diff --git "a/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_13_v1.json" "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_13_v1.json" new file mode 100644--- /dev/null +++ "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_13_v1.json" @@ -0,0 +1,662 @@ +[ + { + "index": 0, + "label": "low_health_literacy", + "original_doc": "This is about a 20-year-old woman. She had a kidney problem since age eight that made protein leak into her urine. The problem first showed up when a big blood clot blocked veins in her brain, and a clot also went to her lungs. She took blood thinners and steroid pills. Later she took a medicine that calms the immune system to help her use fewer steroids. Tests showed no inherited blood-clotting problem. She had several flare-ups of the kidney problem. Steroid pills controlled them until 2017. After that she had no relapses. Her doctors stopped the blood thinner and the immune-calming medicine. One year later she had sudden, very bad belly pain all over. She threw up after eating. Both legs were swollen. Tests showed the kidney problem was back. A special X-ray picture (CT scan) showed a new clot in the main artery that feeds the small intestine. It was like a plug in a pipe that stops water. Blood could not reach the intestines. In surgery, most of her small intestine was dead. Taking out that much bowel would not allow life. She died 48 hours later.", + "wiki_anchor": "Death\nLiu suffered from a narrowed aortic valve. Her husband told the media that she had learnt about her condition purely by chance. Liu had taken her four-year-old daughter to see a doctor for a cold, but the young girl refused to let the doctor place a stethoscope on her chest. The doctor then demonstrated the stethoscope's use to the child by placing the device on Liu's chest. The doctor realised then that Liu had a heart murmur, and advised her to seek further treatment. Liu could have opted for an aortic valve replacement, but it would have required long-term medication after the surgery to prevent blood clots. The medication may also derail her plans to have a second child. On 7 February 2020, while undergoing a heart valve repair surgery at Taipei Veterans General Hospital, Liu had an unexpected sudden cardiac arrest and fell into a coma. Liu was then admitted to the intensive care unit and had been put on extracorporeal membrane oxygenation since then. Despite subsequent operations to deal with a developing cerebral embolism and increased brain pressure, Liu died on 22 March 2020 at the age of 44 after her body had stopped responding to medication and treatment.", + "doc_fkgl": 4.138157894736846, + "wiki_fkgl": 10.80582178217822, + "doc_tree_depth": 4.5, + "wiki_tree_depth": 5.7, + "fkgl_delta": -6.667663887441375 + }, + { + "index": 0, + "label": "intermediate_health_literacy", + "original_doc": "A 20\u2011year\u2011old woman had a 12\u2011year history of idiopathic nephrotic syndrome that initially presented with extensive cerebral venous thrombosis and pulmonary embolism. She was treated with anticoagulation and oral corticosteroids, then mycophenolate mofetil as a steroid\u2011sparing agent. A comprehensive thrombophilia work\u2011up was negative. She experienced multiple relapses controlled with steroids until 2017, then remained in remission; anticoagulation and MMF were discontinued. One year later, she developed sudden diffuse abdominal pain with postprandial vomiting and bilateral leg edema. Laboratory tests confirmed a relapse of nephrotic syndrome. Abdominal CT showed acute superior mesenteric artery thrombosis causing acute mesenteric ischemia. At surgery, there was extensive small\u2011bowel necrosis not compatible with survival. She died 48 hours later.", + "wiki_anchor": "In the US corticotropin is used to treat epileptic spasms in infants, acute exacerbations of multiple sclerosis in adults; acute episodes of psoriatic arthritis and rheumatoid arthritis and ankylosing spondylitis; in acute exacerbations or as maintenance therapy for collagen disorders like systemic lupus erythematosus and systemic dermatomyositis; for skin conditions like severe erythema multiforme and Stevens\u2013Johnson syndrome; for serum sickness; for severe acute and chronic allergic and inflammatory processes involving the eye such as keratitis, iritis and iridocyclitis, diffuse posterior uveitis, choroiditis, optic neuritis, chorioretinitis, and anterior segment inflammation; sarcoidosis in the lungs; and to treat edema in certain nephrotic syndromes.", + "doc_fkgl": 15.20401179941003, + "wiki_fkgl": 48.801980198019805, + "doc_tree_depth": 4.888888888888889, + "wiki_tree_depth": 12.0, + "fkgl_delta": -33.59796839860978 + }, + { + "index": 0, + "label": "proficient_health_literacy", + "original_doc": "A 20\u2011year\u2011old woman had been followed since age eight for idiopathic nephrotic syndrome (NS) inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism, without sequelae and without personal or family thrombotic history. Kidney biopsy was deferred because there was no kidney failure, gross hematuria, hypertension, or extra\u2011renal signs suggestive of secondary NS at presentation. She was treated with an oral vitamin K antagonist and oral corticosteroids with good evolution. Subsequently, she had multiple steroid\u2011dependent relapses and was started on mycophenolate mofetil (MMF) as background therapy to spare corticosteroids and ensure normal growth. An exhaustive thrombophilia assessment was negative: homocysteine, fibrinogen, protein C, protein S, antithrombin III, factor V Leiden, JAK\u20112, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant, and anti\u2011\u03b22\u2011glycoprotein I antibodies were all normal. Anticoagulation was stopped after nine years. Several relapses occurred but were controlled with oral corticosteroids. NS remission was documented from 2017; MMF was gradually discontinued in 2019, and she remained asymptomatic without relapse.\n\nOne year later, she presented to the emergency department with acute intense diffuse abdominal pain without irradiation, associated with postprandial vomiting and bilateral lower\u2011limb edema for six hours. Examination showed intense epigastric tenderness with normal vital signs (BP 120/70 mm Hg, HR 83 bpm, SpO2 100% on room air) and no fever or neurological impairment. Urinalysis detected proteinuria. Hemogasanalysis showed metabolic acidosis with respiratory compensation. Labs revealed hypoalbuminemia, hypercholesterolemia, prothrombin time 90%, elevated D\u2011dimer, LDH, and creatine phosphokinase, with inflammatory markers (CRP 37 mg/L) and leukocytosis (26.4 \u00d7 10^3/\u00b5L); renal and liver function were normal. Urgent abdominal ultrasound showed a low\u2011to\u2011moderate intra\u2011abdominal effusion. Contrast\u2011enhanced CT demonstrated acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. She underwent emergency laparotomy: intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost the entire small bowel, rendering resection incompatible with life. She died 48 hours later.\n\nThis case illustrates catastrophic arterial thrombosis in the setting of NS despite a negative thrombophilia work\u2011up. NS is a hypercoagulable state with multifactorial mechanisms, including urinary loss of anticoagulant proteins (e.g., antithrombin III, protein S), increased fibrinogen, hemoconcentration, dyslipidemia, and systemic inflammation. While venous thromboembolism is more common in NS, superior mesenteric artery thrombosis is rare but often fatal, underscoring the need for high clinical suspicion and rapid imaging when severe acute abdominal pain occurs in patients with active or relapsing NS.", + "wiki_anchor": "Some hematological malignancies exhibit increased numbers of circulating blood eosinophils, increased numbers of bone marrow eosinophils, and/or eosinophil infiltrations into otherwise normal tissues. These malignancies were at first diagnosed as eosinophilia, hypereosinophilia, acute eosinophilic leukemia, chronic eosinophilic leukemia, other myeloid leukemias, myeloproliferative neoplasm, myeloid sarcoma, lymphoid leukemia, or non-Hodgkin lymphomas. Based on their association with eosinophils, unique genetic mutations, and known or potential sensitivity to tyrosine kinase inhibitors or other specific drug therapies, they are now in the process of being classified together under the term clonal hypereosinophilia or clonal eosinophilia. Historically, patients suffering the cited eosinophil-related syndromes were evaluated for causes of their eosinophilia such as those due to allergic disease, parasite or fungal infection, autoimmune disorders, and various well-known hematological malignancies (e.g. Chronic myelogenous leukemia, systemic mastocytosis, etc.) (see causes of eosinophilia). Absent these causes, patients were diagnosed in the World Health Organization's classification as having either 1) Chronic eosinophilic leukemia, not otherwise specified, (CEL-NOS) if blood or bone marrow blast cells exceeded 2% or 5% of total nucleated cells, respectively, and other criteria were met or 2) idiopathic hypereosinophilic syndrome (HES) if there was evidence of eosinophil-induced tissue damage but no criteria indicating chronic eosinophilic leukemia. Discovery of genetic mutations underlining these eosinophilia syndromes lead to their removal from CEL-NOS or HES categories and classification as myeloid and lymphoid neoplasms associated with eosinophilia and abnormalities of PDGFRA, PDGFRB, FGFR1, and, tentatively, PCMA-JAK2. Informally, these diseases are also termed clonal hypereosinophilias. New genetic mutations associated with, and possibly contributing to the development of, eosinophilia have been discovered, deemed to be causes of clonal eosinophilia, and, in certain cases, recommended for inclusion in the category of myeloid and lymphoid neoplasms associated with eosinophilia and abnormalities of PDGFRA, PDGFRB, FGFR1, and, tentatively, PCMA-JAK2. Many of the genetic causes for clonal eosinophilia are rare but nonetheless merit attention because of their known or potential sensitivity to therapeutic interventions that differ dramatically form the often toxic chemotherapy used to treat more common hematological malignancies.", + "doc_fkgl": 17.108284910965327, + "wiki_fkgl": 20.705005476451266, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 8.818181818181818, + "fkgl_delta": -3.5967205654859384 + }, + { + "index": 1, + "label": "low_health_literacy", + "original_doc": "She is 34 years old and pregnant. She had a seizure and trouble speaking clearly. She was sent right away for a head MRI scan. The scan showed a pattern doctors call the \u201cMedusa head.\u201d This means the veins in her brain are arranged in an unusual way that she was born with. There is a small blood clot at the outer part of this vein pattern. The blood is also moving slowly closer to the main vein.", + "wiki_anchor": "The Aga Khan Maternal and Child Care Centre, Hyderabad\n Liaquat University Hospital, Hyderabad/Jamshoro\nNIMRA Cancer Hospital\nNational Institute of Cardiovascular Diseases (NICVD) \n Sir Cowasjee Jehangir Institute of Psychiatry\n St. Elizabeth's Hospital\nSindh Institute of Ophthalmology & Visual Sciences (SIOVS), Hyderabad\nGovernment Skin Hospital\nIsra University Hospital\n Wapda Hospital\n Boulevard Hospital\nG.G Jaghrani Hospital, Hirabad, Hyderabad\nLady Diferal American hospital\nMaa Jee Hospital \nJeejal Maa Hospital\nSindh Government Hospital\nBone Care Center\nAfzal Junejo Hospital", + "doc_fkgl": 3.5813553113553134, + "wiki_fkgl": 22.187671232876713, + "doc_tree_depth": 5.142857142857143, + "wiki_tree_depth": 8.0, + "fkgl_delta": -18.6063159215214 + }, + { + "index": 1, + "label": "intermediate_health_literacy", + "original_doc": "A 34-year-old woman who is 8 weeks pregnant had a first-time generalized seizure with temporary slurred speech. Because she is pregnant and this was her first seizure, doctors obtained an urgent brain MRI. The MRI showed the classic \u201cMedusa head\u201d sign, which indicates a developmental venous anomaly (DVA)\u2014a vein pattern you are born with. Imaging also suggested a partial clot along the peripheral portion of the draining system and slower blood flow closer to the main draining vein. These findings support the diagnosis: a developmental venous anomaly with peripheral partial thrombosis and proximal slow flow.", + "wiki_anchor": "Infantile hemangiomas are the most common benign tumor found in children. They are made up of blood vessels, often called strawberry marks, and are more common in girls than in boys. Babies that are born early are more likely to have a hemangioma. They usually appear on the skin of infants in the days or weeks after birth. They tend to grow quickly for up to a year. Most then shrink or involute without further problem, however some can ulcerate and form scabs which can be painful. Depending on their location and size, they may also be disfiguring.", + "doc_fkgl": 11.942105263157895, + "wiki_fkgl": 6.847551020408165, + "doc_tree_depth": 6.4, + "wiki_tree_depth": 5.714285714285714, + "fkgl_delta": 5.09455424274973 + }, + { + "index": 1, + "label": "proficient_health_literacy", + "original_doc": "A 34-year-old woman, 8 weeks pregnant and without other relevant history, presented with generalized convulsions and postictal dysarthria that resolved within two hours. On examination she was alert, oriented, and without focal language, motor, or sensory deficits; a right lateral tongue bite was noted. Laboratory tests and ECG were unremarkable. Given a first epileptic seizure in pregnancy, an urgent cranial MRI was performed. The protocol included 3D T1 pre- and post-contrast (axial, coronal, sagittal), axial FLAIR, axial T2, VEN BOLD and magnetic susceptibility sequences, as well as axial diffusion and ADC mapping. MRI demonstrated multiple venous cortico-medullary vascular structures converging centripetally to a large central draining vein that emptied via the inferior anastomotic vein into the left transverse sinus, forming the classic \u201cMedusa head\u201d sign. On T1 post-contrast, the drainage vein showed increased signal with central hyphocaptation, suggesting partial thrombosis versus slow flow. On T2 and FLAIR, the parenchyma surrounding the drainage vein was hyperintense, without diffusion restriction, compatible with edema. Overall, the findings are diagnostic of a developmental venous anomaly with signs of partial peripheral thrombosis and more proximal slow flow, causing perilesional edema. Management was initiated with clexane 60 mg every 12 hours and levetiracetam 500 mg every 12 hours, with symptomatic improvement and stability after one week. Contextually, DVAs are typically benign venous variants; however, pregnancy-associated hypercoagulability may predispose to thrombosis. Partial thrombosis and impaired outflow in a DVA can lead to venous congestion and edema, manifesting clinically with seizures.", + "wiki_anchor": "In occipital epilepsy, the hallmark symptoms include both visual and oculomotor. Symptoms may happen spontaneously, or be due to a lesion or injured area of the occipital lobe. For visual symptoms, these may include simple to complex hallucinations, blindness, visions, and palinopsia (seeing a visual stimulus after it has been removed from the visual field). These are usually brief, but can be experienced from 1\u20133 minutes. Oculomotor symptoms include tonic deviation of the eyes, nystagmus (rapid, involuntary movement of the eyes) and repetitive fluttering or closing of the eyelids. In children, they may also have nausea and vomiting during the episode as well. Episodes in total for children usually last less than 10 minutes, and mainly occur at night. Triggers can include turning off lights, and going between dark to light or light to dark areas. It is not uncommon to experience postictal headache, extremely similar to migraines after these seizures. Occipital epilepsy can cause many seizures per day and often in multiple clusters. The seizures may also spread to other areas in the brain.", + "doc_fkgl": 16.247417695473253, + "wiki_fkgl": 11.719688311688312, + "doc_tree_depth": 6.083333333333333, + "wiki_tree_depth": 5.909090909090909, + "fkgl_delta": 4.527729383784941 + }, + { + "index": 2, + "label": "low_health_literacy", + "original_doc": "A 22-year-old woman had painful mouth sores. The sores made eating and drinking hard. The problem started after a fever. Small pimples showed up on her lips. She had been vaping for about one year. The checkup found no spots on the rest of her body. Her lips had crusts with a little blood. The corners of her mouth were raw and bled easily. Inside her mouth there were white sores with yellow edges. The sores were different shapes and sizes and were in several places. A test for the cold-sore virus was negative. The doctor said this was a mouth reaction called oral erythema multiforme. She was treated with salt-water compresses on the lips. She used a mouth rinse with an anti-swelling medicine (dexamethasone) mixed with a coating gel (hyaluronic acid). She put 2% miconazole cream on the sores at the mouth corners. She used petroleum jelly on her dry lips. She was told to stop vaping. Her mouth got better after one week of treatment.", + "wiki_anchor": "Diagnosis\nThe diagnosis is aided by obtaining a history of the circumstances surrounding the bite. The time the bite was experienced, the location of the bite, and examination of the bite is noted. The person may have drainage from the site of the bite. They may also be febrile, and swelling around the wound may occur. Because the wound from the bite may heal too quickly over the punctures, it may need to be opened and explored. Hydrogen peroxide may be used at home to reopen the wound, with pressure being applied around the wound to drain any abscesses. For deep wounds, this process may need to be repeated. At a hospital, you may request that the site be anesthetized prior to exploration. Neurovascular status is assessed. Immune status may determine treatment as does the presence of transplanted tissue or organs, rheumatic disease, diabetes, HIV/AIDS and sickle cell disease. Swollen lymph nodes and red streaks radiating upward may be evident.", + "doc_fkgl": 4.63312375249501, + "wiki_fkgl": 8.667727272727273, + "doc_tree_depth": 5.277777777777778, + "wiki_tree_depth": 6.0, + "fkgl_delta": -4.034603520232263 + }, + { + "index": 2, + "label": "intermediate_health_literacy", + "original_doc": "A 22-year-old woman presented with a month of painful stomatitis that made eating and drinking difficult. The illness began with a fever and pimple-like lesions on the lips. She had been vaping regularly for about one year. Examination showed no skin lesions elsewhere. The lips had serosanguineous crusts and erosions at the labial commissures that tended to bleed. Intraorally, there were multiple irregular white ulcers with yellowish borders on several sites of the oral mucosa. Anti\u2013HSV-1 IgG was non-reactive. The diagnosis was oral erythema multiforme, likely related to vaping. Management included normal saline compresses to the lips, a dexamethasone mouth rinse mixed with hyaluronic acid, 2% miconazole cream applied to the lip corner, petroleum jelly for dry lips, and stopping vaping. Her oral condition improved within one week.", + "wiki_anchor": "Classification \nLip licker's dermatitis which is a subtype of irritant contact cheilitis is caused by an exogenous factor rather than an endogenous one. Irritant contact cheilitis can be separated into different reaction types, so it is an umbrella term and further evaluations are usually needed to properly classify the presenting condition. Cheilitis can have many causes and subtypes, so creating a standard classification and diagnostic procedure is difficult. Since this disease is so broad, it is also best practice to have a multidisciplinary approach to it to rule out the possibility of other diseases that may present as irritant contact cheilitis. The results are usually reproducible but sometimes lack clinical manifestation.", + "doc_fkgl": 10.328562500000004, + "wiki_fkgl": 15.60493693693694, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 7.0, + "fkgl_delta": -5.276374436936937 + }, + { + "index": 2, + "label": "proficient_health_literacy", + "original_doc": "A 22-year-old woman presented to Oral Medicine with a 1-month history of painful oral ulcers causing difficulty eating and drinking. The episode began with fever followed by pimple-like lesions on the lips. She had used pod-type vapes for approximately one year, often trying different e-liquid flavors; she had never smoked conventional cigarettes. She reported no medication exposure prior to onset (no antibiotics, analgesics, anticonvulsants, NSAIDs, or antifungals), no drug or food allergies, and unhealthy eating habits. Extraorally, there were no lesions elsewhere on the body. The lips exhibited serosanguineous crusts with an erosive area at the right labial commissure that tended to bleed. Intraoral examination showed multiple painful white ulcers with yellowish edges, irregular and variable in size, on the labial and buccal mucosa, lateral and ventral tongue, and floor of mouth. Anti-HSV-1 IgG was non-reactive. Based on isolated oral mucosal involvement, absence of cutaneous lesions, and negative HSV serology, a diagnosis of vaping-related oral erythema multiforme, minor type, was established. Management comprised 0.9% NaCl\u2013moistened gauze compresses to the lips three times daily; a dexamethasone mouthrinse (1 mg in 10 mL hyaluronic acid) three times daily with a 30-minute post-rinse fasting period; 2% miconazole cream applied to the wound at the right labial commissure twice daily; and vaseline album (petrolatum) for dry lips. Adjunctive advice included brushing teeth and tongue twice daily (after breakfast and before bed), cessation of vaping, and avoidance of foods containing monosodium glutamate. At 1-week follow-up, the oral condition had improved. Ethical considerations: written informed consent was obtained; the case conformed to the Helsinki Declaration and had institutional approval. Context: Erythema multiforme is a mucocutaneous hypersensitivity reaction classically triggered by infections (e.g., HSV) or drugs; in this case, vaping exposure and frequent e-liquid flavor changes were considered plausible triggers in the absence of medication exposure and with non-reactive anti-HSV-1 serology.", + "wiki_anchor": "Stevens\u2013Johnson syndrome, toxic epidermal necrolysis, and Stevens\u2013Johnson syndrome/Toxic epidermal necrolysis overlap syndrome are a spectrum of Type IV, Subtype IVc, delayed hypersensitivity reactions, i.e. reactions initiated by CD8+ T cells and natural killer T cells. They are characterized initially by fever and flu-like symptoms followed within days by skin as well as mucous membrane blisters and denudation. Differentiation of the three disorders is based on the extent of disease with SJS involving <10%, SGS/TEN involving 10% to 30%, and TEN involving >30% of the total bodily skin area. This spectrum of disorders is complicated by inflammation in and damage to internal organs such as the liver and, less commonly, kidney and heart. More importantly, they are also complicated by sepsis due to the loss of skin and mucous membrane epithelial barriers. In one study, SJS, TEN, and SJS/TEN mortality rates were 4.8%, 19.4%, and 14.8%, respectively, with an important portion of the deaths due to bacterial sepsis, particularly in the acute, early stage of these disorders. The drugs most commonly triggering the SJS, TEN, and SJS/TEN spectrum of disorders are anti-infective sulfonamides, anticonvulsants (e.g. carbamazepine and lamotrigine), non-steroidal anti-inflammatory drugs, allopurinol, nevirapine, and chlormezanone. Allopurinol appears in some studies to be the most common instigator of these disorders. Any new biological or herbal remedy, it is suggested, should be considered a possible cause of these disorders under the proper clinical circumstances.", + "doc_fkgl": 14.527236842105264, + "wiki_fkgl": 13.458614718614719, + "doc_tree_depth": 7.214285714285714, + "wiki_tree_depth": 7.555555555555555, + "fkgl_delta": 1.0686221234905453 + }, + { + "index": 3, + "label": "low_health_literacy", + "original_doc": "At 32 weeks of pregnancy, a routine scan found one small lump inside the baby\u2019s heart. It caused no symptoms. This was the only problem seen. Doctors watched it with clinic visits until 39 weeks plus 1 day. Then the baby was delivered by C-section (a surgery to deliver the baby). After birth, the child had checkups on day 1, day 7, day 30, month 7, and month 12. At each visit, the child\u2019s growth and behavior were healthy for age. The heart lump stayed the same size; it did not grow or shrink. By 1 year old, there were no signs of a related condition called tuberous sclerosis complex.", + "wiki_anchor": "Infantile hemangiomas are the most common benign tumor found in children. They are made up of blood vessels, often called strawberry marks, and are more common in girls than in boys. Babies that are born early are more likely to have a hemangioma. They usually appear on the skin of infants in the days or weeks after birth. They tend to grow quickly for up to a year. Most then shrink or involute without further problem, however some can ulcerate and form scabs which can be painful. Depending on their location and size, they may also be disfiguring.", + "doc_fkgl": 4.623939393939395, + "wiki_fkgl": 6.847551020408165, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 5.714285714285714, + "fkgl_delta": -2.22361162646877 + }, + { + "index": 3, + "label": "intermediate_health_literacy", + "original_doc": "This case describes an isolated, asymptomatic fetal cardiac rhabdomyoma first detected at 32 weeks\u2019 gestation. The pregnancy was monitored as an outpatient until 39 weeks plus one day, when delivery occurred by cesarean section. Postnatal follow-up at day 1, day 7, day 30, 7 months, and 12 months showed normal growth and neurodevelopment. The intracardiac mass remained stable in size across all visits. Up to one year of age, the child did not meet any clinical diagnostic criteria for tuberous sclerosis complex (TSC).", + "wiki_anchor": "Infantile hemangiomas are the most common benign tumor found in children. They are made up of blood vessels, often called strawberry marks, and are more common in girls than in boys. Babies that are born early are more likely to have a hemangioma. They usually appear on the skin of infants in the days or weeks after birth. They tend to grow quickly for up to a year. Most then shrink or involute without further problem, however some can ulcerate and form scabs which can be painful. Depending on their location and size, they may also be disfiguring.", + "doc_fkgl": 11.214120481927715, + "wiki_fkgl": 6.847551020408165, + "doc_tree_depth": 5.4, + "wiki_tree_depth": 5.714285714285714, + "fkgl_delta": 4.36656946151955 + }, + { + "index": 3, + "label": "proficient_health_literacy", + "original_doc": "A 29-year-old gravida V para IV (3 spontaneous vaginal deliveries, prior cesarean for failed induction 4 years earlier) presented for ANC at 32 weeks by LNMP. Maternal labs: VDRL, HBsAg, and urinalysis negative; CBC within normal limits; blood group A Rh-positive. Obstetric ultrasound revealed normal fetal anatomy except the heart. Fetal echocardiography showed normal situs; atria of comparable size; normally positioned atrioventricular and semilunar valves with normal motion; ventricles comparable in size and contractility; left ventricle forming the apex; no ventricular septal defect. Two circumscribed, round, echogenic masses were noted on the left ventricular papillary muscles, measuring 18.2 \u00d7 8.3 mm and 13.5 \u00d7 8.3 mm. LVOT and RVOT anatomy and function were normal on 2D and color flow. Impression: cardiac rhabdomyoma. Given the association with tuberous sclerosis complex (TSC), detailed neurosonography and systemic evaluation were performed and were unremarkable. She continued routine ANC without complications to 39 weeks. At 39 weeks + 1 day, a cesarean section (repeat on request at term) delivered a 3200 g female, Apgar 10 and 10 at 1 and 5 minutes. Postoperative courses for mother and neonate were uneventful; discharge occurred on postoperative day 3. The neonate was evaluated on days 1, 7, and 30: physical examinations were normal; no seizure activity or new cutaneous lesions; mass dimensions were similar to the antenatal findings. At 7 months, development was age-appropriate; pediatric echocardiography showed well-circumscribed hyperechoic masses on both left ventricular papillary muscles measuring 21.8 \u00d7 9.2 mm and 14.7 \u00d7 8.5 mm, without left ventricular inflow obstruction. At 12 months, anthropometric and neurobehavioral development remained normal. Echocardiography again demonstrated well-circumscribed hyperechoic masses on both left ventricular papillary muscles with no size increment and no left ventricular inflow obstruction. Up to one year of age, apart from the persistent intracardiac rhabdomyomas, the child met none of the clinical diagnostic criteria for TSC. Notably, while cardiac rhabdomyomas often regress spontaneously in infancy, these lesions were stable through 12 months.", + "wiki_anchor": "History of pediatric critical care \nPediatric intensive care has been established as a sub-specialty of medicine over the past two decades. It grew out of a need for increasingly complex pediatric care, long-term management of disease, and advancements in medical and surgical sub-specialties, as well as, life-sustaining therapies. The development of pediatric critical care followed the establishment of pediatric intensive care units or PICUs. The first PICU was opened in Europe by Goran Haglund in 1955 at Children's Hospital of Goteburg in Sweden. Advancements in Neonatology and neonatal intensive care, pediatric general surgery, pediatric cardiac surgery, pediatric anesthesiology lead to its opening because of the need to care for critically ill infants and children. Over the next forty years, hundreds of PICUs were established in academic institutions, children's hospitals, and community hospitals. In 1981, the Society of Critical Care Medicine, SCCM, which express guidelines and standards for adult critical care, recognized pediatric critical care as unique from adults and created a separate section within the SSCM for their care. Other institutes followed throughout the 80's, by 1990 there were multiple training programs, certification available, and sub-board on pediatric critical care. Pediatric critical care is now seen as a multidisciplinary field that includes a team of nurse specialists, respiratory therapists, nutritionists, pharmacists, social workers, physical therapists, occupational therapist, and other medical professionals.", + "doc_fkgl": 13.580182389937107, + "wiki_fkgl": 17.960422322775262, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 7.0, + "fkgl_delta": -4.380239932838155 + }, + { + "index": 4, + "label": "low_health_literacy", + "original_doc": "This is about a 13-year-old boy. He has had small growths in his throat since he was two years old. The growths were in his voice box and windpipe. They narrowed his breathing tube, so he had trouble breathing. It was like trying to breathe through a pinched straw. A chest scan showed several small cysts in his lungs. Doctors removed the throat growths. They also placed a breathing tube through a small hole in his neck to help him breathe. He got one dose of a medicine called bevacizumab (400 mg) through a vein. He also had breathing therapy. He got better. The problem has not come back during follow-up.", + "wiki_anchor": "Signs and symptoms\nImmediate manifestations of caustic substance ingestions include erosions of mucosal surfaces of the gastrointestinal tract or airway (which can cause bleeding if the erosions extend to a blood vessel), mouth and tongue swelling, drooling or hypersalivation, nausea, vomiting, dyspnea, dysphonia/aphonia irritation of the eyes and skin. Perforation of the esophagus can lead to mediastinitis or perforation of the stomach or bowel can lead to peritonitis Swelling of the airway or laryngospasm can occur leading to compromised breathing. Injuries affecting the respiratory system include aspiration pneumonia and laryngeal sores. Signs of respiratory compromise include stridor and a change in a person's voice.", + "doc_fkgl": 2.581463963963966, + "wiki_fkgl": 17.69615384615385, + "doc_tree_depth": 4.583333333333333, + "wiki_tree_depth": 7.75, + "fkgl_delta": -15.114689882189886 + }, + { + "index": 4, + "label": "intermediate_health_literacy", + "original_doc": "A 13-year-old boy with recurrent respiratory papillomatosis since age two presented with breathing difficulty, noisy breathing (stridor), and hoarseness. Airway evaluation showed multiple nodules narrowing the larynx and trachea. Chest CT revealed several pulmonary cysts. He underwent surgical removal of the papillomatosis lesions and a tracheostomy. He received a single 400 mg intravenous dose of bevacizumab and respiratory therapy. He recovered well, and there has been no recurrence on follow-up.", + "wiki_anchor": "A bronchial leiomyoma is a relatively rare form of lung tumours. These tumours can form in the lower respiratory tract tissue of the bronchi, trachea and other lung tissue. They may also be derived from blood vessels. These tumors typically form from the smooth muscle tissue lining the bronchi. They grow as a solitary tumor attaching themselves to the sides of the bronchi.", + "doc_fkgl": 12.728571428571431, + "wiki_fkgl": 7.492253968253973, + "doc_tree_depth": 5.166666666666667, + "wiki_tree_depth": 6.4, + "fkgl_delta": 5.2363174603174585 + }, + { + "index": 4, + "label": "proficient_health_literacy", + "original_doc": "A 13-year-old male from Cusco with recurrent respiratory papillomatosis (RRP) since age two (tracheostomy at age three) and a maternal history of genital papilloma presented after 16 days of predominantly nocturnal respiratory difficulty, inspiratory laryngeal stridor, and moderate dysphonia. He had previously received azithromycin and supplemental oxygen without improvement. On exam, there was mild subcostal retraction, decreased vesicular breath sounds over the left hemithorax, and scant wheezes predominating on the right; he required 4 L/min oxygen via binasal cannula. Laboratory studies showed WBC 8.03 \u00d7 10^3/\u03bcL, platelets 209 \u00d7 10^3/\u03bcL, hemoglobin 13.2 g/dL, and CRP 36.6 mg/L. Imaging included a chest study and head and neck tomography; chest tomography visualized several pulmonary cysts. Forty-eight hours after admission, he developed worsening stridor and respiratory distress, prompting emergent OR transfer for tracheostomy, microlaryngoscopy, and excision of papillomatous lesions. Intraoperative findings demonstrated extensive papillomatous disease with appendicular tumor-like lesions and ventricular bands involving the epiglottis, glottic surface, vocal cords, subglottis, and trachea to ring 5. Histopathology showed koilocytotic atypia consistent with HPV and mild focal dysplasia. Postoperatively, he was managed in the PICU with respiratory monitoring and was weaned off oxygen within 48 hours. He received a single intravenous dose of bevacizumab 400 mg and showed prompt clinical improvement. He completed a seven-day hospitalization with normalization of oxygen saturation and progressive oxygen weaning, then was transferred for ongoing care. He also received respiratory therapy. On telemonitoring at eight months, there was no evidence of recurrence or intercurrent events. Clinical context: RRP is typically HPV-related (often low-risk types) and can cause multifocal papillomas leading to airway stenosis; anti-VEGF therapy such as bevacizumab is used off-label to reduce angiogenesis and disease recurrence, and in this case was associated with a favorable short- to mid-term outcome.", + "wiki_anchor": "Learning and utilizing self-examinations of your body, checking for changes or abnormalities in your mouth while performing your oral hygiene as well as routine checks of your genitals after showering can enhance your awareness of changes in your health status. According to the Centers for Disease Control and Prevention (CDC), most sexually active people are likely to acquire at least one HPV infection in their lifetime. It is important that consumers seek routine dental examinations as a part of their health care to allow screening of this type of cancer, as early detection can mean all the difference in treatments. Oral cavity and oropharyngeal cancers can occur anywhere in the mouth but occur most often in the tongue, tonsils, oropharynx (back of the throat), gums, and the floor of the mouth. According to the U.S. Preventative Services Task Force, \"Oropharyngeal cancer is difficult to visualize and is usually located at the base of the tongue (the back third of the tongue), the soft palate (the back part of the roof of the mouth), the tonsils, and the side and back walls of the throat\" and requires a thorough examination by a dental provider or preferably a specialist. Men are twice as likely as women to have oral cancer, regardless of race, as African-Americans and Caucasians are equally likely to develop oral cancer.", + "doc_fkgl": 15.644583333333337, + "wiki_fkgl": 15.807400257400257, + "doc_tree_depth": 6.769230769230769, + "wiki_tree_depth": 7.833333333333333, + "fkgl_delta": -0.16281692406692017 + }, + { + "index": 5, + "label": "low_health_literacy", + "original_doc": "This 54-year-old man had long-term kidney disease. He took steroids and other medicines that weaken the body\u2019s defenses for a long time. He came to the lung department with fever, cough with mucus, and trouble breathing. A scan showed many cloudy spots in both lungs, like frosted glass. Blood tests showed a lot of inflammation. This suggested an infection from germs such as bacteria, a virus, or a fungus. A blood test was positive for RSV antibodies. Tests for other germs were not positive. His immune system was weak. His antibody level (IgG) was low. His infection-fighting T cells (CD4 and CD8) were also low. Doctors gave strong medicines for infection and support to help his breathing. His illness got worse quickly. He died from breathing failure.", + "wiki_anchor": "From 1936, L\u00f6fgren worked mainly at Saint G\u00f6ran Hospital in Stockholm, where he became senior physician at the pulmonary clinic in 1957. He became interested early on in the mysterious disease morbus Schaumann, now known as sarcoidosis. In his thesis, he showed that erythema nodosum, which had always implied tuberculosis in the past, was also present in sarcoidosis. In what came to be known internationally as Lofgren's syndrome, L\u00f6fgren described how erythema nodosum, enlarged lymph nodes on the root of the lung (called hilar lymphadenopathy) and extinguished tuberculin tests were symptoms of an acute but often transient form of sarcoidosis. He became a rallying name at symposia and congresses and, in 1958, helped found the International Sarcoidosis Committee. L\u00f6fgren was honored in 1971 with a professorship for his scientific contributions.", + "doc_fkgl": 5.415573678290215, + "wiki_fkgl": 13.101538461538464, + "doc_tree_depth": 4.785714285714286, + "wiki_tree_depth": 7.166666666666667, + "fkgl_delta": -7.685964783248249 + }, + { + "index": 5, + "label": "intermediate_health_literacy", + "original_doc": "A 54-year-old man with chronic kidney disease on long-term corticosteroids and immunosuppressants was admitted to respiratory medicine with fever, cough with sputum, and shortness of breath. Chest CT showed multiple bilateral ground-glass opacities. Laboratory studies showed elevated inflammatory markers, indicating possible bacterial, viral, or fungal infection. RSV antibodies were positive, while tests for other pathogens were negative. He was immunocompromised from prolonged corticosteroid and immunosuppressant use, with low total IgG and reduced CD4 and CD8 T-lymphocyte counts. Despite intensive anti-infective therapy and escalating respiratory support, his condition deteriorated rapidly, and he died from respiratory failure.", + "wiki_anchor": "Signs and symptoms\nAlimentary toxic aleukia manifests in inflammation of the gastric and intestinal mucosa, a severe progressive leukopenia, anemia, and an increased erythrocyte sedimentation rate. Subsequently petechial hemorrhages of both the skin and mucosa as well as enlarged lymph nodes are seen. Symptoms of the respiratory system include bronchopneumonia, pulmonary hemorrhages, sepsis, and lung abscesses. Vomiting, bloody stools, lassitude, and incoordination are also observed. The severity of the disease and its course was determined by the quantity of the toxin and the various reactive properties of various tissues and organs to the toxin.", + "doc_fkgl": 16.420789473684213, + "wiki_fkgl": 14.96540425531915, + "doc_tree_depth": 6.166666666666667, + "wiki_tree_depth": 7.2, + "fkgl_delta": 1.4553852183650626 + }, + { + "index": 5, + "label": "proficient_health_literacy", + "original_doc": "A 54-year-old male with membranous nephropathy II and nephrotic syndrome on long-term oral glucocorticoids and immunosuppressants (immunocompromised) presented to the Department of Respiratory Medicine with 5 days of fever, cough, expectoration, and progressive dyspnea. He had a 20 pack-year smoking history and no family history of hereditary disease. A chest x-ray one month prior was normal. On admission (August 8, 2016): BMI 24.5 kg/m2, T 39.0\u00b0C, tachypnea 35 breaths/min, severe hypoxemia (SaO2 86%). Auscultation revealed good bilateral air entry with scattered diffuse crackles and rhonchi. Chest CT demonstrated multiple bilateral ground-glass opacities. Initial labs showed a normal WBC count with elevated neutrophils and increased inflammatory markers (CRP, ESR) and elevated (1\u21923)-\u03b2-D-glucan. Serology was positive for RSV antibodies on hospital day 4; other pathogen testing was negative. He had laboratory evidence of immunosuppression with decreased total IgG and reduced CD4 and CD8 T-lymphocyte counts, consistent with chronic exposure to corticosteroids and immunosuppressants.\n\nManagement: Immediate respiratory monitoring and supplemental oxygen were initiated. Empiric anti-infective therapy included antibiotics (moxifloxacin for 4 days, then cefminoxine for 8 days) and antifungal therapy (voriconazole for 10 days). The glucocorticoid and immunosuppressant doses were largely unchanged. After 10 days, clinical status and oxygenation worsened with radiographic progression. He was transferred to the Emergency ICU for noninvasive mechanical ventilation, broad-spectrum antibiotics (i.v. meropenem, oral moxifloxacin, cotrimoxazole), antifungal therapy (micafungin), systemic corticosteroids (methylprednisolone 40 mg bid i.v.), and supportive care. Ganciclovir was added for possible viral coinfection (e.g., CMV). Five days later, chest x-ray showed further aggravation. Despite escalation to invasive ventilator-assisted ventilation, higher-dose methylprednisolone (80 mg bid), additional antibacterials (cefoperazone-sulbactam, tigecycline, cotrimoxazole), and continued micafungin, he developed rapid progression culminating in respiratory failure and death two days later.\n\nInterpretation: The presentation is consistent with severe viral pneumonia due to RSV in an immunocompromised host, with imaging showing multifocal ground-glass opacities and laboratory evidence of systemic inflammation. Elevated (1\u21923)-\u03b2-D-glucan prompted antifungal coverage, while broad-spectrum antibacterial and antiviral regimens addressed possible coinfections. Profound immunosuppression (low IgG, reduced CD4/CD8 T cells) likely contributed to rapid deterioration and refractory hypoxemic respiratory failure despite intensive anti-infective therapy and advanced respiratory support.", + "wiki_anchor": "Some hematological malignancies exhibit increased numbers of circulating blood eosinophils, increased numbers of bone marrow eosinophils, and/or eosinophil infiltrations into otherwise normal tissues. These malignancies were at first diagnosed as eosinophilia, hypereosinophilia, acute eosinophilic leukemia, chronic eosinophilic leukemia, other myeloid leukemias, myeloproliferative neoplasm, myeloid sarcoma, lymphoid leukemia, or non-Hodgkin lymphomas. Based on their association with eosinophils, unique genetic mutations, and known or potential sensitivity to tyrosine kinase inhibitors or other specific drug therapies, they are now in the process of being classified together under the term clonal hypereosinophilia or clonal eosinophilia. Historically, patients suffering the cited eosinophil-related syndromes were evaluated for causes of their eosinophilia such as those due to allergic disease, parasite or fungal infection, autoimmune disorders, and various well-known hematological malignancies (e.g. Chronic myelogenous leukemia, systemic mastocytosis, etc.) (see causes of eosinophilia). Absent these causes, patients were diagnosed in the World Health Organization's classification as having either 1) Chronic eosinophilic leukemia, not otherwise specified, (CEL-NOS) if blood or bone marrow blast cells exceeded 2% or 5% of total nucleated cells, respectively, and other criteria were met or 2) idiopathic hypereosinophilic syndrome (HES) if there was evidence of eosinophil-induced tissue damage but no criteria indicating chronic eosinophilic leukemia. Discovery of genetic mutations underlining these eosinophilia syndromes lead to their removal from CEL-NOS or HES categories and classification as myeloid and lymphoid neoplasms associated with eosinophilia and abnormalities of PDGFRA, PDGFRB, FGFR1, and, tentatively, PCMA-JAK2. Informally, these diseases are also termed clonal hypereosinophilias. New genetic mutations associated with, and possibly contributing to the development of, eosinophilia have been discovered, deemed to be causes of clonal eosinophilia, and, in certain cases, recommended for inclusion in the category of myeloid and lymphoid neoplasms associated with eosinophilia and abnormalities of PDGFRA, PDGFRB, FGFR1, and, tentatively, PCMA-JAK2. Many of the genetic causes for clonal eosinophilia are rare but nonetheless merit attention because of their known or potential sensitivity to therapeutic interventions that differ dramatically form the often toxic chemotherapy used to treat more common hematological malignancies.", + "doc_fkgl": 16.479367816091955, + "wiki_fkgl": 20.705005476451266, + "doc_tree_depth": 6.15, + "wiki_tree_depth": 8.818181818181818, + "fkgl_delta": -4.225637660359311 + }, + { + "index": 6, + "label": "low_health_literacy", + "original_doc": "A 34-year-old woman had new lower back pain. She saw blood in her urine. She also had a big bruise under the skin on her right buttock. She had never had bleeding problems before. Because these bleeding signs were serious, she was sent to the emergency room. Doctors did blood-clotting tests. One test mixed her blood with normal blood to see how it clotted. Another test looked for a blocker against a clotting protein called factor eight. These tests confirmed the diagnosis.", + "wiki_anchor": "Diagnosis\nA physical examination of the hand may show discoloration (blanching, mottling, and/ or cyanosis; gangrene may be present in advanced cases), unusual tenderness/ a callous over the hypothenar eminence, and fingertip ulcerations and splinter hemorrhages over ulnar digits; if an aneurysm is present, there may also be a pulsatile mass. Allen's test will be positive if an occlusion is present and negative if an aneurysm is present. An angiogram may show a \"corkscrew\" ulnar artery or an occlusion or aneurysm at the hook of the hamate.", + "doc_fkgl": 4.512113821138211, + "wiki_fkgl": 16.0648275862069, + "doc_tree_depth": 4.444444444444445, + "wiki_tree_depth": 7.0, + "fkgl_delta": -11.552713765068688 + }, + { + "index": 6, + "label": "intermediate_health_literacy", + "original_doc": "A 34-year-old woman with no prior bleeding history developed lower back pain, passed a kidney stone, and then had three days of haematuria. She later developed painful thigh and right gluteal bruising after an intramuscular injection. Because the bleeding was extensive, she was transferred to the emergency department. Her coagulation work-up showed a markedly prolonged aPTT. A mixing study only partially corrected the aPTT, and factor VIII activity was very low with a measurable factor VIII inhibitor (8.64 BU/mL), confirming acquired haemophilia A, likely postpartum. She was treated with prednisone and cyclophosphamide, and received bypassing therapy (initially FEIBA, then switched to recombinant factor VIIa due to side effects). Her bleeding improved and she was discharged.", + "wiki_anchor": "Awards and honors \n 1993: Dr. Murray Thelin Award, National Hemophilia Foundation\n 1998: International Association Francaise Des Hemophiles Award, \"Prix Henri Chaigneau\"\n 1999: Investigator Recognition Award, Intl. Soc. Thrombosis & Haemostasis (ISTH)\n 2000: Distinguished Investigator Award-MI Hemophilia Society\n 2003: Van Wezel Prize, European Society of Animal Cell Technology (ESACT)\n 2006: Fellow of the American Association for the Advancement of Science\n 2007-2017: NIH NIDDK MERIT Award\n 2014, 2015: Thomson Reuters World's Most Influential Scientific Minds in Biochemistry & Biology\n 2015: Society for Free Radical Research (SFRR), Clinical Science Award\n 2016: Endowed Chair in Cell Biology. SBP Medical Discovery Institute\n 2019: Clarivate's Web of Science Group of Highly Cited Researchers\n 2021: Clarivate's Web of Science Group of Highly Cited Researchers\n 2022: Research.com \u201cBest Scientist Award\u201d\n 2023: Research.com \u201cBiology and Biochemistry in United States Leader Award\u201d", + "doc_fkgl": 11.051032608695653, + "wiki_fkgl": 17.54923076923077, + "doc_tree_depth": 5.0, + "wiki_tree_depth": 5.142857142857143, + "fkgl_delta": -6.498198160535118 + }, + { + "index": 6, + "label": "proficient_health_literacy", + "original_doc": "A 34-year-old female, 2 months post\u2013cesarean section (37 weeks) with persistent postoperative wound bleeding and no childhood/adolescent bleeding history, presented with a 4-week illness. The clinical course began with lower back pain attributed to bilateral renal lithiasis; after spontaneous passage of a stone she had 3 days of haematuria and was given tranexamic acid q12h. Three weeks later she developed progressive pain and induration of the left distal thigh. Following intramuscular diclofenac for persistent pain, she developed ecchymosis and ongoing bleeding in the gluteal area despite compression. An outside \u201cparticular Doppler ultrasound\u201d reportedly showed deep venous thrombosis (left lower limb), and she was started on enoxaparin 30 mg SC q24h plus morphine and hospitalized. The next day she developed epigastralgia, blurred vision, HR 117 bpm, BP 113/85 mmHg, and SpO2 93%; enoxaparin was discontinued. Hemoglobin fell from 10.4 g/dL (day prior to admission) to 6.4 g/dL, prompting 2 units of packed red cells. With a working diagnosis of vasculitis, methylprednisolone was started and she was referred for further evaluation.\n\nOn admission she had severe pallor, extensive ecchymosis of the left thigh and lateral knee, and a right thigh haematoma. Hemogram: Hb 9.8 g/dL, normocytic, normochromic. Chemistry notable for glucose 160 mg/dL; AST 52 U/L, ALT 86 U/L. Coagulation profile showed isolated prolongation of the activated partial thromboplastin time (aPTT) to 91.2 s; the remainder of hemogram, biochemistry, electrolytes, liver profile, and coagulation parameters were within reference limits. Soft-tissue ultrasound of the right gluteal region revealed a subcutaneous collection (TCSC) with oedema extending to the upper third of the thigh. Repeat Doppler ultrasound of the left lower limb showed normal flow without thrombosis in the common femoral, superficial, or deep venous systems. Blood and urine cultures were negative. ANA, C3, C4, and ferritin were within reference ranges.\n\nGiven suspected acquired haemophilia, a mixing test demonstrated partial correction of the aPTT. Factor VIII activity was <1.0 U/dL, and a factor VIII inhibitor was detected at 8.64 Bethesda units/mL, confirming acquired haemophilia A, likely postpartum in onset. Therapy included prednisone 50 mg PO at breakfast plus 10 mg at lunch, cyclophosphamide 50 mg (2 tablets) PO q24h, and FEIBA for haemostasis. After 5 days, FEIBA was discontinued due to chest tightness, dyspnoea, and nausea (suspected adverse drug reaction) and replaced with activated recombinant factor VII (rFVIIa; NovoSeven). Clinical evolution was favourable, with decreasing ecchymoses and no new symptoms, and she was discharged.\n\nContext: Postpartum acquired haemophilia A is mediated by autoantibodies to factor VIII and typically presents with isolated aPTT prolongation, low FVIII activity, and an inhibitor measured in Bethesda units. Partial correction on mixing supports an inhibitor pattern. First-line immunosuppression (e.g., prednisone with or without cyclophosphamide) and bypassing agents (FEIBA or rFVIIa) are standard to control bleeding while eradicating the inhibitor.", + "wiki_anchor": "No liver disease \nIndividuals with this disorder are usually less symptomatic than patients with other fibrinogen disorders because their fibrinogen levels are generally sufficient to prevent spontaneous bleeding. Those with particularly low blood fibrinogen levels (<0.5 gram/liter) may develop serious bleeding spontaneously and many with the disorder do so following trauma or surgery. Depending on their fibrinogen levels, women with the disorder may also bleed excessively during delivery and the postpartum period; in rare cases, they may have an increased risk of suffering miscarriages. Individuals with the disorder also experience thrombotic events which may include blockage of large arteries in relatively young patients who have high levels of cardiovascular risk factors. The thrombi which form in these individuals are unstable, tend to embolize, and may therefore lead to thromboembolic events such as pulmonary embolism. Both bleeding and thrombotic events can occur at separate times or even concurrently in the same individual with the disorder.", + "doc_fkgl": 11.779287370862324, + "wiki_fkgl": 16.283506493506497, + "doc_tree_depth": 6.208333333333333, + "wiki_tree_depth": 7.0, + "fkgl_delta": -4.504219122644173 + }, + { + "index": 7, + "label": "low_health_literacy", + "original_doc": "This is about a 2-day-old newborn boy. He was born at full term by C-section at a private hospital. He came to the children\u2019s hospital because the right side of his scrotum (the sack that holds the testicles) was swollen since birth. In the emergency room, he looked well. His skin was pink and warm. His blood flow looked good. On exam, the right testicle was big and tight. It was not sore when touched. The skin was red and looked rubbed. A light test did not shine through the right side. The light did shine through the left side. There were no signs of a hernia. An urgent ultrasound scan was done. The scan showed the right testicle was larger and looked uneven inside. No blood was flowing to it. The doctors took him quickly to surgery to look inside the scrotum. In surgery, the right testicle was dead because it had twisted, like a kinked hose that stops flow. There was a small amount of fluid. They removed the right testicle. They fixed the left testicle in place to help prevent twisting.", + "wiki_anchor": "The female is very similar to the male in colouration and shape, but is larger. The carapace is between long and wide and the abdomen between long and wide. The carapace is also pear-shaped and dark brown, and has two white stripes on the thorax. The abdomen has a white stripe in the middle which stretches from the front to back, interrupted by two white marks in the middle and ends. The edges of the abdomen are orange and the lighter parts have an orange shine. The spinnerets are yellow. The epigyne is small with a flat plate and the rear sclerotized, with widely separated copulatory openings. The insemination ducts are short and slightly bent toward each other and the spermathecae are round. The conformation of both the epigyne and the spermathecae are particularly distinguishing for the species. The lack of gonopores in the epigyne particularly distinguishes the species from the otherwise similar Stenaelurillus ignobilis.", + "doc_fkgl": 3.26104347826087, + "wiki_fkgl": 9.106612903225805, + "doc_tree_depth": 4.0, + "wiki_tree_depth": 5.7, + "fkgl_delta": -5.8455694249649355 + }, + { + "index": 7, + "label": "intermediate_health_literacy", + "original_doc": "A full\u2011term male newborn, 2 days old and delivered by cesarean section, presented with a congenital right scrotal swelling. On arrival he appeared well perfused and stable. Examination showed the right testis was enlarged, tense, non\u2011tender, and visibly reddish with excoriated overlying skin. Transillumination was negative on the right and positive on the left; both hernia openings were normal. Doppler ultrasound showed the right testis was enlarged with a heterogeneous, darker appearance and no detectable blood flow; the left testis looked normal, with only a small amount of fluid. He was taken urgently to surgery. Intra\u2011operatively, the right testis was frankly nonviable due to intravaginal torsion, with minimal hydrocele. Surgeons removed the right testis (orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to reduce the risk of future twisting.", + "wiki_anchor": "Clinical considerations \nOther structures can be present on the vaginal wall though most of the time these can be differentiated from rugae. Vaginal cysts can be small protrusions into the vagina that can be felt or palpated by a clinician. Vaginal inclusion cysts can appear as small bumps and can develop after childbirth. Other small structures or protrusions can be Gartner duct cysts, patches of endometrial tissue, and benign tumors. These cystic structures can obliterate the rugae and is a clue to their presence. The absence of vaginal rugae seen in the normal vagina of a healthy woman may be an indication of a prolapsed bladder (cystocele) or rectocele. An enterocele, or bulging of the bowel into the vagina can also cause vaginal rugae to disappear. The absence of vaginal rugae may also be an indicator of pelvic organ prolapse. Vaginal rugae disappear in those with an estrogen deficiency.", + "doc_fkgl": 11.784036259541985, + "wiki_fkgl": 11.378076062639824, + "doc_tree_depth": 5.375, + "wiki_tree_depth": 6.444444444444445, + "fkgl_delta": 0.4059601969021607 + }, + { + "index": 7, + "label": "proficient_health_literacy", + "original_doc": "A 2\u2011day\u2011old term male neonate, delivered by cesarean section at a private hospital, was referred for a congenital right scrotal swelling and presented to our children\u2019s hospital one day later. On ED arrival he was well hydrated, pink on room air with good perfusion. Physical exam: right hemiscrotum with an enlarged, tense, non\u2011tender, visibly reddish testis and overlying skin excoriation; transillumination negative on the right and positive contralaterally; both hernial orifices normal. Laboratory studies were obtained, and urgent inguinoscrotal Doppler ultrasonography demonstrated an enlarged right testis measuring 15.6 \u00d7 9.4 mm with heterogeneous hypoechoic echotexture, prominent rete testis, and absent intratesticular color Doppler flow. The left testis was normal in size, shape, and echotexture; there was minimal hydrocele. The patient underwent urgent scrotal exploration. Intra\u2011operatively there was frank necrosis of the right testis secondary to intravaginal testicular torsion, with minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed. Contextually, perinatal testicular torsion often presents at or shortly after birth and Doppler evidence of absent flow with heterogeneous hypoechoic parenchyma correlates with nonviability; salvage rates are low when presentation is delayed. Contralateral orchidopexy is commonly performed to mitigate future torsion risk.", + "wiki_anchor": "Technique and findings\nUnlike arterial ultrasonography, venous ultrasonography is carried out with the probe in a transversal position, (perpendicular to the vein axis), displaying cross-sections of the veins. All collateral veins are better detected this way, including perforator veins, but of most importance is the detection of venous thrombosis. The most reliable sign of thrombosis (even when a good image and color is present) is the absence of compressibility - A vein cannot be compressed when the blood is in a solid state, as with a thrombus, in the same way that a rubber pipe cannot be compressed if the water inside is frozen. However, if the probe is parallel to the vein axis, when the examiner compresses it, the probe can slide to the right or to the left giving a false negative for thrombosis as the probe has moved away and the vein will not then be evident. Nevertheless, when the examiner needs to show the head thrombus in a printout, the probe will be presented parallel to the vein axis.", + "doc_fkgl": 15.11899521531101, + "wiki_fkgl": 16.623674418604654, + "doc_tree_depth": 6.5, + "wiki_tree_depth": 6.8, + "fkgl_delta": -1.5046792032936445 + }, + { + "index": 8, + "label": "low_health_literacy", + "original_doc": "A 4-year-old boy had blood in his pee and swelling for 5 days. He then had headaches, nausea, and vomiting. He came to the hospital with seizures and very high blood pressure. Blood tests showed a low level of a protein called C3 and signs of a recent strep infection. This meant his kidney filters were inflamed after strep. His brain was affected by the very high blood pressure. Doctors suspected a problem called PRES, which is brain swelling from high pressure. A brain MRI confirmed this. His immune system also attacked his red blood cells. This made his blood level drop very low, to 5 g/dL. He was treated with medicines to lower his blood pressure, steps to protect his brain, and steroid medicines. He left the hospital after 31 days. Six months later, he had no symptoms.", + "wiki_anchor": "At 7:00\u00a0a.m. on 2 March, Beria and a group of medical experts were summoned to examine Stalin. Based on their examination, which revealed blood pressure of 190/110 and right-sided hemiplegia, they concluded that Stalin, who had a known history of uncontrolled hypertension, had sustained a hemorrhagic stroke involving the left middle cerebral artery. Over the next two days he received a variety of treatments. In an attempt to decrease his blood pressure, which had risen to 210/120, two separate applications of eight leeches each were applied to his neck and face over the next two days. However, Stalin's condition continued to deteriorate and he died at 9:50\u00a0p.m. on 5 March 1953.", + "doc_fkgl": 4.794388489208632, + "wiki_fkgl": 10.024298356510748, + "doc_tree_depth": 4.923076923076923, + "wiki_tree_depth": 7.2, + "fkgl_delta": -5.229909867302116 + }, + { + "index": 8, + "label": "intermediate_health_literacy", + "original_doc": "A 4-year-old boy presented after 5 days of visible blood in the urine and leg swelling, plus new headaches, nausea, and vomiting. He developed seizures with a hypertensive emergency. Labs showed low complement C3 and a high anti-streptolysin O (ASO) titer, consistent with acute post-streptococcal glomerulonephritis. He developed encephalopathy, and MRI confirmed posterior reversible encephalopathy syndrome (PRES) secondary to the hypertensive crisis. He also developed autoimmune hemolytic anemia, with hemoglobin falling to 5 g/dL. Treatment included antihypertensive therapy, neuroprotective measures, and corticosteroids. He was discharged after 31 days and remained asymptomatic at 6-month follow-up.", + "wiki_anchor": "Moreno is also a noteworthy contributor to research on the neurologic ailment known as Posterior Reversible Encephalopathy Syndrome, or PRES, a rare, poorly understood disease with a number of associated factors but no clearly delineated etiology. During the Covid-19 pandemic, Moreno and a team of clinicians, encountered a patient who contracted SARS-CoV-2 and was treated with tocilizumab, an immunologic agent, and then later went on to develop PRES. Numerous case reports on this same occurrence have since been documented, however Moreno and his coworkers were one of the earlier known to document this specific clinical association.", + "doc_fkgl": 14.753525835866263, + "wiki_fkgl": 19.87541666666667, + "doc_tree_depth": 6.333333333333333, + "wiki_tree_depth": 10.0, + "fkgl_delta": -5.121890830800407 + }, + { + "index": 8, + "label": "proficient_health_literacy", + "original_doc": "A 4-year-old male, two weeks post nasal impetigo treated with topical mupirocin and oral cefadroxil (dose/duration/adherence unknown), presented with 5 days of macroscopic glomerular haematuria and lower-extremity oedema, followed by 12 hours of headache, nausea, and vomiting, and arrived to the ED in convulsive status after 20 minutes of generalized tonic\u2013clonic seizures. On ED arrival he was afebrile, with non-evaluable BP, depressed consciousness, generalized hypertonia, and bilateral pretibial oedema. He was intubated and loaded with phenobarbital 10 mg/kg. In the ICU, BP was 134/94 mmHg (p95 for age 108/66; p95+12 120/78), consistent with hypertensive emergency. Initial labs: urinalysis with haematuria (>100 RBC/hpf), proteinuria 3+, leucocyturia 10\u201325/hpf; creatinine 0.3 mg/dL; anaemia Hct 21%, Hb 7 g/dL with normocytic, normochromic indices; leukocytosis 23,900/mm3; thrombocytosis 756,000/mm3; no elevation of acute-phase reactants; hypocomplementemia with C3 25 mg/dL (VN 80\u2013150) and normal C4. Throat rapid antigen for group A Streptococcus was positive and ASO positive. Non-contrast head CT was unremarkable. Renal ultrasound showed bilateral nephromegaly with increased cortical echogenicity and decreased corticomedullary differentiation. The working diagnosis was nephritic syndrome due to complicated GNAPE with hypertensive emergency and status epilepticus. He required mechanical ventilation and phenobarbital; EEG the next day was normal; CSF was normal. Cefotaxime was started for Streptococcus pyogenes eradication and furosemide for diuresis. By day 2 he developed AKI (creatinine 0.99 mg/dL), hypertension, and 24-hour proteinuria 36.6 mg/m2/h without oliguria. Antihypertensive therapy included amlodipine and IV labetalol with initial control. After extubation at 48 hours, he deteriorated neurologically within 24 hours (GCS 8) with BP > p95+12 despite labetalol infusion up to 3 mg/kg/h, amlodipine 10 mg/day, and furosemide, necessitating reintubation and sodium nitroprusside infusion up to 3 mcg/kg/min with a planned gradual BP reduction of 25% per day to mitigate secondary neurologic injury. Given acute neurologic deficits with severe HTN in GN, PRES was suspected and confirmed by brain MRI on day 5 showing increased subcortical T2/FLAIR signal in bilateral symmetric occipital regions without diffusion restriction, consistent with vasogenic edema. Ophthalmologic exam was normal; repeat EEG showed occasional generalized voltage depression. Enalapril was added. Over 10 days, BP normalized with slow pharmacologic weaning; follow-up MRI on day 12 showed radiologic regression, and he was successfully extubated after 5 days. During the ICU course, Hb fell to 5 g/dL with normocytic, normochromic indices and no thrombocytopenia; hemolytic anemia was diagnosed given a positive direct Coombs test and hemoglobinuria. He required two packed RBC transfusions. Methylprednisolone 1 mg/kg/day was given for 72 hours. Stool culture and urinary antigen for Streptococcus pneumoniae were negative. Serologies for EBV and Parvovirus B19, ENA profile, ANCA, anti-dsDNA, anti-\u03b22 glycoprotein I, anticardiolipin, and lupus anticoagulant were all negative; all cultures (blood, urine, endotracheal aspirate, pharyngeal) were negative. ANA was positive at 1:160. Clinical status improved with BP control, rising complement levels, and resolution of proteinuria and haematuria; the direct Coombs remained positive on hospital day 9. He was discharged on day 31 normotensive, non-anaemic, with preserved renal function, no proteinuria or haematuria, normalized C3, and asymptomatic neurologically. Discharge medications: prednisone, amlodipine, enalapril, and folic acid. He remained asymptomatic with no recurrence at 6 months. Overall, the case represents GNAPE with hypocomplementemia (low C3) and elevated ASO complicated by hypertensive emergency causing encephalopathy and secondary PRES, plus autoimmune hemolytic anemia with Hb nadir 5 g/dL, successfully managed with antihypertensives, neuroprotective measures, and corticosteroids, with full clinical and radiologic recovery.", + "wiki_anchor": "Desidustat (INN, also known as ZYAN1) is a drug for the treatment of anemia of chronic kidney disease. This drug with the brand name Oxemia is discovered and developed by Zydus Life Sciences. Desidustat reduces the requirement of recombinant erythropoietin requirement in anemia, and decreases EPO-resistance, by reducing IL-6, IL-1\u03b2, and anti-EPO antibodies. The subject expert committee of CDSCO has recommended the grant of permission for manufacturing and marketing of Desidustat 25\u00a0mg and 50\u00a0mg tablets in India,based on some conditions related to package insert, phase 4 protocols, prescription details, and GCP. Clinical trials on desidustat have been done in India and Australia. In a Phase 2, randomized, double-blind, 6-week, placebo-controlled, dose-ranging, safety and efficacy study, a mean hemoglobin increase of 1.57, 2.22, and 2.92 g/dL in desidustat 100, 150, and 200\u00a0mg arms, respectively, was observed. The Phase 3 clinical trials were conducted in chronic kidney disease patients which were not on dialysis as well as on dialysis. Desidustat is developed for the treatment of anemia as an oral tablet, where currently injections of erythropoietin and its analogues are drugs of choice. Desidustat is a HIF prolyl-hydroxylase inhibitor. In preclinical studies, effects of desidustat was assessed in normal and nephrectomized rats, and in chemotherapy-induced anemia. Desidustat demonstrated hematinic potential by combined effects on endogenous erythropoietin release and efficient iron utilization. Desidustat can also be useful in treatment of anemia of inflammation since it causes efficient erythropoiesis and hepcidin downregulation. In January 2020, Zydus entered into licensing agreement with China Medical System (CMS) Holdings for development and commercialization of desidustat in Greater China. Under the license agreement, CMS will pay Zydus an initial upfront payment, regulatory milestones, sales milestones and royalties on net sales of the product. CMS will be responsible for development, registration and commercialization of desidustat in Greater China. It has been observed that desidustat protects against acute and chronic kidney injury by reducing inflammatory cytokines like IL-6 and oxidative stress. A clinical trial to evaluate the efficacy and safety of desidustat tablet for the management of COVID-19 patients is ongoing in Mexico, wherein desidustat has shown to prevent acute respiratory distress syndrome (ARDS) by inhibiting IL-6. Zydus has also received approval from the US FDA to initiate clinical trials of desidustat in chemotherapy Induced anemia (CIA).", + "doc_fkgl": 14.958653673835126, + "wiki_fkgl": 14.612631578947369, + "doc_tree_depth": 5.866666666666666, + "wiki_tree_depth": 6.888888888888889, + "fkgl_delta": 0.3460220948877577 + }, + { + "index": 9, + "label": "low_health_literacy", + "original_doc": "This 69-year-old man had heart bypass surgery in the past. For 2 months, he got very short of breath with light activity. Tests\u2014a heart tracing, a blood test, and an X-ray movie with dye of the heart arteries\u2014showed heart failure from poor blood flow after a bypass vein to the right heart artery failed. Doctors first opened a totally blocked artery on the left side of his heart. Then they used tiny natural detours between heart arteries to reach the right heart artery from the far end and open it. His breathing was better when he left the hospital. Six months later, his shortness of breath had not come back.", + "wiki_anchor": "Philip Caves (1940\u20131978) was an Irish cardiothoracic surgeon. In 1972, while at Stanford University, he pioneered the use of the bioptome and transvenous endomyocardial biopsy in the early diagnosis of heart transplant rejection. It was considered the most significant advance in antirejection therapy of the time. Awarded the British American Research Fellowship in 1971, Caves worked with pioneering cardiothoracic surgeon Norman Shumway at Stanford and became staff surgeon leading the transplant programme by 1973. A year later he went to Edinburgh as a senior lecturer in cardiac surgery, where he became particularly interested in pediatric cardiac surgery.", + "doc_fkgl": 6.522207792207791, + "wiki_fkgl": 14.359505154639177, + "doc_tree_depth": 5.571428571428571, + "wiki_tree_depth": 6.8, + "fkgl_delta": -7.837297362431386 + }, + { + "index": 9, + "label": "intermediate_health_literacy", + "original_doc": "A 69-year-old man with prior coronary bypass surgery presented with two months of severe shortness of breath with mild activity (NYHA class III). He was diagnosed with heart failure due to ischemia after failure of a saphenous vein graft to the right coronary artery. This was supported by an abnormal ECG, elevated NT-proBNP, and a coronary angiogram; echocardiography also showed reduced pumping function. The team reopened a chronic total occlusion in the native right coronary artery using a retrograde approach through septal channels (septal surfing). To enable that route, they first re-opened the totally occluded left coronary artery. After the procedure, his dyspnea improved before discharge, and at 6 months he had no recurrence of shortness of breath.", + "wiki_anchor": "Background\nVeins are adapted to an environment of low pressure and low flow. In order to bypass the coronary obstruction and restore blood flow, veins are transferred and integrated into the arterial circulation, where they exposed to high pressure and flow. These new hemodynamic conditions cause intimal hyperplasia and atherosclerosis that cause intermediate and late vein graft failure. The idea of placing an external support on the vein graft was first suggested in 1963. The rational being that it will diminish the circumferential strain of the graft wall, therefore inhibiting intimal hyperplasia and later superimposed atherosclerosis, aiding with the adaptation of the vein toward the arterial environment.", + "doc_fkgl": 13.480000000000004, + "wiki_fkgl": 15.032635514018693, + "doc_tree_depth": 7.166666666666667, + "wiki_tree_depth": 8.2, + "fkgl_delta": -1.5526355140186894 + }, + { + "index": 9, + "label": "proficient_health_literacy", + "original_doc": "A 69-year-old male with prior CABG presented with 2 months of severe dyspnea on mild exertion (NYHA III). ECG showed ST depression in II, III, aVF, and V4\u20136; NT-proBNP was 2640 pg/mL. Echocardiography demonstrated LV systolic dysfunction with LVEF 30%. His history included an inferior STEMI in 2009 with severe 3-vessel disease (proximal LAD CTO, 90% mid/distal LCx stenoses, 95% mid RCA stenosis) treated with CABG (LIMA\u2013LAD; sequential SVG to OM1, OM2, and PL). Current angiography via 6 Fr left radial access showed patent LIMA\u2013LAD and SVG\u2013OM1/OM2, but complete occlusion of the sequential SVG to PL. The native LM was occluded at the ostium and the native RCA was occluded in the mid segment with bridging collaterals. The strategy was to treat the native RCA CTO. Dual arterial access was obtained with an additional 6 Fr right femoral sheath. The right and left coronaries were engaged with 6 Fr AL 0.75 (Launcher; Medtronic) and 6 Fr EBU 3.5 (Launcher; Medtronic) guide catheters, respectively. An antegrade approach from the left radial artery failed: neither a Fielder XTR nor a Gaia 3 with a Finecross microcatheter could enter the distal true lumen. A parallel wire technique with a Crusade microcatheter and two Gaia 3 wires also failed. The team then switched to a retrograde approach via septal channels from the LAD through the occluded left coronary system. A Gaia 3 crossed the occluded LM and LAD to reach the distal LAD true lumen. A Sion wire was exchanged via a Finecross into the distal LAD, followed by dilation of the LM and proximal LAD with a 2.0 \u00d7 15 mm balloon. Septal surfing technique (SST) was then used to identify a viable septal channel. A Sion wire, supported by a 150-cm Finecross, was advanced retrogradely through a distal septal branch into the distal RCA. A Gaia 3 traversed the RCA CTO retrogradely into the proximal RCA true lumen and was advanced into a Guidezilla guide extension catheter positioned in the antegrade guide. The Finecross was delivered to the antegrade guide and an RG3 wire was externalized. The CTO segment was predilated with a 2.0 \u00d7 15 mm balloon and stented with two overlapping DES (2.5 \u00d7 38 mm and 3.0 \u00d7 38 mm), achieving an excellent angiographic result with TIMI 3 flow in all distal branches. Dyspnea was relieved at discharge, and at 6-month follow-up there was no recurrence of dyspnea.", + "wiki_anchor": "REBOA Deployment \nREBOA was developed as a rapidly deployable, minimally invasive alternative to emergency thoracotomy with aortic cross-clamping. Although there is no single indication criteria for the procedure, it is typically performed for patients with either blunt or penetrating traumatic injuries to the torso with severe hemorrhage refractory to blood product resuscitation. REBOA is performed by gaining access to the common femoral artery and inserting a small endovascular catheter with an inflatable balloon within the aorta. Upon inflation of the occluding balloon, blood flow across the descending aorta is either partially or completely obstructed which subsequently stanches downstream bleeding. The adjustable catheter design of the REBOA device allows for variable positioning of the occluding balloon within the aorta based on the suspected source of bleeding. Zone 1 positioning in the descending thoracic aorta minimizes blood flow below the diaphragm and significantly reduces bleeding within the abdomen, pelvis, and lower extremities. Alternatively, Zone 3 placement within the infrarenal descending abdominal aorta reduces bleeding within the pelvis and lower extremities while preserving blood supply within the abdomen. Although REBOA does not replace the need for definitive surgical management, it may act as a temporizing measure by temporarily augmenting cardiac index to preserve cerebral and myocardial perfusion. Immediately following successful REBOA deployment, patients must be considered for emergent surgical intervention.", + "doc_fkgl": 9.065632911392406, + "wiki_fkgl": 19.044669738863288, + "doc_tree_depth": 6.684210526315789, + "wiki_tree_depth": 7.555555555555555, + "fkgl_delta": -9.979036827470882 + }, + { + "index": 10, + "label": "low_health_literacy", + "original_doc": "A 51-year-old man came to us with sudden, painful vision loss in his left eye for three days. His right eye could see clearly (20/20). His left eye could only see hand movements. The back of his left eye showed swelling of the seeing nerve, a bulge in the layer under the retina, several patches of fluid under the retina, and wrinkles in the thin lining there. An MRI scan with contrast dye of the eyes and brain showed a small lump behind the eye where the eye nerve meets the white part of the eye. Tests for cancer and immune diseases were normal. The doctors diagnosed inflammation in the back part of the eye\u2019s white coat that forms a small lump (nodular posterior scleritis). They started high-dose steroid pills by mouth (prednisolone).", + "wiki_anchor": "Signs & symptoms \nCongenital hemifacial enlargement in which mature lipocytes invade adjacent tissue. Phenotypic features include soft-tissue and skeletal hypertrophy and regional macrodontia. The manifestations are variable ranging from mild to severe. The overgrowth is typically present at birth. The most common features, all features on only one affected side of the face, are:\n Increased adipose tissue compared to the other side. The fat is infiltrating with no clear separation from the adjacent tissue.\n Hypertrophy of the skeleton including teeth.\n Early eruption of ipsilateral deciduous and permanent teeth\n The parotid and submandibular gland including accessory tissue is larger.\n Epidermal nevus / nevus sebaceous on the affected side.\n Increased adipose tissue behind the orbital and pterygopalatine fossa.\n Amblyopia of the eye.\n Overgrowth of the ear.\n Mucosal neuromas\n Cutaneous capillary blush\n Ipsilateral macroglossia\n Syndromic hemimegalencaphaly", + "doc_fkgl": 6.597509398496243, + "wiki_fkgl": 11.940000000000001, + "doc_tree_depth": 5.875, + "wiki_tree_depth": 5.076923076923077, + "fkgl_delta": -5.3424906015037585 + }, + { + "index": 10, + "label": "intermediate_health_literacy", + "original_doc": "A 51-year-old man presented with 3 days of sudden, painful vision loss in the left eye. Visual acuity was 20/20 in the right eye and hand motion in the left eye. Left fundus findings included optic nerve head swelling, choroidal bulging, multiple areas of subretinal fluid, and RPE corrugations. Orbital/brain MRI with gadolinium showed a retrobulbar nodular mass enhancing at the junction of the optic nerve and sclera. Oncology and rheumatology evaluations were unremarkable. The clinical diagnosis was nodular posterior scleritis, and oral prednisolone was started.", + "wiki_anchor": "The most common ocular abnormality in encephalocraniocutaneous lipomatosis is a form of benign growth called a choristoma which can occur in one or both eyes. These may effect vision. Other ocular symptoms include abnormally small eyes, small pupils, iris hypoplasia, sclerocornea, hypertrophic conjunctivae, an absent macular reflex and anterior chamber anomalies. There may be eyelid colobomas and short or abnormal palpebral fissures. Skin tags often grow around the eyelids.", + "doc_fkgl": 11.54186046511628, + "wiki_fkgl": 11.852869565217397, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 6.0, + "fkgl_delta": -0.31100910010111704 + }, + { + "index": 10, + "label": "proficient_health_literacy", + "original_doc": "A 51-year-old male presented with acute, painful visual loss of the left eye (LE) for 3 days. Best-corrected distance visual acuity (BCDVA) was 20/20 OD and hand motion (HM) OS. Ocular motility and anterior segment were unremarkable OU. Fundus OS showed optic nerve head (ONH) swelling, choroidal bulging, multiple patches of subretinal fluid (SRF), and retinal pigment epithelial (RPE) corrugations; OD fundus was unremarkable.\n\nMultimodal imaging was obtained: OCT (OptoVue, Inc., Fremont, CA, USA; software version 2018.0.0.18) demonstrated mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid, and mild retinal thickening. Indocyanine green angiography (ICGA) showed a geographic macular hypocyanescent area OS. Blue-autofluorescence (BAF) revealed a geographic macular area with speckled autofluorescence. B-scan ultrasonography showed optic nerve enlargement. Fluorescein angiography (FA) demonstrated vascular leakage at the ONH (hot disc) and a geographic patchy hypofluorescent area with speckled hyperfluorescent margins measuring approximately three disc diameters. Orbital and brain MRI with gadolinium revealed a retrobulbar nodular enhancing mass at the optic nerve\u2013sclera junction. Oncology consultation was unremarkable.\n\nGiven concern for malignancy and the enhancing orbital nodule, the patient underwent transconjunctival lateral orbitotomy one week after presentation. Intraoperatively, a pink localized scleral nodule with edematous Tenon was identified. With a clinical diagnosis of nodular posterior scleritis, sub-Tenon triamcinolone acetonide was administered. The patient declined admission and intravenous corticosteroids; oral prednisolone 50 mg/Kg was initiated. Rheumatologic and infectious work-up, including PPD (tuberculosis), chest X-ray, serum ACE (sarcoidosis), and C-ANCA (Wegener granulomatosis), was unremarkable.\n\nAt the one-week postoperative follow-up, BCDVA was 20/20 OD and counting fingers at 2 meters OS. SRF had resolved, and the macula was atrophic. Oral prednisolone was tapered over three months.", + "wiki_anchor": "Ocular oncology, especially retinoblastoma, has been the principal research area of Honavar and he is known to have contributed to the understanding and treatment of various tumors affecting the ocular surface and orbit. Working on retinoblastoma, he developed various therapeutic and management protocols which included high-dose and periocular chemotherapy, adjuvant therapy to mitigate the high risk of metastasis and multimodal management of orbital affection of the disease and he is reported to have treated over 2000 pediatric retinoblastoma patients with a success rate above of 85%. At L. V. Prasad Eye Institute, he was the first to perform intra-ocular brachytherapy procedure, along with Vijay Anand Reddy. His studies have been documented by way of a number of articles of which many have been listed by online article repositories such as Google Scholar and ResearchGate. Besides, he has contributed chapters to books published by others. He is a section editor for Asia Pacific Academy of Ophthalmology and is a member of the advisory committee of International Council of Ophthalmology. He serves as the scientific program coordinator of Oculoplastic Association of India and has also mentored research scholars in their studies. The invited speeches delivered by him include the BOPSS 2016 of the British Oculoplastic Surgery Society.", + "doc_fkgl": 14.661870129870131, + "wiki_fkgl": 17.77350609756098, + "doc_tree_depth": 5.473684210526316, + "wiki_tree_depth": 8.5, + "fkgl_delta": -3.111635967690848 + }, + { + "index": 11, + "label": "low_health_literacy", + "original_doc": "A 78-year-old man from the Amhara region of Ethiopia had a permanent heart pacemaker because of a complete heart block. He was scheduled for prostate surgery. Before surgery, the anesthesia and heart doctors advised switching his pacemaker to a steady, fixed beat to lower the chance of problems. He could not afford that change. He chose to go ahead with the operation. He signed consent for the plan. After surgery, he also gave permission to share his case. For anesthesia, he got a numbing injection in the lower back (a combined spinal\u2013epidural). The team used 2.5 ml of strong numbing medicine (0.5% bupivacaine) and a tiny dose of fentanyl (50 micrograms). Standard monitors were used, and his heart was watched closely. His vital signs stayed steady, with only small changes. His blood pressure stayed good with IV salt water. After surgery, he went to the recovery room. He got pain medicine after 4 hours and an extra dose through the epidural. Six hours after surgery, he moved to the ward in stable condition. The epidural pain control continued for 72 hours. He went home in stable condition about 88 hours after surgery.", + "wiki_anchor": "Holt's health\nHolt had been in reasonably good health throughout his life, although he had a family history of premature death \u2013 his father had died at the age of 59 and his older brother at the age of 57. He suffered a severe concussion in a road accident in November 1955, in which the driver of his ministerial car was killed. In September 1967, Holt began treatment for a painful shoulder injury that he had originally suffered playing football in his youth; he was prescribed painkillers and twice-weekly physiotherapy. A few days before his death, he had been briefly examined by his personal physician, Marcus Faunce, who advised him to avoid over-exerting himself and to cut back on swimming and tennis. The Prime Minister is Missing, a 2008 docudrama, suggested that Holt's judgement on the weekend of his death had been clouded by his medication, in combination with work-related tiredness and stress. Morphine was named as the drug that he had been prescribed, although \"no direct evidence\" indicated that he had taken any on the day of his death.", + "doc_fkgl": 6.542719298245618, + "wiki_fkgl": 14.371256983240226, + "doc_tree_depth": 4.823529411764706, + "wiki_tree_depth": 8.5, + "fkgl_delta": -7.828537684994608 + }, + { + "index": 11, + "label": "intermediate_health_literacy", + "original_doc": "A 78-year-old man from the Amhara region, Ethiopia, with a permanent pacemaker placed for complete heart block was scheduled for retropubic prostatectomy. The anesthesia and cardiology teams recommended switching his dual-chamber, rate\u2011modulated pacemaker to an asynchronous mode perioperatively to reduce the risk of electromagnetic interference during surgery. He could not afford reprogramming and chose to proceed with the existing plan after informed consent; permission to publish the case was obtained after the operation. He received combined spinal\u2013epidural anesthesia at L3\u2013L4 using 0.5% isobaric bupivacaine 2.5 ml (12.5 mg) plus fentanyl 50 \u00b5g. Standard ASA monitoring was applied with special attention to cardiac stability. Intraoperatively, he remained stable with minimal changes in vital signs; blood pressure was supported with isotonic saline as needed. Postoperatively, he was monitored in the PACU, received analgesia at 4 hours with an epidural top\u2011up, and was transferred to the ward about 6 hours after surgery in stable condition. Epidural analgesia was continued for 72 hours. He was discharged at the 88th postoperative hour in good condition.", + "wiki_anchor": "Ongoing Investigation \nThe safety and efficacy of REBOA in the treatment of severe hemorrhagic shock is an area of ongoing research. Early studies reported conflicting data regarding mortality and failed to establish any clear benefit of REBOA when compared to emergency thoracotomy with aortic cross clamping. However, design improvements of the REBOA device and continuously evolving patient selection criteria have subsequently improved REBOA outcomes. Current literature demonstrates a survival benefit of REBOA deployment in patients with severe hemorrhagic shock who do not require cardiopulmonary resuscitation (CPR). However, despite REBOA demonstrating its greatest efficacy when deployed prior to cardiovascular collapse, recent data has also shown promise when deployed during (CPR). Closed cardiopulmonary compressions with the REBOA device deployed has demonstrated improved cardiac compression fraction and end-tidal when compared to emergency thoracotomy with aortic cross clamping and cardiac massage. Additionally, some centers have promoted REBOA deployment in patients with hypotension at risk for progression to severe hemorrhagic shock but who do not yet meet criteria for emergency thoracotomy with aortic cross clamping. The variability in REBOA outcomes likely reflects the variability in institutional patient selection and indications criteria which highlights the need for ongoing evaluation.", + "doc_fkgl": 12.910294117647059, + "wiki_fkgl": 19.803205958549224, + "doc_tree_depth": 6.444444444444445, + "wiki_tree_depth": 7.875, + "fkgl_delta": -6.8929118409021655 + }, + { + "index": 11, + "label": "proficient_health_literacy", + "original_doc": "A 78-year-old male from the Amhara region of Ethiopia with a 7-year history of a permanent pacemaker for complete heart block was scheduled for retropubic prostatectomy for BPH after prior TURP 3 months earlier. Comorbidities included long-standing hypertension (amlodipine 5 mg daily, enalapril 10 mg BID, atorvastatin 10 mg daily) and type 2 diabetes mellitus (metformin 500 mg BID; NPH insulin 20 IU AM/10 IU PM). Preoperative evaluation showed complete bundle branch block on ECG; electrophysiology assessment demonstrated LVH due to hypertensive heart disease with mild diastolic dysfunction and an EF of 62%. Abdominal ultrasound showed an 82-ml prostate; AP chest X-ray was normal with a left-sided pacemaker in situ; electrolytes and troponin were normal. He had a frailty score of 5.5, METs 3.4, and an RCRI class III, indicating an estimated 10.1% risk of major adverse cardiac events within 30 days and intermediate surgical risk. Multidisciplinary planning recommended reprogramming the dual-chamber, rate\u2011modulated pacemaker to an asynchronous mode to mitigate intraoperative electromagnetic interference risk. Due to financial and logistical constraints, reprogramming was not performed; risks were disclosed, and he consented to proceed. Preoperatively, usual medications were continued (with a lower morning NPH dose at two\u2011thirds); diazepam 5 mg PO was given at midnight for anxiolysis. On the day of surgery, random blood glucose was checked and managed with a sliding scale. Team communication emphasized CIED precautions (electrosurgery pad positioned away from the device; emergency drugs and defibrillator immediately available). Dexamethasone was given for PONV prophylaxis and paracetamol for preemptive analgesia. ASA standard monitoring was applied and baselines recorded. An L3\u2013L4 combined epidural\u2013spinal anesthetic was performed using 0.5% isobaric bupivacaine 12.5 mg (2.5 ml) plus fentanyl 50 \u00b5g, achieving a sensory level to T7. The procedure used a midline infraumbilical incision; monopolar cautery at low voltage (20 mA) with bipolar low\u2011voltage cautery for hemostasis. Intraoperative hemodynamics remained within 10% of baseline without cardiorespiratory events; blood pressure was maintained with isotonic saline. Postoperatively, he was transferred to PACU with vigilant monitoring; analgesia was administered at 4 hours with an epidural top\u2011up, and he was transferred to the ward approximately 6 hours after surgery in stable condition. Epidural analgesia was continued for 72 hours. He was discharged at the 88th postoperative hour in stable condition, with cardiology follow\u2011up advised. Informed consent was obtained, and permission for case report publication was granted after the operation.", + "wiki_anchor": "Although he participated in a great deal of physiological research early in his career, Pickering's research in behavioral determinants and consequences of hypertension formed the heart of the program. Thus, Pickering was one of the earliest researchers to employ ambulatory blood pressure (ABP) monitoring, and contributed to the knowledge that clinic blood pressure measures are prone to both unsystematic and systematic errors, and are hence less useful for the prediction of target organ damage and adverse cardiovascular events than ABP. In the course of this research, he began to examine the nature of the errors more closely; for example, he was one of the first to identify the phenomenon of \"white coat hypertension\", in which patients exhibit poor blood pressure control only in the physician's office, leading to a false diagnosis of hypertension and unnecessary prescription of medication. Pickering was the Principal Investigator of a National Heart Lung and Blood institute Program Project that began in 1993 and has investigated several phenomena related to the behavioral causes and physiological consequences of hypertension, focusing on white coat hypertension, nocturnal blood pressure \"dipping\", race differences in PSG-assessed sleep quality and target organ damage, and the effects of work-related stress on blood pressure and left ventricular hypertrophy (LVH). The latter study remains one of the few prospective demonstrations that environmental stress is associated with hypertension and LVH.", + "doc_fkgl": 13.475840409207162, + "wiki_fkgl": 24.323071428571428, + "doc_tree_depth": 6.2631578947368425, + "wiki_tree_depth": 11.2, + "fkgl_delta": -10.847231019364266 + }, + { + "index": 12, + "label": "low_health_literacy", + "original_doc": "A 52-year-old woman had burning when she peed and had to pee very often for a long time. She tried many treatments for bladder infections, but the problem did not go away. Regular scans and lab tests looked normal. A camera test that looked inside her bladder showed the lining was red and irritated, with tiny bits floating in the urine. Later, the lab saw a live larva (a baby insect) in her urine under the microscope. That finding explained her symptoms. She was told to keep very clean. She was also told to drink plenty of water every day.", + "wiki_anchor": "Description\nLarva carnivorous and can be found from pools with foul water or water with a high organic content. They are well modified to live in any water clogged place for the survival, which includes natural habitats like hollow logs, rock holes, tree holes, bamboo, Pandanus axils, sago palm and banana stumps, fruit shells and husks, fallen leaves and spathes, flower bracts, pitcher plants, and artificial containers having organic matter and small collections of ground water made by humans. Adults are more confined to dark forested areas and active mostly in crepuscular periods. Females are primarily human-biters.", + "doc_fkgl": 6.041, + "wiki_fkgl": 13.574716494845362, + "doc_tree_depth": 5.125, + "wiki_tree_depth": 10.25, + "fkgl_delta": -7.533716494845361 + }, + { + "index": 12, + "label": "intermediate_health_literacy", + "original_doc": "A 52-year-old woman had ongoing dysuria and urinary frequency despite multiple treatments for presumed infections. Cystoscopy showed bladder redness and debris, while imaging and routine lab tests were unremarkable. Eventually, a live larva was identified in the urine, confirming the cause of her symptoms. Management focused on better personal hygiene and increased fluid intake.", + "wiki_anchor": "Symptoms include powdery orange masses on the lower surface of leaves. They often mature into a long columnar shape retaining the same color. The uredinial-telial stages of P. euvitis causes chlorotic and necrotic lesions ranging in shapes and sizes on the upper surface of leaves.", + "doc_fkgl": 12.18240740740741, + "wiki_fkgl": 7.677500000000002, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 6.666666666666667, + "fkgl_delta": 4.5049074074074085 + }, + { + "index": 12, + "label": "proficient_health_literacy", + "original_doc": "A 52-year-old woman presented with a three-year history of urinary frequency, dysuria, and dribbling, along with intermittent passage of red and black thread-like material in the urine. Episodes with these discharges were associated with headache, fever, and chills, and she reported intermittent periurethral and genital pruritus. She had been repeatedly treated for recurrent urinary tract infections without clinical improvement. She denied recent travel, camping, hiking, farming, swimming, or insect bites. Past surgical history included pilonidal sinus surgery (8 years prior) and hysterectomy (7 years prior). Two years before the current visit, she was hospitalized for evaluation. Examination revealed a well-appearing patient with normal vital signs. Laboratory testing, including complete blood count, urinalysis, and serum chemistries, was within normal limits. Abdominopelvic CT was unremarkable. Cystoscopy demonstrated erythema and hyperemia of the bladder mucosa, suspended intravesical debris, and dilatation of the left ureteral orifice. Schistosomiasis was suspected and she received praziquantel at appropriate dose and duration, without improvement. A second infectious diseases consultation raised suspicion for urinary myiasis, and ivermectin was prescribed, again without benefit. She underwent bladder irrigation with polyethylene glycol; no visible larvae were recovered from the washings, and she experienced self-limited hematuria for two days post-procedure. A subsequent random urinalysis was normal. However, a 24-hour urine collection demonstrated a live larva on light microscopy. The specimen was isolated and identified morphologically by an entomologist as Sarcophaga spp. Final management emphasized personal hygiene measures and liberal oral hydration.", + "wiki_anchor": "Pseudoliotia acidalia (Melvill & Standen, 1899)\n Pseudoliotia anaglypta (A. Adams, 1863)\n Pseudoliotia asteriscus (Gould, 1859)\n Pseudoliotia axialis Laseron, 1958\n Pseudoliotia bellatula (W.-M. Feng, 1996)\n Pseudoliotia caelata (Garrett, 1873)\n Pseudoliotia calliglypta (Melvill, 1891)\n Pseudoliotia coronata Rubio & Rol\u00e1n, 2018\n Pseudoliotia cristata (G. B. Sowerby III, 1900)\n Pseudoliotia dispersa Rubio & Rol\u00e1n, 2018\n Pseudoliotia distincta Rubio & Rol\u00e1n, 2018\n Pseudoliotia faceta Rubio & Rol\u00e1n, 2018\n Pseudoliotia fijiensis Rubio & Rol\u00e1n, 2018\n Pseudoliotia gabrielruedai Rubio & Rol\u00e1n, 2018\n Pseudoliotia godeti (Dautzenberg & H. Fischer, 1907)\n Pseudoliotia gowllandi (Brazier, 1874)\n Pseudoliotia granulosa Kuroda & Habe, 1971\n Pseudoliotia hattenbergeri Rol\u00e1n & Rubio, 2002\n Pseudoliotia henjamensis (Melvill & Standen, 1903)\n Pseudoliotia inanis Rubio & Rol\u00e1n, 2018\n Pseudoliotia indicta Rubio & Rol\u00e1n, 2018\n Pseudoliotia intermixta Rubio & Rol\u00e1n, 2018\n Pseudoliotia linguifera (Thiele, 1925)\n Pseudoliotia micans (A. Adams, 1850)\n Pseudoliotia minor Rubio & Rol\u00e1n, 2018\n \u2020 Pseudoliotia motobuensis MacNeil, 1961 \n Pseudoliotia nodenim Rubio & Rol\u00e1n, 2018\n Pseudoliotia nodosa Rubio & Rol\u00e1n, 2018\n Pseudoliotia ocrinium (Melvill & Standen, 1901)\n Pseudoliotia oscostata Rubio & Rol\u00e1n, 2018\n Pseudoliotia philippinensis Rubio & Rol\u00e1n, 2018\n Pseudoliotia philtata (Hedley, 1900)\n Pseudoliotia plurifunis Rubio & Rol\u00e1n, 2018\n Pseudoliotia plusnodosa Rubio & Rol\u00e1n, 2018\n Pseudoliotia pressa Rubio & Rol\u00e1n, 2018\n Pseudoliotia profundi Rubio & Rol\u00e1n, 2018\n Pseudoliotia pulchella (Dunker, 1860)\n Pseudoliotia radians (Laseron, 1958)\n Pseudoliotia reeviana (Hinds, 1843)\n Pseudoliotia rudispiralis Rubio & Rol\u00e1n, 2018\n Pseudoliotia salva Rubio & Rol\u00e1n, 2018\n Pseudoliotia sementis Rubio & Rol\u00e1n, 2018\n Pseudoliotia seposita Rubio & Rol\u00e1n, 2018\n Pseudoliotia speciosa (Angas, 1871)\n Pseudoliotia supremum (Melvill & Standen, 1903)\n Pseudoliotia teresae Rubio & Rol\u00e1n, 2018\n Pseudoliotia tribulationis (Hedley, 1909)\n Pseudoliotia tropica Laseron, 1958\n Pseudoliotia supremum (Melvill & Standen, 1903)\n Pseudoliotia teresae Rubio & Rol\u00e1n, 2018\n Pseudoliotia tribulationis (Hedley, 1909)\n Pseudoliotia tropica Laseron, 1958\n Pseudoliotia vicina Rubio & Rol\u00e1n, 2018", + "doc_fkgl": 14.957394957983198, + "wiki_fkgl": 30.289999999999996, + "doc_tree_depth": 5.411764705882353, + "wiki_tree_depth": 6.25, + "fkgl_delta": -15.332605042016798 + }, + { + "index": 13, + "label": "low_health_literacy", + "original_doc": "A 36-year-old woman had a long-term bowel disease (ulcerative colitis). She came in with chest pain that kept getting worse. She also had shortness of breath, sweating, and felt sick to her stomach. For months she had felt very tired and had night sweats. Her heart test (EKG) showed signs of a heart attack in the lower part of the heart. Doctors did a dye X-ray to look at the heart arteries. It showed bad blockages in two heart pipes. They opened the most blocked pipe right away with a balloon and a tiny mesh tube (stent). While looking, the team worried the main body artery (aorta) was swollen. Blood tests showed mild inflammation. A special CT scan showed the aorta wall looked thick and scarred, with tight narrow spots in several arteries. This pointed to a rare illness that causes swollen big arteries, called Takayasu arteritis. She started strong anti-inflammatory and immune medicines (prednisone and methotrexate). Later she had heart bypass surgery to improve blood flow. She did well after treatment.", + "wiki_anchor": "Hypothesis on development of arteriosclerosis\nIn 2017 Haverich presented a new hypothesis about the pathogenesis of arteriosclerosis. While the potential role of infection and inflammation had been discussed for decades, Haverich noted that only specific arteries were subject to development of arteriosclerotic plaques. He postulated that the formation of plaques is not from inside the vessel, but the result of inflammation of the feeding vessels (vasa vasorum) of arteries that becoming inflamed compromising the integrity of the arterial wall. He noted that arteries with thin walls not having vasa vasorum do not develop arteriosclerosis. He postulated that the damage by inflamed vasa vasorum leads to cell death within the wall and subsequent plaques formation. Vasa vasorum inflammation can be caused by viruses, bacteria, and fine dust among others. According to his view this concept conforms to observations that cardiac infarctions are more common when influenza has occurred or fine particles have been inhaled.", + "doc_fkgl": 5.827348837209307, + "wiki_fkgl": 15.223174603174606, + "doc_tree_depth": 5.066666666666666, + "wiki_tree_depth": 8.285714285714286, + "fkgl_delta": -9.395825765965299 + }, + { + "index": 13, + "label": "intermediate_health_literacy", + "original_doc": "A 36-year-old woman with ulcerative colitis developed a week of worsening chest pressure with autonomic symptoms (such as sweating and nausea). Her electrocardiogram showed ST-segment elevation in the inferior leads, consistent with an inferior-wall heart attack. She also reported several months of fatigue and night sweats.\n\nUrgent coronary angiography found severe two-vessel coronary artery disease. The right coronary artery was the culprit lesion and was opened successfully with a stent. Because the interventional team suspected inflammation of the aorta (aortitis), additional workup was done. Inflammatory markers were mildly elevated, and CT angiography showed fibrotic thickening around the aorta with significant narrowing in multiple arteries, pointing to Takayasu arteritis.\n\nShe started treatment with prednisone and methotrexate. After stabilization, she underwent delayed coronary bypass surgery and did well.", + "wiki_anchor": "Accompanying diseases \nIn spite of being generally considered a benign expression of eosinophilia, isolated cases of family members with familial eosinophilia have been afflicted with tissue dysfunctions that are often associated with more pathological forms of eosinophilia. These dysfunctions include fatal endomyocardial fibrosis, valvular heart disease, and diminished motor and/or sensory function in skin areas served by peripheral nerves. Three patients with heart tissue for pathology examination had eosinophilic infiltration or fibrosis in their heart's endomyocardium. One patient who died suddenly had autopsy findings of eosinophilic infiltration not only in the heart but also in lungs, gastrointestinal tract, and meninges. It is unclear whether these tissue damages were due to primary eosinophil infiltrations or eosinophil infiltrations secondary to other causes.", + "doc_fkgl": 14.593809523809526, + "wiki_fkgl": 16.878333333333334, + "doc_tree_depth": 5.888888888888889, + "wiki_tree_depth": 8.0, + "fkgl_delta": -2.284523809523808 + }, + { + "index": 13, + "label": "proficient_health_literacy", + "original_doc": "A 36-year-old female with ulcerative colitis (well controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares) presented with 1 week of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, the ECG was in sinus rhythm with ST-segment elevation in the inferior wall. She endorsed a 6-month history of general malaise, fatigue, and night sweats, and had experienced exertional precordial pain that progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.\n\nEmergency coronary angiography demonstrated severe 2-vessel coronary disease: a severe 90% ostial lesion in the left coronary trunk (left main) and a severe 99\u2013100% subocclusive ostial lesion in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful placement of a drug-eluting stent. The hemodynamicist noted possible aortitis given arch involvement and vessel friability during balloon advancement and recommended an inflammatory/etiologic evaluation prior to definitive management of the left main lesion.\n\nLaboratory testing showed mild anemia (hemoglobin 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated ESR 42 mm/h, CRP 4.9 mg/L (normal <1), and elevated high-sensitivity troponin. Autoimmunity panel: normal complement C3/C4, negative ANA, anti-DNA, and ENA profile; non-reactive VDRL. Cardiac MRI with contrast demonstrated acute non-transmural infarction of the left ventricular inferior wall and subendocardial ischemia in the anteroseptoapical region at rest, with mild aortic and mitral insufficiency and preserved biventricular systolic function.\n\nComputed tomographic angiography of the chest/abdomen/pelvis showed periaortic fibrotic wall thickening involving the aortic root, arch, and abdominal aorta, with severe left coronary trunk stenosis, mild left subclavian and left vertebral artery stenoses, and severe inferior mesenteric artery stenosis. The differential included IgG4-related disease versus Takayasu arteritis. Total IgG was 1,600 mg/dL (ref 700\u20131,600) with IgG1 1,024 mg/dL (elevated) and normal IgG2 456 mg/dL, IgG3 98.8 mg/dL, and IgG4 13.6 mg/dL, findings not supportive of IgG4-related aortitis. Takayasu arteritis was diagnosed clinically and by imaging.\n\nImmunosuppression was initiated with prednisone 60 mg daily and methotrexate 20 mg weekly (parenteral) with folic acid 1 mg daily. After 3 weeks of therapy, she underwent myocardial revascularization surgery using the left internal mammary artery graft to the descending anterior artery (LAD) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta appeared healthy. She was discharged home in good general condition and remains under ambulatory follow-up.\n\nContext: Takayasu arteritis is a large-vessel granulomatous vasculitis affecting the aorta and its major branches that can produce aorto-ostial coronary lesions (as in this case, involving the left main and right coronary ostia), leading to myocardial ischemia/infarction. The mildly elevated inflammatory indices, periaortic fibrotic thickening, and multifocal arterial stenoses on CTA are characteristic, and the lack of IgG4 elevation argues against IgG4-related aortitis. The staged approach\u2014urgent culprit-vessel PCI followed by immunosuppression and delayed CABG\u2014is consistent with management principles aiming to control vascular inflammation before definitive surgical revascularization.", + "wiki_anchor": "Efficacy of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock have been studied and published first in 2001 Later, the group concluded the ischemic skin lesions (ISL) developed in patients with catecholamine-resistant vasodilatory shock have multi-factorial cause and shall not necessarily been seen a side effect of AVP solely. The presence of septic shock and a history of peripheral arterial occlusive disease are independent risk factors for the development of ISL. In the last decade, in early hyperdynamic septic shock, the administration of high-dose AVP as a single agent proved to fail to increase mean arterial pressure in the first hour but maintains it above 70mmHg in two-thirds of patients at 48h. AVP decreases NE exposure, has no effect on the PrCO(2) - PaCO(2 )difference, and improves renal function and SOFA score. This led to development of a large trial to see theeffect of arginin vasopressin as add-on to norepinephrine in septic shock. It could be shown, if giving vasopressin in early stage of septic shock (norepinephrin < 15 microgramm/min and lactate < 1.4\u00a0mmol/L) there is a statistically significant interaction between vasopressin and corticosteroids. The combination of low-dose vasopressin and corticosteroids was associated with decreased 28 and 90 days mortality and organ dysfunction compared with norepinephrine and corticosteroids.", + "doc_fkgl": 16.972754430379748, + "wiki_fkgl": 16.277884615384615, + "doc_tree_depth": 6.380952380952381, + "wiki_tree_depth": 6.571428571428571, + "fkgl_delta": 0.6948698149951333 + }, + { + "index": 14, + "label": "low_health_literacy", + "original_doc": "A 36-year-old woman had trouble swallowing. Tests found she was born with an unusual shape of the main body artery in her chest. The artery curves to the right in a mirror-image pattern. It wraps around a main branch of the airway. The side branches of the artery come off in the reverse order from normal. Most people with this have no symptoms. Problems happen only if the artery squeezes the space in the middle of the chest. This can press on the food pipe or the windpipe. Surgery may be needed if there is strong pressure on these tubes, a bulge or a tear in the chest artery, or a pouch on the artery bigger than 2 cm. There is no one-size-fits-all treatment. Care is tailored to the person\u2019s symptoms and body anatomy. This patient did not receive any treatment.", + "wiki_anchor": "In this publication Aliu, alongside seven other physicians, discuss the complications that can arise from the placement of a nasogastric tube, a common procedure for patients that are unable to feed themselves. In previous case studies regarding nasogastric tubes, complications such a coiling and knotting are blamed on small bore tubes and are said to be more common in patients with small stomachs. However, Aliu and her colleagues challenge the position that small stomachs are at a greater risk for tube knotting, based on the extreme rarity of related complications in children. Instead, they argue that factors such as excess tube length, gastric surgery, and reduced gastric tone, specifically due to head injury, are the most reasonable predispositions for nasogastric tube knotting.", + "doc_fkgl": 5.730088652482269, + "wiki_fkgl": 16.423032786885248, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 10.25, + "fkgl_delta": -10.692944134402978 + }, + { + "index": 14, + "label": "intermediate_health_literacy", + "original_doc": "A 36-year-old woman had dysphagia due to a congenital right aortic arch with mirror-image branching.\nIn this rare pattern, the aorta runs to the right, wraps around the right main bronchus, and the head-and-arm arteries branch in the reverse order of normal.\nMost people have no symptoms unless the aorta or an associated bulge compresses the esophagus or trachea.\nSurgery is considered for major airway or esophageal compression, aneurysmal disease, thoracic aortic dissection, or a Kommerell diverticulum larger than 2 cm.\nThere is no standard operation; treatment is tailored to the person\u2019s anatomy and symptoms.\nIn this case, imaging showed external compression of the upper esophagus with a small Kommerell diverticulum (about 1.3 cm), so no intervention was performed and her symptoms improved.", + "wiki_anchor": "(Original description) This small, slightly fusiform species is remarkable for the peculiar truncate apex, the pleurotomoid labral sinus, and the columellar plaits being two only in number. Its color is white, sometimes rose-tinged. The shell contains 6 slightly convex whorls, including 2 vitreous whorl in the protoconch. The 16 longitudinal ribs and the transverse lirae (5\u20136 in the penultimate whorl, 18\u201320 in the body whorl) are produced into acute nodules at the points of intersection. The small aperture is narrow. The outer lip is slightly incrassate, distinctly sinuate and shows about six small denticles inside. The wide siphonal canal is very short. The columella is slightly oblique and shows two tubercles in the middle.", + "doc_fkgl": 11.984808362369339, + "wiki_fkgl": 9.530657894736844, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 4.888888888888889, + "fkgl_delta": 2.454150467632495 + }, + { + "index": 14, + "label": "proficient_health_literacy", + "original_doc": "A 36-year-old female presented with dysphagia and longstanding cervical and upper thoracic pain; she also had a multinodular goiter with no other significant history. Esophagogastroduodenal transit after barium ingestion showed a posterior and lateral right impression on the proximal esophagus extending 3.5 cm craniocaudally, with an estimated maximal esophageal stenosis of 60%. Cervical and thoracic CT revealed a congenital anomaly of the aortic arch: a right aortic arch with mirror-image branching. The arch originated from the aortic root, coursed above the right stem bronchus, and gave rise to the three supra-aortic trunks as follows: (1) left brachiocephalic artery (giving rise to the left common carotid artery and the left subclavian artery), (2) right common carotid artery, and (3) right subclavian artery. The aortic arch then passed posterior to the esophagus and exhibited a small anterior saccule measuring 1.3 cm, consistent with a Kommerell diverticulum. This configuration formed a vascular ring around the tracheo-esophageal pair, bounded posterolaterally on the right by the aortic arch, posterolaterally on the left by the Kommerell diverticulum, laterally on the left by the arteriosum ligamentum (or arterial ligament), and anteriorly by the left brachiocephalic artery. Gastroscopy confirmed endoluminal impact of extrinsic compression. Given minimal clinical repercussions and absence of nutritional disorders, no surgical cure was performed. The evolution was favorable with patient-reported spontaneous amelioration of symptoms.\n\nContext: Right aortic arch with mirror-image branching is a rare anomaly of embryologic development. The vast majority of patients are asymptomatic unless mediastinal structures are compressed. Indications for surgery include major compression of the esophagus or trachea, aneurysmal disease, thoracic aortic dissection, or a Kommerell diverticulum larger than 2 cm. There is no standardized treatment; management is individualized according to clinical presentation and anatomic configuration.", + "wiki_anchor": "Unlike other platanistoids, Arktocara had a sagittal crest, and its frontal sinuses were positioned behind the nasals. The nostrils were oriented vertically, and the premaxilla formed a rectangular plateau surrounding them. The nostrils were perhaps . The lacrimal bone in the eye socket wrapped around the outer edge of the brow ridge and was fused to the cheek bones. It further differed from other platanistoids in that it had a smaller process of the squamosal, that is, a projection from its skull. The frontonasal suture between the eyes on the brow ridge, which separates the frontal bone from the nasal bone, was U-shaped. The sutures indicate that the specimen was an adult. It lacked on the upper side of its head a condyloid fossa, a depression between the head and the neck; and had a symmetrical vertex, the upper part of the head. Also contrary to other platanistoids, Arktocara lacked the thin plate which extended from the hard palate in the roof of the mouth and attached to the greater wing of sphenoid bone in the ear. It lacked a maxillary crest, a bony projection from the maxillary and palatine bones in the roof of the mouth that runs along the nasal septum which separates the two nostrils. It did not have a large tympanosquamosal recess, which in cetaceans receives an air-filled sinus originating from the middle ear. The groove for the mandibular branch nerve wrapped around the sides of the pterygoid fossa, which is located behind the eyes laterally on the sphenoid bone.", + "doc_fkgl": 16.455087719298245, + "wiki_fkgl": 10.029337944664032, + "doc_tree_depth": 7.0, + "wiki_tree_depth": 7.583333333333333, + "fkgl_delta": 6.4257497746342125 + }, + { + "index": 15, + "label": "low_health_literacy", + "original_doc": "This story is about a 62-year-old white North African woman. She was diagnosed in 2021 with a rare condition called Von Hippel\u2013Lindau disease. This condition caused growths in several parts of her body. She had a tumor in a bone near her left ear. She had a tumor in the left adrenal gland, which sits above the kidney. She had cancer in her left kidney. Her right kidney had many cysts. She also had growths in her pancreas. She received several treatments. She had radiation treatment. She had surgery to remove the left adrenal gland. She had surgery to remove the left kidney. She had major surgery on the pancreas and nearby small intestine. Later, ultrasound and MRI scans showed a lump with both fluid and solid parts near the left ovary and tube. Keyhole surgery looked inside the pelvis. It found cyst-type tumors in the thin support tissue next to both fallopian tubes. Doctors then removed the uterus and both ovaries and tubes. The lab checked the tissue. It showed tumors of the same type on both sides in the thin support tissue around the tubes and the uterus. These findings fit with Von Hippel\u2013Lindau disease.", + "wiki_anchor": "Marie's cancer diagnosis and death\nIn 1994 Keating experienced breast pain and her doctor diagnosed her with mastitis, providing her with a prescription for antibiotics and telling her to come back if the pain persisted. As she was afraid of hospitals, she did not return for follow-up care even though she was in pain. She discovered a breast lump, and her doctor immediately sent her to Beaumont Hospital in the north of Dublin city for a biopsy where she was told that it was cancer even before tests were run. Over a year and a half later, on , Marie was diagnosed with Paget's disease of the breast which developed into breast cancer as it was not detected early enough. Although this was a shock to both her and her family, she underwent a full mastectomy the following month and began chemotherapy treatment. A year later, in September 1997, she was told that the cancer had gone but, because she rarely did her exercises, she developed lymphedema in her legs, and in the following month, she began to experience back pain and returned to hospital. An MRI scan revealed that she had cancer along her spinal cord so she began radiotherapy which she had completed in January 1998. On , Marie Keating died from breast cancer which had spread to various parts of her body, aged 51.", + "doc_fkgl": 5.262667512690356, + "wiki_fkgl": 13.524527777777777, + "doc_tree_depth": 5.15, + "wiki_tree_depth": 7.25, + "fkgl_delta": -8.26186026508742 + }, + { + "index": 15, + "label": "intermediate_health_literacy", + "original_doc": "A 62-year-old white North African woman with Von Hippel\u2013Lindau (VHL) disease diagnosed in 2021 developed several VHL-related tumors: a left petrous bone tumor, a left pheochromocytoma, left renal cell carcinoma, a multicystic right kidney, and pancreatic masses. She was treated with radiotherapy to the petrous bone lesion, left adrenalectomy, left nephrectomy, and cephalic duodenopancreatectomy for the pancreatic tumors. During surveillance, ultrasound and MRI showed a solid\u2013cystic mass in the left adnexal (ovary/tube) region. Laparoscopy then identified cystic tumors in the mesosalpinx on both the right and left sides. She underwent hysterectomy with removal of both adnexa. Pathology confirmed bilateral clear-cell papillary cystadenomas of the mesosalpinx and broad ligament, a pattern consistent with VHL.", + "wiki_anchor": "The term Vaginitis emphysematosa is related to Women's Reproductive Health and coined by Zweifel in 1877. The cases of Vaginitis emphysematosa are rare. The most important thing is that women never consult with the doctors for particularly Vaginitis emphysematosa but when they visit a doctor for some other reproductive health issue, they diagnose with the Vaginitis emphysematosa fortunately. Vaginitis emphysematosa is not common and Gynaecologists rarely know about it. Basically, this is characterised by gas-filled cysts in the mucosa of the vagina. Vaginitis emphysematosa is usually a self limited cystic disorder of the vagina. It is a very rare condition and has not much specific features to arouse clinical suspicion.", + "doc_fkgl": 13.893053097345135, + "wiki_fkgl": 12.100389610389616, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 6.142857142857143, + "fkgl_delta": 1.7926634869555187 + }, + { + "index": 15, + "label": "proficient_health_literacy", + "original_doc": "A 62-year-old Tunisian Arab postmenopausal woman with Von Hippel\u2013Lindau (VHL) disease (diagnosed 2021) had multisystem involvement. In 2021 she had a 6 cm left petrous bone endolymphatic sac tumor managed with radiotherapy; a 6 cm left pheochromocytoma treated with left adrenalectomy (pathology: pheochromocytoma); and a ruptured left renal mass treated with left nephrectomy (microscopy: multifocal clear-cell renal cell carcinoma, nuclear grade 2). In 2022 she underwent cephalic duodenopancreatectomy for a pancreatic mass; histology showed three serous cystadenomas and two well-differentiated neuroendocrine tumors. In January 2021, surveillance abdominal\u2013pelvic CT incidentally identified a 4 cm solid\u2013cystic left adnexal mass suspected to be malignant; this was confirmed on transvaginal ultrasound and pelvic MRI and classified O-RADS 5. Gynecologic exam was unremarkable. At laparotomy via a midline infraumbilical incision, a well-defined solid\u2013cystic mass was found in the left adnexa. There was no ascites, no peritoneal carcinomatosis, and the right adnexa appeared grossly normal without exocystic vegetations. Peritoneal cytology was obtained. Left adnexectomy was performed and the specimen sent for frozen section, which was inconclusive, raising the differential of a borderline tumor versus a VHL-associated tumor. Given her postmenopausal status, total hysterectomy with right adnexectomy was completed. Final histology demonstrated bilateral clear-cell papillary cystadenomas of the Fallopian tubes and broad ligament, measuring 0.5 cm on the right and 4 cm on the left. The tumors were composed of tightly packed papillae with fibrous cores lined by monolayered epithelium, consistent with VHL-associated mesosalpinx/broad ligament lesions. The postoperative course was uneventful; 1-month postoperative evaluation was normal. She has been followed every 4 months with normal pelvic ultrasound for 2 years, and was recently readmitted to neurosurgery for recurrence of a brain tumor.", + "wiki_anchor": "{| class=\"wikitable sortable\"\n|+\n!Vaginal tumors\n!Benign \n!Synonyms and notes\n!References\n|-\n|Yolk sac tumor\n|no\n|Endodermal sinus tumor\n|\n|-\n|Peripheral primitive neuroectodermal tumor\n|no\n|Ewing's sarcoma \n|\n|-\n|Vaginal melanoma\n|no\n|Melanocytic tumor\n|\n|-\n|Blue nevus\n|yes\n|Melanocytic tumor, blue mole, nevus bleu, \nmelancytic nevus\n|\n|-\n|Carcinosarcoma\n|no\n|Malignant Mullerian Mixed tumors;\nmetaplastic carcinoma\n|\n|-\n|Sarcoma botryoides\n|no\n|botryoid sarcoma, botryoid rhabdomyosarcoma; \nsubtype of embryonal rhabdomyosarcoma\n|\n|-\n|Leimyosarcoma\n|no\n|localized tumor of leukemic cells\n|\n|-\n|Endometrioid stromal sarcoma\n|no\n|endometrial stromal sarcoma\n|\n|-\n|Undifferentiated vaginal sarcoma\n|\n|\n|\n|-\n|Leiomyoma\n|yes\n|fibromyoma\n|\n|-\n|Genital rhabdomyoma\n|\n|\n|\n|-\n|Deep angiomyoxoma\n|\n|\n|\n|-\n|Spindle cell nodule\n|\n|Vaginal Solitary Fibrous Tumor\n|\n|-\n|Undifferentiated carcinoma\n|\n|\n|\n|-\n|Small cell carcinoma\n|no\n|\n|\n|-\n|Carcinoid\n|no\n|\n|\n|-\n|Adenoid basal carcinoma\n|\n|\n|\n|-\n|Adenosquamous carcinoma\n|no\n|\n|\n|-\n|Adenoma\n|yes\n|\n|\n|-\n|Mucinous adenocarcinoma\n|\n|\n|\n|-\n|Squamous papilloma \n|yes\n|vaginal micropapillomatosis\n|\n|-\n|Endometrioid adenocarcinoma\n|no\n|\n|\n|-\n|Mesonephric adenocarcinoma\n|\n|\n|\n|-\n|Clear cell adenocarcinoma\n|no\n|\n|\n|-\n|Fibroepithelial polyp\n|yes\n|\n|\n|-\n|Squamous intraepithelial neoplasia\n|\n|\n|\n|-\n|Genital wart\n|yes\n|Condylomata acuminata\n|\n|-\n|Squamous cell carcinoma\n|no\n|Keratinizing, Nonkeratininzing, Basalaoid,\nVerrucous, Warty\n|\n|-\n|Mesenchymal tumors\n|\n|\n|\n|-\n|Alveolar soft part sarcoma\n|\n|\n|\n|-\n|Mixed epithelial and mesenchymal Tumors\n|\n|\n|\n|-\n|Malignant mixed Tumors resembling synovial sarcoma\n|\n|\n|\n|-\n|Benign mixed tumors\n|\n|\n|\n|-\n|Adenomatoid Tumor\n|yes\n|\n|\n|-\n|Malignant lymphoma\n|no\n|\n|\n|-\n|Granulocytic sarcoma\n|\n|\n|\n|-\n|Fibroepithelial polyp\n|yes\n|\n|\n|-\n|Verrucous carcinoma\n|no\n|\n|\n|-\n|Squamotransitional cell carcinoma\n|\n|\n|\n|}", + "doc_fkgl": 15.117090909090908, + "wiki_fkgl": 48.68629213483146, + "doc_tree_depth": 6.071428571428571, + "wiki_tree_depth": 4.0, + "fkgl_delta": -33.56920122574056 + }, + { + "index": 16, + "label": "low_health_literacy", + "original_doc": "A 59-year-old man with type 1 diabetes came to the hospital with heart failure. A heart ultrasound showed big clumps of germs stuck to two heart valves, the mitral and the aortic valves. His blood test grew a germ called Staphylococcus warneri. This is a kind of staph that usually lives on the skin and is normally harmless. Doctors found he had an infection on his own heart valves (native valve endocarditis). He later had surgery to replace both the mitral and the aortic valves. Looking back, small lab changes and weight loss that began about four months earlier may have been early warning signs. He had not been on immune-weakening medicines and did not have any implanted medical devices.", + "wiki_anchor": "Accompanying diseases \nIn spite of being generally considered a benign expression of eosinophilia, isolated cases of family members with familial eosinophilia have been afflicted with tissue dysfunctions that are often associated with more pathological forms of eosinophilia. These dysfunctions include fatal endomyocardial fibrosis, valvular heart disease, and diminished motor and/or sensory function in skin areas served by peripheral nerves. Three patients with heart tissue for pathology examination had eosinophilic infiltration or fibrosis in their heart's endomyocardium. One patient who died suddenly had autopsy findings of eosinophilic infiltration not only in the heart but also in lungs, gastrointestinal tract, and meninges. It is unclear whether these tissue damages were due to primary eosinophil infiltrations or eosinophil infiltrations secondary to other causes.", + "doc_fkgl": 7.468333333333334, + "wiki_fkgl": 16.878333333333334, + "doc_tree_depth": 6.125, + "wiki_tree_depth": 8.0, + "fkgl_delta": -9.41 + }, + { + "index": 16, + "label": "intermediate_health_literacy", + "original_doc": "A 59-year-old man with long-standing type 1 diabetes presented with acute heart failure. An echocardiogram showed large vegetations on the mitral and aortic valves. Blood cultures were positive for Staphylococcus warneri, a coagulase\u2011negative staphylococcus commonly found on the skin. He was diagnosed with native valve endocarditis. After medical stabilization, he ultimately underwent replacement of both the mitral and aortic valves. In retrospect, mild laboratory abnormalities and several months of weight loss beginning about four months earlier were likely early signs of endocarditis. He had no history of immunosuppressive therapy and no implanted medical devices.", + "wiki_anchor": "Malcolm Winkler is an American biologist currently at Indiana University, Bloomington and an Elected Fellow of the American Association for the Advancement of Science. His work has been important on Streptococcus pneumoniae in studying cell structure, metabolism, pathogenesis and stress responses mediated by regulatory mechanisms, signal transduction and supramolecular complexes. His research has been driven by advanced molecular genetics, cell biology, physiology, tissue culture and biochemistry, leading his papers to be highly cited in consecutive years with highs of 719, 369 and 292.", + "doc_fkgl": 12.996079027355623, + "wiki_fkgl": 20.79036144578313, + "doc_tree_depth": 5.714285714285714, + "wiki_tree_depth": 10.666666666666666, + "fkgl_delta": -7.794282418427507 + }, + { + "index": 16, + "label": "proficient_health_literacy", + "original_doc": "A 59-year-old Japanese man with a 28-year history of type 1 diabetes on intensive multiple-dose insulin therapy (BMI 18.4 kg/m2, undetectable C\u2011peptide, HbA1c ~9.0%) and remote, asymptomatic chronic severe (grade III) aortic regurgitation (diagnosed 16 years earlier without subsequent follow\u2011up) presented with acute decompensated heart failure. He had never undergone surgery or prosthetic device implantation and had no history of immunosuppressive therapies.\n\nEight days after a routine visit, he developed dyspnea and fever >38\u2103. On arrival: BP 192/82 mmHg, HR 118/min, orthopnea, SpO2 80%. Exam: Levine 3/6 systolic murmur; no Osler nodes, Janeway lesions, or conjunctival petechiae. Labs: WBC 20,800/\u03bcL, CRP 6.06 mg/dL, CK\u2011MB 6.0 IU/L, troponin T negative. CXR showed pulmonary congestion with cardiomegaly (CTR 55%). ECG had ST elevation in V1\u2013V4, but emergent echocardiography showed no systolic dysfunction. He was diagnosed with acute heart failure due to valvular disease and treated with non\u2011invasive positive pressure ventilation and nitrates.\n\nTransthoracic echocardiography demonstrated severe aortic regurgitation and severe mitral regurgitation with a mobile mitral vegetation. Transesophageal echocardiography identified a 16.5\u00d76\u2011mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2\u00d75\u2011mm nonmobile vegetation on the noncoronary cusp of the aortic valve, raising strong suspicion for native valve endocarditis (NVE). Head CT and MRI showed no cerebral infarction or hemorrhage.\n\nRetrospective review revealed subtle abnormalities starting four months pre\u2011admission: mildly elevated WBC, albumin decreased to 3.0 g/dL the following month, and gradual hemoglobin decline over two months, with a 4\u2011kg weight loss. EGD and whole\u2011body CT were unrevealing. He partially regained weight and labs nearly normalized except for a CRP of 0.54 mg/dL. At the last pre\u2011admission visit (8 days prior), WBC was 9,300/\u03bcL, Hb 13.1 g/dL, Alb 3.0 g/dL, CRP 4.18 mg/dL, and diastolic BP had fallen; he remained afebrile and asymptomatic aside from weight loss.\n\nEmpiric antibiotics were initiated with ampicillin\u2013sulbactam 12 g/day plus gentamicin 120 mg/day. Three admission blood culture sets all grew Staphylococcus warneri, a coagulase\u2011negative staphylococcus (CoNS) and resident skin flora (MICs: ABPC/S \u22648 \u03bcg/mL; GM \u22641 \u03bcg/mL; CEZ \u22642 \u03bcg/mL), confirming S. warneri IE. Per Japanese Circulation Society guidance, emergency surgery is generally recommended for NYHA III\u2013IV heart failure or urgent surgery for NVE with mobile vegetation >10 mm and severe valve dysfunction. Because heart failure improved rapidly and appropriate antibiotics were started (reducing embolic risk), and given poorly controlled type 1 diabetes increasing operative risk, elective surgery was planned after stabilization of infection and glycemia. Antibiotics were narrowed to cefazolin 6 g/day; dental evaluation showed no periodontitis.\n\nAfter four weeks of antibiotics, surgery revealed a bicuspid aortic valve with intact aortic and mitral annuli and no abscess. Large vegetations were exenterated, and both valves were replaced with mechanical prostheses. The postoperative course was uneventful; he was discharged on postoperative day 22 without apparent embolism and has remained recurrence\u2011free for over two years. This case represents NVE due to the resident CoNS S. warneri in a patient without prosthetic material or immunosuppression, with prodromal laboratory abnormalities and weight loss evident up to four months before presentation.", + "wiki_anchor": "Vigersky RA, McMahon C. The Relationship of Hemoglobin A1C to Time-in-Range in Patients with Diabetes.Diabetes Technol Ther. 2019 Feb;21(2):81-85.\n Vigersky RA, Shin J, Jiang B, Siegmund T, McMahon C, Thomas A. The Comprehensive Glucose Pentagon: A Glucose-Centric Composite Metric for Assessing Glycemic Control in Persons with Diabetes, J. Diab Sci. Tech., 2018 Jan;12(1):114-123.\n Vigersky R, Shrivastav M. Role of continuous glucose monitoring for type 2 in diabetes management and research. J. Diabetes Complicat.2017 Jan;31(1):280-287.\n Powers AC, Wexler JA, Lash RW, Dyer MC, Becker MN, Vigersky RA. . Affordable Care Act Implementation: Challenges and Opportunities to Impact Patients With Diabetes. J. Clin. Endocrinol. Metab. 2016-04-01\n Puckrein GA, Nunlee-Bland G, Zangeneh F, Davidson JA, Vigersky RA, Xu L, Parkin CG, Marrero DG; Diabetes Care. 2016-04-01. Impact of CMS Competitive Bidding Program on Medicare Beneficiary Safety and Access to Diabetes Testing Supplies: A Retrospective, Longitudinal Analysis.\n Fonda, S. J.,Graham, C.,Munakata, J.,Powers, J. M.,Price, D.,Vigersky, R. A.; J Diabetes Sci Technol. 2016 Feb 05. The Cost-Effectiveness of Real-Time Continuous Glucose Monitoring (RT-CGM) in Type 2 Diabetes.\n Development of the Diabetes Technology Society Blood Glucose Monitor System Surveillance Protocol. Klonoff, D. C.,Lias, C.,Beck, S.,Parkes, J. L.,Kovatchev, B.,Vigersky, R. A.,Arreaza-Rubin, G.,Burk, R. D.,Kowalski, A.,Little, R.,Nichols, J.,Petersen, M.,Rawlings, K...; J Diabetes Sci Technol. 2015 Oct 21.\n Effects of \u03b1-Blocker Therapy on Active Duty Military and Military Retirees for Benign Prostatic Hypertrophy on Diabetic Complications. Graybill, S. D.,Vigersky, R. A.; Mil Med. 2015 Mar 04.\n The benefits, limitations, and cost-effectiveness of advanced technologies in the management of patients with diabetes mellitus. Vigersky RA; J Diabetes Sci Technol. 2015-03-01.\n Vigersky RA; J Diabetes Sci Technol. 2015-02-19. Escaping the Hemoglobin A1c-Centric World in Evaluating Diabetes Mellitus Interventions.\n Klonoff, D. C.,Vigersky, R. A.,Nichols, J. H.,Rice, M. J.; Mayo Clin. Proc.. 2014 Sep 10. Timely Hospital Glucose Measurement: Here Today, Gone Tomorrow?\n Vigersky RA, Fish L, Hogan P, Stewart A, Kutler S, Ladenson PW, McDermott M, Hupart KH; J. Clin. Endocrinol. Metab.. 2014-09-01. The clinical endocrinology workforce: current status and future projections of supply and demand.\n Klonoff, D. C.,Lias, C.,Vigersky, R.,Clarke, W.,Parkes, J. L.,Sacks, D. B.,Kirkman, M. S.,Kovatchev, B.; J Diabetes Sci Technol. 2015 Jan 07. The surveillance error grid.\n Salkind, S. J.,Huizenga, R.,Fonda, S. J.,Walker, M. S.,Vigersky, R. A.; J Diabetes Sci Technol. 2014 May 31. Glycemic Variability in Nondiabetic Morbidly Obese Persons: Results of an Observational Study and Review of the Literature.\n Vigersky, R. A.; J. Clin. Endocrinol. Metab.. 2014 May 16. Mad about \"u\".\n Vigersky RA, Fitzner K, Levinson J for the Diabetes Working Group. . Barriers to Providing Optimal Guideline-Driven Care to Patients with Diabetes Mellitus in the United States. 2013;Diabetes Care 36:3843-3849\n Vigersky RA, Fonda SJ, Chellappa M, Walker MS, Ehrhardt N. 2012 Diabetes Care 353: 32\u201338, 2012. Short and Long-Term Effects of Real-Time Continuous Glucose Monitoring in Patients with Type 2 Diabetes Mellitus.\n Vigersky, RA, Loriaux DL., Howards SS, Hodgen GB, Lipsett MB, Chrambach AC. 1975 J Clin Invest 58: 1061\u20131068. Androgen Binding Proteins of Testis, Epididymis and Plasma in Man and Monkey.\n Vigersky RA, Andersen AE, Thompson RH, Loriaux DL. 1977 N Engl J Med 297:1141-1145. Hypothalamic Dysfunction in Secondary Amenorrhea Associated with Simple Weight Loss", + "doc_fkgl": 12.497337640821737, + "wiki_fkgl": 10.725073586684708, + "doc_tree_depth": 5.96, + "wiki_tree_depth": 4.767857142857143, + "fkgl_delta": 1.772264054137029 + }, + { + "index": 17, + "label": "low_health_literacy", + "original_doc": "A 27-year-old woman had many cancers in her large intestine and rectum. She also had an inherited condition that causes many polyps.\n\nShe had robot-assisted surgery to remove the entire colon and rectum. The team also removed lymph nodes from the whole area. They used a surgical robot called Hugo RAS.\n\nThe robot work had three steps.\n\nStep 1: Her head was tilted down. The team removed the right side of the colon with its nearby tissue, up to the bend near the liver.\n\nStep 2: They removed the left side of the colon with its nearby tissue. They also removed the rectum with the tissue around it. They took deeper lymph nodes.\n\nStep 3: Her body was kept flat. The team tied off the main blood vessels along the main artery that feeds the intestines.\n\nAfter the robot part was finished, they took the removed bowel out through the anus. Through a small cut at the belly button, they made a pouch from the small intestine. They connected this pouch to the anus.\n\nThe surgery took about 10 and a half hours. Blood loss was very small. Recovery after surgery went smoothly.", + "wiki_anchor": "Description \nThe Gross Clinic is painted in oil on canvas, and is 240 cm \u00d7 200 cm (8 ft \u00d7 6.5 ft). It portrays surgeon Dr. Samuel D. Gross, the first chief of surgery at Jefferson Medical College, performing surgery on a young man for osteomyelitis of the femur in the surgical amphitheater on the top floor of Jefferson's Ely Building in the company of multiple doctors and medical students. Chief of Clinic Dr. James M. Barton can be seen standing over the patient, probing the incision. Junior assistant Dr. Charles S. Briggs, seen below Gross, is holding the patient's legs while Dr. Daniel M. Appel, seen bottom right, uses a retractor to hold open the incision. The anesthetist, Dr. W. Joseph Hearn, sits at the head of the operating table, holding a chloroform soaked rag over the patient's face. The clinic's clerk, Dr. Franklin West, records the surgery at a desk behind Gross. Gross' son Dr. Samuel W. Gross and orderly Hughey O'Donnell can be seen standing in the hall leading out of the amphitheater. A woman, possibly the patient's mother, can be seen recoiling at the bottom right. A self-portrait of Eakins himself can be seen on the right side of the painting, in the front of the theater, taking notes.", + "doc_fkgl": 5.185050449959093, + "wiki_fkgl": 7.728480450236969, + "doc_tree_depth": 4.526315789473684, + "wiki_tree_depth": 6.8, + "fkgl_delta": -2.5434300002778762 + }, + { + "index": 17, + "label": "intermediate_health_literacy", + "original_doc": "A 27-year-old woman with familial adenomatous polyposis and multiple colorectal cancers underwent robot-assisted total proctocolectomy with complete lymph node dissection using the Hugo RAS system. The robotic work was organized into three steps: 1) in Trendelenburg position, ascending colon complete mesocolic excision up to the hepatic flexure; 2) descending colon complete mesocolic excision and total mesorectal excision with D3 lymph node dissection; and 3) in a flat position, central vessel ligation along the superior mesenteric artery. After undocking, the specimen was removed transanally. An ileal pouch was created through a small umbilical incision and then connected to the anus (ileal pouch\u2013anal anastomosis). The operation lasted 632 minutes with minimal blood loss, and the postoperative course was uneventful.", + "wiki_anchor": "In 2008, Bergamaschi accepted a position as tenured professor and chief of the Division of Colorectal Surgery at State University of New York in Stony Brook, NY. Dr. Bergamaschi served as Chairman of the Education and Training Committee for the European Association for Endoscopic Surgery (EAES) from 2012 through 2015.\n Currently, Bergamaschi is editor of the Colorectal Disease journal and past president of the New York Society of Colon & Rectal Surgeons, where he was elected in 2016. In 2017 Dr Bergamaschi accepted a position as Chief of Colorectal Surgery at Westchester Medical Center and tenured professor of surgery at New York Medical College. In 2023 Dr Bergamaschi accepted a position as Chief of Surgical Oncology and Colorectal Surgery at Jacobi Medical Center, New York City Health Hospitals.", + "doc_fkgl": 16.9342905982906, + "wiki_fkgl": 16.429385826771654, + "doc_tree_depth": 5.8, + "wiki_tree_depth": 8.4, + "fkgl_delta": 0.5049047715189445 + }, + { + "index": 17, + "label": "proficient_health_literacy", + "original_doc": "A 27-year-old woman with multiple colorectal cancers on a background of familial adenomatous polyposis (FAP) underwent robot-assisted total proctocolectomy (TPC) with lymph node dissection of the entire colorectal region using the Hugo RAS system. Preoperative CT showed multiple nodal swellings along the inferior mesenteric artery (IMA) and middle colic artery without distant metastases. After multidisciplinary review, robot-assisted TPC was performed under approvals from the Evaluating Committee for Highly Difficult New Medical Technologies (H-0051) and the Kyoto University IRB.\n\nUnder general anesthesia in lithotomy with arms tucked, a 5-cm vertical umbilical incision was made and a wound protector placed. After pneumoperitoneum, 4 robotic and 2 assistant trocars were inserted. Instruments included a camera, monopolar curved shears (right hand), bipolar fenestrated forceps (left hand), and Cadiere/double-fenestrated forceps (reserve arm). Two table positions (Trendelenburg and flat) were used with specific docking tilts; arm cart angles were unchanged. The robotic procedure comprised three steps, followed by transanal specimen extraction, ileal pouch construction via a small umbilical laparotomy, and ileal pouch\u2013anal anastomosis (IPAA).\n\nStep 1: Ascending colon complete mesocolic excision (CME) from a caudal approach, completed through hepatic flexure mobilization.\n\nStep 2: Central vessel ligation (CVL) of the IMA, descending colon CME to completion of splenic flexure mobilization, and total mesorectal excision (TME) to full exposure of the intersphincteric space. This corresponds to a D3 lymph node dissection of the left colon/rectum.\n\nStep 3: After undocking and repositioning the patient flat, CVL along the superior mesenteric artery (SMA) was performed, ligating the ileocolic, right colic, and middle colic vessels; the inferior mesenteric vein (IMV) was ligated at its root (exposed in Step 2).\n\nTransanal and small laparotomy procedures: After transection of the terminal ileum, a transanal specimen extraction was performed with complete rectal mucosectomy from just below the dentate line due to multiple adenomas in the anal canal. An ileal pouch was constructed via the small umbilical incision, its reach to the anal canal confirmed, and a transanal hand-sewn IPAA was completed. No diverting ileostomy was created.\n\nAll three steps were completed without conversion. Following undocking after Step 3, laparoscopy confirmed hemostasis, specimen extraction, and anastomotic integrity. Total operative time was 632 minutes (Step 1: 36 min; Step 2: 160 min; Step 3: 188 min; positioning/docking/specimen extraction/anastomosis: 248 min). Estimated blood loss was 20 mL. Postoperatively, the course was uneventful: flatus and initiation of liquids on POD 1, advancement to a solid diet on POD 3, with a functional ileal pouch and satisfactory anal function.\n\nFinal pathology identified two sigmoid cancers (S1: Type 0-Ip, 55 \u00d7 50 mm, tub1, T1b, ly0, v0; S2: Type 0-Isp, 55 \u00d7 50 mm, tub1, Tis, ly0, v0) and one rectal cancer (R1: Type 0-Ip, 40 \u00d7 35 mm, tub1, Tis, ly0, v0). Lymph node status: 18/89 positive, all in sigmoid/rectosigmoid stations (#241, #242, #251), yielding UICC pT1bN2b stage.", + "wiki_anchor": "Journals \nThe company currently publishes over 60 medical journals:\n AME Case Reports\n AME Medical Journal\n AME Surgical Journal\n Annals of Blood\n Annals of Breast Surgery\n Annals of Cancer Epidemiology\n Annals of Cardiothoracic Surgery\n Annals of Esophagus\n Annals of Eye Science\n Annals of Infection\n Annals of Joint\n Annals of Laparoscopic and Endoscopic Surgery\n Annals of Lymphoma\n Annals of Nasopharynx Cancer\n Annals of Palliative Medicine\n Annals of Pancreatic Cancer\n Annals of Research Hospitals\n Annals of Thyroid\n Annals of Translational Medicine\n Art of Surgery\n Australian Journal of Otolaryngology\n Biotarget\n Bone & Joint Investigation\n Cardiovascular Diagnosis and Therapy\n Chinese Clinical Oncology\n Current Challenges in Thoracic Surgery\n Digestive Medicine Research\n ExRNA\n Frontiers of Oral and Maxillofacial Medicine\n Gastrointestinal Stromal Tumor\n Gland Surgery\n Gynecology and Pelvic Medicine\n Health Technology\n Hepatobiliary Surgery and Nutrition\n Journal of Emergency and Critical Care Medicine\n Journal of Gastrointestinal Oncology\n Journal of Hospital Management and Health Policy\n Journal of Laboratory and Precision Medicine\n Journal of Medical Artificial Intelligence\n Journal of Public Health and Emergency\n Journal of Spine Surgery\n Journal of Thoracic Disease\n Journal of Visualized Surgery\n Journal of Xiangya Medicine\n Laparoscopic Surgery\n Longhua Chinese Medicine\n Mediastinum\n Mesentery and Peritoneum\n mHealth\n Microphysiological Systems\n Non-coding RNA Investigation\n Pediatric Medicine\n Pharmacogenomics Research and Personalized Medicine\n Precision Cancer Medicine\n Quantitative Imaging in Medicine and Surgery\n Shanghai Chest\n Stem Cell Investigation\n Therapeutic Radiology and Oncology\n Translational Andrology and Urology\n Translational Breast Cancer Research\n Translational Cancer Research\n Translational Gastroenterology and Hepatology\n Translational Lung Cancer Research\n Translational Pediatrics\n Video-Assisted Thoracic Surgery\n \u4e34\u5e8a\u4e0e\u75c5\u7406\u6742\u5fd7\n \u773c\u79d1\u5b66\u62a5", + "doc_fkgl": 14.549020678891925, + "wiki_fkgl": 107.68452674897121, + "doc_tree_depth": 6.681818181818182, + "wiki_tree_depth": 28.5, + "fkgl_delta": -93.13550607007929 + }, + { + "index": 18, + "label": "low_health_literacy", + "original_doc": "A 65-year-old man had a swollen right middle finger after a motorcycle crash 6 months earlier. The middle joint stayed bent, and the fingertip bent backward. He could not fully straighten the finger. An X-ray showed no broken bones. The problem was in the soft tissues and tendon on top of the finger. Before surgery, the middle joint could bend from 45 to 110 degrees but could not straighten. The doctors repaired the top tendon using a small strip from another tendon in the same finger. They put the middle joint in a straight splint for 2 weeks. After 2 weeks, he started gentle bending and straightening exercises for that joint. One month after surgery, the middle joint moved from 0 to 90 degrees. Two months after surgery, movement went back to normal. His hand function score (DASH) improved from 50 to 4.2.", + "wiki_anchor": "Andrew Julian Goldberg , professionally known as Andy Goldberg, is a British orthopaedic surgeon specialising in ankle disorders. He is an honorary consultant orthopaedic surgeon at the Royal National Orthopaedic Hospital in London and Stanmore. He serves as faculty at University College London dealing with ankle and foot surgery. Goldberg runs a research programme focusing on ankle arthritis, the subtalar joint and stem cells. He sits on the AOFAS editorial board for the SAGE Journal, Foot and Ankle Orthopaedics (FAO) as well as the Editorial Committee and Medical Advisory Committee of the National Joint Registry for England & Wales. He has published more than 70 publications and authored the textbooks Surgical Talk, and Surgery: Problems and Solutions, distributed by World Scientific Publishing and is the editor of The Atlas of Ankle Replacements. He consults a startup dealing with improving high heeled shoes.", + "doc_fkgl": 5.560996503496504, + "wiki_fkgl": 13.618571428571432, + "doc_tree_depth": 4.916666666666667, + "wiki_tree_depth": 7.714285714285714, + "fkgl_delta": -8.057574925074928 + }, + { + "index": 18, + "label": "intermediate_health_literacy", + "original_doc": "A 65-year-old man developed persistent swelling and a boutonniere deformity of the right middle finger after a motorcycle fall six months earlier. He could not fully extend the finger. On exam, the finger showed edema with flexion at the proximal interphalangeal (PIP) joint and hyperextension at the distal interphalangeal (DIP) joint. Active PIP range of motion (ROM) was 45\u2013110 degrees. X\u2011rays of the right hand (AP/oblique) showed no bone injury, indicating a soft-tissue problem consistent with a central slip injury. The patient underwent reconstruction of the central slip using a partial ulnar slip of the flexor digitorum superficialis (FDS) tendon. A PIP extension splint was used for 2 weeks. Active and passive PIP ROM exercises began after 2 weeks. One month after surgery, PIP ROM improved to 0\u201390 degrees, and by 2 months it returned to normal. Hand function, measured by the DASH score, improved markedly from 50 to 4.2.", + "wiki_anchor": "In medicine, obligatory synergies occur when spasticity appears, such as following a stroke. It manifests in abnormal and stereotypical patterns across multiple joints called obligatory synergies. They are described as either a flexion synergy or an extension synergy and affect both the upper and lower extremity (see below). When these patterns occur in a patient, he or she is unable to move a limb segment in isolation of the pattern. This interferes with normal activities of daily living. Some aspects of the obligatory synergy patterns however, can be cleverly used to increase function relative to the movement available to the individual. Careful thought should, therefore, be considered in deciding which muscle groups to stretch at specific times during recovery. Obligatory synergy patterns are observed when a patient tries to make a minimal voluntary movement, or as a result of stimulated reflexes.", + "doc_fkgl": 9.454666666666668, + "wiki_fkgl": 13.544742907801421, + "doc_tree_depth": 5.454545454545454, + "wiki_tree_depth": 6.875, + "fkgl_delta": -4.090076241134753 + }, + { + "index": 18, + "label": "proficient_health_literacy", + "original_doc": "A 65-year-old male presented with six months of swelling and boutonniere deformity of the right digit III following a motorcycle accident on January 1, 2023. He initially self-managed with analgesics and did not seek care. He reported inability to fully extend the right middle finger. Examination demonstrated edema and a boutonniere posture (PIP flexion, DIP hyperextension). Active PIP ROM was 45\u2013110 degrees, with passive PIP ROM within normal limits. Radiographs of the right hand (AP/lateral) revealed no osseous pathology, supporting a soft-tissue etiology consistent with a central slip injury. \n\nSurgical technique: Central slip defect reconstruction was performed using the partial ulnar slip of the flexor digitorum superficialis (FDS) tendon. Under anesthesia and tourniquet control in the supine position, a midlateral incision was made on the ulnar aspect of the middle phalanx centered at the PIP joint with dorsal oblique extension, and a transverse incision was made over the MCP flexion crease proximal to the A1 pulley. The ulnar digital neurovascular bundle was identified and protected. Full-thickness dorsal flaps were elevated to expose the central slip and extensor mechanism to the PIPJ. Scar and pseudotendinous tissue were excised. The central slip was not amenable to primary repair; therefore, the ulnar slip of the FDS was selected for reconstruction. The ulnar neurovascular bundle was mobilized to visualize the periosteal insertion of the A3 pulley. The extensor tendon was mobilized and tenolyzed; the dorsal PIP capsule was incised with removal of interposed tissue. The A3 pulley periosteal insertion and the volar capsule of the PIP joint were incised longitudinally. A 2\u20130 non-absorbable monofilament suture was placed around the ulnar FDS slip at the PIP level. Through the proximal incision, the flexor sheath and A1 pulley were incised longitudinally to expose the FDS; the ulnar slip was isolated and transected, preserving the radial slip. The previously placed 2\u20130 suture facilitated delivery of the distally based ulnar FDS slip distally. A 2.8\u2011mm dorsal-to-volar bone tunnel was drilled at the base of the middle phalanx; an elevator protected the FDP, volar plate, and volar structures. With the PIP reduced in full extension, the FDS slip was passed through the tunnel and routed through the intact proximal segment of the central slip/extensor tendon. A tendon weaver completed a Pulvertaft weave under appropriate tension with the PIP in full extension and reduction, secured with 3\u20130 non-absorbable suture. The capsule and central slip reconstruction margins were approximated; adhesions were released and lateral bands mobilized. Tenodesis effect, posture, stability, and motion were assessed. Wounds were irrigated, the tourniquet deflated, hemostasis obtained, and capillary refill confirmed. Skin was closed with horizontal mattress sutures. A sterile dressing and a well-padded PIP extension splint were applied to allow early DIP and MCP motion.\n\nPostoperative course: First wound check at postoperative day 4; the patient received meloxicam 7.5 mg PO BID and doxycycline 100 mg PO BID for 3 days. A second wound visit occurred 3 days later. At 2 weeks, the back slab and external sutures were removed, and active and passive PIP ROM exercises were initiated. By 3 weeks, the wound had healed and PIP ROM was 0\u201390 degrees. At 1 month, PIP ROM improved to 0\u2013100 degrees, with continued functional gains. After 7 weeks of rehabilitation, he returned to work with PIP ROM 0\u2013110 degrees. Overall function improved substantially, with the DASH score decreasing from 50 to 4.2.\n\nInterpretation: Clinical and radiographic findings were concordant with a chronic central slip injury producing boutonniere deformity (PIP flexion, DIP hyperextension due to dorsal apparatus disruption and volar migration of lateral bands). Reconstruction using an ulnar FDS slip via bone tunnel and Pulvertaft weave restored PIP extension and yielded progressive ROM gains and marked functional recovery.", + "wiki_anchor": "Zhongjianosaurus is distinguishable from other microraptorines in the following autapomorphies. Proportionally long ossified uncinate processes are fused to the dorsal ribs. A widely arched furcula is present with slender and posteriorly curved clavicular rami. The humeral proximal end is strongly offset medially from the humeral shaft. The internal tuberosity of the humeral proximal end is short. A large fenestra perforates the humeral deltopectoral crest. The humeral ulnar condyle is hypertrophied. The ulna is slightly longer than the humerus. The ulnar olecranon process has a mediolaterally pinched posterior margin. The ulnar distal end bends anteriorly and is strongly expanded laterally. The proximal end of metacarpal II has a strong ventrolateral extension. Metacarpal III is laterally bowed and adorned with a longitudinal ventral groove. Phalanx II-2 is without a proximodorsal lip and lacks strong dorsal arching. The femoral head is stout and lower than the trochanteric crest. The medial condyle of tibiotarsus distal end has a prominent distal extension. The foot shows the arctometatarsalian condition. Metatarsal II is without ginglymi on its distal end. The authors identify the fingers in the maniraptoran hand as the second, third and fourth, whereas most researchers see them as the first, second and third so that \"metacarpal II\" would become metacarpal I etc.", + "doc_fkgl": 11.863529411764706, + "wiki_fkgl": 10.271811594202902, + "doc_tree_depth": 5.75, + "wiki_tree_depth": 4.833333333333333, + "fkgl_delta": 1.591717817561804 + }, + { + "index": 19, + "label": "low_health_literacy", + "original_doc": "A 23-year-old man came to the emergency room with a sudden, very bad headache. He also felt sick, threw up, and felt heavy pressure in his chest. His blood pressure was high and he was breathing fast. A quick heart test looked like a major heart attack. He was rushed for a procedure to check and open the heart arteries. The heart arteries looked normal. A head CT scan then showed bleeding in the space around his brain. A team of specialists cared for him, but he got worse quickly. He went into cardiac arrest and died.", + "wiki_anchor": "Victims \nSeveral of the injured drove themselves to area hospitals, and some had sustained life-threatening injuries, according to police officials. Eight victims were taken to University of Cincinnati Medical Center, one of whom was in critical condition. Of the remaining, three were seriously injured, and four were stable. Two additional victims were taken to The Christ Hospital with minor injuries. Others were treated at Bethesda North Hospital, Mercy West Hospital and Anderson Mercy Hospital. Officers at the scene attempted to administer CPR to the person who died.", + "doc_fkgl": 4.0628178694158095, + "wiki_fkgl": 11.76614942528736, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 5.5, + "fkgl_delta": -7.70333155587155 + }, + { + "index": 19, + "label": "intermediate_health_literacy", + "original_doc": "A 23-year-old man came to the emergency department with a sudden severe headache, nausea, vomiting, and chest heaviness. His initial vital signs showed high blood pressure and a fast breathing rate. An emergency ECG showed a heart attack pattern (STEMI), so he was urgently sent for percutaneous coronary intervention; the angiogram revealed normal coronary arteries. Further evaluation with a brain CT identified a cisternal subarachnoid hemorrhage (bleeding around the brain). Despite coordinated care by multiple teams, his condition rapidly worsened, leading to cardiac arrest and death.", + "wiki_anchor": "Victims \nSeveral of the injured drove themselves to area hospitals, and some had sustained life-threatening injuries, according to police officials. Eight victims were taken to University of Cincinnati Medical Center, one of whom was in critical condition. Of the remaining, three were seriously injured, and four were stable. Two additional victims were taken to The Christ Hospital with minor injuries. Others were treated at Bethesda North Hospital, Mercy West Hospital and Anderson Mercy Hospital. Officers at the scene attempted to administer CPR to the person who died.", + "doc_fkgl": 13.757534883720933, + "wiki_fkgl": 11.76614942528736, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 5.5, + "fkgl_delta": 1.991385458433573 + }, + { + "index": 19, + "label": "proficient_health_literacy", + "original_doc": "A 23-year-old male with a 23 pack-year smoking history, no alcohol use, and no illicit drug use presented with 2 hours of sudden severe frontal headache, nausea, vomiting, and chest heaviness. He was distressed but alert and oriented. Vitals: BP 178/103 mmHg, RR 26/min, T 38.9\u00b0C, HR 87/min, SpO2 94%. Exam: normal vesicular breath sounds; cardiovascular and abdominal exams inconclusive; neurological exam notable for neck stiffness, dilated but light-reactive pupils, normal plantar reflexes, and no focal deficits. ECG showed ST-segment elevation >2 mm in V2\u2013V5, consistent with STEMI; he received a 300 mg aspirin load and was urgently transferred for PCI. Troponin was elevated at 1.48 mg/dl (normal <0.16 mg/dl). Femoral-access coronary angiography demonstrated normal coronary arteries with TIMI 3 flow. Post-angiography ECG showed normal sinus rhythm with LVH; echocardiography revealed normal ventricular function without RWMA. Subsequent workup found lymphocytosis and mildly elevated CRP. Non-contrast CT brain demonstrated a cisternal subarachnoid haemorrhage with extension anterior to the right temporal lobe. Abdominal ultrasound was negative for polycystic kidney disease; cerebral CT angiography was planned to exclude aneurysm. Nimodipine 60 mg q4h was initiated with a BP target of 160/100 mmHg. On day 2, he acutely deteriorated with cardiac arrest; after CPR, GCS was 6, and he was intubated and mechanically ventilated in the ICU. Owing to instability, repeat CT brain and planned cerebral CTA were not performed. He received multidisciplinary ICU care with NG feeding, IV fluids, antibiotics, a proton pump inhibitor, and nimodipine. On day 8, he developed ventricular fibrillation and, despite CPR and more than five defibrillation attempts, could not be resuscitated and died.", + "wiki_anchor": "Efficacy of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock have been studied and published first in 2001 Later, the group concluded the ischemic skin lesions (ISL) developed in patients with catecholamine-resistant vasodilatory shock have multi-factorial cause and shall not necessarily been seen a side effect of AVP solely. The presence of septic shock and a history of peripheral arterial occlusive disease are independent risk factors for the development of ISL. In the last decade, in early hyperdynamic septic shock, the administration of high-dose AVP as a single agent proved to fail to increase mean arterial pressure in the first hour but maintains it above 70mmHg in two-thirds of patients at 48h. AVP decreases NE exposure, has no effect on the PrCO(2) - PaCO(2 )difference, and improves renal function and SOFA score. This led to development of a large trial to see theeffect of arginin vasopressin as add-on to norepinephrine in septic shock. It could be shown, if giving vasopressin in early stage of septic shock (norepinephrin < 15 microgramm/min and lactate < 1.4\u00a0mmol/L) there is a statistically significant interaction between vasopressin and corticosteroids. The combination of low-dose vasopressin and corticosteroids was associated with decreased 28 and 90 days mortality and organ dysfunction compared with norepinephrine and corticosteroids.", + "doc_fkgl": 12.237704402515725, + "wiki_fkgl": 16.277884615384615, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 6.571428571428571, + "fkgl_delta": -4.04018021286889 + } +] \ No newline at end of file