diff --git "a/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_11_v1.json" "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_11_v1.json" new file mode 100644--- /dev/null +++ "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_11_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": "Nutrients to avoid in dialysis\nThere are some nutrients that are restricted in kidney failure patients because of the body's inability to excrete excessive amounts of them due to the kidneys not functioning properly. In general, these nutrients include:\nPotassium: The kidneys help to regulate potassium levels. When the kidneys are damaged, potassium levels can become elevated. Elevated potassium levels can cause the heart to beat irregularly or even stop.\nPhosphorus: The kidneys also help to regulate phosphorus levels in the body. When the kidneys are damaged, they aren't able to remove excessive phosphorus, causing it to build up in blood. Doctors may prescribe a phosphate binder that is taken with meals to help remove excess phosphorus\nSodium: In patients with kidney failure, sodium can cause excessive fluid retention, which can lead to elevated blood pressure, edema, heart failure, and shortness of breath.\nFluid: As kidney damage worsens so does the ability to excrete fluid. In kidney failure patients, excessive fluid intake can result in the same conditions that excessive sodium intake does.", + "doc_fkgl": 4.138157894736846, + "wiki_fkgl": 13.119383429672446, + "doc_tree_depth": 4.5, + "wiki_tree_depth": 5.454545454545454, + "fkgl_delta": -8.9812255349356 + }, + { + "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": "Publications\n International, multicentre, randomized, double blind study to compare the overall mortality in acutely ill medical patients treated with enoxaprin versus placebo in addition to graduated elastic stockings\n Assessment of Total thrombus load estimation in symptomatic patients with venous thromboembolism\n Takayasu's arteritis: An Indian Perspective\n Pulmonary embolism: A frequent Occurrence in Indian Patients with Symptomatic Lower Limb Venous Thrombosis\n Snapshots in Surgery : Pulsatile Scrotum\n Prevention and treatment of venous thromboembolism. International Consensus Statement (Guidelines according to scientific evidence).\n Cervical Asymmetry: Medical Images.\n Asymptomatic Coronary Artery disease in patients with symptomatic peripheral vascular disease - detected by dobutamine stress echo and coronary angiography.\n Studies on homocysteine demonstrating its significance as a possible tool for differential diagnosis in occlusive vascular disease\n Limb Salvage angioplasty in vascular surgery practice", + "doc_fkgl": 15.20401179941003, + "wiki_fkgl": 22.48, + "doc_tree_depth": 4.888888888888889, + "wiki_tree_depth": 9.0, + "fkgl_delta": -7.275988200589971 + }, + { + "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": "Agranulocytosis, a potentially fatal drop in white blood cell count, basically an exaggerated form of leukopaenia.\n Thrombocytopaenia. A drop in blood platelet counts which are involved in blood clotting. \n Thromboembolism (blood clots; including pulmonary embolism and deep vein thrombosis)\n Rhabdomyolysis (breakdown of muscle tissue leading to the release of myoglobin into the bloodstream which in turn damages the kidneys)\n Alkaline phosphatase increased (an abnormal laboratory parameter)\n Priapism (a painful and enduring erection)\n Urinary hesitation\n Pancreatitis, swelling of the pancreas which supplies the body with insulin. \n Neuroleptic malignant syndrome a potentially fatal complication of antipsychotic drug treatment. Presents with hyperthermia, tremor, tachycardia (high heart rate), mental status change (e.g. confusion), etc.\n Jaundice, which is basically when the body's ability to clear a by product (called bilirubin) of the breakdown of an essential component of the blood called haem, is impaired leading to yellow discolouration of the skin, eyes and mucous membranes. \n Diabetic coma\n Diabetic ketoacidosis. Type II diabetes mellitus is basically where the body cannot effectively utilise sugars to produce energy due to the fact that its cells have become unresponsive to the hormone, insulin, which allows cells to utilise sugars for energy. This in turn forces the body to burn fats for energy and fats require conversion to ketone bodies in order to be utilised by the cells of the body as an energy source. The ketone bodies are acidic hence when the body is entirely reliant on these ketone bodies for energy the levels in the blood reaches a point where it overwhelms the body's natural mechanisms to keep blood pH (a measure of acidity) within a safe range, leading to the blood becoming acidic which is potentially damaging to the tissues of the body due to the ability of acidic environments to denature the proteins of the body. \n Anaphylactic reaction a potentially life-threatening allergic reaction\n Sudden cardiac death", + "doc_fkgl": 17.108284910965327, + "wiki_fkgl": 16.983489736070386, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 8.5, + "fkgl_delta": 0.12479517489494185 + }, + { + "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": "Another of his patients, an adult female former prostitute and I.V. drug user, is informed by him that her child has the disease, indicating that its virus was passed to her child through her blood while she was pregnant, meaning that she became infected before she gave up drugs and prostitution. After her child dies of AIDS, she returns to her former lifestyle.", + "doc_fkgl": 3.5813553113553134, + "wiki_fkgl": 9.644444444444442, + "doc_tree_depth": 5.142857142857143, + "wiki_tree_depth": 5.5, + "fkgl_delta": -6.063089133089129 + }, + { + "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": "Congenital dermal sinus is an uncommon form of cranial or spinal dysraphism. It occurs in 1 in 2500 live births. It occurs as a dermal indentation, found along the midline of the neuraxis and often presents alongside infection and neurological deficit. Congenital dermal sinus form due to a focal failure of dysjunction between the cutaneous ectoderm and neuroectoderm during the third to eight week of gestation. Typically observed in the lumbar and lumbosacral region, congenital dermal sinus can occur from the nasion and occiput region down.", + "doc_fkgl": 11.942105263157895, + "wiki_fkgl": 11.97381395348837, + "doc_tree_depth": 6.4, + "wiki_tree_depth": 6.0, + "fkgl_delta": -0.03170869033047552 + }, + { + "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 \u201cThe Regio Parietalis (of Diencephalon) in Lower Craniates\u201d (1905), Sterzi demonstrates that there are organs which are single (epiphysis and paraphysis) and organs that are originally double (pineal and parapineal organs; Sterzi, 1905). The latter, however, in adult petromyzontes become both asymmetrical acquiring a median location below the cranial vault, which is fissured in their correspondence. They have the structure of a sort of eyes (parietal eyes).\n\u201cGeneral Neuroanatomy\u201d (1912\u20131914) is a series of articles on the development of the longitudinal cerebral fissure (Sterzi, 1912) and that on the significance of the human encephalon and telencephalon (Sterzi, 1914). Concerning the first topic, Sterzi demonstrates that, contrary to earlier reports, the longitudinal fissure is not due to pressure exerted by the falx cerebri but that it is the product of the rapid outgrowth of the cerebral hemispheres from the lateral portions of the telencephalic vesicle. He also maintains that the third ventricle consists, not only of the posterior diencephalic portion, but of a smaller anterior one of telencephalic origin. In the second article (Sterzi, 1914), Sterzi criticizes the concept put forward by Edinger(1911) that the human brain consists of a neoencephalic portion: the cerebral cortex, and of a paleoencephalic one: the remaining encephalon. He demonstrates that even in the portion that Edinger considers paleoencephalon there are neoencephalic derivatives. Concerning whether all portions of the brain really evolve from lower craniates to man, he demonstrates that this is not the case because, in the course of phylogenesis, some parts evolve and others regress.", + "doc_fkgl": 16.247417695473253, + "wiki_fkgl": 16.120476190476193, + "doc_tree_depth": 6.083333333333333, + "wiki_tree_depth": 8.222222222222221, + "fkgl_delta": 0.1269415049970597 + }, + { + "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": "Literature\nRonald D. Gerste [Article in German]: Normaldruckglaukom und vaskul\u00e4re Dysregulationen: Augenleiden mit Tinnitus und kalten Extremit\u00e4ten. Deutsches \u00c4rzteblatt 2014; 111:A 308.\nRonald D. Gerste [Article in German]: Wie ein kalter H\u00e4ndedruck Medizingeschichte schrieb. [How a cold handshake was making medical history]. Schweizer \u00c4rztezeitung 2018; 99:118-120.\nKunin A, Polivka J Jr, Moiseeva N et al.:\"Dry mouth\" and \"Flammer\" syndromes-neglected risks in adolescents and new concepts by predictive, preventive and personalised approach. EPMA Journal 2018, 2;9(3):307-317.\nKonieczka K, Erb C: Diseases potentially related to Flammer syndrome. EPMA J. 2017 Sep 13;8(4):327-332\nPeter Meyer [Article in German]: Geschichte der Universit\u00e4ts-Augenklinik Basel.[History of the University Eye Clinic Basel] In: 100 Jahre SOG und die Entwicklung der Schweizer Augenheilkunde. Le Centenaire de la SSO et le d\u00e9veloppement de l'Ophthalmologie en Suisse. Ed.by Ulrike Novotny and Albert Franceschetti, Horw (Switzerland) 2007.", + "doc_fkgl": 4.63312375249501, + "wiki_fkgl": 9.80298319327731, + "doc_tree_depth": 5.277777777777778, + "wiki_tree_depth": 4.333333333333333, + "fkgl_delta": -5.1698594407823 + }, + { + "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": "Literature\nRonald D. Gerste [Article in German]: Normaldruckglaukom und vaskul\u00e4re Dysregulationen: Augenleiden mit Tinnitus und kalten Extremit\u00e4ten. Deutsches \u00c4rzteblatt 2014; 111:A 308.\nRonald D. Gerste [Article in German]: Wie ein kalter H\u00e4ndedruck Medizingeschichte schrieb. [How a cold handshake was making medical history]. Schweizer \u00c4rztezeitung 2018; 99:118-120.\nKunin A, Polivka J Jr, Moiseeva N et al.:\"Dry mouth\" and \"Flammer\" syndromes-neglected risks in adolescents and new concepts by predictive, preventive and personalised approach. EPMA Journal 2018, 2;9(3):307-317.\nKonieczka K, Erb C: Diseases potentially related to Flammer syndrome. EPMA J. 2017 Sep 13;8(4):327-332\nPeter Meyer [Article in German]: Geschichte der Universit\u00e4ts-Augenklinik Basel.[History of the University Eye Clinic Basel] In: 100 Jahre SOG und die Entwicklung der Schweizer Augenheilkunde. Le Centenaire de la SSO et le d\u00e9veloppement de l'Ophthalmologie en Suisse. Ed.by Ulrike Novotny and Albert Franceschetti, Horw (Switzerland) 2007.", + "doc_fkgl": 10.328562500000004, + "wiki_fkgl": 9.80298319327731, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 4.333333333333333, + "fkgl_delta": 0.5255793067226939 + }, + { + "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": "The CAMBRA system was developed as an evidence-based approach to the prevention, reversal, and treatment of patients with dental caries. The emphasis is on the whole disease process and employs the caries balance method, taking account of all factors that contribute to the development of dental caries (attacking factors) and all factors that research has shown to be protective from dental caries (defense factors). The assessment of this balance not only helps establish risk but suggests the correct strategies to prevent or reverse the process.\nThe CAMBRA system provides a more in-depth assessment tool as a key element of the overall approach and takes account of:\nCaries disease indicators: Socio-economic status, developmental problems, and presence of lesions or restorations placed within the previous 3 years. \nCaries risk factors: Visible accumulations of plaque and quantitative assessment of Streptococcus mutans and Lactobacilli, frequent snacking, saliva flow and salivary modifying factors, fissure anatomy, root surface exposure, and the presence of appliances. \nCaries protective factors: Systemic and topical fluoride sources, adequate saliva flow, xylitol in the diet, use of calcium and phosphate paste or chlorhexidine. \nClinical examination: Presence of white spots, decalcifications, restorations, plaque deposits. \nThe tool assigns patients to low, moderate, high, or extreme risk and offers two formats, one for patients aged 0-5 years, and one for 6 years onward.\nA key benefit of CAMBRA is that it forces both the dental professional and the patient (or their caregiver) to consider all the factors relevant to the patient\u2019s risk and disease state, shifting the focus away from the traditional restorative approach of cavitation and restoration toward the cause of the disease and the need to modify the causes wherever possible. It also allows for greater communication and understanding between all members of the dental team.", + "doc_fkgl": 14.527236842105264, + "wiki_fkgl": 16.98034470989761, + "doc_tree_depth": 7.214285714285714, + "wiki_tree_depth": 9.9, + "fkgl_delta": -2.4531078677923475 + }, + { + "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": "In 2003 an alleged miracle attributed to his intercession had been discovered in the United States of America. The case involved a fetus in the mother's womb which suffered brain defects that would affect the child. The doctor advised the mother to have an abortion but the mother refused to do so and requested the intercession of the late pope at the behest of a nun who gave her a card with a piece of the late pope's cassock on it. When the child was born, there were no defects that could be detected and the child's health was monitored until it became an adolescent. The child in question still shows no signs of defects.", + "doc_fkgl": 4.623939393939395, + "wiki_fkgl": 10.105217391304347, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 7.4, + "fkgl_delta": -5.481277997364952 + }, + { + "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": "Diagnosis\nCraniometaphyseal dysplasia is diagnosed based on clinical and radiographic findings that include hyperostosis. Some things such as cranial base sclerosis and nasal sinuses obstruction can be seen during the beginning of the child's life. In radiographic findings the most common thing that will be found is the narrowing of foramen magnum and the widening of long bones. Once spotted treatment is soon suggested to prevent further compression of the foramen magnum and disabling conditions.", + "doc_fkgl": 11.214120481927715, + "wiki_fkgl": 12.962500000000002, + "doc_tree_depth": 5.4, + "wiki_tree_depth": 6.5, + "fkgl_delta": -1.7483795180722872 + }, + { + "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": "Gopinath was one of the pioneers of open heart surgery and perfusion in India. In 1962, he performed the first successful surgery for closure of an atrial and a ventricular septal defect at Christian Medical College and Hospital. He also introduced pioneering methods in rheumatic heart surgery and cardiac pacemaker implantation. His efforts have been reported behind the introduction of open heart surgery at AIIMS, New Delhi in 1964 when he established the department of cardiothoracic surgery at the institution. The same year, he is known to have started the course for MCh in cardiovascular thoracic surgery. In 1982, when AIIMS opened the Cardiothoracic Sciences Centre, Gopinath became its founder chief. His efforts are reported behind the centre receiving two grants, one from the Swedish International Development Agency (SIDA) and the other from the Department of Science and Technology of the Government of India. The centre has now grown into a 200 bedded independent healthcare facility.\nGopinath's early researches were on the juvenile mitral stenosis, a disease affecting the mitral valve making it shrink, its clinicopathological features and the disease management. Later, he focused his research on aorta, the largest artery and aortic valve and his efforts helped to create a human and animal heart valve bank at AIIMS, New Delhi. Towards later stages, he became interested in preventive cardiology and he undertook an epidemiological study of coronary artery diseases and its pathogenesis to find out how the disease could be modulated through nutrition and antioxidants. His researches have been documented by way of several articles, the first one published in 1952 in the Indian Journal of Medical Research, discussing about the advent of thoracic surgery in India. The first of his medical papers was published in 1953. He also produced many monographs on preventive cardiology.", + "doc_fkgl": 13.580182389937107, + "wiki_fkgl": 14.501660231660232, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 7.642857142857143, + "fkgl_delta": -0.9214778417231244 + }, + { + "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": "Conscious\nSymptoms of airway obstructions includes:\n The person cannot speak or cry out, or has great difficulty and limited ability to do so.\n Breathing, if possible, is labored, producing gasping or wheezing.\n The person has a violent and largely involuntary cough, gurgle, or vomiting noise, though more serious choking victims will have a limited (if any) ability to produce these symptoms since they require at least some air movement.\n The person desperately clutches his or her throat or mouth, or attempts to induce vomiting by putting their fingers down their throat.\n If breathing is not restored, the person's face turns blue (cyanosis) from lack of oxygen.", + "doc_fkgl": 2.581463963963966, + "wiki_fkgl": 11.825169811320759, + "doc_tree_depth": 4.583333333333333, + "wiki_tree_depth": 6.6, + "fkgl_delta": -9.243705847356793 + }, + { + "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": "Microscopy \n Well-demarcated, nodular lesions ranging 2\u20135\u00a0mm in pulmonary parenchyma.\n Type II pneumocytes without nuclear atypia lined thickened alveolar septa and proliferated papillary structures. \n Enlarged cuboidal cells lining mildly thickened alveolar septa.\n Enlarged cuboidal cells have abundant, eosinophilic cytoplasm and large, round nuclei.\n Papillary pattern with irregular margin and lymphocyte infiltration in the stroma.\n No proliferation of immature smooth muscle cells suggestive of lymphangioleiomyomatosis.", + "doc_fkgl": 12.728571428571431, + "wiki_fkgl": 14.198125000000001, + "doc_tree_depth": 5.166666666666667, + "wiki_tree_depth": 5.166666666666667, + "fkgl_delta": -1.4695535714285697 + }, + { + "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": "Medical practice \nAviv had an 18-year academic career as an attending physician at the Columbia University Medical Center and as a Professor of Otolaryngology\u2013Head and Neck Surgery at the Columbia University College of Physicians and Surgeons. In the Department of Otolaryngology\u2013Head and Neck Surgery he served as Director of Microvascular Head and Neck Reconstruction, Director of Head and Neck Surgery and then Director of the Voice and Swallowing Center. He has published medical journal articles on microvascular head and neck reconstruction, tongue reconstruction and developed a method of restoring sensation to the throat using microsurgical techniques. He has also published numerous journal articles related to Flexible Endoscopic Evaluation of Swallowing with Sensory Testing (FEESST),Transnasal esophagoscopy (TNE), acid reflux disease and cough. He has authored or co-authored two textbooks and most recently a health and wellness book designed for the lay public called Killing Me Softly From Inside: The Mysteries and Dangers of Acid Reflux and Its connection to America's Fastest Growing Cancer with a Diet that may save your life. He is licensed to practice medicine in New York and New Jersey. \nIn 2009 he left Columbia to join the largest Ear, Nose and Throat practice in the United States, ENT and Allergy Associates LLP, in New York City, NY. There he founded and became clinical director of the practices Voice and Swallowing Division.", + "doc_fkgl": 15.644583333333337, + "wiki_fkgl": 16.559464285714288, + "doc_tree_depth": 6.769230769230769, + "wiki_tree_depth": 8.25, + "fkgl_delta": -0.9148809523809511 + }, + { + "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": "As Jokke is dying, Cannaerts confesses. The viral outbreak was caused by one of his trainees, who carelessly opened a package of man-made mutated avian flu from Brazil. Cannaerts admits he should have followed protocols for such a dangerous disease, but it was the pathogen he needed to complete his research (before he took a senior position at the United Nations), so he had it delivered secretly by courier. His work and knowledge of the virus helped the authorities put measures in place to quarantine the area around NIID. Angered by these revelations, and the fact that the doctor has no intentions of admitting his culpability, Jokke attacks Cannaerts, deliberately infecting him.", + "doc_fkgl": 5.415573678290215, + "wiki_fkgl": 12.953142857142854, + "doc_tree_depth": 4.785714285714286, + "wiki_tree_depth": 7.6, + "fkgl_delta": -7.537569178852639 + }, + { + "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": "Megaloblastic anaemia\n Methaemoglobinaemia\n Erythema multiforme\n Low blood sugar\n Hepatitis (liver swelling)\n Crystalluria (crystals in the urine)\n Urinary obstruction causing difficulty passing urine\n Lowered mental acuity\n Depression\n Tremor\n Aplastic anaemia\n Haemolytic anaemia\n Hyponatraemia\n Purpura\n Eosinophilia\n Agranulocytosis\n Serum sickness\n Anaphylaxis\n Allergic myocarditis\n Angioedema\n Drug fever\n Periarteritis nodosa\n Hepatic necrosis\n Pancreatitis\n Myelosuppression\n Haemolysis\n Stevens\u2013Johnson syndrome\n Drug reaction with eosinophilia and systemic symptoms\n Toxic epidermal necrolysis\n Ataxia\n Clostridium difficile colitis\n Aseptic meningitis\n Pseudomembranous colitis\n Interstitial nephritis\n Fulminant hepatic necrosis\n Hypersensitivity of the respiratory tract\n Sore throat\n Pallor \n Arthralgia", + "doc_fkgl": 16.420789473684213, + "wiki_fkgl": 47.653333333333336, + "doc_tree_depth": 6.166666666666667, + "wiki_tree_depth": 10.0, + "fkgl_delta": -31.232543859649123 + }, + { + "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": "Leukopaenia a comparatively low white blood cell (the cells that defend the body from foreign invaders) count.\n Neutropaenia a reduced neutrophil (the white blood cells that kill bacteria) count.\n Bradycardia (low heart rate)\n QTc interval prolongation (an abnormality in the electrical cycle of the heart)\n Photosensitivity reaction\n Alopecia (hair loss)\n Urinary incontinence\n Urinary retention, the inability to urinate.\n Amenorrhea the cessation of menses (a woman's menstrual cycles). This is a complication of hyperprolactinaemia.\n Breast enlargement (in either sex). This is a complication of hyperprolactinaemia.\n Galactorrhoea (expulsion of milk from the breasts that's unrelated to pregnancy or lactation. Most likely the result of hyperprolactinaemia)\n High creatine phosphokinase (an abnormal laboratory finding)\n Increased total bilirubin (a by product of the breakdown of haem - a part of blood cells that is used to carry oxygen. In most people this is an indication of impaired liver function)\n Abdominal pain", + "doc_fkgl": 16.479367816091955, + "wiki_fkgl": 12.688448275862072, + "doc_tree_depth": 6.15, + "wiki_tree_depth": 5.909090909090909, + "fkgl_delta": 3.7909195402298828 + }, + { + "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": "Deep vein thrombosis \nDeep vein thrombosis (DVT), or deep venous thrombosis, is the formation of a blood clot (thrombus) within a deep vein, most commonly the legs. Nonspecific signs may include pain, swelling, redness, warmness, and engorged superficial veins. Pulmonary embolism, a potentially life-threatening complication, is caused by the detachment (embolization) of a clot that travels to the lungs. Together, DVT and pulmonary embolism constitute a single disease process known as venous thromboembolism.", + "doc_fkgl": 4.512113821138211, + "wiki_fkgl": 12.864486301369862, + "doc_tree_depth": 4.444444444444445, + "wiki_tree_depth": 7.0, + "fkgl_delta": -8.35237248023165 + }, + { + "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": "The haemostatic (blood clotting) system involves the interaction of proteins in the blood, the blood vessel wall and the flow of blood to control bleeding and blood clotting. Developmental Haemostasis is a term that represents the maturation of the haemostatic system from birth to adulthood. There are differences in the concentration, structure and activity of many proteins involved in blood clotting. These changes play an important role in physiological development and are important in providing appropriate diagnosis and treatment of bleeding and clotting disorders (e.g. thrombosis). The age-specific differences in the blood clotting system may contribute to the fact that children are less prone to developing thrombosis compared to adults.", + "doc_fkgl": 11.051032608695653, + "wiki_fkgl": 14.23, + "doc_tree_depth": 5.0, + "wiki_tree_depth": 8.4, + "fkgl_delta": -3.1789673913043472 + }, + { + "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": "Agranulocytosis, a potentially fatal drop in white blood cell count, basically an exaggerated form of leukopaenia.\n Thrombocytopaenia. A drop in blood platelet counts which are involved in blood clotting. \n Thromboembolism (blood clots; including pulmonary embolism and deep vein thrombosis)\n Rhabdomyolysis (breakdown of muscle tissue leading to the release of myoglobin into the bloodstream which in turn damages the kidneys)\n Alkaline phosphatase increased (an abnormal laboratory parameter)\n Priapism (a painful and enduring erection)\n Urinary hesitation\n Pancreatitis, swelling of the pancreas which supplies the body with insulin. \n Neuroleptic malignant syndrome a potentially fatal complication of antipsychotic drug treatment. Presents with hyperthermia, tremor, tachycardia (high heart rate), mental status change (e.g. confusion), etc.\n Jaundice, which is basically when the body's ability to clear a by product (called bilirubin) of the breakdown of an essential component of the blood called haem, is impaired leading to yellow discolouration of the skin, eyes and mucous membranes. \n Diabetic coma\n Diabetic ketoacidosis. Type II diabetes mellitus is basically where the body cannot effectively utilise sugars to produce energy due to the fact that its cells have become unresponsive to the hormone, insulin, which allows cells to utilise sugars for energy. This in turn forces the body to burn fats for energy and fats require conversion to ketone bodies in order to be utilised by the cells of the body as an energy source. The ketone bodies are acidic hence when the body is entirely reliant on these ketone bodies for energy the levels in the blood reaches a point where it overwhelms the body's natural mechanisms to keep blood pH (a measure of acidity) within a safe range, leading to the blood becoming acidic which is potentially damaging to the tissues of the body due to the ability of acidic environments to denature the proteins of the body. \n Anaphylactic reaction a potentially life-threatening allergic reaction\n Sudden cardiac death", + "doc_fkgl": 11.779287370862324, + "wiki_fkgl": 16.983489736070386, + "doc_tree_depth": 6.208333333333333, + "wiki_tree_depth": 8.5, + "fkgl_delta": -5.204202365208062 + }, + { + "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": "Anjelica's decomposing body was discovered on July 23, 1991, inside a navy blue cooler along the Henry Hudson Parkway in Manhattan, New York. The body was so decomposed that identification was at first impossible, as her face was not recognizable\u2014she soon came to be known as \"Baby Hope\". She was naked, and had been bound with both rope and a Venetian blind cord. She was placed in a fetal position with her hands pressed together. The body was then wrapped in a garbage bag and placed inside the cooler, which was filled with unopened soda cans and water (which was presumably ice at one time). Examiners concluded that \"Baby Hope\" was possibly Hispanic, had dark, wavy hair in a ponytail, was malnourished (weighing only ), was a victim of sexual abuse, and had died on or about July 18. She was initially estimated to have been between three and five years old.", + "doc_fkgl": 3.26104347826087, + "wiki_fkgl": 11.10894985808893, + "doc_tree_depth": 4.0, + "wiki_tree_depth": 7.571428571428571, + "fkgl_delta": -7.847906379828061 + }, + { + "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": "Causes\nMRHK syndrome occurs from an arrest in the embryonic development in the first phase of organogenesis, resulting in underdevelopment of one or both the left and right primitive uterus and vagina (agenesis). Specifically, an arrest in the development of the paramesonephric ducts at week seven of gestation is linked to MRHK syndrome. During embryological development of the first phase, two separate uterine, cervical and vaginal pockets develop, following which a transverse septum forms across the caudal aspect in the upper two thirds of the vagina, which will dissolve when the lower one third of the vagina (developed from the urogenital sinus) fuses with the upper two thirds. An arrest at this stage means midline fusion of pockets do not occur and subsequently are unable to develop into a whole uterus, cervix and vagina.", + "doc_fkgl": 11.784036259541985, + "wiki_fkgl": 18.169029850746274, + "doc_tree_depth": 5.375, + "wiki_tree_depth": 10.0, + "fkgl_delta": -6.384993591204289 + }, + { + "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": "There is limited diagnostic testing in this area. The standard screening tests that take place during pregnancy that can diagnose syndromes such as Down Syndrome do not diagnose WSS. In addition, baseline genetics diagnostic tests conducted after birth do not include testing for WSS. Whole exome sequencing has been used to identify most people with WSS. Often, medical professionals do not offer the option for whole exome testing or the costs associated are not covered by insurance or require a large copay limiting individuals from having the testing done. Frequently, patients are given other incorrect medical explanations or a less specific and broader diagnosis, like autism and Rubinstein\u2013Taybi syndrome. Additionally, once a person reaches a certain age or phase in their lifetime having been mis-diagnosed or gone undiagnosed, he/she may stop looking for answers to their medical trials and tribulations meaning they may never come across a formal WSS diagnosis. There have also been patients with Wiedemann\u2013Steiner syndrome who were initially mis-diagnosed with Kabuki syndrome.", + "doc_fkgl": 15.11899521531101, + "wiki_fkgl": 14.051325757575757, + "doc_tree_depth": 6.5, + "wiki_tree_depth": 6.875, + "fkgl_delta": 1.0676694577352528 + }, + { + "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": "In 2011, Anagnostou reported genetic detection and sequencing of an Adria virus in a boy who was hospitalized because of a simple febrile seizure. This sequence was identical to the one in sandflies detected in a coastal area in Albania. The patient was febrile and had vomited once. He had no previous neurologic or developmental disabilities and no family history of epilepsy or febrile seizures. Clinical examinations including a thorough general and detailed neurologic evaluation revealed no abnormalities except mild rhinitis. Blood levels of various proteins and metabolites were in the physiological level. An electroencephalogram showed no brain malfunctions. After two days of hospitalization, he recovered from the disease, had no symptoms and was discharged from the hospital. One year after discharge from the hospital, his mother reported that the child remained well without any recurrence of febrile or any other type of seizures.", + "doc_fkgl": 4.794388489208632, + "wiki_fkgl": 12.938888888888894, + "doc_tree_depth": 4.923076923076923, + "wiki_tree_depth": 6.111111111111111, + "fkgl_delta": -8.144500399680261 + }, + { + "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": "Bradycardia\n Hypertension (high blood pressure)\n Allergic reactions (e.g. dyspnoea (shortness of breath), bronchospasm, wheezing, angioneurotic oedema)\n Anaphylaxis\n Changes in appetite\n Paraesthesia (pins and needles)\n Hallucinations\n Tremor\n Respiratory depression\n Epileptiform convulsions\n Involuntary muscle contractions\n Abnormal coordination\n Syncope (fainting)\n Blurred vision\n Dyspnoea (shortness of breath)\n Tinnitus (ringing in the ears)\n Migraine\n Stevens\u2013Johnson syndrome/toxic epidermal necrolysis (potentially fatal skin reactions)\n Motorial weakness\n Creatinine increase\n Elevated liver enzymes\n Hepatitis (liver swelling)\n Stomatitis (mouth swelling)\n Liver failure\n Pulmonary oedema (fluid in the lungs)\n Gastrointestinal bleeding\n Pulmonary embolism\n Myocardial ischaemia (lack of blood supply to the heart muscles)\n Speech disorders\n Haemoglobin decrease\n Proteinuria (protein in the urine; usually indicative of kidney damage)", + "doc_fkgl": 14.753525835866263, + "wiki_fkgl": 33.244150943396235, + "doc_tree_depth": 6.333333333333333, + "wiki_tree_depth": 8.0, + "fkgl_delta": -18.490625107529972 + }, + { + "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": "Agranulocytosis, a potentially fatal drop in white blood cell count, basically an exaggerated form of leukopaenia.\n Thrombocytopaenia. A drop in blood platelet counts which are involved in blood clotting. \n Thromboembolism (blood clots; including pulmonary embolism and deep vein thrombosis)\n Rhabdomyolysis (breakdown of muscle tissue leading to the release of myoglobin into the bloodstream which in turn damages the kidneys)\n Alkaline phosphatase increased (an abnormal laboratory parameter)\n Priapism (a painful and enduring erection)\n Urinary hesitation\n Pancreatitis, swelling of the pancreas which supplies the body with insulin. \n Neuroleptic malignant syndrome a potentially fatal complication of antipsychotic drug treatment. Presents with hyperthermia, tremor, tachycardia (high heart rate), mental status change (e.g. confusion), etc.\n Jaundice, which is basically when the body's ability to clear a by product (called bilirubin) of the breakdown of an essential component of the blood called haem, is impaired leading to yellow discolouration of the skin, eyes and mucous membranes. \n Diabetic coma\n Diabetic ketoacidosis. Type II diabetes mellitus is basically where the body cannot effectively utilise sugars to produce energy due to the fact that its cells have become unresponsive to the hormone, insulin, which allows cells to utilise sugars for energy. This in turn forces the body to burn fats for energy and fats require conversion to ketone bodies in order to be utilised by the cells of the body as an energy source. The ketone bodies are acidic hence when the body is entirely reliant on these ketone bodies for energy the levels in the blood reaches a point where it overwhelms the body's natural mechanisms to keep blood pH (a measure of acidity) within a safe range, leading to the blood becoming acidic which is potentially damaging to the tissues of the body due to the ability of acidic environments to denature the proteins of the body. \n Anaphylactic reaction a potentially life-threatening allergic reaction\n Sudden cardiac death", + "doc_fkgl": 14.958653673835126, + "wiki_fkgl": 16.983489736070386, + "doc_tree_depth": 5.866666666666666, + "wiki_tree_depth": 8.5, + "fkgl_delta": -2.0248360622352592 + }, + { + "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": "The theory behind this invasive approach is that the artificial restoration of oxygenation and end-organ perfusion allows treating physicians more time to mitigate and reverse pathology which contributes to cardiac arrest and refractory shock. It has been well documented that the likelihood of return of spontaneous circulation and furthermore eventual discharge from hospital, after ten minutes of CPR falls significantly. Once circulation is established, the patient is able to be transferred, for further investigation and intervention, to facilities such as a cardiac cath lab and an intensive care unit.", + "doc_fkgl": 6.522207792207791, + "wiki_fkgl": 19.049662921348318, + "doc_tree_depth": 5.571428571428571, + "wiki_tree_depth": 9.0, + "fkgl_delta": -12.527455129140527 + }, + { + "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": "Legacy\nAshok Seth is credited with pioneering many cardiological techniques in the Asia Pacific region. He is the first cardiologist in the region to perform an angioscopy and directional atherectomy. He is reported to be the first to use Impella heart support device and Drug-eluting stents, Bioresorbable stents and thrombectomy devices in India. He is known to have contributed to the development of Bioresorbable Scaffold (BRS) Stent as a member of the Advisory Group. The youngest person to receive a doctoral degree (Honoris Causa) from the Banares Hindu University, Seth's tally of angioplasty and angiogram performances is noted by the Limca Book of Records as one of the highest in the world. He is known to perform Percutaneous Myocardial Laser Revascularization, reported to be among the few cardiologists in the World to perform the procedure.", + "doc_fkgl": 13.480000000000004, + "wiki_fkgl": 14.599814814814817, + "doc_tree_depth": 7.166666666666667, + "wiki_tree_depth": 8.166666666666666, + "fkgl_delta": -1.1198148148148128 + }, + { + "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": "In 1977, he published the very first book in the world on Vascular Doppler Exploration (Vascular investigation by Doppler ultrasound) then translated into Italian and Spanish, in which he describes the hemodynamic principles and their expression in terms of Doppler signal. This data remains the undisputed reference for the stenosis quantification and a quality diagnostic. In particular, he worked on the criteria of arterial stenosis of limbs and carotids, Carotid pre-thrombosis, the Pressure-Perfusion Index (Franceschi Index), the Carotid Ratio and the exploration of the Circle of Willis. \n In 1978, he published the first observations of carotid plaque regression. \n In 1980 he described the Fistula Flow Ratio (French 'RDF') to assess the flow of arteriovenous fistulas, especially in renal dialysis.\n In 1981, he invented an interface process which allows for the first time the visualization of supra-aortic arteries by B-Mode echography. A Doppler method for exploring the compensatory ways of the cerebro-cervical vasculature was published the same year. \n In 1986, he published the first book of vascular ultrasound imaging Pr\u00e9cis d'\u00e9chotomographie vasculaire translated into Italian: \u00ab Compendio di ecotomografia vascolare \u00bb\n In 1988, he published the book La cure Conservatrice et H\u00e9modynamique de l'Insuffisance Veineuse en Ambulatoire: CHIVA also translated into English and Italian, where he offers a new approach to the physiology of deep and superficial venous circulation, introducing new concepts such as \u00ab Dynamic hydrostatic pressure fractioning \u00bb, the veno-venous shunts and vicarious evolution of varices.", + "doc_fkgl": 9.065632911392406, + "wiki_fkgl": 18.659737124463522, + "doc_tree_depth": 6.684210526315789, + "wiki_tree_depth": 8.25, + "fkgl_delta": -9.594104213071116 + }, + { + "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 and Symptoms \nThe generalized, common presentation for this broad and inclusive group of diseases is painless, bilateral loss of visual acuity and pallor of the optic disc accompanied with varying degrees of dyschromatopsia and central/cecocentral scatomas. On examination the pupillary responses may be sluggish to light. One would not expect to find an afferent pupillary defect because optic neuropathies are often bilateral and symmetric. The optic disc may appear mildly hyperemic with small splinter hemorrhages on or around the disc, or may appear nearly normal. Optic atrophy typically develops later and may appear mild. In later stages the optic atrophy can become severe, which indicates less opportunity for recovery.", + "doc_fkgl": 6.597509398496243, + "wiki_fkgl": 13.336363636363636, + "doc_tree_depth": 5.875, + "wiki_tree_depth": 5.666666666666667, + "fkgl_delta": -6.738854237867393 + }, + { + "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": "Confluent subpial cortical lesions are the most specific finding for MS, being exclusively present in MS patients. Though this feature can only be detected during an autopsy there are some subrogate markers under study Damage in MS consists also in areas with hidden damage (normal appearing white and gray matters) and two kinds of cortical lesions: Neuronal loss and cortical demyelinating lesions. The neural loss is the result of neural degeneration from lesions located in the white matter areas and the cortical demyelinating lesions are related to meningeal inflammation.", + "doc_fkgl": 11.54186046511628, + "wiki_fkgl": 17.45865168539326, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 9.333333333333334, + "fkgl_delta": -5.916791220276981 + }, + { + "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": "Description\nThe eyed flounder is a flattened, disc-shaped fish which grows to a maximum length of but a more typical size is . As with other members of its family, it lies on its right side, and during its development, its right eye migrates to the left side of its head. The protractile mouth is large and the male fish has a spine on the snout and a bony lump in front of the lower eye. The eyes are large and prominent, the lower one being slightly nearer the snout than the upper one. Both eyes have a fleshy ridge above and behind them. The dorsal fin has 76 to 91 soft rays and has its origin close to the upper eye. It is long and ribbon-like and there is a gap between it and the caudal fin. The anal fin has 58 to 69 soft rays and is also long and distinct from the caudal fin. The color of this fish is pale tan, grey or brown, with patches, mottling and ring-shaped markings, the fish being able to modify its color to match its background. It can change its color in between two and eight seconds. Three larger dark spots lie on the straight portion of the lateral line and there are two fainter ones on the tail. It differs from the slightly darker twospot flounder (Bothus robinsi) because its tail spots are one above the other in this species but one behind the other in the twospot flounder. The underside of this species is pale.", + "doc_fkgl": 14.661870129870131, + "wiki_fkgl": 7.577500000000001, + "doc_tree_depth": 5.473684210526316, + "wiki_tree_depth": 6.384615384615385, + "fkgl_delta": 7.0843701298701305 + }, + { + "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": "Positions\nMani started his career as a faculty member at the Christian Medical College and Hospital, Vellore and moved as the Specialist Surgeon to the Indian Railways Southern Railway HQ Hospital in Perambur in the south Indian state of Tamil Nadu, in 1984. He worked there till 1989 when he returned to Delhi as the Chief Cardiac Surgeon and Director of Cardiac Surgery at the Batra Hospital and Medical Research Centre, a position he held till 1995. The next move was as the Senior Cardiothoracic Consultant of the Apollo Hospital, Indraprastha, a 700 bedded tertiary care hospital in the Indian capital, working there from 1996 to 2003. He has also worked as the visiting consultant at hospitals such as Saroj Hospital, Delhi (2001-2003), Gandhi Medical College, Bhopal (2003), Delhi Heart and Lung Institute (2003-2009), Golden Heart Institute of the Jaipur Golden Hospital (2005-2009), the Mool Chand Hospital, Delhi (2008-2009) and as the Director of the Pushpanjali Institute of Cardiac Sciences and Crosslay Remedies.", + "doc_fkgl": 6.542719298245618, + "wiki_fkgl": 20.138082822085895, + "doc_tree_depth": 4.823529411764706, + "wiki_tree_depth": 9.0, + "fkgl_delta": -13.595363523840277 + }, + { + "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": "Positions\nMani started his career as a faculty member at the Christian Medical College and Hospital, Vellore and moved as the Specialist Surgeon to the Indian Railways Southern Railway HQ Hospital in Perambur in the south Indian state of Tamil Nadu, in 1984. He worked there till 1989 when he returned to Delhi as the Chief Cardiac Surgeon and Director of Cardiac Surgery at the Batra Hospital and Medical Research Centre, a position he held till 1995. The next move was as the Senior Cardiothoracic Consultant of the Apollo Hospital, Indraprastha, a 700 bedded tertiary care hospital in the Indian capital, working there from 1996 to 2003. He has also worked as the visiting consultant at hospitals such as Saroj Hospital, Delhi (2001-2003), Gandhi Medical College, Bhopal (2003), Delhi Heart and Lung Institute (2003-2009), Golden Heart Institute of the Jaipur Golden Hospital (2005-2009), the Mool Chand Hospital, Delhi (2008-2009) and as the Director of the Pushpanjali Institute of Cardiac Sciences and Crosslay Remedies.", + "doc_fkgl": 12.910294117647059, + "wiki_fkgl": 20.138082822085895, + "doc_tree_depth": 6.444444444444445, + "wiki_tree_depth": 9.0, + "fkgl_delta": -7.2277887044388365 + }, + { + "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": "Licensing and clinical development \nEtomoxir has already been through phase II clinical development for the treatment of type 2 diabetes and heart failure. Etomoxir went through preclinical trials by Byk Gulden laboratories (now Altana Pharma AG) from 1981 to 1984. From 1984 to 1993, etomoxir was developed through phase I and II trials that showed favorable effects on the heart and a good safety profile. In 1999, the patent was out-licensed to MediGene for further trials. In 2001, MediGene was granted extended patent rights for the use of etomoxir for the treatment of congestive heart failure. In 2002, MediGene announced that it terminated a phase II trial for the use of etomoxir for heart failure due to adverse side effects. MediGene funded a study of etomoxir as a treatment of heart failure in 2007, but the study was once again terminated prematurely. Four of the 226 patients taking the drug showed unacceptably high liver transaminase levels, which was determined by the experimenters to likely be due to the treatment. The University of Colorado currently holds patents for the use of etomoxir as an anti-inflammatory and anticarcinogenic agent. However, the clinical development of etomoxir has been terminated due to severe hepatotoxicity associated with treatment.", + "doc_fkgl": 13.475840409207162, + "wiki_fkgl": 12.497443349753699, + "doc_tree_depth": 6.2631578947368425, + "wiki_tree_depth": 7.3, + "fkgl_delta": 0.9783970594534637 + }, + { + "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": "Symptoms\nSymptoms vary between individuals and can be dependent upon the stage of growth of the carcinoma. Presence of the carcinoma can lead to be asymptomatic blood in the urine (hematuria), Hematuria can be visible or detected microscopically. Visible hematuria is when urine appears red or brown and can be seen with the naked eye. Other symptoms are not specific. Other inflammatory conditions that affect the bladder and kidney can create similar symptoms. Early detection facilitates curing the disease. Other symptoms can involve:", + "doc_fkgl": 6.041, + "wiki_fkgl": 10.50175559380379, + "doc_tree_depth": 5.125, + "wiki_tree_depth": 5.285714285714286, + "fkgl_delta": -4.460755593803789 + }, + { + "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": "Agitation\n Anxiety\n Emotional lability\n Euphoria\n Nervousness\n Spasticity\n Dyspepsia (indigestion)\n Asthenia (weakness)\n Pruritus (itchiness)\n Dry mouth\n Diarrhea\n Fatigue\n Sweating\n Malaise\n Vasodilation (dilation (widening) of blood vessels)\n Confusion\n Coordination disturbance\n Miosis\n Sleep disorder\n Rash\n Hypertonia\n Abdominal pain\n Weight loss\n Visual disturbance\n Flatulence\n Menopausal symptoms\n Urinary frequency\n Urinary retention (being unable to urinate)", + "doc_fkgl": 12.18240740740741, + "wiki_fkgl": 36.477999999999994, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 6.0, + "fkgl_delta": -24.295592592592584 + }, + { + "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": "Gynecomastia\n Extrapyramidal symptoms (EPS) (dose-dependent). Tends to produce less extrapyramidal side effects than typical antipsychotics but more extrapyramidal side effects than sertindole, clozapine and quetiapine.\n Mild and transient constipation and xerostomia (dry mouth)\n Dizziness\n Weight gain of over 15% of one's initial body weight. Is reported to occur in approximately 7.1% of patients. \n Glucosuria (glucose in the urine. This is a consequence of hyperglycaemia)\n Accidental injury\n Insomnia\n Orthostatic hypotension (a drop in blood pressure that occurs upon standing up) \n Transient, asymptomatic elevations of hepatic aminotransferases (ALT, AST), especially in early treatment. ALT & AST are liver enzymes which are often tested for as a measure of liver function. \n Dyspepsia (indigestion)\n Erectile dysfunction. This is most likely the result of hyperprolactinaemia. \n Decreased libido. This is most likely the result of hyperprolactinaemia. \n Rash\n Asthenia (weakness)\n Fatigue\n Oedema the accumulation of fluid in the tissues of the body leading to swelling\n Akathisia an inner sense of restlessness that presents itself with the inability to stay still\n Parkinsonism tremor, muscle rigidity, reduced ability to move and being unstable on one's feet\n Dyskinesia abnormal, involuntary, repetitive, and pointless movements\n Vomiting \n Coma \n Cardiac arrest", + "doc_fkgl": 14.957394957983198, + "wiki_fkgl": 13.771991978609627, + "doc_tree_depth": 5.411764705882353, + "wiki_tree_depth": 7.230769230769231, + "fkgl_delta": 1.1854029793735705 + }, + { + "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": "Vascular events\nDeep vein thrombosis\nBetween 15 and 25 percent of deep vein thrombosis (DVT) is caused by cancer (often by a tumor compressing a vein). Cancers most likely to cause DVT are pancreatic cancer, stomach cancer, brain tumors, advanced breast cancer and advanced pelvic tumors. DVT may be the first hint that cancer is present. It causes swelling and pain (which varies from intense to vague cramp or \"heaviness\") in the legs, especially the calf, and (rarely) in the arms.\nSuperior vena cava syndrome\nThe superior vena cava (a large vein carrying circulating, de-oxygenated blood into the heart) may be compressed by a tumor, most often non-small-cell lung carcinoma (50 percent), small-cell lung carcinoma (25 percent), lymphoma, or metastasis, causing superior vena cava syndrome. Common symptoms include shortness of breath, swelling of the face and neck, dilation of veins in the neck and chest, and chest wall pain.", + "doc_fkgl": 5.827348837209307, + "wiki_fkgl": 13.260100671140943, + "doc_tree_depth": 5.066666666666666, + "wiki_tree_depth": 7.0, + "fkgl_delta": -7.432751833931636 + }, + { + "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": "Publications\n International, multicentre, randomized, double blind study to compare the overall mortality in acutely ill medical patients treated with enoxaprin versus placebo in addition to graduated elastic stockings\n Assessment of Total thrombus load estimation in symptomatic patients with venous thromboembolism\n Takayasu's arteritis: An Indian Perspective\n Pulmonary embolism: A frequent Occurrence in Indian Patients with Symptomatic Lower Limb Venous Thrombosis\n Snapshots in Surgery : Pulsatile Scrotum\n Prevention and treatment of venous thromboembolism. International Consensus Statement (Guidelines according to scientific evidence).\n Cervical Asymmetry: Medical Images.\n Asymptomatic Coronary Artery disease in patients with symptomatic peripheral vascular disease - detected by dobutamine stress echo and coronary angiography.\n Studies on homocysteine demonstrating its significance as a possible tool for differential diagnosis in occlusive vascular disease\n Limb Salvage angioplasty in vascular surgery practice", + "doc_fkgl": 14.593809523809526, + "wiki_fkgl": 22.48, + "doc_tree_depth": 5.888888888888889, + "wiki_tree_depth": 9.0, + "fkgl_delta": -7.886190476190475 + }, + { + "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": "Apabetalone (development codes RVX 208, RVX-208, and RVX000222) is an orally available small molecule created by Resverlogix Corp. that is being evaluated in clinical trials for the treatment of atherosclerosis and associated cardiovascular disease (CVD). In the phase II clinical trial ASSURE in patients with angiographic coronary disease and low high-density lipoprotein cholesterol (HDL-C) levels, apabetalone showed no greater increase in HDL-cholesterol (HDL-c) and apolipoprotein A-I (ApoA-I) levels or incremental regression of atherosclerosis than administration of placebo, while causing a statistically significant greater incidence of elevated liver enzymes. However, pooled analysis of the effect of apabetalone in three phase II clinical trials ASSERT, ASSURE, and SUSTAIN demonstrated increases in HDL-cholesterol (HDL-c) and apolipoprotein A-I (ApoA-I) levels, as well as decreases in the incidence of major adverse cardiac events (MACE). Reduction of MACE was more profound in patients with diabetes mellitus. In a short-term study in prediabetics, favorable changes in glucose metabolism were observed in patients receiving apabetalone. An international, multicenter phase III trial, \u201cEffect of RVX000222 on Time to Major Adverse Cardiovascular Events in High-Risk Type 2 Diabetes Mellitus Subjects with Coronary Artery Disease\u201d (BETonMACE) commenced in October 2015. The trial is designed to determine whether apabetalone in combination with statins can decrease cardiac events compared to treatment with statins alone.", + "doc_fkgl": 16.972754430379748, + "wiki_fkgl": 18.464022511848345, + "doc_tree_depth": 6.380952380952381, + "wiki_tree_depth": 8.142857142857142, + "fkgl_delta": -1.491268081468597 + }, + { + "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": "The shell is small and thin, with inequally sized and asymmetric valves. It is about 1.5 times as long as high, rounded in the front, subtruncate behind and moderately swollen in the central region. The umbos are small and point out slightly; they are situated nearer to the anterior than the posterior end. The dorsal margin from the umbo to the upper end of the anterior margin is slightly convex, and from the umbo to the posterior region is straight and sloping. The lower margin is convex and evenly curved, and the surface of the upper part of the shell is striated with fine, irregular, transverse concentric markings. The right valve measures in breadth and in height, and the right valve and .", + "doc_fkgl": 5.730088652482269, + "wiki_fkgl": 8.810421545667449, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 6.333333333333333, + "fkgl_delta": -3.0803328931851794 + }, + { + "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": "Medical usage\nFlow diverters are treatment for intracranial aneurysms alternative to endosaccular coil embolization, although the techniques can be combined, especially in large/giant aneurysms. It is mainly effective in wide neck unerupted saccular aneurysms, that are difficult to coil because of the tendency of the coils to fill the parent artery (referred to as prolapse). Another situation is fusiform shape or circumferential aneurysms. \nPrior to flow diverters many intracranial aneurysms went untreated. Flow diverters can be placed in the parent vessel or within the aneurysm, which are called intrasaccular flow diverters. These devices can be used to treat aneurysms by doing a cerebral angiogram via femoral artery or radial artery access.", + "doc_fkgl": 11.984808362369339, + "wiki_fkgl": 12.673648648648651, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 6.5, + "fkgl_delta": -0.6888402862793122 + }, + { + "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": "In \u201cThe Regio Parietalis (of Diencephalon) in Lower Craniates\u201d (1905), Sterzi demonstrates that there are organs which are single (epiphysis and paraphysis) and organs that are originally double (pineal and parapineal organs; Sterzi, 1905). The latter, however, in adult petromyzontes become both asymmetrical acquiring a median location below the cranial vault, which is fissured in their correspondence. They have the structure of a sort of eyes (parietal eyes).\n\u201cGeneral Neuroanatomy\u201d (1912\u20131914) is a series of articles on the development of the longitudinal cerebral fissure (Sterzi, 1912) and that on the significance of the human encephalon and telencephalon (Sterzi, 1914). Concerning the first topic, Sterzi demonstrates that, contrary to earlier reports, the longitudinal fissure is not due to pressure exerted by the falx cerebri but that it is the product of the rapid outgrowth of the cerebral hemispheres from the lateral portions of the telencephalic vesicle. He also maintains that the third ventricle consists, not only of the posterior diencephalic portion, but of a smaller anterior one of telencephalic origin. In the second article (Sterzi, 1914), Sterzi criticizes the concept put forward by Edinger(1911) that the human brain consists of a neoencephalic portion: the cerebral cortex, and of a paleoencephalic one: the remaining encephalon. He demonstrates that even in the portion that Edinger considers paleoencephalon there are neoencephalic derivatives. Concerning whether all portions of the brain really evolve from lower craniates to man, he demonstrates that this is not the case because, in the course of phylogenesis, some parts evolve and others regress.", + "doc_fkgl": 16.455087719298245, + "wiki_fkgl": 16.120476190476193, + "doc_tree_depth": 7.0, + "wiki_tree_depth": 8.222222222222221, + "fkgl_delta": 0.3346115288220517 + }, + { + "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": "Hill's articles give an insight into the range of conditions with which he dealt as a surgeon-apothecary, and his understanding of their causes and treatment. He contributed a case report about a patient who was temporarily \u2018cured\u2019 of syphilis by a \u2018mercurial suffumigation\u2019. After various therapies including laudanum, tonics, claret and Dr Plummer's pills were unsuccessful, he resorted to mercury, a recognised treatment for syphilis and fumes were thought to be the fastest mode of delivery. The symptoms eventually and she survived for more than a year. This report demonstrates that surgeons in Scotland at this time truly acted as surgeon-apothecaries. \nHis report on two cases of hydatid disease describes one patient discharging hydatid cysts via a chronic cutaneous fistula from the liver and the other discharging cysts in the sputum. Both recovered without active treatment. Although able to diagnose hydatid disease he thought the condition arose because \u2018some people have hydatic constitutions.\u2019", + "doc_fkgl": 5.262667512690356, + "wiki_fkgl": 12.615155228758173, + "doc_tree_depth": 5.15, + "wiki_tree_depth": 6.875, + "fkgl_delta": -7.352487716067817 + }, + { + "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 Pacak-Zhuang syndrome is a recently described disease manifestation in females that includes multiple paragangliomas or pheochromocytomas and somatostatinomas (in some), both neuroendocrine tumors, and secondary polycythemia associated with high erythropoietin levels. Paragangliomas in these patients are mainly localized to the abdomen whereas somatostatinomas are found in the second portion of the duodenum, as shown by imaging or biochemistry. This syndrome is of special interest as finding more than one type of neuroendocrine tumor in one individual is unusual. Such co-occurrences are usually seen in patients carrying hereditary syndromes like multiple endocrine neoplasia (MEN), neurofibromatosis 1 (NF1), or von Hippel-Lindau (VHL) disease.", + "doc_fkgl": 13.893053097345135, + "wiki_fkgl": 18.070686274509807, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 7.5, + "fkgl_delta": -4.177633177164672 + }, + { + "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": "Publications\nEdwards has authored and co-authored the following;\nRelief of lymph obstruction by use of a bridge of mesentery and ilieum J.B. Kinmouth, P.A Hurst, J.M. Edwards and D.L. Rutt\nMalignant Melanoma: Treatment by Endolymphatic Radio-Isotope Infusion J.M. Edwards (Annals of the Royal College of Surgeons of England Volume 44-May 1969 Pages 237-254)\nA review of operations for lymphoedema: J.M. Edwards, D. Negus and J.B. Kinmouth\nLymphovenous Shunts in Man: J.M. Edwards: J.B. Kinmouth \nEndolymphatic Radiotherapy: R.W Lloyd-Davies, J.M. Edwards and J.B. Kinmouth\nLymphography of the Testis and its Adnexa in the Normal and in Adiopathic Hydrocele: Michael P. O\u2019Brien, J.M. Edwards and John. B Kinmouth \nThe Value of Lymphography in the Management of Melanoma: J.M. Edwards (Clinical Radiology Vol. XX No. 4 October 1969)\nEndolymphatic Therapy for Malignant Melanoma by J.M. Edwards (from Melanoma and Skin Cancer New South Wales 1972) \nLymphangiography and Surgery in Lymphangioma of the skin: J.M.Edwards, R.D.G. Peachey and J.B. Kinmouth \nSurgical excision of visceral metastases from malignant melanoma: A.R.L May and J.M. Edwards (Clinical Oncology 1976 2, 233-237)\nInvestigation and management of cutaneous artieral insufficiency of the extremities: J.M. Edwards (Clinical and Experimental Dermatology 1982 7, 429-434) \nShearing operation for incompetent perforating veins: J.M. Edwards (Br. J. Surg Vol 63 (1976) \nEndolymphatic Radiotherapy A Comparison of Radiogold and Radioiodine against the VX2 Tumor in the Rabbit: R.W. Lloyd-Davies, J.M. Edwards and J.B. Kinmouth", + "doc_fkgl": 15.117090909090908, + "wiki_fkgl": 10.192606797038163, + "doc_tree_depth": 6.071428571428571, + "wiki_tree_depth": 7.857142857142857, + "fkgl_delta": 4.924484112052745 + }, + { + "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": "Physical characteristics\nOfficials at the Lippe State Museum in Detmold, Germany have revealed that the Detmold child died at the age of eight to nine months after suffering from a rare congenital heart malformation mostly known as hypoplastic left heart syndrome (HLHS), a condition with parts of the left side of the heart not developing completely. The syndrome combined with contracting pneumonia had led to the baby's death. The child was also discovered to have Vitamin D deficiency, and also had an abnormal, conically-shaped skull. The body had been covered by linen and buried with an amulet hung around its neck a CT scan has revealed.", + "doc_fkgl": 7.468333333333334, + "wiki_fkgl": 13.558207547169815, + "doc_tree_depth": 6.125, + "wiki_tree_depth": 6.75, + "fkgl_delta": -6.089874213836481 + }, + { + "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": "Pathogenesis\nStreptococcus tigurinus is generally not a normal part of the human bacteria flora and it is currently unknown where its natural habitat is or its potential for colonization. Capable of causing serious infections if it manages to enter the body's bloodstream, usually through open wounds in the mouth, it was first discovered to cause invasive infections after it was isolated from a patient with infective endocarditis. It was later detected in the blood and cerebrospinal fluid of 14 other patients with varying types of serious invasive infections such as spondylodiscitis, bacteremia, meningitis, and empyema.", + "doc_fkgl": 12.996079027355623, + "wiki_fkgl": 19.117894736842107, + "doc_tree_depth": 5.714285714285714, + "wiki_tree_depth": 10.333333333333334, + "fkgl_delta": -6.121815709486484 + }, + { + "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": "December 3, 1967 (Sunday)\nChristiaan Barnard and a team of surgeons carried out the world's first heart transplant, at Groote Schuur Hospital in Cape Town, South Africa. At 2:20 in the morning, local time, Denise Darvall's heart was removed from her chest, then rushed over to the operating room where 14 surgeons and nurses were ready to transplant it into retired grocer Louis Washkansky. Barnard then removed Washkansky's ailing heart, and Dr. Rodney Hewitson then placed Darvall's heart into Washkansky's chest; Barnard then worked at shaping the aorta, and, at 5:24, connected the new heart. At 5:43, blood was released into the heart muscle, and, at 6:45, the new heart was beating on its own.\nThirty-two people, most of them Thai university students who were on vacation during the birthday of the King, drowned in the sinking of a small river craft in the Gulf of Siam off the coast of the Rayong Province. Another 58 students and the pilot of the craft swam to shore or were rescued by fishing boats from the village of Ban Phe. The pilot was arrested upon arrival on land.\nThe government of Iraq revoked the licenses of all 12 of the nation's daily newspapers as a new press law went into effect.\nAn Arab terrorist group cut the main railway line between Jerusalem and Tel Aviv, with an explosive charge near Beth Shemesh, west of Jerusalem. Two of the saboteurs were killed in the blast.\nGreece and Turkey announced their agreement to UN Secretary General U Thant's request, mediated by Cyrus Vance of the United States, to withdraw their troops from Cyprus and that they would dismantle paramilitary forces on the island. Cyprus agreed the next day to the proposal; Greece returned its troop levels to the limits specified in agreements in 1960, and \"Turkey canceled large-scale preparations for an invasion\", bringing an end to the crisis that had started on November 15.\nForty-two people were injured while riding on one of San Francisco's famed cable cars. The car was traveling in a driving rain on Hyde Street when the grip that held the car steady slipped, sending the vehicle hurtling down the steep hill. After ramming an automobile at the intersection with Bay Street, the car continued until stopping at North Point Street near Fisherman's Wharf. The automobile, which had caught fire, rolled down Hyde Street and struck eight other vehicles.", + "doc_fkgl": 12.497337640821737, + "wiki_fkgl": 11.189594574671972, + "doc_tree_depth": 5.96, + "wiki_tree_depth": 7.375, + "fkgl_delta": 1.307743066149765 + }, + { + "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": "Interventional oncology procedures are generally divided between diagnostic procedures that help obtain tissue diagnosis of suspicious neoplasms and therapeutic ones that aim to cure or palliate the tumour. Therapeutic interventional oncology procedures may be classified further into ablation techniques that destroy neoplastic tissues by delivery of some form of heat, cryo or electromagnetic energy and embolization techniques that aim to occlude the blood vessels feeding the tumour and thereby destroy it by means of ischemia. Both ablation and embolization techniques are minimally invasive treatment, i.e. they may be delivered through the skin (in a percutaneous way) without the need for any skin incisions or other form of open surgery. Hence, most treatments are nowadays offered as day case or outpatient appointments and patients may enjoy rapid recovery and minimal pain and discomfort with low rates of complications.", + "doc_fkgl": 5.185050449959093, + "wiki_fkgl": 17.576291970802917, + "doc_tree_depth": 4.526315789473684, + "wiki_tree_depth": 11.5, + "fkgl_delta": -12.391241520843824 + }, + { + "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": "Legacy and positions\nRawat's contributions are reported in bringing laparoscopic and robotic surgery for Gastrointestinal cancer to Sir Ganga Ram Hospital. He and his team is credited with the first successful performance of robotic and laparoscopic Oesophagectomy in North India, the first robotic hepatico-jejunostomy in India and the first low anterior resection in North India. Reports also credit him with the introduction of an Enhanced recovery programme for cancer Surgery. Besides publishing several articles in peer reviewed journals, he has also contributed to Oxford Handbook of Clinical Surgery and Operative Surgery, two reference books published by Oxford University Press.", + "doc_fkgl": 16.9342905982906, + "wiki_fkgl": 18.377651515151516, + "doc_tree_depth": 5.8, + "wiki_tree_depth": 8.5, + "fkgl_delta": -1.443360916860918 + }, + { + "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": "Ann & Robert H. Lurie Children's Hospital of Chicago\nAtrium Health\nBaptist Health South Florida\nBaylor St. Luke's Medical Center\nBoston Children's Hospital\nBrigham Health/Dana-Farber Cancer Institute\nBroward Health International\nCancer Treatment Centers of America\nCedars-Sinai\nChildren's Hospital Los Angeles\nChildren's Hospital of Philadelphia\nChildren's Mercy Kansas City\nChildren's National Hospital\nCincinnati Children's\nCity of Hope\nCleveland Clinic\nCook Children's Health Care System\nDignity Health International\nGillette Children's Specialty Healthcare\nHenry Ford Health System\nHospital for Special Surgery\nHouston Methodist\nIndiana University Health\nJohns Hopkins Medicine International\nKeck Medicine of the University of Southern California\nKennedy Krieger Institute\nMassachusetts General Hospital\nMayo Clinic\nMD Anderson Cancer Center\nMedStar Georgetown University Hospital\nMemorial Healthcare System\nMemorial Hermann\u2013Texas Medical Center & TIRR Memorial Hermann\nMemorial Sloan Kettering Cancer Center\nMoffitt Cancer Center\nMount Sinai Health System\nNationwide Children's Hospital\nNew York University (NYU) Langone Health\nNewYork-Presbyterian\nNicklaus Children's Hospital\nNorthwell Health\nNorthwestern Medicine\nOchsner Health System\nPenn Medicine\nRush University Medical Center\nSharp HealthCare\nStanford Medicine\nTexas Children's Hospital\nThe James Cancer Hospital at the Ohio State University\nThe Paley Institute at St. Mary's Medical Center\nThe Shirley Ryan AbilityLab\nUChicago Medicine\nUniversity Hospitals Cleveland Medical Center\nUniversity of California, Los Angeles (UCLA) Health\nUniversity of California, San Diego (UCSD) Health\nUniversity of California, San Francisco (UCSF) Health\nUniversity of Pittsburgh Medical Center (UPMC) and Children's Hospital of Pittsburgh of UPMC\nWashington University School of Medicine in St. Louis\nYale International Medicine Program", + "doc_fkgl": 14.549020678891925, + "wiki_fkgl": 29.713087866108783, + "doc_tree_depth": 6.681818181818182, + "wiki_tree_depth": 16.0, + "fkgl_delta": -15.164067187216858 + }, + { + "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": "Tommy John surgery\nAhmad has performed many Tommy John surgeries. This is an elbow surgery most commonly performed on collegiate and professional athletes, especially baseball players. It is known in the medical community as ulnar collateral ligament (UCL) reconstruction, a surgical graft procedure in which the ulnar collateral ligament in the medial elbow is replaced with a tendon from elsewhere in the body. Tommy John surgeries are being performed with greater frequency, leading to questions of whether sports elbow injuries are becoming more common or if players with elbow injuries are undergoing the surgery when it\u2019s not necessary. In 2012 Ahmad published a paper regarding the public\u2019s perception of the surgery. In it, he stated that 33% of coaches, 37% of parents, 51% of high school athletes, and 26% of collegiate athletes believed that Tommy John surgery should be performed on players without elbow injury to enhance performance.", + "doc_fkgl": 5.560996503496504, + "wiki_fkgl": 14.998918918918921, + "doc_tree_depth": 4.916666666666667, + "wiki_tree_depth": 8.166666666666666, + "fkgl_delta": -9.437922415422417 + }, + { + "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": "Tommy John surgery\nAhmad has performed many Tommy John surgeries. This is an elbow surgery most commonly performed on collegiate and professional athletes, especially baseball players. It is known in the medical community as ulnar collateral ligament (UCL) reconstruction, a surgical graft procedure in which the ulnar collateral ligament in the medial elbow is replaced with a tendon from elsewhere in the body. Tommy John surgeries are being performed with greater frequency, leading to questions of whether sports elbow injuries are becoming more common or if players with elbow injuries are undergoing the surgery when it\u2019s not necessary. In 2012 Ahmad published a paper regarding the public\u2019s perception of the surgery. In it, he stated that 33% of coaches, 37% of parents, 51% of high school athletes, and 26% of collegiate athletes believed that Tommy John surgery should be performed on players without elbow injury to enhance performance.", + "doc_fkgl": 9.454666666666668, + "wiki_fkgl": 14.998918918918921, + "doc_tree_depth": 5.454545454545454, + "wiki_tree_depth": 8.166666666666666, + "fkgl_delta": -5.544252252252253 + }, + { + "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": "She first gained real popularity in the sport because she was the first female rider ever to land an \"s-bend\" (wakeboarding trick which is a raley with a 360 -degree overhead rotation) behind a boat. Others had landed it in a cable park, but it is much more difficult to do behind a boat because of the lower angle of the rope. Since then, she has gone on to land many other tricks that other females have not been able to in the past. Her daredevil instincts have also landed her many injuries, but that hasn't stopped her. She has suffered injuries such as torn biceps, a dislocated kneecap, and two broken ankles. Her coach, Fletcher, said that at one tournament, she had an ankle injury that she probably shouldn't have been riding on in the first place, but she wanted to go so bad that when she couldn't find her tape for her ankle, she ended up taping her ankle in duct tape.", + "doc_fkgl": 11.863529411764706, + "wiki_fkgl": 11.618780487804877, + "doc_tree_depth": 5.75, + "wiki_tree_depth": 7.666666666666667, + "fkgl_delta": 0.24474892395982906 + }, + { + "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": "On the morning of January 18, 2015, Olson suffered a near-fatal heart attack at his home. His wife performed CPR until medical help arrived. He was placed in a medically induced coma, after which two stents were put into his heart. Doctors were initially concerned about his condition since his brain had been deprived of oxygen for \"a period of time,\" but Olson came out of the coma about a week after the heart attack, and was released from the hospital a week after that.", + "doc_fkgl": 4.0628178694158095, + "wiki_fkgl": 10.328088235294121, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 6.0, + "fkgl_delta": -6.265270365878312 + }, + { + "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": "A traumatic brain injury (TBI) is a blow, jolt or penetration to the head that disrupts the function of the brain. Most TBIs are caused by falls, jumps, motor vehicle traffic crashes, being struck by a person or a blunt object, and assault. Student-athletes may be put at risk in school sports, creating concern about concussions and brain injury. A concussion can be caused by a direct blow to the head, or an indirect blow to the body that causes reactions in the brain. The result of a concussion is neurological impairment that may resolve spontaneously but may also have long-term consequences.", + "doc_fkgl": 13.757534883720933, + "wiki_fkgl": 10.760117647058824, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 8.4, + "fkgl_delta": 2.997417236662109 + }, + { + "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": "Professional associations\nAshok Seth is a member of Asian Pacific Society of interventional Cardiology (APSIC) Board of Trustees and SCAI Nominating Committee and sits on the advisory boards of ACC India, SCAI Interventional Fellows Institute (IFI), International Andreas Gruentzig Society (IAGS), E-Cypher, USA, Asia-Pacific Society of Interventional Cardiology (Singapore) and ERA Educational Trust and Medical College, Lucknow. He holds the chair of the Indian chapter of the Organization of International Medical Video Interventional Program (IMVIP) and is the co-chairman of SCAI International Committee. He is a voting selector of SCAI (MSCAI) Nominating Committee, Zonal vice president of Asian Pacific Society of Cardiology, associate director of TCT Scientific Sessions and the president of the Delhi branch of the Cardiological Society of India. He is a founding member of Endovascular Intervention Society of India, Academy of TCT, New York and the SAARC Cardiac Society for Research, Training and Exchange of Expertise in Prevention and Treatment of Heart Disease in Asia. He is a trustee of Indo-French Cardiovascular Foundation for Research, Education and Training in the field of Angioplasty and a former trustee of Society of Cardiovascular Angiography and Interventions, USA. He has also served as the vice president of the Cardiological Society of India and as the chairman of the New Delhi branch of Indian Medical Association.", + "doc_fkgl": 12.237704402515725, + "wiki_fkgl": 23.411976744186052, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 11.333333333333334, + "fkgl_delta": -11.174272341670328 + } +] \ No newline at end of file