diff --git "a/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_16_v1.json" "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_16_v1.json" new file mode 100644--- /dev/null +++ "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_16_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": "Donald J Sherrard, Gavril Hercz, York Pei, Norma A Maloney, Celia Greenwood, Arif Manuel, Carl Saiphoo, Stanley S Fenton, Gino V Segre. The spectrum of bone disease in end-stage renal failure\u2014an evolving disorder. Kidney International. 1993.\n Julian Paul Midgley, Andrew Glenday Matthew, Celia Margaret T Greenwood, Alexander Gordon Logan. Effect of reduced dietary sodium on blood pressure: a meta-analysis of randomized controlled trials. JAMA. 1996.\n Brent W Zanke, Celia MT Greenwood, Jagadish Rangrej, Rafal Kustra, Albert Tenesa, Susan M Farrington, James Prendergast, Sylviane Olschwang, Theodore Chiang, Edgar Crowdy, Vincent Ferretti, Philippe Laflamme, Saravanan Sundararajan, St\u00e9phanie Roumy, Jean-Fran\u00e7ois Olivier, Fr\u00e9d\u00e9rick Robidoux, Robert Sladek, Alexandre Montpetit, Peter Campbell, Stephane Bezieau, Anne Marie O'Shea, George Zogopoulos, Michelle Cotterchio, Polly Newcomb, John McLaughlin, Ban Younghusband, Roger Green, Jane Green, Mary EM Porteous, Harry Campbell, Helene Blanche, Mourad Sahbatou, Emmanuel Tubacher, Catherine Bonaiti-Pelli\u00e9, Bruno Buecher, Elio Riboli, Sebastien Kury, Stephen J Chanock, John Potter, Gilles Thomas, Steven Gallinger, Thomas J Hudson, Malcolm G Dunlop. Genome-wide association scan identifies a colorectal cancer susceptibility locus on chromosome 8q24. Nature Genetics. 2007.\n Jean-Philippe Fortin, Aur\u00e9lie Labbe, Mathieu Lemire, Brent W Zanke, Thomas J Hudson, Elana J Fertig, Celia MT Greenwood, Kasper D Hansen. Functional normalization of 450k methylation array data improves replication in large cancer studies. Genome Biology. 2014.", + "doc_fkgl": 4.138157894736846, + "wiki_fkgl": 18.072553317535547, + "doc_tree_depth": 4.5, + "wiki_tree_depth": 6.5625, + "fkgl_delta": -13.934395422798701 + }, + { + "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": "Post-vaccination embolic and thrombotic events, termed vaccine-induced immune thrombotic thrombocytopenia (VITT), vaccine-induced prothrombotic immune thrombocytopenia (VIPIT), thrombosis with thrombocytopenia syndrome (TTS), vaccine-induced immune thrombocytopenia and thrombosis (VITT), or vaccine-associated thrombotic thrombocytopenia (VATT), are rare types of blood clotting syndromes that were initially observed in a number of people who had previously received the Oxford\u2013AstraZeneca COVID\u201119 vaccine (AZD1222) during the COVID\u201119 pandemic. It was subsequently also described in the Janssen COVID\u201119 vaccine (Johnson & Johnson), leading to the suspension of its use until its safety had been reassessed. On 5 May 2022 the FDA posted a bulletin limiting the use of the Janssen Vaccine to very specific cases due to further reassessment of the risks of TTS, although the FDA also stated in the same bulletin that the benefits of the vaccine outweigh the risks.", + "doc_fkgl": 15.20401179941003, + "wiki_fkgl": 23.791729323308278, + "doc_tree_depth": 4.888888888888889, + "wiki_tree_depth": 9.0, + "fkgl_delta": -8.587717523898249 + }, + { + "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": "Publications\nFonseca has over 50 published works as lead author or co-author. They include:\nFonseca AC, Merwick A, Dennis M, et al. European Stroke Organisation (ESO) guidelines on management of transient ischaemic attack. European Stroke Journal. 2021\nFonseca AC, Marto JP, Pimenta D, et al. Undetermined stroke genesis and hidden cardiomyopathies determined by cardiac magnetic resonance. Neurology. 2020\nFonseca AC, Alves P, In\u00e1cio N, Marto JP, Viana-Baptista M, Pinho-E-Melo T, Ferro JM, Almeida AG. Patients with Undetermined Stroke Have Increased Atrial Fibrosis: A Cardiac Magnetic Resonance Imaging Study. Stroke. 2018\nFonseca AC, Marto JP, Alves PN, et al. Women Who Have Ischemic Strokes Have a Higher Burden of Left Atrial Fibrosis Than Men. Stroke. 2018\nFonseca AC, Franco AC, Tavares J. Bilateral parotid gland hemorrhage after intravenous thrombolysis for stroke treatment. J Neuro 2017\nFonseca AC, Ferro JM. Cryptogenic stroke. Eur J Neurol. 2015\nFonseca AC, Melo TP, Ferro JM. Cotard delusion after stroke. Eur J Neurol 2013\nFonseca AC, Matias JS, E Melo TP, Pires C, Geraldes R, Canh\u00e3o P, Brito D, Ferro JM. Time course of NT-proBNP levels after acute ischemic stroke. Acta Neurol Scand 2013\nFonseca AC, Ferro JM. Drug abuse and stroke. Current Neurology and Neuroscience Reports 2013\nFonseca AC, Geraldes R, Pires J, Falc\u00e3o F, Bentes C, Melo TP. Improvement of sleep architecture in the follow up of a patient with bilateral paramedian thalamic stroke. Clin Neurol Neurosurg 2011\nFonseca AC, Canhao P. Diagnostic difficulties in the classification of transient neurological attacks. Eur J Neurol 2011\nFonseca AC, Ferreira JJ, Albuquerque L, Ferro JM. Sneeze as a precipitating factor of cerebral venous thrombosis. Eur J Neurol 2007", + "doc_fkgl": 17.108284910965327, + "wiki_fkgl": 10.33374183006536, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 4.586206896551724, + "fkgl_delta": 6.774543080899967 + }, + { + "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": "A new case was reported in the year 2000, coming from Florian\u00f3polis, Brazil. A male fetus was discovered to have signs of the symptoms, he came from two non-related parents, with the father of the baby being a positive HIV-virus-carrier drug addict. Before the baby was born, pre-natal pectus excavatum, holopresencephaly, hypotonia, polyhydramnios, articular contractures, severe microcephaly and a depressed forehead. After being born, additional symptoms were seen, and the baby developed severe jaundice and petechia throughout his body and died hours later.", + "doc_fkgl": 3.5813553113553134, + "wiki_fkgl": 14.11213855421687, + "doc_tree_depth": 5.142857142857143, + "wiki_tree_depth": 6.75, + "fkgl_delta": -10.530783242861556 + }, + { + "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": "A new case was reported in the year 2000, coming from Florian\u00f3polis, Brazil. A male fetus was discovered to have signs of the symptoms, he came from two non-related parents, with the father of the baby being a positive HIV-virus-carrier drug addict. Before the baby was born, pre-natal pectus excavatum, holopresencephaly, hypotonia, polyhydramnios, articular contractures, severe microcephaly and a depressed forehead. After being born, additional symptoms were seen, and the baby developed severe jaundice and petechia throughout his body and died hours later.", + "doc_fkgl": 11.942105263157895, + "wiki_fkgl": 14.11213855421687, + "doc_tree_depth": 6.4, + "wiki_tree_depth": 6.75, + "fkgl_delta": -2.1700332910589744 + }, + { + "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": "History \nPrior to AG's initiation, the most frequent and best-known types of rare glioneuronal tumors in the brain were dysembryoplastic neuroepithelial tumors and gangliogliomas. In 2002, Wang and his group from the University of Texas recognised a novel neurological pattern in three cerebral hemispheric tumor cases and first published this rare subtype of AG tumor to the American Association of Neuropathologists. In 2005, Lellouch-Tubiana and his team analyzed 204 epilepsy surgery specimens histologically from patients aged 2 to 14 and discovered three very similar cases shown by Wang et al. in terms of pathological appearance and MRI results. AG manifests a distinct architectural neuron pattern and morphologic features, which were subsequently characterized as a new clinicopathologic entity named \"angiocentric neuroepithelial tumors\" within the spectrum of children glioneuronal tumors. Simultaneously in the same month in 2005, Wang et al. also published their further discoveries of five AG cases and indicated the specified histologic, immunohistochemical, and ultrastructural properties of this seizure-producing low growing tumor. In 2007, the Fourth Edition of the World Health Organization Classification of Tumors of the Central Nervous System recognized AG as a new clinicopathologic entity and designated it as an epilepsy-associated Grade I tumor with monomorphous bipolar cells and a unique perivascular growth arrangement in the category of \"other neuroepithelial tumors\". In 2016, WHO made a few amendments in the tumor classification parameter and classified AG, choroid glioma of the third ventricle, and astroblastoma as Grade I \"Other Gliomas\" after revision.", + "doc_fkgl": 16.247417695473253, + "wiki_fkgl": 17.665925925925922, + "doc_tree_depth": 6.083333333333333, + "wiki_tree_depth": 8.571428571428571, + "fkgl_delta": -1.4185082304526695 + }, + { + "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": "1980 - 1983\tResearch Fellow, Medical Immunology, University of Edinburgh Medical School.\n1983 - 1987\tAssistant Professor, Dundee University Dental Hospital and School\n1994\t\tProfessor in Oral Immunology\n1995 \tDirector, Immunology Research Group\n2000\t\tAssociate Dean for Research and Enterprise, University of Glasgow\n1988 - 2002\tChair of Periodontology, University of Glasgow\n2002 - 2009\t University of Louisville\n Centre Director Oral And Systemic Disease\n Endowed Professor, Dept. Periodontology \n Professor, Dept. Immunology. University of Louisville\n2009 - 2017 University of Pennsylvania\n Dean of School of Dental Medicine.\n Professor of Otorhinolaryngology at Penn School of Medicine.\n Professor of Pathology\n Professor of Clinical Periodontology\n2018 - 2020 Professor Invite University of Geneva Dental School.\n2020 - Date\t Professor Adjunct University of Bern Dental School, Switzerland.\n2020 - Date\t Founder and Chief Medical Officer Cignpost Diagnostics Ltd.", + "doc_fkgl": 4.63312375249501, + "wiki_fkgl": 17.502150000000004, + "doc_tree_depth": 5.277777777777778, + "wiki_tree_depth": 5.428571428571429, + "fkgl_delta": -12.869026247504994 + }, + { + "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": "1980 - 1983\tResearch Fellow, Medical Immunology, University of Edinburgh Medical School.\n1983 - 1987\tAssistant Professor, Dundee University Dental Hospital and School\n1994\t\tProfessor in Oral Immunology\n1995 \tDirector, Immunology Research Group\n2000\t\tAssociate Dean for Research and Enterprise, University of Glasgow\n1988 - 2002\tChair of Periodontology, University of Glasgow\n2002 - 2009\t University of Louisville\n Centre Director Oral And Systemic Disease\n Endowed Professor, Dept. Periodontology \n Professor, Dept. Immunology. University of Louisville\n2009 - 2017 University of Pennsylvania\n Dean of School of Dental Medicine.\n Professor of Otorhinolaryngology at Penn School of Medicine.\n Professor of Pathology\n Professor of Clinical Periodontology\n2018 - 2020 Professor Invite University of Geneva Dental School.\n2020 - Date\t Professor Adjunct University of Bern Dental School, Switzerland.\n2020 - Date\t Founder and Chief Medical Officer Cignpost Diagnostics Ltd.", + "doc_fkgl": 10.328562500000004, + "wiki_fkgl": 17.502150000000004, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 5.428571428571429, + "fkgl_delta": -7.1735875 + }, + { + "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": "Samaranayake was born in Sri Lanka and attended the Royal College, Sri Lanka for his secondary education. He then earned his Bachelor of Dental Sciences (BDS) degree from the University of Peradeniya, Sri Lanka, and received his Doctoral Degree (DDS), at the University of Glasgow, UK through research into oral candidal infections, where he served as a Consultant/ Senior Lecturer in Oral Medicine and Pathology; simultaneously he was an honorary consultant in microbiology to the Greater Glasgow Health Board, Scotland (1985-1990). He obtained his training in medical and oral microbiology, at the Glasgow Royal Infirmary, for the Fellowship of the Royal College of Pathologists, UK under Professor Morag Timbury. Subsequently, he became a member, and then a fellow of the college, by examination in clinical microbiology. He was the first dentist from South East Asia to do so, and the fourth, internationally to gain such recognition.\nThen he served as an associate professor at the University of Alberta, Canada (1990-1991), and Reader /Professor University of Hong Kong(1991-2013), University of Queensland, Australia (2014-2016), Kuwait University (2017-2018) and as a Visiting Professor at Sharjah University, UAE through invitation (2018-2020). Currently, he is a Professor Emeritus at the University of Hong Kong and an honorary professor at the Universities of Thailand, Indonesia, Oman, China, and Sri Lanka.", + "doc_fkgl": 14.527236842105264, + "wiki_fkgl": 18.940333778371166, + "doc_tree_depth": 7.214285714285714, + "wiki_tree_depth": 8.285714285714286, + "fkgl_delta": -4.413096936265902 + }, + { + "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": "Etimology \nIt was first discovered in April 1989, when Saito et al. described 2 siblings of the opposite sex (one male and one female) born to healthy, young, non-consanguineous parents. The siblings showed the symptoms mentioned above. When post-mortem examination was performed in the brother, he was found to have truncus arteriosus and a ventricular septal defect. During pregnancy, ultrasounds had shown 2 gestational sacs early on the pregnancy, one contained a fetus (that of the male) and the other started deteriorating and finally disappeared 15 weeks into the pregnancy. When Saito et al. investigated, they found that no other syndrome had features similar to this case, therefore they proposed this case to be part of a brand new, separate autosomal recessive syndrome.", + "doc_fkgl": 4.623939393939395, + "wiki_fkgl": 11.217328687572593, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 7.0, + "fkgl_delta": -6.593389293633198 + }, + { + "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": "Etiology \nThis disorder was first discovered in 1968, when a mother and 3 of her children (4 cases) were described with the symptoms mentioned above. In this case, additional features were found in a majority of the patients; three of the patients had esophageal indentation and left ligamentum arteriosum, two of the patients, a still-born baby, had anencephaly. Another child died due to congenital heart disease. The child in question also had microcephaly. This disorder is suspected to be autosomal dominant.", + "doc_fkgl": 11.214120481927715, + "wiki_fkgl": 11.123061728395061, + "doc_tree_depth": 5.4, + "wiki_tree_depth": 6.0, + "fkgl_delta": 0.09105875353265347 + }, + { + "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": "Abdomen: Dorsally grey, ventrally cream, abdominal tuft light ochreous. Male genitalia with tegumen a wide arch; socii with broad base, weak, setose; median process of transtilla long and slender; valva slender, cucullus tapering in proximal half, parallel sided or slightly tapering in distal half, sacculus short, rounded, protruding; excavation between sacculus and cucullus deep, forming an angle of 90 degrees or slightly less; juxta heart-shaped; phallus of even width, curved at 2/3, with strongly sclerotised ventral plate; vesica with numerous denticles and one strong cornutus with large base. Female genitalia with papillae anales band-like; eighth segment short; sterigma with large cup-shaped anterior part; ductus bursae broad, entirely membranous; corpus bursae with large posterior sclerite and numerous spines, also in the posterior part; some of the spines forming a circle. The position of the sclerite and spines depends in part on how the bursae is compressed on the slide. In most preparations the sclerite is positioned on the right side, causing a membranous portion on the left side. The length of the ductus bursae is variable.", + "doc_fkgl": 13.580182389937107, + "wiki_fkgl": 15.743857142857145, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 7.166666666666667, + "fkgl_delta": -2.1636747529200377 + }, + { + "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": "This disorder was discovered by Macdermot et al. in the early winter of 1989, when he described two brothers that came from consanguineous Moslem Pakistani parents, these brothers showed the symptoms mentioned above, but there were also additional symptoms in this case: a prominent glabella, arched eyebrows, a low frontal hairline, small nose, large ears, camptodactyly and nipples with a wide space in-between, absence of psychomotor development, and a thriving failure. The same siblings didn't live past 1 year of age (one lived to be 21 days old and the other lived to be 7 months old). When one of then were examined (post-mortem), cerebral ventricle dilatation and hydronephrosis were observed. One of the brothers had microcephaly that was detectable by fetal ultrasound when it was 17 weeks into gestation.", + "doc_fkgl": 2.581463963963966, + "wiki_fkgl": 13.157692307692308, + "doc_tree_depth": 4.583333333333333, + "wiki_tree_depth": 7.5, + "fkgl_delta": -10.576228343728342 + }, + { + "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": "Treatment\nPulmonary fibrosis is not currently curable; but some steps can be taken to minimize its effects, such as changing the treatment regimen. Other measures that should be taken into account are quitting smoking (if applicable), oxygen therapy, pulmonary rehabilitation, vaccination against influenza and pneumococcus to prevent lung infections, or in extreme cases, a lung transplant. Under certain circumstances, antifibrotic agents such as pirfenidone or nintedanib can be used.", + "doc_fkgl": 12.728571428571431, + "wiki_fkgl": 16.46695652173913, + "doc_tree_depth": 5.166666666666667, + "wiki_tree_depth": 6.666666666666667, + "fkgl_delta": -3.7383850931677003 + }, + { + "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": "Career \nIn 1932 he became a Fellow of the Royal College of Surgeons of Edinburgh and decided to train in thoracic surgery, a surgical speciality which was then in its infancy. He worked in Newcastle under Professor George Grey-Turner who had pioneered thoracic surgical procedures including blunt oesophagectomy. In 1934 Logan assisted his colleague George Mason at the first pneumonectomy in Britain on a 15-year-old patient with bronchiectasis. This involved detaching the lung but leaving it in the thoracic cavity. Logan later described how he was left to remove the necrotic lung as planned on the 10th post-operative day. During World War II he served in the Royal Army Medical Corps ending with the rank of lieutenant-colonel. He served in Egypt and in Palestine where he was surgeon in charge of a thoracic surgical unit. At the start of the National Health Service in 1948, he was asked to set up a thoracic surgical unit in Edinburgh, initially at the Eastern General Hospital moving to the Edinburgh City Hospital in 1952. This unit became the regional thoracic surgical unit for south east Scotland, initially dealing mainly with pulmonary tuberculosis, lung cancer and oesophageal cancer. As cardiac surgery was developed he established a cardiac surgery unit at the Royal Infirmary of Edinburgh. Logan devised an operation for mitral stenosis for which he gained an international reputation. He designed a mitral valve dilator, introduced through the left ventricle and achieved impressive results with this technique. The instrument was modified by Oswald Tubbs, who added a screw, and by Russell Brock and the procedure became widely used until the advent of open heart surgery. In 1968 he performed the first lung transplant in the UK (the fifth in the world) on a patient whose lungs had been damaged by paraquat poisoning.", + "doc_fkgl": 15.644583333333337, + "wiki_fkgl": 12.747670182166832, + "doc_tree_depth": 6.769230769230769, + "wiki_tree_depth": 6.466666666666667, + "fkgl_delta": 2.8969131511665047 + }, + { + "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": "Use in diagnosis\nCOVID-19 rapid antigen tests (RATs) have been widely used for diagnosis of COVID-19. The World Health Organization (WHO) COVID-19 Case Definition states that a person with a positive RAT (also known as an antigen rapid diagnostic test or Antigen-RDT) can be considered a \"confirmed case of SARS-CoV-2 infection\" in two ways. First, the person with a positive Antigen-RDT could meet a \"probable case definition\" such as having recent loss of smell or taste without any known cause, or could meet certain \"suspect criteria\" such as having a severe acute respiratory illness. Second, the person with a positive Antigen-RDT could be asymptomatic but a \"contact of a probable or confirmed case.\" Nevertheless, individual countries may have different case definitions of COVID-19; for example, in New Zealand a positive PCR test (not just a RAT) is necessary for a person to be considered a \"confirmed case.\"", + "doc_fkgl": 5.415573678290215, + "wiki_fkgl": 15.70321088435374, + "doc_tree_depth": 4.785714285714286, + "wiki_tree_depth": 7.2, + "fkgl_delta": -10.287637206063525 + }, + { + "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": "The most frequently used immunosuppressive drug is cyclosporin, which is commonly prescribed after an organ transplant. Nearly 53% of patients taking cyclosporin after renal transplants presented with gingival growth. Inflammation from bacterial overgrowth in the gingiva and cyclosporin's main metabolite, hydroxyciclosporin, stimulate production of collagen, while simultaneously inhibiting collagen breakdown \u2014 leading to a net increase in production of gingival tissues. Tacrolimus, on the other hand, is less toxic than cyclosporin, causing less severe gingival overgrowth, hepatic and renal toxicity.", + "doc_fkgl": 16.420789473684213, + "wiki_fkgl": 16.011234177215194, + "doc_tree_depth": 6.166666666666667, + "wiki_tree_depth": 7.5, + "fkgl_delta": 0.4095552964690192 + }, + { + "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": "Symptoms \nHepatic hydrothorax has no specific symptoms as it generally occurs with ascites and other manifestations of increased pressure in the portal vein caused by liver disease. Pleural fluid causes symptoms far more easily than ascitic fluid, due to the lower volume of the pleural cavity as compared to the abdominal cavity. The main symptoms are usually related to the symptoms of liver cirrhosis and ascites. Less often, it may be the only manifestation of chronic liver disease. The symptoms depend on many factors, such as the effusion's volume, rate of accumulation, and the co-existence of cardiopulmonary disease. The disease may cause no symptoms and be incidentally detected by medical scans, or it may cause large pleural effusions that result in respiratory symptoms like cough, shortness of breath, low blood oxygen, and respiratory failure. Most people have progressive difficulty breathing and reduced tolerance for exercise. Rarely, there may be acute cases that accumulate fluid rapidly and result in circulatory collapse. In some cases, the main symptoms of people with cirrhosis are respiratory and related to the effusion.", + "doc_fkgl": 16.479367816091955, + "wiki_fkgl": 13.880000000000003, + "doc_tree_depth": 6.15, + "wiki_tree_depth": 7.777777777777778, + "fkgl_delta": 2.599367816091952 + }, + { + "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": "Physical examination reviews clinical symptoms like degree of jaundice, vital signs and sensations of pain, further followed by urine tests, blood analysis and imaging. The degree of yellowish staining of the conjunctiva and skin in jaundice is proportional to hyperbilirubinemia to some extent. Vital signs, such as fever, tachycardia and hypotension, suggest hyperbilirubinemia induced by viral hepatitis. Abdominal pain could indicate biliary tract obstruction and cirrhosis.", + "doc_fkgl": 4.512113821138211, + "wiki_fkgl": 14.445000000000004, + "doc_tree_depth": 4.444444444444445, + "wiki_tree_depth": 6.0, + "fkgl_delta": -9.932886178861793 + }, + { + "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 1977 contamination\nIn 1976 a pregnant woman (referred to as \"Patient X\" in the report of the Finlay Tribunal) was a patient of Dr. McGuinness, assistant master of the Coombe Maternity Hospital.\nHaving had several pregnancies severely affected by haemolytic disease, Patient X was prescribed a therapeutic course of plasma exchange over a 25-week period, to reduce the antibodies that would damage her foetus. The obstetric consultant suggested to one of the BTSB staff that they could off-set the cost of Patient X's treatment by using the plasma extracted from her (which had high concentrations of anti-D) to manufacture anti-D immunoglobulin. Patient X was never asked to consent to her plasma being used in this way.", + "doc_fkgl": 11.051032608695653, + "wiki_fkgl": 13.303521367521366, + "doc_tree_depth": 5.0, + "wiki_tree_depth": 9.25, + "fkgl_delta": -2.252488758825713 + }, + { + "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": "Adverse effects \nBelzutifan was well tolerated, according to the previously available data, and its adverse effect profile was acceptable. Anemia, tiredness, headaches, vertigo, nausea, and dyspnea were the most typical side effects. All participants in the phase II trial reported a hemoglobin reduction of at least 1.9 g/dL; however, only a small number of individuals needed transfusions or erythropoietin-stimulating medications. Because of the downstream effect of HIF-2 inhibition, anemia was a predicted negative outcome of inhibiting the EPO gene. The majority of negative outcomes were grade 1 or 2, while 33% of patients experienced grade 3 to 5 occurrences. In 43% of patients, the course of treatment was discontinued, and in 15% of patients, the dosage had to be adjusted. 2% of patients stopped receiving therapy as a result of a treatment-related. \nfatigue, increased creatinine, headache, dizziness, elevated hyperglycemia, and nausea were the most frequent side effects, including laboratory abnormalities, recorded in 20% or less of patients. Belzutifan has the potential to harm fetuses and embryos during pregnancy and can render some hormonal contraceptives ineffective\nBelzutifan had a good safety profile and was well tolerated throughout the three-year follow-up following the phase I trial. There were no new substantial safety concerns or grade 4 or 5 adverse events.", + "doc_fkgl": 11.779287370862324, + "wiki_fkgl": 14.136468531468534, + "doc_tree_depth": 6.208333333333333, + "wiki_tree_depth": 7.222222222222222, + "fkgl_delta": -2.35718116060621 + }, + { + "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": "Description\nA male and female were described by Levi in 2003. The female had a total length of 15.5\u00a0mm, the carapace being 5.4\u00a0mm long with a maximum width of 5.2\u00a0mm. The carapace was light orange-brown, with three projections with black ends. The sternum was light orange-brown. The abdomen was whitish, with a pair of brown tubercules on the upper surface and a central white rectangle on the lower surface. The first leg was longest, the patella and tibia totalling 10.8\u00a0mm. The male was much smaller, with a total body length of 1.6\u00a0mm, about a tenth of that of the female. Its carapace and the underside of the abdomen were dark brown. The carapace was rough but lacked the projections of the female. The upper surface of the abdomen was spotted with black, grey and white, and had three humps and two hardened discs. The male's palpal bulb had a distinct conductor supporting the embolus. Contrary to an earlier statement by Conrad Akerman that C.\u00a0akermani uses its third leg (a statement repeated by others, e.g. Yeargan), the female handles its bolas with the second leg, swinging it in a horizontal plane.", + "doc_fkgl": 3.26104347826087, + "wiki_fkgl": 6.124837935174071, + "doc_tree_depth": 4.0, + "wiki_tree_depth": 6.333333333333333, + "fkgl_delta": -2.863794456913201 + }, + { + "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": "Background \nThe use of ultrasound and biochemical markers to detect aneuploidies is usually done in the first and / or second trimester of pregnancy. However, both of these approaches have a high rate of false positive results of 2\u20137%. If these tests indicate an increased risk of aneuploidy, then invasive diagnostic testing is used, such as amniocentesis or chorionic villus sampling. Many women, however, feel uncomfortable with the invasive testing, because of the risk associated with miscarriage, which is around 0.5%. Noninvasive prenatal testing is an intermediate step between prenatal screening and invasive diagnostic testing. The only physical risk associated with the procedure is the blood draw and there is no risk of miscarriage.", + "doc_fkgl": 11.784036259541985, + "wiki_fkgl": 13.68420353982301, + "doc_tree_depth": 5.375, + "wiki_tree_depth": 6.285714285714286, + "fkgl_delta": -1.9001672802810248 + }, + { + "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": "Before birth \nTransient myeloproliferative disease develops and may be of concern in fetuses. Features in a review of 39 reported fetal cases include: reduced platelet production often accompanied by significantly reduced levels of circulating platelets; reduced red blood cell production sometimes accompanied by mild anemia; increased levels of circulating megakaryoblasts and white blood cells; grossly enlarged liver and liver dysfunction due to an excessive accumulation of platelet precursor cells; enlarged spleen presumed due mostly to the portal hypertension accompanying liver disease with extramedullary hematopoiesis possibly contributing to the enlargement; accumulation of excessive fluid in bodily compartments such as the pericardial, pleural, abdominal spaces; hydrops fetalis, i.e. the accumulation of excessive fluid in two or more bodily compartments; cardiomegaly and other cardiac abnormalities resulting form atrial septal defects, small ventricular septal defects, and/or, possibly, accumulation of megakaryocytes and secondary cardiac fibrosis. Hydrops fetalis, when accompanied by liver dysfunction, is a particularly poor prognostic combination in TMD.", + "doc_fkgl": 15.11899521531101, + "wiki_fkgl": 24.492822580645164, + "doc_tree_depth": 6.5, + "wiki_tree_depth": 7.0, + "fkgl_delta": -9.373827365334154 + }, + { + "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": "Brain \nBeing highly metabolic with low blood reserves, the brain is the most sensitive organ to ischemia. As a result, any amount of brain ischemia, especially when it is prolonged in cases of cardiac arrest, typically results in brain injury. Increasingly severe injury can lead to long term consequences such as cognitive dysfunction, persistent vegetative state and finally brain death. The brain sustains irreversible injury after about 20 minutes of ischemia. Even after blood flow is restored to the brain, patients can experience hours-days of hypotension, hypoxemia, impaired cerebrovascular autoregulation, brain edema, fever, hyperglycemia and/or seizures which further insult brain tissue. Diagnosis of brain injury involves neurological examination, EEG, brain imaging and/or biomarker evaluation (such as S100B and NSE). For out-of-hospital cardiac arrest, brain injury is the cause of death in most patients who undergo ROSC but ultimately die.", + "doc_fkgl": 4.794388489208632, + "wiki_fkgl": 14.990256937307297, + "doc_tree_depth": 4.923076923076923, + "wiki_tree_depth": 7.142857142857143, + "fkgl_delta": -10.195868448098665 + }, + { + "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": "Pharmacology \nPegcetacoplan acts as a complement inhibitor, specifically targeting complement protein C3, which plays a crucial role in the pathogenesis of paroxysmal nocturnal hemoglobinuria (PNH). In individuals with PNH, there is a heightened and uninhibited complement activity, which may lead to intravascular (inside blood vessels) or extravascular (within the liver or spleen) hemolysis. By binding to and inhibiting C3, pegcetacoplan helps regulate complement activation, thereby reducing red blood cell destruction, anemia, blood clot formation, and improving bone marrow function. This targeted mechanism of action makes pegcetacoplan the first-in-class medication for the treatment of PNH, offering a promising therapeutic approach to address the underlying complement dysregulation in this condition.", + "doc_fkgl": 14.753525835866263, + "wiki_fkgl": 19.414074074074076, + "doc_tree_depth": 6.333333333333333, + "wiki_tree_depth": 8.25, + "fkgl_delta": -4.660548238207813 + }, + { + "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": "Pharmacokinetics \nDasiglucagon rapidly enters the bloodstream upon administration, resulting in a dose-dependent increase in plasma levels within approximately 15 minutes. The maximum concentration of dasiglucagon in the bloodstream is typically attained around 35 minutes after administration, with a half-life (t1/2) of approximately 0.5 hours. Following the time to maximum concentration (tmax), dasiglucagon demonstrates a decline in concentration over a span of approximately 0.4-0.7 hours, as compared to glucagon's t1/2 of 0.25 hours. Consequently, dasiglucagon exhibits significantly greater values for area under the curve (AUC) measurements, such as AUC0-inf, AUC0-30 min, AUC0-240 min, and maximum concentration (Cmax), when administered under euglycemic conditions. These values are approximately 1.4-4 times higher than those observed with glucagon. Comparative analysis with the medication GlucaGen\u00ae (glucagon for injection 1mg/mL) reveals that dasiglucagon demonstrates more prolonged plasma exposure and higher total drug exposure (AUC0-inf). Therapeutic ratios for dasiglucagon doses of 0.6 mg and 0.3 mg, in relation to GlucaGen\u00ae doses of 1.0 mg and 0.5 mg, respectively, indicate superior effects on AUC0-inf, BL (1.59 and 1.46). In contrast, the effects on Cmax,BL are similar (1.03 and 0.91). However, it is worth noting that the upper limit of the 95% confidence interval (CI) for Cmax and AUC0-30 min is slightly lower than 1, potentially due to higher early plasma exposure per milligram observed in the lower-dose group compared to the higher-dose group. In clinical trials (NCT03216226), dasiglucagon showed a similar safety profile to reconstituted glucagon. No serious adverse events or deaths were reported. The most common side effects were nausea and vomiting. In terms of efficacy, dasiglucagon was as effective as reconstituted glucagon in reversing severe hypoglycemia induced by insulin, with a median recovery time of 10 minutes compared to 12 minutes for reconstituted glucagon. The recovery time was significantly shorter compared to the placebo group (median 40 minutes).", + "doc_fkgl": 14.958653673835126, + "wiki_fkgl": 11.15056025369979, + "doc_tree_depth": 5.866666666666666, + "wiki_tree_depth": 7.357142857142857, + "fkgl_delta": 3.808093420135336 + }, + { + "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": "Career\nGreen was the first cardiac surgeon to successfully perform a left coronary artery bypass graft using the internal thoracic artery sutured to the left anterior descending coronary artery to bypass obstruction to the heart circulation in the 1968. At the time, many experts believed that the internal mammary artery was too small for splicing into the coronary arteries. The bypass called for 20 stitches to be taken to attach the vessel. \"Many years ago George Green stood alone in support of the internal mammary artery as a superior conduit,\" Dr. John L. Ochsner of the Ochsner Clinic in New Orleans had written. \"In the years since, many of us have joined his ranks.\"", + "doc_fkgl": 6.522207792207791, + "wiki_fkgl": 12.004210526315791, + "doc_tree_depth": 5.571428571428571, + "wiki_tree_depth": 7.0, + "fkgl_delta": -5.482002734108001 + }, + { + "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": "George E. Green is an American cardiac surgeon best known for pioneering and implementing the first surgical procedure of the left coronary artery bypass graft using the internal thoracic artery sutured to the left anterior descending coronary artery to bypass obstruction to the heart circulation in the late 1960s. He applied these techniques in 1968 at New York University Medical Center and in 1970 he was hired to establish St. Luke's Hospital's (now Mount Sinai Morningside) cardiac surgery program in Manhattan, New York, that by 1982 was seeing approximately 1,800 cases a year, the biggest program in the state. Green has lectured internationally on the topic and has written numerous reports on internal thoracic artery grafting as well as co-authoring, Surgical Revascularization of the Heart: The Internal Thoracic Arteries.", + "doc_fkgl": 13.480000000000004, + "wiki_fkgl": 18.94098837209302, + "doc_tree_depth": 7.166666666666667, + "wiki_tree_depth": 10.0, + "fkgl_delta": -5.460988372093016 + }, + { + "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": "A second major and related focus of Grinspoon\u2019s work has been to investigate the mechanisms and strategies for CVD in HIV. \u00a0In this regard, he led an AHA sponsored State of the Science Symposium on CVD in HIV. The conclusions from this conference called for a better understanding and treatment strategies of CVD in HIV. This work began with epidemiologic studies demonstrating increased myocardial infarction rates in HIV patients in the JCEM. This data was followed by a series of mechanistic studies demonstrating increased prevalence of plaque, particularly noncalcified, lipid rich, plaque. Grinspoon used FDG PET to demonstrate for the first time significant arterial inflammation in asymptomatic low traditional risk HIV patients, compared to Framingham risk matched control subjects, as well as non HIV patients with known CVD, published in JAMA. Of note, increased arterial inflammation was most significantly associated with increased markers of immune activation. He also recently proposed the first use of tilmanocept as a CD206 specific imaging agent for arterial inflammation, with significant success in HIV published in JID. This work was followed by studies in HIV patients in which he phenotyped the morphological characteristics of coronary plaque in HIV patients, demonstrating an increased prevalence of high risk plaque with low attenuation and positive remodeling, more vulnerable to rupture. His studies suggested that treatment with a statin might uniquely target both traditional risk factors including low-density lipoprotein (LDL) but also increased immune activation indices driving atypical noncalcified high risk plaque in this population. This work culminated in a recent paper in Lancet HIV, in which he showed for the first time that a statin can significantly reduce high risk plaque volume as well as improve the high-risk morphological features in coronary lesions in HIV. In recognition of this work, he has led the REPRIEVE trial, a global primary prevention study performed in 12 countries, since 2013 and gave the plenary lecture at CROI 2015 on this topic.", + "doc_fkgl": 9.065632911392406, + "wiki_fkgl": 15.976250000000004, + "doc_tree_depth": 6.684210526315789, + "wiki_tree_depth": 7.833333333333333, + "fkgl_delta": -6.910617088607598 + }, + { + "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": "Association \nThere are several associations of PUK to ocular and systemic diseases. Rheumatoid arthritis (RA),\u00a0 Wegner's granulomatosis (WG), and Polyarteritis Nodosa (PAN) are the most common systemic conditions.\n Rheumatoid arthritis: Approximately 50% of PUK are related to collagen vascular diseases, in which RA is the most common category. Around 34-42% of PUK patients have RA.\n Wegner's granulomatosis: WG is a rare autoimmune disease associated with PUK. It causes vasculitis of the lower and upper respiratory tracts, and it also affects multiple organs, including eyes. Without timely initiation of systemic therapy, WG patients will develop conjunctival and scleral inflammations. The inflammation will eventually cause corneal thinning and worsen PUK.\n Polyarteritis Nodosa: PAN is another autoimmune disease in which the body's immune system attacks small and medium-sized arteries of its own by mistake. PUK is one of the predominant ocular inflammatory manifestations of PAN.", + "doc_fkgl": 6.597509398496243, + "wiki_fkgl": 13.797295774647893, + "doc_tree_depth": 5.875, + "wiki_tree_depth": 5.8, + "fkgl_delta": -7.19978637615165 + }, + { + "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": "In August 1919, Pavel Pototsky lost one eye. Later, the other eye gradually lost its ability to see. In June 1920, Pototsky who had already lost 90% of his vision, had to go to Moscow for treatment of his eyes. Doctors were unable to bring the vision back to Pototsky's eyes. He was suffering from atrophy of the optic nerve and at the time there was no cure for this disease. As a result, at the age of 41, he lost the ability to see in both eyes.", + "doc_fkgl": 11.54186046511628, + "wiki_fkgl": 6.623181818181816, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 5.833333333333333, + "fkgl_delta": 4.918678646934463 + }, + { + "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": "Shimizu S, Lichter PR, Johnson AT, Zhou Z, Higashi M, Gottfredsdottir M, Othman M, Moroi SE, Schertzer RM, Clarke MS, Schwartz AL, Downs CA, Vollrath D, Richards JE: Age-dependent prevalence of mutations at the GLC1A locus in primary open-angle glaucoma. Am. J. Ophthalmol. 130:165-177, 2000.\nLaRoche GR, McIntyre L, Schertzer RM: Epidemiology of severe eye injuries in childhood. Ophthalmology 95(12):1603-1607, 1988.\nMoroi SE, Gottfredsdottir MS, Schteingart MT, Elner SG, Lee CM, Schertzer RM, Abrams GW, Johnson MW: Cystoid Macular Edema Associated with Latanoprost Therapy in a Case Series of Patients with Glaucoma and Ocular Hypertension. Ophthalmology 106(5):1024-1029, 1999.\nCanadian Ophthalmological Society Glaucoma Clinical Practice Guideline Expert Committee; Canadian Ophthalmological Society. Canadian Ophthalmological Society evidence-based clinical practice guidelines for the management of glaucoma in the adult eye. 2009 Aug;44(4):477. PMID 19492005.\nSugar A, Schertzer RM: The Clinical Course of Phacoemulsification Wound Burns. J Cataract Refract Surg 25(5):688-692, 1999.\nEibschitz-Tsimhoni M, Schertzer RM, Musch DC, Moroi SE. Incidence and management of encapsulated cysts following Ahmed glaucoma valve insertion. J Glaucoma. 2005 Aug;14(4):276-9.\nIsbister CM, Schertzer RM, Mackenzie PJ: Comparison of Silicone and Polypropylene Ahmed Glaucoma Valves: Two year follow-up. Canadian Journal Ophthalmology 42: 227-232, April 2007.", + "doc_fkgl": 14.661870129870131, + "wiki_fkgl": 14.134123711340209, + "doc_tree_depth": 5.473684210526316, + "wiki_tree_depth": 4.35, + "fkgl_delta": 0.5277464185299223 + }, + { + "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": "Among others, Schneider\u2019s expertise in intensive care internal medicine concentrated on emergency service for patients with cardiac pacemakers (1972\u20131975) and coronary angiography (1986/1987) as well as consultations for the neurosurgical and orthopedic departments of the University of Leipzig Medical Center (1981\u20131987). When Schneider started to work at the neurological clinic in 1987, the neurocritical emergency service with cephalic CAT scan (1987\u20131999, CAT scan, computed axial tomography or computer-assisted tomography) and consultations at the Leipzig Heart Center (1987\u20131996) followed. In 1993, a modern neurological intensive care unit opened, professionally, structurally prepared and with personnel selected by Schneider, as well as a spatially integrated stroke unit with its initially own personnel in 1998. Both neurocritical units moved to the new building \u201cZentrum f\u00fcr Konservative Medizin\u201d [Center for Conservative Medicine] in 2009 (21 beds with mechanical ventilation, including 12 certified transregional stroke-unit-beds). The internal intensive care department led by Lothar Engelmann was located on the same floor and directly adjacent. In the same year, Schneider handed over the management of the intensive neurological department to his successors (Carsten Hobohm and Dominik Michalski), continued his works on stroke studies with the help of third-party funds (until 2011) and was the manager of the Multiplace HBOT chamber at the clinic for anesthesiology and intensive care therapy until February 28, 2014. He worked on a 24/7 on-call service for emergencies that have to be treated hyperbarically.", + "doc_fkgl": 6.542719298245618, + "wiki_fkgl": 20.465155279503104, + "doc_tree_depth": 4.823529411764706, + "wiki_tree_depth": 8.285714285714286, + "fkgl_delta": -13.922435981257486 + }, + { + "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": "Canada approved the creation of these two units on 25 January 1916, and an organizing committee for XI Canadian Field Ambulance, led by the University of Alberta's President Henry Marshall Tory, was soon formed. The committee chose Major John Douglas McQueen, of Winnipeg, to lead the new unit; Edmonton's Dr. Heber Havelock Moshier became the second-in-command. McQueen, a surgeon, had previously served in France for a year with 3 Canadian Field Ambulance. Moshier was a professor of physiology at the University of Alberta, but had been the medical officer of 103rd Regiment (Calgary Rifles) until moving to Edmonton in 1914. Moshier chose John Ralph Hammond to be the unit's sergeant; Hammond had been a second-year medical student until becoming the hospital sergeant of 66th Battalion (Edmonton Guards) in July 1915, and transferred to 8 Canadian Field Ambulance in February 1916.", + "doc_fkgl": 12.910294117647059, + "wiki_fkgl": 15.087142857142855, + "doc_tree_depth": 6.444444444444445, + "wiki_tree_depth": 7.2, + "fkgl_delta": -2.176848739495796 + }, + { + "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": "By identifying in 1979 the If (\"funny\") pacemaker current in the sinus node, Dario DiFrancesco challenged the prevailing theory and proposed a novel mechanism to explain the origin of cardiac rhythm. Based on the discovery of the new \u201cfunny\u201d channels, carrying an inward (mixed Na+ and K+) current and activating on hyperpolarization, he modified the concept of cardiac pacemaking by demonstrating that the universally accepted \u201cpacemaker\u201d theory of the time, attributed to the deactivation of an outward potassium current (IK2) in Purkinje fibres, was wrong and had to be turned upside-down. He showed that IK2 had been incorrectly interpreted for over a decade as a pure K+ current and was instead a disguised \u201cfunny\u201d current, and pacemaking was not due to deactivation of the outward IK2, but to activation of the inward If. These results showed that the mechanism of pacemaker generation in Purkinje fibres and in sinoatrial node cells was the same, allowing for the first time an integrated view of pacemaking in the heart. Following the discovery of If, DiFrancesco published several studies demonstrating its permeability and gating characteristics, its involvement in the autonomic rate control, and investigated its single-channel properties, providing first evidence for the smallest conductance (1 pS) channel recorded by patch-clamp. Using a macro-patch clamp technique, he showed for the first time that funny channels are directly activated by intracellular cAMP, a mechanism responsible for the If -mediated autonomic modulation of heart rate. The same modulatory mechanism was later confirmed in HCN channels. These experimental studies have been complemented by mathematical and modelling analyses demonstrating the role of If in pacemaker rhythm. In 1985, he developed with Denis Noble a theoretical model incorporating the If -based model of pacemaking and other new experimental results. The model allowed to interpret all experimental data, and represented the paradigm from which subsequent cellular models of the heart were developed. The 1985 model paper was selected in 2015 by the Royal Society, London, as one of the 33 most influential articles published by the Philosophical Transactions of the Royal Society in the 350 years since its foundation in 1665.", + "doc_fkgl": 13.475840409207162, + "wiki_fkgl": 18.969376623376622, + "doc_tree_depth": 6.2631578947368425, + "wiki_tree_depth": 9.545454545454545, + "fkgl_delta": -5.49353621416946 + }, + { + "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": "In larva, abdomen consists with a long anal tube and a urogomphi, both are bent upward. This urogomphi is used to excrete feces. During each moulting, cuticle is partially shed by leaving the exuviae together with the feces. This is visible as a black ball over the body. Early instar grubs are leaf miners and show gregarious behavior called cycloalexy. Fourth instar forms small groups of two or three individuals. Pupation began with one day of pre-pupal period. Pupal case is made of exuviae and feces. Pupal period is about 5 to 6 days.", + "doc_fkgl": 6.041, + "wiki_fkgl": 7.6897163120567384, + "doc_tree_depth": 5.125, + "wiki_tree_depth": 5.111111111111111, + "fkgl_delta": -1.648716312056738 + }, + { + "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": "Larva\nGrubs are whitish translucent in color. The resting posture is C-shaped. Third instar is about 20\u201325\u00a0mm in length. Head reddish brown in color. The last abdominal segment swollen and dark particularly due to the soil ingestion. Spiracles creamy white with 9 pairs in which one pair prothoracic and eight pairs abdominal segments.", + "doc_fkgl": 12.18240740740741, + "wiki_fkgl": 6.494074074074078, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 4.166666666666667, + "fkgl_delta": 5.688333333333333 + }, + { + "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": "The thallus of Punctelia perreticulata measures in diameter. It has either a close or loose attachment to its substrate (either bark, wood, or rock). The upper surface of the thallus is grey to greenish grey, and is often marked with shallow depressions and pits (scrobicules)\u2013but not always. The lobes comprising the thallus are typically wide. The peripheral lobes are covered with pruina (a powdery deposit), which may be abundant, but not always on every lobe. In fresh specimens, the pruina gives the thallus a glaucous (greyish-blue) appearance. Pseudocyphellae are on both the surface of the thallus and its margins. They are point-like (punctiform) or oblong, sometimes elevated and located on ridges of the upper surface, but rarely restricted to the margins. The pseudocyphellae develop into secondary soralia with farinose (mealy) or granular soredia; these sometimes co-occur with phyllidia. Phyllidia are small, leaf-like or scale-like outgrowths from a foliose thallus, which are constricted at the point of attachment and thus readily detached and dispersed by wind or animals. The medulla is white, while the thallus undersurface is a light colour, described as pale buff to creamish, and often darker near the tips. Apothecia are very rarely observed in this species.", + "doc_fkgl": 14.957394957983198, + "wiki_fkgl": 10.030263819095477, + "doc_tree_depth": 5.411764705882353, + "wiki_tree_depth": 6.083333333333333, + "fkgl_delta": 4.92713113888772 + }, + { + "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": "Publications\nOkan has published several articles in many leading journals. Some of his notable contributions are:\n \n Gokhan Okan, Adile Merve Baki, Eda Yorulmaz, Semra Do\u011fru\u2010Abbaso\u011flu, and Pervin Vural. \"Serum Visfatin, Fetuin\u2010A, and Pentraxin 3 Levels in Patients with Psoriasis and Their Relation to Disease Severity\". Journal of clinical laboratory analysis.\n Gokhan Okan, and Halil Ibrahim Canter. \"Nicolau syndrome and perforator vessels: a new viewpoint for an old problem\". Journal of Cutaneous and Ocular Toxicology.\n Gokhan Okan, and Can Baykal. \"Nevoid hyperkeratosis of the nipple and areola: treatment with topical retinoic acid\". Journal of the European Academy of Dermatology and Venereology.\n Gokhan Okan, Serpil Yaylaci, Onder Peker, Sabahattin Kaymakoglu, and Murat Saruc. \"Vanishing bile duct and Stevens-Johnson syndrome associated with ciprofloxacin treated with tacrolimus\". World Journal of gastroenterology.\n Can Baykal, G\u00f6khan Okan, and Rifkiye Sarica. \"Childhood bullous pemphigoid developed after the first vaccination\". Journal of the American Academy of Dermatology.\n G\u00f6khan Okan, \"Atopik dermatitin ba\u015f boyun lokalizasyonlar\u0131nda pityrosporum ovalenin rol\u00fc\". (\"The role of pityrosporum ovalen in head and neck localization of atopic dermatitis.\")\n Gokhan Okan, Adile Merve Baki, Eda Yorulmaz, Semra Dogru-Abbasoglu, Pervin vural. A preliminary study about neurofilament light chain and tau protein levels in psoriasis: Correlation with disease severity. Journal of Clinical Laboratory Analysis", + "doc_fkgl": 5.827348837209307, + "wiki_fkgl": 11.35665505226481, + "doc_tree_depth": 5.066666666666666, + "wiki_tree_depth": 5.1, + "fkgl_delta": -5.529306215055502 + }, + { + "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": "2002: Howard & Jacqueline Chertkof Endowed Fellowship, Johns Hopkins University\n 2003: University Merit Review Award, University of Oxford\n 2004 British Journal of Haematology Research Trust Award\n 2004: Paper of the Year in the Platelets Section of the Journal of Thrombosis and Haemostasis\n 2004: International Society on Thrombosis and Haemostasis Young Investigator Award\n 2005: Gordon Research Conference Speaker Award\n 2007: Paper of the Year in the Platelets Section of the Journal of Thrombosis and Haemostasis\n 2009: American Heart Association Karl Link New Investigator Award in Thrombosis\n 2010: American Heart Association Kenneth M. Brinkhous Young Investigator in Thrombosis Finalist\n 2013: American Heart Association Established Investigator Award\n 2014: Fellow of the American Heart Association\n 2019: Best Basic Science Award at the International Sepsis Forum\n 2021: Douglas Strain Endowed Professorship, OHSU Department of Biomedical Engineering", + "doc_fkgl": 14.593809523809526, + "wiki_fkgl": 34.267692307692315, + "doc_tree_depth": 5.888888888888889, + "wiki_tree_depth": 5.4, + "fkgl_delta": -19.67388278388279 + }, + { + "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": "A second major and related focus of Grinspoon\u2019s work has been to investigate the mechanisms and strategies for CVD in HIV. \u00a0In this regard, he led an AHA sponsored State of the Science Symposium on CVD in HIV. The conclusions from this conference called for a better understanding and treatment strategies of CVD in HIV. This work began with epidemiologic studies demonstrating increased myocardial infarction rates in HIV patients in the JCEM. This data was followed by a series of mechanistic studies demonstrating increased prevalence of plaque, particularly noncalcified, lipid rich, plaque. Grinspoon used FDG PET to demonstrate for the first time significant arterial inflammation in asymptomatic low traditional risk HIV patients, compared to Framingham risk matched control subjects, as well as non HIV patients with known CVD, published in JAMA. Of note, increased arterial inflammation was most significantly associated with increased markers of immune activation. He also recently proposed the first use of tilmanocept as a CD206 specific imaging agent for arterial inflammation, with significant success in HIV published in JID. This work was followed by studies in HIV patients in which he phenotyped the morphological characteristics of coronary plaque in HIV patients, demonstrating an increased prevalence of high risk plaque with low attenuation and positive remodeling, more vulnerable to rupture. His studies suggested that treatment with a statin might uniquely target both traditional risk factors including low-density lipoprotein (LDL) but also increased immune activation indices driving atypical noncalcified high risk plaque in this population. This work culminated in a recent paper in Lancet HIV, in which he showed for the first time that a statin can significantly reduce high risk plaque volume as well as improve the high-risk morphological features in coronary lesions in HIV. In recognition of this work, he has led the REPRIEVE trial, a global primary prevention study performed in 12 countries, since 2013 and gave the plenary lecture at CROI 2015 on this topic.", + "doc_fkgl": 16.972754430379748, + "wiki_fkgl": 15.976250000000004, + "doc_tree_depth": 6.380952380952381, + "wiki_tree_depth": 7.833333333333333, + "fkgl_delta": 0.9965044303797441 + }, + { + "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": "Occurrence and consequences of pendelluft \nAn extreme example of pendelluft is found in a spontaneously breathing patient with an open hemithorax or large flail segment. During the inspiratory phase, the contralateral lung (with a closed / intact chest wall) will expand with most of the tidal volume, with the open plura or paradoxical chest wall movement preventing expansion of the ipsilateral lung. However, during the expiratory phase, there will be gas flow (pendelluft) from the contralateral lung to the lung ipsilateral to the open thorax. Inspiration can also cause gas movement from the ipsilateral to the contralateral lung. This can significantly impair ventilation, and historically was one issue that limited thoracic surgery until more complex methods of mechanical ventilation were available.", + "doc_fkgl": 5.730088652482269, + "wiki_fkgl": 16.288333333333334, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 6.2, + "fkgl_delta": -10.558244680851065 + }, + { + "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": "Esophagogastric junction outflow obstruction (EGJOO) is an esophageal motility disorder characterized by increased pressure where the esophagus connects to the stomach at the lower esophageal sphincter. EGJOO is diagnosed by esophageal manometry. However, EGJOO has a variety of etiologies; evaluating the cause of obstruction with additional testing, such as upper endoscopy, computed tomography (CT imaging), or endoscopic ultrasound may be necessary. When possible, treatment of EGJOO should be directed at the cause of obstruction. When no cause for obstruction is found (functional EGJOO), observation alone may be considered if symptoms are minimal. Functional EGJOO with significant or refractory symptoms may be treated with pneumatic dilation, per-oral endoscopic myotomy (POEM), or botulinum toxin injection.", + "doc_fkgl": 11.984808362369339, + "wiki_fkgl": 14.937300884955754, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 6.333333333333333, + "fkgl_delta": -2.9524925225864145 + }, + { + "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": "Females are millimeters long. In addition to the typical brown tones, fresh adult females show contrasting patterns of almost white, dark brown and black spots. Characteristic is an elongated, strongly tapering ridge medial on the posterior ninth tergite of the abdomen. Also typical of the species are two laterally compressed and rounded teeth on the distal, outer abdominal ridges of the middle and hind legs. The structures on the head are designed as follows. The supra anantals, as well as the anterior and posterior supra occipital, are formed as blunt spines that become shorter towards the rear. The vertex is elongated and raised. The supra orbitals are clearly pronounced, laterally slightly flattened and blunt. The anterior coronals are laterally compressed and lamellar. Their anterior margins extend to the tip of the supraorbital. The centrale coronale is connected to the anterior coronals and is slightly raised. The posterior and lateral coronals are triangular tubercles. A row of three tubercles is located between the lateral coronals and the supra orbitals and further tubercles on the side of the ridge between the lateral and anterior coronals. Behind the eyes there is a distinct edge that reaches the rear edge of the ridge. The antennae, consists of 25 segments, are shorter than the fore legs. There are small tubercles on the body surface. The middle of the abdomen is clearly enlarged laterally.", + "doc_fkgl": 16.455087719298245, + "wiki_fkgl": 9.462518059855523, + "doc_tree_depth": 7.0, + "wiki_tree_depth": 5.529411764705882, + "fkgl_delta": 6.992569659442722 + }, + { + "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": "Presentation\nLPF presents as an ill-defined, slow growing tumor mass located in or below the subcutaneous tissue (area of the skin below the dermis) of an extremity or, less commonly, the thigh, trunk, or head areas. Rare single cases of these tumors have been reported in occur in the heart and eye socket. These tumors are often painless but in some cases become painful when manipulated during examination. LPF tumors occur almost exclusively in children at birth (~18% of cases) up to age 8 years with most cases presenting before age 2 years; they are extremely rare in adults. The disorder has a 2:1 male predominance. LPD tumors are usually 5\u00a0cm. or smaller and obvious on physical examination. Uncommonly, LPF tumors present after they have invaded adjacent underlying structures such as blood vessels, nerves, and muscles although significant functional impairment of the invaded tissues is uncommon. Individuals have also presented with recurrences of these tumors at the site of surgery in up to 1/3 of all surgically treated cases.", + "doc_fkgl": 5.262667512690356, + "wiki_fkgl": 12.322549019607845, + "doc_tree_depth": 5.15, + "wiki_tree_depth": 6.333333333333333, + "fkgl_delta": -7.059881506917488 + }, + { + "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": "Banki syndrome is a rare disorder in which two or more bones are fused. The symptoms may include: abnormality of the long bone of hand; short fingers or toes; permanent curving of the pinkie finger; fusion of wrist bones. The disorder has been reported in three generations of a single Hungarian family. First described by Z. Banki in a 1965 paper, it has been noted as being similar to Liebenberg syndrome, featuring lunatotriquetral fusion of the lunate bone with the triquetral bone, clinodactyly of the fingers, overall short metacarpals, and thin diaphysis of the longer bones, but unlike Liebenberg, no elbow dysplasia is observed.", + "doc_fkgl": 13.893053097345135, + "wiki_fkgl": 11.923923076923078, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 7.75, + "fkgl_delta": 1.9691300204220568 + }, + { + "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": "Presentation\nIndividuals presenting with SEF tumors are 3 to 87 years old (median age 44.6 years) with most individuals aged 30-60\u202fyears. These tumors involve the lower limb and shoulder areas (28.3% of cases), trunk (18.7%), head and neck areas (11.7%), lung and its pleura (10.0%), bone (including the spinal vertebrae) (10.0%), soft tissues (9.1%), upper limb and shoulder areas (7.5%), kidney (3.9%), pancreas (0.9%), liver (0.4%), and brain (0.4%). Rare cases of SEF tumors have developed in the ovary and lower gastrointestinal tract. In two separate studies, 17% and 27% of patients presented with metastases at the time of the initial diagnosis of their disease. While most individuals present with a painless mass, about 33% report having a painful and enlarging mass. The tumor may have been noticed and even painful for a few months to years. Tumors developing in the head, abdominal cavity, or other space-constrained sites often present with symptoms and signs related to their tumors' mass effects. For example, 5 of 5 patients diagnosed with SEF tumors in the spinal vertebrae presented with pain that they had experienced for 3 to 6 months and 2 of 2 patients with a SEF located in the buttock presented with highly painful sciatica. SEF tumors have varied in size from 1 to 25 cm in diameter (average diameter, 8.3 cm). In one small study, all individuals treated with surgical resection of their tumors, re-presented with recurrences of their tumors at the sites of their surgical removal and 91% re-presented with metastases (67% to the lung, 50% to bone, and 1 case each to the liver, brain and abdomen).", + "doc_fkgl": 15.117090909090908, + "wiki_fkgl": 8.355900159320235, + "doc_tree_depth": 6.071428571428571, + "wiki_tree_depth": 8.4, + "fkgl_delta": 6.761190749770673 + }, + { + "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": "The focus of his scientific research was staphylococci and the diseases they cause. His findings on the pathogenesis of foreign body-associated infections by coagulase-negative staphylococci and their ability to form biofilms are considered groundbreaking. His first publication on this topic dates back to 1982, and he consistently championed the diagnosis, prophylaxis and therapy of infections caused by multi-resistant pathogens, such as in particular the methicillin-resistant Staphylococcus aureus strains, the so-called MRSA. His reputation in this field was reflected, among other things, in his election as vice-president (1991) and president (1993) of the \"Gordon Research Conference on Staphylococcal Diseases\".", + "doc_fkgl": 7.468333333333334, + "wiki_fkgl": 17.44459183673469, + "doc_tree_depth": 6.125, + "wiki_tree_depth": 8.25, + "fkgl_delta": -9.976258503401358 + }, + { + "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": "The focus of his scientific research was staphylococci and the diseases they cause. His findings on the pathogenesis of foreign body-associated infections by coagulase-negative staphylococci and their ability to form biofilms are considered groundbreaking. His first publication on this topic dates back to 1982, and he consistently championed the diagnosis, prophylaxis and therapy of infections caused by multi-resistant pathogens, such as in particular the methicillin-resistant Staphylococcus aureus strains, the so-called MRSA. His reputation in this field was reflected, among other things, in his election as vice-president (1991) and president (1993) of the \"Gordon Research Conference on Staphylococcal Diseases\".", + "doc_fkgl": 12.996079027355623, + "wiki_fkgl": 17.44459183673469, + "doc_tree_depth": 5.714285714285714, + "wiki_tree_depth": 8.25, + "fkgl_delta": -4.448512809379068 + }, + { + "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": "Publications\nFonseca has over 50 published works as lead author or co-author. They include:\nFonseca AC, Merwick A, Dennis M, et al. European Stroke Organisation (ESO) guidelines on management of transient ischaemic attack. European Stroke Journal. 2021\nFonseca AC, Marto JP, Pimenta D, et al. Undetermined stroke genesis and hidden cardiomyopathies determined by cardiac magnetic resonance. Neurology. 2020\nFonseca AC, Alves P, In\u00e1cio N, Marto JP, Viana-Baptista M, Pinho-E-Melo T, Ferro JM, Almeida AG. Patients with Undetermined Stroke Have Increased Atrial Fibrosis: A Cardiac Magnetic Resonance Imaging Study. Stroke. 2018\nFonseca AC, Marto JP, Alves PN, et al. Women Who Have Ischemic Strokes Have a Higher Burden of Left Atrial Fibrosis Than Men. Stroke. 2018\nFonseca AC, Franco AC, Tavares J. Bilateral parotid gland hemorrhage after intravenous thrombolysis for stroke treatment. J Neuro 2017\nFonseca AC, Ferro JM. Cryptogenic stroke. Eur J Neurol. 2015\nFonseca AC, Melo TP, Ferro JM. Cotard delusion after stroke. Eur J Neurol 2013\nFonseca AC, Matias JS, E Melo TP, Pires C, Geraldes R, Canh\u00e3o P, Brito D, Ferro JM. Time course of NT-proBNP levels after acute ischemic stroke. Acta Neurol Scand 2013\nFonseca AC, Ferro JM. Drug abuse and stroke. Current Neurology and Neuroscience Reports 2013\nFonseca AC, Geraldes R, Pires J, Falc\u00e3o F, Bentes C, Melo TP. Improvement of sleep architecture in the follow up of a patient with bilateral paramedian thalamic stroke. Clin Neurol Neurosurg 2011\nFonseca AC, Canhao P. Diagnostic difficulties in the classification of transient neurological attacks. Eur J Neurol 2011\nFonseca AC, Ferreira JJ, Albuquerque L, Ferro JM. Sneeze as a precipitating factor of cerebral venous thrombosis. Eur J Neurol 2007", + "doc_fkgl": 12.497337640821737, + "wiki_fkgl": 10.33374183006536, + "doc_tree_depth": 5.96, + "wiki_tree_depth": 4.586206896551724, + "fkgl_delta": 2.1635958107563766 + }, + { + "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": "The story begins with a flashback in 2001 introducing Johnathan Hui, Amos Fong, and Eman Cheung as medical interns. An operation causes a rift between Hui and Fong, leading to them becoming estranged. Flash to the present, Hui and Fong are pediatric surgeons and work at North West Hospital and Princess Anne Hospital, respectively. One day, Hui asks Fong to perform a liver transplant operation jointly. An anesthetic mistake occurs during the procedure where Cheung, a cardiothoracic surgeon, appears timely to rescue. She returns to Hong Kong after being a Doctor Without Borders and is now a newly contracted doctor at Princess Anne Hospital. With the ambitious vision of building a pediatric facility, Fong uses tactics to make Hui join Princess Anne Hospital. He then recruits Hui, Cheung, and a few other doctors, including Max Man, a resident specialist, Kay Mak, pediatric chief of service and Fong's love\u2013interest, and Joey Kwok, an anesthesiologist, to create an \"elite\" surgery team, building themselves an influential reputation to pave the way for Fong's vision. The team faces various obstacles during the process, with Hui and Fong reconciling their friendship. The truth of the operation incident in the past also gets revealed. Although Fong's vision is not yet realized towards the end of the series; the doctors experience growth in both their personal and professional lives.", + "doc_fkgl": 5.185050449959093, + "wiki_fkgl": 12.47910728910729, + "doc_tree_depth": 4.526315789473684, + "wiki_tree_depth": 6.636363636363637, + "fkgl_delta": -7.2940568391481975 + }, + { + "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": "Cripps was well known as teacher and demonstrator; he taught \"with dogmatism, enlivened by caustic wit and shrewd thrusts\". He was an early advocate of inguinal colostomy. He suggested in 1882 that having multiple rectal polyps could be familial. Working with Thomas Claye Shaw, he tried to relieve paralysis and mental symptoms in patients by relieving fluid pressure on the brain. He was responsible for several surgical inventions - an \u00e9craseur for removing sections of the lower rectum (later adapted by oral surgeons for use on the tongue) and a rubber rectal dilator. He published a number of works on rectal and abdominal surgery. A section of his Carcinoma of the Rectum was reprinted in 1986 as part of a series of \"Classic Articles of Colonic and Rectal Surgery\" in the journal Diseases of the Colon & Rectum.", + "doc_fkgl": 16.9342905982906, + "wiki_fkgl": 11.162142857142857, + "doc_tree_depth": 5.8, + "wiki_tree_depth": 7.714285714285714, + "fkgl_delta": 5.772147741147741 + }, + { + "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": "Assignments\nJune 1990 \u2013 June 1991, Surgical Intern, Wilford Hall Medical Center, Lackland AFB, Texas\nJuly 1991 \u2013 June 1992, General Medical Officer, Wilford Hall Medical Center, Lackland AFB, Texas\nJune 1992 \u2013 June 1997, Urological Surgery Resident, Wilford Hall Medical Center, Lackland AFB, Texas\nJuly 1997 \u2013 October 1997, Assistant Chief, Urology, 89th MDG, Andrews AFB, Md.\nNovember 1997 \u2013 September 1999, Chief, Urology, 89th MDG, Andrews AFB, Md.\nOctober 1999 \u2013 September 2000, Chief, Population Health Management, 89th MDG, Andrews AFB, Md.\nOctober 2000 \u2013 July 2001, Analyst, Health Benefits and Policy Division, Office of the Surgeon General, Headquarters Air Force, Bolling AFB, Washington, D.C.\nAugust 2001 \u2013 June 2002, Chief, Operations Branch, Office of the Surgeon General, Headquarters Air Force, Bolling AFB, Washington, D.C.\nJuly 2002 \u2013 May 2003, Chief, Optimization and Integration Division, Air Force Medical Operations Agency (AFMOA), Bolling AFB, Washington, D.C.\nMay 2003 \u2013 May 2005, Commander, 56th Medical Operations Squadron, Luke AFB, Ariz. (September 2004 \u2013 January 2005, Commander, 332nd Expeditionary Aeromedical Operations Squadron, Balad Air Base, Iraq)\nJune 2005 \u2013 April 2006, Chief, Aeromedical and Clinical Services Branches, Headquarters Air Force Space Command, Peterson AFB, Colo.\nMay 2006 \u2013 July 2007, Chief, Medical Operations Division, Headquarters Air Force Space Command, Peterson AFB, Colo.\nAugust 2007 \u2013 June 2008, Student, National War College, Fort McNair, Washington, D.C.\nAugust 2008 \u2013 July 2010, Commander, 3rd Medical Group, 3rd Wing, Elmendorf AFB, Alaska\nJuly 2010 \u2013 July 2011, Commander, 673d Medical Group, 673rd Air Base Wing, JB Elmendorf-Richardson, Alaska\nJuly 2011 \u2013 July 2014, Command Surgeon, HQ Pacific Air Forces, JB Pearl Harbor- Hickam, Hawaii\nJuly 2014 \u2013 June 2016, Vice Commander, AFMOA, JB San Antonio, Lackland, Texas\nJanuary 2015 \u2013 June 2015, Chair, Joint Task Force on High Reliability Organizations, Office of the Assistance Secretary of Defense for Health Affairs, Washington, D.C.\nJune 2016 \u2013 July 2018, Command Surgeon, US Transportation Command, Scott AFB, Ill.\nJuly 2018\u2013 July 2019, Air Combat Command (ACC), Command Surgeon, JB Langley-Eustis, Va.\nJuly 2019\u2013present, Joint Staff Surgeon, the Pentagon, Arlington, Va.", + "doc_fkgl": 14.549020678891925, + "wiki_fkgl": 14.998569217160554, + "doc_tree_depth": 6.681818181818182, + "wiki_tree_depth": 11.5, + "fkgl_delta": -0.4495485382686297 + }, + { + "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": "Legacy in Orthopedics \nDr. Mumford specialized in industrial injuries and was a leading contributor to the literature on mobilization of joint injury publishing hundreds of articles in his lifetime. In 1931 Mumford was one of the eight founders of the American Academy of Orthopedic Surgeons and served as its president for two terms. In 1941 Mumford patented a procedure for distal clavical resection or acromioplasty commonly known as The Mumford Procedure, named in the surgeon's honor. The surgery aims to relieve shoulder pain by removing a small part of the clavicle, or collar bone. Patients with inflammation, swelling, or osteoarthritis in the acromioclavicular (AC) joint elect to have this procedure, if alternative solutions like physical therapy and cortisone injections are unsuccessful. The surgery can be performed using an open or arthroscopic procedure, and typically requires ten weeks recovery time.", + "doc_fkgl": 5.560996503496504, + "wiki_fkgl": 14.396012332990754, + "doc_tree_depth": 4.916666666666667, + "wiki_tree_depth": 8.5, + "fkgl_delta": -8.83501582949425 + }, + { + "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": "Genetic Basis \nMinor severity of said ulnar defect and toe syndactyly in female members of the same family studied in the original discovery suggested that this disorder was transmitted in an X-linked recessive manner, although autosomal dominance with reduced penetrance wasn't excluded as an inheritance pattern. It is more common in males than females. It is hard to characterize the genetic basis of the symptoms of this syndrome, such as the split-foot deformity, due to the lack of occurrence, the wide array of genes involved in limb development, and the complicated interactions of these genes and gene products. While genes and chromosomal loci for other syndromes involving split-hand/split-foot deformities have been identified, specific loci for Van Den Berghe Dequeker syndrome have not been studied.", + "doc_fkgl": 9.454666666666668, + "wiki_fkgl": 17.625806451612906, + "doc_tree_depth": 5.454545454545454, + "wiki_tree_depth": 8.75, + "fkgl_delta": -8.171139784946238 + }, + { + "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": "Personal \nWhite was born on 16 February 1992. She was born and raised in Sydney before moving west to a cattle farm during her teenage years. In 2010, she was involved in a near-fatal head-on motor vehicle accident, where her car was hit by another car that was mistakenly on her side of the road. The accident left her with a broken left foot, broken left ankle, compound fractures of the tibia and fibula, shattered left and right knee caps, broken femur, broken hip, broken ribs, broken collarbone, broken wrist, nose and six vertebrae in her spine. She further had internal injuries, resulting in a damaged kidney, hematoma and extensive scarring. The injuries led to \"a loss of movement and feeling in my left leg, knee, ankle and foot due to nerve damage, steel plates/pins and issues with tendons\" and '\"reduced range of motion and feeling in my right wrist, which also has some steel pins, reduced mobility in my right shoulder, as well as issues with my spine due to the broken vertebrae\". The recovery was extensive, requiring multiple surgeries and rehabilitation.", + "doc_fkgl": 11.863529411764706, + "wiki_fkgl": 12.660359094457458, + "doc_tree_depth": 5.75, + "wiki_tree_depth": 7.714285714285714, + "fkgl_delta": -0.7968296826927528 + }, + { + "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": "Heavy accident\nOn Tuesday 5 May 2020 he was hospitalized with a Arteriovenous Malformation brain bleeding. When he had several headaches in the week before the accident, he felt unwell after he rode a horse. He then got off the horse, after which he collapsed. He was subsequently taken to hospital in a critical condition by helicopter to the La Paz Hospital in Madrid, where he was operated on for his brain haemorrhage. Juan was in an artificial coma for three weeks. On 3 July he left the hospital and was allowed to start his rehabilitation process.", + "doc_fkgl": 4.0628178694158095, + "wiki_fkgl": 9.692319587628866, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 5.714285714285714, + "fkgl_delta": -5.6295017182130564 + }, + { + "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": "Heavy accident\nOn Tuesday 5 May 2020 he was hospitalized with a Arteriovenous Malformation brain bleeding. When he had several headaches in the week before the accident, he felt unwell after he rode a horse. He then got off the horse, after which he collapsed. He was subsequently taken to hospital in a critical condition by helicopter to the La Paz Hospital in Madrid, where he was operated on for his brain haemorrhage. Juan was in an artificial coma for three weeks. On 3 July he left the hospital and was allowed to start his rehabilitation process.", + "doc_fkgl": 13.757534883720933, + "wiki_fkgl": 9.692319587628866, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 5.714285714285714, + "fkgl_delta": 4.065215296092067 + }, + { + "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": "Publications\nFonseca has over 50 published works as lead author or co-author. They include:\nFonseca AC, Merwick A, Dennis M, et al. European Stroke Organisation (ESO) guidelines on management of transient ischaemic attack. European Stroke Journal. 2021\nFonseca AC, Marto JP, Pimenta D, et al. Undetermined stroke genesis and hidden cardiomyopathies determined by cardiac magnetic resonance. Neurology. 2020\nFonseca AC, Alves P, In\u00e1cio N, Marto JP, Viana-Baptista M, Pinho-E-Melo T, Ferro JM, Almeida AG. Patients with Undetermined Stroke Have Increased Atrial Fibrosis: A Cardiac Magnetic Resonance Imaging Study. Stroke. 2018\nFonseca AC, Marto JP, Alves PN, et al. Women Who Have Ischemic Strokes Have a Higher Burden of Left Atrial Fibrosis Than Men. Stroke. 2018\nFonseca AC, Franco AC, Tavares J. Bilateral parotid gland hemorrhage after intravenous thrombolysis for stroke treatment. J Neuro 2017\nFonseca AC, Ferro JM. Cryptogenic stroke. Eur J Neurol. 2015\nFonseca AC, Melo TP, Ferro JM. Cotard delusion after stroke. Eur J Neurol 2013\nFonseca AC, Matias JS, E Melo TP, Pires C, Geraldes R, Canh\u00e3o P, Brito D, Ferro JM. Time course of NT-proBNP levels after acute ischemic stroke. Acta Neurol Scand 2013\nFonseca AC, Ferro JM. Drug abuse and stroke. Current Neurology and Neuroscience Reports 2013\nFonseca AC, Geraldes R, Pires J, Falc\u00e3o F, Bentes C, Melo TP. Improvement of sleep architecture in the follow up of a patient with bilateral paramedian thalamic stroke. Clin Neurol Neurosurg 2011\nFonseca AC, Canhao P. Diagnostic difficulties in the classification of transient neurological attacks. Eur J Neurol 2011\nFonseca AC, Ferreira JJ, Albuquerque L, Ferro JM. Sneeze as a precipitating factor of cerebral venous thrombosis. Eur J Neurol 2007", + "doc_fkgl": 12.237704402515725, + "wiki_fkgl": 10.33374183006536, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 4.586206896551724, + "fkgl_delta": 1.9039625724503644 + } +] \ No newline at end of file