tbuckley/cabot-search huggingface dataset:
SUDDEN AND UNEXPECTED DEATH IN EARLY LIFE
Authors: Samuel S. Morrison
Journal: JAMA (1960)

Reduction of the incidence of sudden death in infants and children depends on prompter recognition, by parents and physicians, of significant symptoms and signs which have preceded such deaths in the past. The author presents an analysis of 17 unexpected deaths at ages ranging from 1 day to 30 months; seven cases are given in some detail. In many cases there was an infection that evolved into fatal septicemia within 48 hours after the first symptom. In three infants he only postmortem finding was mild to moderate pulmonary edema, and the patient had been in apparently normal health before being found dead in the crib. Thus, there remains a significant number of children for whom the precise cause of death cannot as yet be consistently determined.
Localisation of xanthine oxidase to synovial endothelium.
Authors: C R Stevens, M Benboubetra, R Harrison, T Sahinoglu, E C Smith, D R Blake
Journal: Annals of the Rheumatic Diseases (1991)

The presence of the xanthine oxidase enzyme system has been demonstrated in the rheumatoid synovium. This supplies a reactive oxygen species generating system to synovium that is subjected to hypoxic-reperfusion cycles (cf inflamed rheumatoid synovium). An antibody to bovine milk xanthine oxidase has been used to localise the enzyme by immunohistochemistry to synovial endothelium. This implicates the endothelial cell as playing a major part in exacerbations of synovitis, induced by radicals.
Acute, Reversible Respiratory Acidosis in Cardiogenic Pulmonary Edema
Authors: Albert Miller
Journal: JAMA (1971)

Acute, often severe, respiratory acidosis which cleared within several hours was noted in ten patients with classic cardiogenic pulmonary edema. Mental obtundation was present in five. Only three of the ten patients had received narcotics. Treatment was directed at the pulmonary edema and usually included intermittent positive pressure breathing. Coexisting metabolic acidosis was mild; two patients had associated metabolic alkalosis. On presentation, the mean Pco<sub>2</sub>was 64.9 mm Hg and mean pH 7.20; after several hours of treatment, pH was normal and Pco<sub>2</sub>minimally reduced. In view of these findings in pulmonary edema, emphasis should be placed on analysis of the arterial blood gases, a free airway, and supported ventilation.
Proposal of a new nomenclature for budd-chiari syndrome: Hepatic vein thrombosis versus thrombosis of the inferior vena cava at its hepatic portion
Authors: Kunio Okuda, Masayoshi Kage, Santosh M. Shrestha
Journal: Hepatology (1998)

Budd–Chiari syndrome (BCS) was initially defined as a symptomatic occlusion of the hepatic veins, but subsequent reports on various obliterative changes that occur in the hepatic portion of the inferior vena cava (IVC) and hepatic vein orifices have resulted in a broadened and ambiguous definition. Membranous obstruction of the inferior vena cava has been regarded by many as a congenital vascular malformation, but its relation to the classical BCS has remained obscure. With modern imaging and recent histological study of new cases, membranous obstruction of the IVC is now considered to be a sequela to thrombosis. How to classify various forms of occlusion and stenosis of the IVC and hepatic vein ostia is a major challenge. In this review, we emphasize that primary hepatic vein thrombosis (classical Budd–Chiari) and an obliterative disease predominantly affecting the hepatic portion of the IVC, both of which account for most patients with venous outflow block, are clinically quite different. In the West, the former is more common than the latter, which constitutes the vast majority of cases of outflow block in developing countries such as Nepal, South Africa, China, and India. The latter is frequently complicated by hepatocellular carcinoma (HCC), and primary hepatic vein thrombosis is not. The major cause of thrombosis is a hypercoagulable state in hepatic vein thrombosis, but more of the latter cases are idiopathic. The clinical presentation of the latter is milder, and onset is frequently inapparent, whereas the former is more severe, sometimes causing acute hepatic failure. Markedly enlarged subcutaneous veins over the body trunk characterize the latter. We propose that these two disorders be clinically distinguished with a suggested term “obliterative hepato–cavopathy” for the latter against classical BCS.
Intramural haematoma of the oesophagus complicating sclerotherapy for varices.
Authors: F Mosimann, B Bronnimann
Journal: Gut (1994)

A patient is described who developed an intramural haematoma of the oesophagus shortly after variceal endoscopic sclerotherapy. This unusual complication is best imaged by computed tomography or nuclear magnetic resonance and needs conservative treatment. Resolution usually occurs spontaneously and may result in eradication of the varices.
Serological Classification of Viridans Streptococci from Subacute Bacterial Endocarditis, Teeth, and Throats
Authors: F. R. Selbie, R. D. Simon, R. H. M. Robinson
Journal: BMJ (1949)

he rang me up and asked if he could show me how well he was.Certainly, eighteen months after my hopeless forecast, he looked as well as any man of his age in Europe and showed no sign of cancer.Fortunately he was pleased about it and did not threaten to sue me for £6,000 damages. Fallacy of StatisticsSuch experiences, indeed my whole experience, have left me with profound mistrust of statistics.
Presenilin-Dependent Transcriptional Control of the Aβ-Degrading Enzyme Neprilysin by Intracellular Domains of βAPP and APLP
Authors: Raphaëlle Pardossi-Piquard, Agnès Petit, Toshitaka Kawarai, Claire Sunyach, Cristine Alves da Costa, Bruno Vincent, Sabine Ring, Luciano D’Adamio, Jie Shen, Ulrike Müller, Peter St. George Hyslop, Frédéric Checler
Journal: Neuron (2005)
SYSTEMIC FACTORS IN CATARRHAL DEAFNESS.
Authors: SARGENT F. SNOW
Journal: JAMA (1901)

Chronic nonsuppurative inflammation of the middle ear by its very location is a most difficult disease to treat; and when we add to this the fact that it is rare for any of these patients to come to us until the disease is of several years' standing, we do not wonder that a doubtful prognosis has been the rule in the past, but if we are to call ourselves specialists, is it to our credit that we should sit calmly down and accept defeat, with our present facilities for reaching the deeper parts of the head? Without frequent exacerbations an inflamed mucous membrane, even in the most advanced chronic form, is not beyond relief and practical cure. The number of our cases of catarrhal deafness where more than this simple inflammation obtains and the deeper labyrinthine structures are involved, is very small indeed; so what is our proposition but a
Influence of Adiposity on Insulin Resistance and Glycemia Markers Among U.K. Children of South Asian, Black African-Caribbean, and White European Origin
Authors: Claire M. Nightingale, Alicja R. Rudnicka, Christopher G. Owen, Jonathan C.K. Wells, Naveed Sattar, Derek G. Cook, Peter H. Whincup
Journal: Diabetes Care (2013)

Ethnic differences in type 2 diabetes risk between South Asians and white Europeans originate before adult life and are not fully explained by higher adiposity levels in South Asians. Although metabolic sensitivity to adiposity may differ between ethnic groups, this has been little studied in childhood. We have therefore examined the associations among adiposity, insulin resistance, and glycemia markers in children of different ethnic origins.Cross-sectional study of 4,633 9- to 10-year-old children (response rate 68%) predominantly of South Asian, black African-Caribbean, and white European origin (n = 1,266, 1,176, and 1,109, respectively) who had homeostasis model assessments of insulin resistance (HOMA-IR), glycemia markers (HbA1c and fasting glucose), and adiposity (BMI, waist circumference, skinfold thicknesses, and bioimpedance [fat mass]).All adiposity measures were positively associated with HOMA-IR in all ethnic groups, but associations were stronger among South Asians compared to black African-Caribbeans and white Europeans. For a 1-SD increase in fat mass percentage, percentage differences in HOMA-IR were 37.5% (95% CI 33.3-41.7), 29.7% (25.8-33.8), and 27.0% (22.9-31.2), respectively (P interaction < 0.001). All adiposity markers were positively associated with HbA1c in South Asians and black African-Caribbeans but not in white Europeans; for a 1-SD increase in fat mass percentage, percentage differences in HbA1c were 0.04% (95% CI 0.03-0.06), 0.04% (0.02-0.05), and 0.02% (-0.00 to 0.04), respectively (P interaction < 0.001). Patterns for fasting glucose were less consistent.South Asian children are more metabolically sensitive to adiposity. Early prevention or treatment of childhood obesity may be critical for type 2 diabetes prevention, especially in South Asians.
Behavioral toxicity of trihalomethane contaminants of drinking water in mice.
Authors: R L Balster, J F Borzelleca
Journal: Environmental Health Perspectives (1982)

The behavioral toxicity of trichloromethane (TCM), dichlorobromomethane (DCBM), dibromochloromethane (DBCM) and tribromomethane (TBM) was evaluated following oral administration in mice. A variety of dosage regimens and behavioral measures were used. Studies included acute dose effect, 14-and 90-day treatments at 300 and 3000 times the estimated average human daily intake of contaminated drinking water, 30 days of 100 mg/kg/day, and 60 days of 100 and 400 mg/kg/day. In addition, TCM was tested for the production of taste aversions with 10-day administration and for behavioral teratology in offspring following extensive perinatal exposure. The ED50 for acute effects on a screen test of motor performance was about 500 mg/kg for all four trihalomethanes. The 14-day treatments had no effect on swimming behavior and the 90-day treatments had no effect on bar clinging, a test of motor coordination, and a measure of exploratory behavior. None of the compounds produced effects on passive-avoidance learning following 100 mg/kg/day for 30 days. TCM, DBCM and TBM elicited clear effects at both 100 and 400 mg/kg/day on operant behavior when administered for 60 days. DBCM elicited clear effects at 400 mg/kg/day. These effects on operant behavior were seen following the first dose and tolerance tended to develop. Thus, there was no evidence from these studies for a progressive neurotoxicity from trihalomethanes in adult mice. A behavioral teratology study was also conducted with TCM. Both parents were treated with 31.1 mg/kg/day TCM, and treatment of the dam continued throughout gestation and lactation. No clear evidence for behavioral effects in the offspring were observed. The most sensitive measure for the effects of TCM was the taste aversion paradigm in which saccharin aversions were produced after a single treatment of 30 mg/kg.
To (anti-)TNF or not (anti-)TNF? That is the question in pemphigus
Authors: A.A. Sinha
Journal: British Journal of Dermatology (2015)

ORIGINAL ARTICLE, p 760 Pemphigus vulgaris (PV) is a prototypical organ‐specific human autoimmune disease in which autoantibodies in the blood and skin target cell adhesion molecules expressed at the surface of keratinocytes leading to blister formation. Although the widespread use of systemic steroids has improved disease outcomes, mortality remains unacceptably high at 10–15%.1 No consensus guidelines exist for therapeutic management of the disease. An extensive Cochrane review, published first in 20092 and subsequently in 2011,3 could not find support for universally effective and safe treatments. A major issue remains: the limited number of randomized controlled trials and small sample sizes for most studies. Advancement in management strategies will rely on further advancements in our understanding of underlying disease mechanisms. The strong human leucocyte antigen associations reported in PV support a model in which autoreactive T cells are involved in the induction and maintenance of autoantibody production. It thus follows that cytokines are likely to be key players in disease pathogenesis. While an integrated view of cytokine networks in PV is incomplete, qualitative and quantitative alterations in several mediators have been reported (reviewed in Giordano and Sinha4).
The Effect of P-Glycoprotein Function Inhibition With Cyclosporine A on the Biodistribution of Tc-99m Sestamibi
Authors: LEVENT KABASAKAL, METIN HALAĈ, CAVIT NISLI, OYA OGUZ, ĈETIN ÖNSEL, GONCA ĈIVI, İLHAMI USLU
Journal: Clinical Nuclear Medicine (2000)

Purpose The failure to cure persons with cancer is caused primarily by the development of drug resistance by overexpression of p-glycoprotein. Diverse groups of drugs have been identified, including cyclosporine A, which can reverse drug resistance by inhibiting P-glycoprotein transport. Tc-99m sestamibi is a substrate for P-glycoprotein. P-glycoprotein is normally expressed in biliary canalicular surfaces of hepatocytes and is responsible for the excretion of cationic metabolites from the liver. The aim of the current study was to evaluate the effect of cyclosporine A on the biological distribution of Tc-99m sestamibi in vivo. Methods Five patients with alopecia and two renal transplant patients who were treated with cyclosporine A were selected for the study. All patients were examined before and at least 2 weeks after administration of cyclosporine A. Tc-99m sestamibi scintigraphy was performed by obtaining planar abdominal images at 5, 30, 60, 120, and 180 minutes after injection, and the liver–heart ratios were calculated. Results Plasma cyclosporine A, bilirubin levels, liver enzymes, and creatinine clearance values were obtained from all patients. In three, the plasma cyclosporine A level was increased to more than 400 pg/dl. The liver–heart ratio was increased significantly after cyclosporine A administration (P < 0.01). After cyclosporine A administration Tc-99m sestamibi excretion was delayed and the uptake in the liver was increased. The difference was 17% at 5 minutes and 38% at 180 minutes. Liver retention was greatest in patients with cyclosporine A toxicity. Conclusions With a limited number of patients, this study suggests that Tc-99m sestamibi excretion from the liver is mediated by P-glycoprotein, and inhibition of P-glycoprotein transport not only delays liver excretion but also increases the liver uptake of Tc-99m sestamibi. Because this observation deserves further investigation, the inhibition of P-glycoprotein function with nontoxic multidrug-resistance reversing agents may be used as an intervention to increase the tumor uptake of Tc-99m sestamibi and to increase the sensitivity of Tc-99m sestamibi tumor imaging.
Science commentary: Probiotics
Authors: A. Berger
Journal: BMJ (2002)

Probiotics are microbes that protect their host, and in some cases they can prevent disease. They are immunomodulating bacteria that have very low virulence compared with the more pathogenic gut flora such as Escherichia coli and clostridia. Lactobacilli and bifidobacteria are examples of probiotics found in the large intestine.

Lactobacillus GG can prevent diarrhoea and atopy in children.1,2 In the gut, probiotic bacteria are thought to occupy binding sites on the gut mucosa, preventing pathogenic bacteria from adhering to the mucosa. Lactobacilli also produce proteinaceous compounds—bacteriocins—that act as local antibiotics against more pathogenic organisms. But what is known about what happens in vitro cannot necessarily be extrapolated to the complexity of the ecosystem of the human gut.

Diarrhoea associated with antibiotics is presumed to result from the antibiotics disrupting the normal flora in the gut of a healthy person. Such disruptions cause dysfunction of the gut's ecosystem, and they may allow pathogenic bacteria to colonise the gut and gain access to the mucosa. Whether probiotic supplements stop this process by reducing the disruption or by acting as substitutes for the healthy flora is unclear. Probiotics may compete with pathogens for the nutrients the pathogens need to grow, or they may modify toxins produced by pathogens or toxin receptors found in the gut wall, or they may stimulate immune responses to pathogens.

The exact mechanisms by which probiotics prevent atopy are also under debate.3 One suggestion is that the establishment and maintenance of innate immune tolerance is mediated by T helper 1 cells and linked in some way to the faecal flora. If the Th1 response is particularly robust, the allergic response mediated by T helper 2 cells tends not to be so strong. Probiotics may prevent atopy by supporting the faecal flora, strengthening the Th1 response, and reducing the allergic response.

In the countries of continental Europe, probiotics are regarded as medicines, and they are prescribed alongside antibiotics. In other countries, probiotics are marketed as supplements and are sold over the counter—although preparations such as “bioyoghurts” do not always contain probiotic strains proved to be clinically useful.
Expression of human adenosine deaminase in mice transplanted with hemopoietic stem cells infected with amphotropic retroviruses.
Authors: V W van Beusechem, A Kukler, M P Einerhand, T A Bakx, A J van der Eb, D W van Bekkum, D Valerio
Journal: The Journal of Experimental Medicine (1990)

Amphotropic recombinant retroviruses were generated carrying sequences encoding human adenosine deaminase (ADA). Transcription of the human ADA gene was under control of a hybrid long terminal repeat in which the enhancer from the Moloney murine leukemia virus was replaced by an enhancer from the F101 host-range mutant of polyoma virus. Hemopoietic stem cells in murine bone marrow were infected with this virus under defined culture conditions. As a result, 59% of day-12 colony forming unit spleen (CFU-S) stem cells became infected without any in vitro selection. Infected CFU-S were shown to express human ADA before transplantation and this expression sustained upon in vivo maturation. Mice transplanted with infected bone marrow exhibited human ADA expression in lymphoid, myeloid, and erythroid cell types. Moreover, human ADA expression persisted in secondary and tertiary transplanted recipients showing that human ADA-expressing cells were derived from pluripotent stem cells. These characteristics of our amphotropic viruses make them promising tools in gene therapy protocols for the treatment of severe combined immunodeficiency caused by ADA deficiency. In this respect it is also relevant that the viral vector that served as backbone for the ADA vector was previously shown to be nonleukemogenic.
latrogenic Hyperthyroidism Secondary to Dextrothyroxine Administration
Authors: JORDAN H. HANKINS, CLARA M. HEISE, ROBERT J. COWAN
Journal: Clinical Nuclear Medicine (1984)

Two patients are reported who presented with clinical hyperthyroidism, increased serum thyroid function studies, and depressed radioactive iodine uptake, secondary to chronic ingestion of D-T4. Symptoms abated, and function studies returned to normal, following discontinuation of D-T4. This uncommon effect of D-T4 may be more prevalent than is generally realized and must be recognized as another potential cause of low radioiodine uptake in patients with clinical hyperthyroidism.
Safe Drugs and the Cost of Good Intentions
Authors: Hans-Georg Eichler, Eric Abadie, June M Raine, Tomas Salmonson
Journal: New England Journal of Medicine (2009)

Sophisticated data-mining tools are now available that permit real-time analysis of spontaneous reports of adverse drug reactions. These authors from the European Medicines Agency write that these developments are good news, but there are a number of unintended but foreseeable consequences.
CBL mutation in chronic myelomonocytic leukemia secondary to familial platelet disorder with propensity to develop acute myeloid leukemia (FPD/AML)
Authors: Norio Shiba, Daisuke Hasegawa, Myoung-ja Park, Chisato Murata, Aiko Sato-Otsubo, Chitose Ogawa, Atsushi Manabe, Hirokazu Arakawa, Seishi Ogawa, Yasuhide Hayashi
Journal: Blood (2011)
Abortion and miscarriage.
Authors: R F Gardner
Journal: BMJ (1972)

the patient with clear-cut communicating hydrocephalus, the patient with epilepsy, the two patients intoxicated by drugs, the eight depressed patients, and the patient with mania.If we had wished to press the point we might have included 24 other patients in whom the results of investigation could have led to some attempt to treat the patients or their relatives; that is, treatment for the seven hypertensive patients with arteriosclerotic dementia, treatment for the six alcoholics, genetic counselling for the relatives of three patients with Huntington's chorea, symptomatic therapy for the five patients with malignant brain tumours, and even experimental antiviral treatment for the three patients with Creutzfeldt-Jacob's disease.-Weare, etc.,
Detectable minimal residual disease before hematopoietic cell transplantation is prognostic but does not preclude cure for children with very-high-risk leukemia
Authors: Wing Leung, Ching-Hon Pui, Elaine Coustan-Smith, Jie Yang, Deqing Pei, Kwan Gan, Ashok Srinivasan, Christine Hartford, Brandon M. Triplett, Mari Dallas, Asha Pillai, David Shook, Jeffrey E. Rubnitz, John T. Sandlund, Sima Jeha, Hiroto Inaba, Raul C. Ribeiro, Rupert Handgretinger, Joseph H. Laver, Dario Campana
Journal: Blood (2012)
Evaluating and Improving the Quality of Care for Acute Myocardial Infarction
Authors: Edward L. Hannan
Journal: JAMA (2006)

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Do calcium plus vitamin D supplements increase cardiovascular risk?
Authors: B. Abrahamsen, O. Sahota
Journal: BMJ (2011)

Insufficient evidence is available to support or refute the association

Calcium supplements are widely used in the prevention of osteoporosis and as an adjunct to specific osteoporosis treatment but have been associated with a possible increase in the risk of adverse cardiovascular outcomes.1 In the linked study (doi:10.1136/bmj.d2040),2 Bolland and colleagues investigate the effects of personal use of calcium supplements on cardiovascular risk in the Women’s Health Initiative Calcium/Vitamin D (WHI CaD) study and update their meta-analysis of calcium supplements and cardiovascular risk.3 This new analysis is particularly relevant because it includes calcium supplements given with vitamin D.

The meta-analysis extends one previously undertaken by the same group in which calcium supplementation was associated with a significantly increased risk of stroke and myocardial infarction.1 That study was followed by a lively debate on the BMJ website and elsewhere, when it was criticised for reporting individual outcomes when the global end point was not significant, for counting events rather than people with events, and for building on studies that were not designed for cardiovascular outcomes and adjudicated accordingly.

In the …