tbuckley/cabot-search huggingface dataset:
ULCEROMEMBRANOUS ANGINA (VINCENT'S ANGINA) AND STOMATITIS.
Authors: GEORGE H. WEAVER
Journal: JAMA (1906)

The disease to which attention is here directed has been described under several names, "ulcerative angina and stomatitis," "ulceromembranous angina and stomatitis," "pharyngitis ulcerosa," "angina diphtheroides," "angina exsudativa ulcerosa," "Vincent's angina," "angina chancriforme," "pseudomembranous angina," "spirochätenbacillen angina," etc. The name selected for the title of this paper is preferred as designating the principal characteristics of the process, i. e., ulceration and formation of a pseudomembrane. This is not a wholly satisfactory name, as frequently there is no ulceration, a pseudomembrane only being formed, as was observed by us in several cases. Vincent's name is not properly used to designate the angina, since it had been described<sup>1</sup>previous to his studies by French and Russian clinicians (Barthez and Sanné, Simanovsky, Nevejin, Moure and Mendel). All of the cases described are separated sharply by certain clinical and bacteriologic characteristics. On the affected mucous membrane there appear pseudomembranous formations and, as a
Abstract 4771: Molecular, epigenetic, and phenotypic repolarization of human T lymphocytes using 5-aza-2′-deoxycytidine increases CD8 responsiveness and induces Th1 polarity
Authors: Jason A. Dubovsky, John J. Powers, Yang Gao, Javier A. Pinilla-Ibarz, Eduardo M. Sotomayor
Journal: Cancer Research (2010)

Abstract The improper polarization of helper and cytotoxic T lymphocytes is a trademark immunosuppressive strategy employed by a litany of human malignancies. Mounting data implicates chromatin regulation, namely promoter methylation, in the plasticity of naïve human T cells. Very recent in-vitro evidence indicates that this plasticity may be phenotypically replicated by using methylation inhibitors which are approved for clinical use in certain types of cancer, however the longevity and therapeutic potential of repolarized cells remains to be elucidated. These results beg the question: can the ineffective polarization of T lymphocytes in the context of cancer be effectively modulated using methylation inhibitors in a sustainable therapeutic fashion? To answer this question our laboratory has focused on repolarizing helper and cytotoxic T lymphocytes using 5-aza-2′-deoxycytidine (5A2) tracking changes in well characterized molecular and epigenetic signaling pathways involved in effective polarization. Moreover, we sought to investigate the consequences of methylation inhibitor treatment on lymphocyte survival, activation intensity, and naïve cell polarization. Our studies relied upon intracellular staining, methylation specific PCR, and phosflow anlaysis. The data indicates that 5A2 treatment can repolarize Th2 cells to effectively secrete interferon gamma, signal via STAT4, and achieve demethylation of critical Th1 specific promoters. We also show that this repolarization can be maintained. Similar increases in cytotoxic signaling capability were obtained with CD8+ T cells after treatment with 5A2. Moreover, we demonstrate that 5A2 can force Th1 polarization of naïve T cells despite a strong IL-4 stimuli and a lack of IL-12. Finally, we have identified a cytotoxic threshold for 5A2 treatment which is above the concentration necessary to achieve effective and sustained molecular and epigenetic repolarization. All in all our data seeks to define a modality in which improper or ineffective T cell polarization can be altered ex post facto and continued immunotherapeutic intervention may benefit from the naïve polarization of anti-cancer responses. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4771.
Congenital Polyvalvular Disease
Authors: SAROJA BHARATI, MAURICE LEV
Journal: Circulation (1973)

Thirty-six hearts were studied in which all valves were involved in a dysplastic process. This consisted of an increase in spongiosa with vacuolar and lacunar degeneration, and a distinct lack of elastic tissue in the proximalis and in the spongiosa. This process was similar to, but more marked than that seen in a case of a single dysplastic valve as in bicuspid aortic valve. It was completely different than that seen in hemodynamic change. These cases clinically were often associated with trisomy 18 or trisomy 13-15, and called congenital polyvalvular disease. This disease may bear some relationship to Marfan's disease and the "floppy valve".
Clinicopathologic Presentation and Natural History of Anorectal Melanoma
Authors: Caitlin W. Hicks, Emmanouil P. Pappou, Jonathan T. Magruder, Benny Gazer, Sandy Fang, Elizabeth C. Wick, Susan L. Gearhart, Nita Ahuja, Jonathan E. Efron
Journal: JAMA Surgery (2014)

Anorectal melanoma is a rare malignant neoplasm with variable natural history and nonspecific presentation. We describe the clinicopathologic and prognostic parameters of a series of 18 patients (16 [88.9%] white; 10 [55.6%] male; median age, 64.0 years [interquartile range, 45.8-74.3 years]) with histologically proven anorectal melanoma treated at our institution during a 21-year period between October 1991 and August 2012. Late diagnosis was common (44.5% of patients had stage II disease or worse at diagnosis), likely owing to a delay in presentation, nonspecific presenting symptoms, and frequent incorrect diagnoses (16 cases [88.9%]). Overall disease-specific mortality was 66.7% (12 of 18 patients), with a median time to death of 15.5 months (interquartile range, 7.3-25.5 months). Disease-specific survival was significantly better following wide local excision vs abdominoperineal resection (<i>P</i> = .04), although patients undergoing the former tended to have fewer rectal lesions (<i>P</i> = .04), smaller lesions (<i>P</i> = .02), and a trend toward less advanced stage (<i>P</i> = .06). Larger studies assessing optimal medical and surgical management for anorectal melanoma are needed to improve outcomes.
A new variant of type IV glycogenosis: Deficiency of branching enzyme activity without apparent progressive liver disease
Authors: Harry L. Greene, Barbara I. Brown, Daniel T. McClenathan, Rocco M. Agostini, Suzanne R. Taylor
Journal: Hepatology (1988)

Type IV glycogenosis is due to branching enzyme deficiency and is usually manifested clinically by progressive liver disease with cirrhosis and hepatic failure between the second and fourth years of life. We describe a 5-year-old boy who, following an acute febrile illness at 2 years of age, was first noted to have hepatomegaly with mildly elevated serum transaminase levels. Liver biopsy revealed hepatic fibrosis with periodic-acid Schiff-positive, diastase-resistant inclusions in hepatocytes and fibrillar inclusions characteristic of amylopectin by electron microscopy. Enzymatic assay revealed deficient hepatic branching enzyme activity with normal activity of glucose-6-phosphatase, debranching enzyme and phosphorylase activities. During the succeeding 3 years, he grew and developed normally with apparent resolution of any clinical evidence of liver disease and only intermittent elevation in serum transaminase levels associated with fever and prolonged fasting. Repeat liver biopsy at 4 years of age showed persistence of scattered hepatocellular periodic-acid Schiff-positive, diastase-resistant inclusions, but no progression of hepatic fibrosis in spite of persistent deficiency of hepatic branching enzyme activity. Skeletal muscle and skin fibroblasts from the patient also showed deficient enzyme activity. Skin fibroblasts from both parents exhibited half the normal control activity, suggesting a heterozygote state. This is the first documented patient with deficiency of branching enzyme but without evidence of progressive hepatic disease. This patient, coupled with reports of other patients with late onset hepatic or muscle disease with branching enzyme deficiency, suggests that the defect resulting in Type IV glycogen storage disease is more heterogenous and possibly more common than previously suspected.
Are "America's Best Hospitals" America's Best?
Authors: Sherry Glied, Jane E. Meyer
Journal: JAMA (1997)

<h3>To the Editor.</h3> —Dr Green and colleagues<sup>1</sup>describe the limitations of the ranking method used by<i>US News &amp; World Report</i>in their annual survey of "America's Best Hospitals." One component of that ranking is adjusted hospital mortality rates. As the authors point out, concerns about the methods used to make case-mix adjustments in hospital mortality rates led the Health Care Financing Administration (HCFA) to discontinue public release of Medicare hospital mortality rates in 1993.<i>US News &amp; World Report</i>continued to rely on HCFA's published 1991 hospital mortality rates until 1994. Since then,<i>US News &amp; World Report</i>has had a contractor develop casemix-adjusted hospital mortality rates using HCFA's publicly released Medicare claims data.<sup>2</sup> However, there is a fundamental difference between the Medicare claims data now released by HCFA and the data HCFA used to computed hospital mortality rates before 1993. In their internal analyses, HCFA matched Medicare claims data to Social Security records.
Cross-Cultural Medicine
Authors: Helen Chen
Journal: Annals of Internal Medicine (2003)

Medical Writings: Book Notes16 December 2003Cross-Cultural MedicineHelen Chen, MDHelen Chen, MDFrom San Francisco General Hospital, San Francisco, California.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-139-12-200312160-00029 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Bigby JA, ed. 300 pages. Philadelphia: American Coll of Physicians; 2003. $38. ISBN 193051302X. Order phone 215-351-2600.Field of medicine: Internal medicine and public health.Format: Softcover book.Audience: Clinicians, house officers, and students who work with diverse populations in any medical specialty and health services researchers and policymakers who wish to expand their knowledge and skills regarding the care of multicultural populations.Purpose: To serve as a resource guide and framework for internists to provide culturally competent care.Content: The book is divided into 9 chapters. The first is an overview of general strategies that may be used to ... Author, Article, and Disclosure InformationAffiliations: From San Francisco General Hospital, San Francisco, California. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 16 December 2003Volume 139, Issue 12Page: 1048KeywordsArabic peopleCommunication in health careHealth careHispanic peopleImmigrant healthMedical servicesNative American peoplePopulation statisticsPrevention, policy, and public healthSoftware tools ePublished: 16 December 2003 Issue Published: 16 December 2003 Copyright & PermissionsCopyright © 2003 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Antipsychotics and the Risk of Type 2 Diabetes Mellitus in Children and Youth
Authors: William V. Bobo, William O. Cooper, C. Michael Stein, Mark Olfson, David Graham, James Daugherty, D. Catherine Fuchs, Wayne A. Ray
Journal: JAMA Psychiatry (2013)

<h3>Importance</h3> The increased prescribing of antipsychotics for children and youth has heightened concerns that this practice increases the risk of type 2 diabetes mellitus. <h3>Objective</h3> To compare the risk of type 2 diabetes in children and youth 6 to 24 years of age for recent initiators of antipsychotic drugs vs propensity score–matched controls who had recently initiated another psychotropic medication. <h3>Design, Setting, and Participants</h3> Retrospective cohort study of the Tennessee Medicaid program with 28 858 recent initiators of antipsychotic drugs and 14 429 matched controls. The cohort excluded patients who previously received a diagnosis of diabetes, schizophrenia, or some other condition for which antipsychotics are the only generally recognized therapy. <h3>Main Outcomes and Measures</h3> Newly diagnosed diabetes during follow-up, as identified from diagnoses and diabetes medication prescriptions. <h3>Results</h3> Users of antipsychotics had a 3-fold increased risk for type 2 diabetes (HR = 3.03 [95% CI = 1.73-5.32]), which was apparent within the first year of follow-up (HR = 2.49 [95% CI = 1.27-4.88]). The risk increased with cumulative dose during follow-up, with HRs of 2.13 (95% CI = 1.06-4.27), 3.42 (95% CI = 1.88-6.24), and 5.43 (95% CI = 2.34-12.61) for respective cumulative doses (gram equivalents of chlorpromazine) of more than 5 g, 5 to 99 g, and 100 g or more (<i>P</i> &lt; .04). The risk remained elevated for up to 1 year following discontinuation of antipsychotic use (HR = 2.57 [95% CI = 1.34-4.91]). When the cohort was restricted to children 6 to 17 years of age, antipsychotic users had more than a 3-fold increased risk of type 2 diabetes (HR = 3.14 [95% CI = 1.50-6.56]), and the risk increased significantly with increasing cumulative dose (<i>P</i> &lt; .03). The risk was increased for use restricted to atypical antipsychotics (HR = 2.89 [95% CI = 1.64-5.10]) or to risperidone (HR = 2.20 [95% CI = 1.14-4.26]). <h3>Conclusions and Relevance</h3> Children and youth prescribed antipsychotics had an increased risk of type 2 diabetes that increased with cumulative dose.
Complement-induced glomerular epithelial cell injury. Role of the membrane attack complex in rat membranous nephropathy.
Authors: A V Cybulsky, H G Rennke, I D Feintzeig, D J Salant
Journal: Journal of Clinical Investigation (1986)

In passive Heymann nephritis (PHN) in rats, antibody (anti-Fx1A) reacts in situ with a glomerular epithelial antigen and induces complement (C)-mediated cell-independent proteinuria. To assess the role of the membrane attack complex (MAC), we determined the need for C8 in the pathogenesis of proteinuria in an autologous-phase model of PHN. Isolated rat kidneys, containing nonnephritogenic, non-C-fixing gamma 2 sheep anti-Fx1A (planted antigen), when perfused in vitro with C-fixing guinea pig anti-sheep IgG and a source of C (fresh human plasma 50% vol/vol in buffer containing bovine serum albumin), developed marked proteinuria after 20 min (0.58 +/- 0.08 mg/min X g, n = 8) that increased further to 3.20 +/- 0.93 mg/min X g after 80 min. In contrast, identical kidneys perfused with antibody and heat-inactivated or C8-deficient human plasma and normal kidneys perfused with antibody and fresh plasma excreted only 0.27 +/- 0.03 (n = 6), 0.27 +/- 0.04 (n = 5), and 0.40 +/- 0.05 mg/min X g (n = 6) after 20 min, and 0.13 +/- 0.02, 0.22 +/- 0.03, and 0.32 +/- 0.05 mg/min X g after 80 min, respectively. When C8-deficient plasma was reconstituted with sources of C8 (n = 3), proteinuria was restored to the level observed with fresh normal plasma. Differences in protein excretion could not be explained by quantitative differences in glomerular antigen or antibody content. Extensive ultrastructural damage to glomerular visceral epithelial cells was exclusively seen in antigen-containing kidneys perfused with antibody and C8-replete plasma. Thus, glomerular injury in this model results from an antigen-specific, antibody-directed, C8-dependent reaction involving assembly of the MAC. The ultrastructural findings argue in favor of MAC-induced cytotoxicity of the glomerular visceral epithelial cells.
Fatal septicaemia due to Yersinia pseudotuberculosis.
Authors: J Borowski, M L Zaremba, L Wasiluk
Journal: BMJ (1971)

tant about the last patient is that if he had died the coroner would almost certainly have had had to bring in the death as being due to combined drugs, with both the mother and doctor denying that he had more than ordinary doses of sedatives.After recovery he was safely given the combined antidepressant drugs for a fortnight.-Iam, etc.,
Progressive failure of coronary flow during reperfusion of myocardial infarction: Documentation of the no reflow phenomenon with positron emission tomography
Authors: Richmond W. Jeremy, Jonathan M. Links, Lewis C. Becker
Journal: Journal of the American College of Cardiology (1990)

During reperfusion of a myocardial infarct, development of microvascular occlusion may result in regional hypoperfusion ("no reflow") despite a patent infarct-related artery. This study examined the extent and time course of no reflow with use of rubidium-82 positron emission tomography. In 12 anesthetized dogs, the left anterior coronary artery was occluded for 90 min and then freely reperfused. Regional myocardial perfusions was imaged by serial rabidium-82 positron emission tomography during coronary occlusion and every 30 min during reperfusion. After 4 h of reperfusion, infarct size and no reflow zone were measured postmortem by triphenyltetrazolium and thioflavin staining, respectively. Perfusion defects evident on rubidium-82 images during coronary occlusion rapidly resolved during the early reflow period. However, a recurrent perfusion defect appeared after 1 to 2 h of reflow in all dogs. The severity of recurrent perfusion defects progressed with time; after 5 min of reflow, relative perfusion in the left anterior descending artery territory was 97 ± 6% of that in the normal circumflex artery region, but perfusion decreased progressively to 68 ± 5% after 2 h (p < 0.05) and to 55 ± 4% after 4 h of reperfusion (p < 0.05 versus 2 h). As measured by radioactive tracer microspheres, endocardial blood flow decreased similarly in the postischemic left anterior descending artery region from 1.2 ± 0.2 ml/mim per g after 5 min of reflow to 0.4 ± 0.1 ml/min per g after 3 h of reflow (p < 0.01). Residual infarct perfusion, measured by rabidium-82 after 4 h of reflow, was related to both infarct size (r = −0.88) and the extent of the no reflow zone (r = −0.84) in the postmortem left ventricular sections. Thus, serial positron emission tomography with rabidium-82 demonstrates a progressive loss of infarct perfusion, beginning 1 to 2 h after initial restoration of blood flow despite patency of the infarct-related artery. This phenomenon is probably a manifestation of progressive microvascular occlusion within the reperfused myocardium.
Large Right Atrial Thrombi Surrounding Permanent Transvenous Pacemakers
Authors: ANTHONY R. LONDON, PETER J. RUNGE, RICHARD F. BALSAM, MONICA B. BISHOP, GEORGE BOUSVAROS
Journal: Circulation (1969)

Transvenous pacemakers offer advantages but may also lead to complications not seen with transthoracic pacemakers. We have seen two patients in whom at autopsy large right atrial thrombi were found around the catheter. The first patient had signs of increasing right heart failure and oliguria and died 48 hours after implantation of the pacemaker, which functioned normally throughout. At autopsy 80% of the right atrium was filled by a thrombus. This thrombus had caused inadequate filling of the right atrium and seemed responsible for the deterioration and death of the patient. The second patient died suddenly 2 months after insertion of the pacemaker after suprapubic prostatectomy. At autopsy a well-organized thrombus encircled the catheter between the junction of the azygos vein and the superior vena cava to the tricuspid valve. The thrombus may have caused signs of right heart failure before death. Since right atrial thrombi may be detected by angiography and treated by surgery, it is important to be aware of this rare complication of transvenous pacing.
Bill Gates is to urge G20 nations to adopt a financial transaction tax to fund development
Authors: K. McColl
Journal: BMJ (2011)

A small tax on financial trading could raise billions to fund healthcare and other services in developing countries. That’s the message Bill Gates will deliver to leaders of the G20 major economies in Cannes this weekend. 

Mr Gates, who was asked by the G20’s current chairman, President Nicolas Sarkozy of France, to look into new ways of finding money for development, is backing the idea of a financial transaction tax, according to a memo leaked a few weeks ago.

Mr Gates is in good company. Supporters of a financial transaction tax, dubbed the “Robin Hood tax,” range from the Vatican to the Occupy Wall …
Therapeutic Modulation of Akt Activity and Antitumor Efficacy of Interleukin-12 Against Orthotopic Murine Neuroblastoma
Authors: Tahira Khan, Julie A. Hixon, Jimmy K. Stauffer, Erin Lincoln, Timothy C. Back, Jason Brenner, Stephen Lockett, Kunio Nagashima, Douglas Powell, Jon M. Wigginton
Journal: JNCI Journal of the National Cancer Institute (2006)

Patients with advanced neuroblastoma have a poor prognosis. The antiapoptotic protein Akt has been implicated as a possible mediator of the resistance of human neuroblastoma cells to apoptosis; the proapoptotic protein Bid, is inhibited by activated Akt. Neuroblastoma has demonstrated responsiveness to immunotherapeutic approaches in preclinical studies, prompting investigation of new therapeutic strategies based on potentiation of the host immune response, including the use of systemic cytokines.We examined the antitumor efficacy and mechanisms of action of the central immunoregulatory cytokine interleukin-12 (IL-12) in mice bearing established orthotopic neuroblastoma tumors derived from murine TBJ and Neuro-2a cells. Cohorts of mice (10 mice/group) bearing established orthotopic neuroblastoma tumors were injected intraperitoneally with IL-12 or vehicle and monitored for survival. IL-12-induced apoptosis within the tumor microenvironment was investigated using ribonuclease protection assays, nuclear staining, and electron microscopy. Protein expression was determined via Western blot analysis and enzyme-linked immunosorbent assays. Confocal microscopy was used to examine the distribution of overexpressed Bid-enhanced green fluorescent protein fusion protein (Bid-EGFP) in TBJ cells. All statistical tests were two-sided.IL-12 induced complete tumor regression and long-term survival of 8 (80%) of 10 mice bearing established neuroblastoma tumors compared with 1 (10%) of 10 control mice (P = .0055) and profound tumor cell apoptosis in vivo despite the fact that TBJ and Neuro-2a cells were resistant to receptor-mediated apoptosis in vitro. These cells expressed high levels of phosphorylated Akt, a key prosurvival molecule, and Akt inhibitors sensitized neuroblastoma cells to apoptosis mediated by IL-12-inducible cytokines including tumor necrosis factor-alpha and interferon-gamma in vitro. IL-12 increased the expression of proapoptotic genes and decreased Akt phosphorylation within established TBJ tumors in conjunction with activation and subcellular translocation of Bid.Our results suggest that IL-12 overcomes a potentially critical mechanism of tumor self-defense in vivo by inhibiting Akt activity and imply that IL-12 may possess unique therapeutic activity against tumors that express high levels of activated Akt.
Genetic factors in childhood asthma.
Authors: B Sibbald, M E Horn, E A Brain, I Gregg
Journal: Thorax (1980)

The prevalences of asthma and atopy were examined in the families of 77 asthmatic and 87 control children attending a London general practice. The prevalence of asthma in first degree relatives of asthmatic children was found to be significantly higher than in relatives of control children, and this difference was more pronounced for relatives of atopic probands than for relatives of non-atopic probands. Among the relatives of asthmatics, atopic asthma was more common than non-atopic asthma, irrespective of the atopic status of the proband. However, among the relatives of control children, neither the prevalence of asthma nor the atopic status of the asthmatic relatives was influenced by the atopic status of the proband. These findings support the hypothesis that asthma and atopy are inherited independently. Although atopy itself does not predispose to asthma, it may enhance a genetic susceptibility to the condition, thus increasing the likelihood that the latter will be expressed.