tbuckley/cabot-search huggingface dataset:
Review of <i>Public Health Law and Ethics</i>
Authors: Samuel Y. Sessions
Journal: JAMA (2011)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Spontaneous Bilateral Adrenal Hemorrhage
Authors: Lawrence L. Knight, Eleanor H. Valentine
Journal: JAMA (1962)

A 65-yr-old white man was hospitalized for an acute myocardial infarction, and heparin therapy was begun. Except for a mild pneumonitis without overt evidence of septicemia, he improved until the eighth hospital day, when acute abdominal symptoms developed, followed by coma and death. Autopsy disclosed a recent myocardial infarction and massive bilateral adrenal hemorrhage. Recent evidence indicates that excessive corticotropin ( ACTH ) stimulation, by either corticotropin administration or severe stress, may have a lethal effect upon the adrenal cortex; thus, the seriously ill patient may have an increased susceptibility to adrenal damage. The use of anticoagulants in such a patient should be cautious, since it may increase the hazard of adrenal hemorrhage.
Interferon-free antiviral combination therapies without nucleosidic polymerase inhibitors
Authors: Tania Mara Welzel, Georg Dultz, Stefan Zeuzem
Journal: Journal of Hepatology (2014)

The establishment of robust HCV cell culture systems and characterization of the viral life cycle provided the molecular basis for highly innovative, successful years in HCV drug development. With the identification of direct-acting antiviral agents (DAAs), such as NS3/4A protease inhibitors, NS5A replication complex inhibitors, nucleotide and non-nucleoside polymerase inhibitors, as well as host cell targeting agents, novel therapeutic strategies were established and competitively entered clinical testing. The first-in-class NS3/4A protease inhibitors telaprevir and boceprevir, approved in 2011, were recently outpaced by the pan-genotypic nucleotide polymerase inhibitor sofosbuvir that in combination with pegylated interferon and ribavirin, further shortens therapy durations and also offers the first interferon-free HCV treatment option. In the challenging race towards the goal of interferon-free HCV therapies, however, several oral DAA regimens without nucleotide polymerase inhibitors that combine a NS3/4A protease inhibitor, a NS5A inhibitor and/or a non-nucleoside polymerase inhibitor yielded competitive results. Second generation NS3/4A protease and NS5A inhibitors promise an improved genotypic coverage and a high resistance barrier. Results of novel DAA combination therapies without the backbone of a nucleotide polymerase inhibitor, as well as treatment strategies involving host targeting agents are reviewed herein.
Amplification of altered self-reactive cytolytic T lymphocyte responses by cloned, allospecific human Th cells.
Authors: S M Friedman, A Green, C Russo, D N Posnett, D Diffley, M K Crow
Journal: Journal of Clinical Investigation (1988)

The effect of a cloned allospecific human Th cell, termed 86, on the in vitro generation of altered self-reactive cytolytic T lymphocytes (CTL) was investigated. Utilizing the induction of hapten altered self-reactive CTL as a model for virus or tumor-specific cell-mediated immunity, we determined that the presence of small numbers of clone 86 cells markedly amplified the generation of hapten altered self-reactive CTL. The killer cells induced belong to the CD4-, CD8+ subset, are specific for the hapten-modified autologous stimulator cells present in culture, and are MHC class I restricted. The CTL induced under these culture conditions are readily expanded in the presence of IL-2 with maintenance of efficient and specific altered self-killing. Of interest, clone 86 cells preferentially enhance the growth of CD8+ T cells and selectively amplify altered self-cytolysis but not NK cell activity. Although in vitro clone 86 cells mediate help for CTL generation via the production of lymphokines (IL-4 but little IL-2), one can envision immunotherapeutic strategies for human disease that involve the adoptive transfer of Th cells functionally analogous to clone 86.
Bacteroides, Other Nosocomial Bacteria, and Antibiotics
Authors: PETER C. FUCHS
Journal: Annals of Internal Medicine (1971)

Letters, Comments and Corrections1 December 1971Bacteroides, Other Nosocomial Bacteria, and AntibioticsPETER C. FUCHS, M.D.PETER C. FUCHS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-75-6-974_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In the recent exchange of views on antibiotics for bacteroides sepsis between Drs. Kagnoff and Armstrong and Drs. Goodman and Bodner (Ann Intern Med75:316-317, 1971) the latter concluded: "Perhaps the most salient conclusions for the reader to draw from this exchange are that bacteroides should not be assumed to be susceptible to any antimicrobial agent. . . ." Although one cannot argue with this or their other conclusions, I should like to suggest an additional conclusion that I think is even more salient: each hospital should summarize at periodic intervals the antibiotic sensitivity patterns of the...References1. COOKE M, SHOOTER R, and KUMAR P: Hospital food as a possible source of Escherichia coli in patients. Lancet 1:436-437, 1970 CrossrefMedlineGoogle Scholar2. LIDWELL O, POLAKOFF S, and DAVIES J: Nasal acquisition of Staphylococcus aureus in a subdivided and mechanically ventilated ward: endemic prevalence of a single staphylococcal strain. J Hyg (Camb) 68:417-433, 1970 CrossrefMedlineGoogle Scholar3. SELDON R, LEE S, and WARG W: Nosocomial klebsiella infections: intestinal colonization as a reservoir. Ann Intern Med 74:657-665, 1971 LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: PETER C. FUCHS, M.D.Affiliations: Department of Pathology St. Vincent Hospital and Medical Center Portland, Oreg. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 December 1971Volume 75, Issue 6 Page: 974-974 Keywords Antibiotics Antimicrobials Bacteria Bacteroides Sepsis ePublished: 1 December 2008 Issue Published: 1 December 1971 PDF downloadLoading ...
1140-174 Enhanced expression of pro-oxidant enzyme myeloperoxidase is associated with plaque destabilization in human coronary atherosclerotic lesions
Authors: Ryushi Komatsu, Takahiko Naruko, Akira Itoh, Kazuo Haze, Nobuyuki Shirai, Eishu Hai, Yoshihiro Ikura, Masahiko Ohsawa, Makiko Ueda
Journal: Journal of the American College of Cardiology (2004)
Comparative Effectiveness Research: A Progress Report
Authors: Harold C. Sox
Journal: Annals of Internal Medicine (2010)

Sixteen months ago, comparative effectiveness research (CER) began its rapid rise, when the American Recovery and Reinvestment Act of 2009 allocated $1.1 billion for CER. This progress report summarizes how the recipients of the funds—the National Institutes of Health, Agency for Healthcare Research and Quality, and Office of the Secretary of the U.S. Department of Health and Human Services—are spending the $1.1 billion, how the Institute of Medicine priority topics have fared in the agencies' funding programs, and the developing plans for a national CER program. As the United States works to absorb 32 million currently uninsured people into the health care system while simultaneously improving the quality of care and slowing cost increases, CER will increasingly be a necessary component of this change.
Mitral Stenosis in Identical Twins
Authors: Frederic C. Chang
Journal: New England Journal of Medicine (1961)

THE increased incidence of rheumatic fever and A rheumatic heart disease in certain families has been commented on extensively in the literature.1 2 3 4 5 The purpose of this paper is to report the findings of mitral stenosis in a set of identical twins whose twin sisters had previously died of complications of rheumatic heart disease.Case ReportsCase 1. C.B.K. (A-2552), a 36-year-old man, entered the Salt Lake Veterans Administration Hospital for evaluation of rheumatic heart disease. He had been discharged from the Army 17 years previously because of a "heart condition" manifested at that time by dyspnea on exertion and hemoptysis. . . .
Chronic Lymphocytic Leukemia
Authors: Nicholas Chiorazzi, Kanti R. Rai, Manlio Ferrarini
Journal: New England Journal of Medicine (2005)

Our concept of the pathogenesis of chronic lymphocytic leukemia has undergone remarkable changes during the past decade. This review addresses the latest ideas concerning the origin of this common form of leukemia and discusses how molecular investigations are beginning to change the management of the disease.
Cationic polypeptide micelle-based antigen delivery system: A simple and robust adjuvant to improve vaccine efficacy
Authors: Zichao Luo, Ping Li, Jizhe Deng, Ningning Gao, Yijuan Zhang, Hong Pan, Lanlan Liu, Ce Wang, Lintao Cai, Yifan Ma
Journal: Journal of Controlled Release (2013)
The T cell cometh: interplay between adaptive immunity and cytokine networks in rheumatoid arthritis
Authors: Gary S. Firestein
Journal: Journal of Clinical Investigation (2004)

The etiology of autoimmunity in humans remains poorly defined, and animal models provide a unique opportunity to study potential autoimmune mechanisms. A novel model of autoimmune inflammatory arthritis results from a point mutation in the ζ-associated–protein of 70 kDa (ZAP-70), which causes abnormal thymic T cell selection and survival of autoreactive clones. Although the resulting clinical and pathologic abnormalities are clearly T cell–dependent, macrophage and fibroblast cytokines such as IL-1 and TNF-α are required for full expression of the disease. The studies of Hata et al. raise the intriguing possibility that traditional proinflammatory cytokine networks represent common effector mechanisms in inflammatory joint diseases such as rheumatoid arthritis. Hence, effective therapeutic interventions can target either unique etiologic pathways related to adaptive immune responses or shared terminal mechanisms.
Update on Late Relapse of Germ Cell Tumor: A Clinical and Molecular Analysis
Authors: David W. George, Richard S. Foster, Robert A. Hromas, Kent A. Robertson, Gail H. Vance, Thomas M. Ulbright, Troy A. Gobbett, Devan J. Heiber, Nyla A. Heerema, Heather C. Ramsey, Virginia C. Thurston, Sin-Ho Jung, Jianzhao Shen, David E. Finch, Mark R. Kelley, Lawrence H. Einhorn
Journal: Journal of Clinical Oncology (2002)

Purpose: Analysis of patients with late relapse (LR) of germ cell tumor (GCT) with reports on clinical characteristics, outcomes, and molecular and cytogenetic features. Patients and Methods: Eighty-three patients evaluated at Indiana University from 1993 through 2000 for relapse of GCT more than 2 years from initial therapy were reviewed. Available specimens were investigated for expression of the transcription regulator FoxD3 and apurinic/apyrimidinic endonuclease and the presence of chromosome 12 abnormalities. Results: Median interval from initial presentation to LR was 85 months. Forty-three of 49 LR patients who underwent surgery were rendered disease free (NED), and 20 (46.5%) remain continuously NED. Thirty-two patients received chemotherapy, but only six (18.8%) obtained a complete remission. Five of these patients remain continuously NED after chemotherapy alone, including three who were chemotherapy naïve. Eighteen of these 32 patients were successfully rendered NED by postchemotherapy surgery, and 12 remain continuously NED. Two patients continue on observation with no treatment for their LR. Overall, 69 of the 81 treated patients (85.2%) ultimately achieved an NED state, and 38 (46.9%) remain continuously NED with median follow-up from LR therapy of 24.5 months (range, 1 to 83 months), whereas nine other patients are currently NED after therapy for subsequent relapses. Because of the small numbers of specimens tested, we were unable to draw any definitive conclusions from the molecular and cytogenetic analyses. Conclusion: GCT patients require lifetime follow-up. At the time of LR, surgical resection alone remains our preferred therapy.
Evolutionary Diversification of Multigene Families: Allelic Selection of Toxins in Predatory Cone Snails
Authors: Thomas F. Duda Jr, Stephen R. Palumbi
Journal: Molecular Biology and Evolution (2000)

In order to investigate the evolution of conotoxin multigene families among two closely related vermivorous Conus species, we sequenced 104 four-loop conotoxin mRNAs from two individuals of Conus ebraeus and compared these with sequences already obtained from Conus abbreviatus. In contrast to the diversity of conotoxin sequences obtained from C. abbreviatus, only two common sequence variants were recovered from C. ebraeus. Segregation patterns of the variants in these two individuals and restriction digests of four-loop conotoxin amplification products from nine additional individuals suggest that the common variants are alleles from a single locus. These two putative alleles differ at nine positions that occur nonrandomly in the toxin-coding region of the sequences. Moreover, all substitutions are at nonsynonymous sites and are responsible for seven amino acid differences among the predicted amino acid sequences of the alleles. These results imply that conotoxin diversity is driven by strong diversifying selection and some form of frequency-dependent or overdominant selection at conotoxin loci, and they suggest that diverse conotoxin multigene families can originate from duplications at polymorphic loci. Furthermore, none of the sequences recovered from C. ebraeus appeared to be orthologs of loci from C. abbreviatus, and attempts to amplify orthologous sequences with locus-specific primers were unsuccessful among these species. These patterns suggest that venoms of closely related Conus species may differ due to the differential expression of conotoxin loci.
Abstract 3319: Human triple-negative breast cancer stem cells utilized for drug discovery therapeutics for triple-negative breast cancer patients
Authors: Cristian V.R Sharma, Jenna D. Passarini, Mariam W. Majdoub, Christina M. DiMaggio, Omar M. Sobhy, Rubio R. Punzalan, Michael V.R. Sharma, Marni E. Harris-White, Michael W. Warden, Sherven P. Sharma, Jay P. Sharma
Journal: Cancer Research (2010)

Abstract Breast cancer is the most common malignancy among women in developed countries, affecting more than a million women per year worldwide. Of these, triple negative breast carcinoma represents 10-17 %. Triple negative breast carcinomas, characterized by estrogen, progesterone and HER2 receptor negativity are very aggressive tumors with poor prognosis. Breast Cancer Stem derived from triple negative parental Breast Cancer tumors, are a subpopulation of cells within the parental breast cancer population within the individual which are positive for the following markers: CD133+CD44+CD24+ESA+SSEA-1+TRA-1-61+&amp; TRA1-81+ and Oct ¾ these Breast Cancer Stem cells are highly tumorigenic and possess the stem cell-like properties of self-renewal and the ability to produce differentiated progeny. Breast Cancer Stem cells also demonstrate up regulation of SSEA3+, SSEA4+ upon differentiation into parental cancer phenotype. Individualized treatment (tailored therapy) based on molecular biology markers of tumor and patient is the trend in clinical practice these days. However, molecular targets and predictors for the treatment of triple negative breast carcinoma do not currently exist. With the identification and characterization of Breast Cancer Stem Cells from parental triple negative tumors, enables one to screen novel drug candidates for potential development of therapeutics for triple negative Breast Cancer Patients. In this study we have utilized Breast Cancer Stem Cells from triple negative Tumors to screen potential drug candidates. The Breast Cancer Stem Cell based assay system may provide novel therapeutic approaches into treatment of triple negative breast cancer patients, which are resistant to standard chemotherapy and radiation. 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 3319.
Cross-reactivity between streptococcal M surface antigen and human skin
Authors: J. MCFADDEN, H. VALDIMARSSON, L. FRY
Journal: British Journal of Dermatology (1991)

Psoriasis can be triggered by haemolytic streptococcal infections. As M protein is a major pathogenic surface antigen in these streptococci, the cross-reactivity between streptococcal M protein surface antigens and human epidermis was investigated. The conserved component common to the few M proteins investigated consists of an alpha-helical 'coiled-coil' configuration, similar to sub-units of human keratin. The amino acid sequence of protein M6, one of the M proteins that has been fully sequenced, was compared with that of 4721 ubiquitous peptides, by computer-assisted analysis using a protein-sequence data bank. Of all human proteins in the data bank 50-kDa keratin type 1 showed the closest homology with protein M6. Further evaluation revealed that this homology mainly involved the heptapeptide repeat patterns, which form the alpha-helical 'coiled-coil' structure, in both M6 and 50-kDa keratin. Cryostat sections of normal, involved and uninvolved psoriatic skin were studied for cross-reactivity with rabbit antisera raised against 10 different M proteins. All these antisera reacted with the stratum corneum of normal and psoriatic epidermis to a variable extent. Staining of keratinocyte cytoplasm was also observed, but this tended to be more prominent in lesional than in uninvolved and normal skin. Some of the M antisera also stained dendritic cells in the upper dermis as well as endothelium and smooth muscle. These cross-reactivities might be relevant to the pathogenesis of post-streptococcal psoriasis.
Binding of isolated rheumatoid factors to histone proteins and basic polycations.
Authors: R N Hobbs, D J Lea, K K Phua, P M Johnson
Journal: Annals of the Rheumatic Diseases (1983)

A fluorimetric immunoassay has been used to assess reactivity of rheumatoid factor (RF) with both histone proteins and other basic polycations (poly-L-lysine, poly-L-ornithine, and protamine) bound to an immobilised tyrosine-glutamic acid polyanionic copolymer. Isolated RF preparations can bind to histone proteins in this assay, notably to H3 and H4 histones, and this activity was always masked in the original whole seropositive sera. Binding of isolated RF was often noted also to the other large-molecular-weight basic polycations.
Effect of Diabetes Mellitus on the Regulation of Enzyme Secretion by Isolated Rat Pancreatic Acini
Authors: Makoto Otsuki, John A. Williams
Journal: Journal of Clinical Investigation (1982)

The nature and mechanism of the pancreatic exocrine dysfunction in diabetes mellitus were evaluated in vitro using isolated pancreatic acini prepared from streptozotocin-induced diabetic rats. The content of amylase and ribonuclease in diabetic acini was ∼0.5 and 50% of the normal content, respectively. Further, reduced amounts of both enzymes were secreted by diabetic acini in response to both cholecystokinin (CCK) and carbamylcholine. However, when enzyme secretion was normalized relative to initial acinar contents, both normal and diabetic acini released enzymes at a comparable maximal rate. The time course of the release of these enzymes, and newly synthesized protein were similar in both acini. In normal acini, the effect of CCK was maximal at a concentration of 100 pM; higher concentrations led to submaximal enzyme release. The dose-response curve in diabetic acini was similarly shaped, but shifted three-fold towards higher concentration. The mobilization of cellular Ca2+ in response to CCK was also shifted. In contrast to these results with CCK, the dose-response curve to carbamylcholine was unaltered by diabetes. The observed effects were confirmed to be due to insulin deficiency and not due to direct toxic effect of streptozotocin on acinar cells or malnutrition. Streptozotocin had no acute effect on acini when measured 24 h after administration, and alloxan, another beta cell toxin, induced similar changes in acinar enzyme content and secretory response. Moreover, the administration of exogenous insulin to diabetic rats returned the content of pancreatic amylase and the secretory response to CCK towards normal. Starvation for 48 h, although inducing a significant weight loss, did not mimic the effects of diabetes. The present studies demonstrate two major abnormalities in pancreatic exocrine secretion in the diabetic rat: (a) the content of certain digestive enzymes is markedly altered, leading to an altered amount of zymogen secretion, (b) the sensitivity to CCK is selectively reduced, most likely related to a defect in receptor activated transmembrane signaling.
1072-209 PR interval prolongation but not QRS widening is an independent factor of functional intolerance in heart failure patients with dilated cardiomyopathy
Authors: Axel Champagne de la Briolle, Christophe Leclercq, Veronique Sebille, Francois Carre, Christian de Place, Philippe Mabo, Jean-Claude Daubert
Journal: Journal of the American College of Cardiology (2004)
Alzheimer disease β-amyloid activity mimics cholesterol oxidase
Authors: Luigi Puglielli, Avi L. Friedlich, Kenneth D.R. Setchell, Seiichi Nagano, Carlos Opazo, Robert A. Cherny, Kevin J. Barnham, John D. Wade, Simon Melov, Dora M. Kovacs, Ashley I. Bush
Journal: Journal of Clinical Investigation (2005)

The abnormal accumulation of amyloid beta-peptide (Abeta) in the form of senile (or amyloid) plaques is one of the main characteristics of Alzheimer disease (AD). Both cholesterol and Cu2+ have been implicated in AD pathogenesis and plaque formation. Abeta binds Cu2+ with very high affinity, forming a redox-active complex that catalyzes H2O2 production from O2 and cholesterol. Here we show that Abeta:Cu2+ complexes oxidize cholesterol selectively at the C-3 hydroxyl group, catalytically producing 4-cholesten-3-one and therefore mimicking the activity of cholesterol oxidase, which is implicated in cardiovascular disease. Abeta toxicity in neuronal cultures correlated with this activity, which was inhibited by Cu2+ chelators including clioquinol. Cell death induced by staurosporine or H2O2 did not elevate 4-cholesten-3-one levels. Brain tissue from AD subjects had 98% more 4-cholesten-3-one than tissue from age-matched control subjects. We observed a similar increase in the brains of Tg2576 transgenic mice compared with nontransgenic littermates; the increase was inhibited by in vivo treatment with clioquinol, which suggests that brain Abeta accumulation elevates 4-cholesten-3-one levels in AD. Cu2+-mediated oxidation of cholesterol may be a pathogenic mechanism common to atherosclerosis and AD.