tbuckley/cabot-search huggingface dataset:
Cross reaction of antibodies to a glycine/alanine repeat sequence of Epstein-Barr virus nuclear antigen-1 with collagen, cytokeratin, and actin.
Authors: C Baboonian, P.J Venables, D.G Williams, R.O Williams, R.N Maini
Journal: Annals of the Rheumatic Diseases (1991)

P62 is a synthetic peptide which corresponds to the glycine/alanine repeat sequence of Epstein-Barr virus nuclear antigen-1. It is the main epitope recognised by anti-rheumatoid arthritis nuclear antigen antibodies. It was shown previously that anti-P62 antibodies were raised fourfold in patients with rheumatoid arthritis compared with controls. To examine the possibility that this increase was due to cross reactive autoantibodies binding to P62, anti-P62 antibodies from serum samples taken from 10 patients with rheumatoid arthritis and five healthy controls were purified by affinity chromatography. Immunoglobulin G anti-P62 antibodies purified from four of 10 serum samples from patients with rheumatoid arthritis also reacted with human epidermal keratin, denatured collagen type II and actin, but not with influenza antigens, as determined by enzyme linked immunosorbent assay (ELISA). Anti-P62 antibodies in serum samples from healthy controls and patients with rheumatoid arthritis reacted with epidermal keratin by immunoblotting. It is suggested that antibodies to the glycine/alanine repeat sequence of Epstein-Barr nuclear antigen-1 recognise homologous epitopes on keratin, actin, and collagen. It is also possible that molecular mimicry between a major epitope on the Epstein-Barr virus and several autoantigens might contribute to the breakdown of tolerance and autoimmunity in patients with rheumatoid arthritis.
Low-grade dysplasia in Barrett's esophagus has a high risk of progression
Authors: C. Lim, D. Treanor, M. Dixon, A. Axon
Journal: Endoscopy (2007)

See also: Commentaire de travail de C. H. Lim et al., pp. 581Endoscopy 2007; 39(07): 757-757DOI: 10.1055/s-0032-1306948
Familial empirical risks for inflammatory bowel disease: differences between Jews and non-Jews.
Authors: H Yang, C McElree, M P Roth, F Shanahan, S R Targan, J I Rotter
Journal: Gut (1993)

The Jewish population has an increased frequency of inflammatory bowel disease compared with their non-Jewish neighbours. Genetic factors have been implicated in the aetiology of this disorder and may contribute to ethnic differences. This study determined the familial empirical risks for inflammatory bowel disease in the first degree relatives of inflammatory bowel disease probands (for both Jews and non-Jews) for the purpose of accurate genetic counselling and genetic analysis. A total of 527 inflammatory bowel disease patients from Southern California (291 Jews and 236 non-Jews) were questioned about inflammatory bowel disease in their first degree relatives (a total of 2493 individuals). Since inflammatory bowel disease has a variable and late age of onset, age specific incidence data were used to estimate the life time risks and to make valid comparisons between the different groups. In the first degree relatives of non-Jewish probands, the life time risks for inflammatory bowel disease were 5.2% and 1.6% when probands had Crohn9s disease and ulcerative colitis respectively. These values were consistently lower than the corresponding risks for relatives of Jewish patients -7.8% and 4.5% for Crohn9s disease and ulcerative colitis probands respectively (p value for comparison between Jews and non-Jews: 0.028; between ulcerative colitis and Crohn9s disease: 0.005). These data provide the requisite basis for genetic counselling for these disorders in the white American population. In addition, these different empirical risks for relatives of Jewish and non-Jewish probands allow rejection of single Mendelian gene models for inflammatory bowel disease, but are consistent with several alternative genetic models.
Abstract 4886: Targeting WNT1-inducible signaling pathway protein 2 (WISP2) alters human breast cancer cell susceptibility to specific lysis through regulation of KLF-4 and miR-7 expression
Authors: Intissar Akalay, salem chouaib, jean-paul thiery
Journal: Cancer Research (2014)

Abstract The molecular basis for the resistance of tumor cells to cell-mediated cytotoxicity remains poorly understood and thus poses a major challenge for cancer immunotherapy. The present study was designed to determine whether the WNT1-inducible signaling pathway protein-2 (WISP2, also referred to as CCN5), a key regulator of tumor cell plasticity, interferes with tumor susceptibility to Cytotoxic T Lymphocytes (CTL)-mediated lysis. We found that targeting WISP2 signaling in human breast adenocarcinoma MCF7 cells impairs CTL-mediated cell killing by a mechanism involving Kruppel-like factor-4 (KLF-4) induction and microRNA-7 (miR-7)downregulation. Inhibition of TGF-β signaling using the A83-01 inhibitor in MCF7-shWISP2 cells resulted in a significant reversal of the Epithelial-to-Mesenchymal Transition (EMT) phenotype, the expression of stem cell marker KLF-4 and a partial recovery of target susceptibility to CTLs. More importantly, we showed that silencing of KLF-4 was accompanied by a reduction in MCF7-shWISP2 resistance to CTLs. Using human breast cancer tissues, we demonstrated the coexpression of KLF-4 with EMT markers and TGF-β pathway. More importantly, we found that KLF-4 expression was accompanied by miR-7 inhibition, which is partly responsible forimpairing CTL-mediated lysis. Thus, our data indicate that WISP2 plays a role in regulating tumor cell susceptibility through EMT by inducing the TGF-β signaling pathway, KLF-4 expression and miR-7 inhibition. These studies indicate for the first time that WISP2 acts as an activator of CTL-induced killing and suggests that the loss of its function promotes evasion of immunosurveillance and the ensuing progression of the tumor. Citation Format: Intissar Akalay, salem chouaib, jean-paul thiery. Targeting WNT1-inducible signaling pathway protein 2 (WISP2) alters human breast cancer cell susceptibility to specific lysis through regulation of KLF-4 and miR-7 expression. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4886. doi:10.1158/1538-7445.AM2014-4886
Exogenous mesenchymal stem cells localize to the kidney by means of CD44 following acute tubular injury
Authors: M.B. Herrera, B. Bussolati, S. Bruno, L. Morando, G. Mauriello-Romanazzi, F. Sanavio, I. Stamenkovic, L. Biancone, G. Camussi
Journal: Kidney International (2007)
The Homeostasis Model in the San Antonio Heart Study
Authors: Steven M Haffner, Heikki Miettinen, Michael P Stern
Journal: Diabetes Care (1997)

OBJECTIVE Both insulin resistance and decreased insulin secretion have been shown to predict the development of NIDDM. However, methods to assess insulin sensitivity and secretion are complicated and expensive to apply in epidemiological studies. The homeostasis model assessment (HOMA) has been suggested as a method to assess insulin resistance and secretion from the fasting glucose and insulin concentrations. However, this method has not been extensively evaluated, particularly in different ethnic groups. RESEARCH DESIGN AND METHODS We applied the HOMA model to cross-sectional analyses of the San Antonio Heart Study (n = 2,465). RESULTS HOMA insulin resistance (IR) was very strongly correlated with fasting insulin (r = 0.98) and HOMA β-cell function (β-cell) was moderately correlated with the 30-min increment in insulin concentration over the 30-min increment in glucose concentration (Δ I30/Δ G30) in an oral glucose tolerance test (OGTT) (r = 0.44). NIDDM was characterized by both high HOMA IR and low HOMA β-cell function. In Mexican-Americans, HOMA IR in NIDDM subjects was 9.5 compared with 2.7 in normal glucose tolerance (NGT) subjects. In contrast, HOMA β-cell function showed only small differences in Mexican-Americans (176 NIDDM; 257 NGT). However, the ΔI30/ΔG30 (pmol/mmol) showed much larger differences (75 NIDDM; 268 NGT). When modeled separately, impaired glucose tolerance (IGT) was characterized by high HOMA IR and high HOMA β-cell function. However, when analyzed in the same regression model, high HOMA IR and low HOMA β-cell function characterized subjects with IGT. These results were similar in both ethnic groups. Mexican-Americans had increased insulin resistance (as judged by both HOMA IR and fasting insulin) and insulin secretion (by HOMA β-cell and ΔI30/ΔG30) relative to non-Hispanic whites. CONCLUSIONS We conclude that HOMA provides a useful model to assess insulin resistance and β-cell function in epidemiological studies in which only fasting samples are available and that, further, it is critical to take into account the degree of insulin resistance in assessing insulin secretion by the HOMA model.
Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.
Authors: Ralph J Delfino
Journal: Environmental Health Perspectives (2002)

Outdoor ambient air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of asthma. However, the complexity of pollutant mixtures and etiologic heterogeneity of asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g., metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause occupational asthma, only formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific volatile organic compounds (VOCs) identified in association with occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric asthma. In addition, experimental evidence indicates that airborne polycyclic aromatic hydrocarbon (PAH) exposures linked to diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or asthma with exposures to ambient air pollutant mixtures with PAH components, including black smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco smoke. Other particle-phase and gaseous co-pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics from monitored criteria air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on biological mechanisms, particularly irritant and immunological pathways to asthma onset and exacerbation.
The Encyclopaedia of General Practice
Authors: Mildred L. Geiger
Journal: JAMA (1964)

Although only the first two volumes are available at the time of this review, it is obvious that<i>The Encyclopaedia of General Practice</i>is truly a monumental work which is unique in terms of sheer size and scope. It encompasses all conditions, common or rare, likely to be encountered in general practice, with emphasis on those which can be managed by general practitioners. It is unfortunate that such an ambitious undertaking does not have a greater degree of international usefulness.<i>The Encyclopaedia</i>is written and edited by British physicians, most of whom are general practitioners or specialists with personal experience in general practice. While it may be admirably suited to the needs of British generalists, the considerable differences in medical practice between Britain and the United States limit its usefulness for American physicians. For example, the British and American concepts and definitions of bronchitis and emphysema are sufficiently different as
RACIAL AND GENDER DIFFERENCES IN RISK FACTORS AND OUTCOMES ASSOCIATED WITH LONG QTC SYNDROME: INSIGHTS FROM THE NATIONAL INPATIENT SAMPLE DATABASE 2009-10
Authors: Parasuram Krishnamoorthy, Jalaj Garg, Chandrasekar Palaniswamy, Gregg Lanier, Linda Cuomo, Hasan Ahmad, William Frishman
Journal: Journal of the American College of Cardiology (2014)
Neonatal Immune Thrombocytopenia — The Doctor's Dilemma
Authors: Robert I. Handin
Journal: New England Journal of Medicine (1981)

Idiopathic thrombocytopenic purpura (ITP) is a relatively uncommon disorder that has a predilection for women of childbearing age. In fact, a clue to the possible immune nature of ITP came from the observation that many women with ITP bear children with transient thrombocytopenia. The possibility of transplacental passage of antibody prompted Harrington to infuse plasma from patients with ITP into several normal recipients, including himself, thus inducing profound thrombocytopenia.1 This frequently cited study is a classic example of a pioneering clinical experiment that placed ITP on the growing list of antibody-mediated diseases. The Harrington experiments were quickly repeated, and the . . .
Up-regulation of amphotrophic retroviral receptor expression in human peripheral blood CD34+ cells
Authors: Andreas Kaubisch, Maureen Ward, Stuti Schoetz, Charles Hesdorffer, Arthur Bank
Journal: American Journal of Hematology (1999)

Retroviral-mediated gene transfer into hematopoietic stem cells provides the only means of stable transduction of these cells and their progeny for use with a variety of potentially therapeutic genes. Expression of the Moloney amphotropic retroviral receptor—pit-2 or GLVR-2—is critical to the recognition and entry of Moloney leukemia virus-derived viruses into human target cells such as CD34+ hematopoietic cells. GLVR-2 functions as a sodium-dependent phosphate transporter as well as a receptor. We have previously shown that the expression of the murine homologue of the amphotropic receptor Ram 1, also a phosphate transporter, is developmentally regulated in murine hematopoietic fetal liver cells. We also demonstrated that culture of murine fetal liver cells in phosphate-free (PO4-free) medium increases levels of receptor mRNA and makes murine fetal liver cells susceptible to Moloney amphotropic viral gene transfer. We now examine the effect of culture conditions on the expression of GLVR-2 in human CD34+ cells. In this report, we demonstrate that there is a 2–3 fold increase in GLVR-2 mRNA levels in CD34+ cells after 3 days in culture with interleukin 3, interleukin 6, and stem-cell factor. In addition, the use of PO4-free medium increases expression of GLVR-2 an additional 2-fold in these cells during this time. These results indicate that GLVR-2 expression can be up-regulated on these cells, and may permit improved retroviral gene transfer efficiencies. Am. J. Hematol. 61:243–253, 1999. © 1999 Wiley-Liss, Inc.
Role of Fat1 in cell-cell contact formation of podocytes in puromycin aminonucleoside nephrosis and neonatal kidney
Authors: Eishin Yaoita, Hidetake Kurihara, Yutaka Yoshida, Tsutomu Inoue, Asako Matsuki, Tatsuo Sakai, Tadashi Yamamoto
Journal: Kidney International (2005)
The Angel Letters: Lessons That Dying Can Teach Us About Living
Authors: Susan Arjmand
Journal: JAMA (2007)

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
Chronic Excessive Acetaminophen Use and Liver Damage
Authors: JOHN D. BARKER
Journal: Annals of Internal Medicine (1977)

Severe, often fatal liver damage results from extreme overdosage with acetaminophen. In usual dosage, it is considered harmless. We describe three cases of toxic hepatitis associated with the chronic ingestion of excessive doses of acetaminophen. Each patient took approximately 5 to 8 g of acetaminophen per day during a period of several weeks. The transient elevations of serum hepatocellular enzyme concentrations and the histologic evidence of a toxic hepatitis suggest the liver damage was related to the use of acetaminophen. Alcohol abuse in one patient and negative nitrogen balance in another may have increased the susceptibility to acetaminophen toxicity. With the increasing popularity of acetaminophen for mild pain relief, hepatotoxicity from acute or chronic ingestion may be more common than previously recognized, especially in those patients with predisposing conditions.
Phase II Study of Paclitaxel, Carboplatin, and Cetuximab as First Line Treatment, for Patients with Advanced Non-small Cell Lung Cancer (NSCLC): Results of OPN-017
Authors: Hossein Borghaei, Corey J. Langer, Michael Millenson, Karen J. Ruth, Samuel Litwin, Holly Tuttle, Judie Sylvester Seldomridge, Marc Rovito, David Mintzer, Roger Cohen, Joseph Treat
Journal: Journal of Thoracic Oncology (2008)
Studies on the effect of salicylic acid on normal skin
Authors: M. DAVIES, R. MARKS
Journal: British Journal of Dermatology (1976)

This investigation was prompted by our ignorance of the way in which salicyhc acid aids desquamation. Salicylic acid in aqueous cream or white soft paraffin and in concentrations of 2–12%, was applied to normal skin of twenty‐three subjects while the vehicle alone was apphed to the contralateral sites. Biopsies and skin surface biopsies were taken from the test and control sites after 1 week. Histological examination showed that there was less horny layer on the test specimens but that there were no qualitative or quantitative differences in the structure of the viable epidermis. Portions of the biopsies were incubated in the presence of tritiated precursor compounds and subsequent autoradiographic examination showed no difference in the incorporation of thymidine, cytidinc or histidine between test and control preparations. Scanning electron microscopy of skin surface biopsies showed some changes in all specimens—presumably due to hydration—but also showed strking differences between test and control sites and were especially marked with higher concentrations of salicylic acid. It is suggested that salicylic acid causes desquamation by dissolution of intercellular cement material.
The renin-angiotensin-aldosterone system in congestive failure in conscious dogs.
Authors: L Watkins, J A Burton, E Haber, J R Cant, F W Smith, A C Barger
Journal: Journal of Clinical Investigation (1976)

The role of the renin-angiotensin-aldosterone system in the development of congestive failure has been assessed in the conscious dog by use of the nonapeptide converting enzyme inhibitor. Constriction of the pulmonary artery or thoracic inferior vena cava was maintained for 2 wk while daily measurements were made of plasma renin activity, plasma aldosterone, plasma volume, hematocrit, serum sodium and potassium concentrations, sodium and water balance, body weight, and arterial, caval, and atrial pressures. The initial response to constriction was a reduction in blood pressure, a rise in plasma renin activity, plasma aldosterone, and water intake, and nearly complete sodium retention. In the days after moderate constriction plasma volume and body weight increased (with development of ascites and edema); blood pressure, sodium excretion, plasma renin acvitity, and plasma aldosterone returned to normal. In animals in which blood pressure was not restored, plasma renin activity and plasma aldosterone remained elevated throughout the period of constriction. Single injections of converting enzyme inhibitor reduced blood pressure when plasma renin activity was elevated. Chronic infusion of the inhibitor in dogs with thoracic inferior vena caval constriction prevented the restoration of blood pressure and suppressed the rise in plasma aldosterone; sodium retention and volume expansion were less than in control experiments. Thus the renin-angiotensin-aldosterone system plays an essential role in the maintenance of blood pressure during the genesis of congestive failure. Initially, the restoration of blood pressure is dependent upon circulating angiotensin II; in the later stages, blood pressure is dependent upon the increase in plasma volume.
Leucine-induced Hypoglycaemia and Oral Hypoglycaemic Drugs
Authors: R. J. Jarrett, W. J. H. Butterfield
Journal: BMJ (1964)

The trial was designed to test the safety and effectiveness of the drug in patients attending the diabetes clinic at the Royal Victoria Hospital, Belfast.No attempt was made to compare its potency specifically with other hypoglycaemic drugs, although experience was gained in this respect.
Archibald Walter Forbes Erskine
Authors: J. Erskine
Journal: BMJ (2002)

An expert on venomous creatures and one of the great larrikins of Australian medicineIn a country famous for its deadly snakes and spiders, Struan Sutherland became a household name for his expertise on venomous creatures.He was also well known as one of the great larrikins of Australian medicine and as a prolific author.While working at the Commonwealth Serum Laboratories (CSL), Sutherland led efforts to develop an antivenom to the Sydney funnel-web spider and revolutionised treatment of snake bites by developing the pressure-immobilisation first aid technique and venom detection kits.After an acrimonious departure from CSL, Sutherland founded the Australian Venom Research Unit at the University of Melbourne's department of pharmacology in 1994, where he worked until retiring in 1999.But Sutherland, who spent his final years battling a rare, degenerative brain diseasestriatonigral degeneration-was writing until the end.The second edition of the textbook Australian Animal Toxins, which he co-wrote, was published several months before his death.In typical Sutherland style, he wrote asking colleagues to review chapters of the text, offering a multiple choice reply.Recipients could tick either "send me a copy asap" or "stuff off."Sutherland once said that what he enjoyed most about his