tbuckley/cabot-search huggingface dataset:
Psychopathology: A Survey of Modern Approaches
Authors: J. Ernest. Nicole
Journal: JAMA (1934)

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
Placental Cadherin and the Basal Epithelial Phenotype of <i>BRCA1</i>-Related Breast Cancer
Authors: Jarle B. Arnes, Jean-Sébastien Brunet, Ingunn Stefansson, Louis R. Bégin, Nora Wong, Pierre O. Chappuis, Lars A. Akslen, William D. Foulkes
Journal: Clinical Cancer Research (2005)

Abstract Purpose: BRCA1-related breast cancer frequently has a basal epithelial phenotype, and P-cadherin is a basal marker. We undertook a detailed evaluation of the relationship among P-cadherin, prognostic markers in breast cancer, and outcome. Experimental Design: This study was restricted to 292 cases of first primary invasive breast cancer diagnosed in Ashkenazi Jewish women between 1980 and 1995. All available blocks were stained for P-cadherin, and 261 were included in the final statistical analyses, including 27 germ line BRCA1 mutation carriers and 8 BRCA2 mutation carriers. Descriptive analyses were done followed by survival analyses and a Poisson regression analysis. Results: P-cadherin was present in 80 of the 261 breast cancers (31%) and was more frequently present in tumors that have a basal epithelial phenotype [i.e., high-grade, estrogen receptor– and KIP1 (p27Kip1)–negative tumors, with expression of cytokeratin 5/6, cyclin E, TP53, and presence of BRCA1 mutations and vascular nests (all P &amp;lt; 0.001)]. In a univariate survival model, expression of P-cadherin was associated with a relative risk (RR) of death from breast cancer at a 10-year follow-up of 2.9 (95% confidence interval, 1.8-4.7; P &amp;lt; 0.0001) and was a predictor of poor univariate survival in both lymph node–negative and –positive breast cancers. In a multivariate analysis, the effect of P-cadherin levels was not independent of other basal-related markers. Multivariable interaction modeling showed that P-cadherin positivity was highly predictive of a poor prognosis in small, node-negative breast cancers (RR, 7.1; P = 0.006). Conclusions: P-cadherin is a marker for basal-like breast cancers and is strongly associated with the presence of a BRCA1 mutation. It is an adverse prognostic factor, particularly in small, node-negative breast cancers.
Exogenous High-Mobility Group Box 1 Protein Induces Myocardial Regeneration After Infarction via Enhanced Cardiac C-Kit <sup>+</sup> Cell Proliferation and Differentiation
Authors: Federica Limana, Antonia Germani, Antonella Zacheo, Jan Kajstura, Anna Di Carlo, Giovanna Borsellino, Omar Leoni, Roberta Palumbo, Luca Battistini, Raffaella Rastaldo, Susanne Müller, Giulio Pompilio, Piero Anversa, Marco E. Bianchi, Maurizio C. Capogrossi
Journal: Circulation Research (2005)

High-mobility group box 1 protein (HMGB1) is a chromatin protein that is released by inflammatory and necrotic cells. Extracellular HMGB1 signals tissue damage, stimulates the secretion of proinflammatory cytokines and chemokines, and modulates stem cell function. The present study examined exogenous HMGB1 effect on mouse left-ventricular function and myocyte regeneration after infarction. Myocardial infarction was induced in C57BL/6 mice by permanent coronary artery ligation. After 4 hours animals were reoperated and 200 ng of purified HMGB1 was administered in the peri-infarcted left ventricle. This intervention resulted in the formation of new myocytes within the infarcted portion of the wall. The regenerative process involved the proliferation and differentiation of endogenous cardiac c-kit+ progenitor cells. Circulating c-kit+ cells did not significantly contribute to HMGB1-mediated cardiac regeneration. Echocardiographic and hemodynamic parameters at 1, 2, and 4 weeks demonstrated a significant recovery of cardiac performance in HMGB1-treated mice. These effects were not observed in infarcted hearts treated either with the unrelated protein glutathione S-transferase or a truncated form of HMGB1. Thus, HMGB1 appears to be a potent inducer of myocardial regeneration following myocardial infarction.
Hypercholesterolemia in low density lipoprotein receptor knockout mice and its reversal by adenovirus-mediated gene delivery.
Authors: S Ishibashi, M S Brown, J L Goldstein, R D Gerard, R E Hammer, J Herz
Journal: Journal of Clinical Investigation (1993)

We employed homologous recombination in embryonic stem cells to produce mice lacking functional LDL receptor genes. Homozygous male and female mice lacking LDL receptors (LDLR-/- mice) were viable and fertile. Total plasma cholesterol levels were twofold higher than those of wild-type litter-mates, owing to a seven- to ninefold increase in intermediate density lipoproteins (IDL) and LDL without a significant change in HDL. Plasma triglyceride levels were normal. The half-lives for intravenously administered 125I-VLDL and 125I-LDL were prolonged by 30-fold and 2.5-fold, respectively, but the clearance of 125I-HDL was normal in the LDLR-/- mice. Unlike wild-type mice, LDLR-/- mice responded to moderate amounts of dietary cholesterol (0.2% cholesterol/10% coconut oil) with a major increase in the cholesterol content of IDL and LDL particles. The elevated IDL/LDL level of LDLR-/- mice was reduced to normal 4 d after the intravenous injection of a recombinant replication-defective adenovirus encoding the human LDL receptor driven by the cytomegalovirus promoter. The virus restored expression of LDL receptor protein in the liver and increased the clearance of 125I-VLDL. We conclude that the LDL receptor is responsible in part for the low levels of VLDL, IDL, and LDL in wild-type mice and that adenovirus-encoded LDL receptors can acutely reverse the hypercholesterolemic effects of LDL receptor deficiency.
Immediate effects of heavy exercise on the circulating thyroid hormones.
Authors: A. R. Siddiqui, R. B. Hinnefeld, T. Dillon, W. E. Judson
Journal: British Journal of Sports Medicine (1983)

Sera from 20 patients with suspected or known coronary artery disease were measured for thyroxine (T4), tri-iodothyronine (T3), tri-iodothyronine uptake ratio (T3UR), thyroid stimulating hormone (TSH), and reverse tri-iodothyronine (rT3), before and after maximal or near-maximal exercise. On the average the patients achieved 92% (rang 68-108) of the predicted maximum heart rate. There were no statistically significant differences between the pre- and the post-exercise serum levels of thyroid hormones. When five patients who achieved less than 90% of the predicted maximum heart rate were excluded, the results remained unchanged. It appears that the circulating thyroid hormones are not acutely affected after maximal or near-maximal exercise; however, the patient population was highly select.
Intraoperative Microscope-Mounted Spectral Domain Optical Coherence Tomography for Evaluation of Retinal Anatomy during Macular Surgery
Authors: Robin Ray, David E. Barañano, Jorge A. Fortun, Bryan J. Schwent, Blaine E. Cribbs, Chris S. Bergstrom, G. Baker Hubbard, Sunil K. Srivastava
Journal: Ophthalmology (2011)
Monoclonal Proteins and Renal Disease
Authors: Robert A. Kyle
Journal: Annual Review of Medicine (1994)

Renal insufficiency, which is present initially in almost half of patients with multiple myeloma, usually results from myeloma kidney or hypercalcemia. Neither the class of light chain nor the isoelectric point plays an important role in kidney failure. Acute renal failure must be treated with appropriate fluids and with electrolytes and hemodialysis if necessary. Plasma exchange may be helpful, but has not been proven as such. The presence of a nephrotic syndrome and a monoclonal κ or λ light chain in the urine almost always indicates primary amyloidosis (AL) or light-chain deposition disease. Amyloid fibrils must be distinguished from the fibrils of immunotactoid glomerulopathy.
Pancreatic Exocrine Dysfunction in Maturity-Onset Diabetes of the Young Type 3
Authors: Mette Vesterhus, Helge Ræder, Stefan Johansson, Anders Molven, Pål R. Njølstad
Journal: Diabetes Care (2008)

OBJECTIVE—Exocrine pancreas dysfunction is seen in 10–30% of patients with type 1 and 2 diabetes. We have recently identified a syndrome of diabetes and exocrine pancreas dysfunction attributable to mutations in the carboxyl ester lipase (CEL) gene. We wanted to investigate the prevalence of pancreatic exocrine dysfunction in patients with maturity-onset diabetes of the young type 3 (MODY3). RESEARCH DESIGN AND METHODS—All 119 patients with MODY3 in the Norwegian MODY Registry were invited to participate, and 70 (60.5%) responded, among whom 63 were adults. Control groups included 140 subjects with type 1 diabetes and 78 nondiabetic control subjects. Pancreatic dysfunction was defined by fecal elastase deficiency. Fecal fat excretion was measured in 25 patients with fecal elastase deficiency. CEL was investigated for sequence changes. RESULTS—We found a prevalence of fecal elastase deficiency of 12.7% in adult patients with MODY3, compared with 18.6% in patients with type 1 diabetes and 3.8% in nondiabetic control subjects. The six patients with MODY3 with fecal elastase deficiency available for analysis all had increased fecal fat excretion. Fecal elastase decreased with age. Controlled for age, patients with MODY3 still had decreased fecal elastase compared with control subjects. Twelve of 70 patients (17%) had single-base insertions in CEL exon 11. Two of these had fecal elastase deficiency. CONCLUSIONS—The prevalence of pancreatic exocrine dysfunction was 12.7% in a cohort of 63 adult patients with MODY3, similar to the prevalence among type 1 diabetic patients. Fecal fat excretion was increased in all patients with MODY3 with fecal elastase deficiency who were investigated, underscoring the potential clinical importance of the exocrine dysfunction.
Systemic Exposure to Irradiated Apoptotic Cells Induces Autoantibody Production
Authors: Dror Mevorach, Jun Liang Zhou, Xin Song, Keith B. Elkon
Journal: The Journal of Experimental Medicine (1998)

During apoptotic cell death, cell surface ligands initiate phagocytosis of the dying cell. Clearance of these apoptotic cells is thought to occur without an immune response. Since a number of autoantigens are located at the cell surface or within apoptotic blebs, we examined whether exposure of mice to syngeneic apoptotic cells by the intravenous route could induce autoantibody production. Normal mice injected with syngeneic apoptotic thymocytes developed antinuclear autoantibodies and anticardiolipin and anti-ssDNA antibodies. The autoantibody levels were generally lower than those observed in MRL/Faslpr mice and were transient. Surprisingly, six out of six immunized mice demonstrated immunoglobulin G deposition in the glomeruli several months after immunization. These findings indicate that systemic exposure to apoptotic cells can induce an immune response in normal mice, and may help to explain antigen selection and initiation of the immune response in diseases characterized by increased rates of apoptosis such as AIDS and, possibly, systemic lupus erythematosus.
APRIL promotes B-1 cell-associated neoplasm
Authors: Lourdes Planelles, Carla E. Carvalho-Pinto, Gijs Hardenberg, Salette Smaniotto, Wilson Savino, Ruth Gómez-Caro, Melchor Alvarez-Mon, Joan de Jong, Eric Eldering, Carlos Martı́nez-A, Jan Paul Medema, Michael Hahne
Journal: Cancer Cell (2004)
Retinoids exacerbate rat liver fibrosis by inducing the activation of latent TGF-beta in liver stellate cells
Authors: M Okuno
Journal: Hepatology (1997)

Liver stellate cells (SCs) play central roles in both the storage of retinol and the development of liver fibrosis. The present study is aimed to understand the mechanism by which retinoic acid (RA, an active metabolite of retinol) enhances hepatic fibrosis in rats. We tested the effect of 9-cis-RA on several aspects in vitro rat SC cultures, including the activity of cellular plasminogen activator (PA), messenger RNA (mRNA), and protein levels of transforming growth factor-beta (TGF-beta) mRNA level of type-I procollagen, and the activity of type-I collagenase. Employing the rat liver fibrosis model produced by porcine serum, we also estimated the effect of oral administration of a stable RA analog on the progression of the fibrosis, as well as on hepatic TGF-beta contents. In vitro SC cultures, 9-cis-RA enhanced cellular PA and plasmin levels thereby induced plasmin-mediated activation of latent TGF-beta. Active TGF-beta generated self-stimulated its synthesis as well as that of collagen and suppressed the production of collagenase in an autocrine manner. In in vivo rat models, an RA analog accelerated the porcine serum-induced fibrosis by enhancing TGF-beta contents and, thus, collagen levels in the liver, although the RA analog alone was not fibrogenic. These results suggest that RA exacerbated liver fibrosis, at least in part, by inducing the activation and production of latent TGF-beta in liver SCs. (Hepatology 1997 Oct;26(4):913-21)
Selective reporting bias of harm outcomes within studies: findings from a cohort of systematic reviews
Authors: P. Saini, Y. K. Loke, C. Gamble, D. G. Altman, P. R. Williamson, J. J. Kirkham
Journal: BMJ (2014)

<b>Objective</b> To determine the extent and nature of selective non-reporting of harm outcomes in clinical studies that were eligible for inclusion in a cohort of systematic reviews. <b>Design</b> Cohort study of systematic reviews from two databases. <b>Setting</b> Outcome reporting bias in trials for harm outcomes (ORBIT II) in systematic reviews from the Cochrane Library and a separate cohort of systematic reviews of adverse events. <b>Participants</b> 92 systematic reviews of randomised controlled trials and non-randomised studies published in the Cochrane Library between issue 9, 2012 and issue 2, 2013 (Cochrane cohort) and 230 systematic reviews published between 1 January 2007 and 31 December 2011 in other publications, synthesising data on harm outcomes (adverse event cohort). <b>Methods</b> A 13 point classification system for missing outcome data on harm was developed and applied to the studies. <b>Results</b> 86% (79/92) of reviews in the Cochrane cohort did not include full data from the main harm outcome of interest of each review for all of the eligible studies included within that review; 76% (173/230) for the adverse event cohort. Overall, the single primary harm outcome was inadequately reported in 76% (705/931) of the studies included in the 92 reviews from the Cochrane cohort and not reported in 47% (4159/8837) of the 230 reviews in the adverse event cohort. In a sample of primary studies not reporting on the single primary harm outcome in the review, scrutiny of the study publication revealed that outcome reporting bias was suspected in nearly two thirds (63%, 248/393). <b>Conclusions</b> The number of reviews suspected of outcome reporting bias as a result of missing or partially reported harm related outcomes from at least one eligible study is high. The declaration of important harms and the quality of the reporting of harm outcomes must be improved in both primary studies and systematic reviews.
Fasting Plasma Glucose and Clustering of Cardiometabolic Risk Factors in Normoglycemic Outpatient Children and Adolescents
Authors: Procolo Di Bonito, Eduardo Sanguigno, Claudia Forziato, Francesco Saitta, Maria Rosaria Iardino, Brunella Capaldo
Journal: Diabetes Care (2011)

OBJECTIVE To evaluate whether fasting plasma glucose (FPG) within a normoglycemic range is associated with cardiometabolic risk factors (CMRF) among children and adolescents in an outpatient setting. RESEARCH DESIGN AND METHODS Subjects (780; age 6–16 years) with FPG &amp;lt;100 mg/dL were divided into tertiles of FPG. RESULTS BMI, waist circumference, homeostasis model assessment-insulin resistance, systolic blood pressure, and white blood cell (WBC) count (P &amp;lt; 0.0001) increased across tertiles of FPG. Subjects with high-normal FPG (89–99 mg/dL) showed a higher risk of insulin resistance, hypertension, and high WBC count compared with subjects with low-normal FPG, independent of BMI z score. CONCLUSIONS In outpatient children and adolescents, higher FPG within the normal range is associated with several CMRF, independent of obesity. Thus the simple measurement of FPG may help identify subjects who warrant some monitoring in relation to cardiovascular risk.
Tragedy in sport and trial by tabloid
Authors: Domhnall Macauley
Journal: British Journal of Sports Medicine (2000)

Warm upTo be voted favourite advertisement by readers of the Scottish edition of the Sun is no mean feat (p79).Gavin Hastings, sporting hero, led the Health Education Board of Scotland's walking promotion that gained this honour.Winning the award was relatively unimportant, but what really mattered was that so many people noticed it.Rarely does sports medicine reach the national consciousness.Another innovative approach that triggered public awareness was the subway poster campaign (p144) which had two unusual and imaginative ideas that were positive, encouraging and had flair.This is a new approach for a message that could become tedious.
I. RENAL THRESHOLDS FOR HEMOGLOBIN IN DOGS
Authors: John A. Lichty, William H. Havill, George H. Whipple
Journal: The Journal of Experimental Medicine (1932)

We use the term "renal threshold for hemoglobin" to indicate the smallest amount of hemoglobin which given intravenously will effect the appearance of recognizable hemoglobin in the urine. The initial renal threshold level for dog hemoglobin is established by the methods employed at an average value of 155 mg. hemoglobin per kilo body weight with maximal values of 210 and minimal of 124. Repeated daily injections of hemoglobin will depress this initial renal threshold level on the average 46 per cent with maximal values of 110 and minimal values of 60 mg. hemoglobin per kilo body weight. This minimal or depression threshold is relatively constant if the injections are continued. Rest periods without injections cause a return of the renal threshold for hemoglobin toward the initial threshold levels-recovery threshold level. Injections of hemoglobin below the initial threshold level but above the minimal or depression threshold will eventually reduce the renal threshold for hemoglobin to its depression threshold level. We believe the depression threshold or minimal renal threshold level due to repeated hemoglobin injections is a little above the glomerular threshold which we assume is the base line threshold for hemoglobin. Our reasons for this belief in the glomerular threshold are given above and in the other papers of this series.
Element Array by Scanning X-ray Fluorescence Microscopy after <i>Cis</i>-Diamminedichloro-Platinum(II) Treatment
Authors: Mari Shimura, Akira Saito, Satoshi Matsuyama, Takahiro Sakuma, Yasuhito Terui, Kazumasa Ueno, Hirokatsu Yumoto, Kazuto Yamauchi, Kazuya Yamamura, Hidekazu Mimura, Yasuhisa Sano, Makina Yabashi, Kenji Tamasaku, Kazuto Nishio, Yoshinori Nishino, Katsuyoshi Endo, Kiyohiko Hatake, Yuzo Mori, Yukihito Ishizaka, Tetsuya Ishikawa
Journal: Cancer Research (2005)

Abstract Minerals are important for cellular functions, such as transcription and enzyme activity, and are also involved in the metabolism of anticancer chemotherapeutic compounds. Profiling of intracellular elements in individual cells could help in understanding the mechanism of drug resistance in tumors and possibly provide a new strategy of anticancer chemotherapy. Using a recently developed technique of scanning X-ray fluorescence microscopy (SXFM), we analyzed intracellular elements after treatment with cis-diamminedichloro-platinum(II) (CDDP), a platinum-based anticancer agent. The images obtained by SXFM (element array) revealed that the average Pt content of CDDP-resistant cells was 2.6 times less than that of sensitive cells, and the zinc content was inversely correlated with the intracellular Pt content. Data suggested that Zn-related detoxification is responsible for resistance to CDDP. Of Zn-related excretion factors, glutathione was highly correlated with the amount of Zn. The combined treatment of CDDP and a Zn(II) chelator resulted in the incorporation of thrice more Pt with the concomitant down-regulation of glutathione. We propose that the generation of an element array by SXFM opens up new avenues in cancer biology and treatment.
Time Trends and Geographic Disparities in Acute Complications of Diabetes in Ontario, Canada
Authors: Gillian L. Booth, Janet E. Hux, Jiming Fang, Benjamin T.B. Chan
Journal: Diabetes Care (2005)

OBJECTIVE—This study examines whether acute diabetes complication rates have fallen in recent years and whether geographic factors influence these trends. RESEARCH DESIGN AND METHODS—A population-based time-trend analysis of acute complications of diabetes was conducted using linked administrative and census data from Ontario, Canada. The study population included all adults identified through a province-wide electronic diabetes registry between 1994 and 1999 (n = 577,659). The primary outcome was hospitalizations for hyper- and hypoglycemia and emergency department visits for diabetes. RESULTS—Between 1994 and 1999, rates of hospitalization for hyper- and hypoglycemic emergencies decreased by 32.5 and 76.9%, respectively; emergency department visits for diabetes fell by 23.9%. On multivariate analysis, fiscal year was an independent predictor of acute diabetes complications, with individuals in our cohort experiencing a decline in risk of ∼6% per year for either being hospitalized with hyper- or hypoglycemia or requiring an emergency department visit for diabetes. After accounting for variation in physician service use, diabetic individuals living in rural areas or Aboriginal communities were nearly twice as likely to have an acute complication, whereas those residing in remote areas of the province were nearly three times as likely to experience an event. CONCLUSIONS—Although our findings suggest an overall improvement in diabetes care in Ontario, certain subgroups of the population continue to experience higher rates of complications that are potentially preventable through good ambulatory care. Measures to improve access to timely and effective outpatient care may further reduce rates of acute complications among the diabetic population.