tbuckley/cabot-search huggingface dataset:
Surgery for Pelvic Organ Prolapse—Reply
Authors: Ingrid Nygaard
Journal: JAMA (2013)

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
Plaque inflammation in atherosclerotic rabbits can be identified by SPIO; introducing a noninvasive method for imaging macrophage infiltration in active and inflamed vulnerable plaque
Authors: Maziar Azadpour, Silvio Litovsky, Alireza Zarrabi, Ward Casscells, James Willerson, Morteza Naghavi
Journal: Journal of the American College of Cardiology (2002)
Nonpenetrating Abdominal Trauma as Cause of Renal Vascular Hypertension
Authors: Kurt Lange
Journal: JAMA (1966)

THE POSSIBILITY that systolic and diastolic hypertension can be caused by partial ischemia of a kidney or of parts of it is now generally accepted. The basic investigations of Goldblatt et al<sup>1</sup>have clearly demonstrated that reduced blood pressure in the juxtaglomerular apparatus leads to increased renin production, with subsequent increased production of angiotensin I, which by the converting enzyme is rapidly transformed into the highly pressor active angiotensin II. Congenital or acquired narrowing of the renal artery, thrombosis, or external pressure on the renal artery may lead to the mobilization of this mechanism. Boyd and Lewis,<sup>2</sup>and later Howard et al,<sup>3</sup>have called attention to the fact that incomplete infarction of the kidney with ischemic areas in which some, although markedly diminished, blood flow and pressure persist may lead to hypertension and that nephrectomy may relieve the hypertension. The mechanism by which the decreased blood pressure
Tumor Necrosis Factor Inhibitors and Myocardial Infarction in Psoriasis—Reply
Authors: April W. Armstrong
Journal: JAMA (2013)

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
Quantitation of GSTP1 Methylation in Non-neoplastic Prostatic Tissue and Organ-Confined Prostate Adenocarcinoma
Authors: C. Jeronimo, H. Usadel, R. Henrique, J. Oliveira, C. Lopes, W. G. Nelson, D. Sidransky
Journal: JNCI Journal of the National Cancer Institute (2001)

Background: Methylation of regulatory sequences near GSTP1, which encodes the π class glutathione S-transferase, is the most common epigenetic alteration associated with prostate cancer. We determined whether the quantitation of GSTP1 methylation in histopathologically distinct prostate tissue samples could improve prostate cancer detection. Methods: We used a fluorogenic real-time methylation-specific polymerase chain reaction (MSP) assay to analyze cytidine methylation in the GSTP1 promoter in prostate tissue samples from 69 patients with early-stage prostatic adenocarcinoma (28 of whom also had prostatic intraepithelial neoplasia lesions) and 31 patients with benign prostatic hyperplasia. The relative level of methylated GSTP1 DNA in each sample was determined as the ratio of MSP-amplified GSTP1 to MYOD1, a reference gene. We also performed a prospective, blinded investigation to quantitate GSTP1 promoter methylation in sextant prostate biopsy specimens from 21 additional patients with elevated serum prostate-specific antigen levels, 11 of whom had histologically identified adenocarcinoma and 10 of whom had no morphologic evidence of adenocarcinoma. All data were analyzed by using nonparametric two-sided statistical tests. Results: The median ratios (and interquartile ranges) of MSP-amplified GSTP1 to MYOD1 in resected benign hyperplastic prostatic tissue, intraepithelial neoplasia, and adenocarcinoma were 0 (range, 0–0.1), 1.4 (range, 0– 45.9), and 250.8 (range, 53.5–697.5), respectively; all of these values were statistically significantly different (P<.001). The median ratios of MSP-amplified GSTP1 to MYOD1 in the prospectively collected sextant biopsy samples were 410.6 for the patients with adenocarcinoma and 0.0 for the patients with no evidence of adenocarcinoma (P<.001). Conclusion: Quantitation of GSTP1 methylation accurately discriminates between normal hyperplastic tissue and prostatic carcinoma in small samples of prostate tissue and may augment the standard pathologic/histologic assessment of the prostate.
Effects of Glutathione <i>S</i>-Transferase M1, Maternal Smoking during Pregnancy, and Environmental Tobacco Smoke on Asthma and Wheezing in Children
Authors: Frank D. Gilliland, Yu-Fen Li, Louis Dubeau, Kiros Berhane, Edward Avol, Rob McConnell, W. James Gauderman, John M. Peters
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

The rise in childhood asthma prevalence suggests a role for environmental factors in the etiology of this evolving epidemic; however, genetics also influence the occurrence of asthma. Glutathione S-transferase (GST) M1 may play a role in asthma and wheezing occurrence among those exposed to tobacco smoke, as it functions in pathways involved in asthma pathogenesis such as xenobiotic metabolism and antioxidant defenses. Effects of GSTM1 genotype, maternal smoking during pregnancy, and childhood environmental tobacco smoke (ETS) exposure on asthma and wheezing were investigated in 2,950 children enrolled in 4th, 7th, and 10th grade classrooms in 12 Southern California communities. The effects of in utero exposure to maternal smoking on asthma and wheezing occurrence were largely restricted to children with GSTM1 null genotype. Among GSTM1 null children, in utero exposure was associated with increased prevalence of early onset asthma (odds ratio [OR] 1.6, 95% confidence interval [CI] 1.0–2.5), asthma with current symptoms (OR 1.7, 95% CI 1.1–2.8), persistent asthma (OR 1.6, 95% CI 1.1–2.4), lifetime history of wheezing (OR 1.8, 95% CI 1.3–2.5), wheezing with exercise (OR 2.1, 95% CI 1.3–3.3), wheezing requiring medication (OR 2.2, 95% CI 1.4–3.4), and emergency room visits in the past year (OR 3.7, 95% CI 1.9–7.3). Among children with GSTM1 (+) genotype, in utero exposure was not associated with asthma or wheezing. Our findings indicate that there are important long-term effects of in utero exposure in a genetically susceptible group of children.
Coronary Heart Disease Mortality
Authors: Manning Feinleib
Journal: JAMA (1972)

A mortality survey was taken in an affluent suburban Maryland community of 250,000. During calendar year 1969, there were 719 recorded deaths for persons aged 35 to 74 years, of which 257 (36%) were due to coronary heart disease (CHD). Fifty-four (21%) of the CHD deaths were certified as occurring elsewhere than in a hospital. One hundred eighty-seven CHD victims reached local medical facilities; of these, 101 (54%) were either dead on arrival or pronounced dead in emergency rooms. Thus, in a minimum of 155 instances or 60% of the total CHD mortality experience, the patients died before receiving definitive medical care. The median patient delay, from onset of symptoms until hospital arrival, for the 66 persons with fatal CHD who were hospitalized locally was 5.6 hours. Public education and mobile and other ancillary medical facilities play a role in reducing premature CHD mortality.
Cytomegalovirus: Biology and Infection
Authors: Robert F. Betts
Journal: JAMA (1983)

In this book, one of the series<i>Current Topics in Infectious Diseases</i>, edited by William B. Greenough and Thomas C. Merigan, Monto Ho skillfully reviews many aspects of cytomegalovirus. In the early chapters he presents the biochemical makeup of virions and dense bodies and basic replication of the virus. With reference to original publications, he presents the relevant data on replication of the virus in a way that the reader can clearly grasp. In addition, the book compares, where relevant, the features of human cytomegalovirus replication with replication of other members of the herpesvirus group. In fact, the early discussion of the basic biologic characteristics outlined by Dr Ho would allow the book to stand on this information alone. However, the best is yet to come. In later sections of the book, he provides insight for the reader who is partially familiar with the basic characteristics of the virus-host interaction.
Comparative Usefulness of Myocardial Velocity Gradient in Detecting Ischemic Myocardium by a Dobutamine Challenge
Authors: Hiroshi Tsutsui, Masaaki Uematsu, Hiromi Shimizu, Masakazu Yamagishi, Norio Tanaka, Hisao Matsuda, Kunio Miyatake
Journal: Journal of the American College of Cardiology (1998)
Hyperekplexia Phenotype of Glycine Receptor α1 Subunit Mutant Mice Identifies Zn2+ as an Essential Endogenous Modulator of Glycinergic Neurotransmission
Authors: Klaus Hirzel, Ulrike Müller, A. Tobias Latal, Swen Hülsmann, Joanna Grudzinska, Mathias W. Seeliger, Heinrich Betz, Bodo Laube
Journal: Neuron (2006)

Zn2+ is thought to modulate neurotransmission by affecting currents mediated by ligand-gated ion channels and transmitter reuptake by Na+-dependent transporter systems. Here, we examined the in vivo relevance of Zn2+ neuromodulation by producing knockin mice carrying the mutation D80A in the glycine receptor (GlyR) α1 subunit gene (Glra1). This substitution selectively eliminates the potentiating effect of Zn2+ on GlyR currents. Mice homozygous for Glra1(D80A) develop a severe neuromotor phenotype postnatally that resembles forms of human hyperekplexia (startle disease) caused by mutations in GlyR genes. In spinal neurons and brainstem slices from Glra1(D80A) mice, GlyR expression, synaptic localization, and basal glycinergic transmission were normal; however, potentiation of spontaneous glycinergic currents by Zn2+ was significantly impaired. Thus, the hyperekplexia phenotype of Glra1(D80A) mice is due to the loss of Zn2+ potentiation of α1 subunit containing GlyRs, indicating that synaptic Zn2+ is essential for proper in vivo functioning of glycinergic neurotransmission.
The UGDP Study
Authors: David S. Salsburg
Journal: JAMA (1971)

ABSTRACT To the Editor.— It would appear from the Cornfield-Schor exchange (217:1671-1687, 1971) that the major statistical controversy over the UGDP study is whether there is enough evidence of an imbalance between the placebo and tolbutamide patient groups at baseline to account for the imbalance in death patterns that appeared after five years. Schor has examined the published data and believes that the baseline characteristics were sufficiently different. Cornfield has examined both the published data and additional material in the study files and says they were not.I would like to point out that Cornfield has displayed highly significant evidence in favor of Schor's hypothesis.It is fairly easy to pursue imbalances in patient populations that have been randomly assigned to different treatments. One can always find some peculiar ancillary statistic (like the ages at death of the patients' grandmothers) for which the study was not balanced. However, there are
Activation of neutrophils by autocrine IL-17A–IL-17RC interactions during fungal infection is regulated by IL-6, IL-23, RORγt and dectin-2
Authors: Patricia R Taylor, Sanhita Roy, Sixto M Leal, Yan Sun, Scott J Howell, Brian A Cobb, Xiaoxia Li, Eric Pearlman
Journal: Nature Immunology (2013)
Outcome of renal replacement treatment in patients with diabetes mellitus.
Authors: M A McMillan, J D Briggs, B J Junor
Journal: BMJ (1990)

OBJECTIVE--To compare the outcome of renal replacement treatment in patients with diabetes mellitus and in non-diabetic patients with end stage renal failure. DESIGN--Retrospective comparison of cases and matched controls. SETTING--Renal unit, Western Infirmary, Glasgow, providing both dialysis and renal transplantation. PATIENTS--82 Diabetic patients starting renal replacement treatment between 1979 and 1988, compared with 82 matched non-diabetic controls with renal failure and 39 different matched controls undergoing renal transplantation. MAIN OUTCOME MEASURES--Patient characteristics, history of smoking, prevalence of left ventricular hypertrophy and myocardial ischaemia at start of renal replacement treatment; survival of patients with renal replacement treatment and of patients and allografts with renal transplantation. RESULTS--The overall survival of the diabetic patients during the treatment was 83%, 59%, and 50% at one, three, and five years. Survival was significantly poorer in the diabetic patients than the controls (p less than 0.001). Particularly adverse features for outcome at the start of treatment were increasing age (p less than 0.01) and current cigarette smoking (relative risk (95% confidence interval) 2.28 (0.93 to 4.84), p less than 0.05). Deaths were mainly from cardiac and vascular causes. The incidence of peritonitis in patients on continuous ambulatory peritoneal dialysis was the same in diabetic patients and controls (49% in each group remained free of peritonitis after one year), and the survival of renal allografts was not significantly worse in diabetic patients (p less than 0.5). CONCLUSIONS--Renal replacement treatment may give good results in diabetic patients, although the outlook remains less favourable than for non-diabetic patients because of coexistent, progressive vascular disease, which is more severe in older patients.
Functional linkage of cirrhosis-predictive single nucleotide polymorphisms of toll-like receptor 4 to hepatic stellate cell responses
Authors: Jinsheng Guo, Johnny Loke, Feng Zheng, Feng Hong, Steven Yea, Masayuki Fukata, Mirko Tarocchi, Olivia T. Abar, Hongjin Huang, John J. Sninsky, Scott L. Friedman
Journal: Hepatology (2008)

In a recent study, a single nucleotide polymorphism (SNP) of the Toll-like receptor 4 (TLR4) gene (c.1196C>T [rs4986791, p.T399I]) emerged as conferring protection from fibrosis progression compared to a major, wild-type (WT) CC allele (p.T399). The present study examined the functional linkage of this SNP, along with another common, highly cosegregated TLR4 SNP (c.896A>G [rs4986790, p.D299G]), to hepatic stellate cell (HSC) responses. Both HSCs from TLR4(-/-) mice and a human HSC line (LX-2) reconstituted with either TLR4 D299G and/or T399I complementary DNAs were hyporesponsive to lipopolysaccharide (LPS) stimulation compared to those expressing WT TLR4, as assessed by the expression and secretion of LPS-induced inflammatory and chemotactic cytokines (i.e., monocyte chemoattractant protein-1, interleukin-6), down-regulation of bone morphogenic protein and the activin membrane-bound inhibitor expression (an inhibitory transforming growth factor beta pseudoreceptor), and activation of a nuclear factor kappaB (NF-kappaB)-responsive luciferase reporter. In addition, spontaneous apoptosis, as well as apoptosis induced by pathway inhibitors of NF-kappaB, extracellular signal-regulated kinase (ERK), and phosphatidylinositol 3-kinase were greatly increased in HSCs from either TLR4(-/-) or myeloid differentiation factor 88(-/-) (a TLR adaptor protein) mice, as well as in murine HSCs expressing D299G and/or T399I SNPs; increased apoptosis in these lines was accompanied by decreased phospho-ERK and Bcl-2.TLR4 D299G and T399I SNPs that are associated with protection from hepatic fibrosis reduce TLR4-mediated inflammatory and fibrogenic signaling and lower the apoptotic threshold of activated HSCs. These findings provide a mechanistic link that explains how specific TLR4 SNPs may regulate the risk of fibrosis progression.
Genome-wide association study and admixture mapping reveal new loci associated with total IgE levels in Latinos
Authors: Maria Pino-Yanes, Christopher R. Gignoux, Joshua M. Galanter, Albert M. Levin, Catarina D. Campbell, Celeste Eng, Scott Huntsman, Katherine K. Nishimura, Pierre-Antoine Gourraud, Kiana Mohajeri, Brian J. O'Roak, Donglei Hu, Rasika A. Mathias, Elizabeth A. Nguyen, Lindsey A. Roth, Badri Padhukasahasram, Andres Moreno-Estrada, Karla Sandoval, Cheryl A. Winkler, Fred Lurmann, Adam Davis, Harold J. Farber, Kelley Meade, Pedro C. Avila, Denise Serebrisky, Rocio Chapela, Jean G. Ford, Michael A. Lenoir, Shannon M. Thyne, Emerita Brigino-Buenaventura, Luisa N. Borrell, William Rodriguez-Cintron, Saunak Sen, Rajesh Kumar, Jose R. Rodriguez-Santana, Carlos D. Bustamante, Fernando D. Martinez, Benjamin A. Raby, Scott T. Weiss, Dan L. Nicolae, Carole Ober, Deborah A. Meyers, Eugene R. Bleecker, Steven J. Mack, Ryan D. Hernandez, Evan E. Eichler, Kathleen C. Barnes, L. Keoki Williams, Dara G. Torgerson, Esteban G. Burchard
Journal: Journal of Allergy and Clinical Immunology (2014)
Immunohistochemical markers for arthritis in psoriasis.
Authors: D J Veale, L Barnes, S Rogers, O FitzGerald
Journal: Annals of the Rheumatic Diseases (1994)

OBJECTIVES--To examine the immunohistological features in the involved skin of patients with psoriatic arthritis (PA) (n = 15), compared with those in involved skin from patients with psoriasis but no arthritis (n = 5), and with a group with normal skin (n = 4), to identify markers for arthritis in psoriasis. METHODS--Skin was obtained from patients by 6 mm punch biopsy and normal skin was provided by the department of plastic surgery. Samples were stained with monoclonal antibodies against T cells (CD3, CD8, CD4, CD45Ro), B cells (CD20), macrophages (mac387), vascular endothelium (FVIII-related antigen) and a Langerhan9s cell marker (p155). The number of cells/vessels staining with each monoclonal antibody was calculated and serial sections of skin were examined to estimate the presence of DR+ keratinocytes. RESULTS--There were significantly more CD45Ro T-cells and blood vessels in patients with psoriatic arthritis compared with both psoriasis alone, and with normal controls (p &lt; 0.02). While B-cells were not seen in psoriasis without arthritis or in normal skin, a small but significant number were observed in PA (p &lt; 0.02). Furthermore, while DR+ keratinocytes were present in both psoriatic arthritis and psoriasis skin, there were significantly more DR+ cells in the psoriatic arthritis epidermis compared with psoriasis alone (p &lt; 0.02). CONCLUSIONS--This study suggests that increased numbers of CD45Ro T-cells, greater vascularity, the presence of B-cells, and increased numbers of DR+ epidermal cells are markers for arthritis in patients with psoriasis.
Hypoxic ventilatory response in subjects with normal and high oxygen affinity hemoglobins.
Authors: R P Hebbel, R S Kronenberg, J W Eaton
Journal: Journal of Clinical Investigation (1977)

It has still not been shown unequivocally whether a decrement of arterial oxygen content or tension governs the ventilatory response to hypoxia. In an attempt to discriminate between the two possibilities, we have measured the ventilatory response to isocapnic progressive hypoxia in two healthy children with a high oxygen affinity hemoglobin (Hb Andrew-Minneapolis) and in their age- and sex-matched normal siblings. Hypoxic ventilatory response was identical in all subjects, there being no difference in minute ventilation at PAo2 = 40 mm Hg or in k (decrement of PO2 required to increase ventilation by a factor of 2.718). In contrast, at PAo2 = 40 mm Hg, hemoglobin oxygen saturation decreased markedly in controls but only slightly in high affinity subjects. Furthermore the increase in heart rate at PAo2 = 40 mm Hg was significantly less in high affinity subjects, suggesting a concomitant difference in oxygen delivery. Thus, with identical decrements in PAo2 but widely divergent changes in arterial oxygen content and oxygen delivery, controls and high affinity subjects showed virtually identical ventilatory response to hypoxia. We conclude that decrements of oxygen tension are the major stimulus for hypoxic ventilatory response.
Oral Contraceptives and Breast Cancer
Authors: D. B. Thomas
Journal: JNCI Journal of the National Cancer Institute (1993)

Changes in endogenous hormones at various times in life (e.g., early menarche, birth of the 1st child at an advanced maternal age, and late menopause) increase the changes of developing breast cancer. It is reasonable then to expect oral contraceptive (OC) use to increase the risk of breast cancer. It is difficult, however, to prove OC exposure has this effect due to changed OC use patterns plus OCs consist of many different hormones at various doses and compositions. Yet, OC use in the past (even more than 15 years of OC use) had not increased the risk of breast cancer in women of all combined age groups. 3 research groups have identified a small increase in overall risk in low risk women, but unidentified sources of bias or confounding could account for this increased risk. Some recent studies indicate an increased risk of breast cancer with duration of OC use, but the risk depends somewhat on dose of either the estrogen or the progestin. Nonetheless, these findings were weak and inconclusive. Other research shows long-term OC use increases the risk of breast cancer in just young women (under 45 years old). Future epidemiologic studies thus need to address increased breast cancer risk in women under 45 years old who used OCs for a long time. They need to look at whether the risk is due to early use and continues into older age or to longterm use at any time in just young women. Some studies should include women with and without various biological markers of susceptibility. Other studies should measure blood levels of estrogens and progestins in women using the same OCs. BAsed on the information now available, it would be unwise for physicians to warn women against using the highly effective OCs because they do prevent unwanted pregnancy and are protective against ovarian and endometrial cancer.
Asthma: a disease of the innate and adaptive immune systems?
Authors: O Mukhtar
Journal: Thorax (2009)

The paradigm that asthma is a disease solely of the adaptive immune system is gradually being challenged. This study adds weight to the suggestion that the innate immune system may play an equally pivotal role in its pathogenesis.

Using chimeric mice, the authors offer a mechanism by which exposure of the airway epithelium to house dust mite allergen might result in both forms of …