tbuckley/cabot-search huggingface dataset:
Contractions of canine vascular smooth muscle cells caused by ouabain are due to release of norepinephrine from adrenergic nerve endings.
Authors: L L Aarhus, J T Shepherd, G M Tyce, T J Verbeuren, P M Vanhoutte
Journal: Circulation Research (1983)

Experiments were performed to determine whether the contractions of isolated canine blood vessels caused by ouabain are due solely to the release of endogenous norepinephrine. The response of segments of splenic arteries and veins and strips of splenic capsules to ouabain were compared before and after surgical sympathectomy. Successful denervation was demonstrated by absence of a contractile response to electrical stimulation, supersensitivity to exogenous norepinephrine, an extremely low content of endogenous norepinephrine, reduced accumulation of 3H-norepinephrine, and inability of electrical stimulation and tyramine to augment the overflow of 3H-norepinephrine. Ouabain augmented the overflow of 3H-norepinephrine from control but not from denervated splenic capsule. It caused contraction of control but not of denervated splenic arteries, veins, and capsules. Studies were also conducted in the same tissues and in segments of mesenteric and femoral arteries and of circular and longitudinal segments of the portal mesenteric vein before and after chemical sympathectomy with 6-hydroxydopamine. In these tissues, the contractile responses to electrical stimulation but not exogenous norepinephrine and prostaglandin F2 alpha were abolished. In the control tissues, ouabain caused strong contractions, whereas, in the denervated tissues, only a weak or no response to the glycoside occurred. The study demonstrates that, in isolated canine blood vessels, ouabain causes contraction of smooth muscle cells by virtue of its ability to release norepinephrine from the sympathetic nerves.
Aberrant Circulating Levels of Purinergic Signaling Markers Are Associated With Several Key Aspects of Peripheral Atherosclerosis and Thrombosis
Authors: Juho Jalkanen, Gennady G. Yegutkin, Maija Hollmén, Kristiina Aalto, Tuomas Kiviniemi, Veikko Salomaa, Sirpa Jalkanen, Harri Hakovirta
Journal: Circulation Research (2015)

Rationale: Purinergic signaling plays an important role in inflammation and vascular integrity, but little is known about purinergic mechanisms during the pathogenesis of atherosclerosis in humans. Objective: The objective of this study is to study markers of purinergic signaling in a cohort of patients with peripheral artery disease. Methods and Results: Plasma ATP and ADP levels and serum nucleoside triphosphate diphosphohydrolase-1 (NTPDase1/CD39) and ecto-5′-nucleotidase/CD73 activities were measured in 226 patients with stable peripheral artery disease admitted for nonurgent invasive imaging and treatment. The major findings were that ATP, ADP, and CD73 values were higher in atherosclerotic patients than in controls without clinically evident peripheral artery disease ( P &lt;0.0001). Low CD39 activity was associated with disease progression ( P =0.01). In multivariable linear regression models, high CD73 activity was associated with chronic hypoxia ( P =0.001). Statin use was associated with lower ADP ( P =0.041) and tended to associate with higher CD73 ( P =0.054), while lower ATP was associated with the use of angiotensin receptor blockers ( P =0.015). Conclusions: Purinergic signaling plays an important role in peripheral artery disease progression. Elevated levels of circulating ATP and ADP are especially associated with atherosclerotic diseases of younger age and smoking. The antithrombotic and anti-inflammatory effects of statins may partly be explained by their ability to lower ADP. We suggest that the prothrombotic nature of smoking could be a cause of elevated ADP, and this may explain why cardiovascular patients who smoke benefit from platelet P2Y 12 receptor antagonists more than their nonsmoking peers.
Prevalence of the Metabolic Syndrome Defined by the International Diabetes Federation Among Adults in the U.S.
Authors: Earl S. Ford
Journal: Diabetes Care (2005)

OBJECTIVE—The International Diabetes Federation (IDF) has proposed a new definition of the metabolic syndrome that emphasizes central adiposity as determined by ethnic group–specific thresholds of waist circumference. The objective of this study was to estimate the prevalence of this syndrome using the IDF definition among U.S. adults and to compare it with the prevalence estimated using the definition of the National Cholesterol Education Program (NCEP). RESEARCH DESIGN AND METHODS—A total of 3,601 men and women aged ≥20 years from the National Health and Nutrition Examination Survey 1999–2002 were included in the analyses. RESULTS—Based on the NCEP definition, the unadjusted prevalence of the metabolic syndrome was 34.5 ± 0.9% (percent ± SE) among all participants, 33.7 ± 1.6% among men, and 35.4 ± 1.2% among women. Based on the IDF definition, the unadjusted prevalence of the metabolic syndrome was 39.0 ± 1.1% among all participants, 39.9 ± 1.7% among men, and 38.1 ± 1.2% among women. The IDF definition led to higher estimates of prevalence in all of the demographic groups, especially among Mexican-American men. The two definitions similarly classified ∼93% of the participants as having or not having the metabolic syndrome. CONCLUSIONS—In the U.S., the use of the IDF definition of the metabolic syndrome leads to a higher prevalence estimate of the metabolic syndrome than the estimate based on the NCEP definition.
Allele loss, replication errors and loss of expression of E-cadherin in colorectal cancers.
Authors: M Ilyas, I P Tomlinson, A Hanby, I C Talbot, W F Bodmer
Journal: Gut (1997)

Loss of E-cadherin expression has been implicated in the development of invasive characteristics in colorectal carcinomas. Failure to express E-cadherin may result from mutations of the E-cadherin gene (HSECAD).To examine the correlation between E-cadherin expression and genetic changes at HSECAD; and to examine differences in E-cadherin expression and genetic changes at HSECAD between three different groups of colorectal cancer--replication error positive (RER+) sporadic cancers, RER--sporadic cancers and ulcerative colitis associated cancers.Sixty eight colorectal cancers (22 RER+ sporadic cancers, 32 RER- sporadic cancers and 14 ulcerative colitis associated cancers) were studied using immunohistochemistry and for allele loss at the HSECAD locus. Exon 16 of HSECAD contains several mononucleotide repeat tracts which are very similar to microsatellite repeats and which may be susceptible to replication errors (manifest as new alleles). All cases were also examined for new alleles in exon 16.Absent or decreased E-cadherin protein expression was found in 27 (38%) of 68 colorectal cancers and the pattern of expression did not differ significantly among the three tumour groups. Allele loss occurred at HSECAD in four (10%) of 40 informative cancers and there were no differences between the three subgroups. New alleles at exon 16 were detected in three (14%) of 22 RER+ tumours; no new alleles were detected in RER- or ulcerative colitis associated cancers. Overall, there was no correlation between allelic loss or exon 16 replication errors and immunohistochemical E-cadherin expression.(1) Loss of E-cadherin expression probably does not occur as a result of mutation at the HSECAD locus in colorectal cancers. (2) There is no difference in the frequency of loss of heterozygosity at HSECAD among RER+, RER- and ulcerative colitis associated colorectal cancers.
Topical intranasal ioxaglate meglumine 39.3% and ioxaglate sodium 19.6% (Hexabrix) reduces the acute response to nasal challenge with allergen
Authors: Shilpa Vishwanath, Fuad M. Baroody, Mohamad R. Chaaban, Marcella deTineo, Kenneth H. Lasser, Elliot C. Lasser, Robert M. Naclerio
Journal: Journal of Allergy and Clinical Immunology (2011)
Women With Impaired Glucose Tolerance During Pregnancy Have Significantly Poor Pregnancy Outcomes
Authors: Xilin Yang, Bridget Hsu-Hage, Hong Zhang, Cuiping Zhang, Yanni Zhang, Changjun Zhang
Journal: Diabetes Care (2002)

OBJECTIVE—This article tests the hypothesis that women with impaired glucose tolerance (IGT) have the same pregnancy outcomes as those of their counterparts with normal glucose tolerance. RESEARCH DESIGN AND METHODS—From December 1998 to December 1999, 84 of 90 antenatal care base units (ACBUs) under the Tianjin Antenatal Care Network in China participated in the first screening program for gestational diabetes mellitus (GDM). A total of 9,471 pregnant women under the care of participating ACBUs were screened. Of the women screened, 154 were positive for IGT. Of the 154 women, 102 opted for conventional obstetric care. The comparison group was 302 women of normal glucose tolerance (NGT). The initial screening consisted of a 50-g 1-h glucose test, and was carried out at 26–30 gestational weeks. Women with a serum glucose ≥7.8 mmol/l were followed up with a 75-g 2-h oral glucose tolerance test. The World Health Organization’s diagnostic criteria for GDM were used. RESULTS—Women with IGT were at increased risk for premature rupture of membranes (P-ROM) (odds ratio [OR] 10.07; 95% CI 2.90–34.93); preterm birth (6.42; 1.46–28.34); breech presentation (3.47; 1.11–10.84); and high birth weight (90th percentile or 4,000 g) (2.42; 1.07–5.46); adjusting for maternal age, pregravid BMI, hospital levels, and other confounding factors. CONCLUSIONS—The presence of IGT in pregnancy is predictive of poor pregnancy outcomes.
Health Care Scheduling and Access
Authors: Gary S. Kaplan
Journal: JAMA (2015)

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
Variants of the hK2 Protein Gene (<i>KLK2</i>) Are Associated with Serum hK2 Levels and Predict the Presence of Prostate Cancer at Biopsy
Authors: Robert K. Nam, William W. Zhang, Laurence H. Klotz, John Trachtenberg, Michael A.S. Jewett, Joan Sweet, Ants Toi, Seamus Teahan, Vasundara Venkateswaran, Linda Sugar, Andrew Loblaw, Kathy Siminovitch, Steven A. Narod
Journal: Clinical Cancer Research (2006)

Abstract Purpose: Increased levels of serum human kallikrein-2 (hK2) and an hK2 gene (KLK2) variant are positively associated for prostate cancer, but the relationships between them remain unclear. We examined five variants of the KLK2 gene to further define its relevance to prostate cancer susceptibility and hK2 levels. Experimental Design: We genotyped 645 men with biopsy-proven prostate cancer (cases) and 606 males with biopsies negative for prostate cancer (controls) for five additional single nucleotide polymorphisms (SNP) across the KLK2 gene and also tested for serum hK2 levels. These SNPs were identified from sequencing the KLK2 gene among 20 patients with aggressive prostate cancer. Odds ratios (OR) for prostate cancer detection and haplotype analysis were done. Results: Among the SNPs studied, the A allele of the KLK2-SNP1 (G &amp;gt; A, rs2664155) and the T allele of the KLK2-SNP5 (C &amp;gt; T, rs198977) polymorphisms showed positive associations with prostate cancer, adjusted ORs for KLK2-SNP1 AG and AA genotypes being 1.4 [95% confidence interval (95% CI), 1.2-1.8; P = 0.002] and for KLK2-SNP5 TT or CT genotypes being 1.3 (95% CI, 1.1-1.6; P = 0.05). Haplotype analyses also revealed a significant association between prostate cancer and the haplotype containing both risk alleles (ACCTT), OR being 5.1 (95% CI, 1.6-6.5; P = 0.005). Analysis of serum hK2 revealed hK2 levels to be significantly increased in association with KLK2-SNP1 AA and AG risk genotypes compared with the GG genotype (P = 0.001) and also in association with the ACCTT risk haplotype compared with the most common non-risk haplotype (P = 0.05). Conclusions: These findings suggest a role for the KLK2 gene in prostate cancer susceptibility and imply that this role may be realized at least in part by the induction of increases in hK2 production.
Diabetes Incidence and Long-Term Exposure to Air Pollution
Authors: Zorana J. Andersen, Ole Raaschou-Nielsen, Matthias Ketzel, Steen S. Jensen, Martin Hvidberg, Steffen Loft, Anne Tjønneland, Kim Overvad, Mette Sørensen
Journal: Diabetes Care (2011)

Animal and cross-sectional epidemiological studies suggest a link between air pollution and diabetes, whereas the limited prospective data show mixed results. We studied the association between long-term exposure to traffic-related air pollution and incidence of diabetes.We followed 57,053 participants of the Danish Diet, Cancer, and Health cohort in the Danish National Diabetes Register between baseline (1993-1997) and 27 June 2006. We estimated the mean levels of nitrogen dioxide (NO(2)) at the residential addresses of the cohort participants since 1971 and modeled the association between NO(2) and diabetes incidence with a Cox regression model, separately for two definitions of diabetes: all cases and a more strict definition where unconfirmed cases were excluded.Over a mean follow-up of 9.7 years of 51,818 eligible subjects, there were 4,040 (7.8%) incident diabetes cases in total and 2,877 (5.5%) with confirmed diagnoses. Air pollution was not associated with all diabetes cases (hazard ratio 1.00 [95% CI 0.97-1.04] per interquartile range of 4.9 μg/m(3) mean NO(2) levels since 1971), but a borderline statistically significant association was detected with confirmed cases of diabetes (1.04 [1.00-1.08]). Among confirmed diabetes cases, effects were significantly enhanced in nonsmokers (1.12 [1.05-1.20]) and physically active people (1.10 [1.03-1.16]).Long-term exposure to traffic-related air pollution may contribute to the development of diabetes, especially in individuals with a healthy lifestyle, nonsmokers, and physically active individuals.
Giving Up Surgery
Authors: Natalie I. Vokes
Journal: Annals of Internal Medicine (2012)

On Being a Doctor4 December 2012Giving Up SurgeryNatalie I. Vokes, MPhilNatalie I. Vokes, MPhilFrom Harvard Medical School, Boston, MA 02215.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-157-11-201212040-00016 Audio Reading - “Giving Up Surgery” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "Giving Up Surgery," by N.I. Vokes. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail There is a long, hot hallway between the medical student lockers at one end of my hospital and the patient floors at the other. I walked this hallway every morning of the first month of my surgery rotation, and with each sweaty step I felt a growing dread of what was coming: the immediate stress of prerounding; the no-mistakes pace of the surgery team; and most of all, a deep, visceral anxiety about the tasks that I would face and fail to meet. What questions would I be asked that I could not answer? How would my presentations fall short? ... Author, Article, and Disclosure InformationAffiliations: From Harvard Medical School, Boston, MA 02215.Corresponding Author: Natalie I. Vokes, MPhil, Harvard Medical School, 25 Shattuck Street, Boston, MA 02215; e-mail, [email protected]. PreviousarticleNextarticle Advertisement Audio Reading - “Giving Up Surgery” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "Giving Up Surgery," by N.I. Vokes. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ FiguresReferencesRelatedDetails Metrics 4 December 2012Volume 157, Issue 11Page: 829-830KeywordsAnxietyEmotionsFallsForecastingHealth carePatientsResidencySurgeryVisionWalking ePublished: 4 December 2012 Issue Published: 4 December 2012 CopyrightCopyright © 2012 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Magnesium Deficiency Is Associated With Insulin Resistance in Obese Children
Authors: Milagros G. Huerta, James N. Roemmich, Marit L. Kington, Viktor E. Bovbjerg, Arthur L. Weltman, Viola F. Holmes, James T. Patrie, Alan D. Rogol, Jerry L. Nadler
Journal: Diabetes Care (2005)

OBJECTIVE—Magnesium deficiency has been associated with insulin resistance (IR) and increased risk for type 2 diabetes in adults. This study was designed to determine whether obese children exhibit serum or dietary magnesium deficiency and its potential association with IR. RESEARCH DESIGN AND METHODS—We studied 24 obese nondiabetic children (BMI ≥85th percentile) and 24 sex- and puberty-matched lean control subjects (BMI &amp;lt;85th percentile). We measured serum magnesium, indexes of insulin sensitivity, dietary magnesium intake (using a food frequency questionnaire), and body composition (by air displacement plethysmography). RESULTS—Serum magnesium was significantly lower in obese children (0.748 ± 0.015 mmol/l, means ± SE) compared with lean children (0.801 ± 0.012 mmol/l) (P = 0.009). Serum magnesium was inversely correlated with fasting insulin (rs = −0.36 [95% CI −0.59 to −0.08]; P = 0.011) and positively correlated with quantitative insulin sensitivity check index (QUICKI) (0.35 [0.06–0.58]; P = 0.015). Dietary magnesium intake was significantly lower in obese children (obese: 0.12 ± 0.004 vs. lean: 0.14 ± 0.004 mg/kcal; P = 0.003). Dietary magnesium intake was inversely associated with fasting insulin (−0.43 [−0.64 to −0.16]; P = 0.002) and directly correlated with QUICKI (0.43 [0.16–0.64]; P = 0.002). CONCLUSIONS—The association between magnesium deficiency and IR is present during childhood. Serum magnesium deficiency in obese children may be secondary to decreased dietary magnesium intake. Magnesium supplementation or increased intake of magnesium-rich foods may be an important tool in the prevention of type 2 diabetes in obese children.
Immunomodulatory Property of Vitamin D in Allergic Fungal Rhinosinusitis
Authors: Aravind Yadav, Caroline J. Padro, Paul Porter, Ryan P. Drake, Evan D. Corning, Ameerah Wishahy, Faramarz Ashoori, Samer Fakhri, Martin Citardi, David B. Corry, Amber U. Luong
Journal: Journal of Allergy and Clinical Immunology (2015)
Continued inhibition of structural damage over 2 years in patients with rheumatoid arthritis treated with rituximab in combination with methotrexate
Authors: Stanley B Cohen, Edward Keystone, Mark C Genovese, Paul Emery, Charles Peterfy, Paul Peter Tak, Matt Cravets, Tim Shaw, David Hagerty
Journal: Annals of the Rheumatic Diseases (2010)

Background Rituximab inhibited structural damage at 1 year in patients with rheumatoid arthritis (RA) who had had a previous inadequate response to tumour necrosis factor (TNF) inhibitors. Objective To assess structural damage progression through 2 years. Methods Intention-to-treat patients with one post-baseline radiograph (rituximab n=281; placebo n=187) received background methotrexate (MTX) and were randomised to rituximab (2×1000 mg infusions, 2 weeks apart) or placebo; patients were eligible for rituximab re-treatment every 6 months. By week 104, 82% of the placebo population had received ≥1 dose of rituximab. Radiographic end points included the change in total Sharp score (TSS), erosion and joint space narrowing scores at week 104. Results At week 104, significantly lower changes in TSS (1.14 vs 2.81; p&lt;0.0001), erosion score (0.72 vs 1.80; p&lt;0.0001) and joint space narrowing scores (0.42 vs 1.00; p&lt;0.0009) were observed with rituximab plus MTX vs placebo plus MTX. Within the rituximab group, 87% who had no progression of joint damage at 1 year remained non-progressive at 2 years. Conclusions Rituximab plus MTX demonstrated significant and sustained effects on joint damage progression in patients with RA and a previously inadequate response to TNF inhibitors.
Trans-cyclopropanation of mycolic acids on trehalose dimycolate suppresses Mycobacterium tuberculosis-induced inflammation and virulence
Authors: V. Rao
Journal: Journal of Clinical Investigation (2006)

Recent studies have shown that fine structural modifications of Mycobacterium tuberculosis cell envelope lipids mediate host cell immune activation during infection. One such alteration in lipid structure is cis-cyclopropane modification of the mycolic acids on trehalose dimycolate (TDM) mediated by proximal cyclopropane synthase of α mycolates (pcaA), a proinflammatory lipid modification during early infection. Here we examine the pathogenetic role and immunomodulatory function of mycolic acid cyclopropane stereochemistry by characterizing an M. tuberculosis cyclopropane–mycolic acid synthase 2 (cmaA2) null mutant (ΔcmaA2) that lacks trans-cyclopropanation of mycolic acids. Although titers of WT and ΔcmaA2 organisms were identical during mouse infection, ΔcmaA2 bacteria were hypervirulent while inducing larger granulomas than WT M. tuberculosis. The hypervirulence of the ΔcmaA2 strain depended on host TNF-α and IFN-γ. Loss of trans-cyclopropanation enhanced M. tuberculosis–induced macrophage inflammatory responses, a phenotype that was transferable with petroleum ether extractable lipids. Finally, purified TDM lacking trans-cyclopropane rings was 5-fold more potent in stimulating macrophages. These results establish cmaA2-dependent trans-cyclopropanation of TDM as a suppressor of M. tuberculosis–induced inflammation and virulence. In addition, cyclopropane stereochemistries on mycolic acids interact directly with host cells to both positively and negatively influence host innate immune activation.
Nodular lesions due to surgical wires
Authors: S. Shankar, L.S. Ostlere
Journal: British Journal of Dermatology (2002)

Journal Article Nodular lesions due to surgical wires Get access S. Shankar, S. Shankar Kingston Hospital, Galsworthy Road, Kingston, Surrey KT2 7QB, U.K S. Shankar. E‐mail: sonal@shankar‐lall.freeserve.co.uk Search for other works by this author on: Oxford Academic Google Scholar L.S. Ostlere L.S. Ostlere Kingston Hospital, Galsworthy Road, Kingston, Surrey KT2 7QB, U.K Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 147, Issue 1, 1 July 2002, Page 179, https://doi.org/10.1046/j.1365-2133.2002.04730.x Published: 01 July 2002 Article history Accepted: 25 October 2001 Published: 01 July 2002