tbuckley/cabot-search huggingface dataset:
Abstract 740: Statin Prevents Structural and Electrical Atrial Remodeling in Rat Hypertensive Heart Failure Induced by Chronic Inhibition of NO Synthesis
Authors: Hidetoshi Okazaki, Tetsuo Minamino, Masakatsu Wakeno, Osamu Tsukamoto, Jiyoong Kim, Seiji Takashima, Naoki Mochizuki, Masafumi Kitakaze
Journal: Circulation (2007)

Background: The prevalence of atrial fibrillation (AF) increases in patients with hypertension and heart failure in which endothelial function is impaired. Oxidative stress in atrial tissues is involved in the development of AF. Statins have pleiotropic effects including antioxidant effects. Thus, we developed hypertensive heart failure in rats by the chronic inhibition of NO synthesis and we investigated the role of the statin in atrial remodeling. Methods and Results: Ten-week-old male Wistar-Kyoto rats were randomly divided into four groups: the control (no treatment), the L-NAME (received L-NAME, an inhibitor of NO synthase, 1 g/L in drinking water), the L-NAME+atorvastatin (L(a low dose)) (5 mg/kg/day) and the L-NAME+atorvastatin (H(a high dose)) (20 mg/kg/day). Chronic inhibition of NO synthesis increased systolic blood pressure (control group: 138±5 mmHg; L-NAME group: 212±8 mmHg L+atorvastatin (L) group: 210±6 seconds , L+atorvastatin (H): 208±6 seconds) and decreased LV dP/dt max/LVSP (control group: 54±3, L-NAME group: 36±8, L+atorvastatin (L) group: 40±3, L+atorvastatin (H) group: 38±6 1/second), whereas co-administration of atorvastatin did not affect them. The sustained duration of AF was always induced by transesophageal burst pacing (The pacing pulse used for induction of AF was rectanglar in shape, of 60V and 6ms-width. The atrium was paced at a cycle length of 12ms (83Hz) for 30seconds) and it was prolonged by L-NAME, which was prevented by atorvastatin in a dose-dependent manner (control: 8.8 ± 1.0 seconds, L-NAME: 20.7 ± 3.0 seconds, L+atorvastatin (L): 12.8 ± 3.2 seconds , L+atorvastatin (H): 8.8 ± 2.6 seconds). The chronic inhibition of NO synthesis increased the extent of fibrosis and markers of oxidative stresses such as proteins modified with 4-hydroxy-trans-2-nonenal and p47phox and rac1 in left atrial tissue, either of which was prevented by atorvastatin. Conclusion: Atorvastatin attenuates oxidative stresses in atrium and prevents atrial electrical and morphological remodeling in rat hypertensive failing hearts without hemodynamic changes. Statin may be beneficial in patients with coronary heart disease and atrial fibrillation, and may contribute to the prevention of the onset of heart failure.
Abstract 217: Difference of Coronary Artery Lesions or associated Pathogens between the Two Phenotypes of Kawasaki Disease
Authors: Kyung Lim Yoon, Song Ee Youn, Mi Young Han, Sung Ho Cha
Journal: Circulation (2015)

Introduction: There are several reports that coronary artery lesions (CALs) are increased/or not increased in patients who predominantly showed arthritis in patients with Kawasaki disease (KD). Patients with eczematoid skin lesions which seem like atopic dermatitis have not been reported in association with CALs. We intended to evaluate the risk of development of CALs in patients with two different phenotypes. Materials and methods: We retrospectively reviewed the medical records in 220 patients who diagnosed as KD and received IVIG treatment in Kyung Hee University Hospital at Gangdong from August 2006 to December 2013. In both patients groups (6 patients with arthritis and 52 patients with eczematoid skin lesion), we reviewed the state of coronary artery, clinical characteristics, associated viral or bacterial infections. Results: In patients with eczematoid lesions (52/220, 23.6%), the ages of patients were significantly older, the duration of fever was longer, and the prevalence of CAL was significantly higher than that of controls ( P =.000, P =.041, P =.033, respectively). In patients with arthritis (6/220, 3%), there were higher incidence of methylprednisolone or infliximab therapy ( P =.000, P =.004, respectively), and higher incidence of viral infection like influenza A and B, rhinovirus, parainfluenza 2, metapneumovirus, and coronavirus OC43 ( P =.018). Conclusions: The incidence of CAL was higher in group of eczematoid skin lesion in KD patients than in group of patients with arthritis. Associated viral infections were higher in arthritis group, therefore, it is better to find associated pathogens aggressively that might be a certain trigger of the development of KD in this group of patients.
MEDICAL TEMPERANCE.
Journal: JAMA (1895)

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Issue Information
Journal: Medicinal Research Reviews (2021)

The journal publishes timely critical reviews of topics related to medicinal research, broadly defined, to which the authors have made significant contributions.Appropriate topics include, but are not limited to, the underlying pathophysiology of important diseases and disease vectors; therapeutic approaches to the treatment of various diseases; the properties of molecular targets for therapeutic agents; important new methodologies facilitating the search for therapies; genomics and proteomics; structure-activity correlations of drug series; the development of new imaging and diagnostic tools; drug metabolism; drug delivery; and chemical, pharmacological, pharmacokinetic, pharmacodynamic, and clinical characteristics of important drugs.Articles are mainly solicited by the editors; however, voluntary contributions are also encouraged.In the latter case, potential authors are asked to contact the Editor-in-Chief with an outline before beginning to write in order to avoid duplication of effort and to ensure suitability of the topic and the level of coverage.
Effects of vitamin E, ascorbic acid and catalase on bromobenzene- and hydrogen peroxide-induced intracellular oxidation and single strand DNa breakage in HEP G2 cells . Depts. of 1Histology and Cell Biology, 2Clinical Chemistry and 3Medicine, University of Ume�, Ume�, Sweden and 4Dept. of Medicine, Jefferson Medical College, Philadelphia, PA 19107
Journal: Hepatology (1995)

Hyperglycemia-induced oxidative stress has been suggested as a mechanism underlying diabetic complications. Oxidative stress triggers cell death in various cell types, including glomerular mesangial cells which play important roles in diabetic nephropathy. In the present study, we investigated the potential cytoprotective effect of erigeroflavanone, a novel flavanone derivative from the flowers of Erigeron annuus, in cultured mouse mesangial cells using hydrogen peroxide (H2O2) as an oxidative stress inducer. Our data show that hydrogen peroxide induced a decrease in cell viability that was attenuated by erigeroflavanone. Hydrogen peroxide treatment increased formation of dichlorofluorescein (DCF)-sensitive intracellular reactive oxygen species (ROS). This enhanced ROS formation was significantly reduced by pretreatment with erigeroflavanone in a dose-dependent manner. Hydrogen peroxide treatment also induced phosphorylation of the mitogen-activated protein kinases (MAPKs), c-Jun terminal kinase (JNK), extracellular-regulated kinase (ERK) and p38, and activated caspase-3. Pretreatment with erigeroflavanone inhibited hydrogen peroxide-induced activation of MAPKs and caspase-3. From these data we conclude that erigeroflavanone provides a protective effect against oxidative stress-induced cell death in mesangial cells that is associated with its antioxidant action and inhibition of MAPKs and caspase-3. These results suggest that erigeroflavanone has potential as a therapeutic agent in the treatment of renal diabetic complications.
JAMA 75 YEARS AGO
Journal: JAMA (1971)

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THE REACTION OF LIVING CELLS AND TISSUES
Journal: JAMA (1925)

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Correction: Prevalence of diabetes in a predominantly Asian community: preliminary findings of the Coventry diabetes study
Journal: BMJ (1989)

Pi blocker inducing a decrease in glucose disposal mediated by insulin and eventually ends with an increased burden of risk factors for ischaemic heart disease.During this course of events an increased serum triglyceride concentration, decreased serum high density lipoprotein cholesterol concentration, and impaired glucose tolerance or diabetes are direct consequences of insulin resistance and hyperinsulinaemia.People who already have some resistance to insulin when essential hypertension is detected may be particularly susceptible to environmental influences that increase the resistance.The metabolic side effects shown in this study are small, but as 30-50% of people over 60 are treated for hypertension in Sweden the effects of antihypertensive treatment on the incidence of ischaemic heart disease in the whole community should not be underestimated.52The association between antihypertensive treatment and resistance to insulin should be subject to further studies.Non-pharmacological treatments for hypertension should also be investigated, especially as such treatment may influence other risk factors for cardiovascular disease and death.This study was supported by
Archives of Disease in Childhood, London
Journal: JAMA (1966)

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Medical Organization.
Authors: J. N. MCCORMACK
Journal: JAMA (1903)

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Tuberculosis and body build
Authors: D. E. Snider
Journal: JAMA (1987)

In a recent editorial, Comstock<sup>1</sup>said lean, underweight tuberculin reactors have a significantly higher risk of developing tuberculosis than persons above, or at, ideal body weight. Because many physicians may be unfamiliar with the data that support this assertion, a short review of the relevant literature seems appropriate. The notion that a certain kind of body build predisposes a person to tuberculosis dates back at least to Hippocrates.<sup>2</sup>In the early part of this century, Reed and Love<sup>3</sup>studied US Army recruits before and during World War I and found that tuberculosis developed much more frequently among men who were tall and thin than those who were short and heavyset. This build was not thought to be a result of tuberculosis since it was present long before disease became clinically evident. Similar findings were reported by Long and Jablon<sup>4</sup>among men entering the army during World
Specialty Abstracts
Journal: JAMA (1987)

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Abstract 165: Role of the Gut Microbiome in Obesity-Related Vascular Dysfunction
Authors: Micah Battson, Dustin Lee, Shuofei Hou, Dillon Jarrell, Kayl Ecton, Tiffany Weir, Christopher Gentile
Journal: Circulation Research (2017)

Vascular dysfunction, characterized by arterial stiffness and endothelial dysfunction, represents an important link between obesity and cardiovascular disease. Deleterious changes to the gut microbiome, termed dysbiosis, are associated with obesity and may contribute to the development of vascular dysfunction by promoting systemic and arterial inflammation. We tested the hypothesis that antibiotic treatment in diet-induced obese mice would improve vascular function by suppressing potentially harmful gut-derived bacterial products to reduce dysbiosis-related inflammation. Male C57BL/6 mice were fed either a standard diet (SD) or Western diet (WD) for 5 months. Obese WD-fed mice were then randomized to receive 8 weeks of antibiotic treatment via drinking water. Arterial stiffness was measured via in vivo aortic pulse wave velocity and endothelial function assessed via ex vivo pressure myography in isolated mesenteric arteries. Plasma and arterial tissue samples were collected for measures of endotoxemia and inflammation and fecal samples were collected for microbial sequencing. Our results showed that mice fed a WD for 5 months had significantly higher body weight and arterial stiffness compared to SD. Antibiotic treatment significantly reduced arterial stiffness in WD-fed mice without affecting body weight. Endothelial function was impaired in WD-fed mice, whereas WD-Abx mice had similar endothelial function to SD-fed mice. Plasma levels of the pro-inflammatory cytokine IL-6 and endotoxemia marker LPS binding protein (LBP) were significantly increased in WD vs SD, but reduced in WD-Abx vs WD. Gut microbial suppression with antibiotic treatment was confirmed using quantitative PCR and ongoing analyses are being conducted to determine specific diet-induced changes to the composition of the gut microbiome. Overall, our results support the hypothesis that gut dysbiosis contributes the development of vascular dysfunction in obesity and provide evidence that a gut-targeted therapy can improve endothelial function and arterial stiffness in diet-induced obese mice. Future studies will further examine the mechanisms involved in, and help identify potential therapeutic targets for, obesity-related vascular dysfunction.
Curriculum Development
Authors: Glen R. Shepherd
Journal: JAMA (1960)

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Deaths
Journal: JAMA (1924)

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Index to volume 64
Authors: Jacobson Kw, Juto Stranneglrd, K Kaliner, Parillo Je, Hf Klinefelter, Kohn Ba, Twarog Fj, Geha Rs, Lasser Ec, Lang Jh, Lyon Sc, Hamblin Ae, Lawley Tj, See Parillo, Lawton Jm, Shortridge Kf, Wong Rc, Ng Nm, Leiferman Km, Yunginger Jw, Gleich Gj, Lichtenstein Lm, Valentine Md, Sobotka Ak, Lichter Ll, Sigel Mm, Abst Lieberman, Siegle Rl, Light Rw, Taylor Rw, George Rb, Lum Muchmore, Keren Decker, Koski Strober, M Martinez, Santos Stechschulte, Lessof Mh, Kemeneny Dm, Murray Ab, N Nair, See Townley, Nathan Ra, Kinsman Ra, Spector Sl, Rubin Al, Lawley Frank, Kaplan Ap, Fauci Patterson, Paul1 Br, Atassi Mz, Penick Gd, See Richerson, Cohen Mc, Yoshida Cohen, Pruzansky Jj, R Raatgeep, Richerson Hb, Reed Ce, Reinherz El, Rosen Schlossman, Reisman Re, Arbesman Ce, Abst Wypych, Rajtora Dw, Dick Fr, Yoo Tj, Kam Jk, Anuras Js, Rosen Fs, See Fineman, Rosen Jp, Ragni Mc, Saccar Cl, Yaffe Sj, Mathison Da, Rudolph Staud, R-D Baumgarten
Journal: Journal of Allergy and Clinical Immunology (1979)