tbuckley/cabot-search huggingface dataset:
Calcium, Race, and Hypertension
Authors: Stephen Warrenburg, Gary E. Schwartz, Richard Henderson, Paul Crits-Christoph, Patricia Nuzzo
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 June 1986Calcium, Race, and HypertensionSTEPHEN WARRENBURG, Ph.D., GARY E. SCHWARTZ, Ph.D., RICHARD HENDERSON, Ph.D., PAUL CRITS-CHRISTOPH, Ph.D., PATRICIA NUZZO, B.S.STEPHEN WARRENBURG, Ph.D.Search for more papers by this author, GARY E. SCHWARTZ, Ph.D.Search for more papers by this author, RICHARD HENDERSON, Ph.D.Search for more papers by this author, PAUL CRITS-CHRISTOPH, Ph.D.Search for more papers by this author, PATRICIA NUZZO, B.S.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-104-6-892_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In December 1985, McCarron and Morris (1) reported that calcium supplementation leads to a clinically significant lowering ( > 10 mm Hg) of blood pressure in a subset (44%) of hypertensive persons tested in a randomized, placebo, crossover trial. They proposed that impaired calcium metabolism is a critical factor in the pathogenesis of both human and experimental hypertension. In a previous issue ofAnnals(2), McCarron suggested that the elevated prevalence of hypertension in blacks may be calcium related, but there were too few black hypertensive persons in their recent sample to allow testing of this hypothesis....References1. MCCARRONMORRIS DC. Blood pressure response to oral calcium in persons with mild to moderate hypertension. Ann Intern Med. 1985;103:825-31. LinkGoogle Scholar2. MCCARRON D. Calcium and magnesium nutrition in human hypertension. Ann Intern Med. 1983;98:800-5. LinkGoogle Scholar3. WARRENBURGCRITS-CHRISTOPHSCHWARTZ SPG. Stress reduction and diet change treatments of hypertension [Abstract]. Psychophysiology. 1982;19:354-5. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: STEPHEN WARRENBURG, Ph.D.; GARY E. SCHWARTZ, Ph.D.; RICHARD HENDERSON, Ph.D.; PAUL CRITS-CHRISTOPH, Ph.D.; PATRICIA NUZZO, B.S.Affiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 June 1986Volume 104, Issue 6Page: 892-893KeywordsBlood pressureCalciumClinical trial reportingHypertensionPathogenesisRacial and ethnic issues ePublished: 1 December 2008 Issue Published: 1 June 1986 PDF downloadLoading ...
Identification of viral molecules recognized by influenza-specific human cytotoxic T lymphocytes.
Authors: F Gotch, A McMichael, G Smith, B Moss
Journal: The Journal of Experimental Medicine (1987)

Human cytotoxic T cells specific for influenza A virus were tested for recognition of each of the ten influenza A virus proteins expressed in target cells using recombinant vaccinia viruses. They recognized the matrix M1, polymerase PB2, and nucleoproteins of influenza virus in association with MHC class I antigens. These internal viral proteins were seen by CTL in conjunction with one or more of the available dependent HLA gene products. There was no detectable recognition of influenza virus surface glycoproteins in target cells.
A randomized study of adefovir dipivoxil in place of HBIG in combination with lamivudine as post-liver transplantation hepatitis B prophylaxis
Authors: Peter W. Angus, Scott J. Patterson, Simone I. Strasser, Geoffrey W. McCaughan, Edward Gane
Journal: Hepatology (2008)

Abstract Prior to effective prophylaxis, liver transplantation for hepatitis B virus (HBV)-related disease was frequently complicated by recurrence, which could be severe and rapidly progressive. Combination hepatitis B immunoglobulin (HBIG) and lamivudine prophylaxis reduces this rate of recurrence to &lt;5% at 5 years; however, HBIG administration is costly and inconvenient. We conducted a multicenter randomized study of adefovir dipivoxil substitution for low-dose intramuscular (IM) HBIG in patients without HBV recurrence at least 12 months posttransplantation for HBV-related disease. Thirty-four patients were randomized, 16 to adefovir (1 patient withdrew consent at 3 months and is not considered in the results) and 18 to continue HBIG. All continued lamivudine. Groups were well matched by age, sex, and time since transplantation (median, 4.5 years), and background virological risk for HBV recurrence (30% of patients in the adefovir group, 24% in the HBIG group having detectable HBV DNA at transplantation). All patients were alive at study completion without recurrence. One patient in the adefovir group became hepatitis B surface antigen–positive at 5 months but was persistently HBV DNA undetectable via polymerase chain reaction (sensitivity 14 IU/mL) over the following 20 months. Median creatinine was not significantly changed over the course of the study in either group. One patient in the adefovir group with a background of diabetic and hypertensive nephropathy (baseline creatinine 150 μmol/L) developed increased creatinine leading to dose reduction and ultimately cessation of adefovir at 15 months. Yearly cost of combination adefovir/lamivudine prophylaxis was $8,290 versus $13,718 IM HBIG/lamivudine. Conclusion: Compared with combination HBIG plus lamivudine prophylaxis, combination adefovir plus lamivudine provides equivalent protection against recurrent HBV infection but with better tolerability and less cost. (Hepatology 2008.)
The prolyl 4-hydroxylase inhibitor HOE 077 prevents activation of Ito cells, reducing procollagen gene expression in rat liver fibrosis induced by choline-deficient L-amino acid-defined diet
Authors: I Sakaida
Journal: Hepatology (1996)

No effective therapy has yet developed for liver fibrosis by directory inhibiting the accumulation of extracellular matrix. The effect of a newly synthesized prolyl4-hydroxylase (PH) inhibitor, HOE 077 (pyridine- 2, 4-di-carboxylic-di(2-methoxyethyl)amide), was examined using the model of choline-deficient L-amino acid (CDAA) defined diet-induced liver fibrosis in 16-week-old male Wistar rats. HOE 077 at doses up to 200 ppm prevented fibrosis in a dose-dependent manner, as indicated by reduced hydroxyproline content in liver as well as inhibition of increased serum fibrotic markers (PIIIP, 7S, hyaluronic acid). HOE 077 at 200 ppm reduced expression of type III procollagen alpha1, messenger RNA (mRNA) in the liver, with a good correlation with serum PIIIP and hydroxyproline content of the liver. Histologically, HOE 077 at 200 ppm also reduced proliferation of myofibroblastlike cells (activated Ito cells). These results indicate that a PH inhibitor can prevent fibrosis by inhibiting not only the hydroxylation of proline but also the activation of Ito cells, which are considered the main collagen-producing cells, resulting in reduced expression of procollagen mRNA. (Hepatology 1996 Apr;23(4):755-63)
The Effect of Funding Source on Outcome Reporting Among Drug Trials
Authors: Florence T. Bourgeois, Kenneth D. Mandl, Srinivas Murthy
Journal: Annals of Internal Medicine (2011)

Letters18 January 2011The Effect of Funding Source on Outcome Reporting Among Drug TrialsFlorence T. Bourgeois, MD, MPH, Kenneth D. Mandl, MD, MPH, and Srinivas Murthy, MDFlorence T. Bourgeois, MD, MPHFrom Children's Hospital Boston, Boston, MA 02115, and Hospital for Sick Children, Toronto, Ontario M5G 1X9, Canada.Search for more papers by this author, Kenneth D. Mandl, MD, MPHFrom Children's Hospital Boston, Boston, MA 02115, and Hospital for Sick Children, Toronto, Ontario M5G 1X9, Canada.Search for more papers by this author, and Srinivas Murthy, MDFrom Children's Hospital Boston, Boston, MA 02115, and Hospital for Sick Children, Toronto, Ontario M5G 1X9, Canada.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-154-2-201101180-00021 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:We appreciate the opinions and comments on our article, which reflect an important debate over explanations for the higher rate of favorable findings reported among industry-funded trials. Dr. Turner points out that the median anticipated sample sizes were larger among trials funded by industry than among those funded by noncommercial sources and questions whether the increased statistical power alone explains our finding of more favorable results among industry-funded trials. Dr. Turner is correct that in general, larger, more adequately powered trials are more likely to yield statistically significant results. Our multivariate model demonstrated an effect of primary funding ...Reference1. U.S. Food and Drug Administration Amendments Act of 2007. Pub. L. No. 105-185 (2007). Google Scholar Author, Article, and Disclosure InformationAffiliations: From Children's Hospital Boston, Boston, MA 02115, and Hospital for Sick Children, Toronto, Ontario M5G 1X9, Canada.Disclosures: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M10-0087. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoOutcome Reporting Among Drug Trials Registered in ClinicalTrials.gov Florence T. Bourgeois , Srinivas Murthy , and Kenneth D. Mandl The Effect of Funding Source on Outcome Reporting Among Drug Trials Erick H. Turner The Effect of Funding Source on Outcome Reporting Among Drug Trials Adam Jacobs The Effect of Funding Source on Outcome Reporting Among Drug Trials Deborah A. Zarin and Tony Tse Metrics 18 January 2011Volume 154, Issue 2Page: 138KeywordsConflicts of interestDisclosureDrugsFactor analysisMultivariate analysis ePublished: 18 January 2011 Issue Published: 18 January 2011 CopyrightCopyright © 2011 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Epitope-specific T cell tolerance to phospholipase A2 in bee venom immunotherapy and recovery by IL-2 and IL-15 in vitro.
Authors: C A Akdis, M Akdis, T Blesken, D Wymann, S S Alkan, U Müller, K Blaser
Journal: Journal of Clinical Investigation (1996)

Bee venom phospholipase A2 (PLA) is the major allergen in bee sting allergy. It displays three peptide and a glycopeptide T cell epitopes, which are recognized by both allergic and non-allergic bee venom sensitized subjects. In this study PLA- and PLA epitope-specific T cell and cytokine responses in PBMC of bee sting allergic patients were investigated before and after 2 mo of rush immunotherapy with whole bee venom. After successful immunotherapy, PLA and T cell epitope peptide-specific T cell proliferation was suppressed. In addition the PLA- and peptide-induced secretion of type 2 (IL-4, IL-5, and IL-13), as well as type 1 (IL-2 and IFN-gamma) cytokines were abolished, whereas tetanus toxoid-induced cytokine production and proliferation remained unchanged. By culturing PBMC with Ag in the presence of IL-2 or IL-15 the specifically tolerized T cell response could be restored with respect to specific proliferation and secretion of the type 1 T cell cytokines, IL-2 and IFN-gamma. In contrast, IL-4, IL-5, and IL-13 remained suppressed. Treatment of tolerized T cells with IL-4 only partially restored proliferation and induced formation of distinct type 2 cytokine pattern. In spite of the allergen-specific tolerance in T cells, in vitro produced anti-PLA IgE and IgG4 Ab and their corresponding serum levels slightly increased during immunotherapy, while the PLA-specific IgE/IgG4 ratio changed in favor of IgG4. These findings indicate that bee venom immunotherapy induces a state of peripheral tolerance in allergen-specific T cells, but not in specific B cells. The state of T cell tolerance and cytokine pattern can be in vitro modulated by the cytokines IL-2, IL-4, and IL-15, suggesting the importance of microenvironmental cytokines leading to success or failure in immunotherapy.
Maternal Age at First Childbirth and Risk of Low Birth Weight and Preterm Delivery in Washington State
Authors: Michael B. Aldous
Journal: JAMA (1993)

<h3>Objective.</h3> —To study the consequences of delayed first childbearing in a large, population-based US sample, with separate analysis of women aged 40 years or more and adjustment for socioeconomic factors, smoking, medical and reproductive conditions, and route of delivery. <h3>Design and Setting.</h3> —Retrospective survey of Washington State birth certificates from 1984 through 1988. <h3>Subjects.</h3> —First liveborn singleton infants of women aged at least 20 years. Of eligible white infants, all those born to women aged 35 to 39 years (n=4019) and 40 years or more (n=410) and a maternal age-stratified random sample of white infants of younger women were studied. All eligible black infants were studied. <h3>Outcome Measures.</h3> —Low (&lt;2500 g) and very low (&lt;1500 g) birth weight and preterm delivery (&lt;37 weeks of gestation). <h3>Results.</h3> —Adjusted odds ratios for delivering a low-birth-weight white infant increased progressively with each 5-year maternal age group, reaching 2.3 (95% confidence interval, 1.6 to 3.4) for women aged 40 years or more compared with those aged 20 to 24 years. The maternal age effects for very low birth weight and preterm delivery were similar; for each, the odds ratio was 1.8 for the oldest group. No significant maternal age effect was found among births of black infants, but only 127 births to women aged 35 years or more were studied. <h3>Conclusion.</h3> —Increasing maternal age at first childbirth is an independent risk factor for low birth weight and preterm delivery of white infants in the United States. (<i>JAMA</i>. 1993;270:2574-2577)
LYMPHOSARCOMA: DIAGNOSED GASTROSCOPICALLY
Authors: C. Norman Giere
Journal: JAMA (1941)

Sarcomas of the gastrointestinal tract were classified by Ewing<sup>1</sup>as (1) spindle cell myosarcoma, (2) miscellaneous round cell or mixed cell alveolar sarcoma and (3) lymphosarcoma. Lymphosarcoma is the most important type in this classification and is the most frequently seen. The fact that sarcoma seldom involves the gastric mucosa early and therefore produces no characteristic deformity of the stomach on roentgen examination makes early diagnosis difficult. This is particularly unfortunate since the prognosis of gastric lymphosarcoma treated by adequate surgical intervention and follow-up roentgen therapy seems definitely more favorable than that of gastric carcinoma.<sup>2</sup>For these reasons any procedure which may assist in the early diagnosis of this condition should be welcome. The following case is of interest because the lesion was diagnosed correctly by gastroscopic examination one month after roentgen examination had failed to disclose the presence of any abnormality of the stomach. <h3>REPORT OF CASE</h3>
Chronic plus binge ethanol feeding synergistically induces neutrophil infiltration and liver injury in mice: A critical role for E-selectin
Authors: Adeline Bertola, Ogyi Park, Bin Gao
Journal: Hepatology (2013)

Chronic plus binge ethanol feeding acts synergistically to induce liver injury in mice, but the mechanisms underlying this phenomenon remain unclear. Here, we show that chronic plus binge ethanol feeding synergistically up-regulated the hepatic expression of interleukin-1β and tumor necrosis factor alpha and induced neutrophil accumulation in the liver, compared with chronic or binge feeding alone. In vivo depletion of neutrophils through administration of an anti-Ly6G antibody markedly reduced chronic-binge ethanol feeding-induced liver injury. Real-time polymerase chain reaction analyses revealed that hepatic E-selectin expression was up-regulated 10-fold, whereas expression of other neutrophil infiltration-related adhesion molecules (e.g., P-selectin, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1) was slightly up- or down-regulated in this chronic-binge model. The genetic deletion of E-selectin prevented chronic-binge ethanol-induced hepatic neutrophil infiltration as well as elevation of serum transaminases without affecting ethanol-induced steatosis. In addition, E-selectin-deficient mice showed reduced hepatic expression of several proinflammatory cytokines, chemokines, and adhesion molecules, compared to wild-type mice, after chronic-binge ethanol feeding. Finally, the expression of E-selectin was highly up-regulated in human alcoholic fatty livers, but not in alcoholic cirrhosis. Conclusions: Chronic-binge ethanol feeding up-regulates expression of proinflammatory cytokines, followed by the induction of E-selectin. Elevated E-selectin plays an important role in hepatic neutrophil infiltration and injury induced by chronic-binge feeding in mice and may also contribute to the pathogenesis of early stages of human alcoholic liver disease. (Hepatology 2013;58:1814–1823)
Medical Capacity Act 2005 should be invoked
Authors: T. Branton, N. Brindle, T. Zigmond
Journal: BMJ (2009)

A recent report highlights the risks associated with the use of antipsychotic drugs in managing behavioural and psychotic symptoms in dementia.1 We are surprised that it and the government’s response do not refer to the Mental Capacity Act 2005 and its associated code of practice.2

Most patients with dementia who are prescribed antipsychotic …
Leukocyte adhesion receptors are stored in peroxidase-negative granules of human neutrophils.
Authors: D F Bainton, L J Miller, T K Kishimoto, T A Springer
Journal: The Journal of Experimental Medicine (1987)

Previous studies have suggested that the leukocyte adhesion proteins Mac-1 and p150,95 are stored in a latent intracellular pool in neutrophils, and cellular fractionation studies have shown that Mac-1 is localized primarily in the peroxidase-negative specific granules. To determine the subcellular location of leukocyte adhesion receptors (LAR), we used immunocytochemical techniques on frozen thin sections of human blood leukocytes that had been incubated for peroxidase to mark the peroxidase-positive azurophil granules. To enhance the sensitivity of detection, polyclonal antibodies against immunoaffinity-purified p150,95 were raised in rabbits and absorbed with leukocytes from a patient deficient in this protein. The antiserum reacted with p150,95 and two other antigens with the same beta subunit, Mac-1 and lymphocyte function-associated antigen 1 (LFA-1). In neutrophils, we observed immunogold label for LAR predominantly on the membranes of peroxidase-negative granules, and in smaller amounts on the plasma and perinuclear membranes. In double-label experiments, there was colocalization of LAR with lactoferrin in some of the peroxidase-negative granules. We conclude that the latent pool of LAR resides in the membranes of peroxidase-negative granules. A significant increase in label on the plasma membrane of neutrophils stimulated with PMA is consistent with secretion of LAR to the exterior of the cell during degranulation. While LFA-1 appears very early in neutrophil maturation, it is becoming clear that Mac-1 and p150,95 are upregulated from an intracellular storage pool of peroxidase-negative granules that appear during the myelocyte stage of differentiation. Further studies are indicated to determine the significance of these proteins on the plasma membrane of two other granulocytes, eosinophils and basophils.
Disparity in Glycemic Control and Adherence Between African-American and Caucasian Youths With Diabetes: Family and community contexts
Authors: Wendy F Auslander, Sanna Thompson, Daniele Dreitzer, Neil H White, Julio V Santiago
Journal: Diabetes Care (1997)

OBJECTIVE To describe sociodemographic, family, and community factors that contribute to the glycemic control of African-American and Caucasian youths with diabetes, we investigated two questions: 1) Is there a disparity in glycemic control between African-American and Caucasian youths with diabetes, and if so, what sociodemographic, family, and community factors explain the disparity? and 2) Is there a difference in the adherence to treatment between African-American and Caucasian youths with diabetes, and if so, what sociodemographic, family, and community factors explain the difference? RESEARCH DESIGN AND METHODS This cross-sectional study included 146 youths with diabetes (95 Caucasians and 51 African-Americans) and their mothers. The youths were invited to participate if they had been diagnosed with diabetes at least 1 year before the study, did not have another chronic illness, and were &amp;lt; 18 years of age. RESULTS The findings indicate that African-American youths with diabetes are in significantly poorer metabolic control than their Caucasian counterparts (1.5% difference in HbA1c levels). Single-parent household status and lower levels of adherence partially account for the poorer glycemic control. Examination of the adherence subscales indicates that African-Americans report significantly lower adherence to diet and glucose testing than Caucasian youths. CONCLUSIONS This study suggests that African-American youths with diabetes may be at greater risk for poor glycemic control due to the higher prevalence of single parenting and lower levels of adherence found in this population.
In type 2 diabetes, saxagliptin increased HF hospitalizations, regardless of history of HF or CKD
Authors: Danae A. Delivanis, Victor M. Montori
Journal: Annals of Internal Medicine (2015)

Source Citation Scirica BM, Braunwald E, Raz I, et al; SAVOR–TIMI 53 Steering Committee and Investigators. Heart failure, saxagliptin, and diabetes mellitus: observations from the SAVOR-TIMI 53 randomized trial. Circulation. 2014;130:1579-88. 25189213
Abstract 2435: Novel regulators of renal cancer metabolism
Authors: EunYoung Kho, Richard Kirkman, Eun-Hee Shim, Arindam Goash, Sunil Sudarshan
Journal: Cancer Research (2014)

Abstract Renal cell carcinoma (RCC) is among the 10 most common malignancies in the U.S. Clear cell RCC (ccRCC) is the most common histology. Recent analysis of ccRCC by the Cancer Genome Atlas (TCGA) demonstrates the reduced mRNA expression of several enzymes of the tricarboxylic acid (TCA) cycle. Moreover, reduced TCA enzymes expression is associated with worse prognosis. These data indicate a transcriptional program that promotes a bioenergetic shift. These studies prompted us to examine transcription factors that are known regulators of mitochondrial metabolism including the estrogen-related receptors (ERRs) and peroxisome proliferator-activated receptor γ (PPARγ) coactivators 1 (PGC-1s). Interestingly, mRNA analysis of RCC tissues and cell lines demonstrates the reduced expression of ERRγ and PGC-1α. Notably, prior analysis demonstrates putative ERR binding sites in the promoters of FH and MDH2, two genes encoding TCA enzymes with reduced expression in ccRCC. Promoter analysis of these genes with a luciferase reporter assay demonstrates that ERRγ and PGC-1α cooperate to regulate the expression of TCA enzymes indicating that reduced expression of these factors promotes reduced TCA enzyme expression in RCC. Citation Format: EunYoung Kho, Richard Kirkman, Eun-Hee Shim, Arindam Goash, Sunil Sudarshan. Novel regulators of renal cancer metabolism. [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 2435. doi:10.1158/1538-7445.AM2014-2435
793 STRAIN DIFFERENCES IN MICE SUSCEPTIBILITY TO STEATOHEPATITIS INDUCED BY METHIONINE/CHOLINE DEFICIENT DIET UNDERSCORE A ROLE OF IMMUNE MECHANISMS IN NASH
Authors: V. Maina, S. Sutti, M. Vidali, C. Bozzola, C. Mombello, R. Boldorini, E. Albano
Journal: Journal of Hepatology (2010)