tbuckley/cabot-search huggingface dataset:
MicroRNA29
Authors: Kristin Dawson, Reza Wakili, Balázs Ördög, Sebastian Clauss, Yu Chen, Yuki Iwasaki, Niels Voigt, Xiao Yan Qi, Moritz F. Sinner, Dobromir Dobrev, Stefan Kääb, Stanley Nattel
Journal: Circulation (2013)

Background— Congestive heart failure (CHF) causes atrial fibrotic remodeling, a substrate for atrial fibrillation (AF) maintenance. MicroRNA29 (miR29) targets extracellular matrix proteins. In the present study, we examined miR29b changes in patients with AF and/or CHF and in a CHF-related AF animal model and assessed its potential role in controlling atrial fibrous tissue production. Methods and Results— Control dogs were compared with dogs subjected to ventricular tachypacing for 24 hours, 1 week, or 2 weeks to induce CHF. Atrial miR29b expression decreased within 24 hours in both whole atrial tissue and atrial fibroblasts (−87% and −92% versus control, respectively; p &lt;0.001 for both) and remained decreased throughout the time course. Expression of miR29b extracellular matrix target genes collagen-1A1 (COL1A1), collagen-3A1 (COL3A1), and fibrillin increased significantly in CHF fibroblasts. Lentivirus-mediated miR29b knockdown in canine atrial fibroblasts (−68%; p &lt;0.01) enhanced COL1A1, COL3A1, and fibrillin mRNA expression by 28% ( p &lt;0.01), 19% ( p &lt;0.05), and 20% ( p &lt;0.05), respectively, versus empty virus–infected fibroblasts and increased COL1A1 protein expression by 90% ( p &lt;0.05). In contrast, 3-fold overexpression of miR29b decreased COL1A1, COL3A1, and fibrillin mRNA by 65%, 62%, and 61% (all p &lt;0.001), respectively, versus scrambled control and decreased COL1A1 protein by 60% ( p &lt;0.05). MiR29b plasma levels were decreased in patients with CHF or AF (by 53% and 54%, respectively; both p &lt;0.001) and were further decreased in patients with both AF and CHF (by 84%; p &lt;0.001). MiR29b expression was also reduced in the atria of chronic AF patients (by 54% versus sinus rhythm; p &lt;0.05). Adenoassociated viral–mediated knockdown of miR29b in mice significantly increased atrial COL1A1 mRNA expression and cardiac tissue collagen content. Conclusions— MiR29 likely plays a role in atrial fibrotic remodeling and may have value as a biomarker and/or therapeutic target.
Blair unable to fulfil pledge on health spending, says analysis
Authors: G. Yamey
Journal: BMJ (2001)

Saliva is an attractive specimen type for asymptomatic surveillance of COVID-19 in large populations due to its ease of collection and its demonstrated utility for detecting RNA from SARS-CoV-2. Multiple saliva-based viral detection protocols use a direct-to-RT-qPCR approach that eliminates nucleic acid extraction but can reduce viral RNA detection sensitivity. To improve test sensitivity while maintaining speed, we developed a robotic nucleic acid extraction method for detecting SARS-CoV-2 RNA in saliva samples with high throughput. Using this assay, the Free Asymptomatic Saliva Testing (IGI-FAST) research study on the UC Berkeley campus conducted 11,971 tests on supervised self-collected saliva samples and identified rare positive specimens containing SARS-CoV-2 RNA during a time of low infection prevalence. In an attempt to increase testing capacity, we further adapted our robotic extraction assay to process pooled saliva samples. We also benchmarked our assay against the gold standard, nasopharyngeal swab specimens. Finally, we designed and validated a RT-qPCR test suitable for saliva self-collection. These results establish a robotic extraction-based procedure for rapid PCR-based saliva testing that is suitable for samples from both symptomatic and asymptomatic individuals.
Sudden Purpuriform Rash in an Infant
Authors: Helene Sophie Scheer, Lisa Weibel
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
Colorectal Screening after Polypectomy
Authors: Vikram Boolchand, Gregory S. Cooper
Journal: Annals of Internal Medicine (2007)

Letters5 June 2007Colorectal Screening after PolypectomyVikram Boolchand, MD and Gregory S. Cooper, MDVikram Boolchand, MDFrom the University of Arizona, Tucson, AZ 85724, and Case Medical Center, Cleveland, OH 44106.Search for more papers by this author and Gregory S. Cooper, MDFrom the University of Arizona, Tucson, AZ 85724, and Case Medical Center, Cleveland, OH 44106.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-146-11-200706050-00015 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:We are pleased to see the interest of Dr. Antaki and Dr. Otto in our survey study of primary care physicians regarding postpolypectomy surveillance. As we report in our article, constantly changing guidelines from various societies remain an issue for the primary care physician. In 2003, the USMSTF guidelines (1) for colorectal cancer screening and surveillance were developed by a panel of both gastroenterology and primary care societies and the ACS guidelines (2) were from a single society and included recommendations for the early detection of several types of cancer. As Dr. Antaki pointed out, there was an ...References1. Winawer S, Fletcher R, Rex D, Bond J, Burt R, Ferrucci J, et al. Colorectal cancer screening and surveillance: clinical guidelines and rationale. Update based on new evidence. Gastroenterology. 2003;124:544-60. [PMID: 12557158] CrossrefMedlineGoogle Scholar2. Smith RA, Cokkinides V, Eyre HJ. American Cancer Society guidelines for the early detection of cancer, 2003. CA Cancer J Clin. 2003;53:27-43. [PMID: 12568442] CrossrefMedlineGoogle Scholar3. Winawer SJ, Zauber AG, Fletcher RH, Stillman JS, O'Brien MJ, Levin B, et al. Guidelines for colonoscopy surveillance after polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer and the American Cancer Society. Gastroenterology. 2006;130:1872-85. [PMID: 16697750] CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: From the University of Arizona, Tucson, AZ 85724, and Case Medical Center, Cleveland, OH 44106.Disclosures: None disclosed. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoColorectal Screening after Polypectomy: A National Survey Study of Primary Care Physicians Vikram Boolchand , Gregory Olds , Joseph Singh , Pankaj Singh , Amitabh Chak , and Gregory S. Cooper Colorectal Screening after Polypectomy Fadi Antaki Colorectal Screening after Polypectomy Maj Hans F. Otto Metrics 5 June 2007Volume 146, Issue 11Page: 820-821KeywordsAdenomasColonoscopyColorectal cancer screeningConflicts of interestFearReasoning ePublished: 5 June 2007 Issue Published: 5 June 2007 CopyrightCopyright © 2007 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Textbook of Neuropathology
Authors: Moris J. Danon
Journal: JAMA (1985)

This multiauthored textbook of neuropathology is divided into 17 chapters. The first three cover the normal morphology and cellular pathology of neurons, astrocytes, ependyma, oligodendroglia, and microglia. All three chapters contain superb electron micrographs and excellent diagrams describing various cellular functions and myelination in the central nervous system. In addition, there are many examples of animal and experimental neuropathology in relation to human brain disease. The rest of the chapters cover various topics in neuropathology—the meninges, hydrocephalus and edema, congenital malformations, perinatal pathology, inherited metabolic diseases, toxic metabolic disorders, central nervous system manifestations of systemic disease, demyelinating diseases, circulatory disorders, infections of the nervous system, degenerative diseases, Alzheimer's disease, and cerebrospinal trauma. All these chapters are well written and referenced. Illustrations of gross brain pathology, light microscopy, and ultrastructure are of the highest quality. There are excellent diagrams explaining the mechanisms of various nervous disorders in the central nervous system
The Environmental “Riskscape” and Social Inequality: Implicationsfor Explaining Maternal and Child Health Disparities
Authors: Rachel Morello-Frosch, Edmond D. Shenassa
Journal: Environmental Health Perspectives (2006)

Research indicates that the double jeopardy of exposure to environmental hazards combined with place-based stressors is associated with maternal and child health (MCH) disparities. Our aim is to present evidence that individual-level and place-based psychosocial stressors may compromise host resistance such that environmental pollutants would have adverse health effects at relatively lower doses, thus partially explaining MCH disparities, particularly poor birth outcomes. Allostatic load may be a physiologic mechanism behind the moderation of the toxic effect of environmental pollutants by social stressors. We propose a conceptual framework for holistic approaches to future MCH research that elucidates the interplay of psychosocial stressors and environmental hazards in order to better explain drivers of MCH disparities. Given the complexity of the link between environmental factors and MCH disparities, a holistic approach to future MCH research that seeks to untangle the double jeopardy of chronic stressors and environmental hazard exposures could help elucidate how the interplay of these factors shapes persistent racial and economic disparities in MCH.
Fosinopril Versus Amlodipine Comparative Treatments Study
Authors: Marco Pahor, Lonneke V. Franse, Steven R. Deitcher, William C. Cushman, Karen C. Johnson, Ronald I. Shorr, Kandice Kottke-Marchant, Russell P. Tracy, Grant W. Somes, William B. Applegate
Journal: Circulation (2002)

Background — ACE inhibitors and calcium antagonists may modulate fibrinolysis. We conducted a randomized controlled trial to assess the effects of these drugs on plasminogen activator inhibitor-1 (PAI-1) antigen, an inhibitor of fibrinolysis. Methods and Results — Participants with hypertension and type 2 diabetes mellitus (n=96, 51% black) were randomized after an initial 4 weeks of placebo to double-blind 20 or 40 mg fosinopril or 5 or 10 mg amlodipine daily for 4 weeks in a fixed-dose regimen. After 4 weeks of placebo washout, the patients received 4 weeks of crossover treatments. After treatment with placebo, systolic and diastolic blood pressure were 143±2 and 86±1 mm Hg and plasma PAI-1 was 43.4±2.3 ng/mL. Amlodipine achieved a greater systolic and diastolic blood pressure reduction than fosinopril (10 mm Hg versus 8 mm Hg, P =0.029, and 5 mm Hg versus 3 mm Hg, P =0.040, respectively) but tended to increase PAI-1, whereas fosinopril tended to decrease PAI-1 (5.4±3.6 versus −3.8±2.5 ng/mL, P =0.045). The PAI-1 changes depended on drug dose (6.5±6.1 and 3.4±3.9 ng/mL with amlodipine 10 and 5 mg, respectively, and −0.4±3.1 and −7.4±4.0 ng/mL with fosinopril 20 and 40 mg, respectively, P for trend 0.024). No significant differences between fosinopril and amlodipine were found for short-term changes in tissue plasminogen activator antigen, fibrinogen, C-reactive protein, and interleukin-6. The findings were similar in black and white participants. Conclusions — Short-term treatment with fosinopril significantly reduced PAI-1 compared with amlodipine in a dose-dependent fashion. This effect, which was independent of blood pressure reduction, may account for the improved clinical outcomes achieved with ACE inhibitors compared with calcium antagonists.
A simple method for the representative sampling of lungs of diverse size.
Authors: C Langston, E Waszkiewicz, W M Thurlbeck
Journal: Thorax (1979)

The proportion of non-parenchyma (non-gas exchanging tissue) varies with postnatal age and with the distance from the hilum of the lung. We have sampled 11 lungs varying in volume from 24.7 ml to 1308 ml and found that the mid-sagittal slice, or a combination of the two central slices in a lung producing four slices, adequately represents the amount of non-parenchyma and of air in bronchi and bronchioles in the entire lung.
Lipopolysaccharide potentiates the effect of hepatocyte growth factor on hepatocyte replication in rats by augmenting AP-1 activity
Authors: Cuihua Gao, Rodney Jokerst, Prathima Gondipalli, Shi-Rong Cai, Susan Kennedy, Wayne M. Flye, Katherine Parker Ponder
Journal: Hepatology (1999)

The liver regenerates by replication of differentiated hepatocytes after damage or removal of part of the liver. Although several growth factors and signaling pathways are activated during regeneration, it is unclear as to which of these are essential for hepatocyte replication. We show here that low- (1 mg/kg) and high- (10 mg/kg) dose hepatocyte growth factor (HGF) induced replication of 2.1% and 11.1% of hepatocytes in rats, respectively. Lipopolysaccharide (LPS), an inducer of the acute phase response, augmented hepatocyte replication in response to low- and high-dose HGF by 4- and 2-fold, respectively. HGF alone induced moderate levels of c-Jun-N-terminal kinase (JNK) and p44/p42 mitogen-activated protein kinase (MAPK), resulting in moderate levels of AP-1-DNA binding activity. The combination of LPS + HGF increased JNK and AP-1-DNA binding activity more than levels seen with LPS or HGF alone. The activation of Stat3 that was observed after administration of LPS + HGF, but not HGF alone, could contribute to increased transcription of AP-1 components. Because phosphorylation of the c-Jun component of AP-1 by JNK increases its ability to activate transcription, the AP-1 in hepatocytes from animals treated with LPS + HGF may be more active than in rats treated with LPS or HGF alone. LPS may contribute to hepatocyte replication by potentiating the effect of HGF on the activation of both AP-1-DNA binding and transcriptional activity.
Polymorphism in the Angiotensin-Converting Enzyme (ACE) Gene and Sarcoidosis
Authors: HIROSHI TOMITA, YASUTAKA INA, YOSHIKI SUGIURA, SHIGEKI SATO, HARUHIKO KAWAGUCHI, MUNEHIKO MORISHITA, MASAHIKO YAMAMOTO, RYUZO UEDA
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

It has recently been shown that an insertion (I)/deletion (D) polymorphism exists in the angiotensin-converting enzyme (ACE) gene, and that this polymorphism affects the serum ACE level. There are three genotypes: DD, DI, and II, with the ACE level highest in DD, intermediate in DI, and lowest in II. In the present investigation of the possible significance of the polymorphism for sarcoidosis, a total of 207 patients and 314 normal control subjects were examined. There were no significant differences in the I/D ratio and the genotype distribution between the two groups, and no significant variation in organ involvement (i.e., eye, skin, and heart) was noted among the three genotypes. To determine any prognostic influence of the polymorphism, we examined the disappearance ratio of abnormal shadow on chest radiography over 3 and 5 yr. No significant difference among the three genotypes was observed. New normal ranges of serum ACE level were determined for each genotype, and found to be 22% more sensitive overall than the conventional normal range and 39% more so for II type, suggesting an advantage for diagnosis and assessment of the disease activity of sarcoidosis.
Abstract 745: Development of gamma-H2AX assay to assess toxicity and efficacy from chemotherapy in circulating tumor cells (CTCs) and peripheral blood lymphocytes
Authors: Hassan S. Sheikh, Elizabeth Matthew, Wafik S. El-Deiry
Journal: Cancer Research (2012)

Abstract CTC methodology has been recently adopted following FDA approval of the Veridex CellSearch for the detection of CTCs and offers prognostic value in various solid tumors including breast, colorectal, and prostate cancer. gamma-H2AX is an established marker for double strand breaks from DNA damage, and this is particularly evident and has been seen after exposure to ionizing radiation and exposure to topoisomerase inhibitors. Moreover prolonged gamma-H2AX expression has been observed in repair deficiencies after DNA damage where there may be delays in DNA repair and persistence of H2AX. H2AX may therefore serve as an excellent marker not only of toxicity but the efficacy of the chemotherapy. We have been using human tumor cell lines to expose them to chemotherapeutic agents in the laboratory to detect gamma-H2AX levels and the dynamic changes thereof following exposure to cytotoxic chemotherapy. Our results reveal clear time-dependent upregulation of gamma-H2AX in treated cells. This is being adopted for use on CTCs as well as blood lymphocytes with a goal of making correlations with toxicity to chemotherapy in treated patients as well as use of this assay to mark the efficacy of chemotherapy in CTCs. We are applying quantum dot technology to detection of gamma-H2AX in cells recovered from blood and this is being incorporated into a clinical protocol. This assay has potential to impact on monitoring of chemotherapy with regard to both toxicity and efficacy in the clinic. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 745. doi:1538-7445.AM2012-745
New Instructions for JAMA Authors
Authors: Elizabeth Knoll
Journal: JAMA (1985)

Original research studies and case reports, personal essays, and discussions of specialized fields: the articles inThe Journalhave traveled widely by the time they are published. All submissions are read by the editors; most are sent to reviewers in the relevant fields for consultation; and some (11.0% of unsolicited manuscripts in 1984) are accepted for publication. They are then copy edited and sent to the authors for approval; a layout is designed; and the final copy is set in type, ready for timely publication. The manuscript is seen by many eyes during this process; its tables, illustrations, and references may be examined dozens of times atThe Journaland outside it. The ease of every task from review to production is significantly affected by the way in which the manuscript has been prepared by the authors. Missing tables, blurry photographs, or tiny margins in which copy editors cannot make
Moving beyond Round Pegs and Square Holes: Restructuring Medicare To Improve Chronic Care
Authors: Jennifer L. Wolff, Chad Boult
Journal: Annals of Internal Medicine (2005)

Chronic disease is the norm rather than the exception among Medicare beneficiaries, yet Medicare's benefit structure and reimbursement mechanisms are poorly aligned with high-quality chronic care. This disconnect is thought to undermine the quality of chronic care, thereby contributing to excess program spending and placing beneficiaries at risk for undesirable health outcomes. Despite widespread recognition of this mismatch, there is little compelling evidence to suggest that successful quality improvement initiatives would reduce the costs of the Medicare program. This paper describes state-of-the-art chronic care innovations to date, discusses ongoing and planned efforts by the Centers for Medicare & Medicaid Services to test related changes to Medicare's benefit structure and provider reimbursement, and suggests opportunities for future progress in this area.
Biostatistics: The Bare Essentials
Authors: Naomi Vaisrub
Journal: JAMA (2009)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Severe impairment in liver insulin signaling fails to alter hepatic insulin action in conscious mice
Authors: Christoph Buettner, Rima Patel, Evan D. Muse, Sanjay Bhanot, Brett P. Monia, Rob McKay, Silvana Obici, Luciano Rossetti
Journal: Journal of Clinical Investigation (2005)

Insulin exerts its potent effects on hepatic glucose fluxes via direct and indirect mechanisms. Whereas a liver-specific insulin receptor (IR) knockout (LIRKO) mouse exhibits glucose intolerance as well as insulin resistance, it is unclear whether a more acute decrease in the expression of hepatic IR would be sufficient to induce hepatic insulin resistance. Here we report that the downregulation of hepatic IR expression by up to 95% does not modify hepatic insulin action. The i.p. administration (2 injections over 1 week) of an antisense oligodeoxynucleotide (ASO) directed to reduce insulin expression downregulated hepatic IR expression in C57BL6J mice. A high dose of IR-ASO decreased IR protein approximately 95%, while a control-ASO failed to modify IR expression. At this dose, the IR-ASO also decreased IR expression in adipose tissue but did not significantly decrease IR expression in hypothalamus or skeletal muscle. Insulin action was assessed with insulin clamp studies in conscious mice. The rate of glucose infusion during the clamp studies was comparable in control-ASO– and IR-ASO–treated mice. Importantly, the depletion of liver IR protein markedly impaired downstream insulin signaling in the liver, but it failed to modify the rate of glucose production. Thus, near ablation of liver IR does not alter insulin action on glucose production.
Regulated release of nitric oxide by nonhematopoietic stroma controls expansion of the activated T cell pool in lymph nodes
Authors: Veronika Lukacs-Kornek, Deepali Malhotra, Anne L Fletcher, Sophie E Acton, Kutlu G Elpek, Prakriti Tayalia, Ai-ris Collier, Shannon J Turley
Journal: Nature Immunology (2011)