tbuckley/cabot-search huggingface dataset:
Signaling During Epicardium and Coronary Vessel Development
Authors: José María Pérez-Pomares, José Luis de la Pompa
Journal: Circulation Research (2011)

The epicardium, the tissue layer covering the cardiac muscle (myocardium), develops from the proepicardium, a mass of coelomic progenitors located at the venous pole of the embryonic heart. Proepicardium cells attach to and spread over the myocardium to form the primitive epicardial epithelium. The epicardium subsequently undergoes an epithelial-to-mesenchymal transition to give rise to a population of epicardium-derived cells, which in turn invade the heart and progressively differentiate into various cell types, including cells of coronary blood vessels and cardiac interstitial cells. Epicardial cells and epicardium-derived cells signal to the adjacent cardiac muscle in a paracrine fashion, promoting its proliferation and expansion. Recently, high expectations have been raised about the epicardium as a candidate source of cells for the repair of the damaged heart. Because of its developmental importance and therapeutic potential, current research on this topic focuses on the complex signals that control epicardial biology. This review describes the signaling pathways involved in the different stages of epicardial development and discusses the potential of epicardial signals as targets for the development of therapies to repair the diseased heart.
Abstract 4870: High dietary vitamin D prevents dysplastic lesions in an AOM/DSS model of colorectal cancer.
Authors: Doris M. Hummel, Julia Höbaus, Ursula Thiem, Joao Graca, Ildiko Mesteri, Lukas Gober, Barbara Obermayer-Pietsch, Enikö Kallay
Journal: Cancer Research (2013)

Abstract Diet and lifestyle have an important impact on the etiology of colorectal cancer (CRC), one of the leading causes of cancer morbidity and mortality in Western countries. Epidemiological studies suggest that vitamin D might have chemopreventive effects. In this study we investigated the effect of increasing dietary vitamin D3 intake on chemically induced colorectal tumor development in mice. We fed female C57BL/6J mice with a diet containing five different vitamin D3 concentrations ranging from 100 to 5000 IU/kg diet and studied the impact of dietary vitamin D3 on the development of chemically induced colonic dysplasia, a precursor of CRC. To induce dysplasia, we injected mice once with 10 mg/kg azoxymethane (AOM) intraperitoneally, followed by three cycles of dextran sodium sulfate salt (DSS) in the drinking water. Dietary vitamin D3 concentration correlated positively with 25(OH)D3 serum levels (Spearman Correlation Coefficient (SCC) 0.752, p&amp;lt;0.001). Both dietary vitamin D3 concentration and serum 25-hydroxyvitamin D3 levels correlated inversely with the dysplasia score (SCC -0.579, p=0.002; SCC -0.618, p=0.001). Dysplastic regions expressed less vitamin D receptor while the proliferation marker Ki67 was significantly higher expressed in regions with high grade dysplasia compared with the respective normal mucosa of the same colon. Our data show that high dietary vitamin D3 concentrations reduce the development of chemically induced precursors of colorectal cancer in mice. Citation Format: Doris M. Hummel, Julia Höbaus, Ursula Thiem, Joao Graca, Ildiko Mesteri, Lukas Gober, Barbara Obermayer-Pietsch, Enikö Kallay. High dietary vitamin D prevents dysplastic lesions in an AOM/DSS model of colorectal cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4870. doi:10.1158/1538-7445.AM2013-4870
Unexpected Visitor: Hepatic Visualization on Radionuclide Venography
Authors: Yuh-Feng Wang, Chih-Wen Lin, Jainn-Shiun Chiu
Journal: Clinical Nuclear Medicine (2007)

A 56-year-old man with a colectomy for adenocarcinoma of colon 2 years earlier presented with a 5-day history of edema of the lower extremities. Lower extremity radionuclide venography with technetium-99m macroaggregated albumin (Tc-99m MAA) was requested. The results demonstrated circular activity below the bifurcation of the common iliac veins after visualization of uniform hepatic uptake. The concurrent appearance of these characteristics led to a diagnosis of distal inferior vena cava thrombosis with cavoportal collaterals.
Relation Between Work and Labile Phosphate Content in the Isolated Dog Heart
Authors: ALBERT WOLLENBERGER
Journal: Circulation Research (1957)

Starling heart-lung preparations of the dog (with only minor differences in heart rate) were subjected to changes in work load to study their effect on the amount of labile phosphate in the left ventricle. While increasing the work load three to fourfold by increasing output caused no change, doubling the work load by increasing the resistance was accompanied by a marked reduction in labile phosphate. The data suggest that the heart expends phosphate bond energy chiefly in overcoming resistance rather than in systolic emptying.
Arachidonic Acid–Dependent Phosphorylation of Troponin I and Myosin Light Chain 2 in Cardiac Myocytes
Authors: Derek S. Damron, Ahmad Darvish, LeeAnn Murphy, Wendy Sweet, Christine S. Moravec, Meredith Bond
Journal: Circulation Research (1995)

Recent evidence has suggested that arachidonic acid (AA) may be an important signaling molecule in cardiac excitation-contraction coupling. We previously showed that AA and endothelin-1 (ET) inhibit distinct K+ channels via protein kinase C-dependent pathways in rat ventricular myocytes. In addition, we demonstrated that Ca2+ transients in populations of fura 2-loaded myocytes were potentiated by AA and ET via activation of protein kinase C. In this study, we have used suspensions of [32P]orthophosphate (32Pi)-labeled rat ventricular myocytes to study the effects of AA and ET at the level of the myofilaments. After a 10-minute incubation of the labeled cells with phorbol 12-myristate 13-acetate (PMA), AA, or ET in the presence or absence of the protein kinase C inhibitor calphostin C, the myofibrillar proteins were separated by PAGE. Measurement of unloaded cell shortening using video edge detection in single electrically stimulated myocytes was also used to assess the effects of AA and ET on myocyte contractility. Incubation with either PMA, AA, or ET resulted in similar increases in 32Pi incorporation into troponin I (TnI) and myosin light chain 2 (MLC2), which was inhibited by preincubation with the protein kinase C antagonist calphostin C. In addition, the ability of these agonists to stimulate phosphorylation of TnI or MLC2 did not require extracellular Ca2+ or intact intracellular Ca2+ stores. The effects of AA and ET together on phosphorylation of TnI or MLC2 were not additive.(ABSTRACT TRUNCATED AT 250 WORDS)
A Unifying Mutation in Chronic Myeloproliferative Disorders
Authors: John M. Goldman
Journal: New England Journal of Medicine (2005)

In 1892, Louis Vaquez of Paris described a patient with cyanotic polycythemia; the autopsy disclosed massive enlargement of the spleen and liver. In 1903, William Osler, then at Johns Hopkins Hospital, reported on four patients with polycythemia, two of whom had splenomegaly. He gave credit to Vaquez for the earlier description, and the disorder was later named Osler–Vaquez disease, though today it is usually referred to as polycythemia vera.In 1951, William Dameshek drew attention to the relationships among polycythemia vera, idiopathic myelofibrosis, and essential thrombocythemia and proposed that these diseases, as well as chronic myeloid leukemia and erythroleukemia, should . . .
Preventive effect of an E. coli-filtrate (ColibiogenR) in polymorphous light eruption
Authors: B. PRZYBILLA, M. HEPPELER, T. RUZICKA
Journal: British Journal of Dermatology (1989)

Journal Article Preventive effect of an E. coli‐filtrate (Colibiogen®) in polymorphous light eruption Get access B. PRZYBILLA, B. PRZYBILLA Dermatologische Klinik und Poliklinik, der Ludwig‐Maximilians‐Universität, Munich, F.R.G. Priv.‐Doz. Dr Bernhard Przybilla, Dermatologische Klinik und Poliklinik der Ludwig‐Maximilians‐Universität München, Frauenlobstr. 9‐11, D‐8000 München 2, F.R.G. Search for other works by this author on: Oxford Academic Google Scholar M. HEPPELER, M. HEPPELER Dermatologische Klinik und Poliklinik, der Ludwig‐Maximilians‐Universität, Munich, F.R.G. Search for other works by this author on: Oxford Academic Google Scholar T. RUZICKA T. RUZICKA Dermatologische Klinik und Poliklinik, der Ludwig‐Maximilians‐Universität, Munich, F.R.G. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 121, Issue 2, 1 August 1989, Pages 229–233, https://doi.org/10.1111/j.1365-2133.1989.tb01803.x Published: 01 August 1989
Psychological medicine. Stress and distress.
Authors: R C Aitken
Journal: BMJ (1975)

A patient's anxiety or depression can be the natural consequence of change in his life's circumstances, whether the death or departure of a loved one, overcrowding in the home, loss of job owing to retirement or redundancy, financial crisis, or simply loneliness and despondency.It is easy to recognize an anxiety state when it accompanies a reason for intense strain.But feelings of sadness can follow, perhaps after a delay, when it can be more difficult to connect their cause.Indeed stress can precipitate florid depressive illness, when guilt and suicidal feelings determine the clinical picture.Moreover, anxiety and depression can contribute to the distress of many patients-and indeed their relatives-when they suffer from illness and injury, particularly if chronically.Indeed mood disturbance may be the principle cause of distress at some stage in a wide variety of conditions like cancer, coronary artery disease, stroke, viral infections, multiple sclerosis, and personality disorders.Even the patient who denies feeling upset is likely to be afflicted, because all are hyperaroused to some degree.
A conserved surface on Toll-like receptor 5 recognizes bacterial flagellin
Authors: Erica Andersen-Nissen, Kelly D. Smith, Richard Bonneau, Roland K. Strong, Alan Aderem
Journal: The Journal of Experimental Medicine (2007)

The molecular basis for Toll-like receptor (TLR) recognition of microbial ligands is unknown. We demonstrate that mouse and human TLR5 discriminate between different flagellins, and we use this difference to map the flagellin recognition site on TLR5 to 228 amino acids of the extracellular domain. Through molecular modeling of the TLR5 ectodomain, we identify two conserved surface-exposed regions. Mutagenesis studies demonstrate that naturally occurring amino acid variation in TLR5 residue 268 is responsible for human and mouse discrimination between flagellin molecules. Mutations within one conserved surface identify residues D295 and D367 as important for flagellin recognition. These studies localize flagellin recognition to a conserved surface on the modeled TLR5 structure, providing detailed analysis of the interaction of a TLR with its ligand. These findings suggest that ligand binding at the β sheets results in TLR activation and provide a new framework for understanding TLR–agonist interactions.
Puzzles Concerning the Pathogenicity of Human Herpesvirus 6
Authors: Henri Agut
Journal: New England Journal of Medicine (1993)

Human herpesvirus 6 (HHV-6) was discovered in 1986 by Salahuddin and coworkers1 and was initially called human B-lymphotropic virus. The virus was later shown to have a marked tropism for CD4-positive T cells and was renamed HHV-6. HHV-6 is genetically similar to cytomegalovirus,2 and the two viruses share phenotypic properties such as patterns of in vitro sensitivity to antiviral drugs3. This novel herpesvirus was quickly singled out as a potential human pathogen. In 1988, Yamanishi and coworkers4 showed that HHV-6 was the cause of exanthem subitum (roseola infantum, or sixth disease). They isolated the virus from peripheral-blood mononuclear cells . . .
Hypersensitivity to Sunlight
Authors: Amour F. Liber
Journal: JAMA (1961)

<h3>To the Editor:—</h3> In answer to a question concerning "Hypersensitivity to Sunlight" (<i>JAMA</i><b>174</b>:1895 [Dec. 3] 1960), the statement is made that regular window glass provides adequate protection from wave lengths longer than 3,200 A. This is an error. Window glass excludes wave lengths shorter than 3,200 A.
Abstract 385: Potentiating MUC1 expression in human bronchial epithelial cells by cigarette smoke carcinogens through induction of TNF-α secretion from macrophages
Authors: Xiuling Xu, Wenshu Chen, Mabel T. Padilla, Weiyang He, Qiong Wang, Kwang Chul Kim, Yong Lin
Journal: Cancer Research (2012)

Abstract Although an important role of inflammation in the development of lung cancer has been recognized, how inflammation promotes lung epithelial cell transformation and lung cancer development has not been well elucidated. Cigarette smoke (CS), the major cause of lung cancers, potently elicits chronic pulmonary inflammation. Our recent studies have found that CS significantly induces Muc1 (MUC1 for human and Muc1 for nonhuman species) expression in mouse bronchial epithelial cells and macrophages, and MUC1 facilitates Benzo(a)pyrene diolepoxide (BPDE)-induced human lung epithelial cell transformation. In this study, we investigated the role of inflammatory cells in regulating CS carcinogen-induced MUC1 expression in bronchial epithelial cells. BPDE and N-Nitroso-N-methylurea (MNU), an active CS carcinogen and a mimic, strongly induced tumor necrosis factor-alpha (TNF-α) secretion from human macrophages. The TNF-α induction was effectively blocked when ERK, JNK, and NF-κB were blocked, suggesting these pathways are involved in the induction of TNF-α from macrophages by BPDE and MNU. Interestingly, knockdown of MUC1 in macrophages suppressed BPDE- or MNU-induced TNF-α secretion, suggesting MUC1 plays a role in modulating carcinogen-induced and macrophage-mediated inflammatory responses. Conditioned media from BPDE- or MNU-treated macrophages potently induced MUC1 expression in human bronchial epithelial cells (HBECs), which was inhibited by a TNF-α neutralizing antibody, suggesting that TNF-α derived from macrophages contributes to CS carcinogen-induced MUC1 expression in HBECs. Thus, our results establish a dual role of MUC1 in CS-induced and inflammation-associated lung cancer development: to facilitate TNF-α secretion from macrophages and to potentiate transformation of HBECs. Note: This work is supported by NIH/NIEHS grant 1R01ES017328. 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 385. doi:1538-7445.AM2012-385
Nickel-keratinocyte interaction: a possible role in sensitization
Authors: M. PICARDO, CLAUDIA ZOMPETTA, CHIARA LUCA, A. CRISTAUDO, C. CANNISTRACI, A. FAGGIONI, B. SANTUCCI
Journal: British Journal of Dermatology (1990)

Normal human keratinocytes and the keratinocyte‐derived cell lines NCTC 2544 and A 431, were exposed for different periods (i–5 days) to various concentrations (0·023–46.6 μg/ml) of nickel (Ni2+). A dose‐ and time‐dependent inhibition of cell growth and viability was observed. Cultures exposed to 2·3 μg Ni2+/ml showed approximately 50% cell survival at 5 days. An increase in release of interleukin I by keratinocytes was detected following culture for 24 h with a Ni2+ concentration of 2·3–11·5 μg/ml. Short periods of incubation (30 min) with these concentrations induced an activation of lipoxygenase in leucocytes from healthy subjects, without modifying cell viability. The results suggest that the percutaneous penetration of small amounts of Ni2+ can result in damage to keratinocytes and can initiate sensitization.
Effect of Antihypertensive Therapy on the Kidney in Patients with Diabetes: A Meta-Regression Analysis
Authors: Bertram L. Kasiske
Journal: Annals of Internal Medicine (1993)

Objective: To assess the relative effect of different antihypertensive agents on proteinuria and renal function in patients with diabetes. Data Sources: We used MEDLINE and bibliographies in recent articles to identify studies of the effects of antihypertensive agents on renal function in patients with diabetes. Study Selection: We selected 100 controlled and uncontrolled studies that provided data on renal function, proteinuria, or both, before and after treatment with an antihypertensive agent. Data Extraction: Data on blood pressure, renal function, proteinuria, patient characteristics (for example, age, sex, and type of diabetes), and study design (for example, random allocation and the use of a placebo) were extracted from selected studies. Data Synthesis: Multiple linear regression analysis indicated that angiotensin-converting enzyme (ACE) inhibitors decreased proteinuria independent of changes in blood pressure, treatment duration, and the type of diabetes or stage of nephropathy, as well as study design (P < 0.0001). Reductions in proteinuria from other antihypertensive agents could be entirely explained by changes in blood pressure. Blood pressure reduction in itself was associated with a relative increase in glomerular filtration rate (regression coefficient [±SE], 3.70 ±.92 mL/min for each reduction of 10 mm Hg in mean arterial pressure; P = 0.0002); however, compared with other agents, ACE inhibitors had an additional favorable effect on glomerular filtration rate that was independent of blood pressure changes (3.41 ± 1.71 mL/min; P = 0.05). Conclusion: Angiotensin-converting enzyme inhibitors can decrease proteinuria and preserve glomerular filtration rate in patients with diabetes. These effects occur independent of changes in systemic blood pressure.
Oxidized LDL, a critical factor in atherogenesis☆
Authors: D LI, J MEHTA
Journal: Cardiovascular Research (2005)

There is a great deal of experimental, epidemiological, and clinical evidence suggesting that disorders of lipid metabolism play an important role in the pathogenesis of atherosclerosis.To date, there have been many studies investigating the mechanisms by which high levels of LDL-cholesterol affect biology of vessels and cause atherosclerotic lesion formation [1,2].It has become abundantly clear over the last decade that the oxidatively modified form of LDL (ox-LDL) is more important than native LDL in atherogenesis.The study in this issue of Cardiovascular Research by Zhu et al. [3] demonstrates that ox-LDL downregulates ATPbinding cassette transporter-1 (ABCA1) in endothelial cells in a dose-dependent manner by inhibiting liver X receptor (LXR) activation.Ox-LDL also attenuates LXR activation by blocking LXR ligand binding and interfering with the generation of 27-hydroxycholesterol, an LXR endogenous ligand.Further, ox-LDL inhibits exogenous cholesterol and oxysterol-induced endothelial ABCA1 induction.Such activity of ox-LDL may contribute to endothelial dysfunction since ABCA1 mediates the active efflux of cholesterol and phospholipids, playing an important role in cholesterol homeostasis and thereby atherogenesis.
Interleukin 1 stimulates phosphatidylinositol kinase activity in human fibroblasts.
Authors: L R Ballou, S C Barker, A E Postlethwaite, A H Kang
Journal: Journal of Clinical Investigation (1991)

IL-1 mediates multiple cellular immune and inflammatory responses, but little is known of the intracellular biochemical mechanisms involved in IL-1 actions. We studied the effects of IL-1 on phosphatidylinositol (PtdIns) metabolism and confirmed reports indicating that IL-1 does not stimulate increased PtdIns turnover; however, we observed the accumulation of PtdIns-4-phosphate (PtdInsP) in response to IL-1. Using a fibroblast membrane preparation, we were able to detect stimulated PtdInsP accumulation within 10 s of IL-1 addition. Increased PtdInsP accumulation was due to stimulated PtdIns kinase activity, not the inhibition of PtdInsP hydrolysis by phospholipase(s). PtdIns kinase activity was magnesium dependent, increased as a function of IL-1 concentration, and specifically phosphorylated the D4 position of inositol. Stimulated PtdIns kinase activity could be detected at 10(-12) M IL-1 in fibroblast membranes, a concentration within the physiological range for IL-1 action; half-maximal activity was reached at approximately 10(-10) M IL-1. Heat denaturation of IL-1 or treatment of IL-1 with anti-IL-1 antibody abrogated the IL-1 effect. These findings demonstrate the direct, IL-1-mediated, stimulation of PtdIns kinase. IL-1-stimulated PtdIns kinase activity represents an important physiological regulatory effect by IL-1 as it could control the synthesis and/or maintenance of phosphorylated derivatives of PtdIns which comprise only a very small pool of substrates for the generation of the second messengers inositol 1,4,5-triphosphate and diacylglycerol.
Report from the third international consensus meeting to harmonise core outcome measures for atopic eczema/dermatitis clinical trials (HOME)
Authors: J.R. Chalmers, J. Schmitt, C. Apfelbacher, M. Dohil, L.F. Eichenfield, E.L. Simpson, J. Singh, P. Spuls, K.S. Thomas, S. Admani, V. Aoki, M. Ardeleanu, S. Barbarot, T. Berger, J.N. Bergman, J. Block, N. Borok, T. Burton, S.L. Chamlin, S. Deckert, C.C. DeKlotz, L.B. Graff, J.M. Hanifin, A.A. Hebert, R. Humphreys, N. Katoh, R.M. Kisa, D.J. Margolis, S. Merhand, R. Minnillo, H. Mizutani, H. Nankervis, Y. Ohya, P. Rodgers, M.E. Schram, J.F. Stalder, A. Svensson, R. Takaoka, A. Teper, W.L. Tom, L. von Kobyletzki, E. Weisshaar, S. Zelt, H.C. Williams
Journal: British Journal of Dermatology (2014)

This report provides a summary of the third meeting of the Harmonising Outcome Measures for Eczema (HOME) initiative held in San Diego, CA, U.S.A., 6–7 April 2013 (HOME III). The meeting addressed the four domains that had previously been agreed should be measured in every eczema clinical trial: clinical signs, patient‐reported symptoms, long‐term control and quality of life. Formal presentations and nominal group techniques were used at this working meeting, attended by 56 voting participants (31 of whom were dermatologists). Significant progress was made on the domain of clinical signs. Without reference to any named scales, it was agreed that the intensity and extent of erythema, excoriation, oedema/papulation and lichenification should be included in the core outcome measure for the scale to have content validity. The group then discussed a systematic review of all scales measuring the clinical signs of eczema and their measurement properties, followed by a consensus vote on which scale to recommend for inclusion in the core outcome set. Research into the remaining three domains was presented, followed by discussions. The symptoms group and quality of life groups need to systematically identify all available tools and rate the quality of the tools. A definition of long‐term control is needed before progress can be made towards recommending a core outcome measure.
Effect of loratadine on nitrogen dioxide–induced changes in electrical resistance and release of inflammatory mediators from cultured human bronchial epithelial cells☆☆☆★
Authors: Hasan Bayram, Jagdish L. Devalia, Omer A. Khair, Muntasir M. Abdelaziz, Raymond J. Sapsford, Wienia Czarlewski, Alison M. Campbell, Jean Bousquet, Robert J. Davies
Journal: Journal of Allergy and Clinical Immunology (1999)