tbuckley/cabot-search huggingface dataset:
Monitoring the emergence of community transmission of influenza A/H1N1 2009 in England: a cross sectional opportunistic survey of self sampled telephone callers to NHS Direct
Authors: A. J Elliot, C. Powers, A. Thornton, C. Obi, C. Hill, I. Simms, P. Waight, H. Maguire, D. Foord, E. Povey, T. Wreghitt, N. Goddard, J. Ellis, A. Bermingham, P. Sebastianpillai, A. Lackenby, M. Zambon, D. Brown, G. E Smith, O N. Gill
Journal: BMJ (2009)

<b>Objective </b>To evaluate ascertainment of the onset of community transmission of influenza A/H1N1 2009 (swine flu) in England during the earliest phase of the epidemic through comparing data from two surveillance systems. <b>Design </b>Cross sectional opportunistic survey. <b>Study samples </b>Results from self samples by consenting patients who had called the NHS Direct telephone health line with cold or flu symptoms, or both, and results from Health Protection Agency (HPA) regional microbiology laboratories on patients tested according to the clinical algorithm for the management of suspected cases of swine flu. <b>Setting </b>Six regions of England between 24 May and 30 June 2009. <b>Main outcome measure </b>Proportion of specimens with laboratory evidence of influenza A/H1N1 2009. <b>Results </b>Influenza A/H1N1 2009 infections were detected in 91 (7%) of the 1385 self sampled specimens tested. In addition, eight instances of influenza A/H3 infection and two cases of influenza B infection were detected. The weekly rate of change in the proportions of infected individuals according to self obtained samples closely matched the rate of increase in the proportions of infected people reported by HPA regional laboratories. Comparing the data from both systems showed that local community transmission was occurring in London and the West Midlands once HPA regional laboratories began detecting 100 or more influenza A/H1N1 2009 infections, or a proportion positive of over 20% of those tested, each week. <b>Conclusions</b> Trends in the proportion of patients with influenza A/H1N1 2009 across regions detected through clinical management were mirrored by the proportion of NHS Direct callers with laboratory confirmed infection. The initial concern that information from HPA regional laboratory reports would be too limited because it was based on testing patients with either travel associated risk or who were contacts of other influenza cases was unfounded. Reports from HPA regional laboratories could be used to recognise the extent to which local community transmission was occurring.
Fms-like tyrosine kinase 3 ligand/CD135 in arthritis: a new inflammatory system in RA?
Authors: M. I. Ramos, S. Aarrass, L. G. M. van Baarsen, P. P. Tak, M. C. Lebre
Journal: Annals of the Rheumatic Diseases (2011)

<h3>Background</h3> Fms-like tyrosine kinase 3 ligand (Flt3L) is a potent endogenous growth factor for myeloid dendritic cells (mDC) and plasmacytoid dendritic cells (pDC). Its administration to mice and humans leads to dramatic increases of various DC subsets while Flt3L−/− mice show reduced DC numbers. Flt3L and its receptor (CD135) have been poorly studied in the setting of autoimmune diseases in general. Typically, CD135 is expressed on early myeloid and lymphoid progenitors and is activated by its soluble ligand, Flt3L. The highly differentiated cellular pattern in rheumatoid arthritis (RA) synovium made the authors hypothesise that Flt3L, with its ability to induce proliferation and differentiation, could be of importance in induction and/or progression of arthritis. <h3>Material and methods</h3> Patients with active RA, psoriatic arthritis (PsA), spondyloarthritis (SpA), osteoarthritis (OA), gout and healthy donors (HD) were included in this study. Soluble (s)Flt3L levels in synovial fluid (SF) and serum were determined by ELISA. Expression of membrane-bound (m)Flt3L and Flt3L receptor (CD135) in peripheral blood mononuclear cells (PBMC) and SFMC were assessed by FACS. In addition, immunohistochemical analysis of Flt3L and CD135 was performed in RA, PsA, gout, OA and HD synovial tissues. <h3>Results</h3> SF levels of Flt3L in RA (n=103), PsA (n=33), and SpA (n=32), OA (n=8) and gout (n=43) were significantly higher compared to paired serum. In addition, Flt3L levels were significantly higher in RA, PsA and SpA SFs compared to gout SF. In peripheral blood (PB) monocytes, B cells and mDC the expression of mFlt3L in RA was higher compared to HD. Flt3L receptor expression was confined to monocytes and mDC and higher in RA SF compared to PB. Immunohistochemistry and immunofluorescence data showed the presence of Flt3L and CD135 in RA ST. Interestingly, microarray data of RA synovial tissue showed that CD135 expression is increased in patients with high inflammatory gene profile compared to low inflammatory gene profile. There is no different in Flt3L expression between RA and OA confirming the ELISA data. In addition, anti-TNF therapy reduced Flt3L serum levels in RA patients. <h3>Conclusion</h3> The data presented in this study point to inflammatory role for Flt3L/CD135 system. Moreover, as the Flt3L/CD135 system is implicated in the generation of DC and B cells, inflammatory cells important in RA pathogenesis, this system might be of importance in RA. Achieving a detailed understanding of Flt3L function(s) in arthritis may lead to the development of novel immunotherapies for RA and other immune-mediated inflammatory diseases.
Aldosterone increases T-type calcium channel expression and in vitro beating frequency in neonatal rat cardiomyocytes
Authors: N LALEVEE, M REBSAMEN, S BARRERELEMAIRE, E PERRIER, J NARGEOT, J BENITAH, M ROSSIER
Journal: Cardiovascular Research (2005)

Journal Article Aldosterone increases T-type calcium channel expression and in vitro beating frequency in neonatal rat cardiomyocytes Get access Nathalie Lalevé, Nathalie Lalevé aDivision of Endocrinology and Diabetology, Department of Internal Medicine, University Hospital, CH-1211 Geneva 14, Switzerland Search for other works by this author on: Oxford Academic PubMed Google Scholar Michela C. Rebsamen, Michela C. Rebsamen aDivision of Endocrinology and Diabetology, Department of Internal Medicine, University Hospital, CH-1211 Geneva 14, SwitzerlandbLaboratory of Clinical Chemistry, Department of Clinical Pathology, University Hospital, CH-1211 Geneva 14, Switzerland Search for other works by this author on: Oxford Academic PubMed Google Scholar Stéphanie Barrère-Lemaire, Stéphanie Barrère-Lemaire dIGF, CNRS UMR 5203, IGH, Montpellier, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Emeline Perrier, Emeline Perrier aDivision of Endocrinology and Diabetology, Department of Internal Medicine, University Hospital, CH-1211 Geneva 14, SwitzerlandcINSERM U-637, Lab. Cardiovascular Physiopathology, CHU Arnaud de Villeneuve, Montpellier, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Joël Nargeot, Joël Nargeot dIGF, CNRS UMR 5203, IGH, Montpellier, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Jean-Pierre Bénitah, Jean-Pierre Bénitah cINSERM U-637, Lab. Cardiovascular Physiopathology, CHU Arnaud de Villeneuve, Montpellier, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Michel F. Rossier Michel F. Rossier * aDivision of Endocrinology and Diabetology, Department of Internal Medicine, University Hospital, CH-1211 Geneva 14, SwitzerlandbLaboratory of Clinical Chemistry, Department of Clinical Pathology, University Hospital, CH-1211 Geneva 14, Switzerland *Corresponding author. Division of Endocrinology and Diabetology, University Hospital, 24 rue Micheli-du-Crest, CH-1211 Geneva 14, Switzerland. Tel.: +41 22 3729320; fax: +41 22 3729329. Email address: [email protected] Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 67, Issue 2, August 2005, Pages 216–224, https://doi.org/10.1016/j.cardiores.2005.05.009 Published: 01 August 2005 Article history Received: 07 April 2005 Revision received: 06 May 2005 Accepted: 12 May 2005 Published: 01 August 2005
Restenosis after percutaneous transluminal coronary angioplasty: Pathologic observations in 20 patients
Authors: Masakiyo Nobuyoshi, Takeshi Kimura, Hiroto Ohishi, Hisanori Horiuchi, Hideyuki Nosaka, Naoya Hamasaki, Hiroatsu Yokoi, Koutaku Kim
Journal: Journal of the American College of Cardiology (1991)
Intrahepatic expression of HBcAg in chronic HBV hepatitis: Lessons from molecular biology
Authors: Chia-Ming Chu, Yun-Fan Liaw
Journal: Hepatology (1990)

The precore and core proteins of hepatitis B virus have identical deduced amino acid sequences other than a 29-residue amino-terminal extension (precore region) on the precore protein. The first 19 of these residues serve as a signal sequence to direct the precore protein to the endoplasmic reticulum, where they are cleaved off with formation of precore protein derivative P22 for secretion. In this report, we show that P22 can alternatively be transported into the nucleus following signal peptide cleavage. Experiments with deletion mutants indicated that this nuclear transport proceeds via the cytosol and is dependent on the amino-terminal portion of P22. Thus, the hepatitis B virus precore protein is a secreted, cytosolic, and nuclear protein.
Infarct-sparing effect of myocardial postconditioning is dependent on protein kinase C signalling
Authors: A ZATTA, H KIN, G LEE, N WANG, R JIANG, R LUST, J REEVES, J MYKYTENKO, R GUYTON, Z ZHAO
Journal: Cardiovascular Research (2006)

Using non-selective and selective protein kinase C (PKC) epsilon and delta isoform inhibitors, we tested the hypothesis that the cardioprotective phenotype invoked by postconditioning (postcon) is dependent on PKC signalling. Furthermore, we determined whether postconditioning alters pPKCepsilon and/or pPKCdelta in cytosolic and mitochondrial fractions.Male Sprague-Dawley rats underwent 30 min left coronary artery (LCA) occlusion followed by 3 h of reperfusion. Rats were randomised to the following groups: Untreated, no intervention either before or after LCA occlusion; Postcon, 3 cycles of 10-s full reperfusion and 10-s re-occlusion, initiated immediately at the onset of reperfusion; Chelerythrine (non-selective PKC inhibitor, 5 mg/kg)+/-postcon; Rottlerin (PKCdelta inhibitor, 0.3 mg/kg)+/-postcon; KIE1-1 (PKCepsilon inhibitor, 3.8 mg/kg)+/-postcon. A subset of rats was employed to assess pPKCepsilon and/or pPKCdelta in sham, Isch/RP (30-min LCA occlusion followed by 30-min reperfusion), and postcon-treated hearts.Infarct size, expressed as area of necrosis as a percentage of the area at risk, AN/AAR (%), was significantly reduced by postcon compared to control (untreated) rats (39+/-2% vs. 53+/-1% in control, P<0.001). Treatment with chelerythrine alone or the PKCepsilon antagonist KIE1-1 alone at reperfusion had no effect on infarct size compared to control. In contrast, the infarct-sparing effect of postcon was abrogated by non-selective PKC inhibition and PKCepsilon antagonism (50+/-2% and 50+/-1%, respectively, P<0.002). Inhibition of PKCdelta reduced infarct size to values comparable to that in postcon group (36+/-3% vs. 39+/-2%). However, postcon in the presence of PKCdelta inhibitor did not enhance the infarct-sparing effects (38+/-2%). In addition, pPKCepsilon in postcon hearts was significantly higher in the total cell homogenate (10338+/-1627 vs. 4165+/-608 in Isch/RP, arbitrary units), and pPKCdelta translocation to mitochondria was significantly less (>2-fold decrease) compared to Isch/RP.These data suggest that postcon modulates PKC during early reperfusion by increasing PKCepsilon expression and translocation to a site other than the outer mitochondrial membrane, and limits translocation of PKCdelta to mitochondria and associated deleterious signalling.
Utility of specific locus systems in higher plants to monitor for mutagens.
Authors: M J Constantin
Journal: Environmental Health Perspectives (1978)

Plants possess biological and operational attributes that have encouraged geneticists to use them extensively in the development of fundamental genetic concepts. Attributes such as regenerative plasticity, high fecundity, cultural adaptability, range of ploidy, economics of culture and maintenance of specific populations, and versatility make plant genetic systems prime candidates with which to monitor the environment for mutagens. A specific locus (equivalent to a classical Mendelian gene) controls the development of a phenotypic characteristic. It can also mutate to a new allelic form with a consequentially altered phenotypic characteristic and can be separated by crossing over from adjacent loci that govern other specific phenotypic characteristics. Since various plant species have numerous specific loci, one has a rich array of potential systems from which to select. Specific locus systems in higher plants could be used to assess the mutagenicity of single chemical compounds or combinations of chemical compounds. Depending on the circumstances, seeds and/or seedlings could be used; plants could be grown in situ in either containers or plots to assess the immediate environment for one or more mutagens over an extended period. Since plants are eucaryotes, data from such experiments could serve as one more source of information along with that obtained from a battery of other tests used in the tier system.
Subsidies for malaria treatment could save 25,000 lives a month
Authors: Janice Tanne
Journal: BMJ (2006)

Subsidies for combination treatments in countries where malaria is endemic are urgently needed to forestall drug resistance and save lives, warns a paper published this week.

A subsidy of only $100m (£57m; €83m) to $200m for artemisinin based combination drugs might be needed, said Ramanan Laxminarayan, from Resources for the Future, a non-profit, independent organisation based in Washington, DC, and the paper's lead author.

He said that if such a subsidy programme was implemented within three months, up to 25 000 lives a month could be saved ( Health Affairs 2006;25:325-36).

Dr Laxminarayan, whose …
Acquired estrogen independence and antiestrogen resistance in breast cancer
Authors: Robert Clarke, Nils Brunner
Journal: Trends in Endocrinology and Metabolism (1996)

Endocrine-responsive breast tumors appear to follow a predictable pattern of progression from estrogen dependence to estrogen independence, ultimately leading to a phenotype characterized by crossresistance among all endocrine therapies. Cells acquiring a multihormone-resistant phenotype, however, frequently retain expression of the cellular receptors for estrogen (ER) and progesterone (PgR). The proliferation of some of these tumors may be driven by a ligand-independent activation of the remaining steroid hormone receptors. Several intracellular secondary messenger systems can potentially activate ER through altering its pattern of phosphorylation in the absence of estrogens. Emerging evidence suggests that, for many estrogen-regulated genes, both the promoter and cellular contexts are critical factors in regulating their transcription by ER. The cellular context may be important because of the presence/absence of several coregulators of ER function, and this context may be unstable in tumor and some normal cell populations. Thus, the pattern of genes regulated by the transcriptional activities of the ER also may change with time, facilitating the emergence of divergent endocrine-responsive phenotypes. It is this pattern of regulation that may be important for conferring each specific phenotype. The repression or induction of the functionally relevant genes responsible for conferring each of the phenotypic changes represents an estrogen-regulated gene network. These networks will contain genes that are regulated, both directly and indirectly, by the activation of ER. Several growth-regulatory gene networks may exist concurrently, providing a cell with several interrelated pathways for controlling its proliferation. The identity of those estrogen-regulated genes that are responsible, for regulating proliferation remains unknown.
Abstract PL3-2: Translating multiple myeloma stem cells
Authors: William Matsui
Journal: Clinical Cancer Research (2010)

Abstract Emerging evidence suggest that many human cancers consist of phenotypically and functionally heterogeneous cell types. Moreover, the capacity for clonogenic growth and self-renewal may be restricted to specific cell populations. In multiple myeloma, malignant plasma cells make up the vast majority of tumor cells and are responsible for symptoms arising within the disease. However, myeloma plasma cells also appear to be terminally differentiated like their normal counterparts and incapable of long-term proliferation. Similar to other laboratories, we have identified minor populations of B cells that share the identical immunoglobulin gene rearrangements as the malignant plasma cells in most myeloma patients. We have further studied the functional capacity of these clonotypic B cells and found that they have ability to produce ectopic tumor growth both in vitro and in immunodeficient mice in which they recapitulate human disease. Moreover, these cells are relatively resistant to several agents currently used to treat multiple myeloma suggesting that they persist following treatment and are responsible for tumor regrowth and disease relapse. In order to inhibit these drug resistant cancer stem cells, we have studied cellular pathways that regulate the self-renewal of normal adult stem cells and found that several, including the developmental pathway Hedgehog, are potential therapeutic targets. Lastly, we have begun to develop biomarker strategies to serially quantify myeloma stem cells in patients undergoing treatment. We hope that these will serve as useful endpoints as myeloma stem cell directed therapies enter the clinic. Citation Information: Clin Cancer Res 2010;16(7 Suppl):PL3-2
&lt;emph type="ital"&gt;Lilacs With Cup of Milk&lt;/emph&gt;
Authors: Janet M. Torpy
Journal: JAMA (2011)

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
DERMABRASION: AN APPRAISAL.
Authors: J. S. PEGUM, C. M. RIDLEY, BRIAN RUSSELL, N. A. THORNE, S. L. MORRISON
Journal: British Journal of Dermatology (1959)

Journal Article DERMABRASION: AN APPRAISAL. Get access J. S. PEGUM, M.A., M.D. Cantab., M.R.C.P., J. S. PEGUM, M.A., M.D. Cantab., M.R.C.P. Skin Department, The London Hospital Search for other works by this author on: Oxford Academic Google Scholar C. M. RIDLEY, M.A., B.M. Oxon., M.R.C.P., C. M. RIDLEY, M.A., B.M. Oxon., M.R.C.P. Skin Department, The London Hospital Search for other works by this author on: Oxford Academic Google Scholar BRIAN RUSSELL, M.D. Lond., F.R.C.P., D.P.H., BRIAN RUSSELL, M.D. Lond., F.R.C.P., D.P.H. Skin Department, The London Hospital Search for other works by this author on: Oxford Academic Google Scholar N. A. THORNE, M.D. Lond., M.R.C.P., N. A. THORNE, M.D. Lond., M.R.C.P. Skin Department, The London Hospital Search for other works by this author on: Oxford Academic Google Scholar S. L. MORRISON, M.B. St. And., D.P.H. S. L. MORRISON, M.B. St. And., D.P.H. Social Medicine Research Unit of the Medical Research Council, The London Hospital Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 71, Issue 11, 1 November 1959, Pages 371–378, https://doi.org/10.1111/j.1365-2133.1959.tb13366.x Published: 01 November 1959
Severe Lactic Acidosis in an Amnesic Child
Authors: Jonathan Lillie, Finn Coulter, Anusha Ganeshalingham
Journal: JAMA (2014)

An 8-year-old boy presented to the emergency department after he was found unconscious outside his church on a rainy day. He had been seen by his mother 1 hour earlier and was previously fit and well and up to date with immunizations.
Protection against Renal Ischemia Reperfusion Injury by CD44 Disruption
Authors: Kasper M. A. Rouschop, Joris J.T.H. Roelofs, Nike Claessen, Paula da Costa Martins, Jaap-Jan Zwaginga, Steven T. Pals, Jan J. Weening, Sandrine Florquin
Journal: Journal of the American Society of Nephrology (2005)

Inflammation contributes to renal ischemia reperfusion (I/R) injury, potentially causing renal dysfunction. The inflammatory infiltrate mainly consists of neutrophils, which are deleterious for the renal tissue. Because CD44 is expressed by neutrophils and is rapidly upregulated by capillary endothelial cells after I/R injury, it was hypothesized that CD44 might play an important role in the development of I/R injury. This study showed that rapid CD44 upregulation on renal capillary endothelial cells mediates neutrophil recruitment to the postischemic tissue. Hence, CD44 deficiency led to decreased influx of neutrophils regardless of comparable levels in chemotactic factors expressed in the kidney. The reduced influx of neutrophils was associated with preserved renal function and morphology. Adoptive transfer experiments of labeled neutrophils revealed that endothelial CD44 rather than neutrophil CD44 mediates neutrophil migration. Activation of neutrophils increased cell-surface expression of hyaluronic acid (HA). Altogether, a novel mechanism in the recruitment of neutrophils that involves interaction of endothelial CD44 and neutrophil HA was found. Either blocking endothelial CD44 or removal of neutrophil HA decreased rolling and adhesion of neutrophils. Administration of anti-CD44 to mice reduced the influx of neutrophils into the postischemic tissue, associated with renal function preservation. Therefore, anti-CD44-based therapies may contribute to prevent or reduce renal I/R injury.