tbuckley/cabot-search huggingface dataset:
More than half a million people could lose incapacity benefit after welfare changes
Authors: A. O'Dowd
Journal: BMJ (2011)

Around 600 000 people in Britain are set to lose their incapacity benefit and all other benefits because of welfare changes, despite the fact that they have health or disability needs that restrict their ability to work, says a report.

Academics from Sheffield Hallam University’s Centre for Regional Economic and Social Research Centre have calculated that by 2014 there will be nearly one million fewer people on incapacity benefit. At the moment 2.6 million people receive the benefit. Some of the people who receive incapacity benefit will stop doing so because they have reached state pension age, or have died, and some will have returned to work or moved on to other benefits. But 600 000 people will lose out. …
Allelic variations in the human T cell receptor V beta 6.7 gene products.
Authors: Y Li, P Szabo, M A Robinson, B Dong, D N Posnett
Journal: The Journal of Experimental Medicine (1990)

Polymorphisms of human TCR gene products have been suggested by the description of a mAb, OT145, that identifies a subset of TCRs in some individuals but not in others (6). Here we demonstrate that this mAb detects a TCR allotype of the V beta 6.7 gene. Two allelic products of this V gene differ by two nonconservative amino acid substitutions. The mAb OT145 appears to react with V beta 6.7 a gene products ("+" allele), but not with V beta 6.7b gene products ("-" allele). This represents the first direct demonstration that TCR V gene allotypes exist and provides a possible explanation for immune responses under the control of TCR V genes and for disease associations with TCR V genes.
Synchronous superficial spreading lesions of the stomach
Authors: Tsutomu Namikawa, Michiya Kobayashi, Kazuhiro Hanazaki
Journal: Gut (2014)

Coronary artery disease (CAD) causes significant morbidity and mortality. Accurate noninvasive evaluation is important to facilitate appropriate diagnosis and treatment. The ubiquitous nature of CAD requires all practitioners, regardless of their specialty, to be familiar with noninvasive diagnostic modalities. This article reviews currently available tests, including specific features, diagnostic and prognostic value, strengths, and limitations.
OPTIMAL GRADING OF STENOSIS SEVERITY ON CORONARY COMPUTED TOMOGRAPHIC ANGIOGRAPHY IN PATIENTS WITH SUSPECTED CORONARY ARTERY DISEASE
Authors: Hee Tae Yu, Hyuk-Jae Chang, Young Jin Kim, Byung Wook Choi, Donghoon Choi, Namsik Chung
Journal: Journal of the American College of Cardiology (2011)
A prospective randomised multi-centre controlled trial on tight glucose control by intensive insulin therapy in adult intensive care units: the Glucontrol study
Authors: Jean-Charles Preiser, Philippe Devos, Sergio Ruiz-Santana, Christian Mélot, Djillali Annane, Johan Groeneveld, Gaetano Iapichino, Xavier Leverve, Gérard Nitenberg, Pierre Singer, Jan Wernerman, Michael Joannidis, Adela Stecher, René Chioléro
Journal: Intensive Care Medicine (2009)
Functional Myc-Max heterodimer is required for activation-induced apoptosis in T cell hybridomas.
Authors: R P Bissonnette, A McGahon, A Mahboubi, D R Green
Journal: The Journal of Experimental Medicine (1994)

T cell hybridomas respond to activation signals by undergoing apoptotic cell death, and this is likely to represent comparable events related to tolerance induction in immature and mature T cells in vivo. Previous studies using antisense oligonucleotides implicated the c-Myc protein in the phenomenon of activation-induced apoptosis. This role for c-Myc in apoptosis is now confirmed in studies using a dominant negative form of its heterodimeric binding partner, Max, which we show here inhibits activation-induced apoptosis. Further, coexpression of a reciprocally mutant Myc protein capable of forming functional heterodimers with the mutant Max can compensate for the dominant negative activity and restore activation-induced apoptosis. These results imply that Myc promotes activation-induced apoptosis by obligatory heterodimerization with Max, and therefore, by regulating gene transcription.
Response to Letter Regarding Article, “Residential Exposure to Traffic Is Associated With Coronary Atherosclerosis”
Authors: Barbara Hoffmann, Susanne Moebus, Nils Lehmann, Karl-Heinz Jöckel, Stefan Möhlenkamp, Axel Schmermund, Raimund Erbel, Andreas Stang, Nico Dragano, Michael Memmesheimer, Klaus Mann
Journal: Circulation (2008)
Effects of ciclesonide and fluticasone on cortisol secretion in patients with persistent asthma
Authors: E. Derom, R. Louis, C. Tiesler, R. Engelstätter, J-M. Kaufman, G. F. Joos
Journal: European Respiratory Journal (2009)

We compared the systemic and clinical effects of ciclesonide (CIC) and fluticasone propionate (FP) administered, in addition to CIC 160 µg·day −1 and salmeterol 50 µg twice daily, in 32 patients with persistent asthma using a randomised double-blind, placebo-controlled, double-dummy, five-period crossover design. All patients exhibited a provocative concentration leading to a 20% decrease in forced expiratory volume in 1 s (PC 20 ) methacholine &lt;8 mg·mL −1 and a PC 20 adenosine &lt;60 mg·mL −1 . Primary outcome was 24-h serum cortisol suppression after 7 days. Secondary outcomes were changes in PC 20 methacholine and adenosine after 9 days. FP 500 µg·day −1 and 1,000 µg·day −1 significantly suppressed cortisol secretion versus placebo by -46.2 (95% confidence interval (CI) -83.8– -8.5) nmol·L −1 and by -76.1 (95% CI -112.9– -39.3) nmol·L −1 , respectively. Neither dose of CIC (320 nor 640 µg·day −1 ) had a significant suppressive effect (-28.2 (95% CI -65.5–9.2) nmol·L −1 and -37.3 (95% CI -74.7–0.0) nmol·L −1 , respectively). Differences between FP 1,000 µg·day −1 and both CIC treatments were statistically significant (CIC 320 µg·day −1 : -48.0 (95% CI -84.8– -11.1) nmol·L −1 ; CIC 640 µg·day −1 : -38.8 (95% CI -75.7– -1.9) nmol·L −1 ). Compared with placebo, the increase in PC 20 adenosine after the four treatments was small, but significant. Greater improvements in PC 20 adenosine were seen with FP 500 µg·day −1 (1.8 (95% CI 1.0–2.6) doubling concentrations) compared with CIC 320 μg·day −1 (0.9 (95% CI 0.1–1.7) doubling concentrations). No significant difference was seen between CIC 640 μg·day −1 and FP 1,000 μg·day −1 . For a similar decrease in hyperresponsiveness, cortisol secretion was suppressed significantly with moderate-to-high doses of fluticasone propionate, but not with ciclesonide.
Coronary Vessel Development Is Dependent on the Type III Transforming Growth Factor β Receptor
Authors: Leigh A. Compton, Dru A. Potash, Christopher B. Brown, Joey V. Barnett
Journal: Circulation Research (2007)

Transforming growth factor (TGF)beta receptor III (TGFbetaR3), or beta-glycan, binds all 3 TGFbeta ligands and inhibin with high affinity but lacks the serine/threonine kinase domain found in the type I and type II receptors (TGFbetaR1, TGFbetaR2). TGFbetaR3 facilitates signaling via TGFbetaR1/TGFbetaR2 but also has been suggested to play a unique and nonredundant role in TGFbeta signaling. Targeted deletion of Tgfbr3 revealed a requirement for Tgfbr3 during development of the coronary vessels. Coronary vasculogenesis is significantly impaired in null mice, with few vessels evident and numerous, persistent blood islands found throughout the epicardium. Tgfbr3-null mice die at embryonic day 14.5, the time when functional coronary vasculature is required for embryo viability. However, in null mice nascent coronary vessels attach to the aorta, form 2 coronary ostia, and initiate smooth muscle recruitment by embryonic day 14. Analysis of earlier developmental stages revealed defects in the epicardium. At embryonic day 13.5, these defects include an irregular and hypercellular epicardium with abundant subepicardial mesenchyme and a thin compact zone myocardium. Tgfbr3-null mice also displayed other defects in coronary development, including dysmorphic and distended vessels along the atrioventricular groove and subepicardial hemorrhage. In null mice, vessels throughout the yolk sac and embryo form and recruit smooth muscle in a pattern indistinguishable from heterozygous or wild-type littermates. These data demonstrate a requirement for Tgfbr3 during coronary vessel development that is essential for embryonic viability.
Ki67 Measured after Neoadjuvant Chemotherapy for Primary Breast Cancer
Authors: Gunter von Minckwitz, Wolfgang D. Schmitt, Sibylle Loibl, Berit M. Müller, Jens U. Blohmer, Bruno V. Sinn, Holger Eidtmann, Wolfgang Eiermann, Bernd Gerber, Hans Tesch, Jörn Hilfrich, Jens Huober, Tanja Fehm, Jana Barinoff, Thomas Rüdiger, Erhard Erbstoesser, Peter A. Fasching, Thomas Karn, Volkmar Müller, Christian Jackisch, Carsten Denkert
Journal: Clinical Cancer Research (2013)

Abstract Purpose: The value of Ki67 measured on residual disease after neoadjuvant chemotherapy is not sufficiently described. Experimental Design: Participants of the GeparTrio study with primary breast cancer randomly received neoadjuvant response-guided [8 cycles TAC (docetaxel/doxorubicin/cyclophosphamide) in responding and TAC-NX (vinorelbine/capecitabine) in nonresponding patients] or conventional (6 cycles TAC) chemotherapy according to interim response assessment. Ki-67 levels were centrally measured immunohistochemically after neoadjuvant treatment if tumor tissue was available. Here, we analyze 1,151 patients having a pathologic complete response (pCR; n, 484), or residual disease with low (0–15%), intermediate (15.1–35%), or high (35.1–100%) posttreatment Ki67 levels in 488, 77, and 102 patients, respectively. Results: Patients with high posttreatment Ki67 levels showed higher risk for disease relapse (P &amp;lt; 0.0001) and death (P &amp;lt; 0.0001) compared with patients with low or intermediate Ki67 levels. Patients with low Ki67 levels showed a comparable outcome to patients with a pCR (P = 0.211 for disease-free and P = 0.779 for overall survival). Posttreatment Ki67 levels provided more prognostic information than pretreatment Ki67 levels or changes of Ki67 from pre- to posttreatment. Information on pCR plus posttreatment Ki67 levels surmount the prognostic information of pCR alone in hormone–receptor-positive disease [hazard ratios (HR), 1.82–5.88] but not in hormone–receptor-negative disease (HR: 0.61–1.73). Patients with conventional and response-guided treatment did not show a different distribution of posttreatment Ki67 (P = 0.965). Conclusions: Posttreatment Ki67 levels provide prognostic information for patients with hormone–receptor-positive breast cancer and residual disease after neoadjuvant chemotherapy. Levels were not prognostic for outcome after response-guided chemotherapy. High posttreatment Ki67 indicates the need for innovative postneoadjuvant treatments. Clin Cancer Res; 19(16); 4521–31. ©2013 AACR.
Early growth response 1 is an early signal inducing Cav3.2 T-type calcium channels during cardiac hypertrophy
Authors: Shao-Chun Hsu, Ya-Ting Chang, Chien-Chang Chen
Journal: Cardiovascular Research (2013)

The Cav3.2 T-channel plays a pivotal role in inducing calcineurin/nuclear factor of activated T cell (NFAT) signalling during cardiac hypertrophy. Because calcineurin/NFAT signalling is induced early after pressure overload, we hypothesized that Cav3.2 is induced by an early signal. Our aim is to investigate when and how Cav3.2 is induced during cardiac hypertrophy.The evolutionary conserved promoter Cav3.2-3500 from mouse genome was validated to express the reporter gene as endogenous Cav3.2 in cell lines and transgenic (Tg; Cav3.2-3500-Luc) mice. The early induction of luciferase in Tg mice and Cav3.2 mRNA in wild-type mice after transverse aortic banding (TAB) surgery supported our hypothesis that Cav3.2 is induced early during cardiac hypertrophy. The TAB-responding element [-81 to -41 bp upstream of the transcription start site (TSS) of mouse Cav3.2] was identified by in vivo gene transfer by injecting reporter constructs into the left ventricle followed by TAB surgery. Electrophoresis mobility shift assay and chromatin immunoprecipitation assays revealed that Egr1 bound to the TAB-responding element of Cav3.2. Egr1 level was increased with increased Cav3.2 mRNA level at 3 days after TAB. To demonstrate that Egr1 indeed regulates Cav3.2 expression after hypertrophic stimulation, knockdown of Egr1 with short hairpin RNA prevented the phenylephrine-induced up-regulation of Cav3.2 expression and cellular hypertrophy in neonatal rat ventricular myocytes (NRVMs) and H9c2 cells. Furthermore, overexpression of Cav3.2 in Egr1-knockdown cells restored the phenylephrine-induced hypertrophy.Cav3.2 is induced early by Egr1 during cardiac hypertrophy and Cav3.2 is an important mediator of Egr1 in regulating cardiac hypertrophy.
Bridging osteophyte of the anterosuperior sacroiliac joint as a cause of lumbar back pain
Authors: K A Parmar, M Solomon, A Loefler, S Dalton
Journal: British Journal of Sports Medicine (2004)

A case report is presented of a patient with an anterosuperior osteophytic bone bridge of the sacroiliac joint causing lumbar back pain. After prolonged physiotherapy, the bone bridge was excised, with complete resolution of the symptoms. Excision should only be considered in cases of symptomatic sacroiliac joint pain that does not respond to rehabilitation programmes and conservative treatment.
Nuts as a Replacement for Carbohydrates in the Diabetic Diet
Authors: David J.A. Jenkins, Cyril W.C. Kendall, Monica S. Banach, Korbua Srichaikul, Edward Vidgen, Sandy Mitchell, Tina Parker, Stephanie Nishi, Balachandran Bashyam, Russell de Souza, Christopher Ireland, Robert G. Josse
Journal: Diabetes Care (2011)

OBJECTIVE Fat intake, especially monounsaturated fatty acid (MUFA), has been liberalized in diabetic diets to preserve HDL cholesterol and improve glycemic control, yet the exact sources have not been clearly defined. Therefore, we assessed the effect of mixed nut consumption as a source of vegetable fat on serum lipids and HbA1c in type 2 diabetes. RESEARCH DESIGN AND METHODS A total of 117 type 2 diabetic subjects were randomized to one of three treatments for 3 months. Supplements were provided at 475 kcal per 2,000-kcal diet as mixed nuts (75 g/day), muffins, or half portions of both. The primary outcome was change in HbA1c. RESULTS The relative increase in MUFAs was 8.7% energy on the full-nut dose compared with muffins. Using an intention-to-treat analysis (n = 117), full-nut dose (mean intake 73 g/day) reduced HbA1c (−0.21% absolute HbA1c units, 95% CI −0.30 to −0.11, P &amp;lt; 0.001) with no change after half-nut dose or muffin. Full-nut dose was significantly different from half-nut dose (P = 0.004) and muffin (P = 0.001), but no difference was seen between half-nut dose and muffins. LDL cholesterol also decreased significantly after full-nut dose compared with muffin. The LDL cholesterol reduction after half-nut dose was intermediate and not significantly different from the other treatments. Apolipoprotein (apo) B and the apoB:apoA1 ratio behaved similarly. Nut intake related negatively to changes in HbA1c (r = −0.20, P = 0.033) and LDL cholesterol (r = −0.24, P = 0.011). CONCLUSIONS Two ounces of nuts daily as a replacement for carbohydrate foods improved both glycemic control and serum lipids in type 2 diabetes.
An Outbreak of Severe Acute Respiratory Syndrome among Hospital Workers in a Community Hospital in Hong Kong
Authors: Alice S. Ho, Joseph J.Y. Sung, Moira Chan-Yeung
Journal: Annals of Internal Medicine (2003)

During outbreaks, hospital workers are at high risk for nosocomial infection with severe acute respiratory syndrome (SARS)-associated coronavirus.To examine how hospital workers became infected and whether they transmit the virus to their families.Retrospective descriptive study.529-bed community hospital in Hong Kong.40 hospital workers infected with SARS-associated coronavirus over a 6-week period (25 March through 5 May 2003).Percentage of infected hospital workers according to job category.The cumulative incidence was highest among health care assistants, followed by physicians and nurses (8%, 5%, and 4%, respectively). Most hospital workers were infected from direct contact with patients with SARS, who primarily were in general wards and had unsuspected infection. At the time of contact, all hospital workers had used masks but not necessarily other protective devices. Affected hospital workers did not infect their families.Before isolation of all patients with clinically confirmed or suspected SARS, routine use of several protective devices, and training of staff in infection control, many health care workers were infected with SARS from patients with unsuspected cases.
The EGF/CSF-1 Paracrine Invasion Loop Can Be Triggered by Heregulin β1 and CXCL12
Authors: Lorena Hernandez, Tatiana Smirnova, Dmitriy Kedrin, Jeffrey Wyckoff, Liyin Zhu, E. Richard Stanley, Dianne Cox, William J. Muller, Jeffrey W. Pollard, Nico Van Rooijen, Jeffrey E. Segall
Journal: Cancer Research (2009)

Abstract An important step in the process of metastasis from the primary tumor is invasive spread into the surrounding stroma. Using an in vivo invasion assay, we have previously shown that imposed gradients of epidermal growth factor (EGF) or colony-stimulating factor-1 (CSF-1) can induce invasion through an EGF/CSF-1 paracrine loop between cancer cells and macrophages. We now report that invasion induced by other ligands also relies on this EGF/CSF-1 paracrine invasive loop. Using an in vivo invasion assay, we show that MTLn3 breast cancer cells overexpressing ErbB3 exhibit enhanced invasion compared with control MTLn3 cells in response to the ErbB3 ligand HRG-β1. The invasive response of both MTLn3-ErbB3 and transgenic MMTV-Neu tumors to HRG-β1 is inhibited by blocking EGF receptor, CSF-1 receptor, or macrophage function, indicating that invasiveness to HRG-β1 is dependent on the EGF/CSF-1 paracrine loop. Furthermore, we show that CXCL12 also triggers in vivo invasion of transgenic MMTV-PyMT tumors in an EGF/CSF-1–dependent manner. Although the invasion induced by HRG-β1 or CXCL12 is dependent on the EGF/CSF-1 paracrine loop, invasion induced by EGF is not dependent on HRG-β1 or CXCL12 signaling, showing an asymmetrical relationship between different ligand/receptor systems in driving invasion. Our results identify a stromal/tumor interaction that acts as an engine underlying invasion induced by multiple ligands. [Cancer Res 2009;69(7):3221–7]
Fairness Creams in South Asia—A Case of Disease Mongering?
Authors: P. Ravi Shankar, Bishnu Rath Giri, Subish Palaian
Journal: PLoS Medicine (2006)

I am a disease monger.I teach primary care doctors how to identify bipolar disorder.Worse yet, I take money from pharmaceutical companies for doing so.I use it to subsidize my practice so that I can treat patients with no insurance, or little money, who now account for over a third of my patients-in part because the pharmaceutical companies have drained so much money out of the health-care system.Ironic, isn't it?My Web site PsychEducation.org(http:⁄⁄www.psycheducation.org) is number one on Google for searches on "bipolar II."See if you think it looks like disease mongering.Hundreds of people have written thanking me for explaining bipolar II and the concept of a bipolar spectrum, indicating that this new perspective really helps them understand their long-standing symptoms.To my immediate recall, none have complained about being led astray by an overbroad interpretation of bipolarity.Notice that, just like Mr. Moynihan, one of the guest editors of your April 2006 series of articles on disease mongering [1], I could be mongering even now, as I too have a new book.At least I'm not trying to attract attendees to my conference.Tricky, isn't it.Has there been an oversimplifi cation in this analysis?(PsychEducation.org
Prediction of endurance running performance for middle-aged and older runners.
Authors: N Takeshima, K Tanaka
Journal: British Journal of Sports Medicine (1995)

The purpose of this study was to develop regression equations that would sufficiently predict the endurance running performance (ERP) of middle-aged and older runners (n = 55, 43-79 years). Among many independent variables which were selected as possible predictors of the ERP, oxygen uptake corresponding to the lactate threshold (VO2@LT), or age was found to be the single best predictor. Some variables representing training habits correlated significantly but only moderately with the ERP. Linear multiple regression equations developed in this study were: V5km = 4.203 + 0.054X1 - 0.028X2 (r = 0.87) V5km = 4.436 + 0.045X1 - 0.033X2 + 0.005X3 (r = 0.89) V10km = 4.252 + 0.042X1 - 0.026X2 (r = 0.79) V10km = 4.371 + 0.037X1 - 0.031X2 + 0.005X3 (r = 0.82) VM = 3.207 + 0.048X1 - 0.022X2 (r = 0.91) VM = 3.707 + 0.038X1 - 0.031X2 + 0.005X3 (r = 0.93) where V5km, V10km and VM are the mean running velocity at 5 km, 10 km and marathon races, respectively, and X1 = VO2@LT (ml kg-1 min-1), X2 = age (year), and X3 = average running duration per workout (min). We suggest that the ERP of middle-aged and older runners can be predicted from a linear combination of VO2@LT and age or a combination of these variables plus average running duration per workout.
The W620 Polymorphism in PTPN22 Disrupts Its Interaction With Peptidylarginine Deiminase Type 4 and Enhances Citrullination and NETosis
Authors: Hui‐Hsin Chang, Nishant Dwivedi, Anthony P. Nicholas, I‐Cheng Ho
Journal: Arthritis & Rheumatology (2015)

A C-to-T single-nucleotide polymorphism (SNP) located at position 1858 of human protein tyrosine phosphatase PTPN22 complementary DNA carries the highest risk of rheumatoid arthritis (RA) among all non-HLA genetic variants. This C1858T SNP converts an arginine (R620) to a tryptophan (W620), but it is unclear why it has such a strong impact on RA, a disease characterized by anti-citrullinated protein antibodies. The aim of this study was to test the hypothesis that PTPN22 regulates protein citrullination.The level of citrullinated proteins in immune cells was quantified by Western blotting. The physical interaction between PTPN22 and peptidyl arginine deiminase type 4 (PAD-4), which is one of the enzymes that catalyzes protein citrullination, was examined by coimmunoprecipitation. Neutrophils were collected from healthy donors carrying the C1858T SNP and healthy donors not carrying this SNP. The formation of neutrophil extracellular traps (NETs) was examined by immunocytochemistry.PTPN22 physically interacted with PAD-4, and a deficiency in PTPN22 enhanced protein citrullination. This abnormality was reversed by exogenous wild-type PTPN22 or catalytically dead mutant PTPN22. The R-to-W conversion rendered PTPN22 unable to interact with PAD-4 and suppress citrullination. The C1858T SNP was associated with hypercitrullination in peripheral blood mononuclear cells and a heightened propensity for spontaneous formation of NETs, which is a PAD-4-dependent process.PTPN22 is an inhibitor of PAD-4 and protein citrullination. This function of PTPN22 is independent of its phosphatase activity but requires R620. Our data not only establish a molecular link between PTPN22 and PAD-4, but also suggest that the C1858T SNP increases the risk of RA by enhancing protein citrullination and spontaneous formation of NETs.