tbuckley/cabot-search huggingface dataset:
Lispro Mix25 insulin as premeal therapy in type 2 diabetic patients.
Authors: V A Koivisto, J A Tuominen, P Ebeling
Journal: Diabetes Care (1999)

OBJECTIVE: Insulin Mix25 is a new premixed insulin analog containing 25% insulin lispro and 75% neutral protamine lispro (NPL) suspension (NPL insulin). The aim of the study was to compare serum glucose and insulin responses after breakfast in type 2 diabetic patients who received Mix25, premixed regular/NPH (30%/70%), or NPH insulin before the meal. RESEARCH DESIGN AND METHODS: We studied 22 type 2 diabetic patients of age 62 +/- 1 years, BMI 30 +/- 1 kg/m2, duration of diabetes 15 +/- 2 years, duration of insulin therapy 6 +/- 1 years, insulin dose 65 +/- 6 U/day, and HbA1c 7.9 +/- 0.2%. Ten healthy individuals (age 56 +/- 1 years, BMI 28 +/- 1 kg/m2) served as control subjects. Each patient (except healthy subjects, who were studied once each) was studied three times in a double-blind, randomized fashion. After an overnight fast, the patients received 36 +/- 4 U of test insulin. Ten minutes after insulin injection, the patients ingested a breakfast meal (512 kcal, 60% carbohydrate, 20% fat, and 20% protein), identical in all studies. Blood samples were taken before and at 10- to 30-min intervals for 240 min after the breakfast meal. RESULTS: The peak rise in serum glucose was lower after Mix25 (76 +/- 7 mg/dl) than after 30/70 (94 +/- 5 mg/dl, P &amp;lt; 0.05) or NPH (113 +/- 4 mg/dl, P &amp;lt; 0.005) insulin. The incremental area under the serum glucose curve was 36% smaller after Mix25 than after 30/70 (P &amp;lt; 0.01) and 56% smaller than after NPH (P &amp;lt; 0.005) insulin. The peak rise in serum insulin concentration was higher after Mix25 (103 +/- 18 mU/l) than after 30/70 (87 +/- 13 mU/l, P &amp;lt; 0.05) or NPH (62 +/- 12 mU/l, P &amp;lt; 0.01) insulin. The incremental area under the serum insulin curve was higher after Mix25 than after 30/70 during the first 2-3 h (P &amp;lt; 0.02), but the difference disappeared by the end of the 4-h follow-up period. After Mix25 injection, there was an inverse correlation between the glucose response to a meal and insulin dose (r = -0.56, P &amp;lt; 0.01) or the incremental area under the serum insulin curve (r = -0.39, P &amp;lt; 0.05). No such correlations were observed with the other insulins. CONCLUSIONS: Because of its faster initial absorption rate, the new premixed insulin analog Mix25 reduces blood glucose response to a breakfast meal in type 2 diabetic patients compared with premixed 30/70 (regular/NPH) or NPH insulin.
Universal health coverage in Turkey: enhancement of equity
Authors: Rifat Atun, Sabahattin Aydın, Sarbani Chakraborty, Safir Sümer, Meltem Aran, Ipek Gürol, Serpil Nazlıoğlu, Şenay Özgülcü, Ülger Aydoğan, Banu Ayar, Uğur Dilmen, Recep Akdağ
Journal: The Lancet (2013)
Better survival after lung cancer surgery in high-volume hospitals
Authors: Ulrik Sartipy
Journal: Thorax (2013)

Better survival after lung cancer surgery in high-volume hospitalsIn this nationwide database study from England, the association between hospital volume and survival after surgery for non-small cell lung cancer (NSCLC) was investigated.The National Cancer Data Repository was used to extract data on lung cancer diagnosed in England between 2004 and 2008.Survival status was obtained from the National Health Service Central Register and information on surgical resections was acquired from the Hospital Episode Statistics records.Socioeconomic status for each patient was estimated based on the area of residence.Comorbidity information was obtained using diagnosis codes from the Hospital Episode Statistics records and then classified according to Charlson Comorbidity Index.Hospital volume was defined as the number of patients operated on in each hospital in each year of diagnosis.Cox proportional hazards regression models were used to analyse the association between hospital volume and survival.Adjustment was made for age, sex, socioeconomic status, comorbidity and propensity to operate in the area where the patient was diagnosed.The study included 134 293 patients with NSCLC and 12 862 (9.6%) underwent lung cancer surgery at 58 hospitals.Hospital volume ranged from 1 to 194 patients per year.The proportion of NSCLC patients who received surgery varied between 5.5% and 14.3% depending on area of residence.Higher hospital volume was associated with better survival.Specifically, this association was strongest among hospitals operating on more than 150 patients per year compared with hospitals performing less than 70 operations per year (adjusted HR 0.78, 95% CI 0.67 to 0.90).Notably, high-volume hospitals performed surgery in patients who were older and had increased comorbidity compared with low-volume hospitals.Still, early mortality was lower at these centres.The study was limited by lack of information regarding lung cancer stage and adjuvant therapy, factors known to be associated with prognosis.The results presented in this study are consistent with prior studies reporting better survival after surgery in patients with NSCLC, and other cancers, operated on in high-volume hospitals.
Contribution of α-Adrenergic and β-Adrenergic Stimulation to Ischemia-Induced Glucose Transporter (GLUT) 4 and GLUT1 Translocation in the Isolated Perfused Rat Heart
Authors: Silvia Egert, Ngoc Nguyen, Markus Schwaiger
Journal: Circulation Research (1999)

Abstract —The intracellular signaling mechanism of the ischemia-stimulated glucose transporter (GLUT) translocation in the heart is not yet characterized. It has been suggested that catecholamines released during ischemia may be involved in this pathway. The purpose of this study was to evaluate the contribution of α-adrenoceptors and β-adrenoceptors to ischemia-mediated GLUT4 and GLUT1 translocation in the isolated, Langendorff-perfused rat heart. Additionally, GLUT translocation was studied in response to catecholamine stimulation with phenylephrine (Phy) and isoproterenol (Iso). The results were compared with myocardial uptake of glucose analogue [ 18 F]fluorodeoxyglucose (FDG). Subcellular analysis of GLUT4 and GLUT1 protein on plasma membrane vesicles (PM) and intracellular membrane vesicles (IM) using membrane preparation and immunoblotting revealed that α- and β-receptor agonists stimulated GLUT4 translocation from IM to PM (2.5-fold for Phy and 2.1-fold for Iso, P &lt;0.05 versus control), which was completely inhibited by phentolamine (Phe) and propranolol (Pro), respectively. Plasmalemmal GLUT1 moderately rose after Iso exposure, and this was prevented by Pro. In contrast, ischemia-stimulated GLUT4 translocation (2.2-fold, P &lt;0.05 versus control) was only inhibited by α-adrenergic antagonist Phe but not by β-adrenergic antagonist Pro. Similarly, Phe but not Pro inhibited ischemia-stimulated GLUT1 translocation. GLUT data were confirmed by FDG uptake monitored using bismuth germanate detectors. The catecholamine-stimulated FDG uptake (6.9-fold for Phy and 8.9-fold for Iso) was significantly inhibited by Phe and Pro; however, only Phe but not Pro significantly reduced the ischemia-induced 2.5-fold increase in FDG uptake ( P &lt;0.05 versus ischemia). This study suggests that α-adrenoceptor stimulation may play a role in the ischemia-mediated increase in glucose transporter trafficking leading to the stimulation of FDG uptake in the isolated, perfused rat heart, whereas β-adrenergic activation does not participate in this signaling pathway.
American Society of Clinical Oncology Clinical Practice Guideline Update on the Use of Chemotherapy Sensitivity and Resistance Assays
Authors: Harold J. Burstein, Pamela B. Mangu, Mark R. Somerfield, Deborah Schrag, David Samson, Lawrence Holt, Debra Zelman, Jaffer A. Ajani
Journal: Journal of Clinical Oncology (2011)

To update the American Society of Clinical Oncology (ASCO) Technology Assessment guidelines on chemotherapy sensitivity and resistance assays (CSRAs) published in 2004.An Update Working Group reviewed data published between December 1, 2003, and May 31, 2010. MEDLINE and the Cochrane Library were searched. The literature search yielded 11,313 new articles. The limits for "human and English" were used, and then standard ASCO search strings for randomized controlled trials, meta-analyses, guidelines, and reviews were added, yielding 1,298 articles for abstract review. Of these, only 21 articles met predefined inclusion criteria and underwent full text review, and five reports of randomized controlled trials were included for data extraction.Review of the literature does not identify any CSRAs for which the evidence base is sufficient to support use in oncology practice.The use of CSRAs to select chemotherapeutic agents for individual patients is not recommended outside of the clinical trial setting. Oncologists should make chemotherapy treatment recommendations based on published reports of clinical trials and a patient's health status and treatment preferences. Because the in vitro analytic strategy has potential importance, participation in clinical trials evaluating these technologies remains a priority.
Hormonal control of plasma renin substrate; (angiotensinogen).
Authors: L R Krakoff, A J Eisenfeld
Journal: Circulation Research (1977)

The effect of ethinyl estradiol (EE2) and dexamethasone (Dex) upon plasma renin substrate (PRS) was studied in rats in relation to sexual maturation and pituitary function. Normal adult rats had large increases in PRS when given either EE2 or Dex. Prepubescent (25-day-old) rats also had a substantial increase in PRS following Dex, but no increase in PRS after EE2. In adult rats, hypophysectomy prevented the rise in PRS due to EE2 but did not prevent the increase in PRS due to Dex. Hepatic estrogen and glucocorticoid receptors were measured in immature and adult rats. Immature rats had markedly reduced concentration of hepatic estrogen receptors (16%), compared with adults. In contrast, glucocorticoid receptor concentration was not significantly different between immature and adult rats. The results indicate that the effect of estrogens and glucocorticoids upon PRS are mediated by pathways that are separable at the hormone receptor level.
TINEA CAPITIS DUE TO TRICHOPHYTON SULPHUREUM.
Authors: J. MARTIN BEARE
Journal: British Journal of Dermatology (1956)

Journal Article TINEA CAPITIS DUE TO TRICHOPHYTON SULPHUREUM. Get access J. MARTIN BEARE J. MARTIN BEARE Dermatologist, Royal Belfast Hospital for Sick Children, Asst. Physician, Skin Dept., Royal Victoria Hospital, Belfast Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 68, Issue 6, 1 June 1956, Pages 193–199, https://doi.org/10.1111/j.1365-2133.1956.tb13205.x Published: 01 June 1956
Transcriptional Cooperation between the Transforming Growth Factor-β and Wnt Pathways in Mammary and Intestinal Tumorigenesis
Authors: Etienne Labbé, Lisa Lock, Ainhoa Letamendia, Agnieszka E. Gorska, Robert Gryfe, Steven Gallinger, Harold L. Moses, Liliana Attisano
Journal: Cancer Research (2007)

Abstract Transforming growth factor-β (TGF-β) and Wnt ligands function in numerous developmental processes, and alterations of both signaling pathways are associated with common pathologic conditions, including cancer. To obtain insight into the extent of interdependence of the two signaling cascades in regulating biological responses, we used an oligonucleotide microarray approach to identify Wnt and TGF-β target genes using normal murine mammary gland epithelial cells as a model. Combination treatment of TGF-β and Wnt revealed a novel transcriptional program that could not have been predicted from single ligand treatments and included a cohort of genes that were cooperatively induced by both pathways. These included both novel and known components or modulators of TGF-β and Wnt pathways, suggesting that mutual feedback is a feature of the coordinated activities of the ligands. The majority of the cooperative targets display increased expression in tumors derived from either Min (many intestinal neoplasia) or mouse mammary tumor virus (MMTV)–Wnt1 mice, two models of Wnt-induced tumors, with nine of these genes (Ankrd1, Ccnd1, Ctgf, Gpc1, Hs6st2, IL11, Inhba, Mmp14, and Robo1) showing increases in both. Reduction of TGF-β signaling by expression of a dominant-negative TGF-β type II receptor in bigenic MMTV-Wnt1/DNIIR mice increased mammary tumor latency and was correlated with a decrease in expression of Gpc1, Inhba, and Robo1, three of the TGF-β/Wnt cooperative targets. Our results indicate that the TGF-β and Wnt/β-catenin pathways are firmly intertwined and generate a unique gene expression pattern that can contribute to tumor progression. [Cancer Res 2007;67(1):75–84]
Microsatellite alterations and TP53 mutations in plasma DNA of small-cell lung cancer patients: Follow-up study and prognostic significance
Authors: R. Gonzalez, J.M. Silva, A. Sanchez, G. Dominguez, J.M. Garcia, X. qi Chen, M. Stroun, M. Provencio, P. España, P. Anker, F. Bonilla
Journal: Annals of Oncology (2000)
Mortality, CD4 Cell Count Decline, and Depressive Symptoms Among HIV-Seropositive Women
Authors: Jeannette R. Ickovics, Merle E. Hamburger, David Vlahov, Ellie E. Schoenbaum, Paula Schuman, Robert J. Boland, Janet Moore, None for the HIV Epidemiology Research Study Group
Journal: JAMA (2001)

EPRESSION HAS BEEN ASSOciated with immune suppression and other health outcomes in studies of individuals with and without chronic disease. 1-5Although there has been variability in results, the association between depression and immune outcomes are strongest and most consistent in both older and hospitalized patients. 5In the past decade, there has been particular interest in the impact of depression on the health of persons already immunocompromised because of infection with human immunodeficiency virus (HIV).Investigators have examined the relationship of depression with morbidity and mortality among gay and bisexual men with HIV.Studies have documented associations between depression and disease progression, 6-8 HIVrelated symptoms, 9-11 and mortality. 124][15] In contrast, other studies found no association between depression, immune function, and disease progression among gay men with
In normal subjects bracing impairs the function of the inspiratory muscles
Authors: E. Prandi, J Couture, F Bellemare
Journal: European Respiratory Journal (1999)

Normal subjects can increase their capacity to sustain hyperpnoea by bracing their arms on fixed objects, a procedure which is also known to reduce dyspnoea in patients with chronic obstructive pulmonary disease (COPD). In the present study, it was tested whether bracing per se could improve the function of the diaphragm. The effect of bracing on diaphragm function was studied in six normal subjects by recording changes in oesophageal (delta Poes) and transdiaphragmatic (delta Pdi) pressure during inspiratory capacity (IC) manoeuvres in the seated and upright postures, and in the seated posture, also during bilateral phrenic nerve stimulation (BPNS) at functional residual capacity (FRC). The pattern of ribcage motion and deformation associated with bracing and with diaphragm contraction was also evaluated using inductance plethysmography and magnetometers. Bracing increased FRC by >300 mL and reduced IC by approximately 200 mL, in both postures. Delta Pdi during BPNS decreased on average by 15% indicating an impaired diaphragmatic function. The ribcage was deformed with bracing and was more distortable during BPNS. In conclusion, in normal subjects, bracing impairs the function of the inspiratory muscles and reduces ribcage stability. These negative effects cannot explain the improved capacity to sustain hyperpnoea when the arms are braced.
Inflammation and its Resolution as Determinants of Acute Coronary Syndromes
Authors: Peter Libby, Ira Tabas, Gabrielle Fredman, Edward A. Fisher
Journal: Circulation Research (2014)

Inflammation contributes to many of the characteristics of plaques implicated in the pathogenesis of acute coronary syndromes. Moreover, inflammatory pathways not only regulate the properties of plaques that precipitate acute coronary syndromes but also modulate the clinical consequences of the thrombotic complications of atherosclerosis. This synthesis will provide an update on the fundamental mechanisms of inflammatory responses that govern acute coronary syndromes and also highlight the ongoing balance between proinflammatory mechanisms and endogenous pathways that can promote the resolution of inflammation. An appreciation of the countervailing mechanisms that modulate inflammation in relation to acute coronary syndromes enriches our fundamental understanding of the pathophysiology of this important manifestation of atherosclerosis. In addition, these insights provide glimpses into potential novel therapeutic interventions to forestall this ultimate complication of the disease.
Non-steroidal anti-inflammatory drugs in athletes
Authors: G Lippi, M Franchini, G C Guidi
Journal: British Journal of Sports Medicine (2006)

Aspirin and the non-steroidal anti-inflammatory drugs (NSAIDs) have been commercially available for decades, and their ability to reduce pain and inflammation is well established. It was first shown nearly 30 years ago that aspirin strongly inhibits platelet function by acetylation of platelet cyclo-oxygenase (COX) at the functionally important amino acid serine 529. This prevents access of the substrate (arachidonic aid) to the catalytic site of the enzyme at tyrosine 385 and results in irreversible inhibition of platelet dependent formation of thromboxane, a powerful promoter of aggregation, for the lifetime of the platelet (7–10 days). Aspirin is about 150–200-fold more potent as an inhibitor of the constitutive isoform of the platelet enzyme (COX-1) than the inducible isoform (COX-2), which is expressed by cytokines, inflammatory stimuli, and some growth factors.1 This explains the different dose requirements of aspirin as an antithrombotic (COX-1) and an anti-inflammatory drug (COX-2).2 Non-aspirin NSAIDs inhibit the activity of both COX-1 and COX-2 by reversibly blocking the access of arachidonic acid to the active site at the apex of a hydrophobic channel within these enzymes.1 Acetaminophen is a weak, non-selective inhibitor of both COX enzymes, although the precise mechanism of action remains elusive. It has been recently proposed that it might act to reduce the active, oxidised form of both the COX enzymes, which would make it more potent at sites that have low peroxide concentrations, such as the brain and spinal cord.3 Aspirin and NSAIDs are non-selective inhibitors of both COX-1 and COX-2, whereas newer agents termed “coxibs” are selective inhibitors of COX-2.4 The identification of COX-2 selective inhibitory NSAIDs was thought to be a major breakthrough, with the expectation of a significant reduction in side effects. The major controversy with respect to the COX-2 selective inhibitors as a class has been …
Cytotoxic differentiation of mouse gut thymodependent and independent intraepithelial T lymphocytes is induced locally. Correlation between functional assays, presence of perforin and granzyme transcripts, and cytoplasmic granules.
Authors: D Guy-Grand, M Malassis-Seris, C Briottet, P Vassalli
Journal: The Journal of Experimental Medicine (1991)

Mouse gut intraepithelial lymphocytes (IEL), whether thymodependent (CD4+ or CD8 alpha/beta +; TCR-alpha/beta +) or thymoindependent (CD8 alpha/alpha +; TCR-alpha/beta + or -gamma/delta +), all display cytotoxic activity in a "redirected lysis assay" using anti-CD3 or anti-TCR beta or delta chains secreting hybridomas as targets; this is also observed with IEL of germ-free mice, indicating that this activity, which is absent in peripheral T lymphocytes, does not require stimulation by bacterial antigens. Perforin and granzyme transcripts are detectable in unselected gut IEL, in contrast to normal T lymphocytes of peripheral lymphoid organs. Cytological labeling (with [3H]DFP) of IEL smears reveals labeled granules (i.e., containing serine-esterases, presumably granzymes) in all subsets of gut IEL. This indicates that the gut micro-environment has an inductive role on the cytotoxic differentiation of lymphocytes of various origins when they reach the gut wall to become IEL.
Elevations in vascular markers and eosinophils in chronic spontaneous urticarial weals with low‐level persistence in uninvolved skin
Authors: A.B. Kay, S. Ying, E. Ardelean, A. Mlynek, H. Kita, P. Clark, M. Maurer
Journal: British Journal of Dermatology (2014)

In chronic spontaneous urticaria (CSU) mast cell activation together with inflammatory changes in the skin are well documented and may play an important role in mechanisms of tissue oedema. To confirm and extend these observations by measuring microvascular markers, leucocytes and mast cell numbers in lesional and uninvolved skin and to compare findings with a control group. Paired biopsies (one from 4–8‐h spontaneous weals and one from uninvolved skin) were taken from eight patients with CSU and nine control subjects and studied using immunohistochemistry and confocal microscopy using the lectin Ulex europaeus agglutinin 1 (UEA‐1). Lesional skin in CSU contained significantly more CD31+ endothelial cells; CD31+ blood vessels, neutrophils, eosinophils, basophils and macrophages; and CD3+ T cells than nonlesional skin. Increased vascularity was confirmed by confocal imaging using the lectin UEA‐1. Uninvolved skin from CSU contained significantly more CD31+ endothelial cells, CD31+ blood vessels and eosinophils compared with the control subjects. There was a threefold increase in mast cell numbers when CSU was compared with controls but no difference was observed between lesional and uninvolved skin. Increased vascular markers together with eosinophil and neutrophil infiltration are features of lesional skin in CSU and might contribute to tissue oedema. Eosinophils and microvascular changes persist in uninvolved skin, which, together with increased mast cells, suggests that nonlesional skin is primed for further wealing.
Lessons learnt in Europe on tuberculosis surveillance, outbreaks and BCG vaccination in 2011
Authors: Marieke J. van der Werf, Francesco Blasi, Johan Giesecke, Giovanni Battista Migliori
Journal: European Respiratory Journal (2013)

nly a few European scientific journals publish articles on respiratory infectious diseases and tuberculosis (TB).The European Respiratory Journal (ERJ) and Eurosurveillance are two examples with a different focus.Eurosurveillance, which is published by, but editorially independent from, the European Centre for Disease Prevention and Control (ECDC) is a European peer-reviewed scientific journal devoted to the epidemiology, surveillance, prevention and control of communicable diseases, with a focus on topics that are of relevance to Europe.
Infusion of autologous Epstein-Barr virus (EBV)–specific cytotoxic T cells for prevention of EBV-related lymphoproliferative disorder in solid organ transplant recipients with evidence of active virus replication
Authors: Patrizia Comoli, Massimo Labirio, Sabrina Basso, Fausto Baldanti, Paolo Grossi, Milena Furione, Mario Viganò, Roberto Fiocchi, Giorgio Rossi, Fabrizio Ginevri, Bruno Gridelli, Antonia Moretta, Daniela Montagna, Franco Locatelli, Giuseppe Gerna, Rita Maccario
Journal: Blood (2002)