tbuckley/cabot-search huggingface dataset:
Increasing outpatient treatment of mild community-acquired pneumonia: systematic review and meta-analysis
Authors: J.D. Chalmers, A.R. Akram, A.T. Hill
Journal: European Respiratory Journal (2010)

In order to identify, synthesise and interpret the evidence relating to strategies to increase the proportion of low-risk patients with community-acquired pneumonia treated in the community, we conducted a systematic review of intervention studies conducted between 1981–2010. Articles were included if they compared strategies to increase outpatient care with usual care. Outcomes were: the proportion of patients treated as outpatients, mortality, hospital readmissions, health related quality of life, return to usual activities and patient satisfaction with care. The main analysis included six studies. The interventions in these studies were generally complex, but all involved the use of a severity score to identify low-risk patients. Overall, a significantly larger numbers of patients were treated in the community with these interventions (OR 2.31, 95% CI 2.03–2.63). The interventions appear safe, with no significant differences in mortality (OR 0.83, 95% CI 0.59–1.17), hospital readmissions (OR 1.08, 95% CI 0.82–1.42) or patient satisfaction with care (OR 1.21, 95% CI 0.97–1.49) between the intervention and control groups. There was insufficient data regarding quality of life or return to usual activities. All studies had significant limitations. The available evidence suggests that interventions to increase the proportion of patients treated in the community are safe, effective and acceptable to patients.
Are placebo-controlled trials of creams for athlete’s foot still justified?
Authors: F. Crawford, R. Harris, H.C. Williams
Journal: British Journal of Dermatology (2008)

Journal Article Are placebo‐controlled trials of creams for athlete's foot still justified? Get access F. Crawford, F. Crawford Division of Community Health Sciences, General Practice Section, 20 West Richmond Street, Edinburgh EH8 9DX, U.K. Correspondence: Fay Crawford. E‐mail: fay.crawford@ed.ac.uk Search for other works by this author on: Oxford Academic Google Scholar R. Harris, R. Harris Department of Social Medicine, Canynge Hall, 39 Whatley Road, Bristol BS8 2PS, U.K. Search for other works by this author on: Oxford Academic Google Scholar H.C. Williams H.C. Williams Nottingham University Hospital NHS Trust, Queen's Medical Centre Campus, Nottingham NG7 2UH, U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 159, Issue 4, 1 October 2008, Pages 773–779, https://doi.org/10.1111/j.1365-2133.2008.08806.x Published: 01 October 2008
Nurse Navigators in Early Cancer Care: A Randomized, Controlled Trial
Authors: Edward H. Wagner, Evette J. Ludman, Erin J. Aiello Bowles, Robert Penfold, Robert J. Reid, Carolyn M. Rutter, Jessica Chubak, Ruth McCorkle
Journal: Journal of Clinical Oncology (2013)

To determine whether a nurse navigator intervention improves quality of life and patient experience with care for people recently given a diagnosis of breast, colorectal, or lung cancer.
STUDIES ON LYSOSOMES
Authors: Gerald Weissmann, Harold Keiser, Alan W. Bernheimer
Journal: The Journal of Experimental Medicine (1963)

Streptolysins O and S from hemolytic streptococci have been added to granular fractions of tissue homogenates in 0.25 M sucrose prepared from rabbit liver, heart, spleen and lymph nodes. At concentrations ranging from 0.65 microg/ml to 2.0 mg/ml of streptolysin S, and from 10 microg/ml to 1.0 mg/ml of streptolysin O, two lysosomal enzymes (beta glucuronidase and acid phosphatase) and, to a lesser degree, one mitochondrial enzyme (malic dehydrogenase) were released into the supernatants of the reaction mixture. Although the hemolytic action of each lysin paralleled the effect on lysosomes, at equivalent levels of hemolytic activity, SLS was approximately 10 times more active on lysosomes than SLO. SLO was inhibited by cholesterol, cortisol, and specific antibody in vitro; pretreatment of animals with cortisone decreased the susceptibility of their isolated lysosomes to SLO. These agents failed to prevent SLS action on lysosomes. SLO had a pH optimum of 6.5 against lysosomes while SLS was maximally active at 7.5. No other streptococcal extracellular products were as active on lysosomes as the streptolysins, although activated streptococcal proteinase precursor released some hydrolases from the granules. Similarities between the actions of SLO and SLS on red cells and lysosomes suggested that the membranes bounding lysosomes and erythrocytes have common properties.
Misoprostol prior to hysteroscopy in premenopausal and post-menopausal women. A systematic review and meta-analysis
Authors: N. P. Polyzos, A. Zavos, A. Valachis, C. Dragamestianos, C. Blockeel, D. Stoop, E. G. Papanikolaou, H. Tournaye, P. Devroey, I. E. Messinis
Journal: Human Reproduction Update (2012)

Although several randomized controlled trials (RCTs) have examined the effect of misoprostol prior to hysteroscopy for cervical dilatation, no solid conclusion has been reached. We therefore set out to perform a meta-analysis of RCTs. We searched MEDLINE, the ISI Web of Science and the Cochrane Library to identify RCTs comparing misoprostol versus placebo or control prior to hysteroscopy. No restrictions on language or time were applied. Relative risks (RRs) and 95% confidence intervals (CIs) were calculated for all dichotomous outcomes, whereas mean differences (MDs) and 95% CIs were calculated for continuous outcomes using the Mantel–Haenszel or DerSimonian–Laird model according to the heterogeneity. Of the initial 141 potentially relevant articles that were retrieved, 21 RCTs involving 1786 patients were included in the meta-analysis. Subgroup analyses were performed according to menopausal status and according to whether diagnostic or operative hysteroscopy was performed. Premenopausal women treated with misoprostol had a significantly lower risk for further cervical dilatation in the diagnostic setting [RR (95% CI): 0.56 (0.34–0.92)] and a significantly lower risk for cervical laceration in the operative setting [RR (95% CI): 0.22 (0.09–0.54)], compared with placebo. In contrast, post-menopausal patients did not experience any clear benefit from misoprostol compared with placebo regarding the need for further cervical dilatation [RR (95% CI): 0.99 (0.76–1.30)] and the cervical laceration rate [RR (95% CI): 1.15 (0.40–3.29)]. In addition, the mean cervical width prior to hysteroscopy was significantly higher in premenopausal women treated with misoprostol compared with placebo [MD (95% CI): 2.47 mm (1.81–3.13)] but did not differ among post-menopausal patients [MD (95% CI): 0.39 mm (−0.42 to 1.21)]. Misoprostol prior to hysteroscopy appears to facilitate an easier and uncomplicated procedure only in premenopausal women.
Transcription inhibitor actinomycin-D abolishes the cardioprotective effect of ischemic reconditioning
Authors: C Strohm
Journal: Cardiovascular Research (2002)

Objective: Our previous studies have suggested a role of mitogen-activated protein kinases (MAPKs) in cardioprotection in the porcine heart. To investigate, whether this could be due to modification of transcriptional events we studied the influence of actinomycin-D (act-D), a known RNA-synthesis inhibitor on (i) ischemic preconditioning, (ii) (IP)-mediated cardioprotection, (iii) transcription factors levels and MAPKs activation. Methods: The IP-design in our model included two cycles of 10′ LAD occlusion (CO) and 10′ reperfusion (RP), followed by 40′ CO (index ischemia) and 60′ RP. Act-D was infused intramyocardially (i.my.) or systemically (syst.) (0.05 or 0.12 mg/kg) during 15′ before IP and during both RP cycles of the IP-protocol. The i.my. infusions occurred via four pairs of needles into the risk area (RA). Results: Systemic infusion of act-D (0.05 mg/kg) before index ischemia significantly increased the IS from 54.0±2.5 to 78.5±3.8%. IP significantly reduced the IS to 2.5±0.8%. Syst. of act-D completely abolished the IP-induced cardioprotection. At a dose of 0.12 mg/kg the IS was 88.6±1.7% of the risk area; at 0.05 mg/kg IS was 65.6±1.5%. Local infusion of act-D reduced the IP-induced cardioprotection in a concentration dependent manner. Syst. or i.my. infusion of DMSO in KHB did not influence the IP-induced cardioprotection. Western blot analysis with phospho-specific antibodies showed a significant increase in phosphorylation of cytosolic ERK1/2 and SAPK/JNKs at the end of IP procedure and act-D treatment inhibited IP-induced activation of these MAPKs. By Western blot analysis using phospho-specific antibodies against c-Jun, ATF-2, Elk-1 and c-Myc we found increased phosphorylation of all these transcription factors in the myocardial risk area at the end of IP protocol and both local and systemic infusion of act-D significantly (P<0.05) inhibited this increased phosphorylation. Unlike UO, act-D had no influence on the Akt-pathway but inhibited the increased expression of S100 protein induced by IP. Conclusions: We demonstrate in vivo that act-D, completely cancelled the IP-induced cardioprotection. The influence of act-D on cardioprotection, transcription factors, and activities of ERKs and JNKs indicates a possible transcriptional role of these MAPKs signal transduction pathways during ischemia and in IP.
Mechanism of injury of virus-infected cells by antiviral antibody and complement: participation of IgG, F(ab')2, and the alternative complement pathway.
Authors: L H Perrin, B S Joseph, N R Cooper, M B Oldstone
Journal: The Journal of Experimental Medicine (1976)

Antibody-mediated C-dependent lysis of cell lines infected with herpes simplex type 1 virus, influenza A degrees virus, measles virus, and mumps virus occurred by the alternative C pathway with the participation of IgG antibodies. Lysis occurred only with immune human sera, Mg++ EGTA immune sera, and immune sera depleted of C4 or treated with Fab anti-C4. Lysis did not occur with nonimmune sera, Mg++ EDTA immune sera, and immune sera heated 50 degrees C for 25 min, depleted of factor B or treated with Fab antifactor B. Lysis was restored to heated and factor B immunodepleted immune sera by addition of factor B, but not by addition of an excess of C2. Further studies showed that lysis of HeLa cells infected with measles virus was induced by both immune IgG and F(ab')2 but not Fab' in the presence of a nonantibody-containing human C source. Lysis of measles virus-infected cells was also indpendent of movement of viral antigens on the surface of the infected cells, as inhibition of viral antigen capping by cytochalasin B or sodium azide was not associated with abrogation of immune lysis.
THE RELATION BETWEEN AMINO ACIDS AND POTASSIUM IN ISOLATED RAT MUSCLE*
Authors: Norman G. Levinsky, Ian Tyson, Ronald B. Miller, Arnold S. Relman
Journal: Journal of Clinical Investigation (1962)

In previous studies in this laboratory, using in- tact rat diaphragms incubated in an artificial me- dium free of amino acids, it was found that there was essentially no change in steady-state muscle potassium in vitro as external potassium was low- ered from 5.5 to 1.1 mEq per L (1).By con- trast, when plasma potassium fell to comparable levels in vivo in potassium-deficient rats, dia- phragm potassium content was reduced by about one-third.It was therefore concluded that re- duction in external potassium concentration alone is insufficient to produce the loss of muscle potas- sium observed in potassium-deficient rats.Since the striking difference between the in vivo and in vitro behavior of skeletal muscle could not be explained by changes in extracellular acid-base balance, it was evident that other unidentified factors must play a role.A number of observations suggested that cati- onic amino acids might be among these unidentified factors.Qualitative studies by lacobellis, Muntwyler and Dodgen (2) had shown that the amount of lysine and arginine in the muscle of potassium- depleted rats was grossly increased.Quantitative analyses by Eckel, Norris and Pope (3) indicated that about one-third of the potassium lost from such muscle was replaced by cationic amino acids,
Rare Occurrence of Classical Hodgkin's Disease as a T Cell Lymphoma
Authors: Markus Müschen, Klaus Rajewsky, Andreas Bräuninger, Audrey Sylvia Baur, Joost J. Oudejans, Axel Roers, Martin-Leo Hansmann, Ralf Küppers
Journal: The Journal of Experimental Medicine (2000)

Recent work identified Hodgkin and Reed-Sternberg (H/RS) cells in classical Hodgkin's disease (cHD) as clonal progeny of mature B cells. Therefore, it is generally assumed that cHD homogenously represents a B cell lymphoma. In a subset of cHD, however, H/RS cells expressing T cell–associated proteins may be candidates for alternative lineage derivation. Single H/RS cells with cytotoxic T cell phenotype were micromanipulated from three cases of cHD and analyzed by single cell polymerase chain reaction for immunoglobulin heavy (IgH) and light chain (IgL) gene rearrangements, T cell receptor (TCR)-β gene rearrangements, and germline configuration of the IgH and TCR-β loci. H/RS cells from two cases of cHD harbored clonal, somatically mutated Ig gene rearrangements, whereas TCR-β loci were in germline configuration. In contrast, H/RS cells from an additional case harbored clonal TCR-β variable/diversity/joining (VDJ) and DJ gene rearrangements, whereas the IgH locus was in germline configuration on both alleles. Thus, in two cases of cHD with H/RS cells expressing cytotoxic T cell molecules, the tumor cells are derived from mature B cells that aberrantly express T cell markers. In a third case, however, H/RS cells were derived from a T cell, demonstrating that cHD can also occur as a T cell lymphoma.
Superior Outcome of Women With Stage I/II Cutaneous Melanoma: Pooled Analysis of Four European Organisation for Research and Treatment of Cancer Phase III Trials
Authors: Arjen Joosse, Sandra Collette, Stefan Suciu, Tamar Nijsten, Ferdy Lejeune, Ulrich R. Kleeberg, Jan Willem W. Coebergh, Alexander M.M. Eggermont, Esther de Vries
Journal: Journal of Clinical Oncology (2012)

Several studies observed a female advantage in the prognosis of cutaneous melanoma, for which behavioral factors or an underlying biologic mechanism might be responsible. Using complete and reliable follow-up data from four phase III trials of the European Organisation for Research and Treatment of Cancer (EORTC) Melanoma Group, we explored the female advantage across multiple end points and in relation to other important prognostic indicators.Patients diagnosed with localized melanoma were included in EORTC adjuvant treatment trials 18832, 18871, 18952, and 18961 and randomly assigned during the period of 1984 to 2005. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% CIs for women compared with men, adjusted for age, Breslow thickness, body site, ulceration, performed lymph node dissection, and treatment.A total of 2,672 patients with stage I/II melanoma were included. Women had a highly consistent and independent advantage in overall survival (adjusted HR, 0.70; 95% CI, 0.59 to 0.83), disease-specific survival (adjusted HR, 0.74; 95% CI, 0.62 to 0.88), time to lymph node metastasis (adjusted HR, 0.70; 95% CI, 0.51 to 0.96), and time to distant metastasis (adjusted HR, 0.69; 95% CI, 0.59 to 0.81). Subgroup analysis showed that the female advantage was consistent across all prognostic subgroups (with the possible exception of head and neck melanomas) and in pre- and postmenopausal age groups.Women have a consistent and independent relative advantage in all aspects of the progression of localized melanoma of approximately 30%, most likely caused by an underlying biologic sex difference.
Beta-globin mutations are associated with parenchymal siderosis and fibrosis in patients with non-alcoholic fatty liver disease
Authors: Luca Valenti, Elena Canavesi, Enrico Galmozzi, Paola Dongiovanni, Raffaela Rametta, Paolo Maggioni, Marco Maggioni, Anna Ludovica Fracanzani, Silvia Fargion
Journal: Journal of Hepatology (2010)
Parental History and the Risk for Childhood Asthma
Authors: AUGUSTO A. LITONJUA, VINCENT J. CAREY, HARRIET A. BURGE, SCOTT T. WEISS, DIANE R. GOLD
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

Although heredity plays a major role in asthma and in other allergic diseases, mechanisms underlying the inheritance of these disorders are poorly understood, as is the relative contribution of maternal and paternal conditions to risk of disease. We investigated doctor-diagnosed maternal and paternal asthma, eczema, and hay fever as cross-sectional predictors of childhood asthma and allergic disease in 306 children with a median age of 3.5 yr from families in which at least one parent had a history of either asthma or other allergic conditions. For both childhood asthma and eczema, the strongest parental predictors were the same conditions in the parents. For asthma in particular, maternal asthma was most strongly associated with asthma in the child over all ages in both univariate (OR = 3.2, 95% CI = 1.5 to 6.7) and multivariable (OR = 4.1, 95% CI = 1.7 to 10.1) models. Paternal asthma was weakly associated with childhood asthma in the univariate model (OR = 1.4, 95% CI = 0.6 to 3.2), but this association increased in magnitude in the multivariable model (OR = 2.7, 95% CI = 1.0 to 7.2). Among the children < 5 yr of age, the risk for childhood asthma associated with maternal asthma (OR = 5.0, 95% CI = 1.7 to 14.9) was greater than the risk associated with paternal asthma (OR = 1.6, 95% CI = 0.5 to 5.9), whereas both maternal asthma and paternal asthma were associated with similar risks among children ⩾ 5 yr of age (OR = 4.6, 95% CI = 1.1 to 19.0 and OR = 4.1, 95% CI = 1.0 to 16.0, respectively). The odds of having a child with asthma were three times greater in families with one asthmatic parent and six times greater in families with two asthmatic parents than in families where only one parent had inhalant allergy without asthma; furthermore, inhalant allergy in one parent also conferred additional risk in the presence of asthma in the other parent. Further investigation is needed into the relative importance of genetic factors and in utero and postnatal exposures in determining the differential effects of maternal and paternal asthma on the development of childhood asthma.
Analysis of Gene Expression in Early-Stage Ovarian Cancer
Authors: Sergio Marchini, Pietro Mariani, Giovanna Chiorino, Eleonora Marrazzo, Riccardo Bonomi, Robert Fruscio, Luca Clivio, Annalisa Garbi, Valter Torri, Michela Cinquini, Tiziana Dell'Anna, Giovanni Apolone, Massimo Broggini, Maurizio D'Incalci
Journal: Clinical Cancer Research (2008)

Abstract Purpose: Gene expression profile was analyzed in 68 stage I and 15 borderline ovarian cancers to determine if different clinical features of stage I ovarian cancer such as histotype, grade, and survival are related to differential gene expression. Experimental Design: Tumors were obtained directly at surgery and immediately frozen in liquid nitrogen until analysis. Glass arrays containing 16,000 genes were used in a dual-color assay labeling protocol. Results: Unsupervised analysis identified eight major patient partitions, one of which was statistically associated to overall survival, grading, and histotype and another with grading and histotype. Supervised analysis allowed detection of gene profiles clearly associated to histotype or to degree of differentiation. No difference was found between borderline and grade 1 tumors. As to recurrence, a subset of genes able to differentiate relapsers from nonrelapsers was identified. Among these, cyclin E and minichromosome maintenance protein 5 were found particularly relevant, as their expression was inversely correlated to progression-free survival (P = 0.00033 and 0.017, respectively). Conclusions: Specific molecular signatures define different histotypes and prognosis of stage I ovarian cancer. Mucinous and clear cells histotypes can be distinguished from the others regardless of tumor grade. Cyclin E and minichromosome maintenance protein 5, whose expression was found previously to be related to a bad prognosis of advanced ovarian cancer, appear to be potential prognostic markers in stage I ovarian cancer too, independent of other pathologic and clinical variables.
Interleukin-27 Priming of T Cells Controls IL-17 Production In trans via Induction of the Ligand PD-L1
Authors: Kiyoshi Hirahara, Kamran Ghoreschi, Xiang-Ping Yang, Hayato Takahashi, Arian Laurence, Golnaz Vahedi, Giuseppe Sciumè, Aisling O'Hara Hall, Christopher D. Dupont, Loise M. Francisco, Qian Chen, Masao Tanaka, Yuka Kanno, Hong-Wei Sun, Arlene H. Sharpe, Christopher A. Hunter, John J. O'Shea
Journal: Immunity (2012)
Ovarian Follicle Atresia: A Hormonally Controlled Apoptotic Process*
Authors: AARON J. W. HSUEH, HÅKAN BILLIG, ALEX TSAFRIRI
Journal: Endocrine Reviews (1994)

GREATER THAN 99% of ovarian follicles undergo a degenerative process called atresia during reproductive life. Extending earlier morphological analysis, recent studies have demonstrated that apoptotic cell death is the molecular mechanism underlying follicle atresia. The use of DNA 3′-end-labeling methods allows quantitation and identification of internucleosomal degradation of DNA after gel fractionation as well as in situ analysis of specific cell types undergoing DNA fragmentation in histological sections. Using rats as the experimental model, gonadotropins, epidermal growth factor (EGF)/transforming growth factor-α (TGFα), basic fibroblast growth factor (bFGF), insulin-like growth factor-I (IGF-I), and estrogens have been identified as follicle survival factors capable of suppressing apoptotic DNA fragmentation, whereas androgens, interleukin-6 (IL-6), and GnRH are potential atretogenic factors. This review summarizes the historical background of studies on follicle atresia and selection as well as recent advances in the intraovarian hormonal mechanisms that control follicle apoptosis. It is suggested that during the penultimate stage of follicle development, exposure to a survival factor (probably FSH) is responsible for follicle selection.
Proliferative function of cadaveric bone marrow cells
Authors: Paul L. Liu, Makio Ogawa, Lynn Crook, Roland Ochia, Jane K. Upshur
Journal: American Journal of Hematology (1978)

Abstract The proliferative function of human and murine cadaveric bone marrow was studied using methylcellulose clonal cell culture assays and the murine spleen colony technique. The study revealed persistence of hemopoietic functions for as long as 19 postmortem hours in cadaveric marrows of some patients. Studies of murine cadaveric marrows corresponded with those of human marrows. These results strongly suggest that human pluripotent hemopoietic stem cells survive in cadaveric marrows.