tbuckley/cabot-search huggingface dataset:
Leukocytes in ovarian function
Authors: Orhan Bukulmez, Aydin Arici
Journal: Human Reproduction Update (2000)

It has become apparent that in the ovary, the immune system contributes to the regulation of gonadal function. Leukocytes present within the ovary may constitute potential in-situ modulators of ovarian function that act through local secretion of regulatory soluble factors. These factors include numerous cytokines that largely originate by the action of immune cells within the ovary. Actual rupture of the follicle during ovulation may be dependent on tissue remodelling that is characteristic of an acute inflammatory reaction and includes mobilization of thecal fibroblasts, increased leukocyte migration, release of various mediators and loosening of connective tissue elements in the follicle wall. Both corpus luteum formation and luteal regression also involve progressive infiltration of lymphocytes and macrophages, release of chemokines and cytokines, and communication through cell adhesion molecules. In this review, we examine the evidence for the leukocytes and their products in regulation of ovarian function and relate the potential significance of these cells and substances to some ovarian disorders.
Essential Surgery at the District Hospital: A Retrospective Descriptive Analysis in Three African Countries
Authors: Moses Galukande, Johan von Schreeb, Andreas Wladis, Naboth Mbembati, Helder de Miranda, Margaret E. Kruk, Sam Luboga, Alphonsus Matovu, Colin McCord, S. Khady Ndao-Brumblay, Doruk Ozgediz, Peter C. Rockers, Ana Romàn Quiñones, Fernando Vaz, Haile T. Debas, Sarah B. Macfarlane
Journal: PLoS Medicine (2010)

In the first of two papers investigating surgical provision in eight district hospitals in Saharan African countries, Margaret Kruk and colleagues find low levels of surgical care provision suggesting unmet need for surgical services.
Epidermal Growth Factor Receptor (EGFR) Mediates Cell Fusion and Infectivity Of Respiratory Syncytial Virus (RSV)
Authors: Sujin Lee, Michael G. Currier, Anne L. Hotard, Jia Meng, Carla Pretto, Ultan F. Power, Remi Villenave, Michael D. Shields, Michael H. Chi, R. Stokes Peebles, Martin L. Moore
Journal: Journal of Allergy and Clinical Immunology (2014)
The Association of Basal Insulin Glargine and/or n-3 Fatty Acids With Incident Cancers in Patients With Dysglycemia
Authors: Louise Bordeleau, Natalia Yakubovich, Gilles R. Dagenais, Julio Rosenstock, Jeffrey Probstfield, Pan Chang Yu, Lars E. Ryden, Valdis Pirags, Giatgen A. Spinas, Kare I. Birkeland, Robert E. Ratner, Jose A. Marin-Neto, Matyas Keltai, Matthew C. Riddle, Jackie Bosch, Salim Yusuf, Hertzel C. Gerstein
Journal: Diabetes Care (2014)

OBJECTIVE Epidemiologic studies linking insulin glargine and glucose-lowering therapies to cancers and n-3 fatty acids to cancer prevention have not been confirmed. We aimed to assess the effect of insulin glargine and n-3 fatty acids on incident cancers within the context of the ORIGIN (Outcome Reduction with Initial Glargine Intervention) trial. RESEARCH DESIGN AND METHODS The ORIGIN trial is an international, long-term, randomized two-by-two factorial study comparing insulin glargine with standard care and n-3 fatty acids with placebo (double blind) in people with dysglycemia at high risk for cardiovascular events. The primary outcome measure (cancer substudy) was the occurrence of any new or recurrent adjudicated cancer. Cancer mortality and cancer subtypes were also analyzed. RESULTS Among 12,537 people (mean age 63.5 years, SD 7.8; 4,388 females), 953 developed a cancer event during the median follow-up of 6.2 years. In the glargine and standard care groups, the incidence of cancers was 1.32 and 1.32 per 100 person-years, respectively (P = 0.97), and in the n-3 fatty acid and placebo groups, it was 1.28 and 1.36 per 100 person-years, respectively (P = 0.39). No difference in the effect of either intervention was noted within predefined subgroups (P for all interactions ≥0.17). Cancer-related mortality and cancer-specific outcomes also did not differ between groups. Postrandomization HbA1c levels, glucose-lowering therapies (including metformin), and BMI did not affect cancer outcomes. CONCLUSIONS Insulin glargine and n-3 fatty acids have a neutral association with overall and cancer-specific outcomes, including cancer-specific mortality. Exposure to glucose-lowering therapies, including metformin, and HbA1c level during the study did not alter cancer risk.
TCT-485 Paclitaxel Prevented the Intimal Proliferation after Percutaneous Coronary Intervention for Patients with Renal Insufficiency
Authors: Hideyuki Takimura, Toshiya Muramatsu, Reiko Tsukahara, Yoshiaki Ito, Hiroshi Ishimori, Keisuke Hirano, Masatsugu Nakano, Motoharu Araki, Tamon Kato, Norihiro Kobayashi, Yasunari Sakamoto, Shinsuke Mori, Masakazu Tsutsumi, Takuro Takama, Hiroya Takafuji, Takahiro Tokuda
Journal: Journal of the American College of Cardiology (2013)
High short-term mortality following lung biopsy for usual interstitial pneumonia
Authors: J.P. Utz, J.H. Ryu, W.W. Douglas, T.E. Hartman, H.D. Tazelaar, J.L. Myers, M.S. Allen, D.R. Schroeder
Journal: European Respiratory Journal (2001)

Usual interstitial pneumonia (UIP) is a specific histological pattern of interstitial pneumonia most often associated with the clinical syndrome of idiopathic pulmonary fibrosis (IPF). There is controversy regarding the use of surgical lung biopsy in the diagnosis of UIP, and the risk of lung biopsy in these patients is largely unknown. This study investigated the 30 day surgical mortality rate in patients undergoing surgical lung biopsy for UIP. Patients undergoing surgical lung biopsy over a 10-yr period from 1986–1995 with the ultimate diagnosis of UIP (with or without underlying connective tissue disease) were identified. Pathology, computed tomography, medical records, and survival were assessed. Ten of sixty patients with usual interstitial pneumonia were found to be dead within 30 days of surgical biopsy. All of these were patients with idiopathic UIP, unassociated with connective tissue disease (clinical condition of IPF). In conclusion, patients with usual interstitial pneumonia of the idiopathic type, who present with atypical features, may be at higher risk for death following surgical biopsy than patients presenting with more typical features or patients with other interstitial illnesses.
Fluctuation analysis of lung function as a predictor of long-term response to 2-agonists
Authors: C. Thamrin, G. Stern, M-P. F. Strippoli, C. E. Kuehni, B. Suki, D. R. Taylor, U. Frey
Journal: European Respiratory Journal (2008)

The response to β 2 -agonists differs between asthmatics and has been linked to subsequent adverse events, even death. Possible determinants include β 2 -adrenoceptor genotype at position 16, lung function and airway hyperresponsiveness. Fluctuation analysis provides a simple parameter α measuring the complex correlation properties of day-to-day peak expiratory flow. The present study investigated whether α predicts clinical response to β 2 -agonist treatment, taking into account other conventional predictors. Analysis was performed on previously published twice-daily peak expiratory flow measurements in 66 asthmatic adults over three 6-month randomised order treatment periods: placebo, salbutamol and salmeterol. Multiple linear regression was used to determine the association between α during the placebo period and response to treatment (change in the number of days with symptoms), taking into account other predictors namely β 2 -adrenoceptor genotype, lung function and its variability, and airway hyperresponsiveness. The current authors found that α measured during the placebo period considerably improved the prediction of response to salmeterol treatment, taking into account genotype, lung function or its variability, or airway hyperresponsiveness. The present study provides further evidence that response to β 2 -agonists is related to the time correlation properties of lung function in asthma. The current authors conclude that fluctuation analysis of lung function offers a novel predictor to identify patients who may respond well or poorly to treatment.
Silencing of Autocrine Motility Factor Induces Mesenchymal-to-Epithelial Transition and Suppression of Osteosarcoma Pulmonary Metastasis
Authors: Yasufumi Niinaka, Kiyoshi Harada, Masahiro Fujimuro, Masamitsu Oda, Arayo Haga, Misa Hosoki, Narikazu Uzawa, Naoya Arai, Satoshi Yamaguchi, Masashi Yamashiro, Avraham Raz
Journal: Cancer Research (2010)

Phosphoglucose isomerase (PGI) is a multifunctional enzyme that functions in glucose metabolism as a glycolytic enzyme catalyzing an interconversion between glucose and fructose inside the cell, while it acts as cytokine outside the cell, with properties that include autocrine motility factor (AMF)-regulating tumor cell motility. Overexpression of AMF/PGI induces epithelial-to-mesenchymal transition with enhanced malignancy. Recent studies have revealed that silencing of AMF/PGI resulted in mesenchymal-to-epithelial transition (MET) of human lung fibrosarcoma cells and breast cancer cells with reduced malignancy. Here, we constructed a hammerhead ribozyme specific against GUC triplet at the position G390 in the human, mouse, and rat AMF/PGI mRNA sequence. Mesenchymal human osteosarcoma MG-63, HS-Os-1, and murine LM8 cells were stably transfected with the ribozyme specific for AMF/PGI. The stable transfectant cells showed effective downregulation of AMF/PGI expression and subsequent abrogation of AMF/PGI secretion, which resulted in morphologic change with reduced growth, motility, and invasion. Silencing of AMF/PGI induced MET, in which upregulation of E-cadherin and cytokeratins, as well as downregulation of vimentin, were noted. The MET guided by AMF/PGI gene silencing induced osteosarcoma MG-63 to terminally differentiate into mature osteoblasts. Furthermore, MET completely suppressed the tumor growth and pulmonary metastasis of LM8 cells in nude mice. Thus, acquisition of malignancy might be completed in part by upregulation of AMF/PGI, and waiver of malignancy might also be controlled by downregulation of AMF/PGI.
Effect of financial incentives on incentivised and non-incentivised clinical activities: longitudinal analysis of data from the UK Quality and Outcomes Framework
Authors: T. Doran, E. Kontopantelis, J. M. Valderas, S. Campbell, M. Roland, C. Salisbury, D. Reeves
Journal: BMJ (2011)

<b>Objective</b> To investigate whether the incentive scheme for UK general practitioners led them to neglect activities not included in the scheme. <b>Design</b> Longitudinal analysis of achievement rates for 42 activities (23 included in incentive scheme, 19 not included) selected from 428 identified indicators of quality of care. <b>Setting</b> 148 general practices in England (653 500 patients). <b>Main outcome measures</b> Achievement rates projected from trends in the pre-incentive period (2000-1 to 2002-3) and actual rates in the first three years of the scheme (2004-5 to 2006-7). <b>Results</b> Achievement rates improved for most indicators in the pre-incentive period. There were significant increases in the rate of improvement in the first year of the incentive scheme (2004-5) for 22 of the 23 incentivised indicators. Achievement for these indicators reached a plateau after 2004-5, but quality of care in 2006-7 remained higher than that predicted by pre-incentive trends for 14 incentivised indicators. There was no overall effect on the rate of improvement for non-incentivised indicators in the first year of the scheme, but by 2006-7 achievement rates were significantly below those predicted by pre-incentive trends. <b>Conclusions</b> There were substantial improvements in quality for all indicators between 2001 and 2007. Improvements associated with financial incentives seem to have been achieved at the expense of small detrimental effects on aspects of care that were not incentivised.
Allergen immunotherapy induces a suppressive memory response mediated by IL-10 in a mouse asthma model
Authors: Joost L.M. Vissers, Betty C.A.M. van Esch, Gerard A. Hofman, Martien L. Kapsenberg, Frank R. Weller, Antoon J.M. van Oosterhout
Journal: Journal of Allergy and Clinical Immunology (2004)
Up-regulation of circulating miR-20a is correlated with hepatitis C virus-mediated liver disease progression
Authors: Shubham Shrivastava, Jessica Petrone, Robert Steele, Georg M. Lauer, Adrian M. Di Bisceglie, Ratna B. Ray
Journal: Hepatology (2013)

Chronic hepatitis C virus (HCV) infection is one of the major causes of liver fibrosis and liver transplantation in the United States. Circulating microRNAs (miRNAs) in the blood are emerging as biomarkers for pathological conditions. In the present study we performed a systematic screening approach to identify up-regulated miRNAs in the plasma/serum of HCV-infected patients with different stages of hepatic histological disease severity. We initially screened serum samples of HCV-infected patients with fibrosis and compared them with sera of healthy volunteers using serum miRNA array profiling and identified a group of modulated miRNAs. Subsequent study demonstrated that miR-20a and miR-92a in HCV-infected fibrosis patients sera were significantly up-regulated when compared with that of healthy volunteers or non-HCV-associated liver disease. We have also observed an increase of plasma miR-20a and miR-92a in acute and chronic HCV-infected patients as compared to that of healthy volunteers. However, there was no correlation between the plasma/serum levels of any of these miRNAs with HCV viral loads. We next investigated longitudinal plasma samples from HCV-infected patients. Our results suggested that miR-20a and miR-92a remained unaltered in HCV-infected patients who progressed from acute to chronic infection. On the other hand, miR-92a expression was reduced in acute to resolved individuals. These data provide evidence that plasma/serum levels of miR-20a and miR-92a have potential as sensitive and cost-effective biomarkers for early detection of HCV infection. Conclusion: Circulating miR-20a may serve as a potential for predictive biomarker in HCV-mediated fibrosis. (Hepatology 2013;53:863–871)
Skateboarding injuries of today
Authors: L Forsman, A Eriksson
Journal: British Journal of Sports Medicine (2001)

Skateboarding injuries have increased with the rise in popularity of the sport, and the injury pattern can be expected to have changed with the development of both skateboard tricks and the materials used for skateboard construction.To describe the injury pattern of today.The pattern of injuries, circumstances, and severity were investigated in a study of all 139 people injured in skateboarding accidents during the period 1995-1998 inclusive and admitted to the University Hospital of Umeå. This is the only hospital in the area, serving a population of 135 000.Three of the 139 injured were pedestrians hit by a skateboard rider; the rest were riders. The age range was 7-47 years (mean 16). The severity of the injuries was minor (AIS 1) to moderate (AIS 2); fractures were classified as moderate. The annual number of injuries increased during the study period. Fractures were found in 29% of the casualties, and four children had concussion. The most common fractures were of the ankle and wrist. Older patients had less severe injuries, mainly sprains and soft tissue injuries. Most children were injured while skateboarding on ramps and at arenas; only 12 (9%) were injured while skateboarding on roads. Some 37% of the injuries occurred because of a loss of balance, and 26% because of a failed trick attempt. Falls caused by surface irregularities resulted in the highest proportion of the moderate injuries.Skateboarding should be restricted to supervised skateboard parks, and skateboarders should be required to wear protective gear. These measures would reduce the number of skateboarders injured in motor vehicle collisions, reduce the personal injuries among skateboarders, and reduce the number of pedestrians injured in collisions with skateboarders.
Ubiquitin Ligase TRIM62 Regulates CARD9-Mediated Anti-fungal Immunity and Intestinal Inflammation
Authors: Zhifang Cao, Kara L Conway, Robert J Heath, Jason S Rush, Elizaveta S Leshchiner, Zaida G Ramirez-Ortiz, Natalia B Nedelsky, Hailiang Huang, Aylwin Ng, Agnès Gardet, Shih-Chin Cheng, Alykhan F Shamji, John D Rioux, Cisca Wijmenga, Mihai G Netea, Terry K Means, Mark J Daly, Ramnik J Xavier
Journal: Immunity (2015)
Modern Strategies for Hairy Cell Leukemia
Authors: Michael R. Grever, Gerard Lozanski
Journal: Journal of Clinical Oncology (2011)

Enormous progress in the treatment of hairy cell leukemia over the last five decades has emerged as a result of organized clinical investigations. Although interferon represented one of the initial major therapeutic advances in the management of this disease in 1984, the subsequent introduction of purine nucleoside analogs (pentostatin and cladribine) changed the natural history of this rare disease by achieving a high rate of complete and durable remissions. The disease-free survival after effective therapy has not reached a plateau, suggesting control but not cure of the disease. Identification of minimal residual disease in patients achieving a complete hematologic remission provides insight into the potential source for predicting eventual relapse. Modern strategies of targeted therapies directed against immunophenotypic markers on the leukemic cells provide hope that improved long-term control of the disease is possible. Combined chemoimmunotherapy may hold the highest promise for disease eradication, but the optimal strategy for using this approach is under active investigation. Despite the perception by hematologists that this disease has already been conquered, there are critically important unanswered questions that remain. Investigation of the bone marrow microenvironment and its impact on minimal residual disease may ultimately prevent relapse. Consideration of the median age of patients at diagnosis combined with a substantial relapse rate mandates continued pursuit of improved therapy. The ultimate goal will be to achieve cure rather than simple control of the disease.
Maintenance of physical activity and body weight in relation to subsequent quality of life in postmenopausal breast cancer patients
Authors: D.W. Voskuil, J.G.H. van Nes, J.M.C. Junggeburt, C.J.H. van de Velde, F.E. van Leeuwen, J.C.J.M. de Haes
Journal: Annals of Oncology (2010)
Glucose absorption from starch hydrolysates in the human jejunum.
Authors: B J Jones, B E Brown, J S Loran, D Edgerton, J F Kennedy, J A Stead, D B Silk
Journal: Gut (1983)

The intestinal absorption and mucosal hydrolysis of a partial and a complete alpha-amylase hydrolysate of corn starch, simulating the normal intermediary and end products of luminal starch digestion, was studied using an in vivo steady state jejunal perfusion technique in normal human subjects. Alpha-amylase was excluded from the test segment by proximal balloon occlusion. Products of hydrolysis during intestinal perfusion were identified using gel permeation chromatography. Three isocaloric, isotonic sugar saline solutions containing 140 mM glucose, 70 mM maltose and the partial amylase hydrolysate of starch (51.5 +/- 1.4% of glucose content comprising glucose polymers of more than 10 glucose units) were perfused in the first study. Net glucose absorption during perfusion of the partial hydrolysate and free glucose was similar, but significantly faster from maltose (p less than 0.05). Hydrolysis of the polymer fraction containing more than 10 glucose units was significantly slower (29.5 +/- 2.0% of infused load) than the lower molecular weight fraction (56.4 +/- 3.8%, p less than 0.001). As net glucose absorption from the partial hydrolysate was similar to that from glucose, despite the slow hydrolysis of the higher molecular weight fraction, it seemed likely that oligosaccharides in the more rapidly hydrolysed lower molecular weight fractions were exerting a kinetic advantage on glucose absorption. This was confirmed in a second study, where glucose absorption from a complete amylase hydrolysate consisting predominantly of maltose, maltotriose and alpha-limit dextrins, occurred significantly faster (81.8 +/- 4.8 mmol/h/25 cm) than from isocaloric free glucose (55.8 +/- 4.9 mmol/h/25 cm, p less than 0.001). Chromatograms of intestinal aspirates suggested that (1->4), but not 1->6) linked oligosaccharides liberated during luminal and brush-border hydrolysis of dietary starch conferred a kinetic advantage on glucose absorption.
Serum Folate and Risk of Fatal Coronary Heart Disease
Authors: R. Daniel Braun
Journal: JAMA (1996)

<h3>To the Editor.</h3> —Dr Morrison and colleagues<sup>1</sup>take little or no note of what I find to be a very important aspect of the data presented in their article. The folate data for men (in Table 3) show a relative risk (RR) of 1.36 (95% confidence interval [CI], 0.80-2.31) for those in the lowest quartile when compared with those in the highest quartile. In contrast, the data for women (presented in Table 4) show an RR of 2.83 (95% CI, 1.30-6.18) for women in the lowest quartile as compared with those in the highest quartile. Although the authors mention these data, they also comment that, "there was no statistically significant interaction by sex." I am unable to find anything in the article to justify this statement. Moreover, in the "Comment," the authors state, "It is not known if the increased RR in women as compared with men was a
Effect of Wortmannin on Human Eosinophil Responses<i>in Vitro</i>and on Bronchial Inflammation and Airway Hyperresponsiveness in Guinea Pigs<i>in Vivo</i>
Authors: CHARLES I. EZEAMUZIE, JALAJA SUKUMARAN, ELIZABETH PHILIPS
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

Many mediators activate eosinophils via transduction pathways involving the enzyme phosphatidylinositol 3-kinase. The initial investigation of wortmannin, a specific inhibitor of PI3-kinase, was of its effect on human and guinea pig eosinophil superoxide (O2 −) release and degranulation in vitro. Subsequently, the effect on allergen- and Sephadex-induced bronchial inflammation and airway hyperresponsiveness (AHR) in vivo in guinea pigs was investigated. Wortmannin potently inhibited complement C5a-induced O2 − generation and eosinophil peroxidase (EPO) release from human eosinophils, with 50% inhibition produced by a 1–10 nM concentration. Both aerosol allergen challenge of sensitized guinea pigs and intravenous injection of Sephadex beads in normal guinea pigs caused, in 24 h, significant eosinophilia and increased EPO activity in bronchoalveolar lavage fluid (BALF) and AHR to intravenous acetylcholine and histamine. In the allergic model, intranasal pretreatment with wortmannin had no effect on BALF eosinophilia, but dose dependently inhibited BALF EPO activity. At 1 mg/kg, the drug abolished the AHR to histamine, but not acetylcholine. In the Sephadex model, the drug significantly inhibited all three parameters (eosinophilia, increased EPO activity, and AHR to both spasmogens). These results show that wortmannin is a potent inhibitor of human eosinophil degranulation and that when administered intranasally can prevent AHR in allergen-challenged guinea pigs, probably by inhibiting eosinophil degranulation, but not their accumulation in BALF. This may be relevant to the possible clinical utility of wortmannin in conditions involving eosinophilic inflammation and AHR.