tbuckley/cabot-search huggingface dataset:
Grouping of runners during marathon competition.
Authors: K Yamaji, R J Shephard
Journal: British Journal of Sports Medicine (1987)

Marathon runners tend to form clusters during competition, possibly as a means of improving their performance. Studies of international competitors in Fukuoka and Tokyo races have shown a density of 0.44 to 0.80 runners.m2 among those maintaining a pace of 4.8-5.6 m.s-1, clustering being most marked among elite performers. Some 95% of clustered runners maintained a minimum distance of 0.5-1.5 m from other competitors; moreover, such competitors avoided occupying an angle of +/- 15 degrees either before or behind other runners. The phenomenon merits closer study by those interested in the bettering of marathon performance.
Risk factors for pre-eclampsia at antenatal booking: systematic review of controlled studies
Authors: Kirsten Duckitt, Deborah Harrington
Journal: BMJ (2005)

<h3>Abstract</h3> <b>Objective</b> To determine the risk of pre-eclampsia associated with factors that may be present at antenatal booking. <b>Design</b> Systematic review of controlled studies published 1966-2002. <b>Data synthesis</b> Unadjusted relative risks were calculated from published data. <b>Results</b> Controlled cohort studies showed that the risk of pre-eclampsia is increased in women with a previous history of pre-eclampsia (relative risk 7.19, 95% confidence interval 5.85 to 8.83) and in those with antiphospholipids antibodies (9.72, 4.34 to 21.75), pre-existing diabetes (3.56, 2.54 to 4.99), multiple (twin) pregnancy (2.93, 2.04 to 4.21), nulliparity (2.91, 1.28 to 6.61), family history (2.90, 1.70 to 4.93), raised blood pressure (diastolic ≥ 80 mm Hg) at booking (1.38, 1.01 to 1.87), raised body mass index before pregnancy (2.47, 1.66 to 3.67) or at booking (1.55, 1.28 to 1.88), or maternal age ≥ 40 (1.96, 1.34 to 2.87, for multiparous women). Individual studies show that risk is also increased with an interval of 10 years or more since a previous pregnancy, autoimmune disease, renal disease, and chronic hypertension. <b>Conclusions</b> These factors and the underlying evidence base can be used to assess risk at booking so that a suitable surveillance routine to detect pre-eclampsia can be planned for the rest of the pregnancy.
Midpregnancy Serum C-Peptide Concentration and Subsequent Pregnancy-Induced Hypertension
Authors: Ichiro Yasuhi, Joseph W. Hogan, Jacob Canick, Maryellen B. Sosa, Marshall W. Carpenter
Journal: Diabetes Care (2001)

OBJECTIVE—To test the hypothesis that elevated midpregnancy serum insulin (IRI) and C-peptide (CP) concentrations are associated with later development of pregnancy-induced hypertension (PIH), independent of prepregnancy obesity and midpregnancy blood pressure. RESEARCH DESIGN AND METHODS—In this prospective study, a cohort of normotensive women, ages ≥18 years, performed a 50-g glucose challenge test at 24–30 weeks’ gestational age. Blood samples were collected after an overnight fast and 1 h after glucose ingestion. Serum IRI and CP concentrations were measured in each sample. Maternal height, blood pressure, and proteinuria were measured at the time of glucose challenge testing and after 36 weeks’ gestational age. RESULTS—Of 320 subjects enrolled, 44 women (13.8%) had subsequent PIH. Crude odds ratios (ORs) for development of PIH associated with each 1 U rise in log fasting IRI, log fasting CP, and glucose-induced increase in CP (expressed as log [postprandial CP/fasting CP]) were 2.0 (95% CI 1.3–3.3), 1.8 (CI 1.2–2.7), and 2.3 (CI 1.1–4.9), respectively. After controlling for prepregnancy BMI, gestational age, and midpregnancy mean arterial pressure, adjusted ORs corresponding to log fasting IRI and CP for the development of PIH were 1.3 (95% CI 0.7–2.3) and 1.7 (CI 1.1–2.7), respectively, and, after adjustment for fasting CP, the adjusted OR of the glucose-induced rise in log CP was 3.7 (CI 1.5–9.3). CONCLUSIONS—Mid-pregnancy fasting and postoral glucose CP levels are associated with subsequent development of PIH, independent of maternal obesity and midpregnancy baseline blood pressure. These findings may reflect an amplified β-cell response to glycemic stimulus, similar to that found in states of insulin resistance, that appears to be independently associated with PIH.
Occult Axillary Node Metastases in Breast Cancer Are Prognostically Significant: Results in 368 Node-Negative Patients With 20-Year Follow-Up
Authors: Lee K. Tan, Dilip Giri, Amanda J. Hummer, Katherine S. Panageas, Edi Brogi, Larry Norton, Clifford Hudis, Patrick I. Borgen, Hiram S. Cody
Journal: Journal of Clinical Oncology (2008)

In breast cancer, sentinel lymph node (SLN) biopsy allows the routine performance of serial sections and/or immunohistochemical (IHC) staining to detect occult metastases missed by conventional techniques. However, there is no consensus regarding the optimal method for pathologic examination of SLN, or the prognostic significance of SLN micrometastases.In 368 patients with axillary node-negative invasive breast cancer, treated between 1976 and 1978 by mastectomy, axillary dissection, and no systemic therapy, we reexamined the axillary tissue blocks following our current pathologic protocol for SLN. Occult lymph node metastases were categorized by pattern of staining (immunohistochemically positive or negative [IHC+/-], hematoxylin-eosin staining positive or negative [H & E +/-]), number of positive nodes (0, 1, > 1), number of metastatic cells (0, 1 to 20, 21 to 100, > 100), and largest cluster size (<or= 0.2 mm [pN0(i+)], 0.3 to 2.0 mm [pN1(mi)], > 2.0 mm [pN1a]). We report 20-year results as overall survival (OS), disease-free survival (DFS), and disease-specific death (DSD).A total of 23% of patients (83 of 368) were converted to node-positive. Of these, 73% were <or= 0.2 mm in size (pN0(i+)), 20% were 0.3 to 2.0 mm (pN1(mi)), and 6% were more than 2 mm (pN1a). On univariate and multivariate analysis, pattern of staining, number of positive nodes, number of metastatic cells, and cluster size were all significantly related to both DFS and DSD. On multivariate analysis, each of these measures had significance comparable to, or greater than, tumor size, grade or lymphovascular invasion.In breast cancer patients staged node-negative by conventional single-section pathology, occult axillary node metastases detected by our current pathologic protocol for SLN are prognostically significant.
Mutational analysis of the high affinity immunoglobulin E receptor beta subunit gene in asthma
Authors: P. W Dickson, Z. Y H Wong, S. B Harrap, M. J Abramson, E H. Walters
Journal: Thorax (1999)

<h3>BACKGROUND</h3> The gene for the β subunit of the high affinity receptor for immunoglobulin E (FcεRI-β) on chromosome 11q13 is linked with clinical asthma and certain mutations have been identified. A study was undertaken to identify DNA variation in the FcεRI-β gene in a population sample in which linkage between 11q13 and asthma was explained by bronchial hyperreactivity (BHR) but not atopy. <h3>METHODS</h3> DNA samples from 71 subjects with asthma, atopy, or BHR were analysed. The complete coding region, some of the introns, and some of the 5′ untranscribed region of the FcεRI-β gene were sequenced. <h3>RESULTS</h3> In the subjects studied there were no deviations from the published sequence in any of the seven coding exons of the FcεRI-β gene. In particular, the three previously reported mutations (Ile181, Leu183, Glu237) were not detected. Two new polymorphisms were discovered, one at position 243 in the 5′ untranscribed region and one at position 4390 in intron III. Neither of these variants showed significant association with asthma, atopy, or BHR. <h3>CONCLUSIONS</h3> These results suggest that, in the population studied, linkage of asthma and BHR to 11q13 is not explained by mutations in the FcεRI-β gene. Other mutations in the non-coding region of this gene or in adjacent genes must explain the linkage findings in this study.
Seq and CLIP through the miRNA world
Authors: Nitish Mittal, Mihaela Zavolan
Journal: Genome biology (2014)

Abstract High-throughput sequencing of RNAs crosslinked to Argonaute proteins reveals not only a multitude of atypical miRNA binding sites but also of miRNA targets with atypical functions, and can be used to infer quantitative models of miRNA-target interaction strength.
Influence of rugby injuries on players' subsequent health and lifestyle: beginning a long term follow up
Authors: A J Lee, W M Garraway, W Hepburn, R Laidlaw
Journal: British Journal of Sports Medicine (2001)

Objectives —To describe the current rugby playing status of a cohort of 1169 men who had previously participated in an epidemiological survey of rugby injuries during the 1993–1994 season, and assess the consequences of rugby injuries sustained. Methods —In May 1998, 911 (78%) men completed a questionnaire reporting their current involvement in rugby and the influence that the 324 (71%) injuries they had sustained four years earlier had since had on their health and wellbeing. Results —The most common reasons given by the 390 (43%) ex-players for ceasing to play rugby were family (10%), employment (25%), and an injury sustained while playing rugby (26%), 80% of which were dislocations, strains, and sprains, mainly to the knee (35%), back (14%), and shoulder (9%). A significantly (χ 2 test 21.7, df = 1, p&lt;0.001) higher proportion of current players (90%) undertook (non-rugby) sporting activities compared with ex-players (78%). Few ex-players undertook coaching (12%) and refereeing (2%). Only 22 (9%) men reported significant negative effects to employment, family life, and health up to mid-1998 from injuries that occurred during the 1993–1994 season, although the impact on their lifestyle had been substantial in some cases. Conclusions —With the recent increase in the incidence of dislocation, strain, and sprain injuries in rugby football, the findings of this follow up could have a great impact on the game in the future. Although this survey has shown that, so far, only a small proportion of players suffer significant effects of rugby injuries, four years is not long enough to assess the long term effects. This cohort of rugby players need to be followed up for at least a further 20 years to determine whether there is a higher incidence of subsequent degenerative joint disease or other long term sequelae to injuries sustained while playing rugby.
COMPARATIVE STUDIES IN ROUS SARCOMA WITH VIRUS, TUMOR CELLS AND CHICK EMBRYO CELLS TRANSFORMED IN VITRO BY VIRUS
Authors: Herbert R. Morgan, Angelo P. Andrese
Journal: The Journal of Experimental Medicine (1962)

Chick embryo fibroblasts infected with Rous sarcoma virus in vitro are rendered malignant for such cells produce typical Rous sarcomas when injected into susceptible chicks since the tumors produced predominantly retain the sex chromatin patterns of the donor cells when such cells are injected into a recipient of the opposite sex. However, examination of the sex chromatin of cells at the periphery of the tumor shows presence of recipient cells though the bulk of the tumor is clearly of donor cell origin. Such tumors grow and cause death of the recipient. Injection of RSV induces tumors of the sex of the recipient as also does the injection of transformed cells rendered incapable of multiplication by x-rays. Following their injection into susceptible chicks, the cells transformed in vitro by virus behave in the same manner as tumor cells obtained from tumors induced by virus in vivo and cultivated in the same conditions in vitro. When such tumors induced by transformed cells are serially transferred in recipients of the opposite sex, they gradually convert to the sex of the recipient indicating that the tumors are not indefinitely transplantable. These chick embryo fibroblasts transformed in vitro show the same neo-plastic properties as tumor cells when they are introduced into the cheek pouch of the hamster or the eye of the guinea pig.
Macrophage-derived foam cells freshly isolated from rabbit atherosclerotic lesions degrade modified lipoproteins, promote oxidation of low-density lipoproteins, and contain oxidation-specific lipid-protein adducts.
Authors: M E Rosenfeld, J C Khoo, E Miller, S Parthasarathy, W Palinski, J L Witztum
Journal: Journal of Clinical Investigation (1991)

Pure macrophage-derived foam cells (MFC) were isolated from the aortas of rabbits made atherosclerotic by balloon deendothelialization followed by diet-induced hypercholesterolemia. The MFC were isolated under sterile conditions using an enzymatic digestion procedure and discontinuous density gradient centrifugation. The purity of the MFC preparations was verified immunocytochemically with the macrophage specific monoclonal antibody RAM-11. MFC plated in medium containing 0.5% FCS for 24 h contained approximately 600 micrograms cholesterol per mg cell protein, 80% of which was esterified cholesterol. The MFC specifically degraded low density lipoprotein (LDL), acetyl-LDL, copper oxidized LDL, and beta-very low density lipoprotein (beta-VLDL) at rates comparable to mouse peritoneal macrophages (MPM) in 5-h assays. MFC within sections of the atherosclerotic lesions from the ballooned rabbits as well as the MFC isolated from the same lesions in the presence of antioxidants, exhibited positive immunoreactivity with polyclonal guinea pig antisera and mouse monoclonal antibodies directed against malondialdehyde-LDL, and 4-hydroxynonal-LDL. The MFC also exhibited the capacity to induce the oxidation of LDL at rates comparable to those exhibited by MPM and rabbit aortic endothelial cells. These data provide direct evidence that arterial wall macrophages express modified LDL receptors in vivo, contain epitopes found in oxidized-LDL and are capable of oxidizing LDL even when maximally loaded with cholesterol.
Cerebral Blood Flow Velocity and Periventricular White Matter Hyperintensities in Type 2 Diabetes
Authors: Vera Novak, David Last, David C. Alsop, Amir M. Abduljalil, Kun Hu, Lukas Lepicovsky, Jerry Cavallerano, Lewis A. Lipsitz
Journal: Diabetes Care (2006)

Diabetes increases the risk for cerebromicrovascular disease, possibly through its effects on blood flow regulation. The aim of this study was to assess the effects of type 2 diabetes on blood flow velocities (BFVs) in the middle cerebral arteries and to determine the relationship between white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI) and BFVs.We measured BFVs in 28 type 2 diabetic and 22 control subjects (aged 62.3 +/- 7.2 years) using transcranial Doppler ultrasound during baseline, hyperventilation, and CO(2) rebreathing. WMHs were graded, and their volume was quantified from fluid-attenuated inversion recovery images on a 3.0 Tesla MRI.The diabetic group demonstrated decreased mean BFVs and increased cerebrovascular resistance during baseline, hypo- and hypercapnia (P < 0.0001), and impaired CO(2) reactivity (P = 0.05). WMH volume was negatively correlated with baseline BFV (P < 0.0001). A regression model revealed that baseline BFVs were negatively associated with periventricular WMHs, HbA(1c) (A1C), and inflammatory markers and positively associated with systolic blood pressure (R(2) = 0.86, P < 0.0001).Microvascular disease in type 2 diabetes, which manifests as white matter abnormalities on MRI, is associated with reduced cerebral BFVs, increased resistance in middle cerebral arteries, and inflammation. These findings are clinically relevant as a potential mechanism for cerebrovascular disease in elderly with type 2 diabetes.
Liver cancer: EphrinA2 promotes tumorigenicity through Rac1/Akt/NF-κB signaling pathway
Authors: Yu-Xiong Feng, Jiang-Sha Zhao, Jing-Jing Li, Tao Wang, Shu-Qun Cheng, Yunfei Yuan, Fudi Wang, Xiao-Fan Wang, Dong Xie
Journal: Hepatology (2009)

Eph/Ephrin family, one of the largest receptor tyrosine kinase families, has been extensively studied in morphogenesis and neural development. Recently, growing attention has been paid to its role in the initiation and progression of various cancers. However, the role of Eph/Ephrins in hepatocellular carcinoma (HCC) has been rarely investigated. In this study, we found that the expression of EphrinA2 was significantly up-regulated in both established cell lines and clinical tissue samples of HCC, and the most significant increase was observed in the tumors invading the portal veins. Forced expression of EphrinA2 in HCC cells significantly promoted in vivo tumorigenicity, whereas knockdown of this gene inhibited this oncogenic effect. We further found that suppression of apoptosis, rather than accelerating proliferation, was responsible for EphrinA2-enhanced tumorigenicity. In addition, EphrinA2 endowed cancer cells with resistance to tumor necrosis factor alpha (TNF-alpha)-induced apoptosis, thus facilitating their survival. Furthermore, we disclosed a novel EphrinA2/ras-related c3 botulinum toxin substrate 1 (Rac1)/V-akt murine thymoma viral oncogene homolog (Akt)/nuclear factor-kappa B (NF-kappaB) pathway contributing to the inhibitory effect on apoptosis in HCC cells.This study revealed that EphrinA2 played an important role in the development and progression of HCC by promoting the survival of cancer cells, indicating its role as a potential therapeutic target in HCC.
Hospice Referral Practices for Children With Cancer: A Survey of Pediatric Oncologists
Authors: Kimberly Fowler, Katherine Poehling, Dean Billheimer, Rodney Hamilton, Huiyun Wu, John Mulder, Haydar Frangoul
Journal: Journal of Clinical Oncology (2006)

To examine hospice referral patterns among pediatric oncologists and identify barriers to referral.A self-administered survey was sent to 1,200 pediatric oncologists who are members of Children's Oncology Group. Two electronic mail messages followed by traditional mail surveys were sent to eligible physicians. Pediatricians and pediatric oncologists developed, pretested, and modified the survey for item clarification.Of 944 eligible pediatric oncologists surveyed, 632 replied, yielding a response rate of 67%. Most respondents reported having access to palliative care programs (65%) and hospice services (85%), but few (27%) had access to inpatient hospice services. More respondents reported feeling comfortable managing end-of-life pain than psychological issues (86% v 67%, respectively). Many pediatric oncologists (62%) reported that half or more of their patients died in the hospital. In multivariate analysis, physicians with access to hospice that accepts patients receiving chemotherapy had more patients die at home than in hospital compared with physicians without access to such services (P = .007). The probability of hospice referral was positively associated with the presence of a hospice facility (P < .001) and with a larger size oncology group (P = .024). Only 2.5% of respondents referred patients at the time of relapse. Continued therapy was cited as the most common reason for not making a referral, and was significantly higher when hospice did not admit children receiving chemotherapy (P = .002).Hospice referral for children with cancer is usually made late in the course of their disease and might improve if hospice admits patients who are actively receiving chemotherapy.
PHARMACOLOGIC PROPHYLAXIS FOR VENOUS THROMBOEMBOLISM: THE MOST FREQUENT REASON FOR OMITTING ORDERED DOSES IS PATIENT REFUSAL
Authors: John Fanikos, Leslie-Ann Stevens, Gregory Piazza, Mathew Labreche, Elaine Catapane, Lena Novack, Samuel Z. Goldhaber
Journal: Journal of the American College of Cardiology (2010)
Glioblastoma Cells Require Glutamate Dehydrogenase to Survive Impairments of Glucose Metabolism or Akt Signaling
Authors: Chendong Yang, Jessica Sudderth, Tuyen Dang, Robert G. Bachoo, Jeffrey G. McDonald, Ralph J. DeBerardinis
Journal: Cancer Research (2009)

Abstract Oncogenes influence nutrient metabolism and nutrient dependence. The oncogene c-Myc stimulates glutamine metabolism and renders cells dependent on glutamine to sustain viability (“glutamine addiction”), suggesting that treatments targeting glutamine metabolism might selectively kill c-Myc–transformed tumor cells. However, many current or proposed cancer therapies interfere with the metabolism of glucose, not glutamine. Here, we studied how c-Myc–transformed cells maintained viability when glucose metabolism was impaired. In SF188 glioblastoma cells, glucose deprivation did not affect net glutamine utilization but elicited a switch in the pathways used to deliver glutamine carbon to the tricarboxylic acid cycle, with a large increase in the activity of glutamate dehydrogenase (GDH). The effect on GDH resulted from the loss of glycolysis because it could be mimicked with the glycolytic inhibitor 2-deoxyglucose and reversed with a pyruvate analogue. Furthermore, inhibition of Akt signaling, which facilitates glycolysis, increased GDH activity whereas overexpression of Akt suppressed it, suggesting that Akt indirectly regulates GDH through its effects on glucose metabolism. Suppression of GDH activity with RNA interference or an inhibitor showed that the enzyme is dispensable in cells able to metabolize glucose but is required for cells to survive impairments of glycolysis brought about by glucose deprivation, 2-deoxyglucose, or Akt inhibition. Thus, inhibition of GDH converted these glutamine-addicted cells to glucose-addicted cells. The findings emphasize the integration of glucose metabolism, glutamine metabolism, and oncogenic signaling in glioblastoma cells and suggest that exploiting compensatory pathways of glutamine metabolism can improve the efficacy of cancer treatments that impair glucose utilization. [Cancer Res 2009;69(20):7986–93]
Delayed hepcidin response explains the lag period in iron absorption following a stimulus to increase erythropoiesis
Authors: D M Frazer
Journal: Gut (2004)

<b>Introduction:</b> The delay of several days between an erythropoietic stimulus and the subsequent increase in intestinal iron absorption is commonly believed to represent the time required for body signals to programme the immature crypt enterocytes and for these cells to migrate to the villus. Recent data however suggest that signals from the body to alter absorption are mediated by circulating hepcidin and that this peptide exerts its effect on mature villus enterocytes. <b>Methods:</b> We have examined the delay in the absorptive response following stimulated erythropoiesis using phenylhydrazine induced haemolysis and correlated this with expression of hepcidin in the liver and iron transporters in the duodenum. <b>Results:</b> There was a delay of four days following haemolysis before a significant increase in iron absorption was observed. Hepatic hepcidin expression did not decrease until day 3, reaching almost undetectable levels by days 4 and 5. This coincided with the increase in duodenal expression of divalent metal transporter 1, duodenal cytochrome b, and Ireg1. <b>Conclusion:</b> These results suggest that the delayed increase in iron absorption following stimulated erythropoiesis is attributable to a lag in the hepcidin response rather than crypt programming, and are consistent with a direct effect of the hepcidin pathway on mature villus enterocytes.