tbuckley/cabot-search huggingface dataset:
Evaluation of cricket helmet performance and comparison with baseball and ice hockey helmets
Authors: A S McIntosh, D Janda
Journal: British Journal of Sports Medicine (2003)

Protective helmets in sport are important for reducing the risk of head and facial injury. In cricket and other sports with projectiles, national test standards control the minimum helmet performance. However, there are few field data showing if helmets are effective in reducing head injury.(a) To examine the performance of cricket helmets in laboratory tests; (b) to examine performance with regard to test standards, game hazards, and helmet construction; (c) to compare and contrast these findings with baseball and ice hockey helmets.Impact tests were conducted on a selection of helmet models: five cricket, two baseball, and two ice hockey. Ball to helmet impacts at speeds of 19, 27, 36, and 45 m/s were produced using an air cannon and a Hybrid III dummy headform and neck unit. Free fall drop tests with a rigid headform on to a selection of anvils (flat rigid, flat deformable, and hemispherical rigid) were conducted. Resultant headform acceleration was measured and compared between tests.At the lower speed impacts, all helmets produced a good reduction in headform acceleration, and thus injury risk. At the higher speed impacts, the effectiveness was less. For example, the mean maximum headform accelerations for all cricket helmets at each speed were: 67, 160, 316, and 438 g for 19, 27, 36, and 45 m/s ball speeds respectively. Drop tests on to a hemispherical anvil produced the highest accelerations. The variation in performance increased as the magnitude of the impact energy increased, in both types of testing.The test method used for baseball helmets in which the projectile is fired at the helmet may be superior to helmet drop tests. Cricket helmet performance is satisfactory for low speed impacts, but not for impacts at higher, more realistic, speeds. Baseball and ice hockey helmets offer slightly better relative and absolute performance at the 27 m/s ball and puck impacts.
Obesity, Inflammation, and Cancer
Authors: Tuo Deng, Christopher J. Lyon, Stephen Bergin, Michael A. Caligiuri, Willa A. Hsueh
Journal: Annual Review of Pathology Mechanisms of Disease (2016)

Obesity, a worldwide epidemic, confers increased risk for multiple serious conditions, including cancer, and is increasingly recognized as a growing cause of preventable cancer risk. Chronic inflammation, a well-known mediator of cancer, is a central characteristic of obesity, leading to many of its complications, and obesity-induced inflammation confers additional cancer risk beyond obesity itself. Multiple mechanisms facilitate this strong association between cancer and obesity. Adipose tissue is an important endocrine organ, secreting several hormones, including leptin and adiponectin, and chemokines that can regulate tumor behavior, inflammation, and the tumor microenvironment. Excessive adipose expansion during obesity causes adipose dysfunction and inflammation to increase systemic levels of proinflammatory factors. Cells from adipose tissue, such as cancer-associated adipocytes and adipose-derived stem cells, enter the cancer microenvironment to enhance protumoral effects. Dysregulated metabolism that stems from obesity, including insulin resistance, hyperglycemia, and dyslipidemia, can further impact tumor growth and development. This review describes how adipose tissue becomes inflamed in obesity, summarizes ways these mechanisms impact cancer development, and discusses their role in four adipose-associated cancers that demonstrate elevated incidence or mortality in obesity.
After portal branch ligation in the rat, cellular proliferation in associated with selective induction of c-Ha-ras, p53, cyclin E, and Cdk2
Authors: P Starkel
Journal: Gut (2001)

<h3>BACKGROUND</h3> In liver regeneration after portal branch ligation we previously showed that early cellular changes are observed in both the proliferating and atrophying liver lobes. They are therefore not indicative of future proliferative response. In this study we attempted to define precisely, in the same model, the time at which the cellular processes diverge between the lobes by measuring various parameters associated with cellular proliferation. We also investigated the possible role of inhibitors of cell proliferation in the absence of progression towards the S phase in the atrophying lobes. <h3>AIMS</h3> Expression of p53, c-Ha-ras, cyclin E, cyclin dependent kinase (Cdk2), transforming growth factor (TGF)-β, and interleukin (IL)-1α and IL-1β were assessed in relation to their potential role in proliferating and atrophying cellular phenomenons. <h3>METHODS</h3> Immunohistochemistry, northern blotting, western blotting, and reverse transcription-polymerase chain reaction were performed, mainly at time points corresponding to mid-G1/S phase progression (8–24 hours after surgery). <h3>RESULTS</h3> The common and thus most likely non-specific response was still evident 5–8 hours after surgery and included an increase in IL-1 mRNA as well as p53 and cyclin E proteins. From 12 hours onwards, p53, c-Ha-ras, cyclin E, and Cdk2 were selectively induced in proliferating lobes whereas IL-1β was predominantly activated in atrophying lobes. No changes in TGF-β or IL-1α expression were observed at the same time points in any of the liver lobes. <h3>CONCLUSIONS</h3> The initial response to portal branch ligation and thus probably to partial hepatectomy seems to be non-specific for at least eight hours. Thereafter, p53, c-Ha-ras, cyclin E, and Cdk2 seem to drive cellular proliferation while IL-1β is associated with cellular atrophy. In contrast, TGF-β and IL-1α do not seem to play a role in determining the commitment of cells towards atrophy or proliferation.
Circulating Vitamin D Metabolites and Subclinical Atherosclerosis in Type 1 Diabetes
Authors: Michael C. Sachs, John D. Brunzell, Patricia A. Cleary, Andrew N. Hoofnagle, John M. Lachin, Mark E. Molitch, Michael W. Steffes, Bernard Zinman, Ian H. de Boer
Journal: Diabetes Care (2013)

OBJECTIVE People with type 1 diabetes are at high risk of premature atherosclerosis. Existing evidence suggests that impaired vitamin D metabolism may contribute to the development of atherosclerosis. We tested associations of circulating vitamin D metabolite concentrations with subclinical atherosclerosis among 1,193 participants with type 1 diabetes in the DCCT/EDIC study. RESEARCH DESIGN AND METHODS We measured plasma concentrations of 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D, and 24,25-dihydroxyvitamin D by mass spectrometry at the end of the DCCT. In a staggered cross-sectional design, we tested associations with coronary artery calcium (CAC), measured by computed tomography a median of 10 years later, and with common and internal carotid intima-media thickness (IMT), measured by B-mode ultrasonography on two occasions a median of 4 years later and a median of 10 years later. We hypothesized that lower concentrations of each vitamin D metabolite would be associated with increased risk of CAC and greater carotid IMT. RESULTS At the time metabolites were measured, mean age was 32.4 years and mean duration of diabetes was 7.5 years. The prevalence and severity of CAC tended to be lower—not higher—with lower concentrations of each vitamin D metabolite. For instance, in a fully adjusted multinomial logistic model, a 25 nmol/L lower 25-hydroxyvitamin D was associated with a 0.8-fold decrease in the odds of having higher CAC (95% CI 0.68–0.96, P = 0.01). No vitamin D metabolite was associated with either common or internal mean IMT. CONCLUSIONS We did not find evidence linking impaired vitamin D metabolism with increased subclinical atherosclerosis in type 1 diabetes.
Bronchoalveolar lavage cell analysis in measles viral pneumonia
Authors: S Myou, M Fujimura, M Yasui, T Ueno, T Matsuda
Journal: European Respiratory Journal (1993)

Although the immunological changes due to measles virus infection, such as suppression of delayed skin reactivity and increase in soluble CD8 in peripheral blood, have been demonstrated, the immunological changes in the lung during measles viral pneumonia (MVP) have not been reported. The aim of this study was to clarify the intrapulmonary immunological changes in MVP. We analysed cell differentials and lymphocyte surface antigens of bronchoalveolar lavage (BAL) cells, both in the acute and the convalescent phase of MVP by flow-cytometry, using CD4+, CD8+, CD8+CD11b+ and CD8+CD11b- monoclonal antibodies in five patients and six healthy control subjects. The absolute numbers of CD8+ and CD8+CD11b- cells were significantly greater both in the acute and the convalescent phase compared with those in controls. The percentages of CD8+ and CD8+CD11b- cells in the acute phase were significantly greater than those in controls and the convalescent phase. The CD4/CD8 ratios in the acute phase were significantly smaller than those in the convalescent phase and controls. In conclusion, the intrapulmonary immunological changes with an increase in CD8+ and CD8+CD11b- cells in BAL fluid of MVP are thought to be the primary reaction in measles virus-infected lungs.
A Family Intervention to Delay Nursing Home Placement of Patients With Alzheimer Disease
Authors: Mary S. Mittelman
Journal: JAMA (1996)

To determine the long-term effectiveness of comprehensive support and counseling for spouse-caregivers and families in postponing or preventing nursing home placement of patients with Alzheimer disease (AD).Randomized controlled intervention study.Outpatient research clinic in the New York City metropolitan area.Referred, volunteer sample of 206 spouse-caregivers of AD patients who enrolled in the study during a 3 1/2-year period. All patients were living at home at baseline and had at least 1 relative living in the area.Caregivers in the treatment group were provided with 6 sessions of individual and family counseling within 4 months of enrollment in the study and were required to join support groups. In addition, counselors were available for further counseling at any time.Time from enrollment of caregivers in the study to placement of the AD patients in a nursing home.Using Kaplan-Meier survival analysis, we estimated that the median time (weighted average of estimates for male and female caregivers) from baseline to nursing home placement of AD patients was 329 days longer in the treatment group than in the control group (z=2.29; P=.02). The relative risk (RR) from a Cox proportional hazard model of nursing home placement (intent-to-treat estimate) after adjusting for caregiver sex, patient age, and patient income was 0.65 (95% confidence interval [CI], 0.45 to 0.94; P=.02), indicating that caregivers were approximately two thirds as likely to place their spouses in nursing homes at any point in time if they were in the treatment group than if they were in the control group. Treatment had the greatest effect on risk of placement for patients who were mildly demented (RR, 0.18; 95% CI, 0.04 to 0.77) or moderately demented (RR, 0.38; 95% CI, 0.17 to 0.82).A program of counseling and support can substantially increase the time spouse-caregivers are able to care for AD patients at home, particularly during the early to middle stages of dementia when nursing home placement is generally least appropriate.
Safety and efficacy of weekly nab®-paclitaxel in combination with carboplatin as first-line therapy in elderly patients with advanced non-small-cell lung cancer
Authors: M.A. Socinski, C.J. Langer, I. Okamoto, J.K. Hon, V. Hirsh, S.R. Dakhil, R.D. Page, J. Orsini, H. Zhang, M.F. Renschler
Journal: Annals of Oncology (2012)

BackgroundThis analysis evaluates safety and efficacy in elderly (≥70 years old) versus younger patients enrolled in a phase III advanced non-small-cell lung cancer (NSCLC) trial.Patients and MethodsUntreated stage IIIB/IV patients with PS 0/1 were randomly assigned (1:1) to carboplatin AUC6, day 1 every 3 weeks, and either nab-paclitaxel (Abraxane) 100 mg/m2 weekly (nab-P/C) or solvent-based paclitaxel (Taxol) 200 mg/m2 day 1 every 3 weeks (sb-P/C). The primary end-point was overall response rate (ORR).ResultsFifteen percent of 1052 enrolled patients were elderly: nab-P/C, n = 74; sb-P/C, n = 82. In both age cohorts, the ORR was higher with nab-P/C versus sb-P/C (age ≥70: 34% versus 24%, P = 0.196; age <70: 32% versus 25%, P = 0.013). In elderly patients, progression-free survival (PFS) trended in favor of nab-P/C (median 8.0 versus 6.8 months, hazard ratio (HR) 0.687, P = 0.134), and overall survival (OS) was significantly improved (median 19.9 versus 10.4 months, HR 0.583, P = 0.009). In younger patients, PFS (median 6.0 versus 5.8 months, HR 0.903, P = 0.256) and OS (median 11.4 versus 11.3 months, HR 0.999, P = 0.988) were similar in both arms. Adverse events were similar in both age groups, with less neutropenia (P = 0.015), neuropathy (P = 0.001), and arthralgia (P = 0.029), and increased anemia (P = 0.007) with nab-P/C versus sb-P/C.ConclusionsIn elderly NSCLC patients, nab-P/C as first-line therapy was well tolerated and improved the ORR and PFS, with substantially longer OS versus sb-PC.
Altered Monocyte Responses to Defined TLR Ligands in Patients With Primary Biliary Cirrhosis *
Authors: Tin Ky Mao, Zhe-Xiong Lian, Carlo Selmi, Yasunori Ichiki, Paul Ashwood, Aftab A. Ansari, Ross L. Coppel, Shinji Shimoda, Hiromi Ishibashi, Eric M. Gershwin
Journal: Hepatology (2005)

The role of the adaptive immune response, with regard to the development of autoantibodies, has been extensively studied in primary biliary cirrhosis (PBC). However, the importance of innate immunity has been noted only recently. Based on the proposed role of microorganisms in the pathogenesis of the disease, we hypothesize that patients with PBC possess a hyper-responsive innate immune system to pathogen-associated stimuli that may facilitate the loss of tolerance. To address this issue, we isolated peripheral blood monocytes from 33 patients with PBC and 26 age-matched healthy controls and stimulated such cells in vitro with defined ligands for toll-like receptor (TLR) 2 (lipoteichoic acid; LTA), TLR3 (polyIC), TLR4 (lipopolysaccharide; LPS), TLR5 (flagellin), and TLR9 (CpG-B). Supernatant fluids from the cultures were analyzed for levels of 5 different pro-inflammatory cytokines, interleukin (IL)-1beta, IL-6, IL-8, IL-12p70, and TNF-alpha. After in vitro challenge with TLR ligands, PBC monocytes produced higher relative levels of pro-inflammatory cytokines, particularly IL-1beta, IL-6, IL-8, and TNF-alpha, compared with controls. In conclusion, monocytes from patients with PBC appear more sensitive to signaling via select TLRs, resulting in secretion of selective pro-inflammatory cytokines integral to the inflammatory response that may be critical in the breakdown of self-tolerance.
Integrative oncology in the Middle East: from traditional herbal knowledge to contemporary cancer care
Authors: E. Ben-Arye, E. Schiff, E. Hassan, K. Mutafoglu, S. Lev-Ari, M. Steiner, O. Lavie, A. Polliack, M. Silbermann, E. Lev
Journal: Annals of Oncology (2011)
The domain on the Duffy blood group antigen for binding Plasmodium vivax and P. knowlesi malarial parasites to erythrocytes.
Authors: C E Chitnis, A Chaudhuri, R Horuk, A O Pogo, L H Miller
Journal: The Journal of Experimental Medicine (1996)

Plasmodium vivax and the related simian malarial parasite P. knowlesi use the Duffy blood group antigen as a receptor to invade human erythrocytes and region II of the parasite ligands for binding to this erythrocyte receptor. Here, we identify the peptide within the Duffy blood group antigen of human and rhesus erythrocytes to which the P. vivax and P. knowlesi ligands bind. Peptides from the NH2-terminal extracellular region of the Duffy antigen were tested for their ability to block the binding of erythrocytes to transfected Cos cells expressing on their surface region II of the Duffy-binding ligands. The binding site on the human Duffy antigen used by both the P. vivax and P. knowlesi ligands maps to a 35-amino acid region. A 34-amino acid peptide from the equivalent region of the rhesus Duffy antigen blocked the binding of P. vivax to human erythrocytes, although the P. vivax ligand expressed on Cos cells does not bind rhesus erythrocytes. The binding of the rhesus peptide, but not the rhesus erythrocyte, to the P. vivax ligand was explained by interference of carbohydrate with the binding process. Rhesus erythrocytes, treated with N-glycanase, bound specifically to P. vivax region II. Thus, the interaction of P. vivax ligand with human and rhesus erythrocytes appears to be mediated by a peptide-peptide interaction. Glycosylation of the rhesus Duffy antigen appears to block binding of the P. vivax ligand to rhesus erythrocytes.
Asthma inhaler adherence determinants in adults: systematic review of observational data
Authors: Alexandra L. Dima, Gimena Hernandez, Oriol Cunillera, Montserrat Ferrer, Marijn de Bruin
Journal: European Respiratory Journal (2014)

Nonadherence to inhaled medication leads to poor asthma control and increased healthcare utilisation. Many studies exploring adherence determinants have been conducted, but summaries of the evidence are scarce. We performed a systematic review of observational research on determinants of asthma inhaler adherence among adults. We searched for articles in English reporting quantitative observational studies on inhaler adherence correlates among adults in developed countries, published in EMBASE, Medline, PsychInfo and PsychArticles in 1990–2014. Two coders independently assessed eligibility and extracted data, and assessed study quality. Results were summarised qualitatively into social and economic, and healthcare-, therapy-, condition- and patient-related factors. The 51 studies included mainly examined patient-related factors and found consistent links between adherence and stronger inhaler-necessity beliefs, and possibly older age. There was limited evidence on the relevance of other determinants, partly due to study heterogeneity regarding the types of determinants examined. Methodological quality varied considerably and studies performed generally poorly on their definitions of variables and measures, risk of bias, sample size and data analysis. A broader adoption of common methodological standards and health behaviour theories is needed before cumulative science on the determinants of adherence to asthma inhalers among adults can develop further.
Ambient particulate matter accelerates coagulation via an IL-6–dependent pathway
Authors: Gökhan M. Mutlu, David Green, Amy Bellmeyer, Christina M. Baker, Zach Burgess, Nalini Rajamannan, John W. Christman, Nancy Foiles, David W. Kamp, Andrew J. Ghio, Navdeep S. Chandel, David A. Dean, Jacob I. Sznajder, G.R. Scott Budinger
Journal: Journal of Clinical Investigation (2007)

The mechanisms by which exposure to particulate matter increases the risk of cardiovascular events are not known. Recent human and animal data suggest that particulate matter may induce alterations in hemostatic factors. In this study we determined the mechanisms by which particulate matter might accelerate thrombosis. We found that mice treated with a dose of well characterized particulate matter of less than 10 μM in diameter exhibited a shortened bleeding time, decreased prothrombin and partial thromboplastin times (decreased plasma clotting times), increased levels of fibrinogen, and increased activity of factor II, VIII, and X. This prothrombotic tendency was associated with increased generation of intravascular thrombin, an acceleration of arterial thrombosis, and an increase in bronchoalveolar fluid concentration of the prothrombotic cytokine IL-6. Knockout mice lacking IL-6 were protected against particulate matter–induced intravascular thrombin formation and the acceleration of arterial thrombosis. Depletion of macrophages by the intratracheal administration of liposomal clodronate attenuated particulate matter–induced IL-6 production and the resultant prothrombotic tendency. Our findings suggest that exposure to particulate matter triggers IL-6 production by alveolar macrophages, resulting in reduced clotting times, intravascular thrombin formation, and accelerated arterial thrombosis. These results provide a potential mechanism linking ambient particulate matter exposure and thrombotic events.
Socioeconomic status and indicators of asthma in children.
Authors: P Ernst, K Demissie, L Joseph, U Locher, M R Becklake
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

Differential access and utilization of medical care by the poor and rich may contribute to differences in asthma prevalence. We therefore studied the relationship of socioeconomic status (SES) to various indicators of asthma in the Canadian context of universal access to medical care. Information on respiratory symptoms, demographics, and home exposures of 1,111 primary school children was collected by questionnaire. Parental occupation was used to establish SES. Exercise-induced bronchospasm (EIB) after a 6-min free-running test was our measure of airways responsiveness and was available for 989 children. As compared with children from the most advantaged homes, children from the least advantaged homes were more likely to present EIB (OR: 2.26, 95% CI: 1.12 to 4.58) and to report night cough (OR: 2.30, 95% CI: 1.04 to 5.06) and cough with mucus (OR: 3.15, 95% CI: 1.06 to 9.33), while there was no significant excess of the report of wheeze or diagnosed asthma. Among factors potentially linked to SES, the presence of a cat at home (OR: 1.63, 95% CI: 1.02 to 2.61) and lower respiratory infection before 2 yr of age were associated with an excess of EIB (OR: 1.71, 95% CI: 1.16 to 2.52). Our results suggest that unidentified environmental factors contribute to the excess asthma morbidity in poor children.
Clinical Dutch-English Lambert-Eaton Myasthenic Syndrome (LEMS) Tumor Association Prediction Score Accurately Predicts Small-Cell Lung Cancer in the LEMS
Authors: Maarten J. Titulaer, Paul Maddison, Jacob K. Sont, Paul W. Wirtz, David Hilton-Jones, Rinse Klooster, Nick Willcox, Marko Potman, Peter A.E. Sillevis Smitt, Jan B.M. Kuks, Bart O. Roep, Angela Vincent, Silvère M. van der Maarel, J. Gert van Dijk, Bethan Lang, Jan J.G.M. Verschuuren
Journal: Journal of Clinical Oncology (2011)

Approximately one half of patients with Lambert-Eaton myasthenic syndrome (LEMS) have small-cell lung carcinomas (SCLC), aggressive tumors with poor prognosis. In view of its profound impact on therapy and survival, we developed and validated a score to identify the presence of SCLC early in the course of LEMS.We derived a prediction score for SCLC in LEMS in a nationwide cohort of 107 Dutch patients, and validated it in a similar cohort of 112 British patients. A Dutch-English LEMS Tumor Association Prediction (DELTA-P) score was developed based on multivariate logistic regression.Age at onset, smoking behavior, weight loss, Karnofsky performance status, bulbar involvement, male sexual impotence, and the presence of Sry-like high-mobility group box protein 1 serum antibodies were independent predictors for SCLC in LEMS. A DELTA-P score was derived allocating 1 point for the presence of each of the following items at or within 3 months from onset: age at onset ≥ 50 years, smoking at diagnosis, weight loss ≥ 5%, bulbar involvement, erectile dysfunction, and Karnofsky performance status lower than 70. The area under the curve of the receiver operating curve was 94.4% in the derivation cohort and 94.6% in the validation set. A DELTA-P score of 0 or 1 corresponded to a 0% to 2.6% chance of SCLC, whereas scores of 4, 5, and 6 corresponded to chances of SCLC of 93.5%, 96.6%, and 100%, respectively.The simple clinical DELTA-P score discriminated patients with LEMS with and without SCLC with high accuracy early in the course of LEMS.