tbuckley/cabot-search huggingface dataset:
Low risk of concussions in top-level karate competition
Authors: Rafael Arriaza, Dusana Cierna, Patricia Regueiro, David Inman, Franco Roman, Benjamin Abarca, Mercé Barrientos, Miguel A Saavedra
Journal: British Journal of Sports Medicine (2016)

Background Although it is well known that injuries occur in combat sports, the true incidence of concussions is not clearly defined in the literature for karate competition. Aim To determine the incidence of concussions in top-level (World Karate Federation World Championships) karate competition. Methods Injuries that took place in 4 consecutive World Karate Championships (from 2008 to 2014) were prospectively registered. A total of 4625 fights (2916 in the male category and 1709 in the female category) were scrutinised, and concussions were identified and analysed separately for frequency (rate per fight) and injury risk. Results A total of 4 concussions were diagnosed by the attending physicians after carrying out athlete examinations. Globally, there was 1 concussion in every 1156 fights, or 0.43/1000 athlete-exposures (AE). In male athletes, the rate of concussion was 1/5832 min of fighting, and in female athletes, it was 1/6836 min. OR for concussion in women is 0.57 (95% CI 0.06 to 5.47; z=0.489; p=0.6249) and risk ratio for concussions in men is RR 1.478 (95% CI 0.271 to 8.072), p=0.528, representing a higher risk of definite concussions in men than in women, but not statistically significant. There is not a significantly higher risk of concussions in team competition (no weight limit) when compared with individual competition (held with strict weight limits for each category). Conclusion The risk of concussions in top-level karate competition is low, with a tendency for an increased risk for men and for competition without weight limits, but not statistically significant with respect to women or individual competition.
Dose-escalation of REgorafenib for patients with previously treated metastatic colorectal cancer - DEREGULATE study
Authors: Ryuta Nishitai, Dai Manaka, Hisashi Amaike, Akira Nozaki, Masashi Kanai, Daisuke Yamaguchi, Takeshi Yazawa, Kazuhiko Kawashima, Fusao Ikeda
Journal: Annals of Oncology (2015)
PTH-069 Alcohol and liver diseases: recognition and impact on admissions in a district general hospital
Authors: M H Chapman, S Mangaleswaran, A R R Henderson, E M Alstead
Journal: Gut (2010)

<h3>Introduction</h3> Self reported alcohol intake in the 2005 UK census suggests that 38% of men and 18% of women drink an average of &gt;20 g of alcohol per day. The recently published National Plan for Liver Services in the UK1 documents the increasing problem of alcohol and liver related diseases and recommends that all UK district general hospitals should have hepatologists and alcohol services on site. <h3>Methods</h3> We assessed the burden of alcohol and liver related admissions in a busy DGH by examining a random sample of case notes of adult general medical and surgical admissions over a 7-day period. Stroke, elderly care, obstetric and paediatric wards were excluded. An Alcohol Attributable Fraction (ICD-10 figures) was calculated for each case according to primary and secondary diagnoses. <h3>Results</h3> Our hospital is a typical DGH with 596 beds (60% medicine), with an average of 70 patients admitted per day for average of 9 days. At the time of the audit there was no dedicated alcohol liaison service. Notes were reviewed for 246 patients (143 medicine, 37 surgery, 66 orthopaedics: 111 male, 135 female). An alcohol history (simple yes/no) was documented in 120 (49%) and smoking history in 137 (56%). Any more thorough alcohol history (eg, occasional, binge or units) was documented in only 52 (21%). A history of illicit drug use was documented in 1 (0.4%). The primary diagnosis was reported as directly alcohol related in 12 (5%) (alcohol related liver disease/cirrhosis 10; head injury while intoxicated 2) and liver related in 1 (0.4%, cryptogenic cirrhosis). Less overt diagnoses associated with alcohol were either not recognised or reported, none being documented in medical notes. The mean Alcohol Attributable Fraction for admission diagnoses was 8.0%, or 12.4% when including all those with a fall/fracture as per ICD-10 classification. Documentation of referral to alcohol services was found in 5 (42% of those recognised as alcohol related). Hepatitis or metabolic liver disease were not causes for admission (0%). 29 (12%) of non-liver related admissions had abnormal liver biochemistry. Of these, 13 (45%) had evidence of further investigation for a cause (ultrasound, hepatitis, autoantibody and/or metabolic screen). <h3>Conclusion</h3> Alcohol associated illness is a common cause of hospital admission (Alcohol Attributable Fraction 8%–12%) but recognition and documentation of alcohol use is poor. Hepatitis and metabolic liver diseases are uncommon reasons for admission. Better recognition, implementation of brief intervention strategies and/or referral to alcohol services may reduce the predicted future harmful impact of alcohol on personal and public health.
SPARC contributes to Leukemia Growth and Aggressive Disease in Acute Myeloid Leukemia (AML)
Authors: Houda Alachkar, Kati Maharry, Ramasamy Santhanam, Paolo Neviani, Stefano Volinia, Jessica Kohlschmidt, Klaus H. Metzeler, Adrienne M Dorrance, Sebastian Schwind, Heiko Becker, Jason H. Mendler, Ann-Kathrin Eisfeld, Susan Whitman, Krzysztof Mrózek, Ramiro Garzon, Danilo Perrotti, Michael A. Caligiuri, Richard M. Stone, Guido Marcucci, Clara D. Bloomfield
Journal: Blood (2012)
Abstract 3111: JNK/c-Jun- and NF-κB-mediated microRNA-221 governs tumor suppressor HDAC6 to potentiate malignant progression of liver cancer
Authors: Hyung Seok Kim, Qingyu Shen, Jung Woo Eun, Woo Chan Shin, Hee Doo Yang, Won Sang Park, Joung Young Lee, Suk Woo Nam
Journal: Cancer Research (2015)

Abstract Many clinical studies of cancer patients have established that the most common reason behind changes in HDAC function is its overexpression. However, among HDACs in liver cancer, HDAC6, a cytoplasmic tubulin deacetylase, is uniquely endowed with a tumor suppressor, but the mechanism underlying HDAC6 inactivation has yet to be uncovered. In this study we show that genetic and epigenetic dysregulation was not part of the HDAC6 inactivation mechanism. Instead, microRNA-221-3p (miR-221) directly suppressed HDAC6 in hepatocellular carcinoma (HCC) cells. A comprehensive miRNA profiling analysis identified seven putative endogenous miRNAs that are significantly upregulated in HCC. Ectopic expression of miRNA mimics in Dicer knockdown cells evidenced miR-221 to suppress HDAC6 in HCC cells. Notably, targeted-disruption of miR-221 repressed cancer cell growth and proliferation, and it recapitulated HDAC6 overexpression effects in HCC cells. Our results also demonstrate that c-Met-mediated c-Jun NH2-terminal kinase (JNK)/c-Jun signaling induced miR-221 to suppress HDAC6 and was sustained in liver cancer cells but not in normal hepatic cells. In addition, cytokine-induced NF-κBp65 independently regulated miR-221, thereby suppressing HDAC6 expression in liver cancer cells. HCC tissues derived from chemical-induced rat liver cancer models validated that JNK/c-Jun activation and NF-kBp65 nuclear translocation are essential for the transcriptional activation of oncogenic miR-221 to repress tumor suppressor HDAC6 in HCC. In conclusion, our finding suggest that the functional loss or suppression of the tumor suppressor HDAC6 is caused by miR-221 through coordinated JNK/c-Jun- and NF-κB-signaling pathways during liver tumorigenesis, providing a novel target for the molecular treatment of liver malignancies. Citation Format: Hyung Seok Kim, Qingyu Shen, Jung Woo Eun, Woo Chan Shin, Hee Doo Yang, Won Sang Park, Joung Young Lee, Suk Woo Nam. JNK/c-Jun- and NF-κB-mediated microRNA-221 governs tumor suppressor HDAC6 to potentiate malignant progression of liver cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3111. doi:10.1158/1538-7445.AM2015-3111
Abstract 2346: Targeting the tumor immune response for pro-senescence therapy in prostate cancer
Authors: Diletta Di Mitri, JingJing Chen, Andrea Alimonti
Journal: Cancer Research (2015)

Abstract Cellular senescence is a stable growth arrest that constrains cell cycle progression in case proliferation becomes aberrant, thus limiting tumorigenesis. Oncogenic mutations and loss of tumor suppressor genes that cause uncontrolled cell-cycle progression are required events in tumor development. Nevertheless, many of these genetic alterations retain an intrinsic tumor-suppressive potential that gives rise to oncogene-induced senescence and tumor suppressor loss-induced senescence. Interestingly, many evidences support the idea that a strong interplay occurs between senescence, cancer cells, and tumor infiltrating immune populations, thus opening at the possibility to tune such interplay for cancer treatment. Indeed, tumor infiltrating T helper 1 cells can drive senescence in cancers in a cytokine-induced manner, by secreting IFNγ and TNFα in the tumor microenvironment. In addition, we recently described a model where Pten loss induced senescence is hindered in prostate tumor by non-cell-autonomous mechanisms. Our study support a model where tumor-infiltrating CD11b+Gr-1+ myeloid cells paracrinally triggers tumor senescence evasion in the prostate of Pten null mice, eventually promoting tumor progression. These findings we’ll be discussed. Interestingly, we will present new evidences from our lab indicating that M1 macrophages are polarized to the M2 phenotype in both Pten pc-/- and that treatments that interfere with the M1-M2 polarization and switch the skewing to the M1 polarization profile can induce senescence in Pten; Trp53pc-/- invasive prostate cancer tumours thereby arresting tumour progression. These findings open at the possibility that M1 directly control senescence in tumor cells. Finally, we have identified a gene expression signature that distinguishes myeloid infiltration in tumors and can be used as a predictive marker for tumor progression in prostate cancer patients. These evidences we’ll be also discussed. Citation Format: Diletta Di Mitri, JingJing Chen, Andrea Alimonti. Targeting the tumor immune response for pro-senescence therapy in prostate cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2346. doi:10.1158/1538-7445.AM2015-2346
What Lengths Should We Go to for Fluoroscopy-Free Resuscitative Endovascular Balloon Occlusion of the Aorta?
Authors: Michael D. Goodman, Timothy A. Pritts
Journal: JAMA Surgery (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Surgery HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Surgery journal
The Insulin Treatment of Diabetes Mellitus.
Journal: JAMA (1924)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Genome-wide association study of immunoglobulin light chain amyloidosis in three patient cohorts: comparison with myeloma
Authors: M I da Silva Filho, A Försti, N Weinhold, I Meziane, C Campo, S Huhn, J Nickel, P Hoffmann, M M Nöthen, K-H Jöckel, S Landi, J S Mitchell, D Johnson, G J Morgan, R Houlston, H Goldschmidt, A Jauch, P Milani, G Merlini, D Rowcieno, P Hawkins, U Hegenbart, G Palladini, A Wechalekar, S O Schönland, K Hemminki
Journal: Leukemia (2016)
A gene network regulated by the transcription factor VGLL3 as a promoter of sex-biased autoimmune diseases
Authors: Yun Liang, Lam C Tsoi, Xianying Xing, Maria A Beamer, William R Swindell, Mrinal K Sarkar, Celine C Berthier, Philip E Stuart, Paul W Harms, Rajan P Nair, James T Elder, John J Voorhees, J Michelle Kahlenberg, Johann E Gudjonsson
Journal: Nature Immunology (2016)
145. Rational Design of Aptazyme Based Riboswitches Using the Strand Displacement Mechanism
Authors: Jiawen Wang, Jingxian Feng, Yong Diao
Journal: Molecular Therapy (2015)

Aptazymes are self-cleaving ribozymes whose activity is regulated by binding of the ligand. Recently the aptazyme based riboswitches have emerged as a powerful tool for gene regulation independent of transcription factors and could meet the challenge of precise regulation of therapeutic gene expression in vivo. However, the most popular way to generate these artificial riboswitches relies on a time-consuming screening process. Here, based on the strand displacement mechanism (Fig.A,B), we engineered a series of theophylline responsive aptazymes by joining a theophylline-binding aptamer to a hammerhead ribozyme that derived from the trematode Schistosoma mansoni (Fig.C).
Procoagulant and inflammatory mediators in small cell lung carcinoma: Potential role in thromboembolic complications.
Authors: I. Thethi, D. Hoppensteadt, H. Khan, M. Demir, C. Adiguzel, E. Litinas, J. Fareed
Journal: Journal of Clinical Oncology (2011)

2553 Background: Small Cell Lung Carcinoma (SCLC) patients exhibit a higher prevalence of thromboembolic complications. We hypothesized that in this malignancy, procoagulant and inflammatory mediators contribute to the pathogenesis of such complications and warfarin may down regulate these levels. Methods: In a prospective, randomized, controlled study, patients with inoperable lung cancer (n=100) were randomized to receive chemotherapy and radiation with and without warfarin (INR 1.5 – 2.5). Blood samples were drawn prior to and after the 2nd treatment cycle with warfarin or control and retrospectively analyzed for microparticles and thrombin generation markers such as fibrinopeptide A (FPA), thrombin-antithrombin complex (TAT) and prothrombin fragment F1.2 (F1.2). In addition, biochip array for C-reactive protein (CRP), D Dimer, neuron specific enolase (NSE), neutrophil gelatinase associated lipocalin (NGAL), tumor necrosis factor receptor 1 (TNFR1), and thrombomodulin (TM) were measured. The results were compared with a normal population (N=50). Results: The microparticles were markedly increased in the SCLC patients (3 fold increase) at baseline. Similary, the thrombin generation markers showed variable increase (1.5-3.2 fold increase). In the biochip array analysis, variable increase was noted. CRP (2.4 fold), D DIMER (11.6 fold), NSE (1.8 fold), NGAL (1.7 fold), TNFR1 (2 fold) and TM (1.3 fold) were all increased as compared to normal controls. All of the markers exhibited a decrease after warfarin treatment with a most pronounced decrease in the D Dimer and TNFR1. Conclusions: These results validate the hypothesis that SCLC patients exhibit a hypercoagulable state that is associated with simultaneous upregulation of inflammatory mediators. Warfarin treatment results in a down regulation of these mediators. Our results provide a rationale for prophylactic anticoagulant therapy in this group of patients.
Abstract 3612: Study of the functional importance of PPARγ in honokiol-induced apoptosis of hepatoma cells
Authors: Chin-Wen Chi, Hui-Tzu Hsu, Jia-Dong Hou, Chih-Chun Lee, Ying-Ju Kuo, Hsin-Chen Lee, Cheng-Yuan Hsia
Journal: Cancer Research (2015)

Abstract Hepatocellular carcinoma (HCC) is the leading cause of death in male cancer patients in Asia. PPARγ exhibited an inhibitory role in hepatocarcinogenesis in vitro and in vivo. Recently, it was found that honokiol functions not only as a RXR agonist but also a PPARγ agonist, and is capable of potentiating the activation of PPARγ in the presence of PPARγ agonist rosiglitazone in HLE human hepatoma cells. It also has been reported that honokiol exerts inhibitory effects on the growth and migration in hepatoma cells. However, whether PPARγ overexpression modulates the honokiol-induced growth inhibition in hepatoma cells is not known. Firstly, we examined the expression of PPARγ in tumor samples from 83 HCC patients by immunohistochemical staining. Our results showed that 53 samples had no PPARγ and the clinical parameters including tumor number, stages, and macroscopic vascular invasion (MVI) showed significant negative correlation with PPARγ expression. However, the expression of PPARγ was not associated with disease free survival or overall survival of patients with HCC. Using PPARγ overexpressed SK-Hep1 cells (SK-Hep1-PPARγ) for in vitro analyses, we found that 40 μM honokiol treatment of SK-Hep1-PPARγ cells induced a 20% increase of growth inhibition at 48 hour as compared to vector control cells by MTT assay. This corresponded well with the 15% increase in G0/G1 phase after honokiol treatment at 24 hour compared to vector control cells. In addition, honokiol treatment resulted in decreased cyclin D1, increased p21 and KLF4 expressions in SK-Hep1-PPARγ cells. Moreover, miRNA array analyses showed that increased expression of miR-222, let-7i, miR-628-3p and miR-664 as well as decreased miR-1291, miR184 and miR1249 were observed in SK-Hep1-PPARγ cells. In conclusion, PPARγ is not only a biomarker for prognosis of patients with HCC but also play an important role in the honokiol-induced growth inhibition of hepatoma cells. The functional importance of PPARγ regulated miRNA is currently under further investigation. Citation Format: Chin-Wen Chi, Hui-Tzu Hsu, Jia-Dong Hou, Chih-Chun Lee, Ying-Ju Kuo, Hsin-Chen Lee, Cheng-Yuan Hsia. Study of the functional importance of PPARγ in honokiol-induced apoptosis of hepatoma cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3612. doi:10.1158/1538-7445.AM2015-3612
Phase 2 placebo-controlled, double-blind trial of dasatinib added to gemcitabine for patients with locally-advanced pancreatic cancer
Authors: T.R.J. Evans, E. Van Cutsem, M.J. Moore, I.S. Bazin, A. Rosemurgy, G. Bodoky, G. Deplanque, M. Harrison, B. Melichar, D. Pezet, A. Elekes, E. Rock, C. Lin, L. Strauss, P.J. O’Dwyer
Journal: Annals of Oncology (2016)
The era of research collaborations: new models for working together
Authors: Ratko Djukanović, Guy Brusselle, Samantha Walker, Stephen T. Holgate, Sabina Škrgat, Piotr Kuna, Liam G. Heaney, G. Walter Canonica, Jørgen Vestbo
Journal: European Respiratory Journal (2017)

The past two decades have seen the creation of several European collaborations focusing on asthma and chronic obstructive pulmonary disease (COPD). The growth of the collaboration model for research began in the late 1990s with the Framework Programme (FP)-4-funded project on severe asthma, ENFUMOSA (European Network for Understanding Mechanisms of Severe Asthma), a cross-sectional observational study that provided the proof of principle for large collaborations. Soon after, two more in-depth projects were established, focusing on mechanisms and biomarkers of severe asthma and COPD in two longitudinal cohort studies: BIOAIR (Longitudinal Assessment of Clinical Course and Biomarkers in Severe Chronic Airway Disease) project, funded by FP-5, FP-6 and several national funding bodies; and the GlaxoSmithKline-funded project on COPD, the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE). More recently, the Unbiased Biomarkers in Prediction of Respiratory Disease Outcomes (U-BIOPRED) programme, funded by the European Union (EU) Innovative Medicines Initiative, and the FP-7-funded AirPROM (Airway Disease Predicting Outcomes through Patient Specific Computational Modelling) project have sought to provide a step-change in phenotyping of chronic airways disease through the use of multidimensional clinical outcomes, 'omics biomarkers and sophisticated lung imaging. This editorial proposes the establishment of a registry of European centres with expertise in asthma research <http://ow.ly/OPHY304Cr9h> The authors are very grateful to Judit Varkonyi-Sepp and Blanka Varkonyi for their excellent conduct of the online survey, canvassing views from across Europe about the needs, opportunities and challenges of a European network of asthma research centres.