tbuckley/cabot-search huggingface dataset:
SAT0410 Hla-b27 role in ankylosing spondylitis phenotype: results from the regisponser database
Authors: M Arevalo, P Font, M Moreno, D Ruiz, M Castro, P Carreto, M Larrosa, E Collantes, J Gratacόs
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Objectives</h3> To assess if there are different phenotypical patterns of Ankylosing Spondylitis (AS) patients depending on the positivity or negativity of HLAB27. <h3>Methods</h3> This is a multicentric, observational, transversal and descriptive study of AS patients from the spanish database REGISPONSER. We compared HLAB27 positive and HLAB27 negative patients regarding clinical and demographical data, disease activity and structural damage. In order to assess disease activity we used the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and acute phase reactants (VSG and PCR). Functional disability was measured by Bath Ankylosing Spondylitis Functional Index (BASFI), and structural damage by Bath Ankylosing Spondylitis Radiology Score (BASRI). For qualitative variables we used the Chi square test and for quantitative ones the t test. An univariate and multivariate comparative analyisis was performed, in order to define which variables were related to the negativity or positivity of HLAB27. <h3>Results</h3> Data of 1235 AS pacients were analysed. Of them 1029 (83.3%) were HLAB27 positive and 206 (17.7%) HLAB27 negative. 924 (74.8%) were men. AS patients with HLAB27+ presented significantly more familiar history of spondyloarhritis (p=0.002), were younger (p=0.012) and had earlier disease onset and disease diagnosis (p&lt;0.001), with a longer disease duration (p=0.037) and a trend to a higher percentage of uveitis compared to those with HLAB27-. On the other hand, AS patients with HLAB27- also presented significantly more peripheral arthritis (p=0.0022), dactylitis (p=0.001) and extraarticular manifestations (psoriasis, palmoplantar pustulosis, inflammatory bowel disease (IBD) and balanitis (p&lt;0.001)) compared with those of HLAB27+. AS patients with HLAB27- also presented higher scores of BASDAI and BASFI (p=0.047 and p=0.005 respectively). The study didn9t show differences between both groups of patients regarding sex distribution, axial manifestations, enthesitis nor radiological damage (assessed by BASRI). In the multivariate analysis, the family history of spondyloarthritis (OR 2.10, IC95% 1.27–3.49, p=0.004), the age at diagnosis (OR 0.97, IC95% 0.96–0.98, p&lt;0.001), the presence of dactylitis (OR 0.16, IC95% 0.05–0.56, p=0.004), extraarticular manifestation specially IBD (OR 0.22, IC95% 0.12–0.40, p&lt;0.001) and peripheral arthritis (OR 0.53, IC95% 0.32–0.89, p=0.016) were the variables independently associated with the presence of HLAB27. <h3>Conclusions</h3> The presence of HLAB27 in AS patients is associated to an earlier disease onset, a higher frequency of familiar history of spondyloarthritis, and a lower frequency of dactylitis, extraarticular manifestations and peripheral arthritis. <h3>Disclosure of Interest</h3> None declared
Elevated serum carcinoembryonic antigen and prediction of poor survival of patients with small cell lung cancer.
Authors: Hui Zhu, Hongbo Guo, Li Kong, Jinming Yu
Journal: Journal of Clinical Oncology (2015)

e18561 Background: Serum levels of tumor marker may be related to tumor burden, but the prognostic value of these markers remains controversial.We conducted a retrospective study to evaluate the prognostic utility of biomarkers in patients with small cell lung cancer (SCLC). Methods: The serum levels of biomarkers such as carcinoembryonic antigen(CEA), nerve cell specific enolase (NSE), and lactate dehydrogenase (LDH) in 281 patients who were diagnosed with SCLC between January 2004 and December 2009 were analyzed in this study . Overall survival (OS) was the primary endpoint, the role of biomarkers, clinical factors and treatment modalities on prognosis was further evaluated. Univariate survival analysis was performed using the Kaplan–Meier method. Multivariate survival analysis was performed using the Cox proportional hazards model. Results: Elevated serum CEA levels were observed in 92 (32.7%) patients. Survival was superior in patients with normal serum CEA levels compared to those with elevated serum CEA levels. The median survival time (MST), 2-year overall survival (OS) rate, and 3-year (OS) rate were 19.1 months versus 14.6 months, 42.7% versus 28.3%, and 30.6% versus 14.1%, respectively (p = 0.002). In multivariate analysis, extensive-stage SCLC (hazard ratio [HR] = 1.936, p = 0.001), an elevated serum CEA level (HR = 1.432, p = 0.021) at diagnosis and < 4 cycles of chemotherapy (HR = 0.432, p = 0.001) were independent negative prognostic factors of the OS. Additionally, normal CEA level (HR = 1.678, p = 0.012) , treatment modalities including surgery(HR = 1.595, p = 0.049) and ≥ 4 cycles of chemotherapy (HR = 1.880, p = 0.004) were independent positive prognostic factors of OS in patients with local disease. In the subgroup of extensive stage, normal serum CEA level (HR = 1.608, p = 0.043) , thoracic radiotherapy (HR = 1.744, p = 0.005) and ≥ 4 cycles of chemotherapy (HR = 2.626, p = 0.001) was independent positive prognostic factors of OS. Conclusions: An elevated serum level of CEA can act as a predicative factor of poor prognosis for SCLC patients.
Randomized phase 2 study of low-dose decitabine vs low-dose azacitidine in lower-risk MDS and MDS/MPN
Authors: Elias Jabbour, Nicholas J. Short, Guillermo Montalban-Bravo, Xuelin Huang, Carlos Bueso-Ramos, Wei Qiao, Hui Yang, Chong Zhao, Tapan Kadia, Gautam Borthakur, Naveen Pemmaraju, Koji Sasaki, Zeev Estrov, Jorge Cortes, Farhad Ravandi, Yesid Alvarado, Rami Komrokji, Mikkael A. Sekeres, David P. Steensma, Amy DeZern, Gail Roboz, Hagop Kantarjian, Guillermo Garcia-Manero
Journal: Blood (2017)
01.07 Control of chronic inflammation by t-bet expressed in th cells
Authors: Jakob Zimmermann, Andreas Radbruch, Hyun-Dong Chang
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> The transcription factor 'T-box expressed in T cells' (T-bet) is highly expressed by Th cells isolated from the inflamed tissue in many chronic inflammatory diseases. Here we have analysed in detail the contribution of T-bet in shaping the inflammation in the T-cell transfer induced colitis model as a prototypic model for T cell mediated chronic, progressive inflammation. <h3>Methods</h3> To induce colitis<i> Tbx21</i>-deficient Th cells were adoptively transferred into <i>Rag</i>-deficient mice. Intestinal inflammation was characterised by quantitative and qualitative analysis of lamina propria-infiltrating cells, Th cell phenotyping and histology. <h3>Results</h3> Here we show that the requirement for T-bet expression by Th cells for the manifestation of clinical symptoms of T cell-induced colitis is absolutely dependent on the composition of the intestinal microbiota. When colitis develops, T-bet exerts several non-redundant functions in shaping the inflammation. T-bet expressed by Th cells promotes the survival and positioning of the Th cells in the colon and their repertoire of chemokine and chemokine receptor expression, the recruitment of myeloid cells to the inflamed colon, and the differentiation of macrophages/monocytes. Remarkably, in T cell-induced colitis, T-bet-deficient Th cells differentiate into Th1/17 cells, able to express IFN-γ and IL-17 upon restimulation. Th cell-derived IFN-γ or IL-17, however, are not required to induce colitis. <h3>Conclusions</h3> We demonstrate that while T-bet shapes the type of the intestinal inflammatory reaction, it is not an essential pre-requisites for T cell-induced colitis. Our data show that the key cytokines IFN-γ and IL-17 play a subordinate role in colitis induction and suggest that the type of inflammation is determined by the chemokine expression profile of the Th cells. In addition, whether Th cells are pathogenic is largely determined by the composition of the intestinal microbiota. Thus, our data shed light on the heterogeneity of inflammatory bowel diseases and their variable response to therapy depending on the microbiota composition and the Th cells involved.
INJURY RISK AMONG FEMALE SOCCER PLAYERS IN ZIMBABWE
Authors: Risk Matiya
Journal: British Journal of Sports Medicine (2017)

Background Women soccer is proving to be popular the world over and in African countries as well. However in spite of its popularity there is always the attendant high risk of injury. The risk of injury is associated with many factors which include personality factors and coping skills. Objective The purpose of the current study is to explore the relationship between personality traits, coping skills and risk of injury. Design The study was a retrospective cross sectional survey. Setting The study was carried out in Zimbabwe among women soccer players belonging to the elite division of the premier league. Patients (or Participants) All the participants were female soccer players whose age ranges were 18 through 35.200 participants were selected based on stratified random sampling from the national football association register. Interventions (or Assessment of Risk Factors) Four questionnaires were administered among 200 female soccer players in the current competitive season. The four questionnaires included the personality inventory questionnaire, B-COPE and the athletic injury questionnaire. Main Outcome Measurements A descriptive and inferential analysis was conducted examining the influence of personality traits and coping skills on injury frequency and severity. Results Descriptive and inferential analysis indicated that personality and coping skills were significant predictors of sporting injury among female soccer players, accounting for 30% of the variance. Conclusions The findings highlight the need to enhance prevention of athletes injuries by identifying athletes who are injury prone given their personality traits and coping styles. Athletes, coaches and sports medicine practitioners need to identify the role of stress, coping skills and personality in sport injuries, especially those relating to women's soccer.
Discrepant Expectations About Benefits and Harms—Reply
Authors: Tammy C. Hoffmann, Chris Del Mar
Journal: JAMA Internal Medicine (2017)

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 Internal Medicine 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 Internal Medicine journal
Genomic analysis of hairy cell leukemia identifies novel recurrent genetic alterations
Authors: Benjamin H. Durham, Bartlomiej Getta, Sascha Dietrich, Justin Taylor, Helen Won, James M. Bogenberger, Sasinya Scott, Eunhee Kim, Young Rock Chung, Stephen S. Chung, Jennifer Hüllein, Tatjana Walther, Lu Wang, Sydney X. Lu, Christopher C. Oakes, Raoul Tibes, Torsten Haferlach, Barry S. Taylor, Martin S. Tallman, Michael F. Berger, Jae H. Park, Thorsten Zenz, Omar Abdel-Wahab
Journal: Blood (2017)
The Changing Tides of the Type 2 Diabetes Epidemic—Smooth Sailing or Troubled Waters Ahead? Kelly West Award Lecture 2016
Authors: Edward W. Gregg
Journal: Diabetes Care (2017)

The Kelly West Award for Outstanding Achievement in Epidemiology is given in memory of Kelly M. West, widely regarded as the “father of diabetes epidemiology,” to an individual who has made significant contributions to the field of diabetes epidemiology. Edward W. Gregg, PhD, of the Division of Diabetes Translation, Centers for Disease Control and Prevention, Atlanta, GA, received the prestigious award at the American Diabetes Association's 76th Scientific Sessions, 10–14 June 2016, in New Orleans, LA. He presented the Kelly West Award Lecture, “Changing Tides of the Type 2 Diabetes Epidemic—Smooth Sailing or Troubled Waters Ahead?” on Sunday, 12 June 2016.
Regulation of the PU.1 Gene by Sense and Functional Antisense RNAs Generated through the Same Chromatin Architecture.
Authors: Alex Ebralidze, Pu Zhang, Frank Rosenbauer, Gang Huang, Ulrich Steidl, Tajhal Dayaram, Florence Guibal, Johanna Klupp, Dana Neel, Constanze Bonifer, Daniel G. Tenen
Journal: Blood (2006)
Résection muqueuse endoscopique pour néoplasme superficiel de l’ésophage: comparaison entre résultats macoscopiques, histologiques et résultats du suivi
Authors: T Ponchon, M Ciocirlan, JC Saurin, B Napoléon, C Lefort, JC Souquet, B Pujol, A Chavaillon
Journal: Endoscopy (2004)

Introduction: La résection muqueuse endoscopique (RME) permet d’obtenir une pièce pour contrôle histologique. Dans une série de RME pour néoplasme superficiel de l’ésophage, nous avons analysé en particulier les résultats du contrôle histologique par rapport aux résultats macroscopiques et à ceux du suivi. Patients et Méthodes: Soixante dix neuf patients (pts), avec 84 lésions, ont été traités par RME pour une dysplasie ou un cancer épidermoïde superficiel (epi) (38 pts, âge moyen 64 ans) ou pour une dysplasie de haut grade ou un adénocarcinome superficiel sur Barrett (Ba) (41 pts, âge moyen 70 ans), par la technique du capuchon transparent. Les lésions étaient traitées par RME si classées uT1m ou uT1sm1 en EE. Des marques ont été réalisées à environ 2 mm du pourtour de la lésion par électrocoagulation. La résection a été considérée complète macroscopiquement si les marques ont été enlevées. En histologie, la pièce a été traitée comme une pièce chirurgicale: 4 bandes latérales ont été coupées et analysées séparément. La résection a été considérée complète si les bandes latérales et si le plan de coupe profond ne contenaient pas de cellules néoplasiques. Un contrôle a été réalisé à 1 mois avec biopsies de la zone de traitement puis le pt a été suivi si le contrôle était normal. Résultats: Cent deux séances de RME ont été réalisées sur 84 lésions. Les complications ont été de 17%: une perforation asymptomatique, une sténose traitée efficacement par dilatation, 15 hémorragies arrêtées immédiatement par clips. Soixante douze pour cent des résections (épi 73%, Ba 71%) ont été considérées comme macroscopiquement complètes et seulement 30% histologiquement complètes (épi 22%, Ba 37,5%). La majorité (74%) des réponses incomplètes était liée à un envahissement des bandes latérales et seulement 26% à un envahissement du plan profond. Cependant, le contrôle endoscopique à 1 mois était normal chez 76% des pts (épi: 71%, Ba 80,5%). Quatorze pts (18%) avaient un envahissement de la sous muqueuse sur la pièce et ont eu chirurgie ou radiothérapie. Les autres pts ont été suivis (suivi moyen: 18,6 mois épi, 12,5 mois Ba): il a été observé une récidive chez 8,8% des pts (épi 7,9%, Ba 9,8%) et l’apparition d’autres lésions à distance chez 11,4% des pts (épi 15,8%, Ba 7,3%). Ce qui fait qu’en intention de traiter, 58% des pts (épi 47,4%, Ba 63,4%) ont été traités par endoscopie seule avec suivi normal > 1 an. Conclusion: La RME est adaptée au traitement des néoplasmes superficiels de l’ésophage. Sa morbidité cliniquement significative est faible. Elle permet de traiter près de 60% des lésions par endoscopie seule. Elle fournit une pièce permettant d’orienter les pts vers un autre traitement si nécessaire (18% dans cette série). Cependant, une résection histologique complète (avec marges de sécurité) est très difficile à obtenir et le résultat macroscopique reste un élément déterminant.
Surveillance in Germline <i>TP53</i> Mutation Carriers Utilizing Whole-Body Magnetic Resonance Imaging
Authors: Mandy L. Ballinger, Nicholas J. Ferris, Kate Moodie, Gillian Mitchell, Sue Shanley, Paul A. James, David M. Thomas
Journal: JAMA Oncology (2017)

Phuong L. Mai; Payal P. Khincha, MD; Jennifer T. Loud; Rosamma M. DeCastro, CRNP; Renée C. Bremer; June A. Peters; Chia-Ying Liu; David A. Bluemke; Ashkan A. Malayeri; Sharon A. Savage, MD
Macrophage Migration Inhibitory Factor Limits Renal Inflammation and Fibrosis by Counteracting Tubular Cell Cycle Arrest
Authors: Sonja Djudjaj, Ina V. Martin, Eva M. Buhl, Nina J. Nothofer, Lin Leng, Marta Piecychna, Jürgen Floege, Jürgen Bernhagen, Richard Bucala, Peter Boor
Journal: Journal of the American Society of Nephrology (2017)

Renal fibrosis is a common underlying process of progressive kidney diseases. We investigated the role of macrophage migration inhibitory factor (MIF), a pleiotropic proinflammatory cytokine, in this process. In mice subjected to unilateral ureteral obstruction, genetic deletion or pharmacologic inhibition of MIF aggravated fibrosis and inflammation, whereas treatment with recombinant MIF was beneficial, even in established fibrosis. In two other models of progressive kidney disease, global Mif deletion or MIF inhibition also worsened fibrosis and inflammation and associated with worse kidney function. Renal MIF expression was reduced in tubular cells in fibrotic compared with healthy murine and human kidneys. Bone marrow chimeras showed that Mif expression in bone marrow-derived cells did not affect fibrosis and inflammation after UUO. However, Mif gene deletion restricted to renal tubular epithelial cells aggravated these effects. In LPS-stimulated tubular cell cultures, Mif deletion led to enhanced G2/M cell-cycle arrest and increased expression of the CDK inhibitor 1B (p27Kip1) and of proinflammatory and profibrotic mediators. Furthermore, MIF inhibition reduced tubular cell proliferation in vitro . In all three in vivo models, global Mif deletion or MIF inhibition caused similar effects and attenuated the expression of cyclin B1 in tubular cells. Mif deletion also resulted in reduced tubular cell apoptosis after UUO. Recombinant MIF exerted opposing effects on tubular cells in vitro and in vivo . Our data identify renal tubular MIF as an endogenous renoprotective factor in progressive kidney diseases, raising the possibility of pharmacologic intervention with MIF pathway agonists, which are in advanced preclinical development.
Adverse Heart–Lung Interactions in Ventilator-induced Lung Injury
Authors: Bhushan H. Katira, Regan E. Giesinger, Doreen Engelberts, Diana Zabini, Alik Kornecki, Gail Otulakowski, Takeshi Yoshida, Wolfgang M. Kuebler, Patrick J. McNamara, Kim A. Connelly, Brian P. Kavanagh
Journal: American Journal of Respiratory and Critical Care Medicine (2017)

Rationale: In the original 1974 in vivo study of ventilator-induced lung injury, Webb and Tierney reported that high Vt with zero positive end-expiratory pressure caused overwhelming lung injury, subsequently shown by others to be due to lung shear stress.Objectives: To reproduce the lung injury and edema examined in the Webb and Tierney study and to investigate the underlying mechanism thereof.Methods: Sprague-Dawley rats weighing approximately 400 g received mechanical ventilation for 60 minutes according to the protocol of Webb and Tierney (airway pressures of 14/0, 30/0, 45/10, 45/0 cm H2O). Additional series of experiments (20 min in duration to ensure all animals survived) were studied to assess permeability (n = 4 per group), echocardiography (n = 4 per group), and right and left ventricular pressure (n = 5 and n = 4 per group, respectively).Measurements and Main Results: The original Webb and Tierney results were replicated in terms of lung/body weight ratio (45/0 > 45/10 ≈ 30/0 ≈ 14/0; P < 0.05) and histology. In 45/0, pulmonary edema was overt and rapid, with survival less than 30 minutes. In 45/0 (but not 45/10), there was an increase in microvascular permeability, cyclical abolition of preload, and progressive dilation of the right ventricle. Although left ventricular end-diastolic pressure decreased in 45/10, it increased in 45/0.Conclusions: In a classic model of ventilator-induced lung injury, high peak pressure (and zero positive end-expiratory pressure) causes respiratory swings (obliteration during inspiration) in right ventricular filling and pulmonary perfusion, ultimately resulting in right ventricular failure and dilation. Pulmonary edema was due to increased permeability, which was augmented by a modest (approximately 40%) increase in hydrostatic pressure. The lung injury and acute cor pulmonale is likely due to pulmonary microvascular injury, the mechanism of which is uncertain, but which may be due to cyclic interruption and exaggeration of pulmonary blood flow.
システイナーゼ/シスチナーゼによるL‐システイン/シスチンの全身的枯渇は活性酸素種を増加させて腫瘍の増殖を抑制する
Authors: Cramer Shira L, Triplett Kendra, Lamb Candice, Georgiou George, Saha Achinto, Digiovanni John, Liu Jinyun, Huang Peng, Tadi Surendar, Tiziani Stefano, Yan Wupeng, Zhang Yan Jessie, Stone Everett, Alters Susan E, Rowlinson Scott, Keating Michael J
Journal: Nature Medicine (2017)
PPARγ in dendritic cells and T cells drives pathogenic type-2 effector responses in lung inflammation
Authors: Samuel Philip Nobs, Sara Natali, Lea Pohlmeier, Katarzyna Okreglicka, Christoph Schneider, Michael Kurrer, Federica Sallusto, Manfred Kopf
Journal: The Journal of Experimental Medicine (2017)

Type-2 immune responses are well-established drivers of chronic inflammatory diseases, such as asthma, and represent a large burden on public health systems. The transcription factor PPARγ is known to promote M2-macrophage and alveolar macrophage development. Here, we report that PPARγ plays a key role in both T cells and dendritic cells (DCs) for development of type-2 immune responses. It is predominantly expressed in mouse Th2 cells in vitro and in vivo as well as human Th2 cells from allergic patients. Using conditional knockouts, we show that PPARγ signaling in T cells, although largely dispensable for IL-4 induction, is critical for IL-33–driven Th2 effector function in type-2 allergic airway responses. Furthermore, we demonstrate that IL-4 and IL-33 promote up-regulation of PPARγ in lung-resident CD11b+ DCs, which enhances migration to draining lymph nodes and Th2 priming capacity. Thus, we uncover a surprising proinflammatory role for PPARγ and establish it as a novel, important mediator of DC–T cell interactions in type-2 immunity.
強化RFと化学療法相乗的腫瘍治療のためのRGD活性標的化と高周波増強された透過性の相乗的保持戦略【Powered by NICT】
Authors: Zhang Kun, Li Pei, He Yaping, Bo Xiaowan, Li Xiaolong, Li Dandan, Chen Hangrong, Xu Huixiong
Journal: Biomaterials (2016)