tbuckley/cabot-search huggingface dataset:
Analysis of mammalian gene function through broad-based phenotypic screens across a consortium of mouse clinics
Authors: Martin Hrabě de Angelis, George Nicholson, Mohammed Selloum, Jacqueline K White, Hugh Morgan, Ramiro Ramirez-Solis, Tania Sorg, Sara Wells, Helmut Fuchs, Martin Fray, David J Adams, Niels C Adams, Thure Adler, Antonio Aguilar-Pimentel, Dalila Ali-Hadji, Gregory Amann, Philippe André, Sarah Atkins, Aurelie Auburtin, Abdel Ayadi, Julien Becker, Lore Becker, Elodie Bedu, Raffi Bekeredjian, Marie-Christine Birling, Andrew Blake, Joanna Bottomley, Michael R Bowl, Véronique Brault, Dirk H Busch, James N Bussell, Julia Calzada-Wack, Heather Cater, Marie-France Champy, Philippe Charles, Claire Chevalier, Francesco Chiani, Gemma F Codner, Roy Combe, Roger Cox, Emilie Dalloneau, André Dierich, Armida Di Fenza, Brendan Doe, Arnaud Duchon, Oliver Eickelberg, Chris T Esapa, Lahcen El Fertak, Tanja Feigel, Irina Emelyanova, Jeanne Estabel, Jack Favor, Ann Flenniken, Alessia Gambadoro, Lilian Garrett, Hilary Gates, Anna-Karin Gerdin, George Gkoutos, Simon Greenaway, Lisa Glasl, Patrice Goetz, Isabelle Goncalves Da Cruz, Alexander Götz, Jochen Graw, Alain Guimond, Wolfgang Hans, Geoff Hicks, Sabine M Hölter, Heinz Höfler, John M Hancock, Robert Hoehndorf, Tertius Hough, Richard Houghton, Anja Hurt, Boris Ivandic, Hughes Jacobs, Sylvie Jacquot, Nora Jones, Natasha A Karp, Hugo A Katus, Sharon Kitchen, Tanja Klein-Rodewald, Martin Klingenspor, Thomas Klopstock, Valerie Lalanne, Sophie Leblanc, Christoph Lengger, Elise le Marchand, Tonia Ludwig, Aline Lux, Colin McKerlie, Holger Maier, Jean-Louis Mandel, Susan Marschall, Manuel Mark, David G Melvin, Hamid Meziane, Kateryna Micklich, Christophe Mittelhauser, Laurent Monassier, David Moulaert, Stéphanie Muller, Beatrix Naton, Frauke Neff, Patrick M Nolan, Lauryl M J Nutter, Markus Ollert, Guillaume Pavlovic, Natalia S Pellegata, Emilie Peter, Benoit Petit-Demoulière, Amanda Pickard, Christine Podrini, Paul Potter, Laurent Pouilly, Oliver Puk, David Richardson, Stephane Rousseau, Leticia Quintanilla-Fend, Mohamed M Quwailid, Ildiko Racz, Birgit Rathkolb, Fabrice Riet, Janet Rossant, Michel Roux, Jan Rozman, Edward Ryder, Jennifer Salisbury, Luis Santos, Karl-Heinz Schäble, Evelyn Schiller, Anja Schrewe, Holger Schulz, Ralf Steinkamp, Michelle Simon, Michelle Stewart, Claudia Stöger, Tobias Stöger, Minxuan Sun, David Sunter, Lydia Teboul, Isabelle Tilly, Glauco P Tocchini-Valentini, Monica Tost, Irina Treise, Laurent Vasseur, Emilie Velot, Daniela Vogt-Weisenhorn, Christelle Wagner, Alison Walling, Marie Wattenhofer-Donze, Bruno Weber, Olivia Wendling, Henrik Westerberg, Monja Willershäuser, Eckhard Wolf, Anne Wolter, Joe Wood, Wolfgang Wurst, Ali Önder Yildirim, Ramona Zeh, Andreas Zimmer, Annemarie Zimprich, Chris Holmes, Karen P Steel, Yann Herault, Valérie Gailus-Durner, Ann-Marie Mallon, Steve D M Brown
Journal: Nature Genetics (2015)
Correlation of prostate-specific antigen (PSA) levels and survival in men with bone metastatic hormone-refractory prostate cancer (HRPC) and normal alkaline phosphatase (ALK)
Authors: W. Xie, M. M. Regan, M. Nakabayashi, W. K. Oh
Journal: Journal of Clinical Oncology (2007)

5140 Background: PSA and ALK are recognized factors for predicting survival in men with metastatic HRPC. However, few studies have evaluated the combined effects of PSA and ALK on survival of patients with metastatic HRPC. Methods: 224 patients treated with chemotherapy for bone metastatic HRPC between 1999 and 2006 were identified from an institutional database. 143 patients had ALK as well as PSA values at start of chemotherapy. There were no statistically significant differences in baseline characteristics (including age, Gleason score, PSA, clinical stage at diagnosis or at the initiation of chemotherapy) between groups with and without available ALK (p&gt;0.05). The primary endpoint was overall survival (OS) after chemotherapy. ALK was dichotomized to normal and abnormal groups based on institutional normal range (38–126 U/L). The effect of PSA was evaluated both as categorical (low, median and high group using the 33%, 66% cut-off values) and continuous values with log transformation in Cox regression. Results: Of 143 eligible patients, median ALK was 159 U/L (range: 52–2,020 U/L); 89 (62%) had elevated ALK. Median PSA at start of chemotherapy was 147 ng/mL; 93 ng/mL in patients with normal ALK and 171 ng/mL in those with elevated ALK. With median follow-up of 30 months after chemotherapy, 93 patients have died. Median OS after chemotherapy was 15.8 (range 0–57) months and was significantly longer if ALK was in the normal range (21.3 vs. 14 months, p=0.005). For the group with normal ALK, median OS was 12.5, 24.5 and 36.9 months for patients with low, median and high PSA, respectively; while there was no effect of PSA on survival if ALK was beyond the normal range (16.5 vs. 11.9 vs. 12.1 months) (p=0.21 for the interaction). In multivariable analysis after adjusting for age, the interaction effect of PSA and ALK on OS was statistically significant (p=0.02). The relative risk due to one unit increase in the value of Ln(PSA) was 0.68 (95% CI: 0.51–0.92) if ALK in the normal range, compared to 1.07 (95% CI: 0.85–1.35) in the group with elevated ALK. Conclusions: ALK was a significant factor in predicting OS for men with bone metastatic HRPC. In patients with normal ALK, a higher PSA was associated with improved survival. No significant financial relationships to disclose.
10 year trends in urban–rural disparities in treatments and outcomes after ST-elevation myocardial infarction in China: insights from the China PEACE-Retrospective Acute Myocardial Infarction Study
Authors: Xi Li, Karthik Murugiah, Jing Li, Qing Wang, Shuang Hu, Frederick A Masoudi, John A Spertus, Nicholas S Downing, Paul Chan, Harlan M Krumholz, Lixin Jiang
Journal: The Lancet (2015)
Can Mobile Health Applications Facilitate Meaningful Behavior Change?
Authors: Zubin J. Eapen, Eric D. Peterson
Journal: JAMA (2015)

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Authors: Paul Michel Mertes, Pascal Demoly, Annick Alperovitch, Agnes Bazin, Jacques Bienvenu, Cyril Caldani, Bernard Lamy, Dominique Laroche, Marie Françoise Leconte des Floris, Jean-Yves Py, Christian Drouet, Monique Carlier, Andre Lienhart
Journal: Journal of Allergy and Clinical Immunology (2013)
Abstract 17018: β-Catenin Interacts with both FoxO1 and TCF-4 to Suppress NaV1.5 Expression after Myocardial Infarction
Authors: Ning Wang, Benzhi Cai, Yan Lu, Bo Ye, Xiang Li, Faqian Li, Haodong Xu
Journal: Circulation (2014)

Introduction:  Ventricular tachycardia and fibrillation (VT/VF) are the leading causes of morbidity and mortality after myocardial infarction (MI). Dysfunction of ion channels is the main mechanism underlying VT/VF. Reactive oxidative species (ROS) promote the interaction between β-catenin and FoxO1 that affects the targeting gene expression. Our previous study revealed that both TCF-4 and FoxO1 are required for β-catenin to suppress Na V 1.5 expression in cardiomyocytes, but it is unknown if this process contributes to the development of VT/VF after MI.   Hypothesis:  We hypothesized that β-catenin interacts with FoxO1 and TCF-4 to suppress cardiac Na V 1.5 expression after MI.   Methods:  Immunohistochemistry was used to determine the cellular localization of β-catenin, FoxO1 and TCF-4 in 3 human hearts with ischemic heart disease (IHD) and 3 relatively normal controls. Mouse MI was induced by ligation of the left anterior descending coronary artery (LAD). Na V 1.5 expression in the peri-infarct zone (PIZ) of mouse hearts one week after MI and in H 2 O 2 -treated HL-1 cells were detected by qRT-PCR and Western blot, respectively. Distribution of β-catenin and expression of Na V 1.5 protein in HL-1 cells were determined using confocal microscopy. Immunoprecipitation (IP) was performed to define the interaction of β-catenin with FoxO1 and TCF-4 in HL-1 cells.   Results:  The expression of Na V 1.5 was reduced at both mRNA and protein levels in PIZ, compared to the sham group. Na V 1.5 protein was significantly decreased in HL-1 cells after 100 μM and 200 μM H 2 O 2  treatment mimicking oxidative stress. β-catenin and FoxO1 were more localized in the nuclei of cardiomyocytes in human IHD, compared to controls, but TCF-4 was not altered. Although 200 μM H 2 O 2  treatment did not affect β-catenin protein levels in HL-1 cells, it promoted β-catenin translocation from the cytoplasm into the nucleus. IP revealed that β-catenin interacted with FoxO1 and TCF-4 protein in HL-1 cells.   Conclusions:  β-catenin interacts with FoxO1 and TCF-4 to suppress Na V 1.5 expression after MI. These findings provide a new insight into the molecular mechanisms underlying the ROS-induced the decrease of Na V 1.5 related to the development of VT/VF in MI.
Comparative study of sequential intravesical chemotherapy using gemcitabine and mitomycin C with mitomycin C alone for non-muscle invasive bladder carcinoma- a randomized trial
Authors: Kumar Jayant, Santosh Kumar, Shrawan kumar Singh, Swati Agrawal, Rajendra Agrawal
Journal: Journal for ImmunoTherapy of Cancer (2015)

Meeting abstracts This study was conducted to investigate the ablative efficacy and safety of sequential intravesical gemcitabine and mitomycin C with mitomycin C alone in refractory non-muscle invasive bladder cancer (NMIBC). A total of 219 patients with refractory NMIBC were prospectively
Toll-like receptor 4–mediated lymphocyte influx induces neonatal necrotizing enterocolitis
Authors: Charlotte E. Egan, Chhinder P. Sodhi, Misty Good, Joyce Lin, Hongpeng Jia, Yukihiro Yamaguchi, Peng Lu, Congrong Ma, Maria F. Branca, Samantha Weyandt, William B. Fulton, Diego F. Niño, Thomas Prindle, John A. Ozolek, David J. Hackam
Journal: Journal of Clinical Investigation (2015)

The nature and role of the intestinal leukocytes in necrotizing enterocolitis (NEC), a severe disease affecting premature infants, remain unknown. We now show that the intestine in mouse and human NEC is rich in lymphocytes that are required for NEC development, as recombination activating gene 1–deficient (Rag1–/–) mice were protected from NEC and transfer of intestinal lymphocytes from NEC mice into naive mice induced intestinal inflammation. The intestinal expression of the lipopolysaccharide receptor TLR4, which is higher in the premature compared with full-term human and mouse intestine, is required for lymphocyte influx through TLR4-mediated upregulation of CCR9/CCL25 signaling. TLR4 also mediates a STAT3-dependent polarization toward increased proinflammatory CD3+CD4+IL-17+ and reduced tolerogenic Foxp3+ Treg lymphocytes (Tregs). Th17 lymphocytes were required for NEC development, as inhibition of STAT3 or IL-17 receptor signaling attenuated NEC in mice, while IL-17 release impaired enterocyte tight junctions, increased enterocyte apoptosis, and reduced enterocyte proliferation, leading to NEC. Importantly, TLR4-dependent Th17 polarization could be reversed by the enteral administration of retinoic acid, which induced Tregs and decreased NEC severity. These findings identify an important role for proinflammatory lymphocytes in NEC development via intestinal epithelial TLR4 that could be reversed through dietary modification.
Clinical characteristics and genotype-phenotype correlations in C3 deficiency
Authors: Yuka Okura, Ichiro Kobayashi, Masafumi Yamada, Satoshi Sasaki, Yutaka Yamada, Ichiro Kamioka, Rie Kanai, Yutaka Takahashi, Tadashi Ariga
Journal: Journal of Allergy and Clinical Immunology (2015)
B Cell Reconstitution after Rituximab Treatment in Idiopathic Nephrotic Syndrome
Authors: Manuela Colucci, Rita Carsetti, Simona Cascioli, Federica Casiraghi, Annalisa Perna, Lucilla Ravà, Barbara Ruggiero, Francesco Emma, Marina Vivarelli
Journal: Journal of the American Society of Nephrology (2015)

The pathogenesis of nephrotic syndrome is unclear. However, the efficacy of rituximab, a B cell–depleting antibody, in nephrotic syndrome suggests a pathogenic role of B cells. In this retrospective study, we determined by flow cytometry levels of B and T cell subpopulations before and after rituximab infusion in 28 pediatric patients with frequently relapsing or steroid–dependent nephrotic syndrome. At baseline, patients had lower median percentages of transitional and mature B cells than age–matched healthy controls ( P &lt;0.001). Rituximab induced full depletion of B cells (&lt;1% of lymphocytes). At 1 year, most patients exhibited complete total and mature B cell recovery, whereas memory B cell subsets remained significantly depleted. Total T cell concentration did not change with rituximab, whereas the CD4 + /CD8 + T cell ratio tended to increase. Fourteen patients relapsed within 24 months, with a median follow-up of 11.2 months (interquartile range, 8–17.7 months). We observed no difference at baseline between nonrelapsing and relapsing patients in several clinical parameters and cell subset concentrations. Reconstitution of all memory B cell subpopulations, number of immunosuppressive drugs, and dose of tacrolimus during the last 4 months of follow-up were predictive of relapse in univariate Cox regression analysis. However, only delayed reconstitution of switched memory B cells, independent of immunosuppressive treatment, was protective against relapse in multivariate ( P &lt;0.01) and receiver operator characteristic ( P &lt;0.01 for percentage of lymphocytes; P =0.02 for absolute count) analyses. Evaluation of switched memory B cell recovery after rituximab may be useful for predicting relapse in patients with nephrotic syndrome.
Tumor-specific pH-responsive peptide-modified pH-sensitive liposomes containing doxorubicin for enhancing glioma targeting and anti-tumor activity
Authors: Yang Zhao, Wei Ren, Ting Zhong, Shuang Zhang, Dan Huang, Yang Guo, Xin Yao, Chao Wang, Wei-Qiang Zhang, Xuan Zhang, Qiang Zhang
Journal: Journal of Controlled Release (2015)
Stress fracture risk factors in female football players and their clinical implications
Authors: Stuart J Warden, Mark W Creaby, Adam L Bryant, Kay M Crossley
Journal: British Journal of Sports Medicine (2007)

A stress fracture represents the inability of the skeleton to withstand repetitive bouts of mechanical loading, which results in structural fatigue, and resultant signs and symptoms of localised pain and tenderness. Reports of stress fractures in female football players are not prevalent; however, they are probably under-reported and their importance lies in the morbidity that they cause in terms of time lost from participation. By considering risk factors for stress fractures in female football players it may be possible to reduce the impact of these troublesome injuries. Risk factors for stress fractures in female football players include intrinsic risk factors such as gender, endocrine, nutritional, physical fitness and neuromusculoskeletal factors, as well as extrinsic risk factors such as training programme, equipment and environmental factors. This paper discusses these risk factors and their implications in terms of developing prevention and management strategies for stress fractures in female football players.
Hypertensive disorders of pregnancy, respiratory outcomes and atopy in childhood
Authors: Seif O. Shaheen, Corrie Macdonald-Wallis, Debbie A. Lawlor, A. John Henderson
Journal: European Respiratory Journal (2015)

Few epidemiological studies have investigated the role of hypertensive disorders of pregnancy in the aetiology of childhood respiratory and atopic outcomes. In the Avon Longitudinal Study of Parents and Children we examined associations of maternal gestational hypertension, hypertension before pregnancy and pre-eclampsia with wheezing at 18 months, wheezing and asthma at 7 years and lung function at 8–9 years, after controlling for potential confounders (n=5322–8734, depending on outcome). Gestational hypertension was not associated with any of the outcomes. There was weak evidence for a positive association between pre-eclampsia and early wheezing (adjusted OR 1.31, 95% CI 0.94–1.82, compared to normotensive pregnancies) and for negative associations between pre-eclampsia and forced expiratory volume in 1 s (adjusted mean difference in sd score −0.14, 95% CI −0.33–0.06) and maximal mid-expiratory flow (−0.15, 95% CI −0.34–0.04). Hypertension before pregnancy was positively associated with wheezing (OR 1.63, 95% CI 1.16–2.31) and asthma (OR 1.34, 95% CI 1.00–1.79). Gestational hypertension is unlikely to be a risk factor for childhood respiratory disorders; hypertension before pregnancy may be a risk factor for childhood wheezing and asthma, but this finding needs replication. Larger studies are needed to confirm whether pre-eclampsia is associated with impaired childhood lung function.
Effects of Alcohol Consumption on Hepatocarcinogenesis in Japanese Patients With Fatty Liver Disease
Authors: Yusuke Kawamura, Yasuji Arase, Kenji Ikeda, Norio Akuta, Masahiro Kobayashi, Satoshi Saitoh, Fumitaka Suzuki, Yoshiyuki Suzuki, Mie Inao, Satoshi Mochida, Hiromitsu Kumada
Journal: Clinical Gastroenterology and Hepatology (2015)
What defines latent infection with <i>Mycobacterium tuberculosis</i> in patients with autoimmune diseases?
Authors: Martina Sester, Beate Kampmann
Journal: Thorax (2015)

Screening for latent infection with Mycobacterium tuberculosis (LTBI) and treatment of test-positives is the cornerstone in the prevention of TB and should be performed preferably among individuals with risk for progression. Progression from LTBI to active TB is highest in recent contacts of patients with active TB. Moreover, it is considered particularly high in latently infected patients if they are also immunodeficient. Therefore, screening for evidence of LTBI is recommended for HIV-infected individuals, patients with chronic renal failure, individuals receiving immunosuppressive drug therapy following solid organ or stem cell transplantation, and patients with autoimmune diseases.1 ,2 Since by definition LTBI lacks the gold standard of bacteriological confirmation, the condition is diagnosed indirectly by detection of an immune response towards mycobacterial antigens with either the tuberculin skin test (TST) or interferon-γ release assays (IGRA) performed from whole blood. IGRA may have test-intrinsic and operational advantages over the TST: due to the use of M. tuberculosis -specific antigens, IGRA have been shown to be more specific than the TST and allow distinction of infections with M. tuberculosis from immunity towards bacille Calmette–Guerin (BCG) or most non-tuberculous mycobacteria.3 Moreover, unlike the TST, which has been shown to be of low sensitivity in immunocompromised patients, IGRA seem to be less affected by immunodeficiency, as frequently reflected by a higher percentage of positive test results in IGRA compared with TST in head-to-head comparative analyses.4 Finally, as IGRA are performed along with negative and positive controls, indeterminate results due to failure of responses in the positive control (phytohaemagglutinin) may increase with increasing immunodeficiency and potentially allow to discriminate true negative from falsely negative test results. Our knowledge about the effect of immunosuppressive drugs on TST and IGRA results remains somewhat limited as the individual studies published to date suffer from sample sizes, …
A Post-QRS Potential in Brugada Syndrome
Authors: Yoshifusa Aizawa, Masaomi Chinushi, Minoru Tagawa, Hiroshi Furushima, Shinsuke Okada, Kenichi Iijima, Daisuke Izumi, Hiroshi Watanabe, Satoru Komura
Journal: Journal of the American College of Cardiology (2008)
COX-1-selective inhibitors are new attractive agents for cancer treatment without the gastric damage: Design, in vitro and in vivo evaluation of a structurally-simple benzamide-type COX-1 selective inhibitor, TFAP
Authors: Hiroki Kakuta, Xiaoxia Zheng, Hiroyuki Oda, Shun Harada, Hideko Nagasawa, Yukio Sugimoto, Kenji Sasaki, Akihiro Tai
Journal: Cancer Research (2008)

AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA

1308 

Pain relaxation care of terminal cancer patients is recommended by the World Health Organization (WHO). Ones of widely used painkillers for cancer patients are non-steroidal anti-inflammatory drugs (NSAIDs). However, NSAIDs produce a serious problem, gastric disturbance. This problem is thought to be caused by inhibition of cyclooxygenase-1 (COX-1), a prostaglandin (PG) synthesis enzyme, by NSAIDs. Nevertheless, it has been reported that a limited number of COX-1-selective inhibitors tend to exhibit strong analgesic effects without gastric damage. In order to show the usefulness of COX-1 selective inhibitors, we developed new structurally simple COX-1-selective inhibitors by structural mimicry of the s-trans conformation in COX-1 of indomethacin (1). As a result, N-(5-amino-2-pyridinyl)-4-(trifluoromethyl)benzamide (TFAP: 2) was discovered as a potent COX-1-selective inhibitor (COX-1 IC50 = 0.99 I¼M, COX-2 IC50 = 230 I¼M). TFAP (2) causes little gastric damage in rats even at a dose of 300 mg/kg by oral administration and has an apparent analgesic effect even at a dose of 10 mg/kg. In addition, TFAP (2) showed anti-angiogenesis effect. Our results indicate clearly that COX-1-selective inhibitors can be attractive agents for cancer treatment without causing gastric damage.
Scatter Photocoagulation Does Not Reduce Macular Edema or Treatment Burden in Patients with Retinal Vein Occlusion
Authors: Peter A Campochiaro, Gulnar Hafiz, Tahreem A Mir, Adrienne W Scott, Sharon Solomon, Ingrid Zimmer-Galler, Akrit Sodhi, Elia Duh, Howard Ying, Adam Wenick, Syed Mahmood Shah, Diana V Do, Quan D Nguyen, Saleema Kherani, Raafay Sophie
Journal: Ophthalmology (2015)
Phase II calm extension study: Coxsackievirus A21 delivered intratumorally to patients with advanced melanoma induces immune-cell infiltration in the tumor microenvironment
Authors: Robert HI Andtbacka, Brendan D Curti, Sigrun Hallmeyer, Zipei Feng, Christopher Paustian, Carlo Bifulco, Bernard Fox, Mark Grose, Darren Shafren
Journal: Journal for ImmunoTherapy of Cancer (2015)

Meeting abstracts CAVATAK, an oncolytic immunotherapy, is a bio-selected oncolytic strain of Coxsackievirus A21 (CVA21). Following intratumoral (IT) injection, CVA21 preferentially infects ICAM-1 expressing tumor cells, resulting in viral replication, cell lysis, and a systemic anti-tumor immune