tbuckley/cabot-search huggingface dataset:
Abstract 11919: A Potent and Selective Covalent Inhibitor of JNK Protects Heart From Both Ischemia/Reperfusion- and Hypertension-induced Heart Failure
Authors: Xu Chen, Nanhu Quan, Lin Wang, Dongyang Chu, Peng Zhao, Mei Xue, Yanping Bi, Courtney Cates, Ji Li
Journal: Circulation (2016)

Introduction: c-Jun NH 2 -terminal kinases (JNKs) are critical mediators of a variety of detrimental stimuli including ischemia-reperfusion (I/R) and mechanical stress induced by pressure overload. A novel synthesized highly selective JNK inhibitor, JNK-IN-8, can form an ATP site-directed covalent bond with a conserved cysteine residual in all JNKs, therefore, it may be broadly useful as a pharmacological tool for inhibiting JNK-dependent signal transduction that is involved in various pathological conditions. Hypothesis: The potent JNK inhibitor, JNK-IN-8, could act as a cardioprotectant against ischemia/reperfusion (I/R)- or hypertension-induced heart failure. Methods: The effects of JNK-IN-8 were monitored in a mouse I/R models with the left anterior descending coronary artery occluded and subsequently released, and a mouse model of transverse aortic constriction (TAC), in which pressure overload hypertrophy was induced in 4 weeks. Results: JNK-IN-8 treatment significantly reduced myocardial infarct area by 40% in mouse ischemia and reperfusion (I/R) model as compared to the vehicle groups (p&lt;0.01). Interestingly, the immunohistochemistry data showed that JNK-IN-8 treatment attenuated the macrophage infiltration and caspase-3 executed apoptosis signaling in TAC-induced heart failure mice (p&lt;0.01 vs. vehicle groups). Moreover, the staining of wheat germ agglutinin (WGA) and Masson trichrome staining revealed that there are significant decreases in hypertrophy and fibrosis in the hearts of JNK-IN-8 treated TAC-induced heart failure mice. Furthermore, the immunoblotting data demonstrated that JNK-IN-8 treatment selectively attenuated both I/R- and pressure overload-induced JNK and downstream oxidative stress p-SHC (p66), inflammatory NF-kappaB signaling pathways, while the levels of other mitogen protein kinase family signals (p-p38 and p-ERK) remained unchanged, indicating the specificity of JNK-IN-8 on JNK signaling in the heart. Conclusions: JNK-IN-8 reduces myocardial infarction caused by ischemia and reperfusion, and attenuates pressure overload-induced inflammation, apoptosis, hypertrophy and fibrosis. Thus JNK-IN-8 is a potential therapeutic drug for I/R- and pressure overload-induced heart failure.
Chemoconnectomics: Mapping Chemical Transmission in Drosophila
Authors: Bowen Deng, Qi Li, Xinxing Liu, Yue Cao, Bingfeng Li, Yongjun Qian, Rui Xu, Renbo Mao, Enxing Zhou, Wenxia Zhang, Juan Huang, Yi Rao
Journal: Neuron (2019)
Modulation of TET2 Activity By Ascorbic Acid and Factors Affecting Lysine Acetylation
Authors: Yihong Guan, Edward F Greenberg, Metis Hasipek, Cassandra M. Hirsch, Amy C Graham, Tomas Radivoyevitch, Shi Chen, Xiaochen Liu, Valeria Visconte, Dewen You, Eiju Negoro, Bartlomiej P. Przychodzen, Hideki Makishima, Aziz Nazha, Daniel Gackowski, Ewelina Zarakowska, Mridul Mukherji, Mikkael A. Sekeres, Mingjiang Xu, Ryszard Ólinski, Jaroslaw P. Maciejewski, Babal K. Jha
Journal: Blood (2018)
Sedentary Behavior and Cardiovascular Disease in Older Women
Authors: John Bellettiere, Michael J. LaMonte, Kelly R. Evenson, Eileen Rillamas-Sun, Jacqueline Kerr, I-Min Lee, Chongzhi Di, Dori E. Rosenberg, Marcia L. Stefanick, David M. Buchner, Melbourne F. Hovell, Andrea Z. LaCroix, Jacques Rossouw, Shari Ludlam, Dale Burwen, Joan McGowan, Leslie Ford, Nancy Geller, Garnet Anderson, Ross Prentice, Charles Kooperberg, JoAnn E. Manson, Barbara V. Howard, Rebecca Jackson, Cynthia A. Thomson, Jean Wactawski-Wende, Marian Limacher, Robert Wallace, Lewis Kuller, Sally Shumaker, Sally Shumaker
Journal: Circulation (2019)

Background: Evidence that higher sedentary time is associated with higher risk for cardiovascular disease (CVD) is based mainly on self-reported measures. Few studies have examined whether patterns of sedentary time are associated with higher risk for CVD. Methods: Women from the OPACH Study (Objective Physical Activity and Cardiovascular Health; n=5638, aged 63–97 years, mean age 79±7 years) with no history of myocardial infarction or stroke wore accelerometers for 4 to 7 days and were followed up for up to 4.9 years for CVD events. Average daily sedentary time and mean sedentary bout duration were the exposures of interest. Cox regression models were used to estimate hazard ratios (HRs) and 95% CIs for CVD using models adjusted for covariates and subsequently adjusted for potential mediators (body mass index, diabetes mellitus, hypertension, and CVD risk biomarkers [fasting glucose, high-density lipoprotein, triglycerides, and systolic blood pressure]). Restricted cubic spline regression characterized dose-response relationships. Results: There were 545 CVD events during 19 350 person-years. With adjustment for covariates, women in the highest (≈11 h/d or more) versus the lowest (≈9 h/d or less) quartile of sedentary time had higher risk for CVD (HR, 1.62; 95% CI, 1.21–2.17; P trend &lt;0.001). Further adjustment for potential mediators attenuated but did not eliminate significance of these associations ( P trend &lt;0.05, each). Longer versus shorter mean sedentary bout duration was associated with higher risks for CVD (HR, 1.54; 95% CI, 1.27–2.02; P trend=0.003) after adjustment for covariates. Additional adjustment for CVD risk biomarkers attenuated associations, resulting in a quartile 4 versus quartile 1 HR of 1.36 (95% CI, 1.01–1.83; P trend=0.10). Dose-response associations of sedentary time and bout duration with CVD were linear ( P nonlinear &gt;0.05, each). Women jointly classified as having both high sedentary time and long bout durations had significantly higher risk for CVD (HR, 1.34; 95% CI, 1.08–1.65) than women with low sedentary time and short bout duration. All analyses were repeated for incident coronary heart disease (myocardial infarction or CVD death), and associations were similar, with notably stronger HRs. Conclusions: Both high sedentary time and long mean bout durations were associated in a dose-response manner with increased CVD risk in older women, which suggests that efforts to reduce CVD burden might benefit from addressing either or both components of sedentary behavior.
Abstract 4771: Epigenetic modification of LY6K in CGI shore and CGI regulates LY6K gene activation and metastatic function in breast cancer
Authors: Hyun Kyung Kong, Sae Jeong Park, Ye Sol Kim, Jong Hoon Park
Journal: Cancer Research (2015)

Abstract LY6K is associated with development of the immune response and carcinogenesis. Elevated LY6K by AP-1 activation induces invasion and metastasis by activating the ERK signaling pathway. However, the exact epigenetic mechanism of LY6K gene expression has not been clarified. The CpG island and 5′CGI shore in the region around the transcription start site of the LY6K were predicted using the UCSC genome browser and Methprimer software to elucidate the epigenetic mechanism of LY6K gene regulation and expression. We performed the methylation-specific PCR, bisulfite pyro-sequencing, and bisulfite sequencing to investigate the DNA methylation status of CpG sites from −400 to +500 on the LY6K CpG island and 5′CGI shore. ChIP and ChIP-MSP analysis were performed to confirm the histone modification and DNA methylation status. To validate the inverse correlation between LY6K 5′CGI shore methylation and LY6K expression in vivo, we performed bisulfite pyro-sequencing and tissue microarray using breast carcinoma samples. LY6K expression was inversely correlated with methylation status of CGI and 5′CGI shore in the LY6K of human breast cancer. Moreover, DNA methylation status of LY6K was correlated with histone modification. Treatment of 5-Aza-dC with low LY6K expression caused elevated LY6K expression leading to wound healing. An understanding of epigenetic changes in LY6K may contribute to diagnosing carcinogenic risk and to predict the outcome of patients with breast cancer. Citation Format: Hyun Kyung Kong, Sae Jeong Park, Ye Sol Kim, Jong Hoon Park. Epigenetic modification of LY6K in CGI shore and CGI regulates LY6K gene activation and metastatic function in breast 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 4771. doi:10.1158/1538-7445.AM2015-4771
A Report by the Editor-in-Chief for MBE, Volume 33
Authors: Sudhir Kumar
Journal: Molecular Biology and Evolution (2017)

MBE serves a broad community of researchers, undivided by organismal allegiances, who conduct research at the intersection of molecular biology and evolution.In addition to publishing innovative and broad-interest research discoveries, MBE focuses on providing our research community with access to new and improved methods, resources, technologies, and theories that will significantly advance evolutionary research.Journal impact factor (JIF) is considered to be an important metric for scientific journals, reflecting the contribution of journal content to broader scientific progress.More simply, JIF reflects how often articles published in MBE are cited.Conventionally, impact factor for a given year (e.g., 2016) is calculated as the number of citations recorded that year (2016) for articles published in the preceding 2 years (2014 and 2015).Although debate exists among the scientific community regarding the overall importance of JIF, it is widely discussed, reported, and used by researchers in choosing where to publish and evaluating the importance of a particular study.The Journal Citations Reports (JCR) database, released by Thomson Reuters, reported the 2016 JIF of MBE as 6.202.It is important to note that MBE's impact factor has been quite volatile over the past 5 years, which is largely attributable to the disproportionate impact of articles describing widely used tools and resources on JIF calculations.When these articles become part of the calculations, MBE's JIF increases.We find that a modified JIF, which excludes all articles with more than 100 citations in the focal year, reveals that the impact of Discoveries and Methods published in MBE has been growing over the past 5 years.MBE also performs well under alternative metrics.Eigenfactor is calculated through usage-weighted analysis of 5-year citation data.Normalized eigenfactor scores (which scale the average journal score to 1) for MBE have risen steadily from 9.6 in 2013 to 12 in 2016.The SCImago Journal Rankings incorporate both numerical citation data and an assessment of the "prestige" of citing journals; MBE ranks sixth in the category Ecology, Evolution, and Behavioral Sciences (fourth if review-focused journals are excluded) and 13th among Molecular Biology Journals (seventh if reviewfocused journals are excluded).Google Scholar journal rankings are based on median and 5-year H-index, which should
Angiopoietin-like protein 1 suppresses SLUG to inhibit cancer cell motility
Authors: Tsang-Chih Kuo, Ching-Ting Tan, Yi-Wen Chang, Chih-Chen Hong, Wei-Jiunn Lee, Min-Wei Chen, Yung-Ming Jeng, Jean Chiou, Pei Yu, Pai-Sheng Chen, Ming-Yang Wang, Michael Hsiao, Jen-Liang Su, Min-Liang Kuo
Journal: Journal of Clinical Investigation (2017)

During the assembly of Figure 3H, an incorrect image was inadvertently included for the CL1-5GL/ANGPTL1 +pLKO_AS2.neo/SLUGsample in the lower panel.The correct tail vein injection panel is below.
Conduits harnessing spatially controlled cell-secreted neurotrophic factors improve peripheral nerve regeneration
Authors: Aaron X. Sun, Travis A. Prest, John R. Fowler, Rachel M. Brick, Kelsey M. Gloss, Xinyu Li, Michael DeHart, He Shen, Guang Yang, Bryan N. Brown, Peter G. Alexander, Rocky S. Tuan
Journal: Biomaterials (2019)
Clinical Impact of Clonal and Subclonal TP53 Mutations in Chronic Lymphocytic Leukemia
Authors: Riccardo Bomben, Maria Francesca Rossi, Tiziana D'Agaro, Tamara Bittolo, Antonella Zucchetto, Erika Tissino, Federico Pozzo, Filippo Vit, Pietro Bulian, Massimo Degan, Eva Zaina, Ilaria Cattarossi, Paola Nanni, Hillarj Chivilò, Giovanni Francesco D'Arena, Annalisa Chiarenza, Enrico Santinelli, Francesco Zaja, Gabriele Pozzato, Francesco Di Raimondo, Giovanni Del Poeta, Valter Gattei
Journal: Blood (2018)
Long‐term fostamatinib treatment of adults with immune thrombocytopenia during the phase 3 clinical trial program
Authors: James B. Bussel, Donald M. Arnold, Michael A. Boxer, Nichola Cooper, Jiri Mayer, Hany Zayed, Sandra Tong, Anne‐Marie Duliege
Journal: American Journal of Hematology (2019)

Two randomized, double-blind, placebo-controlled studies demonstrated responses (≥50 000/μL) to fostamatinib in adults with long-standing immune thrombocytopenia (ITP). The long-term safety and efficacy of fostamatinib were evaluated in a follow-on, open-label extension (OLE) study. Patients received double-blind fostamatinib in the randomized trials, and responders continued the same dose, 100 to 150 mg BID, in the OLE study. Nonresponders received 100 mg BID for 4 weeks and could escalate to 150 mg BID at week 4. Endpoints included stable response, platelet count ≥50 000/μL at 4/6 biweekly (randomized trials) or 2/3 monthly visits (OLE), and overall response, ≥1 platelet count ≥50 000/μL during weeks 1 to 12. A total of 146 patients received fostamatinib including 123 in the OLE study. Median treatment duration was 6.7 months. Baseline median ITP duration was 8 years and median platelet count was 16 000/μL; prior treatments included thrombopoietic (TPO) agents (47%), splenectomy (35%), and rituximab (32%). Twenty-seven (18%) patients achieved a stable response with median duration of >28 months and a median platelet count of 89 000/μL. Sixty-four (44%) patients achieved an overall response (including stable responders) with a median platelet count of 63 000/μL and a median response duration of >28 months. Twenty-four of 71 (34%) patients who had failed TPO agents achieved overall responses to fostamatinib. The most common adverse events (AEs) were diarrhea, hypertension, nausea, epistaxis, and abnormal liver function tests. Most AEs were mild/moderate and resolved or were managed with dose reduction, dose interruption, and/or secondary medication. Almost half of the patients achieved an overall response, and most of these maintained their responses for >2 years. No new or increased frequency of AEs was seen at up to 31 months of treatment.
Allergen immunotherapy improves defective follicular regulatory T cells in patients with allergic rhinitis
Authors: Yin Yao, Zhi-Chao Wang, Nan Wang, Peng-Cheng Zhou, Cai-Ling Chen, Jia Song, Li Pan, Bo Liao, Xin-Hao Zhang, Yong-Shi Yang, Xiao-Yan Xu, Rong-Fei Zhu, Di Yu, Zheng Liu
Journal: Journal of Allergy and Clinical Immunology (2019)
Medical Devices to Prevent Opioid Use Disorder
Authors: Sandra D. Comer, Robert H. Dworkin, Eric C. Strain
Journal: JAMA Psychiatry (2019)

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 Psychiatry 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 Psychiatry journal
Multimodal Single-Cell Profiling Defines the Epigenetic Determinants of Chronic Lymphocytic Leukemia Evolution
Authors: Ronan Chaligne, Federico Gaiti, Franco Izzo, Steven Kothen-Hill, Hongcang Gu, Kevin Huang, Davide Risso, Rafael Schulman, Ryan M Brand, Stanley C Lee, Asaf Poran, Kye-Tae Kim, Alessandro Pastore, Alicia Alonso, Andreas Gnirke, Catherine J. Wu, Omar I Abdel-Wahab, Alexander Meissner, Dan A. Landau
Journal: Blood (2018)
Bronchial hyperresponsiveness in children with allergic rhinitis and the associated risk factors
Authors: Betul Karaatmaca, Pınar Gur Cetinkaya, Saliha Esenboga, Murat Ozer, Ozge Soyer, Erdem Karabulut, Bulent Enis Sekerel, Umit Murat Sahiner
Journal: Allergy (2019)

Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
241. Lentivirus Mediated Dystrophin Expression in mdx Muscles
Journal: Molecular Therapy (2004)

Top of pageAbstract
To study candidate treatments for Duchenne muscular dystrophy, we have generated a series of lentiviral vectors that express various reporter genes and mini-dystrophin cassettes and tested their ability to transduce a variety of cell types in vitro and in vivo. Direct injection of lentiviral vectors into adult skeletal muscle resulted in significantly lower levels of gene expression than were obtained using either AAV or adenoviral vectors.

Since an advantage of lentiviral vectors is stable expression of a transgene that has integrated into host genomic DNA, stem cells are considered a good target of lentiviral vectors. During myogenesis, activated-satellite cells or muscle progenitor cells proliferate in the muscle microenvironment. Most of these cells become differentiated and form myofibers, while small numbers of them are stored adjacent to myofibers as mitotically quiescent satellite cells for future muscle regeneration. Skeletal muscle of newborn mice may be a good target for lentiviral vectors, because of relatively high numbers of activated muscle progenitor cells contributing to muscle growth and satellite cell pools. Therefore, we tried targeting satellite cells or muscle progenitor cells using lentivirual vectors expressing dystrophin mini-gene.

We demonstrated that relatively higher levels of transuction were obtained with intra-muscular injection into neonatal muscles, and that both muscle fibers and primary cultured satellite cells stably expressed a GFP marker gene. We also demonstrated that lentiviral mediated truncated mini-dystrophin expression in mdx muscles may be useful for correction of pathological changes in dystrophic muscle.

These data suggest that myogenic stem cells can be stably transduced with lentiviral vectors and may contribute to stable muscle regeneration in dystrophic muscle by enabling continuous expression of mini-dystrophin, which may have implications for gene therapy of Duchenne muscular dystrophy.
Sex Differences in Heart Failure With Preserved Ejection Fraction Pathophysiology
Authors: Anna L. Beale, Shane Nanayakkara, Louise Segan, Justin A. Mariani, Micha T. Maeder, Vanessa van Empel, Donna Vizi, Shona Evans, Carolyn S.P. Lam, David M. Kaye
Journal: JACC Heart Failure (2019)
AMA House of Delegates Adopts Resolutions, Part 1
Journal: JAMA (1998)

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
Chronic Kidney Disease (CKD) in the U.S. Hemophilia Population: A Cohort Study
Authors: Suman L. Sood, Dunlei Cheng, Amy Shapiro, Craig M. Kessler, Nigel S. Key, Doris Quon, M. Elaine Eyster, Marilyn J Manco-Johnson, Christine L. Kempton, Adam Cuker, Margaret V. Ragni, Philip Kuriakose, Annette von Drygalski, Peter A. Kouides, Miguel A Escobar, Allison P. Wheeler, Tzu-Fei Wang, Cindy A. Leissinger, Sarah Galdzicka, Barbara A Konkle
Journal: Blood (2018)