tbuckley/cabot-search huggingface dataset:
Ten-year trends in colorectal cancer (CRC) control in Texas.
Authors: Davor Vugrin
Journal: Journal of Clinical Oncology (2012)

e12044 Background: The 2015 colorectal cancer control goals are to reduce age-adjusted incidence to 34.8/100,000 and mortality to 12.0/100,000 and to increase the number of 50 year and older undergoing screening per national guidelines up to 75%. Methods: In order to determine progress and trends toward meeting the 2015 objectives we have reviewed Texas Cancer Registry 2000 – 2009 data for incidence, 1999 – 2008 data for mortality, and BRFSS 2002 0 2010 data for screening rates. Results: 91,260 Texans were diagnosed with CRC and 32,840 died from it. Non-Hispanics represent 50.1% of population they account for 66.4% of cases diagnosed with it. Hispanics account for 34.7% of population and contribute to 18.7% of diagnoses. Blacks, 12.1% of population contribute 12.6% of cases. Male and female contribution to diagnosed CRC was 53.5 % and 46.% of cases. Black male incidence rates were highest 74.7 and Hispanic females lowest 32.7/100,000. While NH White and Blacks reduced incidence rates by about 1% per year, Hispanics rate of decrease was 0.5/yr. Gender and race played role in this decrease. Mortality rates declined most in Blacks and NH Whites, while no appreciable improvement was observed in Hispanics. Race and gender mortality rates varied. Black male mortality rates were highest, 36.0 and Hispanic females lowest, 10.5. Frequency of sigmoidoscopy-colonoscopy increased in all 3 racial/ethnic groups, but was lowest among Hispanics. Lack of insurance is big obstacle to progress. Conclusions: Major coordinated screening push will be needed to reach 2015 goals.
Abstract 15663: Gender Differences in Circulating Progenitor Cells and Regenerative Capacity
Authors: Matthew L Topel, Salim S Hayek, Yi-An Ko, Greg S Martin, Edmund K Waller, Arshed A Quyyumi
Journal: Circulation (2016)

Introduction: Lower levels of circulating progenitor cells (PCs) are reflective of reduced endogenous regenerative capacity and are associated with aging, subclinical vascular disease and higher mo...
Procalcitonin to Guide Antibiotic Decisions—Reply
Authors: Philipp Schuetz, Beat Mueller
Journal: JAMA (2018)

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
Annals Story Slam - Getting to Know My People
Authors: Sarah G. Candler
Journal: Annals of Internal Medicine (2018)

Web Exclusives17 July 2018Annals Story Slam - Getting to Know My PeopleFREESarah G. Candler, MD, MPHSarah G. Candler, MD, MPHMichael E. DeBakey VA Medical Center, Baylor College of Medicine, Houston, Texas (S.G.C.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/W18-0016 SectionsAboutVisual Abstract ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Video. Annals Story Slam - Getting to Know My People "Getting to Know My People," by Sarah G. Candler (Duration 7:00)Building on the popular Annals feature “On Being a Doctor,” storytellers share stories about the experience of doctoring on video.For more videos from and information on Annals Story Slam, visit go.annals.org/StorySlam. Comments0 CommentsSign In to Submit A Comment Author, Article, and Disclosure InformationAffiliations: Michael E. DeBakey VA Medical Center, Baylor College of Medicine, Houston, Texas (S.G.C.)Corresponding Author: Sarah G. Candler, MD, MPH; e-mail, [email protected]com. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 17 July 2018Volume 169, Issue 2Page: SS1 ePublished: 17 July 2018 Issue Published: 17 July 2018 Copyright & PermissionsCopyright © 2018 by American College of Physicians. All Rights Reserved.Loading ...
Identifying demographic, social and clinical predictors of biologic therapy effectiveness in psoriasis: a multicentre longitudinal cohort study
Authors: R.B. Warren, A. Marsden, B. Tomenson, K.J. Mason, M.M. Soliman, A.D. Burden, N.J. Reynolds, D. Stocken, R. Emsley, C.E.M. Griffiths, C. Smith
Journal: British Journal of Dermatology (2018)

Biologic therapies have revolutionized the treatment of moderate‐to‐severe psoriasis. However, for reasons largely unknown, many patients do not respond or lose response to these drugs. To evaluate demographic, social and clinical factors that could be used to predict effectiveness and stratify response to biologic therapies in psoriasis. Using a multicentre, observational, prospective pharmacovigilance study (BADBIR), we identified biologic‐naive patients starting biologics with outcome data at 6 (n = 3079) and 12 (n = 3110) months. Associations between 31 putative predictors and outcomes were investigated in univariate and multivariable regression analyses. Potential stratifiers of treatment response were investigated with statistical interactions. Eight factors associated with reduced odds of achieving ≥ 90% improvement in Psoriasis Area and Severity Index (PASI 90) at 6 months were identified (described as odds ratio and 95% confidence interval): demographic (female sex, 0·78, 0·66–0·93); social (unemployment, 0·67, 0·45–0·99); unemployment due to ill health (0·62, 0·48–0·82); ex‐ and current smoking (0·81, 0·66–0·99 and 0·79, 0·63–0·99, respectively); clinical factors (high weight, 0·99, 0·99–0·99); psoriasis of the palms and/or soles (0·75, 0·61–0·91); and presence of small plaques only compared with small and large plaques (0·78, 0·62–0·96). White ethnicity (1·48, 1·12–1·97) and higher baseline PASI (1·04, 1·03–1·04) were associated with increased odds of achieving PASI 90. The findings were largely consistent at 12 months. There was little evidence for predictors of differential treatment response. Psoriasis phenotype and potentially modifiable factors are associated with poor outcomes with biologics, underscoring the need for lifestyle management. Effect sizes suggest that these factors alone cannot inform treatment selection.
2018 AATS/ACC/SCAI/STS Expert Consensus Systems of Care Document: Operator and Institutional Recommendations and Requirements for Transcatheter Aortic Valve Replacement
Authors: Joseph E. Bavaria, Carl L. Tommaso, Ralph G. Brindis, John D. Carroll, G. Michael Deeb, Ted E. Feldman, Thomas G. Gleason, Eric M. Horlick, Clifford J. Kavinsky, Dharam J. Kumbhani, D. Craig Miller, A. Allen Seals, David M. Shahian, Richard J. Shemin, Thoralf M. Sundt, Vinod H. Thourani
Journal: Journal of the American College of Cardiology (2018)
Abstract 432: MCUB Regulates Mitochondrial Calcium Uniporter Channel Gating and Modulates Bioenergetics and Cell Death
Authors: Jonathan P Lambert, TImothy S Luongo, Pooja Jadiya, Erhe Gao, Xueqian Zhang, Anna Maria Lucchesee, John W Elrod
Journal: Circulation Research (2017)

The mitochondrial calcium uniporter (MCU) is a high-capacity, inward-rectifying channel in the inner mitochondrial membrane and is required for mitochondrial Ca 2+ ( m Ca 2+ ) uptake. m Ca 2+ signaling regulates bioenergetics and activates the mitochondrial permeability transition pore (MPTP) which are cellular processes implicated in cardiac pathophysiology warranting further research into the molecular regulation of the MCU. Recently, a MCU gene paralog, MCUB , was identified as a possible component of the channel. To investigate MCUB’s contribution to uniporter regulation we created a MCUB -/- HeLa cell line using CRISPR-Cas9n. Here, we report that loss of MCUB increased m Ca 2+ transient amplitude after IP3R stimulation (52% vs. con) suggesting MCUB negatively regulates m Ca 2+ uptake. Mitoplast patch-clamping confirmed that loss of MCUB increases MCU current density, suggesting MCUb modulates channel capacitance. Permeabilized MCUB -/- and WT cells exposed to various levels of Ca 2+ (0.5-20μM) revealed that MCUB -/- cells exhibited m Ca 2+ uptake at lower Ca 2+ concentrations than controls, suggesting MCUB contributes to channel gating. In m Ca 2+ retention capacity experiments MCUB -/- cells required ~30% less bath Ca 2+ to induce depolarization, suggesting a predisposition to m Ca 2+ overload. Next, we generated a cardiac-specific, tamoxifen-inducible MCUB overexpression mouse model ( MCUB -Tg). Cardiomyocytes isolated from MCUB -Tg hearts exhibited decreased m Ca 2+ uptake at low-Ca 2+ (59% vs. con) and isolated mitochondria exhibited a reduction in Ca 2+ -induced swelling (37% vs. con), suggesting a resistance to permeability transition. MCUB -Tg mice displayed a significant impairment in isoproterenol-induced contractile reserve and this correlated with a loss of isoproterenol-mediated activation of pyruvate dehydrogenase. In summary, our results suggest that MCUB limits m Ca 2+ uptake by altering channel-gating and thereby regulates bioenergetics and MPTP opening.
Diagnosis and Treatment of Acute Respiratory Distress Syndrome
Authors: Brian M. Fuller, Nicholas M. Mohr, Marin H. Kollef
Journal: JAMA (2018)

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
High-throughput identification of noncoding functional SNPs via type IIS enzyme restriction
Authors: Gang Li, Marta Martínez-Bonet, Di Wu, Yu Yang, Jing Cui, Hung N. Nguyen, Pierre Cunin, Anaïs Levescot, Ming Bai, Harm-Jan Westra, Yukinori Okada, Michael B. Brenner, Soumya Raychaudhuri, Eric A. Hendrickson, Richard L. Maas, Peter A. Nigrovic
Journal: Nature Genetics (2018)
Treatment of Acute Stanford Type B Aortic Dissection With a Novel Cylindrical Balloon Catheter in Dogs
Authors: HiromuTerai, NobushigeTamura, TatsuoNakamura, KazunobuNishimura, NorimasaTsutsui, YasuhikoShimizu, MasashiKomeda
Journal: Circulation (2000)

Background—Despite recent progress in medical and surgical treatment, acute type B aortic dissection still carries a high mortality rate. We have developed a novel cylindrical balloon catheter for less invasive treatment to block the entry of the dissection and induce thrombotic occlusion of the false lumen. The balloon has the shape of a sheet when deflated but a double-cylinder shape when inflated. Therefore, aortic blood flow is maintained through the cylindrical lumen during balloon inflation. Methods and Results—Six beagle dogs underwent a left thoracotomy at the 6th intercostal space. An acute dissection of 4-cm length was created surgically on the descending aorta. The balloon catheter was inserted through the distal descending aorta and advanced to the entry site. The balloon catheter was inflated for 6 hours. The blood flow in the descending aorta and the position of the balloon was monitored by color Doppler echovasculography. Four dogs were killed humanely on the following day and 2 dogs 10 day...
Critical role of histone demethylase Jumonji domain-containing protein 3 in the regulation of neointima formation following vascular injury
Authors: XiaoLing Luo, Di Yang, WeiJun Wu, Fen Long, ChenXi Xiao, Ming Qin, Betty YuenKwan Law, Rinkiko Suguro, Xin Xu, LeFeng Qu, XinHua Liu, Yi Zhun Zhu
Journal: Cardiovascular Research (2018)

Jumonji domain-containing protein 3 (JMJD3), also called lysine specific demethylase 6B (KDM6b), is an inducible histone demethylase which plays an important role in many biological processes, however, its function in vascular remodelling remains unknown. We aim to demonstrate that JMJD3 mediates vascular neointimal hyperplasia following carotid injury, and proliferation and migration in platelet-derived growth factor BB (PDGF-BB)-induced vascular smooth muscle cells (VSMCs).By using both genetic and pharmacological approaches, our study provides the first evidence that JMJD3 controls PDGF-BB-induced VSMCs proliferation and migration. Furthermore, our in vivo mouse and rat intimal thickening models demonstrate that JMJD3 is a novel mediator of neointima formation based on its mediatory effects on VSMCs proliferation, migration, and phenotypic switching. We further show that JMJD3 ablation by small interfering RNA or inhibitor GSK J4 can suppress the expression of NADPH oxidase 4 (Nox4), which is correlated with H3K27me3 enrichment around the gene promoters. Besides, deficiency of JMJD3 and Nox4 prohibits autophagic activation, and subsequently attenuates neointima and vascular remodelling following carotid injury. Above all, the increased expression of JMJD3 and Nox4 is further confirmed in human atherosclerotic arteries plaque specimens.JMJD3 is a novel factor involved in vascular remodelling. Deficiency of JMJD3 reduces neointima formation after vascular injury by a mechanism that inhibits Nox4-autophagy signalling activation, and suggesting JMJD3 may serve as a perspective target for the prevention and treatment of vascular diseases.
Occupational hand eczema and job change
Authors: T.K. Carøe, N.E. Ebbehøj, J.P.E. Bonde, S.G. Vejlstrup, T. Agner
Journal: British Journal of Dermatology (2018)

Occupational hand eczema is a type of eczema specifically affecting the hands and caused by a person's work. It often affects people whose hands get wet a lot or are exposed to chemicals when working, such as hairdressers and cleaners. It can cause a great deal of distress to people, affecting their health‐related quality of life (HRQoL) and often meaning they have to leave work or change jobs. It is a major reason for people seeking disability benefit in countries including the UK, so as well as having a negative impact on the patient, it also impacts on society more widely. In theory, occupational hand eczema should heal when the exposure is removed; however, several studies have shown that this is unfortunately not the case in reality, and some patients may continue to have severe hand eczema symptoms. This study involved 1496 people who were suffering from occupational hand eczema in Denmark in 2010 and 2011, who then completed a questionnaire 5 years later, asking questions about their job, their eczema and their quality of life. 48.7% were still in the same profession, 32.6% had changed profession and 18.8% were not working (outside the labour market, e.g. retired, unemployed, on parental leave). Healing of hand eczema (meaning their hands were now clear of eczema) was reported by 19.5% of the participants who changed their profession and 27.3% of the participants who outside the labour market, compared with 15.8% of those still in the same profession. Looking at improvement (but not healing) of their eczema, 64.9% of the participants who had changed profession and 58.2% of the participants outside the labour market reported improvement in their hand eczema compared with 53.1% of the participants still in the same profession. However, health related quality of life was not improved by changing jobs or leaving work, and in fact worsened. Also, the authors did not ask if the participants changed to a profession with more or less exposure than the previous profession, so it is possible that some participants have changed to another high risk profession, thereby diminishing the effect of change. These two points both need further research.
Endothelial Cell–Specific Liver Kinase B1 Deletion Causes Endothelial Dysfunction and Hypertension in Mice In Vivo
Authors: WenchengZhang, QilongWang, YueWu, CateMoriasi, ZhaoyuLiu, XiaoyanDai, QiongxinWang, WeiminLiu, Zu-YiYuan, Ming-HuiZou
Journal: Circulation (2014)

Background—Liver kinase B1 (LKB1), a tumor suppressor, is a central regulator of cell polarity and energy homeostasis. The role of LKB1 in endothelial function in vivo has not been explored. Methods and Results—Endothelium-specific LKB1 knockout (LKB1endo−/−) mice were generated by cross-breeding LKB1flox/flox mice with VE-Cadherin-Cre mice. LKB1endo−/− mice exhibited hypertension, cardiac hypertrophy, and impaired endothelium-dependent relaxation. LKB1endo−/− endothelial cells exhibited reduced endothelial nitric oxide synthase activity and AMP kinase (a downstream enzyme of LKB1) phosphorylation at Thr172 compared with wild-type (WT) cells. In addition, the levels of caveolin-1 were higher in the endothelial cells of LKB1endo−/− mice, and knockdown of caveolin-1 by siRNA normalized endothelial nitric oxide synthase activity. Human antigen R bound with the adenylate-uridylate-rich elements of caveolin-1 mRNA 3′ untranslated region, resulting in the increased stability of caveolin-1, and genetic knockdown...
FUN14 Domain‐Containing 1–Mediated Mitophagy Suppresses Hepatocarcinogenesis by Inhibition of Inflammasome Activation in Mice
Authors: Wenhui Li, Yanjun Li, Sami Siraj, Haojie Jin, Yuyuan Fan, Xinrong Yang, Xiaowu Huang, Xiaohui Wang, Jun Wang, Lei Liu, Lei Du, Quan Chen
Journal: Hepatology (2018)

Mitochondria lie at the heart of innate immunity, and aberrant mitochondrial activity contributes to immune activation and chronic inflammatory diseases, including liver cancers. Mitophagy is a selective process for removing dysfunctional mitochondria. The link between mitophagy and inflammation in tumorigenesis remains largely unexplored. We observed that FUN14 domain-containing 1 (FUNDC1), a previously characterized mitophagy receptor, accumulates in most human hepatocellular carcinomas (HCCs), and we thus explored the role of FUNDC1-mediated mitophagy in HCC initiation and progression in a mouse model in which HCC is induced by the chemical carcinogen, diethylnitrosamine (DEN). We showed that specific knockout of FUNDC1 in hepatocytes promotes the initiation and progression of DEN-induced HCC, whereas FUNDC1 transgenic hepatocytes protect against development of HCC. Hepatocyte-specific FUNDC1 ablation results in the accumulation of dysfunctional mitochondria and triggers a cascade of events involving inflammasome activation and hyperactivation of Janus kinase/signal transducer and activator of transcription signaling. Specifically, cytosolic mitochondrial DNA (mtDNA) release and caspase-1 activation are increased in FUNDC1-depleted hepatocytes. This subsequently results in the elevated release of proinflammatory cytokines, such as interleukin-1β (IL1β) and hyperproliferation of hepatocytes. Conclusion: Our results suggest that FUNDC1 suppresses HCC initiation by reducing inflammasome activation and inflammatory responses in hepatocytes, whereas up-regulation of FUNDC1 expression at the late stage of tumor development may benefit tumor growth. Our study thus describes a mechanistic link between mitophagic modulation of inflammatory response and tumorigenesis, and further implies that FUNDC1-mediated mitophagy and its related inflammatory response may represent a therapeutic target for liver cancer.
Is Venous Thromboembolism in Asian Patients Undergoing Gastrectomy Different From Venous Thromboembolism in Their Western Counterparts?
Authors: Oluwafemi P. Owodunni, Matthew J. Weiss, Elliott R. Haut
Journal: JAMA Surgery (2018)

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
Prophylactic Haloperidol for Critically Ill Adults
Authors: Jacqueline J. M. H. Strik, Jan N. M. Schieveld
Journal: JAMA (2018)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Clinical Trial Evidence Supporting FDA Approval of Drugs Granted Breakthrough Therapy Designation
Authors: Jeremy Puthumana, Joshua D. Wallach, Joseph S. Ross
Journal: JAMA (2018)

This study used the Drugs@FDA database to review FDA-approved “breakthrough” therapies from 2012 to 2017 (characterizing the pivotal clinical trials that serve as the basis of FDA approval), and premarket development and review times to assess the strength of evidence supporting breakthrough approvals.