tbuckley/cabot-search huggingface dataset:
Abstract 20796: Effect of in Situ Automatic Implantable Cardioverter-Defibrilator(AICD) on the in Hospital Outcomes in the Patients With Takotsubo Cardiomyopathy
Authors: Ronak G Soni, Mohit Pahuja, Badal Thakkar, Savdeep Singh, Dhara G Patel
Journal: Circulation (2016)

Introduction: Hospitalizations of takotsubo cardiomyopathy (TTC) have been rising in last decade. There is limited data reporting mortality associated with the disease. It can occasionally present ...
Patients with self‐reported HS in a cohort of Danish blood donors
Authors: P. Theut Riis, O.B. Pedersen, V. Sigsgaard, C. Erikstrup, H.M. Paarup, K.R. Nielsen, K.S. Burgdorf, H. Hjalgrim, K. Rostgaard, K. Banasik, H. Ullum, G.B. Jemec
Journal: British Journal of Dermatology (2019)

Hidradenitis suppurativa (HS) is a distressing skin condition in which patients suffer from repeated eruptions of boils in the armpit, groin, under the breast, and in the perineum. The disease is suspected to affect around 1 in 100 people, but studies are conflicting on how many actually suffer from this disease. The unique nature of the disease makes it possible to diagnose the disease using questionnaires. Danish blood donors received the questionnaire, and 27,765 answered it. Approximately 1.8 % (almost 1 in 50) of blood donors seemed to suffer from HS. Donors with HS had a higher body mass index and were younger than donors without; female to male ratio was approximately 1:1. Smoking frequency and body mass index of donors with HS were between that of blood donors without HS and patients with HS from other studies. The questionnaire also revealed that HS patients were more depressed, but their life quality was the same as non‐HS donors. The unique civil registration number in Denmark allowed us to compare publicly registered information about the participants. More HS donors received educational support and cash benefits (both are government support) than non‐HS donors. HS did not, however, seem to affect income of donors. Only 2.2 % of the HS donors were registered with the disease. We interpreted this as a need for better diagnosis of mild cases of the disease. If the blood donors continue to give blood, we can follow them to see how much their HS condition affects their life.
Understanding the Financial Consequences of Smoking During Cancer Treatment in the Era of Value-Based Medicine
Authors: Cara M. Petrucci, Andrew Hyland
Journal: JAMA Network Open (2019)

Graham W. Warren, MD, PhD; Kathleen B. Cartmell, PhD; Elizabeth Garrett-Mayer, PhD; Ramzi G. Salloum, PhD; K. Michael Cummings, PhD, MPH
Molecular Corroboration of Type 2 Segmental Mosaicism in Various Types of Porokeratosis
Authors: Rudolf Happle
Journal: JAMA Dermatology (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 Dermatology 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 Dermatology journal
Exosomes in gastric cancer: roles, mechanisms, and applications
Authors: Min Fu, Jianmei Gu, Pengcheng Jiang, Hui Qian, Wenrong Xu, Xu Zhang
Journal: Molecular Cancer (2019)

Exosomes are nanosized extracellular vesicles that can be released by almost all types of cells. Initially considered as the garbage bins acting to discard unwanted products of cells, exosomes are now recognized as an important way for cellular communication by transmitting bioactive molecules including proteins, DNA, mRNAs, and non-coding RNAs. The recent studies have shown that exosomes are critically involved in human health and diseases including cancer. Exosomes have been suggested to participate in the promotion of tumorigenesis, tumor growth and metastasis, tumor angiogenesis, tumor immune escape, and tumor therapy resistance. Increasing evidence indicate that exosomes play important roles in gastric cancer development and progression. In this review, we summarized the current understanding of exosomes in gastric cancer with an emphasis on the biological roles of exosomes in gastric cancer and their potential as biomarkers for gastric cancer diagnosis as well as potential targets for gastric cancer therapy.
Another Warning for Febuxostat
Authors: Rebecca Voelker
Journal: JAMA (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 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
Infographic. Tramadol: should it be banned in athletes while competing, particularly in road cycling?
Authors: Joao Gabriel Baltazar-Martins, María del Mar Plata, Jesús Muñoz-Guerra, Gloria Muñoz, Daniel Carreras, Juan Del Coso
Journal: British Journal of Sports Medicine (2019)

Tramadol is a synthetic opioid widely used for the management of pain in sport setting.1 Tramadol is considered an effective substance to reduce acute and chronic pain because it acts by binding to the μ-opioid receptor to induce analgesia and sedation. However, tramadol also inhibits serotonin and norepinephrine reuptake and thus, it might play a role in the regulation of mood. In the past years, tramadol has caught attention of media and antidoping authorities because this substance might be the subject of abuse in some sports, notably cycling.2 WADA determined that the use of some narcotics are …
Abstract 130: Clinical Efficacy Of Modified RAISE Protocol In Acute Kawasaki Disease
Authors: Satoshi Ikehara, Shinichi Takatsuki, Kazuyuki Naoi, Tomotaka Nakayama, Hiroyuki Matsuura, Tohru Kobayashi, Tsutomu Saji
Journal: Circulation (2015)

Backgrounds and Objectives: RAISE protocol demonstrated that IVIG plus prednisolone (PSL) therapy reduced the incidence of coronary artery abnormalities (CAAs) in children with high risk of refractory Kawasaki disease (KD). However, this protocol has longer hospital stay because PSL is tapered over the next 15 days when CRP was under 5mg/L. We proposed modified RAISE protocol which PSL is tapered over 9 days. The aim of this study was to evaluate clinical utility of modified RAISE protocol. Methods: This is a retrospective study to evaluate clinical data from KD between May, 2012 and August, 2014. Composite outcomes included incidence of relapse and coronary arterial abnormalities. Using Kobayashi score, children were divided into high and low risk group. Results: We enrolled 36 KD patients with high risk group in total 147 patients with KD. Median of age was 33 months (range 2-83 months), 13 males. Median days of illness were 4.0 (range 2-7) and Kobayashi score was 6.0 (range 5-9). Overall, 31 children (86.1%) were responders, whereas 5 children were non-responders (resistance; 1 (2.8%) relapse; 4 (11.1%)). Among 5 non-responders, 4 patients received methylprednisolone pulse therapy (mPSL) and the remaining one patient administrated two times mPSL and infliximab. During follow-up (1-29 months), 3 children (8.3%) had CAAs (dilatation: 3 patients). Modified RAISE protocol was not inferior to conventional RAISE protocol (CAAs 3.3%, p=0.68, responder 84.3%, p=1.0, resistance 5.0%, p=0.92, relapse 10.7%, p= 0.66). Conclusions: Clinical safety and efficacy of modified RAISE protocol (3days х3) were similar to conventional RASIE protocol(5days х3).
Prevalence of Carriers of Intermediate and Pathological Polyglutamine Disease–Associated Alleles Among Large Population-Based Cohorts
Authors: Sarah L. Gardiner, Merel W. Boogaard, Stella Trompet, Renée de Mutsert, Frits R. Rosendaal, Jacobijn Gussekloo, J. Wouter Jukema, Raymund A. C. Roos, N. Ahmad Aziz
Journal: JAMA Neurology (2019)

<h3>Importance</h3> Nine hereditary neurodegenerative diseases are known as polyglutamine diseases, including Huntington disease, 6 spinocerebellar ataxias (SCAs) (SCA1, SCA2, SCA3, SCA6, SCA7, and SCA17), dentatorubral-pallidoluysion atrophy, and spinal bulbar muscular atrophy. <h3>Objective</h3> To determine the prevalence of carriers of intermediate and pathological polyglutamine disease–associated alleles among the general population. <h3>Design, Setting, and Participants</h3> This observational cross-sectional study included data from 5 large European population–based cohorts that were compiled between 1997 and 2012, and the analyses were conducted in 2018. In total, 16 547 DNA samples were obtained from participants of the 5 cohorts. Individuals with a lifetime diagnosis of major depression were excluded (n = 2351). In the remaining 14 196 participants without an established polyglutamine disease diagnosis, the CAG repeat size in both alleles of all 9 polyglutamine disease–associated genes (PDAGs) (ie,<i>ATXN1</i>,<i>ATXN2</i>,<i>ATXN3</i>,<i>CACNA1A</i>,<i>ATXN7</i>,<i>TBP</i>,<i>HTT</i>,<i>ATN1</i>, and<i>AR</i>) was determined. <h3>Exposure</h3> The number of CAG repeats in the alleles of the 9 PDAGs. <h3>Main Outcomes and Measures</h3> The number of individuals with alleles within the intermediate or pathological range per PDAG, as well as differences in sex, age, and body mass index between individuals carrying alleles within the normal or intermediate range and individuals carrying alleles within the pathological range of PDAGs. <h3>Results</h3> In the 14 196 analyzed participants (age range, 18-99 years; 56.3% female), 10.7% had a CAG repeat number within the intermediate range of at least 1 PDAG. Moreover, up to 1.3% of the participants had a CAG repeat number within the disease-causing range, predominantly in the lower pathological range associated with elderly onset. No differences in sex, age, or body mass index were found between individuals with CAG repeat numbers within the pathological range and individuals with CAG repeat numbers within the normal or intermediate range. <h3>Conclusions and Relevance</h3> These results indicate a high prevalence of individuals carrying intermediate and pathological ranges of polyglutamine disease–associated alleles among the general population. Therefore, a substantially larger proportion of individuals than previously estimated may be at risk of developing a polyglutamine disease later in life or bearing children with a de novo mutation.
Targeting Intracellular Signaling Cascades for Patients with Relapsed, Refractory Multiple Myeloma: A Systematic Review of Clinical Trials
Authors: Shehroz Aslam, Mustafa Nadeem Malik, Abdul Rafae, Rida Riaz, Seren Durer, Ceren Durer, Faisal Mahfooz, Muhammad Jahanzeb Khalil, Jemin Aby Jose, Zunairah Shah, Chaudhry Saad Sohail, Maaz Ahmed Yusufi, Faiz Anwer
Journal: Blood (2018)
Peroral intraductal cholangioscopy-guided laser lithotripsy via endoscopic ultrasound-guided hepaticogastrostomy for intrahepatic bile duct lithiasis
Authors: Adrien Sportes, Sarah Leblanc, Benoit Bordacahar, Maximilien Barret, Frederic Prat
Journal: Endoscopy (2019)

A 25-year-old man was referred for recurrent cholangitis. At the age of 5, he had undergone surgery for a Todani Type 1 choledochal cyst, with a Roux-en-Y hepaticojejunostomy reconstruction. He experienced several bouts of cholangitis in 2016. Magnetic resonance cholangiopancreatography (MRCP) showed dilated intrahepatic ducts, with bile duct stones in the right posterior sector and above a stenosis at the hepaticojejunal anastomosis ([Video 1]).
Platelet GPIbα is a mediator and potential interventional target for NASH and subsequent liver cancer
Authors: Mohsen Malehmir, Dominik Pfister, Suchira Gallage, Marta Szydlowska, Donato Inverso, Elena Kotsiliti, Valentina Leone, Moritz Peiseler, Bas G. J. Surewaard, Dominik Rath, Adnan Ali, Monika Julia Wolf, Hannah Drescher, Marc E. Healy, Daniel Dauch, Daniela Kroy, Oliver Krenkel, Marlene Kohlhepp, Thomas Engleitner, Alexander Olkus, Tjeerd Sijmonsma, Julia Volz, Carsten Deppermann, David Stegner, Patrick Helbling, César Nombela-Arrieta, Anahita Rafiei, Martina Hinterleitner, Marcel Rall, Florian Baku, Oliver Borst, Caroline L. Wilson, Jack Leslie, Tracy O’Connor, Christopher J. Weston, Abhishek Chauhan, David H. Adams, Lozan Sheriff, Ana Teijeiro, Marco Prinz, Ruzhica Bogeska, Natasha Anstee, Malte N. Bongers, Mike Notohamiprodjo, Tobias Geisler, Dominic J. Withers, Jerry Ware, Derek A. Mann, Hellmut G. Augustin, Alexandros Vegiopoulos, Michael D. Milsom, Adam J. Rose, Patricia F. Lalor, Josep M. Llovet, Roser Pinyol, Frank Tacke, Roland Rad, Matthias Matter, Nabil Djouder, Paul Kubes, Percy A. Knolle, Kristian Unger, Lars Zender, Bernhard Nieswandt, Meinrad Gawaz, Achim Weber, Mathias Heikenwalder
Journal: Nature Medicine (2019)
Thymic stromal lymphopoietin production induced by skin irritation results from concomitant activation of protease‐activated receptor 2 and interleukin 1 pathways
Authors: D. Redhu, K. Franke, V. Kumari, W. Francuzik, M. Babina, M. Worm
Journal: British Journal of Dermatology (2019)

Thymic stromal lymphopoietin (TSLP) mediates proallergic T helper 2‐type responses by acting on leucocytes. Endogenous pathways regulating TSLP production are poorly defined. To uncover the mechanisms by which skin barrier disruption elicits TSLP production and to delineate the level at which individual mechanistic components may converge. A combination of primary keratinocytes, skin explants and in vivo strategies was employed. Murine skin was tape stripped in the presence of neutralizing antibodies or antagonists. Cells and explants were stimulated with interleukin (IL)‐1 and protease‐activated receptor 2 agonist (PAR‐2‐Ag). TSLP levels were quantified by enzyme‐linked immunosorbent assay and real‐time quantitative polymerase chain reaction. Chromatin immunoprecipitation and promoter reporter assays were used to examine recruitment and functional activity of nuclear factor kappa B (NF‐κB) at the TSLP promoter. TSLP induction in mouse skin occurred in a PAR‐2‐ and IL‐1‐dependent manner. This scenario was duplicated by exogenous IL‐1 plus PAR‐2‐Ag vs. each stimulus alone. Joint activity of PAR‐2 and IL‐1 was also observed in human keratinocytes. The TSLP promoter was identified as the target of PAR‐2/IL‐1, whereby PAR‐2 activation augmented the recruitment of NF‐κB and transcriptional activation over IL‐1 alone. Combined treatment showed activity at concentrations of IL‐1 unable to elicit NF‐κB activity on their own. Skin barrier disruption activates the IL‐1 and the PAR‐2 pathways, which act in concert to activate the TSLP promoter and possibly other inflammatory genes. Awareness of this combined activity may permit a more flexible clinical management by selective targeting of either pathway individually or collectively. What's already known about this topic? Thymic stromal lymphopoietin (TSLP) is rapidly induced upon skin perturbation and mediates proallergic T helper 2‐type responses by acting on leucocytes. Endogenous control of TSLP expression is poorly understood, but interleukin (IL)‐1 is one regulator in the cutaneous environment In addition to IL‐1, protease‐activated receptor 2 (PAR‐2) organizes central inflammatory pathways in the skin. What does this study add? IL‐1 and PAR‐2 pathways cooperate in driving TSLP production in mice and humans. Pathway integration occurs at the level of the TSLP promoter through enhanced recruitment and transcriptional activation of nuclear factor kappa B. When PAR‐2 is co‐stimulated, very low IL‐1 levels (inactive by themselves) can induce biologically meaningful responses in the skin environment. What is the translational message? Physical skin irritation results in robust TSLP production by simultaneous activation of PAR‐2 and IL‐1 pathways.
Liver-directed gene therapy results in long-term correction of progressive familial intrahepatic cholestasis type 3 in mice
Authors: Sem J. Aronson, Robert S. Bakker, Xiaoxia Shi, Suzanne Duijst, Lysbeth ten Bloemendaal, Dirk R. de Waart, Joanne Verheij, Giuseppe Ronzitti, Ronald P. Oude Elferink, Ulrich Beuers, Coen C. Paulusma, Piter J. Bosma
Journal: Journal of Hepatology (2019)

Progressive familial intrahepatic cholestasis type 3 (PFIC3), for which there are limited therapeutic options, often leads to end-stage liver disease before adulthood due to impaired ABCB4-dependent phospholipid transport to bile. Using adeno-associated virus serotype 8 (AAV8)-mediated gene therapy, we aimed to restore the phospholipid content in bile to levels that prevent liver damage, thereby enabling stable hepatic ABCB4 expression and long-term correction of the phenotype in a murine model of PFIC3.Ten-week-old Abcb4-/- mice received a single dose of AAV8-hABCB4 (n = 10) or AAV8-GFP (n = 7) under control of a liver specific promoter via tail vein injection. Animals were sacrificed either 10 or 26 weeks after vector administration to assess transgene persistence, after being challenged with a 0.1% cholate diet for 2 weeks. Periodic evaluation of plasma cholestatic markers was performed and bile duct cannulation enabled analysis of biliary phospholipids. Liver fibrosis and the Ki67 proliferation index were assessed by immunohistochemistry.Stable transgene expression was achieved in all animals that received AAV8-hABCB4 up to 26 weeks after administration. AAV8-hABCB4 expression restored biliary phospholipid excretion, increasing the phospholipid and cholesterol content in bile to levels that ameliorate liver damage. This resulted in normalization of the plasma cholestatic markers, alkaline phosphatase and bilirubin. In addition, AAV8-hABCB4 prevented progressive liver fibrosis and reduced hepatocyte proliferation for the duration of the study.Liver-directed gene therapy provides stable hepatic ABCB4 expression and long-term correction of the phenotype in a murine model of PFIC3. Translational studies that verify the clinical feasibility of this approach are warranted.Progressive familial intrahepatic cholestasis type 3 (PFIC3) is a severe genetic liver disease that results from impaired transport of lipids to bile, which makes the bile toxic to liver cells. Because therapeutic options are currently limited, this study aims to evaluate gene therapy to correct the underlying genetic defect in a mouse model of this disease. By introducing a functional copy of the missing gene in liver cells of mice, we were able to restore lipid transport to bile and strongly reduce damage to the liver. The proliferation of liver cells was also reduced, which contributes to long-term correction of the phenotype. Further studies are required to evaluate whether this approach can be applied to patients with PFIC3.
Circular RNA circ-DONSON facilitates gastric cancer growth and invasion via NURF complex dependent activation of transcription factor SOX4
Authors: Lixian Ding, Yuying Zhao, Shuwei Dang, Yue Wang, Xinglong Li, Xiaotong Yu, Zhongsheng Li, Jiufeng Wei, Ming Liu, Guodong Li
Journal: Molecular Cancer (2019)

Circular RNAs (circRNAs) are a novel type of noncoding RNAs and play important roles in tumorigenesis, including gastric cancer (GC). However, the functions of most circRNAs remain poorly understood. In our study, we aimed to investigate the functions of a new circRNA circ-DONSON in GC progression. The expression of circ-DONSON in gastric cancer tissues and adjacent normal tissues was analyzed by bioinformatics method, qRT-PCR, Northern blotting and in situ hybridization (ISH). The effects of circ-DONSON on GC cell proliferation, apoptosis, migration and invasion were measured by using CCK8, colony formation, EdU, immunofluorescence (IF), FACS and Transwell assays. qRT-PCR and Western blotting were utilized to validate how circ-DONSON regulates SOX4 expression. ChIP, DNA fluorescence in situ hybridization (DNA-FISH) and DNA accessibility assays were used to investigate how circ-DONSON regulates SOX4 transcription. The interaction between circ-DONSON and NURF complex was evaluated by mass spectrum, RNA immunoprecipitation (RIP), pulldown and EMSA assays. Xenograft mouse model was used to analyze the effect of circ-DONSON on GC growth in vivo. Elevated expression of circ-DONSON was observed in GC tissues and positively associated with advanced TNM stage and unfavorable prognosis. Silencing of circ-DONSON significantly suppressed the proliferation, migration and invasion of GC cells while promoting apoptosis. circ-DONSON was localized in the nucleus, recruited the NURF complex to SOX4 promoter and initiated its transcription. Silencing of the NURF complex subunit SNF2L, BPTF or RBBP4 similarly attenuated GC cell growth and increased apoptosis. circ-DONSON knockdown inhibited GC growth in vivo. circ-DONSON promotes GC progression through recruiting the NURF complex to initiate SOX4 expression.