tbuckley/cabot-search huggingface dataset:
Genetic Studies Help Clarify the Complexities of Lipid Biology and Treatment
Authors: Allan D. Sniderman, Eric D. Peterson
Journal: JAMA (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 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
Biomarker-Guided vs Guideline-Directed Titration of Medical Therapy for Heart Failure
Authors: Gregg C. Fonarow
Journal: JAMA (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 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
A nosocomial measles outbreak in Italy, February-April 2017
Authors: Andrea Porretta, Filippo Quattrone, Francesco Aquino, Giulio Pieve, Beatrice Bruni, Giulia Gemignani, Maria Linda Vatteroni, Mauro Pistello, Gaetano Pierpaolo Privitera, Pier Luigi Lopalco
Journal: Eurosurveillance (2017)

We describe a nosocomial outbreak of measles that occurred in an Italian hospital during the first months of 2017, involving 35 persons and including healthcare workers, support personnel working in the hospital, visitors and community contacts. Late diagnosis of the first case, support personnel not being promptly recognised as hospital workers and diffusion of the infection in the emergency department had a major role in sustaining this outbreak.
The Practical Implications of the New Metaphysics of Race for a Postracial Medicine: Biomedical Research Methodology, Institutional Requirements, Patient–Physician Relations
Authors: Joanna K. Malinowska, Tomasz Żuradzki
Journal: The American Journal of Bioethics (2017)

This article refers to:Now is the Time for a Postracial Medicine: Biomedical Research, the National Institutes of Health, and the Perpetuation of Scientific Racism
CD177 modulates human neutrophil migration through activation-mediated integrin and chemoreceptor regulation
Authors: Ming Bai, Ricardo Grieshaber-Bouyer, Junxia Wang, Angela B. Schmider, Zachary S. Wilson, Liling Zeng, Olha Halyabar, Matthew D. Godin, Hung N. Nguyen, Anaïs Levescot, Pierre Cunin, Craig T. Lefort, Roy J. Soberman, Peter A. Nigrovic
Journal: Blood (2017)
Procedural Anticoagulation in Myocardial Infarction
Authors: Gregg W Stone
Journal: New England Journal of Medicine (2017)

The prognosis for patients with ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI) is improved with the use of percutaneous coronary intervention (PCI). Choosing the best procedural anticoagulation regimen to balance the risks of ischemia and bleeding during PCI is essential to optimize outcomes. Heparin, a nonspecific indirect thrombin inhibitor, was the only anticoagulant agent used during PCI for several decades, first with aspirin alone and then with aspirin plus a platelet P2Y12 receptor inhibitor (ticlopidine or clopidogrel). Adding a platelet glycoprotein IIb/IIIa receptor inhibitor to heparin therapy further reduced the risk of stent thrombosis, reinfarction, and death among patients . . .
In vivo evaluation of urokinase-loaded hollow nanogels for sonothrombolysis on suture embolization-induced acute ischemic stroke rat model
Authors: Yuming Teng, Haiqiang Jin, Ding Nan, Mengnan Li, Chenghe Fan, Yuanyuan Liu, Pu Lv, Wei Cui, Yongan Sun, Hongjun Hao, Xiaozhong Qu, Zhenzhong Yang, Yining Huang
Journal: Bioactive Materials (2017)

The urokinase-type plasminogen activator (uPA) loaded hollow nanogels (nUK) were synthesized by a one-step reaction of glycol chitosan and aldehyde capped poly (ethylene oxide). The resultant formulation is sensitive to diagnostic ultrasound (US) of 2 MHz. Herein, we evaluated the in vivo sonothrombolysis performance of the nUK on acute ischemic stroke rat model which was established by suture embolization of middle cerebral artery (MCA). Via intravenous (i.v.) administration, the experimental data prove a controlled release of the therapeutic protein around the clots under ultrasound stimulation, leading to enhanced thrombolysis efficiency of the nUK, evidenced from smaller infarct volume and better clinical scores when compared to the i.v. dose of free uPA no matter with or without US intervention. Meanwhile, the preservation ability of the nanogels not only prolonged the circulation duration of the protein, but also resulted in the better blood-brain barrier protection of the nUK formulation, showing no increased risk on the hemorrhagic transformation than the controls. This work suggests that the nUK is a safe sonothrombolytic formulation for the treatment of acute ischemic stroke.
Open Access Data Tool for Cancer Research
Authors: Jeff Lyon
Journal: JAMA (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 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
Optical imaging of MMPSense as a biomarker of matrix metalloprotease activity in vivo
Authors: Jeffrey Peterson, Sylvie Kossodo, Houari Korideck, Jennifer Jeschke, Agnieszka Blusztajn, Milind Rajopadhye, Jun Zhang, Anthony Catalano
Journal: Cancer Research (2008)

1130  Matrix metalloproteases (MMP) are a family of zinc-containingendopeptidases known to degrade extracellular matrix (ECM) components such as collagens, fibronectin, and laminin. As such, they play a key role in various normal and pathological settings, for example in turnover of the ECM, joint tissue remodeling in rheumatoid arthritis, and tumor development/metastasis. We developed a novel near infrared (NIR) fluorescent probe, designed to be selectively activated in the presence of disease-associated MMPs. This agent contains a peptide sequence (GPLGVRGKC) labeled with a NIR fluorophore and conjugated to a pegylated polylysine scaffold. In its native state, the MMP probe is optically quenched and becomes fluorescent upon enzymatic cleavage (predominantly by MMPs 7, 9, 12, and 13), yielding a four- to eight-fold increase in signal. In vivo, using either planar or tomographic imaging, this probe can be used to detect and quantify MMP activity associated with a variety of disease states. Interestingly, in vivo tomographic imaging, but not planar imaging, of HT-29 colon adenocarcinoma tumor xenografts revealed the predominantly tumor margin distribution of MMP activity, in agreement with the known biology. As a control for the inflammatory component of tumor growth, we also determined that this probe is effective in detecting and quantifying macrophage/synoviocyte MMP activity associated with arthritic disease progression. This probe could also be used as a mechanistic biomarker for therapeutic MMP inhibitory activity in HT-29 tumor xenografts. Intravenous injection of MMPSense in established disease (using an MMP inhibitor regimen insufficient to modify clinical disease severity) allowed the non-invasive quantification of mechanistic MMP inhibition (60-65%), showing a robust technique for establishing target coverage in living animals.  The ability to non-invasively quantify the underlying biology of tumor progression in real time is critical in the development and monitoring of anti-tumor therapies.
PADI2-Mediated Citrullination Promotes Prostate Cancer Progression
Authors: Lin Wang, Guanhua Song, Xiang Zhang, Tingting Feng, Jihong Pan, Weiwen Chen, Muyi Yang, Xinnuo Bai, Yu Pang, Jindan Yu, Jinxiang Han, Bo Han
Journal: Cancer Research (2017)

Onset of castration-resistance prostate cancer (CRPC) after long-term androgen deprivation therapy remains a major obstacle in the treatment of prostate cancer. The peptidylarginine deiminase PADI2 has been implicated in chronic inflammatory diseases and cancer. Here we show that PADI2 is an androgen-repressed gene and is upregulated in CRPC. PADI2 expression was required for survival and cell-cycle progression of prostate cancer cells, and PADI2 promoted proliferation of prostate cancer cells under androgen-deprived or castration conditions in vitro and in vivo Cytoplasmic PADI2 protected the androgen receptor (AR) against proteasome-mediated degradation and facilitated AR binding to its target genes after nuclear translocation and citrullination of histone H3 amino acid residue R26. In contrast, mutant PADI2 D180A failed to affect AR stability, nuclear translocation, or transcriptional activity. PADI2 mediated AR control in a manner dependent on its enzymatic activity and nuclear localization, as correlated with increased histone H3 citrullination. Notably, coadministration of the PADI inhibitor Cl-Amidine and the AR signaling inhibitor enzalutamide synergized in inhibiting CRPC cell proliferation in vitro and tumor growth in vivo Overall, our results establish PADI2 as a key mediator for AR in prostate cancer progression, especially CRPC, and they suggest PADI as novel therapeutic targets in this disease setting. Cancer Res; 77(21); 5755-68. ©2017 AACR.
Mutations in KEOPS-complex genes cause nephrotic syndrome with primary microcephaly
Authors: Daniela A Braun, Jia Rao, Geraldine Mollet, David Schapiro, Marie-Claire Daugeron, Weizhen Tan, Olivier Gribouval, Olivia Boyer, Patrick Revy, Tilman Jobst-Schwan, Johanna Magdalena Schmidt, Jennifer A Lawson, Denny Schanze, Shazia Ashraf, Jeremy F P Ullmann, Charlotte A Hoogstraten, Nathalie Boddaert, Bruno Collinet, Gaëlle Martin, Dominique Liger, Svjetlana Lovric, Monica Furlano, I Chiara Guerrera, Oraly Sanchez-Ferras, Jennifer F Hu, Anne-Claire Boschat, Sylvia Sanquer, Björn Menten, Sarah Vergult, Nina De Rocker, Merlin Airik, Tobias Hermle, Shirlee Shril, Eugen Widmeier, Heon Yung Gee, Won-Il Choi, Carolin E Sadowski, Werner L Pabst, Jillian K Warejko, Ankana Daga, Tamara Basta, Verena Matejas, Karin Scharmann, Sandra D Kienast, Babak Behnam, Brendan Beeson, Amber Begtrup, Malcolm Bruce, Gaik-Siew Ch'ng, Shuan-Pei Lin, Jui-Hsing Chang, Chao-Huei Chen, Megan T Cho, Patrick M Gaffney, Patrick E Gipson, Chyong-Hsin Hsu, Jameela A Kari, Yu-Yuan Ke, Cathy Kiraly-Borri, Wai-ming Lai, Emmanuelle Lemyre, Rebecca Okashah Littlejohn, Amira Masri, Mastaneh Moghtaderi, Kazuyuki Nakamura, Fatih Ozaltin, Marleen Praet, Chitra Prasad, Agnieszka Prytula, Elizabeth R Roeder, Patrick Rump, Rhonda E Schnur, Takashi Shiihara, Manish D Sinha, Neveen A Soliman, Kenza Soulami, David A Sweetser, Wen-Hui Tsai, Jeng-Daw Tsai, Rezan Topaloglu, Udo Vester, David H Viskochil, Nithiwat Vatanavicharn, Jessica L Waxler, Klaas J Wierenga, Matthias T F Wolf, Sik-Nin Wong, Sebastian A Leidel, Gessica Truglio, Peter C Dedon, Annapurna Poduri, Shrikant Mane, Richard P Lifton, Maxime Bouchard, Peter Kannu, David Chitayat, Daniella Magen, Bert Callewaert, Herman van Tilbeurgh, Martin Zenker, Corinne Antignac, Friedhelm Hildebrandt
Journal: Nature Genetics (2017)
Abstract 15511: A Novel Mitochondrial Targeted DNA Repair Enzyme Attenuates Maladaptive Myocardial Remodeling and Preserves Cardiac Function in Heart Failure
Authors: Jessica M Bradley, Hiroyuki Otsuka, Chelsea L Organ, Shashi Bhushan, David J Polhemus, Glenn L Wilson, David J Lefer
Journal: Circulation (2015)

Background: Sustained increases in mitochondrial oxidative stress results in mitochondrial DNA (mtDNA) damage further worsening oxidative damage and cellular injury. These cellular events are pivotal in development and progression of myocardial damage and heart failure. We investigated the effects of a novel mitochondrial targeted fusion protein that traffics endonuclease III (Exscien1-III) and repairs mtDNA in the setting of pressure overload heart failure. Methods: Male C57/BL6J mice (n=10) were subjected to transverse aortic constriction (TAC; 27 g needle) and Exscien1-III (4 mg/kg/d, i.p.) or VEH were administered daily starting at 3 wks post TAC. Left ventricular (LV) function (Vevo 2100) was assessed at baseline and biweekly for 12 weeks post TAC. At the 12 wk endpoint, mice were sacrificed and hearts were collected for biochemical and molecular assessment of cellular injury. Results: Exscien1-III significantly attenuated TAC-induced LV dilation at 12 wks post TAC (LVEDD: 3.9 ± 0.1 vs. 4.6 ± 0.1 mm, p &lt; 0.05; LVESD: 3.1 ± 0.2 vs. 3.9 ± 0.1 mm, p &lt; 0.05) compared to VEH. Exscien1-III displayed a reduced LV wall thickness (LVPWd: 1.1 ± 0.1 vs. 1.4 ± 0.1 mm, p &lt; 0.05) at 8 wks post TAC compared to VEH. In comparison to VEH, LV ejection fraction (LVEF) was preserved in the Exscien1-III treated mice at 8-12 weeks post TAC compared to VEH (*p &lt; 0.05; **p &lt; 0.01). Treatment with Exscien1-III resulted in a reduction in heart weights (9.7 ± 0.4 vs. 12.15 ± 1.2 mg/mm, p &lt; 0.05) compared to VEH. Picrosirius Red staining of LV collagen revealed that Exscien1-III significantly decreased myocardial interstitial collagen volume fraction by 55% (p &lt; 0.05 vs. VEH). Conclusion: Delayed treatment with Exscien1-III attenuated interstitial myocardial collagen deposition and preserved LVEF following the onset of TAC-induced cardiac hypertrophy and heart failure. Current studies are underway to further investigate the mechanisms by which this novel mtDNA repair enzyme protects the failing heart.
ステント内再狭窄の予防のためのTGFβ_1発現をダウンレギュレートするために低分子ヘアピン型RNAをコードするpDNAベクターの表面媒介トランスフェクション【Powered by NICT】
Authors: Zhang He, Ren Ke-feng, Chang Hao, Wang Jin-lei, Ji Jian
Journal: Biomaterials (2017)
Relationship of Kidney Injury Biomarkers with Long-Term Cardiovascular Outcomes after Cardiac Surgery
Authors: Chirag R. Parikh, Jeremy Puthumana, Michael G. Shlipak, Jay L. Koyner, Heather Thiessen-Philbrook, Eric McArthur, Kathleen Kerr, Peter Kavsak, Richard P. Whitlock, Amit X. Garg, Steven G. Coca
Journal: Journal of the American Society of Nephrology (2017)

Clinical AKI, measured by serum creatinine elevation, is associated with long-term risks of adverse cardiovascular (CV) events and mortality in patients after cardiac surgery. To evaluate the relative contributions of urine kidney injury biomarkers and plasma cardiac injury biomarkers in adverse events, we conducted a multicenter prospective cohort study of 968 adults undergoing cardiac surgery. On postoperative days 1-3, we measured five urine biomarkers of kidney injury (IL-18, NGAL, KIM-1, L-FABP, and albumin) and five plasma biomarkers of cardiac injury (NT-proBNP, H-FABP, hs-cTnT, cTnI, and CK-MB). The primary outcome was a composite of long-term CV events or death, which was assessed via national health care databases. During a median 3.8 years of follow-up, 219 (22.6%) patients experienced the primary outcome (136 CV events and 83 additional deaths). Compared with patients without postsurgical AKI, patients who experienced AKI Network stage 2 or 3 had an adjusted hazard ratio for the primary composite outcome of 3.52 (95% confidence interval, 2.17 to 5.71). However, none of the five urinary kidney injury biomarkers were significantly associated with the primary outcome. In contrast, four out of five postoperative cardiac injury biomarkers (NT-proBNP, H-FABP, hs-cTnT, and cTnI) strongly associated with the primary outcome. Mediation analyses demonstrated that cardiac biomarkers explained 49% (95% confidence interval, 1% to 97%) of the association between AKI and the primary outcome. These results suggest that clinical AKI at the time of cardiac surgery is indicative of concurrent CV stress rather than an independent renal pathway for long-term adverse CV outcomes.
AB0922 Clinical manifestations and outcomes of acute septic arthritis in songklanagarind hospital: a 10-year retrospective study
Authors: T Yaowmaneerat, D Aiewruengsurat
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Septic arthritis is a rheumatologic emergency. Its delayed diagnosis and treatment cause joint morbidity and mortality.<sup>1</sup> Cases involving antimicrobial-resistant bacteria have been reported.<sup>2,3</sup> <h3>Objectives</h3> To determine the clinical manifestations and outcomes of septic arthritis, find the factors associated with mortality, and discover the incidence of drug-resistant organisms in our institution <h3>Methods</h3> A retrospective study was performed. Septic arthritis was defined as the presence of acute inflammatory arthritis indicated by a positive synovial fluid or synovial tissue culture for bacteria. A total of 116 septic arthritis patients, who visited Songklanagarind Hospital from January 2005 to December 2014, were reviewed. <h3>Results</h3> The patient median age was 58 (IQR: 46, 72). Sixty-one patients (52%) were female. The median onset of symptoms and symptoms until diagnosis were 5 (IQR: 2, 7) and 6 (IQR: 3, 10) days, respectively. Eighty-eight cases (76.7%) had underlying diseases that might predispose to joint infection. Sixty-nine cases (59.5%) had pre-existing joint disease. Joint pain was the most common presenting symptom, and 58% of the cases had fever. The most common presentation was monoarthritis (87%), which was predominantly associated (78%) with knee joint involvement. The median synovial fluid leukocyte counts were 64,460 cells/μL (IQR: 30,300; 129,000). Blood cultures were positive in 53 patients (49.1%). Synovial fluid cultures commonly had <i>Streptococcus spp.</i> growth (41%). Seven cases (7%) involved drug-resistant organisms. All of them either were diagnosed with septic arthritis during hospitalization or had a history of previous surgery. Twenty-five percent of the cases obtained the empirical antibiotic, ceftriaxone, and 86 patients (80%) underwent arthrotomy drainage. The mortality rate was 12%, and its associated factors were cancer, liver disease and advanced age. <h3>Conclusions</h3> <i>Streptococcus spp.</i> is an emerging cause of septic arthritis in Southern Thai patients. Physicians should be aware of this in patients presenting with fever and acute monoarthritis, particularly those with comorbidities and underlying joint diseases. The proper empirical antibiotic of choice is ceftriaxone. <h3>References</h3> Garcia-Arias M, Balsa A, Mola EM. Septic arthritis. Best practice &amp; research Clinical rheumatology. 2011;25(3):407–21. Frazee BW, Fee C, Lambert L. How common is MRSA in adult septic arthritis? Annals of emergency medicine. 2009;54(5):695–700. Chao CM, Lai CC, Hsueh PR. Bacteriology of septic arthritis at a regional hospital in Southern Taiwan. Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi. 2013;46(3):241–2. <h3>Disclosure of Interest</h3> None declared
Reassessment of gamma-glutamyl transpeptidase to platelet ratio (GPR): a large-sample, dynamic study based on liver biopsy in a Chinese population with chronic hepatitis B virus (HBV) infection
Authors: Wei Zhang, MiMi Sun, Gang Chen, Yong An, ChunLei Lv, YongQing Wang, QingHua Shang
Journal: Gut (2017)

Recently, Lemoine and colleagues1 presented a novel marker of liver fibrosis, the gamma-glutamyl transpeptidase to platelet ratio (GPR), as a more accurate non-invasive marker than either the aspartate aminotransferase to platelet ratio index (APRI) or the fibrosis index based on four factors (FIB-4) for diagnosing liver fibrosis in patients with chronic hepatitis B virus (HBV) infection in West Africa, and a simple and inexpensive alternative to transient elastography and liver biopsy. Boyd and colleagues2 demonstrated good results for GPR in the diagnosis of liver fibrosis in patients with HBV/HIV co-infection in France. However, Stockdale and colleagues3 reported that in patients with HBV / human immunodeficiency virus (HIV) co-infection in West Africa, GPR showed poor correlation with transient elastography. Lemoine and colleagues4 subsequently responded that the diagnostic accuracy of GPR differed when using liver biopsy or transient elastography as the reference. These inconsistent opinions indicated that the value of GPR for diagnosing liver fibrosis was still uncertain and needed further validation, not to mention its value for dynamic assessment of treatment response in patients with chronic HBV infection.

To further evaluate the accuracy of GPR for diagnosing liver fibrosis, we undertook a retrospective study in China of 1168 patients, with chronic HBV infection and without alcoholic …