tbuckley/cabot-search huggingface dataset:
Abstract 224: Reducing Fluoroscopy Times and Contrast Volume Significantly in the Therapy of Acute Coronary Syndromes by Performing Angioplasty Through Cordis 6F Diagnostic Catheters - Changing the Interludes
Authors: Mark C Arokiaraj
Journal: Circulation Research (2018)

Aims: To reduce fluoroscopy times and contrast volume in the therapy of acute coronary syndromes by performing angioplasty and stenting through 6F Cordis diagnostic catheters in acute coronary syndromes. Methods: 414 patients underwent angioplasty and stenting with acute coronary syndromes with 6F Cordis diagnostic catheters. Primary angioplasty was seen in 124 cases. Baseline renal failure or elevated creatinine &gt;2mg/dl was seen in 15 cases. Baseline creatinine more than 4mg/dl was seen in 6 cases. N acetyl cystenine was given to patients orally for 2 days when creatinine was &gt;1.3mg/dl. All procedures were performed through femoral route only using 6F Cordis diagnostic catheters only. The details of the patients and fluoroscopy times were analysed retrospectively. All patients were followed up at 30 days after discharge. Results: In total 511 lesions and 575 stents were used in the angioplasty procedures. Retrospective analysis showed the mean contrast volume per patient was 27±8 ml. Also, the mean fluoroscopy time was 5.8±2.7 min/patient including the angiogram prior to the angioplasty. In 11% cases where the procedure time was &gt;10 mins, and if these cases were eliminated from analysis the mean fluoroscopy time was 4.4±1.8 min/patient including the angiogram before the angioplasty. There were 4 patients who expired, and 3 of these patients had cardiogenic shock, one patient expired due to possible acute stent thrombosis after discharge. In total, 14 cardiogenic shock patients were treated. Two patients had acute stent thrombosis and were treated with an additional stent. One patient required dialysis who had a baseline creatinine of 5.6mg/dl at presentation. Congestive cardiac failure was seen in 21 cases who were treated with oxygen and early BIPAP ventilation, and frusemide injections and infusion. A variety of stents from various companies could be used in the procedures. Buddy wires were used in 12 patients. Proximal mild edge dissection was seen in two patients after stenting and it was treated with a additional stent. Also, it is feasible to perform IVUS during the procedures. Conclusion: It is feasible to safely reduce the fluoroscopy times and contrast volume by performing angioplasty through 6F Cordis diagnostic catheters in acute coronary syndromes.
COMPARISON OF POLYMER-COATED, PACLITAXEL-ELUTING STENT (ELUVIA) IMPLANTATION AND POLYMER-FREE, PACLITAXEL-COATED STENT (ZILVER PTX) IMPLANTATION ON VASCULAR RESPONSE IN THE FEMOROPOPLITEAL ARTERY LESION ASSESSED ON INTRAVASCULAR ULTRASOUND
Authors: Yusuke Tomoi, Yoshimitsu Soga, Kenji Ando
Journal: Journal of the American College of Cardiology (2019)
Abstract 16095: Is the Arachidonic Acid Pathway Adequately Inhibited in Shunted Infants on Aspirin?
Authors: Dongngan T Truong, Joyce T Johnson, David K Bailly, Jason R Clawson, Madolin K Witte, L. LuAnn Minich
Journal: Circulation (2014)

Introduction: Prevention of shunt thrombosis is vital in infants who require a reliable source of pulmonary blood flow. Aspirin (ASA) prophylaxis is used to inhibit the platelet arachidonic acid (AA) pathway, but dosing is extrapolated from adults, and no therapeutic monitoring guidelines exist. We sought to determine the percentage of infants on ASA after shunt surgery with adequate AA inhibition using thromboelastography with platelet mapping (TEG-PM) and to describe adverse events (AE). Methods: We performed a prospective observational study of infants treated with ASA after shunt (12/2012-5/2014). ASA was dosed at 3-5 mg/kg enterally starting postop day 1. TEG-PM was obtained at 5 intervals: 1) baseline (before cardiopulmonary bypass), 2) prior to 1st ASA dose, 3) after 3rd ASA dose, 4) 1st postop clinic visit, and 5) 2-6 months postop. Adequate AA inhibition was defined as ≥70%, the target parameter in the pediatric Berlin Heart protocol. Bleeding and thrombotic events were recorded as AEs. Clinician...
Abstract 105: Tuning EC-Coupling: <i>β</i> -Adrenergic Receptor Activation Stimulates Dynamic Augmentation of Ca <sub>V</sub> 1.2 Channel Sarcolemmal Abundance and Cooperativity
Authors: Danica W Ito, Karen I Hannigan, Luis F Santana, Rose E Dixon
Journal: Circulation Research (2018)

Voltage-gated L-type Ca V 1.2 channels play an essential role in cardiac excitation-contraction coupling. These channels decorate the z-lines of ventricular myocytes where they form discrete clusters on the t-tubule membrane. We have previously reported that groups of channels within these clusters are capable of influencing each other’s gating behavior and undergo dynamic, cooperative interactions. This occurs via Ca 2+ -calmodulin-dependent, physical interactions between the C-terminal tails of adjacent channels. The interactions increase the open probability ( P o ) of adjoined channels, and thus amplify Ca 2+ influx into the myocytes. It has long been known that activation of β -adrenergic receptors during the ‘fight or flight’ response, leads to increased mean open time and P o of Ca V 1.2 channels, and thus enhanced Ca 2+ influx. Given our previous finding that Ca V 1.2 channel cooperativity is triggered by Ca 2+ -influx, we predicted that β -AR stimulation could affect Ca V 1.2 channel cooperativity in ventricular myocytes. To test this hypothesis, we investigated the effect of the β -agonist isoproterenol (ISO) on Ca V 1.2 channel clustering and cooperativity using a combination of optical and electrophysiological approaches. Ground State Depletion super-resolution nanoscopy revealed ‘super-clustering’ of Ca V 1.2 channels in ISO-stimulated adult mouse ventricular myocytes. Channels within these super-clusters display enhanced physical interactions compared to control unstimulated cells as revealed by Bimolecular fluorescence complementation. To visualize this process, we performed live cardiomyocyte imaging and observed a robust, dynamic increase in sarcolemmal Ca V 1.2 channel abundance in response to ISO. Functionally, optical and electrophysiologicaI recordings of Ca V 1.2 channel activity revealed that ISO-stimulated cells display enhanced Ca V 1.2 channel cooperativity, and amplified Ca 2+ influx. On the basis of these data, we propose that stimulation of β ARs initiates dynamic augmentation of Ca V 1.2 channel abundance, and enhanced cooperative gating of Ca V 1.2 channels, in the sarcolemma of ventricular myocytes, to amplify Ca 2+ influx into these cells and tune EC-coupling in times of high metabolic or hemodynamic demand.
ADOPTION OF CONTINUOUS BEAT-TO-BEAT NOCTURNAL BLOOD PRESSURE MEASUREMENT IN AMBULATORY BLOOD PRESSURE MONITORING
Authors: Sebastian Estrada, Younghoon Kwon, Martin Baruch, Elizabeth Harrison, Ronald Williams, Yeilim Cho, David Gerdt, Heather Bonner, Sula Mazimba, Richard Berry
Journal: Journal of the American College of Cardiology (2019)
Finding Benefit in n-of-1 Trials—Reply
Authors: Richard L. Kravitz, Christopher H. Schmid, Ida Sim
Journal: JAMA Internal Medicine (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 Internal Medicine 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 Internal Medicine journal
SUB-CLINICAL IMPAIRED VENTRICULAR-ARTERIAL COUPLING IN PATIENTS WITH LEFT VENTRICULAR HYPERTROPHY PLUS ELEVATED BIOMARKERS
Authors: Michinari Hieda, Satyam Sarma, Christopher M. Hearon, Katrin A. Dias, Dean Palmer, Jose Martinez Diaz, Mitchel Samels, Braden Everding, Sheryl Livingston, Margot Morris, Benjamin D. Levine
Journal: Journal of the American College of Cardiology (2019)
Abstract 171: Effect of Shock Delivery After Conversion to Shockable Arrest From Out-of-Hospital Non-shockable Cardiac Arrest
Authors: Tsukasa Yagi, Ken Nagao, Eizo Tachibana, Kei Nishikawa, Naohiro Yonemoto, Shinichi Shirai, Morimasa Takayama, Hiroshi Nonogi, Takeshi Kimura
Journal: Circulation (2013)

Background: The 2005 guidelines for cardiopulmonary resuscitation (CPR) with electrical therapy recommended a single shock plus an immediate 2 minutes of CPR instead of 3-shock sequences recommende...
Signal Transducing Adaptor Protein (STAP) Family Accelerates Gut and Thymic Graft-Versus-Host-Disease in Murine Model
Authors: Hideaki Saito, Michiko Ichii, Jun Toda, Yuichi Kitai, Ryuta Muromoto, Jun-ichi Kashiwakura, Kodai Saitoh, Hirohiko Shibayama, Tadashi Matsuda, Kenji Oritani, Yuzuru Kanakura
Journal: Blood (2018)
Biallelic mutations in PALB2 cause Fanconi anemia and predispose to childhood cancer
Authors: Sarah Reid, Detlev Schindler, Helmut Hanenberg, Marc Tischkowitz, Sandra Hanks, Karen Barker, Patrick Kelly, Sheila Seal, Sat Dev Batish, Francis Lach, Reinhard Kalb, Kornelia Neveling, Chris Mathew, Arleen Auerbach, Nazneen Rahman
Journal: Cancer Research (2007)

4922  PALB2 was recently identified as a nuclear binding partner of BRCA2. Biallelic BRCA2 mutations cause Fanconi anemia subtype FA-D1 and predispose to childhood malignancies. We identified pathogenic truncating PALB2 mutations in seven families affected with Fanconi anemia, demonstrating that PALB2 mutations cause a new subtype of Fanconi anemia. The phenotype of PALB2 is, in many ways, typical of Fanconi anemia as all cases showed increased chromosome breakage with interstrand crosslinking agents, growth retardation and variable congenital malformations. However, PALB2 appears to be associated with unusually severe disease and early mortality due to childhood cancer. All seven cases developed cancer in early childhood including three Wilms tumors, five medulloblastomas, two cases of AML and one neuroblastoma. One individual developed three malignancies within the first year of life and three individuals had two cancers. Cancer treatment was unsuccessful in five patients, all of whom died before 3 years of age. One individual is currently alive at 4.5 years but is in the early stages of treatment for medulloblastoma. The cancer spectrum of biallelic PALB2 mutations is therefore very similar to that associated with biallelic BRCA2 mutations, which also confer high risks of embryonal tumors. Mutations in BRCA2 and PALB2 together account for almost all our individuals with both Fanconi anemia and childhood solid tumors. The reasons for the association between childhood solid tumors and the deficiency of BRCA2 or PALB2 are unclear. To investigate whether somatic mutations in PALB2 and BRCA2 occur in embryonal tumors we will screen 30 Wilms tumor, 30 medulloblastoma and 30 neuroblastoma for PALB2 and BRCA2 mutations and the results will be presented. These data identify a new Fanconi subtype and a cause of childhood solid tumors.
Abstract 294: Investigating the Small Heat Shock Proteins Impact on Aggregate Inhibition
Authors: Andrew Roth, Hays Rye
Journal: Circulation Research (2018)

The small heat shock proteins (sHsp) are a highly conserved protein chaperone family needed for ischemia/reperfusion recovery and mitigation of protein aggregation. Without them, environmental stressors, like hypoxia and oxidative stress, can cause highly toxic protein aggregation, leading to cardiomyopathy. Nevertheless, the mechanisms by which sHsps protect cell viability are poorly understood. sHsp mechanism remains elusive due to their highly heterogeneous and dynamic nature making them difficult to study with current methods. To solve this problem, we use a single particle technique called Burst Analysis Spectroscopy (BAS). BAS provides a powerful approach, permitting the real-time observation of size population-resolved kinetics under non-perturbing, free solution conditions. This method allow us to observe events like protein aggregation as well as the interacting sHsp complexes. To study the mechanism of aggregate inhibition by sHsps, we utilize the E. coli sHsps IbpA and IbpB (IbpAB) with two established protein substrates, RuBisCO from R. Rubrum and PepQ from E. coli . Prior work, in vivo and in vitro , has established that IbpAB play a similar role in E. coli as sHsp do in higher eukaryotes suggesting all sHsps may share common mechanistic properties. Using BAS, we established PepQ and RuBisCO form large heterogeneous amorphous aggregates, with RuBisCO also capable of forming fibril-like aggregates under different aggregation conditions. When IbpAB are present during aggregation, both aggregate types decrease in size and form a very specific homogenous aggregate size distribution suggesting IbpAB activity is independent of protein aggregate substrate or structure. Remarkably, binding of IbpAB to RuBisCO aggregates differs dramatically depending on the aggregate structure. The amorphous aggregates appear to bind IbpAB at a RuBisCO monomer-to-IbpAB ratio of 1:1 while the fibril-like RuBisCO aggregates display a bifurcation, where two, distinct aggregate sub-populations bind IbpAB at very different stoichiometries. This data has uncovered the unknown capability of IbpAB/sHsps to inhibit ongoing aggregation of two substrates and structures through two different mechanistic processes all to the same homogenous aggregate size.
David Oliver: Can doctors be too politicised?
Authors: David Oliver
Journal: BMJ (2019)

The Conservative MP Johnny Mercer, a former army officer, is concerned that doctors have become “too politicised.” He told the Health Service Journal in December 2018 that he was “really worried” that this politicisation had led to “unprofessional behaviour” and started to “affect patient care.”1 He didn’t provide any examples beyond recounting that a GP’s child on a school visit had told him, “My daddy says the Tories kill more people than cancer.”

I’d like to challenge the notion that doctors can somehow be “too politicised.”

Doctors have a long and noble tradition of influencing public policy that affects the public’s health. …
IMPACT OF THE CLINICAL FRAILTY SCALE ON ADVERSE EVENTS IN PATIENTS WITH ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION IMPACT OF THE CLINICAL FRAILTY SCALE ON ADVERSE EVENTS IN PATIENTS WITH ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
Authors: Masanari Kurobe, Yasuhiro Uchida, Jun Yonekawa, Yuichiro Makino, Akinori Satake, Wataru Suzuki, Koji Mizutani, Yoshiaki Mizutani, Hitoshi Ichimiya, Junji Watanabe, Masaaki Kanashiro, Satoshi Ichimiya
Journal: Journal of the American College of Cardiology (2019)
Abstract 321: Miat Long Non-coding Rna Regulates Cardiac Hypertrophy and Ribosomal Expression in Cardiomyocytes
Authors: He (Iris) Wang, Zhihua Wang, Yifan Wang, Shuxun Ren, Christopher Rau, Yibin Wang
Journal: Circulation Research (2018)

Cardiac hypertrophy is characterized by elevated protein synthesis and pathological cardiomyocyte enlargement. The mechanisms underlying the stress response in ribosomal remodeling at organelle level during cardiac hypertrophy is not fully established. We have identified a long non-coding RNA, Myocardial Infarction Associated Transcript (MIAT), that is significantly associated with pathological cardiac hypertrophy through a systems genetic analysis. MIAT expression is induced by hypertrophic signal, and silencing of the MIAT gene significantly blocks myocyte hypertrophy in response to hypertrophic stimuli associated with diminished global protein synthesis activities. Furthermore, MIAT inactivation significantly reduces ribosomal genes at mRNA and protein levels, and reduces protein synthesis activity at basal and post-hypertrophic stimulation in vitro and in vivo . Using a MIAT knockout mouse model, we investigated the in vivo pathophysiological impact of MIAT in pressure-overload induced cardiac hypertrophy and heart failure. Remarkably, we find that the MIAT knockout mice show significantly blunted cardiac hypertrophy and preserved cardiac function following pressure-overload. This study highlights a novel mechanism of translational regulation by a lncRNA MIAT. The outcome will expand functional role of lncRNAs in heart diseases and advance our current understanding of the complexity of regulatory circuits in cardiac hypertrophy and heart failure. It will provide novel insights to protein synthesis and ribosomal regulation and reveal potential therapeutic targets for pathological hypertrophy.
Long term hormone therapy may increase Alzheimer’s risk, study finds
Authors: Gareth Iacobucci
Journal: BMJ (2019)

Long term use of oral hormone therapy is associated with a slightly increased risk of Alzheimer’s disease in postmenopausal women, a study published by The BMJ has found.1

The study authors from Finland emphasised that the absolute risk is small (9-18 extra cases per 10 000 women per year) and that the age at which hormone therapy is started has no bearing on future risk. But they advised that women should be informed of the potential risk associated with prolonged use.

Several observational studies have shown that postmenopausal hormone therapy may protect against Alzheimer’s disease. But a subsequent placebo controlled clinical trial23 did not confirm this benefit and in fact implied …
Abstract 409: Ablation of Endothelial Sirt3 Exacerbates Pressure Overload-induced Heart Failure
Authors: Xiaochen He, Heng Zeng, Jian Xiong Chen
Journal: Circulation Research (2018)

Cardiovascular disease leads to cardiac dysfunction and eventually heart failure which is the leading cause of death in the United States. Our previous data indicates that global ablation of SIRT3 exacerbates acute injury after myocardial ischemia and that deletion of endothelial SIRT3 (SIRT3 ECKO) leads to development of cardiac dysfunction. In the present study, we demonstrates that loss of SIRT3 in endothelial cells results in upregulation of TIGAR, but downregulation of HIF-1α, HIF-2α, glucose transport GLUT-1, glycolytic enzymes PFK-1, and PFKFB3. To further investigate the role of endothelial SIRT3 on cardiac hypertrophy and heart failure during chronic stress, SIRT3 ECKO and their control SIRT3 LoxP mice were subjected to pressure overload-induced by transverse aortic constriction (TAC) for 7 weeks. Our results demonstrate that the ratio of heart weight to tibia length was increased in both strains of mice, in which SIRT3 ECKO + TAC mice exhibited more severe cardiac hypertrophy. In addition, systolic function was significantly decreased in SIRT3 ECKO + TAC mice compared to SIRT3 LoxP + TAC mice, as evidenced by lower EF and FS at week 7. In contrast, diastolic function decreased after TAC surgery in a similar manner in both strains of mice, despite that pre-existing diastolic dysfunction was found in SIRT3 ECKO mice. Similarly, there was no difference in coronary flow reserve between both strains of mice subjected to TAC. Moreover, pressure overload-induced upregulation of Apelin, Angiopoietin-1, GLUT-4, and ERK phosphorylation were decreased in SIRT3 ECKO + TAC mice, whereas the expression of pro-inflammatory molecules, ICAM-1 and VCAM-1, was significantly increased in SIRT3 ECKO + TAC mice. These results implicate a critical role of SIRT3 in regulating glucose uptake and glycolytic function in endothelial cells. Ablation of endothelial SIRT3 exacerbates pressure overload-induced cardiac hypertrophy and heart failure via impaired glucose metabolism and increased pro-inflammatory molecules.
Hydrogel-Based Strategies to Advance Therapies for Chronic Skin Wounds
Authors: Lucília P. da Silva, Rui L. Reis, Vitor M. Correlo, Alexandra P. Marques
Journal: Annual Review of Biomedical Engineering (2019)

Chronic skin wounds are the leading cause of nontraumatic foot amputations worldwide and present a significant risk of morbidity and mortality due to the lack of efficient therapies. The intrinsic characteristics of hydrogels allow them to benefit cutaneous healing essentially by supporting a moist environment. This property has long been explored in wound management to aid in autolytic debridement. However, chronic wounds require additional therapeutic features that can be provided by a combination of hydrogels with biochemical mediators or cells, promoting faster and better healing. We survey hydrogel-based approaches with potential to improve the healing of chronic wounds by reviewing their effects as observed in preclinical models. Topics covered include strategies to ablate infection and resolve inflammation, the delivery of bioactive agents to accelerate healing, and tissue engineering approaches for skin regeneration. The article concludes by considering the relevance of treating chronic skin wounds using hydrogel-based strategies.
Abstract 308: <i>Wls</i> Inhibits Fibrosis Through Wnt Secretion From the Cardiomyocytes During Heart Regeneration
Authors: Shijie Liu, Tanner Monroe, Matthew Hill, James F Martin
Journal: Circulation Research (2018)

Because cardiomyocytes lose their capacity for self-renewal shortly after birth, the heart cannot regenerate muscle lost due to injury or heart failure. Instead, dead myocardium is replaced with a fibrotic scar. Recent studies have demonstrated that blocking the Hippo pathway specifically in cardiomyocytes promotes heart functional recovery after injury, not only by stimulating cardiomyocyte proliferation, but also by preventing fibrosis. The mechanism through which YAP activates the cell cycle is widely studied; however, the mechanism through which it inhibits fibrosis is unknown. Here, we identified Wntless ( Wls ) to be a downstream target of YAP in regenerating cardiomyocytes; Wls plays a role in regulating the secretion of Wnt ligands, which influences interstitial cells through paracrine effects. By using Adeno-Associated Virus 9 (AAV9) to deliver guide RNAs (gRNAs) that target the Wls locus exclusively in cardiomyocytes that express the Cas9 protein, we generated a cardiomyocyte-specific Wls knock out mouse (Wls-Cas9 CKO). After myocardial infarction at the neonatal stage (regenerative stage), cardiomyocyte deletion of Wls detrimental the heart regeneration as showed decreased heart function and increased fibrosis in Wls-Cas9 CKO mice. Mechanistically, by performing nuclear RNA-Seq technology, we revealed that non-canonical Wnt ligands are enriched in cardiomyocytes suggest cardiomyocytes influence fibroblasts through non-canonical signaling during heart regeneration. We will further use the single-cell sequencing technology to investigate the cell to cell communication during heart regeneration.
COMPARISON OF OUTCOMES WITH DRUG ELUTING VERSUS BARE METAL STENT IN VERY ELDERLY POPULATION
Authors: Abhishek Mishra, Sushruth Edla, Byomesh Tripathi, Shilpkumar Arora, Abdel Rahman Omer, Varun Kumar, Kanika Parashar, Edo Kaluski
Journal: Journal of the American College of Cardiology (2019)