tbuckley/cabot-search huggingface dataset:
TRANSCATHETER REPLACEMENT OF THE SAPIEN 3 VALVE IN A SURGICALLY PLACED SAPIEN XT VALVE IN THE MITRAL POSITION AND ROLE OF PULMONARY ARTERY SENSOR MONITORING
Authors: Maya Safarova, Amandeep Goyal, Steven Bormann, Peter Tadros, George Zorn, Bhanu Gupta
Journal: Journal of the American College of Cardiology (2021)
Sodium-glucose co-transporter 2 inhibitors: game changers when handled with care?
Authors: Zay M Htet, Mahzuz Karim
Journal: Journal of the Royal Society of Medicine (2021)

Recent years have seen a paradigm shift in the management of patients with diabetes mellitus. Rather than good glycaemic control being the sole primary aim, the therapeutic focus has broadened to consider potential additional cardiovascular and renal benefits. Sodium-glucose co-transporter 2 inhibitors, such as empagliflozin, canagliflozin and dapagliflozin, have gained increasing prominence, with evidence suggesting significant improvement in outcomes in patients with established cardiovascular and renal disease. Here, we discuss the benefits and relative risks of these novel agents and highlight important clinical issues of relevance to general physicians.
Inducible nitric oxide synthase is an endogenous neuroprotectant after traumatic brain injury in rats and mice
Authors: Elizabeth H. Sinz, Patrick M. Kochanek, C. Edward Dixon, Robert S.B. Clark, Joseph A. Carcillo, Joanne K. Schiding, Minzhi Chen, Stephen R. Wisniewski, Timothy M. Carlos, Debra Williams, Steven T. DeKosky, Simon C. Watkins, Donald W. Marion, Timothy R. Billiar
Journal: Journal of Clinical Investigation (1999)

Nitric oxide (NO) derived from the inducible isoform of NO synthase (iNOS) is an inflammatory product implicated both in secondary damage and in recovery from brain injury. To address the role of iNOS in experimental traumatic brain injury (TBI), we used 2 paradigms in 2 species. In a model of controlled cortical impact (CCI) with secondary hypoxemia, rats were treated with vehicle or with 1 of 2 iNOS inhibitors (aminoguanidine and L-N-iminoethyl-lysine), administered by Alzet pump for 5 days and 1.5 days after injury, respectively. In a model of CCI, knockout mice lacking the iNOS gene (iNOS–/–) were compared with wild-type (iNOS+/+) mice. Functional outcome (motor and cognitive) during the first 20 days after injury, and histopathology at 21 days, were assessed in both studies. Treatment of rats with either of the iNOS inhibitors after TBI significantly exacerbated deficits in cognitive performance, as assessed by Morris water maze (MWM) and increased neuron loss in vulnerable regions (CA3 and CA1) of hippocampus. Uninjured iNOS+/+ and iNOS–/– mice performed equally well in both motor and cognitive tasks. However, after TBI, iNOS–/– mice showed markedly worse performance in the MWM task than iNOS+/+ mice. A beneficial role for iNOS in TBI is supported.
ECHOCARDIOGRAPHY-BASED CONVOLUTIONAL NEURAL NETWORK MODEL SUPERSEDES THE CARDIOTOXICITY RISK SCORE IN PREDICTING CHEMOTHERAPY-INDUCED CARDIOMYOPATHY
Authors: Chieh Ju Chao, Hau-Lun Wu, Timothy Barry, Amith Reddy Seri, Megan Meyer, Pradyumna Agasthi, Merna Abdou, Michael O’Shea, Megan Campany, Hana Newman, Olubadewa Fatunde, Carolyn Larsen, Julie Rosenthal, Brian Hardaway, Hemalatha Narayanasamy, Shimoli Shah, Reza Arsanjani
Journal: Journal of the American College of Cardiology (2021)
Integration of Functional Dependencies and Molecular Alterations of Myeloma Cells
Authors: Ricardo De Matos Simoes, Geoffrey Matthews, Ryosuke Shirasaki, Hu Yiguo, Michal Sheffer, Olga Dashevsky, Sara Gandolfi, Paul Hengeveld, Johanna Bruggenthies, Eugen Dhimolea, Huihui Tang, Megan Bariteau, Andrew Aguirre, Quinlan Sievers, Benjamin L. Ebert, Brian Glassner, Christopher J. Ott, Dennis Buckley, Nicholas P. Kwiatkowski, Jonathan D. Licht, Nathanael Gray, Joshua Dempster, Richard W. J. Groen, Francisca Vazquez, Aviad Tsherniak, William C. Hahn, Aedin Culhane, Constantine S. Mitsiades
Journal: Blood (2017)
HIGH ON-TREATMENT PLATELET REACTIVITY WITH CLOPIDOGREL VS TICAGRELOR IN PATIENTS WITH AND WITHOUT CHRONIC KIDNEY DISEASE - A RANDOMIZED CONTROLLED TRIAL
Authors: Andre Franci, Carlos Barbosa, Talia Dalcoquio, Paulo Genestreti, Rocío Salsoso, Aline Ferrari, Viviane Lima, Luciano Baracioli, Remo Furtado, Jose Nicolau
Journal: Journal of the American College of Cardiology (2021)
The effect of diet in infancy on asthma in young adults: the Merthyr Allergy Prevention Study
Authors: Sadiyah Hand, Frank Dunstan, Ken Jones, Iolo Doull
Journal: Thorax (2021)

Introduction Early infant diet might influence the risk of subsequent allergic disease. Methods The Merthyr Allergy Prevention Study (MAPS) was a randomised controlled trial in infants at high risk of allergic disease. The trial determined whether a cow’s milk exclusion diet for the first 4 months of life decreased the risk of allergic disease including asthma compared with a normal diet. A soya milk preparation was offered to those in the intervention group. A standardised questionnaire for allergic disease was completed at ages 1, 7, 15 and 23 years, with clinical assessment at 1, 7 and 23 years. The effect of the intervention on the risk of atopy, asthma and wheeze at age 23 years was determined. Findings 487 subjects entered the study; at age 23 years 299 completed the questionnaire, of which 119 attended clinical assessment. Subjects randomised to the intervention group had a significantly increased risk of atopy (adjusted OR 2.97, 95% CI 1.30 to 6.80; p=0.01) and asthma (OR 2.07, 95%CI 1.09 to 3.91; p=0.03) at age 23 years, but not wheeze (OR 1.43, 95%CI 0.87 to 2.37; p=0.16). Earlier exposure to cow’s milk was associated with a decreased risk of wheeze and asthma at age 23 years, while earlier exposure to soya milk was associated with an increased risk of atopy and asthma. Interpretation In infants at high risk of allergic disease, either cow’s milk exclusion or early soya milk introduction for the first 4 months of life increases the risk of atopy, wheeze and asthma in adulthood.
Development of novel nanofibers targeted to smoke-injured lungs
Authors: Alexandra I. Mercel, Kathleen Marulanda, David C. Gillis, Kui Sun, Tristan D. Clemons, Smaranda Willcox, Jack Griffith, Erica B. Peters, Mark R. Karver, Nick D. Tsihlis, Rob Maile, Samuel I. Stupp, Melina R. Kibbe
Journal: Biomaterials (2021)
Germline and somatic mutation in the HGF gene promoter causes its aberrant expression in human carcinoma and establishes an HGF-Met autocrine loop.
Authors: Jihong Ma
Journal: Cancer Research (2005)

43  Hepatocyte growth factor (HGF) is a multifunctional growth factor that is essential for normal growth and differentiation of a variety of epithelial tissues. Unregulated expression of HGF and/or its receptor Met protooncogene is known to contribute to neoplastic growth. The expression of the HGF gene is controlled at the transcriptional level and is restricted to the mesenchymal cells of a given tissues. In normal epithelial cells, expression of this gene is extinguished. Thus, the HGF-Met signaling axis constitutes a tightly controlled paracrine circuit between the mesenchymal and epithelial components of tissues. Several studies have shown that in human carcinomas such as breast, the HGF gene becomes activated and expressed. However, the molecular mechanisms in this process involved have remained unknown. In the present work, we have identified an important regulatory region in the human HGF gene promoter that is mutated in human breast and uterine cervical carcinoma tissues as compared to the adjacent normal tissue counterparts. To understand the global effects of the mutation on the whole promoter region, we performed in vivo footprinting, DNA binding and ChIP assays. We found that mutation of the regulatory element profoundly changes the DNA-protein interaction pattern making several cis-acting regulatory sites within the promoter accessible /inaccessible to their cognate factors. Genotyping indicated that approximately 10 percent of the normal population overall carries the mutated genotype; when stratified according to race (African American versus Caucasian), African Americans had a significantly higher frequency of harboring the mutated element than Caucasians. Based on these data, the HGF promoter mutation we identified may constitute a functional polymorphism. This could be of importance since African Americans have a higher mortality in some epithelial cancers such as breast and prostate cancer. Overall, these results not only shed light on our understanding of the genetic basis of human carcinogenesis but also may have led to the identification of a potential marker in the diagnosis/prognosis of some human cancers.
Hyaluronic acid coated bilirubin nanoparticles attenuate ischemia reperfusion-induced acute kidney injury
Authors: Zhi-Wei Huang, Yannan Shi, Yuan-Yuan Zhai, Chu-Chu Du, Jiaoyuan Zhai, Run-Jie Yu, Longfa Kou, Jian Xiao, Ying-Zheng Zhao, Qing Yao
Journal: Journal of Controlled Release (2021)
Abstract 10549: The Impact of Area Deprivation on the Cardiac Mortality Among Young People: A Longitudinal Analysis of Scottish Linkage Data From 1991-2010
Authors: Kai Jin, Lis Neubeck, Iain Atherton
Journal: Circulation (2019)

Introduction: Socioeconomic status is a strong contributor to disparities in cardiac outcomes. However, little is known about the impact of area deprivation on cardiac mortality among young people....
Further Prognostic Factors for Stratification of Patients in the High-Risk HCT-CI Group Undergoing Allogeneic HCT
Authors: Yasuhiko Shibasaki, Tatsuya Suwabe, Shun Uemura, Takayuki Katagiri, Tomoyuki Tanaka, Takashi Ushiki, Kyoko Fuse, Miwako Narita, Hirohito Sone, Masayoshi Masuko
Journal: Blood (2017)
APABETALONE (RVX-208) REDUCES ACE2 PROTEIN ABUNDANCE AND PREVENTS SARS-COV-2 SPIKE PROTEIN BINDING TO HUMAN LUNG CELLS, A MOA THAT COULD ATTENUATE VIRAL ENTRY
Authors: Li Fu, Dean Gilham, Laura Tsujikawa, Brooke D. Rakai, Sylwia Wasiak, Stephanie Stotz, Christopher D. Sarsons, Michael Sweeney, Jan Johansson, Norman Wong, Ewelina Kulikowski
Journal: Journal of the American College of Cardiology (2021)
HIGHER TRIGLYCERIDE LEVEL IS ASSOCIATED WITH HIGHER FREQUENCY OF PLAQUE WITH MACROPHAGE ACCUMULATION IN CORONARY PLAQUES AMONG PATIENTS WITH LOW LOW-DENSITY LIPOPROTEIN CHOLESTEROL LEVEL
Authors: Kiyoshi Asakura, Yoshiyasu Minami, Ayami Kato, Aritomo Katsura, Masahiro Katamine, Takuya Hashimoto, Daisuke Kinoshita, Junya Ako
Journal: Journal of the American College of Cardiology (2021)
Abstract 18792: Treatment With an EET Agonist in a Post Myocardial Infarction Model Increases Left Ventricular Ejection Fraction and Attenuates Cardiac Remodeling by Induction of HMOX1
Authors: Jian Cao, Ellen Thompson, Nader G Abraham, Stephen J Peterson, Darryl C Zeldin, Michal L Schwartzman
Journal: Circulation (2013)

Rationale: Myocardial Infarction (MI) leads to a progressive decline in cardiac function, an increase in patient morbidity and is an event expanding burden on the health care system. Failure of myocardial regeneration, insufficient blood flow and enhanced oxidative stress all contribute to this pathological outcome. Objective: Since epoxyeicosatrienoic acids (EETs) agonists increase angiogenesis and vasodilation in ischemic heart, we examined if cross talk between EET and heme oxygenase-1(HMOX1) could reduce post infarcted cardiac remodeling resulting in an improvement of cardiac function in a model of post-MI. Methods: C57B16 mice were divided into 4 groups: sham, mice with myocardial infarction (MI) via LAD ligation and mice with MI treated with an EET-agonist (NUDSA) with and without the HO activity inhibitor stannous mesoporphyrin (SnMP). NUDSA was administered 5 days after MI for 30 days (0.5 mg/kg). Myocardial echocardiography was performed to assess blood volume, velocity, LVend-diastolic and ejection fractions. Microvessel density, inflammation and pericardial fibrosis were compared among the groups. Results: Echocardiography showed that left ventricle dilatation, measured as end diastolic area (EDA), was reduced in the NUDSA treated group compared to the MI group (EDA: MI: 0.314 ±0.01 cm 2 ; MI+NUDSA: 0.193±0.02 cm 2 ; p&lt;0.01). Cardiac Index, decreased by MI, was restored by NUDSA. NUDSA treatment increased serum adiponectin levels and decreased IL-6 and MCP-1 levels (p&lt;0.05 vs. MI), reduced fibrosis in the peri-infarct myocardium and decreased apoptosis. Immunoblot analysis of cardiac tissue demonstrated increased expression of HMOX1, VEGF and FGF along with decreased expression of TXA2 and 3NT in mice treated with NUDSA as compared to the MI group (p&lt;0.02). All these beneficial effects were reversed by SnMP. Conclusion: This study demonstrates that cross talk between EET and HMOX1 ameliorates cardiac remodeling in the post infarcted myocardium and increases angiogenesis, suggesting EET as a potential therapeutic strategy in the preservation of cardiac function in this animal model of post MI.
THE LONG PATH TO YOUR HEART: AN UNCOMMON DIAGNOSIS OF ANOMALOUS CORONARY ARTERIES
Authors: Migdoel Cruz-Rodriguez, Steven Garcia Santiago, Erica Otero-Cardenas, Jonathan Cordero-Jiménez, Jorge Ballester-Maldonado, Jose Martinez-Toro, Pedro Vargas Otero
Journal: Journal of the American College of Cardiology (2021)
Circulating Small Extracellular Vesicles Activate TYRO3 to Drive Cancer Metastasis and Chemoresistance
Authors: Miso Park, Ji Won Kim, Kyu Min Kim, Seungmin Kang, Wankyu Kim, Jin-Ki Kim, Youngnam Cho, Hyungjae Lee, Moon Chang Baek, Ju-Hyun Bae, Seung Hyun Lee, Sung Baek Jeong, Sung Chul Lim, Dae Won Jun, Sung Yun Cho, Yeonji Kim, Yong June Choi, Keon Wook Kang
Journal: Cancer Research (2021)

Abstract Extracellular vesicles (EV) in the tumor microenvironment have emerged as crucial mediators that promote proliferation, metastasis, and chemoresistance. However, the role of circulating small EVs (csEV) in cancer progression remains poorly understood. In this study, we report that csEV facilitate cancer progression and determine its molecular mechanism. csEVs strongly promoted the migration of cancer cells via interaction with phosphatidylserine of csEVs. Among the three TAM receptors, TYRO3, AXL, and MerTK, TYRO3 mainly interacted with csEVs. csEV-mediated TYRO3 activation promoted migration and metastasis via the epithelial–mesenchymal transition and stimulation of RhoA in invasive cancer cells. Additionally, csEV–TYRO3 interaction induced YAP activation, which led to increased cell proliferation and chemoresistance. Combination treatment with gefitinib and KRCT-6j, a selective TYRO3 inhibitor, significantly reduced tumor volume in xenografts implanted with gefitinib-resistant non–small cell lung cancer cells. The results of this study show that TYRO3 activation by csEVs facilitates cancer cell migration and chemoresistance by activation of RhoA or YAP, indicating that the csEV/TYRO3 interaction may serve as a potential therapeutic target for aggressive cancers in the clinic. Significance: These findings demonstrate that circulating extracellular vesicles are a novel driver in migration and survival of aggressive cancer cells via TYRO3 activation.
Ligand-dependent activation of the nuclear orphan receptor DAX-1
Authors: Sabitha Papineni, Sudhakar R. Chintharlapalli, Paolo Sassone-Corsi, Enzo Lalli, Stephen Safe
Journal: Cancer Research (2005)

1208  DAX-1 is an atypical orphan nuclear receptor that plays a key role in steroidogenesis, reproduction and mammalian sex development. DAX-1 does not directly bind to cognate promoter elements but contains a C-terminal ligand binding domain and three N-terminal single-stranded DNA/RNA binding motifs. Ligand-dependent activation of DAX-1 has previously not been reported. Initial screening for ligand-dependent activation of DAX-1 used the SW-480 (colon) cancer cell line transfected with a luciferase reporter construct containing five tandem GAL4 response elements (pGAL45) and a GAL4-DAX-1 chimera which expresses the yeast GAL4-DBD(1-147) and the C-terminal region (207-470) of DAX-1. Cells were transfected with pGAL4-DAX-1 and treated with four different series of >60 compounds derived from 1,1-bis(3’-indolyl)-1-(p-substituted-phenyl)methanes (C-DIMs) containing variable indole and phenyl substituents as well as a series of heteroaromatic analogs. C-DIMs containing p-CF3 (DIM-C-pPhCF3), p-bromo (DIM-C-pPhBr) and p-t-butyl (DIM-C-pPhtBu) substituents and some of their ring substituted analogs induced transactivation in SW-480 as well as in RKO (colon), MCF-7 (breast) and CV-1 (monkey kidney) cell lines. The corresponding N-methyl C-DIMs were inactive suggesting that a free indole moiety was essential for ligand-dependent activation of DAX-1. Ligand dependent interactions of DAX-1 with coactivators were also investigated in SW-480 cells transfected with pGAL45 and plasmids expressing GAL4-coactivator and VP-DAX-1 chimeras. In this mammalian two hybrid assay, DIM-C-pPhCF3 induced DAX-1 interactions with steroid receptor coactivator-1 (SRC-1), SRC-2, TRAP 220 and PGC-1, but not with SRC-2, the methyltransferase CARM-1, or the corepressor SMRT. The results demonstrate that selected C-DIMs activate DAX-1 and induce interactions with coactivators, and current studies are focused on domains of DAX-1 required for transactivation and functional aspects of ligand-induced DAX-1.
Research progress in the effects of terahertz waves on biomacromolecules
Authors: Liu Sun, Li Zhao, Rui-Yun Peng
Journal: Military Medical Research (2021)

With the rapid development of terahertz technologies, basic research and applications of terahertz waves in biomedicine have attracted increasing attention. The rotation and vibrational energy levels of biomacromolecules fall in the energy range of terahertz waves; thus, terahertz waves might interact with biomacromolecules. Therefore, terahertz waves have been widely applied to explore features of the terahertz spectrum of biomacromolecules. However, the effects of terahertz waves on biomacromolecules are largely unexplored. Although some progress has been reported, there are still numerous technical barriers to clarifying the relation between terahertz waves and biomacromolecules and to realizing the accurate regulation of biological macromolecules by terahertz waves. Therefore, further investigations should be conducted in the future. In this paper, we reviewed terahertz waves and their biomedical research advantages, applications of terahertz waves on biomacromolecules and the effects of terahertz waves on biomacromolecules. These findings will provide novel ideas and methods for the research and application of terahertz waves in the biomedical field.
Kinetics and correlates of the neutralizing antibody response to SARS-CoV-2 infection in humans
Authors: Kanika Vanshylla, Veronica Di Cristanziano, Franziska Kleipass, Felix Dewald, Philipp Schommers, Lutz Gieselmann, Henning Gruell, Maike Schlotz, Meryem S. Ercanoglu, Ricarda Stumpf, Petra Mayer, Matthias Zehner, Eva Heger, Wibke Johannis, Carola Horn, Isabelle Suárez, Norma Jung, Susanne Salomon, Kirsten Alexandra Eberhardt, Birgit Gathof, Gerd Fätkenheuer, Nico Pfeifer, Ralf Eggeling, Max Augustin, Clara Lehmann, Florian Klein
Journal: Cell Host & Microbe (2021)
A positive feedback loop reinforces the allergic immune response in human peanut allergy
Authors: Xiaoying Zhou, Wong Yu, Shu-Chen Lyu, Claudia Macaubas, Bryan Bunning, Ziyuan He, Elizabeth D. Mellins, Kari C. Nadeau
Journal: The Journal of Experimental Medicine (2021)

Food allergies are a leading cause of anaphylaxis, and cellular mechanisms involving antigen presentation likely play key roles in their pathogenesis. However, little is known about the response of specific antigen-presenting cell (APC) subsets to food allergens in the setting of food allergies. Here, we show that in peanut-allergic humans, peanut allergen drives the differentiation of CD209+ monocyte-derived dendritic cells (DCs) and CD23+ (FcєRII) myeloid dendritic cells through the action of allergen-specific CD4+ T cells. CD209+ DCs act reciprocally on the same peanut-specific CD4+ T cell population to reinforce Th2 cytokine expression in a positive feedback loop, which may explain the persistence of established food allergy. In support of this novel model, we show clinically that the initiation of oral immunotherapy (OIT) in peanut-allergic patients is associated with a decrease in CD209+ DCs, suggesting that breaking the cycle of positive feedback is associated with therapeutic effect.
Abstract 13067: When Are 3 ECG Leads Better Than 12? Streamlining and Optimizing ECG Assessment in Sudden Death Prediction
Authors: Isabelle Ruedisueli, Joyce Ma, Karishma Lakhani, Randy Nguyen, Jeffrey Gornbein, Holly R Middlekauff
Journal: Circulation (2020)

Introduction: Prolonged Tpeak to Tend (Tp-e) interval, an index of repolarization on the 12-lead ECG, is associated with increased risk for sudden cardiac death. However, there is no current consensus on which of the 12 leads is the most sensitive to measure the longest Tp-e interval. Aim: The aim of this study was to measure all 12 ECG leads and to analyze whether there are leads that are most sensitive to detect prolongation of Tp-e in order to optimize methodology for future investigations. Methods: Fifteen healthy volunteers (F/M 6/9; mean age 25 yrs) were included in our study. We recorded the 12-lead ECG for 5-minutes. Tp-e was defined as the interval from the peak of the T wave to the end of the T wave. QT is the interval from QRS complex onset to the end of the T wave. Using commercially available software (AdInstruments), three primary outcomes, Tp-e interval, Tp-e/QT, Tp-e/QTc ratios, and two secondary outcomes, QT, QTc intervals, were determined. Results: The location of maximum value for primary outcomes (Tp-e, Tp-e/QT, Tp-e/QTc) were not evenly distributed across the 12 leads, but most frequently was located in leads V2, V3 &amp; V4. The maximum Tp-e was located in one of these three leads 79.7% of the time (CI 69.4, 89.9%) vs other leads (p=0.007, Figure). Conversely, maximum values for the secondary outcomes (QT, QTc) were located in AVL, AVR and III (Figure). Two of the leads, V5 and V6, never had a maximum value for any outcomes. Conclusion: Preliminary findings in our study suggest that investigators should focus on leads V2, V3 &amp; V4 to detect prolongation of Tp-e intervals and leads AVL, AVR &amp; III for prolongation of QT interval when investigating associations with sudden cardiac death.