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mice echocardiography

Manar D Samad, Alvaro Ulloa, Gregory J Wehner, Linyuan Jing, Dustin Hartzel, Christopher W Good, Brent A Williams, Christopher M Haggerty, Brandon K Fornwalt
OBJECTIVES: The goal of this study was to use machine learning to more accurately predict survival after echocardiography. BACKGROUND: Predicting patient outcomes (e.g., survival) following echocardiography is primarily based on ejection fraction (EF) and comorbidities. However, there may be significant predictive information within additional echocardiography-derived measurements combined with clinical electronic health record data. METHODS: Mortality was studied in 171,510 unselected patients who underwent 331,317 echocardiograms in a large regional health system...
June 9, 2018: JACC. Cardiovascular Imaging
Dai Kimura, Jordy Saravia, Sridhar Jaligama, Isabella McNamara, Luan D Vu, Ryan D Sullivan, Salvatore Mancarella, Dahui You, Stephania A Cormier
Pulmonary hypertension (PH) has been observed in up to 75% of infants with moderate to severe respiratory syncytial virus (RSV) bronchiolitis and is associated with significant morbidity and mortality in infants with congenital heart disease. The purpose of this study was to establish a mouse model of PH secondary to RSV bronchiolitis that mimics the disease etiology as it occurs in infants. Neonatal mice were infected with RSV at 5 days of age, and then re-infected 4 weeks later. Serum free medium was administered to age-matched mice as control...
June 15, 2018: American Journal of Physiology. Heart and Circulatory Physiology
Ji-Gang He, Hong-Rong Li, Jin-Xiu Han, Bei-Bei Li, Dan Yan, Hong-Yuan Li, Ping Wang, Ying Luo
This study aimed to investigate whether exosomes secreted by mouse GATA-4-expressing bone marrow mesenchymal stem cells (BMSCs) could induce BMSC differentiation into myocyte precursors, decrease cardiomyocyte apoptosis, and improve cardiac function following myocardial infarction (MI). BMSCs were transduced with a lentivirus carrying a doxycycline (DOX)-inducible GATA-4 or control lentivirus, and secreted exosomes from these BMSCs were collected and co-cultured with BMSCs or cardiomyocytes under hypoxic and serum free conditions...
June 13, 2018: Scientific Reports
Xiaxia Wang, Chunming Yong, Kai Yu, Renchao Yu, Rui Zhang, Lingfan Yu, Shan Li, Shanglang Cai
BACKGROUND Abnormally expressed long noncoding RNAs (lncRNAs) are recognized as one of the key causes of cardiac diseases. However, the role of lncRNA in cardiac fibrosis remains largely unknown. MATERIAL AND METHODS The experiment was divided into 4 groups: a sham operation group, a myocardial infarction (MI) group, a lentivirus group (LV-si-n379519), and a lentivirus control (LV-NC) group. The adenovirus expression vectors LV-si-n379519 and LV-NC were constructed and transfected into mice. Echocardiography, HE staining, and Masson staining were performed to detect the heart function and collagen volume fraction in each group...
June 11, 2018: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
Emmanuel Rineau, Thomas Gaillard, Naïg Gueguen, Vincent Procaccio, Daniel Henrion, Fabrice Prunier, Sigismond Lasocki
BACKGROUND: Iron deficiency (ID), with or without anemia, is frequent in heart failure patients, and iron supplementation improves patient condition. However, the link between ID (independently of anemia) and cardiac function is poorly understood, but could be explained by an impaired mitochondrial metabolism. Our aim was to explore this hypothesis in a mouse model. METHODS AND RESULTS: We developed a mouse model of ID without anemia, using a blood withdrawal followed by 3-weeks low iron diet...
September 1, 2018: International Journal of Cardiology
Qiancheng Wang, Zhenhuan Chen, Xiaobo Huang, Lin Chen, Baihe Chen, Yingqi Zhu, Shiping Cao, Wangjun Liao, Jianping Bin, Masafumi Kitakaze, Yulin Liao
Either angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor 1 blocker (ARB) attenuates cardiac remodeling. However, the overall molecular modulation of the reversing remodeling process in response to the ACEI or ARB treatment is not yet well determined. In this study, we examined whether gene expressions are modulated by ACEI (temocapril), ARB (olmesartan) or both in a murine model with transverse aortic constriction (TAC) and confirm whether periostin is a target gene of olmesartan in mice with myocardial infarction (MI)...
May 15, 2018: Oncotarget
Tingting Sui, Yeh Siang Lau, Di Liu, Tingjun Liu, Li Xu, Yandi Gao, Liangxue Lai, Zhanjun Li, Renzhi Han
Duchenne muscular dystrophy (DMD) is an X-linked muscle-wasting disorder caused by mutations in the dystrophin gene, with an incidence of 1 in 3500 in new male births. Mdx mice are widely used as an animal model for DMD. However, these mice do not faithfully recapitulate DMD patients in many aspects, rendering the preclinical findings in this model questionable. Although larger animal models of DMD, such as dogs and pigs, have been generated, usage of these animals is expensive and only limited to several facilities in the world...
June 4, 2018: Disease Models & Mechanisms
Linda Cambier, Jorge F Giani, Weixin Liu, Takeshi Ijichi, Antonio K Echavez, Jackelyn Valle, Eduardo Marbán
Hypertension often leads to cardiovascular disease and kidney dysfunction. Exosomes secreted from cardiosphere-derived cells (CDC-exo) and their most abundant small RNA constituent, the Y RNA fragment EV-YF1, exert therapeutic benefits after myocardial infarction. Here, we investigated the effects of CDC-exo and EV-YF1, each administered individually, in a model of cardiac hypertrophy and kidney injury induced by chronic infusion of Ang (angiotensin) II. After 2 weeks of Ang II, multiple doses of CDC-exo or EV-YF1 were administered retro-orbitally...
June 4, 2018: Hypertension
Rong-Rong Gao, Xiao-Dong Wu, Hui-Min Jiang, Yu-Jiao Zhu, Yan-Li Zhou, Hai-Feng Zhang, Wen-Ming Yao, Yong-Qin Li, Xin-Li Li
Background: Clinical study has demonstrated that the traditional Chinese medicine Qiliqiangxin (QLQX) has protective effects on heart failure. Phenylephrine (PE) is an important inducing factor for cardiac hypertrophy and our previous studies have showed that QLQX attenuates PE-induced cardiac hypertrophy. Besides, QLQX protects against cardiac remodeling after myocardial infarction via activating PPARγ. However, whether QLQX prevents PE-induced cardiac hypertrophy through PPARγ and its coactivator PGC-1α is still unknown...
April 2018: Annals of Translational Medicine
Nina Divorty, Graeme Milligan, Delyth Graham, Stuart A Nicklin
BACKGROUND: The orphan receptor G protein-coupled receptor 35 (GPR35) has been associated with a range of diseases, including cancer, inflammatory bowel disease, diabetes, hypertension, and heart failure. To assess the potential for GPR35 as a therapeutic target in cardiovascular disease, this study investigated the cardiovascular phenotype of a GPR35 knockout mouse under both basal conditions and following pathophysiological stimulation. METHODS: Blood pressure was monitored in male wild-type and GPR35 knockout mice over 7-14 days using implantable telemetry...
May 31, 2018: American Journal of Hypertension
Ying-Nan Wang, Lei Gao, Shi-Yong Wu, Shu Qin
BACKGROUND Revascularization is a successful therapeutic strategy for myocardial infarction. However, restoring coronary blood flow can lead to ischemia-reperfusion (I/R) injury. Low-dose 4-hydroxy-2-nonenal (HNE) therapy appears to play a key role in myocardial tolerance to I/R injury. We hypothesized that the positive effects of HNE on myocardial I/R injury may be UCP3-dependent. MATERIAL AND METHODS Adult male wild-type (WT) or UCP3 knockout (UCP3-/-) mice were pre-treated with the UCP inhibitor genipin or saline 1 h before ischemia and underwent 30-min coronary artery ligation followed by 24-h reperfusion...
June 2, 2018: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
Michael F Bode, Alyson C Auriemma, Steven P Grover, Yohei Hisada, Alex Rennie, Weeranun D Bode, Rashi Vora, Saravanan Subramaniam, Brian Cooley, Patricia Andrade-Gordon, Silvio Antoniak, Nigel Mackman
INTRODUCTION: Rivaroxaban selectively inhibits factor Xa (FXa), which plays a central role in blood coagulation. In addition, FXa activates protease-activated receptor-2 (PAR-2). We have shown that PAR-2-/- mice exhibit less cardiac dysfunction after cardiac injury. MATERIAL AND METHODS: Wild-type (WT) and PAR-2-/- mice were subjected to left anterior descending artery (LAD) ligation to induce cardiac injury and heart failure. Mice received either placebo or rivaroxaban chow either starting at the time of surgery or 3 days after surgery and continued up to 28 days...
May 17, 2018: Thrombosis Research
Fengdan Dai, Yan Zhang, Qiang Wang, De Li, Yongjian Yang, Shuangtao Ma, Dachun Yang
BACKGROUND/AIMS: Activation of stromal interaction molecule 1 (STIM1) and Orai1 participates in the development of cardiac hypertrophy. Store-operated Ca2+ entry-associated regulatory factor (SARAF) is an intrinsic inhibitor of STIM1-Orai1 interaction. Thus, we hypothesized that SARAF could prevent cardiac hypertrophy. METHODS: Male C57BL/6 mice, aged 8 weeks, were randomly divided into sham and abdominal aortic constriction surgery groups and were infected with lentiviruses expressing SARAF and GFP (Lenti-SARAF) or GFP alone (Lenti-GFP) via intramyocardial injection...
May 22, 2018: Cellular Physiology and Biochemistry
Christian Jung, Bernhard Wernly, Mikael Bjursell, John Wiseman, Therese Admyre, Johannes Wikström, Malin Palmér, Frank Seeliger, Michael Lichtenauer, Marcus Franz, Charlotte Frick, Ann-Katrin Andersson, Margareta Elg, John Pernow, Per-Ove Sjöquist, Mohammad Bohlooly-Y, Qing-Dong Wang
BACKGROUND: Oxytocin (Oxt) and its receptor (Oxtr) gene system has been implicated in cardiomyogenesis and cardioprotection; however, effects of chronic activation of Oxtr are not known. We generated and investigated transgenic (TG) mice that overexpress Oxtr specifically in the heart. METHODS AND RESULTS: Cardiac-specific overexpression of Oxtr was obtained by having the α-major histocompatibility complex promoter drive the mouse Oxtr gene (α-Mhc-Oxtr). Left ventricular (LV) function and remodeling were assessed by magnetic resonance imaging and echocardiography...
May 23, 2018: Journal of Cardiac Failure
Zhu-Xia Shen, Qing-Zhen Yang, Chao Li, Lin-Juan Du, Xue-Nan Sun, Yan Liu, Jian-Yong Sun, Hui-Hui Gu, Yu-Min Sun, Jun Wang, Sheng-Zhong Duan
BACKGROUND AND AIMS: Agonists of peroxisome proliferator-activated receptor gamma (Pparγ) have been demonstrated to reduce the risk of myocardial infarction (MI) in clinical trials and animal experiments. However, the cellular and molecular mechanisms are not completely understood. We aimed to reveal the functions of myeloid Pparγ in MI and explore the potential mechanisms in this study. METHODS: Myeloid Pparγ knockout (MPGKO) mice (n = 12) and control mice (n = 8) underwent coronary artery ligation to induce MI...
May 5, 2018: Atherosclerosis
Antoinette Bugyei-Twum, Christopher Ford, Robert Civitarese, Jessica Seegobin, Suzanne L Advani, Jean-Francois Desjardins, Golam Kabir, Yanling Zhang, Melissa Mitchell, Jennifer Switzer, Kerri Thai, Vanessa Shen, Armin Abadeh, Krishna K Singh, Filio Billia, Andrew A Advani, Richard E Gilbert, Kim A Connelly
Aims: Transforming growth factor β1 (TGF-β1) is a prosclerotic cytokine involved in cardiac remodeling leading to heart failure (HF). Acetylation/de-acetylation of specific lysine residues in Smad2/3 has been shown to regulate TGF-β signaling by altering its transcriptional activity. Recently, the lysine de-acetylase sirtuin 1 (SIRT1) has been shown to have a cardioprotective effect; however SIRT1 expression and activity are paradoxically reduced in HF. Here, we investigate whether pharmacological activation of SIRT1 would induce cardioprotection in a pressure overload model and assess the impact of SIRT1 activation on TGF-β signaling and the fibrotic response...
May 25, 2018: Cardiovascular Research
Xiao-Wei Song, Lu-Lu Zou, Ling Cui, Song-Hua Li, Yong-Wen Qin, Xian-Xian Zhao, Qing Jing
Due to the lack of typical clinical symptoms, the average delay time for diagnosis of pulmonary hypertension (PH) is longer than 2 years. It is urgent to find biomarkers for PH diagnosis. In this study we investigated whether plasma microRNAs (miRNAs) can be used as biomarkers for PH diagnosis. We used microarray to identify dynamic miRNAs between PH and non-PH patients. The candidate miRNAs were verified using qRT-PCR in a mouse model of PH, which was induced by monocrotaline (MCT) injection. We observed that miR-21, miR-126, miR-145, miR-191 and miR-150 had no differences between control mice and MCT-treated mice; but plasma miR-451 was significantly decreased in the 2wk-MCT group, with no further decrease in the 4wk-MCT group...
May 24, 2018: Acta Pharmacologica Sinica
Yihui Yu, Zuoying Hu, Bing Li, Zhimei Wang, Shaoliang Chen
This study aimed to investigate the effects and molecular mechanisms of ivabradine in preventing cardiac hypertrophy in an established transverse aortic constriction (TAC) mouse model. A total of 56 male C57BL/6 mice were randomly assigned into the following seven groups (8 mice per group): sham, TAC model, Iva-10 (10 mg/kg/day ivabradine), Iva-20 (20 mg/kg/day ivabradine), Iva-40 (40 mg/kg/day ivabradine), Iva-80 (80 mg/kg/day ivabradine), and Rap (rapamycin, a positive control). Echocardiography and left ventricular hemodynamics were performed...
May 22, 2018: Molecular and Cellular Biochemistry
Xiangming Wang, Junhong Wang, Tiantian Tu, Zakaria Iyan, Deeraj Mungun, Zhijian Yang, Yan Guo
Background: The aim of the present study was to observe the effect of RAGE-HMGB1 signal pathway on remote ischemic postconditioning in mice with myocardial ischemia reperfusion injury. Methods: Mice model of MIRI was established and randomly divided into three groups: control group, ischemia reperfusion group, and remote ischemic postconditioning group. Infarction size was detected by Evans blue and TTC staining. Cardiac function was detected by echocardiography measurement...
2018: BioMed Research International
Alice E Kane, Kaitlyn M Keller, Stefan Heinze-Milne, Scott A Grandy, Susan E Howlett
A frailty index based on clinical deficit accumulation (FI-Clinical) quantifies frailty in aging mice. We aimed to develop a laboratory test-based murine FI tool (FI-Lab) and to investigate the effects of age and sex on FI-Lab scores, FI-Clinical scores and the combination (FI-Combined), as well as to explore links between frailty and inflammation. Studies used older (17 & 23-months) C57BL/6 mice of both sexes. We developed an FI-Lab (blood pressure, blood chemistry, echocardiography) based on deviation from reference values in younger adults (12 months), which showed similar characteristics to a human FI-Lab tool...
May 18, 2018: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
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