Database : MEDLINE Search on : infarction [Words] References found : 275055 [refine] Displaying: 1 .. 10   in format [Detailed]

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[PMID]: 29524682 [Au] Autor: Ghosh K; N I [Ad] Address: Unit of Toxicology, Department of Zoology, School of Life Sciences, Bharathiar University, Coimbatore, 641046, Tamil Nadu, India; Department of Zoology, Annamalai University, Annamalainagar, Chidambaram, 608002, Tamil Nadu, India. Electronic address: kavisa9@gmail.com. [Ti] Title: Cadmium treatment induces echinocytosis, DNA damage, inflammation, and apoptosis in cardiac tissue of albino Wistar rats. [So] Source: Environ Toxicol Pharmacol;59:43-52, 2018 Feb 27. [Is] ISSN: 1872-7077 [Cp] Country of publication: Netherlands [La] Language: eng [Ab] Abstract: Cadmium (Cd), a potent carcinogen present in almost all foods, poses a major health risk to humans. Major routes of exposure to Cd for humans are occupation, diet, and tobacco use. Cd elicits various deleterious effects on cellular molecules mainly by causing oxidant-antioxidant imbalance. Cd has been implicated in the pathogenesis of many cancers, Itai-itai disease, diabetic nephropathy, hypertension, peripheral artery disease, and myocardial infarction. This study was designed to investigate the effects of Cd intake on erythrocytes and cardiac tissue in male albino Wistar rats. We treated male albino Wistar rats with cadmium chloride (CdCl ) by intra-gastric administration for 30 days and examined Cd burden and changes in blood constituents and antioxidant status of blood and cardiac tissue. We also studied the structural alterations in the erthrocytes, elemental changes and Cd burden in cardiac tissue using scanning electron microscope (SEM/EDX). Inflammation and apoptosis were analysed in the cardiac tissue by polymerase chain reaction (PCR), western blotting, and DNA fragmentation assay. Cd treatment resulted in echinocytosis of erythrocytes and distorted myofibrils arrangement, vacuolization and congestion in the vessels. Cd administration has also induced inflammation and apoptosis in the cardiac tissue. At molecular level, Cd administration caused oxidative damage to DNA, lipids, and proteins and diminished the activities of various antioxidants. The present study provides a compelling evidence of Cd-induced imbalance in oxidant-antioxidant system with damage to erythrocytes and cardiac tissue that may contribute to various cardiac diseases. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1803 [Cu] Class update date: 180310 [Lr] Last revision date: 180310 [St] Status: Publisher

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[PMID]: 29524572 [Au] Autor: Zhang Z; Li Y; Yang X; Wang L; Xu L; Zhang Q [Ad] Address: Heart Canter, Beijing Chao Yang Hospital, Capital Medical University, Beijing, China. [Ti] Title: Susceptibility of multiple polymorphisms in ADIPOQ, ADIPOR1 and ADIPOR2 genes to myocardial infarction in Han Chinese. [So] Source: Gene;, 2018 Mar 07. [Is] ISSN: 1879-0038 [Cp] Country of publication: Netherlands [La] Language: eng [Ab] Abstract: We aimed to investigate the association of 12 extensively studied polymorphisms in adiponectin (ADIPOQ), adiponectin receptor-1 (ADIPOR1) and adiponectin receptor-2 (ADIPOR2) genes with myocardial infarction in Han Chinese. This is a hospital-based, cross-sectional, case-control study, including 717 myocardial infarction patients and 612 controls. Myocardial infarction was confirmed through electrocardiogram/anatomopathological examinations. All polymorphisms met the Hardy-Weinberg equilibrium (p > 0.05). The genotype/allele counts of ADIPOQ gene rs2241766 (p = 0.001/0.003) and ADIPOR2 gene rs10773989 (p < 0.001/=0.008) differed significantly between patients and controls. Under the recessive model, rs2241766 (odds ratio [OR] = 4.16, 95% confidence interval [CI]: 1.83-9.49, p = 0.001) and rs10773989 (OR = 8.40, 95% CI: 2.54-27.8, p < 0.001) were associated with the significantly increased risk of myocardial infarction. Haplotype analysis revealed none or marginal significance, and there was no likelihood of genetic interaction as indicated by multifactor dimensionality reduction (MDR). Logistic regression analysis indicated that age, total cholesterol, hypertension, rs2241766, rs1342387, rs10773989 and rs1044471 were significant contributors, and a nomogram based on these contributors exhibited a good predictive utility (C-index: 0.795, p < 0.001). Our findings demonstrate that two polymorphisms, rs2241766 in ADIPOQ gene and rs10773989 in ADIPOR2 gene, especially under the recessive model of inheritance, played independent leading roles in susceptibility to myocardial infarction in Han Chinese. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1803 [Cu] Class update date: 180310 [Lr] Last revision date: 180310 [St] Status: Publisher

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[PMID]: 29524504 [Au] Autor: Qiu F; Dong C; Liu Y; Shao X; Huang D; Han Y; Wang B; Liu Y; Huo R; Paulo P; Zhang Z; Zhao D; Chu WF [Ad] Address: Department of Pharmacology (the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China. [Ti] Title: Pharmacological inhibition of SUMO-1 with ginkgolic acid alleviates cardiac fibrosis induced by myocardial infarction in mice. [So] Source: Toxicol Appl Pharmacol;, 2018 Mar 07. [Is] ISSN: 1096-0333 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: BACKGROUND AND PURPOSE: Protein modification by small ubiquitin-like modifier (SUMO) plays a critical role in the pathogenesis of heart diseases. The present study was designed to determine whether ginkgolic acid (GA) as a SUMO-1 inhibitor exerts an inhibitory effect on cardiac fibrosis induced by myocardial infarction (MI). EXPERIMENTAL APPROACH: GA was delivered by osmotic pumps in MI mice. Masson staining, electron microscopy (EM) and echocardiography were used to assess cardiac fibrosis, ultrastructure and function. Expression of SUMO-1, PML, TGF-ß1 and Pin1 was measured with Western blot or Real-time PCR. Collagen content, cell viability and myofibroblast transformation were measured in neonatal mouse cardiac fibroblasts (NMCFs). Promyelocytic leukemia (PML) protein was over-expressed by plasmid transfection. KEY RESULTS: GA improved cardiac fibrosis and dysfunction, and decreased SUMO-1 expression in MI mice. GA (>20 µM) inhibited NMCF viability in a dose-dependent manner. Nontoxic GA (10 µM) restrained angiotensin II (Ang II)-induced myofibroblast transformation and collagen production. GA also inhibited expression of TGF-ß1 mRNA and protein in vitro and in vivo. GA suppressed PML SUMOylation and PML nuclear body (PML-NB) organization, and disrupted expression and recruitment of Pin1 (a positive regulator of TGF-ß1 mRNA), whereas over-expression of PML reversed that. CONCLUSIONS AND IMPLICATIONS: Inhibition of SUMO-1 by GA alleviated MI-induced heart dysfunction and fibrosis, and the SUMOylated PML/Pin1/TGF-ß1 pathway is crucial for GA-inhibited cardiac fibrosis. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1803 [Cu] Class update date: 180310 [Lr] Last revision date: 180310 [St] Status: Publisher

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[PMID]: 29524460 [Au] Autor: Gupta K; Phan N; Wang Q; Liu B [Ad] Address: Department of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI, USA. [Ti] Title: Necroptosis in cardiovascular disease - a new therapeutic target. [So] Source: J Mol Cell Cardiol;, 2018 Mar 07. [Is] ISSN: 1095-8584 [Cp] Country of publication: England [La] Language: eng [Ab] Abstract: Contrary to the apoptosis-necrosis binary view of cell death, recent experimental evidence demonstrates that several forms of necrosis, represented by necroptosis, are regulated or programmed in nature. Multiple death stimuli known to be associated with cardiovascular disease are capable of causing either apoptosis or necroptosis. Whether a cell dies from apoptosis or necroptosis has distinct consequences on inflammation. It is known that apoptosis, a non-lytic form of death mediated by the caspase family of proteases, does not generally evoke an immune response. Necroptosis, on the other hand, is a lytic form of cell death. Due to the rapid loss of plasma membrane integrity, cells dying from necroptosis release proinflammatory intracellular contents and subsequently cause inflammation. Our review delineates various genetic and biochemical evidence that demonstrates a compelling role of necroptosis in the pathogenesis and/or progression of cardiovascular disease including myocardial infarction, atherosclerosis, and aortic aneurysm. Through recent studies of necroptosis in cardiovascular diseases, we attempt to discuss the role of necroptosis in vascular inflammation as well as the potential of necroptosis inhibitors in future clinical management of cardiovascular events. Inhibiting necroptosis in the vasculature has an overall protective role and necroptosis may represent a new therapeutic target to prevent the development and progression of cardiovascular diseases. [Pt] Publication type: JOURNAL ARTICLE; REVIEW [Em] Entry month: 1803 [Cu] Class update date: 180310 [Lr] Last revision date: 180310 [St] Status: Publisher

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[PMID]: 29520182 [Au] Autor: Wang L; Chen Y; Zhang B; Chen W; Wang C; Song L; Xu Z; Zheng J; Gao F [Ad] Address: Molecular Imaging Center, West China Hospital of Sichuan University, Chengdu 610041, China. [Ti] Title: Self-Gated Late Gadolinium Enhancement at 7T to Image Rats with Reperfused Acute Myocardial Infarction. [So] Source: Korean J Radiol;19(2):247-255, 2018 Mar-Apr. [Is] ISSN: 2005-8330 [Cp] Country of publication: Korea (South) [La] Language: eng [Ab] Abstract: Objective: A failed electrocardiography (ECG)-trigger often leads to a long acquisition time (TA) and deterioration in image quality. The purpose of this study was to evaluate and optimize the technique of self-gated (SG) cardiovascular magnetic resonance (CMR) for cardiac late gadolinium enhancement (LGE) imaging of rats with myocardial infarction/reperfusion. Materials and Methods: Cardiovascular magnetic resonance images of 10 rats were obtained using SG-LGE or ECG with respiration double-gating (ECG-RESP-gating) method at 7T to compare differences in image interference and TA between the two methods. A variety of flip angles (FA: 10°-80°) and the number of repetitions (NR: 40, 80, 150, and 300) were investigated to determine optimal scan parameters of SG-LGE technique based on image quality score and contrast-to-noise ratio (CNR). Results: Self-gated late gadolinium enhancement allowed successful scan in 10 (100%) rats. However, only 4 (40%) rats were successfully scanned with the ECG-RESP-gating method. TAs with SG-LGE varied depending on NR used (TA: 41, 82, 154, and 307 seconds, corresponding to NR of 40, 80, 150, and 300, respectively). For the ECG-RESP-gating method, the average TA was 220 seconds. For SG-LGE images, CNR (42.5 ± 5.5, 43.5 ± 7.5, 54 ± 9, 59.5 ± 8.5, 56 ± 13, 54 ± 8, and 41 ± 9) and image quality score (1.85 ± 0.75, 2.20 ± 0.83, 2.85 ± 0.37, 3.85 ± 0.52, 2.8 ± 0.51, 2.45 ± 0.76, and 1.95 ± 0.60) were achieved with different FAs (10°, 15°, 20°, 25°, 30°, 35°, and 40°, respectively). Optimal FAs of 20°-30° and NR of 80 were recommended. Conclusion: Self-gated technique can improve image quality of LGE without irregular ECG or respiration gating. Therefore, SG-LGE can be used an alternative method of ECG-RESP-gating. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1803 [Cu] Class update date: 180311 [Lr] Last revision date: 180311 [St] Status: In-Data-Review [do] DOI: 10.3348/kjr.2018.19.2.247

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[PMID]: 29511372 [Au] Autor: Yu J; Xu N; Zhao Y; Yu J [Ad] Address: Department of Surgery and Operating Room, The First Hospital of Jilin University, Changchun, 130021, China. [Ti] Title: Clinical importance of the anterior choroidal artery: a review of the literature. [So] Source: Int J Med Sci;15(4):368-375, 2018. [Is] ISSN: 1449-1907 [Cp] Country of publication: Australia [La] Language: eng [Ab] Abstract: The anterior choroidal artery (AChA) is a critical artery in brain physiology and function. The AChA is involved in many diseases, including aneurysm, brain infarct, Moyamoya disease (MMD), brain tumor, arteriovenous malformation (AVM), etc. The AChA is vulnerable to damage during the treatment of these diseases and is thus a very important vessel. However, a comprehensive systematic review of the importance of the AChA is currently lacking. In this study, we used the PUBMED database to perform a literature review of the AChA to increase our understanding of its role in neurophysiology. Although the AChA is a small thin artery, it supplies an extremely important region of the brain. The AChA consists of cisternal and plexal segments, and the point of entry into the choroidal plexus is known as the plexal point. During treatment for aneurysms, tumors, AVM or AVF, the AChA cisternal segments should be preserved as a pathway to prevent the infarction of the AChA target region in the brain. In MMD, a dilated AChA provides collateral flow for posterior circulation. In brain infarcts, rapid treatment is necessary to prevent brain damage. In Parkinson disease (PD), the role of the AChA is unclear. In trauma, the AChA can tear and result in intracranial hematoma. In addition, both chronic and non-chronic branch vessel occlusions in the AChA are clinically silent and should not deter aneurysm treatment with flow diversion. Based on the data available, the AChA is a highly essential vessel. [Pt] Publication type: JOURNAL ARTICLE; REVIEW [Em] Entry month: 1803 [Cu] Class update date: 180311 [Lr] Last revision date: 180311 [St] Status: In-Process [do] DOI: 10.7150/ijms.22631

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[PMID]: 29510122 [Au] Autor: Wei J; Yang RX; Ye Q; Xiao XL; Zang XL; Zhao ZJ; Cai ZZ; Wang M; Xu J; Jiang L [Ad] Address: Department of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China. [Ti] Title: Higher risk of myocardial injury in chest pain patients with elevated red blood cell distribution width. [So] Source: Clin Chim Acta;481:121-125, 2018 Mar 03. [Is] ISSN: 1873-3492 [Cp] Country of publication: Netherlands [La] Language: eng [Ab] Abstract: BACKGROUND: High level of red blood cell distribution width (RDW) has been associated with adverse outcomes in coronary artery disease patients. We aimed to investigate the relationship between RDW and the risk of myocardial injury in chest pain patients. METHODS AND RESULTS: We retrospectively reviewed 2078 chest pain patients with suspected acute myocardial infarction. Myocardial injury was defined as high-sensitivity cardiac troponin T (hs-cTnT) >14 ng/L. RDW was associated with hs-cTnT (r = 0.607) and the risk of myocardial injury stepwise increased across increasing RDW quartiles in all subgroups based on age and sex. The receiver operating characteristic curve analysis was calculated to assess the elevated RDW to predict myocardial injury, with the cutoff value of 13.25%. RDW had a high sensitivity (78.10%), specificity (87.44%), as well as positive predictive value (77.48%). The area under the curve (AUC) for all patients was 0.88 (95%CI 0.87, 0.90) and there is no statistical significant in AUCs for all subgroups. CONCLUSIONS: Elevated RDW was significantly associated with a higher risk of myocardial injury in chest pain patients with potential acute myocardial infarction. The RDW may be helpful to identify myocardial injury in such patients. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1803 [Cu] Class update date: 180310 [Lr] Last revision date: 180310 [St] Status: Publisher

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[PMID]: 29506472 [Au] Autor: Yogendranathan N; Herath HMMTB; Jayamali WD; Matthias AT; Pallewatte A; Kulatunga A [Ad] Address: National hospital, Colombo, Sri Lanka. ynilu6@gmail.com. [Ti] Title: A case of anterior spinal cord syndrome in a patient with unruptured thoracic aortic aneurysm with a mural thrombus. [So] Source: BMC Cardiovasc Disord;18(1):48, 2018 Mar 05. [Is] ISSN: 1471-2261 [Cp] Country of publication: England [La] Language: eng [Ab] Abstract: BACKGROUND: Spinal cord infarction is an uncommon condition. Anterior cord syndrome present with paraparesis or quadriparesis with sparing of vibration and proprioceptive senses. The common causes of anterior cord syndrome are aortic dissection and aortic surgical interventions. Spontaneous unruptured nondissected aortic aneurysms with intramural thrombus can rarely cause anterior cord infarctions. CASE PRESENTATION: We report a case of anterior spinal cord syndrome due to aneurysm of the thoracic aorta with a mural thrombus. A 64 year old male presented with sudden onset paraparesis with a sensory level at T1 with preserved sense of proprioception and vibration. The MRI panspine revealed increased T2 intensity in the anterior portion of the spinal cord from C5 to T10 level with characteristic 'owl eye' appearance on axial imaging. The CT aortogram detected aneurysmal dilatation of the ascending aortic, arch and descending thoracic aorta with significant intimal irregularities, calcified atherosclerotic plaques and a small mural thrombus. CONCLUSION: The possible mechanisms postulated are occlusion of ostia of radicular arteries by the atherosclerotic plaques and mural thrombus or thromboembolism to the anterior spinal artery. Nondissected atherosclerotic aortic aneurysms should be considered in patients presenting with spinal cord infarctions especially in the presence of vascular risk factors and smoking. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1803 [Cu] Class update date: 180311 [Lr] Last revision date: 180311 [St] Status: In-Data-Review [do] DOI: 10.1186/s12872-018-0786-4

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[PMID]: 29499335 [Au] Autor: Gopoju R; Panangipalli S; Kotamraju S [Ad] Address: Centre for Chemical Biology, CSIR-Indian Institute of Chemical Technology, Uppal Road, Hyderabad 500007, India; Academy of Scientific and Innovative Research, Training and Development Complex, Chennai 600113, India. [Ti] Title: Metformin treatment prevents SREBP2-mediated cholesterol uptake and improves lipid homeostasis during oxidative stress-induced atherosclerosis. [So] Source: Free Radic Biol Med;118:85-97, 2018 Mar 02. [Is] ISSN: 1873-4596 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Lipids are responsible for the atheromatous plaque formation during atherosclerosis by their deposition in the subendothelial intima of the aorta, leading to infarction. Sterol regulatory element-binding protein 2 (SREBP2), regulating cholesterol homeostasis, is suggested to play a pivotal role during the early incidence of atherosclerosis through dysregulation of lipid homeostasis. Here we demonstrate that oxidative stress stimulates SREBP2-mediated cholesterol uptake via low density lipoprotein receptor (LDLR), rather than cholesterol synthesis, in mouse vascular aortic smooth muscle cells (MOVAS) and THP-1 monocytes. The enhancement of mature form of SREBP2 (SREBP2-M) during oxidative stress was associated with the inhibition of AMP-activated protein kinase (AMPK) activation. In contrast, inhibition of either SREBP2 by fatostatin or LDLR by siLDLR resulted in decreased cholesterol levels during oxidative stress. Thereby confirming the role of SREBP2 in cholesterol regulation via LDLR. Metformin-mediated activation of AMPK was able to significantly abrogate cholesterol uptake by inhibiting SREBP2-M. Interestingly, although metformin administration attenuated angiotensin (Ang)-II-impaired lipid homeostasis in both aorta and liver tissues of ApoE mice, the results indicate that SREBP2 through LDLR regulates lipid homeostasis in aorta but not in liver tissue. Taken together, AMPK activation inhibits oxidative stress-mediated SREBP2-dependent cholesterol uptake, and moreover, metformin-induced prevention of atheromatic events are in part due to its ability to regulate the SREBP2-LDLR axis. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1803 [Cu] Class update date: 180310 [Lr] Last revision date: 180310 [St] Status: Publisher

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[PMID]: 29479056 [Au] Autor: Zhong Z; Wu H; Ye M; Yang Y; Luo W; Wu Y; Wu H; Zhong M; Zhao P [Ad] Address: Center for Cardiovascular Diseases, Meizhou People's Hospital (Huangtang Hospital), Meizhou Hospital Affiliated to Sun Yat-sen University, Meizhou, Guangdong, China (mainland). [Ti] Title: Association of APOE Gene Polymorphisms with Cerebral Infarction in the Chinese Population. [So] Source: Med Sci Monit;24:1171-1177, 2018 Feb 26. [Is] ISSN: 1643-3750 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: BACKGROUND Apolipoprotein E (ApoE) is a multifunctional protein that plays an important role in lipoprotein metabolism. However, the relationship between APOE gene polymorphisms and cerebral infarction in the Chinese population remains unclear. Therefore, we studied the role of APOE gene polymorphisms in patients with cerebral infarction in a Chinese population. MATERIAL AND METHODS This study involved 906 patients with cerebral infarction and 1,141 individuals without cerebral infarction who served as controls. APOE genotypes were identified in all participants who participated in the study. Factors influencing cerebral infarction were also analyzed. RESULTS Statistically significant variances in the distribution and frequencies of the APOE genotypes in the patients were observed (ε2/ε3 versus ε2/ε4 versus ε3/ε3=22.85% versus 7.62% versus 56.95%) and controls (ε2/ε3 versus ε2/ε4 versus ε3/ε3=17.27% versus 2.72% versus 66.87%; p<0.001). Univariate analysis showed that the APOE ε3/ε3 genotype [OR, 0.393 (95% CI, 0.237-0.653); p<0.001] and ε3/ε4 genotype [OR, 0.376 (95% CI 0.221-0.637); p<0.001] played a protective role against cerebral infarction in Chinese men. CONCLUSIONS Statistically significant variances in the distribution and frequencies of the APOE genotypes of the patients and controls were observed. The study demonstrated that the APOE ε3/ε3 and ε3/ε4 genotypes played a protective role against cerebral infarction in Chinese men, but not women. Additionally, the ε2/ε4 genotype may be a potential risk factor in men, whereas ε3/ε4 genotype may play a potential protective role against this disease in women. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1802 [Cu] Class update date: 180311 [Lr] Last revision date: 180311 [St] Status: In-Process

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