NF-κB directs dynamic super enhancer formation in inflammation and atherogenesis.

Proinflammatory stimuli elicit rapid transcriptional responses via transduced signals to master regulatory transcription factors. To explore the role of chromatin-dependent signal transduction in the atherogenic inflammatory response, we characterized the dynamics, structure, and function of regulatory elements in the activated endothelial cell epigenome. Stimulation with tumor necrosis factor alpha prompted a dramatic and rapid global redistribution of chromatin activators to massive de novo clustered enhancer domains. Inflammatory super enhancers formed by nuclear factor-kappa B accumulate at the expense of immediately decommissioned, basal endothelial super enhancers, despite persistent histone hyperacetylation. Mass action of enhancer factor redistribution causes momentous swings in transcriptional initiation and elongation. A chemical genetic approach reveals a requirement for BET bromodomains in communicating enhancer remodeling to RNA Polymerase II and orchestrating the transition to the inflammatory cell state, demonstrated in activated endothelium and macrophages. BET bromodomain inhibition abrogates super enhancer-mediated inflammatory transcription, atherogenic endothelial responses, and atherosclerosis in vivo.

Brd4 participates in epigenetic regulation of the extinction of remote auditory fear memory.

BACKGROUND: Inaccurate fear memories can be maladaptive and potentially portrait a core symptomatic dimension of fear adaptive disorders such as post-traumatic stress disorder (PTSD), which is generally characterized by an intense and enduring memory for the traumatic events. Evidence exists in support of epigenetic regulation of fear behavior. Brd4, a member of the bromodomain and extra-terminal domain (BET) protein family, serves as a chromatin "reader" by binding to histones in acetylated lysine residues, and hence promotes transcriptional activities. However, less is known whether Brd4 participates in modulating cognitive activities especially memory formation and extinction. Here we provide evidence for a role of Brd4 in modulation of auditory fear memory. Auditory fear conditioning resulted in a biphasic Brd4 activation in the anterior cingulate cortex (ACC) and hippocampus of adult mice. Thus, Brd4 phosphorylation occurred 6 h and 3-14 days, respectively, after auditory fear conditioning. Systemic inhibition of Brd4 with a BET inhibitor, JQ1, impaired the extinction of remote (i.e., 14 days after conditioning) fear memory. Further, conditional Brd4 knockout in excitatory neurons of the forebrain impaired remote fear extinction as observed in the JQ1-treated mice. Herein, we identified that Brd4 is essential for extinction of remote fear in rodents. These results thus indicate that Brd4 potentially plays a role in the pathogenesis of PTSD.

Fendrr involves in the pathogenesis of cardiac fibrosis via regulating miR-106b/SMAD3 axis.

Cardiovascular diseases (CVDs) is the first cause of death worldwide, generally exhibiting a high morbidity, high disability rate and high mortality especially in the elderly persons (>50 years old). Previously, extensive studies have demonstrated that cardiac fibrosis plays cardinal roles in the pathogenesis of CVDs. However, due to the unclear underlying mechanisms of cardiac fibrosis, its clinical intervention remains very lacking. Long non-coding RNAs (lncRNAs), a class of non-coding RNA but differing from microRNAs, are generally considered as transcripts with a length ranging 200 to 100 nucleotides. Recently, accumulating evidence showed that lncRNAs involve in the pathogenesis of cardiac fibrosis. Fendrr (FOXF1 adjacent non-coding developmental regulatory RNA), is a spliced long non-coding RNA transcribed bi-directionally with FOXF1 on the opposite strand. Fendrr has been demonstrated to be essential for normal development of the heart and body wall in mouse, and shows a good anti-fibrotic activity in pulmonary fibrosis. In this study, we aimed to explore the effects of Fendrr on cardiac fibrosis. Intriguingly, we first observed that lncRNA Fendrr was up-regulated in the heart tissues of transverse aortic constriction (TAC) induced cardiac fibrosis mouse models, determined by RT-QPCR. Loss-function of Fendrr significantly alleviated the cardiac fibrosis phenotypes induced by TAC, indicating that Fendrr is required for the pathogenesis of cardiac fibrosis. In mechanism, we demonstrated experimentally that Fendrr directly targeting miR-106b, by which the lncRNA promotes cardiac fibrosis (indicated by the elevation of Col1a1, Col3a1, CTGF and ACTA2 expression) in a miR-106b mediated manner. Collectively, our findings highlight the axis of Fendrr/miR-106b/Samd3 in the pathogenesis of cardiac fibrosis, which may be a promising target for clinical intervention target of cardiac fibrosis.

P-selectin (CD62P) and soluble TREM-like transcript-1 (sTLT-1) are associated with coronary artery disease: a case control study.

BACKGROUND: Platelet activation plays a crucial role in the pathogenesis of coronary artery disease (CAD). Platelet P-selectin (CD62P) is a classic platelet activation indicator on the platelet surface, and soluble TREM-like transcript-1 (sTLT-1) is a new indicator. However, the relationship between these two markers and CAD, especially in acute coronary syndrome (ACS), has not been elucidated. This study aimed to investigate CD62P expression on the platelet surface and sTLT-1 expression in serum, as well as to assess their relationship with CAD. METHODS: We measured the levels of CD62P and sTLT-1 in 83 patients with CAD compared to 49 controls. The association of these indicators with age, blood pressure, lipid profile, body mass index, and liver injury marker level were also examined. RESULTS: CD62P concentration was higher in CAD patients than in the control group (P < 0.01), especially in acute myocardial infarction (AMI) patients (P < 0.01). Serum sTLT-1 concentration was higher in the AMI and unstable angina pectoris (UAP) groups than in the normal control (NC) group (P < 0.01). CONCLUSIONS: The consistency of sTLT-1 and CD62P expression levels in CAD patients indicates that sTLT-1 level, the same as CD62P, may be a new marker of platelet activation that is positively related to CAD.

Bromodomain-containing protein 4 contributes to renal fibrosis through the induction of epithelial-mesenchymal transition.

Fibrosis is a common pathology in renal disease. Hypertensive nephropathy (HN) is one of the most common secondary nephropathies that often progresses to severe renal fibrosis with limited treatment options beyond hypertension control. Bromodomain-containing protein 4 (Brd4) was recently recognized as a target in signaling pathways that underlie the pathologies of inflammatory diseases and tumors. A recently developed inhibitor of Brd4, JQ1, has been shown to exert antifibrotic effects and is being clinically explored as an anti-inflammatory and antitumor drug. Here, using human kidney biopsies and Angiotensin II-induced mouse fibrotic kidney samples, we show that Brd4 was upregulated in renal tissue from HN patients and hypertensive mouse models. In mice, JQ1 alleviated Angiotensin II-induced kidney fibrosis and blocked epithelial-mesenchymal transition (EMT) by altering the expression of EMT-related proteins. Using an in vitro model of HK2 cells exposed to Angiotensin II, we also demonstrated that JQ1 suppressed the protein expression of fibrotic genes in these cells. These results further implicate Brd4 in the fibrotic response in HN and reveal that Brd4 is a potential antifibrotic target. BET inhibitors are currently being investigated in clinical trials as antitumor agents and show potent pharmacological effects. Our findings suggest that BET inhibitors may also be potential translational therapies for HN.

Cerebral infarction as the first symptom in acute promyelocytic leukemia: A case report and literature review. / ä»¥è„‘æ¢—æ­»ä¸ºé¦–å‘ç—‡çŠ¶çš„æ€¥æ€§æ—©å¹¼ç²’ç»†èƒžç™½è¡€ç— 1例及文献回顾.

In the clinical settings, disseminated intravascular coagulation (DIC) and complications such as hemorrhage are commonly seen in acute promyelocytic leukemia patients, whereas thrombosis is rarely reported. We reported a case here that the patient presented with cerebral infarction as the first manifestation. During the admission, the patient encountered differentiation syndrome, pulmonary embolism, pulmonary hemorrhage, and myocardial ischemia, as well as bleeding and thrombosis complications. Hence the patient was diagnosed as DIC. After the treatment of blood transfusion instead of anticoagulation, his condition was stable and the remission was completely achieved. The treatment experience provides guides for other patients with similar complications of simultaneous bleeding and thrombosis.

Lovastatin attenuates angiotensin II induced cardiovascular fibrosis through the suppression of YAP/TAZ signaling.

Angiotensin II (ANG II) is associated with fibrosis in both clinical and basic studies. Thus, we aimed to explore a mechanism by which ANG II induces fibrosis. 5 µM of ANG II was used in the in vitro study. The mouse cardiovascular fibrosis model was established by infused with AngII (1000 ng/kg/min) for 7 days and cotreated with lovastatin (10 mg/kg daily) or vehicle control (DMSO in saline). We found that ANG II activated yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), two transcription factors that were shown to induce fibrosis. Inhibition of ras homolog gene family member A (RhoA) reduced ANG II-induced YAP/TAZ transcriptional activity, which suggests that the upregulation of YAP/TAZ signaling by ANG II is RhoA-dependent. Furthermore, studies have shown that the inhibition of YAP/TAZ by either siRNA or small molecule inhibitor suppressed ANG II-induced expression of fibrogenic genes, indicating that ANG II upregulates YAP/TAZ to initiate fibrosis. The mevalonate pathway, which is targeted by statins, has also been shown to control YAP/TAZ. Here, we found that the suppression of YAP/TAZ signaling by lovastatin attenuates ANG II-induced fibrosis, both in vitro and in vivo. These data reveal a novel mechanism for ANG II in the induction of fibrosis. In addition, our findings provide a reasonable explanation regarding the mechanism by which statins improve fibrosis in patients with cardiovascular and renal diseases.

Beta 2-Microglobulin and the Severity of Coronary Stenosis in Patients With Acute Coronary Syndrome.

BACKGROUND: Previous studies have shown that beta 2-microglobulin (B2M) could predict all-cause mortality and cardiovascular mortality in various groups of people. However, the relationship between B2M and severity of coronary stenosis in patients with acute coronary syndrome has not been established. METHODS: We enrolled 872 consecutive patients admitted with acute coronary syndrome in our study. All participants underwent coronary angiography examination or stent implantation after admission. The severity of coronary stenosis was assessed by Gensini score and the presentation of triple-vessel disease. B2M and other biochemical parameters were measured. All subjects were divided into quartiles of B2M. Multivariate linear regression and logistic regression were applied in the analysis. RESULTS: Gensini score and the prevalence of triple-vessel disease were elevated in accordance with increasing B2M quartiles (p=0.002 and p<0.001, respectively). Multivariate regression showed diabetes (p=0.031), high-sensitivity C-reactive protein (hs-CRP, p=0.043) and B2M (p=0.006) were positively correlated with Gensini score. Logistic regression analysis revealed that the crude and fully adjusted odds ratios of triple-vessel disease were 2.34 (95% CI: 1.58-3.46) and 1.97 (95% CI: 1.14-3.40) in the fourth quartile of B2M compared with the first quartile, respectively. However, no interactive relationships were found in subgroup analysis by estimated glomerular filtration rate or hs-CRP in the above associations, neither in the distribution of Gensini score (p for interaction>0.05 for both). CONCLUSION: Our data indicated that B2M was an independent risk factor of coronary stenosis in patients with acute coronary syndrome.

MicroRNA-126 alleviates endothelial cells injury in atherosclerosis by restoring autophagic flux via inhibiting of PI3K/Akt/mTOR pathway.

MicroRNAs (miRNAs) have emerged as critical modulators of ECs function and play a vital role in the development of cardiovascular disease. Among them, miR-126 is a crucial regulator of atherosclerosis. Endothelial cells (ECs) death and autophagy have been described in cells to cope with the progression of atherosclerosis. Hence, the aim of this study is to investigate the effects of miR-126 on atherosclerosis in oxidized low-density lipoprotein (ox-LDL)-stimulated human umbilical vein endothelial cells (HUVECs) and the potential roles of autophagy flux in these processes. Our results showed that miR-126 level was significantly reduced in ox-LDL-treated HUVECs and miR-126 overexpression induced by miR-126 mimics remarkably blocked ox-LDL-induced HUVECs injury as evidenced by the reduced cell viability, and the increased LDH release, caspase-3 activity and apoptosis ratio. In addition, ox-LDL increased LC3-II, Beclin 1, and p62 expressions in HUVECs, while these changes were nullified in the presence of treatment with bafilomycin A1 (BafA1, an inhibit autophagic flux inhibitor). However, we found that ox-LDL-induced impaired autophagy flux was recused by miR-126 mimics. Subsequently, we found that Bafi A1 pretreatment reversed the protection of miR-126 mimics against ox-LDL-induced HUVECs injury. Finally, our results showed that miR-126 mimics rescued ox-LDL-induced impaired autophagy flux through inhibiting PI3K/Akt/mTOR signaling. Taken together, our findings suggested that miR-126 alleviates ox-LDL-induced HUVECs injury through restoring autophagy flux via repressing PI3K/Akt/mTOR pathway, and further implicate the potential therapeutic targets to reverse atherosclerosis.

MicroRNA-21 suppresses ox-LDL-induced human aortic endothelial cells injuries in atherosclerosis through enhancement of autophagic flux: Involvement in promotion of lysosomal function.

Atherosclerosis is a common pathological basis of cardiovascular disease and remains the leading cause of mortality. Endothelial cell (EC) injury and autophagy dysfunction have been proved to contribute to the development of atherosclerosis. Recently, accumulating evidence confirms that microRNAs (miRNAs) have emerged as vital regulators and fine-tuners of various pathophysiological cellular impacts and molecular signaling pathways involved in atherosclerosis. Herein, the objective of the present study was to explore the biological function of miR-21 in oxidized low-density lipoprotein (ox-LDL)-induced human aortic endothelial cells (HAECs) injury and the underlying molecular mechanism. The results showed that ox-LDL treatment significantly decreased HAECs viability, increased caspase-3 activity, apoptosis ratio and Bax protein expression, and reduced Bcl-2 protein expression resulting in EC injuries. Simultaneously, ox-LDL treatment obviously reduced miR-21 level in a time-and dose-dependent manner. Notably, ox-LDL-induced EC injuries were abolished by miR-21 mimics transfection. In addition, miR-21 mimics alleviated ox-LDL-induced impaired autophagic flux as illustrated by the increases in LC3-II/LC3-I ratio and Beclin-1 protein expression, and the decrease in p62 protein expression in HAECs. Moreover, ox-LDL suppressed the expressions of lysosomal membrane protein (LAMP1) and cathepsin D proteins, and attenuated cathepsin D activity in HAECs, leading to lysosomal dysfunction, while these effects were also blocked by miR-21 mimics. These findings indicated that miR-21 restored impaired autophagic flux and lysosomal dysfunction, thereby attenuating ox-LDL-induced HAECs injuries.

Super enhancers at the miR-146a and miR-155 genes contribute to self-regulation of inflammation.

Inflammatory response is essential to host defense and repair, and requires tight regulation as excessive and constant inflammatory response is deleterious. We recently identified that one of the general but key mechanisms for inflammatory gene transcription regulation is controlled by the formation of super enhancers mediated by NF-κB, and bromodomain and extraterminal (BET) proteins. Given that microRNA transcription shares a similar mechanism to mRNA, we assume that the inflammatory microRNAs transcription could be NF-κB and BET bromodomain dependent. In the present study, we confirmed that inflammatory stimuli changed human umbilical vein endothelial cells (HUVEC) microRNA profile. Among these microRNAs, miR-146a and miR-155, two well-established inflammatory microRNAs, are both downregulated at transcriptional level by NF-κB and BET bromodomain inhibition. To pursue this mechanism, we analyzed the ChIP-seq data and found that NF-κB, BRD4 and RNA POL II were rapidly distributed at the upstream regions of miR-146a and miR-155, and more importantly mediated the formation of the super enhancers that drive miR-146a and miR-155 transcription. These microRNAs transcription driven by super enhancers in turn downregulate both in vitro and in vivo canonical inflammatory genes expression through targeting inflammatory mediators. This novel finding demonstrated how the host self-regulates inflammatory genes expression at both transcriptional and post-transcriptional level to ensure the appropriate level of the host inflammatory response.

BET bromodomain is a novel regulator of TAZ and its activity.

Transcriptional coactivator with PDZ-binding motif (TAZ) is a key transcriptional mediator of Hippo signaling that has been recently reported to mediate Wnt-activated transcription and serve as a component to suppress canonical Wnt/ß-catenin activity. The Bromodomain and Extra-terminal domain (BET) family of proteins can recognize the acetylated lysine chain on histones and plays a critical role in transcriptional regulation. However, the mechanisms underlying transcriptional repression by the BET bromodomain are poorly understood. Here, we found that BET bromodomain inhibition upregulated TAZ protein and its transcriptional output, independent of its well-established role as a mediator of Hippo and Wnt signaling. Additionally, JQ1, a synthetic BET inhibitor, suppressed Wnt/ß-catenin activity by upregulating TAZ. Although JQ1 upregulated TAZ, which is known to promote cell proliferation, it drastically suppressed the growth of colon cancer cells by inducing cell cycle arrest. Collectively, our study identified an unexpected transcriptional repression function of the BET bromodomain and a novel mechanism for TAZ upregulation.

Association of Serum Prealbumin with Angiographic Severity in Patients with Acute Coronary Syndrome.

BACKGROUND Serum prealbumin (PA), which is a nutritional index, has been found to be associated with severities and prognoses of various diseases. However, there are no reports about the relationship between PA and angiographic severity of coronary artery disease. MATERIAL AND METHODS This cross-sectional study included 867 patients with acute coronary syndrome (ACS) who underwent coronary angiography. Patients were divided into quartiles of PA and coronary artery stenosis was determined by angiographic Gensini score, the presence of high Gensini score (Gensini score ≥120), and triple-vessel disease. Multivariate linear and logistic regression analyses were performed to explore the relationship between PA and disease severity in a coronary angiogram. RESULTS There was a significant and independent negative correlation between PA and Gensini score in multivariate linear regression (p=0.015). Logistic regression analysis revealed that crude odds ratios of triple-vessel disease and high Gensini score were 2.47 (95% CI: 1.66-3.67) and 1.83 (95% CI: 1.50-3.49), respectively, in the first quartile of PA compared with the fourth quartile and the results remained significant for high Gensini score after adjustment for confounding factors. In addition, estimated glomerular filtration rate, liver function, and high-sensitivity C-reactive protein (hs-CRP) had no interactive relationships in the above associations. Patients with lower levels of albumin or higher levels of hs-CRP or the ratio of hs-CRP to PA (hs-CRP/PA) also had more severe coronary atherosclerosis. CONCLUSIONS PA is negatively and independently associated with angiographic severity in patients with ACS, indicating for potential use in estimating the burden of coronary atherosclerosis.

[Comparison of differentiated endothelial cells from the embryonic stem cells with human umbilical vein endothelial cells].

OBJECTIVE: To compare the differentiated endothelial cells from the embryonic stem cells in vitro with human umbilical vein endothelial cells (HUVECs).
 Methods: Induction of the stem cells HUES9 to endothelial cells follows 2 steps. Stem cells were treated with CHIR99021 (10 µmol/L) and bone morphogenetic protein 4 (25 ng/mL) for 3 days to keep mesoderm state, then subsequent exposure them to VEGF165 (200 ng/mL) and Forskolin (2 µmol/L) to differentiate into endothelial cells. The morphology of differentiated endothelial cells were compared with HUVECs. The surface marker CD144 on differentiated cells and HUVECs were detected. The capabilities of two types of endothelial cells in migration and angiogenesis were examined.
 Results: The differentiated endothelial cells show the same morphology with HUVECs. After 6 days of differentiation, the efficiency reached 73.4%. The positive percentage of CD144 for the differentiated endothelial cells and HUVECs was 86.6% and 94.4%, respectively. Both of them show capabilities of migration and angiogenesis, especially when they were treated with SB431542 to inhibit TGF-ß signal pathway.
 Conclusion: The method for induction of stem cells to endothelial cells is productivity and it can be used for further study.

[Progress in research on obstructive sleep apnea syndrome with hypertension].

Obstructive sleep apnea syndrome (OSAS) is a complicated chronic disease caused by certain reasons, characterized by obstruction of the upper airway and apnea or hypopnea during sleep, which can be followed by anoxia, snoring and daytime sleepiness. Recent studies have shown that hypertension is closely connected to OSAS. OSAS can lead to hypertension by several possible mechanisms. The diagnosis of OSAS mainly depends on the medical history, sign, polysomnogram (PSG) result and the frequency of apnea and hypopnea. OSAS can be relieved by continuous positive airway pressure (CPAP), oral orthodontic treatment, medicine, change of lifestyles and others. This brief review focuses on the mechanism of hypertension due to OSAS and the diagnosis criteria and treatment of OSAS.

[Y-27632 reduces the MMP2 and MMP9 expression in endothelial cell via inhibition of ROCK signal pathway].

OBJECTIVE: To explore the effect of ROCK inhibitor Y-27632 on the matrix metalloproteinase 2 and 9 (MMP2 and MMP9) gene expression and activity in tumor necrosis factor α (TNF-α)-treated human umbilical vein endothelial cell (HUVEC).
 METHODS: HHUVEC was divided into 3 groups, a control group, a TNF-α group, and a TNF-α plus Y-27632 group. The expressions of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), MMP2 and MMP9 were examined by real-time PCR. The MMP2/9 activity was measured by gelatin zymography.
 RESULTS: Compared to the control group, the mRNA expressions of ICAM-1, VCAM-1, MMP2 and MMP9 were increased TNF-α-treated cells, which were suppressed by ROCK inhibitor (P<0.01). The MMP2/9 activity was elevated in TNF-α-treated cells, which was reversed by ROCK inhibitor (P<0.05).
 CONCLUSION: ROCK inhibitor can suppress TNF-α-induced inflammation in endothelial cells through down-regulation of MMP2/9.

Efficacy of folic acid therapy in primary prevention of stroke among adults with hypertension in China: the CSPPT randomized clinical trial.

IMPORTANCE: Uncertainty remains about the efficacy of folic acid therapy for the primary prevention of stroke because of limited and inconsistent data. OBJECTIVE: To test the primary hypothesis that therapy with enalapril and folic acid is more effective in reducing first stroke than enalapril alone among Chinese adults with hypertension. DESIGN, SETTING, AND PARTICIPANTS: The China Stroke Primary Prevention Trial, a randomized, double-blind clinical trial conducted from May 19, 2008, to August 24, 2013, in 32 communities in Jiangsu and Anhui provinces in China. A total of 20,702 adults with hypertension without history of stroke or myocardial infarction (MI) participated in the study. INTERVENTIONS: Eligible participants, stratified by MTHFR C677T genotypes (CC, CT, and TT), were randomly assigned to receive double-blind daily treatment with a single-pill combination containing enalapril, 10 mg, and folic acid, 0.8 mg (n = 10,348) or a tablet containing enalapril, 10 mg, alone (n = 10,354). MAIN OUTCOMES AND MEASURES: The primary outcome was first stroke. Secondary outcomes included first ischemic stroke; first hemorrhagic stroke; MI; a composite of cardiovascular events consisting of cardiovascular death, MI, and stroke; and all-cause death. RESULTS: During a median treatment duration of 4.5 years, compared with the enalapril alone group, the enalapril-folic acid group had a significant risk reduction in first stroke (2.7% of participants in the enalapril-folic acid group vs 3.4% in the enalapril alone group; hazard ratio [HR], 0.79; 95% CI, 0.68-0.93), first ischemic stroke (2.2% with enalapril-folic acid vs 2.8% with enalapril alone; HR, 0.76; 95% CI, 0.64-0.91), and composite cardiovascular events consisting of cardiovascular death, MI, and stroke (3.1% with enalapril-folic acid vs 3.9% with enalapril alone; HR, 0.80; 95% CI, 0.69-0.92). The risks of hemorrhagic stroke (HR, 0.93; 95% CI, 0.65-1.34), MI (HR, 1.04; 95% CI, 0.60-1.82), and all-cause deaths (HR, 0.94; 95% CI, 0.81-1.10) did not differ significantly between the 2 treatment groups. There were no significant differences between the 2 treatment groups in the frequencies of adverse events. CONCLUSIONS AND RELEVANCE: Among adults with hypertension in China without a history of stroke or MI, the combined use of enalapril and folic acid, compared with enalapril alone, significantly reduced the risk of first stroke. These findings are consistent with benefits from folate use among adults with hypertension and low baseline folate levels. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00794885.

[Circulating miR-214 level and its correlation with the extent of coronary lesion in patients with acute myocardial infarction].

OBJECTIVE: To examine the circulating levels of miR-214 in acute myocardial infarction (AMI) patients and to explore the relationship between the circulating levels of miR-214 and the degree of coronary lesion. METHODS: A total of 45 patients with AMI (AMI group) were enrolled from Xiangya Hospital of Central South University between September, 2011 and January, 2012. Twenty healthy volunteers served as a normal control group (n=20). According to the coronary artery lesion area, AMI group was also divided into a single-branch group, a double-branch group and a triple-branch group (n=20, 13, 12 respectively). Circulating levels of miR-214 and plasma levels of placental growth factor (PLGF) were measured by real time-PCR assay and enzyme-linked immunosorbent assay respectively on the day when the patients admitted to the hospital. The plasma levels of miR-214 and PLGF were compared among the various branch groups. The correlation between miR-214 and PLGF was analyzed in AMI subgroups. RESULTS: The miR-214 levels in the AMI subgroups were lower than that in the control group. The more decrease in miR-214 level, the larger size of coronary lesion. There was significant difference in the different groups (all P<0.05). Compared with the control group, the levels of plasma PLGF were significantly higher in the AMI subgroups. The more increase in PLGF level, the larger size of coronary lesion. There was significant difference in the different groups (all P<0.05). The plasma levels of miR- 214 were negatively correlated with that of PLGF in the AMI group (r=-0.588, P<0.01). CONCLUSION: The circulating level of miR-214 was significantly decreased in the AMI group, which might be correlated with the extent of the coronary lesion. Circulating miR-214 may be a promising biomarker for the diagnosis and prognosis of severe AMI.

[Five-case report for transvenous epicardial pacemaker implantation via coronary sinus in patients after prosthetic tricuspid valve replacement].

Five patients after prosthetic tricuspid valve, who received pacemaker implantation via coronary sinus during Oct, 2011 and Jul, 2014, were enrolled. Pacemakers were implanted via coronary vein in 5 patients without complications. The stimulation thresholds keep stable and symptoms (such as short breath and fatigue) were disappeared during the follow-up. For patients after tricuspid valve replacement, implantation of pacemaker via coronary sinus provides a safe and invasive approach and avoids opening the chest again.

[An improved method of electrode placement for ECG monitoring in children].

OBJECTIVE: This study examines the impacts of an improved electrode placement on the electrocardiogram (ECG) results in order to determine a better electrode placement for ECG monitoring in children. METHODS: ECG was recorded using the traditional electrode placement and the modified electrode placement (with shortened electrode distance) respectively in 50 pediatric patients. The amplitudes of P wave and QRS wave on ECG by the two measurements were compared. Furthermore, the impacts of different body positions on the amplitudes of P wave and QRS wave were studied after applying the modified electrode placement. RESULTS: There were no significant differences in the amplitudes of P wave and QRS wave on ECG by the traditional electrode placement and the modified electrode placement (P>0.05). When modified electrode placement was utilized, the body position change did not lead to significant changes in the amplitudes of P wave and QRS wave (P>0.05). CONCLUSIONS: A satisfactory ECG can be obtained with the modified electrode placement independent of patient's body position, suggesting that the modified electrode placement can be used instead of the traditional placement in children.