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.
Blood Coagulation ; Cerebral Infarction ; Disseminated Intravascular Coagulation ; etiology ; Humans ; Leukemia, Promyelocytic, Acute ; complications ; Thrombosis

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 ceils 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-β signal pathway.Conclusion:The method for induction of stem cells to endothelial cells is productivity and it can be used for further study.

Objective:To explore bromodomain and extra-terminal (BET) inhibition in the regulation of vascular endothelial cells activation and early atherosclerosis formation and its potential molecular mechanisms.Methods:1.Human umbilical vein endothelial cells (HUVEC) and mouse heart endothelial cells (MHEC) were isolated,and tumor necrosis factor α (TNFα) was used to activate in flammatory genes transcription in the presence or absence of JQ1,a specific BET inhibitor.The groups are as follows:(1)Normal control group;(2) TNFα(25 ng/mL)group;(3) TNFα+JQ 1 group.The gene mRNA and protein expression of inflammatory cytokines were measured by both real-time PCR and flow cytometry (FCM).2.LDL receptor-deficient (LDLR-/-) mice were randomly divided into 2 groups:JQ1 group (n=8,JQlintraperitoneal,50 mg/kg,daily) and control group (n=8,DMSO,daily).After 8 weeks feeding with high cholesterol diet,vascular cell adhesion molecule-1 (VCAM-1) expression in aortic arch was measured by immunohistochemistry.The activity of nuclear factor kappa B (NF-κB) signaling was monitored by 5XκB luciferase reporter assay in HEK293.Results:TNFα dramatically induced the mRNA and protein expression of inflammatory genes and JQ 1 significantly downregulated the induction of them (E-selectin,P-selectin,VCAM-1,IL-8)(P＜0.01).Immunohistochemistry detection indicated that JQ1 significantly downregulated the expression of VCAM-1 in aortic arch induced by 8 weeks high cholesterol diet feeding comparing to control group.In addition,BET bromodomain inhibition downregulated TNFα upregulated NF-κB transcriptional activity (P＜0.01).Conclusions:Our study demonstrated that BET bromodomain was involved in NF-κB mediated inflammatory genes expression;inhibition of BET bromodomain suppressed vascular endothelial activation in vitro,and attenuated early atherogenesis in vivo.

With the popularity of heart disease and obesity,as an important part of the integrated management of heart disease,weight gradually attracting attention from all walks of life.This paper summarizes the 2013 to 2016,American College of Cardiology/American Heart Association (ACC/AHA) jointly launched by the obese patients lose weight guide and aimed at overweight or obese patients with the fone management based on the weight of the specific steps,and by the AHA and international diabetes groups put forward the treatment of type 2 diabetes and overweight or obesity surgery.

On June 20,2014 in Washington for a meeting of the heart,a think-tank.As a call to action,the meeting to define the cardiovascular disease~ prevention and control of new mode and method,to help solve the problem of merging high metabolic risk of cardiovascular disease.More than 20 representative groups participate in the discussion and meet the following consensus that metabolic syndrome is a complex pathophysiological state,is a process of gradual change,consisting of a series of known and unknown risk factors,and is associated with the severity of the disease.Treatment is the ideal mode of the metabolic syndrome,before the disease can accurately determine risk,identify the subtypes of disease,and identify the different stages of the disease,in order to better carry out prevention and treatment of cardiovascular disease.This new mode of prevention and control of determination needs establishment of consensus,and sustainable development of this control mode,the mode of authentication,in the future continue to optimize the mode.

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.
Amides ; Cells, Cultured ; Down-Regulation ; Endothelial Cells ; Humans ; Intercellular Adhesion Molecule-1 ; Matrix Metalloproteinase 2 ; Matrix Metalloproteinase 9 ; Pyridines ; Signal Transduction ; Tumor Necrosis Factor-alpha ; Umbilical Veins ; Vascular Cell Adhesion Molecule-1 ; rho-Associated Kinases

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.
Continuous Positive Airway Pressure ; Humans ; Hypertension ; epidemiology ; Polysomnography ; Sleep Apnea, Obstructive ; epidemiology ; Snoring

Objective: To investigate the effect of interleukin-8 (IL-8) on survival and apoptosis of hypoxic human umbilical vein endothelial cells (HUVECs) with its mechanisms.
Methods: Hypoxic HUVECs were induced by CoCl2. HUVECs were cultured with different concentrations of CoCl2 or IL-8 and the survival rates of HUVECs were examined. Normal or hypoxic HUVECs were incubated with IL-8 or simultaneously incubated with anti-IL-8 or Akt inhibitor LY294002 for 48h. The HUVECs survival rate was detected by MTT method, apoptosis rate was measured by Annexin V-FITC/PI method, the protein expressions of Caspase-3, phosphorylated Akt (pAkt) and GSK-3βser9 (pGSK-3βser9) were evaluated by Western blot analysis.
Results: By 12 h incubation with low concentration of CoCl2 (50, 100 μmol/L), HUVECs proliferation were improved, P<0.01; while by 24h and 48 h incubation with high concentration of CoCl2 (200, 400 μmol/L) HUVECs survival were decreased. By 48h and 72h incubation with IL-8 at (10, 50, 100 ng/ml), the hypoxia induced cell apoptosis was decreased and the survival was increased,P<0.01. IL-8 at 10 ng/ml may obviously inhibit the normal and hypoxic HUVECs apoptosis, down-regulate caspase-3 and up-regulate pAkt and pGSK-3βser9 expressions in HUVECs,P<0.01, while the above effects could be reversed by LY294002 and anti-IL-8,P<0.01.
Conclusion: IL-8 could down-regulate caspase-3 and up-regulate pAkt and pGSK-3βser9 expressions in HUVECs and therefore, inhibit the apoptosis and improve the survival of hypoxic HUVECs.

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.
Biomarkers ; blood ; Case-Control Studies ; Enzyme-Linked Immunosorbent Assay ; Humans ; MicroRNAs ; blood ; Myocardial Infarction ; pathology ; Placenta Growth Factor ; Pregnancy Proteins ; blood ; Prognosis

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.
Cardiac Surgical Procedures ; Coronary Sinus ; Heart Valve Prosthesis Implantation ; Humans ; Pacemaker, Artificial ; Tricuspid Valve