Progressing from acute kidney injury (AKI) to chronic kidney disease (CKD) is acknowledged as a significant clinical challenge. Our recent works indicated that PR domain-containing 16 (PRDM16) impedes the progression of AKI and DKD. Nonetheless, the specific function and regulatory mechanism of PRDM16 during the AKI to CKD transition remain incompletely understood. In this investigation, it was identified that PRDM16 mitigates TGF-β1-induced renal tubulointerstitial fibrosis in BUMPT cells. From a mechanistic perspective, PRDM16 was found to enhance the expression of eif6, which subsequently suppressed TGF-β, CTGF, and NLRP3 levels via the suppression of the Wnt/β-catenin/SP1 signaling cascade. Additionally, knock-in of PRDM16 in kidney proximal tubules resulted in increased expression of eIF6, thereby restraining the stimulation of the Wnt/β-catenin/SP1 pathway, reducing the production of TGF-β, CTGF, and NLRP3, and consequently limiting renal tubulointerstitial fibrosis progression in both unilateral ureteral obstruction and ischemia-reperfusion-injury mouse models.Moreover, overexpression of PRDM16 following ischemia-induced AKI was shown to attenuate renal tubulointerstitial fibrosis and the eIF6/Wnt/β-catenin/SP1/TGF-β, CTGF, and NLRP3 axis. Finally, the PRDM16/eIF6/Wnt/β-catenin/SP1/TGF-β, CTGF, and NLRP3 axis were analyzed in renal biopsies from individuals with minimal change disease and severe obstructive nephropathy. Collectively, these findings indicate that PRDM16-mediated eIF6 induction serves to impede the transition from AKI to CKD by suppressing the Wnt/β-catenin/SP1/TGF-β, CTGF, and NLRP3 axis.

Currently, evidence concerning the link between maximal aortic diameter and in-hospital mortality in cases of acute type B aortic dissection (ATBAD) is insufficient. Thus, this study aimed to explore the relationship between the maximal aortic diameter at the time of admission and the early prognosis of patients diagnosed with ATBAD. A total of 678 patients with ATBAD were included between January 2016 and December 2018, during which their clinical data was gathered. The independent variable analyzed was the maximal diameter of the aorta, while the dependent variable was mortality during hospitalization. Factors considered in this analysis included the patients' age, gender, body mass index (BMI), medical history of hypertension, stroke, diabetes, atherosclerosis, smoking habits, chronic kidney insufficiency, time until presentation, systolic and diastolic blood pressures, ejection fraction, presence of aortic regurgitation, symptoms, involvement of abdominal vessels, laboratory findings, and treatment approaches. Of these patients collected, the mean age was 56.03 +/- 12.22 years, and approximately 82.45% of them were male. After analysis, it was found that the maximal aortic diameter of patients with ATBAD was positively correlated with in-hospital mortality (OR = 1.06, 95% CI 1.03 to 1.10). Surprisingly, a J curve relationship was detected between maximal aortic diameter (point 31 mm) and in-hospital death for patients with ATBAD. The effect sizes and confidence intervals of the right (maximal aortic diameter > 31 mm) and left (maximal aortic diameter <= 31 mm) aspects of the inflection point were 1.06 (1.02-1.11) and 1.03 (0.83-1.28), respectively. In addition, the stratified analysis showed a stable relationship between maximal aortic diameter and in-hospital mortality, while there was no significant difference in the interaction between different subgroups. In patients with ATBAD, a J-curve relationship was identified between the maximal aortic diameter and in-hospital mortality. Specifically, when the maximal aortic diameter exceeds 31 mm, a positive correlation with in-hospital death was observed.

LncRNAs are reported to participate in multiple biological and pathological processes, including renal fibrosis due to obstructive nephropathy. However, the function and mechanisms of each lncRNA in this context differ. In this study, we created a fibrosis model in vitro using TGF-β1 treatment and in vivo through unilateral ureteral obstruction. We demonstrated that lncRNA6524 expression increased in both models, as confirmed by qPCR. Additionally, we discovered that lncRNA6524 mediates the TGF-β1-induced accumulation of extracellular matrix (ECM) proteins in BUMPT cells. We investigated the mechanism using dual luciferase reporter assays, immunofluorescence, and qPCR. Our results indicate that lncRNA6524 acts as a sponge for miR-92a-2-5p, promoting renal fibrosis by upregulating the Dvl1/Wnt/β-catenin signaling pathway. In summary, our findings demonstrate a linear regulatory relationship among lncRNA6524, miR-92a-2-5p, and the Dvl1/Wnt/β-catenin axis in renal epithelial cells during kidney obstruction. This highlights a new potential target for treating obstruction-related renal fibrosis.

AIMS:Studies on objectively measured physical activity (PA) have investigated acute cardiovascular outcomes but not cardiac arrest (CA). Our study aimed to investigate the dose-response relationship between accelerometer-measured PA and CA by intensity of PA. METHODS AND RESULTS:This prospective cohort study included 98 893 UK Biobank participants whose PA data were measured using wrist-worn accelerometers. Total PA volume was measured using the average overall acceleration. Minutes per week of light PA (LPA), moderate PA (MPA), and vigorous PA (VPA) were recorded. The incident CA was identified using diagnostic codes linked to hospital encounters and death records. Cox proportional hazard models with restricted cubic splines were used to study the associations, including sex differences. During the follow-up period (median: 7.31 years; interquartile range: 6.78-7.82 years), 282 incident CAs (0.39 per 1000 person-years) occurred. Total PA was inversely related to CA risk. The CA risk decreased sharply until the time spent in MPA or VPA reached ∼360 min or 20 min per week, respectively, after which it was relatively flat. The LPA was not associated with CA risk. Subgroup analyses showed a more pronounced association between PA and a reduced risk of CA in women compared to men. CONCLUSION:Accelerometer-measured PA, particularly MPA and VPA, was associated with a lower CA risk. Furthermore, a stronger association was observed in women than men.

The pathogenesis of Diabetic kidney disease(DKD) involves pathological changes in both tubulo-interstitium and the glomerulus. Surprisingly, tubulo-interstitial fibrosis (TIF), does not develop significantly until the late stage of DKD. Here, it is demonstrated that PR domain-containing 16 (PRDM16) is a key to the low level of TIF in DKD. In the experiments, PRDM16 is upregulated in high glucose-treated renal tubular cells, DKD mouse kidneys, and renal biopsy of human DKD patients via activation of NF-κB signal pathway. High glucose-induced expression of fibrotic proteins in renal tubular cells is suppressed by PRDM16. Mechanistically, PRDM16 bound to the promotor region of Transient receptor potential ankyrin 1 (TRPA1) to transactivate its expression and then suppressed MAPK (P38, ERK1/2) activation and downstream expression of TGF-β1. Knockout of PRDM16 from kidney proximal tubules in mice blocked TRPA1 expression and enhanced MAPK activation, TGF-β1 production, TIF development, and DKD progression, whereas knock-in of PRDM16 has opposite effects. In addition, overexpression of PRDM16 or its induction by formononetin ameliorated renal dysfunction and fibrosis in db/db diabetic mice. Finally, the above finding are detected in renal biopsies of DKD patients. Together, these results unveil PRDM16/TRPA1 as the mechanism responsible for the low level of TIF in the early stage of DKD by suppressing and TGF-β1 expression.

Several studies have reported that long non-coding RNAs (LncRNAs) were associated with the progression of acute kidney injury (AKI). However, the role and regulation mechanism of lncRNA122049 in ischemic AKI remains unknown. In the present study, we found that lncRNA 122049 protected against the ischemia/reperfusion (I/R) induced apoptosis in BUMPT cells. Mechanistically, the lncRNA 122049 directly sponged miR-330-5p, then increased the expression of ELK1(ETS transcription factor ELK1) to decrease renal cell apoptosis. In addition, miR-330-5p inhibitor completely reversed the pro-apoptotic effect of LncRNA 122049 siRNA on I/R-induced BUMPT cells apoptosis. Finally, overexpression of lncRNA 122049 attenuated ischemic mice AKI via targeting of the miR-330-5p/ELK1 axis. Collectively, the data demonstrated that LncRNA 122049 prevented the I/R-induced renal cell apoptosis via regulation of the miR-330-5p/ELK1 axis, which brings new insights into the pathogenesis and potential targeted treatment of ischemic AKI.

Apoptosis of alveolar epithelial cells is a critical initial link in the pathogenesis of acute lung injury (ALI), recent studies have revealed that Methyl-CpG binding domain protein 2 (MBD2) was involved in the execution of apoptosis, yet its role in ALI remained unclear. In the present study, we aim to explore the role and mechanism of MBD2 in the pathogenesis of ALI. We have found that MBD2 expression, in parallel to apoptosis, increased in alveolar epithelial cells of mice treated with LPS, knockout of MBD2 reduced apoptosis and protected mice from LPS-induced ALI. In MLE-12 cells, a cell line of murine alveolar epithelial cells, LPS induced MBD2 expression and apoptosis in a dose- and time-dependent manner. Knockdown of MBD2 with shRNA alleviated, while overexpression of MBD2 increased LPS-induced apoptosis. Mechanistically, intracellular zinc level decreased when MLE-12 cells were treated with LPS. MBD2 knockdown restored intracellular zinc level after LPS treatment, and MBD2 overexpression further aggravated LPS-induced intracellular zinc loss. Metal transcription factor 1 (MTF1) is a critical transcription factor in charge of intracellular zinc efflux. LPS treatment induced MTF1 expression both in vivo and in vitro. Inhibition of MTF1 reduced LPS-induced apoptosis in MLE-12 cells. MBD2 could bind to the promoter region of MTF1 and promote MTF1 expression. Collectively, these data indicated that loss of MBD2-ameliorated LPS-induced alveolar epithelial cell apoptosis and ALI in mice via modulating intracellular zinc homeostasis by upregulating MTF1.

Previous studies reported that RAGE participated in the process of kidney fibrosis, but the function and regulation pathway of RAGE in proximal tubular cells in this process remains unclear. Here, we found that expression of RAGE was increased by TGF-β1 treatment and unilateral ureteral obstruction (UUO). Knock down of RAGE ameliorated renal fibrosis by TGF-β1 treatment, the expression of vimentin, Collagen I&III, and fibronectin are decreased. Mechanistically, RAGE mediated TGF-β1-induced phosphorylation of Stat3 and directly upregulated the Atg7 to increase the level of autophagy, and ultimately resulting in renal fibrosis. Furthermore, PT-RAGE-KO mice reduced kidney fibrosis in UUO model via inhibiting Stat3/Atg7 axis by knocking down RAGE. Furthermore, the above findings were confirmed in kidney of patients with obstructive nephropathy. Collectively, RAGE in proximal tubular cells promotes the autophagy to increase renal fibrosis via upregulation of Stat3/Atg7 axis.

In this study, we investigated the role of circular RNA_30032 (circRNA_30032) in renal fibrosis and the underlying mechanisms. The study was carried out using TGF-β1-induced BUMPT cells and unilateral ureteral obstruction (UUO)-induced mice, respectively, as in vitro and in vivo models. CircRNA_30032 expression was significantly increased by 9.15- and 16.6-fold on days 3 and 7, respectively, in the renal tissues of UUO model mice. In TGF-β1-treated BUMPT cells, circRNA_30032 expression was induced by activation of the p38 mitogen-activated protein kinase signaling pathway. Quantitative real-time PCR, western blotting and dual luciferase reporter assays showed that circRNA_30032 mediated TGF-β1-induced and UUO-induced renal fibrosis by sponging miR-96-5p and increasing the expression of profibrotic proteins, including HBEGF, KRAS, collagen I, collagen III and fibronectin. CircRNA_30032 silencing significantly reduced renal fibrosis in UUO model mice by increasing miR-96-5p levels and decreasing levels of HBEGF and KRAS. These results demonstrate that circRNA_30032 promotes renal fibrosis via the miR-96-5p/HBEGF/KRAS axis and suggest that circRNA_30032 is a potential therapeutic target for treatment of renal fibrosis.

目的 探讨胆碱酯酶、乳酸对脓毒症患者病情严重程度及预后的评估作用.方法 选择2018年1月至2018年12月入住中南大学湘雅二医院急诊ICU的86例脓毒症患者,根据患者病情的严重程度将86例患者分为脓毒症组(62例)和脓毒性休克组(24例);再根据患者28 d生存情况将86例患者分为存活组(57例)和死亡组(29例).记录所有患者的年龄、性别、生命体征、呼吸机使用情况、血管活性药物使用情况、胆碱酯酶、乳酸、急性病生理学和长期健康评价(APACHE)Ⅱ评分、序贯器官衰竭估计(SOFA)评分及28 d预后情况.采用多因素Logistic回归分析影响脓毒症患者病情严重程度及预后的危险因素;绘制受试者工作特征(ROC)曲线,分析胆碱酯酶、乳酸评估脓毒症患者病情严重程度及预后的价值.结果 脓毒症组患者胆碱酯酶水平[3897.30(2970.70,4760.15)U/L vs.2718.05(2080.25,3182.05)U/L]显著高于脓毒性休克组患者,而乳酸水平[2.09(1.15,2.99)mmol/L vs.3.00(2.10,7.00)mmol/L]、APACHEⅡ评分[9.00(6.00,15.00)分vs.15.50(9.00,19.75)分]及SOFA评分[4.00(2.00,7.50)分vs.9.50(6.25,13.75)分]均显著低于脓毒性休克组患者(P均<0.05).存活组患者胆碱酯酶水平[(3933±1484)U/L vs.(2678±756)U/L]显著高于死亡组患者,而乳酸水平[2.14(1.24,2.98)mmol/L vs.4.55(1.72,12.13)mmol/L]、APACHEⅡ评分[9.00(6.00,14.50)分vs.17.50(15.00,19.75)分]及SOFA评分[5.00(2.50,8.50)分vs.10.50(7.50,13.75)分]均显著低于死亡组患者(P均<0.05).将胆碱酯酶、乳酸、APACHEⅡ评分及SOFA评分纳入多因素Logistic回归分析,结果显示,胆碱酯酶是脓毒症患者病情严重程度及预后的保护因素,而乳酸、APACHEⅡ评分及SOFA评分则是脓毒症患者严重程度及预后的独立危险因素(P均<0.05).ROC曲线结果显示,胆碱酯酶、乳酸、胆碱酯酶联合乳酸、APACHEⅡ评分及SOFA评分均对脓毒症病情的严重程度及预后具有预测价值(P均<0.05).结论 胆碱酯酶和乳酸对脓毒症患者病情的严重程度及预后均具有预测价值,可协助临床医生做出准确、快速的判断.

The prediction of mortality for septic acute kidney injury (AKI) has been assessed by a number of potential biomarkers, including long noncoding RNAs (lncRNAs). However, the validation of lncRNAs as biomarkers, particularly for the early stages of septic AM, is still warranted. Our results indicate that the lncRNA TCONS_00016233 is upregulated in plasma of sepsis-associated non-AKI and AKI patients, but a higher cutoff threshold (9.5 x 10(5), copy number) provided a sensitivity of 71.9% and specificity of 89.6% for the detection of AKI. The plasma TCONS_00016233 was highly correlated with serum creatinine, tissue inhibitor metalloproteinase-2 (TIMP-2), insulin-like growth factor binding protein-7 (IGFBP7), interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), C-reactive protein (CRP), and urinary TCONS_00016233. Lipopolysaccharide (LPS) induced the expression of lncRNA TCONS_00016233 via the Toll-like receptor 4 (TLR4)/p38 mitogen-activated protein kinase (MAPK) signal pathway in human renal tubular epithelial (HK-2) cells. Furthermore, TCONS_00016233 mediates the LPS-induced HK-2 cell apoptosis and the expression of IL-1 beta and TNF-alpha. Mechanistically, TCONS_00016233 acts as a competing endogenous RNA (ceRNA) to prevent microRNA (miR)-22-3p-mediated downregulation of the apoptosisinducing factor mitochondrion-associated 1 (AIFM1). Finally, overexpression of TCONS_00016233 is capable of aggravating the LPS- and cecal ligation and puncture (CLP)-induced septic AKI by targeting the miR-22-3p/AIFM1 axis. Taken together, our data indicate that TCONS_00016233 may serve as an early diagnosis marker for the septic AM, possibly acting as a novel therapeutic target for septic AKI.

Our previous study demonstrated that the methyl-CpG-binding domain protein 2 (MBD2) mediates vancomycin (VAN)-induced acute kidney injury (AKI). However, the role and regulation of MBD2 in septic AKI are unknown. Herein, MBD2 was induced by lipopolysaccharide (LPS) in Boston University mouse proximal tubules (BUMPTs) and mice. For both in vitro and in vivo experiments, we showed that inhibition of MBD2 by MBD2 small interfering RNA (siRNA) and MBD2-knockout (KO) substantially improved the survival rate and attenuated both LPS and cecal ligation and puncture (CLP)-induced AKI, renal cell apoptosis, and inflammatory factor production. Global genetic expression analyses and in vitro experiments suggest that the expression of protein kinase C eta (PKCη), caused by LPS, is markedly suppressed in MBD2-KO mice and MBD2 siRNA, respectively. Mechanistically, chromatin immunoprecipitation (ChIP) analysis indicates that MBD2 directly binds to promoter region CpG islands of PKCη via suppression of promoter methylation. Furthermore, PKCη siRNA improves the survival rate and attenuates LPS-induced BUMPT cell apoptosis and inflammatory factor production via inactivation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK)1/2, which were further verified by PKCη siRNA treatment in CLP-induced AKI. Finally, MBD2-KO mice exhibited CLP-induced renal cell apoptosis and inflammatory factor production by inactivation of PKCη/p38MAPK and ERK1/2 signaling. Taken together, the data indicate that MBD2 mediates septic-induced AKI through the activation of PKCη/p38MAPK and the ERK1/2 axis. MBD2 represents a potential target for treatment of septic AKI.

Several studies have suggested that long intergenic noncoding RNAs are involved in the progression of diabetic nephropathy (DN). However, the exact role and regulatory mechanism of long noncoding RNA (lncRNA) NR_038323 in diabetic nephropathy (DN) remain largely unclear. In the present study, we found that lncRNA NR_038323 overexpression ameliorated the high glucose (HG)-induced expression levels of collagen I, collagen IV, and fibronectin, whereas lncRNA NR_038323 knockdown exerted the opposite effects. Moreover, the results of bioinformatic prediction, luciferase assay, and fluorescence in situ hybridization (FISH) demonstrated that lncRNA NR_038323 directly interacted with miR-324-3p. Additionally, miR-324-3p mimic aggravated the HG-induced expression levels of collagen I, collagen IV, and fibronectin by dual-specificity protein phosphatase-1 (DUSP1) expression to activate p38 mitogen-activated protein kinase (MAPK) and ERK1/2 pathways. In contrast, overexpression of DUSP1 attenuated the HG-induced expression levels of collagen I, collagen IV, and fibronectin via inactivation of p38 MAPK and ERK1/2 pathways. In addition, lncRNA NR_038323 knockdown increased the expression levels of collagen I, collagen IV, and fibronectin by upregulating DUSP1 expression during HG treatment, which were markedly reversed by miR-324-3p inhibitor. Furthermore, these molecular changes were verified in the human kidney samples of DN patients. Finally, overexpression of lncRNA NR_038323 ameliorated the interstitial fibrosis in STZ-induced diabetic nephrology (DN) rat via miR-324-3p/DUSP1/p38MAPK and ERK1/2 axis. In conclusion, our data indicate that overexpression of lncRNA NR_038323 may suppress HG-induced renal fibrosis via the miR-324-3p/DUSP1/p38MAPK and ERK1/2 axis, which provides new insights into the pathogenesis of DN.

Despite DNA methylation occurred in acute kidney injury (AKI), how it influenced progression of AKI remains unclear. Methyl-CpG-binding domain protein 2 (MBD2), a protein readers of methylation, was used to analyze the impact of DNA methylation on vancomycin (VAN)-induced AKI. Here, in cultured human kidney tubular epithelial cells (HK-2), we show that knockdown of MBD2 by siRNA attenuated VAN-induced apoptosis, caspase activity, and the expression of BAX and cleaved caspase 3. Interestingly, knockdown of MBD2 by siRNA was associated with the suppression of miR-301a-5p. Mechanistic studies confirmed MBD2 binds to these methylated CpG elements of miR-301a-5p promoter, and then activates miR-301a-5p promoter by suppressing methylation. Furthermore, anti-miR-301a-5p significantly blocked VAN-induced apoptosis and caspase activity in HK-2 cells, which was accompanied by downregulation of p53, and upregulation of MITF, HDGF and MDM-4 together. The latter genes were further identified as target genes of miR-301a-5p, and silencing of MDM-4 promoted p53 accumulation. In vivo, mice with MBD2 knockout (MBD2-KO) were counteracted to VAN-induced AKI, indicated by the analysis of renal function, histology, apoptosis and inflammation. MBD2-KO also significantly suppressed the expression of miR-301a-5p, p53, BAX and cleaved caspase 3, and restored the expression of MDM-4, MITF and HDGF. Finally, in vivo inhibition of miR-301a-5p also ameliorated VAN-induced AKI. Together, these results show the novel MBD2/miR-301a-5p/MITF, HDGF and MDM-4/p53 pathway in VAN-induced AKI.

Objective To investigate the clinical features of aortic dissection (AD) and emergency treatments. Methods Data from 784 patients with aortic dissection were collected in the Department of Emergency from January 2000 through December 2009. A retrospective analysis was carried out to determine the survival rate, mortality rate and treatment efficiency. Results Pain was the most common onset symptom (77.7% , 609/784). The majority of patients (86.5%) had essential hypertension (678/784). All the patients with preoperative diagnosis of aortic dissection underwent emergency medical intervention by internists resulting in 81.5% survival rate (639/784) and 18.5% mortality rate (145/784). There were 157 patients without improvement (20.0% ) and the total efficiency rate was (83. 1% ). The efficiency rate of conventional treatment was 76.4% , while the efficiency rate of triple four-procedure treatment was 89. 8% (P<0.05). Of them, 139 patients (17. 7% ) died in the hospital. Among them,. 26 patients died within 24 hours (18.4% ) and 47 cases died within 48 hours (33. 8% ) and 66 patients died within 72 hours (47.2% ). There were 92 patients who refused treatments after diagnosis, and among them, 81 patients died within 72 hours (88.04% ). The difference in mortality rate between two groups was significant (P<0.05). Conclusions The diagnosis of aortic dissection depends on detailed history, physical examination and CT or MRI imaging. Analgesia, sedation and control of blood pressure are essential for emergency treatments. Early diagnosis and effective emergency treatments are the critical strategy for the early surgical intervention and time window for further treatment to improve the survival rate of AD.

Objective To study the therapy efficacy of basic and further life support recommended in the 2005 international cardiopulmonary resuscitation guide. Methods A total of 386 patients with cardiac arrest admitted to the emergency department of our hospital from September 2007 to September 2009 were randomly divided into control group (group A,n=196) and observation group (group B,n=190). Patients in group A were treated following the 2005 international cardiopulmonary resuscitation guide. Patients in group B were treated following the improved 2005 international cardiopulmonary resuscitation guide. In brief,mentality→respiration→position→open airway→artificial circulation→artificial respiration (artificial circulation/artificial respiration=30/2)were assessed with the traditional ABC adjusted to ACB during basic life support. A cardiopulmonary resuscitation group including 2 physicians and 3 nurses was established to use resuscitation drugs following the improved 2005 international cardiopulmonary resuscitation guide,complete electric defibrilation within 1 min and endotracheal intubation within 3 min,etc. Autonomous circulation and respiration recovery rate and time,24 h survival rate and survival rate after discharge were recorded in patients of two groups. Results The autonomous circulation and respiration recovery rates were higher in group A than in group B (15.82% and 26.84% vs 14.80% and 25.26%,P<0.05). The autonomous circulation recovery time was 12.38±3.96 min and 7.52±2.87 min respectively in groups A and B. The autonomous respiration recovery time was longer in group A than in group B group (152.70±10.80 min vs 76.56±8.29 min). The 24h survival rate and the survival rate after discharge were higher in group B than in group A(15.82% vs 26.84%,13.27% vs 21.58%,P<0.05). Conclusion The improved 2005 international cardiopulmonary resuscitation guide can significantly increase the autonomous circulation and respiration recovery rate,the 24 h survival rate and the survival rate after discharge,and shorten the autonomous circulation and respiration recovery time during cardiopulmonary resuscitation compared with the 2005 international cardiopulmonary resuscitation guide.

BACKGROUND:Bone morphogenetic protein-2 (BMP-2) plays a key role both in vascular development and pathophysiological processes. However, the effects of oxidized low-density lipoprotein (ox-LDL) combined with atorvastatin on BMP-2 expression are entirely unknown in human umbilical vein endothelial cells (HUVECs). The present study investigates the effects of ox-LDL on BMP-2 expression. Furthermore, the influence of atorvastatin on ox-LDL-induced BMP-2 expression is also examined.METHODS AND RESULTS:The HUVECs were treated by ox-LDL or combined with pyrrolidine dithiocarbamate (PDTC) or atorvastatin. The expression level of BMP-2 mRNA was examined by real-time PCR and RT-PCR analysis. The expression of BMP-2 protein was assayed by enzyme-linked immunosorbent assay. The malondialdehyde (MDA) and activities of total superoxide dismutase (SOD) were detected by routine methods. The activation of nuclear factor kappaB (NF-kappaB) in HUVECs was determined using an assay kit from active motif and western blot analysis. Ox-LDL treatment significantly increased BMP-2 expression, which is associated with NF-kappaB activation, but BMP-2 expression was suppressed by treatment with PDTC or atorvastatin. Furthermore, the increase in MDA levels and decrease in activities of total SOD caused by ox-LDL treatment were reversed by the treatment of PDTC or atorvastatin.CONCLUSIONS:Ox-LDL-induced BMP-2 expression was suppressed by PDTC or atorvastatin treatment. The effects of atorvastatin might contribute to the mechanisms by inhibiting NF-kappaB activation.

Objective To compare the clinical effect of mask ventilation and intubation ventilation in cardiopulmonary resuscitation.Methods We observed 43 patients using balloon mask ventilation and 35 using intubation ventilation in cardiopulmonary resuscitation,and compared,between the two groups,the time of receiving timely oxygen supply after cardiopalmus and respiration arrest,the rate and the required time of oxygen saturation(SaO3) rising up to more than 85% after rescue,and anti-flow rate of stomach contents and successful rate of cardiopulmonary resuscitation.Results There was significant difference in time of timely oxygen supply,the required time of SaO285% and anti-flow rate of stomach contents between two groups(P0.01),and no significant difference was noted in rate of SaO285% and successful rate of recovery between them(P0.05).Conclusion Each method of ventilation has advantages and disadvantages,and can be used at its discretion in actual operation.

[ABSTRACT] AIM To investigate the effects and the safety of extended-release niacin. METHODS Eighty-five patients with hyperlipidemia were randomly assigned into atorvastatin group (n = 42) and extended-release niacin group ( n = 43) . They were treated with atorvastatin and extended-release niacin, 10 mg·d-1 and 500 mg·d-1,respectively for 4 wk. Lipid profile and physical laboratory investigations for adverse drug reactions were also assessed. Serum levels of total cholesterol (TC), triglyceride (TG),low density lipoprotein cholesterol ( LDL-C ) , high density lipoprotein cholesterol ( HDL-C ) and a-lipoprotein were measured at the end of 4 wk of the trial period. RESULTS Extended-release niacin treatment was more effective than atorvastatin in reducing serum levels of TC, TG, LDL-C and a-lipoprotein and in raising HDL-C. Extended-release niacin group had more adverse drug reactions than atorvastatin group during the period of treatment,while most of patient's tolerance was good in both groups. CONCLUSION①Extended-release niacin has full-scale lipid-regulating effects , especially in reducing serum levels of TG and a-lipoprotein and raising HDL-C.②Extended-release niacin has more flushing and gastrointestinal symptoms than atorvastatin , but it is also safe.