Association of cardiometabolic multimorbidity with all-cause and cardiovascular disease mortality among Chinese hypertensive patients

BACKGROUND Hypertension usually clusters with multiple comorbidities.However,the association between cardiometabolic multimorbidity(CMM)and mortality in hypertensive patients is unclear.This study aimed to investigate the association between CMM and all-cause and cardiovascular disease(CVD)mortality in Chinese patients with hypertension.METHODS The data used in this study were from the China National Survey for Determinants of Detection and Treatment Status of Hypertensive Patients with Multiple Risk Factors(CONSIDER),which comprised 5006 participants aged 19–91 years.CMM was defined as the presence of one or more of the following morbidities:diabetes mellitus,dyslipidemia,chronic kidney disease,coronary heart disease,and stroke.Cox proportional hazard models were used to calculate the hazard ratios(HR)with 95%CI to determine the association between the number of CMMs and both all-cause and CVD mortality.RESULTS Among 5006 participants[mean age:58.6±10.4 years,50%women(2509 participants)],76.4%of participants had at least one comorbidity.The mortality rate was 4.57,4.76,8.48,and 16.04 deaths per 1000 person-years in hypertensive patients without any comorbidity and with one,two,and three or more morbidities,respectively.In the fully adjusted model,hypertensive participants with two cardiometabolic diseases(HR=1.52,95%CI:1.09–2.13)and those with three or more cardiometabolic diseases(HR=2.44,95%CI:1.71–3.48)had a significantly elevated risk of all-cause mortality.The findings were similar for CVD mortality but with a greater increase in risk magnitude.CONCLUSIONS In this study,three-fourths of hypertensive patients had CMM.Clustering with two or more comorbidities was associated with a significant increase in the risk of all-cause and cardiovascular mortality among hypertensive patients,suggesting more intensive treatment and control in this high-risk patient group.

TrkA regulates the regenerative capacity of bone marrow stromal stem cells in nerve grafts

We previously demonstrated that overexpression of tropomyosin receptor kinase A(TrkA)promotes the survival and Schwann celllike differentiation of bone marrow stromal stem cells in nerve grafts,thereby enhancing the regeneration and functional recovery of the peripheral nerve.In the present study,we investigated the molecular mechanisms underlying the neuroprotective effects of TrkA in bone marrow stromal stem cells seeded into nerve grafts.Bone marrow stromal stem cells from Sprague-Dawley rats were infected with recombinant lentivirus vector expressing rat TrkA,TrkA-shRNA or the respective control.The cells were then seeded into allogeneic rat acellular nerve allografts for bridging a 1-cm right sciatic nerve defect.Then,8 weeks after surgery,hematoxylin and eosin staining showed that compared with the control groups,the cells and fibers in the TrkA overexpressing group were more densely and uniformly arranged,whereas they were relatively sparse and arranged in a disordered manner in the TrkA-shRNA group.Western blot assay showed that compared with the control groups,the TrkA overexpressing group had higher expression of the myelin marker,myelin basic protein and the axonal marker neurofilament 200.The TrkA overexpressing group also had higher levels of various signaling molecules,including TrkA,pTrkA(Tyr490),extracellular signal-regulated kinases 1/2(Erkl/2),pErk1/2(Thr202/Tyr204),and the anti-apoptotic proteins Bcl-2 and Bcl-xL.In contrast,these proteins were downregulated,while the pro-apoptotic factors Bax and Bad were upregulated,in the TrkA-shRNA group.The levels of the TrkA effectors Akt and pAkt(Ser473)were not different among the groups.These results suggest that TrkA enhances the survival and regenerative capacity of bone marrow stromal stem cells through upregulation of the Erk/Bcl-2 pathway.All procedures were approved by the Animal Ethical and Welfare Committee of Shenzhen University,China in December 2014(approval No.AEWC-2014-001219).

钴互连化学机械抛光浆料中的界面腐蚀行为研究

芯片互连层进行化学机械抛光(CMP)时,抛光液对互连金属的腐蚀问题是影响抛光后表面质量的重要因素。本文在含有氧化剂过硫酸钾(KPS)、络合剂甘氨酸(Gly)和缓蚀剂苯骈三氮唑(BTA)的抛光液体系中,对互连金属钴的界面腐蚀行为进行了研究。结果显示,强氧化剂KPS在互连层抛光液中并不能使钴表面形成稳定钝化,需要进一步引入BTA以抑制过度腐蚀。静态腐蚀实验和扫描电子显微镜观察显示,BTA能有效地降低钴在抛光液中的腐蚀,提高表面质量,电化学测试计算出其缓蚀效率最高可达99.02%。电化学阻抗谱和X射线光电子能谱揭示了腐蚀过程机理:Gly的加入可以溶解钴表面的二价及三价氧化物,破坏KPS形成的钝化层,BTA的引入会大幅增加电化学腐蚀过程的电荷转移电阻,从而抑制抛光液对钴的腐蚀。