Expression of Nemo-Like Kinase (NLK) in the Brain in a Rat Experimental Subarachnoid Hemorrhage Model

This study aimed to investigate the expression of the Nemo-like kinase (NLK) in the brain after experimental subarachnoid hemorrhage (SAH) in rats. A total of 90 rats were randomly divided into six groups: control group, day 1, day 3, day 5, day 7, and day 14. Day 1, day 3, day 5, day 7, and day 14 groups were all SAH groups in which the rats were killed on days 1, 3, 5, 7, and 14, respectively. In SAH groups, autologous arterial blood was injected into cisterna magna once on day 0. Cross-sectional area of basilar artery was measured by H&E staining. Immunostaining and immunoblotting experiments were performed to detect the expression of NLK protein. Real-time polymerase chain reaction was used to analyze the presence and quantity of NLK mRNA. The level of oxidative stress in the artery was also measured. The basilar arteries exhibited vasospasm after SAH and became the most severe on day 3. The expressions of NLK protein and mRNA were decreased remarkably in SAH groups compared with the control group. The down-regulated expression of NLK was detected after SAH and the low ebb was on day 3, which was oppositely the peak time of oxidative stress. The expression of NLK was present mainly in the neurons in the brain and smooth muscle cells in the basilar artery. NLK is decreasingly expressed in an opposite time-course to the development of cerebral vasospasm (CVS) and SAH-induced brain injury in this rat experimental model of SAH and these findings might have important implications during the administration of specific NLK agonist to prevent or reduce CVS or neuronal apoptosis caused by SAH.     

Vascular progenitor cell senescence in patients with Marfan syndrome

Vascular progenitor cells (VPCs) present in the adventitia of the vessel wall play a critical role in the regulation of vascular repair following injury. This study aimed to assess the function of VPCs isolated from patients with Marfan syndrome (MFS). VPCs were isolated from control and MFS donors and characterized. Compared with control‐VPCs, MFS‐VPCs exhibited cellular senescence as demonstrated by increased cell size, higher SA‐β‐gal activity and elevated levels of p53 and p21. RNA sequencing showed that several cellular process‐related pathways including cell cycle and cellular senescence were significantly enriched in MFP‐VPCs. Notably, the expression level of TGF‐β1 was much higher in MFS‐VPCs than control‐VPCs. Treatment of control‐VPCs with TGF‐β1 significantly enhanced mitochondrial reactive oxidative species (ROS) and induced cellular senescence whereas inhibition of ROS reversed these effects. MFS‐VPCs displayed increased mitochondrial fusion and decreased mitochondrial fission. Treatment of control‐VPCs with TGF‐β1 increased mitochondrial fusion and reduced mitochondrial fission. Nonetheless, treatment of mitofusin2 (Mfn2)‐siRNA inhibited TGF‐β1‐induced mitochondrial fusion and cellular senescence. Furthermore, TGF‐β1‐induced mitochondrial fusion was mediated by the AMPK signalling pathway. Our study shows that TGF‐β1 induces VPC senescence in patients with MFS by mediating mitochondrial dynamics via the AMPK signalling pathway.     

GhL1L1 affects cell fate specification by regulating GhPIN1‐mediated auxin distribution

Auxin is as an efficient initiator and regulator of cell fate during somatic embryogenesis (SE), but the molecular mechanisms and regulating networks of this process are not well understood. In this report, we analysed SE process induced by Leafy cotyledon1‐like 1 (GhL1L1), a NF‐YB subfamily gene specifically expressed in embryonic tissues in cotton. We also identified the target gene of GhL1L1, and its role in auxin distribution and cell fate specification during embryonic development was analysed. Overexpression of GhL1L1 accelerated embryonic cell formation, associated with an increased concentration of IAA in embryogenic calluses (ECs) and in the shoot apical meristem, corresponding to altered expression of the auxin transport gene GhPIN1. By contrast, GhL1L1‐deficient explants showed retarded embryonic cell formation, and the concentration of IAA was decreased in GhL1L1‐deficient ECs. Disruption of auxin distribution accelerated the specification of embryonic cell fate together with regulation of GhPIN1. Furthermore, we showed that PHOSPHATASE 2AA2 (GhPP2AA2) was activated by GhL1L1 through targeting the G‐box of its promoter, hence regulating the activity of GhPIN1 protein. Our results indicate that GhL1L1 functions as a key regulator in auxin distribution to regulate cell fate specification in cotton and contribute to the understanding of the complex process of SE in plant species.     

Diabetic HDL Is Dysfunctional in Stimulating Endothelial Cell Migration and Proliferation Due to Down Regulation of SR-BI Expression

Background

Diabetic HDL had diminished capacity to stimulate endothelial cell (EC) proliferation, migration, and adhesion to extracellular matrix. The mechanism of such dysfunction is poorly understood and we therefore sought to determine the mechanistic features of diabetic HDL dysfunction.

Methodology/Principal Findings

We found that the dysfunction of diabetic HDL on human umbilical vein endothelial cells (HUVECs) was associated with the down regulation of the HDL receptor protein, SR-BI. Akt-phosphorylation in HUVECs was induced in a biphasic manner by normal HDL. While diabetic HDL induced Akt phosphorylation normally after 20 minutes, the phosphorylation observed 24 hours after diabetic HDL treatment was reduced. To determine the role of SR-BI down regulation on diminished EC responses of diabetic HDL, Mouse aortic endothelial cells (MAECs) were isolated from wild type and SR-BI (−/−) mice, and treated with normal and diabetic HDL. The proliferative and migratory effects of normal HDL on wild type MAECs were greatly diminished in SR-BI (−/−) cells. In contrast, response to diabetic HDL was impaired in both types suggesting diminished effectiveness of diabetic HDL on EC proliferation and migration might be due to the down regulation of SR-BI. Additionally, SR-BI down regulation diminishes diabetic HDL’s capacity to activate Akt chronically.

Conclusions/Significance

Diabetic HDL was dysfunctional in promoting EC proliferation, migration, and adhesion to matrix which was associated with the down-regulation of SR-BI. Additionally, SR-BI down regulation diminishes diabetic HDL’s capacity to activate Akt chronically.     

自然保护区管理中生态与娱乐属性的权衡:一个选择实验的应用

随着自然保护区多样化的发展以及旅游需求的日益增长,保护区管理者面临着保护生态环境与满足娱乐需求的双重压力,这使得保护区管理者需要更多的信息进行决策。以中国东北部的扎龙国家级自然保护区为例,进行了一项选择实验,选取生物多样性、预期游客数量、景区的环境教育设施、门票价格等4个属性,分别采用多项logit模型、随机参数logit模型和潜在分类模型,探究游客在可能存在冲突的管理优先级之间的偏好。目的是揭示游客如何评价保护区不同的管理属性,以及各属性的边际支付意愿和偏好,并根据这些信息制定有效的保护区管理指南。研究结果表明生物多样性是保护区游客最关注的属性,并且游客对于生态属性的关注度高于娱乐属性。因此,保护区管理者应首先维持并改善生物多样性及其生态环境,在不破坏生态环境的基础上开发具有环境教育作用的娱乐服务。此外,研究发现游客可分为生态友好型和价格敏感型两种类别,不同类型的群体对游览保护区存在不同偏好,女性和年轻的受访者对生态更友好,男性和年长的受访者对价格更敏感。本文的贡献是将某一方面属性价值的描述扩展到涵盖多个管理属性的研究,并为保护区管理中生态与娱乐的权衡问题提供了更具体的见解。     

云南高黎贡山蚤类的生态区系

本文报道了１９８５年以来对我甸横断山南端高黎贡山东、西坡蚤类生态区系的调查及研究结果。共发现蚤类５科２３属４７种（亚种）。文中对该山脉蚤类在不同森林植物带的群落结构、种的多样性及均匀度,各种蚤的栖境幅度、宿主多样性进行了陈述和比较,并对蚤类的区系特征、特有种的区系划分等问题进行了讨论。     

滇金丝猴（Rhinopithecus bieti）食性的分析

由野外大猴群摄食行为观察、捕获个体摄食偏好度观察、它们粪便的显微鉴定及定量分析、消化能力测定和寄生虫鉴定等五方面证据汇聚的信息表明:滇金丝猴的主要食物是被子植物类型;而曾被误认为是其主食的冷杉等寒带裸子植物叶则几乎不是其食物。故滇金丝猴应更适应热带亚热带被子植物环境而非高山寒温带云冷杉植物群;故该种猴现代高山分布成因需深入研究。鉴于研究现状,本文特别把方法学问题提到一个不宜忽略的位置上。     

Lifetime risk of developing diabetes in Chinese people with normoglycemia or prediabetes: A modeling study

BackgroundLittle is known about the lifetime risk of progression to diabetes in the Asian population. We determined remaining lifetime risk of diabetes and life years spent with diabetes in Chinese people with normoglycemia and prediabetes.Methods and findingsUsing territory-wide diabetes surveillance data curated from electronic medical records of Hong Kong Hospital Authority (HA), we conducted a population-based cohort study in 2,608,973 individuals followed from 2001 to 2019. Prediabetes and diabetes were identified based on laboratory measurements, diagnostic codes, and medication records. Remaining lifetime risk and life years spent with diabetes were estimated using Monte Carlo simulations with state transition probabilities based on a Markov chain model. Validations were performed using several sensitivity analyses and modified survival analysis. External replication was performed using the China Health and Retirement Longitudinal Survey (CHARLS) cohort (2010 to 2015).The expected remaining lifetime risk of developing diabetes was 88.0 (95% confidence intervals: 87.2, 88.7)% for people with prediabetes and 65.9 (65.8, 65.9)% for people with normoglycemia at age 20 years. A 20-year-old person with prediabetes would live with diabetes for 32.5 (32.0, 33.1) years or 51.6 (50.8, 52.3)% of remaining life years, whereas a person with normoglycemia at 20 years would live 12.7 (12.7, 12.7) years with diabetes or 18.4 (18.4, 18.5)% of remaining life years. Women had a higher expected remaining lifetime risk and longer life years with diabetes compared to men. Results are subjected to possible selection bias as only people who undertook routine or opportunistic screening were included.ConclusionsThese findings suggest that Hong Kong, an economically developed city in Asia, is confronted with huge challenge of high lifetime risk of diabetes and long life years spent with diabetes, especially in people with prediabetes. Effective public health policies and targeted interventions for preventing progression to diabetes are urgently needed.

Xinge Zhang and colleagues estimate remaining lifetime risk of diabetes and life years spent with diabetes in Chinese people with normoglycaemia and prediabetes.     

大气污染物致突变研究中的Breakpoint回归

本文在用Ames试验和SOS显色法两个细菌短期测试系统研究广州地区1991年的大气总悬浮颗粒（TSP）二氯化烷（DCM）提取物遗传毒性的基础上,建立了气温（T）,气压（P）,风速（W）,降雨量（R）,相对湿度（RH）5种主要气象因素与诱变力和诱导力之间的Breakpoint回归模型,回归效果显著。     

利用不同方法测定红松人工林叶面积指数的季节动态

采用2种异速生长方程法、凋落物法、综合法(对光学仪器法进行木质部分及集聚效应校正后结合凋落物法)和光学仪器法测定了小兴安岭红松(Pinus koraiensis)人工林的叶面积指数(LAI)。首先利用光学仪器法测定有效叶面积指数(Le)的季节动态;其次为获得相对准确LAI,基于生长季节(5—8月)的展叶调查,结合凋落物法、综合法和2种异速生长方程法分别测定LAI的季节动态。结果表明:生长季节红松叶片8月初停止生长,迟于其他树种约两周;不同方法测定红松人工林LAI的季节变化均呈单峰型,且在8月初达到峰值,分别为异速生长方法-B(10.58)凋落物法(7.90)异速生长方法-A(6.70)综合法(4.41)光学仪器法(1.81);在整个调查期内(5月至11月),相对于异速生长方法-B、凋落物法、异速生长方法-A和综合法,光学仪器法分别平均低估81.69%、75.50%、70.18%和48.90%。本研究探讨了非破坏条件下测定红松人工林LAI季节动态的直接方法,并比较了不同方法之间的差异,研究结果可为有效测定常绿针叶林LAI提供参考。