Immuno-electron microscopical studies on the retinal basement membrane of chick embryo

Retinal basement membrane (RBM), also called inner limiting membrane of retina, is constituted by extracellular matrix. It was reported that neurite outgrowth of a neuron was closely related to extracellular matrix, particularly the laminin. In this laboratory RBM was used as the optimal substrate for retinal cells in culture. We have studied the surface of RBM and its relation to neurite outgrowth by scanning electronmicroscopy and immunogold transmission electronmicroscopy. RBM could be separated by mechanical disruption of the retina mounted between 2 adhesive substrata (membrane filter and poly-L-lysine coated glass). The surface of RBM studied was the side of RBM facing the optic fiber layer and ganglion cell layer. Small particles densely distributed on surface of RBM (Plate I, Fig. 1 and 2) were shown to be chrysanthemum-like structures with radiative arms under the scanning electronmicroscopy (Plate I, Fig. 3 and 4). The radiative arms of RBM of 12-day old chick embryo (E 12) were more in number and longer in length than that of the 6-day old chick embryo (E 6). The axons of ganglion cell from E 6 retinal strip extended out very well on RBM (Plate I, Fig. 5). Growth cone was active with filopodia. The chrysanthemum-like structures changed to ball-particles when the RBM was cultured for 24 hr. Some of ball-particles lay over the growth cone, and some beside it. Over and beside the nerve fiber could also be seen some ball-particles. When many neurites grew on RBM, a lot of ball-particles were shown to be displaced and piled up (Plate I, Fig. 6). The whole amount RBM labeled by indirect immunogold staining of Müller glial cell could be observed by transmission electronmicroscopy. The gold particles wer located at the chrysanthemum-like structure of E 6 RBM (Plate II, Fig. 7) and E 12 RBM (Plate II, Fig. 8). It was suggested that those structures were the end foot of Müller glial cells. Staining of PBS control or mouse serum control was negative (Plate II, Fig. 9 and 10).(ABSTRACT TRUNCATED AT 250 WORDS)     

退化高寒草甸关键生态属性对多途径恢复措施的响应特征

高寒草甸是青藏高原的主体植被类型,但退化态势较为严峻,严重威胁青藏高原生态屏障的战略地位。退化高寒草甸的复健是世界性难题,治理效果也因退化状态、恢复措施及气候环境而异。以春季休牧、秋季休牧、畜群结构优化、减畜轮牧、围栏封育及翻耕改建等典型多途径恢复措施下的退化高寒草甸为对象,系统探讨主要生态要素和生态功能的响应特征及潜在过程。结果表明,典型恢复措施下退化高寒草甸的植被生产力、土壤有机碳密度及土壤饱和持水量等生态要素都得到一定程度的提升,而恢复效果与实施年限及恢复措施密切相关。围栏封育和翻耕改建下土壤有机碳密度及饱和持水量随恢复年限均表现为对数饱和型的响应特征,退化高寒草甸固碳持水功能的基本恢复年限约为6—10年。春季休牧、秋季休牧、畜群结构优化、减畜轮牧、围栏封育等放牧管理恢复措施应适用于轻度退化至重度退化的高寒草甸,而翻耕改建则是极度退化高寒草甸的适宜治理措施。由于多途径恢复措施的关注目标不同,今后研究应集中在恢复措施的组合优化和综合评价等方面。     

Single-cell transcriptomic atlas of primate cardiopulmonary aging

Aging is a major risk factor for many diseases,especially in highly prevalent cardiopulmonary comorbidities and infectious diseases including Coronavirus Diseas...     

LRP6 downregulation promotes cardiomyocyte proliferation and heart regeneration

The adult mammalian heart is thought to be a terminally differentiated organ given the postmitotic nature of cardiomyocytes. Consequently, the potential for cardiac repair through cardiomyocyte proliferation is extremely limited. Low-density lipoprotein receptor-related protein 6 (LRP6) is a Wnt co-receptor that is required for embryonic heart development. In this study we investigated the role of LRP6 in heart repair through regulation of cardiomyocyte proliferation. Lrp6 deficiency increased cardiomyocyte cell cycle activity in neonatal, juvenile and adult mice. Cardiomyocyte-specific deletion of Lrp6 in the mouse heart induced a robust regenerative response after myocardial infarction (MI), led to reduced MI area and improvement in left ventricular systolic function. In vivo genetic lineage tracing revealed that the newly formed cardiomyocytes in Lrp6-deficient mouse hearts after MI were mainly derived from resident cardiomyocytes. Furthermore, we found that the pro-proliferative effect of Lrp6 deficiency was mediated by the ING5/P21 signaling pathway. Gene therapy using the adeno-associated virus (AAV)9 miRNAi-Lrp6 construct promoted the repair of heart injury in mice. Lrp6 deficiency also induced the proliferation of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). Our study identifies LRP6 as a critical regulator of cardiomyocyte proliferation, which may lead to the development of a novel molecular strategy to promote myocardial regeneration and repair.Subject terms: Cell-cycle exit, Cytokinesis     

piR-823 inhibits cell apoptosis via modulating mitophagy by binding to PINK1 in colorectal cancer

Mitophagy plays a vital role in the maintenance of mitochondrial homeostasis and tumorigenesis. Noncoding RNA piR-823 contributes to colorectal tumorigenesis. In this study, we aim to evaluate piR-823-mediated mitophagy and its mechanistic association with colorectal cancer (CRC). Digital gene expression analysis was performed to explore the potential functions of piR-823. A piR-823 antagomir (Ant-823) was used to inhibit piR-823 expression, and piR-823 mimics (mimics-823) were used to increase piR-823 expression. Mitophagy was measured in vivo and in vitro by immunofluorescence and western blot analysis. JC-1 staining, ATP production, real-time PCR, and western blot analysis were used to measure changes in mitochondrial quality and number. siRNA transfection was used to inhibit mitophagy, and CCCP was used to induce mitophagy. RNA pull-down assays and RNA-binding protein immunoprecipitation assays were conducted to investigate the molecular mechanisms. Here, we found that CRC cells transfected with Ant-823 presented an altered expression of autophagic and mitophagy genes by Digital gene expression analysis. Ant-823 could promote Parkin activation and mitophagy in vitro and in vivo, followed by mitochondrial loss and dysfunction of some mitochondria, whereas mimics-823 exerted the opposite effects in CRC cells. The inhibition of mitophagy by siParkin alleviated Ant-823-induced mitochondrial loss and dysfunction, as well as apoptosis to a certain extent. Furthermore, piR-823 was found to interact with PINK1 and promote its ubiquitination and proteasome-dependent degradation, thus alleviating mitophagy. Finally, these findings were verifed in samples obtained by patients affected by colorectal cancer. In conclusion, we identify a novel mechanism by which piR-823 regulates mitophagy during CRC tumorigenesis by increasing PINK1 degradation. Subject terms: Colorectal cancer, Gastrointestinal cancer     

Genomic Shifts,Phenotypic Clines,and Fitness Costs Associated With Cold Tolerance in the Asian Tiger Mosquito

Climatic variation is a key driver of genetic differentiation and phenotypic traits evolution, and local adaptation to temperature is expected in widespread species. We investigated phenotypic and genomic changes in the native range of the Asian tiger mosquito, Aedes albopictus. We first refine the phylogeographic structure based on genome-wide regions (1,901 double-digest restriction-site associated DNA single nucleotide polymophisms [ddRAD SNPs]) from 41 populations. We then explore the patterns of cold adaptation using phenotypic traits measured in common garden (wing size and cold tolerance) and genotype–temperature associations at targeted candidate regions (51,706 exon-capture SNPs) from nine populations. We confirm the existence of three evolutionary lineages including clades A (Malaysia, Thailand, Cambodia, and Laos), B (China and Okinawa), and C (South Korea and Japan). We identified temperature-associated differentiation in 15 out of 221 candidate regions but none in ddRAD regions, supporting the role of directional selection in detected genes. These include genes involved in lipid metabolism and a circadian clock gene. Most outlier SNPs are differently fixed between clades A and C, whereas clade B has an intermediate pattern. Females are larger at higher latitude yet produce no more eggs, which might favor the storage of energetic reserves in colder climate. Nondiapausing eggs from temperate populations survive better to cold exposure than those from tropical populations, suggesting they are protected from freezing damages but this cold tolerance has a fitness cost in terms of egg viability. Altogether, our results provide strong evidence for the thermal adaptation of A. albopictus across its wide temperature range.     

A Human Active Lower Limb Model for Chinese Pedestrian Safety Evaluation

A subsystem impactor test for pedestrian lower limb injury evaluation has been brought in China New Car Assessment Protocol(CNCAP).Concerning large anthropometr...     

Hg2+对南极冰藻Chlorophyceae L-4生长和抗氧化系统的影响及藻体富集Hg2+的规律

南极冰藻Chlorophyceae L-4是南极生态系统重要的初级生产力和组成部分,其长期生长在极地环境中,有着特殊的生理机制。在生存环境和生长条件发生变化时,冰藻的膜脂系统和蛋白含量都会发生变化,而在受到重金属胁迫时,冰藻的超微结构也会发生明显变化。【目的】研究Chlorophyceae L-4在重金属离子Hg2+胁迫条件下的状态和Hg2+富集以及对其抗氧化系统的影响,为南极环境监测提供依据。【方法】绘制南极冰藻细胞在重金属离子Hg2+不同浓度胁迫条件下的生长曲线,观察其超微结构;测定丙二醛含量和SOD酶活性变化;ICP-MS法研究藻体富集Hg2+规律。【结果】Hg2+在低浓度时(≤100μg/L),细胞个数较正常条件明显偏少;在高浓度时(≥250μg/L),出现细胞死亡。丙二醛含量随Hg2+浓度升高而升高,SOD酶活性则先增强再减弱。藻体富集Hg2+在1 h达到峰值,而在Hg2+浓度持续升高时,富集量轻微降低。【结论】Hg2+离子对冰藻生长有抑制毒害作用;对Chlorophyceae L-4抗氧化系统有明显不利影响;L-4富集Hg2+在1 h内饱和,Hg2+过高时,富集量稍微降低。