温度对亚热带地区常见树种叶片甲烷排放的影响

以亚热带常见树种米槠、木荷、浙江桂、罗浮栲、杉木和柑橘为对象,利用控制试验研究了温度对树木叶片甲烷(CH4)排放的影响.结果表明:当温度在10℃时,供试的6种树木中,仅木荷、柑橘和罗浮栲的叶片排放CH4;温度高于20℃时,所有树木叶片均可排放CH4.温度高于30℃时,叶片排放CH4的平均排放速率(1.010ngCH4·g-1DM·h-1)是10～30℃时平均排放速率(0.255ngCH4·g-1DM·h-1)的3.96倍.增温对柑橘和杉木CH4排放速率的影响显著高于其他4种树木.培养时间对叶片排放CH4速率有显著影响,温度胁迫对树木排放CH4的影响受植物活性的控制.在低温或高温条件下,树木干叶均不能排放CH4.高温胁迫对树木叶片排放CH4有重要影响,全球变暖可能增加植物的CH4排放.     

Annual cycle of activity of the neurons of the anterior preoptic area in the brain of Rana esculenta L.

Abstract

Sexually mature male and female Rana esculenta L. were captured in their natural habitat in six phases of the annual cycle. Nuclear volumes in APOA cells were found to fluctuate distinctly in the course of the year. In both sexes nuclear volumes were maximal in the phases preceding the breeding season (IIIrd decade of January, and 1st decade of April), and minimal throughout the phases of active life (IIIrd decade of May, IInd decade of July, and 1st decade of September). No aldehydefuchsin or Gomori‐positive material was found in the APOA perikaryons.     

Lysosomal membrane permeabilization is involved in oxidative stress-induced apoptotic cell death in LAMP2-deficient iPSCs-derived cerebral cortical neurons

Patients with Danon disease may suffer from severe cardiomyopathy, skeletal muscle dysfunction as well as varying degrees of mental retardation, in which the primary deficiency of lysosomal membrane-associated protein-2 (LAMP2) is considerably associated. Owing to the scarcity of human neurons, the pathological role of LAMP2 deficiency in neural injury of humans remains largely elusive. However, the application of induced pluripotent stem cells (iPSCs) may shed light on overcoming such scarcity.In this study, we obtained iPSCs derived from a patient carrying a mutated LAMP2 gene that is associated with Danon disease. By differentiating such LAMP2-deficient iPSCs into cerebral cortical neurons and with the aid of various biochemical assays, we demonstrated that the LAMP2-deficient neurons are more susceptible to mild oxidative stress-induced injury.The data from MTT assay and apoptotic analysis demonstrated that there was no notable difference in cellular viability between the normal and LAMP2-deficient neurons under non-stressed condition. When exposed to mild oxidative stress (10 μM H₂O₂), the LAMP2-deficient neurons exhibited a significant increase in apoptosis. Surprisingly, we did not observe any aberrant accumulation of autophagic materials in the LAMP2-deficient neurons under such stress condition.Our results from cellular fractionation and inhibitor blockade experiments further revealed that oxidative stress-induced apoptosis in the LAMP2-deficient cortical neurons was caused by increased abundance of cytosolic cathepsin L. These results suggest the involvement of lysosomal membrane permeabilization in the LAMP2 deficiency associated neural injury.     

MicroRNAs as regulators of cell death mechanisms in amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder affecting upper and lower motor neurons (MNs), resulting in paralysis and precocious death from respiratory failure. Although the causes of ALS are incompletely understood, the role of alterations in RNA metabolism seems central. MicroRNAs (miRNAs) are noncoding RNAs implicated in the regulation of gene expression of many relevant physiological processes, including cell death. The recent model of programmed cell death (PCD) encompasses different mechanisms, from apoptosis to regulated necrosis (RN), in particular necroptosis. Both apoptosis and necroptosis play a significant role in the progressive death of MNs in ALS. In this review, we present key research related to miRNAs that modulate apoptosis and RN pathways in ALS. We also discuss whether these miRNAs represent potential targets for therapeutic development in patients.     

Spinal cord tissue affects sprouting from aortic fragments in ex vivo co‐culture

It is a well‐known fact, that there is a close interconnection between vascular and neural structures in both embryonic development and postnatal life. Different models have been employed to dissect the mechanisms of these interactions, ranging from in vitro systems (e.g., co‐culture of neural and endothelial cells) to in vivo imaging of central neural system recovery in laboratory animals after artificially induced trauma. Nevertheless, most of these models have serious limitations. Here, we describe an ex vivo model, representing an organotypic co‐culture of aortic fragments (AF) with longitudinal slices of mouse neonatal spinal cord (SC) or dorsal root ganglia (DRG). The samples were co‐cultured in a medium adapted for SC tissue and lacking any pro‐angiogenic or neurotrophic growth factors. It was found, that cultivation of AFs in the SC injury zone (transversal dissection of a SC slice) resulted in the initiation of active aortic sprouting. Remarkably, the endothelial cells exiting the AFs never invaded the SC tissue, concentrating in a nearby area (negative taxis). In contrast, the DRGs, while also promoting the sprouting, were a target of active endothelial CD31⁺ cell invasion (positive taxis). Thus, the tissues of both central and peripheral nervous systems have a prominent positive effect on aortic sprouting, while the vector of endothelial cell expansion is strictly nervous‐tissue‐type dependent. The ex vivo AF co‐culture with SC or DRG appeared to be a useful and promising model for a further endeavor into the mechanisms driving the complex interactions between neural and endothelial tissues.     

稳定性氮肥配合秸秆还田对水稻产量及N2O和CH4排放的影响

以中国科学院辽宁沈阳农田生态系统国家野外科学观测研究站连续两年的试验平台为依托,以潮棕壤为供试土壤,开展了稳定性氮肥配合秸秆还田对水稻产量及N₂O和CH₄排放的影响研究,设置对照(CK)、尿素(U)、尿素+脲酶抑制剂+硝化抑制剂(U+I)、秸秆还田(S)、秸秆还田+尿素(S+U)、秸秆还田+尿素+脲酶抑制剂+硝化抑制剂(S+U+I)6个处理.结果表明: 与CK相比,尿素显著提高了水稻产量、N₂O和CH₄累积排放及全球增温潜势.硝化抑制剂和脲酶抑制剂与尿素配施可显著减缓N₂O的累积排放.秸秆还田显著增加了N₂O和CH₄累积排放、全球增温潜势和温室气体排放强度.S+U+I处理水稻产量最高,但温室气体排放强度也显著高于其他处理;U+I处理产量略低于S+U+I,但温室气体排放强度最小.秸秆单独还田处理作物产量与对照相比无显著差异.在东北潮棕壤发育的水田中,S+U+I和U+I是相对较优的施肥模式.     

全球变化对森林土壤甲烷吸收的影响及其机制研究进展

大气CO₂浓度升高、降水格局改变、全球氮沉降增加和土地覆盖变化等全球变化不仅改变了森林土壤理化性质,而且影响了植物的生长和微生物活性,导致森林土壤碳、氮循环发生改变,进而影响土壤CH₄的吸收.本研究综述了森林土壤CH₄吸收的重要性,森林土壤CH₄吸收对大气CO₂浓度升高、降水格局改变、全球氮沉降增加和土地覆盖变化等全球变化的响应差异及驱动机制.大气CO₂浓度升高抑制土壤CH₄吸收;降水减少倾向于促进土壤CH₄吸收;外源氮输入抑制富氮森林土壤CH₄吸收,而对贫氮森林土壤CH₄吸收则表现为促进或不影响;森林转化为草地、农田或人工林会减少土壤CH₄的吸收量,而植树造林则会增加土壤CH₄的吸收量.今后的研究重点是探讨全球变化对森林土壤CH₄吸收产生长期影响和综合效应,并借助分子生物学方法进一步探究土壤CH₄吸收的微生物学机制.     

Acute Complexin Knockout Abates Spontaneous and Evoked Transmitter Release

1. Download high-res image (151KB)
2. Download full-size image