内蒙古典型草原植物叶片碳氮磷化学计量特征的季节动态

分析植物叶片(C)、氮(N)、磷(P)含量及其比值的季节动态, 不仅有助于认识植物生长发育和养分吸收利用等生理生态过程, 也有利于认识植物化学计量的动态平衡关系。该文选择内蒙古典型温带草原18种常见植物, 在生长季的6-9月, 每半月一次进行连续采样, 在此基础上分析了叶片C、N、P含量及其比值在生长季内的变化。主要结果: 1)植物叶片C、N、P含量及其比值的季节性变化在不同功能类群间不同步, 其中叶片N、P含量的季节变化体现了明显的稀释作用。2)叶片C、N、P含量及其比值在不同功能类群间差异显著, 单子叶、多年生禾草类的叶片N、P含量显著低于双子叶和多年生杂类草植物, 而其叶片C:N、C:P则高于双子叶和多年生杂类草植物。3)叶片N、P含量显著正相关, 叶片C:N和C:P分别与N和P含量显著负相关, 可能体现了植物体内营养元素间的内在耦合机制。4)叶片N含量与C:N, 叶片P含量与C:P以及叶片N含量与P含量均呈现等速生长关系, 且等速生长关系在生长季保持稳定。     

Poloxamer-188 Attenuates TBI-Induced Blood–Brain Barrier Damage Leading to Decreased Brain Edema and Reduced Cellular Death

Neurochemical Research - Plasmalemma permeability plays an important role in the secondary neuronal death induced by traumatic brain injury (TBI). Previous works showed that Poloxamer 188 (P188)...     

ERK通路在脑缺血及缺血预处理沙土鼠海马神经元中的作用

目的：探讨细胞外信号调节激酶（ERK）通路在脑缺血及缺血预处理海马神经元中的作用。方法：雄性蒙古沙土鼠,随机分为假手术组（SH）、缺血/再灌注组（I/R）、缺血预处理组（IP）、PD98059组（PD）、溶剂对照组（VE组）、PD98059复合IP组（PIP）,每组按再灌注15 min、2 h、4 h、6 h、1 d、3 d、5 d及7 d又分8个亚组。建立前脑缺血再灌注损伤模型,观察对行为学、组织学、p-ERK、HSP70、Fos及NF-κB表达的影响。结果：IP组鼠探索活动、CA1区凋亡神经元数及NF-κB阳性神经元数较I/R组明显减少（P〈0.05）,CA1区Fos阳性神经元数、HSP70及CA3/DG区p-ERK表达水平较I/R组明显增加（P〈0.05）。PD组再灌注各点Fos阳性神经元数较I/R组明显减少（P〈0.05）。再灌注1 d、3 d凋亡神经元数较I/R组明显增多（P〈0.05）。PIP组各观察指标介于IP组及IR组间。结论：ERK通路在缺血后海马CA3/DG区的激活可能与该区的缺血耐受有关 诱导CA1区神经元Fos、HSP70表达,减少NF-κB生成是缺血预处理神经元保护作用的分子机制之一。     

植物叶片形态的生态功能、地理分布与成因

叶片是植物与环境进行水气交换的重要场所, 形态多变。叶片形态可直接影响植物的生理生化过程, 反映植物的资源获取策略。该文以叶片大小、叶形、叶缘特征(有无叶齿)和叶型(单、复叶)等形态性状为例, 总结了当前叶片形态的研究进展, 分析了叶形态性状的生态功能, 综述叶片形态的地理分布, 探讨叶片形态性状变化的驱动因素及其对生态系统功能的影响。现有研究主要聚焦于局域尺度的特定类群, 关注叶大小、叶缘具齿性以及叶型的地理分布与生态成因, 发现叶片的形态发育受基因调控, 叶形态性状与其他性状相互权衡, 其空间变异受气温和降水量共同驱动。以叶大小为代表的叶片形态性状影响水分和养分循环, 能够反映气候变化下的群落响应, 也可用于预测生态系统初级生产力。今后应结合新方法获得覆盖度高且区域无偏的数据, 探索叶形态在长时间尺度上的适应性进化, 研究叶形态特征及其对生态系统功能影响的尺度推绎。该文有助于从叶片的角度认识植物对环境变化的响应, 以性状为桥梁将个体适合度、群落动态与生态系统功能联系起来, 能够加深对植物群落生态学和功能生物地理学等相关领域研究进展的了解。     

Spatiotemporal quantification of metastatic tumour cell growth and distribution in lymph nodes by whole-mount tissue 3D imaging

Lymph nodes (LNs) are a common site of metastasis in many solid cancers. Tumour cells can migrate to LNs for further metastatic colonization of distant organs, indicating poor prognosis and requiring different clinical interventions. The histopathological diagnostic methods currently used to detect clinical lymph node metastasis (LNM) have limitations, such as incomplete visualization. To obtain a complete picture of metastatic LNs on the spatial and temporal scales, we used ultimate 3D imaging of solvent-cleared organs (uDISCO) and 3D rapid immunostaining. MC38 cells labelled with EGFP were injected into the left footpads of C57BL/6 mice. Draining lymph nodes (DLNs) harvested from these mice were cleared using the uDISCO method. Metastatic colorectal cancer (CRC) cells in various regions of DLNs from mice at different time points were quantified using 3D imaging of whole-mount tissue. Several stages of tumour cell growth and distribution in LNs were identified: 1) invasion of lymphatic vessels (LVs) and blood vessels (BVs); 2) dispersion outside LVs and BVs for proliferation and expansion; and 3) re-entry into BVs and efferent lymphatic vessels (ELVs) for further distant metastasis. Moreover, these data demonstrated that mouse fibroblast cells (MFCs) could not only promote LNM of tumour cells but also metastasize to LNs together with tumour cells, thus providing a “soil” for tumour cell colonization. In conclusion, 3D imaging of whole-mount tissue and spatiotemporal analysis of LNM may collectively constitute an auxiliary method to improve the accuracy of clinical LNM detection.     

A new peptide with membrane-permeable function derived from human circadian proteins

Recently, the small regions of some proteins suchas human immunodeficiency virus type 1 (HIV-1) Tat-(48-60) and Drosophila Antennapedia-(43-58) have beenreported to have the ability to translocate through the cellmembranes and carry the exogenous molecules into cyto-plasm and nucleus, and are called membrane-permeablepeptides (MPPs) [1–14]. Delivery of bioactive peptidesacross the blood-brain barrier is generally restricted to small(6 amino acids or less) or highly lipophilic peptides. But…     

铁死亡的生化过程及对肿瘤的影响

铁死亡(ferroptosis）是近年提出的一种调节性细胞死亡方式,主要依赖于细胞内铁和脂质活性氧（reactive oxygen species, ROS）积累所引起的细胞死亡。铁死亡的发生与多种生物化学过程密切相关,包括多不饱和脂肪酸、铁和氨基酸代谢,以及谷胱甘肽、磷脂、烟酰胺腺嘌呤二核苷酸磷酸（nicotinamide adenine dinucleotide phosphate, NADPH）和辅酶Q10的生物合成。与正常细胞相比,肿瘤细胞内ROS水平通常较高,因而与ROS有关的铁死亡对肿瘤疾病的影响引人注目。在调节肿瘤细胞如卵巢恶性肿瘤、头颈部癌、弥漫性大B细胞淋巴瘤、肝癌,以及横纹肌肉瘤的生长和增殖中,铁死亡发挥了不可忽视的作用。本文主要阐述了各种生物化学过程对铁死亡的影响,以及铁死亡在肿瘤疾病中的研究进展,为肿瘤疾病的治疗提供新思路。     

线粒体功能障碍与神经病理性疼痛的关系相关研究进展

神经病理性疼痛是由外周或中枢神经系统受损引起的慢性疼痛,是神经系统疾病的一种,其发病机制尚未完全清楚,目前缺乏有效的治疗策略.线粒体是细胞的重要组成部分,在ATP合成、氧化应激、细胞内Ca2+稳态维持和细胞信号转导过程上发挥着重要作用.最近研究发现,线粒体数量、形态和功能的改变与神经病理性疼痛的发生发展密切相关.因此,...     

Necrostatin-1 Suppresses Autophagy and Apoptosis in Mice Traumatic Brain Injury Model

Traumatic brain injury (TBI) results in neuronal apoptosis, autophagic cell death and necroptosis. Necroptosis is a newly discovered caspases-independent programmed necrosis pathway which can be triggered by activation of death receptor. Previous works identified that necrostatin-1 (NEC-1), a specific necroptosis inhibitor, could reduce tissue damage and functional impairment through inhibiting of necroptosis process following TBI. However, the role of NEC-1 on apoptosis and autophagy after TBI is still not very clear. In this study, the amount of TBI-induced neural cell deaths were counted by PI labeling method as previously described. The expression of autophagic pathway associated proteins (Beclin-1, LC3-II, and P62) and apoptotic pathway associated proteins (Bcl-2 and caspase-3) were also respectively assessed by immunoblotting. The data showed that mice pretreated with NEC-1 reduced the amount of PI-positive cells from 12 to 48?h after TBI. Immunoblotting results showed that NEC-1 suppressed TBI-induced Beclin-1 and LC3-II activation which maintained p62 at high level. NEC-1 pretreatment also reversed TBI-induced Bcl-2 expression and caspase-3 activation, as well as the ratio of Beclin-1/Bcl-2. Both 3-MA and NEC-1 suppressed TBI-induced caspase-3 activation and LC3-II formation, Z-VAD only inhibited caspase-3 activation but increased LC3-II expression at 24?h post-TBI. All these results revealed that multiple cell death pathways participated in the development of TBI, and NEC-1 inhibited apoptosis and autophagy simultaneously. These coactions may further explain how can NEC-1 reduce TBI-induced tissue damage and functional deficits and reflect the interrelationship among necrosis, apoptosis and autophagy.