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991.
992.
目的:建立皮质酮诱导的PC12细胞梯度应激损伤模型,为细胞应激水平的评估和细胞应激损伤调控研究提供实验基础和对象。方法:通过检测不同浓度皮质酮(0~1 000μmol/L)在经过不同干预时间(8~48 h)后PC12细胞活力,观察皮质酮对细胞活力的影响,筛选最佳干预条件的细胞模型。分光光度法和微量法检测细胞模型的关键应激指标(MDA、SOD、NADH、LDH),对模型进行评价。结果:当皮质酮浓度在200μmol/L以下且干预时间为12 h时,细胞活力在半数失活率以下,可减少各组由于细胞活力下降而产生的混杂因素。与空白对照组比较,皮质酮浓度依赖性地升高模型组的MDA、NADH和LDH水平,降低SOD水平(P<0.01),符合梯度应激模型的构建要求。结论:成功建立了PC12细胞梯度应激损伤模型,在干预时间为12 h的情况下,干预浓度为0μmol/L、25μmol/L、50μmol/L、100μmol/L、150μmol/L、200μmol/L,使得细胞模型应激损伤程度梯度增加,可作为开展细胞应激损伤评估及调控实验的基础和对象。 相似文献
993.
Alberto Fernando Oliveira Justo Claudia Kimie Suemoto 《Journal of cell communication and signaling》2022,16(2):155
The accumulation and propagation of misfolded proteins in the brain is a pathological hallmark shared by many neurodegenerative diseases, such as the depositions of β-amyloid and hyperphosphorylated tau proteins in Alzheimer''s disease. Initial evidence shows the role of nitric oxide synthases in the development of neurodegenerative diseases. A recent, in an exciting paper (Bourgognon et al. in Proc Natl Acad Sci USA 118, 1–11, 2021. 10.1073/pnas.2009579118) it was shown that the inducible nitric oxide synthase plays an important role in promoting oxidative and nitrergic stress leading to neuroinflammation and consequently neuronal function impairments and decline in synaptic strength in mouse prion disease. In this context, we reviewed the possible mechanisms of nitric oxide synthase in the generation of neurodegenerative diseases. 相似文献
994.
995.
Arnaud Di Franco Denis Baurain Gernot Glckner Michael Melkonian Herv Philippe 《Molecular biology and evolution》2022,39(1)
It is commonly assumed that increasing the number of characters has the potential to resolve evolutionary radiations. Here, we studied photosynthetic stramenopiles (Ochrophyta) using alignments of heterogeneous origin mitochondrion, plastid, and nucleus. Surprisingly while statistical support for the relationships between the six major Ochrophyta lineages increases when comparing the mitochondrion (6,762 sites) and plastid (21,692 sites) trees, it decreases in the nuclear (209,105 sites) tree. Statistical support is not simply related to the data set size but also to the quantity of phylogenetic signal available at each position and our ability to extract it. Here, we show that this ability for current phylogenetic methods is limited, because conflicting results were obtained when varying taxon sampling. Even though the use of a better fitting model improved signal extraction and reduced the observed conflicts, the plastid data set provided higher statistical support for the ochrophyte radiation than the larger nucleus data set. We propose that the higher support observed in the plastid tree is due to an acceleration of the evolutionary rate in one short deep internal branch, implying that more phylogenetic signal per position is available to resolve the Ochrophyta radiation in the plastid than in the nuclear data set. Our work therefore suggests that, in order to resolve radiations, beyond the obvious use of data sets with more positions, we need to continue developing models of sequence evolution that better extract the phylogenetic signal and design methods to search for genes/characters that contain more signal specifically for short internal branches. 相似文献
996.
Habitat loss and fragmentation are widely acknowledged as the main driver of the decline of giant panda populations. The Chinese government has made great efforts to protect this charming species and has made remarkable achievements, such as population growth and habitat expansion. However, habitat fragmentation has not been reversed. Protecting giant pandas in a large spatial extent needs to identify core habitat patches and corridors connecting them. This study used an equal‐sampling multiscale random forest habitat model to predict a habitat suitability map for the giant panda. Then, we applied the resistant kernel method and factorial least‐cost path analysis to identify core habitats connected by panda dispersal and corridors among panda occurrences, respectively. Finally, we evaluated the effectiveness of current protected areas in representing core habitats and corridors. Our results showed high scale dependence of giant panda habitat selection. Giant pandas strongly respond to bamboo percentage and elevation at a relatively fine scale (1 km), whereas they respond to anthropogenic factors at a coarse scale (≥2 km). Dispersal ability has significant effects on core habitats extent and population fragmentation evaluation. Under medium and high dispersal ability scenarios (12,000 and 20,000 cost units), most giant panda habitats in the Qionglai mountain are predicted to be well connected by dispersal. The proportion of core habitats covered by protected areas varied between 38% and 43% under different dispersal ability scenarios, highlighting significant gaps in the protected area network. Similarly, only 43% of corridors that connect giant panda occurrences were protected. Our results can provide crucial information for conservation managers to develop wise strategies to safeguard the long‐term viability of the giant panda population. 相似文献
997.
组学分析技术的发展推动生物学逐渐成为一门以数据分析为中心的科学。依托生物数据在细胞整体系统水平建立数字细胞模型,对于理解细胞系统组织原理和生命产生进化规律,预测各种环境和基因扰动对细胞功能的影响并指导设计人工生命具有重要意义,因此数字细胞的构建模拟设计已成为合成生物学的核心研究内容与底层支撑技术。本文重点对天津工业生物技术研究所创立十年来在数字细胞研究方面的进展进行回顾介绍,重点包括基因组尺度代谢网络模型的构建、质控以及其在途径设计和指导菌种代谢工程改造方面的应用,进一步结合近年来细胞模型研究的前沿趋势,对整合多种约束的模型的构建和分析研究方面的最新成果进行了介绍,最后对数字细胞研究的未来发展方向进行展望。数字细胞技术将与基因组测序、合成和编辑等合成生物学前沿技术一起提升人们对生命进行读写改创的能力。 相似文献
998.
999.
I. Walker 《International Review of Hydrobiology》1988,73(2):229-234
WANGERSKY and WANGERSKY'S (1980, 1981, 1983) Manna models on algal patchiness and competition are essentially stochastic models. Analysis of their phase-spatial properties, however, reveals complementary, deterministic features: interspecific competition is relatively ineffective because of the high degree of compartmentalization of resource supply and consumption; the probability of consumption in a given place at a given time is largely independent of the rate of consumption in other places. 相似文献
1000.
Jie Zhang Lei Wang Qianqian Song Mingbing Xiao Jie Gao Xiaolei Cao Wenjie Zheng 《International journal of biological sciences》2022,18(7):2729
Environmental and exogenous/ endogenous factors, in a setting of individual genetic predisposition, contribute to the cancer development. Over the years, epidemical evidence increasingly highlights the correlations of multiple cancer incentives and genetic alterations with cancer incidence. Unraveling the pivotal carcinogenesis events prompted by particular risk factors remarkably advances early surveillance and oncogenesis intervening. Traditional cell-based models and animal-based models are unrealistic and unreliable for translational study, respectively ascribing to the limited tumor heterogeneity and species-related variation. Organoid emerged as a fidelity model that well preserves the properties of its origin. With inherent quality of holistic perspective, organoid is therefore ideally suited for delineating the carcinogenesis under risk exposure, in favor of understanding pathogen-host interactions and alleviating cancer initiation. In this review, we have summarized the organoid model-based evidence that identified or validated carcinogenic risks, mainly including diet, aging, microbial infection, and chemical exposure. In addition, we envisioned the exciting prospect of organoid model in screening promising treatment and/or prevention during tumorigenesis. As a robust 3D in vitro system, organoid has been widespread applied in basial and clinical cancer research, which may elucidate crucial mechanisms of oncogenesis and develop novel targeting strategies. 相似文献