松嫩平原不同生境蝴蝶群落多样性及其保护建议

随着气候变化加剧和人类活动影响,生物多样性变化及其保护逐渐受到广泛关注。蝴蝶作为开花植物的传粉媒介和生态环境监测及评价的关键指示者,其多样性变化能够在一定程度上反映生境状况,因此,有必要清晰认识不同生境中的蝴蝶多样性变化。为明确松嫩平原蝴蝶资源和不同生境的群落多样性差异,采用样线法于2016年5月-2018年8月对松嫩平原的割草草地、湿地、农田、放牧利用草地及恢复草地共五种生境类型进行调查研究。结果发现,调查共记录蝴蝶5108头,隶属于6科21属26种,其中牧女珍眼蝶（Coenonympha amaryllis）和红珠灰蝶（Plebejus argyrognomon）为优势种类,分别占蝴蝶个体总数的25.61%和31.66%,且在五种生境类型中均有分布。不同生境类型中,蝴蝶群落的物种丰富度指数和均匀度指数无明显差异,而恢复草地生境的蝴蝶群落Shannon-Wiener多样性指数较高,优势度指数较低。农田生境中的蝴蝶个体数量较少,且群落组成与其他四种生境之间均具有显著差异。五种生境类型中的蝴蝶数量和多样性均呈现一定的月动态和年动态变化趋势。除湿地和农田外,其余三种生境中蝴蝶物种和个体数量从5月到8月均持续升高。四种生境的蝴蝶物种数量、个体数量（除农田外）在2018年均出现明显下降趋势。物种丰富度指数等指标的月动态和年动态在不同生境类型间存在较大差异。这些结果表明,生境类型和人类活动与蝴蝶多样性变化关系密切,表现为单一生境中蝴蝶多样性较低,复杂生境有利于保护蝴蝶多样性。本研究有助于厘清松嫩平原蝴蝶资源的基础数据,并为该地区蝴蝶多样性保护和利用及评估该区域生态环境提供一定理论支撑。     

黄河三角洲芦苇湿地底栖无脊椎动物与环境因子的关系研究——以石油开采区与淡水补给区为例

分别于2018年5月和8月对黄河三角洲芦苇湿地19(淡水补给区11处,石油开采区8处)处采样点的底栖无脊椎动物和水体理化指标进行调查采样,运用统计方法分析两个区域物种组成、优势种、多样性、群落结构以及与环境因子的关系。结果表明:两季共采集到底栖无脊椎动物54种,主要以水生昆虫、腹足纲和软甲纲为主,淡水补给区和石油开采区各类群组成差异明显。独立样本T检验表明淡水补给区和石油开采区水体理化指标间差异显著(P<0.05)。双因子方差分析显示,昆虫纲和腹足纲密度在两区域差异显著(P<0.05),软甲纲和腹足纲密度在季节上差异明显(P<0.05)。底栖无脊椎动物优势种共10种,淡水补给区指示物种8种,而石油开采区未发现有指示物种。聚类和非参数多维排序(nM DS)显示,底栖无脊椎动物群落结构相似性较低; RDA结果表明:淡水补给区底栖无脊椎动物群落结构主要受Cond,TDS,Sal,pH,Eh,HCO₃^-,SO₄^2-等环境因子的影响。石油开采区底栖无脊椎动物群落结构影响较大的环境因子为HCO...     

全球啄木鸟濒危格局及研究现状

啄木鸟科物种作为初级洞巢者与蛀干害虫控制者,对森林高度依赖,是森林生态系统重要的伞护种和环境指示物种。自20世纪以来,由于全球范围的栖息地丧失和片段化,啄木鸟科物种的森林生境急剧萎缩,威胁着该类群物种的生存和繁衍。为探究啄木鸟科动物濒危情况和研究现状,本研究利用世界自然保护联盟濒危物种红色名录(IUCN Red List)和国际鸟盟(BirdLife International)在线数据库,检索并整理出1988年到2023年以下内容：(1)全球啄木鸟的物种数、濒危等级及其变化情况;(2)各大洲的啄木鸟物种数及其受威胁物种的比例;(3)啄木鸟的主要威胁因素;(4)通过Google学术搜索等方式检索并统计啄木鸟相关文章的研究内容。结果显示：(1)目前现存254种啄木鸟,33年间全球受威胁啄木鸟由7种增加至18种,受威胁物种数占当年已命名啄木鸟物种数的比例由3.4%上升至7.0%。(2)亚洲、南美洲和北美洲各分布了83种、93种和56种啄木鸟,受威胁物种占比分别为12.0%、6.4%、5.3%。非洲和欧洲分别分布了36种和11种啄木鸟,当前没有受威胁物种。(3)农业和生物资源利用以及放牧是啄木鸟的主要威胁因素。(4)共检索到研究啄木鸟的有关文章1 024篇,研究覆盖了140种啄木鸟,其中,文章数最多的物种是红顶啄木鸟(Leuconotopicus borealis)(162篇)。研究主要集中在巢相关特征(129篇)、生境选择特征(122篇)、取食行为(112篇)、繁殖行为(99篇)和种群状况(66篇)等基础生态学内容。这些研究为啄木鸟生物学、生态学积累了一定的基础,但物种覆盖程度还远远不够。在生物多样性急剧丧失的大背景下,亟需开展更为广泛和深入的研究。本研究对全球啄木鸟的濒危格局与研究现状进行了全面的分析,以期为后续啄木鸟的研究与保护工作提供参考。     

Ungulate bocaparvovirus 4 and rodent bocavirus are different genotypes of the same species of virus

Bocaviruses are associated with many human infectious diseases, such as respiratory tract infections, gastroenteritis, and hepatitis. Rats are known to be reservoirs of bocaviruses, including rodent bocavirus and rat bocavirus. Recently, ungulate bocaparvovirus 4, a known porcine bocavirus, has also been found in rats. Thus, investigating bocaviruses in rats is important for determining the origin of the viruses and preventing and controlling their transmission. To the best of our knowledge, no study to date has investigated bocaviruses in the livers of rats. In this report, a total of 624 rats were trapped in southern China between 2014 and 2017. Liver and serum samples from rats were tested for the prevalence of bocaviruses using PCR. Sequences related to ungulate bocaparvovirus 4 and rodent bocavirus were detected in both liver and serum samples. Interestingly, the prevalence of ungulate bocaparvovirus 4 (reference strain:KJ622366.1) was higher than that of rodent bocavirus (reference strain:KY927868.1) in both liver (2.24% and 0.64%, respectively) and serum samples (2.19% and 0.44%, respectively). The NS1 regions of ungulate bocaparvovirus 4 and rodent bocavirus related sequences displayed over 84% and 88% identity at the nucleic acid and amino acid levels, respectively. Furthermore, these sequences had similar genomic structure, genomic features, and codon usage bias, and shared a common ancestor. These viruses also displayed greater adaptability to rats than pigs. Our results suggested that ungulate bocaparvovirus 4 and rodent bocavirus may originate from rats and may be different genotypes of the same bocavirus species.     

NEDD4 promotes cell growth and motility in hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related death worldwide. In China, the situation is even worse as cancer incidence and mortality continue to increase rapidly. Although tremendous progress has been made toward HCC treatments, the benefits for liver cancer patients are still limited. Therefore, it is necessary to identify and develop novel therapeutic methods. Neuronally expressed developmentally downregulated 4 (NEDD4), an E3 ubiquitin ligase, plays a critical role in the development and progression of various types of human cancers. In our study, NEDD4 acts as an oncoprotein in both QGY7703 and SMMC7721 liver cancer cell lines. We found that depletion of NEDD4 by siRNA transfection led to inhibition of cell growth, invasion and migration, and promotion of apoptosis. In contrast, overexpression of NEDD4 via plasmid transfection resulted in facilitated cell proliferation, invasion and migration, and decreased apoptosis. Importantly, we observed that tumor suppressor LATS1, also a core component of Hippo pathway, was negatively regulated by NEDD4 in liver cancer cells. Our findings suggested that NEDD4 may be involved in the HCC progression via regulating LATS1 associated signaling pathway. Therefore, targeting NEDD4-LATS1 signaling could be a potential therapeutic option for HCC treatment.     

Oxidative stress and NF-κB signaling are involved in LPS induced pulmonary dysplasia in chick embryos

Inflammation or dysbacteriosis-derived lipopolysaccharides (LPS) adversely influence the embryonic development of respiratory system. However, the precise pathological mechanisms still remain to be elucidated. In this study, we demonstrated that LPS exposure caused lung maldevelopment in chick embryos, including higher embryo mortality, increased thickness of alveolar gas exchange zone, and accumulation of PAS⁺ immature pulmonary cells, accompanied with reduced expression of alveolar epithelial cell markers and lamellar body count. Upon LPS exposure, pulmonary cell proliferation was significantly altered and cell apoptosis was inhibited as well, indicating a delayed progress of pulmonary development. LPS treatment also resulted in reduced CAV-1 expression and up-regulation of Collagen I, suggesting increased lung fibrosis, which was verified by Masson staining. Moreover, LPS induced enhanced Nrf2 expression in E18 lungs, and the increased reactive oxygen species (ROS) production was confirmed in MLE-12 cells in vitro. Antioxidant vitamin C restored the LPS induced down-regulation of ABCA3, SP-C and GATA-6 in MLE-12 cells. Furthermore, LPS induced activation of NF-κB signaling in MLE-12 cells, and the LPS-induced decrease in SP-C expression was partially abrogated by blocking NF-κB signaling with Bay-11–7082. Bay-11–7082 also inhibited LPS-induced increases of ROS and Nrf2 expression. Taken together, we have demonstrated that oxidative stress and NF-κB signaling are involved in LPS induced disruption of pulmonary cell development in chick embryos.     

Bovine and human insulin activate CD8+-autoreactive CTL expressing both type 1 and type 2 cytokines in C57BL/6 mice

CD8+ T cells down-regulate a variety of immune responses. For example, porcine and human insulin do not stimulate Abs in C57BL/6 mice because CD8+ T cells inhibit CD4+ helper T cells. By contrast, bovine insulin induces Ab in C57BL/6 mice, and removal of CD8+ T cells does not alter this response. This raises the question of whether porcine, but not bovine, insulin activates CD8+ T cells or whether both insulins activate CD8+ T cells but CD4+ helper T cells are differentially inhibited by them. In this study, we show that insulin-specific CD8+ CTL can be cultured from C57BL/6 mice primed with either bovine or human insulin in CFA. Thus, exogenous Ags, besides OVA, induce CD8+ CTL when administered in an adjuvant, suggesting this is a typical response. These CTL are H-2Kb restricted and produce IL-5, IL-10, IFN-gamma, and small amounts of IL-4, which is distinct from IFN-gamma and TNF-alpha that are typically secreted by virus-specific CTL. Moreover, the CTL primed with either bovine or human insulin recognize an A-chain peptide that is identical to the mouse insulin sequence. That foreign proteins, which are closely related to self-proteins, activated autoreactive, CD8+ T cells in vivo is a novel finding. It raises the possibility that self-reactive CTL may be activated by cross-reacting Ags and once activated they might participate in autoimmunity. These results also suggest that down-regulation of insulin-specific responses by autoreactive CD8+ T cells is most likely due to the differential sensitivity of bovine and human insulin-specific CD4+ T cells.     

HCV编码病毒结构蛋白的DNA免疫研究

应用HCVC (pC)和HCVCE1E2 (pCE1E2 )重组体转染真核细胞并且通过肌注免疫BALB/C小鼠 ,对其体液免疫和细胞免疫进行检测。所用的 pC和 pCE1E2 均可在真核细胞内表达出特异性HCVC蛋白 ;肌注DNA免疫后均可诱导出BALB/C小鼠的体液和细胞免疫反应 ,抗体反应的A值 :pC组为 0 .358± 0 .0 96 ,pCE1E2 组为 0 .4 15± 0 .12 7;CTL活力 pC组为 18.6 5%± 5.72 % ,pCE1E2 组为 2 0 .0 7%± 11.11% ;通过免疫鼠荷瘤检测体内CTL反应 ,可观察到免疫组鼠发瘤时间滞后 ,发瘤部位减少和存活时间延长。在开发和研制HCV疫苗的过程中 ,DNA免疫是在快速构建、评价和筛选免疫原方面的有效办法。