青藏高原东缘的锈菌资料Ⅱ.裸堆串孢锈菌属在我国的首次记录

裸堆串孢锈菌属以冬孢子单孢串生为主要特征,孢子堆裸露缺包被,外观酷似柄锈属的孢子堆。此属已知7种。寄生于菊科,大戟科和荨麻科植物,6种分布美洲,1种分布东亚.本文报告亚洲仅知的一种,即寄生于宽叶孢麻Urtica laetevirens Maxim.的川息尔堆串孢锈菌Baeodromus tranzschelii Azbukina,标本采自四川九寨沟(岷山).     

淡色库蚊对敌百虫的抗药性研究——抗性谱及联合作用

1973年采集于上海闸北区的淡色库蚊幼虫在室内以敌百虫选育抗性品系(RD品系)获得成功,F₁₂代的LC₅₀已为室内正常品系(SEN)的240多倍。RD品系的抗性谱表明,对有机磷杀虫剂均具有不同程度的交互抗性;对有机氯如DDT、丙体666和氨基甲酸酯类等杀虫剂无明显的交互抗性;对天然除虫菊和拟除虫菊酯类有低度的负交互抗性。并测定了29种药剂与敌百虫混用对RD品系和SEN品系的增效作用。还测定了对敌百虫有较高交互抗性的杀虫剂分别与TPP,TOCP、稻瘟净、异稻瘟净和增效醚混用后的增效作用。     

Indication of dynamic neurovascular coupling from inconsistency between EEG and fMRI indices across sleep–wake states

Sleep and Biological Rhythms - Neurovascular coupling (NVC), the transient regional hyperemia following the evoked neuronal responses, is the basis of blood oxygenation level-dependent techniques...     

病毒感染对角质形成细胞CCL20表达的影响及其机制

目的:既往研究发现,趋化因子CCL20在银屑病、白癜风等在内的多种自身免疫性皮肤疾病的病理过程中扮演了重要的角色,同时病毒感染也被认为是自身免疫性疾病的重要参与者。皮肤组织是机体抵御外界病原体的第一道屏障,其中角质形成细胞被认为在启动免疫中发挥了关键的作用。视黄酸诱导基因蛋白I(RIG-I)是固有免疫模式识别受体家族的重要成员,其能够被病毒复制的中间产物激活。然而,病毒感染是否会通过RIG-I信号通路影响角质形成细胞中CCL20的表达,进而参与自身免疫性皮肤疾病的病理过程仍不清楚。本文使用聚肌胞苷酸(Poly(I:C))来体外模拟病毒感染,探究病毒感染对皮肤角质形成细胞CCL20表达的影响,并且通过小干扰RNA沉默关键分子来探究相应的分子机制。方法:首先,体外细胞实验使用Poly(I:C)刺激角质形成细胞系HaCaT,通过Western-blot实验和qRT-PCR实验探究Poly(I:C)对HaCat中RIG-I表达的影响;接下来,通过实时荧光定量PCR(qRT-PCR)以及酶联免疫吸附测定实验(ELISA)检测Poly(I:C)对角质形成细胞CCL20分泌的影响;线粒体抗病毒信号蛋白(MAVS)在RIG-I的下游发挥着重要作用,我们通过小干扰RNA(si-RNA)阻断RIG-I-MAVS-NF-κB信号通路关键分子,探究Poly(I:C)诱导角质形成细胞CCL20表达升高的分子机制。结果:Poly(I:C)能够明显促进角质形成细胞中RIG-I的表达及CCL20的表达和分泌;Poly(I:C)诱导角质形成细胞CCL20分泌是由RIG-I-MAVS-NF-κB信号通路介导的。结论:Poly(I:C)模拟病毒感染能够通过RIG-I-MAVS-NF-κB信号通路介导CCL20表达增加,进而参与自身免疫性皮肤疾病的病理过程。     

不同释放密度和高度对稻螟赤眼蜂防控两种水稻螟虫效果的影响

稻螟赤眼蜂Trichogramma japonicum Ashmead是二化螟Chilo suppressalis(Walker)和稻纵卷叶螟Cnaphalocrocis medinalis(Guenée)的优势卵寄生蜂。为优化稻螟赤眼蜂田间释放技术,作者分别在安徽、福建和贵州进行了稻螟赤眼蜂不同释放高度和密度对防控两种水稻螟虫效果影响的田间试验。结果表明,对于防控稻纵卷叶螟,释放量一定时,赤眼蜂在稻株顶部以上5 cm高度、8点/0.07 hm 2释放密度的防治效果优于其他释放密度和高度的处理。而对于防控二化螟,不同释放高度对赤眼蜂防治效果差异不显著。     

大熊猫国家公园四川片区自然保护地空间关系对大熊猫分布的影响

理清自然保护地的空间关系与分布格局是加强空间管控、整合优化自然保护地体系的基础。以大熊猫国家公园四川片区内的自然保护地为案例,基于ArcGIS空间数据的处理、分析与可视化表达等功能,结合韦恩(Venn)图在空间层面上量化分析了公园范围内各类自然保护地的空间关系,并进一步揭示了不同保护情景下大熊猫(Ailuropoda melanoleuca)的分布格局。研究结果表明:(1)研究区内含有6类自然保护地,占研究区总面积的75.13%,其中40.68%为交叉重叠区域。(2)各类自然保护地皆存在大面积的交叉重叠。自然保护区为研究区面积最大的自然保护地类型,占自然保护地总面积的72.53%,其中45.89%为交叉重叠区域;其他类自然保护地占自然保护地总面积的60.87%,其中66.48%为交叉重叠区域。(3)猫点密度与自然保护地的交叉重叠程度呈现逆向增长趋势,区域的重叠水平越高,猫点密度越低。(4)自然保护地整体非重叠区的猫点密度高于重叠区。自然保护区是整体猫点密度最高的自然保护地类型,其非重叠区密度明显高于重叠区;森林公园非重叠区与水利风景区重叠区呈现较高的猫点密度。(5)与自然保护区交叉重叠的自然保护地中,位于自然保护区的猫点密度远高于其他重叠区。由此可见,大熊猫国家公园四川片区内原有自然保护地体系体量大但空间关系复杂,不同区域间的保护效能既不平衡也不充分。建议将研究区内自然保护区的非重叠区、位于自然保护区的世界遗产地区域、森林公园的非重叠区以及水利风景区的重叠区等作为大熊猫的核心保护区,施行严格保护;将自然保护区的重叠区、世界遗产地的其他区域作为生态保育区,恢复受损退化的大熊猫栖息地及所在的自然生态系统;将其他区域作为一般控制区,在有效维护大熊猫种群及其栖息地的前提下适度开展人为活动。同时,建议对空间重叠和邻近相接的区域开展科学评估,明确自然保护地的唯一属性。另一方面,我们期待健全自然保护地管理体制,统筹自然保护地的空间布局,为以国家公园为主体的自然保护地体系建设"松体制之绑"。     

Whole‐genome resequencing reveals the pleistocene temporal dynamics of Branchiostoma belcheri and Branchiostoma floridae populations

Global climatic fluctuations governed the ancestral demographic histories of species and contributed to place the current population status into a more extensive ecological and evolutionary context. Genetic variations will leave unambiguous signatures in the patterns of intraspecific genetic variation in extant species since the genome of each individual is an imperfect mosaic of the ancestral genomes. Here, we report the genome sequences of 20 Branchiostoma individuals by whole‐genome resequencing strategy. We detected over 140 million genomic variations for each Branchiostoma individual. In particular, we applied the pairwise sequentially Markovian coalescent (PSMC) method to estimate the trajectories of changes in the effective population size (N_e) of Branchiostoma population during the Pleistocene. We evaluated the threshold of sequencing depth for proper inference of demographic histories using PSMC was ≥25×. The PSMC results highlight the role of historical global climatic fluctuations in the long‐term population dynamics of Branchiostoma. The inferred ancestral N_e of the Branchiostoma belcheri populations from Zhanjiang and Xiamen (China) seawaters was different in amplitude before the first (mutation rate = 3 × 10^?9) or third glaciation (mutation rate = 9 × 10^?9) of the Pleistocene, indicating that the two populations most probably started to evolve in isolation in their respective seas after the first or third glaciation of the Pleistocene. A pronounced population bottleneck coinciding with the last glacial maximum was observed in all Branchiostoma individuals, followed by a population expansion occurred during the late Pleistocene. Species that have experienced long‐term declines may be especially vulnerable to recent anthropogenic activities. Recently, the industrial pollution and the exploitation of sea sand have destroyed the harmonious living environment of amphioxus species. In the future, we need to protect the habitat of Branchiostoma and make full use of these detected genetic variations to facilitate the functional study of Branchiostoma for adaptation to local environments.     

奇异变形杆菌中基因岛介导的多重耐药传播研究进展

奇异变形杆菌是导致医院内感染的重要条件致病菌,广泛分布于自然环境及人和动物的肠道中。基因岛是细菌染色体上约10-200 kb独立的DNA片段,能促进宿主细菌适应复杂多变的环境,与细菌适应性进化密切相关。近年来在奇异变形杆菌基因组中发现了多个与多重耐药密切相关的基因岛,包括沙门菌基因岛1及其相关基因岛、SXT/R391整合性接合元件、PmGRI1等,表明基因岛在奇异变形杆菌多重耐药形成和传播中具有重要作用。本文对奇异变形杆菌中与耐药相关基因岛的结构特征、传播机制、流行情况等进行综述,以期为奇异变形杆菌中多重耐药相关基因岛的深入研究提供参考。     

Endometrial extracellular matrix rigidity and IFNτ ensure the establishment of early pregnancy through activation of YAP

BackgroundIn mammals, early pregnancy is a critical vulnerable period during which complications may arise, including pregnancy failure. Establishment of a maternal endometrial acceptance phenotype is a prerequisite for semiheterogeneous embryo implantation, comprising the rate‐limiting step of early pregnancy.MethodsConfocal fluorescence, immunohistochemistry and western blot for nuclear and cytoplasmic protein were used to examine the activation of yes‐associated protein (YAP) in uterine tissue and primary endometrial cells. The target binding between miR16a and YAP was verified by dual‐luciferase reporter gene assay. The mouse pregnancy model and pseudopregnancy model were used to investigate the role of YAP in the maternal uterus during early pregnancy in vivo.ResultsWe showed that YAP translocates into the nucleus in the endometrium of cattle and mice during early pregnancy. Mechanistically, YAP acts as a mediator of ECM rigidity and cell density, which requires the actomyosin cytoskeleton and is partially dependent on the Hippo pathway. Furthermore, we found that the soluble factor IFNτ, which is a ruminant pregnancy recognition factor, also induced activation of YAP by reducing the expression of miR‐16a.ConclusionsThis study revealed that activation of YAP is necessary for early pregnancy in bovines because it induced cell proliferation and established an immunosuppressive local environment that allowed conceptus implantation into the uterine epithelium.     

SETD2 epidermal deficiency promotes cutaneous wound healing via activation of AKT/mTOR Signalling

ObjectivesCutaneous wound healing is one of the major medical problems worldwide. Epigenetic modifiers have been identified as important players in skin development, homeostasis and wound repair. SET domain–containing 2 (SETD2) is the only known histone H3K36 tri‐methylase; however, its role in skin wound healing remains unclear.Materials and MethodsTo elucidate the biological role of SETD2 in wound healing, conditional gene targeting was used to generate epidermis‐specific Setd2‐deficient mice. Wound‐healing experiments were performed on the backs of mice, and injured skin tissues were collected and analysed by haematoxylin and eosin (H&E) and immunohistochemical staining. In vitro, CCK8 and scratch wound‐healing assays were performed on Setd2‐knockdown and Setd2‐overexpression human immortalized keratinocyte cell line (HaCaT). In addition, RNA‐seq and H3K36me3 ChIP‐seq analyses were performed to identify the dysregulated genes modulated by SETD2. Finally, the results were validated in functional rescue experiments using AKT and mTOR inhibitors (MK2206 and rapamycin).ResultsEpidermis‐specific Setd2‐deficient mice were successfully established, and SETD2 deficiency resulted in accelerated re‐epithelialization during cutaneous wound healing by promoting keratinocyte proliferation and migration. Furthermore, the loss of SETD2 enhanced the scratch closure and proliferation of keratinocytes in vitro. Mechanistically, the deletion of Setd2 resulted in the activation of AKT/mTOR signalling pathway, while the pharmacological inhibition of AKT and mTOR with MK2206 and rapamycin, respectively, delayed wound closure.ConclusionsOur results showed that SETD2 loss promoted cutaneous wound healing via the activation of AKT/mTOR signalling.