中国林蛙蝌蚪的口器发育

采用扫描电镜和组织学技术观察了中国林蛙(Rana chensinensis)蝌蚪发育过程中口器外部形态结构的变化,以及中国林蛙蝌蚪口器内部结构特征.结果表明,在口器发育的初期,角质颌最先出现,接着出现唇乳突以及唇齿;在变态高峰期(G4l～G42),口器结构如唇齿、角质颌和唇乳突则是按以下顺序消失的,即唇齿最先消失,其次...     

不同盐胁迫对外来植物黄顶菊生理特征的影响

以外来植物黄顶菊幼苗为材料,通过室内盆栽实验比较不同盐度中性盐(NaCl)和碱性盐(Na2CO3)胁迫对其生长和生理指标的影响。结果表明:(1)两种盐胁迫均能不同程度引起黄顶菊叶片细胞膜的完整性损伤和叶片电解质外渗率升高,且Na2CO3的伤害更严重;黄顶菊植株叶内丙二醛含量在各盐度NaCl胁迫处理下无显著变化,而在Na2CO3处理下却显著升高,且150 mmol/L Na2CO3处理叶内达到最高值(2.284×10-2μmol.g-1FW)。(2)黄顶菊的生长在低盐度的NaCl(50 mmol/L)处理下受到一定的促进,而相同盐度的Na2CO3下却受到明显抑制;经NaCl处理的黄顶菊地上部分和地下部分日相对生长率均大于相同盐度的Na2CO3处理。(3)黄顶菊叶内可溶性糖和游离脯氨酸含量在NaCl胁迫处理中变化不显著,而它们在Na2CO3处理植株中却变化显著,两者在200mmol/L Na2CO3处理植株叶内分别达到177.3μmol.g-1FW和4.21 mg.g-1DW;NaCl处理的黄顶菊地上部分含水量明显高于相同盐度下的Na2CO3处理,而两种盐对黄顶菊地下部分相对含水量的影响不显著。研究发现,黄顶菊对于中性盐渍土具有较强的耐性和抗性,而在碱性盐渍土上的侵入和发展均受到一定的抑制。     

河南新郑望京楼遗址出土的动物骨骼及其反映的家养动物的差异化

聚落考古研究表明,二里头文化时期（1750~1530 BC）中原腹地出现了都邑和大、中、小型四级聚落系统,东亚地区由此进入了早期广域王权国家时代。二里头文化时期的生业经济研究对于理解中华文明形成与早期发展过程中的关键时期的社会变革与文化演进的骤然提速具有重要意义。家养动物及其副产品的开发和利用、管理和分配是生业经济研究和社会复杂化发展的重要内容。在以往研究中,尽管学界已对二里头文化时期的核心都邑二里头遗址和若干中小型聚落遗址开展了多项动物考古学研究,但是针对大型聚落的系统分析较少。鉴于此,本文以河南省新郑市望京楼遗址发掘出土的动物骨骼为研究对象,通过种属鉴定、数量统计、测量数据分析、死亡年龄推算等方法,尝试探讨居于大型聚落的先民对动物资源的消费和利用。结果显示,该遗址的家养动物有猪、黄牛、绵羊、山羊和狗,家养动物数量占多数。遗址的猪多数为未成年个体,说明肉食消费是遗址先民养猪的主要目的;绵羊多数为成年个体,说明获取羊毛是遗址先民养羊的主要目的。通过与二里头、南洼、煤山和皂角树等其他等级聚落遗址的比较可知,早期国家的都邑和大中型聚落的家养动物的种类更丰富,绵羊的数量比例随聚落等级的降低而减少,绵羊的身体尺寸随聚落等级的降低而变小,以获取羊毛为主要目的养羊业更容易在高等级聚落中出现。这一研究揭示了早期国家大型聚落和国家内部不同等级聚落开发利用动物资源的特点和差异,为从动物考古的角度探讨早期社会复杂化提供了可能性。     

Intersectin-Cdc42 interaction is required for orderly meiosis in porcine oocytes

Intersectins (ITSNs) have been shown to act as adaptor proteins that govern multiple cellular events via regulating Cdc42 activity. However, it remains to be determined whether the ITSN-Cdc42 pathway is functional in porcine oocytes. To address this question, we used a small molecule, ZCL278, to selectively disrupt the ITSN2-Cdc42 interaction. In the present study, we find that porcine oocytes exposed to ZCL278 are unable to completely progress through meiosis. Meanwhile, the spindle defects and chromosomal congression failure are frequently detected in these oocytes. In support of this, we observed the accumulated distribution of vesicle-like ITSN2 signals around the chromosome/spindle region during porcine oocyte maturation. In addition, our results also showed that inhibition of the ITSN-Cdc42 interaction impairs the actin polymerization in porcine oocytes. In summary, the findings support a model where ITSNs, through the interaction with Cdc42, modulates the assembly of meiotic apparatus and actin polymerization, consequently ensuring the orderly meiotic progression during porcine oocyte maturation.     

高糖环境下持续性牵张力对子宫平滑肌细胞白介素-1和白介素-6表达的影响

目的:探讨高糖环境下持续性牵张力对大鼠子宫平滑肌细胞白介素-1(IL-1)、白介素-6(IL-6)表达的影响。方法:体外培养大鼠子宫平滑肌细胞,高糖作用不同时间后,观察高糖状态下大鼠子宫平滑肌细胞IL-1、IL-6表达变化情况。对高糖状态下的肌细胞施加持续性牵张力,明确牵张力对肌细胞IL-1、IL-6表达的影响以及高糖和牵张力之间的协同作用,同时采用晚期糖基化终末产物(AGEs)抑制剂拮抗高糖作用作为参照,并对结果进行分析。结果:随着高糖作用时间增加,肌细胞IL-1、IL-6表达也随之升高。牵张力也可促进肌细胞IL-1、IL-6表达增加,并可与高糖状态产生协同作用,这一过程可被高糖抑制剂部分阻断,但不能完全阻断。结论:高糖状态及牵张力均可促进肌细胞IL-1、IL-6表达增加,并有一定协同作用,AGEs参与了这一过程,但并不是唯一途径。     

濒危植物毛瓣金花茶遗传多样性的ISSR分析

采用ISSR分子标记对毛瓣金花茶6个自然居群的遗传多样性进行了分析。利用11个引物对150个个体进行了扩增,共扩增出92条条带,其中多态性条带74条。毛瓣金花茶在物种水平和居群水平都表现出相对较高的遗传多样性,在物种水平上,多态位点百分率(PPB)为80.43%,Nei’s基因多样性指数(h)为0.245 1,Shannon多样性指数(I)为0.377 6;在居群水平上,PPB为58.70%~66.30%,h为0.199 7~0.229 3,I为0.300 9~0.343 8。Nei’s遗传多样性分析和AMOVA分析表明,毛瓣金花茶的遗传变异主要存在于居群内,居群间的遗传分化程度较低(Gst=0.126 6,Φst=11.37%),基因流(Nm)为3.448 0。Mantel检测表明,居群间的遗传距离和地理距离之间存在显著的相关关系(r=0.755 1,P0.05)。研究认为,毛瓣金花茶较高的遗传多样性和较低的遗传分化可能与其异交型繁育系统和鸟类传粉有关。     

民勤绿洲荒漠过渡带植物群落数量分类和排序研究

绿洲-荒漠过渡带作为绿洲与荒漠的连接区域,在干旱区生态环境退化与恢复研究中具有重要意义。该研究以民勤绿洲荒漠过渡带为例,在47个植物群落调查样地的基础上,应用双向指示种分类法(TWINSPAN)和除趋势对应分析法(DCA)对研究区典型植物群落进行数量分类和排序,并讨论了影响植物群落类型及空间分布的环境因子。结果表明:(1)研究区植物群落结构简单,植物种以旱生耐盐植物为主。(2)TWINSPAN分类将研究区的植物群落划分为11个群丛类型,即白刺+盐生草群丛、白刺+芦苇群丛、白刺+盐爪爪群丛、盐爪爪+黑果枸杞群丛等,分类结果在空间上反映了民勤绿洲荒漠过渡带植物群落的演替变化趋势。(3)DCA排序结果验证了TWINSPAN分类结果的合理性,同时指出制约民勤绿洲荒漠过渡带植物群落类型及空间分布的重要环境因子是地下水埋深和地貌形态。     

Genetic deficiency of neuronal RAGE protects against AGE-induced synaptic injury

Synaptic dysfunction and degeneration is an early pathological feature of aging and age-related diseases, including Alzheimer''s disease (AD). Aging is associated with increased generation and deposition of advanced glycation endproducts (AGEs), resulting from nonenzymatic glycation (or oxidation) proteins and lipids. AGE formation is accelerated in diabetes and AD-affected brain, contributing to cellular perturbation. The extent of AGEs'' involvement, if at all, in alterations in synaptic structure and function is currently unknown. Here we analyze the contribution of neuronal receptor of AGEs (RAGE) signaling to AGE-mediated synaptic injury using novel transgenic neuronal RAGE knockout mice specifically targeted to the forebrain and transgenic mice expressing neuronal dominant-negative RAGE (DN-RAGE). Addition of AGEs to brain slices impaired hippocampal long-term potentiation (LTP). Similarly, treatment of hippocampal neurons with AGEs significantly decreases synaptic density. Such detrimental effects are largely reversed by genetic RAGE depletion. Notably, brain slices from mice with neuronal RAGE deficiency or DN-RAGE are resistant to AGE-induced LTP deficit. Further, RAGE deficiency or DN-RAGE blocks AGE-induced activation of p38 signaling. Taken together, these data show that neuronal RAGE functions as a signal transducer for AGE-induced synaptic dysfunction, thereby providing new insights into a mechanism by which the AGEs–RAGE-dependent signaling cascade contributes to synaptic injury via the p38 MAP kinase signal transduction pathway. Thus, RAGE blockade may be a target for development of interventions aimed at preventing the progression of cognitive decline in aging and age-related neurodegenerative diseases.Advanced glycation endproducts (AGEs) are members of a heterogeneous class of molecules, which modify cellular function by distinct mechanisms, including ligation and activation of signal transduction receptors. The products of non-enzymatic glycation (or oxidation) of proteins and lipids, AGEs contribute to the normal aging process and when accelerated have a causative role in the vasculature complications of diabetes mellitus and several neurodegenerative diseases, including Alzheimer''s (AD), Parkinson''s, and Huntington''s diseases.^{1, 2, 3, 4, 5} In diabetic patients, the concentration of circulating AGEs (serum AGE level) has been reported at 7.2–22 mU/ml (equivalent to 30–88 μg/ml AGE-BSA), which is significantly higher than that of non-diabetic patients (3 mU/ml, equivalent to 12 μg/ml AGE-BSA).^{6, 7, 8} The brain AGE level was also increased to 5-6 μM (equivalent to 325–390 μg/ml AGE-BSA) in the diabetic animal model.⁹ Excess AGE accumulation is detrimental to neurons and is believed to be a key to the pathogenesis of cognitive decline in normal aging and specific chronic diseases of aging. For example, in a recent clinical study, peripheral AGE levels were associated with cognitive decline in older adults with and without diabetes.¹⁰ Diabetes complications affect the brain, increasing risk for depression, dementia, and AD. In fact, patients with type 2 diabetes are at twofold to threefold increased relative risk for AD^{11, 12, 13, 14, 15, 16, 17, 18} and accelerated cognitive dysfunction.Long-lived proteins such as β-amyloid peptide (Aβ) and hyperphosphorylated tau protein that accumulate in AD brain are highly susceptible to AGE modification.^{19, 20, 21, 22} AGE-modified Aβ or tau protein results in increased oxidative stress and chronic inflammation, accelerating AD pathology and neuronal perturbation.^{19, 20, 22, 23, 24, 25} Moreover, Aβ or tau glycation results in increased aggregation and subsequent formation of senile plaques or neurofibrillary tangles, the major pathological feature of AD,^{19, 22} suggesting that AGE modification is an important risk factor for neurodegenerative diseases.²⁶ Although increased accumulation of AGEs in brain, as seen in aging, diabetes, or neurodegenerative diseases, speeds up oxidative damage to neurons contributing to synaptic dysfunction and cognitive decline, its underlying mechanisms are not well understood.Receptor for advanced glycation endproduct (RAGE) was first identified as a cell surface receptor of the immunoglobulin superfamily for AGEs.^{27, 28} Increased expression of RAGE occurs in neuronal and non-neuronal cells in the peripheral and central nervous system in aging, diabetes, and AD-affected individuals, where RAGE ligands are upregulated.^{29, 30} Although it has been shown that AGEs–RAGE interaction contributes to cellular perturbation relevant to the pathogenesis of the cardiovascular disease and the diabetes vascular complications,^{31, 32, 33} little is known about the role of AGEs and its interaction with RAGE on synaptic dysfunction. To understand the mechanisms involved in AGE-mediated synaptic damage, the following questions need to be addressed: (1) ‘Do AGEs alter synaptic structure and function? If so, are these changes dependent on RAGE signaling?'' (2) ‘Does RAGE blockage by genetic depletion protect from AGE-induced synaptic dysfunction and loss?'' and (3) ‘What is the impact of neuronal RAGE in AGE-induced aberrant synaptic function?''. Thus it is important to evaluate the impact of AGEs–RAGE interaction on synaptic dysfunction and to explore the mechanism underlying AGE–RAGE-dependent signal transduction and its contribution to synaptic damage.Here we investigate neuronal RAGE signaling in AGE-induced synaptic injury using our novel conditional RAGE knockout mice targeted to cortical neurons as well as transgenic mice that overexpress signal transduction-deficient mutants of RAGE in neurons. Given that neuronal and non-neuronal cells in the brain may contribute to AGE-induced sustained neuronal and synaptic stress and dysfunction, we assessed the impact of global RAGE deletion in this setting and further delineated the mechanism by which RAGE-dependent activation of p38 MAP kinase potentiates AGE-insulted synaptic injury.     

香菇液体发酵高产多糖菌株筛选

通过评价香菇野生菌株发酵产多糖性能,筛选高产香菇多糖菌株.以采自长白山野生香菇通过组织分离获得的6株菌株和2株人工栽培菌株为出发菌株,对不同发酵培养时间菌丝体生物量、胞内多糖含量、胞外多糖含量等进行测试分析,结果表明,8株菌株随着培养时间的延长,菌丝体生物量均有不同程度的增加,但胞内多糖含量和胞外多糖得率变化趋势不同,...     

Inactivation of the Cullin (CUL)-RING E3 ligase by the NEDD8-activating enzyme inhibitor MLN4924 triggers protective autophagy in cancer cells

The multiunit Cullin (CUL)-RING E3 ligase (CRL) controls diverse biological processes by targeting a mass of substrates for ubiquitination and degradation, whereas its dysfunction causes carcinogenesis. Post-translational neddylation of CUL, a process triggered by the NEDD8-activating enzyme E1 subunit 1 (NAE1), is required for CRL activation. Recently, MLN4924 was discovered via a high-throughput screen as a specific NAE1 inhibitor and first-in-class anticancer drug. By blocking CUL neddylation, MLN4924 inactivates CRL and causes the accumulation of CRL substrates that trigger cell cycle arrest, senescence and/or apoptosis to suppress the growth of cancer cells in vitro and in vivo. Recently, we found that MLN4924 also triggers protective autophagy in response to CRL inactivation. MLN4924-induced autophagy is attributed partially to the inhibition of mechanistic target of rapamycin (also known as mammalian target of rapamycin, MTOR) activity by the accumulation of the MTOR inhibitory protein DEPTOR, as well as reactive oxygen species (ROS)-induced stress. Moreover, the blockage of autophagy response enhances apoptosis in MLN4924-treated cells. Together, our findings not only reveal autophagy as a novel cellular response to CRL inactivation by MLN4924, but also provide a piece of proof-of-concept evidence for the combination of MLN4924 with autophagy inhibitors to enhance therapeutic efficacy.