墨兰幼叶和成熟叶不同部位叶绿体超微结构和光合作用

墨兰试管苗植株成熟叶片叶绿体基粒较发达,类囊本膜垛叠较紧密。幼叶叶绿体中少有亲锇颗粒,成熟叶的叶绿体中往往既有亲锇颗粒又有淀粉粒。幼叶中基粒数目比成熟叶的少,叶绿体也比成熟叶的小。幼叶的光合放氧速率比成熟叶的低。幼叶中叶尖部叶绿体最大而叶基部最小,但叶尖部的光合放氧速率比叶基部小。成熟叶中叶绿体大小及光合放氧速率区别不明显。通过对各部位叶绿素含量的测定发现,叶绿素含量与光合放氧速率之间没有正相关性     

农业生态系统可持续发展趋势度的评价方法研究

在对农业生态系统时间演替过程分析的基础上,以评价指标年际变异性、评价指标的时间发展斜率变化率和评价指标的初如阈值水平为评价领域,提出了可持续发展趋势度的概念。并以德清县为例进行了案例分析,结果表明该县的可持续度为0.657,属中上水平。     

湿加松无性系表型遗传多样性研究

以35个湿加松（Pinus elliottii×P.caribaea Morelet var.hondurensis）无性系为试验材料,对其8个表型性状进行相关性分析、聚类分析及主成分分析研究,并深入探讨了遗传多样性水平,为湿加松无性系利用及良种选育提供科学依据。结果表明：（1）生长性状变异系数介于12.31~29.28%,均值为22.90%;多样性指数介于1.61~1.80,均值为1.69。形质性状变异系数介于13.34~47.25%,均值为26.86%;多样性指数介于1.50~1.94,均值为1.77。表明湿加松无性系遗传变异较为丰富,遗传多样性水平较高。（2）8对表型性状两两间有11对呈极显著正相关,5对呈显著正相关。选定材积为该材料育种选择的主要指标,其次为树高。（3）采用系统聚类法在欧式距离为12的时候将35个无性系分为6大类群,部分来源相同或父本相同的聚为一类,说明它们在表型上的变异较小。（4）针对8个表型性状做主成分分析提取了3个主成分,累积贡献率达86.00%,主要代表了6个性状,以此来表达所有供试材料的综合变异情况。     

氮素形态对杉木幼苗侧根生长和叶片光合特性的影响

以3月龄的杉木实生苗为试验材料,分析了不同氮素形态——硝态氮(NO₃^- N)、铵态氮(NH4⁺ N)和硝酸铵(NH₄NO₃)(氮素浓度均为3 mmol·L^-1)对杉木幼苗侧根生长、叶片光合气体交换参数和叶绿素荧光参数的影响,以揭示杉木幼苗对不同形态氮的偏好性,以及不同形态氮肥下杉木幼苗侧根生长和光合生理的响应特征,为杉木苗期氮肥管理提供理论依据。结果显示：(1)不同氮素形态对杉木幼苗地上部和侧根生物量具有显著影响,其中NH₄⁺ N处理下幼苗地上部和侧根生物量最大,NO₃^- N处理次之,而NH₄NO₃处理最小。(2)NH₄⁺ N和NO₃^- N处理下杉木幼苗总根长、根系总表面积和根系总体积均显著高于NH₄NO₃处理(P＜0.05),且NH₄⁺ N处理又显著高于NO₃^- N处理,但不同氮形态处理间侧根数量差异不显著。(3)NH₄⁺ N处理下杉木幼苗叶片净光合速率、气孔导度和蒸腾速率明显高于NO₃^- N和NH₄NO₃处理,但NO₃^- N和NH₄NO₃处理之间无明显差异。(4)NH₄⁺ N处理下杉木叶片初始荧光强度低于NO₃^- N处理,而最大荧光强度、可变荧光强度和PSⅡ潜在活性却高于全硝氮和硝铵氮处理。上述结果表明,NH₄⁺ N处理不仅有利于杉木幼苗侧根生长发育,且其叶片具有较强的光合能力,较高的PSⅡ中心稳定性、光化学活性以及电子传递效率,从而更有利于植株生长。因此,从根系生长和光合特性来看,杉木幼苗对铵态氮具有偏好性。     

P38α/β在黑色素瘤细胞辐射应急响应中的作用

P38有丝分裂原激活蛋白激酶(MAPK)在肿瘤的发生发展中的作用仍然存在争议。实验结果显示,P38α/β特异性抑制剂SB202190可以显著增加黑色素瘤细胞的倍增时间、降低细胞的微核率,但对γH2AX foci的形成和克隆存活率并没有明显影响。提示P38α/β可能不影响人黑色素瘤细胞的DNA损伤修复能力及细胞的辐射敏感性,而是通过提高细胞的增殖速率、增加基因组不稳定性来促进人黑色素瘤细胞的恶性发展。     

Phenology of high-arctic butterflies and their floral resources： Species-specific responses to climate change

Current global warming is particularly pronounced in the Arctic and arthropods are expected to respond rapidly to these changes. Long-term studies of individual arthropod species from the Arctic are, however, virtually absent. We examined butterfly specimens collected from yellow pitfall traps over 14 years （1996-2009） at Zackenberg in high-arctic, north-east Greenland. Specimens were previously sorted to the family level. We identified them to the species level and examined long-term species-specific phenological responses to recent summer wanning. Two species were rare in the samples （Polaris fritillary Boloria polaris and Arctic blue Plebejus glandon） and statistical analyses of phenological responses were therefore restricted to the two most abundant species （Arctic fritillary, B. chariclea and Northern clouded yellow Colias hecla）. Our analyses demonstrated a trend towards earlier flight seasons in B. chariclea, but not in C. hecla. The timing of onset, peak and end of the flight season in B. chariclea were closely related to snowmelt, July temperature and their interaction, whereas onset, peak and end of the flight season in C. hecla were only related to timing of snowmelt. The duration of the butterfly flight season was significantly positively related to the temporal overlap with floral resources in both butterfly species. We further demonstrate that yellow pitfall traps are a useful alternative to transect walks for butterfly recording in tundra habitats. More phenological studies of Arctic arthropods should be carded out at the species level and ideally be analysed in context with interacting species to assess how ongoing climate change will affect Arctic biodiversity in the near future [Current Zoology 60 （2）： 243-251, 2014].     

针对T315I 突变的Bcr-Abl 酪氨酸激酶抑制剂研究进展

BCR-ABL 是一种由bcr 基因和c-abl 原癌基因融合产生的致癌基因。该基因表达的Bcr–Abl 癌蛋白是慢性粒细胞白血病的病理学基础。因此研发选择性的Bcr–Abl 酪氨酸激酶抑制剂成为治疗慢性粒细胞白血病的一种有效策略。目前已有数个Bcr–Abl 酪氨酸激酶抑制剂获准上市。然而,Abl 激酶结构域的突变或其他原因导致肿瘤耐药性的出现,其中T315I 突变是最重要的突变之一,引发的耐药性更是难以克服。重点介绍了针对T315I 突变的Bcr–Abl 酪氨酸激酶抑制剂的研究进展。     

胸腺法新联合恩替卡韦治疗慢性病毒性乙型肝炎的疗效及对患者血清HA、Ⅳ-C、LN和免疫功能的影响

目的:探讨胸腺法新联合恩替卡韦(ETV)治疗慢性病毒性乙型肝炎(CVHB)的临床效果及对患者血清透明质酸(HA)、Ⅳ型胶原(Ⅳ-C)、层黏蛋白(LN)水平和免疫功能的影响。方法:选取我院2013年6月～2016年7月收治的102例CVHB患者,采取随机数字表法均分为两组。对照组(51例)予以恩替卡韦抗病毒治疗,观察组(51例)在此基础上加用胸腺法新治疗。比较两组的临床疗效,治疗前后血清HA、Ⅳ-C、LN水平及外周血T细胞亚群水平的变化和不良反应的发生情况。结果:治疗48周后,观察组总有效率为84.3%,较对照组明显升高(66.7%,P0.05)。与治疗前相比,两组治疗48周后血清HA、Ⅳ-C、LN水平均显著降低(P0.01),外周血CD3~+、CD4~+、CD4~+/CD8~+水平较治疗前均显著提高(P0.01),且观察组血清HA、Ⅳ-C、LN水平显著低于对照组(P0.01)。外周血CD3~+、CD4~+、CD4~+/CD8~+水平较对照组显著升高(P0.01)。治疗过程中,对照组和观察组不良反应率分别为7.8%和11.8%,差异无统计学意义(P0.05)。结论:与单用ETV治疗相比,胸腺法新联合ETV治疗CVHB更能有效消除/缓解患者的症状体征,提高其免疫功能和疗效,且安全性高,可能与其降低血清HA、Ⅳ-C、LN水平有关。     

Bcl-2/Beclin-1复合体在自噬中的调节作用

自噬(autophagy)是一种进化保守的溶酶体依赖性分解代谢途径,是细胞维持自稳态的重要机制之一,并参与多种疾病的发生. Beclin-1作为自噬体成核的关键分子之一,是1个调节自噬的关键靶点. Beclin-1有1个BH3结构域,Bcl-2、Bcl-XL等可以通过这个BH3结构域与Beclin-1结合而影响其活性. 抗凋亡Bcl-2家族蛋白和Beclin-1的表达水平、磷酸化、分子的亚细胞定位以及BH3-only蛋白等,均可调节Beclin-1蛋白和Bcl-2家族蛋白结合水平,进而调控自噬的发生,并可能对细胞最终走向自噬还是凋亡起着关键作用.     

TGBp3 triggers the unfolded protein response and SKP1‐dependent programmed cell death

The Potato virus X (PVX) triple gene block protein 3 (TGBp3), an 8‐kDa membrane binding protein, aids virus movement and induces the unfolded protein response (UPR) during PVX infection. TGBp3 was expressed from the Tobacco mosaic virus (TMV) genome (TMV‐p3), and we noted the up‐regulation of SKP1 and several endoplasmic reticulum (ER)‐resident chaperones, including the ER luminal binding protein (BiP), protein disulphide isomerase (PDI), calreticulin (CRT) and calmodulin (CAM). Local lesions were seen on leaves inoculated with TMV‐p3, but not TMV or PVX. Such lesions were the result of TGBp3‐elicited programmed cell death (PCD), as shown by an increase in reactive oxygen species, DNA fragmentation and induction of SKP1 expression. UPR‐related gene expression occurred within 8 h of TMV‐p3 inoculation and declined before the onset of PCD. TGBp3‐mediated cell death was suppressed in plants that overexpressed BiP, indicating that UPR induction by TGBp3 is a pro‐survival mechanism. Anti‐apoptotic genes Bcl‐xl, CED‐9 and Op‐IAP were expressed in transgenic plants and suppressed N gene‐mediated resistance to TMV, but failed to alleviate TGBp3‐induced PCD. However, TGBp3‐mediated cell death was reduced in SKP1‐silenced Nicotiana benthamiana plants. The combined data suggest that TGBp3 triggers the UPR and elicits PCD in plants.