Saving face: the emotional costs of the Asian immigrant family myth

Access to resources through ethnic group membership is often presumed to affect the intensity of ethnic identification. We examine this premise using survey data on three ethnic groups in Mauritius: Creoles, Hindus, and Muslims. Two key findings emerge from our research. First, access to material resources explains only a modest proportion of total variation in ethnic identification within each group. Second, the resources that affect ethnic identification differ significantly across groups. Access to political goods through group membership affects Hindu identification but is unrelated to ethnic identification among Creoles or Muslims. Conversely, access to economic goods affects Creole and Muslim identification but has no effect on Hindu identification. Explaining these group differences leads us beyond a basic means–ends instrumentalist model to identify conditions that likely mediate the relationship between individual interests and collective identification including the divisibility of economic goods relative to political goods in Mauritius.     

Potentilla jiaozishanensis sp. nov. (sect. Leptostylae,Rosaceae) from southwest China

Potentilla jiaozishanensis, a distinct new species of Rosaceae from Yunnan, China, is described and illustrated. Morphologically, it is closely related to P. stenophylla var. stenophylla but clearly differs from the latter by its bidentate leaflets, lanceolate epicalyx‐segments that are longer than the sepals, villose ovaries and achenes. Moreover, the pollen grains of P. jiaozishanensis are markedly different from those of P. stenophylla var. stenophylla in size and shape. The newly described species is endemic to the Jiaozishan Mountains, southwest China.     

PI3K and Notch signal pathways coordinately regulate the activation and proliferation of T lymphocytes in asthma

AimsIn the present study, we determined whether Phosphoinositide 3-kinase (PI3K) and Notch signal pathways are involved in the expression of cyclinD1, cyclinA and p27kip1 which were key molecules in controlling cell cycling from CD4⁺ T lymphocyte in animal model of asthma.Main methodsOvalbumin (OVA) sensitized murine model of asthma was used to investigate the expression of cyclin D1, cyclin A, and p27kip1 by splenic CD4⁺ T lymphocytes. We further observed the effect of specific inhibitor of PI3K(LY294002) and specific inhibitor of Notch(DAPT) on the proliferation of such CD4⁺ T lymphocytes.Key findingsWe found that the expression of cyclinD1 and cyclinA was upregulated at both protein and mRNA levels in asthma group while p27kip1 was down-regulated. Both LY294002 and DAPT inhibit the proliferation of CD4⁺ T lymphocytes in a time- and dose-dependent manner. Furthermore, LY294002 and DAPT have additive effect in down-regulation of cyclinD1 and upregulation of p27kip1. An upregulation of cyclinA, although not statistically significant, was also observed.SignificanceThese data suggested that PI3K signal pathway and Notch signal pathway may coordinately regulate the cell proliferation and differentiation processes through up-regulating cyclinD1 and down-regulating p27kip1 of CD4⁺ T lymphocytes.     

Comparison of population genetic patterns in two widespread freshwater mussels with contrasting life histories in western North America

We investigate population genetic structuring in Margaritifera falcata, a freshwater mussel native to western North America, across the majority of its geographical range. We find shallow rangewide genetic structure, strong population‐level structuring and very low population diversity in this species, using both mitochondrial sequence and nuclear microsatellite data. We contrast these patterns with previous findings in another freshwater mussel species group (Anodonta californiensis/A. nuttalliana) occupying the same continental region and many of the same watersheds. We conclude that differences are likely caused by contrasting life history attributes between genera, particularly host fish requirements and hermaphroditism. Further, we demonstrate the occurrence of a ‘hotspot’ for genetic diversity in both groups of mussels, occurring in the vicinity of the lower Columbia River drainage. We suggest that stream hierarchy may be responsible for this pattern and may produce similar patterns in other widespread freshwater species.     

Functional consequences of retro-inverso isomerization of a miniature protein inhibitor of the p53–MDM2 interaction

Peptide retro-inverso isomerization is thought to be functionally neutral and has been widely used as a tool for designing proteolytically stable d-isomers to recapitulate biological activities of their parent l-peptides. Despite success in a wide range of applications, exceptions amply exist that clearly defy this rule of thumb when parent l-peptides adopt an α-helical conformation in their bound state. The detrimental energetic effect of retro-inverso isomerization of an α-helical l-peptide on its target protein binding has been estimated to be 3.0–3.4 kcal/mol. To better understand how the retro-inverso isomer of a structured protein works at the molecular level, we chemically synthesized and functionally characterized the retro-inverso isomer of a rationally designed miniature protein termed stingin of 18 amino acid residues, which adopts an N-terminal loop and a C-terminal α-helix stabilized by two intra-molecular disulfide bridges. Stingin emulated the transactivation peptide of the p53 tumor suppressor protein and bound with high affinity and via its C-terminal α-helix to MDM2 and MDMX—the two negative regulators of p53. We also prepared the retro isomer and d-enantiomer of stingin for comparative functional studies using fluorescence polarization and surface plasmon resonance techniques. We found that retro-inverso isomerization of l-stingin weakened its MDM2 binding by 720 fold (3.9 kcal/mol); while enantiomerization of l-stingin drastically reduced its binding to MDM2 by three orders of magnitude, sequence reversal completely abolished it. Our findings demonstrate the limitation of peptide retro-inverso isomerization in molecular mimicry and reinforce the notion that the strategy works poorly with biologically active α-helical peptides due to inherent differences at the secondary and tertiary structural levels between an l-peptide and its retro-inverso isomer despite their similar side chain topologies at the primary structural level.¹     

ERK介导的炎性反应参与肾缺血再灌注损伤

目的研究小鼠肾缺血再灌注损伤的发病机制。方法建立小鼠肾缺血再灌注损伤模型。12只雄性C57BL／6随机分为2个组（n=6）,分别为假手术组（Sham）,肾缺血再灌注损伤模型组（IRI）。IRI组血管夹夹闭左肾动脉,置于32℃温箱后1h松开血管夹,去除右肾。Sham组操作同上,但不夹闭左肾动脉。再灌注24h后处死小鼠,收集血清和肾脏标本。测定血清肌酐（Cr）和血尿素氮（BUN）。PAS染色后显微镜下观察肾脏形态学变化,Western印迹分析ERK、p-ERK的表达,PCR检测MCP-1、IFN-γ。结果与假手术组（Sham）相比,IRI组血清肌酐、血尿素氮明显升高,病理检查可见肾脏内肾小管上皮细胞明显肿胀坏死、蛋白管型形成明显,还可观察到炎性细胞浸润明显增加。ERK、p-ERKWestern印迹结果PCR显示MCP-1、TNF-α也明显上调,但ERK表达不变。结论在肾缺血再灌注中,ERK激活介导的炎性后府可能参与了肾扣伤。     

EZH2在乳腺癌中的表达及其临床意义

目的 探讨EZH2在乳腺癌中的表达及其临床意义.方法 用免疫组化的方法研究105例乳腺癌中EZH2蛋白表达情况,并进一步探讨其与乳腺癌临床病理因素及其预后的关系.结果 EZH2蛋白在乳腺癌组织中表达明显高于乳腺良性疾病,其表达与患者年龄、肿瘤大小、TNM分期、PR和c-erbB-2表达无关(P＞0.05),与淋巴结转移、病理组织学分级、ER表达及乳腺癌预后相关(P＜0.05).EZH2蛋白表达在三阴性乳腺癌中表达明显高于非三阴性乳腺癌(P＜0.05).结论 EZH2在乳腺癌淋巴结转移及侵袭中扮演一定的角色,其与乳腺癌预后相关,与ER阴性的乳腺癌发生发展有关.     

食用菌加工产业研究现状与前景

食用菌加工是利用物理、化学和生物方法处理食用菌子实体或菌丝体,生产食用菌制品。它可以解决食用菌从生产到商品出售所存在的时间矛盾,提高食用菌的商品价值。详细介绍了食用菌的干制加工、盐渍加工及罐藏加工技术,概括了食用菌深加工产业的发展现状及研究进展,提出了对食用菌加工的展望。     

医学真菌基因组学研究进展(上)

近年来,一系列重要医学致病真菌全基因组数据陆续被公布,使人类对这些致病菌的认识提高到全新水平.本文在回溯医学真菌基因组学和基因组测序技术发展历程、综述其发展现状及应用的基础上,再分别介绍重要医学真菌全基因组测序的进展.     

Senescence evasion in melanoma progression: uncoupling of DNA‐damage signaling from p53 activation and p21 expression

The best‐established function of the melanoma‐suppressor p16 is mediation of cell senescence, a permanent arrest following cell proliferation or certain stresses. The importance of p16 in melanoma suggests indolence of the other major senescence pathway through p53. Little or no p53 is expressed in senescent normal human melanocytes, but p16‐deficient melanocytes can undergo p53‐mediated senescence. As p16 expression occurs in nevi but falls with progression toward melanoma, we here investigated whether p53‐dependent senescence occurs at some stage and, if not, what defects were detectable in this pathway, using immunohistochemistry. Phosphorylated checkpoint kinase 2 (CHEK2) can mediate DNA‐damage signaling, and under some conditions senescence, by phosphorylating and activating p53. Remarkably, we detected no prevalent p53‐mediated senescence in any of six classes of lesions. Two separate defects in p53 signaling appeared common: in nevi, lack of p53 phosphorylation by activated CHEK2, and in melanomas, defective p21 upregulation by p53 even when phosphorylated.