仙人掌红色素的研究

仙人掌红色素是从仙人掌科(Gactaceae)仙人掌属植物(Opuntia dillenii (Ker-Gawl.) Hawl)的成熟果实中提取的一种天然食用色素。在pH2—8范围内呈鲜艳的紫红色。色素的主要化学成份是甜菜花青素(betacyanines):甜菜甙(betanin)。本色素为水溶性色素,对光、热不稳定,抗坏血酸能提高色素的热稳定性。     

CO2倍增对不同基因型大豆光合色素含量和荧光诱导动力学参数的影响

研究了CO_2倍增对大豆(Glycine max L.)Bragg(野生型)及其不同单基因突变品系Nts 382(超结瘤突变体)和Nod 49(不结瘤突变体)某些光合特性的影响。结果表明,CO_2倍增能提高Bragg、Nts 382和Nod 49的叶绿素(Chl)和类胡萝卜素(Car)的含量,但不同品系提高的幅度有所不同。荧光诱导动力学测定结果表明,CO_2倍增均能提高其PSⅡ活性、PSⅡ原初光能转化效率和光合作用潜在量子转化效率。CO_2倍增更有利于提高Nts 382的荧光光化学猝灭系数(qp)和PSⅡ总的光化学量子产量,以及较大幅度地降低荧光非光化学猝灭系数(qN),有助于把所捕获的光能用于进行光合作用。这可能与Nts 382是超结瘤突变体,比Bragg和Nod 49能更充分地利用空气中的氮素有关。     

A combined A431 cell membrane chromatography and online high performance liquid chromatography/mass spectrometry method for screening compounds from total alkaloid of Radix Caulophylli acting on the human EGFR

We have developed an online analytical method that combines A431 cell membrane chromatography (A431/CMC) with high performance liquid chromatography and mass spectrometry (LC/MS) for identifying active components from Radix Caulophylli acting on human EGFR. Retention fractions on A431/CMC model were captured onto an enrichment column and the components were directly analyzed by combining a 10-port column switcher with an LC/MS system for separation and preliminary identification. Using Sorafenib tosylate as a positive control, taspine and caulophine from Radix Caulophylli were identified as the active molecules which could act on the EGFR. This A431/CMC-online-LC/MS method can be applied for screening active components acting on EGFR from traditional Chinese medicines exemplified by Radix Caulophylli and will be of great utility in drug discovery using natural medicinal herbs as a source of novel compounds.     

乐至黑山羊PRLR基因外显子10多态性与产羔数的关系研究

设计2对特异性引物对乐至黑山羊PRLR基因第10外显子进行了PCR-SSCP检测,并研究该基因与产子性能的相关性。结果表明,P1引物扩增片段不存在多态性;P2引物扩增片段存在多态性,表现为AA,AB,AD和CD 4种基因型,测序结果表明,4种基因型都在该片段第89、94、146和157位存在C→T、A→C、C→G、G→C的突变;此外AA型还在61位发生C→T的突变;AD型还在175位发生A→G的突变;CD型还在24位发生T→C的突变,96位发生C→T的突变,通过统计分析发现AD型平均产羔数优于其他3种基因型,并且与AB型差异达到显著水平(P<0.05)。因此认为PRLR基因对于乐至黑山羊产子性能有一定的影响。     

中国表珠甲螨属二新记录种记述（甲螨亚目：珠甲螨科）

记述表珠甲螨属Epidamaeus 2中国新记录种:变表珠甲螨Epidamaeus variabilis Fujikawa & Fujita,1985及蒙古表珠甲螨Epidamaeus mongolicus Bayartogtokh, 2000,并分别对两种做了重新描述。     

重组干扰素γ的中间试制

用带有表达质粒ＰＢＶ２２０（含有γ干扰素基因）的大肠杆菌ＤＨ５α株进行发酵培养,３批中试的菌产量平均为１４．１克／Ｌ,γ干扰素的表达量平均为１．０２±１０＾９ＩＵ／Ｌ,收集的菌体经高压匀质破菌后收集包涵体,用７ｍｏｌ／Ｌ盐酸胍提取干扰素,此过程中去除７８．４％菌体蛋白,而干扰素活性仅损失１０．４１％,粗制干扰素经复性可使干扰素活性提高４０５％,比活也有明显提高,３批平均为１．７６×１０＾７ＩＵ／ｍ     

Spred2 Modulates the Erythroid Differentiation Induced by Imatinib in Chronic Myeloid Leukemia Cells

Differentiation induction is currently considered as an alternative strategy for treating chronic myelogenous leukemia (CML). Our previous work has demonstrated that Sprouty-related EVH1 domainprotein2 (Spred2) was involved in imatinib mediated cytotoxicity in CML cells. However, its roles in growth and lineage differentiation of CML cells remain unknown. In this study, we found that CML CD34⁺ cells expressed lower level of Spred2 compared with normal hematopoietic progenitor cells, and adenovirus mediated restoration of Spred2 promoted the erythroid differentiation of CML cells. Imatinib could induce Spred2 expression and enhance erythroid differentiation in K562 cells. However, the imatinib induced erythroid differentiation could be blocked by Spred2 silence using lentiviral vector PLKO.1-shSpred2. Spred2 interference activated phosphorylated-ERK (p-ERK) and inhibited erythroid differentiation, while ERK inhibitor, PD98059, could restore the erythroid differentiation, suggesting Spred2 regulated the erythroid differentiation partly through ERK signaling. Furthermore, Spred2 interference partly restored p-ERK level leading to inhibition of erythroid differentiation in imatinib treated K562 cells. In conclusion, Spred2 was involved in erythroid differentiation of CML cells and participated in imatinib induced erythroid differentiation partly through ERK signaling.     

Ginsenoside Re reduces insulin resistance through inhibition of c-Jun NH2-terminal kinase and nuclear factor-kappaB

Ginsenoside Re (Re), a compound derived from Panax ginseng, shows an antidiabetic effect. However, the molecular basis of its action remains unknown. We investigated insulin signaling and the antiinflammatory effect by Re in 3T3-L1 adipocytes and in high-fat diet (HFD) rats to dissect its anti-hyperglycemic mechanism. Glucose uptake was measured in 3T3-L1 cells and glucose infusion rate determined by clamp in HFD rats. The insulin signaling cascade, including insulin receptor (IR) beta-subunit, IR substrate-1, phosphatidylinositol 3-kinase, Akt and Akt substrate of 160 kDa, and glucose transporter-4 translocation are examined. Furthermore, c-Jun NH(2)-terminal kinase (JNK), MAPK, and nuclear factor (NF)-kappaB signaling cascades were also assessed. The results show Re increases glucose uptake in 3T3-L1 cells and glucose infusion rate in HFD rats. The activation of insulin signaling by Re is initiated at IR substrate-1 and further passes on through phosphatidylinositol 3-kinase and downstream signaling cascades. Moreover, Re demonstrates an impressive suppression of JNK and NF-kappaB activation and inhibitor of NF-kappaBalpha degradation. In conclusion, Re reduces insulin resistance in 3T3-L1 adipocytes and HFD rats through inhibition of JNK and NF-kappaB activation.