匙羹藤叶中匙羹藤酸的含量测定

匙羹藤叶中匙羹藤酸的含量测定＠秦民坚＠叶文才＠张健＠田中俊弘￥中国药科大学￥岐阜药科大学匙羹藤;匙羹藤酸;含量测定匙羹藤叶中匙羹藤酸的含量测定秦民坚叶文才张健田中俊弘（中国药科大学,南京２１００３８）（岐阜药科大学,岐阜５０２日本）Ｄｅｔｅｒｍｉｎａｔｉｏ...     

鸢尾科药用根茎类16种植物的异黄酮含量测定

鸢尾科药用根茎类１６种植物的异黄酮含量测定秦民坚王强巫弘罡徐国钧（中国药科大学,南京２１００３８）田中俊弘（岐阜药科大学,日本国岐阜市５０２）Ｄｅｔｅｒｍｉｎａｔｉｏｎｏｆｉｓｏｆｌａｖｏｎｅｓｉｎ１６ｓｐｅｃｉｅｓｏｆｒｈｉｚｏｍａｔｏｕｓｍｅｄｉ...     

射干和鸢尾的挥发性成分

射干和鸢尾的挥发性成分秦民坚王强徐珞珊徐国钧（中国药科大学,南京２１００３８）田中俊弘（岐阜药科大学,日本国岐阜市５０２）ＶｏｌａｔｉｌｅｃｏｎｓｔｉｔｕｅｎｔｓｏｆＢｅｌａｍｃａｎｄａｃｈｉｎｅｎｓｉｓａｎｄＩｒｉｓｔｅｃｔｏｒｕｍＱｉｎＭｉｎＪ...     

Screening for Drought Resistance of Rice Recombinant Inbred Populations in the Field

In a 2-year experiment, 187 genotypes were grown under well-watered and drought stress conditions, imposed at panicle initiation stage. The relationship of genotypic variation in yield under drought conditions to potential yield, heading date and flowering delay, reduction in plant height, and to a drought response index （DRI） was detected. Grain yield under drought stress conditions was associated with yield under well-watered conditions （r= 0.47^＊＊, and r= 0.61^＊＊ during 2 years of tests）. The delay of heading date ranged from -1 （no delay） to 24days, and was negatively associated with grain yield （r =-0.40^＊）, spikelet fertility percentage （r =-0.40^＊＊）, harvest index （r =-0.58^＊＊）, but positively associated with yield reduction percentage （r = 0.60^＊＊）. The reduction in plant height was negatively associated with grain yield （r =-0.24^＊＊, and r=-0.29^＊＊）, spikelet fertility percentage （r = -0.23^＊＊, and r= -0.21^＊）, harvest index （r = -0.37^＊＊, and r= -0.54^＊＊）, and positively associated with yield reduction percentage （r = 0.58^＊＊, and r= 0.58^＊＊） in 2003 and 2004, respectively. The DRI of genotypes was strongly associated with grain yield （r = 0.87^＊＊, and r= 0.77^＊＊）, fertility percentage （r = 0.66^＊＊ and r= 0.54^＊＊）, harvest index （r= 0.67^＊＊ and r= 0.61^＊＊）, and negatively associated with grain reduction percentage （r=-0.70^＊＊, and r=-0.73^＊＊） under drought stress. The results indicate that genotypes with drought resistance can be identified by measuring yield potential, delay in flowering, reduction in plant height, or DRI under test environments of well-watered and drought stress.     

青柿子可降低血液中胆固醇含量

日本岐阜生物工程学研究所科研人员经动物实验发现，未成熟的柿子具有降低血液中胆固醇含量的功效。     

多瘤病毒分离株的研究

多瘤病毒注入新生小鼠体内后，可刺激小鼠组织细胞分裂繁殖、产生多种肿瘤。用肿瘤药物治疗后，从缩小的肿瘤块组织细胞中分离的多瘤病毒株有的已经不再能诱发肿瘤。本文研究了这种不能产生肿瘤的多瘤病毒株和野生型病毒株在分子遗传学上的区别。1材料与方法5一氟胞咯咤（5－F。）购于美国SIGMA公司，［’H卜胸腺喀＠、［‘’S〕一甲硫氨酸购一千英国RadiocheAncalCentreAmrsharn，兔抗鼠多瘤病毒幻灯免疫荧光试剂购于法国巴斯德研究所。1．且分离多瘤病毒的方法小鼠为NIH小鼠，新生小鼠皮下接种或腹腔内接种多瘤病毒悬液。有肿瘤生长…     

裸爪螯蜂属一新种(膜翅目：螯蜂科，裸爪螯蜂亚科)

裸爪螯蜂属一新种＊（膜翅目：螯蜂科,裸爪螯蜂亚科）许再福＊＊（华南农业大学昆虫生态室广州５１０６４２）何俊华（浙江农业大学植保系杭州３１００２９）＊国家自然科学基金资助项目＊＊浙江农业大学九五届毕业博士生１９９５－０９－１２收稿,１９９６－０３－０１...     

虎眼万年青的快速繁殖

RapldPropopHonofDrni量ogal艺界mca已丞dalumYINDOng，HUANGBat－on（haitlaeof（lejle。ndqstaim，ha～A，ffe＊＊＊＊＊＊－t｝lzl；wrwi，CfollocmDz130024）1植物名称虎眼万年青（Drnitogalumcaudatum）。2材料类别子鳞茎。3塔共条件（l）MS＋NAA3．0ms／L（单位下同）＋6     

抑制性差减杂交PCR：一种寻找有差别表达基因的方法

抑制性差减杂交ＰＣＲ：一种寻找有差别表达基因的方法蒋小陵＊鲁林荣＊＊陈诗书＊郑仲承＊＊（＊上海第二医科大学生物化学教研室,上海２０００２５;＊＊中国科学院上海生物化学研究所,上海２０００３１）测定高等生物（包括人类）基因组序列是一个现实和预期的目标。...     

带有饱和接触率和垂直传染的两病株病原体的共存性（英文）

讨论了带有饱和接触率和垂直传染的两病株病原体的共存性,获得了共存性存在的充要条件R_2（N_2~＊）〈R_1（N_2~＊）,R_1（N_1~＊）〈R_2（N_1~＊）,并且在共存平衡点存在的条件下证明得到其局部稳定.     

Common elements in growth factor stimulation and oncogenic transformation: 85 kd phosphoprotein and phosphatidylinositol kinase activity

The phosphorylation of proteins on tyrosine in vivo and in vitro was examined in 3T3 cells stimulated by platelet-derived growth factor (PDGF) and transformed by polyoma middle T antigen (MTAg) by using an antibody directed against phosphotyrosine (P-tyr). Two common events were observed upon PDGF stimulation or MTAg transformation of cells: the appearance in the immunoprecipitates of an 85 kd phosphoprotein, and increased phosphatidylinositol (PI) kinase activity. In PDGF-stimulated cells, the 85 kd phosphoprotein and PI kinase activity appeared rapidly, within 1 min of growth factor addition. The PI kinase activity and 85 kd phosphorylation were also increased in anti-P-tyr immunoprecipitates from cells transformed by v-fms and v-sis, but not by SV40 T antigen. The presence of the tyrosine-phosphorylated 85 kd protein correlated with PI kinase activity during several purification steps. These results suggest that the 85 kd phosphoprotein, a putative PI kinase, is a substrate for both the PDGF receptor and MTAg/pp60c-src tyrosine kinase activities.     

Pathway of phospholipase C activation initiated with platelet-derived growth factor is different from that initiated with vasopressin and bombesin

The mode of phospholipase C activation initiated with platelet-derived growth factor (PDGF) has been studied in comparison with that initiated with vasopressin and bombesin in a rat fibroblast line, WFB. Stimulation of WFB cells by PDGF, vasopressin, and bombesin elicites rapid hydrolysis of polyphosphoinositides and an increase in cytoplasmic free Ca2+ concentration ([Ca2+]i). On stimulation by PDGF, there was a lag period of about 10 s before an increase in [Ca2+]i. No measurable lag period was observed in the [Ca2+]i response induced by vasopressin or bombesin. Pretreatment of WFB cells with phorbol 12-myristate 13-acetate profoundly inhibited inositol phosphate formation evoked by vasopressin and bombesin, but enhanced to some extent inositol phosphate formation stimulated by PDGF. In membranes prepared from WFB cells, GTP markedly augmented inositol polyphosphate formation induced by vasopressin and bombesin. It was not successful in showing the PDGF-stimulated formation of inositol phosphates in the membrane preparation. The effects of GTP, guanosine 5'-O-(2-thiodiphosphate) (GDP beta S), and guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) on polyphosphoinositide hydrolysis stimulated by growth factors were studied in WFB cells made permeable to nucleotides by treatment with either saponin or Pseudomonas aeruginosa cytotoxin. PDGF, vasopressin, and bombesin elicited inositol phosphate production in the permeabilized WFB cells in the absence of added GTP. GDP beta S, a competitive inhibitor of GTP-binding proteins (G-proteins), markedly reduced the bombesin- and vasopressin-stimulated production of inositol phosphates. However, the PDGF-stimulated production of inositol phosphates was not affected by the addition of GDP beta S. GTP gamma S, an agonist of G-proteins, largely enhanced the vasopressin- and bombesin-stimulated hydrolysis of inositol lipids when added at 10-100 microM. In the presence of GTP gamma S, the PDGF-stimulated hydrolysis of inositol lipids was not enhanced, but was reduced: 100 microM GTP gamma S reduced the stimulated hydrolysis to about a half of the control level. Only GTP gamma S, and no other nucleoside triphosphates, was found to have these effects. Activation of G-proteins in WFB cells by fluoroaluminate resulted in the inhibition of inositol phosphate production elicited with not only PDGF, but also with vasopressin and bombesin. These results indicate that a G-protein couples vasopressin and bombesin receptors to the activation of phospholipase C. Moreover, these results suggest that coupling of the PDGF receptor to phospholipase C is not mediated through a G-protein.(ABSTRACT TRUNCATED AT 400 WORDS)     

The lack of PDGE-stimulated PGE2 release from ras-transformed NIH-3T3 cells results from reduced phospholipase C but not phospholipase A2 activity

Our previous work demonstrated that NIH-3T3 cells expressing high levels of the mutated cellular ras oncogene (EJ-ras gene) exhibited reduced hormone-sensitive adenylate cyclase and platelet-derived growth factor-stimulated (PDGF) phospholipase A2/C activities. We now report that although the ras-transformed cells display markedly reduced phospholipase C activity, as measured by the levels of inositol 1,4,5-trisphosphate synthesized after PDGF-stimulation, normal levels of phospholipase A2 activity can be uncovered; thus, similar levels of prostaglandin E2 were synthesized in EJ-ras transformed and control cells after stimulation with phorbol myristate acetate (PMA) and/or the calcium ionophore A-23187, agents which stimulate protein kinase C and intracellular Ca2+ levels, respectively. These data suggest that the EJ-ras gene product uncouples the PDGF receptor from the phospholipase C, resulting in reduced PDGF-stimulated Ca2+ mobilization, protein kinase C stimulation and an apparent decrease in Ca2+-dependent phospholipase A2.     

Activation of the platelet-derived growth factor receptor by the bovine papillomavirus E5 transforming protein.

The bovine papillomavirus E5 gene encodes a 44 amino acid membrane-associated protein that can induce tumorigenic transformation of rodent fibroblast cell lines. Genetic studies suggest that the E5 protein may transform cells by influencing the activity of cellular proteins involved in growth regulation. We report here that the endogenous cellular beta type receptor for the platelet-derived growth factor (PDGF) is constitutively activated in C127 and FR3T3 cells stably transformed by the E5 protein, but not in these cell types transformed by a variety of other oncogenes. In C127 cells, a metabolic precursor as well as the mature form of the receptor is activated by E5 transformation. Activation of the receptor also occurs upon acute E5-mediated transformation of these cells and precedes mitogenic stimulation in this system. Moreover, activation of the receptor by addition of PDGF or the v-sis gene to untransformed cells is sufficient to induce DNA synthesis and stable growth transformation. We propose that the PDGF receptor is an important cellular intermediate in the transforming activity of the bovine papillomavirus E5 protein. There is a short region of sequence similarity between the fibropapillomavirus E5 proteins and PDGF, suggesting that the E5 proteins may activate the PDGF receptor by binding directly to it.     

Platelet-derived growth factor or basic fibroblast growth factor induce anchorage-independent growth of human fibroblasts

Anchorage-independent growth, i.e., growth in semi-solid medium is considered a marker of cellular transformation of fibroblast cells. Diploid human fibroblasts ordinarily do not exhibit such growth but can grow transiently when medium contains high concentrations of fetal bovine serum. This suggests that some growth factor(s) in serum is responsible for anchorage-independent growth. Much work has been done to characterize the peptide growth factor requirements of various rodent fibroblast cells for anchorage-independent growth; however, the requirements of human fibroblasts are not known. To determine the peptide growth factor requirements of human fibroblasts for anchorage-independent growth, we used medium containing serum that had had its peptide growth factors inactivated. We found that either platelet-derived growth factor (PDGF) or the basic form of fibroblast growth factor (bFGF) induced anchorage-independent growth. Epidermal growth factor (EGF) did not enhance the growth induced by PDGF, or did so only slightly. Transforming growth factor beta (TGF-beta) decreased the growth induced by PDGF. EGF combined with TGF-beta induced colony formation in semi-solid medium at concentrations at which neither growth factor by itself was effective, but the combination was much less effective in stimulating anchorage-independent growth than PDGF or bFGF. This work showed that PDGF, or bFGF, or EGF combined with TGF-beta can stimulate anchorage-independent growth of nontransformed human fibroblasts. The results support the idea that cellular transformation may reduce or eliminate the need for exogenous PDGF or bFGF.     

Analysis of middle tumor antigen and pp60c-src interactions in polyomavirus-transformed rat cells.

The relative abundance of pp60c-src molecules associated with polyomavirus (Py) middle tumor antigen (MTAg) and the relative abundance of MTAg associated with pp60c-src in a variety of Py-transformed rat cells was determined by quantitative immunoblot analyses which detect pp60c-src or Py MTAg. The results demonstrate that approximately 5 to 10% of the total immunoprecipitable pp60c-src molecules in Py-transformed rat cells are stably associated with MTAg and have elevated protein kinase activities. In these same cells, it was found that approximately 10 to 15% of the detectable MTAg molecules are stably associated with pp60c-src. Other results presented in this report demonstrate that approximately 50 to 75% of the total MTAg-associated cellular tyrosine kinase activity potentially represents the enzymatic activity of pp60c-src, while the remaining 25 to 50% represents the activity of other cellular tyrosine kinases. Our results also show that most pp60c-src molecules associated with Py MTAg do not possess electrophoretic mobilities that are altered from those of pp60c-src molecules not associated with MTAg or pp60c-src molecules obtained from normal rodent cells.     

In vitro association and phosphorylation of polyoma virus middle T antigen by cellular tyrosyl kinase activity

We have observed increased phosphorylation of tyrosine residues on the polyoma virus middle tumor antigen (MTAg) in in vitro kinase assays of the immune complexes immunoprecipitated from lysates of polyoma virus-infected mouse embryo cells to which increasing amounts of uninfected mouse embryo cell lysate had been added. The components from uninfected mouse cells responsible for increased MTAg phosphorylation were localized by subcellular fractionation to the plasma membrane and found to be sensitive to protease digestion, N-ethylmaleimide, and 5'-p-fluorosulfonylbenzoyladenosine inactivation. The majority of the membrane-associated activity responsible for the increased MTAg phosphorylation in these assays could be cleared from lysates of uninfected mouse cell lysates by centrifugation after reaction with Sepharose-bound monoclonal antibodies which recognize pp60c-src. These results suggest that MTAg can associate with cellular tyrosyl kinases in vitro and be phosphorylated by these enzymes in immune-complex kinase assays. The identity of at least one of these cellular tryosyl kinases which can associate with MTAg in vitro is likely to be pp60c-src.     

Platelet-derived growth factor receptor can mediate tumorigenic transformation by the bovine papillomavirus E5 protein.

We showed previously that the beta receptor for platelet-derived growth factor (PDGF) is constitutively activated in fibroblasts transformed by the 44-amino-acid bovine papillomavirus type 1 (BPV) E5 protein and that the E5 protein and the PDGF receptor exist in a stable complex in E5-transformed fibroblasts. On the basis of these results, we proposed that activation of the PDGF receptor by the BPV E5 protein generates a sustained proliferative signal, resulting in fibroblast transformation. In this study, we used a gene transfer approach to provide functional evidence that the PDGF receptor can mediate transformation by the E5 protein. We show that normal mouse mammary gland (NMuMG) cells, a murine mammary epithelial cell line that does not express PDGF receptors, are not susceptible to transformation by the E5 protein. Coexpression of the PDGF beta receptor and E5 genes in these cells results in markedly increased tyrosine phosphorylation of an immature PDGF receptor species and the formation of a stable complex between the E5 protein and this immature PDGF receptor form. Importantly, introduction of the PDGF receptor gene into NMuMG cells renders them highly susceptible to E5-mediated tumorigenic transformation. In contrast, the E5 protein does not induce transformation via the endogenous epidermal growth factor receptor pathway in these cells. These results demonstrate that the PDGF receptor, a cellular protein with a well-characterized role in the positive control of cell proliferation, can mediate transformation by a DNA virus transforming protein.     

The phenotypic characteristics of simian sarcoma virus-transformed human fibroblasts suggest that the v-sis gene product acts solely as a PDGF receptor agonist in cell transformation.

Previous studies have indicated that the oncogene v-sis of simian sarcoma virus (SSV) encodes a growth factor that is structurally and functionally similar to platelet-derived growth factor (PDGF). In the present investigation we have analysed the phenotypic characteristics of human foreskin fibroblasts transformed by SSV. It was found that the PDGF receptors were extensively down-regulated. This finding is consistent with a high, local, extracellular concentration of a PDGF-like factor, synthesized by the transformed cell. The receptors were up-regulated by suramin, a drug that is known to dissociate PDGF and the v-sis product from the PDGF receptors. A cell-associated v-sis product of mol. wt 24,000 was identified by immunoprecipitation with PDGF antibodies; release of this component was induced by a high concentration of exogenous PDGF, indicating that a fraction of the product is associated with the PDGF receptors. SSV was not found to be an immortalizing virus; when serially passaged, SSV-transformed cells had essentially the same life-span as their non-transformed counterparts. Moreover, SSV did not induce growth in soft agar beyond the level afforded by exogenously added PDGF. Thus, the present study favors the notion that SSV transformation is mediated by a growth factor that mimics PDGF but has no further cellular effects.