中药金樱子的研究应用概况

本文就国内外对中药金樱子的化学成分及其提取分离方法、药理学研究和临麻应用作了综述,为金樱子的综合开发提供依据。     

固定化酵母细胞生产1,6-二磷酸果糖研究

本文研究了固定化酵母细胞制备果糖1,6二磷酸(FDP)的方法及其生产。用卡拉胶包埋方法固定化酿酒酵母(Sacchromyces cerevisae),对含葡萄糖1.0M,磷酸盐0.8M的糖磷液,pH6.5,在37℃下进行磷酸化反应。反复分批转化20天以上,可达到平均产FDPH_427.58mg/ml,最高为59.94mg/ml。用100ml固定化细胞生物反应器连续运转309h,稀释速率D=0.097h~(-1),平均产FDPH_4 21.51mg/ml。20L反应器连续运转,生产能力达到1.7g/h.L。用层析方法制备FDPNa_3结晶粉,提取收率为72.08％,制备质量达到或超过了国内外同类产品的质量要求。     

金黄色葡萄球菌L型和人乳头瘤病毒与宫颈癌关系的研究

应用改良革兰氏染色和免疫组化染色（ＡＢＣ法）,对２７０例宫颈癌和３３例慢性宫颈炎进行了研究。结果发现,宫颈癌革兰氏染色切片中细菌Ｌ型感染率（７５．１％）明显高于慢性宫颈炎（４５．５％）（Ｐ＜０．０５）,金黄色葡萄球菌Ｌ型抗原阳性率（７６．２％）明显高于人乳头瘤病毒（ＨＰＶ）抗原阳性率（５７．１％）。Ｌ型、ＨＰＶ混合感染率为４２．８％。上述结果表明宫颈癌中金葡菌Ｌ型与ＨＰＶ感染均常见,尤其金葡菌Ｌ型感染更为多见;金葡菌Ｌ型与ＨＰＶ感染的致病特征相似,两者均有不同程度的空泡细胞出现。提示金葡菌Ｌ型感染可能也是宫颈癌的致癌重要因素之一。     

应用离体叶片法鉴定棉花种质抗螨性的研究

应用离体叶片法,对9个棉花种质进行了鉴定,试验结果表明;种质间抗生性和忌避性差异显著;同株棉花不同部位的叶片对朱砂叶螨的抗生性无显著性差异。通过对叶螨在不同棉花种质上种群增长动态进行系统聚类,可将9个棉花种质划分为3类:斯字棉825-91、杞县86789、鄂棉314、苏联8911为1类,中棉164、潼南接龙棉、新库861517-2、南农NAC90-2为1类,美棉7-15独立为1类。依据朱砂叶螨在不同种质上的种群增长曲线和高峰期螨量增长倍数,可将9个种质划分为3个类型;斯字棉825-91、新库861517-2为抗性类型,潼南接龙棉、美棉7-15、南农NAC90-2为感性类型,其余为中抗类型。从忌避性看:斯字棉825-91、美棉7-15表现出较高的忌避性。     

铽离子与RNA的荧光反应及RNA测定的研究

核糖核酸（ＲＮＡ）与稀土铽离子在ｐＨ５．０～６．５条件下能形成具有较强荧光的络合物,其激发峰在２８８ｎｍ处,发射峰为４９４ｎｍ及５４５ｎｍ处．ＲＮＡ在０．１～１０ｍｇ／Ｌ范围内与其荧光强度呈线性关系,其检出限为６．０×１０￣（－８）ｍｏｌ／Ｌ．腺苷酸,尿苷酸,胞苷酸对ＲＮＡ的干扰比较小,因此可在其存在下选择性地测定ＲＮＡ．     

广州抽水蓄能电站蓄水库蓄水初期浮游生物调查

对我国首座核电站配套工程的抽水蓄能电站水库蓄水初期的浮游生物进行了调查。蓄水水库由上下两水库组成。两水库的浮游生物种类组成显著不同。上水库浮游植物共记录到３０种（属）,浮游动物１２种（属）;下水库浮游植物１９种（属）;浮游动物２５种（属）。上下两水库浮游生物数量均较贫乏,表明浮游生物群落尚处于初期发育阶段,但在局部浅水处已出现小规模的蓝藻水花,认为是水库蓄水初期必然的结果     

A NEW SPECIES OF GENUS HABROPHLEBIODES ULMER (EPHEMEROPTERA: LEPTOPHLEBIIDAE)

Abstract  The present paper deals with a new species Habrophlebiodes zijinensis sp. nov. collected in Nanjing, Jiangsu Povince, China.     

Poly(ADP-Ribose) Synthetase Activation: An Early Indicator of Neurotoxic DNA Damage

Abstract: DNA damage activates a nuclear enzyme poly(ADP-ribose) synthetase (PARS) that facilitates DNA repair by adding multiple ADP-ribose groups to nuclear proteins such as histones and PARS itself. N -Methyl- d -aspartate neurotoxicity may involve DNA damage excessively activating PARS to deplete its substrate NAD, as PARS inhibitors prevent this toxicity. We now show that PARS is rapidly and markedly activated in PC12 cells following treatment with neurotoxic agents, including the amyloid β-protein, hydrogen peroxide, N -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and its active metabolite N -methyl-4-phenylpyridine (MPP⁺). With MPP⁺, PARS activity is increased fivefold in 1 h and 20-fold by 3 h. By contrast, direct measurement of DNA damage by the terminal-deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling assay shows no significant increase by 3 h and less than fourfold by 24 h. These findings indicate that PARS activity can provide a simple, sensitive, and early index of DNA damage following neurotoxic insults.     

Differential requirement of protein tyrosine kinase and protein kinase C in the generation of IL-2-induced LAK cell and αCD3-induced CD3-AK cell responses

This study examined the role of protein tyrosine kinase (PTK) and protein kinase C (PKC) in the signal transduction pathways for lymphocyte activation through IL-2R to generate LAK cells and through TCR—CD3 to generate CD3-AK cells. Two PTK inhibitors [herbimycin A and genistein (PTK-I)] and two PKC inhibitors [calphositin C and staurosporine (PKC-I)] were used in the experiments. It was found that the primary activation pathway through IL-2R was PTK-dependent; that is, generation of both the IL-2-induced proliferative and the cytotoxic responses was completely abrogated by PTK-I and not by PKC-I. Quite different results were obtained with the αCD3-induced CD3-AK cell response. First, the αCD3-induced proliferation was only partially inhibited by PTK-I or PKC-I alone. Second, generation of CD3-AK cytotoxic response was primarily PKC-dependent; that is, only PKC-I induced significant inhibition. Genistein was found to reduce protein tyrosine phosphorylation in both LAK cells and CD3-AK cells, indicating that CD3-AK cells were also susceptible to PTK-I treatment. Further studies showed that PTK-I and not PKC-I suppressed perforin mRNA expression and N-2-benzyoxycarbonyl-l-lysine thiobeneylester esterase production in LAK cells, and the opposite was true for CD3-AK cells. These results indicate that different pathways were employed in lymphocyte activation through IL-2R and TCR—CD3. The former pathway is primarily PTK-dependent. Activation through TCR—CD3 is a more complex event. Induction of a proliferative response can employ either a PTK- or a PKC-dependent pathway, whereas induction of a cytotoxic response is primarily PKC-dependent. Furthermore, it appears that a PTK-independent pathway exists for the induction of a CD3-AK response and thus suggests that activation of the second messenger PKC may not necessarily be preceded by PTK activation.     

Inherited non-autosomal effects on body fat in F2 mice derived from an AKR/J × SWR/J cross

In this study we describe the contribution of matrilineal and patrilineal effects on the adiposity, body weight, and on the weights of individual fat pads in F₂ male mice derived from an SWR/J × AKR/J cross. AKR/J mice become obese after 12 weeks on a high-fat diet, whereas SWR/J mice remain relatively lean. Here we report that mice with AKR maternal and AKR paternal grandmothers have significantly larger epidydimal and retroperitoneal fat pads than those with SWR maternal and paternal grandmothers. However, grandparental strain had no effect on the overall adiposity (AI) or the weights of the inguinal, subcutaneous or mesenteric fat pads. The strain of the paternal grandparents had a small but significant effect on body weight. These effects can be attributed to in utero effects, imprinting effects, cytoplasmic and/or Y chromosome transmission of factors controlling body fat. We also describe the presence of a quantitative trait locus (QTL) on Chromosome X, close to DXMit174, which is linked to adiposity, body weight, and to the weights of the individual fat depots. However, this QTL is not responsible for the grandparental strain effects described above. Received: 3 March 1997 / Accepted: 5 May 1997