赤霉素及机械处理的相互作用对破除Sandersonia aurantiaca种子休眠的研究

在预备试验的基础上，选用了21种促进种子发芽的方法，结果显示，完整的s．aurantiaca种子对任何处理都无响应，砂纸磨擦 近胚根处切除小部分可使种子发芽率提高至11％。以上处理结合300mg／L GA3溶液的使用可破除种子休眠，使种子发芽率提高到69％以上。结果还表明，S．aurantiaca种子发芽的适宜温度为20℃；25℃ 16h／d光照及30℃的条件可降低种子的发芽率。研究还对S．aurantiaca种子的吸胀能力以及所含抑制物对生菜种子发芽的影响进行了比较。初步得出，S．aurantiaca种子具有种皮限制和种胚休眠的双重休眠机制，GA3和机械处理的相互作用可破除种子休眠。     

绢丝昆虫茧丝蛋白酶抑制剂含量的比较分析

以 6种绢丝昆虫的茧壳为材料 ,对茧丝蛋白酶抑制剂的含量及热稳定性进行了研究。结果表明 :家蚕品种间茧丝蛋白酶抑制剂的含量差异极显著 ,外层丝中含量较多 ,F1代的含量呈双亲中间型 ,偏向于含量较多的亲本 ,雌雄间含量无显著差异 ;家蚕茧丝蛋白酶抑制剂对热稳定性较强 ;天蚕绿茧、野蚕的茧丝中有少量的蛋白酶抑制剂存在 ,蓖麻蚕的茧丝中有微量蛋白酶抑制剂存在 ,天蚕黄茧、柞蚕茧、樗蚕茧的茧丝中基本无蛋白酶抑制剂存在。     

组氨醇脱氢酶抑制剂的研究动态

组氨醇脱氢酶(HDH)是组氨酸生物合成过程中最后两步反应的催化酶。对组氨醇脱氢酶的结构、催化机理、组氨醇脱氢酶抑制剂等方面的研究动态进行了较为详细的综述。     

水稻与稻瘟病菌非亲和性互作中重要防御酶活性变化规律研究

 选以CO39为背景的水稻抗稻瘟病近等基因系,与稻瘟菌生理小种ZC₁₃(菌株97-151a)组成的3类典型非亲和性互作,以亲和性互作为对照,对各互作中过氧化物酶(POD)、苯丙氨酸解氨酶(PAL)、几丁质酶及β-1,3-葡聚糖酶的活性变化规律进行了系统研究。完全非亲和性互作C101A51/97-151a、高度非亲和性互作C101L AC/97-151a及中度非亲和性互作C104 PKT/97-151a,POD比活性接种后即开始明显升高,48h前达到高峰,升高趋势一直持续到7d完全显症时,幅度基本与各互作非亲和程度呈正相关;亲和性互作CO39/97-151a接种后40 h POD比活性才开始升高,4~6 d达到高峰,峰值也较大。3类非亲和性互作PAL比活性在接种后0 h或16 h开始较明显升高,整个互作中形成3~4个较明显的峰;亲和性互作中PAL比活性一直明显下降。3类非亲和性互作外切几丁质酶比活性接种后即开始升高,基本一直保持升高趋势,在40 h前幅度较大,并形成1~3个较高的峰;亲和性互作外切几丁质酶比活性接种后即开始大幅度升高直至完全显症,48h后幅度远高于非亲和性互作。3类非亲和性互作β-1,3-葡聚糖酶比活性在24 h内开始较明显升高,在48h前形成2~3个较明显的峰;亲和性互作在接种后β-1,3-葡聚糖酶比活性即开始升高,在48h后显著高于非亲和性互作。讨论了POD、PAL、几丁质酶及β-1,3-葡聚糖酶参与水稻抗稻瘟病的可能性。     

转基因水稻对稻瘟病的抗性研究

 采用苗期初筛、复筛、抗谱测定和田间自然诱发试验等不同鉴定方法,对经分子检测证明已整合有碱性几丁质酶基因和β-1,3-葡聚精酶基因的22个转化系的转基因水稻植株进行稻瘟病抗性鉴定研究,筛选出对稻瘟病的抗性比原种对照七丝软占有明显提高的一系列转基因水稻品系,其中表现高抗的有来自F4-9转化株系的7个品系。高抗材料的R7代品系,经室内抗谱测定及田间病圃试验结果,仍然表现高抗稻瘟病。本研究通过转基因技术,成功地将优质感病品种改良成高抗品系,研究结果证明了利用基因工程手段培育抗病水稻新品种是一个非常有希望的育种途径。     

Transgenic cucumber expressing an endogenous class III chitinase gene has reduced symptoms from Botrytis cinerea

A class III chitinase gene (CHI2) is induced in cucumber plants (Cucumis sativa L.) in response to infection by pathogenic microorganisms. Infection of Botrytis cinerea, causal agent of gray mold disease on cucumber, also induces CHI2 expression. To investigate whether CHI2 is involved in resistance to gray mold disease, transgenic cucumber plants were produced to overexpress the CHI2 gene. One line was analyzed in detail in terms of disease resistance. The transgenic cucumber plant (CC2) constitutively expressed CHI2 and reduced the symptoms of B. cinerea for 4 days after inoculation compared with nontransgenic plants. However, this inhibitory effect was not absolute, and CC2 eventually developed serious disease symptoms. Chitinase activity of the crude extract from CC2 leaves was higher than that from nontransgenic plants. A high-molecular-weight fraction containing CHI2 from CC2 leaves had fungistatic activity against B. cinerea. Interestingly, the low-molecular-weight fraction from CC2 leaves with CHI2 removed also had fungistatic activity against B. cinerea. Not only the introduced chitinase activity but also the endogenous defense reactions activated by overexpression of CHI2 may be involved in the enhanced gray mold disease resistance in CC2.     

Gly-Gly肽和Gly-L-Leu肽在蛋鸡肠道内水解的研究

采用蛋鸡离体外翻肠段培养法,将小肠分为十二指肠、空肠前段、中段、后段和回肠五个部位肠段,洗净外翻。2种二肽培养液(Gly-Gly肽和Gly-L-Leu肽溶液)作为两组对照培养液,每种二肽培养液中添加肽酶抑制剂(Bestatin和Amastatin),作为试验培养液,39.5℃培养25min,每5min取样一次,测定培养液中的二肽含量。结果表明,培养5min后,含Gly-Gly肽的对照和试验培养液中均未能检测到完整Gly-Gly肽。而含Gly-L-Leu肽的对照培养液Gly-L-Leu肽的含量降低到16.75％,试验培养液则下降到43.40％。而试验培养液中Gly-L-Leu肽的含量10min后无显著降低(P>0.05)。各培养时段试验培养液Gly-L-Leu含量均显著高于对照培养液(P<0.05)。由此认为,离体肠囊在培养过程中能够迅速释放肠肽酶及一些生物活性物质,快速水解2种二肽。肽酶抑制剂(Bestatin和Amastatin)能抑制Gly-L-Leu的水解,但不能抑制Gly-Gly的水解。     

几种脲酶抑制剂对大豆脲酶和绵羊瘤胃微生物脲酶的抑制作用

本文研究了脲酶抑制剂乙酰氧肟酸 (AHA)、邻苯二酚、氢醌 (HQ)和硼砂对大豆脲酶和绵羊瘤胃微生物脲酶的抑制作用。结果表明 ,在浓度为 0 .0 0 0 1,0 .0 0 1,0 .0 1和 0 .1mmol/L时 ,4种脲酶抑制剂对大豆脲酶的抑制率分别为 :AHA为 6 % ,6 .2 % ,9.6 6 %和 2 9.79% ;HQ为 8.4 % ,13.0 3% ,19.79%和 4 4 .75 % ;邻苯二酚为 2 0 .34% ,19.12 % ,83.16 %和 93.78% ;而硼砂为 16 .5 5 % ,17.18% ,18.95 %和 35 .5 0 %。在相同浓度下 ,4种脲酶抑制剂对绵羊瘤胃微生物脲酶的抑制率分别为 :AHA为 9.5 8% ,14 .0 4 % ,4 1.30 %和 72 .73% ;HQ为 12 .2 1% ,39.99% ,6 4 .6 2 %和 78.87% ;邻苯二酚为 6 .0 7% ,9.36 % ,31.2 9%和 5 0 .4 4 % ;而硼砂分别为 4 .97% ,8.6 3% ,2 1.78%和 32 .0 2 %。     

Treatment of canine haemangiosarcoma with suberoylanilide hydroxamic acid, a histone deacetylase inhibitor

A case report is presented by describing the treatment of a 12‐year‐old dog – diagnosed with haemangiosarcoma (HSA) – with suberoylanilide hydroxamic acid (SAHA), a histone deacetylase (HDAC) inhibitor. The drug was administered orally, on a daily basis, approximately 2 weeks post‐splenectomy at a dose of 3 mg kg^?1. HSA is a lethal malignancy of the endothelium, which is usually disseminated by the time it is diagnosed. Median survival time, usually, is no longer than 80 days. Following treatment with SAHA, no sign of malignant growth could be discerned by means of diagnostic abdominal ultrasound, chest X‐ray or with the help of clinical symptoms, over a period of >1000 days. The precise mechanism by which HDAC inhibitors exert their anti‐cancer effects is uncertain, but evidence suggests that exposure to SAHA generates hyperacetylated chromosomal histones, which, in turn, facilitates the expression of tumour suppressor genes turned off by epigenetic mechanisms during neoplastic transformation of the endothelium.     

Effect of benazepril and pimobendan on serum angiotensin‐converting enzyme activity in dogs

To support their combined use, the objective of the study was to evaluate the effects of benazepril and pimobendan on serum angiotensin‐converting enzyme (ACE) activity in dogs. A total of 48 healthy beagle dogs were randomized into four groups (n = 12 per group) in a parallel‐group design study: A (control, placebo twice daily (BID)); B (0.5–1.0 mg/kg benazepril once daily (SID) in the morning, placebo in the evening); C (0.25–0.5 mg/kg benazepril BID); D (0.25–0.5 mg/kg benazepril and 0.125–0.25 mg/kg pimobendan, both BID). The test items were administered orally for 15 days. Serum ACE activity was measured on days 1 and 15. Groups B, C and D had significantly lower average serum ACE activity compared to baseline and to the control group, on both days 1 and 15. There were no significant differences in average ACE activity between groups B, C and D. Noninferiority of group C to B was demonstrated. In conclusion, 0.25–0.5 mg/kg benazepril administered BID produced noninferior inhibition of serum ACE activity compared to 0.5–1.0 mg/kg benazepril dosed SID. Pimobendan had no significant effect on benazepril's action on serum ACE activity. The results support the use of benazepril BID in dogs and in combination with pimobendan.