首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 109 毫秒
1.
李锦山 《生物学通报》2012,47(10):32-35
要提高课堂教学的有效性,需要充分考虑学生的需求.学生的需求来自学生所缺的、学生所怕的、学生所惑的3个方面.列举“孟德尔定律”一章中学生所缺、所怕、所惑的具体知识、方法和能力,分析其成因,并提供了弥补所缺、消除所怕和所惑的教学方法或策略.  相似文献   

2.
植物绿原酸的研究动态   总被引:2,自引:0,他引:2  
阐述了近些年来国内外关于植物绿原酸所做的研究工作.植物绿原酸的提取、纯化、鉴定和药理活性及其应用开发所取得成果.揭示了绿原酸具有潜在的、广阔的应用前景.  相似文献   

3.
左心室与体动脉的匹配模型   总被引:1,自引:0,他引:1       下载免费PDF全文
柳兆荣  吴驰 《中国科学C辑》1997,27(5):469-474
为揭示左心室及其后负荷耦合模型如何影响主动脉根部的压力和流量,比较3种不同的匹配模型所确定压力和流量波形与实测波形的差异情况.结果表明,与匹配模型1和匹配模型2比之,所建立的匹配模型3所确定的压力和流量波形与相应的实验波形吻合得最好.说明匹配模型3是一种较合适表征左心室与体动脉匹配耦合的模型.  相似文献   

4.
生物多样性保护现状及其研究   总被引:2,自引:0,他引:2  
生物多样性是地球上所有生命的总和,是40亿年以来生物进化的最终结果,也是世界上的自然财富.它包括几百万不同种类的植物、动物和微生物以及它们所拥有的基因和由这些生物与所在地环境所构成的生态系统.因此,生物多样性包括三个层次的概念,即遗传多样性、物种多样性和生态系统多样性.此外,人们还重视更高层次的多样性即景观多样性.生物多样性是人类的生物资源,有的已为人类所利用,而大部分它的潜在价值尚未被人们所发现.自然保护在20世纪40年代已开始受到重视.自80年代初以来,有关生物多样性国际会议频频召开,1992年,世界资源研究所(WRI)、  相似文献   

5.
寄生于南非金钟花(PhygeliuscapensisE.May)上的白粉菌属新种:南非金钟花白粉菌ErysiphephygeliiWangetZhangsp.nov.。模式标本分别保存于云南农业大学植病所真菌标本室(MHYAU)和中科院微生物所真菌标本室(HMAS)。  相似文献   

6.
寄生于南非金钟花(PhygeliuscapensisE.May)上的白粉菌属新种:南非金钟花白粉菌ErysiphephygeliiWangetZhangsp.nov.。模式标本分别保存于云南农业大学植病所真菌标本室(MHYAU)和中科院微生物所真菌标本室(HMAS)。  相似文献   

7.
目的:从青藏高原冰川雪中筛选出一菌多酶的菌株.方法:对恢复出的4个细菌,通过平板透明法研究其产淀粉酶、脂肪酶和蛋白酶的特性.结果:LHG-C-9为惟一可以产淀粉酶的菌株,所产脂肪酶活性最高.4个菌株均不产蛋白酶.结论:LHG-C-9最适生长温度为15℃,属于耐冷菌.对该菌所产淀粉酶和脂肪酶的性质进行了初步研究,其随产淀粉酶的最适作用温度为50℃;最佳产酶pH值为7.0,该pH值所产酶活为83.9U/mL;在60℃的高温下温浴10min后酶活为0%.该菌株所产脂肪酶的最适作用温度为20℃;最佳产酶pH值为7.0,该pH值所产酶活为9.2U/mL;50℃温浴1h后酶活力不足34%.  相似文献   

8.
研究4种食物对真水狼蛛发育和繁殖的影响.结果表明:单喂果蝇时,幼蛛世代存活率最低;喂混合食物时幼蛛历期最短;单喂果蝇时,历期最长.幼蛛腹部体色与所喂食物颜色相近.喂混合食物的幼蛛,其背甲宽度和体重均大于其他3种食物.雌蛛所产卵袋数和产卵总量均以喂混合食物时为最高.多种食物混合喂养,有利于真水狼蛛的个体发育和繁殖.  相似文献   

9.
美国生物医学工程学会主席 R.Plonsey教授和 J.T.Mortimer 教授向中国同行们介绍了美国的生物医学工程的教育概况:目前,美国有65所大学招收生物医学工程学生,其中27所大学招收本科生,其余只招收研究生。另有35所左右的大学开设了生物医学工程选修课。  相似文献   

10.
太白红杉顶芽动态及其对分枝格局的影响   总被引:1,自引:0,他引:1  
应用计盒维数方法比较研究了与太白红杉顶芽动态相关的不同分枝格局对空间占据能力的差异.结果表明,Ⅰ型分枝有利于对所拥有的空间进行有效填充和利用,Ⅱ型分枝有利于扩展枝条所占的面积,Ⅲ型分枝既扩展了面积,又实现了对所拥有空间的有效填充和利用.总的来讲,顶芽的死亡使分枝对空间的占据能力和对光能利用的效率有所提高,同时对植株冠型的调整也有重要作用.太白红杉枝条顶芽的死亡是外界严酷环境条件的被迫“产物”.  相似文献   

11.
Feeding in starfish of the species Asterias rubens involves eversion of the cardiac stomach over prey such as mussels and oysters. For eversion to be accomplished the cardiac stomach must be relaxed. Here we show that two neuropeptides (S1 and S2) belonging to a family of echinoderm neuropeptides called SALMFamides cause concentration-dependent relaxation of the cardiac stomach in vitro, with S2 being 10 to 20 times more potent than S1. Previously, we have obtained evidence that nitric oxide mediates neural control of cardiac stomach relaxation in Asterias. However, S2-induced relaxation of the cardiac stomach is not affected by an inhibitor of the nitric oxide ''receptor'' soluble guanylyl cyclase. Therefore, cardiac stomach relaxation in starfish appears to be controlled by at least two neural signalling pathways acting in parallel. To assess the involvement of the SALMFamides in mediating cardiac stomach eversion in Asterias, experiments were performed in which water (control) or S1 or S2 was injected into the perivisceral coelom. Cardiac stomach eversion was observed after 5 min in 3% of tests with water, in 11% of tests with S1 and in 57% of tests with S2. Importantly, the effectiveness of S1 and S2 in promoting eversion corresponds with their relative potency as cardiac stomach relaxants in vitro. Collectively, these data indicate that SALMFamide neuropeptides may be involved in regulating the process of cardiac stomach eversion in starfish.  相似文献   

12.
To assess the genotoxicity of chemicals on the stomach, we developed in vivo assays that can detect micronucleus induction and gene expression changes in epithelial cells of the glandular stomach in mice. Male BALB/c mice were orally given a single dose (100 mg/kg) of N-nitroso-N-methylurea (MNU) or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) as stomach-targeted carcinogens. The glandular stomach was excised at 4h, 3 and 4 days after administration, and a single cell suspension of epithelial cells was prepared from the everted glandular stomach by EDTA treatment. For determination of micronucleus induction, gastric epithelial cells on days 3 and 4 after administration were fixed with 10% neutral-buffered formalin, stained with a combination of AO-DAPI, and analyzed under fluorescence microscopy. We also examined the induction of micronuclei in peripheral blood of these mice on days 2 and 3 after administration. Moreover, total RNA was extracted from gastric epithelial cells at 4h after administration, and p21 and plk2 expression was analyzed using a quantitative RT-PCR technique. 1) A significant increase of micronucleated cells was observed in the glandular stomach in mice treated with N-nitroso-N-methylurea (MNU) or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) compared to mice treated with vehicle. 2) In peripheral blood, induction of micronuclei was observed in mice treated with MNU but not with MNNG. 3) p21 and plk2, which related to cell cycle arrest, were up-regulated in the glandular stomach in mice treated with MNU or MNNG compared to mice treated with vehicle. The present study showed that these assays using glandular stomach may help to evaluate the genotoxicity of chemicals after oral administration.  相似文献   

13.
Ghrelin is a recently discovered stomach hormone that stimulates pituitary growth hormone (GH) secretion potently. The purpose of these experiments was to test the hypothesis that a stomach-ghrelin-pituitary-GH axis exists in which either an elevation or reduction in systemic GH levels will exert a negative or positive feedback action, respectively, on stomach ghrelin homeostasis. In rats, GH administration decreased stomach ghrelin mRNA levels and plasma ghrelin levels significantly. In GH-releasing hormone (GHRH) transgenic mice, GHRH overexpression decreased stomach ghrelin peptide levels when compared with control mice. In aged rats (25 months) stomach ghrelin mRNA and peptide levels and plasma ghrelin levels were decreased when compared with young rats (5 months). Because GH secretion is reduced in aged rats, the elevated stomach ghrelin production and secretion may reflect a decreased GH feedback on stomach ghrelin, homeostasis, and secretion. Together, these findings suggest that endogenous pituitary GH exerts a feedback action on stomach ghrelin homeostasis and support the hypothesis that a stomach-ghrelin-pituitary GH axis exists.  相似文献   

14.
Presence and release of calcitonin gene-related peptide in rat stomach   总被引:1,自引:0,他引:1  
Immunoreactive (IR)-calcitonin gene-related peptide (CGRP) was identified throughout the entire stomach of rats, being most highly concentrated in the pyloric region, and the concentrations in muscular layers being higher than those in mucosal layers. In addition, IR-CGRP was also present in the venous effluent from isolated perfused rat stomach, and its release was stimulated by dibutyryl cyclic AMP or theophylline but not by glucagon. Gel chromatography as well as HPLC of both tissue extracts and gastric perfusate showed three identical major peaks of IR-CGRP, one of which coeluted with synthetic CGRP. These results suggest that CGRP in the stomach plays a role in the regulation of gastric function.  相似文献   

15.
Gastrointestinal ulcerogenic effect of indomethacin is causally related with an endogenous prostaglandin (PG) deficiency, yet the detailed mechanism remains unknown. We examined the effect of various PGE analogues specific to EP receptor subtypes on these lesions in rats and mice, and investigated which EP receptor subtype is involved in the protective action of PGE(2). Fasted or non-fasted animals were given indomethacin s.c. at 35 mg/kg for induction of gastric lesions or 10-30 mg/kg for intestinal lesions, and they were killed 4 or 24 h later, respectively. Various EP agonists were given i.v. 10 min before indomethacin. Indomethacin caused hemorrhagic lesions in both the stomach and intestine. Prior administration of 16,16-dimethyl PGE(2) (dmPGE(2)) prevented the development of damage in both tissues, and the effect in the stomach was mimicked by 17-phenyl PGE2 (EP1), while that in the small intestine was reproduced by ONO-NT-012 (EP3) and ONO-AE-329 (EP4). Butaprost (EP2) did not have any effect on either gastric or intestinal lesions induced by indomethacin. Similar to the findings in rats, indomethacin caused gastric and intestinal lesions in both wild-type and knockout mice lacking EP1 or EP3 receptors. However, the protective action of dmPGE(2) in the stomach was observed in wild-type and EP3 receptor knockout mice but not in mice lacking EP1 receptors, while that in the intestine was observed in EP1 knockout as well as wild-type mice but not in the animals lacking EP3 receptors. These results suggest that indomethacin produced damage in the stomach and intestine in a PGE(2)-sensitive manner, and exogenous PGE(2) prevents gastric and intestinal ulcerogenic response to indomethacin through different EP receptor subtypes; the protection in the stomach is mediated by EP1 receptors, while that in the intestine mediated by EP3/EP4 receptors.  相似文献   

16.
We have previously suggested that an origin of a stomach cancer is from a progenitor cell specializing toward exocrine cell (Exo-cell) lineages. To clarify whether our hypothesis is correct or not, we analyzed the expression of Exo-cell and endocrine cell (End-cell) markers in a series of lesions for comparison. We evaluated chromogranin A (CgA) expression in 37 early and 73 advanced stomach cancers, in 30 stomach adenomas, in 8 carcinoid tumors, and in 4 endocrine cell carcinomas (ECCs) with assessment of gastric and/or intestinal (G/I) phenotypes in both Exo-cell and End-cell by immunohistochemistry. CgA expression was observed in 10.8% of the early and 16.4% of the advanced stomach cancers, respectively. The End-cell G/I phenotypes were in line with the Exo-cell counterparts in the CgA-positive stomach cancerous areas, and there was strong association between Cdx2 expression and the intestinal End-cell markers. All of the adenoma cases had the intestinal Exo-cell phenotypic expression, with the positive link between Exo-cell and End-cell G/I phenotypes. All stomach carcinoids had CgA expression but no expression of Exo-cell markers. In conclusion, most stomach cancers might develop from a progenitor cell specializing towards Exo-cell lineages, but some cases possessed both Exo-cell and End-cell markers with maturely differentiated phenotypes. In such cases, Exo-cell and End-cell phenotypes were found to correlate strongly, suggesting the possibility of histogenesis from "cancer stem cells".  相似文献   

17.
We investigated the regulatory mechanism of acid-induced HCO(3)(-) secretion in the slightly permeable rat stomach after an exposure to hyperosmolar NaCl. Under urethane anesthesia, a rat stomach was mounted on a chamber and perfused with saline, and the secretion of HCO(3)(-) was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. Acidification of the normal stomach with 100 mM HCl increased HCO(3)(-) secretion, and this response was totally inhibited by pretreatment with indomethacin but not N(G)-nitro-l-arginine methyl ester (l-NAME) or chemical ablation of capsaicin-sensitive afferent neurons. Exposure of the stomach to 0.5 M NaCl deranged the unstirred mucus gel layer without damaging the surface epithelial cells. The stomach responded to 0.5 M NaCl by secreting slightly more HCO(3)(-), in an indomethacin-inhibitable manner, and responded to even 10 mM HCl with a marked rise in HCO(3)(-) secretion, although 10 mM HCl did not have an effect in the normal stomach. The acid-induced HCO(3)(-) response in the NaCl-treated stomach was significantly but partially attenuated by indomethacin, l-NAME, or sensory deafferentation and was totally abolished when these treatments were combined. These results suggest that gastric HCO(3)(-) secretion in response to acid is regulated by two independent mechanisms, one mediated by prostaglandins (PGs) and the other by sensory neurons and nitric oxide (NO). The acid-induced HCO(3)(-) secretion in the normal stomach is totally mediated by endogenous PGs, but, when the stomach is made slightly permeable to acid, the response is markedly facilitated by sensory neurons and NO.  相似文献   

18.
Xeroderma pigmentosum group G (XPG) protein plays an important role in the DNA repair process by cutting the damaged DNA at the 3′ terminus. Previous studies have indicated some polymorphisms in the XPG gene are associated with stomach cancer susceptibility. We performed this hospital‐based case–control study to evaluate the association of four potentially functional XPG polymorphisms (rs2094258 C>T, rs751402 C>T, rs2296147 T>C and rs873601G>A) with stomach cancer susceptibility. The four single nucleotide polymorphisms (SNPs) were genotyped in 692 stomach cancer cases and 771 healthy controls. Logistic regression analysis was conducted, and odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the association of interest. Of the studied SNPs, XPG rs873601G>A polymorphism was found to significantly associate with stomach cancer susceptibility (AA versus GG/AG: OR = 1.31, 95% CI = 1.03–1.66, P = 0.027). Combined analysis of all SNPs revealed that the individuals with two of risk genotypes had a significantly increased stomach cancer risk (OR = 1.52, 95% CI = 1.13–2.06). In the stratification analysis, the association between the rs873601AA genotype and stomach cancer risk was observed in older group (>59 year), as well as patients with non‐cardia stomach cancer. Further combined analysis indicated men, smokers, or non‐drinkers more than one risk genotypes had a significantly increased stomach cancer risk. Our results indicate that XPG rs873601G>A polymorphism may be associated with the risk of stomach cancer. Further prospective studies with different ethnicities and large sample sizes are needed to validate our findings.  相似文献   

19.
The hormone leptin and the gut peptide CCK synergistically interact to enhance the process of satiation. Although this interaction may occur at several levels of the neuroaxis, our previous results indicate that leptin can specifically enhance the satiation effect of CCK by acting on subdiaphragmatic vagal afferent neurons. Because of this localized action, we hypothesized that a high proportion of vagal afferent neurons innervating the stomach or duodenum would be responsive to leptin and/or CCK. To test this hypothesis, we measured changes in cytosolic calcium levels induced by leptin and CCK in cultured nodose ganglion neurons labeled with a retrograde neuronal tracer injected into either the stomach or the duodenum. In the neurons labeled from the stomach, CCK activated 74% (39 of 53) compared with only 35% (34 of 97) of nonlabeled cells. Of the CCK-responsive neurons 60% (18 of 30) were capsaicin-sensitive. Leptin activated 42% (22 of 53) of the stomach innervating neurons compared with 26% of nonlabeled neurons. All of the leptin-sensitive neurons labeled from the stomach also responded to CCK. In the neurons labeled from the duodenum, CCK activated 71% (20 of 28). Of these CCK-responsive neurons 80% (12 of 15) were capsaicin sensitive. Leptin activated 46% (13 of 28) of these duodenal innervating neurons, of which 89% (8 of 9) were capsaicin-sensitive. Among neurons labeled from the duodenum 43% (12 of 28) were responsive to both leptin and CCK, compared with only 15% (15 of 97) of unlabeled neurons. Our results support the hypothesis that vagal afferent sensitivity to CCK and leptin is concentrated in neurons that innervate the stomach and duodenum. These specific visceral afferent populations are likely to comprise a substrate through which acute leptin/CCK interactions enhance satiation.  相似文献   

20.
The sensory innervation of the postpharyngeal foregut was investigated by injecting the enzyme horseradish peroxidase (HRP) into the walls of the esophagus, stomach, or duodenum. The transported HRP was identified histochemically, labeled neurons in the spinal and vagal ganglia were counted, and the results were plotted using an SAS statistical program. The spinal sensory fields of each viscus were defined using three determinations: craniocaudal extent, principal innervation field, and peak innervation field. The data revealed that innervation fields are craniocaudally extensive, the sensory field of each viscus overlaps significantly with its neighbor, yet each viscus can be characterized by a field of peak innervation density. Craniocaudal innervation of the esophagus spans as many as 22-23 paired spinal ganglia (C1-L2). There are two peak innervation fields for the cervical (C2-C6 and T2-T4) and for the thoracic (T2-T4 and T8-T12) sectors of the esophagus. The sensory innervation of the stomach extends craniocaudally over as many as 25 paired spinal ganglia (C2-L5). The peak innervation field of the stomach spans a large area comprising the cranial, middle, and the immediately adjoining caudal thoracic ganglia (T2-T10). The duodenum is innervated craniocaudally by as many as 15 paired thoracolumbar ganglia (T2-L3). Peak innervation originates in the middle and caudal thoracic ganglia and cranial lumbar (T6-L1) ganglia. There is a recognizable viscerotopic organization in the sensory innervation of the postpharyngeal foregut; successively more caudal sectors of this region of the alimentary canal are supplied with sensory fibers from successively more caudal spinal dorsal root ganglia. Vagal afferent innervation of the esophagus, stomach, and duodenum is bilateral and originates predominantly, but not exclusively, from vast numbers of neurons in the nodose (distal) ganglia. The esophagus is innervated bilaterally and more abundantly by jugular (proximal) ganglia neurons than is either the stomach or duodenum. The physiological significance of the findings are discussed in relation to the phenomena of visceral pain and referred pain.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号