千里光提取物体外抗阴道毛滴虫的效果观察

目的研究千里光提取物对体外培养的阴道毛滴虫的杀虫效果。结论体外培养阴道毛滴虫,选择千里光提取物进行体外抗阴道毛滴虫实验,千里光药液浓度经稀释后分别为4,2,1,0.5,0.25mg/ml。同时以甲硝唑为阳性对照,乙醇及RPMI-1640为阴性对照。结果体外实验表明千里光在24h时杀灭阴道毛滴虫的最低有效浓度为2mg/ml,其杀虫效果与甲硝唑近似;阴道毛滴虫在RPMI-1640培养液中生长良好,增值3倍。结论千里光提取物在体外具有杀灭和抑制阴道毛滴虫生长的作用。     

麝香保心丸在冠心病治疗中的临床研究进展

麝香保心丸目前已是治疗冠心病最常用的药物之一,不但能用于冠心病的长期治疗与预防,还能用于心绞痛发作时的急救.近年的研究又发现了麝香保心丸减少脂质浸润、抗动脉壁炎症、稳定易损斑块等作用,特别是促进治疗性血管新生作用的发现.使得对麝香保心丸治疗冠心病的临床作用开始重新认识     

肾康丸对早期糖尿病肾病大鼠肾脏晚期糖基化终产物及其受体表达的影响

目的：观察肾康丸对糖尿病肾病（DN）大鼠晚期糖基化终产物（AGEs）及其受体（RAGEs）表达的影响，探讨肾康丸对DN的肾保护作用机制。方法:应用链脲佐菌素建立大鼠DN模型，将DN模型大鼠随机分为4组：DN模型对照组、肾康丸组、厄贝沙坦组、肾康丸和厄贝沙坦合用组；另设正常对照组。各组分别干预8周后，观察24 h尿蛋白量、血清和肾组织AGEs含量变化，免疫组化法检测肾组织RAGEs的表达，RT-PCR法检测肾组织RAGEs mRNA的表达，光镜观察肾脏病理改变。结果:应用肾康丸、厄贝沙坦干预后，DN大鼠24 h尿蛋白量、血清及肾组织AGEs含量明显减少，肾组织RAGEs含量及其mRNA表达水平明显降低，肾脏病理改变显著减轻，肾康丸和厄贝沙坦合用组效果更为显著。结论:肾康丸对DN的肾保护作用与厄贝沙坦作用相当，且二者具有协同作用，其机制可能与其降低DN大鼠血清、肾组织AGEs水平以及肾组织RAGEs含量，抑制肾组织RAGEs mRNA的表达有关。     

枸橼酸铋雷尼替丁三联疗法根除幽门螺杆菌的临床观察

目的 观察以枸橼酸铋雷尼替丁(Ranitidine Bismuth Citrate)为基础的三联疗法对幽门螺杆菌(Hp)根除疗效及安全性.方法 将确诊为Hp阳性65例患者随机分为三组,即枸橼酸铋雷尼替丁组(简称枸雷组),奥美拉唑组和雷尼替丁组,疗程一周,应用14C-尿素呼气试验及荧光定量PCR法检测(由泸州医学院检验科检测),判断Hp根除效果.结果 根据意图治疗(ITT)分析Hp根除率分别为枸雷组84%、奥美拉唑组85.79%、雷尼替丁组68.4%.根据试验方案分析(PP)Hp根除率分别为88%、90.5%及73.7%.枸雷组Hp根除率与奥美拉唑组相近,但两组均较雷尼替丁组明显升高.枸雷组和奥美拉唑组较雷尼替丁组消化道症状明显改善,但枸雷组与奥美拉唑两组间无明显差异.枸雷组与奥美拉唑组不良反应均较雷尼替丁组轻微.结论 枸雷组三联疗法根Hp的临床疗效优于雷尼替丁三联疗法,但与奥美拉唑三联疗法相当,副反应发生情况也与奥美拉唑三联疗法无显著性差异,且因枸雷组相对价格低廉,值得作为一线药物推广使用.     

麝香保心丸在冠心病治疗中的临床研究进展

麝香保心丸目前已是治疗冠心病最常用的药物之一,不但能用于冠心病的长期治疗与预防,还能用于心绞痛发作时的急救。近年的研究又发现了麝香保心丸减少脂质浸润、抗动脉壁炎症、稳定易损斑块等作用,特别是促进治疗性血管新生作用的发现。使得对麝香保心丸治疗冠心病的临床作用开始重新认识     

锌对体外培养淋巴细胞功能的影响研究

本文研究不同锌离子浓度对体外培养淋巴细胞增殖功能的影响及其作用的可能机制.结果表明10~(-4)mmol/L,10~(-5)mmol/L Zn~(2+)使淋巴细胞增殖指数明显增加,但其作用弱于PHA.同时在该浓度下,淋巴细胞分泌IL-2增多,三磷酸肌醇(IP_3)含量增加,但对[Ca~(2+)]i浓度无显著影响.结果显示锌离子促使淋巴细胞分泌IL-2,引起淋巴细胞增殖,而IP_3可能与锌离子引起淋巴细胞增殖的部分功能有关.     

生血丸对环磷酰胺所致小鼠骨髓抑制的影响

目的:研究生血丸对小鼠骨髓造血功能的增强作用。方法:将小鼠分成4组:对照组、环磷酰胺模型组、生血丸低剂量组、生血丸高剂量组。模型组、生血丸组腹腔注射环磷酰胺造模, 同时生血丸组给不同剂量生血丸灌胃, 对照组、模型组生理盐水灌胃。结果:高、低剂量生血丸对环磷酰胺所致小鼠外周血像、骨髓有核细胞数的降低均有升高作用(P<0.01)。对骨髓微核细胞增加有明显的拮抗作用(P<0.05)。生血丸组小鼠骨髓细胞染色体畸变率显著低于模型组, 低剂量组和高剂量组抑制率分别为51.2%、61.5%。结论:生血丸可拮抗环磷酰胺诱发的小鼠造血功能损伤。     

生物杀虫剂球形赖氨酸芽孢杆菌的研究进展

自从20世纪60年代分离得到第1株具有杀灭蚊幼虫的细菌后,陆续出现了很多具有作为生物杀虫潜力的菌株.球形赖氨酸芽孢杆菌Lysinibacillus sphaericus（又称球型芽孢杆菌Bacillus sphaericus）和苏云金芽孢杆菌Bacillus thuringiensis是目前研究最为深入,在我国应用最广泛的生物杀虫剂.本文旨在通过对以往有关L.sphaericus的研究进行总结综述,包括其关键特性、灭蚊毒素及作用机制等,为进一步研究新型无污染的生物杀虫剂产品提供研究的视角.     

八味丸方药对代谢综合征患者治疗效应的临床观察

目的：考察八味丸方药（汤剂）对代谢综合征患者血糖、血压、血脂、血胰岛素及血浆过氧化脂质等的影响。方法：将60例代谢综合征患者随机分为实验组和对照组,对照组服卡托普利和二甲双胍,实验组在此基础上加服八味丸方汤剂,疗程印天,观察两组治疗前后血糖、血压、血脂、血胰岛素及血浆过氧化脂质等指标变化。结果：实验组有效率明显高于对照组（p〈0．01）。与对照组相比,实验组治疗后的血糖、血压、血脂、血胰岛索及血浆过氧化脂质等指标的改善更明显（p〈0．05or p〈O．01）。结论：本研究结果提示,八味丸方药对代谢综合征的降糖、降脂、降胰岛素和降压作用主要是通过改善IR而实现的;八味丸方药较好的改善IR及相关病理生理改变的作用,可能与其降低血浆过氧化脂质有关。     

腺嘌呤核苷酸活化蛋白激酶与哺乳动物雷帕霉素靶蛋白信号转导通路的相互作用

背景：腺嘌呤核苷酸活化蛋白激酶的下游靶分子哺乳动物雷帕霉素靶蛋白对细胞生长、分裂和蛋白质合成有重要意义。 目的：综述腺嘌呤核苷酸活化蛋白激酶与哺乳动物雷帕霉素靶蛋白信号转导相互调节的最新研究进展,以期揭示腺嘌呤核苷酸活化蛋白激酶和哺乳动物雷帕霉素靶蛋白信号转导的交互作用对蛋白质合成的影响。 方法：以“(mammalian target of rapamycin OR mTOR) AND (AMP activated protein kinase OR AMPK) AND signal transduction”为检索式,计算机检索PubMed数据库相关内容的文献,最终纳入30篇可反映腺嘌呤核苷酸活化蛋白激酶与哺乳动物雷帕霉素靶蛋白信号转导通路相互作用的文献,并进行归纳总结。 结果与结论：腺嘌呤核苷酸活化蛋白激酶活化导致哺乳动物雷帕霉素靶蛋白信号转导减弱一定程度上抑制蛋白质合成,腺嘌呤核苷酸活化蛋白激酶通过多个位点磷酸化和活化而调节哺乳动物雷帕霉素靶蛋白信号转导。腺嘌呤核苷酸活化蛋白激酶磷酸化马铃薯球蛋白会抑制Akt,ERK1/ERK2和p90rsk等其他蛋白激酶的作用。明确腺嘌呤核苷酸活化蛋白激酶对哺乳动物雷帕霉素靶蛋白的调节过程所起的作用,对揭示腺嘌呤核苷酸活化蛋白激酶-哺乳动物雷帕霉素靶蛋白途径调控能量代谢和蛋白合成方面有重要意义。     

Toward an analysis of conscious activity: 2. The functions of sleep and wakefulness

What we generally call information is created through interference between regular information and reverse information. In this process, conscious activity is the creator of information. We can assume that the following five-stage mechanism exists inside the brain: 1) a mechanism that creates consciousness and recognizes information; 2) a mechanism that accumulates information in the neural circuits; 3) a mechanism that combines and separates the self-conscious mind and fragments of accumulated information; 4) a mechanism that accesses the operating system or distributes information to localized neural circuits; and 5) a mechanism that allows the operating system to modify itself with an increase in the amount of information. These mechanisms can be considered to belong to the category of conscious activity, which is created by a combination of potentialization of sleep and potentialization of wakefulness.     

大学生个性与防御机制的关系研究

目的：观察大学生个性与防御机制的关系。方法：按不同专业分层抽样共抽取大学生541例，分别采用艾森克个性问卷（EPQ）和防御方式问卷（DSQ）进行测试。结果：精神病质（EPQ－P）与大部分的不成熟防御机制呈正相关，与成熟防御机制呈负相关；神经质（EPQ－N）与大部分的不成熟防御机制、中间型防御机制呈正相关；内外向（EPQ－E）与大部分的不成熟防御机制呈负相关，与成熟防御机制呈正相关，与中间型防御机制表现出比较复杂的关系。结论：精神病质个性倾向的学生更多采用不成熟防御机制，神经质个性倾向的学生更多采用不成熟和中间型防御机制，而外向个性倾向的学生更多混合采用成熟的和一些中间型防御机制。提示一定类型人格常具有相应的防御机制，二者间存在一种复杂的相互关系。     

Evidence that cytotoxic T cells and natural cytotoxic cells use different lytic mechanisms to lyse the same targets

There is evidence that natural cytotoxic (NC) cells are in the T cell lineage. To lyse targets, cytotoxic T cells (T^K) must recognize any of the myriad antigens plus syngeneic major histocompatibility complex (MHC) determinants. In spite of the evidence which indicates T^K and NC are in the same lineage, NC cells can recognize few determinants (perhaps only one) and do not require recognition of MHC determinants. In addition to differences in the requirement for target recognition, in this report we show that T^K cells and NC cells also use different lytic mechanisms to lyse the same targets. NC effectors initiate a lytic mechanism in NC-sensitive and NC-resistant targets. This lytic mechanism requires approximately 4 h before target lysis is apparent in NC-sensitive targets; it is inactivated by a protein synthesis-dependent counterlytic mechanism in NC-resistant targets. In contrast the T^K lytic mechanism causes a rapid release of ⁵¹Cr from both NC-sensitive and NC-resistant targets and is not inhibited by the NC counterlytic mechanism present in NC-resistant cells. These findings lead to the conclusion that the mechanism used by NC cells to lyse targets is fundamentally different from that used by T^K cells.     

Harvey Cushing and the regulation of blood pressure in giraffe, rat and man: introducing 'Cushing's mechanism'

The fundamental mechanism that underlies essential hypertension is a high total peripheral resistance. We review here possible origins of high total peripheral resistance in physiologically hypertensive giraffes, spontaneously hypertensive rats and humans with essential hypertension. We propose that a common link could be reduced brainstem perfusion, as first suggested by Cushing in 1901. Any tendency towards reduction of cerebral blood flow to the cardiovascular control centres in rest and sleep will be prevented by activation of a response arising in the brainstem. The response will proportionately increase systemic blood pressure and return cerebral blood flow to a new homeostatic level. New evidence we review here supports this idea and leads us to suggest that central regulation of blood pressure has two components: the classic Cushing's response, which is a terminal event, and a Cushing's mechanism, which is a physiological mechanism for long-term control of mean arterial pressure. In giraffes, Cushing's mechanism is activated by increasing neck length during growth and subsequent gravitational hypotension that stimulates a rise in basal arterial blood pressure. In man and rats, the mechanism is activated by narrowing of the arteries supplying the brainstem. If we are correct, future successful treatment of essential hypertension in man will include methods of reducing cerebral arterial resistance.     

Osteoblast differentiation stage-specific expression of the pyrophosphate-generating enzyme PC-1

Fibroblast growth factor (FGF) signaling plays a critical role in skeletal development, yet the mechanism by which FGFs affect bone mineralization is not well understood. Review of the literature investigating effects of FGF signaling on bone mineralization indicates that FGFs may stimulate expression of factors that prevent mineralization in the short term and enhance mineralization in the long term. Pyrophosphate is an ideal example of a factor that, dependent upon environment, has the capacity to inhibit or enhance mineralization. PC-1 is the primary generator of pyrophosphate in osteoblastic cells; therefore, regulated expression of PC-1 by FGFs may be a principal mechanism by which FGF signaling affects bone mineralization. We previously showed that FGF2 induces PC-1 expression in preosteoblastic cells and that this induction is differentiation stage dependent. In order to more directly investigate the mechanism by which PC-1 expression is regulated, we have cloned a 2.8-kb region of the PC-1 gene promoter and constructed a PC-1 gene promoter/firefly luciferase reporter construct. Results indicate that this construct is specifically responsive to FGF2 or ascorbate (an inducer of osteoblast differentiation). Promoter responsiveness to FGF2 is significantly diminished upon osteoblast differentiation, and increases in promoter activity that occur with osteoblast differentiation are inhibited by FGF2 treatment. These results indicate that the mechanism of PC-1 induction by FGF2 in preosteoblastic cells is distinct from the mechanism of induction that occurs with osteoblast differentiation. These results also indicate that PC-1 may play multiple and distinct roles in the development of mineralized tissues.     

The balance of deletion and regulation in allograft tolerance

Summary:  Although the precise mechanisms involved in the establishment and maintenance of peripheral allograft tolerance are still not fully understood, it is now clear that acquisition of transplantation tolerance is an active, highly regulated, multistep process. According to the pool size model of allograft tolerance, the allograft outcome, rejection, or tolerance, often depends on the balance between cytopathic and regulatory T cells (Tregs). Although both deletion and regulation play important roles in allograft tolerance, our recent studies showed that the quantitative details for each mechanism differ from model to model. Therefore, we hypothesize that there is a delicate balance between deletion and regulation in allograft tolerance. In a model of allograft tolerance in which the deletional mechanism plays a dominant role, e.g. tolerance produced via creation of mixed chimeras, the regulatory mechanism, albeit sometimes present, is far less important. Whilst in a model in which the regulation mechanism plays a critical role, e.g. donor-specific transfusion plus MR1-induced allograft tolerance, a deletional mechanism lowers the threshold for effective Treg action.     

Repetitive transients in intracellular Ca2+ in cultured human vascular smooth muscle cells.

Human uterine vascular smooth muscle cells have been isolated and maintained in culture. When these cells are exposed to bathing solutions with nominally zero sodium, using potassium, N-methyl-D-glucamine or Tris as substitutes, repetitive transient increases in intracellular calcium are observed. These transients are abolished when the calcium concentration of the bathing solution is reduced to nominally zero suggesting a role for extracellular calcium in the activation or maintenance of the transients. The hypothesis is proposed that the underlying mechanism involves a calcium influx through the reversed operation of a sodium-calcium exchange mechanism and the cyclical activation of calcium-induced calcium release from the sarcoplasmic reticulum. Noradrenaline (10(-6) M) and caffeine (20-30 mM) reversibly inhibited the transients. The inhibitory action of these agents could not be mimicked by dibutyryl cAMP suggesting that cAMP does not mediate the inhibition. Caffeine alone had no effect on resting calcium. Thimerosal (1-100 microM), an agent thought to activate a second type of calcium-induced calcium release mechanism activated repetitive transient increases in intracellular calcium which behave in a similar manner to those activated by sodium removal. These data are consistent with the presence of a thimerosal-activated calcium-induced calcium release mechanism in these cultured human cells. It is proposed that this mechanism is different from the calcium-induced calcium release mechanism, described in other cell types, which is activated by caffeine.     

The telomere lengthening mechanism in telomerase-negative immortal human cells does not involve the telomerase RNA subunit

According to the telomere hypothesis of senescence, the progressive shortening of telomeres that occurs upon division of normal somatic cells eventually leads to cellular senescence. The immortalisation of human cells is associated with the acquisition of a telomere maintenance mechanism which is usually dependent upon expression of the enzyme telomerase. About one third of in vitro immortalised human cell lines, however, have no detectable telomerase but contain telomeres that are abnormally long. The nature of the alternative telomere maintenance mechanism (referred to as ALT, for Alternative Lengthening of Telomeres) that must exist in these telomerase-negative cells has not been elucidated. It has previously been shown that abnormal lengthening of yeast telomeres may occur due to mutations in the yeast telomerase RNA gene. That this is not the mechanism of the abnormally long telomeres in ALT cell lines was demonstrated by the finding that seven of seven ALT lines have wild-type human telomerase RNA (hTR) sequence, including a novel polymorphism that is present in 30% of normal individuals. We found that two ALT cell lines have no detectable expression of the hTR gene. This shows that the ALT mechanism in these cell lines is not dependent on hTR. Expression of exogenous hTR via infection of these cells with a recombinant hTR-adenovirus vector did not result in telomerase activity, indicating that their lack of telomerase activity is not due to absence of hTR expression. We conclude that the ALT mechanism is not dependent on the expression of hTR, and does not involve mutations in the hTR sequence.      

Metabolism and antiviral activity of ribavirin

Thirty years after its synthesis, the mechanism of action of ribavirin is still not completely understood. Although much is known about the metabolism and biochemical effects of ribavirin in human cells, there is still much to be learned about the precise mechanism of action of ribavirin with the various viruses. New information about its ability to induce mutations in viral genomes has led to new questions about its mechanism of action. There is considerable evidence that indicates that ribavirin triphosphate (RTP) can interact with the various viral RNA polymerases, and it seems likely that this interaction is important to the mechanism of action of ribavirin. It seems likely that ribavirin will not have one universal mechanism of action, but will inhibit different viruses in different ways. In some cases, inhibition of IMP dehydrogenase may be sufficient for antiviral activity. Whereas, in other cases, inhibition of viral RNA polymerases by RTP may be more important. It is also likely that RTP will interact with the different viral RNA polymerases in different ways leading to different mechanisms of actions. More comprehensive studies are needed that address all aspects of ribavirin metabolism and biochemical actions to gain a thorough understanding of the activity of this agent. Finally, the differences in the metabolism and biochemical actions of ribavirin, selenazofurin, and tiazofurin indicate that small structural changes can have profound effects on biological activity. This observation is well known by investigators familiar with nucleoside analogs, but indicate that one should not assume that agents of similar structure have identical activities.     

The fundamental role of hyaluronidase in tissue

The interstitial ground substance plays an essential role in the physiological processes of the capillary and the cell. Together they form a fundamental unit of function in which the cell is the most important part. Therefore the fundamental unit is called: THE CELLULAR UNIT. It is proposed central role and that this enzyme is indispensible for normal healthy cells as well as for the reactive mechanism in critical situations. The reactive mechanisms can be divided into a local reactive mechanism and a general reactive mechanism. The local reactive mechanism has a function of RESTORATION. The general reactive mechanism is especially for PROTECTION AGAINST ISCHAEMIA and REDISTRIBUTION OF TOTAL BODY NUTRIENTS in order to stimulate the restoration. These two mechanisms may have important clinical consequences.