不同证型老年男性高血压病患者性激素相关调控因素的比较研究

目的:探讨男性老年人高血压病肾气亏虚证、肝火上炎证与性激素相关调控因素的关联性,从而为研究老年人高血压病肾气亏虚证、肝火上炎证证候表现的病理生理基础提供依据。方法:根据高血压诊断与分级标准、中医辨证标准选择了男性高血压病肾气亏虚证、肝火上炎证患者各30例和健康老年男性30例,采用酶联免疫吸附法检测白介素-2(IL-2)、瘦素(Leptin)、肿瘤坏死因子(TNF-α)、促性腺激素释放激素(GnRH)和硫酸脱氢表雄酮(DHEA-S)的水平。结果:男性老年人高血压肾气亏虚证患者的性激素相关调控因素水平的异常变化与男性老年人高血压病肾气亏虚证的发病有关,预示血清白介素-2、瘦素、促性腺激素释放激素和硫酸脱氢表雄酮水平的异常变化可能是男性老年人高血压病肾气亏虚证形成的病理基础之一。

不同证型老年女性高血压病患者性激素相关调控因素的比较研究

目的:探讨女性老年人高血压病肾气亏虚证、肝火上炎证与性激素相关调控因素的关联性,从而为研究老年人高血压病肾气亏虚证、肝火上炎证证候表现的病理生理基础提供依据。方法:根据高血压诊断与分级标准、中医辨证标准选择了女性高血压病肾气亏虚证、肝火上炎证患者各30例和健康老年女性30例,采用酶联免疫吸附法检测白介素-2(IL-2)、瘦素(Leptin)、肿瘤坏死因子(TNF-α)、促性腺激素释放激素(GnRH)和硫酸脱氢表雄酮(DHEA-S)的水平。结果:女性老年人高血压肾气亏虚证患者的性激素相关调控因素水平的异常变化与女性老年人高血压病肾气亏虚证的发病有关,预示血清白介素-2水平的异常变化可能是女性老年人高血压病肾气亏虚证形成的病理基础之一。

老年男性高血压病肾气亏虚证特征性性激素与其相关调控因素的相关性研究

目的:探讨老年男性高血压病肾气亏虚证特征性性激素与其相关调控因素的的关联性,从而为研究老年高血压病肾气亏虚证证候表现的病理生理基础提供依据。方法:对30例老年男性高血压病肾气亏虚证患者首先采用电化学发光免疫法检测血清卵泡刺激素、雌二醇水平,其次采用放射免疫分析法和酶联免疫吸附法检测血清白介素-2、瘦素、促性腺激素释放激素和硫酸脱氢表雄酮水平,最后应用多重线性回归法建立多重线性回归模型,深入探析老年男性高血压病肾气亏虚证特征性性激素指标与特征性性激素相关调控因素之间的相关程度。结果:白介素-2是老年男性高血压病肾气亏虚证患者血清雌激素的敏感性调控因素,雌二醇含量变异的20.50%可由白介素-2的变化来解释,且二者呈负相关关系;瘦素是老年男性高血压病肾气亏虚证患者血清卵泡刺激素的敏感性调控因素,卵泡刺激素含量变异的18.30%可由瘦素的变化来解释,且二者呈正相关关系。结论:老年男性高血压病肾气亏虚证患者的白介素-2对雌二醇具有负向调控作用,瘦素对卵泡刺激素具有正向调控作用。

Cloning and Expression of Gonadotrophin Releasing Hormone Receptor in Apis cerana cerana

[Objective] This study was to clone the GnRH （gonadotropin-releasing hormone）, and to investigate its expression in Apis cerana cerana. [Method] The cDNA sequence of GnRHR gene was amplified from Apis cerana cerana by using RT-PCR techniques. It was conducted with bioinformatics analysis and the in situ hybridization histochemistry of its expression products was studied. [Result] The sequence analy- sis showed that the full cDNA sequence was 1 050 bp with the open reading frame of 1 050 bp, and it encoded 349 amino acid residues. The deduced amino sequence included 7 transmembrane regions, and the predicted molecular mass and isoelectric point were 40.6 kD and 9.54, respectively. The cluster analysis showed that the GnRHR from ＇,4. cerana cerana had close relationship to the GnRHR II from other insects. In situ hybridization showed that Bee-GnRHR staining was specifically localized to the brain, intestine, fat body and testis. [Conclusion] The results indicated that the GnRHR provided molecular bond for the reproduction and metabolism for insects, and suggested a functional role for bee-GnRHR signaling in the coupling of reproduction activities and environment conditions.

Sex Hormones and Androgen Receptor:Risk Factors of Coronary Heart Disease in Elderly Men

Objective To investigate the variation of sex hormone and its receptor level in elderly male patients with coronary heart disease (CHD) and to evaluate the correlations between CHD and sex hormone as well as sex hormone receptor. Methods Altogether 139 male CHD patients (CHD group) aged 60-92 years and 400 healthy men (control group) aged 60-90 years were included in this cross sectional study. The plasma concentrations of dehydroepiandrosterone sulfate (DHEAS),total testosterone (TT),free testosterone (FT),estradiol (E2),sex hormone binding globulin (SHBG),luteinizing hormone (LH),and follicle-stimulating hormone (FSH) were measured. The androgen receptor (AR) was tested by flow cytometry. Correlations between CHD and levels of sex hormones and AR were analyzed. Results Compared with the control group,the levels of DHEAS,TT,FT,SHBG,and the fluorescence intensity of AR in the CHD group significantly reduced (P<0.05),while the levels of FSH and E2 significantly increased (P<0.01). Age was negatively correlated with TT (r=-0.28,P=0.00) and FT (r=-0.17,P=0.01),while it was positively correlated with SHBG (r=0.14,P=0.04) and E2 (r=0.33,P=0.00). AR fluorescence intensity was negatively correlated with systolic blood pressure (r=-0.12,P=0.01). Binary logistic regression analysis showed that TT,SHBG,and AR were all negatively correlated with CHD (P<0.05). Conclusions Elderly male patients with CHD are found to have low levels of DHEAS,TT,FT,SHBG,and AR,while high concentrations of E2 and FSH. Low levels of TT and SHBG may be the potential risk factors of CHD in elderly men.

Problems associated with glucose toxicity:Role of hyperglycemia-induced oxidative stress

Glucose homeostasis deficiency leads to a chronic increase in blood glucose concentration. In contrast to physiological glucose concentration, chronic super-physiological glucose concentration negatively affects a large number of organs and tissues. Glucose toxicity means a decrease in insulin secretion and an increase in insulin resistance due to chronic hyperglycemia. It is now generally accepted that glucose toxicity is involved in the worsening of diabetes by affecting the secretion of B-cells. Several mechanisms have been proposed to explain the adverse effects of hyperglycemia. It was found that persistent hyperglycemia caused the functional decline of neutrophils. Infection is thus the main problem resulting from glucose toxicity in the acute phase. In other words, continued hyperglycemia is a life-threatening risk factor, not only in the chronic but also the acute phase, and it becomes a risk factor for infection, particularly in the perioperative period.

Estrogen,male dominance and esophageal adenocarcinoma:Is there a link?

Esophageal adenocarcinoma is a cancer with poor prognosis, and its incidence has risen sharply over recent decades. Obesity is a major risk factor for developing this cancer and there is a clear male gender bias in the incidence that cannot be fully explained by known risk factors. It is possible that a difference in the expression of estrogen, or its signaling axes, may contribute to this gender bias. We undertook a com- prehensive literature search and analyzed the available data regarding estrogen and estrogen receptor expres- sion, and the possible sex-specific links with esopha- geal adenocarcinoma development. Potentially relevant associations between visceral vs subcutaneous fat deposition and estrogen expression, and the effect of crosstalk between estrogen and leptin signaling were identified. We also found limited studies suggesting a role for estrogen receptor 13 expression in esophageal adenocarcinoma development. The current literature supports speculation on an etiological role for estrogen in the male gender bias in esophageal adenocarcino- ma, but further studies are required.

Is the iron regulatory hormone hepcidin a risk factor for alcoholic liver disease?

Despite heavy consumption over a long period of time, only a small number of alcoholics develop alcoholic liver disease. This alludes to the possibility that other factors, besides alcohol, may be involved in the progression of the disease. Over the years, many such factors have indeed been identified, including iron. Despite being crucial for various important biological processes, iron can also be harmful due to its ability to catalyze Fenton chemistry. Alcohol and iron have been shown to interact synergistically to cause liver injury. Iron-mediated cell signaling has been reported to be involved in the pathogenesis of experimental alcoholic liver disease. Hepcidin is an iron-regulatory hormone synthesized by the liver, which plays a pivotal role in iron homeostasis. Both acute and chronic alcohol exposure suppress hepcidin expression in the liver. The sera of patients with alcoholic liver disease, particularly those exhibiting higher serum iron indices, have also been reported to display reduced prohepcidin levels. Alcohol-mediated oxidative stress is involved in the inhibition of hepcidin promoter activity and transcription in the liver. This in turn leads to an increase in intestinal iron transport and liver iron storage. Hepcidin is expressed primarily in hepatocytes. It is noteworthy that both hepatocytes and Kupffer cells are involved in the progression of alcoholic liver disease. However, the activation of Kupffer cells and TNF-α signaling has been reported not to be involved in the down-regulation of hepcidin expression by alcohol in the liver. Alcohol acts within the parenchymal cells of the liver to suppress the synthesis of hepcidin. Due to its crucial role in the regulation of body iron stores, hepcidin may act as a secondary risk factor in the progression of alcoholic liver disease. The clarification of the mechanisms by which alcohol disrupts iron homeostasis will allow for further understanding of the pathogenesis of alcoholic liver disease.

The Characteristics of vasa Gene from Japanese Sea Bass(Lateolabrax japonicas) and Its Response to the External Hormones

The RNA helicase Vasa is an important regulator of primordial germ cell development. Its function in mature fish, espe- cially the hormone-related differences in maturing male fish has seldom been documented. In this study, a full length cDNA sequence of the vasa gene was cloned from Japanese sea bass, Lateolabraxjaponicas, and it was namedjsb-vasa. Homology analysis showed thatjsb-vasa was closely related to its teleost homologs. The spatial distribution ofjsb-vasa indicated that it was only highly ex- pressed in testis, showing its germ cell-specific expression pattern. During the testicular development cycle, jsb-vasa was highly expressed during early period of spermatogenesis, and reduced when spermatogenesis advanced. In addition, the jsb-vasa gene ex- pression was significantly inhibited at 6 h, 12 h and 24 h after injecting hCG （human ehorionic gonadotropin） and GnRHa （Gonad- otropin-releasing hormone analogue）, indicating thatjsb-vasa gene may play an important role in spermatogenesis of Japanese sea bass, and be under the regulation of external sex hormones.

Effects of quercetin on hepatocyte stimulating factor production by mouse peritoneal macrophages

Objective: To study the effects of quercetin on hepatocyte stimulating factor production from mouse peritoneal macrophages. Methods: Hepatocyte stimulating factor was evaluated by the amount of fibrinogen synthesized in Hep3B cells. Interleukin-6 activity was measured by B9 cell proliferation methyl thiazolyl tetrazolium colorimetric method. Hep3B cell supernatant fibrinogen was quantitated with ELISA. Results: LPS induced the synthesis of hepatocyte stimulating factor in mouse peritoneal macrophages, and hepatocyte stimulating factor promotes the synthesis of fibrinogen from Hep3B cells. Quercetin(5 to 40μmol/ L) inhibited the synthesis of hepatocyte stimulating factor stimulated by LPS. Quercetin(5 to 20μmol/ L) inhibited release of interleukin-6 from mouse peritoneal macrophages induced by 0. 5 g/ L fibrin fibrinogen degradation products. Conclusion: Quercetin inhibits the synthesis of hepatocyte stimulating factor in macrophages.

Hormones and phenotypic plasticity： Implications for the evolution of integrated adaptive phenotypes

It is generally accepted that taxa exhibit genetic variation in phenotypic plasticity, but many questions remain unan- swered about how divergent plastic responses evolve under dissimilar ecological conditions. Hormones are signaling molecules that act as proximate mediators of phenotype expression by regulating a variety of cellular, physiological, and behavioral re- sponses. Hormones not only change cellular and physiological states but also influence gene expression directly or indirectly, thereby linking environmental conditions to phenotypic development. Studying how hormonal pathways respond to environ- mental variation and how those responses differ between individuals, populations, and species can expand our understanding of the evolution of phenotypic plasticity. Here, we explore the ways that the study of hormone signaling is providing new insights into the underlying proximate bases for individual, population or species variation in plasticity. Using several studies as exem- plars, we examine how a ＇norm of reaction＇ approach can be used in investigations of hormone-mediated plasticity to inform the following： 1） how environmental cues affect the component hormones, receptors and enzymes that comprise any endocrine sig- naling pathway, 2） how genetic and epigenetic variation in endocrine-associated genes can generate variation in plasticity among these diverse components, and 3） how phenotypes mediated by the same hormone can be coupled and decoupled via independent plastic responses of signaling components across target tissues. Future studies that apply approaches such as reaction norms and network modeling to questions concerning how hormones link environmental stimuli to ecologically-relevant phenotypic re- sponses should help unravel how phenotypic plasticity evolves