中药熏洗治疗老年性阴道炎61例临床观察

目的研究老年性阴道炎的中药疗法。方法 61例老年性阴道炎患者,用中药熏洗治疗,观察治疗前后症状缓解情况。结果治疗后白带增多、外阴阴道瘙痒、阴道干燥、性交疼痛等临床症状消退明显,治疗效果肯定且费用低廉,患者易于接受。结论中药熏洗治疗老年性阴道炎,疗效肯定,值得基层临床推广应用。     

知柏地黄丸配合中药熏洗对老年性阴道炎的疗效

目的：探讨老年性阴道炎治疗中,知柏地黄丸联合中药熏洗的应用效果。方法：选取我院老年性阴道炎患者54例,随机分为对照组与观察组,各组27例,分别行中药熏洗与知柏地黄丸联合中药熏洗治疗,观测两组治疗效果及不良反应。结果：对照组治疗总有效率为88.89%,不良反应率为3.70%;观察组治疗总有效率为96.30%,不良反应率为3.70%。结论：在老年性阴道炎治疗中,知柏地黄丸联合中药熏洗疗效确切,值得推广。     

中西医结合治疗老年性阴道炎93例分析

目的 :老年性阴道炎是绝经后妇女和卵巢功能早衰妇女的常见病 ,治疗效果欠佳。本文意在探讨治疗老年性阴道炎的有效方法。方法 :本文采用中西医结合的治疗方法 :内服中药 (知柏地黄汤加减 ) ,外用西药 ,治疗老年性阴道炎。结果 :本组治疗老年性阴道炎 93例 ,痊愈 77例 ,显效 11例 ,好转 4例 ,无效 1例 ,总有效率为 98.9% ;较对照组只用西医治疗的效果 91.9%为好。结论 :中药滋阴补阳 ,可调节绝经期和卵巢功能早衰妇女的机体阴阳平衡 ,增加机体抵抗力。中西医结合的治疗方法能达到“标本同治”的效果 ,避免了长期使用雌激素药物引起的不良反应。临床观察 ,疗效好 ,副作用少 ,是老年性阴道炎的一种有效治疗方法。     

中西医结合治疗老年性阴道炎60例

目的 探讨老年性阴道炎的有效治疗方法.方法 对我院门诊2008 年1 月至2010 年1 月的60 例老年性阴道炎患者在中药外洗配合西药外用进行治疗,观察有效率.结果 60 例中治愈54 例,有效6 例,总有效率100%.结论 中西医结合治疗老年性阴道炎疗效确切,经济简便,无不良反应.尤适应基层医疗单位应用.     

中西医结合治疗老年性阴道炎100例疗效观察

目的观察中西医结合治疗老年性阴道炎的疗效。方法选择来本院治疗的老年性阴道炎患者200例,随机分为对照组与治疗组,各100例,对照组单用西医治疗,治疗组是在对照组的基础上内外兼治,口服中药知柏地黄汤,外用复方桃仙合剂。结果治疗组总有效率为98％,对照组总有效率为75％,两组比较差异有统计学意义（P〈0．05）。结论采用中西医结合内外兼治,治疗老年性阴道炎疗效显著,复发率低,值得临床推广应用。     

中西医结合法治疗老年性阴道炎的临床疗效分析

目的探讨中西医结合法治疗老年妇女阴道炎的临床特征及治疗。方法回顾性分析自2008年6月至2009年12月间共收治36例老年性阴道炎患者的临床资料,随机分为治疗组和对照组。治疗组采用中西医结合的治疗方法:内服中药(知柏地黄汤加减),外用西药,治疗老年性阴道炎。结果治疗组18例患者中,痊愈14例,显效2例,好转1例,无效1例,总有效率为94.44%;较对照组只用西医治疗的效果77.78%为好。结论中药滋阴补阳,可调节绝经期和卵巢功能早衰妇女的机体阴阳平衡,增加机体抵抗力。中西医结合的治疗方法能达到"标本同治"的效果,避免了长期使用雌激素药物引起的不良反应。临床观察,疗效好,不良反应少,是老年性阴道炎的一种有效治疗方法。     

中药熏洗配合康妇特栓治疗老年性阴道炎80例疗效察

目的了解中药熏洗配合康妇特栓对老年性阴道炎的疗效。方法采集老年性阴道炎患者80例,予中药（苦参30g,黄柏30g,地肤子30g,蛇床子30g,白鲜皮15g）水煎去渣,取汁2500ml左右,先熏蒸外阴及阴道、再坐浴,每次30min,之后用康妇特栓（太阳石药业生产的）1枚塞入阴道深部。结果 80例患者,治愈66例,有效11例,无效3例。治愈率82.5%,总有效率96.3%。结论中药熏洗配合康妇特栓治疗老年性阴道炎临床效果明显,值得推广应用。     

老年性阴道炎行臭氧治疗的护理

目的总结老年性阴道炎患者行臭氧治疗的护理措施,以提高患者的治疗效果。方法采用妇科臭氧治疗仪,进行老年性阴道炎的治疗。结果回顾性总结300例老年性阴道炎患者,行臭氧治疗的护理措施。结论老年性阴道炎行臭氧治疗,安全、无不良反应。疗效明显,复发率低。     

中药组方治疗老年性阴道炎和尿道炎的临床观察

老年性阴道炎和尿道炎是老年妇女常见病,老年性阴道炎在绝经妇女中的发病率为26．3％～30％,老年性尿道炎在50岁以上妇女中发病率约为34％。现代医学认为,两者的发病机理均与绝经后体内雌激素水平下降有关,治疗上均以补充雌激素替代治疗为主要措施,老年性尿道炎使用雄激素治疗同样有效。但在临床工作中,常有一部分老年患者因担心使用雌激素引起副作用而不愿接受雌激素治疗,一部分老年患者自感阴道局部上药非常不适及不便,也不愿接受使用雌激素阴道局部放置。2006年1月至2008年12月我们对53例老年性阴道炎和尿道炎患者采用中药组方薰洗及坐浴治疗,取得较好疗效,现报告如下。     

老年性阴道炎的激素治疗临床疗效分析

目的探讨老年性阴道炎的临床治疗与临床疗效分析。方法选取临床160例老年性阴道炎患者的临床资料进行分析。结果160例老年性阴道炎,痊愈155例,好转5例,总有效率100％。结论使用雌激素治疗,增加阴道对细菌的抵抗力,改变阴道局部的易感染特性,减低或避免发生老年性阴道炎。     

The efficacy and safety of calcitriol and/or Caltrate D in elderly Chinese women with low bone mass

Aim： To observe the efficacy and safety of Rocaltrol （calcitriol） and/or Caltrate D （calicum carbonate plus vitamin D） in elderly Chinese women with osteopenia or osteoporosis.
Methods： One hundred fifty Chinese women aged over 65 years with osteopenia or osteoporosis from three centers were randomly divided into two groups. Seventy-six participants received Caltrate D as one pill daily; the other 74 participants received 0.25 μg Caltrate D plus Rocaltrol daily. The changes in bone mineral density （BMD） served as primary end-points. Height changes, the presence of new vertebral fractures, muscle strength and balance were evaluated.
Results： The following are the mean percentage changes （and SD） in BMD over 12 months： at L2-L4, 0.83±3.88 in the Caltrate D group and 2.84±4.04 in the Rocaltrol＋Caltrate D group （P=0.003, by ANCOVA ）; at the femoral neck, 0.04±3.94 in the Caltrate D group and 2.01±5.45 in the Rocaltrol＋Caltrate D group （P=0.085, by ANCOVA）; and in the trochanter, 1.59±4.57 in the Caltrate D group and 3.76±6.25 in the Rocaltrol＋Caltrate D group （P=0.053, by ANCOVA）. The stand and maximal forward reach test （SMFRT） was significantly enhanced in both groups during the 12 months of treatment, but no significant differences were found between these two groups. No severe adverse event related to these medications occurred throughout the study.
Conclusion： Treatment with Rocaltrol plus Caltrate D or Caltrate D for 12 months in elderly Chinese postmenopausal women effectively increased BMD at the lumbar spine. Rocaltrol plus Caltrate D was more effective at the lumbar spine than Caltrate D alone.     

Addictive evaluation of cholic acid-verticinone ester,a potential cough therapeutic agent with agonist action of opioid receptor

Aim： The purpose of this work was to search for potential drugs with potent antitussive and expectorant activities as well as a low toxicity, but without addictive properties. Cholic acid-verticinone ester （CA-Ver） was synthesized based on the clearly elucidated antitussive and expectorant activities of verticinone in bulbs of Fritillaria and different bile acids in Snake Bile. In our previous study, CA-Ver showed a much more potent activity than codeine phosphate. This study was carried out to investigate the central antitussive mechanism and the addictive evaluation of CA-Ver. Methods： Testing on a capsaicin-induced cough model of mice pretreated with naloxone, a non-selective opioid receptor antagonist, was performed for the observation of CA-Ver＇s central antitussive mechanism. We then took naloxone-induced withdrawal tests of mice for the judgment of CA-Ver＇s addiction. Lastly, we determined the opioid dependence of CA-Ver in the guinea pig ileum. Results： The test on the capsaicin-induced cough model showed that naloxone could block the antitussive effect of CA-Ver, suggesting the antitussive mechanism of CA-Ver was related to the central opioid receptors. The naloxone-urged withdrawal tests of the mice showed that CA-Ver was not addictive, and the test of the opioid dependence in the guinea pig ileum showed that CA-Ver had no withdrawal response. Conclusion： These findings suggested that CA-Ver deserved attention for its potent antitussive effects related to the central opioid receptors, but without addiction, and had a good development perspective.     

Allosteric activation mechanism of the cys-loop receptors

Binding of a neurotransmitter to its ionotropic receptor opens a distantly located ion channel, a process termed allosteric activation. Here we review recent advances in the molecular mechanism by which the cys-loop receptors are activated with emphasis on the best studied nicotinic acetylcholine receptors （nAChRs）. With a combination of affinity labeling, mutagenesis, electrophysiology, kinetic modeling, electron microscopy （EM）, and crystal structure analysis, the allosteric activation mechanism is emerging. Specifically, the binding domain and gating domain are interconnected by an allosteric activation network. Agonist binding induces conformational changes, resulting in the rotation of a β sheet of aminoterminal domain and outward movement of loop 2, loop F, and cys-loop, which are coupled to the M2-M3 linker to pull the channel to open. However, there are still some controversies about the movement of the channel-lining domain M2. Nine angstrom resolution EM structure of a nAChR imaged in the open state suggests that channel opening is the result of rotation of the M2 domain. In contrast, recent crystal structures of bacterial homologues of the cys-loop receptor family in apparently open state have implied an M2 tilting model with pore dilation and quaternary twist of the whole pentameric receptor. An elegant study of the nAChR using protonation scanning of M2 domain supports a similar pore dilation activation mechanism with minimal rotation of M2. This remains to be validated with other approaches including high resolution structure determination of the mammalian cys-loop receptors in the open state.     

The impact of extracellular and intracellular Ca2＋ on ethanol-induced smooth muscle contraction

Aim： To evaluate the impact of extracellular and intracellular Ca2＋ on contractions induced by ethanol in smooth muscle. Methods： Longitudinal smooth muscle strips were prepared from the gastric fundi of mice. The contractions of smooth muscle strips were recorded with an isometric force displacement transducer. Results： Ethanol （164 mmol/L） produced reproducible contractions in isolated gastric fundal strips of mice. Although lidocaine （50 and 100 μmol/L）, a local anesthetic agent, and hexamethonium （100 and 500 μmol/L）, a ganglionic blocking agent, failed to affect these contractions, verapamil （1-50 μmol/L） and nifedipine （1-50 pmol/L）, selective blockers of L-type Ca2＋ channels, significantly inhibited the contractile responses of ethanol. Using a Ca2＋-free medium nearly eliminated these contractions in the same tissue. Ryanodine （1-50 μmol/L） and ruthenium red （10-100 pmol/L）, selective blockers of intracellular Ca2＋ channels/ryanodine receptors; cyclopiazonic acid （CPA; 1-10 μmol/L）, a selective inhibitor of sarcoplasmic reticulum （SR） Ca2＋-ATPase; and caffeine （0.5-5 mmol/L）, a depleting agent of intracellular Ca2＋ stores, significantly inhibited the contractile responses induced by ethanol. In addition, the com- bination of caffeine （5 mmol/L） plus CPA （10 μmol/L）, and ryanodine （10 μmol/L） plus CPA （10 μmol/L）, caused further inhibition of contractions in response to ethanol. This inhibition was significantly different from those associated with caffeine, ryanodine or CPA. Furthermore the combination of caffeine （5 mmol/L）, ryanodine （10 μmol/L） and CPA（IO pmol/L） eliminated the contractions induced by ethanol in isolated gastric fundal strips of mice. Conclusion： Both extracellular and intracellular Ca2＋ may have important roles in regulating contractions induced by ethanol in the mouse gastric fundus.     

The peroxisome proliferator-activated receptor-α （PPAR-α） agonist,AVE8134, attenuates the progression of heart failure and increases survival in rats

Aim： To investigate the efficacy of the peroxisome proliferator-activated receptor-α （PPARa） agonist, AVE8134, in cellular and experimental models of cardiac dysfunction and heart failure.
Methods： In Sprague Dawley rats with permanent ligation of the left coronary artery （post-MI）, AVE8134 was compared to the PPARy agonist rosiglitazone and in a second study to the ACE inhibitor ramipril. In DOCA-salt sensitive rats, efficacy of AVE8134 on cardiac hypertrophy and fibrosis was investigated. Finally, AVE8134 was administered to old spontaneously hypertensive rats （SHR） at a nonblood pressure lowering dose with survival as endpoint. In cellular models, we studied AVE8134 on hypertrophy in rat cardiomyocytes nitric oxide signaling in human endothelial cells （HUVEC） and LDL-uptake in human MonoMac-6 cells.
Results： In post-MI rats, AVE8134 dose-dependently improved cardiac output, myocardial contractility and relaxation and reduced lung and left ventricular weight and fibrosis. In contrast, rosiglitazone exacerbated cardiac dysfunction. Treatment at AVE8134 decreased plasma proBNP and arginine and increased plasma citrulline and urinary NOx/creatinine ratio. In DOCA rats, AVE8134 prevented development of high blood pressure, myocardial hypertrophy and cardiac fibrosis, and ameliorated endothelial dysfunction. Compound treatment increased cardiac protein expression and phosphorylation of eNOS. In old SHR, treatment with a low dose of AVE8134 improved cardiac and vascular function and increased life expectancy without lowering blood pressure. AVE8134 reduced phenylephrine-induced hypertrophy in adult rat cardiomyocytes. In HUVEC, Ser-1177-eNOS phosphorylation but not eNOS expression was increased. In monocytes, AVE8134 increased the expression of CD36 and the macrophage scavenger receptor 1, resulting in enhanced uptake of oxidized LDL.
Conclusion： The PPARa agonist AVE8134 prevents post-MI myocardial hypertrophy, fibrosis and cardiac dysfunction. AVE8134 has beneficial effects against hy     

Nicotinic acetylcholine receptor α7 subunits with a C2 cytoplasmic loop yellow fluorescent protein insertion form functional receptors

Aim： Several nicotinic acetylcholine receptor （nAChR） subunits have been engineered as fluorescent protein （FP） fusions and exploited to illuminate features of nAChRs. The aim of this work was to create a FP fusion in the nAChR α7 subunit without compromising formation of functional receptors, Methods： A gene construct was generated to introduce yellow fluorescent protein （YFP）, in frame, into the otherwise unaltered, large, second cytoplamsic loop between the third and fourth transmembrane domains of the mouse nAChR α7 subunit （α7Y）. SH-EP1 cells were transfected with mouse nAChR wild type α7 subunits （α7） or with α7Y subunits, alone or with the chaperone protein, hRIC-3. Receptor function was assessed using whole-cell current recording. Receptor expression was measured with 125I-labeled α-bungarotoxin （I-Bgt） binding, laser scanning confocal microscopy, and total internal reflectance fluorescence （TIRF） microscopy. Results： Whole-cell currents revealed that α7Y nAChRs and α7 nAChRs were functional with comparable EC50 values for the α7 nAChR-selective agonist, choline, and IC50 values for the α7 nAChR-selective antagonist, methyllycaconitine. I-Bgt binding was detected only after co-expression with hRIC-3. Confocal microscopy revealed that α7Y had primarily intracellular rather than surface expression. TIRF microscopy confirmed that little α7Y localized to the plasma membrane, typical of α7 nAChRs. Conclusion： nAChRs composed as homooligomers of α7Y subunits containing cytoplasmic loop YFP have functional, ligand binding, and trafficking characteristics similar to those of α7 nAChRs, α7Y nAChRs may be used to elucidate properties of α7 nAChRs and to identify and develop novel probes for these receptors, perhaps in high-throughput fashion.     

Central cholinergic regulation of respiration： nicotinic receptors

Nicotinic acetylcholine receptors （nAChRs） are expressed in brainstem and spinal cord regions involved in the control of breathing. These receptors mediate central cholinergic regulation of respiration and effects of the exogenous ligand nicotine on respiratory pattern. Activation of α4＊ nAChRs in the preBotzinger Complex （preBotC）, an essential site for normal respiratory rhythm generation in mammals, modulates excitatory glutamatergic neurotransmission and depolarizes preBotC inspiratory neurons, leading to increases in respiratory frequency, nAChRs are also present in motor nuclei innervating respiratory muscles. Activation of post- and/or extra-synaptic α4＊ nAChRs on hypoglossal （XII） motoneurons depolarizes these neurons, potentiating tonic and respiratory-related rhythmic activity. As perinatal nicotine exposure may contribute to the pathogenesis of sudden infant death syndrome （SIDS）, we discuss the effects of perinatal nicotine exposure on development of the cholinergic and other neurotransmitter systems involved in control of breathing. Advances in understanding of the mechanisms underlying central cholinergic/nicotinic modulation of respiration provide a pharmacological basis for exploiting nAChRs as therapeutic targets for neurological disorders related to neural control of breathing such as sleep apnea and SIDS.     

Pivotal effects of phosphodiesterase inhibitors on myocyte contractility and viability in normal and ischemic hearts

Phosphodiesterases （PDEs） are enzymes that degrade cellular cAMP and cGMP and are thus essential for regulating the cyclic nucleotides. At least 11 families of PDEs have been identified, each with a distinctive structure, activity, expression, and tissue distribution. The PDE type-3, -4, and -5 （PDE3, PDE4, PDE5） are localized to specific regions of the cardiomyocyte, such as the sarcoplasmic reticulum and Z-disc, where they are likely to influence cAMP/cGMP signaling to the end effectors of contractility. Several PDE inhibitors exhibit remarkable hemodynamic and inotropic properties that may be valuable to clinical practice. In particular, PDE3 inhibitors have potent cardiotonic effects that can be used for short-term inotropic support, especially in situations where adrenergic stimulation is insufficient. Most relevant to this review, PDE inhibitors have also been found to have cytoprotective effects in the heart. For example, PDE3 inhibitors have been shown to be cardioprotective when given before ischemic attack, whereas PDE5 inhibitors, which include three widely used erectile dysfunction drugs （sildenafil, vardenafil and tadalafil）, can induce remarkable cardioprotection when administered either prior to ischemia or upon reperfusion. This article provides an overview of the current laboratory and clinical evidence, as well as the cellular mechanisms by which the inhibitors of PDE3, PDE4 and PDE5 exert their beneficial effects on normal and ischemic hearts. It seems that PDE inhibitors hold great promise as clinically applicable agents that can improve cardiac performance and cell survival under critical situations, such as ischemic heart attack, cardiopulmonary bypass surgery, and heart failure.     

Response of mesenchymal stem cells to shear stress in tissueengineered vascular grafts

Aim： Recent studies have demonstrated that mesenchymal stem cells （MSCs） can differentiate into endothelial cells. The effect of shear stress on MSC differentiation is incompletely understood, and most studies have been based on two-dimensional systems. We used a model of tissue-engineered vascular MSC differentiation. grafts （TEVGs） to investigate the effects of shear stress on Methods： MSCs were isolated from canine bone marrow. The TEVG was constructed by seeding MSCs onto poly-ε- caprolactone and lactic acid （PCLA） scaffolds and subjecting them to shear stress provided by a pulsatile bioreactor for four days （two days at 1 dyne/cm^2 to 15 dyne/cm^2 and two days at 15 dyne/cm^2）. Results： Shear stress significantly increased the expression of endothelial cell markers, such as platelet-endothelial cell adhesion molecule-1 （PECAM-1）, VE-cadherin, and CD34, at both the mRNA and protein levels as compared with static control cells. Protein levels of alpha-smooth muscle actin （α-SMA） and calponin were substantially reduced in shear stresscultured cells. There was no significant change in the expression of α-SMA, smooth muscle myosin heavy chain （SMMHC） or calponin at the mRNA level. Conclusion： Shear stress upregulated the expression of endothelial cell-related markers and downregulated smooth muscle-related markers in canine MSCs. This study may serve as a basis for further investigation of the effects of shear stress on MSC differentiation in TEVGs.