会阴局麻术松弛会阴的效果评价

目的:评价会阴局麻术松弛会阴的效果.方法:56例实验组对宫口开全的产妇用0.5％普鲁卡因行双侧加正中会阴局麻,以使会阴松弛,使产妇免于侧切或严重撕裂;50例对照组按产科常规执行.结果:侧切率明显降低,会阴完好率明显提高.结论:此法简单、易行、经济,具有临床实用价值.     

分别基于行为疗法和口服帕罗西汀在治疗功能性腹痛综合征中的临床研究

目的探讨功能性腹痛综合征（FAPS）患者症状与精神心理状态的联系,比较分别基于行为疗法与口服帕罗西汀在治疗FAPS中的作用。方法以症状自评量表（SCL-90）评价FAPS患者和健康志愿者的心理状态,并与国内常模比较。将确诊为FAPS患者随机分为松弛行为疗法组和口服帕罗西汀组,记录每位患者治疗前后的症状（严重程度及影响程度）评分及相关因子分值,采用样本非参数检验进行统计学分析。记录患者及健康志愿者性别、是否绝经、年龄、文化程度、经济状况、对目前工作生活满意度及过去6个月有无重大负性事件,采用非条件Logistic回归分析发病危险因素。结果FAPS患者SCL90评价阳性率显著高于健康志愿者,部分因子分值高于国内常模,焦虑因子与FAPS症状严重程度呈显著相关,精神病性与强迫因子呈显著相关（P〈0.05）。治疗2周后,组内比较显示帕罗西汀组症状显著改善,组间比较显示帕罗西汀改善疼痛优于松弛疗法。治疗8周后,组内比较显示松弛疗法和口服帕罗西汀改善症状与焦虑因子分值差异均有统计学意义（P〈0.01）;组间比较差异无统计学意义（P〉0.05）。非条件Logistic回归分析,负性事件为密切相关危险因素。结论口服帕罗西汀治疗FAPS的短期疗效优于行为疗法,8周后2种方法总体疗效无显著差异;松弛行为疗法更易于患者接受,且成本/效益比优于口服药物。     

放松训练对化疗期乳腺癌患者情绪的影响

目的探讨放松训练疗法对化疗期乳腺癌患者情绪障碍的影响。方法住院的化疗期乳腺癌患者48例,均伴较强的情绪障碍,随机分为研究组和对照组,各24例,研究组进行隔天放松训练,共12周,两组采用HAMA及HAMD量表评估疗效。结果治疗12周后,研究组HAMA、HAMD总分低于对照组(P<0.01)。结论有目的、有计划地放松训练治疗能明显改善化疗期乳腺癌患者的负性情绪。     

Effect of relaxation on the level of nursing internshipstudents＇ stress

Objective： To explore how relaxation reduce the effect of stress in Iranian nursing students. Methods： A total of 40 nursing students were randomly selected and divided into two groups of test and control each with 20 students. An exam questionnaire consisting of the stress test of Spilberger and control of physiological determinants （blood pressure, pulse respiration, temperature） was performed to two groups. The practice of relaxation continued for two weeks and three times a day. Data were collected and analysed using t-test and Chi-square. Results： Two groups did not show any difference in relation to the average of physiological determinants before and after investigation. However, pulse was significantly different between the two groups. The average scores of stress before and after relaxation were significantly differed between the two groups investigation so that the level of stress was reduced in the test group （t= 2.5, df =39, P= 0.02）. Conclusion： To alleviate stressors associated with clinical practice and create a healthy work environment for practice it is recommended that nursing students have some relaxation before entering practical environments.     

亚急性衰老大鼠逼尿肌舒缩功能变化的实验研究

目的观察D—gal致亚急性衰老大鼠膀胱逼尿肌舒缩功能的变化。方法在初筛合格的sD大鼠颈背部皮下注射浓度为5％的D—gaI生理盐水溶液125mg·kg^-1·d^-1连续8周。用离体逼尿肌条实验观察动物逼尿肌舒缩功能,并进行组织病理形态学观察。结果与正常对照组比较,模型组动物逼尿肌自发性收缩频率加快（P〈0．01）．顺应性、弹力下降（P〈0．05～0．01）,但收缩性没有明显改变（P〉0．05）;ATP对亚急性衰老逼尿肌中的收缩作用增强,ISO在亚急性衰老动物逼尿肌中的抑制收缩作用减弱（P〈0．05～0．01）;病理形态学观察显示,模型动物膀胱形态改变明显,逼尿肌中胶原纤维组织所占比例增加（P〈0．01）。结论亚急性衰老大鼠逼尿肌舒缩功能及神经受体敏感性发生显著改变。     

Transient receptor potential A1 (TRPA1) activity in the human urethra--evidence for a functional role for TRPA1 in the outflow region

Background

A role for the transient receptor potential (TRP) A1 ion channel in rat lower urinary tract (LUT) sensation and disease has been proposed, but in the human LUT no information on TRPA1 activity is available.

Objectives

To investigate the distribution of TRPA1 in the human urethra and to study the effect of TRPA1 agonists on isolated urethral strip preparations.

Design, settings, and participants

Urethral specimens were obtained preoperatively from 10 patients and were freshly prepared for Western blot, immunohistochemistry, and functional in vitro investigations.

Measurements

The expression patterns of TRPA1 were studied with Western blot and immunohistochemistry. The effects of allyl isothiocyanate (AI), cinnamaldehyde (CA), and NaHS (donor of H₂S) on tension of urethral strips were investigated in tissue baths.

Results and limitations

TRPA1 immunoreactivity (-IR) was found in nerve fibres in the suburothelial space and was also located to nerve fibres of the muscle layer. Single TRPA1-IR nerves extended into the urothelium. A majority, but not all TRPA1-IR nerves also expressed immunoreactivity for CGRP or TRPV1. In the urothelium, TRPV1 was located to the outer layers whereas TRPA1 was observed in basal urothelial cells. Interspersed between strands of smooth muscle cells of the urethral wall, TRPA1- and vimentin-IR cells containing central nuclei and slender cytoplasmatic extensions were observed.In functional experiments, TRPA1-agonists had no contractile effect in urethral preparations. After precontraction with phenylephrine, AI, CA, and NaHS caused concentration-dependent relaxations of urethral strip preparations.

Conclusions

The localization of TRPA1 to nerves that also express TRPV1 and CGRP, and in urothelial cells and interstitial cells, as well as the findings that TRPA1 agonists can modify tone of urethral preparations, propose a role for TRPA1 in afferent and efferent sensory signaling of the human outflow region.     

放松训练对康复期精神分裂症患者的对照研究

目的探讨放松训练对康复期精神分裂症患者的治疗效果。方法将120例康复期精神分裂症患者,随机分为两组即实验组和对照组。两组在接受常规治疗和护理的同时,实验组进行3个月的放松训练。采用简明精神病评定量表（BPRS）、社会功能缺陷筛选量表（SDSS）和日常生活能力量表（ADL）对放松前和放松后3个月进行量化评定。结果放松训练3个月后实验组BPRS、SDSS及ADL评分明显低于对照组（P〈0.01）。结论放松训练技术能改善精神分裂症患者社会功能和日常生活能力,对于提高生活质量,延缓衰退,促进疾病的恢复很有帮助,值得在精神科推广。     

Temporal dissociation of frequency-dependent acceleration of relaxation and protein phosphorylation by CaMKII

Frequency-dependent acceleration of relaxation (FDAR) is an important intrinsic mechanism that allows for diastolic filling of the ventricle at higher heart rates, yet its molecular mechanism is still not understood. Previous studies showed that FDAR is dependent on functional sarcoplasmic reticulum (SR) and can be abolished by phosphatase or by Ca/CaM kinase (CaMKII) inhibition. Additionally, CaMKII activity/autophosphorylation has been shown to be frequency-dependent. Thus, we tested the hypothesis that CaMKII phosphorylation of SR Ca(2+)-handling proteins (Phospholamban (PLB), Ca(2+) release channel (RyR)) mediates FDAR. Here we show that FDAR occurs abruptly in fluo-4 loaded isolated rat ventricular myocytes when frequency is raised from 0.1 to 2 Hz. The effect is essentially complete within four beats (2 s) with the tau of [Ca(2+)](i) decline decreasing by 42+/-3%. While there is a detectable increase in PLB Thr-17 and RyR Ser-2814 phosphorylation, the increase is quantitatively small (PLB<5%, RyR approximately 8%) and the time-course is clearly delayed with regard to FDAR. The low substrate phosphorylation indicates that pacing of myocytes only mildly activates CaMKII and consistent with this CaMKIIdelta autophosphorylation did not increase with pacing alone. However, in the presence of phosphatase 1 inhibition pacing triggered a net-increase in autophosphorylated CaMKII and also greatly enhanced PLB and RyR phosphorylation. We conclude that FDAR does not rely on phosphorylation of PLB or RyR. Even though CaMKII does become activated when myocytes are paced, phosphatases immediately antagonize CaMKII action, limit substrate phosphorylation and also prevent sustained CaMKII autophosphorylation (thereby suppressing global CaMKII effects).     

CaMKII inhibition targeted to the sarcoplasmic reticulum inhibits frequency-dependent acceleration of relaxation and Ca2+ current facilitation

Cardiac Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in heart has been implicated in Ca(2+) current (I(Ca)) facilitation, enhanced sarcoplasmic reticulum (SR) Ca(2+) release and frequency-dependent acceleration of relaxation (FDAR) via enhanced SR Ca(2+) uptake. However, questions remain about how CaMKII may work in these three processes. Here we tested the role of CaMKII in these processes using transgenic mice (SR-AIP) that express four concatenated repeats of the CaMKII inhibitory peptide AIP selectively in the SR membrane. Wild type mice (WT) and mice expressing AIP exclusively in the nucleus (NLS-AIP) served as controls. Increasing stimulation frequency produced typical FDAR in WT and NLS-AIP, but FDAR was markedly inhibited in SR-AIP. Quantitative analysis of cytosolic Ca(2+) removal during [Ca(2+)](i) decline revealed that FDAR is due to an increased apparent V(max) of SERCA. CaMKII-dependent RyR phosphorylation at Ser2815 and SR Ca(2+) leak was both decreased in SR-AIP vs. WT. This decrease in SR Ca(2+) leak may partly balance the reduced SERCA activity leading to relatively unaltered SR-Ca(2+) load in SR-AIP vs. WT myocytes. Surprisingly, CaMKII regulation of the L-type Ca(2+) channel (I(Ca) facilitation and recovery from inactivation) was abolished by the SR-targeted CaMKII inhibition in SR-AIP mice. Inhibition of CaMKII effects on I(Ca) and RyR function by the SR-localized AIP places physical constraints on the localization of these proteins at the junctional microdomain. Thus SR-targeted CaMKII inhibition can directly inhibit the activation of SR Ca(2+) uptake, SR Ca(2+) release and I(Ca) by CaMKII, effects which have all been implicated in triggered arrhythmias.