郭志强教授运用"提壶揭盖"法治疗多囊卵巢综合征的经验

多囊卵巢综合征(polycystic ovary syndrome,PCOS)为临床上常见的生殖内分泌代谢性疾病,根据其临床表现,中医常将其归为闭经、月经后期、月经过少、不孕症等范畴.目前中医治疗PCOS思路多从肝、脾、肾的调理入手.郭志强教授根据多年临床经验提出应用"提壶揭盖"法从肺论治PCOS."提壶揭盖"法主要适用于PCOS中的两种实证:肺失宣降,痰湿内蕴;肺气闭郁,气滞血瘀."提壶揭盖"多为宣肺之法,临床多用辛味、发散之药,并常佐以健脾、养血之品顾护气血.     

郭志强教授运用崇阳理论治疗反复胚胎移植着床失败的经验

本文介绍郭志强教授运用崇阳理论治疗反复胚胎移植着床失败的经验.郭老认为妇人体质"阴常不足,阳亦常虚",形成"阴阳相济,阴基阳主"的崇阳理论.认为反复胚胎移植着床失败的主要病机为肾阳不足,胞宫寒冷,不能摄精成孕,提出治疗应从阳气着手,并秉持着求子先调经的原则,在胚胎移植前采用中药序贯疗法调经促孕,胚胎移植后予两固汤补肾温阳,顾护阳气,促进着床.     

Learning to nurse in China--structural factors influencing professional development in practice settings: a phenomenological study

This paper describes findings from a stratified phenomenological investigation into Chinese nursing students' experiences of learning in practice placements. The investigation was undertaken in China whilst studying at an English University for a post-graduate degree. With the transition of Chinese nursing education into higher education institutions, clinical nursing experience remains a fundamental factor in students' preparation for qualification. This small phenomenological study sought to understand the kinds of experiences students encounter, the factors that supported or inhibited their learning and the ways in which learning in practice could be enhanced. This paper concentrates on the structural factors that influenced students' learning. These structural factors included; the opportunities available for students to learn, students' participation in clinical nursing activities; the relationship that placement staff were willing to engage in with the students and the prevailing learning climate of the placement setting.     

Clinico-radiological spectrum of reversible splenial lesions in children

Recently, many cases of children presenting reversible splenial lesions during febrile illness (RESLEF) have been reported; however, their overall clinico-radiological features are unclear.     

小组干预模式治疗大学生抑郁的效果

目的:探讨小组干预模式对大学生抑郁的干预效果,观察治疗前后组员的焦虑、抑郁、自我评价及行为改善情况,进行自身前后对照。方法:选择2004-05/07北京友谊医院临床心理科诊断为抑郁或抑郁状态的北京不同大学的1～4年级的在校学生10例。男5例,女5例,年龄19～24岁。采用小组治疗的方法对其进行干预。小组由组长和副组长两位治疗师带领,治疗1次/周,3h/次,干预8次。每次干预设有主题,采取半结构式治疗形式,安排活动,引发组员思考、讨论和领悟,并对组员引发出的问题给予关注和指导,去除一些情绪和不合理思维,增加彼此的共鸣与支持。治疗前后采用症状自评量表评估心理健康水平,采用焦虑自评量表评估患者的焦虑状态,采用抑郁自评量表评估患者抑郁程度,采用小组成员自我评价表进行成员的自我评定。数据进行配对t检验。结果:10例参加小组治疗的学生无脱落,全部进入结果分析。①小组治疗后症状自评量表的强迫因子评分比治疗前极显著降低(2.94±0.38,1.86±0.59,t=5.07,P<0.01),人际关系、抑郁、焦虑、偏执等因子评分比治疗前明显降低(t=2.83,3.90,3.53,3.28,P<0.05)。②治疗后焦虑自评量表、抑郁自评量表总分比较治疗前均显著降低(32.20±3.82,40.30±6.34,t=4.126,P<0.01;35.50±5.31,48.60±7.16,t=4.701,P<0.01)。③组员在对自己了解自己、了解别人、信赖自己、信任别人、关心别人、帮助别人、与他人沟通、与他人合作方面都有较高评价,自觉比以前开朗、自信,相信自己能够面对各种问题,掌握了一些调节情绪的技术和沟通的方法,对小组过程和活动比较喜欢。结论:小组治疗对于大学生抑郁是一种较有效的心理干预模式。治疗后小组成员自我评价升高,自觉有信心、有能力面对各种困难和问题。能有效改善抑郁大学生的情绪、行为、自我认知和应对模式。     

Organization and cellular arrangement of two neurogenic regions in the adult ferret (Mustela putorius furo) brain

In the adult mammalian brain, two neurogenic regions have been characterized, the subventricular zone (SVZ) of the lateral ventricle (LV) and the subgranular zone (SGZ) of the dentate gyrus (DG). Despite remarkable knowledge of rodents, the detailed arrangement of neurogenic regions in most mammals is poorly understood. In this study, we used immunohistochemistry and cell type‐specific antibodies to investigate the organization of two germinal regions in the adult ferret, which belongs to the order Carnivora and is widely used as a model animal with a gyrencephalic brain. From the SVZ to the olfactory bulb, doublecortin‐positive cells tended to organize in chain‐like clusters, which are surrounded by a meshwork of astrocytes. This structure is homologous to the rostral migratory stream (RMS) described in other species. Different from rodents, the horizontal limb of the RMS emerges directly from the LV, and the anterior region of the LV extends rostrally and reached the olfactory bulb. In the DG, glial fibrillary acidic protein‐positive cells with long radial processes as well as doublecortin‐positive cells are oriented in the SGZ. In both regions, doublecortin‐positive cells showed characteristic morphology and were positive for polysialylated‐neural cell adhesion molecule, beta‐III tubulin, and lamin B1 (intense staining). Proliferating cells were detected in both regions using antibodies against proliferating cell nuclear antigen and phospho‐histone H3. These observations demonstrate that the two neurogenic regions in ferrets have a similar cellular composition as those of other mammalian species despite anatomical differences in the brain. J. Comp. Neurol. 522:1818–1838, 2014. © 2013 Wiley Periodicals, Inc.     

New-onset psychiatric disorders after corticosteroid therapy in systemic lupus erythematosus: an observational case-series study

The objective of this study was to clarify the incidence, clinical characteristics, and courses of new-onset psychiatric manifestations after corticosteroid therapy in patients with systemic lupus erythematosus (SLE), including possible ways of differentiating between corticosteroid-induced psychiatric disorders (CIPDs) and central nervous system manifestations of SLE (CNS-SLE). We prospectively followed for 8 weeks 139 consecutive episodes in 135 in-patients who had a non–CNS-SLE flare treated with corticosteroids. Psychiatric events were evaluated once a week using DSM-IV criteria. We then conducted a post hoc etiological analysis of any newly developed psychiatric events during this follow-up period. In the 8 weeks of corticosteroid administration, new psychiatric events occurred in 20 (14.4 %) of the 139 episodes. The mean dosage of corticosteroids administered was prednisolone at 0.98 (range 0.24–1.39) mg/kg/day. Of the 20 psychiatric events, 14 (10.1 %) were suitable for the strict definition of CIPDs, accompanied by mood disorders in 13 (depressive in 2, manic in 9, and mixed in 2) and psychotic disorder in one. Two (1.4 %), both presenting delirium, were diagnosed as CNS-SLE on the basis of evidence of abnormal CNS findings even before psychiatric manifestations, all of which improved in parallel with these patients’ recoveries through augmentation of immunosuppressive therapy. The other four events (2.9 %) could not be etiologically identified. This study suggests that corticosteroid therapy triggers CIPDs and CNS-SLE in patients with SLE. Delirium may be suggestive of CNS-SLE, while mood disorders may be more suggestive of CIPDs. Electroencephalographic abnormalities may possibly be predictive of CNS-SLE.     

Disruption of actin‐binding domain‐containing Dystonin protein causes dystonia musculorum in mice

The Dystonin gene (Dst) is responsible for dystonia musculorum (dt), an inherited mouse model of hereditary neuropathy accompanied by progressive motor symptoms such as dystonia and cerebellar ataxia. Dst‐a isoforms, which contain actin‐binding domains, are predominantly expressed in the nervous system. Although sensory neuron degeneration in the peripheral nervous system during the early postnatal stage is a well‐recognised phenotype in dt, the histological characteristics and neuronal circuits in the central nervous system responsible for motor symptoms remain unclear. To analyse the causative neuronal networks and roles of Dst isoforms, we generated novel multipurpose Dst gene trap mice, in which actin‐binding domain‐containing isoforms are disrupted. Homozygous mice showed typical dt phenotypes with sensory degeneration and progressive motor symptoms. The gene trap allele (Dst^Gt) encodes a mutant Dystonin‐LacZ fusion protein, which is detectable by X‐gal (5‐bromo‐4‐chloro‐3‐indolyl‐β‐D‐galactoside) staining. We observed wide expression of the actin‐binding domain‐containing Dystonin isoforms in the central nervous system (CNS) and peripheral nervous system. This raised the possibility that not only secondary neuronal defects in the CNS subsequent to peripheral sensory degeneration but also cell‐autonomous defects in the CNS contribute to the motor symptoms. Expression analysis of immediate early genes revealed decreased neuronal activity in the cerebellar‐thalamo‐striatal pathway in the homozygous brain, implying the involvement of this pathway in the dt phenotype. These novel Dst^Gt mice showed that a loss‐of‐function mutation in the actin‐binding domain‐containing Dystonin isoforms led to typical dt phenotypes. Furthermore, this novel multipurpose Dst^Gt allele offers a unique tool for analysing the causative neuronal networks involved in the dt phenotype.