精神分裂症患者的社交技能训练小组活动方案

目的:通过社交技能训练让精神分裂症患者明确正确的沟通方式,锻炼自己的交谈能力,学会社会交往技巧,体会人与人之间的关系,学会分析解决社交过程中出现的问题,从而掌握社会交往的技能,防止或延缓发生严重的社会功能衰退。方法:选择早期精神分裂症患者(5年内),在住院治疗达到临床治愈出院后立即开始训练。活动以小组为单位(10人1组)进行,小组成员相对固定。前3个月每个月1次,以后每3个月1次,持续1年。活动过程中以游戏为主导,让组员在游戏中领会人际交往过程中的要领。具体训练方案包括6个方面:①训练一:语言表达能力,正确的沟通方式。②训练二:如何寻找帮助。③训练三:指导患者学习人际交往的基本技巧。④训练四:如何与人打交道。⑤训练五:合作。⑥训练六:社交问题的解决。结果:通过增加对社交时恐惧的暴露及社交技巧训练,对精神分裂症伴发社交恐惧症有效;但对精神分裂症意志活动减退所致社交时主动性不足效果较差。结论:对精神分裂症患者的社交训练应尽早进行,同时在设计精神分裂症社交训练时应加强对患者主动性不足的针对性。     

应用事件相关电位技术考察正常人名词和动词的脑区分布特征

目的：应用事件相关电位技术考察正常人脑区名词和动词的分布特征. 方法：实验于2006-03在徐州师范大学完成.选择在校大学生16名作为受试者,男女各8名,年龄19～22岁,进行词语搭配判断实验.①刺激材料包括180个启动刺激（“一Q”和“不M”,Q为名量词,M为能愿动词）,以及180个目标刺激（名词和动词）.启动词和目标词构成4组不同搭配的短语,其中2组为正确搭配,另2组为错误搭配.②实验任务：要求被试判断启动词和目标词的搭配是否正确.刺激材料为随机编排,启动词和目标词的呈现时间均为200 ms,启动词和目标词之间的时间间隔为300 ms,相邻两个trail间的时间间隔为2 500 ms.③实验评估：采用Neuroscan Synamps 2记录脑电,并使用Neuroscan 4.3对采集的脑电进行离线分析处理.最后用两因素重复测量的方差分析法对数据进行分析. 结果：16名被试的实验数据均纳入统计分析.①反应时和正确率：两种正确搭配短语“一Q＋名词”和“不M＋动词”反应时比较差异显著[F（1,30）=5.475,P=0.026];而二者的正确率未见显著效应.②Nd400的平均幅值：在目标刺激呈现后350～750 ms,额区Nd400的类型主效应十分显著[F（1,15）=14.211,P=0.002],“不M＋名词”-“不M＋动词”差异波Nd400成分在额区显著.在目标刺激呈现后450～530 ms,后部脑区Nd400的类型主效应十分显著[F（1,15）=11.042,P=0.005],“一Q＋动词”-“一Q＋名词”差异波Nd400更负.③潜伏期：在后部脑区,两个差异波的Nd400在潜伏期上差异也十分显著[F（1,15）=29.512,P=0.000],差异波“一Q＋动词”-“一Q＋名词”所诱发的Nd400更加延迟.④脑区电压分析：在目标词呈现后400～600 ms,差异波“不M＋名词”-“不M＋动词”在额区的电压更负,而“一Q＋动词”-“一Q＋名词”则在中央顶区有更负的电压值. 结论：对于正常人而言,名词和动词具有不同的大脑皮质表征,额区主要负责动词的加工,而后部脑区在名词的表征中起主要作用.     

PROSTATIC CANCER PRESENTING AS DYSPHAGIA

SUMMARY Neurological dysfunction from base of skull metastasis of prostate cancer is rare. In this case, dysphagia was the presenting symptom and relief occurred after orchidectomy. Improvement of neurological symptoms usually occurs only after local radiotherapy.     

Evaluation of 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid in the inhibition of rouleaux formation

BACKGROUND: DIDS (4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid) inhibits the formation of serum-or plasma-induced rouleaux through its ability to bind to band 3 on red cell membranes. This property of DIDS was evaluated in the serologic testing of specimens exhibiting rouleaux. STUDY DESIGN and METHODS: Optimal test conditions for DIDS treatment of reagent red cells were determined by varying the volume and concentration of DIDS solution and the incubation temperature and duration and comparing the results of antibody screening procedures using specimens that exhibit macroscopically visible rouleaux. Blind titration studies compared untreated and DIDS-treated red cells to evaluate the maintenance of antigen integrity. The use of DIDS-treated red cells for antibody detection and identification was evaluated by comparing the results in donor specimens containing antibodies with those in untreated and DIDS-treated selected panel cells. In addition, 4-percent (wt/vol) dextran in serum was used to induce rouleaux formation as a way of determining the capability of DIDS to resolve ABO serum grouping discrepancies. RESULTS: Complete inhibition of rouleaux formation occurred when reagent red cells were treated by incubation at 37 degrees C for 10 minutes with 150 microliter (approx. 5 drops) of 0.05 mg per mL of DIDS in 0.9-percent NaCl. There were no significant differences in titration scores of untreated and DIDS-treated red cells tested with the 19 antisera used to assess antigen integrity. Antibody identification studies showed that DIDS-treated reagent red cells reacted similarly to untreated reagent red cells. In addition, DIDS resolved dextran-induced ABO serum grouping discrepancies. CONCLUSION: DIDS effectively resolved the serologic problems associated with the presence of rouleaux, without affecting the results of the test system itself. Implementation of this method to inhibit the rouleaux-forming properties of serum and plasma specimens can be useful in serologic testing.     

Regulatory mechanisms in cell-mediated immune responses. VI. Interaction of H-2 and non-H-2 genes in elaboration of mixed leukocyte reaction suppressor factor

Previous studies have shown that alloantigen-activated spleen T cells produce a soluble factor which suppresses mixed lymphocyte reaction proliferative responses, and that the interaction between suppressor and responder cells is controlled by genes of the H-2 complex. However a defect in the expression of suppressor activity was identified in the mouse strain C57BL/6J. Factor prepared from alloactivated B6 spleen cells failed to suppress MLR responses of syngeneic or H-2 compatible responder cells. Unimpaired suppressor factor production by other H-2 (b) strains and failure of suppressor factor production by a B6 congenic strain, B6.C-H-2(d) isolated the defective gene to the non-H-2 portion of the genome. In addition, the defect appeared to be related specifically to inability to produce an active factor, while the capacity to respond to suppressor molecules was unimpaired. The genetic character of the non-H-2 gene action was identified in F1 hybrid studies. Initially F(1) hybrids of the nondefective histoincompatible strains were studied. Suppressor factor from F1 cells suppressed the responses of both parental strains, and parental factors each suppressed the response of F(1) cells. Adsorption of F(1) factor with Con A-activated thymocytes of either parental strain removed suppressor activity specific for that strain, leaving activity against the other parental strain intact. The data support cedominant expression and production of distinct, parental H-2 haplotype-specific suppressor molecules by F(1) suppressor cells. An F(1) hybrid of the defective B6 strain with nondefective BALB/c produced suppressor factor which was also capable of suppressing both parental strains. Production of a suppressive B6-reactive factor by F(1) cells was verified by adsorption studies. Thus it appears that non-H-2 genes of the BALB/c parent acted in a genetically dominant fashion to provide the function required for expression of B6 suppressor molecules. We conclude that multiple genes control the expression of alloactivated suppressor cell activity, with at least one gene mapped to the I-C subregion of the murine major histocompatibility complex and one or more genes mapped to the non-H-2 gene complement.     

Role of prostaglandin E in the biphasic fever response to endotoxin

Biphasic fevers were induced in sheep with intravascular infusions or injections of 4-10 μg (80-200 ng/kg) of endotoxin, whereas monophasic fevers were obtained with doses of 1-2/μg (20-40 ng/kg). A marked increase in arterial blood pressure invariably accompanied the onset of fever; the latency of responses to the higher and lower doses of endotoxins averaged 26 min and 42 min, respectively. Prostaglandin (PG) assays of plasma from the carotid artery and jugular vein during fever episodes revealed a surge of PGE and PGF coincident with the pressor response and the first phase of fever, but PG were not detected in plasma samples taken throughout the second phase of fever. PG measurements of arterial and venous plasma collected at a distal site (hind limb) showed a similar surge of PGE and PGF in association with the early fever response, indicating that intravascular PG synthesis and release represents a generalized systemic response to circulating endotoxin. Carotid arterial infusions of PGE(2) produced immediate monophasic fevers and pressor responses, whereas PGD(2) infusions produced an immediate pressor effect but no fever. Infusions of PGF(2α) or prostacyclin, however, evoked neither fever nor pressor effects. Intracarotid infusions of leukocyte pyrogen (LP) caused monophasic fevers with latent periods of 15-20 min but pressor responses were not seen and neither PGE nor PGF were detected in plasma samples from the carotid artery or jugular vein before or during fever. Indomethacin, a potent inhibitor of arachidonic acid metabolism, blocked fever responses to endotoxin and to LP. These findings implicate PGE as the mediator of the early phase of endotoxin fever and imply a role for another pyrogenic metabolite ofarachidonic acid in the mediation of the second phase of fever, i.e., the phase associated with circulating LP. It is possible that both pyrogenic metabolites are generated within the vascular compartment, reaching thermoregulatory centers of the brain by transfer across the blood-brain interface.     

Hyperinsulinemia,obesity, and diabetes mellitus

International Journal of Diabetes in Developing Countries -     

Suppression of mouse skin tumor promotion and induction of apoptosis in HL-60 cells by Alpinia oxyphylla Miquel (Zingiberaceae)

There have been considerable efforts to search for naturally occurring substances for the intervention of carcinogenesis. Many components from dietary or medicinal plants have been identified that possess substantial chemopreventive properties. An example is curcumin (Curcuma longa Linn., Zingiberaceae), which has been shown to inhibit tumor promotion in experimental carcinogenesis. Alpinia oxyphylla Miquel, another plant of the ginger family used in oriental herbal medicine, contains diarylheptanoids whose structures are analogous to that of curcumin. In the present study, we have tested A.oxyphylla for its ability to suppress tumor promotion. Thus, topical application of the methanolic extract of dried fruits of A.oxyphylla significantly ameliorated 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin tumor promotion as well as ear edema in female ICR mice. In another study, treatment of HL-60 cells with the methanolic extract of A.oxyphylla significantly reduced the viability of the cells and also inhibited DNA synthesis. Microscopic examination of the treated cells showed characteristic morphology of apoptosis. Furthermore, cells treated with the extract of A.oxyphylla exhibited internucleosomal DNA fragmentation in time- and concentration-dependent manners. TPA- stimulated generation of superoxide anion in differentiated HL-60 cells was also blunted by A.oxyphylla. Taken together, these findings suggest that A.oxyphylla possesses potential chemopreventive and antitumorigenic activities.