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。     

人胎肺间充质干细胞分离培养条件及向心肌细胞诱导分化的可能关联

目的:观察分离培养得到人胎肺间充质干细胞的条件,并分析诱导其转分化为心肌细胞的可能性及其相关因素。方法:实验于2003-01/2005-12在西北农林科技大学陕西省干细胞工程技术研究中心完成。取10周龄人工流产胎儿肺组织,0.25%胰蛋白酶消化,经培养得到人胎肺间充质干细胞。观察细胞形态及增殖,测细胞生长曲线。将人胎肺间充质干细胞以1.8×104/孔接种于明胶预处理的24孔板中。加Dulbecco修正Eagle’s基础培养液培养24h后弃去培养液,磷酸盐缓冲液(-)洗两三次。每14孔为1组,分别加入Dulbecco修正Eagle’s基础培养液和先进的Dulbecco修正Eagle’s(分别添加2%、5%、8%和10%新生牛血清)5种不同的培养液,其后方法同上,每天选任意两孔计数,求平均值。用流式细胞仪对所分离第8代细胞进行以下细胞表面标志检测:CD45、CD11a、CD14、CD90、CD34、CD71、CD25、CD105、CD117、CD166和CD44。人胎肺间充质干细胞向心肌细胞诱导分化:将第12代人胎肺间充质干细胞以500个/孔接种于明胶预处理的24孔板中。每6孔为1组,分别在Dulbecco修正Eagle’s基础培养液中添加0、5、10、20μmol/L5-氮胞苷,每组中每2孔为一诱导时间段,分别诱导培养24,48,72h后换成Dulbecco修正Eagle’s基础培养液,以后每3d换液1次。观察细胞在各组中变化情况,诱导12d后固定进行糖元染色和α平滑肌肌动蛋白免疫组化染色。结果:成功分离了人胎肺间充质干细胞,细胞已扩增至26代,流式细胞仪检测CD25、CD105、CD166和CD44表达阳性;CD71(39.1%)和CD117(29.8%)弱阳性。Dulbecco修正Eagle’s培养液比先进的Dulbecco修正Eagle’s培养液更适合于这类细胞生长。经10μmol/L5-氮胞苷诱导48h后,糖元染色、心肌α平滑肌肌动蛋白免疫组化染色阳性细胞率达60%以上。结论:①人胎肺间充质干细胞在Dulbecco修正Eagle’s基础培养液中能够大量扩增。②并表达CD25,CD105,CD166和CD44等细胞表面标志。③10μmol/L5-氮胞苷诱导48h对该细胞向心肌细胞分化有明显促进作用。     

Lesion progression and plaque composition are not altered in older apoE-/- mice lacking tumor necrosis factor-alpha receptor p55

BACKGROUND: Inflammatory processes are an integral component of the initiation, progression, and destabilization of atherosclerotic lesions. Tumor necrosis factor-alpha (TNF-alpha) is considered a primary mediator of inflammatory processes. METHODS AND RESULTS: The role of TNF-alpha in plaque progression and plaque destabilization was investigated in the innominate arteries of older TNF-alpha receptor p55 deficient mice that were generated on a hyperlipidemic apolipoprotein E deficient background (p55-/- apoE-/-). There were no significant differences in levels of circulating cytokines, plaque progression, plaque composition or features of plaque destabilization in p55-/- apoE-/- compared to wild type (p55+/+ apoE-/-) mice. CONCLUSIONS: Progression and destabilization of advanced atherosclerotic lesions does not seem to be mediated via the TNF-alpha receptor p55.     

Angiotensin II receptor antagonists in heart failure: Rationale and design of the evaluation of losartan in the elderly (ELITE) trial

Summary Angiotensin-converting enzyme inhibitors (ACE-I) have been proven to be effective in reducing morbidity and mortality in patients with heart failure or post-myocardial infarction left ventricular dysfunction. Despite evidence from several large-scale randomized trials, the use of ACE-I in patients with heart failure remains relatively low. In part, the failure to achieve more widespread use of ACE-I in patients with heart failure may be due to physician's perceptions of the side effects associated with ACE-I, such as angioedema, renal dysfunction, cough, and hypotension. Many of these side effects are thought to be due to ACE-I-induced bradykinin accumulation. It is possible to inhibit the effect of angiotensin II without increasing bradykinin levels using an angiotensin II type I blocking agent such as losartan. How effective losartan is compared with an ACE-I is uncertain, however. Some of the beneficial effects of ACE-I have been attributed to bradykinin accumulation, and therefore ACE-I might have an advantage compared with an angiotensin II type I receptor antagonist such as losartan. On the other hand, angiotensin II may be produced by non-ACE-I-dependent mechanisms, which would suggest that an angiotensin II type I receptor blocking agent would be advantageous. To determine the relative safety and efficacy of an ACE-I, which results in bradykinin accumulation and inhibitors of angiotensin II, versus an angiotensin II type I receptor blocking agent, which does not result in bradykinin accumulation, we have begun the Evaluation of Losartan In The Elderly (ELITE) trial, which will compare the safety and efficacy of captopril and losartan in elderly patients with heart failure.     

Canine model for gene therapy: inefficient gene expression in dogs reconstituted with autologous marrow infected with retroviral vectors

Successful retroviral gene transfer into murine hematopoietic stem cells indicates the potential for somatic gene therapy in the treatment of certain human hereditary diseases. We developed a canine model to test the applicability of these techniques to a preclinical model of human marrow transplantation. Previously we reported that canine CFU-GM could be infected with retroviral vectors carrying either the gene for a mutant dihydrofolate reductase (DHFR) or neomycin phosphotransferase (NEO). This study reports six lethally irradiated dogs transplanted with autologous marrow cocultivated with retroviral vector-producing cells. This procedure conferred drug resistance to 3% to 13% of the CFU- GM. Three dogs infected with either the NEO or DHFR virus engrafted, but we detected no drug-resistant CFU-GM. Three dogs were given marrow infected with a DHFR virus and received methotrexate (MTX) as in vivo selection; all three had evidence of engraftment. In the surviving dog, we detected 0.03% to 0.1% MTX-resistant CFU-GM at 3 to 5 weeks posttransplant during in vivo selection. These results indicate that we can reconstitute lethally irradiated dogs with autologous marrow exposed to retroviral vectors and suggest that gene transfer into hematopoietic cells is feasible on a large scale. However, the low- level transient gene expression indicates that considerable obstacles remain before human gene therapy can be considered.     

Goblet cell carcinoid of the appendix.

We have reviewed all cases of goblet cell carcinoid in the Department of Pathology, Edinburgh University. Of the 10 cases identified, two had died as a result of the tumour. This would suggest a poorer prognosis than is generally recognized. Those patients who subsequently had progression of their disease were not predicted by histological criteria. Because of the unpredictable behaviour of these tumours we recommend that such patients should correctly be treated by a right hemicolectomy.     

Cisplatin, vinblastine, and bleomycin in advanced and recurrent ovarian germ-cell tumors. A trial of the Gynecologic Oncology Group

STUDY OBJECTIVE: To evaluate the efficacy of cisplatin-based combination chemotherapy in patients with advanced ovarian germ-cell tumors. DESIGN: Nonrandom prospective trial with endpoints of tumor response, results of repeat surgical exploration, progression-free interval, and survival. SETTING: Cooperative university-based cancer study comprising 27 participating institutions. PATIENTS: Ninety-seven patients were treated and all were evaluable. Of these, 8 had dysgerminoma and 89 had other cell types. INTERVENTIONS: Patients received 3 to 4 courses of cisplatin. vinblastine, and bleomycin (PVB). After chemotherapy, suitable patients had re-staging laparotomy. Maintenance vinblastine therapy was originally given but was discontinued for all patients in 1981. Patients with persistent or recurrent disease were treated with vincristine, dactinomycin, and cyclophosphamide (VAC) or etoposide plus cisplatin (EP). RESULTS: Of 35 patients with tumors other than dysgerminoma who had clinically measurable disease, 15 (43%; CI, 26% to 61%) had complete responses. Forty of fifty-six second-look laparotomies (71%; CI, 58% to 83%) revealed no tumor or mature teratoma. Forty-seven patients are still disease-free and 59 are alive. The survival rate is 71% (CI, 62% to 89%) and the disease-free rate is 51% (CI, 41% to 62%) at 2 years. Eight patients had durable remissions with second- or third-line therapy. Seven of eight patients with dysgerminoma are also disease-free. CONCLUSIONS: Cisplatin-based chemotherapy is effective for patients with ovarian germ-cell tumors, is superior to previous regimens, and will cure a substantial number of patients.     

Ventricular arrhythmias triggered by alerting stimuli in conscious rabbits pre-treated with dofetilide

We tested whether normally benign alerting/arousing stimuli provoke cardiac arrhythmias in conscious rabbits with electrically unstable myocardium. Alerting stimuli (loud sound, tapping and moving the cage, pinprick, inhalation of formaldehyde vapour) were presented before and after administration of dofetilide to conscious unrestrained rabbits (New Zealand White). Dofetilide (0.28-3.0 mg/kg i. v.) caused prolongation of QT interval (from 131 +/- 9 to 217 +/- 11 ms; p < 0.01, n = 6) and Tpeak-Tend interval (from 34 +/- 5 to 81 +/- 9 ms; p < 0.01, n = 6), altered ventricular conductance, and caused appearance of spontaneous ventricular ectopic beats. Alerting stimuli elicited ventricular ectopic beats in 18/30 trials in all dofetilide-treated animals, with a short latency (3.1 +/- 0.4 s). Formaldehyde vapour, in addition, elicited profound bradycardia, and precipitated non-sustained polymorphic ventricular tachycardia (torsades de points) lasting 0.6-8.5 s in 5/6 animals. These arrhythmias occurred also with a short latency (mean 8.7 +/- 1.6 s). Betaadrenergic blockade with propranolol (1.5 mg/kg i. v.) abolished spontaneous ventricular ectopy, suppressed torsades de points precipitated by formaldehyde, and significantly (p < 0.05) reduced the number of ventricular ectopic beats triggered by alerting stimuli. In predisposed hearts, alerting stimuli precipitate arrhythmias by producing transient increases in sympathetic discharge in the ventricular myocardium. Vagally induced bradycardia with concurrent ventricular beta-adrenoreceptor activation may underlie development of torsades de points in patients with long QT syndrome precipitated by swimming, diving or facial immersion.