阿片类依赖者的社会心理因素分析

本文对２８４例自愿戒毒的阿片类依赖者的部分社会心理因素进行分析。３０ａ以下、初中以下文化的青年，特别是待业和个体户，性格不稳定者是阿片类物质滥用的高危人群，为预防的重点对象。阿片类依赖戒断治疗后的高复吸率，反映出目前的治疗仅注重戒断，忽视康复和回归社会后的随访工作。今后应在人力、财力方面向康复和社会随访方面转移和倾斜，方能真见成效。     

Teratogen-induced apoptosis may be affected by immunopotentiation

Intra-uterine immunization of mice with paternal allogeneic or xenogeneic (rat) splenocytes was found to increase embryo tolerance to cyclophosphamide (CP)-induced teratogenesis. As the CP-induced teratogenic effect was shown to be associated with apoptosis, the present study was designed to investigate whether the protective effect of immunopotentiation may be realized via an alteration of CP-induced apoptosis. Various doses of CP were injected intraperitoneally into ICR mice on day 12 of pregnancy. Intra-uterine immunization with xenogeneic rat splenocytes was carried out 3 weeks before mating. Implantation sites, resorptions, live and dead fetuses, as well as soft tissue anomalies and external malformations, were recorded to evaluate the CP-induced embryotoxic effect. In parallel, flow cytometric analysis and DNA fragmentation assay were used for evaluation of CP-induced apoptosis in limbs, tail and whole embryos. The treatment of mothers with a high dose of CP induced the death of almost all embryos and striking fetal growth retardation in survivors. This strong embryotoxic effect was accompanied by very prominent DNA degradation in cells collected from whole embryos. Immunostimulation caused a dramatic decrease of embryonal loss (by ˜ 50%) and a significant (about 30%) increase in fetal weight. Such an increase in fetal survival and in fetal weight was found to be accompanied by a clear decrease in apoptosis level in embryo cell populations as judged by DNA gel electrophoresis with subsequent quantitation of DNA fragmentation in negatives by an image analysis technique. After treatment with a low dose of CP, a decrease in the proportion of fetuses with limb and tail anomalies in immunized females was accompanied by a decrease in the proportion of apoptotic nuclei in cells taken from limbs and tails. The results of this study suggest that the teratogen-induced apoptosis may, at least partly, be dependent on fetomaternal immune interactions.     

穹隆-海马伞切断对大鼠脑内TrkA表达的影响

①目的　探讨穹隆 海马伞切断对大鼠脑内不同部位神经生长因子受体TrkA表达的影响及临床意义。②方法　成年健康雌性Wistar大鼠 10只 ,随机分为穹隆 海马伞切断模型组和假手术组。两组大鼠均常规取海马CA1区、皮质区、杏仁复合体区、基底前脑Meynert核等部位脑组织与假手术组比较TrkA阳性细胞表达情况。③结果　假手术组大脑各观察区有基础水平的TrkA表达。模型组大脑海马CA1区、大脑皮质区、杏仁复合体区以及Meynert核区TrkA阳性细胞数明显减少 (t=3.94 4～ 8.4 4 2 ,P <0 .0 5 )。 ④结论　穹隆 海马伞切断可致大鼠脑内多部位TrkA表达减少 ,其可能是导致认知和情绪损伤的原因之一。     

肺癌组织中血管内皮生长因子受体Flt1及KDR的表达及其与肿瘤转移和预后的关系

①目的　探讨肺癌中血管内皮生长因子受体Flt1、KDR的表达与其转移及预后的关系。②方法　应用免疫组织化学PowerVisionTM PV90 0 0法 ,测定 75例肺癌标本中Flt1、KDR的表达。③结果　肺癌组织中Flt1、KDR的表达较为广泛 ,主要位于肿瘤细胞胞浆及胞膜上 ,纤维母细胞和血管内皮细胞胞浆中亦有表达。Flt1、KDR在肿瘤细胞中的阳性率均显著高于在间质纤维母细胞中的表达 (χ2 =6 .0 7、5 .88,P <0 .0 5 )。肿瘤细胞及纤维母细胞中该两种受体的阳性率在不同年龄、不同性别及不同病理类型、不同病理分级之间差异均无显著性 (χ2 =0 .0 1～4 .84 ,P >0 .0 5 ;P =0 .2 9～ 0 .79)。肿瘤细胞中Flt1、KDR的阳性表达率在 3组不同大小的肿瘤间差异均有显著性(χ2 =1 0 .35、7.2 9,P <0 .0 5 ) ,而纤维母细胞中差异均无显著性 (χ2 =2 .86、2 .5 6 ,P >0 .0 5 ) ;肿瘤细胞及纤维母细胞中Flt1、KDR的阳性率在淋巴结有、无转移两组间的差异均有显著性 (χ2 =4 .72～ 9.32 ,P <0 .0 5 ) ,在 3组不同术后生存时间病人间亦均有显著性差异 (χ2 =8.81～ 1 9.1 9,P <0 .0 5 )。肿瘤细胞中Flt1、KDR的表达呈极显著性正相关 (r =0 .4 4 ,P <0 .0 1 )。④结论　肺癌的生长主要依赖自分泌机制 ,联合检测Flt1、KDR可能对肺癌转移     

参附注射液对肠缺血-再灌注大鼠肿瘤坏死因子α的影响

目的观察肿瘤坏死因子α(TNF-α)在大鼠肠缺血-再灌注损伤过程中的作用及参附注射液对TNF-α的影响,探讨参附注射液防治肠缺血-再灌注损伤机制。方法 SD大鼠随机分为肠缺血-再灌注组(IR组)、参附注射液预处理组(SF组)和假手术组(C组)。采用阻断肠系膜上动脉(SMA)的方法制造肠缺血-再灌注模型。分别测定各组动物血浆、肠组织TNF-α含量及血液动力学变化;光镜观察肠粘膜损伤情况。结果IR组再灌注后MAP下降,与C组和SF组比有显著性差异(P<0.01);SF组肠粘膜损伤程度减轻,与IR组比有显著性差异(P<0.01);SF组血浆及肠组织TNF-α水平降低,与IR组比有显著性差异(P<0.01)。结论参附注射液可明显防治大鼠肠缺血-再灌注导致的肠粘膜损伤,这种作用可能是通过抑制TNF-α的释放实现的。     

Neurotoxic effects of MDMA (“ecstasy”) administration to neonatal rats

3,4-Methylenedioxymethamphetamine damages fine serotonergic fibers and nerve terminals in adult organisms. Developing animals seem to be less susceptible to this effect, possibly due to a lack of drug-induced hyperthermia. We tested this hypothesis by producing hyperthermia in neonatal rats for 2 h after each of twice-daily MDMA (10 mg/kg s.c.) or saline injections administered from postnatal days 1–4. Other drug-treated and control litters were maintained at normothermic temperatures following injection. Changes in forebrain serotonergic innervation were assessed at postnatal day 25 (serotonin transporter binding and serotonin levels), postnatal day 60 (serotonin transporter binding), and 9 months of age (serotonin transporter immunohistochemistry). We also determined the influence of MDMA treatment on apoptotic activity by means of immunohistochemistry for cleaved caspase-3 at postnatal day 5. The hippocampus showed significant MDMA-related reductions in serotonergic markers at postnatal day 25 and postnatal day 60. At 9 months, there was no effect of prior MDMA exposure on serotonin transporter-immunoreactive fiber density in the hippocampus; however, significant reductions in fiber density were observed in two neocortical areas and a hyperinnervation was found in the caudate-putamen and nucleus accumbens shell. MDMA treatment also produced a two-fold increase in the number of cleaved caspase-3-immunoreactive cells in the rostral forebrain and hippocampus. All of these effects were completely independent of pup body temperature. These findings demonstrate that neonatal MDMA administration exposure stimulates apoptotic cell death in various forebrain areas and also leads to a long-term reorganization of the forebrain serotonergic innervation. Consequently, offspring of MDMA-using women may be at heightened risk for abnormal neural and behavioral development.     

Inflammatory biomarkers in blood of patients with acute brain ischemia

Although many failed surrogate markers are provided in the literature, inflammation may contribute to the outcome of ischemic stroke. In 50 consecutive patients with acute ischemic stroke, in the absence of symptoms and signs of concomitant infection, we evaluated a panel of biomarkers reported to be variably associated with brain ischemia, and correlate their serum level with the brain lesion volume and clinical outcome. Infarct size was calculated on computed tomography (CT) scans by means of the Cavalieri's method. Neurological impairment was scored by using the Glasgow Coma Scale, Glasgow Outcome Scale and National Institutes of Health (NIH) scales at stroke onset and 3-month follow-up. Some markers showed a direct significant correlation with both initial and final NIH scale and with infarct size, particularly tumor necrosis factor alpha (TNF-alpha) (P=0.002), intercellular adhesion molecule-1 (P<0.01) and matrix metalloproteinase-2/9 (P=0.001). In contrast to previous reports, interleukin-6 (IL-6) serum level showed a significant inverse correlation with both final neurological impairment and infarct size (P<0.001). This novel finding allows us suggesting that IL-6, in the context of a complex pro-inflammatory network occurring during stroke, is associated with neuroprotection rather than neurotoxicity in patients with ischemic brain injury.     

Pemphigus Vulgaris Associated with Autoimmune Hemolytic Anemia and Elevated TNFα

A 76-year-old female was admitted with many bullae and erythema on her trunk and extremities. A biopsy specimen showed significant intercellular edema in the lower epidermis and eosinophilic infiltration into the dermis and the epidermis. Immunofluorescent staining revealed the deposition of IgG in the intercellular area of her prickle cells. From these histologic findings and the typical clinical features, we diagnosed her as having pemphigus vulgaris. Examination of her blood revealed that she also suffered from autoimmune hemolytic anemia. Despite intensive treatment with prednisolone, she finally died. This case is of interest because of its rarity and the TNFα detected significantly in the blister fluid of this patient.     

Hereditary plasma thromboplastin antecedent (PTA,FXI)

A rare case of factor XI (PTA) deficiency was discovered in a Saudi family in the Riyadh area. Nine members of the family were studied. Two were found to have a severe PTA deficiency’ levels of factor XI clotting activity were 0.01 i.u./ml and 0.02 i.u./ml respectively. Both plasmas were markedly deficient in factor XI antigen and appeared to be negative for cross-reactive material (CRM-). The parents were first cousins and both were found to have a minor PTA deficiency. Factor XI levels were: mother 0.048 i.u./ml and father 0.33 i.u./ml. Another sibling was found to have a FXI level of 0.47 i.u./ml. Menorrhagia and bleeding for 1 day after tooth extraction were the main bleeding manifestations found in one member with severe PTA deficiency. Clinically this member presented with iron deficiency anaemia. Other family members had no significant history of bleeding tendency. This is the first report of a Saudi Arabian family with PTA deficiency.     

Vascular cell adhesion molecule-1 modulation by tumor necrosis factor in experimental allergic encephalomyelitis

Anti-tumor necrosis factor (TNF) antibodies inhibit passively transferred experimental allergic encephalomyelitis (EAE) in SJL mice. The possibility that this occurs through interference in TNF's upregulation of endothelial cell adhesion molecules was investigated. Expression of both vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on spinal cord vessels increased during EAE. The upregulation of VCAM-1 was markedly reduced or prevented by anti-TNF treatment. Leukocytic infiltration was 15-fold lower in anti-TNF-treated than diseased animals. Spinal cord endothelial expression of VCAM-1, though not ICAM-1 or fibronectin, positively correlated with the extent of T cell, B cell or monocyte infiltration in each animal.