血清SOD、MDA、NO与突发性聋的相关研究

目的：通过对突发性聋病人血中一氧化氮（NO）、丙二醛（MDA）、超氧化物歧化酶（SOD）含量的检洲，探讨突聋与血氧自由基和自由基的清除剂SOD之间的关系。方法：采用硝酸还原酶法测定了30例突聋病人血中NO含量，并以25例同期体检正常的健康人为对照组；同时还用硫代巴比妥酸比色法测定MDA含量，用黄嘌呤氧化酶法测定SOD含量。砖呆；应用金纳多、能量合剂、克林臭（即马来酸桂哌齐特，钙通道阻滞药）联合静脉输入，突聋各组的听力均有不同程度提高，有效率在78．57％以上。治疗后同对照组相比，血清NO、MDA水平明显低于患病之初，而SOD活性明显高于治疗之前，P〈0．01。结论；检测突聋病人血中N0、MDA、SOD的含量，能帮助我们探讨突聋的发病机理，估计预后。血氧自由基的升高可能是突聋发病因素之一，而SOD的含量可以帮助我们估计预后。     

Primary osteosarcoma of the skull

Primary osteogenic sarcoma of the skull is an exceedingly rare condition. An adult male patient is described, who had a painless swelling in the right forehead that had rapidly enlarged in the previous 6 months. Radiological investigations showed a large destructive mass lesion involving the right side of the frontal bone with extension into the frontal sinus, causing marked extradural compression of brain parenchyma. Histopathological examination confirmed the lesion to be primary osteogenic sarcoma.     

Left-lung-collapse bronchial deformation in giant omphalocele

Five infants with giant omphalocele had persistent collapse of the left lung and required prolonged respiratory support. Narrowing of the left main bronchus, reversible with positive end-expiratory pressure, was identified radiographically in 3 infants, and we postulate that this relates to distortion of the bronchus within the constraints of the elongated, narrow thoracic cavity characteristic of these patients. The lung collapse may be precipitated by manipulation (reduction or attempted reduction) of the omphalocele. J Pediatr Surg 36:846-850.     

维甲酸和联合应用神经营养因子对新生大鼠神经干细胞分化的影响

目的研究全反式维甲酸（ATRA）及联合应用神经营养因子（BDNF，GDNF）对体外培养的神经干细胞（NSCs）分化的影响。方法取新生SD大鼠的前脑室下带（SVZ）区，按NSCs的常规培养方法分离、培养。用免疫细胞化学法鉴定巢蛋白（nestin）、微管相关蛋白-2（MAP-2）、胶质原纤维酸性蛋白（GFAP）的表达，以此来观察ATRA、BDNF、GDNF单独或联合应用对次代神经球细胞分化的作用。结果原代及次代神经球均显示nestin阳性，并可分化为MAP-2阳性神经元样细胞及GFAP阳性胶质细胞样细胞。1μmol／LATRA可促进NSCs分化为MAP-2阳性细胞的比例达（29．14±5．00）％，显著高于对照组的（7．19±1．21）％，差异有高度统计学意义（P〈0．001）。ATRA联合应用10ng／ml的BDNF或GDNF，与单独使用ATRA比较，并不显著提高NSCs分化为MAP-2阳性细胞的比例。结论ATRA可促进神经干细胞向神经元方向分化，ATRA联合应用BDNF或GDNF无明显的协同作用。     

MDR1 基因单靶点双荧光素酶报告基因系统的建立

目的通过构建以MDR1启动子为启动序列的双荧光素酶报告基因系统并进行活性分析，为MDR1基因表达的单靶点调控研究和逆转剂的筛选提供一种有效的方法。方法从HCT-8细胞中提取DNA并克隆含有MDR1基因启动子中Y—box序列。将该序列重组到萤光素酶报告基因载体pGL-3．Basic的启动区域中，从而构建报告基因载体pGL-MDR1。将pGL-MDR1和pRL-TK载体共转染到HCT-8和HCT-8／VCR细胞中。通过调节不同载体的比例来优化转染效率。利用MDRI基因激活剂（热诱导）和抑制剂（EGCG）等处理来分析其启动转录活性受外界因素的影响。结果通过直接测序法验证了pGL-MDR1含有MDR1基因启动子Y—box序列且没有出现碱基突变。在pGL-MDR1和pRL-TK的转染比例为5：5时，转染效率最高并具有最高的萤光素酶活性。通过MDR1基因激活处理后表现为时间依赖性地激活MDR1基因的表达，而MDR1基因抑制剂的作用则相反。结论MDR1启动子为启动序列的双荧光素酶报告基因系统建立成功。该系统不但可以用于研究活体生物发光成像和MDRI基因表达的机理，而且可用于单靶点的多药耐药抑制剂的筛选。     

Relations between age, metabolic control, disease adjustment and psychological aspects in insulin-dependent diabetes mellitus

The relations between age, metabolic control, disease adjustment, and psychological factors in boys and girls with recently diagnosed insulin-dependent diabetes mellitus (IDDM) were studied. Older girls had significant higher postremission glycosylated haemoglobin A (Hb A_lc) levels ( p = 0.008). Girls with more hospitalizations had a lower developmental level ( p = 0.05), and had significantly more problems in the behavioural rating ( p = 0.05). Boys with more hospitalizations had a more external locus of control ( p = 0.01), more difficulties with disease adjustment, more emotional problems, and were also clinically assessed as having more behavioural problems. Boys showing more difficulties in psychological adjustment to the disease also had higher postremission Hb A_1clevels ( p = 0.02). Although Swedish children with IDDM of short disease duration do not differ from healthy children in important psychological aspects, older girls and a small group of problematic younger boys are at risk of developing metabolic imbalance after a short disease duration.     

Metabolic effects of growth hormone treatment: an early predictor of growth response?

Fourteen children receiving one year of recombinant human growth hormone (rhGH) treatment underwent measurement of serial changes in body composition (measured by skinfold thickness, bioelectrical impedance, and H2(18)O dilution), resting energy expenditure (REE, estimated by ventilated hood indirect calorimetry), and total free living daily energy expenditure (TEE, measured by the doubly labelled water technique). Mean height velocity increased from 4.9 to 8.6 cm/year after six months of treatment. Fat free mass (FFM) increased more during the first six weeks (24.4 g/day) than from six to 26 weeks of treatment (6.8 g/day); fat mass decreased by 7.2 g/day and 1.1 g/day respectively. The six week increase in REE (kJ/day) was maintained after six months of treatment, though expressed per kilogram FFM (kJ/kgFFM/day), returned to pretreatment values by three months. Height velocity increases at six months correlated with six week changes in fat mass measured by skinfold thickness and REE, though use of this relationship to predict growth response in individuals is limited by the wide 95% prediction intervals. No significant changes in growth, body composition, or energy expenditure were observed between six and 12 months of treatment, in either patients who had initially responded well to treatment or those who were poor initial responders to treatment and who had their dose of rhGH doubled after six months.     

HIV-1tat induced apoptosis of T-cells is not mediated by TGF-β

Recent reports have demonstrated that the HIV-1 transactivator protein,tat, induces apoptosis in T-lymphocyte cell lines, as well as in peripheral blood mononuclear cells, and stimulates a cascade of events resulting in up-regulation of the potent immunosuppressive cytokine, transforming growth factor-β (TGF-β). In this study we evaluated the ability of TGF-β to mediatetat induced apoptosis in T-lymphocyte cell lines. T-cells treated exogenously with either TGF-β1 or a combination of tat and pan-specific TGF-β neutralizing antibodies showed little change in the amount of apoptosis. When treated with pan-specific TGF-β neutralizing antibodies, Jurkat cells that stably expresstat protein (Jurkat-tat) showed only a modest decrease in apoptosis, while CEM-TART cells (CEM T-cells expressing both HIV-1tat andrev) demonstrated little change in the amount of apoptosis. In conclusion, we have demonstrated that TGF-β does not play a significant role in mediatingtat induced T-cell apoptosis.