塔里木油田地区地表温度分布规律的研究

选用塔里木盆地外围 1 5个站 36年地表温度观测资料和油田地区 4个短期观测站短期地表温度观测资料 ,应用气候统计方法 ,将油田地区的短期地表温度资料订正到长年同期 ,并加以分析研究。结果表明 ;塔里木油田地区年平均地表温度由周围向油田地区增加。夏季 ( 7月 )最高 ,冬季 ( 1月 )最低。     

Progress in autoantibodies to platelet and idiopathic thrombocytopenic purpura

The onset of idiopathic thrombocytopenic purpura (ITP) is related to excessive destruction of platelet resulting from antiplatelet autoantibody. The immunity with ITP is imbalance, so the hypofunction of suppressor T cell (Ts) can't restrain B lymphocytes producing antibody, as a result, autoant ibody is produced, the clearance of platelet in blood circulation is accelerated. The different antibodies have different functions on ITP. The measuring of platelet antibody has its significance in diagnosis, therapeutic evaluat ion and expectation of prognosis.     

Effect of Liucha extract on tumor K562 cell growth

AIM:To investigate the effects of Liucha extract on the growth of tumor cells in vitro and its possible mechanism.METHODS:The capability of colony forming of human leukemia K562 cell in vitro and the cells metabolism were studied by semi-solid agar culture and MTT staining. Then , the changes in morphology in the tumor cells were examined using electronic microscope.RESULTS:Semi-solid agar culture and MTT colorimetric analysis showed that Liucha extrats could significantly inhibit the growth of the tumor cells and their capability of colony forming. Also,under the electronic microscope,it was found that the tumor K562 cell had a narrower perinuclear space,condensation of chromatin and an enlarged mitochondria , in which the cristase disappeared.CONCLUSION:The extract from Liucha possesses an inhibitory effect on K562 cell growth in vitro through affecting the metabolism of the tumor cells.     

陕甘宁老区脆弱生态环境定量评价——以榆林、延安两市为例

位于黄土高原中部的陕甘宁老区生态环境极为脆弱 ,近年来由于气候、人类开发资源等自然和人为原因 ,使生态环境的脆弱程度升高。选定年降水量、年均温、蒸发量等 8个指标 ,定量评价各县 1 970 - 2 0 0 0年的脆弱度状况 ,结果表明榆林、延安两市生态环境整体脆弱 ,脆弱度存在空间差异但差异不明显 ,时间段上的波动幅度不大。陕甘宁老区脆弱生态环境具有不稳定性 ,对外界干扰较敏感。     

不同粘度矿物油助剂对除草剂活性的影响

室内及温室内测定了10种不同粘度矿物油助剂对除草剂防除苘麻和稗草药效的影响及对玉米苗期的安全性。结果表明,10种矿物油助剂均不同程度地增加了氰草津和烟嘧磺隆防除两种杂草的活性。其中粘度为46 mm2/s (40℃)的矿物油乳剂(MOC46)对供试除草剂药效的增强作用最为明显,其次为粘度32 mm2/s (40℃)的矿物油乳剂。10种助剂对氰草津药效的增强作用大于对烟嘧磺隆。MOC46对除草剂活性的增加由高到低依次为:莠去津、氰草津＞莠去津+氰草津、莠去津+烟嘧磺隆、氰草津+烟嘧磺隆＞烟嘧磺隆;对玉米苗期安全性依次为:莠去津、烟嘧磺隆、莠去津+烟嘧磺隆＞莠去津+氰草津、氰草津+烟嘧磺隆＞氰草津。氰草津与MOC46混用对玉米苗期药害较重。     

姬松茸与双孢蘑菇不同菌株的RAPD扩增研究

以4个姬松茸菌株和2个双孢蘑菇菌株为材料，用20个随机引物对它们进行RAPD扩增，通过对供试菌株遗传相似系数的估算和系统聚类分析，构建姬松茸和双孢蘑菇遗传相关树状聚类图谱，结果表明，进行RAPD扩增的20个随机引物中，有12个能产生三种带型，当遗传相似系数升至0.8713时，这6个菌株被分为3类，第一类为菌株18和26，第二类为菌株13和12，第三类为菌株33和45。     

Role of calcineurin in airway remodeling in guinea pig model of asthma

AIM:To investigate the role of calcineurin (CaN) in airway remodeling in guinea pig model of asthma.METHODS:Male guinea pigs were randomly divided into three groups: control, asthma group and CsA group. The following parameters were measured: 1. The protein content, cell count and differential count of BALF; 2. The amount of [³H]-TdR incorporation into central airway smooth muscle; 3. The mean thickness of airway wall and airway smooth muscle of small airwaysl; 4.CaN activity of trachea and lung tissue.RESULTS:1. The protein content, cell count and eosinophil of BALF in CsA group were 46%, 51% and 60% lower than those in asthma group, respectively (P＜0.01); 2. [³H]-TdR incorporation in CsA group was 22% lower than that in asthma group (P＜0.05);3. The mean thickness of airway wall and airway smooth muscle were 34% and 37% less in CsA group than those in asthma group, respectively (P＜0.01); 4. CaN activity of lung tissue and trachea were 52% and 44% lower in CsA group than those in asthma group, respectively (P＜0.01).CONCLUSION:CsA reduced airway remodeling in guinea pig model of asthma, indicating the role of CaN in the airway remodeling.     

Establishment of chronic obstructive pulmonary disease rat models by passive cigarette smoking and intratracheal instillation of lipopolysaccharide

AIM:To establish rat chronic obstructive pulmonary disease(COPD) models by passive cigarette smoking plus intratracheal instillation of lipopolysacchride(LPS) or passive cigarette smoking only, which would be similar to the pathogenesis of human COPD. METHODS:48 Wistar rats were randomly divided into 4 groups.(1) Healthy control I group(n=12), rats were bred 4 weeks;healthy control II group(n=12), rats were bred for 3months. (2) Model group I (n=12), 200μg lipopolysaccharide(LPS) was instilled intratracheally once for every two weeks and the rats were exposured to 5% of cigarette smoke, 0.5 h/d for 4 weeks.(3) Model group II(n=12),rats were exposed to 5% of cigarette smoke, 0.5 h/d for 3 months. The pathologic changes of airways and lung tissues, pulmonary function and blood gas analysis were determined. The airway wall lymphocytes and alveolar macrophages were counted. The cross areas of epithelial layer, smooth muscle layer and lamina propria of bronchi were measured. The hydroxyproline of lung tissue homogenates was determined by biochemistry method.RESULTS:The pathologic changes of airways and lung tissue of two models were similar to but milder than those of COPD patients(biopsy data). The collagen deposition and the cross areas of epithelial layer and smooth muscle layer in airway walls of two model groups were significantly increased than those of control groups(P＜0.01,P＜0.05).FEV_0.3/FVC% of two model groups, PaO₂ and SaO₂ of model I group were significantly decreased, while R_i and R_e in model I group were significantly increased than that of control I group(P＜0.05). The PaCO₂ and the counts of lymphocytes and alveolar macrophages of both model groups were significantly increased than those of the control groups (P＜0.01). Lots of alveolar macrophages had phagocyted smoke granules. The amounts of hydroxyproline of two model groups were significantly increased than those of control group((P＜0.05) and were negatively related to the FEV_0.3/FVC%, respectively (P＜0.01,P＜0.01) and positively related to airway resistance of model I group(P＜0.01). CONCLUSIONS:COPD rat models were successfully established by passive cigarette smoking plus intratracheal instillation of LPS and cigarette smoking only. The pathologic changes were similar but milder than those of COPD patients. The airway obstruction of model I group was more severe than that of model II group, but they have no significant difference.     

Expression of alpha-smooth muscle actin in scar tissue and its relationship with apoptosis

AIM: To examine the expression of alpha-smooth muscle actin in scar tissue, and observe the phenomenon of apoptosis and its involvement in the process of pathological scarring and the presence of myofibroblasts or absence of cell in the dermis. To investigate the potential role of reparative cell apoptosis in hyperplastic scar formation. METHODS: The samples of scar were obtained from post-burn patients undergoing plastic operation in our burn unit recently, and the samples of control came from skin donor site of the same patient correspondingly. TUNEL assays were performed to evaluate the number of apoptotic cells in scar versus normal skin. In situ hybridization and immunohistochemistry staining technique were employed to determine the expression of different dermis cells markers in scar tissue and normal skin. RESULTS: There existed evident difference in apoptotic cells in the dermis between scars tissue and normal human skin. The expression positive cells were much more in hyperplastic scars than that in normal human skin; the apoptotic cells of proliferative stage were slight more than that of mature stage. However, in proliferative stage, the number of apoptotic cells was higher for the combination of hyperplastic scar than normally healed flat scars. But in mature stage, no obviously difference was detected between hyperplastic scar and normally healed flat scar. The monoclonal anti-α smooth muscle actin (ASMA) expression was significantly stronger in proliferative stage than that of mature stage. CONCLUSIONS: With reconstitution of dermal tissue, myofibroblasts containing alpha-SM actin disappear under normal wound healing, probably as a result of apoptosis. The myofibroblast play a critical role in wound closure and in the pathologic sequelae of healing.