锌及复合微量营养素的营养干预对学龄前儿童蛋白质营养状况的影响

选择重庆市近郊农村学龄前儿童１４０名，男、女各半，随机分为单纯补锌组、补锌及复合微量营养素组和单纯补充微量营养素组，另一组为对照。实验组每组４０人，对照组为２０人，进行１０周营养干预实验。结果显示，在补锌的同时服用硒、锰、维生素Ａ等多种微量营养素或单纯补充多种微量营养素均能有效改善受试儿童体内锌营养状况，使血浆中前白蛋白、转铁蛋白、铜蓝蛋白含量增加，血清中多种必需及非必需氨基酸，３甲基组氨酸浓度下降。提示，儿童营养状况改善后其体内蛋白质合成代谢加强，而分解减少，这种变化除缘于血清锌含量增加外，可能还与其它微量营养素的作用有关。而单纯补锌儿童血清锌变化并不显著，血清中几种转运蛋白与对照均无明显差异。     

达乌尔黄鼠种群繁殖特征的研究

本文根据1983～1986年在松辽平原区通辽地区的调查,研究了达乌尔黄鼠种群繁殖特征。结果表明:在松辽平原地区,各年份达乌尔黄鼠的怀孕率多在90％以上,平均胚胎数多在8.0以上,胚胎分布呈正态分布。黄鼠在怀孕过程中,有5.48—16.26％的雌体发生胚胎吸收,平均吸收胚胎2.0个左右,吸收胚胎分布呈poisson分布。1984年观察,平均每只雌鼠实际产仔鼠7.622±0.154只,其分布仍为正态分布。     

支气管扩张症肺组织内降钙素表达的临床意义

目的　了解支气管扩张症肺组织降钙素 (CT)蛋白表达水平与其病变特点的关系。方法　应用免疫组化方法定量分析 4 5例支气管扩张症患者手术切除的肺组织 ,对其气道上皮内神经内分泌细胞 (NEC)计数 ,并与 19例无肺部疾患的尸检肺组织进行比较。结果　 2组均可见被染成棕红色的CT阳性细胞 ,它们分布于肺内各级支气管上皮细胞间 ,以支气管分叉处较多见。支气管扩张症组肺组织内5 0 0 0个上皮细胞中CT阳性细胞数为 (6 7.4 8± 11.0 3)个 ,非支气管扩张症组肺组织内CT阳性细胞数仅为 (5 .0 2± 1.0 0 )个 ,2组比较有非常显著性差异 (P <0 .0 0 1)。结论　支气管扩张症肺组织高水平CT表达可能与其慢性炎症改变有关 ,其局部CT表达增高可能系机体对支气管扩张病变的一种局部性代偿或调节机制。     

脂质比值与代谢综合征的关联及预测价值评价：基于多阶段横断面研究

背景 随着代谢性疾病发病率的上升,代谢综合征(MS)的预防与控制引起广泛的关注。而脂质比值是重要的筛查指标之一,与MS之间的关系成为热点研究话题。目的 基于贵州省多阶段横断面研究人群分析三酰甘油/高密度脂蛋白胆固醇(TG/HDL-C)、总胆固醇/HDL-C(TC/HDL-C)、低密度脂蛋白胆固醇/HDL-C(LDL-C/HDL-C)及非高密度脂蛋白胆固醇(non-HDL-C)与MS发病风险的关联及预测价值评价。方法 回顾性选取贵州省参与2010年全国疾病监测地区慢性病及危险因素调查、2013年中国慢性病及其危险因素监测、2015年中国成人慢性病与营养监测和2018年中国成人慢性病与营养监测的21 727例自然人群为研究对象,收集研究对象的基线资料,根据是否患有MS将研究对象分为MS组(n=4 981)和非MS组(n=16 746)。绘制受试者工作特征曲线(ROC曲线)分别评价男性和女性TG/HDL-C、TC/HDL-C、LDL-C/HDL-C和non-HDL-C对MS的预测价值。通过Delong检验比较脂质比值预测MS发生的ROC曲线下面积(AUC)的差异。采用多因素Logistic回...     

陡脉冲电场对荷瘤BALB/c小鼠癌细胞杀伤效应的实验研究

观测陡脉冲电场对荷瘤BALB/c小鼠癌细胞的杀伤效应。处理后的癌细胞在光镜下表现为细胞核固缩、核碎裂、核溶解;在电镜下表现为异染色质增加,边集,呈团块样改变,细胞质肿胀,脂滴数量增加,质膜破裂;核固缩,碎裂,线粒体肿胀。实验揭示了陡脉冲电场能有效地杀伤癌细胞,明显抑制了荷瘤小鼠恶性肿瘤的生长、增殖,有着良好的应用前景。     

Multiplex PCR for the detection of genes encoding aminoglycoside modifying enzymes and methicillin resistance among Staphylococcus species

We developed multiplex polymerase chain reaction (PCR) to detect aac(6 ')/aph(2 "), aph(3 ')-IIIa, and ant(4 ')-Ia, the genes encoding the most clinically relevant amino-glycoside modifying enzymes (AME), and simultaneously, the methicillin resistant gene, mecA, in Staphylococcus species. Clinical isolates of 45 S. aureus and 47 coagulase negative staphylococci (CNS) from tertiary university hospitals were tested by conventional susceptibility testing, using the agar dilution method and by multiplex PCR. Of a total of 92 isolates, 61 isolates were found to be methicillin-resistant. Of these, 54 isolates (89%) were found to be harboring mecA. Seventy-five percent of the 92 isolates demonstrated resistance to at least one of the aminoglycosides tested. Moreover, resistance to aminoglycosides was closely associated with methicillin-resistance (p<0.05). The most prevalent AME gene was aac(6 ')/aph(2 ") which was found in 65% of the isolates, and ant(4 ')-Ia and aph(3 ')-IIIa were present in 41% and 9% of the isolates, respectively. The concordance between methicillin-resistance and the presence of mecA gene was 98% in S. aureus and 81% in CNS. The concordance between gentamicin resistance and the presence of aac(6 ')/aph(2 ") gene was 100% in S. aureus and 85% in CNS. The multiplex PCR method that we developed appears to be both a more rapid and reliable than conventional method.     

Calcineurin B1 is essential for positive but not negative selection during thymocyte development

During development, discrete cell fates often result from variation in the intensity of a particular signal. The mechanisms underlying these seemingly analog-to-digital switches are not understood. In developing T lymphocytes, low-intensity signals through the antigen receptor result in positive selection while more intense signals give rise to negative selection. By deleting the genetic locus encoding the regulatory B1 subunit of calcineurin specifically in thymocytes, we found an absolute requirement for calcineurin in positive selection. In contrast, calcineurin activity was dispensable in several models of negative selection. Unexpectedly, we found that removal of calcineurin activity from thymocytes results in inefficient ERK activation at the double-positive stage of thymocyte development, when selection occurs. These studies clarify the mechanism by which graded signals are converted to discrete outcomes in T cell development and further indicate that the developmental roles of calcineurin likely contribute to immunosuppression by calcineurin inhibitors.     

Circulating inflammatory mediators during start of fever in differential diagnosis of gram-negative and gram-positive infections in leukopenic rats

Gram-negative and gram-positive infections have been considered the most important causes of morbidity and mortality in patients with leukopenia following chemotherapy. However, discrimination between bacterial infections and harmless fever episodes is difficult. Because classical inflammatory signs of infection are often absent and fever is frequently the only sign of infection, the aim of this study was to assess the significance of serum interleukin-6 (IL-6), IL-10, macrophage inflammatory protein-2 (MIP-2), procalcitonin (PCT), and C-reactive protein (CRP) patterns in identifying bacterial infections during start of fever in normal and cyclophosphamide-treated (leukopenic) rats following an injection of lipopolysaccharide (LPS) or muramyl dipeptide (MDP) as a model for gram-negative and gram-positive bacterial infections. We found that, compared to normal rats, immunosuppressed animals exhibited significantly higher fevers and lesser production of all mediators, except IL-6, after toxin challenge. Moreover, compared to rats that received MDP, both groups of animals that received an equivalent dose of LPS showed significantly higher fevers and greater increase in serum cytokine levels. Furthermore, in contrast to those in immunocompetent rats, serum levels of IL-6 and MIP-2 were not significantly changed in leukopenic animals after MDP injection. Other serum markers such as PCT and CRP failed to discriminate between bacterial stimuli in both groups of animals. These results suggest that the use of the analyzed serum markers at an early stage of fever could give useful information for the clinician for excluding gram-negative from gram-positive infections.     

Fibroblast growth factor 2 induces differentiation and apoptosis of Askin tumour cells

Peripheral primitive neuroectodermal tumour (PNET)/Ewing's sarcoma (ES) and neuroblastoma (NB) are related tumours of neural crest origin with primitive neural characteristics. Fibroblast growth factor 2 (FGF2) is a critical signalling molecule for primitive neural crest cells. The treatment of NB cells with FGF2 variably affects biological characteristics such as growth and differentiation, while in PNET/ES, FGF2 predominantly induces apoptosis. The JK-GMS Askin tumour cell line can be induced to differentiate upon treatment with nerve growth factor (NGF), indicating the integrity of the cellular machinery necessary for differentiation. The present study assesses whether FGF2 can induce differentiation in JK-GMS cells. JK-GMS cells expressed high-affinity FGF receptors (FGFRs), and treatment with FGF2 induced phosphorylation of FGFR1 together with activation of extracellular signal-regulated kinases (ERK1/ERK2) and c-Jun N-terminal kinase (JNK). Subsequent biological effects were growth inhibition, neuronal differentiation, and apoptosis, and these changes were associated with increased expression of neurofilaments, reduction of c-myc and bcl-2 expression, and activation of caspase 3. Treatment of the cells with a specific inhibitor of the MAPK/extracellular signal-regulated kinase (MEK)-1, PD98059, predominantly inhibited the effects of FGF2 on growth, differentiation, and apoptosis, while an inhibitor of JNK reduced apoptosis, indicating that the ERK1/2 and JNK pathways are critical components of FGF2-mediated effects in JK-GMS cells. Additional comparative analyses of FGF2-mediated effects in two ES cell lines (CADO-ES, RD-ES) and a PNET cell line (SK-N-MC) showed pronounced differentiation in SK-N-MC, but not in CADO-ES or RD-ES cells. This study demonstrates that FGF2 can induce neuronal differentiation of PNET including Askin tumour. These findings clearly indicate that the FGF2-mediated signalling pathway plays a critical role in controlling the major properties of PNET cells and may provide a potential therapeutic target for PNET.     

药物从多孔骨架聚合物系统中恒速释放的机理

以组分的连续性方程为基础 ,建立了药物从多孔骨架聚合物系统中释放的数学模型。在模型中引入相对渗透速度来刻画药物释放过程中不同机理的影响。对药物从多孔骨架聚合物系统中non -Fickian扩散现象进行了研究 ,特别对药物溶出机制控制的恒速释药现象进行了解释。