从一名国内感染的艾滋病人分离人免疫缺陷病毒（HIV）

从一名国内感染的艾滋病人采血,分离其外周血单核细胞（ＰＭＣｓ）。首先与正常的ＰＭＣｓ共培养,４周后检测其ＨＩＶ－１ｐ２４抗原（ＥＬＩＳＡ）达到峰值。用此时的细胞及其上清分别感染Ｊｕｒｋａｔ－ｔａｔ、ＣＥＭ、ＭＴ４细胞,可很快地在这三株细胞中检测到ＨＩＶ生长,ＨＩＶ在Ｊｕｒｋａｔ－ｔａｔ细胞中生长情况最好,同时用病人血清直接感染Ｊｕｒｋａｔ－ｔａｔ和ＭＴ４细胞,４周后检测其细胞上清ＨＩＶ－１ｐ２４抗原（ＥＬＩＳＡ法）为阳性,但ＯＤ值很低（约为ＰＭＣ共培养组的一半）。用病人的少量全血与正常ＰＭＣｓ共培养,得到的结果与分离病人ＰＭＣｓ法相近。应用间接免疫荧光法（ＩＦＡ）、免疫酶法（ＩＥＡ）、蛋白印迹法及ＨＩＶ－１ＰＯｌ基因和Ｅｎｖ基因特异引物的聚合酶链反应（ＰＣＲ）等证实为ＨＩＶ－１病毒。分离的ＨＩＶ在Ｊｕｒｋａｔ－ｔａｔ细胞中连续传代,细胞被感染后２－３天即出现以大量融合细胞为主的细胞病变,感染后７－１０天细胞几乎全部死亡。病毒在连续传代过程中的生长特征及致细胞病变特征不变。此病毒命名为ＣＡ－２毒株。     

一级吸收药物的生物利用度估计的两点法

本文应用系统分析方法,建立了一种一级吸收药物的生物利用度的简便估计的两点法。这种方法,只需测量血管内和血管外给药后的两个相同时点的血药浓度值。不论该药的处置系统是多少室,均能得到较好的结果。这种方法不仅比目前常用的点一点法和点一面法简单,而且结果更精确。     

津白_3侏儒小鼠垂体前叶生长激素细胞的免疫细胞化学研究

津白_３侏儒小鼠（ｄＷ~ｔ）是１９８２年从津白_３纯系小鼠（ＴＡ_３）中发现,进而培育成侏的变种。本实验应用免疫细胞化学技术,对ｄｗ￣ｔ小鼠垂体前叶生长激素（ＧＨ）细胞进行观察,并根据体视学原理进行定量分析,以探讨ｄｗ~ｔ小鼠是否存在垂体发育缺陷。实验结果显示,ｄｗ~ｔ小鼠ＧＨ细胞的体积密度（Ｖｖ）和数密度（Ｎｖ）值均低于正常对照组,Ｐ＜０．０１～０．００１。表明ｄｗ~ｔ小鼠由于垂体前叶ＧＨ细胞数量减少,导致ＧＨ分泌不足,从而形成侏儒。     

HBIG,无环鸟苷,干扰素联合对慢性乙型肝炎抗病毒效应观察

本文报道血清ＨＢＶ复制标志阳性的慢乙肝５４例,随机分为治疗组及对照组各２７例进行ＨＢＩＧ、无环鸟苷、干扰素联合近、远期抗病毒效应观察。治疗组为无环鸟苷第一周按２５～２０ｍｇ／ｋｇ／ｄ计后改１７～１５ｍｇ／ｋｇ／ｄ×５３天,共６０天;人白细胞干扰素１×１０６Ｕ肌注每周３次×４周,后改１．０×１０６Ｕ肌注每周２次×６周,共１０周;ＨＢＩＧ４００Ｕ肌注隔日１次,共１０周,对照组仅给予一般“保肝”药物。其中治疗组１８例,对照组１９例进行治后半年到２年追踪观察,结果近、远期ＨＢｃＡｇ、ＤＮＡＰ、ＨＢＶ－ＤＮＡ阴转率治疗组均高于对照组,其中治疗组近、远期ＨＢｃＡｇ,ＨＢＶ－ＤＮＡ阴转率均达４０％以上,明显高于对照组（Ｐ＜０．０５～０．０１）,治疗组近、远期各有４例及２例ＨＢｓＡｇ阴转,而对照组则无一例阴转,从近、远期综合抗病毒效应观察,治疗组全阴率分别为３３．３％、４４．４％,而对照组分别为３．７９％及０％,Ｐ＜０．０１,治疗组无明显毒副反应。对比单用无环鸟苷,全阴率３１．８％;无环鸟苷加干扰素两药联合全阴率３７．５％,均有所提高,达到４４．４％,值得进一步研究。     

冷锻炼和ABA诱导水稻幼苗提高抗冷性期间膜保护系统的变化

冷锻炼和ＡＢＡ处理提高了水稻幼苗叶绿体ＳＯＤ和ＧＲ活性及叶片抗氧化剂ＡｓＡ和ＧＳＨ的含量,降低了膜电解质泄漏,增强了幼苗的抗冷性．等电聚焦电泳分析表明,冷锻炼和ＡＢＡ处理苗叶绿体ＳＯＤ三条同工酶带和ＧＲ１、２、３和６同工酶带都有不同程度的增强．低温胁迫后,处理和未处理首的ＳＯＤ、ＧＲ活性和ＡＳＡ、ＧＳＨ含量均有所下降．但处理苗的水平仍维持在未处理苗之上．亚胺环已酮可抑制因冷锻炼和ＡＢＡ诱导增加的ＳＯＤ和ＧＲ活性,并使叶片电解质泄漏增大．本试验结果表明冷锻炼或ＡＢＡ诱导水稻幼苗抗冷性提高时,对防御活性氧的保护系统有类似的影响。     

岩豆凝集素的圆二色性与生物学活性关系的研究

岩豆凝集素（ＭＤＬ）的远紫外圆二色性谱（ＣＤ谱）显示２１６－２１７ｎｍ处的单一负峰。此时ＭＤＬ分子含有１６．２％的α螺旋,４６．３％的β折叠和３７．５％的无规卷曲。ｐＨ９．０时负峰红移至２２０ｎｍ,且在２１７－２２２ｎｍ处的峰值几乎相同;在２０－４０℃范围内,ＣＤ谱的变化甚微;６０℃时谱峰蓝移;在８０℃或１００℃时,２１２ｎｍ处出现一大负峰。１ｍｏｌ／Ｌ或２ｍｏｌ／Ｌ脲时,ＭＤＬ的ＣＤ谱已发生明显变化,二级结构单元也有变化,凝集兔红细胞的活性也随之减弱;随脲浓度的增加,ＭＤＬ的谱峰蓝移,最终在２１２ｎｍ处出现大负峰。当胍浓度为０．７５ｍｏｌ／Ｌ时,ＭＤＬ的ＣＤ谱即有明显变化和活性丧失;胍浓度继续增加,ＣＤ谱逐渐成为特征的无规卷曲的谱形。在ｐＨ９．０、温度超过８０℃、脲或胍浓度分别高于２ｍｏｌ／Ｌ和０．７５ｍｏｌ／Ｌ时,ＭＤＬ的ＣＤ谱发生显著变化的同时,其凝集兔红细胞的生物学活性全部丧失,分子的二级结构单元也发生很大改变。     

大鼠出生后脑内钙调神经磷酸酶的研究

本文用BA-ELISA.immunoblotting及酶活力测定等方法,研究了大鼠脑中钙调神经磷酸酶在大鼠出生后的变化情况。结果表明,钙调神经磷酸酶的含量在大鼠出生后第二周和第三周显著增加,其活力也在出生后第二周达到顶峰。钙调神经磷酸酶这种有规律的变化与脑中突触形成在时间上是一致的,暗示钙调神经磷酸酶可能参与突触功能的调节。     

Bisphenol S induces oxidative stress-mediated impairment of testosterone synthesis by inhibiting the Nrf2/HO-1 signaling pathway

Bisphenol S (BPS) is an environmental endocrine disruptor widely used in industrial production. BPS induces oxidative stress and exhibits male reproductive toxicity in mice, but the mechanisms by which BPS impairs steroid hormone synthesis are not fully understood. Nuclear factor erythroid 2-related factor 2(Nrf2)/HO-1 signaling is a key pathway in improving cellular antioxidant defense capacities. Therefore, this study explored the effects of exposure to BPS on testosterone synthesis in adult male mice and its mechanisms with regard to the Nrf2/HO-1 signaling pathway. Adult male C57BL/6 mice were orally exposed to BPS (2, 20, and 200 mg/kg BW) with sesame oil as a vehicle (0.1 ml/10 g BW) per day for 28 consecutive days. The results showed that compared with the control group, serum testosterone levels were substantially reduced in the 20 and 200 mg/kg BPS treatment groups, and testicular testosterone levels were reduced in all BPS treatment groups. These changes were accompanied by a prominent decrease in the expression levels of testosterone synthesis-related enzymes (STAR, CYP11A1, CYP17A1, HSD3B1, and HSD17B3) in the mouse testis. In addition, BPS induced oxidative stress in the testis by upregulating the messenger RNA and protein levels of Keap1 and downregulating the levels of Nrf2, HO-1, and downstream antioxidant enzymes (CAT, SOD1, and Gpx4). In summary, our results indicate that exposure of adult male mice to BPS can inhibit Nrf2/HO-1 signaling and antioxidant enzyme activity, which induces oxidative stress and thereby may impair testosterone synthesis in testicular tissues, leading to reproductive damage.     

GPD1L inhibits renal cell carcinoma progression by regulating PINK1/Parkin-mediated mitophagy

Few approaches have been conducted in the treatment of renal cell carcinoma (RCC) after nephrectomy, resulting in a high mortality rate in urological tumours. Mitophagy is a mechanism of mitochondrial quality control that enables selective degradation of damaged and unnecessary mitochondria. Previous studies have found that glycerol-3-phosphate dehydrogenase 1-like (GPD1L) is associated with the progression of tumours such as lung cancer, colorectal cancer and oropharyngeal cancer, but the potential mechanism in RCC is still unclear. In this study, microarrays from tumour databases were analysed. The expression of GPD1L was confirmed by RT–qPCR and western blotting. The effect and mechanism of GPD1L were explored using cell counting kit 8, wound healing, invasion, flow cytometry and mitophagy-related experiments. The role of GPD1L was further confirmed in vivo. The results showed that GPD1L expression was downregulated and positively correlated with prognosis in RCC. Functional experiments revealed that GPD1L prevented proliferation, migration and invasion while promoting apoptosis and mitochondrial injury in vitro. The mechanistic results indicated that GPD1L interacted with PINK1, promoting PINK1/Parkin-mediated mitophagy. However, inhibition of PINK1 reversed GPD1L-mediated mitochondrial injury and mitophagy. Moreover, GPD1L prevented tumour growth and promoted mitophagy by activating the PINK1/Parkin pathway in vivo. Our study shows that GPD1L has a positive correlation with the prognosis of RCC. The potential mechanism involves interacting with PINK1 and regulating the PINK1/Parkin pathway. In conclusion, these results reveal that GPD1L can act as a biomarker and target for RCC diagnosis and therapy.     

底栖生物影响下的潮滩微地貌演化数值模拟

潮滩是海岸带湿地的主要类型之一,其中分布的底栖生物对生态环境具有重要的调节作用。潮滩底栖微藻、泥沙与水动力之间存在相互作用,影响潮滩微地貌形态,明晰底栖生物对潮滩微地貌的演化机制至关重要。以黄河三角洲潮滩湿地为研究区,通过构建潮滩微地貌动力模型,探究底栖生物对微地貌格局演化的作用机制,分析底栖生物对微地貌系统稳定性的影响。结果表明(1)底栖微藻生长与泥沙扩散、水流再分配过程交互作用驱动下,潮滩上可形成底栖微藻覆盖的高丘与积水洼地交替分布的规则性微地貌斑图;(2)微地貌斑图的形成提高了潮滩生态系统初级生产力和泥沙淤积高度;(3)底栖微藻与泥沙、水流的交互作用使得潮滩微地貌系统对侵蚀扰动呈现非线性响应行为,系统存在临界点,且在一定侵蚀率范围内存在双稳态;(4)黄河口泥螺入侵使得微地貌系统抵抗侵蚀扰动能力减小,且系统稳定性随泥螺生物量的增加而降低。