自然感染鼠痘的小鼠肝脾内病毒超微结构的观察

应用自然感染鼠痘存档5年蜡块转制超薄切片，在电镜下观察发现鼠痘病毒的复制部位是在肝脾细胞浆的基质区和包涵体的周围。此部位有大量不同发育阶段的病毒颗粒。未成熟病毒颗粒可分为球状颗粒和含有拟核的球状颗粒。成熟病毒颗粒的典型形态呈年椭圆形，外被双层囊膜，中心含有哑铃形核心，核心两侧各有一个测体。本实验结果证实应用存档蜡块转制超薄切片，可成功地应用于鼠痘感染及追溯性鼠痘病原和传染源的电镜诊断。并在电镜下证实光镜下A、B型包涵体及免疫酶组化病毒抗原的阳性部位与鼠痘病毒生物合成和装配的部位是一致的。     

腐植酸对鼠胶原脯氨酸及赖氨酸羟化的影响

目的：探讨腐植酸对NMRI鼠关节软骨胶原分子直径的影响及其机制。方法：用含30mg／L腐植酸的饮水饲养二代NMRI鼠，应用形态学、生物化学的方法对子代鼠关节软骨胶原的分子直径、糖基化率进行观察。结果与对照组相比，实验组关节软骨胶原分子直径明显增粗（P〈0．01），糖基化产物GHH明显下降（P〈0．01）。结论：鼠关节软骨胶原分子直径的改变与腐植酸对胶原分子糖基化率的影响有关。     

鼠肝高尔基体双向凝胶电泳的建立

目的分离纯化鼠肝高尔基体,初步建立一套相对完善、分辨率和重复性均较高的高尔基体双向凝胶电泳技术。方法应用蔗糖密度梯度超离心法分离纯化高尔基体,通过电镜观察和标志酶分析鉴定其形态及纯度,双向凝胶电泳分离高尔基体蛋白质,用PDQuest8.0软件分析电泳图谱。结果电镜观察显示大部分为高尔基体,纯化高尔基体标志酶TPP酶比活力提高了120倍,得到了分辨率和重复性均较好的双向凝胶电泳图谱。结论已成功建立了鼠肝高尔基体双向凝胶电泳技术。     

双甲敌鼠铵盐的研制

本文介绍了双甲敌鼠铵盐的性质、结构、生产工艺及其应用;通过对比,提出其优越于敌鼠钠盐之处。     

紫外分光光度法测定毒鼠饵中杀鼠迷含量

本文用无水乙醇提取样品中杀鼠迷,在308.2纳米处进行分析测定,其提取率,准确度、精密度和灵敏度均高。     

微生物合成鼠李糖脂生物表面活性剂的研究进展

微生物合成的鼠李糖脂是一类重要的生物表面活性剂,具有易被生物降解、表面活性良好等优点,应用前景广阔。目前用于发酵合成鼠李糖脂的菌株主要为假单胞菌属。综述了产鼠李糖脂菌株的发现与筛选、鼠李糖脂的生物合成途径与代谢调控关系、鼠李糖脂发酵过程的优化与控制、高产鼠李糖脂工程菌株的构建等方面的研究进展,并对其研究趋势进行了展望。     

生肖"鼠壶"创作随想

鼠在十二生肖中排行为首,关于鼠的创作题材被艺人们广泛运用.庚子鼠年,新年伊始我国遇到了新冠肺炎的爆发,在这突如其来的这场抗疫中,对中国政府、中国人民都是一场大考验,因而产生了这款壶的创作灵感,记录这一历史事件.     

发酵液中鼠李糖脂的活性炭吸附-酸沉淀分离

采用活性炭吸附-酸沉淀法从铜绿假单胞菌发酵液中提取鼠李糖脂。探讨了活性炭吸附鼠李糖脂的热、动力学规律,研究了p H值对活性炭吸附鼠李糖脂的影响及洗脱剂与洗脱时间的选择。结果表明:p H 7.0、吸附温度40—80℃时果壳活性炭的吸附平衡时间为60—140 min,80℃得到最大吸附量40.2 mg/g;酸沉淀能显著提高吸附量,p H 2.0时,果壳活性炭对鼠李糖脂的平衡吸附量提高至120.6 mg/g,一次吸附回收率达76.1%。适宜的洗脱剂为体积分数95%乙醇,洗脱时间为2 h,鼠李糖脂一次洗脱回收率为30.2%。该方法避免了有毒挥发性有机溶剂的使用,是一种经济环保的鼠李糖脂分离提取工艺。     

氯鼠酮农田灭鼠试验

氯鼠酮(氯敌鼠)是一种新型高效的抗凝血杀鼠剂,国外已广泛应用。1985年我国辽宁省化工研究所研制成功,1988年江苏省无锡洛社卫生用品厂合成此药,目前已进行批量生产。为了了解氯鼠酮的灭鼠效果,1989年3月我们在小海乡进行了试验观察,结果报告如下。     

鼠李糖脂在石油工业中的应用研究进展

鼠李糖脂是一种具有良好乳化作用、增溶作用以及可降低界面张力的生物表面活性剂。介绍了鼠李糖脂的结构及生产方法,综述了鼠李糖脂在石油工业中应用的研究进展,探讨了目前的研究热点及存在的问题,展望了鼠李糖脂今后的发展方向。     

检查传代细胞致肿瘤因子动物模型的研究

以Vero传代细胞系为例，用一种严重联合免疫缺陷小鼠（SevereCombinedImmunodeficintMice，SCID）及棵鼠（NudeMice），以10~7／0.2ml的传代细胞注射于胸部皮下。同时用Hela细胞作为阳性肿瘤细胞对照，并接种于免疫功能正常的BALB／c小鼠和昆明种小鼠。结果表明Vero细胞（P_(137)代）无论在SCID小鼠或探鼠都未引起肿瘤。而Hela细胞注射的SCID小鼠及裸鼠，于注射后第7天，在注射部位有进行性的肿瘤生长，到21天解剖时长至15×20mm，局部淋巴结也受累；而在免疫功能正常的小鼠则未引起肿瘤生长。证明SCID小鼠及探鼠可作为致肿瘤试验的动物模型。     

西洋参根多糖对免疫抑制小鼠免疫功能的影响

应用环磷酰胺引起免疫抑制小鼠模型，观察了西洋参根多糖（PQRP）对其免疫功能的影响。结果表明，PQRP不仅能抗免疫抑制小鼠外周血白细胞减少、胸腺和脾脏重量的减轻，并能增强正常和免疫抑制小鼠网状内皮系统的吞噬功能；可明显促进免疫抑制小鼠牌淋巴细胞转化，并提高白细胞介素－2活性。提示PQRP可作为一种新的免疫调节剂。     

非肥胖型糖尿病小鼠胸腺异位基因及MHC-Ⅱ类分子的表达

目的研究非肥胖型糖尿病(NOD)小鼠胸腺异位基因及MHC-Ⅱ类分子表达水平,探讨胸腺异位基因及MHC-Ⅱ类分子在中枢免疫耐受中的作用。方法对NOD小鼠用GA-PAP试剂盒检测血糖;尿糖试纸检测尿糖;ELISA间接法检测IAA的含量;光镜观察胰岛的组织学改变情况;MTT法检测胸腺T淋巴细胞功能;ELISA夹心法检测胸腺细胞IL-4、IFN-γ分泌水平;流式细胞术检测胸腺细胞MHC-Ⅱ类分子表达水平;RT-PCR法检测胸腺异位基因的表达水平。结果NOD小鼠血糖水平与正常BALB/c小鼠差异无显著意义,尿糖水平均为阴性;NOD小鼠自身抗体水平与正常BALB/c小鼠差异无显著意义;与对照组相比,NOD小鼠胰岛数量减少,分布稀疏,胰岛细胞数亦减少,同时有大量炎细胞浸润;NOD小鼠胸腺细胞对ConA刺激的应答水平与正常BALB/c小鼠差异无显著意义;NOD小鼠胸腺细胞IFN-γ的分泌与正常BALB/c小鼠差异无显著意义,而IL-4的分泌能力明显低于正常BALB/c小鼠;NOD小鼠胸腺内Insulin水平显著减少,而GAD67和PLP水平无显著变化;NOD小鼠MHC-Ⅱ类分子的表达水平明显下降。结论NOD小鼠在糖尿病发病前期存在着胸腺异位基因及MHC-Ⅱ类分子表达缺陷,表明胸腺异位基因及MHC-Ⅱ类分子在中枢免疫耐受中起着重要作用。     

Restoration of Immune Responsiveness to Glioma by Vaccination of Mice with Established Brain Gliomas with a Semi-Allogeneic Vaccine

Prior studies had shown the clinical efficacy of a semi-allogeneic glioma vaccine in mice with lethal GL261 gliomas. This was confirmed in the present study. As subcutaneous vaccination resulted in protection against tumor in the brain, the present study assessed the impact of this vaccination of mice bearing established GL261 brain gliomas on their cytokine production upon in vitro exposure to tumor-derived products. Mice with established GL261 brain gliomas were vaccinated subcutaneously with H-2^b GL261 glioma cells fused with H-2^d RAG-neo cells or with a mock vaccine of phosphate-buffered saline. The results of these analyses show that the presence of GL261 tumor-conditioned medium resulted in increased production of Th1, inflammatory and inhibitory cytokines by spleen cells from control mice and from vaccinated glioma-bearing mice. In contrast, spleen cells of tumor-bearing, mock-vaccinated mice produced lower levels of cytokines in the presence of tumor-conditioned media. However, these results also show that there was not a heightened level of cytokine production in the presence of tumor-conditioned medium by spleen cells of vaccinated mice over the production by spleen cells of control mice. Overall, these results show that vaccination slows growth of the GL261 tumors to the point where GL261-vaccinated mice do not show the signs of morbidly or splenic dysfunction exhibited by unvaccinated, late stage glioma-bearing mice.     

Altered Induction of Reactive Oxygen Species by X-rays in Hematopoietic Cells of C57BL/6-Tg (CAG-EGFP) Mice

Previous work pointed to a critical role of excessive production of reactive oxygen species (ROS) in increased radiation hematopoietic death in GFP mice. Meanwhile, enhanced antioxidant capability was not demonstrated in the mouse model of radio-induced adaptive response (RAR) using rescue of radiation hematopoietic death as the endpoint. ROS induction by ex vivo X-irradiation at a dose ranging from 0.1 to 7.5 Gy in the nucleated bone marrow cells was comparatively studied using GFP and wild type (WT) mice. ROS induction was also investigated in the cells collected from mice receiving a priming dose (0.5 Gy) efficient for RAR induction in WT mice. Significantly elevated background and increased induction of ROS in the cells from GFP mice were observed compared to those from WT mice. Markedly lower background and decreased induction of ROS were observed in the cells collected from WT mice but not GFP mice, both receiving the priming dose. GFP overexpression could alter background and induction of ROS by X-irradiation in hematopoietic cells. The results provide a reasonable explanation to the previous study on the fate of cells and mice after X-irradiation and confirm enhanced antioxidant capability in RAR. Investigations involving GFP overexpression should be carefully interpreted.     

Mfn2 Overexpression Attenuates MPTP Neurotoxicity In Vivo

Mitochondrial dysfunction represents a critical event in the pathogenesis of Parkinson’s disease (PD). Increasing evidence demonstrates that disturbed mitochondrial dynamics and quality control play an important role in mitochondrial dysfunction in PD. Our previous study demonstrated that MPP⁺ induces mitochondrial fragmentation in vitro. In this study, we aimed to assess whether blocking MPTP-induced mitochondrial fragmentation by overexpressing Mfn2 affords neuroprotection in vivo. We found that the significant loss of dopaminergic neurons in the substantia nigra (SN) induced by MPTP treatment, as seen in wild-type littermate control mice, was almost completely blocked in mice overexpressing Mfn2 (hMfn2 mice). The dramatic reduction in dopamine neuronal fibers and dopamine levels in the striatum caused by MPTP administration was also partially inhibited in hMfn2 mice. MPTP-induced oxidative stress and inflammatory response in the SN and striatum were significantly alleviated in hMfn2 mice. The impairment of motor function caused by MPTP was also blocked in hMfn2 mice. Overall, our work demonstrates that restoration of mitochondrial dynamics by Mfn2 overexpression protects against neuronal toxicity in an MPTP-based PD mouse model, which supports the modulation of mitochondrial dynamics as a potential therapeutic target for PD treatment.     

Modulation of Endocannabinoids by Caloric Restriction Is Conserved in Mice but Is Not Required for Protection from Acute Kidney Injury

Acute kidney injury (AKI) is a frequent and critical complication in the clinical setting. In rodents, AKI can be effectively prevented through caloric restriction (CR), which has also been shown to increase lifespan in many species. In Caenorhabditis elegans (C. elegans), longevity studies revealed that a marked CR-induced reduction of endocannabinoids may be a key mechanism. Thus, we hypothesized that regulation of endocannabinoids, particularly arachidonoyl ethanolamide (AEA), might also play a role in CR-mediated protection from renal ischemia-reperfusion injury (IRI) in mammals including humans. In male C57Bl6J mice, CR significantly reduced renal IRI and led to a significant decrease of AEA. Supplementation of AEA to near-normal serum concentrations by repetitive intraperitoneal administration in CR mice, however, did not abrogate the protective effect of CR. We also analyzed serum samples taken before and after CR from patients of three different pilot trials of dietary interventions. In contrast to mice and C. elegans, we detected an increase of AEA. We conclude that endocannabinoid levels in mice are modulated by CR, but CR-mediated renal protection does not depend on this effect. Moreover, our results indicate that modulation of endocannabinoids by CR in humans may differ fundamentally from the effects in animal models.     

Fatty acid composition of triglycerides from adipose tissue transplanted between obese and lean mice

The subcutaneous adipose tissue of genetically obese mice (ob/ob) differs from that of lean litter-mates not only by virtue of its larger cells but also in its fatty acid composition; it contains a higher proportion of palmitoleic acid and a lower proportion of linoleic acid. To determine whether these differences in fatty acid composition were inherent in fat cells, subcutaneous adipose tissue from obese and lean mice was transplanted under the kidney capsules of lean and obese host mice and the fatty acid composition of the neutral lipids of the graft and of the host perirenal and subcutaneous fat was determined 1 or 2 months later. The fatty acid composition of grafts from lean donors in obese mice resembled that of the perirenal adipose tissue of the obese hosts after 1 month, with a lower proportion of linoleic acid and a higher proportion of palmitoleic acid than in lean mice. Grafts from obese mice in lean mice had fatty acid compositions which were either unchanged, partially changed or which completely resembled that of the host. The use of grafts prelabeled by feeding the donor margaric acid indicated that total lack of fatty acid turnover, rather than selective metabolic processes, was responsible for the failure of some grafts from obese mice in lean mice to acquire the fatty acid composition of the perirenal adipose tissue of the host.