第三丁基过氧化氢诱导MIN6细胞损伤

目的 通过第三丁基过氧化氢(t-BHP)诱导小鼠胰腺β细胞,模拟体外氧化应激的细胞模型,观察氧化损伤对β细胞生长的影响.方法 体外培养小鼠β细胞株MIN6,MTT法测定细胞存活率,AO-EB荧光显微镜观测,Annexin-Ⅴ-PI染色流式细胞技术定量定性分析细胞凋亡率及坏死率. 结果 MTT显示,t-BHP(12.5～200 μmol/L)作用不同时间后可明显抑制MIN6细胞的生长,并呈现一定的时效和量效关系;AO-EB荧光显微镜及Annexin-Ⅴ-PI流式细胞检测证实,25μmol/L浓度的t-BHP诱导β细胞的损伤作用以凋亡为主,而更高浓度的t-BHP使细胞由凋亡转向坏死.结论 t-BHP可用于体外模拟β细胞氧化应激损伤的模型.     

地塞米松对小鼠MIN6细胞增殖和凋亡的影响

目的 探讨地塞米松对小鼠胰岛β细胞株MIN6细胞增殖和凋亡的影响.方法实验分对照组和不同浓度地塞米松(50,100,200,400,800 nmol/L)组诱导刺激MIN6细胞1～4 d,MTT法观察地塞米松作用后细胞的存活率;hochest/PI染色荧光显微镜观测细胞凋亡率.结果地塞米松作用1～4 d可明显抑制MIN6细胞的生长;>100 nmol/L组的地塞米松处理48 h后,细胞凋亡明显,凋亡率高达(30.44±4.52)%,与对照组比较差别有统计学意义(P<0.01),800 nmol/L组地塞米松使细胞由凋亡转向坏死.结论地塞米松对小鼠MIN6细胞增殖有明显影响,并能够引起MIN6细胞凋亡.     

美国住院病人髋膝关节置换术后谵妄发生率及危险因素

目的 探讨基于大样本量的髋膝关节置换(TJA)术后谵妄的发生率及危险因素.方法 基于2005～2014年美国的全国住院病人样本(NIS)数据库进行了回顾性分析.分别纳入并分析行全髋关节置换术(THA)和全膝关节置换术(TKA)且在2005～2014年NIS数据库中信息完整的病例.排除年龄不足18岁、急诊入院、合并骨骼感...     

Physical mechanisms of photoinduced charge transfer in neutral and charged donor–acceptor systems

In this paper, we provide visualization methods to reveal the physical mechanisms of photoinduced charge transfer in neutral and charged donor–acceptor systems. These visualization methods use the charge density difference and transition density matrix, which can promote deeper understanding of photoinduced charge transfer in donor–acceptor systems.

In this paper, we provide visualization methods to reveal the physical mechanisms of photoinduced charge transfer in neutral and charged donor–acceptor systems.     

白芍总苷对佐剂关节炎大鼠足爪组织病理的影响及MMP-9蛋白表达的抑制作用

目的:探讨白芍总苷(total glucosides of paeonia:TGP)对佐剂关节炎大鼠足爪组织中基质金属蛋白酶-9(MMP-9)蛋白表达的抑制作用和对大鼠足爪组织病理改变的影响及血清中血管内皮生长因子(VEGF)和白介素-1β(IL-1β)含量的影响。方法:建立Ⅱ型胶原诱导的佐剂关节炎大鼠模型,用免疫组化染色法检测足爪组织中MMP-9蛋白的表达,病理切片观察不同剂量的TGP对佐剂关节炎大鼠的治疗效果,用ELISA法检测佐剂关节炎大鼠血清中VEGF和IL-1β的含量。结果:白芍总苷中(50 mg/kg)、大(100 mg/kg)剂量组的胞浆内MMP-9的阳性表达比模型对照组明显降低,TGP中、大剂量治疗组与地塞米松组能明显改变佐剂关节炎大鼠皮下组织细胞排列、炎性细胞浸润及血管增生现象,TGP 25 mg/kg组对改善佐剂关节炎大鼠足部皮肤的病理状况无明显作用。中、大剂量的TGP组和地塞米松组血清VEGF和IL-1β的含量明显降低。结论:TGP对佐剂关节炎大鼠炎症的抑制作用,可能与其下调MMP-9蛋白的表达,抑制炎性细胞浸润及血管增生,降低炎性细胞因子VEGF和IL-1β的产生有关。     

Comparison of Physical and Biochemical Characterizations of SARS-CoV-2 Inactivated by Different Treatments

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused huge social and economic distress. Given its rapid spread and the lack of specific treatment options, SARS-CoV-2 needs to be inactivated according to strict biosafety measures during laboratory diagnostics and vaccine development. The inactivation method for SARS-CoV-2 affects research related to the natural virus and its immune activity as an antigen in vaccines. In this study, we used size exclusion chromatography, western blotting, ELISA, an electron microscope, dynamic light scattering, circular dichroism, and surface plasmon resonance to evaluate the effects of four different chemical inactivation methods on the physical and biochemical characterization of SARS-CoV-2. Formaldehyde and β-propiolactone (BPL) treatment can completely inactivate the virus and have no significant effects on the morphology of the virus. None of the four tested inactivation methods affected the secondary structure of the virus, including the α-helix, antiparallel β-sheet, parallel β-sheet, β-turn, and random coil. However, formaldehyde and long-term BPL treatment (48 h) resulted in decreased viral S protein content and increased viral particle aggregation, respectively. The BPL treatment for 24 h can completely inactivate SARS-CoV-2 with the maximum retention of the morphology, physical properties, and the biochemical properties of the potential antigens of the virus. In summary, we have established a characterization system for the comprehensive evaluation of virus inactivation technology, which has important guiding significance for the development of vaccines against SARS-CoV-2 variants and research on natural SARS-CoV-2.     

中西医结合治疗胆道蛔虫症67例报告

目的:探讨中西医结合在治疗胆道蛔虫疾病中的作用.方法:67例胆道蛔虫症患者进行辨证施治,并给予解痉止痛、利胆驱虫、抗感染等手段处理.结果:本组67例患者全部治愈,住院时间2～20 d,平均5 d.结论:中西医结合治疗胆道蛔虫症驱虫彻底,复发率低,可有效地预防或减少胆管结石、胆源性胰腺炎、肝脓肿和急性胆管炎的发生.     

Low density lipoprotein undergoes oxidation within lysosomes in cells

The oxidized low density lipoprotein (LDL) hypothesis of atherosclerosis proposes that LDL undergoes oxidation in the interstitial fluid of the arterial wall. We have shown that aggregated (vortexed) nonoxidized LDL was taken up by J774 mouse macrophages and human monocyte-derived macrophages and oxidized intracellularly, as assessed by the microscopic detection of ceroid, an advanced lipid oxidation product. Confocal microscopy showed that the ceroid was located in the lysosomes. To confirm these findings, J774 macrophages were incubated with acetylated LDL, which is internalized rapidly to lysosomes, and then incubated (chase incubation) in the absence of any LDL. The intracellular levels of oxysterols, measured by HPLC, increased during the chase incubation period, showing that LDL must have been oxidized inside the cells. Furthermore, we found that this oxidative modification was inhibited by lipid-soluble antioxidants, an iron chelator taken up by fluid-phase pinocytosis and the lysosomotropic drug chloroquine, which increases the pH of lysosomes. The results indicate that LDL oxidation can occur intracellularly, most probably within lysosomes.