28例脑脓肿的CT与MRI表现分析

28例经手术或脑穿刺病理证实的脑脓肿病例，均行CT平扫和增强检查，其中23例行MRI检查。其CT与MRI表现为：单发24例，多发4例。CT平扫示各个时期的脑脓肿表现不完全相同，典型病灶主要表现为低密度囊性病灶或等低混杂密度的囊实性病灶(20～42Hu)，其中2例病灶内含气体，增强后病灶中央无强化。周围有明显强化的壁，除6例囊壁欠光整外，其余病灶囊壁较光整。MRI平扫示病灶中央呈低T1WI、高T2WI信号灶，有环形的高信号的壁，增强后壁强化明显，病灶中央无强化。认为脑脓肿CT与MRI表现有一定特征性，CT、MRI对脑脓肿有极高的诊断价值。     

肾宁口服液对兔膜性肾病模型肾保护作用的实验研究

目的观察肾宁口服液治疗膜性肾病的实验研究.方法用阳离子牛血清白蛋白(C-BSA)制备家免膜性肾病模型,设立正常对照组、中药治疗组、激素治疗组和模型组.每周测定一次24h尿蛋白,实验结束时测定血浆白蛋白、血脂和肾功能等生化指标.结果肾宁口服液中药治疗组的24h尿蛋白、血脂和肾功能等生化指标较模型组明显改善(P＜0.01或P＜0.05),而激素治疗组与模型组比较无明显差异(P＞0.05).结论肾宁口服液能降低尿蛋白,提高血浆白蛋白,改善肾功能,对膜性肾病有显著疗效.     

乙型肝炎患者可溶性白细胞介素2受体水平变化

本研究应用酶联免疫吸附试验(ELISA)检测了103例乙型肝炎各型患者及26倒乙肝病毒(HBV)携带者血清中可溶性白细胞介素2受体(sIL-2R)水平,并结合临床资料进行分析。结果发现:各型患者及HBV 携带者sIL-2R 水平均明显高于正常对照(P<0.01～0.001),其升高程度与病情轻重呈正比,在去除危重患者酶—胆分离时谷丙转氨酶(ALT)过低的影响后,sIL-2R 水平与ALT 有良好的正相关关系(r=0.38.p<0.05);作者认为sIL-2R 能够较好地反映疾病的活动状况,动态观察血清sIL-2R 水平的变化,对判断和评价HBV 感染后的病情演变及免疫失衡状态具有重要意义。     

三七总皂苷眼用凝胶在兔眼部的组织分布研究

[目的] 研究三七总皂苷眼用凝胶在兔眼组织的药物分布。[方法] 选取12只新西兰大白兔,随机分为4组,每组3只兔子。每只兔眼分别给予凝胶41.67 μL/kg（即三七皂苷R1 0.132 mg/kg,人参皂苷Rg1 0.452 mg/kg）。给药后于0.5、1、1.5、2 h空气栓塞各处死1组兔子。取眼球,分离各眼组织。采用UPLC-MS检测不同时间点各眼组织的药物含量。[结果] 兔眼给予三七总皂苷眼用凝胶后,三七皂苷R1在兔角膜、晶状体、房水、玻璃体中的最大含量分别为13.16、1.16、0.86、0.10 μg/g,人参皂苷Rg1在角膜、晶状体、房水、玻璃体中的最大含量分别为38.49、4.50、3.38、0.28 μg/g。[结论] 三七总皂苷眼用凝胶滴到兔眼后,三七皂苷R1和人参皂苷Rg1可透过角膜分散到各眼组织。在0~2 h内,各眼组织中的药物含量由高到低依次为角膜、晶状体、房水、玻璃体,表明三七皂苷R1和人参皂苷Rg1可透过角膜,到达眼后部组织,在2 h时各眼部组织的药物含量依然较高,在眼组织的保留时间长。     

Immunoglobulin mimicry by Hepatitis C Virus envelope protein E2

Hepatitis C virus (HCV) establishes persistent infection in the majority of infected individuals. The currently accepted hypothesis of immune evasion by antigenic variation in hypervariable region 1 (HVR1) of glycoprotein E2 does not however, explain the lack of subsequent immune recognition. Here, we show that the N-terminal region of E2 is antigenically and structurally similar to human immunoglobulin (Ig) variable domains. E2 is recognized by anti-human IgG antibodies and also possesses common amino acid (aa) sequence features of the conserved v-gene framework regions of human Ig light chains in particular but also heavy chains and T cell receptors. Using a position specific scoring system, the degree of similarity of HVR1 to Ig types correlated with immune escape and persistence in humans and experimentally infected chimpanzees. We propose a unique role for threshold levels of Ig molecular mimicry in HCV biology that not only advances our concept of viral immune escape and persistent infection but also provides insight into host-dependent disease patterns.     

IL-18 Receptor Expression on Epithelial Cells is Upregulated by TNF Alpha

IL-18 is a multifunctional cytokine that augments both innate and acquired immunity and potentiates Th1 and Th2 reactions. We studied the expression of IL-18 receptor (IL-18R) on renal and respiratory epithelial cell lines. Both cell lines upregulated IL-18R mRNA and IL-18R membrane expression in response to TNF alpha and other proinflammatory cytokines. The function of IL-18R was confirmed by induction of IL-8 release from epithelial cells in response to recombinant IL-18. Epithelial cells may represent an important target for IL-18, mainly under inflammatory conditions associated with TNF alpha release.     

Comparison of protein tyrosine phosphorylation and morphological changes induced by IL-2 and IL-3.

We constructed cell lines which can proliferate in response to IL-2 or IL-3 by introducing a wild-type and mutant forms of cDNAs encoding the human IL-2R p75 chain into an IL-3 dependent hematopoietic cell line which expresses the p55 chain of the IL-2R. We compared early events that were induced in these cells by IL-2 and IL-3. Analysis of protein tyrosine phosphorylation showed that two common protein bands, pp95 and pp90, were phosphorylated by stimulation of either IL-2 or IL-3, suggesting the possible sharing of part of a signal transduction pathway between IL-2R and IL-3R. Comparison of protein tyrosine phosphorylation profiles induced by IL-2 and IL-3 among a variety of cell lines revealed that the pp90 band is the common tyrosine phosphorylation substrate in the cell lines examined, although the general tyrosine phosphorylation pattern differed in each cell line. Mutant p75 molecules incapable of inducing tyrosine phosphorylation could bind and internalize IL-2, but could not support cell growth. We also found that swift changes of cytoskeletal protein organization are one of the early events caused by signal transduction through either IL-2R and IL-3R. Reorganization of cytoskeletal proteins seems to be associated with protein phosphorylation, as a significant portion of pp90 was found in a detergent-soluble fraction in IL-2 or IL-3 treated cells.     

Comparative study of pituitary and bacteria-derived human growth hormone by monoclonal antibodies

We have established hybridoma lines which secrete mouse monoclonal antibodies (Mabs) to human pituitary growth hormone, hGH. Using indirect competitive ELISA and indirect passive hemagglutination inhibition twelve different Mabs were characterized with regard to cross-reactivity with the hGH-related hormones, human chorionic somatomammotropin, hCS, and human prolactin, hPRL. The reactivity of these Mabs with pituitary hGH was compared to that with either bacterially-produced methionyl-hGH or to that of reduced and S-carboxymethylated hGH, which has an altered conformation. None of the Mabs reacted with hPRL. Four did not react with hCS whereas the others showed varying degree of cross-reactivity with hCS. All Mabs reacted more weakly with reduced and S-carboxymethylated hGH than with the native form of the hormone, which was not seen with conventional rabbit antisera to hGH. Thus in the case of hGH the Mabs are superior to conventional antisera in revealing small conformational differences. However the pituitary and bacterially-derived methionyl-hGH were indistinguishable as determined by the 12 Mabs.     

MicroRNA155 Plays a Critical Role in the Pathogenesis of Cutaneous Leishmania major Infection by Promoting a Th2 Response and Attenuating Dendritic Cell Activity

Interferon (IFN)-γ is indispensable in the resolution of cutaneous leishmaniasis (CL), while the Th2 cytokines IL-4, IL-10, and IL-13 mediate susceptibility. A recent study found that miR155, which promotes CD4⁺ Th1 response and IFN-γ production, is dispensable in the control of Leishmania donovani infection. Here, the role of miR155 in CL caused by L. major was investigated using miR155-deficient (miR155^−/−) mice. Infection was controlled significantly quicker in the miR155^−/− mice than in their wild-type (WT) counterparts, indicating that miR155 contributes to the pathogenesis of CL. Faster resolution of infection in miR155^−/− mice was associated with increased levels of Th1-associated IL-12 and IFN-γ and reduced production of Th2- associated IL-4, IL-10, and IL-13. Concentrations of IFN-γ⁺CD8⁺ T cells and natural killer cells in draining lymph nodes were significantly higher in the L. major−infected miR155^−/− mice than in the infected WT mice, as indicated by flow-cytometry. After in vitro IFN-γ stimulation, nitric oxide and IL-12 production were increased, IL-10 production was decreased, and parasite clearance was enhanced in L. major−infected miR155^−/− DCs compared to those in WT DCs. Furthermore, IFN-γ production from activated miR155^−/− T cells was significantly enhanced in L. major−infected miR155^−/− DCs. Together, these findings demonstrate that miR155 promotes susceptibility to CL caused by L. major by promoting Th2 response and inhibiting DC function.

Leishmania are obligate intracellular protozoans that infect phagocytes and cause a spectrum of clinical diseases such as cutaneous leishmaniasis (CL) and visceral leishmaniasis. Common in the tropical and subtropical regions, leishmaniasis affects over 1 billion people worldwide, with an incidence of up to 1 million cases per year.¹ CL is the most common type of Leishmania infection, manifesting as localized skin lesions that can become chronic, leading to significant tissue destruction and disfigurement.^2,3 It is well documented that the induction of a Th1 response and interferon (IFN)-γ are indispensable in the resolution of CL caused by Leishmania major,⁴ whereas disease progression is associated with the induction of a Th2 response and the production of cytokines such as IL-4 and IL-10.⁵ Establishing a disease-resolving response in the host is largely dependent on the ability to mount an appropriate Th1 immune response.⁴ Crucial in this response is the stimulation and activation of DCs that direct T-cell proliferation and differentiation toward IFN-γ–producing Th1 cells.^6,7 In addition to activating of phagocytic cells, IFN-γ induces the production of reactive nitrogen species, specifically nitric oxide (NO), leading to enhanced parasite clearance.⁴miR155 is a recognized regulator of immune cell function and immune response. miR155 enhances macrophage and DC activation and induces inflammatory response,^8,9 and up-regulation of miR155 in CD4⁺ T cells promotes preferential Th1 differentiation and IFN-γ production¹⁰ by suppressing the expression of suppressor of cytokine signaling (SOCS)-1.11, 12, 13, 14 Conversely, miR155 gene–deficient mice exhibit diminished levels of Th1/Th17 cells, macrophages, and DCs.¹⁵ miR155 has also been shown to play a role in regulating effector Th2 response.16, 17, 18 Collectively, these findings suggest that miR155 regulates both Th1 and Th2 responses, which control the outcome of CL caused by L. major. Therefore, the role of miR155 in immunity to L. major using miR155^−/− mice was investigated in the present study. The findings show that miR155 is not required for the induction of a Th1 response and IFN-γ in L. major infection. Rather, miR155 plays a disease-exacerbating role in CL by attenuating DC function and Th1 response and promoting Th2 response.