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目的 研究甲基苯丙胺（methamphetamine, METH）对脂多糖（LPS）诱导小鼠血清和脾脏IL-1β、IL-6和TGF-β表达的影响。方法 选用C57BL/6小鼠，模拟人类药物成瘾模式，分段式渐进性递增剂量隔天给予小鼠腹腔注射（i.p.）METH（第1周0.5mg/kg、第2周1.0mg/kg、第3周2.0mg/kg、第4周4.0mg/kg）或生理盐水（10.0mL/kg），在最后一剂METH之后24h给小鼠i.p. LPS（0.33mg/kg）或生理盐水（10.0mL/kg），给予LPS 2h后摘除眼球采血并分离脾脏，检测血清及脾脏匀浆中IL-1β、IL-6和TGF-β的表达水平。结果 METH单独作用使血清中TGF-β的表达显著下降（P〈0.001），对IL-6的表达没有影响；给予LPS刺激后，METH使小鼠血清中IL-6的表达显著升高（P〈0.001），对TGF-β的表达没有影响；而IL-1β在血清中表达水平较低，未检测到。在脾脏中，METH单独作用对IL-1β、IL-6和TGF-β的表达没有影响；给予LPS刺激后，METH显著升高了IL-6的表达水平（P〈0.001），而使TGF-β的表达明显下降（P〈0.001），IL-1β的表达水平没有变化。结论 METH作用可以改变LPS诱导小鼠血清和脾脏IL-1β、IL-6和TGF-β的表达水平。

目的探讨模拟微重力对猕猴脾脏结构及免疫细胞表面分子和相关细胞因子表达的影响。方法在特殊装置上将猕猴置于头低位–10°以模拟微重力。将15只猕猴随机均分为对照组（NC组）、模拟微重力组（SM组）和模拟微重力后恢复组（MR组）,每组5只。完成实验后,猕猴在麻醉状态下放血处死,取脾脏组织标本进行HE和免疫组化染色。观察各组猕猴脾脏大体结构,检测脾脏免疫细胞表面分子CD3、CD4、CD8、CD20、CD68及相关细胞因子（IL-1β、IL-5、IL-6、IL-17、IL-18、IL-22、IL-23）的表达。结果 NC组脾脏组织结构正常,SM组脾脏红、白髓分界不清,白髓缩小,动脉周围淋巴鞘减小,淋巴细胞排列紊乱,MR组改变较SM组轻。免疫组化结果显示,与NC组和MR组比较,SM组脾脏表达CD3^＋、CD4^＋、CD20^＋的免疫细胞数目降低,CD8＋免疫细胞数目增高,IL-5分泌水平降低,差异有统计学意义（P〈0.05）。结论模拟微重力可引起猕猴脾脏组织结构损伤,对CD3^＋T细胞、CD4^＋T细胞、CD8^＋T细胞和CD20＋B细胞数目有一定影响,并能影响细胞因子IL-5分泌,这可能与模拟微重力引起免疫系统功能受损有关。

目的 研究T淋巴细胞亚群在不同周龄的自发性高血压大鼠（spontaneously hypertensive rat,SHR）和正常Wistar京都（Wistar-Kyoto,WKY）大鼠脾脏中的表达差异。方法 选取16周龄和40周龄雄性SHR和WKY大鼠各8只,监测血压后,通过苏木素-伊红（HE）染色观察大鼠脾脏病理学变化,应用流式细胞术检测WKY大鼠和SHR脾脏中T淋巴细胞亚群的表达变化。结果 与相同周龄WKY大鼠比较,SHR脾脏中央动脉血管壁增厚,管腔狭窄,且40周龄SHR脾脏病变较16周龄严重;相同周龄的SHR与WKY大鼠比较,脾脏中CD3＋、CD3＋CD4＋和CD3＋CD8＋T淋巴细胞比例均无统计学差异（P〉0.05）;与16周龄WKY大鼠比较,40周龄WKY大鼠脾脏CD3＋和CD3＋CD8＋T淋巴细胞比例显著降低（P〈0.01）,CD3＋CD4＋T淋巴细胞比例和CD4＋/CD8＋比值显著升高（P〈0.01）;40周龄SHR脾脏CD3＋、CD3＋CD4＋、CD3＋CD8＋T淋巴细胞以及CD4＋/CD8＋比值的变化趋势同WKY大鼠相一致。结论 高血压可引起脾脏病理改变,但其对脾脏T淋巴细胞亚群比例可能无显著影响,然而随着周龄的增加,脾脏T淋巴细胞亚群均发生紊乱。

近年来,随着对脾脏组织结构、细胞功能、分泌功能和神经支配的深入研究,对于脾脏的功能有了更深层次的认识。脾脏是机体免疫-神经-内分泌网络调节中心的一个重要组成部分,它不仅具有滤血、免疫、造血和储血等功能,而且其免疫功能具有“双向性”和“时相性”的特点。然而,要确切评价脾脏的功能尤其是病理状态下的脾脏功能,明确阐述脾功能亢进的机制、脾脏与其他脏器的关系等一系列问题还有待于对其进行进一步的深入研究。本文将从多个角度对脾脏的基础研究进展进行简要的介绍。

目的研究三叶因子3（TFF3）在胃溃疡大鼠脾脏不同部位的表达。方法胃前壁黏膜下注射冰乙酸制备大鼠胃溃疡模型,免疫组织化学法分别检测正常组（6只）和溃疡组（42只）雄性大鼠脾脏TFF3的表达。结果①溃疡组大鼠脾脏明显肿大、充血;与正常组相比白髓面积明显增大（P〈0.05或P〈0.01）,至6 d组最大,边缘区增厚（P〈0.05或P〈0.01）,至10 d组最厚;红髓面积减少。②TFF3阳性反应物呈棕黄色颗粒状分布于胞质中。③TFF3在正常组大鼠脾脏中呈弱阳性表达,在溃疡组表达明显增高（P〈0.05或P〈0.01）。溃疡组白髓中阳性细胞TFF3平均吸光度值各组与正常组相比明显增高（P〈0.05）,以10 d组增高最为明显;边缘区阳性细胞TFF3吸光度值1、2 d和6 d组与正常组相比明显增高（P〈0.05或P〈0.01）,以6 d组增高最为明显;红髓阳性细胞TFF3吸光度值1、2、6 d和14 d组与正常组相比明显增高（P〈0.05或P〈0.01）,以6 d组增高最为明显。④溃疡组边缘区TFF3表达与损伤时间呈负相关（P〈0.05）。结论 TFF3在胃溃疡大鼠脾脏各部位呈高水平表达,可能通过提高脾脏免疫反应性促进胃溃疡的愈合

目的 研究甲基苯丙胺(methamphetamine,ma)急性处理对lps诱导的小鼠脾脏il-6、il-10和tnf-α表达的影响.方法 选用c57bl/6j小鼠,分别腹腔注射(intraperitoneally,i.p.)生理盐水(ns)或ma(5 mg/kg),10 min后,再分别i.p.ns和lps(150 μg/kg),予lps后30 min和60 min,取脾脏,检测这两个时间点小鼠脾脏il-6、il 10和tnf-α的水平.结果 ma可显著提高lps诱导的脾脏il-6和il-10的表达(p＜0.01).对于脾脏il-6的水平存在ma+ lps的交互效应(p＜0.01),在i.p.lps60min后ma+ lps组脾脏il-6水平较ns+ lps组明显升高(p＜0.01).对于脾脏il -10的水平也存在ma+ lps的交互效应(p＜0.01),在i.p.lps30min后ma+ lps组脾脏il-10水平较ns+ lps组明显升高(p＜0.01).对于tnf-α,在这两个时间点既无显著的ma的主效应,也无ma+ lps的交互效应,ma组较ns组几乎没有差异(p=1.00).同一组别两个时间点的比较发现,无lps刺激,小鼠脾脏il-6、il-10和tnf-α的水平在两个时间点无差异；给予lps刺激,i.p.lps后60 min小鼠脾脏il-6、il-10和tnf-α的水平较30 min显著增高(p＜0.01).结论 ma处理小鼠后短时间内可显著增加lps诱导的脾脏il-6和il-10的表达,但对tnf-α表达无影响.

目的:对比分析脾脏、腹腔和骨髓源性巨噬细胞(SPMs、PCMs和BMs)在安静及极化状态下的差异。创新点:首次对比分析脾脏、腹腔和骨髓源性巨噬细胞在安静(M0)及极化状态(M1和M2)下的特征。方法:通过小鼠脾脏研磨及单细胞贴壁获得脾源性巨噬细胞;腹腔灌洗及细胞贴壁获得腹腔源性巨噬细胞;骨髓贴壁细胞在巨噬细胞集落刺激因子体外刺激下培养7天获得骨髓源性巨噬细胞。三种细胞即为M0型巨噬细胞,M0在干扰素及脂多糖刺激下获得M1型巨噬细胞,M0在白介素4(IL-4)刺激下获得M2型巨噬细胞。通过流式细胞仪分析三种类型巨噬细胞在三种状态下的Ⅱ类主要组织相容性复合体(MHC Ⅱ)和CD86表达差异。通过实时荧光定量聚合酶链式反应(q PCR)检测肿瘤坏死因子α(TNF-α)、白介素1β(IL-1β)、甘露糖受体(MR)和类几丁质酶3样分子(Ym1)的表达变化。结论:骨髓贴壁细胞培养能获得最大量的同源巨噬细胞(图1和2),但表型偏向于M2型巨噬细胞(图3和4)。三种巨噬细胞均能极化为M1和M2型巨噬细胞(图5),其中SPMs具有更强的M1型极化能力,而M2型极化能力之间未见明显差异(图6)。综上所述,三种细胞无论在安静及极化状态下均具有不同的特征,骨髓可以获得大量同源性巨噬细胞,但性质不同于组织源性的脾脏和腹腔巨噬细胞。

Dendritic cells （DCs） and monocyte subpopulations present in the human spleen were analyzed by flow cytometry in an attempt to identify the presence of a novel dendritic-like cell subset described previously in mice and named L-DCs. In this study, an equivalent of this novel murine subset was characterized in the human spleen, thus increasing our knowledge of the antigen-presenting cell types present in the human spleen. Human L-DCs were identified as a hCD11c~hCD11b＋HLA-DR-hCD86＋ subset in the spleen, along with the previously described subsets of hCDlc＋ DCs, hCD123＋ plasmacytoid DCs （pDCs）, hCD16＋ DCs and hCD141＋ DCs. Three subsets of monocytes were also characterized. DC and monocyte subsets in human spleen had phenotypes similar to those of subsets in human blood. In line with murine studies, the presence of L-DC progenitors within the spleen was also investigated. When human splenocytes depleted of T and B cells were cocultured with the murine stromal line 5G3, hematopoiesis ensued and hCD11c＋HLA-DR＋ and hCD11c＋HLA-DR- cells were produced. The latter resemble L-DCs, which are also produced in murine spleen cocultures. Both subsets expressed hCDSO and hCD86, which identifies them as antigen-presenting cells, particularly DCs, and were highly endocytic. It is noteworthy that murine splenic stroma can serve as a support matrix for human hematopoiesis and DC production. These results support the hypothesis that 5G3 must express both cell-associated and soluble factors that can signal hematopoiesis in human and murine progenitors.

Background： Postresuscitation immune dysfunction contributes to the low survival rate after successful resuscitation, but its mechanism remains poorly understood. The purpose of this study was to investigate whether splenic regulatory T-cell （Treg） apoptosis was involved in the postresuscitation immune dysfunction. Methods： Thirty-eight pigs were randomly divided into sham-operated group （SHAM group, n - 8）, 12 h post return of spontaneous circulation （ROSC） group, 24 h post-ROSC group, and 48 h post-ROSC group （n = 10 per group）. A Wuzhishan miniature porcine model of 8-min ventricular fibrillation cardiac arrest （CA） was established. The apoptosis rates of Treg in the spleen were tested by flow cytometry; the expressions of forkhead/winged helix transcription factor （Foxp3） of Treg in the spleen were detected by real-time polymerase chain reaction; and the levels ofinterleukin-4 （IL-4）, IL- 10, and interferon gamma （IFN-γ） of Treg in the spleen were detected by enzyme-linked immunosorbent assay. Results： The apoptosis rates of Treg in all post-ROSC groups were significantly lower than that of SHAM group （7.7% ± 1.9%, 7.1% ±1 .8%, 6.2% ± 0.4% vs. 13.1% ± 1.6%： P 〈 0.05）; the expression levels of Foxp3 and IL- 10 were also decreased with the increase ofapoptosis rates of Treg. Helper T-cells CD4^＋ lymphocyte subsets were significantly lower in the post-ROSC groups compared with SHAM group （29. 1% ± 2.2%, 24.3% ± 2.2%, 24.1% ± 2.5% vs. 43.8%± 4.5%; P 〈 0.01 ） at 12, 24, and 48 h after ROSC. Compared with SHAM group, the levels of IFN-,/（161.0 ± 12.9, 167.7 ± 10.5, 191.2 ± 7.7 vs. 7.6 ± 0.9 rig/L） and 1L-4 （27.7 ± 6.2, 35.9 ± 3.5, 50.6 ± 6.1 vs. 13.3 i 2.3 ng/L） and the ratio of IFN-y/IL-4 （8.6 ± 2.3, 4.9 ± 0.4, 4.5 ± 0.9 vs. 0.8 ± 0.2） were all greatly elevated in all post-ROSC groups （P 〈 0.05）. Conclusions： Apoptosis rate of Treg was significantly decreased after CA, and thus the proportion of Treg was increased and the inhibitory effects were enhanced, which further led to the decrease of the amount ofCD4^＋ T-cells. In addition, the T helper type 2/T helper type 1 （Th2/Th 1） cell drift of Treg in the spleen caused postresuscitation immune dysfunction.

INTRODUCTION Despite a higher incidence of postoperative complications, splenectomy is a commonly performed procedure for splenic space-occupying lesions. A retrospective analysis of 2796 splenectomy patients showed that 119 patients （4.25%） had postoperative bacterial infections,