目的 初步观察脓毒症小鼠脾脏树突状细胞(DC)焦亡情况及其与炎性因子水平、DC免疫功能的相关性.方法 70只BALB/c小鼠随机分为假手术组(n=20)、脓毒症模型组(CLP组,n=30)与胱天蛋白酶(CASP)-1抑制剂干预组(CLP+YVAD组,n=20),CLP组和CLP+YVAD组按术后不同时间点分为CLP 12 h组、CLP 24 h组、CLP 48 h组、CLP 72 h组及CLP+YVAD 24 h组、CLP+YVAD 72 h组.所有小鼠于术后预定时间眼眶取血、处死并取脾脏组织.流式细胞仪测定脾脏DC焦亡率及表面标志物(CD80、CD86、MHC-Ⅱ)表达水平,激光共聚焦显微镜观察CASP-1在小鼠脾脏DC中的活化情况,Western blotting检测DC中CASP-1的表达情况,ELISA法检测血清中肿瘤坏死因子(TNF)-α、白细胞介素(IL)-12、IL-1β、IL-6浓度;观察CLP术后小鼠死亡情况.提取BALB/c小鼠T细胞与各组小鼠脾脏DC共培养,采用流式细胞仪测定T细胞增殖率,ELISA法检测共培养上清中γ干扰素(IFN-γ)、IL-4、IL-10浓度.结果 与假手术组比较,DC焦亡率在CLP术后12 h升高(P<0.05),于24 h达高峰(P<0.01),随后呈下降趋势,至72 h仍高于假手术组(P<0.01).激光共聚焦显微镜观察显示,CLP术后小鼠脾脏DC CASP-1活化明显.Western blotting检测结果显示,DC中焦亡蛋白CASP-1表达在脓毒症早期(12 h和24 h)较假手术组明显上调(P<0.01).而给予CASP-1特异性抑制剂Ac-YVAD-cmk后,CLP+YVAD 24 h组DC焦亡率较CLP 24 h组下降(P<0.01),CLP+YVAD 72 h组DC表面标志物CD80、MHC-Ⅱ表达水平较CLP 72 h组上调(P<0.01),术后7 d小鼠生存率提高(P<0.01).ELISA法检测结果显示,CLP小鼠血清TNF-α、IL-12、IL-1β和IL-6浓度在脓毒症早期(24 h)和后期(72 h)均较假手术组明显升高(P<0.01),而CLP+YVAD组血清内上述因子浓度明显下降(P<0.01).共培养实验结果显示,与DC-CLP 24 h组比较,DC-CLP+YVAD 24 h组T细胞增殖率明显增高(P<0.01),共培养上清中IFN-γ水平下降,而IL-4、IL-10水平上升(P<0.01).结论 DC焦亡在脓毒症早期启动并持续存在,可能是脓毒症状态下炎性因子水平异常增高和DC免疫功能抑制的病理生理机制之一,且与脓毒症预后不良相关.

目的 探究脓毒症状态下老年小鼠脾脏树突状细胞(dendritic cell,DC)功能状态的异常改变及其与高尔基体应激反应和自噬反应的内在联系.方法 不同年龄小鼠(青年鼠 8周龄,老年鼠18 月龄)分别随机分为假手术组与脓毒症模型组(CLP组)(n =4).CLP组小鼠于术后24h处死并取脾脏组织.采用免疫磁珠法分离纯化脾脏DC,流式细胞术检测各组DC表面标志物及共刺激分子(CD80、CD86、MHC-Ⅱ)表达水平.分离纯化不同年龄小鼠脾脏DC,各自分为空白对照组、LPS刺激组(1 μg/mL)(n =4).免疫印迹法检测各组细胞高尔基体应激反应相关蛋白——高尔基体磷蛋白 3(Golgi phosphoprotein 3,GOLPH3)、高尔基体重组堆积蛋白 2(Golgi reassembly stacking protein of 55 kDa,GRASP55)以及高尔基体自噬相关蛋白高尔基体蛋白亚家族A成员2(Golgi matrix protein,GM130)、微管相关蛋白 1A和 1B(microtubule-associated proteins 1A and 1B,MAP1LC3B)表达水平.激光共聚焦显微镜检测高尔基体红色荧光探针(Golgi-tracker Red)在各空白对照组中的显示情况.进一步应用抑制高尔基体蛋白转运的莫能菌素(monensin,MON)(1 μg/mL)预处理,检测扰乱高尔基体稳态对小鼠DC功能分化的影响.结果 与青年小鼠比较,老年脓毒症模型小鼠脾脏DC活化障碍显著.CLP术后 24h老年小鼠脾脏DC表面标志分子CD80、CD86、MHC-Ⅱ表达升高水平明显低于青年小鼠(P<0.05).对比健康小鼠脾脏DC胞内高尔基体的结构功能状态发现,与青年小鼠比较,老年DC胞内高尔基体结构蛋白GRASP55、GM130 呈高表达(P<0.001),提示高尔基体结构肿胀;高尔基体外膜蛋白GOLPH3表达减弱(P<0.001),提示蛋白修饰及转运功能低下.分离提取不同年龄小鼠脾脏DC进行体外培养并给予LPS刺激,发现脓毒症老年小鼠DC胞内高尔基体应激反应增强、自噬明显,与DC功能障碍密切相关.给予MON抑制高尔基体蛋白转运,观察到青年、老年小鼠DC胞内高尔基体均发生显著应激与自噬反应,青年小鼠DC免疫功能活化障碍,老年小鼠功能障碍则更为显著.结论 老年小鼠DC中高尔基体结构肿胀且功能受损,造成DC免疫功能活化障碍,与老年脓毒症免疫抑制密切相关.

脓毒症是由于感染引起机体宿主反应失调，最终导致多脏器功能障碍的临床综合征，是当今重症监护病房（ICU）患者的主要死亡原因之一。据统计，2017年全球脓毒症患者病死率已达到22.5%，约占全球总死亡患者的五分之一 [1]。脓毒症发病机制复杂，主要涉及过度炎症反应、免疫功能紊乱、凝血功能障碍等，多系统功能失调相互影响、相互促进，通过网络状效应加剧脓毒症的恶性发展 [2]。免疫应答与凝血系统相互作用失调时，易导致多级血管中形成微小的免疫血栓（immunothrombosis），是诱发弥散性血管内凝血（DIC）和多器官衰竭的主要原因。临床资料显示，30%~50%的脓毒症患者会发生DIC，其病死率高达28%~43% [3]。因此，免疫血栓发病本质和干预途径问题日益受到关注与重视，已成为脓毒症研究的重要领域之一。

目的:研究严重烧伤小鼠体内高水平高迁移率族蛋白B1(HMGB1)诱导脾脏树突状细胞(DC)凋亡与内质网应激(ERS)的关系.方法:①复制严重烧伤小鼠模型,检测脾脏与血清中HMGB1的表达.②烧伤模型小鼠和假烫组(37℃水浴)均随机分为3组,分别给予抗HMGB1中和抗体、未免疫兔血清IgG和生理盐水,观察烧伤各组及生理盐水处理假伤组小鼠7 d生存率,并测定各组脾脏DC细胞ERS相关蛋白GRP78和XBP-1的表达.③正常小鼠尾静脉注射10或20μg重组HMGB1,48 h后处死,测定脾脏GRP78和XBP-1的表达.④以1、10、100 ng/ml HMGB1体外刺激健康小鼠的脾脏DC,并进一步应用细胞凋亡抑制剂Salubrinal(Sal)于HMGB1刺激1 h前进行干预,流式细胞术检测DC凋亡;Western blot法检测DC内ERS相关因子GRP78和CHOP的表达水平.分析HMGB1诱导DC细胞凋亡与ERS的内在联系.结果:小鼠烧伤后HMGB1蛋白表达水平增高.抗HMGB1中和抗体对严重烧伤小鼠有明确保护作用,可提高严重烧伤小鼠7 d存活率,显著降低烧伤小鼠脾脏DC内ERS标志分子GRP78以及ERS介导细胞凋亡的关键分子CHOP的蛋白水平.HMGB1(10 ng/ml)刺激可直接诱导DC凋亡以及ERS相关细胞凋亡关键分子CHOP蛋白表达升高;Sal干预可缓解ERS并抑制HMGB1诱导的DC凋亡(P<0.05).结论:HMGB1刺激诱导DC凋亡与ERS相关性细胞凋亡通路激活密切相关,是严重烧伤小鼠脾脏DC功能障碍的重要发病机制.

Objective To investigate the effect of skin-resident regulatory T cells (Tregs) on wound healing after burn injury. Methods 60 Foxp3DTR mice and 60 wild-type C57BL/6 mice were included in the present study. The Foxp3DTRdiphtheria toxin (DT) injection group (F-DT group) and the wild-type DT injection group (C-DT group) were further divided into early (n=9) and late (n=9) groups according to the random number table method. In the early group, mice were injected intraperitoneally with DT during the early stage (–1, 0 and 3rd days ofter injury) after burns, while in the late group, mice were injected at the late stage (5th, 7th and 9th days after injury). We took photos of mouse wounds at different time points, and measured the wound area to assess wound healing rate. After HE staining, re-epithelialization of the wound was observed under light microscope. In addition, flow cytometry was used to analyze changes in local infiltration and functional expression of Tregs in skin of wild-type mice at different time points after burns. Results Compared with the C-DT group, the rate of burn wound healing in the F-DT early group was significantly reduced (P 0.05). In comparison to the C-DT group, HE staining in the F-DT early group revealed slower wound closure process and slower scar formation and crusting process, together with faster granulation tissue formation and obvious slower angiogenesis and re-epithelialization. Using flow cytometry to analyzing the infiltration of skin Tregs, CD4+ Foxp3+ T cells were significantly increased after burns, and gradually returned to basal level after reaching peak on day 5 (P<0.05). While CD25+ Treg cells were markedly decreased to baselines after peaking on day 3 (P<0.05). In addition, CTLA-4 expressions of skin Tregs was significantly enhanced after burns, and peaked on day 3 after burns, then gradually decreased to baseline values (P<0.05), while ICOS reached peak on day 5 postburn, and gradually decreased to normal range on day 11 (P<0.05). Conclusion The skin Tregs appear to be infiltrated into the wounds during the early stage after injury, which might contributes to promoting wound healing following burns. DOI: 10.11855/j.issn.0577-7402.2020.06.02

目的:探讨白细胞介素(IL)-33对小鼠脾脏树突状细胞(DC)功能的影响及其与脓毒症免疫抑制的关系.方法:小鼠随机分为3组:盲肠结扎穿孔(CLP)组采用CLP方法复制脓毒症小鼠模型;假伤组除不行盲肠穿孔外,其他处理方法同CLP组;可溶性IL-33受体(sST2)干预组于CLP术后1 h经腹腔注射重组sST2(每只10μg,溶于200μl PBS中),同批对照CLP组同时给予200μl PBS腹腔注射.应用免疫磁珠分离提纯小鼠脾脏DC.正常小鼠脾脏DC体外培养并给予不同浓度(0、1、10、100 ng/ml)、不同时间(12和24 h)重组IL-33刺激.应用流式细胞术检测各样本DC表面标志、共刺激分子CD80、CD86、主要组织相容性复合物-Ⅱ(MHC-Ⅱ)表达水平.Western blot检测小鼠脾脏IL-33蛋白表达.结果:与假伤组比较,CLP小鼠脾脏组织IL-33蛋白水平术后24～72 h明显升高,虽然DC表面CD80表达水平有所升高,但CD86、MHC-Ⅱ表达水平均显著降低(P＜0.01).CLP术后1 h给予sST2以中和IL-33可改善DC功能状态,DC表面CD80、CD86、MHC-Ⅱ表达水平均显著增强(P＜0.01),小鼠存活率也有一定程度的提高.正常小鼠脾脏DC体外培养,重组IL-33体外刺激(10 ng/ml,24 h)可直接诱导DC表面CD86、MHC-Ⅱ表达降低(P＜0.05),与CLP模型小鼠脾脏DC体内改变趋势相似.结论:IL-33可直接诱导DC成熟分化障碍,是引发脓毒症小鼠免疫细胞功能抑制的重要因素;拮抗IL-33生物效应可有效地改善DC功能状态,对脓毒症动物发挥保护作用.

Objective: To explore influence of vagus nerve on multiple organ function and immune reaction of T lymphocytes in septic rats. Methods: Forty Sprague-Dawley rats were divided into sham injury group, sepsis group, vagus nerve stimulation (VNS) group, and vagotomy (VGX) group, according to the random number table, with 10 rats in each group. Rats in sepsis group, VNS group, and VGX group were inflicted with sepsis by cecal ligation and puncture (CLP). Rats in VNS group were given electrical stimulation on left cervical vagus nerve for 15 min right after CLP. Rats in VGX group underwent vagotomy of left cervical vagus nerve at 30 min before CLP. At 24 h after CLP, serum of rats was collected to detect levels of alanine transaminase (ALT), aspartate aminotransferase (AST), glycocholic acid (CG), creatine kinase (CK), myocardial creatine kinase (CK-MB), blood urea nitrogen (BUN), and serum creatinine by fully automatic biochemistry analyzer. The left lung of rats was collected to determine wet or dry mass, and wet to dry (W/D) ratio was calculated. The right lung of rats was collected to measure the activity of pulmonary myeloperoxidase (MPO) by enzyme linked immunosorbent assay (ELISA). Spleen of rats was collected to determine the proliferative activity of CD4(+) T lymphocytes by cell counting kit 8, and real-time fluorescence quantitative polymerase chain reaction and ELISA were used to quantify mRNA expressions and levels of interleukin 2 (IL-2), interferon-γ, and IL-4, respectively. Data were processed with one-way analysis of variance and Tukey's honest significant difference test. Results: (1) The levels of serum ALT, AST, CG, CK, CK-MB, BUN, and creatinine, pulmonary W/D ratio, as well as MPO activity of rats in sepsis group were significantly higher than those in sham injury group and VNS group (P<0.01) and were significantly lower than those in VGX group (P<0.01). (2) The proliferative activity of CD4(+) T lymphocytes of rats in sepsis group was 0.93±0.03, which was significantly lower than 1.54±0.07 of rats in sham injury group (P<0.01). The proliferative activity of CD4(+) T lymphocytes of rats in VNS group was 1.15±0.15, which was significantly higher than that of rats in sepsis group (P<0.01). The proliferative activity of CD4(+) T lymphocytes of rats in VGX group was 0.75±0.06, which was obviously lower than that of rats in sepsis group (P<0.01). (3) In comparison with those of rats in sham injury group, the levels of IL-2 and interferon-γ in CD4(+) T lymphocytes of rats in sepsis group were markedly decreased (P<0.01), while the level of IL-4 was significantly increased (P<0.01). In comparison with those of rats in sepsis group, the levels of IL-2 and interferon-γ in CD4(+) T lymphocytes of rats in VNS group were obviously increased (P<0.01), while the level of IL-4 was markedly decreased (P<0.01). As compared with those of rats in sepsis group, the levels of IL-2 and interferon-γ in CD4(+) T lymphocytes of rats in VGX group were markedly decreased (P<0.01), while the level of IL-4 was significantly increased (P<0.01). (4) As compared with those of rats in sham injury group, expressions of IL-2 and interferon-γ mRNA in CD4(+) T lymphocytes of rats in sepsis group were markedly decreased (P<0.01), while expression of IL-4 mRNA was significantly increased (P<0.01). Expressions of IL-2 and interferon-γ mRNA in CD4(+) T lymphocytes of rats in VNS group were obviously increased when compared with those of rats in sepsis group (P<0.01), while expression of IL-4 mRNA was markedly decreased (P<0.01). In comparison with those of rats in sepsis group, expressions of IL-2 and interferon-γ mRNA in CD4(+) T lymphocytes of rats in VGX group were markedly decreased (P<0.01), while expression of IL-4 mRNA was significantly increased (P<0.01). Conclusions: Electrical stimulation of vagus nerve can significantly improve multiple organ dysfunction and reverse immunosuppression of T lymphocytes in septic rats, while vagotomy of vagus nerve may enhance the susceptibility of rats to sepsis.

目的:探讨IL-6对脓毒症小鼠脾脏调节性树突状细胞(DCregs)的免疫调节作用.方法:85只雄性BALB/c小鼠随机分为5组:假手术组(n=5),除不行盲肠结扎穿孔(CLP)外,其余操作同模型组;CLP组和3个IL-6治疗组(n=20)均采用CLP方法制备脓毒症模型.假手术组于手术当天处死,其余4组小鼠分别于CLP模型制作后1、2、3、4d处死,获取脾脏DC细胞和T细胞,3个IL-6治疗组细胞分别给予IL-6(50、100、200u g/kg)体外刺激24 h,收集DC细胞和T细胞,并进一步分离和培养DCregs(CD11c-CD45RBhighDCregs)和CD4+T淋巴细胞,观察各组小鼠DCregs细胞比例和DCregs分泌IL-10的变化.以假手术组CD4+T细胞为对照组,将CLP小鼠的DCregs分别和CLP小鼠CD4+T淋巴细胞(IL-6未刺激组)、经IL-6刺激的CLP小鼠CD4+T淋巴细胞+IL-10抗体、经IL-6刺激的CLP小鼠CD4+T淋巴细胞+IL-10同型对照抗体混合培养24 h,观察各组CD4+T淋巴细胞增殖及细胞培养上清中IFN-γ、IL-4水平的变化.结果:IL-6可呈剂量依赖性促进DCregs分化及促进Dcregs分泌IL-10;IL-6还抑制了CLP小鼠CD4+T淋巴细胞增殖和诱导Th2极化,降低CLP小鼠IL-4的水平,这一作用与IL-10的分泌相关.结论:IL-6可诱导CLP小鼠DC向调节性DC细胞亚群分化并诱导IL-10的分泌,诱导CD4+T淋巴细胞向Th2分型,从而调节机体免疫功能.

脓毒症 ( sepsis) 是创伤、 烧伤、 大手术及严重感染等临床急危重症患者的主要并发症之一, 以机体对感染的异常应答为显著特征, 进一步发展可诱发休克及多器官功能障碍综合征 ( MODS ) , 甚至死亡. 2012 年脓毒症与脓毒性休克 ( septic shock) 处理指南特别推荐早期目标导向治疗( EGDT) 的液体复苏方案, 然而近几年的临床资料表明, EGDT方案并不能改善脓毒性休克患者预后[ 1?4]. 2016年新版指南给予脓毒性休克新的定义, 即有效的容量复苏后, 仍出现低血压 (升压药维持下平均血压 ≥60 mmHg ) , 血乳酸 >2 mmol/L; 同时, 进一步明确改善循环功能是缓解脓毒性休克的主要措施, EGDT 方案虽被移除,但最优的液体管理方案及时机尚无明确定论[5].深入探讨脓毒性休克的发病机制, 将为探寻有效的临床救治方案提供新的契机.

目的 观察特异性拮抗高迁移率族蛋白B1(HMGB1)对烫伤小鼠白细胞介素-35(IL-35)表达及T淋巴细胞免疫功能的影响.方法 选择成年雄性BALB/c小鼠30只,按随机数字表法分为正常组、假伤组、烫伤组、Abox干预组,正常组6只,其余各组每组8只.将小鼠背部皮肤置于97℃恒温热水中6s造成约15％体表面积烫伤模型,Abox干预组小鼠烫伤后2h和12h腹腔注射HMGBl特异性拮抗剂Abox 300μg.烫伤后24 h处死小鼠,取心、肝、脾、肺等组织,用酶联免疫吸附试验(ELISA)测定各组织中HMGB1和IL-35含量;用实时荧光定量反转录-聚合酶链反应(qRT-PCR)分析IL-35亚基p35和EB病毒诱导基因3(EBI3)的mRNA表达水平;由脾脏提取单个核细胞检测HMGB1和IL-35分泌水平,分离脾脏淋巴细胞检测效应T细胞增殖活性及IL-2、γ-干扰素(IFN-γ)、IL-4分泌水平.结果 与烫伤组比较,Abox干预后,各器官HMGB1含量和脾脏单个核细胞HMGB1分泌水平显著降低[心脏(mg/g):65.78±4.42比110.49±11.19,肝脏(mg/g):50.90±3.72比117.77±8.10,脾脏(mg/g):83.34±3.90比149.84±11.93,肺脏(mg/g):125.15±8.75比236.20±17.51,脾脏单个核细胞(μg/L):34.57±0.69比73.66±19.03];各器官组织p35和EBI3的mRNA表达[相对定量(RQ)值]及IL-35蛋白水平均有不同程度下降[p35 mRNA(RQ值):心脏为0.91±0.62比19.74±18.05,肝脏为0.42±0.19比14.85±8.39,脾脏为1.99±1.12比21.94±6.90,肺脏为0.50±0.21比5.15±3.46;EBI3 mRNA(RQ值)心脏为0.63±0.61比74.25±15.19,肝脏为0.64±0.09比56.59±19.99,脾脏为1.24±0.48比32.72±3.34,肺脏为0.30±0.06比2.41±1.43;IL-35蛋白(μg/g:心脏为142.40±19.95比241.64±12.40,肝脏为272.68±14.90比409.76±21.60,脾脏为66.94±9.60比92.28±8.82,肺脏为235.88±15.65比193.50±27.06;均P＜0.05),脾脏T淋巴细胞增殖活性增强(A值:1.26±0.26比1.03±0.05)及IL-2分泌水平也显著升高(ng/L:153.48±26.64比101.77±34.55),IFN-γ/IL-4比值显著增加(7.44±1.70比0.33±0.07),差异均有统计学意义(均P＜0.01).结论 特异性拮抗HMGB1可显著下调烧伤小鼠重要组织IL-35表达水平,有效促进脾脏T细胞增殖及Thl功能极化,从而有助于改善严重烧伤后免疫抑制状态.

为观察微电极射频电化学疗法治疗内痔的疗效,将内痔患者120例随机分为治疗组和对照组,每组60例.治疗组采用微电极射频电化学疗法治疗,对照组采用铜离子电化学疗法治疗.结果显示,两组对痔出血疗效相近(P＞0.05),但治疗组凝固点少,治疗时间短(P＜0.05).两组对痔脱出近期有效率相近(P＞0.05).但治疗组术后肛管黏膜溃疡发生率少于对照组(P＜0.05).结果表明,微电极射频电化学疗法使内痔的手术治疗由微创向无创的方向迈进了一步,其更具有实用性.

目的 探讨小针刀侧方内括约肌切断术治疗肛裂的临床疗效.方法 对我院2008年6月至2010年6月收治的60例肛裂患者采用小针刀侧方内括约肌切断术的临床资料作回顾性分析.结果 治愈57例,好转2例,未愈1例,治愈率为95%,无外科需要处理的并发症.结论 小针刀侧方内括约肌切断术治疗肛裂具有安全、有效、创伤小、恢复快、并发症少等优点.

目的:探讨痔上黏膜环切钉合术联合消痔灵注射治疗重度痔脱垂的临床疗效。方法:36例重度痔脱垂患者均采用痔上黏膜环切钉合术联合消痔灵注射治疗,观察临床疗效、术后并发症、术后1年复发率。结果:36例中治愈35例,好转1例,无需外科处理的并发症,术后1年复发1例。结论:痔上黏膜环切钉合术联合消痔灵注射治疗重度痔脱垂具有安全、有效、疼痛轻、恢复快等优点。

Objective To evaluate the efficacy and patient satisfaction of the deroofing technique for perianal hidradenities suppurativa(HS) lesions.Methods An open study consisted of 12 HS patients treated by Deroofing technique by follow-up of 13-60 months.Results 2 patients treated lesions recurrenced after a median of 6 months.10 patients treated lesions did not show a recurrence after a median follow-up 33 moths.Conclusion The deroofing technique is an effective,simple,minimally invasive,and tissue-saving surgical intervention for the treatment of perianal HS lesions.

Objective To explore the clinical features of Fournier's gangrene and the prognostic factors.Methods Retrospective analyzed medical records of patients with Fournier gangrene over the last 5 years in our hospital.Results 30 patients were studied in the study.After aggressive surgical debridement,29 cases were cured,and 1case died.Conclusion Early diagnosis of disease and aggressive surgical debridement combined use of broad spectrum antibiotics,and general supportive therapy is the key to successful treatment of Fournier gangrene.

<正>慢性肛瘘继发黏液腺癌是临床上一种非常罕见的直肠癌,由于对本病认识不足,难以早期诊断。回顾性分析我院1995—2010年收治的4例慢性肛瘘继发黏液腺癌患者的临床资料,总结诊治经验,报告

Objective To evaluate the clinical features,pathology,treatment,and outcome of patients with fistula-associated anal adenocarcinoma.Methods A retrospective study was made to analyze clinical,treatment,and pathological features of 4 cases mucinous adenocarcinoma from chronic anal fistula.Results The canceration of anal fistula was due to chronic inflammation and scarring.The definitive diagnosis of the carcinoma depends on biopsy of the fistula and the related tumor.Conclusion If surgical treatment for perineal abscess or anorectal fistula is not successful for a long time,mucinous adenocarcinoma should be suspected.Biopsy of fistulous tracts and perianal abscesses are thus paramount in the early diagnosis and subsequent treatment of these tumours.

目的 观察丙酮酸乙酯(EP)对肝脏热缺血再灌注损伤是否具有保护作用.方法 20只Wistar大鼠随机均分为正常对照组(A组)和假手术组(B组).肝I/R损伤模型采用钳夹除肝脏尾叶血管外的肝蒂90min,然后切除未缺血的尾叶方法制备,此模型可使95%肝脏缺血.另120只随机均分为肝缺血再灌注损伤(HIRI组,C组,接受HIRI),Ringer氏液组(D组,HIRI前尾静脉注射Ringer氏液),EP治疗组(E组,HIRI前尾静脉注射浓度为3.262mg/ml的EP4ml).A组取静脉血检测血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)水平,随即处死取肝脏标本测丙二醛(MDA)含量;B组假手术后2h取标本;C、D、E组于术后2、8、24、48h取血,每组每个时间点处死10只取肝组织检测.结果 与A组比较,B组血清ALT、AST水平和肝组织MDA含量仅轻度变化.与C组比较,D和E组在灌注8 h、24 h时血清ALT、AST水平均显著降低(均P<0.01),尤其是E组.同时,EP治疗组在2h时肝组织MDA含量显著低于D和C组(均P<0.01).结论 肝脏热缺血再灌注损伤早期EP可显著降低脂质过氧化损伤,从而发挥其对肝脏的保护作用.

目的 探讨高迁移率族蛋白B1(HMGB1)在大鼠肝脏热缺血/再灌注(I/R)损伤中的作用.方法 90只Wistar大鼠被随机分为正常对照组、林格液组、丙酮酸乙酯(EP)治疗组.采用夹闭左、右肝蒂使95%肝脏缺血90 min再恢复血流并切除未缺血的尾叶肝脏制模.林格液组和EP治疗组制模前分别经阴茎背静脉注射林格液4 ml或EP 3.26 g/L(溶于林格液4 ml中),于术后2、8、24、48 h取下腔静脉血检测血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)水平,处死动物后检测肝组织HMGB1、肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10)含量.结果 林格液组和EP治疗组血清ALT、AST水平均显著高于正常对照组,EP治疗组各时间点ALT及术后2 h、8 h AST水平均显著低于林格液组(P<0.05或P<0.01).林格液组8、24、48 h肝组织HMGB1水平显著高于正常对照组,EP治疗组仅48 h显著升高;EP治疗组在8 h、24 h时HMGB1水平显著低于林格液组;林格液组和EP治疗组在8 h时TNF-α水平均高于正常对照组,而EP治疗组显著低于林格液组(P<0.05或P<0.01).各组IL-10水平无明显差异.结论 HMGB1参与了肝I/R损伤的病理过程.