带蒂筋膜管的耳大神经移植治疗面神经缺失性损伤

Inthepresentstudy，greatauricularnervecoatedbypediculatedfascialtubenearfacialnervetrunkwasusedtotreatdefectivedamageoffacialnerve．Andthefunctionalrecoveryoffacialnervewasmoreapparentthangraftinggreatauricularnervealone．Thestudyisre－portedasfollowing．１Subjectandmethod１．１Subject（１）Threecasesofotogenicfacialparalysis．Case１，male，８yearsold．Hasnecrotizingexternalotitisintherightearandfacialparalysisfor１２months．Case２，female，３６yearsold．Haspa－pillomaofexternalauditorycanal…     

奇曼丁治疗晚期癌症疼痛的疗效

Itisestimatedthat７０％patientssufferedfromadvancedtumorsdevelopedpainofdifferentextent．Painaffectsqualityoflifedirect－ly，mind，psychology，socialandpersonalrelationandleadtodis－comfort犤１犦．WiththespreadingofWHOthree－stepmanagement，ad－ministrationwaysaretransformedfromdemanddependanttotimedepend犤１犦．Tramcontin（slowreleasedtramadol），theweakthebaicdrug，cancontrolmoderatepain．１Subjectandmethod１．１Subject１１６caseswithpathologicallyandradiologicallyprovedadvancedtumors（６…     

高压氧对动物有机磷中毒后神经损害恢复的实验研究

１Subjectandmethod１．１Subject１６healthyNewZealandrabbitsaging６monthsandweightingfrom１．５kgto２．０kg，meanweight：（１．６７±２．０）kg，wereprovidedbyAnimalcenterDepartmentofGeneralHospitalofFuzhouMilitaryRegion．５０％oxidizingorgor（orgonicphospho－rus）wereperfusedintorabbit＇sstomach，５０mg／kg．Acutepoisoningmodelsofratswereestablished．Allratswererandomlydividedintohyperbaricoxygenandcontrolgroups．１．２MethodRabbitsinhyperbaricoxygengroupweretreatedwithHBO，２０minutesea…     

大叶性肺炎并中毒性休克病人的护理

护理评估１．１一般资料：李某某，男，５６岁，已婚，干部。１．２活动运动型态：１．２．１全身皮肤湿冷，肢体末梢紫绀，烦躁不安，血压１１／６ｋＰａ。１．２．２端坐呼吸。血气分析：氧分压降低，二氧化碳分压上升，氧饱和度下降。１．２．３由于吸氧、发热及机械通...     

焦虑情绪与海员高血压及相关因素的分析

FromAugusttoOctober１９９７，wefoundanxietycorrelatewithbloodpressureapparently．Sowemakefurtherstudyontherela－tionshipofanxietyandprevalencerateofmarinehypertensionandmarinehypertensionrelatedsusceptiblefactors．１Subjectsandmethod１．１Subjects４２０１seamenreceivedSASandquestionnaireinquiry，４０４８caseswerevalid．Allthecasesweremale，averageagewas（２３．８１±４．３２）．Allthecasesworknormally１weekbeforeinquirywithoutspecialmissioninfluencesuchasdistalsail，longsail．１．２Method（…     

献血员手臂消毒效果检测的实验报告

搞好献血员手臂消毒是防止血液污染及献血员感染的重要措施。２０００年１月至６月，我们对１００名无偿献血员手臂进行细菌监测和消毒效果对比观察，现报道如下：１材料和方法１．１材料１．１．１普通肥皂、流动自来水、０．２％过氧乙酸、１：２００的“８４”消毒液、１：５００的“８４”液。１．１．２１％Na２S２O３、３％吐温８０１．２方法１．２．１分组方法：第一组，献血员手臂未清洗采样；第二组，献血员用肥皂流动水洗手３分钟，洗至肘部１０厘米以上，３分钟后采样；第三组，用肥皂流动水洗手３分钟后，用０．２％过氧乙酸…     

间歇导尿术对糖尿病神经原性膀胱治疗效果的评价

FromJanuary２０００toJanuary２００１，２１patientswithin－tractablediabeticneurogenicbladderweretreatedusingintermittenturethralcatheterization，２０patientsofthesameperiodwereselectedascontrols．Weobtainedgoodtherapeuticeffect，hereisthereport．１Subjectandmethod１．１Subject４１inpatientswithdiabeticneurogenicbladderconfirmedbyclinicalandexperimentalexaminationenteredourstudy．DiabeteswasdiagnosedaccordingtoADAcriteria．５patientswerediabetestype１，２６werediabetestype２．Thesepatientsin…     

软组织肿瘤的组织学分类

软组织肿瘤的组织学分类１纤维组织肿瘤１．１良性１．１．１纤维瘤１．１．２瘢痕瘤或称瘢痕疙瘩１．１．３结节性筋膜炎１．１．４增生性肌炎及增生性筋膜炎（与增生性肌炎相似病变，发生于浅筋膜及皮下）１．１．５弹力纤维瘤１．１．６婴儿纤维性错构瘤１．１．７孤立...     

尼莫地平对脑梗死患者康复期认知功能干预的临床和实验研究

Rehabilitationofpatientswithcerebralinfarctionreliesondrugtherapyprimarily．Nimodipine，asthebrain－protectingdrugfortreatmentofdementia犤１犦isoneofwidelyuseddrugsinclinicinChina．However，recently，therewasmuchmorecontroversiesovertheeffectofnimodipineoncognitivefunctioninavarietyofre－ports犤２～５犦．Combininganimalexperimentwithclinicalfingidngs，weinvestigateimpactofnimodipineoncognitionrehabilitation．１Materialandmethod１．１Material（１）Animals：IsolatedWistarratswereprovidedbyAni…     

肉毒素和肿瘤坏死因子对大白鼠肝功能的影响

１MaterialsandMethods１．１ExperimentalanimalsSDmaleratswiththeageof１monthproducedinShanghai，weightedfrom９０gto１００g．１．２MainreagentsandinstrumentsDMEMmedium（providedbyGIBCOcompanyofUSA），０．０３％collagenaseⅠsolutions５０ml（SigmaCorporation，withDMEMassolvent），phosphoricbuffersolution（PBS）２５０ml，RDB－７８peristalsispump（InstrumentCorporationofZhangjiaganginJiangsu），cen－trifugalapparatusofBiofuge１５R，productionofGermanycompa－ny．１．３Separationandcultu…     

大鼠视网膜缺血再灌注损伤中ICAM-1 mRNA的表达及意义

【目的】为了解视网膜缺血再灌注损伤中不同时期ICAM-1表达的动态变化,探讨其在视网膜缺血再灌注损伤中的作用。【方法】建立结扎颈总动脉的视网膜缺血再灌注损伤模型。35只SD大鼠被随机分为缺血再灌注1h,6h,12h,24h,48h,72h及对照组,以原位杂交法(ISH法)检测视网膜组织中的ICAM-1的表达状态。【结果】在缺血再灌注损伤1h,未见ICAM-l的表达,在缺血再灌注6h,ICAM-1开始表达,至第24h表达最强,第48h开始减弱,但第72h仍有表达。【结论】ICAM-1在视网膜缺血再灌注损伤中可能发挥着重要作用。     

大鼠深Ⅱ度烫伤后创面自噬及凋亡的表达规律

目的 观察大鼠深Ⅱ度烫伤后72 h内创面自噬及凋亡的表达规律,探讨其与深Ⅱ度创面早期加深之间的关系.方法 Wistar大鼠背部10％ TBSA深Ⅱ度烫伤,观察烫伤后1h、6h、12 h、24 h、48 h、72 h创面组织自噬标志蛋白LC3、Beclin-1的表达及变化规律;TUNEL法检测创面凋亡水平的变化规律;HE染色及Masson染色显示创面组织形态和创面深度的变化.结果 烫伤后创面组织LC3、Beclin-1蛋白水平持续下降,至伤后24h达到最低,此后稍有升高,但仍远低于正常水平;伤后创面组织TUNEL阳性细胞持续增多,至伤后48 h达到最高,此后稍有下降,但仍远高于正常水平;创面组织真皮深层自噬被激活;烫伤后创面深度随着时间的推移进行性加深.结论 大鼠深Ⅱ度烫伤后早期创面组织自噬减少,凋亡增加,可能是参与创面加深的因素;真皮深层自噬的激活,可能是一种保护机制.     

黏附分子与树突状细胞在大鼠肝和肾缺血-再灌注损伤中作用及抗黏附干预的影响

目的 探讨黏附分子P-选择素、ICAM-1及树突状细胞(DC)在大鼠肝和肾缺血-再灌注损伤中作用，以及抗P-选择素单抗的抗黏附抑制及其防治效果。方法 分别建立肝和肾缺血-再灌流损伤大鼠模型，随机分为P-选择素单抗治疗组(n=20)和非治疗组(n=20)，按不同再灌注时间(1，3，6和24h)再分为4组，每组5只，另设两组另设假手术组(n=5)作为对照。采用免疫组化LSAB法和免疫双染与荧光图像分析法，分别观察和比较各组大鼠肝、肾组织P-选择素、ICAM-1表达及DC分布变化。结果 (1)缺血-再灌注1h起，P-选择素即以肝窦内皮细胞或肾小管上皮细胞为主于肝和肾内广泛高表达，至24h仍维持一定水平；ICAM-1于缺血-再灌注6h起持续以肝窦和肾血管为主表达上调和明显增强。(2)CDla^ CD80^ DC白再灌注1h起以肝窦和肾小管间质为主分布数量逐渐增多，至24h达峰，并与大鼠肝、肾功能密切相关。(3)经抗P-选择素单抗处理后，大鼠肝、肾组织P-选择素和ICAM-1表达受到抑制，CDla^ CD80^ DC分布及数量减少，组织病理损伤及肝、肾功能也相应减轻和改善。结论 DC可能通过黏附分子尤其P-选择素早期介导的肝、肾组织内迁移聚集，参与启动了肝、肾缺血-再灌注时的免疫病理损伤过程，而抗P-选择素单抗对此具有抗黏附调抑和防治效果。     

Recovery from glycerol-induced acute kidney injury is accelerated by suramin

Acute kidney injury (AKI) is a common and potentially life-threatening complication after ischemia/reperfusion and exposure to nephrotoxic agents. In this study, we examined the efficacy and mechanism(s) of suramin in promoting recovery from glycerol-induced AKI, a model of rhabdomyolysis-induced AKI. After intramuscular glycerol injection (10 ml of 50% glycerol per kilogram) into male Sprague-Dawley rats, serum creatinine maximally increased at 24 to 72 h and then decreased at 120 h. Creatinine clearance (CrCl) decreased 75% at 24 to 72 h and increased at 120 h. Suramin (1 mg/kg i.v.) administered 24 h after glycerol accelerated recovery of renal function as demonstrated by increased CrCl, decreased renal kidney injury molecule-1, and improved histopathology 72 h after glycerol injection. Suramin treatment decreased interleukin-1β (IL-1β) mRNA, transforming growth factor-β(1) (TGF-β(1)), phospho-p65 of nuclear factor-κB (NF-κB), and cleaved caspase-3 at 48 h compared with glycerol alone. Suramin treatment also decreased glycerol-induced activation of intracellular adhesion molecule-1 (ICAM-1) and leukocyte infiltration at 72 h. Urinary/renal neutrophil gelatinase-associated lipocalin 2 (NGAL) levels, hemeoxygenase-1 expression, and renal cell proliferation were increased by suramin compared with glycerol alone at 72 h. Mechanistically, suramin decreases early glycerol-induced proinflammatory (IL-1β and NF-κB) and growth inhibitory (TGF-β(1)) mediators, resulting in the prevention of late downstream inflammatory effects (ICAM-1 and leukocyte infiltration) and increasing compensatory nephrogenic repair. These results support the hypothesis that delayed administration of suramin is effective in abrogating apoptosis, attenuating inflammation, and enhancing nephrogenic repair after glycerol-induced AKI.     

The cytokine-adhesion molecule cascade in ischemia/reperfusion injury of the rat kidney. Inhibition by a soluble P-selectin ligand.

Ischemia/reperfusion (I/R) injury associated with renal transplantation may influence both early graft function and late changes. The initial (</= 7 d) events of warm and in situ perfused cold ischemia of native kidneys in uninephrectomized rats were examined. mRNA expression of the early adhesion molecule, E-selectin, peaked within 6 h; PMNs infiltrated in parallel. T cells and macrophages entered the injured kidney by 2-5 d; the associated upregulation of MHC class II antigen expression suggested increased immunogenicity of the organ. Th1 products (IL-2, TNFalpha, IFNgamma) and macrophage-associated products (IL-1, IL-6, TGFbeta) remained highly expressed after 2 d. To examine directly the effects of selectins in I/R injury, a soluble P-selectin glycoprotein ligand (sPSGL) was used. Ischemic kidneys were perfused in situ with 5 microg of sPSGL in UW solution; 50 microg was administered intravenously 3 h after reperfusion. E-selectin mRNA remained at baseline, leukocytes did not infiltrate the injured organs throughout the 7-d period, and their associated products were markedly inhibited. Class II expression did not increase. No renal dysfunction secondary to I/R occurred. The early changes of I/R injury may be prevented by treatment with soluble P- and E-selectin ligand. This may reduce subsequent host inflammatory responses after transplantation.     

Burn injury induces an early activation response by lymph node CD4+ T cells

Several reports have shown that burn injury primes the immune system for an early and vigorous proinflammatory CD4 T cell response, suggesting that injury might signal CD4 T cell activation. We addressed this possibility by investigating changes in CD4 T cell activation marker expression, proliferation, and T cell receptor (TCR) usage at several early time points after burn injury. Using a sensitive flow cytometry approach to measure changes in the expression of Ki-67 antigen, a nuclear protein detected only in proliferating cells, we observed an early burst of proliferation by lymph node, but not spleen, CD4 T cells 12 h after burn injury. In contrast, mice that were treated with the bacterial superantigen staphylococcal enterotoxin B (SEB) as a positive control for in vivo T cell activation did not show this early proliferation. Instead, we observed a significant increase in proliferating lymph node and spleen CD4 and CD8 T cells by 3 days after SEB treatment. Burn injury induced higher cell surface CD25 and CD152 expression on lymph node CD4 T cells, whereas SEB treatment increased CD25 and CD69 expression on CD4 and CD8 T cells. Finally, we found that burn injury induced a proliferative response at 12 h by an oligoclonal subset of TCR Vbeta-chain-expressing CD4 T cells (Vbeta4, Vbeta6, Vbeta11, and Vbeta14). Interestingly, CD4 T cells expressing the Vbeta11-TCR remained significantly increased in the lymph nodes 3 days after burn injury. Taken together, these findings indicate that burn injury induces an early proliferation and activation of CD4 T cells in the regional lymph nodes and that these proliferating cells show restricted TCR Vbeta-chain usage consistent with the idea that injury triggers an early T cell activation signal.     

Endogenous interleukin-6 enhances the renal injury, dysfunction, and inflammation caused by ischemia/reperfusion

Here, we investigate the effects of renal ischemia/reperfusion (I/R) on the degree of renal injury, dysfunction, and inflammation in interleukin (IL)-6 knockout (IL-6(-/-)) mice and mice administered a monoclonal antibody against IL-6. IL-6(-/-) mice were subjected to bilateral renal artery occlusion (30 min) and reperfusion (24 h). At the end of experiments, indicators and markers of renal dysfunction, injury, and inflammation were measured. Kidneys were used for histological evaluation of renal injury. Renal expression of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and P-selectin, as well as nitration of proteins in the kidney, were determined using immunohistochemistry. In addition, wild-type mice were pretreated (24 and 1 h before ischemia) with an IL-6 antibody to mimic the effects that would be seen in IL-6(-/-) mice. IL-6(-/-) mice and wild-type mice administered the IL-6 antibody demonstrated significantly reduced plasma urea and creatinine levels, indicating reduction of renal dysfunction caused by I/R. Neutrophil infiltration was also significantly reduced in IL-6(-/-) mice and wild-type mice administered the IL-6 antibody subjected to renal I/R. Proinflammatory cytokines (tumor necrosis factor-alpha and IL-1beta) in renal tissues were significantly attenuated in IL-6(-/-) mice to levels seen in wild-type mice. IL-6(-/-) mice demonstrated reduced histological evidence of tubular injury and markedly reduced immunohistochemical evidence of ICAM-1, P-selectin, and nitrotyrosine when subjected to renal I/R. We propose that endogenous IL-6 enhances the degree of renal injury, dysfunction, and inflammation caused by I/R of the kidney by promoting the expression of adhesion molecules and subsequent oxidative and nitrosative stress.     

高密度脂蛋白对严重烧伤大鼠肝组织保护的组织学观察

目的：探讨高密度脂蛋白（HDL）对严重烧伤大鼠肝脏的保护作用。方法：制作大鼠30％体表Ⅲ度烫伤模型，观察正常对照组（不作任何处理），烧伤组（烫伤后30min补充平衡溶液）及实验组（烫伤后立即静脉注入HDL）。伤后12、24、48、72h4个时间点的肝组织学变化和细胞间粘附分子1（ICAml）的表达。结果：（1）组织学观察：烫伤后各组大鼠肝细胞均有不同程度损伤，其中以烧伤组伤后24h最重，肝窦扩张充血，窦内炎细胞浸润，肝细胞变性，点灶性坏死，实验组24h肝组织学改变与烧伤组比较上述损伤明显改善。正常对照组肝组织结构基本正常。（2）ICAm-1免疫组化检测：正常对照组无表达，烧伤组与实验组ICAm-1平均表达率分别为81．6％（49／60）及36．6％（22／60），两组24h时段的表达率分别为86．6％（13／15）及20％（3／15），烧伤组表达强度明显高于实验组（P〈O．01），而两组各其他时段表达强度差异无显著性（P〉0．05）。结论：严重烧伤大鼠早期应用HDL对抑制肝细胞中ICAm-1的表达，减少肝细胞免疫损伤有良好的效果。     

Cardiomyocyte function after burn injury and lipopolysaccharide exposure: single-cell contraction analysis and cytokine secretion profile

A component of multiorgan dysfunction in burned patients is heart failure. Burn trauma induces cytokine synthesis of interleukin (IL) 1beta, IL-6, and tumor necrosis factor alpha (TNF-alpha) which can negatively impact cardiac function. Infectious complications are common following severe burn injury. We hypothesized that burn injury and lipopolysaccharide (LPS) exposure independently influence peak cardiomyocyte contraction and cytokine secretion. Rats underwent a full-thickness 30% total body surface area scald or sham burn. At 1, 6, 12, and 24 h after burn, cardiomyocytes were isolated and incubated with increasing LPS doses. Peak sarcomere shortening and contractile velocity parameters were recorded using a variable-rate video camera with sarcomere length detection software. Supernatants were assayed for IL-1beta, IL-6, and TNF-alpha by ELISA. Peak sarcomere shortening was decreased in the burn group at 1, 6, 12, and 24 h after burn. IL-1beta, IL-6, and TNF-alpha levels were increased in cardiomyocytes isolated 1 h after burn compared with sham controls, but returned to sham levels at 6, 12, and 24 h after burn. LPS exposure caused dose-dependent decreases in sarcomere shortening in sham and burn animals. LPS exposure did not produce increased cardiomyocyte cytokine expression. Burn injury diminished peak sarcomere shortening. Whereas exposure to LPS did not have an effect on cardiomyocyte cytokine expression, LPS significantly inhibited sarcomere shortening in a dose-dependent fashion. Combined burn and LPS exposure inhibited sarcomere shortening more than each alone. These results demonstrate that LPS exposure and burn injury independently decrease peak cardiac shortening. These decreases did not directly correlate with the levels of cytokines released in response to each stressor.     

Differential activation of coronary and pulmonary endothelial cells by thermal injury.

Remote organ dysfunction during resuscitation of severe thermal injury is characterized by early, transient pulmonary insufficiency and cardiac contractile dysfunction. Thermal injury is typified by profound systemic alterations of endothelial immunological, vasoactive, and barrier functions. The unique location of this ubiquitous, fragile monolayer makes it vulnerable to circulating serum factors created at remote cutaneous wounds. We examined endothelial "activation" in 2 distinct cell types, human coronary and pulmonary endothelial cells (EC), after severe thermal injury. By using human serum isolated at specific times after thermal injury ("early" [2 h post-burn] or "late" [26 h post-burn]), the endothelial release of vasoactive mediators, ICAM-1 expression, and monolayer permeability were assessed in vitro. Early burn serum enhanced coronary EC vasoconstrictor (ET-1) release and ICAM expression, inhibited vasodilator (PGI2) release, but had no effect on permeability. Conversely, under similar conditions, pulmonary EC PGI2 release and permeability were enhanced, ET-1 release was diminished, but ICAM was unaffected. Late burn serum enhanced vasodilator (NO) release and permeability to albumin in both coronary and pulmonary EC, whereas ET-1 release was inhibited. Under these conditions, only pulmonary ICAM expression was significantly enhanced. These data suggest that human endothelium isolated from divergent vascular beds are activated by burn injury in a unique manner for time post-burn and vascular site of cell origin.