牙周炎患者龈沟液白细胞介素—1β检测及意义

目的：检测牙周炎患者龈沟液（gingival crevicular fluid,GCF)中白细胞介素－1β(interleukin-1β,IL-1β)的含量,探讨IL－1β在牙周炎发病中的作用。方法：用滤纸条浸润法采集正常成年人及成年人牙周炎患者治疗前后GCF样本,用酶联免疫吸附法（ELISA）检测GCF中IL－1β含量变化,牙周炎患者龈沟液中IL－1β水平显著高于正常对照组（P＜0．01）,牙周炎治疗组患者龈沟液中IL－1β水平较牙周炎组显著降低（P＜0．01）,龈沟液中IL－1β水平分别与牙龈指数,探诊出血指数,牙周袋深呈显著正相关,结论：IL－1β参与牙周炎的发生和发展,GCF中IL－1β可作为检查牙周病活动情况的一项较为敏感的指标。     

听宫穴针刺及注射利多卡因治疗神经性耳鸣

目的：探讨针刺听宫穴注射昨多卡因治疗神经性耳鸣的效果。方法：对神经性耳鸣80例采用针刺听宫穴得气后注射2％利多卡因1ml。结果：80例中治愈58例、66耳,显效10例、12耳、有效6例、6耳,无效6例、8耳。结论：突聋伴耳鸣及噪声性耳鸣且病程短短者疗效好,外伤性耳鸣及原因不明耳鸣者疗效较差。此法简便易行、安全,无毒副作用。     

Effect of high-BDNF microenvironment stem cells therapy on neurogenic bladder model in rats

BackgroundThe purpose of this study is to explore the effects of high-BDNF microenvironment produced by engineered immortalized mesenchymal stem cells (imMSCs) on the neurogenic bladder (NB) and investigate underlying mechanism.MethodsMale Sprague-Dawley rat (12-week-old, weighing about 370–400 g) were purchased from a Korean company (Orient Bio Co. Seongnam, Korea) and divided into the following groups (n=32): sham control group (n=8), NB group (n=8), NB + ImMSCs group (n=8), NB + ImMSCs (BDNF) group (n=8). The major pelvic ganglion (MPG) was observed under anesthesia. Three NB groups of rats were then subjected to bilateral MPG injury. The sham control group of rats was treated with sham surgery. Cystometry were performed before the rats were sacrificed, and then MPG and bladder were collected for histochemical and Western blot analysis.ResultsMSCs treatment improves lower urinary tract function, and the NB + ImMSCs (BDNF) group is better than the NB + ImMSCs group (P<0.01). MSCs treatment accelerates recovery of injured nerve tissue, and the NB + ImMSCs (BDNF) group is better than the NB + ImMSCs group (P<0.01). In high BDNF environment, apoptosis was reduced more significantly and muscle tissue recovered more rapidly (P<0.01). High-BDNF microenvironment activates more BDNF/TrkB/CREB signaling pathways (P<0.01).ConclusionsIn a rat NB model caused by nerve injury, imMSCs have certain effects on nerve tissue repair. At the same time, it was proved that increasing the expression of BDNF which had specific effect on nerve injury repair could more effectively repair injured MPG in local microenvironment. The mechanism may be related to the activation of the BDNF/TrkB/CREB signaling pathway and the reduction of apoptosis by highly expressed BDNF.     

p53基因突变与肺癌发生的早期遗传学损害

在进行肺癌与ｐ５３基因关系的系列研究过程中，发现１例支气管粘膜上皮不典型增生和１例原位癌，运用免疫组织化学方法进行ｐ５３蛋白表达检测，结果发现支气管上皮不典型增生和原位癌组织中有明显的ｐ５３蛋白阳性染色细胞，从而进一步证实了ｐ５３基因突变可能是肺癌发生的早期遗传学损害。     

不同组织来源的成纤维细胞的生物学特性比较

目的 探讨来自政治家皮肤、增生性瘢痕和瘢痕疙瘩组织的成纤维细胞的生物学特性。方法 对三种组织均采用组织块法进行细胞的原代培养,采用胰蛋白酶消化传代,分别利用绘制细胞生长曲线,^H-胸腺嘧啶掺入及^3H-脯氨酸掺入等方法观察细胞的增殖,DNA合成代谢及胶原合成等情况。并比较它们之间的差异。结果 瘢痕疙瘩成纤维细胞在细胞增殖、DNA合成代谢及胶原合成量等方面均明显高于正常皮肤及增生性瘢痕组织来源的成纤维细胞。后两者之间有一定区别但无统计学意义。结论 不同组织来源的成纤维细胞其生物学行为亦有所区别,因此,在进行实验研究时应有一定的针对性。     

面神经颅外段局部解剖与临床应用

目的：为颌面部外科手术、整形及美容手术提供面神经颅外段的应用解剖学资料。方法：在20具成人尸体、50具新生儿、1－6岁儿童尸体的139例头面部标本上,对面神经颅外段的根、干、支、丛等进行解剖观察分析。结果：（1）面神经出颅以后以一根型为主,共为138侧,占99．28％。（2）面神经干以二干为主,共122例,占87．77％。（3）上干的分支以颞支（T）、颧支（Z）、颊支（B）为主,即TZB型113侧,占89．68％。下干分支以颊支（B）、下颌缘支（M）、颈支（C）即（BMC）为主85侧,占77．98％;（4）分支形成的神经丛以TZB型最多见为87侧,占55．41％。颊支以2支为主共77例,占55．40％。结论：根据颌面部手术及整形、美容术的不同要求,对面神经加以保护和选择性应用。     

Clinical observation on treatment of tubal pregnancy by chinese herbal medicine combined with tubal intubation administration of methotrexate under uteroscope

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IL-2对小鼠脾淋巴细胞体内迁移的影响

目的:观察白细胞介素-2(Interleukin-2,IL-2)对淋巴细胞体内迁移的影响.方法:选用近交系小鼠为实验动物,背部剃毛,皮内注射细胞因子,同时尾静脉输注3H-UR标记的淋巴细胞.20h后,切取注射区皮块,制样后测定样品计数率.经计算后将计数率转换成细胞浓度因子(Cell concentration factor,CCF),用CCF值反应淋巴细胞迁移的水平.结果:IL-2注射区淋巴细胞迁移量与对照组无明显差异(P＞0.05),而且IL-2与肿瘤坏死因子-α联合应用时,亦没有协同作用.结论:提示在复杂的体内环境中,IL-2对小鼠脾淋巴细胞体内迁移无明显诱导作用.     

TNF-α和IFN-α对淋巴细胞迁移至小鼠皮肤区的影响

目的　体内观察TNF -α和IFN -α两种细胞因子对淋巴细胞迁移至小鼠皮肤区的影响。方法　以近交系BALB/C小鼠为实验动物 ,皮内注射细胞因子 ,尾静脉输注标记的淋巴细胞 ,然后切取注射区皮块 ,制样后行乳化计数测量。测量值计算后转化成细胞浓度因子 (CCF) ,用CCF值反应淋巴细胞迁移的水平。结果　TNF -α和IFN -α注射区CCF值均高于对照(P <0 0 1) ;且TNF -α与IFN -α联合应用的CCF值是TNF -α和IFN -α各自应用之和的 137%。结论　TNF -α及IFN-α可以体内诱导淋巴细胞迁移至小鼠皮肤区内。     

Proteomics reveals a global phenotypic shift of NK cells in HCV patients treated with direct-acting antivirals

Chronic hepatitis C virus (HCV) infections compromise natural killer (NK)-cell immunity. Direct-acting antivirals (DAA) effectively eliminate HCV, but the long-term effects on NK cells in cured patients are debated. We conducted a proteomic study on CD56⁺ NK cells of chronic HCV-infected patients before and 1 year after DAA therapy. Donor-variation was observed in NK-cell proteomes of HCV-infected patients, with 46 dysregulated proteins restored after DAA therapy. However, 30% of the CD56⁺ NK-cell proteome remained altered 1 year post-therapy, indicating a phenotypic shift with low donor-variation. NK cells from virus-negative cured patients exhibited global regulation of RNA-processing and pathways related to “stimuli response”, “chemokine signaling”, and “cytotoxicity regulation”. Proteomics identified downregulation of vesicle transport components (CD107a, COPI/II complexes) and altered receptor expression profiles, indicating an inhibited NK-cell phenotype. Yet, activated NK cells from HCV patients before and after therapy effectively upregulated IFN-γ and recruited CD107a. Conversely, reduced surface expression levels of Tim-3 and 2B4 were observed before and after therapy. In conclusion, this study reveals long-term effects on the CD56⁺ NK-cell compartment in convalescent HCV patients 1 year after therapy, with limited abundance of vesicle transport complexes and surface receptors, associated with a responsive NK-cell phenotype.