退行性腰椎侧凸的炎症反应

BACKGROUND: Degenerative lumbar scoliosis patients will appear to have abnormal changes in various cytokines in the serum of the body, which is closely related to patient’s pathogenesis. OBJECTIVE: To monitor the changes in the serum levels of tumor necrosis factor-α, interleukin-6 and interleukin-1β during the onset of degenerative lumbar scoliosis. METHODS: Sixty-six patients with degenerative lumbar scoliosis were enrolled as observation group, and according to Schwab evaluation system, there were 16 cases of type I, 32 of type II, and 18 of type III. Additionally, 60 healthy persons undergoing homochronous physical examination were extracted as control group. Blood samples were taken at preoperative 1, 2, 3 weeks and at postoperative 1, 2, 3, 4, 5, 6 weeks to determine serum levels of tumor necrosis factor-α, interleukin-6 and interleukin-1β as well as to observe the relevant changes. RESULTS AND CONCLUSION: In the observation group, the levels of tumor necrosis factor-α, interleukin-6 and interleukin-1β were increased gradually at 1-3 weeks before treatment, and then showed a decrease trend at 6 weeks after treatment. Compared with the control group, in the observation group, the levels of tumor necrosis factor-α were significantly higher at 1-4 weeks after admission (P < 0.05); the levels of interleukin-6 and interleukin-1β were significantly higher at 1-5 weeks after admission (P < 0.05). These findings indicate that the levels of tumor necrosis factor-α, interleukin-6 and interleukin-1 reached the peak at 1 week before treatment, and then gradually decreased. Changes in the levels of tumor necrosis factor-α, interleukin-6 and interleukin-1β have an important role to assess disease development, which can be used to determine the severity of inflammation based on which we can select the appropriate treatment.      

急性不完全脊髓损伤模型大鼠相关炎症因子的表达

背景：随着现代交通和工矿事业的发展,脊髓损伤成为临床常见的多发病,严重的影响了人类身心健康和生活质量。 目的：检测在大鼠急性脊髓损伤模型中磷酸化信号转导与转录激活因子3（p-STAT3）介导的IL-1β、IL-6、IL-17等炎症因子的表达变化情况,探讨IL-1β、IL-6、IL-17等炎症因子在急性脊髓损伤后炎症反应过程中的作用。 方法：雄性成年SD大鼠75只,随机分为对照组和脊髓损伤1h、6h、24h和72h四个亚组（n=15只）。采用改良Allen氏法建立脊髓损伤模型,对照组仅行椎板全切除术。在建模之后相应的时间点获取损伤段脊髓、脾脏组织,免疫组织化学染色法检测IL-6和IL-17在损伤段脊髓组织中的分布及表达情况,蛋白免疫印迹法检测p-STAT3在损伤段脊髓组织中的表达变化,采用RT-PCR法检测IL-1βmRNA、IL-6mRNA和IL-17AmRNA在脾脏组织中的表达情况。 结果与结论：脊髓损伤后p-STAT3、IL-1β、IL-6和IL-17的表达明显高于对照组（P＜0.05）。损伤后炎症因子表达量立即升高,IL-1β和IL-6在损伤后6h小时到达高峰,随后开始下降;p-STAT3和IL-17在损伤后24h到达高峰,随后开始下降,至损伤后72h表达量仍高于对照组。损伤早期p-STAT3介导的促炎因子IL-1β和IL-6表达增加,可能导致损伤区域炎症级联放大,诱导继发性脊髓损伤;促炎因子IL-17的异常升高,可能在继发性损伤炎症反应中起着重要作用。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

转化生长因子β信号与肌肉调控

BACKGROUND: Transforming growth factor-β signaling widely existing in cells mediates cell growth, proliferation, migration, differentiation, and apoptosis. The activation of transforming growth factor-β signaling can result in muscular dystrophy. However, there have been some contradictions regarding the effects of the transforming growth factor-β signaling on muscular dystrophy. OBJECTIVE: To summarize the latest progress in the effects of the transforming growth factor-β signaling on muscle mass and function regulation to provide the solutions for the treatment of muscular dystrophy. METHODS: A computer-based online search was conducted in PubMed and Wanfang databases from 2005 to 2015 to screen the relevant literatures using Chinese and English key words “transforming growth factor-β, muscle, regulation mechanism, treatment”. A total of 102 literatures were retrieved, and 22 eligible literatures were included, summarized, and analyzed. RESULTS AND CONCLUSION: The activation of transforming growth factor-β signaling as a common cause of most muscle disorders promotes the activation of muscle satellite cells, differentiation of myocytes, myoblast infusion, the expression of muscle-specific proteins, and the inhibition of collagen synthesis, which facilitates muscular fibrosis and scar formation. Transforming growth factor-β signaling is involved in Duchenne muscular dystrophy, spinal scoliosis, type I diabetes induced skeletal muscle regenerative disorders, myocardial and cardiac remodeling. The inhibition of transforming growth factor-β signaling may result in incomplete muscle recovery. 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

神经调节蛋白1β与卡托普利对慢性心衰大鼠心肌纤维化及转化生长因子β1的影响

目的:探讨神经调节蛋白1β(neuregulin-1β,NRG-1β)与卡托普利联合应用对慢性心力衰竭大鼠心肌纤维化及转化生长因子β1(transforming growth factor-β1,TGF-β1)表达的影响。方法:将青年雄性SpragueDawley大鼠随机分为假手术组、心衰组、NRG组、卡托普利组和联合用药组,采用腹主动脉-下腔静脉穿刺造瘘法制备心衰模型。通过超声心动图评价大鼠心功能;Masson染色检测心肌纤维化程度,并计算胶原容积分数(collagen volume fraction,CVF);放射免疫法检测血浆中血管紧张素II(Ang II)的浓度;Western blot检测各组大鼠左心室心肌组织中TGF-β1和α-平滑肌肌动蛋白(α-SMA)的蛋白表达水平;透射电镜观察左室心肌的超微结构。结果:与心衰组比较,NRG组、卡托普利组及联合用药组左心室舒张末直径和心肌纤维化程度明显降低,射血分数明显升高(P0.05);TGF-β1和α-SMA蛋白表达明显降低(P0.05);电镜下显示,NRG组、卡托普利组及联合用药组心肌纤维化程度较心衰组明显减轻,而与NRG组和卡托普利组相比,联合用药组效果更加显著(P0.05)。结论:神经调节蛋白1β与卡托普利单用及联合应用均可有效改善心功能、抑制心肌纤维化,且联合用药的疗效优于单独用药。     

高加速度环境作用颞下颌关节软骨基质成分与相关生长因子及炎性因子的变化

背景：强大的加速性能可产生持续性高正加速度(+Gz),使颞下颌骨关节内部受到各种方向的压力和撞击,引起微小创伤,进而引发颞下颌关节紊乱病症。目的：观察颞颌关节紊乱后软骨关节基质成分Ⅱ型胶原、多糖聚糖体、胶原酶以及胰岛素样生长因子1、转移生长因子β1、肿瘤坏死因子α、白细胞介素2与白细胞介素3的变化。方法：建立不同持续性正高加速度(+Gz)环境和作用时间下的大鼠模型,分成阴性对照组,+5 G加速度组,+10 G加速度组。按不同+Gz值进行正高加速度模拟处理,离心5 min,4 d/周,每天连续离心5次,共持续3周;阴性对照组大鼠按相同时间和频次只在离心机的固定装置上固定5 min,不做持续高正加速度离心处理,每天离心前所有动物均空腹12 h。分离并体外培养各组大鼠的颞下颌软骨细胞,提取总蛋白,Western Blot检测。结果与结论：与阴性对照组比较,在持续性高加速度下,颞下颌关节软骨细胞的软骨基质成分Ⅱ型胶原、多糖聚糖体、胶原酶以及胰岛素样生长因子1、转移生长因子β1明显减少,肿瘤坏死因子α、白细胞介素2与白细胞介素3显著增高。结果说明在持续性高正加速度下,颞下颌关节软骨基质成分受到严重影响,修复能力下降,炎症反应增加。 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程全文链接：     

全髋关节置换后早期创伤局部引流血和循环血中的相关细胞因子水平

背景：对于全髋关节置换后创伤早期的应激阶段,创伤局部和全身细胞因子动态变化规律的研究还鲜见报道。 目的：观察全髋关节置换后早期无菌性炎症阶段创伤局部引流血和全身循环血中相关细胞因子水平的动态变化。 方法：选取行全髋关节置换患者9例,分别在关闭伤口时、置换后1,4和24 h采集静脉血样本以及创伤局部引流血液样本;采用酶联免疫吸附法分别测定血清中白细胞介素6,肿瘤坏死因子α,白细胞介素1β和白细胞介素17水平。 结果与结论：全髋关节置换后早期创伤局部引流血和循环血中白细胞介素6水平均明显升高,并且在各个时间点上创伤局部引流血中白细胞介素6水平均高于循环血(P < 0.05);置换后早期循环血中肿瘤坏死因子α水平明显升高,创伤局部引流血肿瘤坏死因子α的水平无明显变化,但仍高于循环血中的水平(P < 0.05);白细胞介素1β和白细胞介素17的水平在置换后无显著改变,且在创伤局部和循环中的含量无显著性差异。结果提示在全髋关节置换后急性无菌性炎症阶段,循环血中炎性细胞因子的水平不会直接反映局部的炎症反应。     

转化生长因子-β1,2在不同发育阶段皮肤组织中的定位及表达量的变化

目的:探讨转化生长因子-β_{1, 2}(TGF-β₁和TGF-β₂)与α-平滑肌肌动蛋白(α-ASMA)在胎儿和成人皮肤中的分布和表达变化规律。方法:20例被测标本中包括不同胎龄的胎儿皮肤15例和成人皮肤5例。用免疫组化方法和病理技术确定这3种蛋白在不同发育阶段皮肤中的定位和表达量。结果:在妊娠早期的胎儿皮肤中, TGF-β_{1, 2}和α-ASMA呈弱阳性表达, 随着胎儿生长发育, 这3种蛋白的阳性细胞率逐渐增大;在妊娠晚期胎儿和成人皮肤中这3种蛋白的表达量明显多于妊娠早期胎儿皮肤(P＜0.01)。TGF-β_{1, 2}的阳性信号主要存在于表皮细胞, 内皮细胞和部分成纤维细胞中, α-ASMA蛋白定位于肌成纤维细胞和汗腺上皮细胞内。结论:TGF-β₁和TGF-β₂可能在皮肤的发生、结构和功能的维持以及皮肤损伤后的修复中起重要作用。     

大鼠皮肤创伤修复过程中转化生长因子β1和β3的表达

背景：转化生长因子β在组织创伤修复中发挥核心和关键作用。 目的：观察转化生长因子β1和转化生长因子β3在大鼠皮肤瘢痕性创伤愈合过程中表达量及表达部位的变化。 方法：制备大鼠皮肤全层切伤模型,长度1.5-2.0 cm,深及筋膜层。于伤后0 h,12 h,1 d,2 d,3 d,4 d,5 d,6 d,7 d处死大鼠,取损伤部位皮肤,采用免疫组织化学染色检测各时间点转化生长因子β1和转化生长因子β3的表达,并进行定量分析。 结果与结论：免疫组织化学染色显示,在创伤愈合的早期阶段(伤后1-5 d),转化生长因子β1和转化生长因子β3免疫阳性颗粒主要出现在上皮细胞、上皮基底层细胞胞浆、巨噬细胞等免疫细胞胞浆及肉芽组织中;随着创伤修复时间的持续,免疫阳性颗粒主要出现在真皮层的成纤维细胞及细胞外基质中。其中转化生长因子β1的表达在创伤后1-5 d最强,而转化生长因子β3在创伤后六七天时开始明显表达。可见在大鼠皮肤瘢痕性创伤愈合过程中,转化生长因子β1的表达先于转化生长因子β3,提示转化生长因子β1与胶原形成及创伤修复关系密切,而转化生长因子β3在愈合后期表达量有升高趋势,其可能与创伤后期的组织改建密切相关。     

大鼠急性心肌梗死后NLRP3炎性体-IL-1β信号轴激活与End-MT的关系

目的:研究在急性心肌梗死(acute myocardial infarction,AMI)引发的心肌纤维化过程中,NLRP3炎性体-IL-1β信号轴的激活与内皮-间充质转化(endothelial-mesenchymal transition,End-MT)是否存在同一性。方法:30只成年雄性SD大鼠随机分为假手术组(n=15)与AMI组(n=15),术后28 d采用Masson染色检测心肌纤维化水平;Western blot检测NLRP3炎性体(NLRP3、ASC、pro-caspase-1和caspase-1)、内皮细胞标志物(CD31和VE-cadherin)及间充质细胞标志物(α-SMA和FSP1)的表达;酶联免疫吸附法检测NLRP3炎性体下游因子IL-1β的表达。结果:与假手术组相比,冠脉结扎组AMI大鼠心肌纤维化水平、End-MT进展程度、NLRP3炎性体活性及caspase-1和IL-1β的表达均显著增加(P0.05)。结论:NLRP3炎性体-IL-1β信号轴的激活与End-MT进程具有显著同一性,提示NLRP3炎性体-IL-1β作为激活End-MT的潜在靶点将为研究AMI后心肌纤维化及心力衰竭提供新的理论依据。     

不同浓度尿酸钠对大鼠滑膜细胞炎性因子的影响

背景：利用尿酸钠刺激滑膜细胞制备体外急性痛风性关节炎滑膜模型,在评价治疗这类疾病药物作用机制方面有重要意义。 目的：通过不同浓度尿酸钠体外直接刺激滑膜细胞后滑膜细胞细胞因子的浓度变化,探讨急性痛风性关节炎滑膜模型制备条件。 方法：培养大鼠滑膜细胞,分别添加终浓度为0(空白组),50,125,250,500,1 000 μmol/L的尿酸钠进行干预,于培养24,48 h后测定细胞活力及培养液中细胞因子白细胞介素1β、白细胞介素8、肿瘤坏死因子α的浓度。 结果与结论：各组在24,48 h内药物对细胞活力无影响。与空白组比较,尿酸钠干预组在24,48 h培养液中细胞因子白细胞介素1β、白细胞介素8、肿瘤坏死因子α浓度均提高,尿酸钠浓度为500 μmol/L,给药时间为24 h,培养液中各细胞因子浓度最高。说明利用一定浓度尿酸钠和刺激时间,便于筛选理想的急性痛风性关节炎体外模型。     

Histological changes in the genital tract in transsexual women following androgen therapy

Thirty-two young women who desired sexual reassignment were treated with large doses of androgen for a period of 1 year or more, followed by total hysterectomy. Histological examination revealed marked atrophy of cervical epithelium which could mimic dysplasia, and variable degrees of endometrial atrophy. The ovaries showed occasional corpora lutea indicating that even in the face of long term androgen therapy, ovulation may occur.     

Histological skeletal muscle damage and surface EMG relationships following eccentric contractions

This study examined the effects of a different number of eccentric contractions (ECs) on histological characteristics, surface electromyogram (EMG) parameters (integral EMG, iEMG; muscle fiber conduction velocity, MFCV; and action potential waveform), and isometric peak torque using the rat EC model. Male Wistar rats (n = 40) were anesthetized, and ECs were initiated in the tibialis anterior muscle via electrical stimulation while the muscle was being stretched by electromotor. The rats were grouped according to the number of ECs (EC1, EC5, EC10, EC20, EC30, EC40, and EC100). Three days after the ECs, surface EMG signals and isometric peak torque were measured during evoked twitch contractions via electrical stimulation of the peroneal nerve. The muscle damage was evaluated from hematoxylin-eosin (HE) stained cross sections as a relative number of damaged fibers to intact fibers. Intense histological muscle damage (approximately 50% to 70% of the fiber), loss of isometric peak torque, disturbance of action potential waveform, and depression of iEMG (approximately -60% to -70%) were observed at EC20, EC30, EC40, and EC100. On the other hand, the MFCV did not change in any EC group. Although muscle damage and pathological surface EMG signals were not found at EC10, isometric peak torque was reduced significantly. In conclusion, the extent of histological muscle damage is not proportionally related to the number of ECs. Muscle damage was reflected by iEMG and action potential waveforms, but not by MFCV, which remained unaffected even though approximately 50% to 70% of the fiber demonstrated injury.     

Histological changes in the hypofunctional pituitary gland following conventional radiotherapy for adenoma

AIMS: Although delayed hypopituitarism is a common complication of conventional radiotherapy of sellar tumours, histological changes that may account for it have been rarely reported. To elucidate the changes, hypofunctional pituitary glands following irradiation were studied. METHODS AND RESULTS: Two pituitary glands obtained at autopsy from patients who had been irradiated for adenoma and exhibited hypopituitarism were examined. In both cases diffuse fibrosis was observed in the adenohypophysis, whereas the neurohypophysis remained unchanged. Immunohistochemistry showed that stellate-shaped S100 protein-positive cells were increased in number and distributed among the endocrine cells. Some irradiated endocrine cells showed dense granular immunoreactivity for mitochondrial protein, cytochrome oxidase and manganese-superoxide dismutase. In addition to faint reactivity with anti-cytokeratin 8, 18 antibody, many cells were densely positive with anti-cytokeratin 1, 5, 10, 14 antibody. CONCLUSIONS: These results indicate that radiation- induced fibrosis is associated with an increased number of folliculo-stellate cells and the presence of metabolic dysfunctional mitochondria resembling mitochondria in oncocytes. Squamous metaplasia in the irradiated endocrine cells was also noted. Various intracellular changes may participate in delayed pituitary hypofunction following radiotherapy.