早期先天性肌性斜颈38例诊治体会

先天性肌性斜颈是一侧胸锁乳突肌发生纤维变性后引起挛缩而形成的畸形,病因和发病机制目前尚未确定。早期发现有一定的困难,治疗方法颇多,但以早期为佳。笔者自1980年以来,用普鲁卡因和强的松龙注射液注射挛缩的胸锁乳突肌,治疗早期先天性肌性斜颈38例,方法简便安全,疗效满意。体会如下:     

MMP-2、MMP-7、MMP-9在先天性肌性斜颈中的表达及意义

目的观察基质金属蛋白酶-2,7,9（MMP-2、MMP-7、MMP-9）在先天性肌性斜颈胸锁乳突肌的表达情况,探讨先天性肌性斜颈胸锁乳突肌纤维化的发生机制。方法免疫组织化学染色法观察先天性肌性斜颈病变组和正常对照组胸锁乳突肌MMP-2、7、9的表达情况。结果免疫组织化学染色法可见对照组绿色的胶原纤维极少,肌肉型组和纤维型组胶原纤维明显增多。MMP-2,7,9在纤维型组中表达比在对照组及肌肉型组中明显减少（P〈0.01）;在肌肉型组中表达略有增加,与对照组相比无统计学意义（P〉0.05）。结论 MMP-2,7,9表达下降可能是导致胶原过度沉积、SCM细胞外基质纤维化加重的重要因素。     

小儿先天性斜颈矫正术的护理

先天性肌性斜颈是一侧胸锁乳突肌发生纤维性挛缩后形成的畸形,是小儿常见的先天性疾病之一。发病原因是一侧胸锁乳突肌在难产时受伤发生出血、机化,以致纤维变性后引起该肌挛缩。患儿出现斜颈畸形,重者面部不对称。长葛市人民医院自2002年以来,对18例先天性斜颈患儿行矫正术,经过随访及信访,效果满意。现将笔者对18例先天性斜颈患儿的护理报告如下。     

先天性肌性斜颈—临床类型,病因与术式关系探讨

对２２３例经手术矫治的先天性肌性斜颈的临床资料进行分析，对该病的发生原因提出了新的观点，在临床上分为纤维型和肌肉型，纤维型者可能系肌筋膜室综合征引起，胸锁乳突肌仅切除起点处２ｃｍ即可。肌肉型者以为先天性肌肉短缩畸形，胸锁乳突肌起点应楔形切除，认为保守治疗效果不佳者应早期手术矫治斜颈，预防继发畸形的发生和发展，强调手术松的彻底性和术后有效的功能锻炼。     

高频超声在婴幼儿先天性肌性斜颈诊断中的价值

目的 探讨高频超声在婴幼儿先天性肌性斜颈诊断中的价值。方法 选取2015年1月～2018年12月在我院行高频超声检查并经临床证实的疑似先天性肌性斜颈体检者共60例,按是否系先天性肌性斜颈分为先天性肌性斜颈组(CM组,n=38)和非先天性肌性斜颈组(NCM组,n=22)。采用单因素分析婴幼儿先天性肌性斜颈的高频超声声像图特征,采用二分类Logistic回归分析婴幼儿先天性肌性斜颈的独立预测因素;用独立预测因素构建预测婴幼儿先天性肌性斜颈可能的回归方程模型,采用受试者工作特征曲线分析本模型对婴幼儿先天性肌性斜颈的诊断效能。结果 两组患侧的回声强度比较,差异无统计学意义(P 0.05);两组回声质地、血流信号、包膜、边缘和胸锁乳突肌横径比较,差异有统计学意义(P 0.05)。二分类Logistic回归分析显示,回声质地、血流信号、包膜和胸锁乳突肌横径是婴幼儿先天性肌性斜颈的独立预测因素。本模型最佳截点值为395.884,其曲线下面积为0.924,此截点值下本模型对婴幼儿先天性肌性斜颈的敏感度、特异度、阳性预测值、阴性预测值和符合率分别为94.70%、95.50%、97.30%、91.30%和95.00%。结论 高频超声对婴幼儿先天性肌性斜颈具有较高的诊断效能,能用于筛查婴幼儿先天性肌性斜颈,还能够进一步为临床制定治疗方案提供参考依据。     

小儿先天性斜颈17例诊治体会

先天性肌性斜颈是由于出生后一侧的胸锁乳突肌挛缩和纤维变性所致的一种畸形，其原因是难产时损伤了一侧胸锁乳肌，治疗越早越好，年龄越大畸形越难完全矫正。我们收治17例，现将诊治情况报告如下。1临床资料     

婴儿先天性肌性斜颈治疗的护理

我院骨科专科门诊从１９９８年～２００１年开展了糖皮质激素胸锁乳突肌局部注射治疗辅以手法矫正 ,效果满意。现将３８０例总结分析 ,有关护理问题的讨论。１临床资料１ １一般资料 :３８０例中男１３９例 ,女２４１例。年龄在２～６月。１ ２临床表现 :病例胸锁乳突肌均有包块 ,最早在出生后５天 ,最长３９天 ,包块多数位居胸锁乳突肌中下位 ,包块较大者累及整块肌肉 ,患儿均以头颈偏斜或颈部包块来院就诊。检查发现患侧面部发育比健则差 ,有典型先天性肌性斜颈的临床表现。首诊病例常规行两侧Ｂ超对比检查 ,其资料作以后治疗随访动态观察…     

先天性肌性斜颈

<正> 先天性肌性斜颈是指一侧胸锁乳突肌发生纤维性挛缩后所形成的畸形。发病率在我国并不低,若早期得不到合理的治疗,日后将对病人的心理、工作、婚姻等方面,带来一定的影响。一、局部解剖胸锁乳突肌位于颈部两侧,左右各一,每个胸锁乳突肌包括五个以上的肌束,包于颈外筋膜内。起     

小儿先天性斜颈17例诊治体会

先天性肌性斜颈是由于出生后一侧的胸锁乳突肌挛缩和纤维变性所致的一种畸形,其原因是难产时损伤了一侧胸锁乳肌,治疗越早越好,年龄越大畸形越难完全矫正。我们收治17例,现将诊治情况报告如下。     

超声对先天性肌性斜颈的诊断价值

目的探讨超声检查对先天性肌性斜颈的应用价值。方法69例先天性肌性斜颈用彩色多普勒超声检查,观察两侧胸锁乳突肌大小、形态和回声的变化。观察肿块血流及周围血管情况。结果先天性肌性斜颈的胸锁乳突肌局限性增厚58例．均匀性增厚11例;声像图表现：肌束纹理紊乱,回声强弱不一,分布不均匀;肌外膜均保持连续。临床未扪及肿块而超声发现异常回声7例。结论超声能早期正确诊断本病。并且在指导治疗和疗效的观察上有重要价值。有助于与其他原因引起的斜颈相鉴别。     

单切口手术治疗儿童先天性肌性斜颈疗效观察

目的探讨儿童先天性肌性斜颈（CMT）单切121手术治疗的疗效。方法选2002年7月至2011年3月CMT患儿176例,年龄10个月-15岁,中位年龄4．8岁。右侧112例,左侧64例。所有患儿均行单切口胸锁乳突肌起点锁骨头及胸骨头松解,术后早期功能锻炼同时结合枕颌牵引。佩戴颈托或支具保持颈部在矫枉过正姿势。结果术后随访1～7．5年,中位随访时间为4．2年。所有患儿术后外观及颈部活动受限明显改善,斜视和面部发育异常逐步近于正常,优良率达96．0％（169／176）。结论CMT患儿无论年龄大小,只要严格掌握手术适应证,采用单切口手术治疗配合术后积极的康复锻炼可获得满意的疗效。     

Effects of arginine vasopressin on growth of rat cardiac fibroblasts: role of V1 receptor

The abnormal proliferation of cardiac fibroblasts is involved in the pathophysiologic process of left ventricular hypertrophy (LHV) associated with essential hypertension. Arginine vasopressin (AVP) has been reported to contribute significantly to the pathogenesis of hypertension. In this study, the authors investigated the effects of AVP and its V1 receptor antagonist [d(CH2)5Tyr2(Me)]AVP on the growth of rat cardiac fibroblasts. Cardiac fibroblasts of neonatal Sprague-Dawley rats were isolated, and growth-arrested cardiac fibroblasts were stimulated with 2.5% fetal calf serum in the presence and absence of AVP (0.001, 0.01, 0.1, and 1 microM) and [d(CH2)5Tyr2(Me)]AVP (0.1 microM). DNA synthesis was measured by [3H]thymidine incorporation. Thiazolyl blue assay and flow cytometry techniques were adopted to measure cell numbers and analyze cell cycle, respectively. Arginine vasopressin (0.1 and 1 microM) significantly increased DNA synthesis in cardiac fibroblasts. Moreover, AVP (0.1 and 1 microM) significantly increased the number of cardiac fibroblasts. Analysis of cell cycle showed that AVP (0.1 microM) increased S-stage percentage and proliferation index (PI). The V1 receptor antagonist [d(CH2)5Tyr2(Me)]AVP (0.1 microM) significantly inhibited DNA synthesis in cardiac fibroblasts. The cell number, S-stage percentage, and PI induced by AVP (0.1 microM) were significantly decreased by [d(CH2)5Tyr2(Me)]AVP (0.1 microM). These findings suggest that AVP might promote the proliferation of rat cardiac fibroblasts, which seems to be mediated via the V1 receptor. Arginine vasopressin may be involved in the pathophysiologic process of LVH by promoting cardiac fibroblast proliferation.     

吡格列酮对高糖高胰岛素诱导的心肌成纤维细胞增殖的影响

目的利用体外培养的乳鼠心肌成纤维细胞,观察噻唑烷二酮(TZD)类药物吡格列酮对高浓度葡萄糖与高浓度胰岛素共同诱导的心肌成纤维细胞增殖的影响,进一步推测TZD类药物对糖尿病并发心肌肥厚的可能作用机制。方法以培养的乳鼠心肌成纤维细胞为模型分组给药后。利用结晶紫染色法测定细胞的数量;利用[3H]thym id ine标记法测定细胞DNA的合成;利用流式细胞仪分析细胞周期。结果吡格列酮可以抑制高糖高胰岛素诱导的心肌成纤维细胞数量、DNA合成及S+G2+M期细胞的百分比增加,并呈一定的剂量依赖性。结论吡格列酮能有效抑制高糖高胰岛素诱导的心肌成纤维细胞的增殖,这种作用可能是通过作用于PPARγ来实现的。     

洛伐他汀对醛固酮诱导大鼠心肌成纤维细胞增殖的影响

目的:探讨洛伐他汀对醛固酮诱导的大鼠心肌成纤维细胞增殖的影响及其作用机制。方法:采用胰酶消化法分离培养SpragueDawley大鼠心肌成纤维细胞,以3H胸腺嘧啶核苷(3HTdR)掺入法、四氮唑蓝比色法和流式细胞仪观察洛伐他汀对醛固酮诱导心肌成纤维细胞增殖的DNA合成、细胞数目和细胞周期的影响。结果:(1)0.1,1,10μmol·L-1浓度的洛伐他汀抑制醛固酮诱导的心肌成纤维细胞3HTdR掺入率和A490值,其中1,10μmol·L-1组的3HTdR掺入率[(1292±s152),(1030±163)counts·min-1]和A490值[(0.287±0.008),(0.231±0.007)]显著低于对照组、0.1和0.01μmol·L-1组(P<0.01);(2)洛伐他汀可增加G0/G1期细胞百分率,降低S期细胞百分率、增殖指数和DNA含量;(3)甲羟戊酸可逆转洛伐他汀的上述作用。结论:洛伐他汀可抑制醛固酮诱导的心肌成纤维细胞增殖及DNA合成,阻止其由G1期进入S期,其机制可能与甲羟戊酸代谢途径有关。     

白细胞介素—1阻滞剂CK—119和CK—122地成纤维样细胞增生的抑制

AIM: To study potent and nontoxic agents to inhibit fibroblast proliferation. METHODS: Fibroblast-like corneal and conjunctival cells were cultured and inhibited by interleukin-1 (IL-1) blockers, dihydropyridazino-pyridazines CK-119 and CK-122. The cell growth and syntheses of DNA, RNA, and protein after IL-1 blocker incubation were determined. RESULTS: CK-119 and CK-122 inhibited cell growth of corneal fibroblast at 30 mg.L-1. DNA and RNA syntheses in corneal fibroblasts were markedly inhibited by CK-119 and CK-122 whereas protein synthesis was either unaffected or mostly enhanced at 30-100 mg.L-1 and 100-300 mg.L-1, respectively. Similar results were obtained in conjunctival cell cultures by CK-119 and CK-122 at 3-10 mg.L-1 and 30-100 mg.L-1, respectively. CONCLUSION: CK-119 and CK-122 are potent IL-1 blockers to inhibit cell growth of fibroblast-like corneal and conjunctival cells mainly through the inhibition of DNA and RNA syntheses but not protein synthesis.     

推拿配合斜颈矫正托佩戴治疗先天性肌性斜颈200例

目的:探讨推拿配合斜颈矫正托佩戴治疗先天性肌性斜颈的疗效.方法:将300例先天性肌性斜颈患儿随机分成治疗组200例和对照组100例,其中治疗组采用推拿治疗配合斜颈矫正托佩戴,对照组只进行推拿治疗,分别观察治疗结束后的疗效和2年后随访的远期疗效.结果:治疗结束后疗效及远期疗效比较,治疗组痊愈率和显效率均高于对照组(P<0.01).结论:推拿配合斜颈矫正托佩戴治疗先天性肌性斜颈的疗效优于单纯推拿治疗.     

Selective inhibition of collagen accumulation by N-(3,4-dimethoxycinnamoyl)anthranilic acid (N-5') in granulation tissue

The effect of topically applied N-5', an inhibitor of chemical mediator release from mast cells, on the carrageenin-air-pouch inflammation was studied. The formation of granulation tissue, the accumulation of exudate and the number of infiltrating cells were significantly reduced by the treatment with N-5' (100 mg/kg). The collagen content in granulation tissue was dose-dependently reduced without affecting the noncollagen protein and DNA content by treatment with N-5'. At a dose of 100 mg/kg of N-5', prolyl hydroxylase activity in the tissue was significantly decreased. The selective inhibition of collagen accumulation in granulation tissue resulted from reduction of collagen biosynthesis in vivo. N-5' did not directly inhibit collagen synthesis by diploid fibroblasts, but inhibited fibroblast proliferation in culture. Such results indicate that one of the inhibitory mechanisms of collagen accumulation by N-5' in inflamed sites may involve the inhibition of fibroblast proliferation.     

大于7岁儿童肌性斜颈的手术疗效

目的：观察大年龄同性斜颈的手术疗效,方法：手术治疗肌性斜颈患儿４９例,对大年龄患称部分切除胸锁乳突肌远端,对２２例手术时年龄〉７岁（平均１１岁８个月）者随访１年以上（平均３年４个月）结果：所有患儿的功能和外观均有改善,但有些病事遗脊柱侧凸畸形,尤其是女孩,结论：大年龄儿童尤其女孩可继发脊柱畸形。     

Differential Inhibition of DNA Synthesis in Human T Cells by the Cigarette Tar Components Hydroquinone and Catechol

Hydroquinone (HQ), catechol, and phenol exist in microgram quantitiesin cigarette tar and represent the predominant form of humanexposure to benzene. Exposure of human T lymphoblasts (HTL)in vitro to 50 µM HQ or 50 µM catechol decreasedIndependent DNA synthesis and cell proliferation by >90%with no effect on cell viability. Phenol had no effect on HTLproliferation at concentrations up to 1 mM. The addition ofHQ or catechol to proliferating HTL blocked ³H-TdR uptake by>90% within 2 hr without significantly affecting ³H-UR uptake,suggesting that both compounds inhibit a rate-limiting stepin DNA synthesis. However, the effects of HQ and catechol appearto involve different mechanisms. Ferric chloride (FeCl₃) reversedthe inhibitory effect of catechol, but not HQ, correspondingwith the known ability of catechol to chelate iron. HQ, butnot catechol, caused a decrease in transferrin receptor (TfR,CD71) expression, comparable to the level observed in IL-2-starvedcells. HQ also inhibited DNA synthesis in cultures of transformedJurkat T lymphocytes, primary and transformed fibroblasts, andmink lung epithelial cells, indicating that its antiproliferativeeffect was not restricted to IL-2 mediated proliferation. However,DNA synthesis by primary lymphocytes was more sensitive to HQ(1C50 = 6 µM) than that of the transformed Jurkat T cellline (IC50 = 37 (µM) or primary human fibroblasts (IC50= 45 µM), suggesting that normal lymphocytes may be particularlysensitive to HQ. The effects of HQ and catechol on DNA synthesiscould be partially reversed by a combination of adenosine deoxyriboseand guanosine deoxyribose, suggesting that both compounds mayinhibit ribonucleotide reductase.