无张力疝修补术后慢性疼痛的原因及防治

目的：探讨腹股沟疝无张力修补术后慢性疼痛的原因及防治。方法：选取131例腹股沟疝患者行无张力疝修补术,分析其术后疼痛原因及防治方法。结果：随访时间3～12个月,术后出现3个月以上局部慢性疼痛不能缓解并需进一步治疗的患者8例,发生率为6.1%。结论：开放性无张力疝修补术中熟练的手术操作、部分可吸收材料的应用、材料使用个体化等可以减少术后慢性疼痛的发生,提高患者术后的生活质量。     

子宫内膜异位症致盆腔疼痛与病灶特点的相关性

目的 探讨子宫内膜异位症患者盆腔疼痛与病灶部位、粘连程度、浸润深度间的关系.方法 对湖州市菱湖人民医院2010年1月至2014年5月间妇科住院部确诊为子宫内膜异位症且经手术治疗的168例患者进行临床研究,观察痛经、排便痛、肛门坠痛、性交痛及慢性盆腔痛与病灶部位、粘连程度、浸润深度间的关系.结果 子宫内膜异位症发生部位在子宫骶韧带、子宫直肠凹部的肛门坠痛、排便痛、痛经、性交痛及慢性盆腔痛发生率均明显高于其它部位(子宫韧带:x2值分别为23.60、65.83、65.58、37.00、25.63,均P＜0.01;子宫直肠凹;x2值分别为17.98、56.41、54.49、27.93、40.90,均P＜0.01).术中见131例患者存在粘连,且多为复合粘连,卵巢粘连发生率明显高于其它部位(x2=115.43,P＜0.01),病灶浸润深度在≥5mm者,肛门坠痛、排便痛、痛经、性交痛及慢性盆腔疼痛患者发生率均明显高于＜5mm患者(x2值分别为6.62、11.83、10.62、10.66、7.29,均P＜0.05).结论 子宫内膜异位症患者盆腔疼痛与病灶部位、浸润深度及粘连程度为正相关性.     

缝隙连接与神经病理性痛的研究进展

缝隙连接是介导相邻细胞间物质转运、化学或电信号传递的专用跨膜通道,维持着细胞内环境的稳定。在神经系统中,缝隙连接不仅介导神经元和胶质细胞的胞间偶合,还参与病理条件下继发性损害。目前,研究证明缝隙连接在由神经系统损伤引起的神经病理性痛中发挥作用。对缝隙连接与神经病理性痛的关系进行研究有助于更深层次的了解神经病理性痛的发病机制,为治疗神经病理性痛提供新的研究方向。     

Effect of oxymatrine on CaMKII expression in sciatic nerve ligation-induced neuropathic pain in mice北大核心CSCD

Aim To observe the analgesic effect of oxymatrine (OMT) and its mechanism. Methods A peripheral mononeuropathy was produced in adult mice by placing loosely constrictive ligatures around the common sciatic nerve. The antinociceptive effects of the OMT were assessed in mechanical allodynia and cold allodynia tests. The CAMKII inhibitor KN-93 and AIP were adopted to investigate the influence of OMT on the analgesic effect and analyze its analgesic mechanisms. Western blot was used to evaluate the expressions of tCaMKII and pCaMKII protein. Results The intraperitoneal administration of OMT (160, 80 mg · kg-1) increased the paw withdrawal threshold in the mechanical allodynia test (P < 0. 05), OMT (160, 80, 40 mg · kg-1 , ip) remarkably decreased the paw lifts in the cold allodynia test (P < 0. 05). Ith KN-93 (1. 25 (μg/site), AIP (0. 02 μg/site) significantly enhanced the analgesic effect of OMT (35 mg · kg-1) (P<0. 01). Protein expression of pCaMKII was decreased by OMT(160 mg · kg-1). Conclusion OMT has significant protective effects on chronic constriction injury(CCI) in mice, and the effective mechanism of OMT inhibits the expression of CaMKII receptor.     

Tat-LK15运载siRNA沉默RGC-5神经细胞nNOS基因的实验研究

目的探讨离体条件下细胞穿透肽Tat-LK15运载小干扰RNA(small interference RNA,siRNA)沉默RGC-5视神经节细胞(retinal ganglion cell line,RGC-5)神经元型一氧化氮合酶(neuronal nitric oxide synthase,n NOS)基因的可行性,为在体条件下研究Tat-LK15运载siRNA沉默n NOS表达治疗神经病理性疼痛提供理论依据。方法 1通过凝胶阻滞分析测定Tat-LK15与siRNA的最佳交联比。流式细胞术检测Tat-LK15/FAM-siRNA以最佳交联比转染RGC-5细胞的转染效率;不同剂量Tat-LK15(1、2.5、5、10和20μg)孵育RGC-5细胞24 h,流式细胞术检测细胞凋亡率。2制备n NOS高表达的RGC-5细胞模型。3将RGC-5细胞随机分为5组:对照组、模型组、Tat-S组(Tat-LK15运载n NOS/siRNA转染模型细胞)、Lipo-S组(LipofectamineTMRNAi MAX运载n NOS/siRNA转染模型细胞)及Tat-N组(Tat-LK15运载NCsiRNA转染模型细胞),通过Q-PCR及Western blot检测各组nN OS表达水平。结果 Tat-LK15与siRNA质量比为2∶1时可完全包裹siRNA,达到最佳交联,此时其转染效率为(84.4±3.9)%。当Tat-LK15剂量为20μg(6.1μmol·L-1)时才出现一定细胞毒性,细胞凋亡率高于对照组[(10.3±1.1)%vs(7.4±0.9)%,P<0.05]。造模后RGC-5细胞nN OS表达水平明显升高(P<0.05)。与模型组相比,Tat-S组nN OS mRNA及蛋白表达水平降低(P<0.05),Tat-S组与Lipo-S组相比无差异(P>0.05)。结论Tat-LK15能高效转染siRNA,细胞毒性低,离体条件下可有效运载siRNA沉默nN OS的基因表达。     

学龄儿童功能性腹痛的临床特点分析与治疗

目的：探讨分析学龄儿童功能性腹痛的临床特点与治疗方法及效果。方法选取2012年1月～2013年12月间收治的100例功能性腹痛学龄儿童（6岁～12岁）,随机分为观察组和对照组各50例。观察组给予化积颗粒治疗,对照组给予消旋山莨菪碱片治疗,分析两组患儿的临床特点,观察比较两组患儿的疗效和安全性。结果学龄儿童功能性腹痛的临床特点为男性少于女性（40/60,1∶1.5）,6～7岁患儿多于8～12岁（65/35,1.86∶1）,病程多为2～3个月;观察组治疗后在总有效率、中医症候评分、不良反应发生率方面均明显优于对照组,差异具统计学意义（P＜0.05）。结论学龄儿童功能性腹痛的临床特点为多为女性患儿,年龄在6～7岁患儿,病程在2～3个月。给予化积颗粒治疗的疗效显著,安全性高。     

A Cross-sectional Survey of Patients with Suspected Diabetic Peripheral Neuropathic Pain in Japan

Objective The burden of diabetic peripheral neuropathic pain (DPNP) is poorly understood. The present study reported on the current status of DPNP in Japan, to improve our understanding of this condition among healthcare providers and inform future clinical research on its prevalence, diagnosis, and management. Methods A cross-sectional, observational study (UMIN000037023) was conducted via a web-based survey. The primary endpoints were the frequency of patients with bilateral foot symptoms, consulting a doctor, understanding DPNP, and reporting problems in daily life, as well as the treatment awareness of patients. Patients Adults ≥20 years old who were registered in the Rakuten Insight Disease Panel and receiving anti-diabetic therapy in Japan were included. Results Bilateral foot pain symptoms were reported by 1,768/7,754 (22.8%) respondents, most commonly intense numbness (13.0%). Of those with symptoms, 55.3% consulted a doctor; the most common reason for not seeking consultation was feeling that symptoms were insufficiently severe to bother their doctor (89.4%). Nearly 60% reported understanding the causes of their symptoms, with diabetes-associated neurologic deficits (58.8%) most commonly identified. About one-quarter reported daily life problems, including an inability to walk for long periods (58.3%) and feeling anxious (58.1%). Treatment awareness was reported by 18.2%; oral medications were commonly recognized (64.6%). Conclusion In Japan, 22.8% of patients with diabetes have bilateral foot pain symptoms; some experience problems in their daily life without understanding the causes of their symptoms. This supports the importance of actions to increase awareness and minimize DPNP-associated impairment of daily life in patients with diabetes.     

Normocalcemic Primary Hyperparathyroidism Presenting with Muscle Weakness and Body Pain

We herein report a 39-year-old woman who had aggravated body pain, waddling gait, and fatigability for the past 2 years. A neurological examination showed hyperreflexia and proximal muscle weakness. The serum calcium level was normal (10.1 mg/dL). However, serum alkaline phosphatase (3,855 IU/I) and parathyroid hormone (1,008 pg/mL) levels were remarkably high. Cervical ultrasonography revealed parathyroid goiter. The patient was diagnosed with hyperparathyroidism. Her muscle weakness and pain improved within three months after parathyroidectomy. Our findings suggest that clinicians should consider hyperparathyroidism as a differential diagnosis in patients with proximal muscle weakness, even if the serum calcium level is normal.