Alpha2-adrenergic receptor activation reinstates motor deficits in rats recovering from cortical injury

Norepinephrine plays an important role in motor functional recovery after a brain injury caused by ferrous chloride.Inhibition of norepinephrine release by clonidine is correlated with motor deficits after motor cortex injury.The aim of this study was to analyze the role ofα-adrenergic receptors in the restoration of motor deficits in recovering rats after brain damage.The rats were randomly assigned to the sham and injury groups and then treated with the following pharmacological agents at 3 hours before and 8 hours,3 days,and 20 days after ferrous chloride-induced cortical injury:saline,clonidine,efaroxan(a selective antagonist ofα-adrenergic receptors)and clonidine+efaroxan.The sensorimotor score,the immunohistochemical staining forα-adrenergic receptors,and norepinephrine levels were evaluated.Eight hours post-injury,the sensorimotor score and norepinephrine levels in the locus coeruleus of the injured rats decreased,and these effects were maintained 3 days post-injury.However,20 days later,clonidine administration diminished norepinephrine levels in the pons compared with the sham group.This effect was accompanied by sensorimotor deficits.These effects were blocked by efaroxan.In conclusion,an increase inα-adrenergic receptor levels was observed after injury.Clonidine restores motor deficits in rats recovering from cortical injury,an effect that was prevented by efaroxan.The underlying mechanisms involve the stimulation of hypersensitiveα-adrenergic receptors and inhibition of norepinephrine activity in the locus coeruleus.The results of this study suggest thatαreceptor agonists might restore deficits or impede rehabilitation in patients with brain injury,and therefore pharmacological therapies need to be prescribed cautiously to these patients.

Chx10+V2a interneurons in spinal motor regulation and spinal cord injury

Chx10-expressing V2 a(Chx10+V2 a) spinal interneurons play a large role in the excitatory drive of motoneurons. Chemogenetic ablation studies have demonstrated the essential nature of Chx10+V2 a interneurons in the regulation of locomotor initiation, maintenance, alternation, speed, and rhythmicity. The role of Chx10+V2 a interneurons in locomotion and autonomic nervous system regulation is thought to be robust, but their precise role in spinal motor regulation and spinal cord injury have not been fully explored. The present paper reviews the origin, characteristics, and functional roles of Chx10+V2 a interneurons with an emphasis on their involvement in the pathogenesis of spinal cord injury. The diverse functional properties of these cells have only been substantiated by and are due in large part to their integration in a variety of diverse spinal circuits. Chx10+V2 a interneurons play an integral role in conferring locomotion, which integrates various corticospinal, mechanosensory, and interneuron pathways. Moreover, accumulating evidence suggests that Chx10+V2 a interneurons also play an important role in rhythmic patterning maintenance, leftright alternation of central pattern generation, and locomotor pattern generation in higher order mammals, likely conferring complex locomotion. Consequently, the latest research has focused on postinjury transplantation and noninvasive stimulation of Chx10+V2 a interneurons as a therapeutic strategy, particularly in spinal cord injury. Finally, we review the latest preclinical study advances in laboratory derivation and stimulation/transplantation of these cells as a strategy for the treatment of spinal cord injury. The evidence supports that the Chx10+V2 a interneurons act as a new therapeutic target for spinal cord injury. Future optimization strategies should focus on the viability, maturity, and functional integration of Chx10+V2 a interneurons transplanted in spinal cord injury foci.

Deep learning-based activity recognition and fine motor identification using 2D skeletons of cynomolgus monkeys

Video-based action recognition is becoming a vital tool in clinical research and neuroscientific study for disorder detection and prediction.However,action recognition currently used in non-human primate(NHP)research relies heavily on intense manual labor and lacks standardized assessment.In this work,we established two standard benchmark datasets of NHPs in the laboratory:Monkeyin Lab(Mi L),which includes 13 categories of actions and postures,and MiL2D,which includes sequences of two-dimensional(2D)skeleton features.Furthermore,based on recent methodological advances in deep learning and skeleton visualization,we introduced the Monkey Monitor Kit(Mon Kit)toolbox for automatic action recognition,posture estimation,and identification of fine motor activity in monkeys.Using the datasets and Mon Kit,we evaluated the daily behaviors of wild-type cynomolgus monkeys within their home cages and experimental environments and compared these observations with the behaviors exhibited by cynomolgus monkeys possessing mutations in the MECP2 gene as a disease model of Rett syndrome(RTT).Mon Kit was used to assess motor function,stereotyped behaviors,and depressive phenotypes,with the outcomes compared with human manual detection.Mon Kit established consistent criteria for identifying behavior in NHPs with high accuracy and efficiency,thus providing a novel and comprehensive tool for assessing phenotypic behavior in monkeys.

Bilateral carpal tunnel syndrome and motor dysfunction caused by gout and type 2 diabetes:A case report

BACKGROUND Carpal tunnel syndrome(CTS)has been associated with gout and type 2 diabetes mellitus(T2DM).However,due to insufficient clinical understanding of goutrelated CTS and reliance on the diagnostic importance of elevated serum uric acid levels,such cases are prone to missed diagnosis,misdiagnosis,and delayed treatment.In addition,the effect of T2DM on gout-induced carpal tunnel syndrome has not been reported.CASE SUMMARY Herein,we present an unusual case of CTS and motor dysfunction caused by miliary tophaceous gout and T2DM.The patient presented to the hand and foot clinic with paresthesia of the fingers of both hands,especially at night.The patient was diagnosed with type 2 diabetes a month ago.Ultrasonography revealed bilateral transverse carpal ligament thickening with median nerve compression during hospitalization.The patient was successfully treated with carpal tunnel decompression and tendon release.The postoperative pathological examination revealed typical gout nodules.This case suggests that the presence of T2DM could accelerate tophi formation and worsen CTS symptoms,although no definitive proof in this regard has been described previously.CONCLUSION Tophi formation may most likely cause the co-occurrence of CTS and flexor dysfunction in gout and incipient diabetes patients.

A Stable Fuzzy-Based Computational Model and Control for Inductions Motors

In this paper,a stable and adaptive sliding mode control(SMC)method for induction motors is introduced.Determining the parameters of this system has been one of the existing challenges.To solve this challenge,a new self-tuning type-2 fuzzy neural network calculates and updates the control system parameters with a fast mechanism.According to the dynamic changes of the system,in addition to the parameters of the SMC,the parameters of the type-2 fuzzy neural network are also updated online.The conditions for guaranteeing the convergence and stability of the control system are provided.In the simulation part,in order to test the proposed method,several uncertain models and load torque have been applied.Also,the results have been compared to the SMC based on the type-1 fuzzy system,the traditional SMC,and the PI controller.The average RMSE in different scenarios,for type-2 fuzzy SMC,is 0.0311,for type-1 fuzzy SMC is 0.0497,for traditional SMC is 0.0778,and finally for PI controller is 0.0997.

T_(2)-mapping定量评估脊髓性肌萎缩症严重程度

目的:探讨磁共振T_(2)-mapping技术定量评估儿童脊髓性肌萎缩症(SMA)严重程度的临床价值。方法:前瞻性将28例在本院经基因检测确诊的SMA患儿纳入本研究。记录每例患儿的年龄、体质指数(BMI)和汉默史密斯功能运动量表扩展版(HFMSE)评分。所有患儿行大腿常规序列MRI和T_(2)-mapping扫描,测量右侧骨盆和大腿部位的13块肌肉(右侧臀大肌、阔筋膜张肌、股直肌、股内侧肌、股外侧肌、股中间肌、缝匠肌、半膜肌、半腱肌、股二头肌长头肌、大收肌、长收肌和股薄肌)的T_(2)值,并得到彩色编码的肌肉组织T_(2)值分布图,以确定受累最严重的肌肉。采用两独立样本t检验比较Ⅱ和Ⅲ型SMA患者13块肌肉的T_(2)值、平均T_(2)值、HFMSE评分、年龄及BMI的组间差异,并采用Spearman秩相关分析评估肌肉T_(2)值与各项临床指标的相关性。结果:13块肌肉中,臀大肌的平均T_(2)值最高[(63.3±11.9)ms],长收肌的平均T_(2)值最低[(42.5±4.5)ms],长收肌的平均T_(2)值明显低于其它肌肉(P均<0.05)。彩色编码的T_(2)值分布图提供了对肌肉T_(2)值异质性分布的有效视觉评估。Ⅱ型SAM患者的阔筋膜张肌T_(2)值明显高于Ⅲ型(P<0.01),年龄及HFMSE评分均明显低于Ⅲ型(P<0.01)。在Ⅱ型、Ⅲ型及所有SMA患者中,肌肉平均T_(2)值均与HFMSE呈高度负相关(r=-0.696、-0.724、-0.657,P均<0.01)。13块肌肉中,阔筋膜张肌的T_(2)值与HFMSE评分的相关性最高(r=-0.743,P<0.001)。结论:磁共振T_(2)-mapping技术能客观定量评估SMA患儿疾病的严重程度,有助于识别该疾病的肌肉受累模式。阔筋膜张肌的T_(2)值可较准确地鉴别Ⅱ型与Ⅲ型SMA患者,此条肌肉可能是评估SMA疾病严重程度的最理想的目标肌肉。

Dysregulated cortical synaptic plasticity under methyl-CpG binding protein 2 deficiency and its implication in motor impairments

Caused by the mutation of methyl-CpG binding protein 2(MeCP2),Rett syndrome leads to a battery of severe neural dysfunctions including the regression of motor coordination and motor learning.Current understanding has revealed the motor cortex as the critical region mediating voluntary movement.In this review article,we will summarize major findings from human patients and animal models regarding the cortical synaptic plasticity under the regulation of MeCP2.We will also discuss how mutation of MeCP2 leads to the disruption of cortical circuitry homeostasis to cause motor deficits.Lastly,potential values of physical exercise and neuromodulation approaches to recover neural plasticity and motor function will be evaluated.All of this evidence may help to accelerate timely diagnosis and effective interventions for Rett syndrome patients.

Type-2 Fuzzy Logic Controllers Based Genetic Algorithm for the Position Control of DC Motor

Type-2 fuzzy logic systems have recently been utilized in many control processes due to their ability to model uncertainty. This research article proposes the position control of (DC) motor. The proposed algorithm of this article lies in the application of a genetic algorithm interval type-2 fuzzy logic controller (GAIT2FLC) in the design of fuzzy controller for the position control of DC Motor. The entire system has been modeled using MATLAB R11a. The performance of the proposed GAIT2FLC is compared with that of its corresponding conventional genetic algorithm type-1 FLC in terms of several performance measures such as rise time, peak overshoot, settling time, integral absolute error (IAE) and integral of time multiplied absolute error (ITAE) and in each case, the proposed scheme shows improved performance over its conventional counterpart. Extensive simulation studies are conducted to compare the response of the given system with the conventional genetic algorithm type-1 fuzzy controller to the response given with the proposed GAIT2FLC scheme.

Double-target neural circuit-magnetic stimulation improves motor function in spinal cord injury by attenuating astrocyte activation

Multi-target neural circuit-magnetic stimulation has been clinically shown to improve rehabilitation of lower limb motor function after spinal cord injury. However, the precise underlying mechanism remains unclear. In this study, we performed double-target neural circuit-magnetic stimulation on the left motor cortex and bilateral L5 nerve root for 3 successive weeks in a rat model of incomplete spinal cord injury caused by compression at T10. Results showed that in the injured spinal cord, the expression of the astrocyte marker glial fibrillary acidic protein and inflammatory factors interleukin 1β, interleukin-6, and tumor necrosis factor-α had decreased, whereas that of neuronal survival marker microtubule-associated protein 2 and synaptic plasticity markers postsynaptic densification protein 95 and synaptophysin protein had increased. Additionally, neural signaling of the descending corticospinal tract was markedly improved and rat locomotor function recovered significantly. These findings suggest that double-target neural circuit-magnetic stimulation improves rat motor function by attenuating astrocyte activation, thus providing a theoretical basis for application of double-target neural circuit-magnetic stimulation in the clinical treatment of spinal cord injury.

Establishing motor disorder mouse models of Parkinson disease Comparison of 6-hydroxydompamine and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine

At present, pathogenesis and mechanism of Parkinson disease （PD） are still unclear. Animal models of PD are essential tools in studies on etiology and therapy and should mimic the chronic pathological process, histological characteristics and motor behavior dysfunction. In recent years, transgenic mice have been widely utilized to study the mechanism of PD, and it has become imperative that a PD mouse model of motor behavioral dysfunction be established. OBJECTIVE： To compare the behavioral and histochemical characters of two neurotoxic mice model induced with 6-hydroxydopamine （6-OHDA） or 1-methyl-4-phenyl-1, 2, 3, 6 -tetrahydropyridine （MPTP）, and a better method to mimic Parkinson disease will be found out. DESIGN： Parallel experiment. SETTING： Laboratory of Molecular Genetics, Department of Medical Genetics, Shanghai Jiao Tohg University. MATERIALS： Sixty 129Sv/C57BL6J male wild mice, SPF grade, 8 - 12 weeks old, weighing 20 - 25 g, were provided by Experimental Animal Center, Shanghai Jiao Tong University. All the surgery operation was performed according to the rules of Shanghai Jiaotong University Animal Committee. METHODS： The experiment was carried out in the Laboratory of Molecular Genetics （National Key Laboratory）, Department of Medical Genetics, Shanghai Jiao Ttong University from March to August 2006. ①Thirty-two male mice were randomly divided into control group and drug treatment group with 16 mice in each group. Surgery was carried out and 6-OHDA was administrated to substantia nigra pars compacta （SNpc） and nigra-striatum pathway according to the different parameters with intoxication apparatus. Saline was injected to the other 16 mice according to the same paradigm. 1 mg/kg apomorphine was injected intraperitoneally 2 weeks later after surgery to induce the imbalanced rotation behavior for 40 minutes. ②Twenty-eight mice were randomly divided into 4 groups with 7 in each group, including low-dose, moderate-dose, high-dose groups and negative control group. Then, mice in the drug treatment group were injected intraperitoneally with 5, 10 and 15 mg/kg MPTP for 9 successive days. In addition, mice in the control group were injected with the same volume of saline for 9 days. Pole test and stride length test were utilized to detect coordinative behavioral dysfunction. Mice were sacrificed 20 days after MPTP treatment, and histochemical staining of tyrosine hydroxynase （TH） was used to observe the loss of dopaminergic neuron in SNpc. MAIN OUTCOME MEASURES： ① Success ratio of each model establishment method; ② inducible asymmetric cycle behavior test 2 weeks after 6-OHDA injection; ③behavioral dysfunction in pole test and stride length, morphological changes in brain tissue. RESULTS： Totally sixty mice were used in this experiment and 3 mice were excluded because of the hypersensitivity or the clumsy reaction in motor behavioral detection before MPTP treatment, therefore, data was analyzed with the rest 57 mice. ① Lethal ratio： Three out of 16 mice died in striatum injection group and 5 out of 16 mice died in nigro-striatal pathway group. No mouse died in MPTP treatment groups. ② Locomotor behavior： No dysfunction of locomotor was found in 6-OHDA treatment groups. However, several motor behavioral dysfunction were start to present at the 4th day of MPTP injection. ③ Asymmetric cycle behavior： No asymmetric cycle was induced successfully two weeks after 6-OHDA surgery. Mice show hypersensitive behavior 10 minutes after apomorphine injection, which lasted for about 20 minutes. ④ Pole test： From the 4^th day of MPTP treatment, mice started to display coordinate dysfunction, such as climbing down along the pole in spiral, moving slowly with hesitation. Some mice could not grab the pole and slide down along the pole at 4th day post injection. Comparing with 0 dose control group, all the threedrug treatment groups show significant different dysfunction from the 4th day to the 20th day post injection （P 〈 0.01）. ⑤ stride length test： Mice＇s stride length decreased, when treated with MPTP, and the mice in the high dose group displayed obviously. ⑥ Dopaminergic neuron stained with TH in nigra pars compacta： The results indicated that administrated MPTP （from low dose to high dose） by intraperitoneal cause chronic lesions on the dopaminergic neuron in the SNpc. CONCLUSION： PD mice models induced with 6-OHDA show high mortality ratio and no asymmetric cycle was found after apomorphine injection. However, injection of MPTP intraperitoneally can simulate the chronic pathway of PD, typical histological changes are found and stable motor behavioral dysfunctions are displayed.

多学科支持下的运动处方对老年2型糖尿病患者运动功能、骨骼肌量、肌力及血糖水平的改善效果

目的:探究多学科支持下的运动处方对老年2型糖尿病患者运动功能、骨骼肌量、肌力及血糖水平的改善效果。方法:选取2020年1月—2022年11月河南省人民医院内分泌科收治的127例老年2型糖尿病患者作为研究对象,采用随机数表法将其分为对照组(n=63)和观察组(n=64)。对照组:实施常规护理管理;观察组:实施多学科支持下的运动处方干预。对比两组患者的运动功能、骨骼肌量及肌力以及血糖水平。结果:干预后观察组糖化血红蛋白、空腹血糖低于对照组,四肢运动功能评分、6m步行速度、四肢骨骼肌质量(ASM)、四肢骨骼肌质量指数(ASMI)、握力均高于对照组,差异有统计学意义(P<0.05)。结论:采用多学科支持下的运动处方对老年2型糖尿病患者进行干预,可有效控制患者的血糖水平,提高其骨骼肌质量、肌力,促进患者运动能力的恢复。

Eph receptor A4 regulates motor neuron ferroptosis in spinal cord ischemia/reperfusion injury in rats

Previous studies have shown that the receptor tyrosine kinase Eph receptor A4(EphA4) is abundantly expressed in the nervous system. The EphA4 signaling pathway plays an important role in regulating motor neuron ferroptosis in motor neuron disease. To investigate whether EphA4 signaling is involved in ferroptosis in spinal cord ischemia/reperfusion injury, in this study we established a rat model of spinal cord ischemia/reperfusion injury by clamping the left carotid artery and the left subclavian artery. We found that spinal cord ischemia/reperfusion injury increased EphA4 expression in the neurons of anterior horn, markedly worsened ferroptosis-related indicators, substantially increased the number of mitochondria exhibiting features consistent with ferroptosis, promoted deterioration of motor nerve function, increased the permeability of the blood-spinal cord barrier, and increased the rate of motor neuron death. Inhibition of EphA4 largely rescued these effects. However, intrathecal administration of the ferroptosis inducer Erastin counteracted the beneficial effects conferred by treatment with the EphA4 inhibitor. Mass spectrometry and a PubMed search were performed to identify proteins that interact with EphA4, with the most notable being Beclin1 and Erk1/2. Our results showed that inhibition of EphA4 expression reduced binding to Beclin1, markedly reduced p-Beclin1, and reduced Beclin1-XCT complex formation. Inhibition of EphA4 also reduced binding to p-Erk1/2 and markedly decreased the expression of c-Myc, transferrin receptor 1, and p-Erk1/2. Additionally, we observed co-localization of EphA4 and p-Beclin1 and of EphA4 and p-ERK1/2 in neurons in the anterior horn. In conclusion, EphA4 participates in regulating ferroptosis of spinal motor neurons in the anterior horn in spinal cord ischemia/reperfusion injury by promoting formation of the Beclin1-XCT complex and activating the Erk1/2/c-Myc/transferrin receptor 1 axis.

永磁无刷电机中平行充磁2极气隙磁场的解析计算

永磁无刷电机中,平行充磁的2极磁环产生的气隙磁场是正弦分布的。推延了一个通用的解析公式来计算气隙磁场。有限元计算和实验都证明了该解析计算的可靠性。

Alberta婴儿运动量表与Peabody运动发育量表-2在脑损伤高危儿中的一致性研究

目的探讨Alberta婴儿运动量表(AIMS)与Peabody运动发育量表-2(PDMS-2)在1-9个月脑损伤高危儿的平行效度。方法 1-9个月脑损伤高危儿60例,均接受AIMS和PDMS-2评估。AIMS总分与PDMS-2粗大运动原始总分(GMS)进行Spearman相关性分析,AIMS百分位与粗大运动商(GMQ)根据Kappa值进行定性分析。并对两个量表检查时间进行比较。结果 AIMS总分与PDMS-2 GMS的相关系数为0.91(P<0.001),AIMS百分位与PDMS-2 GMQ的相关系数为0.6。AIMS评估时间平均(10.47±3.63)min,PDMS-2评估时间平均(26.5±7.77)min(t=28.895,P<0.001)。结论 AIMS与PDMS-2在1-9个月脑损伤高危儿的运动发育评估中具有较高的一致性。

大鼠脊髓损伤后MAP-2的表达及与运动功能恢复的相关性

目的研究大鼠脊髓损伤后MAP-2表达的变化及与运动功能恢复的相关性。方法健康成年Wistar大鼠36只,随机取6只作为正常对照组,余30只制作成脊髓打击伤动物模型,随机分为5组,每组6只。伤后1、3、7、14、28d取材,应用免疫组织化学方法观察MAP-2的表达,采用计算机图像分析系统,进行定量分析;用改良的Tarlov评分、斜板试验观察大鼠脊髓损伤后运动功能的恢复情况及MAP-2的表达和二者的相关程度。结果大鼠脊髓损伤后MAP-2的表达在损伤后1-14d呈进行性升高,并在损伤后14d达到高峰,损伤后28d较损伤后14d明显下降(P<0.01),但仍明显高于正常对照组(P<0.01),呈高水平表达;大鼠脊髓损伤后1-28d改良的Tarlov评分、斜板试验进行性升高,并在损伤后28d达到高峰,但仍明显低于正常对照组(P<0.01)。MAP-2的表达和改良的Tarlov评分、斜板试验在损伤后呈正相关(|r1|=0.81,P<0.01;|r2|=0.79,P<0.01)。结论大鼠脊髓损伤后MAP-2的表达和运动功能的恢复呈正相关,MAP-2很可能参与了大鼠脊髓损伤后运动功能的恢复。

2-甲氧基雌二醇对脊髓损伤大鼠运动功能及神经细胞凋亡的影响

目的:探讨2-甲氧基雌二醇(2ME2)对脊髓损伤(SCI)大鼠运动功能及细胞凋亡的影响。方法:将成年雄性SD大鼠72只随机分为假手术组(n=24)、脊髓损伤组(n=24)、2ME2治疗组(n=24)。采用改良的Allen法制作脊髓损伤模型,造模成功后1、3、7、14、21、28d应用BBB运动评分系统对各组大鼠运动功能进行评估,造模成功后连续7天对2ME2治疗组大鼠腹腔注射2ME2(24mg/kg),第7天应用免疫荧光技术检测各组大鼠caspase-3表达,应用TUNEL染色进行凋亡细胞计数。结果:脊髓损伤组及2ME2治疗组损伤后随时间延长BBB评分升高,其中2ME2治疗组损伤后第14、21、28天BBB评分显著高于脊髓损伤组,差异具有显著性意义(P<0.05)。与假手术组(4.583±2.234)比较,脊髓损伤组(33.417±4.274)及2ME2治疗组(22.250±4.048)免疫荧光染色caspase-3蛋白表达阳性细胞数显著增加,2ME2治疗组caspase-3蛋白表达阳性细胞数较脊髓损伤组显著减少,差异具有显著性意义(P<0.05)。与假手术组(12.25±2.67)相比,脊髓损伤组(49.17±4.75)及2ME2治疗组(38.67±4.44)凋亡细胞数显著增多,2ME2治疗组凋亡细胞数较脊髓损伤组显著减低,差异具有显著性意义(P<0.05)。结论:2ME2改善脊髓损伤大鼠模型脊髓损后的运动功能,具有神经保护作用;2ME2降低脊髓损伤大鼠模型脊髓损后caspase-3蛋白表达,抑制神经细胞凋亡。

运动诱发电位对2型糖尿病马尾神经近端损害的诊断价值

目的：探讨运动诱发电位对2型糖尿病马尾神经近端损害的诊断价值。方法：107例2型糖尿病患者分为无周围神经病变组（NDPN组）60例、有周围神经病变组（DPN组）47例,另选正常对照33例,检测指标包括腘窝、S1、T12三点刺激的踇展肌运动诱发电位潜时及波幅,S1-腘窝、T12-腘窝、T12-S1的运动传导速度;并采用logistic回归分析DPN的危险因素。结果：DPN组较NDPN组及对照组的运动诱发电位腘窝刺激的潜时延长,波幅降低;S1刺激的潜时延长,波幅降低;T12刺激的潜时延长,波幅降低;T12-S1传导速度减慢,S1-腘窝传导速度减慢,T12-腘窝传导速度减慢（P〈0.05）。与NDPN组相比,DPN组的年龄、病程、FPG、Hb A_1c升高（P〈0.05）。Logistic回归分析结果显示,年龄（OR=1.079,95%CI=1.032～1.129）、病程（OR=1.099,95%CI=1.019～1.185）、FPG（OR=1.195,95%CI=1.026～1.390）、Hb A_1c（OR=1.416,95%CI=1.113～1.802）为DPN的危险因素。结论：2型糖尿病神经病变存在马尾及周围神经近端损害,年龄、病程、FPG、Hb A_1c是影响DPN的危险因素。

电针治疗对MCAO大鼠运动功能及梗死对侧大脑皮层GAP-43、MAP-2表达的影响

目的观察局灶性脑梗死大鼠梗死对侧皮层不同时期生长相关蛋白GAP-43(growth associated protein-43)及微管相关蛋白MAP-2(microtubule associated protein-2)表达的动态变化,探讨电针调节GAP-43和MAP-2表达与神经可塑性及大鼠运动功能改善的可能关系。方法 60只雄性SD大鼠随机分为假手术组(n=6)、模型组和电针组,模型组和电针组再随机分为3d、7d、14d、28d等4个亚组(剔除耗损或死亡,n=6)。运用Longa改良线栓法制备右侧大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)大鼠模型,电针组取双侧"曲池""足三里"针灸治疗,余两组同一时间捆绑,不做治疗。采用Bederson法评定大鼠神经功能缺损情况、免疫组化法检测梗死对侧皮层GAP-43、MAP-2的表达变化。结果与模型组比较,电针组术后第3天神经功能缺损评分差异无统计学意义(P>0.05),随着治疗时间的延长,术后第7、14、28天神经功能评分逐渐降低,差异有统计学意义(P<0.05)。免疫组化结果显示,电针组术后第3天GAP-43、MAP-2阳性细胞表达量与模型组比较差异无统计学意义(均P>0.05);术后第7、14天GAP-43、MAP-2阳性细胞表达量明显高于模型组(均P<0.05),术后第28天GAP-43阳性细胞表达量明显高于模型组(P<0.05)。结论电针治疗增加梗死对侧皮层MAP-2、GAP-43的表达,改善了大鼠的运动功能,促进神经功能重塑,可能与加快启动梗死对侧皮层的保护机制、减少病灶对侧的远隔继发性损害有关。

纳米TiO_2填料对变频电机耐电晕电磁线绝缘性能的影响

测试和分析了某型耐电晕电磁线绝缘漆中无机填料的化学组成和微观形貌 ,并测试该电磁线绝缘漆的紫外 可见光吸收谱。从无机填料效用的角度研究了纳米TiO2 在绝缘破坏过程中的电、光及热效应。纳米TiO2 填充改性绝缘的电磁线遭受电晕破坏时 ,析出的纳米TiO2 微粉层可以改善电场分布 ,提高热传导能力 ,并在绝缘表面形成电子和紫外线屏障 ,捕获电晕放电产生的电荷 ,吸收紫外线。这些研究可为开发变频电机用耐电晕电磁线提供理论参考依据。

Ghrelin对CKD大鼠十二指肠消化间期移行性复合运动和Bcl-2/Bax表达的影响

目的观察ghrelin对慢性肾功能不全(CKD)大鼠十二指肠消化间期移行性复合运动变化和Bcl-2/Bax表达的影响。方法 SD大鼠18只,体重(180±20)g,雌雄不拘,随机分为对照组(CKD+生理盐水)、ghrelin 1组(CKD+ghrelin 10μg/kg)和ghrelin 2组(CKD+ghrelin 50μg/kg),每组6只。采用5/6肾切除法建立CKD大鼠模型。模型建立成功后分别采用多道生理记录仪和免疫组织化学方法观察十二指肠消化间期移行性复合运动变化和凋亡相关基因Bcl-2/Bax的表达。结果 CKD大鼠普遍存在十二指肠运动功能障碍;ghrelin可以明显增加CKD大鼠十二指肠消化间期移行性复合运动出现的频率,包括呈剂量依赖性增加Ⅲ相出现的时间、频率和振幅,各参数在对照组、ghrelin 1组和ghrelin 2组分别为:Ⅲ相出现的时间[(0.81±0.12)minvs.(0.84±0.13)minvs.(0.99±0.17)min];频率[(22.68±1.00)次/minvs.(23.55±1.08)次/minvs.(29.31±1.51)次/min];振幅[(249.71±13.98)μVvs.(258.49±13.12)μVvs.(318.85±20.10)μV](P<0.05)。同时ghrelin可以明显减少Bcl-2和Bax的表达,其中以Bax的减少更明显(P<0.05),Bcl-2/Bax比值增加(P<0.05)。结论 ghrelin可以明显改善CKD大鼠十二指肠的运动功能,有可能成为一种新型胃肠动力药物。