Monotropein Improves Dexamethasone-Induced Muscle Atrophy via the AKT/mTOR/FOXO3a Signaling Pathways

The present study aimed to investigate the effects of monotropein (MON) on improving dexamethasone (DEX)-induced muscle atrophy in mice and C2C12 mouse skeletal muscle cells. The body weights, grip strengths, and muscle weights of mice were assessed. The histological change in the gastrocnemius tissues was also observed through H&E staining. The expression of myosin heavy chain (MyHC), muscle ring finger 1 (MuRF1), and muscle atrophy F-box (Atrogin1) and the phosphorylation of AKT, mTOR, and FOXO3a in the muscle tissues of mice and C2C12 myotubes were analyzed using Western blotting. MON improved muscle atrophy in mice and C2C12 myotubes by regulating catabolic states via the AKT/mTOR/FOXO3a signaling pathways, and enhanced muscle function by the increases of muscle mass and strength in mice. This suggests that MON could be used for the prevention and treatment of muscle atrophy in patients.     

Noninvasive measures of bone bending rigidity in the monkey (M. nemestrina)

Summary The in vivo bending rigidity and bone mineral content of monkey ulnae and tibiae were measured. Bending rigidity in the anteroposterior plane was measured by an impedance probe technique. Forced vibrations of the bones were induced with an electromechanical shaker, and force and velocity at the driving point were determined. The responses over the range of 100–250 Hz were utilized to compute the bending rigidity. Bone mineral content in the cross section was determined by a photon absorption technique. Seventeen male monkeys (Macaca nemestrina) weighing 6–14 kg were evaluated. Repeatability of the rigidity measures was 4%. Bone mineral content was measured with a precision of 3.5%. Bending rigidity was correlated with the mineral content of the cross section,r=0.899. Two monkeys were evaluated during prolonged hypodynamic restraint. Restraint produced regional losses of bone most obviously in the proximal tibia. Local bone mineral content declines 17 to 24% and the average bending rigidity declines 12 to 22%. Changes in bones leading to a reduction in mineral content and stiffness are discussed.     

研究缺血对失神经支配骨骼肌萎缩的影响

目的　研究缺血对失神经支配骨骼肌萎缩的影响。方法　选用 SD大鼠 2 4只 ,建立右下肢缺血加腓肠肌失神经支配的动物模型 (实验组 ) ,左侧为对照组。术后 2、4周取双侧腓肠肌 ,另取 6只正常大鼠腓肠肌作正常对照 ,观察组织学、肌电图及酶组织化学的变化。结果　术后 2、4周 ,实验组肌细胞直径比正常对照组减少 5 1.1%和 6 3.6 % (t =2 .94,P <0 .0 5 ) ,截面积减少 5 3.6 %和 6 2 .0 % (t =2 .88,P <0 .0 5 )。实验组肌细胞线粒体呈空泡状、数量减少 ;肌质网明显扩张退变。肌肉出现纤颤电位 ,和对照组比 ,其波幅无明显差异 (t=2 .11,P<0 .0 5 )。术后 2周实验组的 Na,K- ATP酶活性比正常对照组增高 74.6 % ,术后 4周则下降至对照组的 88.0 % (t=7.6 4,2 .2 4,P<0 .0 1、<0 .0 5 )。术后2周 Ca- ATP酶活性比正常对照组下降 2 8.32 % ,术后 4周下降至 35 .8% (t=2 .98、2 .2 1,P<0 .0 5 )。结论　缺血可加速失神经支配肌肉萎缩的发生与发展     

颞叶癫痫颅内EEG记录定位与海马病理变化的关系

目的探讨颞叶癫痫颅内EEG记录与颞叶海马病变程度的关系。方法视频EEG证实为颞叶癫痫并经MRI检查的病人序贯进入本研究,采用硬膜下电极及深部电极联合纪录,确定领先发作释放(initialictaldischarge,IID)部位。37例病人中,无或轻度海马萎缩(hippocampalatrophy,HA阴性组)27例,中至中度HA(HA阳性组)者10例。海马病理变化依据MRI检查的海马容积测量及术后组织病理学的海马硬化分级。结果本组HA阴性组27例病人中,9例病人IID广泛出现在海马区、内侧旧皮层及外侧新皮层;3例在海马区及内侧古皮层;14例完全出现在海马区以外的颞叶皮层;仅1例局限于海马区。在HA阳性组中,90%的病人IID局限于海马区(P<0.05),在25例低级别海马硬化(HS)中,IID局限于海马区显著低于12例HS高级别病人(P<0.05)。结论颞叶癫痫的抽搐发作放电定位与海马的病理变化存在着密切关系,无HA和低级别HS病人的IID多出现在海马、颞叶内侧皮层、颞叶新皮层的部位,而HA明显者和高级别的HS病人出现的IID往往仅局限于海马(HF)。     

优选短串联重复序列应用于脊肌萎缩症产前诊断的连锁分析

目的 建立完整的适合汉族人群的脊肌萎缩症(SMA)产前基因诊断体系.方法 对30名正常汉族人的外周血样本进行基因多态性分析,评估位于运动神经元存活基因1(SMN1)两侧的短串联重复序列(STR)位点的多态信息含量;并通过在6个SMA产前诊断家系连锁中的应用,优选出STR位点,并结合PCR-酶切法(PCR-RFLP)进一步评价STR位点与SMN1基因的连锁紧密性.结果 从7个STR位点中优选出D5S435、D5S629、D5S610和D5S351四个STR位点用于家系连锁分析,联合PCR-RFLP,在6名待检胎儿中检出2例患者和4例携带者.结论 通过优选出的4个多态性强、与SMN1基因紧密连锁的STR位点,联合家系连锁和PCR-RFLP,建立起稳定可靠的适合汉族人群的SMA产前基因诊断体系.     

细胞外三磷腺苷对失神经大鼠腓肠肌细胞中FoxO3a通路的影响

目的 探讨细胞外三磷腺苷(ATP)对失神经大鼠腓肠肌细胞中FoxO3a/MAFbx通路的影响.方法 雌性成年Wistar大鼠54只随机分为3组:失神经对照组,ATP治疗组,健康对照组.其中失神经对照组和ATP治疗组在右侧梨状肌下缘切断坐骨神经,制作失神经动物模型.术后ATP治疗组于右侧腓肠肌内注射ATP0.1mg/d,左侧腓肠肌内注射等量生理盐水;失神经对照组双下肢注射等量的生理盐水;健康对照组不做任何处理.在术后0、2、7、14、28d分别处死一组大鼠,取其两侧腓肠肌,称肌湿重,计算肌失重比(右侧/左侧),采用实时荧光定量PCR和Western Blot检测大鼠腓肠肌FoxO3a和MAFbx的mRNA和蛋白表达水平以及253位磷酸化的FoxO3a(p-FoxO3a)蛋白表达.结果 ATP治疗组肌湿重比高于失神经对照组,差异有统计学意义(P＜0.01);ATP治疗组FoxO3a的mRNA和蛋白表达略低于失神经对照组,差异无统计学意义(P＞0.05);MAFbx的mRNA和蛋白表达低于失神经对照组,差异有统计学意义(P＜0.05);p-FoxO3a的蛋白表达量较对照组明显增加,不同时段差异均有统计学意义(P＜0.05).结论 细胞外ATP可能通过磷酸化FoxO3a进而抑制MAFbx蛋白的表达来延缓大鼠骨骼肌失神经萎缩.     

多系统萎缩患者的证候规律(167例)

目的:本研究旨在临床观察并分析多系统萎缩(Multiple System Atrophy,MSA)证候规律。方法:采用横断面分析方法,收集所有符合西医诊断标准的MSA患者一般情况及四诊信息,不设定证候类型,辨别每个病例具体证型,提取证候要素。统计证候要素频次,百分比,归纳证候要素组成分布;采用以类型或平均值为界进行证素的分组比较,探讨证候要素与病程、疾病严重程度、疾病分型的相关性。结果:167例MSA患者总体病机虚多实少,寒多热少。P型热证多见,C+P型寒证多见;气虚最多见于C+P型,血虚多见于P型;气虚常与寒证并见,且多见于疾病中晚期,热证常与血虚并见,且多见于疾病早期。肾虚最多见于C+P型,肝病、心病多见于P型,脾虚及胃病多见于C型。痰、湿多见于C+P型和P型,血瘀多见于C+P型,而气陷只见于C+P型。随着病情加重、混合型的出现,虚证与实证并见,正虚和邪实皆增加。结论:MSA核心病机为肾阳虚,总体治则在于温肾助阳。