盐酸二甲双胍治疗Ⅱ型糖尿病疗效评价

为比较盐酸二甲双胍和糖适平对Ⅱ型糖尿病的治疗效果，通过３３例Ⅱ型糖尿病患者服用二甲双胍和３５例Ⅱ型糖尿病患者服用糖适平，观察４ｍｏ后发现二甲双胍在降低血糖、２４ｈ尿糖定量，降低血脂及逆转外周神经病变方面有显著疗效。但二甲双胍不能升高血浆Ｃ—肽水平，不能降低２４ｈ尿蛋白质定量。如能将二甲双胍和糖适平联合应用将会提高疗效，减轻副作用。     

赖诺普利与氯沙坦预防压力负荷性心肌肥厚的实验研究

目的 探讨大鼠心肌肥厚时心血管重构的结构、生化改变及赖诺普利与氯沙坦对心血管重构的预防作用。方法 膈下腹主动脉缩窄法建立大鼠心肌肥厚模型。假手术组、模型组、降压和非降压剂量赖诺普利与氯沙坦在术后第2天用药至30天后，检测平均动脉压(MAP)、心肌肥厚程度及局部心肌组织一氧化氮(N0)、一氧化氮合酶(NOS)和胶原蛋白含量。结果 (1)与假手术组相比，模型组MAP、左室重量(LVW)、左室重量指数(LVMI)、心肌细胞横径(TDM)、胶原蛋白分别提高28．6％、20．5％、26．9％、17．9％、54．4％(P＜0．01)；NO、NOS分别降低53．4％、51．2％(P＜0．01)。(2)降压剂量赖诺普利与氯沙坦和非降压剂量氯沙坦干预后，LVW、LVMI、TDM、NO、NOS、胶原蛋白含量与假手术组无明显差异。非降压剂量赖诺普利可使LVW、LVMI和TDM下降，但仍高于假手术组(P＜0．01)，NO、NOS改善不明显；(3)LVMI与MAP、胶原蛋白含量均呈正相关(分别为γ=0．7841，γ=0．8177，P＜0．01)，与NO显负相关(γ=-0．7730，P＜0．01)。结论 心血管重构与血压、心脏间质成分及NO有密切关系；赖诺普利预防心肌肥厚可能是血流动力学和非血流动力学因素共同作用的结果；氯沙坦可能主要依靠非血流动力学因素抗心肌肥厚。     

Salvianolic acid A demonstrates cardioprotective effects in rat hearts and cardiomyocytes after ischemia/reperfusion injury

Salvianolic acid A (Sal A), the water-soluble component from the root of the Salvia miltiorrhiza plant, possesses antioxidant, antiproliferative, and antiplatelet properties. However, whether it plays a role in the protection against ischemia-reperfusion (I/R) injury in rat hearts has yet to be elucidated. In the present study, we tested cell viability, shortening amplitude, necrosis, apoptosis, and the expression levels of Akt, phosphorylated Akt, Bcl-2, Bax, and caspase-3 after 3-hour simulated ischemia and 2- or 6-hour simulated reperfusion in cardiomyocytes. We further observed the contractile function and infarct size in isolated hearts after they were subjected to global 30-minute ischemia and 120-minute reperfusion. Pretreatment with Sal A markedly increased cell viability and shortening amplitude while reducing evidence of necrosis and apoptosis in the cells. In addition, the expression of Bcl-2 was upregulated and Bax was downregulated, thereby increasing the Bcl-2/Bax ratio. Sal A inhibited the activation of caspase-3 as well. The results also showed that Sal A significantly increased phosphorylation of Akt and that this phosphorylation can be partially inhibited by phosphoinositide 3-kinase/Akt inhibitor. Furthermore, Sal A improved I/R-induced myocardial contractile function and reduced infarct size. In summary, our results showed that Sal A prevents I/R-induced myocardial damage by reducing necrosis and apoptosis in isolated rat hearts and cardiomyocytes.     

50岁以上甲状腺机能亢进症70例临床分析

本文分析50岁以上甲亢患者70例,显示老年前期及老年期患者病程长,临床表现多不典型。浸润性突眼少于中青年组,结节性甲肿显著高于中青年组,而甲状腺摄取(131)碘率及血清T T_s、T T_4 FT_4~1均显著低于中青年组(P<0.01)。口服他巴唑抗甲状腺治疗达到症状控制所需剂量及总天数均少于中青年组(P<0.01)。提示老年甲亢在治疗上要区别于中青年甲亢。     

不同磷脂肽段诱导的实验性自身免疫性脑脊髓炎模型病理特征多样性的研究

目的:探索是否不同磷脂肽段可以诱导Lewis大鼠产生不同的病理学表现。方法:采用髓鞘碱性蛋白82-99(MBP82-99)、MBP68-86、髓鞘少突胶质细胞糖蛋白35-55(MOG35-55)免疫Lewis大鼠,每天进行神经功能评分。免疫后取各组大鼠大脑、小脑、脑干和脊髓组织,观察炎性细胞浸润部位和浸润程度、有无脱髓鞘和轴索损害。结果:MBP68-86和MBP82-99两组大鼠的大脑、脑干、小脑和脊髓组织均有炎性细胞浸润,脊髓炎症程度重于其他部位;MBP68-86和MBP82-99诱导的脊髓炎症程度无统计学差异;MOG35-55组大鼠仅脊髓组织受累,且炎症程度明显低于MBP组,其余各组未见炎性细胞浸润。各组大鼠神经组织均未见脱髓鞘和轴索受累。结论:不同磷脂肽段诱导Lewis大鼠神经组织炎性细胞浸润的分布和程度不同。     

静脉注射尼卡地平对重度高血压患者血压和心功能的影响

目的研究静脉注射尼卡地平对重度高血压患者血压和左心功能的影响。方法用尼卡地平持续２４ｈ静脉滴注（１．５～３ｍｇ／ｈ）治疗２０例重度高血压患者，观察给药前后血压、心率、左心功能以及自觉症状变化。结果降压显效率１００％，５ｍｉｎ起效，０．５～１ｈ血压降至理想水平，同时全部病例脑循环障碍症状消失，２４ｈ降压效果平稳，心率轻度增快（＜１０ｍｉｎ－１），左心收缩功能明显改善，而舒张功能未见变化。结论静脉注射尼卡地平可迅速、显著而平稳降低重度高血压患者的血压，改善左心收缩功能。     

房颤对高血压心脏病心电图的影响

对 18例高血压心脏病合并房颤病人房颤转复前后的心电图进行比较 ,发现房颤时 Q RS波振幅较窦性心律时明显下降 ,Σ QRS平均下降 17.9% (182 .5± 40 .7比 14 9.2± 33.6 m m ,P <0 .0 5 )。同期超声心动图提示房颤时 QRS波振幅降低与左室容积减少有关。建议对房颤状态下心电图判断左室肥厚的 QRS波振幅标准应相应降低 ,否则影响敏感性     

Suppression of autophagy by FIP200 deletion leads to osteopenia in mice through the inhibition of osteoblast terminal differentiation

Autophagy is a conserved lysosomal degradation process that has important roles in both normal human physiology and disease. However, the function of autophagy in bone homeostasis is not well understood. Here, we report that autophagy is activated during osteoblast differentiation. Ablation of focal adhesion kinase family interacting protein of 200 kD (FIP200), an essential component of mammalian autophagy, led to multiple autophagic defects in osteoblasts including aberrantly increased p62 expression, deficient LC3‐II conversion, defective autophagy flux, absence of GFP‐LC3 puncta in FIP200‐null osteoblasts expressing transgenic GFP‐LC3, and absence of autophagosome‐like structures by electron microscope examination. Osteoblast‐specific deletion of FIP200 led to osteopenia in mice. Histomorphometric analysis revealed that the osteopenia was the result of cell‐autonomous effects of FIP200 deletion on osteoblasts. FIP200 deletion led to defective osteoblast terminal differentiation in both primary bone marrow and calvarial osteoblasts in vitro. Interestingly, both proliferation and differentiation were not adversely affected by FIP200 deletion in early cultures. However, FIP200 deletion led to defective osteoblast nodule formation after initial proliferation and differentiation. Furthermore, treatment with autophagy inhibitors recapitulated the effects of FIP200 deletion on osteoblast differentiation. Taken together, these data identify FIP200 as an important regulator of bone development and reveal a novel role of autophagy in osteoblast function through its positive role in supporting osteoblast nodule formation and differentiation. © 2013 American Society for Bone and Mineral Research.