益肝明目汤治疗糖尿病黄斑水肿的疗效分析

目的 观察益肝明目汤治疗糖尿病黄斑水肿的临床疗效。方法 将49例（91眼）糖尿病黄斑水肿患者随机分为两组,观察组25例49眼,口服益肝明目汤治疗;对照组24例42眼,采用醋酸曲安奈德球后注射治疗,疗程6个月。观察两组患者治疗后视力及黄斑水肿的变化情况,比较两组的综合疗效。结果 治疗6个月后,观察组总有效率93.9%;对照组总有效率76.2%,观察组综合疗效优于对照组,差异有统计学意义（P<0.05）。结论 益肝明目汤治疗糖尿病黄斑水肿远期疗效优于曲安奈德,值得临床推广应用。     

糖尿病足溃疡高危体质的临床特征及对伤口愈合影响的研究

目的 研究中医体质类型与糖尿病足溃疡（diabetic foot ulcers,DFU）的相关性,为糖尿病足溃疡的防治提供新思路。方法 随机收集住院2型糖尿病足溃疡患者73例,采用标准化的中医体质量表判定患者体质类型,并进行身高、体质量、血糖、血脂等指标的测量和观察记录伤口愈合速率、愈合时间、预后结局等情况。分析中医体质对2型糖尿病足溃疡伤口愈合的影响。结果 DFU患者以痰湿质、血瘀质和湿热质为多。其中血瘀质相对其他两种体质足溃疡程度较重,湿热质感染程度较重。湿热质的年龄最低,血瘀质相对年龄偏大。痰湿质的身体质量指数（BMI）最大,糖尿病病程最短（P<0.05）。血瘀质伤口愈合速率和时间较慢（P<0.05）。结论 痰湿质、血瘀质和湿热质是2型糖尿病足溃疡的高危体质,不同DFU患者临床特征不同,血瘀质的伤口愈合较慢,提示不同体质下DFU的预防及治疗应有侧重。     

人参白虎汤对糖尿病大鼠周围神经病变的影响

目的:探讨人参白虎汤对实验性糖尿病大鼠周围神经病变的影响。方法:四氧嘧啶尾静脉注射复制高血糖大鼠模型,以大鼠机械刺激痛阈、大鼠坐骨神经传导速度与坐骨神经病理形态学改变为主要指标,观察人参白虎汤对糖尿病大鼠周围神经病变的影响。结果:人参白虎汤可明显提高糖尿病大鼠痛阈值(P<0.05或P<0.01),提高坐骨神经传导速度P<0.01),明显地改善高血糖引起的神经纤维髓鞘变性(P<0.05或P<0.01),具有一定的抗糖尿病周围神经病变的作用。     

不同剂量链脲佐菌素及不同性别大鼠糖性白内障模型的比较研究

本试验旨在研究不同剂量链脲佐菌素(streptozocin,STZ)及不同性别在建立大鼠糖性白内障模型方面的差异。将65、70和75 mg/kg 3个浓度STZ通过一次性腹腔注射建立雌、雄性大鼠糖性白内障模型,36 h后尾静脉采血测血糖,3周后进行裂隙灯检查,每天测量动物饮食量及排粪尿量变化,每周测定体重。试验结果显示,70 mg/kg STZ比65 mg/kg STZ糖性白内障发生时间缩短约1周,且比75 mg/kg STZ死亡率低。同浓度STZ腹腔注射后雌性大鼠糖尿病发生时间为72 h,雄性大鼠为36 h,白内障发生时间雌性比雄性大鼠慢约1周。试验结果表明,腹腔注射70 mg/kg STZ在糖性白内障模型建立所需时间及模型稳定性等方面具有优势,雄性大鼠较雌性更易于建立糖性白内障模型。     

降糖益肾方干预胰岛素信号通路改善转基因 2型糖尿病1VIKR鼠肾损伤的研究

目的观察降糖益肾方对高脂饮食转基因2型糖尿病MKR鼠血糖、血胰岛素及肾皮质中胰岛素受体、磷脂酞肌醇-3一激酶蛋白表达的影响、方法选取MKR鼠40只经鉴定后,随机分为MKR鼠组、MKR鼠高脂组、降糖益肾方组和糖适贝那组〔MKR鼠组用基础饲料喂养,MKR鼠高脂组、降糖益肾方组和糖适贝那组用高脂饲料喂养,连续喂养8周后,降糖益肾方组给予降糖益肾方,糖适贝那组给予糖适平加贝那普利,同时MKR鼠组和MKR鼠高脂组分别给予蒸馏水灌胃4周〔4周后处死小鼠收集标本,免疫组织化学SABC法检测肾小球中胰岛素受体1(IRS-1),磷脂酞肌醇-3一激}(PI-3K)的蛋白表达〔结果降糖益肾方明显降低高脂饮食MKR鼠肾小球中IRS-1和PI-3 K的蛋白表达水平,与MKR鼠高脂组比较,差异有统计学意义(P<0.01)、结论降糖益肾方改善糖尿病肾病系膜细胞增殖的机制可能与千预胰岛素信号通路有关、     

一例猫肥厚性心肌病的诊断与治疗

针对合肥市某宠物医院接诊的一例猫肥厚性心肌病病例,阐述了其临床诊断和治疗措施。     

Echocardiographic assessment of feline false tendons and their relationship with focal thickening of the left ventricle

Background

False tendons (FTs) are string-like structures in the left ventricle. A FT might produce focal thickening at its insertion region of the left ventricle, which could be mistaken for focal hypertrophic cardiomyopathy.

Comparisons of 3‐, 2‐Dimensional,and M‐Mode Echocardiographical Methods for Estimation of Left Chamber Volumes in Dogs with and without Acquired Heart Disease

Background: Real‐time 3‐dimensional echocardiography (RT3D) is a recent technique based on volumetric scanning, eliminating the need for geometric modeling of the cardiac chambers and minimizing the errors caused by foreshortened views. Hypothesis: Estimations of left ventricular (LV) end‐diastolic (EDV) and end‐systolic volume (ESV), and left atrial (LA) size, differ depending on the echocardiographic technique of estimation. Animals: Fifty‐one dogs with acquired heart disease and 34 healthy control dogs. Methods: Prospective observational study by M‐mode (Teichholz method), Simpson's modified 2‐dimensional (2D) method, and RT3D methods for estimation of LV volumes. LA size was evaluated by 2D and RT3D methods. Results: RT3D showed good agreement with 2D for EDV and ESV, whereas Teichholz method overestimated LV volumes in comparison with the other 2 methods by approximately a factor 2. There were no statistically significant differences among the 3 methods in estimating ejection fraction. Comparison between RT3D assessment of LA end‐systolic volume per kilogram (LAs/kg) and LA to aortic ratio (LA/Ao) measured by 2D relative to each other showed that the RT3D method underestimated LAs/kg at lower values, and overestimated it at higher values. The difference between methods increased with increasing LA size. Conclusions and Clinical Importance: There was good agreement between RT3D and 2D methods of estimating EDV and ESV, whereas the Teichholz method overestimated LV volumes by approximately a factor 2. In comparison with RT3D, LA/Ao underestimated LA size, especially when LA was enlarged.     

Oxygen free radical injury of myocardial mitochondria in the experimental type 2 diabetic rats

AIM: To study the mechanism of diabetic cardiomyopathy and abnormality of oxygen free radicals. METHODS: The contents of myocardial cytosolic cytochrome C, mitochondria cytochrome C, mitochondrial calcium, NO, MDA and the activity of SOD and NOS were determined in diabetic rats induced by STZ. The pathological changes were observed under transmission electron microscope. RESULTS: Compared to the normal and ganoderma group, the levels of mitochondrial NO, iNOS, MDA, calcium and plasma Cyt-C in rat myocardium were higher (P<0.05), while mitochondrial Cyt-C and SOD were lowered in model group (P<0.05). The bouncary indistinct, disorganization, a focal loss of muscular fibril, myocardium mitochondria swelling, pulmonary vascular endothelial cellular swelling and obstructed lumen of the capillary were also observed under transmission electronic microscope. CONCLUSION: The findings indicate that oxyradical and lipid peroxidation might be associated with the damage of myocardial mitochondria in NIDDM rats. Cyt-C and mitochondrial calcium is also involved in the process.     

Comparison of the effects of ivabradine and atenolol on heart rate and echocardiographic variables of left heart function in healthy cats

Background: Ivabradine is a novel negative chronotropic drug used for treatment of ischemic heart disease in people. Little is known about its effects and safety in cats. Hypothesis/Objectives: Ivabradine is not inferior to atenolol with regard to clinical tolerance, heart rate (HR) reduction, and effects on cardiac function in healthy, lightly sedated cats. Animals: Ten healthy laboratory cats. Methods: Physical examination, systolic blood pressure measurement, and transthoracic echocardiography were performed in all cats at baseline and after oral administration (4 weeks each) of ivabradine (0.3 mg/kg q12h) and atenolol (6.25 mg/cat q12h; 1.0–1.7 mg/kg) in a prospective, double‐blind, randomized, active‐control, fully crossed study. A priori noninferiority margins for the effects of ivabradine compared with atenolol were set at 50% (f= 0.5) based on predicted clinical relevance, observer measurement variability, and in agreement with FDA guidelines. Variables were compared by use of 2‐way repeated measures ANOVA. Results: Ivabradine was clinically well tolerated with no adverse events observed. HR (ivabradine, P < .001; atenolol, P < .001; ivabradine versus atenolol, P= .721) and rate‐pressure product (RPP) (ivabradine, P < .001; atenolol, P= .001; ivabradine versus atenolol, P= .847) were not different between treatments. At the dosages used, ivabradine demonstrated more favorable effects than atenolol on echocardiographic indices of left ventricular (LV) systolic and diastolic function and left atrial performance. Conclusions and Clinical Importance: Ivabradine is not inferior to atenolol with regard to effects on HR, RPP, LV function, left atrial performance, and clinical tolerance. Clinical studies in cats with hypertrophic cardiomyopathy are needed to validate these findings.