The evaluation of secondary stress response of grass carp (Ctenopharyngodon idella, Val. 1844) after exposing to the saline water

The stress response of grass carp to salinity was evaluated assessing the levels of hematocrit, leucocrit, plasma glucose, sodium, potassium and calcium. Mean hematocrit values increased following exposure to salinity. Mean leucocrit values elevated after exposure to salinity for 24 h, then decreased. Mean plasma glucose increased during saline exposure for 48 h and then decreased to normal values. Plasma sodium and chloride levels were increased to their highest values after 48 h. While plasma potassium value increased with the exposure time, plasma calcium values were not affected by salinity exposure.     

Hydrogen sulfide ameliorates high glucose-induced endothelial cell senescence by suppressing oxidative stress

AIM：To explore the effect of hydrogen sulfide on the senescence of human umbilical vein endothelial cells (HUVECs) induced by high glucose. METHODS：Senescence model was established by treating HUVECs with 33 mmol/L glucose for 48 h. The parameters were detected to demonstrate the effect of hydrogen sulfide on senescence and the mechanism involved was also investigated. RESULTS：In the cells treated with high glucose, the proliferation was attenuated with a higher number of senescence-associated β-galactosidase (SA-β-Gal) positive cells, and plasminogen activator inhibitor 1 (PAI-1) protein expression, malondialdehyde (MDA) production and NF-κB p65 activity were increased significantly, but the expression of superoxide dismutase 1 (SOD1) was decreased. However, the cell number and SOD1 expression were increased, and the number of SA-β-Gal positive cells, PAI-1 protein expression, MDA production and the activity of NF-κB p65 were decreased after sodium hydrosulfide (100 and 200 μmol/L) treatment.CONCLUSION：Exo-genous hydrogen sulfide prevents HUVECs against high glucose-induced senescence by suppressing oxidative stress and NF-κB p65 activity.     

Mechanisms of hyperglycemia induced by immunosuppressant FK506

AIM：To investigate the effect of immunosuppressant FK506 on serum glucose in rats and to explore its mechanism. METHODS：Sprague-Dawley rats (n=12) were randomly divided into drug group and normal group. The rats in drug group were intraperitoneally injected with FK506 at dose of 1 mg·kg-1·d-1 and the rats in normal group received saline (1 mL·kg-1·d-1, ip) for 14 d. The fasting weight and fasting glucose were regularly measured every 2 d. Visceral fat was isolated from the rats at the end of experiment. The mRNA expression of adiponectin, leptin, visfatin, resistin, retinol-binding protein 4 (RBP4) and peroxisome proliferator-activated receptors γ (PPAR-γ) was determined by real-time fluorescence quantitative PCR. The protein expression of PPAR-γ and adiponectin was measured by Western blotting. RESULTS：Compared with normal group, the concentration of fasting blood glucose in model group was significantly increased from the 10th day (P<0.05). At day 14, the fasting blood glucose of the model group increased from (5.10±062) mmol/L to (7.73 ± 0.73) mmol/L. No significant change of blood glucose in normal group between the 10th day and the 14th day ［from (4.66 ± 0.32) mmol/L to (5.80±0.10) mmol/L］ was observed. Compared with normal group, the mRNA expression of PPAR-γ, adiponectin and leptin in the adipose tissue of model group was significantly decreased (P<001), whereas the expression of visfatin, resistin and RBP4 was significantly increased (P<005). Compared with normal group, the expression of PPAR-γ and adiponectin in model group was decreased (P<001). CONCLUSION：FK506 may decrease the expression of PPAR-γ to change the expression of adipocytokines and induce hyperglycemia in rats.     

亚麻籽油对糖尿病大鼠辅助降血糖功能的研究

[目的]探讨亚麻籽油对糖尿病大鼠空腹血糖及糖耐量的影响。[方法]高脂饲料喂养SD雄性大鼠建立肥胖模型;将肥胖模型大鼠一次性腹腔注射40 mg/kg链脲菌素建立糖尿病模型;将糖尿病模型大鼠随机分为模型对照组以及亚麻籽油低、中、高剂量组,每组8只,连续灌胃30 d后测定模型大鼠空腹血糖和糖耐量。[结果]亚麻籽油高剂量组可以降低糖尿病大鼠的空腹血糖和糖耐量。[结论]亚麻籽油具有辅助降低糖尿病大鼠血糖的功能。     

Influence of stem canker (Rhizoctonia solani Kühn) on tuber yield,tuber size,reducing sugars and crisp colour in cv. Record

Summary In eight experiments in 4 years, inoculating seed tubers withR. solani caused stem canker and in seven experiments decreased the total yield and the yield of tubers 40–70 mm. Yields of larger tubers were usually increased. In most experiments inoculating increased the reducing sugar content of the tubers and darkened the colour of crisps, but did not consistently affect the amounts of sucrose. Treating soil with aldicarb or oxamyl before planting also slightly increased the total reducing sugars.     

绵羊Musclin基因真核表达载体的构建及其对肌细胞糖代谢和胰岛素作用的影响

为了研究绵羊Musclin对糖代谢和胰岛素作用的影响,本试验运用生物信息学软件对其结构特征进行预测,并构建绵羊Musclin基因真核表达载体。分4组对绵羊胎儿成肌细胞进行处理：空载体组（pcDNA3.1）、Musclin过表达组（pcDNA3.1-Musclin）、空载体+胰岛素组（pcDNA3.1+Insulin）、Musclin过表达+胰岛素组（pcDNA3.1-Musclin+Insulin）。然后分别在分化48和72 h时收集细胞,检测Musclin对正常或添加胰岛素培养的分化状态绵羊肌细胞糖代谢的影响,并利用荧光定量PCR检测相关基因表达的变化。酶切鉴定和测序结果表明,成功构建了表达载体pcDNA3.1-Musclin。生物信息学分析表明,绵羊Musclin蛋白含有一个信号肽,并在28氨基酸位点处存在一个酶切位点。亚细胞定位在胞外,属于分泌蛋白。其二级和三级结构以α螺旋和无规则卷曲为主。细胞试验表明,绵羊Musclin基因过表达明显减少了正常或胰岛素处理的绵羊肌细胞糖原含量并增加了培养液中葡萄糖含量。诱导分化72 h时,过表达Musclin抑制了Musclin过表达组和Musclin过表达+胰岛素组绵羊肌细胞中IRS1、AKT1、AKT2、GLUT1、GLUT4基因mRNA表达,并促进了GSK3β mRNA表达;而诱导分化48 h时,只有GLUT4基因的表达受到抑制。综上所述,绵羊Musclin基因过表达可以影响肌细胞糖代谢并减弱胰岛素的作用,二者相互协调以维持糖代谢稳态。其作用机制涉及到上述相关基因的表达变化,且与绵羊成肌细胞的分化状态有关。     

高浓度葡萄糖对猪卵母细胞体外成熟和早期胚胎发育的影响

试验旨在探究高浓度葡萄糖对猪卵母细胞体外成熟及早期胚胎发育能力的影响。取体外分离处于生发泡期的猪卵丘卵母细胞复合体(COCs),分为3个处理组。分别用含葡萄糖浓度为5.6 mmol/L(C组)、10 mmol/L(G-1组)、15 mmol/L(G-2组)的培养液,进行体外成熟(IVM)处理,42 h后观察,并统计卵丘细胞扩散情况和第一极体排出率;对体外成熟42 h后的卵母细胞孤雌激活,统计2-细胞、4-细胞和第7天囊胚发育。结果发现,G-1组和G-2组卵丘细胞扩散度显著低于C组(P<0.05);G-1组和G-2组的MII期卵母细胞死亡率和存活率与C组相比无显著差异(P>0.05),但G-1组极体率显著降低(P<0.05),G-2组极体率极显著低于C组(P<0.01)。孤雌激活后,与C组相比,G-1组和G-2组的2-细胞分裂率显著降低(P<0.05),4-细胞分裂率以及囊胚发育率均极显著降低(P<0.01),但G-1、G-2组囊胚细胞数量与C组相比无显著性差异(P>0.05)。进一步线粒体染色发现,G-1组和G-2组的线粒体与C组相比分布不均。与C组相比,荧光结果显示G-1组和G-2组不仅活性氧(ROS)水平极显著升高(P<0.01),而且G-1组与G-2组谷胱甘肽(GSH)含量显著降低(P<0.05),虽然G-1组丙二醛(MDA)无显著性差异(P>0.05),但G-2组丙二醛(MDA)含量显著升高(P<0.05)。研究结果表明,葡萄糖浓度高会影响猪卵母细胞线粒体分布,氧化应激水平升高,成熟效率降低,损害早期胚胎的发育潜能。     

Electroencephalographic alterations in a mare with presumed intermittent neuroglycopenia caused by severe hypoglycaemia-associated with nonislet cell tumour

The focus of this report was to document the electroencephalogram (EEG) findings associated with nonislet cell tumour-induced hypoglycaemia (NICTH) in a racing Thoroughbred mare subsequently diagnosed with renal carcinoma and carcinomatosis. We evaluated cortical cerebral activity and confirmed paroxysmal activity consistent with subclinical seizures by performing an EEG prior to onset of clinical signs of seizures. We showed that the electrical activity pattern progressed in a similar fashion as in humans with severe, progressive hypoglycaemia and presumed neuroglycopenia. The glycaemic threshold for abnormalities detected in EEG showed that abnormal electrical cortical activity appeared when blood glucose dropped to 44 mg/dL (2.4 mmol/L) and paroxysmal activity spread, becoming generalised when blood glucose dropped to 23 mg/dL (1.3 mmol/L). NICTH is an uncommon paraneoplastic phenomenon in several species. In horses, NICTH has been reported most frequently in primary renal tumours, followed by primary hepatic tumours. This report highlights the importance of investigating the possibility of hypoglycaemia in cases of horses that present altered state of consciousness with or without intermittent seizures. This case report also highlights that the diagnostic work-up for horses presenting with episodic hypoglycaemia should comprise investigation of possible neoplasia, as paraneoplastic hypoglycaemia should be included in the list of differentials of horses with hypoglycaemia.     

添加铬、铁及葡萄糖对土壤中异化铁还原的影响

采用水稻土为供试土壤,通过添加氧化铁、铬酸盐和葡萄糖的模拟试验,在厌氧培养条件下测定了土壤中可浸提态的亚铁和铬( )浓度的变化,探讨了有机碳源及Cr( )、Fe对厌氧条件下水稻土中微生物铁还原的影响及Fe( )和Cr( )还原的竞争关系。结果表明,添加碳源和氧化铁后,能有效促进厌氧条件下水稻土中铁的异化还原过程,显著减小土壤中铬( )浓度;添加Cr( ),将导致土壤中铁还原滞后;厌氧水稻土中Fe( )和Cr( )的竞争还原机制为,有机电子供体导致氧化铁发生微生物还原,产生的Fe( )引起土壤中Cr( )的化学还原。