闭锁群体BLUP选择下遗传方差和近交系数的变化

采用计算机随机模拟方法模拟了在一个闭锁群体内连续对单个性状进行 1 5个世代选择的情况。选择过程中世代不重叠 ,每个世代的种畜根据动物模型最佳线性无偏预测 (BLUP)法估计的育种值进行选留 ,并在此基础上系统地比较了不同群体规模、公母比例和性状遗传力对群体遗传方差和近交系数变化的影响。结果表明 ,扩大育种群规模、增加公畜比例以及对低遗传力性状进行选择时 ,群体遗传方差降低的速度和近交系数上升的速度会更慢 ,在长期选择时可望获得更大的持续进展和适宜的近交增量     

利用体外培养法建立饲料营养成分与瘤胃丙酸产量的回归模型

根据美国康乃尔净碳水化合物和蛋白质体系 (CNCPS) ,分析测定了 4类 2 4种饲料的营养成分 ,利用体外批次培养技术测定了它们在体外培养一定时间后的丙酸产量 ,并由此建立了饲料中产丙酸的营养成分和瘤胃丙酸产量的回归方程     

Rat mesenchymal stem cells differentiate into neuron-like cells induced by berberine in vitro

AIM: To investigate whether berberine can induce rat mesenchymal stem cells (MSCs) to differentiate into neuron -like cells in vitro. METHODS: MSCs were separated from young rat femurs marrow and expanded in culture medium. MSCs were induced to differentiate by berberine. The morphological changes of MSCs were evaluated by light microscope.Neuron-spcific enolase (NSE), neurofilament (NF), glial fibrillary acidic protein (GFAP) were detected by immunohistochemistry. RESULTS: Induced by berberine for 8 hours,MSCs exhibited neurotype . The expression of NSE and NF in the neuron-like cells was positive, but the glial astrocyte marker GFAP didn't express. CONCLUSION: Berberine may induce adult rat MSCs to differentiate into neuron-like cells in vitro.     

Relation between TNF-α,TNFR I expression and apoptosis in oral lichen planus

AIM: To examine the expression and distribution of tumor necrosis factor-α (TNF-α), tumor necrosis factor receptor I (TNFR I) and apoptosis in oral lichen planus, and evaluate their roles and relation in the oral lichen. METHODS: Immunohistochemical technique and TUNEL were employed to study the expression of TNF-α, TNFR I and apoptosis in 50 cases of oral lichen planus and 10 normal oral mucosa specimens. RESULTS: Compared with the normal control group, TNF-α expression was upregulated in mononuclear cells in lamina propria and decreased in keratinocytes in oral lichen planus lesion (P<0.05). On the contrary, TNFR I expression was increased in keratinocytes and decreased in lamina propria in oral lichen planus lesion (P<0.05). The increased apoptosis index in keratinocytes and the decreased apoptosis index in lamina propria were found in oral lichen planus (P<0.05). CONCLUSION: The accelerated apoptosis of keratinocytes and the inhibition of lymphocytes apoptosis may contribute to the formation and progression of oral lichen planus.     

Nitric oxide-mediated the cardioprotection of tumor necrosis factor-alpha on cultured neonatal rat cardiomyocytes during hypoxia/reoxygenation

AIM: To investigate the role of nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC) and protein kinase C (PKC) signaling in tumor necrosis factor-α (TNF-α)-induced cardioprotection against hypoxia/reoxygenation (H/R) injury. METHODS: Neonatal rat ventricular myocytes were pretreated with TNF-α or sodium nitroprusside (SNP) or L-arginine (L-Arg), respectively, for 12 h and then subjected to continuous hypoxia for 12 h, followed by reoxygenation for 6 h. The manganese superoxide dismutase (Mn-SOD) activity of the cells was measured after H/R. Myocyte injury was determined by the release of lactic dehydrogenase (LDH). RESULTS: TNF-α (10⁵ U/L) significantly increased the Mn-SOD activity and decreased release of LDH from ventricular myocytes. The cardioprotection against H/R injury was induced by the pretreatment with SNP (5 μmol/L) or L-Arg (5 mmol/L), which was blocked by ODQ (10 μmol/L), the specific sGC inhibitor, and Chel (5 μmol/L), the specific PKC inhibitor. Pretreatment with L-NAME (100 μmol/L), ODQ, Chel, antoxidant 2-MPG (400 μmol/L) or tyrosine kinase inhibitor genistein (50 μmol/L) attenuated the increased Mn-SOD activity and reduced LDH level induced by TNF-α. CONCLUSION: The results suggest that NO may play a role in TNF-α-induced cardioprotection, which is mediated by sGC and PKC.     

Effects of 11, 12-EET and ischemic preconditioning on phosphorylated ERK and p38 MAPK during ischemia and reperfusion in rat myocardium

AIM: In order to study the relationship between the ERK and p38 MAPK activation and the protection of 11, 12-epoxyeicosatrienoic acid (11, 12-EET) and ischemia preconditioning (IP), the effects of 11, 12-EET and ischemic preconditioning on phosphorylated ERK and p38 MAPK during ischemia and reperfusion in rat myocardium were examined. METHODS: The rat heart was subjected to ischemia for 5 min by ligating the left anterior descending coronary artery followed by reperfusion for 5 min (two times) to undergo ischemia preconditioning. The rats were divided into 5 groups: (1) control; (2) sham group; (3) ischemia/reperfusion (I/R) group, in which the rat heart suffered from 60 min ischemia followed by 30 min reperfusion; (4) IP plus I/R group; (5) EET plus I/R group, in which 6.28×10^-8 mol/L 11, 12-EET was injected intravenously 20 min before I/R. The heart function was examined, and phosphorylated ERK and p38 MAPK were detected by Western blot. RESULTS: At 30 min reperfusion, +dp/dt_max, -dp/dt_max and LVDP decreased significantly in I/R group compared with sham group, IP plus I/R group and EET plus I/R group; Phosphorylated ERK1/2 level was higher in I/R group than sham group, but was lower in I/R group than IP plus I/R group and EET plus I/R group; Phosphorylated p38 MAPK level was lower in control, sham, IP plus I/R and EET plus I/R group than I/R group. CONCLUSION: 11,12-EET protects rat heart against ischemia/reperfusion injury, the mechanism may be related to activation of ERK1/2 and inhibition of p38 MAPK.     

Changes of potassium currents in rabbit ventricle with healed myocardial infarction

AIM: To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), and to investigate the changes of action potential duration (APD),transient outward potassium current (I_to), delayed rectifier potassium current (I_K) and inward rectifier potassium current (I_K1) of left ventricular myocytes in noninfarcted zone of HMI. METHODS: 12 rabbits were randomly assigned in two groups: HMI group (thoracotomy and ligation of the circumflex coronary); sham-operated group (thoracotomy but no conorary ligation). 3 months after operation, whole cell patch clamp technique was used to record APD, I_to, I_K and I_K1 of ventricular myocytes in non-infarcted zone. RESULTS: Membrane capacitance was larger in HMI group than that in sham-operated group. Action potential duration was lengthened significantly in HMI group and early after depolarization (EAD) appeared in HMI group. The densities of I_to, I_K,tail and I_K1 were reduced significantly in HMI group (P<0.01), from (6.72±0.42) pA/pF, (1.54±0.13) pA/pF and (25.6±2.6) pA/pF in Sham-operated group to (4.03±0.33) pA/pF, (1.14±0.11) pA/pF and (17.6±2.3) pA/pF, respectively. CONCLUSION: The reduced densities of I_to, I_K,tail and I_K1 in ventricular myocytes of non-infarcted zone in HMI are responsible for the prolongation of APD and the presentation of EAD, which play important roles in the malignant arrhythmia of HMI.     

BsC3-41杀蚊幼制剂对蚊幼虫毒杀效果研究

通过以BsC3- 41杀蚊幼制剂对 3种蚊幼虫进行生物活性测定和野外灭蚊试验 ,结果表明 :该制剂对致乏库蚊CulexfatigansWiedemann的毒杀效果最好、对中华按蚊AnophelessinensisWiedemann次之、对白纹伊蚊AedesalbopictusSkuse的效果较差 ,2 4小时LC50值分别为 0 2 0 2 5 μg/ml、 2 5 363μg/ml和 5 9 730 2 μg/ml。野外水体灭蚊使用 3ml/m2 的浓度防治淡色库蚊效果可达 98 88%～ 1 0 0 0 0 % ,使用 1 0ml/m2 的浓度防治中华按蚊效果可达96 81 %～ 1 0 0 0 0 % ,使用 2 0 0ml/m2 的浓度防治白纹伊蚊效果达到 90 64%以上。     

噻二唑基-3-哒嗪酮类化合物的合成及生物活性

将取代的二酰基肼环合后,得到中间体2-芳基-5-氯甲基-1,3,4-噻二唑,然后与2-叔丁基-4-氯-5-羟基-3(2H)-哒嗪酮反应,合成了8个未见文献报道的含噻二唑基哒嗪酮类化合物,其化学结构经1H NMR、高分辩质谱和元素分析确认。生物活性测试结果表明,部分化合物对粘虫P.separate W.有较好的抑制生长活性,其中化合物 3b 的EC50值为21 mg/L。     

Osmolarity,cell volume and proliferation in nasopharyngeal carcinoma cells

AIM: To investigate the relationship between osmolarity, cell volume and cell proliferation in nasopharyngeal carcinoma cells. METHODS: MTT method was applied to detect the proliferation ability of the poorly-differentiated nasopharyngeal carcinoma cell (CNE-2Z) under various osmolarity conditions. The flow cytometry was used to analyse cell cycle distribution. Cell volume was obtained by the image analysis of living cells and cell viability was determined by the trypan blue assay. RESULTS: Cultivation of cells under the hypertonic conditions of 370 and 440 mOsmol/L increased cell volume by 8.7% and 27.8% and facilitated cell proliferation by 22.2% and 33.9%, respectively. However, hypotonic incubation of cells with osmolarity of 160 and 230 mOsmol/L decreased cell volume by 12.8% and 4.1% and inhibited cell proliferation by 34.0% and 15.6%, respectively. Cell volume was positively correlated with cell proliferation rate. Long-term cultivation of cells under anisotonic conditions did not significantly alter cell cycle distribution, but hypotonic cultivation decreased cell viability. CONCLUSION: Proliferation of nasopharyngeal carcinoma cells was closely correlated with the osmolarity of culture medium and cell volume. Hypotonic cultivation may inhibit cell proliferation by decreasing cell volume to facilitate cell death mechanisms.