五酸肽对蛋鸡产蛋性能及其饲料养分消化率的影响

为研究五酸肽对蛋鸡产蛋性能及其饲料养分消化率的影响．试验选择640只53-54周龄海兰褐壳蛋鸡。随机分为4组，每组5个重复，每重复32只鸡。对照组不添加酸化剂、酸化剂组添加市售酸化剂3kg／t、柠檬酸组添加柠檬酸5kg／t和试验组添加五酸肽10kg／t。预试期8d。正试期90d。结果表明：日粮中添加酸化剂3、柠檬酸5和五酸肽10kg／t后，试验组蛋鸡产蛋率比对照组分别提高1．51％（P〉0．05）、1．99％（P〉0．05）和5．11％（P〈0．05），采食量比对照组分别提高5．20％（P〉0．05）、5．92％（P〉0．05）和l0．09％（P〈0．05），破蛋率比对照组分别下降5．20％（P〉0．05）、7．33％（P〉0.05）和19．39％（P〈0．05），脏蛋率比对照组分别下降5．23％（P〉0．05）、10．69％（P〈0．05）和12．23％（P〈0．05），病死率比对照组分别下降17．07％（P〉0．05）、17．56％（P〉0．05）和39．02％（P〈0．05），料蛋比比对照组分别下降1．80％（P〉0．05）、2．70％（P〉0．05）和3．60％（P〈0．05）。添加酸化剂、柠檬酸和五酸肽有增加蛋质量的趋势，但各组平均蛋质量差异不显著（P〉0．05）。与添加酸化剂相比，日粮中添加五酸肽10kg／t后，蛋鸡产蛋率和采食量分别提高3．54％和4．65％（P〉0．05），破蛋率、脏蛋率、病死率和料蛋比分别显著降低14．96％、7．39％、26．47％和1．84％（P〈0．05），粗脂肪表观消化率比对照组分别提高4．51％（P〉0．05）、6．78％（P〉0．05）和8．95％（P〈0．05），粗蛋白表观消化率比对照组分别提高4．31％（P〉0．05）、4．58％（P〉0．05）和8．57％（P〈0．05），钙表观消化率比对照组分别提高1．55％（P〉0．05）、1．78％（P〉0．05）和8．98％（P〈0．05），磷表观消化率比对照组分别提高3．56％（P〉0．05）、4．56％（JP〉0．05）和9．11％（P〈0．05）。与添加酸化剂相比。日粮中添加五酸肽10kg／t后，粗脂肪、粗蛋白、钙和磷的表观消化率分别提高4．25％（P〉0．05）、4．08％（P〉0．05）、7．32％（P〈0．05）和5．36％（P〈0．05）。结果表明：五酸肽能够明显提高蛋鸡的产蛋性能（P〈0．05或P〉0．05），且饲喂效果好于市售酸化剂。

丙氨酸-α-五肽构象稳定性的快速预测

定义了丙氨酸-α-多肽中的特殊氢原子,对构象中与特殊氢原子有关的主要非键作用进行分析,提出使用与特殊氢原子有关的主要非键作用预测多肽构象稳定性,并将之称为特殊氢方法.基于丙氨酸-α-二肽和三肽分子共12个构象,我们确定了与特殊氢原子有关的7个非键作用参数.利用特殊氢方法定量预测丙氨酸-α-五肽分子65个低能构象的相对稳定性,与B3LYP/6-31G*方法比较,得到了满意的结果.

敲低富含亮氨酸的三角状五肽重复结构蛋白(LRPPRC)促进激素抵抗性前列腺癌细胞凋亡

目的研究富含亮氨酸的三角状五肽重复结构蛋白(LRPPRC)对激素抵抗性前列腺癌细胞凋亡的影响。方法Western blot法检测前列腺癌DU145细胞和LNCaP细胞LRPPRC和雄激素受体(AR)蛋白水平;在DU145细胞中瞬转LRPPRC小干涉RNA(siLRPPRC);反转录PCR检测转染细胞LRPPRC mRNA水平;Western blot法检测LRPPRC蛋白水平;噻唑蓝(MTT)法检测细胞存活率;Hoechst33258法和流式细胞术检测细胞凋亡率;荧光素酶法检测细胞ATP水平;Western blot法检测Bcl2、BAX和胱天蛋白酶3(caspase-3)蛋白水平。结果 LRPPRC在DU145细胞和LNCaP细胞均高表达,但DU145细胞不表达AR。敲低DU145细胞LRPPRC水平后,细胞存活率显著降低、细胞凋亡增加、 ATP水平下降、活化的caspase-3蛋白水平增高、Bcl2蛋白水平降低。结论敲低激素抵抗性前列腺癌DU145细胞LRPPRC促进细胞凋亡。

YIGSR五肽及RGD三肽对肝窦内皮细胞窗孔的调节作用

目的 探讨酪氨酸 -异亮氨酸 -甘氨酸 -丝氨酸 -精氨酸 (Tyr- Ile- Gly- Ser- Arg,YIGSR)五肽及精氨酸 -甘氨酸 -天门冬氨酸 (Arg- Gly- Asp,RGD)三肽对肝窦内皮细胞 (SEC)窗孔的影响。方法 用胶原酶原位灌注、Percoll不连续密度梯度离心法分离大鼠的 SEC,并加入包被有 型胶原或层粘连蛋白 (lam inin,L N)基质的盖玻片上培养。采用扫描电镜技术及放免方法 ,分别观察 YIGSR五肽及 RGD三肽对 SEC窗孔数目、大小 ,以及 SEC分泌 型胶原能力的影响。结果 生长在包被 L N的盖玻片上 48小时的 SEC,其窗孔数目及大小均比生长在 型胶原上的 SEC明显降低 (P<0 .0 5 ) ;但同时加入 YIGSR五肽 (5 0 μg/ ml)及 RGD三肽 (5 0 μg/ m l)作用 48小时后 ,SEC窗孔数目及大小均有明显增加 (P<0 .0 5 ) ,同样地 ,经 YIGSR五肽及 RGD三肽作用后 ,生长在 L N上的 SEC分泌 型胶原的能力亦明显下降 (P<0 .0 5 )。结论 YIGSR五肽及 RGD三肽对 SEC的形态 (如窗孔 )及功能 (如分泌 型胶原 )

An accelerated method to evaluate thymopentin release from microspheres in vitro

To design an accelerated method to evaluate thymopentin release from PLGA microspheres in vitro. Microspheres were prepared by double emulsion technique, using poly（lactide-co-glycolide） （PLGA） as carrier. At higher medium temperature （45℃, 50℃ and 55℃）, an accelerated release testing in short time was studied and correlated with the conventional release （37℃） in vitro. The release in vitro of thymopentin from PLGA microspheres at 45 ℃, 50℃ and 55℃ was significantly accelerated （P 〈 0.05）. In particular, at 50℃, an accelerated release （30 h） of the hydrophilic peptide from the PLGA matrix was achieved and correlated well with the conventional release （30 d）. An accelerated release testing in vitro at higher temperature could be used to monitor thymopentin release from PLGA microspheres.

Effect of somatostatin analogue octreotide injected into the third cerebral ventricle on pentagastrin-induced gastric acid secretion in rats

AIM： To investigate the effect of long-lasting somatostatin analogue octreotide （Oct） injected into the third cerebral ventricle （TCV） on gastric acid secretion in rats. METHODS： TCVs were cannulated in male Wistar rats anesthetized with sodium pentobarbital. One week later acute gastric lumen perfusion was carried out and gastric acid was continuously washed with 37℃ saline by a perfusion pump. Gastric perfusion samples were collected every 10 min and titrated by 0.01 moL/L NaOH to neutral. On the basis of subcutaneous （sc） injection of pentagastrin （G-5, 160 μg/kg）, Oct （0.025 μg, 0.05 μg, 0.1 μg, n=12 in each group） or vehicle （pyrogen-free physiological saline, n = 10） was injected into the TCV, Before and after the TCV injection, 1 h total acid output （TAO） was determined and experimental data were expressed in change rate （%） of TAO. RESULTS： Oct （0.025, 0.05 and 0.1 μg） injected into the TCV resulted in change rate of 1.56% （P〉0.05）, 20.21% （P〈 0.01） and 37.82% of TAO （P〈 0.001）, respectively. Moreover, comparison in change rate of TAO among these 3 doses showed P〈 0.05 between 0.025μg and 0.05 μg, P〈 0.01 between 0.025 μg and 0.ling, and P〈 0.05 between 0.05μg and 0.1 μg. However, sc injection of 0.05 μg Oct had no effect on G-5 stimulated gastric acid secretion. CONCLUSION： Octreotide injected into the third cerebral ventricle inhibits gastrin-induced gastric acid secretion in a dose-dependent manner.

Influence of gastric inhibitory polypeptide on pentagastrinstimulated gastric acid secretion in patients with type 2 diabetes and healthy controls

AIM： Gastric inhibitory polypeptide is secreted from intestinal K-cells in response to nutrient ingestion and acts as an incretin hormone in human physiology. While animal experiments suggested a role for GIP as an inhibitor of gastric secretion, the GIP effects on gastric acid output in humans are still controversial. METHODS： Pentagastrin was administered at an infusion rate of 1 μg . kg^-1 . h^-1 over 300 min in 8 patients with type 2 diabetes （2 female, 6 male, 54± 10 years, BMI 30.5 ± 2.2 kg/m^2; no history of autonomic neuropathy） and 8 healthy subjects （2/6, 46 ± 6 years., 28.9 ± 5.3 kg/ m^2）. A hyperglycaemic clamp （140 mg/dl） was performed over 240 min. Placebo, GIP at a physiological dose （1 pmol . kg^-1 . min^-1）, and GIP at a pharmacological dose （4 mol . kg^-1 . min^-1） were administered over 60 min each. Boluses of placebo, 20 pmol GIP/kg, and 80 pmol GIP/kg were injected intravenously at the beginning of each infusion period, respectively. Gastric volume, acid and chloride output were analysed in 15-min intervals. Capillary and venous blood samples were drawn for the determination of glucose and total GIP. Statistics were carried out by repeated-measures ANOVA and one-way ANOVA. RESULTS： Plasma glucose concentrations during the hyperglycaemic clamp experiments were not different between patients with type 2 diabetes and controls. Steady-state GIP plasma levels were 61 ±8 and 79 ± 12 pmol/I during the low-dose and 327±35 and 327± 17 pmol/I during the high-dose infusion of GIP, in healthy control subjects and in patients with type 2 diabetes, respectively （P= 0.23 and p 0.99）. Pentagastrin markedly increased gastric acid and chloride secretion （P〈 0.001）. There were no significant differences in the rates of gastric acid or chloride output between the experimental periods with placebo or any dose of GIP. The temporal patterns of gastric acid and chloride secretion were similar in patients with type 2 diabetes and healthy controls （P= 0.86 and P= 0.61, respectively）. CONCLUSION： Pentagastrin-stimulated gastric acid secretion is similar in patients with type 2 diabetes and healthy controls. GIP administration does not influence gastric acid secretion at physiological or pharmacological plasma levels. Therefore, GIP appears to act as an incretin rather than as an enterogastrone in human physiology.

Pernicious anemia: What are the actual diagnosis criteria?

A gastric intrinsic factor output under 200 U/h after pentagastrin stimulation (N > 2000 U/h) is specific for pernicious anemia. The other findings are either variable or non specific. Serum intrinsic factor antibodies, considered as specific in general practice, are present only in half of the patients with pernicious anemia. In their absence, since the disappearance of the Schilling tests, the gastric tubage currently used for the study of gastric acid secretion, is obligatory for the simultaneous study of intrinsic factor output. This study is important to eliminate another disease much more frequent than pernicious anemia, the protein bound to cobalamin malabsorption was observed in achlorhydric simple atrophic gastritis in the presence of intrinsic factor secretion.

光谱法研究Leu-ENK与ct-DNA的相互作用

亮氨酸脑啡五肽是动物体内一种具有很强生物活性的阿片肽,在生物体内有极其重要的作用。利用紫外光谱和荧光光谱法研究了亮氨酸脑啡五肽(Leu-ENK)与小牛胸腺DNA(ct-DNA)的相互作用。研究表明,Leu-ENK-ct-DNA体系随着Leu-ENK浓度增大,体系的紫外光谱呈增色效应;随着ct-DNA浓度的增加,体系Leu-ENK的荧光逐渐猝灭;这两种方法的实验结果都表明两者的作用模式主要为嵌入结合,根据Stern-Volmer方程可知Leu-ENK-ct-DNA体系的作用属于静态猝灭。计算得到两者作用的结合常数达到2.54×104L/mol,结合位点数为1.014。