Peptides with CCK-like activity administered intracranially elicit satiety in sheep

Cholecystokinin (CCK) peptides and receptors have been shown to be present in the brain as well as in gastrointestinal organs. While functions for peripheral CCK are well recognized, those for central CCK peptides are only now being investigated. We have shown previously that CCK-octapeptide (CCK-OP) is a very potent and specific suppressor of feeding when administered in the cerebral ventricles of sheep. In the present study the objective was to determine the relative potency of several CCK analogues in inhibiting feeding when administered as 75 min continuous injections into the lateral cerebral ventricles of 2-hr fasted sheep. In comparing feeding response during CCK-OP injections to that during caerulein injections, it was found that feed intakes were similar only at an equal molar dose (0.638 pmole/min); whereas three times as much CCK-33 (1.91 pmoles/min) as CCK-OP (0.638 pmoles/min) was required to produce similar feed intakes. Both caerulein (0.638 pmoles/min) and CCK-33 (1.91 pmoles/min) caused significant decreases in feeding compared to control (sCSF). Desulfated CCK-OP had no effect on feeding at a dose (0.638 pmoles/min) that causes 80–100% decreases in feeding when the C-7 tyrosine is sulfated. Feed intake was significantly less with 2.55 pmoles/min CCK-OP than with an equal dose of desulfated CCK-OP. These results concur with those of previous studies on specific CCK receptors in the pancreas and in the brain, and therefore support the concept of specific CCK receptors in brain having a role in satiety.     

Relationship between prostagandin E1, polyphloretin phosphate and alpha and beta adrenoceptor-bound feeding loci in the hypothalamus of sheep

We have previously proposed that prostaglandins (PG) may play a modulating role on hypothalamic areas controlling feeding and energy balance. In the present experiment we have tested in the medial hypothalamus of sheep for interactions between α and β adrenoceptors, PGE₁ and a PG antagonist polyphloretin phosphate (PPP). Sheep were prepared with 6 cannula guides in the hypothalamus. In each sheep following preliminary injection with 1-norepinephrine (1-NE) and dl-isoproterenol (dl-Isop), loci were selected that showed preferentially either α or β adrenoceptor-bound feeding. In the subsequent experiment PGE₁ blocked the 1-NE (α-agonist) elicited feeding in the α-bound feeding loci but PGE₁ elicited feeding when injected into the β-bound feeding loci. The PGE₁-elicited feeding was specifically blocked by a β antagonist (LB-46). The PPP elicited feeding in both α and β-bound feeding loci but the responses were blocked only by the α antagonist (phentolamine) in the α loci and by the β antagonist (LB-46) in the β loci. These responses lend support to our previous conclusions that injection of α agonists into some and β agonists into other hypothalamic sites, but not vice versa will elicit feeding. PGE₁, injected into loci showing differences in sensitivity to adrenoceptor agonists which elicit feeding, results in increased feeding, as in this experiment, or decreased feeding as shown in a previous report. Thus, we conclude that although it is unlikely that systematically produced PG modulate hypothalamic controls on feeding and energy balance because of the dual effect on feeding, there may be an interaction of endogenous hypothalamic PG and adrenoceptors.     

Catch-up growth up to ten years of age in children born very preterm or with very low birth weight

Background  

Improved survival due to advances in neonatal care has brought issues such as postnatal growth and development more to the focus of our attention. Most studies report stunting in children born very preterm and/or small for gestational age. In this article we study the growth pattern of these children and aim to identify factors associated with postnatal catch-up growth.     

Influence of dietary conjugated linoleic Acid and fat source on body fat and apoptosis in mice

OBJECTIVE: To determine whether altered dietary essential fatty acid (linoleic and arachidonic acid) concentrations alter sensitivity to conjugated linoleic acid (CLA)-induced body fat loss or DNA fragmentation. RESEARCH METHODS AND PROCEDURES: Mice were fed diets containing soy oil (control), coconut oil [essential fatty acid deficient (EFAD)], or fish oil (FO) for 42 days, and then diets were supplemented with a mixture of CLA isomers (0.5% of the diet) for 14 days. Body fat index, fat pad and liver weights, DNA fragmentation in adipose tissue, and fatty acid profiles of adipose tissue were determined. RESULTS: The EFAD diet decreased (p < 0.05) linoleic and arachidonic acid in mouse adipose tissue but did not affect body fat. Dietary CLA caused a reduction (p < 0.05) in body fat. Mice fed the EFAD diet and then supplemented with CLA exhibited a greater reduction (p < 0.001) in body fat (20.21% vs. 6.94% in EFAD and EFAD + CLA-fed mice, respectively) compared with mice fed soy oil. Dietary FO decreased linoleic acid and increased arachidonic acid in mouse adipose tissue. Mice fed FO or CLA were leaner (p < 0.05) than control mice. FO + CLA-fed mice did not differ in body fat compared with FO-fed mice. Adipose tissue apoptosis was increased (p < 0.001) in CLA-supplemented mice and was not affected by fat source. DISCUSSION: Reductions in linoleic acid concentration made mice more sensitive to CLA-induced body fat loss only when arachidonic acid concentrations were also reduced. Dietary essential fatty acids did not affect CLA-induced DNA fragmentation.     

World health system performance revisited: the impact of varying the relative importance of health system goals

Background

In 2002, the World Health Organization published a health system performance ranking for 191 member countries. The ranking was based on five indicators, with fixed weights common to all countries.

Methods

We investigate the feasibility and desirability of using mathematical programming techniques that allow weights to vary across countries to reflect their varying circumstances and objectives.

Results

By global distributional measures, scores and ranks are found to be not very sensitive to changes in weights, although differences can be large for individual countries.

Conclusions

Building the flexibility of variable weights into calculation of the performance index is a useful way to respond to the debates and criticisms appearing since publication of the ranking.     

Ventral hernia repair: a study of current practice

Ventral wall hernias are common; despite this, there are no guidelines on the best surgical management. The aim of this study was to examine the types of repair in use for abdominal wall hernias in the West of Scotland over a 3-month period. Data were gathered on 120 patients. There were 60 incisional, 32 umbilical, and 28 epigastric hernias. The main indication for repair was pain (78%), while 12 patients (10%), presented acutely with incarceration or strangulation. The most common method of repair was sutured (55%), followed by mesh (29%) and Mayo repair (16%). There was no correlation between use of mesh and hernia size or whether repair was for a recurrent hernia. Surgical practice varies widely in the repair of ventral wall hernias. Clinical trials are required to establish the best method of repair for this common condition. Electronic Publication     

医用高等数学函数图形动画库的制作

利用专业数学软件将医用高等数学中一些常见的函数制作成图形动画,并建立一个“高等数学函数图形动画库”,该库包括了函数图形的生成、概率分布函数的动态变化和高数概念的几何刻划等三个方面的动画。该动画库可供教师在编写多媒体课件时直接引用,也可作为学生自学时调用播放。     

hTEFT重组绿色荧光表达载体的构建与表达

目的构建人端粒酶逆转录酶(hTERT)片段的真核表达质粒。方法用RT-PCR方法从肝癌组织中提取总RNA扩增出hTERT基因片段,将其连接pGEM-TEasy质粒上,将重组质粒pGEM-T-hTERT和pEGFP-C3真核绿色荧光蛋白表达载体同时用HindⅢ和BamHⅠ双酶切后进行连接,再将重组的pEGFP-C3-hTERT基因片段转染NIH3T3细胞,经G418筛选获得稳定转染的细胞系,荧光倒置显微镜观察并检测转染细胞的hTERTmRNA表达水平。结果DNA序列分析证实了重组载体pGEM-T-hTERT和pEGFP-C3-hTERT内插入片段的碱基组成与公开发表的hTERT序列一致。转染pEGFP-C3-hTERT的NIH3T3细胞可见绿色荧光,并检出高水平表达的hTERT。结论成功构建高效表达hTERT的真核表达载体,为以hTERT为靶点的肿瘤治疗打下实验基础。     

急性肺损伤幼鼠肺泡Ⅱ型上皮细胞和SP-A变化相关性的研究

目的：该实验旨在研究急性肺损伤（ALI）时肺泡Ⅱ型上皮细胞（AEC-Ⅱ）超微结构变化和肺组织表面活性蛋白SP-A含量的变化关系，从而探讨ALI的发病机制。方法：48只Sprague-Dawley幼鼠被随机分为正常对照组和ALI组。 腹腔注射脂多糖（LPS，4 mg/kg）建立ALI模型，正常对照组注射等量生理盐水。 LPS注射后24，48，72 h每亚组各处死8只大鼠。 取左肺下肺组织待透射电镜检查。 用Western blot方法测定肺组织SP-A的相对含量。结果：ALI 24 h时，AEC-Ⅱ微绒毛消失。24 h及48 h时板层小体（lamellar body, Lb）数量增加，体积增大，密度减低，排空明显增强，呈指环状绕核排列，细胞增生活跃，代谢旺盛。48 h时Lb呈巨大空泡样变性。肺组织SP-A含量明显高于对照组（24 h时ALI组为6.52±0.62，对照组为5.02±0.35， P< 0.01；48 h时ALI组为6.65±0.62，对照组为5.01±0.36，P< 0.01）。72 h时Lb破溃，数目明显减少，细胞核形态不规则，部分核边界不清，肺组织SP-A含量下降(ALI组为3.87±0.50，对照组为5.22±0.36，P<0.01)。结论： LPS致幼鼠ALI时AEC-Ⅱ和肺组织SP-A的变化为时间依赖性，随AEC-Ⅱ损伤程度的加重肺组织SP-A由代偿转为失代偿，可能是发生ARDS的重要机制之一。