Fatty acid balance studies in term infants fed formula milk containing long-chain polyunsaturated fatty acids

Long-chain polyunsaturated fatty acids (LCP) are thought to be required for optimal nervous system development in the newborn. A commercial milk formula containing LCP (Aptamil-LCP) with a fatty acid profile closely resembling breast milk, has recently been introduced for term infants. The absorption of fatty acids in term infants was examined in a double-blind randomized controlled trial comparing Aptamil-LCP ( n = 20) and standard Aptamil ( n = 20). Formula-fed newborn infants were studied from birth for 14 d. Fat balances (3 d) were performed from d 10. A 3-d stool collection was performed from d 10 in a parallel breastfed group ( n = 21). Plasma samples were taken on d 6. Median fat excretion (mg kg⁻¹) was 897.1, 615.0 and 355.2 with Aptamil, Aptamil-LCP and breastfeeding, respectively. The median total fat absorption coefficient in Aptamil-LCP-fed infants was higher than in those fed standard Aptamil ( p < 0:01). These findings were accounted for by differences in the excretion and absorption of long-chain saturated fatty acids (C14:0, C16:0 and C18:0). Higher fat excretion was associated with bulkier and firmer stools. Only trace amounts of LCP were detected in the stools of all groups. This accounted for less than 4% of dietary intake in Aptamil-LCP-fed infants. No differences in the utilization of LCP from Aptamil-LCP and breast milk feeding were apparent. Plasma phospholipid fatty acid composition data reflected differences in dietary LCP intake. Thus, PL LCP levels were highest in the breastfed infants and lowest in the Aptamil-fed infants, with values for the Aptamil-LCP-fed group falling in between.     

代谢综合症基线调查

目的：通过对豫宛市30岁以上人群代谢综合症（MS）发病率的词查、统计和分析，旨在唤起人们对此病的重视和预防。方法：利用年度体检之机采用三级分组法对30岁以上人群进行有关MS指标的检测和统计，依据亚洲及我国体重指数标准及2004年中华医学会糖尿病分会诊断代谢综合症标准。共计调查人数3987人（男1981人，女2006人）。结果：30岁以上MS患病率，青年有10％～13％，中老年后可渐增至20％～30％。结论：MS是中老年多见的代谢异常疾病。已严重威胁着人们的生命健康。     

羊肚菌属群体遗传学和基因组进化的研究进展

羊肚菌Morchella esculenta是子囊菌亚门的一种大型药食两用真菌,具有重要的经济价值和药用价值。然而近年来全球气候变化,导致羊肚菌属物种的栖息地破碎和片段化,加上消费者对羊肚菌美食的喜爱,过渡采挖造成羊肚菌属野生资源急剧减少,因此,急需对羊肚菌属物种资源进行保护。遗传多样性的时空分布是保护生物学的重要内容,遗传多样性关系到一个物种或类群的进化潜力和未来命运。生物基因组和进化的研究能够辅助挖掘物种深层次的优异基因资源,有利于从本质上对物种进行科学保护。从羊肚菌属的遗传多样性、遗传结构和家系关系以及基因组进化等的研究进展进行综述,以期为羊肚菌属资源的科学保护提供重要依据。     

丁香水溶性化学成分的研究

目的：研究丁香水溶性化学成分。方法：利用HP-20大孔吸附树脂、反相硅胶柱色谱、反相制备薄层色谱、制备型反相高效液相色谱进行分离,NMR和MS等方法进行结构鉴定。结果：从丁香干燥花蕾的水提物中分离鉴定了5个化合物,分别为槲皮素-3-O-葡萄糖醛酸苷（1）,槲皮素-3-O-葡萄糖醛酸苷6″-甲酯（2）,槲皮素-3-O-葡萄糖苷（3）,丁香酚-β-芸香糖苷（4）,杨梅酮（5）。结论：化合物1～4为首次从丁香属植物中分离得到。     

蒙药胃舒安对束缚-水浸应激致胃溃疡的预防作用及对TGF-β1表达的影响

[目的]评价蒙药胃舒安对束缚-水浸应激所致大鼠胃溃疡的预防作用。[方法]将Wistar实验大鼠,分正常组、给药组和对照组3组,正常组不给药,无束缚-水浸应激压力,对照组给淀粉,给药组灌胃给蒙药胃舒安,给药剂量为0．9～1．3mL／只（82．5g／L）,连续给胃舒安7d后,停食24h,建立3h束缚-水浸应激性胃溃疡模型,取胃,肉眼观察胃黏膜损伤,用Image J图像分析法测定胃黏膜溃疡面积,并进行比较。用酶联免疫吸附测定法检测胃溃疡大鼠血清转化生长因子（TGF-β1）含量并进行比较。[结果]蒙药胃舒安对3h束缚-水浸应激所致大鼠胃溃疡形成有抑制作用。胃舒安组大鼠血清TGF-β1含量明显低于对照组。[结论]蒙药胃舒安对实验大鼠束缚-水浸应激3h所致胃溃疡的形成有显著抑制作用。     

膜联蛋白A1在非小细胞肺癌组织中的表达及意义

  目的  检测膜联蛋白A1（annexin A1,ANXA1）在人非小细胞肺癌组织中的表达情况,并探讨其临床意义。  方法  通过实时荧光定量PCR、蛋白免疫印迹和免疫组织化学技术检测非小细胞肺癌患者肺癌组织和癌旁组织（距肿瘤边缘>5 cm）中膜联蛋白A1的表达水平,并分析其与临床病理参数之间的关系。  结果  实时荧光定量PCR显示,膜联蛋白A1 mRNA在肺癌组织中的表达水平（0.574±1.403）高于癌旁组织（0.240±0.893）,差异具有统计学意义（t=2.060,P=0.045）。肺癌组织中膜联蛋白A1的表达与其分化程度、淋巴结转移、TNM分期相关（P < 0.05）;与性别、年龄、吸烟史、肿瘤直径、组织学类型无关（P > 0.05）。蛋白免疫印迹和免疫组织化学结果均显示,膜联蛋白A1蛋白在肺癌组织中的表达高于癌旁组织。  结论  ANXA1在非小细胞肺癌患者肺癌组织中呈高表达,可能与其发生发展和侵袭转移有一定关系。      

Substrate for endothelial prostacyclin production in the presence of platelets exposed to collagen is derived from the platelets rather than the endothelium

Interactions between vascular endothelial cells and blood platelets have been investigated using a model microcirculation consisting of microcarrier beads colonized with human umbilical vein endothelial cells (HUVECs) and perfused with washed platelet suspensions. To simulate the effects of endothelial desquamation and exposure of subendothelium, fibrillar collagen in suspension was coinjected with the platelets. In this model, neither the passage of platelets alone nor collagen alone stimulated prostacyclin (PGI2) production by the HUVECs. Platelets activated by coinjection with collagen released thromboxane A2 (TXA2), and this was associated with the simultaneous production of PGI2 by the HUVECs. By means of double-isotope experiments with [3H]arachidonic acid (AA) incorporated into platelets and [14C]-AA into HUVECs, it was shown that all the PGI2 generated was derived from platelet AA and/or endoperoxides. This interpretation was strengthened by the finding that PGI2 production was not prevented by treatment of HUVECs with indomethacin followed by perfusion with collagen-stimulated platelets. AA metabolites in double-isotope label experiments were further characterized by reverse-phase chromatography, and it was shown that both cyclooxygenase and lipoxygenase products of the HUVECs were derived from platelet membrane lipid. Thrombin regularly produced transient PGI2 release, but showed rapid tachyphylaxis. Platelet-derived compounds including ADP, ATP, and platelet-activating factor (PAF) did not produce PGI2 release by HUVECs in this system. Thus, the transfer of AA and metabolites from collagen- stimulated platelets is likely to be the mechanism for PGI2 production in the context of minor degrees of endothelial desquamation.     

T-cell origin of Lennert''s lymphoma

The arrangement of the T-cell receptor and immunoglobulin genes has been analysed in five cases of Lennert's lymphoma. All cases showed rearrangement of the gene coding for the beta chain of the T-cell receptor and a germline configuration of the immunoglobulin genes. This provides strong evidence that Lennert's lymphoma is a T-cell lymphoma.     

Parental origin of mutation and the risk of breast cancer in a prospective study of women with a BRCA1 or BRCA2 mutation

The objective is to estimate the risk of breast cancer in women who carry a deleterious BRCA1 or BRCA2 mutation, according to parental origin of mutation. We conducted a cohort study of women with a BRCA1 mutation (n = 1523) or BRCA2 mutation (n = 369) who had not been diagnosed with breast or ovarian cancer. For each woman, the pedigree was reviewed and the origin of the mutation was assigned as probable paternal or maternal. The hazard ratio (HR) for developing breast cancer in the follow‐up period was estimated for women with a paternal mutation compared to a maternal mutation. The risk of breast cancer was modestly higher in women with a paternal BRCA1 mutation compared to women with a maternal BRCA1 mutation (HR = 1.46; 95% CI = 0.99–2.16) but the difference was not significant (p = 0.06). The parental mutation origin did not affect the risk in women with a BRCA2 mutation. Our results are consistent with the hypothesis that there is an increased risk of breast cancer among women with a paternally inherited BRCA1 mutation compared to a maternally inherited mutation. However, the data are not sufficiently compelling to justify different screening recommendations for the two subgroups.