头孢匹胺在重症急性胰腺炎小鼠中血胰屏障通透性的实验观察

目的：研究头孢匹胺（CPM）在重症急性胰腺炎（SAP）小鼠血胰屏障的通透性,为头孢匹胺防治胰腺组织感染提供理论依据。方法以20%L-精氨酸2 g·kg-1体重腹腔注射方法复制SAP模型。正常对照组和SAP模型组小鼠均尾静脉注射头孢匹胺42.5 mg·kg-1,在规定时间点取样,用高效液相色谱法（HPLC）测定血浆和胰腺组织中药物的浓度。结果头孢匹胺在正常动物组和SAP模型组血浆和胰腺中的处置均符合一室模型。正常动物组CPM对血胰屏障平均穿透率（PR）可达（49.2±38.4）%,血浆和胰腺组织中的t1/2分别为1.42 h和1.14 h,AUC分别为122.73 mg·h·L-1和69.88 mg·h·kg-1。SAP模型组PR平均可达（56.±34.7）%,与正常动物组相比无显著性差异,胰腺组织中t1/2、C0及AUC0-∞与正常动物组相近。结论头孢匹胺在SAP小鼠胰腺中有良好的分布,值得向临床推荐用于预防和治疗胰腺感染。     

瑞舒伐他汀钙片溶出度研究

目的建立瑞舒伐他汀钙片溶出度研究方法。方法HPLC法,色谱柱：AgilentExtendC18（4．6×250mm,5μm）;流动相：以乙腈为流动相A,以0．02％三氟乙酸溶液为流动相B,0～13min,A：37％,13—27min,A：37％--90％;检测波长：242nm;流速：1．0mL·min-1;发生降解行为的溶出度样品经碱中和前处理后以瑞舒伐他汀钙与瑞舒伐他汀非对映异构体峰面积之和计算累积溶出量（％）。结果瑞舒伐他汀钙在pH1．0盐酸溶液不稳定,降解生成瑞舒伐他汀非对映异构体,瑞舒伐他汀-5S-内酯和瑞舒伐他汀-5R-内酯,后两者经碱中和处理后重新生成瑞舒伐他汀及瑞舒伐他汀非对映异构体,且瑞舒伐他汀钙片在pH1．0盐酸溶液中溶出速率最慢。结论瑞舒伐他汀钙在pH1．0盐酸溶液中溶出曲线可作为处方筛选的依据。     

Cumulative effects of genetic markers and the detection of advanced colorectal neoplasias by population screening

Genetic markers associated with colorectal cancer may be used in population screening for the early identification of patients at elevated risk of disease. We genotyped 3059 individuals with no cancer family history for eight markers previously associated with colorectal cancer. After colonoscopy, the genetic profile of cases with advanced colorectal neoplasia (213) was compared with the rest (2846). rs2066847 and rs6983267 were significantly associated with the risk of advanced colorectal neoplasia but with limited effect on their own [odds ratio (OR) 1.59; 95% confidence interval (CI) 1.02–2.41; p = 0.033 and OR 1.45; 95% CI 1.02–2.12; p = 0.044, respectively]. Cumulative effects, in contrast, were associated with high risk: the combination of rs2066847, rs6983267, rs4779584, rs3802842 and rs4939827 minimized the number of markers considered, while maximizing the relative size of the carrier group and the risk associated to it, for example, for at least two cumulated risk markers, OR is 2.57 (95% CI 1.50–4.71; corrected p‐value 0.0079) and for three or more, OR is 3.57 (95% CI 1.91–6.96; corrected p‐value 0.00074). The identification of cumulative models of – otherwise – low‐risk markers could be valuable in defining risk groups, within an otherwise low‐risk population (no cancer family history).     

基于2D电阻抗成像的位置误差和相对数量指数的后处理方法

本文提出了一种基于2D电阻抗成像的位置误差和相对数量指数的后处理方法,用于多种电导率分布的确定、组织成分的识别以及位置信息的确定。此外,还介绍了一种基于现有两种重建算法的混合正则化算法,并将三种重建算法重建的结果进行了比较。结果证明,这种后处理方法可以提高2D电阻抗成像的位置精度和空间分辨率,使得电阻抗成像适用于临床检查和过程监测。     

Prospective relations between alexithymia,substance use and depression: findings from a National Birth Cohort

Abstract

Purpose: This study examined a developmental model that links affect-regulation difficulties in childhood with three dimensions of alexithymia in adolescence (difficulty identifying feelings, difficulty describing feelings, and externally oriented thinking) and substance use and depression in adulthood, while accounting for cumulative contextual risk in childhood, and testing potential gender moderation.

Methods: Multiple group path analyses were conducted using data from the Northern Finland Birth Cohort 1986 (N?=?6963). Analyses used data collected during prenatal/birth, childhood, adolescence, and young adulthood periods.

Results: Our examination of early precursors for alexithymia indicated that the associations of affect-regulation problems in childhood with alexithymia were stronger for girls, potentially putting girls with affect-regulation difficulties in childhood at higher risk for developing alexithymia in adolescence. The associations of cumulative contextual risk in childhood with alexithymia, substance use disorder, and depression diagnosis in adulthood were significant for both girls and boys. Our findings in regard to substance use and depression disorders revealed that alexithymia in adolescence predicted depression diagnosis in adulthood, particularly due to a contribution from the alexithymia domain of ‘difficulties identifying feelings.’ However, none of the alexithymia domains was directly associated with substance use disorder in adulthood.

Conclusions: Our study contributes to research that links alexithymia with difficulties in affect regulation and cumulative contextual risk in childhood, yielding findings that may be relevant for preventive interventions.     

骨髓涂片有核细胞量减少的真实性研究

目的研究骨髓涂片有核细胞的假阳性和假阴性减少,提高对涂片评估有核细胞量不足的认识。方法用骨髓穿刺针抽吸髓液涂片272例,随后同步以活检术获取组织块置于载玻片上制成印片,组织块入Bouin液固定,以骨髓印片和切片为对照,评估涂片对检查有核细胞量的价值。结果272例骨髓涂片有核细胞减少和增多级别均显著低于骨髓印片和切片(P<0.05~<0.01)。以印片和切片为对照,124例涂片有核细胞减少中,58.9%和66.1%为假阳性减少,常见误诊疾病为再生障碍性贫血、造血减低;而印片和切片细胞量增加中,涂片仍有26%和36%为假阴性减少,常见疾病或结论为脾功能亢进、真性红细胞增多症、特发性血小板增多症等;印片和切片细胞减低者中,涂片符合率(91.2%和97.9%),以及涂片细胞增加者中,印片和切片符合率(95%和100%)均高。涂片诊断细胞量真性减少疾病或结论(再生障碍性贫血和造血减低)的假阳性分别为29.0%和37.1%,诊断真性增加疾病(脾功能亢进、特发性血小板增多症、真性红细胞增多症等)假阴性率为22.6%和21.8%,诊断指标性能评价均不佳。结论骨髓涂片评估有核细胞量差,常造成假阳性和假阴性结果,建议将印片作为常规项目以弥补涂片的不足。     

大理市售不锈钢餐具中铬铅溶出量的测定

目的:了解大理市售不锈钢餐具中重金属铅、铬的溶出量,并为卫生监督部门提供相关参考。方法:选择大理市紫云市场、泰兴市场、新桥市场、珠海市场为采样点,对样品处理后,经4%的乙酸溶液浸泡并放置24h后,用火焰原子吸收光谱法(F-AAS)测定不锈钢餐具浸泡液中铬、铅溶出量。结果:紫云市场、泰兴市场、新桥市场、珠海市场四个市场抽样合格率分别是75%、87.5%、75%、100%;抽查中发现的主要质量问题是部分不锈钢产品铬溶出量大于0.5 mg/L,有超标现象,样品的铬溶出量有统计学意义(t=5.488,P<0.05),样品的铅溶出量均小于1 mg/L,没有超标,符合国家标准。结论:大理市售不锈钢餐具中有重金属铬溶出量超标的产品,有关部门应引起重视,保护人们的健康。     

Cell-kinetic analysis of pancreatic cancers in syrian golden hamsters

Cell-kinetic analysis of pancreatic cancers using bromodeoxyuridine (BrdU) was performed on four transplantable pancreatic ductal adenocarcinomas, which were experimentally induced by givingN-nitrosobis (2-hydroxypropyl) amine (BHP) to Syrian golden hamsters. The volume-doubling time (Td)of the tumor was 0.43, 1.03, 2.30, and 3.50 d for tumor lines J, D, B, and F, respectively. In the pulse-labeling study, the labeling index was 15.8, 23.3, 27.9, and 31.7, respectively. The most rapidly growing tumor line, J, unexpectedly showed the lowest BrdU-labeling index (LI). The further study of tumor using the cumulative-labeling method revealed that the duration of S phase (Ts), the generation time (Tg) and the growth fraction (GF) were 2 h, 14 h, and 90% for tumor J and 12 h, 37 h, and 85% for slowly growing tumor B, respectively. Cells of limited life span (CLLS) of these lines did not differ from each other. These results conclude that the marked difference ofTg between tumor lines J and B resulted in a distinction of their growth rates. The disagreement ofTs/Tg also lead to a reversion of LI between the two lines. Furthermore, LI of BrdU with one-point pulse labeling did not seem to be a sufficient indicator of the growth characteristics, at least, in the present experiment.     

Vascular dysfunction induced by AGE is mediated by VEGF via mechanisms involving reactive oxygen species, guanylate cyclase, and protein kinase C

OBJECTIVE: These experiments were designed to elucidate mechanisms mediating vascular dysfunction induced by advanced glycation end products (AGEs). METHODS: Skin chambers were mounted on the backs of Sprague-Dawley rats and 1 week later, granulation tissue that formed in the bottom of the chamber was exposed twice daily for 7 days to glycated rat serum albumin in the presence and absence of inhibitors of reactive oxygen intermediates, nitric oxide synthase and guanylate cyclase, protein kinase C (PKC), and a neutralizing vascular endothelial growth factor (VEGF) antibody. Vascular (125)I-albumin clearance and blood flow were quantified by use of a double isotope-dilution technique and radiolabeled microspheres, respectively. RESULTS: Albumin permeation and blood flow were increased dose-dependently to a maximum of 2 to 3 times controls by increasing the extent of glucose modification, the concentration, or the duration of exposure to glycated albumin. These increases were significantly attenuated by probucol and superoxide dismutase; N(G)-nitro-L-arginine-methyl ester (L-NAME), a nitric oxide synthase inhibitor; LY83583, a guanylate cyclase inhibitor; and LY333531, a beta-isoform-selective protein kinase C inhibitor. A neutralizing VEGF monoclonal antibody also markedly attenuated the permeability and blood flow increases induced by glycated albumin. CONCLUSIONS: These observations indicate potentially important roles for oxygen free-radicals and nitric oxide in mediating permeability and blood flow changes induced by glycated proteins via mechanisms involving increased protein kinase C activity and VEGF production. Striking similarities in the mechanism by which hyperglycemia and glycated proteins induce vascular dysfunction suggest that a common pathway mediates effects of these different metabolic imbalances on vascular dysfunction.