血中乙醇质量浓度与神经行为能力的关系

目的 研究血中乙醇质量浓度与神经行为能力的关系。方法 采用中文第三版计算机化神经行为测试评价系统（NES-C3）,通过自身对照的方式,对233名饮酒者进行神经行为能力的测试。结果 当血中乙醇质量浓度I〉0．157mg／mL时,视简单反应时和数字筛选能力指数有显著性下降;当血中乙醇质量浓度I〉0．204mg／mL时,心算、视觉保留、线条判断能力指数有显著性下降。结论 神经行为能力随着血中乙醇质量浓度的升高而下降,然后随着乙醇的不断代谢,血中乙醇质量浓度的降低,神经行为能力逐渐恢复。     

Changing patterns of income among blacks and whites before and after executive order 11246

Some suggest that affirmative action has contributed to the widening gap between better-off and worse-off blacks. Analyses of census data challenge the claim.     

论保险业集中度的演变及其对策

从演进趋势看,发达国家保险业集中度较高,这是由竞争规律决定的。然而,发展中国家保险业的集中度却呈现逐渐降低的趋势。由于历史原因,中国保险业的集中度一直过高,这不利于中国保险业竞争力的提升。可通过降低保险市场的进入壁垒和引进民营资本等途径降低中国保险业的集中度。     

改进行政事业单位会计集中核算问题探讨

会计集中核算是以会计核算中心为单位集中办理会计核算工作和实行会计监督的一项新举措。这项制度的实施效果显著。改革构想:一是要做到国库集中收付与会计集中核算的相互渗透和有效融合,二是各统管单位切实加强报账会计队伍建设,三是加快实行部门科学预算的进度,四是会计核算中心职能应从核算型向管理型转化,五是构建新型的财政稽查监督机制,六是完善内外监控制度,七是健全完善会计法规体系。     

Stability studies of ALD-52 and its homologue 1P-LSD

With the emergence of new psychoactive substances (NPSs) over the years, the substances detected on stamps (also known as blotter papers) have also evolved from the traditional drug—lysergic acid diethylamide (LSD) to the multiple variants of lysergamides such as ALD-52 and 1P-LSD. The analysis of such blotter papers is usually done by solvent extraction followed by identification using gas chromatography–mass spectrometry (GC-MS). This study has shown that hydrolysis to form LSD was observed in GC-MS analysis when ALD-52 was extracted with methanol. The extraction of ALD-52 using other solvents such as acetonitrile, ethanol, isopropyl alcohol, ethyl acetate, and acetone, followed by GC-MS analysis, was investigated. It is shown that alcoholic solvents such as methanol and ethanol will result in the conversion of ALD-52 to LSD during GC-MS analysis, whereas the sterically hindered isopropyl alcohol will prevent this conversion. Investigation also shows that the hydrolysis of ALD-52 to LSD occurs at the GC injector port. It was also observed that the degree of hydrolysis was more pronounced at a lower concentration (0.1 mg/mL). The study was extended to a close analog—1P-LSD, and the results showed that 1P-LSD similarly hydrolyzes to LSD. However, 1P-LSD was observed to be more stable than ALD-52 due to steric hindrance because of the propanoyl group.     

大鼠死后心血中吗啡浓度变化的HPLC检测

本文采用高效液相色谱（HPLC）分析技术检测了治疗量及中毒量吗啡肌注大鼠死后心血中吗啡浓度变化．结果表明．以治疗量吗啡肌注大鼠死后96h内，心血中吗啡浓度随死后时间增加而显著升高（P<0.01），吗啡浓度水平与死后时间呈显著正相关．以中毒量吗啡肌注大鼠死后12h内，心血中吗啡浓度无明显变化．死后24h、48h及96h．随死后时间延长，心血中吗啡浓度逐渐升高（P＞0.01），其递增强度不如治疗量吗啡组大鼠的明显．本研究证实死后尸体心血吗啡浓度明显受生前剂量的影响，且死后96h内，随死后时间延长心血中吗啡浓度不断增高．本文初步探讨了死后心血吗啡浓度变化发生的可能机制．为海洛因或吗啡中毒死亡的血液检测结果评判及死因分析提供理论依据．     

涉嫌酒后驾驶交通事故人体损伤与驾驶员血中乙醇质量浓度关系研究

目的探讨涉嫌酒后驾驶所致道路交通事故中人体损伤情况与驾驶员血中乙醇质量浓度关系,为预防、控制道路交通事故及人体损伤提供依据。方法对467例涉嫌酒后驾驶机动车的道路交通事故损伤人员相关鉴定资料与肇事驾驶员血中乙醇质量浓度进行系统分析性研究。结果涉嫌酒后驾驶发生道路交通事故的损伤人员中,以20~39岁男性居多;事故中驾驶员损伤机率最高;酒后交通事故以长头小车及摩托车最多,而驾驶员血中乙醇质量浓度（BAC）为0.1~20mg/100mL浓度的摩托车驾乘人员伤亡构成比最高;酒后驾驶机动车肇事导致的人体致命性损伤及人员死亡的饮酒组危险程度均高于未饮酒组,在驾驶员血中乙醇质量浓度（BAC）为0.1~20mg/100mL组与20.1~80mg/100mL组比较无明显差异。结论酒后驾驶肇事导致的人员伤亡比未饮酒驾车交通事故严重;未达酒后驾车组（BAC为0.1~20mg/100mL）和酒后驾车组（BAC为20.1~80mg/100mL）交通事故导致的人员伤亡无明显差异。研究结果提示,应降低饮酒后驾车血中乙醇质量浓度（BAC）法定标准阈值,进一步控制和减少道路交通事故人身伤亡率。     

不同温度下兔玻璃体液K~+浓度与死亡时间的关系研究

目的探索在不同环境温度条件下,玻璃体液中钾离子浓度变化规律与死亡时间的关系。方法家兔处死后分别置于5℃、15℃、25℃和35℃温度下保存,在0~120h内每12h双眼交替微量提取玻璃体液80~100μL;应用罗氏DPPI生化分析仪检测玻璃体液中K~+的浓度;应用插值函数进行分析拟合,建立死亡时间推断方程。结果各温度组家兔玻璃体液中K~+浓度随死亡时间延长均呈上升趋势,对所得数据进行插值拟合,在5℃~35℃的温度变化区间内,K~+浓度变化与PMI关系的三元五次曲面方程:f(x,y)=-1.998e~(14)+1.345e~(12)x+5.902e~(13)y+0.005 585x~2-4.509e~(11)xy-3.876e~(12)y~2-0.000 286 8x~3+0.003 545x~2y+4.406e~(10)xy~2-1.746e~(10)y~3+2.669e~(-6)x~4-1.568e~(-5)x~3y-0.000 177 1x~2y~2-1.64e~9xy~3+6.669e~9y~4-8.672e~(-9)x~5+4.467e~(-8)x~4y+2.354e~(-7)x~3y~2+2.459e~(-6)x~2y~3+2.05e~7xy~4-1.214e~8y~5(R~2=0.995 6),其中温度为自变量x,K~+浓度值为自变量y,PMI为因变量f(x,y)。结论在5℃~35℃的环境温度区间内,家兔眼玻璃体液中K~+浓度变化与死亡时间关系符合三元五次方程分布,利用插值函数拟合的方法可将环境温度作为参数,实现在环境温度变化条件下进行死亡时间推断。     

Death of a 10‐Month‐Old Boy After Exposure to Ethylmorphine

Abstract: Ethylmorphine, an opiate that is partially metabolized to morphine, is a common ingredient in antitussive preparations. We present a case where a 10‐month‐old boy was administered ethylmorphine in the evening and found dead in bed the following morning. Postmortem toxicological analyses of heart blood by gas chromatography‐mass spectrometry and liquid chromatography‐mass spectrometry revealed the presence of ethylmorphine and morphine at concentrations of 0.17 μM (0.054 mg/L) and 0.090 μM (0.026 mg/L), respectively. CYP2D6 genotyping showed that the deceased had an extensive metabolizer genotype, signifying a “normal” capacity for metabolizing ethylmorphine to morphine. The autopsy report concluded that death was caused by a combination of opiate‐induced sedation and weakening of respiratory drive, a respiratory infection, and a sleeping position that could have impeded breathing. This is the first case report where the death of an infant has been linked to ethylmorphine ingestion.