1.A CASE REPORT OF AUTOPSY FROM ACUTE WATER INTOXICATION
Chenghan TANG ; Yuanyuan CHEN ; Xi XIN
Journal of Xi'an Jiaotong University(Medical Sciences) 1982;0(01):-
Case report of autopsy from acute water intoxication is very rare. It accounts for 0.1% of allautopsys done in our University. Recently forensic autopsy was made in a case of acute water intoxication. Water intoxication often causes medical dispate resulted from transfusion. Thus a forensic appraisal standard was advanced, including: ① There was history of reduction of exterocellular osmotic pressure ② Cerebral edema, lung edema and more excretion are shown in clinic. ③ Concentration of the blood sodium was lower than 120mmol/L. ④ The transfusion order or speed was not proper. ⑤ Cause of death from general disease, injury and poisoning can be ruled out by autopsy.
2.Postmortem redistribution of morphine in rats with chronic morphine poisoning
Lixia MA ; Huiling WANG ; Junfeng ZHANG ; Ping ZHANG ; Chenghan TANG
Journal of Xi'an Jiaotong University(Medical Sciences) 1982;0(01):-
Objective To investigate the postmortem redistrib ution of morphine in rat model of chronic morphine poisoning. Methods Samples including cardiac blood, liver, heart, kidney, lung and brain tissues were collected in the rats with chronic morphine poisoning at 0~96 h after death, respectively. The morphine amount was measured with solid phase ext raction-gas chromatography. Results The study showed an increase in morphine concentrat ion of postmortem cardiac blood. Significant increase in morphine level was also observed 24~96 h after death in liver, heart and brain tissues, while the kid ney morphine levels decreased at 96 h after death. In the liver there was the g reatest increase (25-fold) in morphine levels 96 h after death. All the sample s showed marked alterations in morphine concentration within 96 h after death c ompared with cardiac blood at time of death. The postmortem morphine levels in b rain were closely related to those in the heart blood. Conclusion The postmortem redistribution of morphine exists in rats with chronic morphine poisoning. The brain tissues may better represent morphine levels in heart blood at the time of death.
3.Bidirectional relationship between type 2 diabetes mellitus and coronary artery disease: Prospective cohort study and genetic analyses
Wenqiang ZHANG ; Li ZHANG ; Chenghan XIAO ; Xueyao WU ; Huijie CUI ; Chao YANG ; Peijing YAN ; Mingshuang TANG ; Yutong WANG ; Lin CHEN ; Yunjie LIU ; Yanqiu ZOU ; Ling ZHANG ; Chunxia YANG ; Yuqin YAO ; Jiayuan LI ; Zhenmi LIU ; Xia JIANG ; Ben ZHANG
Chinese Medical Journal 2024;137(5):577-587
Background::While type 2 diabetes mellitus (T2DM) is considered a putative causal risk factor for coronary artery disease (CAD), the intrinsic link underlying T2DM and CAD is not fully understood. We aimed to highlight the importance of integrated care targeting both diseases by investigating the phenotypic and genetic relationships between T2DM and CAD.Methods::We evaluated phenotypic associations using data from the United Kingdom Biobank ( N = 472,050). We investigated genetic relationships by leveraging genomic data conducted in European ancestry for T2DM, with and without adjustment for body mass index (BMI) (T2DM: Ncase/ Ncontrol = 74,124/824,006; T2DM adjusted for BMI [T2DM adjBMI]: Ncase/ Ncontrol = 50,409/523,897) and for CAD ( Ncase/ Ncontrol = 181,522/984,168). We performed additional analyses using genomic data conducted in multiancestry individuals for T2DM ( Ncase/ Ncontrol = 180,834/1,159,055). Results::Observational analysis suggested a bidirectional relationship between T2DM and CAD (T2DM→CAD: hazard ratio [HR] = 2.12, 95% confidence interval [CI]: 2.01–2.24; CAD→T2DM: HR = 1.72, 95% CI: 1.63–1.81). A positive overall genetic correlation between T2DM and CAD was observed ( rg = 0.39, P = 1.43 × 10 -75), which was largely independent of BMI (T2DM adjBMI–CAD: rg = 0.31, P = 1.20 × 10 –36). This was corroborated by six local signals, among which 9p21.3 showed the strongest genetic correlation. Cross-trait meta-analysis replicated 101 previously reported loci and discovered six novel pleiotropic loci. Mendelian randomization analysis supported a bidirectional causal relationship (T2DM→CAD: odds ratio [OR] = 1.13, 95% CI: 1.11-1.16; CAD→T2DM: OR = 1.12, 95% CI: 1.07-1.18), which was confirmed in multiancestry individuals (T2DM→CAD: OR = 1.13, 95% CI: 1.10-1.16; CAD→T2DM: OR = 1.08, 95% CI: 1.04-1.13). This bidirectional relationship was significantly mediated by systolic blood pressure and intake of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, with mediation proportions of 54.1% (95% CI: 24.9-83.4%) and 90.4% (95% CI: 29.3-151.5%), respectively. Conclusion::Our observational and genetic analyses demonstrated an intrinsic bidirectional relationship between T2DM and CAD and clarified the biological mechanisms underlying this relationship.