Forensic Identification of Diving Deaths / 法医学杂志

Investigation of the cause of death during diving is one of the contents of forensic pathology. In this article, relevant foreign literature is reviewed to summarize the techniques and methods used in the identification of diving deaths, such as accident reconstruction, diving monitoring data, postmortem CT examination and gas analysis (location and quantity) in the body of the corpse, in order to provide a reference for forensic identification of such cases.

Association between overweight/obesity in parents and autism spectrum disorders in offspring / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the association between overweight/obesity in parents before maternal pregnancy and the development of autism spectrum disorders (ASD) in offspring.</p><p><b>METHODS</b>A total of 36 children who were diagnosed with ASD (ASD group) and 72 normal children matched for sex and age (control group) were enrolled. A questionnaire survey was performed to collect the general information, including body height and body weight of parents before maternal pregnancy and maternal weight gain during pregnancy. Univariate and multivariate logistic regression analyses were used to investigate the association between overweight/obesity in parents before maternal pregnancy and ASD in offspring.</p><p><b>RESULTS</b>The ASD group had a significantly higher detection rate of overweight/obesity in the father than the control group (56% vs 32%; P=0.018) before maternal pregnancy. The univariate and multivariate logistic regression analyses showed that overweight/obesity of the father before maternal pregnancy was a risk factor for ASD in offspring (OR=2.66 and 2.58 respectively; P<0.05).</p><p><b>CONCLUSIONS</b>Overweight/obesity of the father before maternal pregnancy is an independent risk factor for ASD in offspring, and therefore, it is important for the father to control his body mass index within the normal range before maternal pregnancy.</p>

Oncogenic induction of cellular high CpG methylation by Epstein-Barr virus in malignant epithelial cells / 癌症

Epstein-Barr virus (EBV) is a well-known human herpesvirus associated with virtually all nasopharyngeal carcinoma (NPC) and approximately 10% of gastric cancer (GC) worldwide. Increasing evidence shows that acquired genetic and epigenetic alterations lead to the initiation and progression of NPC and GC. However, even deep whole exome sequencing studies showed a relatively low frequency of gene mutations in NPC and EBV-associated GC (EBVaGC), suggesting a predominant role of epigenetic abnormities, especially promoter CpG methylation, in the pathogenesis of NPC and EBVaGC. High frequencies of promoter methylation of tumor suppressor genes (TSGs) have been frequently reported in NPC and EBVaGC, with several EBV-induced methylated TSGs identified. Further characterization of the epigenomes (genome-wide CpG methylation profile--methylome) of NPC and EBVaGC shows that these EBV-associated tumors display a unique high CpG methylation epigenotype with more extensive gene methylation accumulation, indicating that EBV acts as a direct epigenetic driver for these cancers. Mechanistically, oncogenic modulation of cellular CpG methylation machinery, such as DNA methyltransferases (DNMTs), by EBV-encoded viral proteins accounts for the EBV-induced high CpG methylation epigenotype in NPC and EBVaGC. Thus, uncovering the EBV-associated unique epigenotype of NPC and EBVaGC would provide new insight into the molecular pathogenesis of these unique EBV-associated tumors and further help to develop pharmacologic strategies targeting cellular methylation machinery in these malignancies.

Immunohistochemical study of tumor necrosis factor-alpha expression in the lungs and small intestines in hyperthermia-LPS co-stressed rats / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effects of co-exposure to hyperthermia and lipopolysaccharides (LPS) on tumor necrosis factor-alpha (TNF-alpha) expression in the lungs and small intestines of rats.</p><p><b>METHODS</b>Male pathogen-free Wistar rats were randomly assigned into saline-injected normothermic control (C), saline heat exposure (H), LPS normothermic control (L), and LPS plus heat exposure (HL) groups. The rats in H and HL groups were exposed in a chamber at an ambient dry bulb temperature (Tdb) of 35.0-/+0.5 degrees celsius;, and those in C and L groups to 26-/+0.5 degrees celsius;. In L and HL groups, the rats were given an intravenous injection of LPS 10 mg/kg via the tail vein to induce endotoxemia, and those in C and H group received 10 ml/kg injection. The plasma levels of sTNFrI and sTNFrII were detected at different time points using ELISA. The expression of TNF-alpha in the lungs and small intestines was detected by immunohistochemical SABC method, and the damage of the lungs and small intestines evaluated histologically 120 min after the treatment.</p><p><b>RESULTS</b>Co-exposure to hyperthermia and LPS caused significantly enhanced expressions of TNF-alpha and its receptor sTNFrI and sTNFrII in the plasma and tissues and obvious histopathological damage in the lung and small intestines.</p><p><b>CONCLUSION</b>Co-stress of hyperthermia and LPS-induced toxicity is associated with the expression of TNF-alpha in the lung and small intestines.</p>