Search

A 56-year-old man with a long history of alcoholism and a palpable raised mass about 23 cm × 12 cm in size on his neck was diagnosed with Madelung’s disease (MD); the patient also had hyperuricemia. On day 1, he underwent neck lipoma tissue resection and suddenly had dyspnea 9 h after the operation, which was followed by cardiac arrest. After heart rate resuscitation, he developed a heartbeat, but he remained in a coma and died 9 days after the operation. No obvious pathological tracheal compression from a hematoma was observed while evaluating the patient’s neck on autopsy. On microscopy, the patient had an extensive pulmonary fat embolism, partial alveolar septal rupture and hemorrhage, and fat particles, and there was extensive infiltration of macrophages, which had phagocytosed fat particles, in the alveolar cavity. There was also evidence of pulmonary infection and hypoxic-ischemic encephalopathy. The cause of death was postoperative pulmonary fat embolism resulting in pneumonia and central nervous system injury. This is the first report of a patient with MD who died of a fatal pulmonary fat embolism after neck lipoma tissue resection. Medicolegal experts and clinicians should pay sufficient attention to this case.

Methamphetamine (METH) is a major psychostimulant drug of abuse worldwide, and its neurotoxicity has been studied extensively. In addition to neurotoxicity, METH can also induce hepatotoxicity. The underlying mechanism of intestinal microorganisms in METH-induced hepatotoxicity remains unclear. In this study, mice have received antibiotics intragastrically or PBS once each day for 1 week, followed by METH or saline. The antibiotics attenuated METH-induced hepatotoxicity as evidenced by histopathological observation and biochemical analysis; furthermore, they alleviated METH-induced oxidative stress. The effect of antibiotics on METH-induced hepatotoxicity was investigated using RNA-sequencing (RNA-seq). The RNA-seq results demonstrated that antibiotics could regulate 580 differentially expressed genes (DEGs), of which 319 were upregulated after METH treatment and then downregulated with antibiotic pretreatment and 237 were first downregulated after METH administration and then upregulated after antibiotic pretreatment, in addition to 11 upregulated and 13 downregulated ones simultaneously in METH and antibiotic-pretreated groups. RNA-seq analyses revealed that TLR4 is one of the hub genes. Western blot analysis indicated that antibiotics inhibited the increase of TLR4, MyD88 and Traf6 induced by METH. This research suggests that antibiotics may play an important role in preventing METH-induced liver injury by regulating oxidative stress and TLR4/MyD88/Traf6 axis, though further investigation is required.

A full-term female baby born with an Apgar score of 10 exhibited a continual decrease in blood glucose and acid-base imbalance until she died at 40 h postpartum despite emergency rescue efforts. Autopsy showed a highly oedematous brain and a swollen liver. The cells of the myocardium, liver and kidney exhibited extensive microscopic vacuolar degeneration. The cardiac muscle and liver and kidney tissues were positive for Sudan III staining. Tandem mass spectrometry analysis revealed that the deceased was deficient in free carnitine, accompanied by an increase in multiple acylcarnitines. Genetic testing showed the parents of the deceased to be ETFDH mutation carriers, and the deceased carried a complex heterozygous mutation in ETFDH. Therefore, based on the results of autopsy, specific staining, genetic metabolic disease testing and genetic testing, we speculated that glutaric aciduria type IIc was the cause of death.

Misuse of the psychostimulant methamphetamine (METH) could induce serious hepatotoxicity. Our previous study revealed the effects of luteolin on alleviating METH-induced hepatotoxicity, however, the detailed mechanisms have not been elucidated. In this study, rats were orally pretreated with 100 mg/kg luteolin or sodium dodecyl sulfate water, and then METH (15 mg/kg, intraperitoneal [i.p.]) or saline was administered. Histopathological and biochemical analyses were used to determine the alleviative effects of luteolin. Based on the RNA-sequencing data, METH induced 1859 differentially expressed genes (DEGs) in comparison with the control group, which were enriched into 11 signaling pathways. Among these DEGs, 497 DEGs could be regulated through luteolin treatment and enriched into 16 pathways. The p53 signaling pathway was enriched in both METH administered and luteolin pretreated rats. Meanwhile, luteolin significantly suppressed METH-induced elevation of p53, caspase9, caspase3, cleaved caspase3, the ratio of Bax/Beclin-2, as well as autophagy-related Beclin-1, Atg5, and LC3-II. Luteolin also relieved METH-induced hepatotoxicity by decreasing inflammation factors, including TNF-α, IL-1β, and IL-18. Moreover, the levels of PI3K, p-Akt, and the normalized ratio of p-Akt/Akt declined after METH administration, whereas luteolin pretreatment failed to reverse these effects. Our results suggest that luteolin alleviates METH-induced hepatic apoptosis, autophagy, and inflammation through repressing the p53 pathway. It further illustrates the protective mechanisms of luteolin on METH-induced hepatotoxicity and provides a research basis for clinical treatment.

We report a case of nontraumatic fat embolism syndrome with large amounts of macrophages with phagocytized fat droplets in the alveoli. A 46-year-old male presented with a glass-cut injury in his little finger. The wound was debrided and sutured at the hospital, but he was found dead 43 h after treatment. Autopsy results showed that the patient had steatohepatitis, accompanied by histological findings of fat droplets in the pulmonary capillaries. In the alveoli, we found a large number of macrophages with phagocytized fat droplets that showed stained. To the best of our knowledge, this is the first report of such a case, and the paper proposes that fat droplets phagocytized by a large number of macrophages may be a characteristic feature of fat embolism, which may be relevant to forensic pathology practice.

Methamphetamine (MA) is a highly abused amphetamine-like psychostimulant. At present, the mechanisms underlying MA-induced cardiotoxicity are poorly understood. The cardiotoxic effects have yet not been clearly elucidated with respect to the apoptotic pathway. Insulin-like growth factor binding protein-5 (IGFBP5) is important for cell growth control and the induction of apoptosis. The aim of the present study was to analyze whether IGFBP5 is involved in MA-induced apoptosis as a novel target. MA-induced apoptosis was observed in neonatal rat ventricular myocytes (NRVMs) in a concentration-dependent manner using a terminal deoxyribonucleotide transferase-mediated dUTP nick end-labeling assay. Using reverse transcription polymerase chain reaction and western blotting, MA was demonstrated to induce concentration-dependent increases in the expression of IGFBP5. Silencing IGFBP5 with small interfering RNA significantly reduced apoptosis and suppressed the expression of caspase-3 in NRVMs following treatment with MA. To the best of our knowledge, the present study provided the first evidence suggesting that IGFBP5 is a potential therapeutic target in MA-induced apoptosis in vitro, providing a foundation for future in vivo studies. [ABSTRACT FROM AUTHOR]

The clinical features suggest that genetic factors may have a strong influence on susceptibility to coronary artery disease (CAD). The aim of this study was to investigate the association between FokI (rs2228570) and BsmI (rs1544410) of the vitamin D receptor ( VDR) gene polymorphisms and patients with CAD in a Chinese population. One hundred and fifty-two CAD patients and 212 healthy controls were genotyped for the FokI and BsmI polymorphisms in VDR gene using polymerase chain reaction–restriction fragment length polymorphism. No significant differences were observed in the genotype and allele frequencies of the FokI and BsmI polymorphisms between the cases and controls (For FokI: odds ratio = 1.11, 95% confidence interval 0.83–1.50; for BsmI: odds ratio = 0.74, 95% confidence interval 0.44–1.23). There was no significant difference in the genotype distribution or the allele frequencies of VDR FokI and BsmI between two groups in a Chinese population. [ABSTRACT FROM AUTHOR]

Abstract  The present study analyzed serum levels of urea nitrogen (UN), creatinine (Cr), and C-reactive protein (CRP), which are very stable during the early postmortem period, for investigation of the cause of death with special regard to hyperthermia (heat stroke) in serial medico-legal autopsy cases (n = 429), excluding fatal injury, intoxication, and fire fatality. In this series, mechanical asphyxiation, drowning, and sudden cardiac death cases (n = 56, n = 43, and n = 212, respectively) usually showed low levels within postmortem reference ranges for these serum markers, although UN and CRP levels were mildly elevated in cases of sudden cardiac death and cerebrovascular stroke. There were concomitant significant elevations in serum levels of UN (>50 mg/dL), Cr (>2 mg/dL), and CRP (>2 mg/dL) for chronic renal failure, gastrointestinal bleeding, pneumonia, and hypothermia (cold exposure). UN and CRP were especially high for chronic renal failure and pneumonia, respectively. However, hyperthermia cases showed an isolated elevation in the serum Cr level, suggesting an influence of systemic skeletal muscle damage. These serum markers may be practically useful for postmortem investigation of death due to hyperthermia (heat stroke), for which specific pathological and toxicological evidence may not be available. [ABSTRACT FROM AUTHOR]

Abstract??Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in the blood are clinical markers for the diagnosis of cardiac failure. This study was a comprehensive analysis of the postmortem pericardial levels of the natriuretic peptides in serial medico-legal autopsy cases (n=263, within 72?h postmortem) to assess their validity in investigating cardiac function. There was no significant relationship of pericardial ANP or BNP levels with postmortem time or the age of the subjects. The ANP and BNP levels showed negative correlations with the pericardial cardiac troponin T level. The ANP level was significantly elevated in drowning cases. Pericardial BNP and the BNP/ANP ratio were significantly higher for chronic congestive heart disease. However, asphyxiation, sharp instrument injury, hyperthermia, and fatal MA poisoning cases showed lower levels for both markers. These observations suggest that elevations in the postmortem pericardial ANP and BNP may mainly depend on acute atrial overload and subacute or chronic cardiac failure, respectively, and may be reduced by advanced myocardial damage. [ABSTRACT FROM AUTHOR]

Abstract Although the EpsteinBarr virus (EBV) causes acute infection accompanied by a high fever in young people, there appears to be few reports of a fatal outcome involving myocarditis. We report two cases of unexpected sudden death due to acute myocarditis possibly caused by the EBV. They each visited a hospital due to common cold-like symptoms and unexpectedly died several days later. In both cases, autopsy revealed myocardial necrosis with marked lymphocytic infiltration. Polymerase chain reaction (PCR) screening was positive for the EBV, whereas immunohistochemistry and in situ hybridization for the EBV were negative. Serological investigations showed a mild elevation in antiviral capsid antigen IgG and anti-EBV nuclear antigen IgG in both cases. Immunohistochemical study of lymphocytic infiltrates showed strong positivity for a T-cell marker (CD45R0) in the myocardium and pharyngeal mucosa. These cases suggest the potential risk of mortality from acute EBV infection in young people, even without severe clinical manifestations, and the importance of microbiological investigations, including PCR procedures, in postmortem diagnosis of infectious diseases. [ABSTRACT FROM AUTHOR]