Sudden death due to traumatic ascending aortic pseudoaneurysms ruptured into the esophagus: 2 case reports.

We present 2 rare cases of patients with uncontrolled hemorrhagic shock induced by traumatic ascending aortic pseudoaneurysm rupture into the esophagus. Two men were presented to the hospital after traffic accidents. Their chest radiograph showed no obvious signs of aortic damage or aortic pseudoaneurysms but only a small amount of high-density shadow in the mediastinum and no specific clinical signs besides chest tightness or chest tenderness. The first case was misdiagnosed as pulmonary contusion and pleural effusion, and the second case was misdiagnosed as mediastinal lesions in the mediastina. They were given symptomatic and supportive treatment. Unfortunately, they died suddenly after >1 month of traumatic accident. At autopsy, ascending aortic pseudoaneurysms that broke into the esophagus and multiple organ hematocele were detected by gross examination. In histopathological examination, inflammatory cells and proliferated fibrous connective tissue were detected in the ascending aortic pseudoaneurysms, and the pathological gastrointestinal bleeding was not seen. The drugs and poisons were not found on toxicological analysis. The 2 patients died as a result of hemorrhagic shock from traumatic ascending aortic pseudoaneurysm rupture into the esophagus. We suggest that thoracic surgeon should be aware of the possibility of aortic injury after chest trauma to reduce misdiagnosis and prevent similar accidents.

Fatal barium chloride poisoning: four cases report and literature review.

Barium is an alkaline earth metal which has a variety of uses including in the manufacturing industry and in medicine. However, adverse health effects and fatalities occur due to absorption of soluble barium compounds, notably the chloride, nitrate, and hydroxide, which are toxic to humans. Although rare, accidental and suicidal modes of poisoning are sporadically reported in the literature.We describe 4 cases of poisoning due to barium chloride in China. In witnessed cases, severe gastrointestinal symptoms, hypokalemia leading to muscle weakness, cardiac arrhythmias, and respiratory failure were noted. Autopsy showed some nonspecific but common findings, such as subendocardial hemorrhage in the ventricles, visceral petechiae, and fatty changes in the liver. Interestingly, microscopic examination showed degenerative changes and amorphous, flocculent foamy materials in the renal tubules. Toxicology was relevant for barium in blood and tissues. Three of the cases were accidental and 1 homicidal in nature. A round-up of relevant literature on fatal barium compounds poisoning is also provided. Forensic pathologists should be aware of the clinical presentations of barium compound poisoning and especially look for any evidence of hypokalemia. Still, postmortem toxicological and histological studies are essential for an accurate identification of the cause of death.

Role of neuropeptide Y and peroxisome proliferator-activated receptor γ coactivator-1α in stress cardiomyopathy.

Death following situations of intense emotional stress has been linked to the cardiac pathology described as stress cardiomyopathy, whose pathomechanism is still not clear. In this study, we sought to determine, via an animal model, whether the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and the amino peptide neuropeptide Y (NPY) play a role in the pathogenesis of this cardiac entity. Male Sprague-Dawley rats in the experimental group were subjected to immobilization in a plexy glass box for 1 h, which was followed by low voltage electric foot shock for about 1 h at 10 s intervals in a cage fitted with metallic rods. After 25 days the rats were sacrificed and sections of their hearts were processed. Hematoxylin-eosin staining of cardiac tissues revealed the characteristic cardiac lesions of stress cardiomyopathy such as contraction band necrosis, inflammatory cell infiltration and fibrosis. The semi-quantitative RT-PCR analysis for PGC-1α mRNA expression showed significant overexpression of PGC1-α in the stress-subjected rats (P<0.05). Fluorescence immunohistochemistry revealed a higher production of NPY in the stress-subjected rats as compared to the control rats (P=0.0027). Thus, we are led to conclude that following periods of intense stress, an increased expression of PGC1-α in the heart and an overflow of NPY may lead to stress cardiomyopathy and even death in susceptible victims. Moreover, these markers can be used to identify stress cardiomyopathy as the cause of sudden death in specific cases.

Distribution of methamphetamine and its metabolite amphetamine in acute and subacute ethanol-methamphetamine combination abuse model rats.

The aim of this study is to investigate the distribution of methamphetamine (MA) and its metabolite amphetamine (AP) in rat models of acute and subacute MA-ethanol combination abuse. Rats were fed with 20% ethanol for 4 weeks (chronic active-drinking group), and MA was injected intraperitoneally into chronically drinking and normal rats over 5 and 14 days, respectively. Then the rats from the acute and subacute combination abuse groups were euthanized, and ethanol, MA, and AP concentrations in samples were quantified. Except for the similar ethanol concentrations among acute and subacute groups, the MA and AP levels between groups were quite different. The concentrations of MA and AP in rats' liver, lung, kidney, and brain were much higher than other tissues, regardless of combination with ethanol. Also, MA and AP levels in subacute rats groups were higher than those in acute groups, and the levels of MA and the formation of AP in rats subjected to the combination abuse with ethanol were higher than in MA-only intoxicated rats. We conclude that ethanol has no bearing on the MA and AP distribution in body fluids and tissues, yet it can increase MA levels and markedly accelerate the formation of AP in combination-abuse rats. Comparing the acute and subacute combination-abuse rats' samples, it can be deduced that various accumulated amounts of MA and AP were unaffected by ethanol, even after multi-dose injection, regardless of acute or subacute use.

Involvement of oxidative stress in the mechanism of triptolide-induced acute nephrotoxicity in rats.

Triptolide is one of the most widely used and one of the most potent Chinese traditional herbal medicines. However, side effects, especially nephrotoxicity, limit the use of triptolide. It has been reported that oxidative stress is involved in drug-induced nephrotoxicity. In the present study, we focused on observing triptolide-induced acute nephrotoxicity in rats and investigating whether or not oxidative stress is involved in the pathogenesis of this process. The results showed that a single large dose peritoneal injection of triptolide caused severe oxidative stress characterized by significant decreases of renal SOD and GSH-Px activities, as well as significant increase of renal MDA content and also led to severe impairment of renal structure and function characterized by injury of renal tubules observed in HE-stained and TUNEL-stained slides and increases of Cre and BUN concentrations in a short time. However, pretreatment with the antioxidant vitamin C significantly ameliorated triptolide-induced depletion in renal SOD and GSH-Px activities, caused marked normalization of renal MDA content and also blunt the impairment of renal tubules and renal function. These results suggest that triptolide induces oxidative stress via impairing the antioxidant system, and oxidative stress contributes, at least in part, to the mechanism of triptolide-induced acute nephrotoxicity.

Role of reactive oxygen species in triptolide-induced apoptosis of renal tubular cells and renal injury in rats.

This study investigated the role of reactive oxygen species (ROS) in the pathogenesis of triptolide-induced renal injury in vivo. Rats were randomly divided into 4 groups (n=5 in each): triptolide group in which the rats were intraperitoneally injected with triptolide solution at a dose of 1 mg/kg of body weight on day 8; control group in which the rats received a single intraperitoneal injection of 0.9% physiological saline on day 8; vitamin C group in which the rats were pretreated with vitamin C by gavage at a dose of 250 mg/kg of body weight per day for 7 days before the same treatment as the control group on day 8; triptolide+vitamin C group in which the rats were first subjected to an oral administration of vitamin C at a dose of 250 mg/kg of body weight per day for 7 days, and then to the same treatment as the triptolide group on day 8. All the rats were sacrificed on day 10. Blood samples were collected for detection of plasma creatinine (Pcr) and plasma urea nitrogen (PUN) concentrations. Both kidneys were removed. The histological changes were measured by haematoxylin-eosin (HE) staining. The production of ROS was determined by detecting the fluorescent intensity of the oxidation-sensitive probe rhodamine 123 in renal tissue. Renal malondialdehyde (MDA) content was measured to evaluate lipid peroxidation level in renal tissue. TUNEL staining was performed to assess apoptosis of renal tubular cells. Renal expression of apoptosis-related proteins Bcl-2, Bax, Bid, Bad, Fas and FasL, as well as corresponding encoding genes were assessed by Western Blotting and real-time PCR. The results showed that triptolide treatment promoted the generation of a great amount of ROS, up-regulated the expression of Bax, Bid, Bad, Fas and FasL at both protein and mRNA levels, as well as the ratio of Bax to Bcl-2, and caused the apoptosis of renal tubular cells and renal injury. However, pretreatment with an antioxidant, vitamin C, significantly reduced the generation of ROS and effectively inhibited the triptolide-induced apoptosis of renal tubular cells and renal injury. It was concluded that ROS plays a critical role in triptolide-induced apoptosis of renal tubular cells and renal injury. The protective administration of vitamin C may help alleviate triptolide-induced renal injury and nephrotoxicity.

HIV-negative drug addict diagnosed with AIDS and tuberculosis at autopsy: a case report and brief review of literature.

Human Immunodeficiency Virus (HIV) infection is a true plague and a major health concern globally. It is one of the most significant pandemics in recorded history. Despite worldwide efforts to fight the pandemic, and now with the re-emergence of tuberculosis, those clinicians, personnel performing autopsies and medical caregivers are again at risk in the work place, especially in developing countries. We describe a case where a drug abuser, whose addiction was concealed by his parents, died in hospital. He was tested HIV-negative there. A medical tangle ensued and forensic autopsy was carried out. Autopsy confirmed he was an intravenous drug addict and had tuberculosis. Post-mortem blood was positive for HIV antibodies and he was diagnosed with AIDS. Due to social stigmas, lack of knowledge or inefficient medical laboratory procedures etc, such type of cases can become a hazard to those attending the sick and to autopsy pathologists alike. We provide the case description, autopsy findings and review of pertinent literature.

Role of Reactive Oxygen Species in Triptolide-induced Apoptosis of Renal Tubular Cells and Renal Injury in Rats / 华中科技大学学报（医学）（英德文版）

This study investigated the role of reactive oxygen species (ROS) in the pathogenesis of triptolide-induced renal injury in vivo.Rats were randomly divided into 4 groups (n=5 in each):triptolide group in which the rats were intraperitoneally injected with triptolide solution at a dose of 1 mg/kg of body weight on day 8; control group in which the rats received a single intraperitoneal injection of 0.9％ physiological saline on day 8; vitamin C group in which the rats were pretreated with vitamin C by gavage at a dose of 250 mg/kg of body weight per day for 7 days before the same treatment as the control group on day 8; triptolide+vitamin C group in which the rats were first subjected to an oral administration of vitamin C at a dose of 250 mg/kg of body weight per day for 7 days,and then to the same treatment as the triptolide group on day 8.All the rats were sacrificed on day 10.Blood samples were collected for detection of plasma creatinine (Pcr) and plasma urea nitrogen (PUN) concentrations.Both kidneys were removed.The histological changes were measured by haematoxylin-eosin (HE)staining.The production of ROS was determined by detecting the fluorescent intensity of the oxidation-sensitive probe rhodamine 123 in renal tissue.Renal malondialdehyde (MDA) content was measured to evaluate lipid peroxidation level in renal tissue.TUNEL staining was performed to assess apoptosis of renal tubular cells.Renal expression of apoptosis-related proteins Bcl-2,Bax,Bid,Bad,Fas and FasL,as well as corresponding encoding genes were assessed by Western Blotting and real-time PCR.The results showed that triptolide treatment promoted the generation of a great amount of ROS,up-regulated the expression of Bax,Bid,Bad,Fas and FasL at both protein and mRNA levels,as well as the ratio of Bax to Bcl-2,and caused the apoptosis of renal tubular cells and renal injury.However,pretreatment with an antioxidant,vitamin C,significantly reduced the generation of ROS and effectively inhibited the triptolide-induced apoptosis of renal tubular cells and renal injury.It was concluded that ROS plays a critical role in triptolide-induced apoptosis of renal tubular cells and renal injury.The protective administration of vitamin C may help alleviate triptolide-induced renal injury and nephrotoxicity.

Fatal renal failure due to the Chinese herb "GuanMu Tong" (Aristolochia manshuriensis): autopsy findings and review of literature.

Herbal remedies have been used since ancient times and it is now known that they are not completely free of adverse effects. We present the case of a 41-year-old Chinese man, who died in renal failure because he consumed a herbal preparation called "Fen Qing Wu Lin Wan", having GuanMu Tong as main ingredient, for about 1 month. GuanMu Tong is derived from the plant Aristolochia manshuriensis which contains aristolochic acid. Aristolochic acid is being reported as the causative agent of what is now called aristolochic acid nephropathy (AAN) which includes Chinese herb nephropathy (CHN) and Balkan endemic nephropathy (BEN), all having renal impairment as hallmark for the disease. The gross autopsy showed multiple punctate hemorrhages over the limbs, pleural effusion, and edematous lungs with consolidation, mild myocardial hypertrophy and normal-looking kidneys. Microscopic renal tissue examination showed severe degeneration, necrosis and desquamation of renal tubular epithelial cells, presence of protein cast and a widened, edematous interstitium with interstitial fibrosis. We also provide the clinical presentation of the deceased as reported in the medical records and briefly review the literature pertinent to similar cases.

Characterization of protein in old myocardial infarction by FTIR micro-spectroscopy / 华中科技大学学报（医学）（英德文版）

The aim of the present study was to assess whether Fourier transform infrared spectrometry (FTIR) micro-spectroscopy could produce distinct spectral information on protein of old myocardial infarction (OMI) and to set them as molecular markers to diagnose atypical OMI. Paraffin-embedded heart samples were derived from victims dying of OMI. In combination with histological stain, FTIR and infrared micro-spectroscopy, the characteristics of OMI were analyzed morphologically and molecularly. The most relevant bands identified were the amide A, B, I and, II showing crucial spectral differences between apparent normal region and OMI region, including the peak position blue shift and the increased intensity of OMI, moreover relative increase in alpha-helix and decrease in beta-sheet of protein secondary structures in OMI. Comparing to single spectral band, the I1650/I1550 ratio was increased and rationally used as a molecular marker for diagnosing OMI. These novel preliminary findings supported further exploration of FTIR molecular profiling in clinical or forensic study, and were in accordance with histopathology.

Noncompaction of ventricular myocardium and its medicolegal evaluation / 法医学杂志

Noncompaction of ventricular myocardium (NVM) is a rare cardiomyopathy. For the past few years, there have been more clinical reports and related scientific researches on NVM. It is one of the hottest topics in the field of clinical cardiovascular science. NVM is rare, but usually leads to fatal results, such as sudden unexpected death. Most forensic medical examiners in China have not recognized the importance of this disease. There are no good forensic pathological methods yet to identify this disease. Furthermore, NVM is easily to be confused with other types of heart diseases. As a result, we should be very careful about NVM, and understand the importance of making right diagnosis of NVM. This review focuses on NVM's pathological features, clinical diagnostic methods, and differential diagnosis from other cardiac disease. The key points on how to make right forensic pathological diagnosis of NVM have also been summarized.