Lung is the largest organ of the respiratory system. During hypoxia, pulmonary cells undergo rapid damage changes and activate the self-rescue pathways, thus leading to complex biomacromolecule modification. Death from mechanical asphyxia refers to death due to acute respiratory disorder caused by mechanical violence. Because of the absence of characteristic signs in corpse, the accurate identification of mechanical asphyxia has always been the difficulty in forensic pathology. This paper reviews the biomacromolecule changes under the pulmonary hypoxia condition and discusses the possibility of application of these changes to accurate identification of death from mechanical asphyxia, aiming to provide new ideas for related research.
Humans ; Asphyxia/pathology* ; Cause of Death ; Hypoxia/pathology* ; Lung/pathology* ; Forensic Pathology

In recent years, the increase in the number of cases of postural asphyxia has gradually attracted the attention and discussion of forensic scientists domestically and internationally, but a systematic, comprehensive and recognized expert consensus and identification standard has not been established at home and abroad. This paper reviews the case characteristics, occurrence, mechanism of death, and identification criteria of postural asphyxia, to provide reference for future research.
Asphyxia/etiology* ; Forensic Medicine ; Forensic Pathology ; Humans

Mitochondria are the special organelle in eukaryotic cells. Their main functions are to synthesize energy required for cell activity by oxidative phosphorylation. Most of the oxygen absorbed by the body is consumed in the mitochondria. The precise diagnosis of mechanical asphyxia is one of the difficulties in forensic pathology practice. Forensic pathologists have been trying to find a reliable and sensitive marker for the diagnosis of mechanical asphyxia. Mitochondria are very sensitive to hypoxic environments, and the markers of mitochondrion damage can be used as a basis for the diagnosis of mechanical asphyxia. The purpose of this paper is to review the research progress on mitochondrial damage in hypoxic environments and to explore the possibility of using markers of mitochondrion damage in forensic pathological practice.
Asphyxia ; Forensic Pathology ; Humans ; Hypoxia ; Mitochondria ; Oxygen

Investigating neonatal deaths in the toilets is challenging for forensic pathologists. During the postmortem examination, they should evaluate whether the baby was alive or a stillbirth and determine any causes of death, such as prenatal cause, infection, anatomical abnormalities, birth or other blunt force injury, drowning, and asphyxia. We retrieved two cases of neonatal deaths in the toilets and reviewed their autopsy findings and circumstances. However, findings from the postmortem examination were insignificant. Their lung examinations revealed non-expanded alveoli, and hydrostatic tests were negative. However, the cases cannot be confirmed as stillbirths because of the possibility that they might be alive for a short period of time after birth and then exposed into the water in the toilet or to accidental or non-accidental asphyxia or that they might have died because of neglect. These cases illustrate that the death scene and the associated circumstances should be meticulously and carefully investigated.
Asphyxia ; Autopsy ; Cause of Death ; Drowning ; Forensic Pathology ; Humans ; Infant, Newborn* ; Lung ; Parturition ; Perinatal Death ; Stillbirth ; Water

Under hypoxia condition, microRNA （miRNA） can interact with transcription factors for regulating the cell metabolism, angiogenesis, erythropoiesis, cellular proliferation, differentiation and apoptosis. The biological processes above may play an important role in mechanical asphyxia death. This article reviews the regulating function of miRNA under hypoxia condition and the influence of hypoxia to biosynthesis of miRNA, which may provide some new ideas to the research of miRNA on determining the cause of mechanical asphyxia death in the field of forensic medicine.
Accidents ; Airway Obstruction/physiopathology* ; Apoptosis ; Asphyxia/pathology* ; Cause of Death ; Death ; Forensic Medicine ; Humans ; Hypoxia/physiopathology* ; MicroRNAs/metabolism* ; Oxygen

OBJECTIVETo study the effect of leptin on the expression of calcium-activated neutral protease 1 (calpain-1) and B cell lymphoma-2 (Bcl-2) and apoptosis in the myocardial tissue of neonatal rats after asphyxia.

METHODSA total of 48 neonatal rats were randomly and equally divided into normal control group, asphyxia group, leptin treatment groups, and calpain-1 inhibitor (CAI-1) group. The neonatal rat model of asphyxia under normal atmospheric condition was established in all groups except the control group. For the leptin treatment groups, rats received 20, 80, and 160 μg/kg leptin by intraperitoneal injection immediately after model establishment, respectively. For the CAI-1 group, rats received 10 mg/kg CAI-1 by intraperitoneal injection immediately after model establishment. For all the groups, the myocardial tissue was collected at 2 hours after model establishment. Immunohistochemistry was used to measure the expression of calpain-1 and Bcl-2. The TUNEL method was used to evaluate apoptosis of myocardial cells.

RESULTSThe expression of calpain-1 and Bcl-2 and apoptosis index (AI) were significantly higher in the asphyxia group than in the normal control group (P˂0.05). The leptin treatment groups and the CAI-1 group had significantly lower expression of calpain-1, significantly lower AI, and significantly higher expression of Bcl-2 than the asphyxia group (P˂0.05). The CAI-1 group had the largest changes in all the indices compared with the asphyxia group. However, there were no significant differences in all indices between the 160 μg/kg leptin treatment group and the CAI-1 group. After asphyxia, the expression of calpain-1 was positively correlated with AI, while the expression of Bcl-2 was negatively correlated with AI and the expression of calpain-1 (P˂0.05).

CONCLUSIONSLeptin reduces apoptosis of myocardial cells in asphyxiated neonatal rats by the inhibition of calpain-1 activation and upregulation of Bcl-2 expression.

Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Asphyxia Neonatorum ; metabolism ; pathology ; Calpain ; analysis ; antagonists & inhibitors ; Leptin ; pharmacology ; Myocardium ; metabolism ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; analysis ; Rats ; Rats, Sprague-Dawley

BACKGROUNDMorbidity and mortality after resuscitation largely depend on the recovery of brain function. Ventricular fibrillation cardiac arrest (VFCA) and asphyxial cardiac arrest (ACA) are the two most prevalent causes of sudden cardiac death. Up to now, most studies have focused on VFCA. However, results from the two models have been largely variable. So, it is necessary to characterize the features of postresuscitation cerebral metabolism of both models.

METHODSForty-four Wuzhishan miniature inbred pigs were randomly divided into three groups: 18 for VFCA group, ACA group, respectively, and other 8 for sham-operated group (SHAM). VFCA was induced by programmed electric stimulation, and ACA was induced by endotracheal tube clamping. After 8 min without treatment, standard cardiopulmonary resuscitation (CPR) was initiated. Following neurological deficit scores (NDS) were evaluated at 24 h after achievement of spontaneous circulation, cerebral metabolism showed as the maximum standardized uptake value (SUVmax) was measured by 18 F-fluorodeoxyglucose positron emission tomography/computed tomography. Levels of serum markers of brain injury, neuron specific enolase (NSE), and S100β were quantified with an enzyme-linked immunosorbent assay.

RESULTSCompared with VFCA group, fewer ACA animals achieved restoration of spontaneous circulation (61.1% vs. 94.4%, P < 0.01) and survived 24-h after resuscitation (38.9% vs. 77.8%, P < 0.01) with worse neurological outcome (NDS: 244.3 ± 15.3 vs. 168.8 ± 9.71, P < 0.01). The CPR duration of ACA group was longer than that of VFCA group (8.1 ± 1.2 min vs. 4.5 ± 1.1 min, P < 0.01). Cerebral energy metabolism showed as SUVmax in ACA was lower than in VFCA (P < 0.05 or P < 0.01). Higher serum biomarkers of brain damage (NSE, S100β) were found in ACA than VFCA after resuscitation (P < 0.01).

CONCLUSIONSCompared with VFCA, ACA causes more severe cerebral metabolism injuries with less successful resuscitation and worse neurological outcome.

Animals ; Asphyxia ; complications ; physiopathology ; Brain ; metabolism ; Cardiopulmonary Resuscitation ; Heart Arrest ; metabolism ; pathology ; therapy ; Positron-Emission Tomography ; Swine ; Ventricular Fibrillation ; metabolism ; pathology ; therapy

BACKGROUNDThe two most prevalent causes of sudden cardiac death are ventricular fibrillation cardiac arrest (VFCA) and asphyxiation cardiac arrest (ACA). Profound postresuscitation myocardial dysfunction has been demonstrated in both VFCA and ACA animal models. Our study aimed to characterize the two porcine models of cardiac arrest and postresuscitation myocardial metabolism dysfunction.

METHODSThirty-two pigs were randomized into two groups. The VFCA group (n = 16) were subject to programmed electrical stimulation and the ACA group (n = 16) underwent endotracheal tube clamping to induce cardiac arrest (CA). Once induced, CA remained untreated for a period of 8 minutes. Two minutes following initiation of cardiopulmonary resuscitation (CPR), defibrillation was attempted until return of spontaneous circulation (ROSC) was achieved or animals died. To assess myocardial metabolism, (18)F-FluoroDeoxyGlucose Positron Emission Tomography was performed at baseline and 4 hours after ROSC.

RESULTSROSC was 100% successful in VFCA and 50% successful in ACA. VFCA had better mean arterial pressure and cardiac output after ROSC than ACA. Arterial blood gas analysis indicated more detrimental metabolic disturbances in ACA compared with VFCA after ROSC (ROSC 0.5 hours, pH: 7.01 ± 0.06 vs. 7.21 ± 0.03, P < 0.01; HCO3(-): (15.83 ± 2.31 vs. 20.11 ± 1.83) mmol/L, P < 0.01; lactate: (16.22 ± 1.76 vs. 5.84 ± 1.44) mmol/L, P < 0.01). Myocardial metabolism imaging using Positron Emission Tomography demonstrated that myocardial injuries after ACA were more severe and widespread than after VFCA at 4 hours after ROSC (the maximum standardized uptake value of the whole left ventricular: 1.00 ± 0.17 vs. 1.93 ± 0.27, P < 0.01). Lower contents of myocardial energy metabolism enzymes (Na(+)-K(+)-ATPase enzyme activity, Ca(2+)- ATPase enzyme activity, superoxide dismutase and phosphodiesterase) were found in ACA relative to VFCA.

CONCLUSIONSCompared with VFCA, ACA causes more severe myocardium injury and metabolism hindrance, therefore they should be treated as different pathological entities.

Animals ; Asphyxia ; pathology ; Cardiomyopathies ; pathology ; Cardiopulmonary Resuscitation ; Disease Models, Animal ; Female ; Heart Arrest ; pathology ; Heart Injuries ; pathology ; Male ; Swine ; Ventricular Fibrillation ; pathology

OBJECTIVETo study the effects of erythropoietin (EPO) on cardiomyocyte apoptosis and endoplasmic reticulum stress (ERS)-related proteins, glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP), in neonatal rats with asphyxia.

METHODSA total of 120 newborn Sprague-Dawley rats (7 days old) were randomly divided into sham-operated (n=40), asphyxia (n=40) and EPO-treated asphyxia groups (n=40). A neonatal rat model of normobaric asphyxia was established in the asphyxia and EPO-treated asphyxia groups. The rats in the EPO-treated asphyxia group received intraperitoneal injection of recombinant human erythropoietin (500 U/mL) immediately after the model was established, while the other two groups received the same volume of normal saline (0.9%). Heart blood and myocardial tissue samples were collected from 8 rats in each group at 2, 6, 12, 24 or 48 hours after the model was established. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) levels were measured; cardiomyocyte apoptosis was evaluated, and expression of myocardial GRP78 and CHOP was measured.

RESULTSCompared with the sham-operated and EPO-treated asphyxia groups, the asphyxia group had significantly increased serum CK and LDH levels, number of apoptotic cells, and expression of myocardial GRP78 and CHOP at each time point (P<0.01), and all the indices were significantly higher in the EPO-treated asphyxia group than in the sham-operated group (P<0.01). At 24 hours after asphyxia, the expression of myocardial CHOP was positively correlated with the myocardial apoptosis index (r=0.944, P<0.01).

CONCLUSIONSEPO exerts a protective effect on the myocardium of neonatal rats with hypoxic-ischemic injury by regulating ERS-related proteins GRP78 and CHOP and reducing cardiomyocyte apoptosis.

Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Asphyxia Neonatorum ; drug therapy ; pathology ; Creatine Kinase ; blood ; Endoplasmic Reticulum Stress ; physiology ; Erythropoietin ; pharmacology ; Heat-Shock Proteins ; analysis ; L-Lactate Dehydrogenase ; blood ; Myocytes, Cardiac ; drug effects ; pathology ; Rats ; Rats, Sprague-Dawley ; Transcription Factor CHOP ; analysis

OBJECTIVE: To summarize the solved homicide cases taking place in Suzhou city and to find out the characteristics and commonness of them in order to analyze the key points of investigation at the scene. METHODS: The data of 483 solved homicide cases occurring from January 2006 to March 2010 in the city were analyzed. RESULTS: Most cases involved 1 victim and 1 suspect, with young male adults dominated. Most of them were non-local residents. The majority of suspects were intentional by passion due to quarrel and dispute. The most common weapons were sharp instruments generally carried by the suspects. Mechanical asphyxia and mechanical injury were the two most common causes of death in these cases. CONCLUSION The social characteristics of suspects, criminal motivation, injury instruments, distribution of injuries, cause of death, and manner of death in Suzhou showed similar general characteristics as the experience for detecting homicide cases in the future.
Adult ; Age Distribution ; Asphyxia/mortality* ; Cause of Death ; Crime Victims/statistics & numerical data* ; Criminal Psychology ; Female ; Forensic Pathology ; Homicide/statistics & numerical data* ; Humans ; Male ; Retrospective Studies ; Sex Distribution ; Shock, Hemorrhagic/mortality* ; Socioeconomic Factors ; Weapons/statistics & numerical data* ; Wounds and Injuries/pathology*