Arrhythmia onsets triggered by acute myocardial ischemia are not mediated by lysophosphoglycerides accumulation in ventricular myocardium.

Lysophosphoglycerides (LPLs) have been reported to accumulate in myocardium and serve as a cause of arrhythmias in acute myocardial ischemia. However, in this study we found that LPLs level in the ventricular myocardium was decreased by the onset of acute myocardial ischemia in vivo in rats. Decreasing of LPLs level in left ventricular myocardium, but not right, was observed within 26 min of left myocardial ischemia, regardless of whether arrhythmias were triggered. Lower LPLs level in the ventricular myocardium was also observed in aconitine-simulated ventricular fibrillation (P < 0.0001) and ouabain-simulated III° atrioventricular block (P < 0.0001). Shot-lasting electric shock, e.g., ≤ 40 s, decreased LPLs level, while long-lasting, e.g., 5 min, increased it (fold change = 2.27, P = 0.0008). LPLs accumulation was observed in long-lasting myocardial ischemia, e.g., 4 h (fold change = 1.20, P = 0.0012), when caspase3 activity was elevated (P = 0.0012), indicating increased cell death, but not coincided with higher frequent arrhythmias. In postmortem human ventricular myocardium, differences of LPLs level in left ventricular myocardium was not observed among coronary artery disease- and other heart diseases-caused sudden death and non-heart disease caused death. LPLs level manifested a remarkable increasing from postmortem 12 h on in rats, thus abolishing the potential for serving as biomarkers of sudden cardiac death. Token together, in this study we found that LPLs in ventricular myocardium were initially decreased by the onset of ischemia, LPLs accumulation do not confer arrhythmogenesis during acute myocardial ischemia. It is necessary to reassess the roles of LPLs in myocardial infarction.

The down-regulation of STC2 mRNA may serve as a biomarker for death from mechanical asphyxia.

Death from mechanical asphyxia (DMA) is a common cause of death in forensic pathology. However, due to the lack of biomarkers, the authentication of DMA now relies on a series of non-specific signs, which may cause troubles in the judicial trials, especially when the criminal scene is not fully elucidated. To search for the potential biomarkers for DMA, brain samples of DMA and craniocerebral injury groups were screened by microarray. The obtained mRNAs were validated by animal and human samples. Primary cell culture was conducted to explore the biochemical changes under hypoxia. 415 differentially expressed mRNAs between two groups were discovered. Ten mRNAs were examined in both human and animal samples died of different causes of death. Stanniocalcin-2 (STC2) showed significant down-regulation in DMA samples compared to other groups, regardless of PMI, age, or temperature. Cellular experiments indicated that ROS level peaked after 15-min-hypoxic culture, when the expression level of STC2 was significant down-regulated simultaneously. The ER-stress-related proteins also showed potential connection with STC2. In general, it is indicated that the down-regulation of STC2 may serve as a biomarker for DMA.

Research Progress on Molecular Changes in Pulmonary Hypoxia and Cause of Death Identification in Mechanical Asphyxia.

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.

Characteristics of road traffic accident types and casualties in Guangzhou, China, from 2007 to 2020: A retrospective cohort study based on the general population.

Introduction: This study aimed to explore the trend and main influencing factors of road traffic accidents in Guangzhou, China, from 2007 to 2020 and to provide a reference and guidance for government decision-making. Methods: A retrospective cohort study was used to describe road traffic accidents in Guangzhou. According to the population types, all people with road traffic accidents were divided into migrant workers and the control population. We divided road users, administrative districts, motorcycle types and injury levels into subgroups to investigate the characteristics of road traffic accidents in Guangzhou. The road traffic accident data were derived from the Guangzhou Public Security Traffic Management Integrated System. Results: The incidence rate of road traffic accidents per 10,000 vehicles in Guangzhou decreased from 36.55 in 2007 to 10.07 in 2012, remained relatively stable at 9.47 in 2017, and finally rose to 11.12 in 2020. The injury rate showed the same trend as the incidence rate, while the mortality rate gradually decreased from 14.21 in 2007 to 5.19 in 2020. Vulnerable road users such as motorized two-to-three-wheeler drivers and migrant workers were casualties in more than 80% of the cases. The proportion of casualties involving mopeds and electric bicycles increased rapidly after 2018. Motor vehicle drivers frequently caused road traffic accidents and were most often uninjured. Conclusion: Road safety in Guangzhou has shown a clear trend of improvement, but casualties are uneven across administrative districts. More attention should be given to motorized two-to-three-wheelers, migrant workers, and road traffic violations by uninjured individuals.

Mechanism of transverse fracture of the skull base caused by blunt force to the mandible.

Transverse fracture of the skull base is common both in the crushing of temporal regions of the skull and in the case of force acting on one temporal region. However, the mechanism of transverse skull base fracture caused by maxillofacial force has not been fully clarified. To provide an injury identification basis for forensic pathologists and clinicians, this paper combines accident reconstruction and finite element analysis methods to study the injury mechanism of an incomplete transverse fracture of skull base after the injured individual's mandible was subjected to violence in a traffic accident. The results show that after the injured individual's mandible was subjected to violence, forces in the direction of the left mandibular fossa and the right mandibular fossa were generated, creating the component forces. The combination of the two forces can produce a crushing effect toward the center of the skull base, as if the left and right temporal regions are being crushed, and the stress is concentrated at the joint of the mandible, the middle cranial fossa and the hypophyseal fossa. When the stress exceeds a certain limit, it will cause a transverse fracture of the skull base.

Sudden Death from Ischemic Heart Disease While Driving: Cardiac Pathology, Clinical Characteristics, and Countermeasures.

BACKGROUND Sudden death from ischemic heart disease while driving is an important cause of traffic accidents. This study discusses causes of traffic accidents in relation to risk factors for acute myocardial infarction such as hypertension and overwork and provides references for the early prevention and regulation of drivers' health conditions. MATERIAL AND METHODS Data on 21 cases of sudden death by ischemic heart disease while driving from January 2015 to December 2019 were collected. Age, symptoms, and cardiac pathological changes of patients were summarized by systematic anatomical and medical history data. RESULTS Patients were 21 men with an average age of 47±7.27 years (most aged 40 to 60 years), and the average weight of their hearts was 439.45±76.3 g. Twelve patients had a history of hypertension, 8 had previous myocardial infarction, and 4 had fatty liver. All had at least 1 severe narrowing of a major coronary artery. Twelve patients died within a short period; 9 died more than 12 h after myocardial infarction onset. Ten patients had worked more than 80 h of overtime per month, 4 patients, more than 45 h, and 7 patients, less than 45 h. CONCLUSIONS Regular physical examination and information about ischemic heart disease should be emphasized for men aged 40 to 60 years who drive frequently, especially for those with hypertension, overwork, or previous myocardial infarction. Incorporating objective evaluation criteria for the severity of ischemic heart disease and overwork into health condition-related driving regulations is needed.

Three Cases of Karoshi Without the Typical Pathomorphological Features of Cardiovascular/Cerebrovascular Disease.

Karoshi is a term used to describe unexplained sudden death associated with overwork and has become a serious public health issue in China. Cases have occurred in physicians, university professors, engineers in high-tech companies, and blue-collar workers. The mechanisms associated with death by overwork are very complex. According to most researchers, karoshi is considered to be caused by an excessive workload that induces deterioration of underlying hypertension or atherosclerosis. These conditions inevitably lead to death from cardiovascular or cerebrovascular diseases. However, in our own experience, we have found that in some cases, the victims of karoshi were in a chronic state of overwork but without a history of cardiovascular or cerebrovascular diseases. In support of this, we have found that even autopsies have revealed few positive findings except for cardiac hypertrophy. In this article, we report 3 typical cases of karoshi but without the typical pathomorphological features of cardiovascular or cerebrovascular disease.

Nontraumatic Multiple-Organ Fat Embolism: An Autopsy Case and Review of Literature.

The patient was an 88-year-old woman with a 10-year history of hypertension. She was suspected to have been hit by a car. At the time of the event, she was conscious and able to stand on her own and had no obvious injuries. She was sent home, but she lapsed into unconsciousness and was nonresponsive after 2 hours. She was sent to the hospital, and her heartbeat and breathing stopped. After half an hour of rescue attempts, her heartbeat did not recover, and she was declared dead. During the autopsy, a small subcutaneous hemorrhage was observed below the right knee joint. No obvious internal organ injuries or bone fractures were observed. The deceased also had mild atherosclerosis in the coronary arteries and an old cerebral infarction in the right cerebellum. The tissue histopathological tests showed distinct fat embolism in multiple organs, including the brain, lungs, kidneys, liver, and pancreas. A postmortem blood biochemistry test of the heart blood showed that the levels of low-density lipoprotein, cholesterol, triglycerides, and free fatty acids in the blood were increased, and the level of C-reactive protein was elevated. According to the autopsy results, the direct cause of death was multiorgan fat embolism. This case suggests that aging, hypertension, and hyperlipidemia may be risk factors for nontraumatic fat embolism under stressful conditions.

Karoshi May Be a Consequence of Overwork-Related Malignant Arrhythmia.

BACKGROUND Karoshi, which is sudden death associated with overwork, has become a serious problem in China. Many studies have examined the relationship between cardiovascular risks and karoshi, but there is little evidence that explains the exact mechanism by which overwork induces sudden death. In these cases, there are few obvious positive findings from forensic autopsies except for histories of overwork prior to death. Therefore, we assume that abnormalities, such as cardiac arrhythmia, rather than organic changes are the cause of karoshi. MATERIAL AND METHODS In the present study, the forced swim test (FST) was used to establish models of overwork. The myocardial tissues of SD rats taking FST (1 h per day, for 30 consecutive days) were collected. The arrhythmia-related molecule CX43 as well as its upstream regulation molecule Cav-1 and cSrc were tested by Western blot (WB) and immunohistochemistry (IHC). HE staining and Masson's staining were performed in the myocardium tissue section. RESULTS We observed downregulation of caveolin-1 (Cav1) followed by cSrc activation, resulting in the decrease of connexin43 (Cx43) levels in overwork models. Myocardial interstitial fibrosis, which is associated with electrophysiological aberrances that result in arrhythmia, was also found in the overwork models. CONCLUSIONS These data provide a mechanistic explanation for the speculated link between karoshi and cardiac arrhythmias.

Surface tyre imprints caused by a motorcycle collision rather than by being run over.

Tyre imprints on the skin are usually considered to be the result of being run over by a motor vehicle. This article reports a traffic accident in which tyre marks on the victim's skin were caused by a collision rather than by being run over. The mechanism of the injury in this case is analysed and discussed. A 23-year-old male drove a motorcycle while under the influence of alcohol and collided with a sign pillar on the side of the road. Both the victim and the motorcycle careened into the bottom of a tractor-trailer. No witnesses or surveillance videos could confirm the process of the accident. Because tyre imprints were found on the victim's skin, traffic police believed that he had been run over during the accident. However, forensic autopsy and analysis of the accident process revealed that the true cause of the imprints was a collision between the victim's body and a tyre.

Blunt Trauma-Induced Pericardial Tamponade After Video-Assisted Thoracoscopic Surgery.

This report describes a case of blunt cardiac injury and pericardial tamponade after video-assisted thoracoscopic surgery in a patient with lung cancer, hypertension, and cardiac hypertrophy. Anatomic findings included massive hemorrhage in the pericardium, cardiac hypertrophy, and a superficial contusion with a ruptured blood vessel on the epicardium at the lateral wall of the left ventricle. The patient died of pericardial tamponade secondary to blunt trauma from the tip of the thoracoscopic instrument. This case suggests that detailed assessment of the cardiovascular system, especially cardiac hypertrophy, careful preoperative preparation, and careful monitoring of postoperative conditions are important.

Fatal spontaneous rupture of common iliac artery associated with fibromuscular dysplasia.

A previously healthy 25-year-old man with no known risk factors was presented at the emergency room with a 3 h history of abdominal and loin pain. Physical examination and lab data showed no specific findings except tenderness, slight white cell count elevation and decreased haemoglobin level. The patient's condition deteriorated over the following hours and he died despite resuscitation attempts. Autopsy revealed a 2.5-cm longitudinal tear in the intima of the right common iliac artery, which formed a thrombosed false lumen extending to the abdominal aorta proximally and to the left common iliac artery. Histopathologic examination revealed the characteristic changes of fibromuscular dysplasia (FMD). FMD involving the common iliac arteries is extremely rare; only six cases have been reported previously, and only two of those included forensic findings. The presented case is the first case of FMD with intimal tearing in the right common iliac artery, with propagation to the left common iliac artery and abdominal aorta. When a previously healthy young adult without hypertension or other risk factors presents with acute abdominal and loin pain, systemic vascular disease should be on the list of differential diagnoses. Careful and complete evaluation of multiple arteries can be critical.

[Morphological analysis of cardiac rupture due to blunt injury, cardiopulmonary resuscitation and myocardial infarction in forensic pathology].

OBJECTIVE: To analyze the morphological features and forensic pathological characteristics of cardiac ruptures of different causes for their differential diagnosis. METHODS: We analyzed the data of 44 autopsy cases of cardiac rupture from 2014 to 2017 in our institute, including 11 cases caused by blunt violence with intact pericardium, 4 caused by cardiopulmonary resuscitation (CPR), 9 by myocardial infarction, and 20 by aorta dissection rupture.The gross features and histopathological characteristics of cardiac rupture and pericardial effusion were analyzed and compared. RESULTS: Cardiac ruptures caused by blunt violence varied in both morphology and locations, and multiple ruptures could be found, often accompanied with rib or sternum fractures; the volume of pericardial effusion was variable in a wide range; microscopically, hemorrhage and contraction band necrosis could be observed in the cardiac tissue surrounding the rupture.Cardiac ruptures caused by CPR occurred typically near the apex of the right ventricular anterior wall, and the laceration was often parallel to the interventricular septum with frequent rib and sternum fractures; the volume of pericardial blood was small without blood clots; microscopic examination only revealed a few hemorrhages around the ruptured cardiac muscular fibers.Cardiac ruptures due to myocardial infarction caused massive pericardial blood with blood clots, and the blood volume was significantly greater than that found in cases of CPR-induced cardiac rupture (P < 0.05);lacerations were confined in the left ventricular anterior wall, and the microscopic findings included myocardial necrosis, inflammatory cell infiltration, and mural thrombus.Cardiac tamponade resulting from aorta dissection rupture was featured by massive pericardial blood with blood clots, and the blood volume was much greater than that in cases of cardiac ruptures caused by blunt violence, myocardial infarction and CPR (P < 0.05). CONCLUSIONS: Hemorrhage, inflammatory cell infiltration, and lateral thrombi around the cardiac rupture, along with pericardial blood clots, are all evidences of antemortem injuries.

Sudden infant death from neonate carnitine palmitoyl transferase II deficiency.

A full-term female baby born to parents who gave birth three years prior to a girl who survived only 31h postpartum died 36h after birth. An autopsy showed that the heart was markedly hypertrophic (32g). Microscopically, the myocardium, liver and kidney cells exhibited extensive vacuolar degeneration. Sudan III staining was positive in cardiac muscle, liver and kidney tissue. Tandem mass spectrometry analysis revealed that the deceased patient had a carnitine palmitoyl transferase II (CPT2) deficiency or a carnitine-acylcarnitine translocase deficiency. Genetic testing of the parents revealed heterozygous CPT2 mutations, indicating that their offspring would have a 25% chance of having a CPT2 deficiency. Therefore, we speculated that CPT2 deficiency might be the cause of death based on the results of staining, tandem mass spectrometry analysis and parental genetic testing.

Postmortem Serum Tryptase Levels with Special Regard to Acute Cardiac Deaths.

An elevated serum tryptase concentration is considered a specific marker for systemic mast cell activation, a central feature of anaphylaxis. However, in some cases of acute cardiovascular death, high concentrations of serum tryptase are also observed. We compared the postmortem serum tryptase concentrations in 74 cases assigned to the following four groups: anaphylactic deaths (Group A, n = 20), acute cardiac deaths (Group ACD, n = 30), acute dissecting aneurysm ruptures (Group ADA, n = 10), and controls (Group C, n = 14). Additionally, the cutoff between Group A and the other groups was calculated using receiver-operating characteristic (ROC) curve analysis. Tryptase concentrations were markedly elevated in Group A (p < 0.001), Group ACD (p = 0.015), and Group ADA (p = 0.005). The optimal cutoff was 43 ng/mL, the sensitivity was 90%, and the specificity was 98%. While elevated concentrations of tryptase were noted in practical autopsy cases, due attention should be paid to the differential diagnosis between anaphylactic and acute cardiovascular deaths.

Electrocution-related mortality: a review of 71 deaths by low-voltage electrical current in Guangdong, China, 2001-2010.

The aim of this study was to investigate the epidemiological characteristics of low-voltage electrocution deaths in Guangdong, China. Three thousand three hundred seventy autopsy reports from the Department of Forensic Pathology, Zhongshan School of Medicine, Sun Yat-Sen University, over a period of 10 years (2001-2010) were reviewed, of which 71 low-voltage electrocution cases were identified. The descriptive statistical analyses were carried out with the application of SPSS 19.0 software. Electrocution accounted for 2.11% of all autopsied cases. The age range was 3 to 57 years with a mean age of 31.77 ± 11.0 years. The average age of male victims was 33.08 ± 10.77 years, and that of female victims was 22.63 ± 11.06 years. The majority of the victims (87.33%) were male. Among the circumstances leading to electrocution, most of them occurred in factory and in the street. Considering the contact details, deaths were caused most frequently by touching electrical wires (n = 27, 38.02%), followed by touching charged machine (n = 20, 28.17%). There were no suicide and homicide cases. Of all electrocution cases, 50.70% occurred during the summer period from June through August. The upper extremity was the most frequently involved contact site (59.72%). No electrical burn marks were present in 14 cases (19.72%). Our results indicated that most deaths from electrocution occur more often in factories, in summer seasons, and to young male workers, which can help in the development of a differentiated strategy for the prevention of electrocution, while taking into consideration sex, age, occupation, and season of the year.

Association of common variants in NOS1AP gene with sudden unexplained nocturnal death syndrome in the southern Chinese Han population.

Here, we investigate the association of common polymorphisms of the NOS1AP gene with sudden unexplained nocturnal death syndrome (SUNDS) in the southern Chinese Han population. We genetically screened five common NOS1AP polymorphisms (rs10918594, rs12143842, rs16847548, rs12567209, and rs10494366) previously reported to be associated with QT interval variation and sudden cardiac death (SCD) in 123 sporadic SUNDS cases and 166 healthy controls using polymerase chain reaction (PCR) and direct DNA sequencing. In the present study, the A allele of rs12567209 was more common in controls than in SUNDS cases, which was associated with 0.656-fold decreased risk of SUNDS (95% confidence interval 0.431 to 0.998, P = 0.048) compared with G allele. Under the dominant genetic model, GA + AA genotype of rs12567209 was also more common in controls than in SUNDS cases, which was associated with 0.604-fold decreased risk of SUNDS (95 % confidence interval 0.368 to 0.991, P = 0.045) compared with GG genotype. No significant associations of rs10918594, rs12143842, rs16847548, and rs10494366 with SUNDS were observed (P > 0.05). In haplotype analyses, the distribution of haplotype GCTA was significantly overrepresented in controls compared to SUNDS cases (P = 0.040). This is the first report of the association of common NOS1AP polymorphisms with SUNDS in the southern Chinese Han population. These findings suggest that the A allele of rs12567209 and haplotype GCTA may serve as a protective modifier.

Impact of traumatic muscle crush injury as a cause of cardiomyocyte-specific injury: an experimental study.

BACKGROUND: Muscle crush injury commonly occurs after earthquakes, collapse of buildings and sjambok beatings, and it often induces crush syndrome if not treated promptly. The general manifestation of crush syndrome is the presence of myoglobinuria with acute renal failure. However, whether cardiomyocyte injury is induced after muscle crush injury has not been investigated. The aim of this study was to observe the effects of muscle crush injury on cardiomyocyte injury and its relationship to the changes of ANP and ET-1 levels after muscle crush injury in rats. METHODS: Muscle crush injury was produced in Male Sprague-Dawley rats. Forty-eight rats were divided into six groups. The changes of electrocardiogram (ECG) were recorded. The serum levels of K(+), Ca(2+), urea, creatinine (CR), creatine kinase (CK), creatine kinase-myocardial band (CK-MB) and cardiac troponin I (cTnI) were detected by automated biochemical analysis and automated chemiluminescence assay, respectively. The myocardial and plasma levels of ANP and ET-1 were investigated by radioimmunoassay. Myocardial apoptosis and caspase-3 protein expression were quantitatively analysed by TUNEL-staining and Western blotting, respectively. RESULTS: After six hours of decompression, the serum levels of K(+) and urea increased and ST-segment elevated and heart rates decreased pronouncedly over 48h, CR increased and Ca(2+) decreased considerably over 24h. The serum levels of CK-MB and cTnI increased significantly from 6h to 24h and CK increased markedly from 0h to 24h after decompression and then decreased slowly. However, after 48h of decompression, the serum levels of cTnI were still higher than those of the control group. Plasma levels of ANP and ET-1 increased and myocardial ANP and ET-1 decreased progressively over 48h, and changed significantly from 6h to 48h after decompression. The number of TUNEL-positive myocytes and caspase-3 protein expression were higher from 6h to 48h after decompression. Moreover, the levels of K(+), urea, CR, CK, CK-MB, cTnI and caspase-3 reached their highest values after 12h of decompression. There were significant correlations between the plasma ANP elevation and the myocardial ANP decline, between the plasma ANP elevation and the plasma ET-1 increase, and between the plasma ET-1 increase and the myocardial ET-1 decline. CONCLUSIONS: Cardiomyocyte injury was induced by muscle crush injury at the early stage of decompression but not at compression. The most dangerous period of cardiomyocyte injury was at the 12th hour of decompression. Cardiomyocyte injury may partly relate to the changes of ANP and ET-1.

[Changes of left ventricular myocardial collagen fibers and osteopontin expression in hypertrophic cardiomyopathy].

OBJECTIVE: To investigate the changes of collagen fibers and the expression of osteopontin in the left ventricle in cases of hypertrophic cardiomyopathy (HCM), along with the significance of their potential forensic application. METHODS: Fifteen cases of HCM, 15 cases of coronary heart disease with cardiac hypertrophy and 20 cases of traffic accidents were selected as HCM group, coronary heart disease group and control group, respectively. Collagen volume fraction and osteopontin expression were observed and compared by HE staining, Masson trichrome staining and immunohistochemistry methods. Imaging and statistical methods were used for quantitative analysis. RESULTS: Collagen volume fraction in left ventricle of HCM and coronary heart disease were significantly higher than that in the control group (P < 0.05), which was not significantly different between the HCM group and the coronary heart disease group. The integral light density value of osteopontin in left ventricular cardiomyocytes of the HCM group and the coronary heart disease group were significantly higher than that of the control group (P< 0.05), and the value of the HCM group was also significantly higher than that of coronary heart disease group (P < 0.05). CONCLUSION: The increased contents of collagen fibers and the overexpression of osteopontin may play an important role in myocardial fibrosis, and they can be used as markers in aid of diagnosing sudden death due to HCM.

[The role of diaphgram fatigue in the death from hanging with bound upper limbs of rabbits].

OBJECTIVE: To explore the role of diaphgram fatigue in the death from hanging with bound upper limbs of rabbits. METHODS: Rabbits were hanged with upper limbs bound, then the data of EMGdi were gathered RESULTS: By analyzing power spectral of EMGdi in experiment, we compare the ratio change of H/L between pre-experiment and post-experiment. There is a significance decrease of the ratio of H/L, so it indicates that diaphgram fatigue does exist. CONCLUSION: Diaphgram fatigue plays an important role in the death from hanging with limbs of rabbits bound.