Research Status and Prospects of Non-Traumatic Fat Embolism in Forensic Medicine.

In the practice of forensic pathology, fat embolism is one of the common causes of death, which can be divided into two categories: traumatic and non-traumatic. Non-traumatic fat embolism refers to the blockage of small blood vessels by fat droplets in the circulatory blood flow caused by non-traumatic factors such as underlying diseases, stress, poisoning and lipid metabolism disorders. At present, it is believed that the production of non-traumatic fat embolism is related to the disturbance of lipid metabolism, C-reactive protein-related cascade reaction, the agglutination of chylomicron and very low-density lipoprotein. The forensic identification of the cause of death of non-traumatic fat embolism is mainly based on the case, systematic autopsy, HE staining and fat staining, but it is often missed or misdiagnosed by forensic examiners because of its unknown risk factors, hidden onset, the difficulty of HE staining observation and irregular implementation of fat staining. In view of the lack of attention to non-traumatic fat embolism in forensic identification, this paper reviews the concepts, pathophysiological mechanism, research progress, existing problems and countermeasures of non-traumatic fat embolism, providing reference for forensic scholars.

Characteristics of human movement and injury in a side collision between the front of a small car and a bicycle.

OBJECTIVE: Our research groups have studied the movement and injury characteristics of the human body in a side collision between the front of a small car and a pedestrian. This study discusses the movement and injury characteristics of the human body in a side collision between the front of a small car and bicycle. METHODS: A total of 31 cases of traffic accidents caused by small car collisions when riding a bicycle across a road were collected. Through on-site inspection and trace inspection of the accident vehicles and bicycles, the speed of the car during the collision was calculated, the collision relationship between the small car and bicycle was determined, and the injury site and degree were determined through autopsy. The car speed was divided into two groups: <60 km/h and >60 km/h. Injuries of the skull, cervical spine, ribs, pelvis, femur and tibiofibular were analysed, and the correlations with the height of the bicycle controller, the height of the bicycle seat, the height of the car hood and the length of hood were discussed. PC-Crash was used for simulation analysis to further clarify the injury process. RESULTS: The ratio of the height of the bicycle seat to the height of the hood plus the length of the hood in the windshield-damaged group was larger than that in the undamaged windshield group (P < 0.05). No cervical fracture was found when V < 60 km/h, and 52.94% of cases had cervical fracture when V > 60 km/h. The ratio of the height of the bicycle seat to the height of the hood in the pelvic fracture group was smaller than that in the nonpelvic fracture group (P < 0.05). The incidence of tibiofibular fracture was less than 65%. CONCLUSIONS: When a side impact between a car front and a bicycle occurs, the resulting human injury is related not only to the speed but also to the height of the bicycle seat and the height and length of the hood of the car. The incidence of tibiofibular fractures was significantly lower than that of small car front-pedestrian side impacts.

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.

Analysis of Pedestrian Fractures in Collisions Between Small Cars and Pedestrians Based on Surveillance Videos.

OBJECTIVE: To discuss the collision relationship and the cause of the fracture caused by traffic accidents in which the front of a small car collides with the side of a pedestrian while braking. METHODS: The surveillance videos of 42 traffic accidents involving the front of a small car colliding with the side of a pedestrian while braking were collected. By analyzing the surveillance videos and the paths, the speed of the collision, the relationship between the vehicle and the pedestrian upon collision, and the movement trajectory of the human body were clearly identified. The type and severity of the injuries were also determined through autopsy. The characteristics of the human injuries and vehicle paths were analyzed according to the collision speed (<40 km/h, 40-60 km/h, 60-90 km/h), and the correlations between the fracture and the height of the pedestrian, the height of the hood and the length of the hood were discussed. RESULTS: When a small car hits the side of a pedestrian, the front bumper first hits the lower limbs of the pedestrian, and then, the human body falls to the side of the vehicle, causing a secondary collision with the hood and front windshield; thus, the pedestrian is thrown at a speed similar to the speed of the vehicle, finally falling to the ground and sliding forward a certain distance. (1) When V is less than 40 km/h (n = 10), the pedestrian's head did not collide with the windshield, and the fatal injuries were caused by the individual striking the ground. (2) When V is greater than 40 km/h (n = 32), the majority (97%) of cases showed collision with the windshield. (3) When 40 to 60 km/h (n = 16), the pedestrian's head collided with the windshield, which can cause fatal injuries, and pelvic fractures and rib fractures occurred in 56.25% of patients. (4) When V is less than 60 km/h (n = 26), the ratio of the height of the pedestrian to the height of the hood was significantly smaller in the pelvic fracture group than in the nonpelvic fracture group (P < 0.01). (5) When 60 to 90 km/h (n = 16), there were holes in the windshield, and the pedestrians experienced severe head injuries, with cervical spine fracture occurring in 37.5% of patients, pelvic fractures occurring in 43.75% of patients, and rib fractures occurring in 31.25% of patients. CONCLUSIONS: When V is less than 40 km/h, the vehicle does not cause severe injuries in pedestrians; when V is greater than 40 km/h, the collisions of the pedestrian's head with the windshield lead to severe head injuries and the accident can cause severe pelvic and rib fractures; when V is greater than 60 km/h, the collisions of the pedestrian's head with the windshield can cause cervical spine fracture in addition to head injuries. The occurrence of human injuries is related to not only the vehicle speed but also factors such as the height of the pedestrian, the height of the hood and the length of the hood.

Antibiotics Attenuate Methamphetamine-Induced Hepatotoxicity by Regulating Oxidative Stress and TLR4/MyD88/Traf6 Axis.

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.

Luteolin Alleviates Methamphetamine-Induced Hepatotoxicity by Suppressing the p53 Pathway-Mediated Apoptosis, Autophagy, and Inflammation in Rats.

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-1ß, 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.

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.

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.

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.

Decreased mRNA levels of cardiac Cx43 and ZO1 in sudden cardiac death related to coronary atherosclerosis: a pilot study.

Sudden cardiac death (SCD) is the most frequent cause of sudden unexplained death in forensic practice. The most common cause of SCD is coronary artery disease related to coronary atherosclerosis. Previous study suggested the possible application of connexin 43 (Cx43) and zonula occludens-1 (ZO1) immunostaining in the early diagnosis of myocardial ischemia. However, there appears to be insufficient data with regard to their mRNA levels. The present study investigated the cardiac mRNA levels of Cx43 and ZO1, using forensic autopsy materials consisting of 41 control cases without any disease or structural abnormality of the heart (group 1), 32 deaths due to acute ischemic heart disease related to coronary atherosclerosis without apparent myocardial necrosis (group 2), and 29 traumatic deaths with coronary atherosclerosis (group 3). Ten candidate reference genes were evaluated in the left ventricles of 10 forensic autopsy cases. EEF1A1, PPIA, TPT1, and RPL13A were identified as the most stable reference genes. Using these validated reference genes, mRNA levels of Cx43 and ZO1 were examined in the bilateral ventricles and atria of the heart. Relative mRNA quantification demonstrated decreased calibrated normalized relative quantity (CNRQ) values of Cx43 and ZO1 in bilateral ventricles of group 2. When using one conventional reference gene (GAPDH or ACTB) for normalization, nearly no difference was detected among the three groups. These findings indicate that ventricular gap junction remodeling may be a key contributor to rhythm disturbances. Analysis of cardiac Cx43 and ZO1 using real-time PCR is useful in diagnosis of SCD, and validation of reference genes is crucial.

Critical role of insulin­like growth factor binding protein­5 in methamphetamine­induced apoptosis in cardiomyocytes.

Methamphetamine (MA) is a highly abused amphetamine­like psychostimulant. At present, the mechanisms underlying MA­induced cardiotoxicity are poorly understood. The cardiotoxic effects have yet not been clearly elucidated with respect to the apoptotic pathway. Insulin­like growth factor binding protein­5 (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 MA­induced apoptosis as a novel target. MA­induced apoptosis was observed in neonatal rat ventricular myocytes (NRVMs) in a concentration­dependent manner using a terminal deoxyribonucleotide transferase­mediated dUTP nick end­labeling assay. Using reverse transcription polymerase chain reaction and western blotting, MA was demonstrated to induce concentration­dependent increases in the expression of IGFBP5. Silencing IGFBP5 with small interfering RNA significantly reduced apoptosis and suppressed the expression of caspase­3 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 MA­induced apoptosis in vitro, providing a foundation for future in vivo studies.

Remodeling of ion channel expression may contribute to electrophysiological consequences caused by methamphetamine in vitro and in vivo.

Methamphetamine (MA) is a psychostimulant. MA may induce numerous cardiotoxic effects, leading to cardiac arrhythmias, heart failure, eventually leading to sudden cardiac death. The deleterious effects of methamphetamine work in tandem to disrupt the coordinated electrical activity of the heart and have been associated with life-threatening cardiac arrhythmias. Remodeling of ion channels is an important mechanism of arrhythmia. Although arrhythmogenic remodeling involves alterations in ion channel expression, it is yet unknown whether MA induced electrical remodeling by affecting gene expression, and whether the changes in protein expression are paralleled by alterations in mRNA expression. Our study focused on the expression of ion channels which were correlated to the electrical remodeling caused by MA. We used RT-PCR and western blot to assess of the transcript and translate levels of ion channel subunits, including Ito: kv1.4, kv1.7, kv3.4, kv4.2; IK1: kir2.1, kir2.2, kir2.3, kir2.4; and ICa-l: Ca(2+)α1, Ca(2+)ß, respectively. The reversible effect of these changes after MA withdrawal was also evaluated. MA caused decrease in mRNA and protein levels in all ion channel subunits in vitro and also in vivo, is at this work. The kv3.4 and all 4 subunits of Kir2.0 family showed significant decrease than the other genes. Most of the channel subunit expression started to reverse after MA withdrawal for 4 weeks and significantly reverse in all of the channel subunits after MA withdrawal for 8 weeks. We found that CACNA1C and Kir2.0 family showed lower recoverability than the others after MA withdrawal for 8 weeks. The reduction of the ion channel expression levels may be the molecular mechanism that mediates the electrical remodeling caused by methamphetamine.

[Latest progress in postmortem interval estimation].

Accurate estimation of the postmortem interval (PMI) has been one of the most important and complicated issues in the forensic practice. In order to provide novel perspectives for the future research concerning PMI, the advantages and disadvantages of related traditional methods, postmortem degradation of nucleic acid and tissue, the componential change of vitreous humor and histological biochemistry since 2002 have been introduced and compared in this review.

Quantitative analysis of GFAP- and S100 protein-immunopositive astrocytes to investigate the severity of traumatic brain injury.

Previous studies have shown that diffuse cortical astrocyte damage is seen in acute deaths due to brain injury and mechanical asphyxiation. The present study quantitatively investigated the number of astrocytes that showed GFAP- and S100-protein immunopositivity in the cerebral white matter and hippocampus at the sites distant from primary injury with regard to survival time, complication, and the immediate cause of death of brain injury cases. Autopsy cases of brain injury (8-48 h postmortem) comprising acute/subacute deaths (survival time, <3/6 h-3 days; n=27/42) and delayed deaths (survival time >3 days) with/without complications (n=30/22) were examined. Delayed death cases with complications were subdivided into those in which the immediate cause of death had been determined as cerebral dysfunction (n=22) and those that had been determined as due to fatal complications (n=8). For controls, natural deaths from pneumonias (n=12) and sudden cardiac deaths (n=27) were used. In brain injury cases, the numbers of astrocytes in the cerebral white matter and hippocampal CA4 region were significantly lower for subacute death and delayed death without complications (p<0.05-0.001). Delayed death with fatal complications showed a significant increase in the number of astrocytes (p<0.05). Among delayed death cases, the numbers of astrocytes were higher in the cases with fatal complications than in those without complications and with non-fatal complications, although the latter cases showed large variations in the numbers of these astrocytes. These findings suggest that critical brain injury causes acute death without evident astrocyte pathology and that subacute death is associated with progressive brain damage accompanied by an astrocyte loss. In delayed death cases, the numbers astrocytes might be closely related to the severity of posttraumatic brain injury. GFAP and S100-immunopositivity might be useful for elucidating the cause and process of deaths due to brain injury.

Unexpected sudden death due to intracranial chordoma: an autopsy case.

Intracranial chordoma is a locally invasive, relatively rare tumour at the base of the skull. The tumour usually grows slowly but there have been several case reports of sudden death, all of which were due to tumour-associated haemorrhages. We report an autopsy case of a sudden unexpected death due to clinically undiagnosed intracranial chordoma in the brainstem without haemorrhage. A 44-year-old man was found dead at home. The autopsy revealed two small gelatinous and semi-translucent greyish tumours on the ventral surface of the brainstem between the midbrain and pons. The tumours were not attached to the dura or bone. The brain was markedly swollen, with enlarged lateral and third ventricles, but the aqueduct was compressed and narrowed. Microscopically, the tumour invaded the cerebral peduncles, and was classified as a chordoma. The cause of death was diagnosed as acute obstructive hydrocephalus due to a ventral brainstem tumour. Even a minor intracranial tumour that is not primarily life-threatening may cause sudden death due to subsequent obstructive hydrocephalus. The brainstem is one of the most vulnerable regions in the brain, and careful examination of this region is important for forensic pathologists.

Cardiothoracic ratio in postmortem chest radiography with regard to the cause of death.

It is difficult to examine the intact in situ status of thoracic organs, including the heart and lungs, after opening the chest at autopsy. The present study investigated the pathological diagnostic significance of the cardiothoracic ratio (CTR) with regard to heart and lung weight in postmortem plain chest radiography. The pathological diagnostic significance of the CTR in postmortem plain chest radiography using serial forensic autopsy cases of adults (>19 years of age, n=367, within 72 h postmortem) was retrospectively investigated. In natural deaths, CTR was larger for heart diseases, and was smaller for pulmonary infection and gastrointestinal bleeding, showing correlations to the heart weight except in cases of hemopericardium. In traumatic deaths, CTR was larger in cases of fire fatality and acute methamphetamine intoxication, and varied in cases of blunt injury, showing correlations to the heart weight. However, CTR was smaller for sharp instrument injury and drowning, independently of the heart weight. These findings suggest that postmortem CTR (median, 55.6%, measured using a mobile X-ray apparatus) primarily depends on the heart weight, but is substantially modified during the process of death: the CTR may be enlarged by cardiac dilatation due to terminal congestive heart failure, but may be reduced by inflated lungs in drowning or hypovolemia due to fatal hemorrhage. CTR showed a mild correlation to the right diaphragm level, which was also related to the cause of death, but was independent of the left diaphragm level. Plain chest radiographic findings may also be helpful in investigating the pathophysiology of death, and are to some extent comparable with clinical findings. This also suggests the potential usefulness of postmortem CT and MRI for analysis of terminal cardiac function.

Morphological analysis of astrocytes in the hippocampus in mechanical asphyxiation.

The present study investigated the morphology of astrocytes in the hippocampus and serum S100B levels in cases of mechanical asphyxia due to neck compression (n=23: atypical hanging, n=7; ligature/manual strangulation, n=16) with regard to the classical autopsy findings, compared with those of other types of asphyxiation (n=9) and acute myocardial infarction/ischemia (AMI, n=20). The decrease in intact astrocyte number, as shown by S100 and GFAP-immunostaining, was larger for asphyxiation due to neck compression compared with that for other asphyxiation and AMI, showing a correlation with the increase in the serum S100B levels. The decrease in intact astrocyte number and increase in serum S100B were closely related to the severity of conjunctival petechial hemorrhage and fracture(s) of the hyoid bone and/or thyroid cartilage in asphyxia due to neck compression. These findings suggest that hippocampal astrocyte injury is caused by cerebral hypoxia accompanied by congestion, especially in mechanical asphyxia due to neck compression.