Na Zheng

Commotio Cordis – A Report of Two Similar Cases

Commotio cordis is a rare and fatal mechano‐electric arrhythmogenic syndrome, occurring mainly during sports activities. The present study describes two similar cases of sudden death caused by commotio cordis associated with homicide. The two decedents were both 15‐year‐old male teenagers. Both collapsed within several minutes after being punched in the precordial region, as observed by witnesses at the scenes. Although electrocardiograms were not recorded at the scenes or the hospitals, the sudden onset of cardiovascular, respiratory, and neural symptoms were consistent with sudden cardiac death caused by commotio cordis. Autopsy and forensic morphology both revealed no cardiac or pericardiac structural damage, evident lesions of other internal organs, or underlying diseases, along with negative toxicological analysis, conforming to criteria for diagnosis of commotio cordis. The diagnosis of commotio cordis by forensic pathologists is important in deliberating a verdict of homicide, especially involuntary homicide. In rare instances, a death caused by commotio cordis may have a homicide manner of death.

Characterization of protein in old myocardial infarction by FTIR micro-spectroscopy

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 α-helix and decrease in β-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.SummaryThe 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 α-helix and decrease in β-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.

Bioluminescent assay of microbial ATP in postmortem tissues for the estimation of postmortem interval

To study the relationship between changes of microbial ATP in four kinds of murine tissues and the postmortem interval (PMI), healthy SD rats were sacrificed and their muscles, livers, spleens and kidneys were sampled at different postmortem intervals. The concentration of microbial ATP was detected using bioluminescent assay and the data was statistically analyzed. The concentration of microbial ATP in muscle increased with PMI time. The peak appeared at the 7th day after death, and at the 10th day, microbial ATP in muscle tissue increased again. In internal organs, the peaks of microbial ATP were observed at the 8th day after death and the level decreased during 8–10 d. The differences in microbial ATP concentration in liver, spleen and kidney were not statistically significant. During day 0 to day 9 after death, the correlation was best between PMI and microbial ATP in muscle. With PMI as the independent variable, the cubic polynomial regression equation was Y=0.02X3-0.166X2-0.666X+13.412 (R 2=0.989, P<0.01). In internal organs, the best correlation was found between PMI and microbial ATP during day 0 to day 10. With PMI as the independent variable, the cubic polynomial regression equation was Y=0.016X3-0.127X2-0.809X+13.324 (R 2=0.986, P<0.01). There existed high correlations between PMI and microbial ATP concentration in rat tissues. Since only a small amount of tissue was needed for the detection and the sample was not affected by self-decomposition, the method may extend the time range of PMI estimation.SummaryTo study the relationship between changes of microbial ATP in four kinds of murine tissues and the postmortem interval (PMI), healthy SD rats were sacrificed and their muscles, livers, spleens and kidneys were sampled at different postmortem intervals. The concentration of microbial ATP was detected using bioluminescent assay and the data was statistically analyzed. The concentration of microbial ATP in muscle increased with PMI time. The peak appeared at the 7th day after death, and at the 10th day, microbial ATP in muscle tissue increased again. In internal organs, the peaks of microbial ATP were observed at the 8th day after death and the level decreased during 8–10 d. The differences in microbial ATP concentration in liver, spleen and kidney were not statistically significant. During day 0 to day 9 after death, the correlation was best between PMI and microbial ATP in muscle. With PMI as the independent variable, the cubic polynomial regression equation was Y=0.02X3-0.166X2-0.666X+13.412 (R2=0.989, P<0.01). In internal organs, the best correlation was found between PMI and microbial ATP during day 0 to day 10. With PMI as the independent variable, the cubic polynomial regression equation was Y=0.016X3-0.127X2-0.809X+13.324 (R2=0.986, P<0.01). There existed high correlations between PMI and microbial ATP concentration in rat tissues. Since only a small amount of tissue was needed for the detection and the sample was not affected by self-decomposition, the method may extend the time range of PMI estimation.

Chemical Analysis in the Corpus Callosum Following Traumatic Axonal Injury using Fourier Transform Infrared Microspectroscopy: A Pilot Study.

Evaluating traumatic axonal injury remains challenging in clinical and forensic sciences as its identification is difficult using routine diagnostic methods. This study used Fourier transform infrared microspectroscopy to detect TAI within the corpus callosum in an animal model. Protein conformational analysis revealed significantly increased β‐sheet and β‐turn contents paralleled by a decrease in α‐helix content at 24 h postinjury, while the antiparallel β‐sheet content was decreased at 12 h postinjury. Compared with the control group, the lipid/protein ratio was significantly reduced in all of the injured groups. At 24 h postinjury, there were increases in the olefinic=CH and CH3 group of lipids accompanied by the decreased CH2 group, but the results at 12 and 72 h were contrary to that at 24 h. Our study showed that FTIRM could differentiate injured from normal white matter at different time points following TBI via examination of these infrared spectral parameters.

Imprudent blow, catastrophic consequence: a case of commotio cordis associated with violence

Commotio cordis is a rare and catastrophic mechano-electric feedback syndrome, and it is especially apt to occur in male children, adolescents and youths during sports activities. The authors present a case of unexpected sudden death due to commotio cordis associated with violence. In a house of detention, a 19-year-old boy was punched and kicked in the face, neck and chest during a fight with another suspect in their ward. Unfortunately, his precordium was the major injured region. The victim turned pale, then lost the ability to resist and lost consciousness immediately. When the emergency medical personnel arrived, the victim was found in a condition of cardiac and respiratory arrest and he was pronounced dead at the scene without cardiopulmonary resuscitation. Both autopsy signs and forensic morphology were in accord with the criteria for commotio cordis diagnosis, showing no cardiac or other organic fatal lesions and no underlying cardiac diseases; moreover, the toxicological screening was negative for alcohol, drug and common toxicants. In the present case, the whole fight was seen by some witnesses in their ward, and it was recorded by the monitoring unit. Based on the statements of the witnesses and the monitoring videotape, combined with the forensic pathological and toxicological examinations, all the testimonies supported the conclusion that the cause of death was commotio cordis.

Neurotoxicity of quinolinic acid to spiral ganglion cells in rats

Our study investigated the neurotoxicity of quinolinic acid (QA) to spiral ganglion cells (SGCs), observed the protective effects of N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 and magnesium ions on the QA-induced injury to SGCs, and analyzed the role of QA in otitis media with effusion (OME)-induced sensorineural hearing loss (SNHL). After culture in vitro for 72 h, SGCs were exposed to different media and divided into 4 groups: the blank control group, the QA injury group, the MK-801 treatment group, and the MgCl2 protection group. The apoptosis rate of SGCs was analyzed by Annexin V and PI double staining under the fluorescence microscopy 24 h later. SGCs were cultured in vitro for 72 h and divided into four groups: the low concentration QA group, the high concentration QA group, the MK-801 group, the MgCl2 group. The transient changes of intracellular calcium concentration were observed by the laser scanning confocal microscopy. Apoptosis rate in QA injury group was higher than that in blank control group and MgCl2 protection group (both P<0.05), but there was no significant difference between MK-801 treatment group and blank control group (P>0.05). In high concentration QA group, there was an obvious increase of the intracellular calcium concentration in SGCs, which didn’t present in low concentration QA group. In MgCl2 group, the peak values of the intracellular calcium concentration in SGCs were reduced and the duration was shortened, but the intracellular calcium concentration in SGCs had no significant change in MK-801 group. It was concluded that QA could injure SGCs by excessively activating NMDA receptors on the cell membrane, which might be the mechanism by which OME induced SNHL, while Mg2+ could protect the SCGs from the neurotoxicity of QA.SummaryOur study investigated the neurotoxicity of quinolinic acid (QA) to spiral ganglion cells (SGCs), observed the protective effects of N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 and magnesium ions on the QA-induced injury to SGCs, and analyzed the role of QA in otitis media with effusion (OME)-induced sensorineural hearing loss (SNHL). After culture in vitro for 72 h, SGCs were exposed to different media and divided into 4 groups: the blank control group, the QA injury group, the MK-801 treatment group, and the MgCl2 protection group. The apoptosis rate of SGCs was analyzed by Annexin V and PI double staining under the fluorescence microscopy 24 h later. SGCs were cultured in vitro for 72 h and divided into four groups: the low concentration QA group, the high concentration QA group, the MK-801 group, the MgCl2 group. The transient changes of intracellular calcium concentration were observed by the laser scanning confocal microscopy. Apoptosis rate in QA injury group was higher than that in blank control group and MgCl2 protection group (both P<0.05), but there was no significant difference between MK-801 treatment group and blank control group (P>0.05). In high concentration QA group, there was an obvious increase of the intracellular calcium concentration in SGCs, which didn’t present in low concentration QA group. In MgCl2 group, the peak values of the intracellular calcium concentration in SGCs were reduced and the duration was shortened, but the intracellular calcium concentration in SGCs had no significant change in MK-801 group. It was concluded that QA could injure SGCs by excessively activating NMDA receptors on the cell membrane, which might be the mechanism by which OME induced SNHL, while Mg2+ could protect the SCGs from the neurotoxicity of QA.