Résumé
Objective To discuss the methods and strategies to identify the causes of dependents' deaths, as well as provide the experiences that can be used for reference and scientific basis for the forensic identification of the potentially growing deaths of the same kind in the future. Methods The 13 cases concerning death of dependents accepted by Sun Yat-sen University Forensic Center were collected, and the basic information of the dependents were statistically described. The nutritional status, environmental condition and medical care condition were evaluated according to dietary energy, living space, environment and medical treatment condition. Results Among the 13 dependents, there were 11 males and 2 females, with the oldest 74 and the youngest 9 and dwelling time was from 0.4 to 5.6 years. Forensic pathological examination showed that 13 dependents had infectious diseases and 11 were severely dystrophic. There were no fatal mechanical injuries or poisoning in dependents. Molecular pathological screening of 4 cases revealed no pathogenic variants of sudden death susceptible genes. The poor status of the diet, nutrition, living environment and medical care of these dependents were discovered. The direct cause of death of all 13 dependents was identified to be disease. The lack of nutrition, poor living environment and lack of medical care were thought to play a dominant role in causing the deaths of 12 dependants. Conclusion The death identification should follow the judicial procedure. In identification of the causes of death and analysis of the proportion of the affecting factors resulting in death, all factors, including nutrition,environment, medical care, injury and diseases, need to be considered.
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Femelle , Humains , Mâle , Cause de décès , Mort subiteRésumé
OBJECTIVE@#To explore the changes of c-fos in apoptosis of cerebellar granular neuron of neonatal SD rats induced by heroin and the mechanisms of neuronal injury caused by heroin.@*METHODS@#Primary cerebellar granular neuron were cultured in vitro, the model of apoptosis induced by heroin was established. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were adopted to investigate the changes of c-fos in cell models.@*RESULTS@#Ten microg/mL of heroin was the optimal dose to induce the apoptosis of cerebellar granular neuron at 48 h. Both Western blotting and RT-PCR showed down regulation of c-fos expression.@*CONCLUSION@#Heroin could induce apoptosis of cerebellar granular neuron and down regulation of c-fos, which may be one of the apoptosis mechanisms.
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Animaux , Mâle , Rats , Animaux nouveau-nés , Apoptose/effets des médicaments et des substances chimiques , Technique de Western , Cellules cultivées , Cervelet/métabolisme , Relation dose-effet des médicaments , Régulation négative , Régulation de l'expression des gènes/effets des médicaments et des substances chimiques , Héroïne/pharmacologie , Neurones/métabolisme , Protéines proto-oncogènes c-fos/métabolisme , ARN messager/métabolisme , Rat Sprague-Dawley , RT-PCRRésumé
<p><b>OBJECTIVE</b>To investigate the effects of matrine on the anti-tumor efficiency of H22 murine hepatocarcinoma cell-based vaccine modified by TIM2 gene in vivo.</p><p><b>METHOD</b>The combinant eukaryotic expression vector pIRES2-EGFP-TIM2 was constructed and transfected into H22 cells by lipofectamin. The monoclone of the positive H22-TIM2 cells and negative control H22-EGFP cells were selected by G418 pressure and limited dilution method in turn. The H22 whole-cell-based vaccine were inoculated to establish the tumor-bearing mouse model, and its oncogenicity and immunogenicity were observed in vivo. Then the matrine was administered to the tumor-bearing mice inoculated by H22-TIM2 cells, H22-EGFP cells and H22 cells, and the inhibitory effect of matrine on tumor was studied.</p><p><b>RESULT</b>The co-expression of EGFP protein and TIM2 mRNA were detected in H22-TIM2 cells. The rate of tumor formation in mice injected of H22-TIM2 cells was 41%, lower than that of H22 cells and H22-EGFP cells injection (92%) in mice. The growth of tumor were significantly inhibited vaccinated with H22-TIM2 cells in mice. The inhibitory rate of tumor (IR) was 69.2% in mice of H22-TIM2 group, higher than that of mice treated with matrine and H22 cells injection, the later was 67.5%. Matrine could dramatically strengthen the anti-tumor efficiency of H22 cells modified by TIM2 gene, with the highest tumor inhibitory rate (IR) (90.6%) in all the experimental mice. The spleen index, populations of CD4-positive lymphocytes and the ratio of CD4-positive to CD8-positive lymphocytes of spleen in mice vaccinated of H22-TIM2 cells were obviously higher than those in the other groups.</p><p><b>CONCLUSION</b>The oncogenicity of H22 cells is markedly impaired after modified by TIM2 gene. Matrine can strengthen the inhibitory effect of H22-TIM2 cells on tumor in mice. These data give us important clues to further study the biological role of TIM2 gene in tumor immunity and explore the molecular mechanism of matrine in suppressing tumor.</p>
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Animaux , Femelle , Humains , Mâle , Souris , Alcaloïdes , Pharmacologie , Antinéoplasiques d'origine végétale , Pharmacologie , Carcinome hépatocellulaire , Traitement médicamenteux , Génétique , Allergie et immunologie , Métabolisme , Lignée cellulaire tumorale , Expression des gènes , Protéines membranaires , Génétique , Métabolisme , Souris de lignée BALB C , Tumeurs expérimentales , Quinolizines , Pharmacologie , Rate , Allergie et immunologieRésumé
<p><b>OBJECTIVE</b>To investigate the effects of matrine on the anti-tumor efficiency of TIM2 gene-modified murine hepatocarcinoma H22 cells.</p><p><b>METHODS</b>A combined eukaryotic expression vector pIRES2-EGFP-TIM2 was constructed and transfected into H22 cells by lipofectamin. The monoclone of positive H22-TIM2 cells and negative control H22-EGFP cells transfected with pIRES2-EGFP vector were selected by G418 pressure and limited dilution method in turn and were inoculated to establish the tumor-bearing mouse model. Next, matrine was administered to the tumor-bearing mice and the inhibitory effect of matrine was determined.</p><p><b>RESULTS</b>The co-expression of EGFP protein and TIM2 gene was detected in H22 cells selected after TIM2 gene transfecion. After subcutaneous injection of H22-TIM2 cells, the rate of tumor formation (41%) was lower than that of H22 cells and H22-EGFP cells injection (92%) in mice. The tumor growth was significantly inhibited in mice vaccinated with H22-TIM2 cells. After the experiment was completed, the volume of tumors in mice of H22-TIM2 group was 31.34 +/- 9.21 mm3, smaller than those in H22-EGFP group (98.25 +/- 25.23)mm3 and H22 cells group (114.08 +/- 36.45)mm3 (P < 0.01). Matrine dramatically enhanced the anti-tumor efficiency of TIM2 gene-modified H22 cells, with the highest tumor inhibitory rate (IR) 90.6% among the H22-TIM2 group, matrine treatment group and H22-EGFP cells combined with matrine treatment group (69.2%, 67.5% and 70.8%, respectively) in the experimental mice.</p><p><b>CONCLUSION</b>The tumorigenesity of H22 cells has been markedly impaired after modification by TIM2 gene. Matrine can enhance its inhibitory effect on tumors of H22-TIM2 cells in vivo. These data indicate importance to further study on the biological role of TIM2 gene in tumor immunity and explore the molecular mechanism of matrine in suppressing of tumor growth.</p>
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Animaux , Souris , Alcaloïdes , Pharmacologie , Antinéoplasiques d'origine végétale , Pharmacologie , Lignée cellulaire tumorale , Vecteurs génétiques , Protéines à fluorescence verte , Génétique , Métabolisme , Tumeurs expérimentales du foie , Métabolisme , Anatomopathologie , Protéines membranaires , Génétique , Métabolisme , Souris de lignée BALB C , Transplantation tumorale , Quinolizines , Pharmacologie , Protéines recombinantes , Génétique , Métabolisme , Transfection , Charge tumoraleRésumé
OBJECTIVE@#To investigate whether heroin can directly induce apoptosis in primary cultured cortical neurons of rat's brain.@*METHODS@#Cultured primary neurons cultures were obtained from cerebral cortex of embryo rats. After 7 days, the cells were incubated with different concentrations of heroin (purity-80%) for 24 hours. The neuronal survival was assessed by cell viability counting with fluorescent diacetate (FDA) staining. The morphological and biochemical changes were observed with Hoechst 33258 fluorescent staining and then analyzed by agarose gel electrophoresis, respectively.@*RESULTS@#After treatment with different concentrations of heroin, the neurons showed a decreased survival rate in a dose dependent manner, and there was a significant difference in the survival rate between the heroin group and the control group (P < 0.05). When exposed to different concentrations of heroin, neurons exhibited the morphological and biochemical features of apoptosis, including cell shrinkage, neurite degeneration, network disappearance, condensation and aggregation of nuclear chromatin, and the formation of DNA ladders. With the increase of heroin concentration of rat's brain more apoptotic bodies were seen.@*CONCLUSION@#Heroin can directly induce apoptosis in primary cultured cortical neurons in rat's brain.
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Animaux , Femelle , Mâle , Rats , Apoptose/effets des médicaments et des substances chimiques , Noyau de la cellule/anatomopathologie , Survie cellulaire/effets des médicaments et des substances chimiques , Cellules cultivées , Cortex cérébral/anatomopathologie , Fragmentation de l'ADN/effets des médicaments et des substances chimiques , Relation dose-effet des médicaments , Électrophorèse sur gel d'agar/méthodes , Héroïne/pharmacologie , Neurones/anatomopathologie , Rat Sprague-Dawley , Coloration et marquageRésumé
Virtopsy is a non-invasive technique to reconstruct 3 dimensional (3-D) images of human organs and tissues using digitized radiographic imaging and may provide clues for forensic identification of the cause and manner of death. Because of its nature of minimally invasive, objective, and accurate, virtopsy has recently been a research focus of forensic pathology in developed countries. In this review article, the authors will discuss the principle, advantage, disadvantage, and recent proceeding of virtopsy as well as its potential application in forensic practice in China.
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Humains , Autopsie , Médecine légale/méthodes , Anatomopathologie légale , Imagerie tridimensionnelle/méthodes , Imagerie par résonance magnétique/méthodes , Tomodensitométrie/méthodesRésumé
OBJECTIVE@#To investigate the effects of serum from crush injury rats on vascular endothelial cell apoptosis and their potential mechanism.@*METHODS@#Bovine aorta endothelial cells were cultured in vitro and the effects of serum from crush injury rats on cell apoptosis and intracellular calcium concentration ([Ca2+]i) were observed. Meanwhile, the levels of rat blood plasma endothelin-1 (ET-1) and atrial natriuretic peptide(ANP) were measured.@*RESULTS@#Compared with normal rat serum treatment, the cell apoptosis rate decreased from (8.26+/-1.75)% to (2.75+/-0.90)%, while the concentration of [Ca2+]i increased from (96.98+/-3.95) to (118.79+/-3.22) nmol/L in serum from crush injury rats, respectively. The concentration of ET-1 and ANP increased significantly in crush injury rat serum.@*CONCLUSION@#Serum from crush injury rats could inhibit apoptosis of the vascular endothelial cells. These effects may be related to increased level of [Ca2+]i mediated by ET-1 and ANP.
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Animaux , Bovins , Rats , Apoptose/effets des médicaments et des substances chimiques , Facteur atrial natriurétique/sang , Calcium/métabolisme , Cellules cultivées , Milieux de culture/composition chimique , Modèles animaux de maladie humaine , Cellules endothéliales/métabolisme , Endothéline-1/sang , Membres/traumatismes , Cytométrie en flux , Rat Sprague-DawleyRésumé
OBJECTIVE@#To observe the effects of heroin on intracellular free Ca2+ in rat myocardium.@*METHODS@#The effects of heroin on intracellular free Ca2+ were observed in cultured neonatal rat myocardium by measuring intracellular free Ca2+ concentration using calcium fluorescent probe Flou-3/AM and laser scanning confocal microscope.@*RESULTS@#Different doses and concentrations of heroin appeared to have different effects on intracellular free Ca2+ concentrations, with a dosage dependent short linear increase in the fluorescence intensity (i.e., Ca2+ concentration) leading to [Ca2+]i peak.@*CONCLUSION@#Heroin could affect concentrations of [Ca2+]i in myocardium and its dosage related effect needs further investigation.
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Animaux , Rats , Calcium/métabolisme , Signalisation calcique , Cellules cultivées , Relation dose-effet des médicaments , Héroïne/pharmacologie , Microscopie confocale/méthodes , Microscopie de fluorescence , Myocytes cardiaques/métabolisme , Rat Sprague-DawleyRésumé
OBJECTIVE@#To study cellular mechanism of cardiomyocytes injury in the early stage of crush injury by observing some effects of crush injury rat sera on cultured neonatal rat cardiomyocytes.@*METHODS@#One to three days old neonatal rat cardiomyocytes were cultured in vitro and some effects of crush injury rat sera on beating rate, cell surface area, total protein content, 3H-Leu incorporation, intracellular calcium concentration ([Ca2+]i) and Fos protein expression were observed in cultured rat cardiomyocytes.@*RESULTS@#Compared with normal rat serum group, crush injury rat sera decreased beating rate(beats/min) of cardiomyocytes from 88.3 to 26.4, cell surface area, total protein content, 3H-Leu incorporation, [Ca2+]i (nmol/L) and PI of Fos protein expression were increased.@*CONCLUSION@#Crush injury rat sera suppress cell beating, increase intracellular calcium, induce Fos protein synthesis and cause cell hypertrophy, which may cause cardiac injury in the early stage of rush injury.
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Animaux , Rats , Calcium/métabolisme , Taille de la cellule/effets des médicaments et des substances chimiques , Cellules cultivées , Modèles animaux de maladie humaine , Membres/traumatismes , Lésions traumatiques du coeur/anatomopathologie , Rythme cardiaque/effets des médicaments et des substances chimiques , Sérums immuns/pharmacologie , Myocytes cardiaques/anatomopathologie , Protéines proto-oncogènes c-fos/métabolisme , Rat Sprague-DawleyRésumé
<p><b>OBJECTIVE</b>To construct an eukaryotic expression vector of open reading frame of unknown KH gene (KH-ORF), and investigate its effect on cell proliferation.</p><p><b>METHODS</b>The pCI-neo-KH-ORF expression vector was constructed by DNA recombinant technique and was introduced into COS-7 cells and K562 cells by lipofectactin-mediated DNA transfection. Expression of KH-ORF mRNA was detected by RT-PCR. The effect of KH-ORF on cell cycle of COS-7 cells and K562 cells was evaluated by flow cytometry (FCM). Effect on cell proliferation of COS-7 cells was tested by MTT assay and that on K562 cells was analyzed by growth curves and LDH activity measurement.</p><p><b>RESULTS</b>(1) KH-ORF mRNA was expressed both in COS-7 cells and K562 cells. (2) The cell cycle and cell proliferation of COS-7 cells were unaffected significantly. (3) The proportion of cells in S phase was increased in pCI-neo-KH-ORF-transfected K562 cells; and growth curves and LDH activity indicated enhanced cell proliferation.</p><p><b>CONCLUSION</b>KH gene may be a leukemia gene related to proliferation of K562 cells.</p>
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Animaux , Humains , Cellules COS , Prolifération cellulaire , Chlorocebus aethiops , Régulation de l'expression des gènes tumoraux , Gènes tumoraux , Génétique , Physiologie , Vecteurs génétiques , Cellules K562 , L-Lactate dehydrogenase , Métabolisme , Cadres ouverts de lecture , Génétique , Physiologie , Plasmides , ARN messager , Génétique , Protéines de liaison à l'ARN , Génétique , Phase S , TransfectionRésumé
<p><b>OBJECTIVE</b>To investigate the inhibitory effect of matrine on tumor growth in tumor-bearing mice and explore its possible mechanisms of anti-tumor action in vivo.</p><p><b>METHODS</b>Hepatocellular carcinoma cells H(22) were subcutaneously injected into BALB/c mice and matrine was administered to the tumor-bearing mice. The kinetics of tumor formation and tumor growth were measured, tumor growth inhibition rate (IR) was calculated, and tumor tissue samples were taken and examined by light and electron microscopy to assess the inhibitory effects of matrine on tumor growth in the mice.</p><p><b>RESULTS</b>Marked inhibitory effect of matrine on the transplanted hepatocellular carcinoma H(22) was observed in the tumor-bearing mice. The inhibitory rates were 62.5% and 60.7% in the groups treated with high and low dosage of matrine, respectively (P < 0.01 vs. control group). The tumor formation was significantly retarded and tumor growth was inhibited in matrine-treated groups compared with those in control mice. Histopathological examination revealed widespread necrosis with massive accumulation of infiltrating lymphocytes and plasmacytes in the tumors. Numerous apoptotic cells and apoptotic bodies were observed in the tumors under the electron microscope.</p><p><b>CONCLUSION</b>Matrine has marked inhibitory effects on tumor growth in vivo, which is probably related to inhibition of cell division and tumor cell proliferation, directly killing of tumor cells and/or induction of apoptosis and modulation of anti-tumor immune responses.</p>
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Animaux , Souris , Alcaloïdes , Utilisations thérapeutiques , Antinéoplasiques d'origine végétale , Utilisations thérapeutiques , Apoptose , Tumeurs expérimentales du foie , Traitement médicamenteux , Anatomopathologie , Souris de lignée BALB C , Transplantation tumorale , Quinolizines , Utilisations thérapeutiquesRésumé
OBJECTIVE@#To study the changes of electrocardiograms (ECG) and myocardial ultrastructure in heroin dependence in rats, in order to reveal the mechanisms of the myocardial injury by heroin.@*METHODS@#Establish heroin addict model in SD mice, investigate the changes in electrocardiograms, HE staining and myocardial ultrastructure.@*RESULTS@#The electrocardiograms of the addict group had prominently changes, main expressions: heart rate decreased, P wave and T wave amplitude reduced and duration increased, S-T reduced and duration increased, QT interval prolongation, these changes indicated that myocardium had been injured, myocardial ischemia, ventricle function declined. These difference was significant (P<0.05) between before inject heroin and after inject heroin. Transformations in the ultrastructure: nuclear concentrate, reduce, nuclear membrane shrink, chromatin agglutinate, mitochondria cristal had disorder formation, disappeared or hollowed, these indicated that heroin could cause pathological changes in myocardial ultrastructure.@*CONCLUSION@#Above-mentioned changes indicated that heroin can injure myocardium, and the changes of myocardial ultrastructure suggested that myocardial apoptosis may be one of the mechanisms of the myocardial injury by heroin.
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Animaux , Rats , Modèles animaux de maladie humaine , Électrocardiographie , Rythme cardiaque , Dépendance à l'héroïne/physiopathologie , Ischémie myocardique/physiopathologie , Myocarde/ultrastructure , Rat Sprague-DawleyRésumé
The heroin abuses can seriously damage human body system, among them the damage of cardiovascular system is various. In this paper those damages involved heart rate, blood pressure, electrocardiogram, heart function, blood circulation, the changes of some material inside, and complications of cardiovascular system are reviewed.
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Humains , Troubles du rythme cardiaque/étiologie , Circulation sanguine , Pression sanguine , Maladies cardiovasculaires/physiopathologie , Mort subite/étiologie , Électrocardiographie , Rythme cardiaque , Dépendance à l'héroïne/physiopathologie , Ischémie myocardique/étiologieRésumé
OBJECTIVE@#To study the expression of the glycoprotein in atrioventricular cell membrane of the acute myocardial infarction.@*METHODS@#The glycoprotein changes occurred at the atrioventricular cell membrane of the acute myocardial infarction of 8 cases were observed by using immunohistochemical methods.@*RESULTS@#Positive staining of PNA could be observed in atrioventricular cell membrane.@*CONCLUSION@#This experiment proved that atrioventricular cell membrane expressed D-galactose as same as myocardial cell membrane in the acute myocardial infarction.