OBJECTIVE: To observe the changes of electrocardiogram and serum cardiac troponin I at the early stage of severe crush injury in rats. METHODS: Crush injury was produced in Sprague-Dawley rats. The changes of electrocardiogram were recorded with the standard II, the serum levels of cardiac troponin I were studied by automated chemiluminescence assay. RESULTS: The ST segment elevated considerably after crush injury and lasted 24 h, the levels of serum cTnI were much higher than those of the control groupes after 6 h of injury. CONCLUSION Cardiomyocyte injury was induced in the early phase of crush injury.
Animals ; Crush Syndrome/physiopathology* ; Electrocardiography ; Extremities/injuries* ; Female ; Heart Injuries/physiopathology* ; Male ; Rats ; Rats, Sprague-Dawley ; Troponin I/blood*

The interaction between adults and children during shared reading contributes to the conversation and reading in hand and makes the activity interactive. It is, therefore, imperative to understand parents’ goals for shared reading with their children as it will influence their behaviour and, in turn, affect their children’s development of language and literacy skills. In Malaysia, no local psychometric instrument identifying parent goals for shared reading is available. This study aims to translate the English version of the Parent Goals for Shared Reading Questionnaire (PGSRQ) into Malay and validate the translated questionnaire. Four qualified translators carried out the translation processes, and a panel of eight experts subsequently validated the Malay-translated version of PGSRQ. Of 33 items, the validation assessment revealed that 17 items had a content validity ratio (CVR) value of 1.0, while 12 items had a CVR value of 0.8. Only four items had a CVR value lower than 0.78 and were retranslated and modified. The findings of this study can pave the way for more research efforts in the field of shared reading in Malaysia. The questionnaire can also assist a speech therapist in assessing the goals that parents have on shared reading to come up with better designs for shared book reading intervention.

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.
Animals ; Calcium/metabolism* ; Cell Size/drug effects* ; Cells, Cultured ; Disease Models, Animal ; Extremities/injuries* ; Heart Injuries/pathology* ; Heart Rate/drug effects* ; Immune Sera/pharmacology* ; Myocytes, Cardiac/pathology* ; Proto-Oncogene Proteins c-fos/metabolism* ; Rats ; Rats, Sprague-Dawley

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.
Animals ; Apoptosis/drug effects* ; Atrial Natriuretic Factor/blood* ; Calcium/metabolism* ; Cattle ; Cells, Cultured ; Culture Media/chemistry* ; Disease Models, Animal ; Endothelial Cells/metabolism* ; Endothelin-1/blood* ; Extremities/injuries* ; Flow Cytometry ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To study the changes of serum creatinine kinase(CK) and its cardiac-specific isoenzyme compound(CK-MB) levels in crush injury rats. METHODS: Crush injury was produced in SD rats, the serum levels of CK and CK-MB were studied by automated biochemical analyzer. RESULTS: The levels of plasma CK and CK-MB were much higher in crush injury rats than those of the control group. CONCLUSIONS Cardiomyocyte injury may be induced in the early stage of crush injury rats.
Animals ; Creatine Kinase/blood* ; Creatine Kinase, MB Form ; Crush Syndrome/enzymology* ; Female ; Isoenzymes/blood* ; Male ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To investigate the changes of the activity of tryptase of sera, lungs and bronchial tubes in the guinea-pigs which suffered from hetero-serum anaphylactic shock. METHODS: Sera and tissues were collected from anaphylactic shock guinea-pigs, and the enzyme activity was tested colormetrically using special substrate, BAPNA. RESULTS: The activity of tryptase of sera, lungs and bronchial tubes increased significantly in Anaphylactic guinea-pigs compared with control group. CONCLUSION The changes of tryptase activity are helpful to diagnose anaphylactic shock.
Anaphylaxis/enzymology* ; Animals ; Female ; Forensic Medicine ; Guinea Pigs ; Male ; Serine Endopeptidases/metabolism* ; Tryptases

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.
Animals ; Apoptosis/drug effects* ; Cell Nucleus/pathology* ; Cell Survival/drug effects* ; Cells, Cultured ; Cerebral Cortex/pathology* ; DNA Fragmentation/drug effects* ; Dose-Response Relationship, Drug ; Electrophoresis, Agar Gel/methods* ; Female ; Heroin/pharmacology* ; Male ; Neurons/pathology* ; Rats ; Rats, Sprague-Dawley ; Staining and Labeling

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.
Animals ; Calcium/metabolism* ; Calcium Signaling ; Cells, Cultured ; Dose-Response Relationship, Drug ; Heroin/pharmacology* ; Microscopy, Confocal/methods* ; Microscopy, Fluorescence ; Myocytes, Cardiac/metabolism* ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To explore the mechanism that how human enterovirus 71 (EV71) invades the brainstem and how intercellular adhesion molecules-1 (ICAM-1) participates by analyzing the expression and distribution of human EV71, and ICAM-1 in brainstem of infants with brain stem encephalitis. METHODS: Twenty-two brainstem of infants with brain stem encephalitis were collected as the experimental group and 10 brainstems of fatal congenital heart disease were selected as the control group. The sections with perivascular cuffings were selected to observe EV71-VP1 expression by immunohistochemistry method and ICAM-1 expression was detected for the sections with EV71-VP1 positive expression. The staining image analysis and statistics analysis were performed. The experiment and control groups were compared. RESULTS: (1) EV71-VP1 positive cells in the experimental group were mainly astrocytes in brainstem with [dark]-brown particles, and the control group was negative. (2) ICAM-1 positive cells showed [dark]-brown. The expression in inflammatory cells (around blood vessels of brain stem and in glial nodules) and gliocytes increased. The results showed statistical difference comparing with control group (P < 0.05). CONCLUSION The brainstem encephalitis can be used to diagnose fatal EV71 infection in infants. EV71 can invade the brainstem via hematogenous route. ICAM-1 may play an important role in the pathogenic process.
Astrocytes/pathology* ; Brain Stem/virology* ; Case-Control Studies ; Encephalitis, Viral/virology* ; Enterovirus A, Human/metabolism* ; Female ; Hand, Foot and Mouth Disease/virology* ; Humans ; Immunohistochemistry ; Infant ; Intercellular Adhesion Molecule-1/metabolism* ; Male

Objective To explore the causes and characteristics of medical disputes caused by death after cardiac surgery and to analyze the pathological changes after cardiac surgery and the key points of forensic anatomy, thus to provide pathological evidence for clinical diagnosis and treatment of cardiac surgery and judicial appraisal as well as reference for the prevention of medical disputes in such cases. Methods Forensic pathological cases of medical disputes caused by death after cardiac surgery which were accepted by the Center for Medicolegal Expertise of Sun Yat-Sen University from 2013 to 2018 were analyzed retrospectively from aspects such as causes of death, pathological diagnosis, surgery condition, medical misconduct, and so on. Results The causes of death after cardiac surgery of 43 patients were abnormal operation, low cardiac output syndrome, postoperative infection, postoperative thrombosis, and other diseases. Among the 43 cases, there were 18 cases without medical fault while 25 cases had medical fault. Conclusion The medical disputes caused by death after cardiac surgery are closely related to the operative technique and postoperative complications. The causes of medical faults include defects in diagnosis and treatment technique, as well as unfulfillment of duty of care.
Cardiac Surgical Procedures/adverse effects* ; Dissent and Disputes ; Forensic Medicine ; Forensic Pathology ; Humans ; Retrospective Studies