RESUMO
Acute carbon dioxide (CO2) poisoning causes no specific features that are revealed upon autopsy, and the pathophysiological mechanism of this syndrome is unclear. To address this issue, in the present study, we exposed rats to CO2 concentrations ranging from 10% to 60% and determined the effects on mRNA expression. According to the results of Gene Ontology (GO) and cluster analyses of microarrays data, we selected the following genes for further analysis: alkylglycerone phosphate synthase (Agps), hypocretin (Hcrt), tyrosine hydroxylase (Th), heat shock protein beta 2 (Hspb2), and opioid receptor delta 1 (Oprd1) expressed in the frontal cortex and renin (Ren), pancreatic polypeptide (Ppy), corticotropin releasing hormone receptor 2 (Crhr2), carbonic anhydrase 1 (Car1), and hypocretin receptor 1 (Hcrtr1) expressed in the hypothalamus. We found significant differences between the expression levels of Agps and Hspb2 mRNAs in the frontal cortex and that of Ppy, Crhr2 mRNAs in the hypothalamus in the presence of high concentrations of CO2. Further investigation of these genes may clarify the pathophysiology of acute CO2 poisoning and facilitate the development of novel forensic tests that can diagnose the cause of death.
Assuntos
Dióxido de Carbono/intoxicação , Lobo Frontal/metabolismo , Hipotálamo/metabolismo , RNA Mensageiro/metabolismo , Animais , Modelos Animais de Doenças , Masculino , Ratos , Ratos WistarRESUMO
We report the case of 2-year-old girl who died of precursor B-cell acute lymphoblastic leukaemia (ALL), the most common cancer in children. She had no remarkable medical history. She was transferred to a hospital because of respiratory distress and died 4 hours after arrival. Two weeks before death, she had a fever of 39 degrees C, which subsided after the administration of a naturopathic herbal remedy. She developed jaundice 1 week before death, and her condition worsened on the day of death. Laboratory test results on admission showed a markedly elevated white blood cell count. Accordingly, the cause of death was suspected to be acute leukaemia. Forensic autopsy revealed the cause of death to be precursor B-cell ALL. With advancements in medical technology, the 5-year survival rate of children with ALL is nearly 90%. However, in this case, the deceased's parents preferred complementary and alternative medicine (i.e., naturopathy) to evidence-based medicine and had not taken her to a hospital for a medical check-up or immunisation since she was an infant. Thus, if she had received routine medical care, she would have a more than 60% chance of being alive 5 years after diagnosis. Therefore, we conclude that the parents should be accused of medical neglect regardless of their motives.
Assuntos
Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia , Autopsia , Pré-Escolar , Terapias Complementares , Evolução Fatal , Feminino , Febre/etiologia , Medicina Herbária , Humanos , Icterícia/etiologia , Leucemia-Linfoma Linfoblástico de Células Precursoras/complicações , Leucemia-Linfoma Linfoblástico de Células Precursoras/terapiaRESUMO
Diagnosis of fatal hypothermia is considered to be difficult in forensic practice because of the lack of any specific pathological findings. The mechanism that induces abnormal behavior such as undressing or hiding during the state of hypothermia has not been clarified. In order to solve these problems, we made a rat model of fatal hypothermia and investigated the expression of some mRNA within the hypothalamus and the frontal cortex. The expression of aldehyde dehydrogenase 6 family, member A1 (ALDH6A1), cocaine- and amphetamine-regulated transcript peptide (CARTPT), desmin (DES), heat shock 70kDa protein 4 (HSPA4), serotonin receptor 2A (HTR2A), opioid receptor, delta 1 (OPRD1) and transthyretin (TTR) supposedly related to fatal hypothermia was determined using quantitative real-time PCR. The expression of OPRD1 in the hypothalamus of fatal hypothermia was significantly increased, while the expression of TTR within the frontal cortex was significantly decreased compared to that in the control. These findings suggest that OPRD1 and TTR may be involved in thermoregulation at a low ambient temperature.
Assuntos
Lobo Frontal/metabolismo , Hipotálamo/metabolismo , Hipotermia/metabolismo , RNA Mensageiro/metabolismo , Aldeído Desidrogenase/genética , Aldeído Desidrogenase/metabolismo , Animais , Desmina/genética , Desmina/metabolismo , Patologia Legal , Proteínas de Choque Térmico HSP110/genética , Proteínas de Choque Térmico HSP110/metabolismo , Masculino , Modelos Animais , Proteínas do Tecido Nervoso/genética , Proteínas do Tecido Nervoso/metabolismo , Reação em Cadeia da Polimerase , Pré-Albumina/genética , Pré-Albumina/metabolismo , Ratos , Ratos Wistar , Receptores Opioides delta/genética , Receptores Opioides delta/metabolismo , Receptores de Serotonina/genética , Receptores de Serotonina/metabolismoRESUMO
BACKGROUND: Betel quid chewing is a common habit widely practiced in Southern Asian populations. However, variations are seen in the content of a betel quid across the different countries. Factors associated with commencement and cessation of this habit has been numerously studied. Unfortunately, data on Malaysian population is non-existent. This study aims to determine the factors associated with the inception and also cessation of betel quid chewing behaviour among Malaysian adults. METHOD: This study is part of a nationwide survey on oral mucosal lesions carried out among 11,697 adults in all fourteen states in Malaysia. The questionnaire included sociodemographic information and details on betel quid chewing habit such as duration, type and frequency. The Kaplan-Meier estimates were calculated and plotted to compare the rates for the commencement and cessation of betel quid chewing behaviour. Cox proportional hazard regression models were used to calculate the hazard rate ratios for factors related to commencement or cessation of this habit. RESULTS: Of the total subjects, 8.2% were found to be betel quid chewers. This habit was more prevalent among females and, in terms of ethnicity, among the Indians and the Indigenous people of Sabah and Sarawak. Cessation of this habit was more commonly seen among males and the Chinese. Females were found to be significantly more likely to start (p < 0.0001) and less likely to stop the quid chewing habit. Females, those over 40 years old, Indians and a history of smoking was found to significantly increase the likelihood of developing a quid chewing habit (p < 0.0001). However, those who had stopped smoking were found to be significantly more likely to promote stopping the habit (p = 0.0064). Cessation was also more likely to be seen among those who chewed less than 5 quids per day (p < 0.05) and less likely to be seen among those who included areca nut and tobacco in their quid (p < 0.0001). CONCLUSION: Factors that influence the development and cessation of this behaviour are gender, age, ethnicity, and also history of smoking habit while frequency and type of quid chewed are important factors for cessation of this habit.
Assuntos
Areca , Mastigação , Plantas Medicinais , Transtornos Relacionados ao Uso de Substâncias/epidemiologia , Adolescente , Adulto , Criança , Feminino , Humanos , Estimativa de Kaplan-Meier , Malásia/epidemiologia , Masculino , Pessoa de Meia-Idade , Transtornos Relacionados ao Uso de Substâncias/etnologia , Inquéritos e Questionários , Adulto JovemRESUMO
Oxyfunctionalization of the bioactive terpenoids, ursolic acid acetate (1), oleanolic acid acetate (5), lupeol acetate (12), and kaurenic acid (17), with dimethyldioxirane (DMDO) was investigated. Treatment of the terpenoids with DMDO under mild conditions afforded a variety of oxidation and oxydegradation products to yield naturally occurring and/or novel compounds in one step. After chromatographic separation, the structures of the individual isolated products were determined using spectroscopic methods including several homonuclear (1H-1H) and heteronuclear (1H-13C) shift-correlated 2D-NMR techniques. The inhibitory activity of the terpenoid derivatives against alpha-glucosidase was investigated and compounds 1, 3, 7, and 9 were found to exhibit potent activity.
Assuntos
Compostos de Epóxi/farmacologia , Plantas Medicinais , Terpenos/farmacologia , alfa-Glucosidases/metabolismo , Acetatos/química , Acetatos/farmacologia , Diterpenos/química , Diterpenos/farmacologia , Compostos de Epóxi/química , Espectroscopia de Ressonância Magnética , Ácido Oleanólico/química , Ácido Oleanólico/farmacologia , Oxirredução , Triterpenos Pentacíclicos , Terpenos/química , Triterpenos/química , Triterpenos/farmacologia , Ácido UrsólicoRESUMO
We previously demonstrated that pulmonary fat embolism was induced by elevation of the core body temperature, in rats with a fatty liver. The aim of the present examination was to investigate the core body temperature at which pulmonary fat embolism developed capillaries through exposure to a high temperature, in rats with a fatty liver. Following heat stress, pulmonary fat embolism was observed to a slight degree at a core body temperature of 41 and 42 degrees C, whereas the severity of pulmonary fat embolism was greatly increased and was classified as severe at a core body temperature of 43 degrees C. Moreover, the concentrations of aspartate aminotransferase and alanine aminotransferase within plasma were significantly increased at a core body temperature of 43 degrees C. These results clearly indicate that the development of pulmonary fat embolism could be related to hyperthermia at above 42 degrees C following heat stress, and that fat emboli may be derived from the fatty liver itself. It is thus likely that pulmonary fat embolism can be considered as one form of evidence of hyperthermia in an individual with a fatty liver.
Assuntos
Temperatura Corporal , Embolia Gordurosa/etiologia , Fígado Gorduroso/complicações , Temperatura Alta/efeitos adversos , Embolia Pulmonar/etiologia , Animais , Embolia Gordurosa/patologia , Eosinófilos/patologia , Fígado Gorduroso/patologia , Hemorragia/patologia , Hipertermia Induzida/efeitos adversos , Fígado/patologia , Pulmão/patologia , Masculino , Embolia Pulmonar/patologia , Ratos , Ratos Sprague-DawleyRESUMO
A 50-year-old man was admitted to the emergency room complaining oppression on his chest, sweating and vomiting. He had drunk a 30 ml volume nutrition supplement 60 minutes before. As myosis and decrease of serum choline esterase activity were observed on admission examination, poisoning was suspected and toxicological analyses were carried out on the heeltap of the drink. Drug screening by gas chromatography-mass spectrometry (GC/MS) revealed the presence of methomyl and the concentration of methomyl in the heeltap determined by liquid chromatography was 2.1 mg/ml. Methomyl concentrations in the serum and urine were determined after converting methomyl to its oxime form followed by derivatization and GC/MS. Methomyl concentration in the serum collected 6 hours after ingestion was 0.63 microg/ml, and that in the urine collected 7-20 hours after ingestion was 0.10 microg/ml. Based on these values and reported data, the amount of methomyl contaminated to the drink was considered to be a toxic dose.