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Objective To compare the differences of blood glucose detected by four methods with different instruments and specimen types at early stage in severely burned rats.Methods 24 Sprague-Dawley (SD) rats were randomly divided into two groups:control group 1 (Sham scald group,n=8) and scald injury group 1 (n=16).Blood samples of scald injury group 1 were collected at 12,and 24 hours after scald (n=8,each time).Another 20 SD rats were randomly divided into two groups:control group 2 (Sham scald group,n=10) and scald injury group 2 (n=10).Blood samples of scald injury group 2 were collected at 12 hours after scald.The rats in scald injury group 1 and 2 were placed into scalding water (95.0±0.5)℃ for 15 seconds to model third-degree burn with 30% total burn surface area (TBSA).The rats in scald injury group 1 were given intraperitoneal injection with normal saline(40 ml/kg) immediately,while those in scald injury group 2 were given intraperitoneal injection with normal saline (40 ml/kg) 6 hours after scald.The rats in Sham scald group 1 and 2 were placed into warm water 37℃ for 15 seconds,and did not received injection.Portable glucometer/caudal artery (vein) blood,portable glucometer/abdominal aorta blood,spectrophotometer/femoral venous plasma,and spectrophotometer/abdominal aorta plasma were used to detect blood glucose.Results ①Compared with Sham scald group 1,the levels of blood glucose detected by portable glucometer/caudal artery (vein) blood and spectrophotometer/femoral venous plasma in scald injury group1 at 12,24 hours after scald were significantly increased(P<0.05).Compared with Sham scald group 2,the levels of blood glucose detected by portable glucometer/abdominal aorta blood and spectrophotometer/abdominal aorta plasma in scald injury group 2 at 12 hours after scald were significantly increased(P<0.05).②The comparison of portable glucometer/caudal artery (vein) blood and spectrophotometer/femoral venous plasma in Sham scald group 1,portable glucometer/abdominal aorta blood and spectrophotometer/abdominal aorta plasma in Sham scald group 2 had no statistical significance (P>0.05).The levels of blood glucose detected by portable glucometer/caudal artery (vein) blood were significantly lower than those detected by spectrophotometer/femoral venous plasma (P<0.05) in scald injury group 1.The comparison of blood glucose detected by portable glucometer/abdominal aorta blood and spectrophotometer/abdominal aorta plasma had no statistical significance in scald injury group 2 (P>0.05).Conclusion Four kinds of methods used in this study shows that the levels of blood glucose were significantly increased at early stage in severely burned rats,and the portable glucometer/abdominal aorta blood is a relatively simple and fast method to detect blood glucose.
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<p><b>OBJECTIVE</b>To evaluate the renal function of 298 liver cirrhosis cases among the patient population of Beijing Ditan Hospital.</p><p><b>METHODS</b>The medical database of Beijing Ditan Hospital was retrospectively searched for patients with liver cirrhosis (compensated and decompensated). Patients were excluded from the study according to the presence of concomitant serious diseases, such as hypertension, diabetes, and malignancies.The consistency of renal insufficiency was evaluated by the glomerular filtration rate (eGFR) or serum creatinine (SCr) level, which were applied to the simplified modification of diet in renal disease (MDRD) equation.The renal function was compared between groups stratified according to compensated/decompensated status, sex, and age.The factors affecting renal insufficiency were screened.Measurement data were compared using the t-test and count data were compared using the chi-square test.Multiple sets of data were compared using analysis of variance.Correlations were assessed using multivariate logistic regression analysis, and the confounding variables were controlled with the Mantel-Haenszel method.</p><p><b>RESULTS</b>A total of 298 hospitalized patients with liver cirrhosis were included in the study, among which 41 had compensated cirrhosis and 257 had decompensated cirrhosis.Twenty patients (6.7%) with renal insufficiency were identified by SCr measurement and 62 patients (20.8%) were identified by eGFR, and the number identified was significantly different between the two groups (x2=42.00, P less than 0.05).Fifty-six (21.8%) patients had decompensated cirrhosis and 6 (14.6%) patients had decompensated cirrhosis with renal dysfunction; the eGFR levels for these two groups were (117.75 +/- 32.60) ml/min/(1.73 m2)-1 and (112.72 +/- 24.01) ml/min/(1.73 m2) respectively and the difference was not statistically significant (P more than 0.05).The incidence of renal dysfunction among female patients was 22.7% (17/75), and the incidence among male patients was 20.2% (45/223); the eGFR levels for these two groups were (110.07 +/- 26.60) ml/min/(1.73 m2)1 and (112.49 +/- 33.05) ml/min/(l.73 m2) respectively, and the difference was not statistically significant (P more than 0.05).The rate of renal dysfunction among patients aged 20 to 40 years-old, more than 40 to 60 years-old, and more than 60 years years-old was 5.7% (4/70), 22.5% (40/178), and 36.0%(18/50) respectively; the eGFR values for these two groups were (123.43 +/- 24.42) ml min/(l.73 m2), (111.18+/- 33.57) ml/min/(1.73 m2), and (98.20 +/- 27.04) ml/min/(1.73 m2), and the differences were not statistically significant (P less than 0.05).After stratification of the study population by age, the patient sex and the cirrhosis stage were not significantly different (P more than 0.05).Multivariate logistic regression analysis identified age as a risk factor of hepatitis B-related cirrhosis and renal dysfunction (P less than 0.05).</p><p><b>CONCLUSION</b>The simplified MDRD equation can help clinicians determine whether patients have kidney injury.Development of renal dysfunction in patients with liver cirrhosis is not associated with patient sex and cirrhosis stage, but is precisely correlated with patient age.</p>
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Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Tasa de Filtración Glomerular , Enfermedades Renales , Cirrosis Hepática , Estudios Retrospectivos , Factores de RiesgoRESUMEN
<p><b>AIM</b>To explore sodium selenite-induced oxidative stress and apoptosis in human promyelocytic leukemia NB4 cells.</p><p><b>METHODS</b>The growth inhibition of NB4 cells was measured by MTT test. Apoptosis was determined morphologically by Giemsa stain and by DNA ladder formation in electrophoresis. Quantitation of apoptosis was determined by percentage of PI stained cells containing subdiploid amount of DNA measured by flow cytometry. Generation of reactive oxidative species (ROS) in NB4 cells was determined by lucigenin dependent chemoluminescent (CL) test. Spectrophotometer was used to measure the level of reduced glutathione, superoxide dismutase (SOD) and glutathione peroxidase in the cell.</p><p><b>RESULTS</b>Sodium selenite was shown to inhibit the growth of NB4 cells. Sodium selenite induced apoptosis with dose and time dependency: the ratio of subdiploid cells in control group was 1.3% +/- 0.7%. The 5 mumol.L-1 group was 10.4% +/- 1.4%, 10 mumol.L-1 group was 16% +/- 1%, and the 20 mumol.L-1 group was 27.3% +/- 0.8%. Sodium selenite (> or = 5 mumol.L-1) enhanced the ROS level markedly in NB4 cells (in 20 mumol.L-1 group ROS level was increased by 17 times, compared with control group), accompanied with decrease of reduced intracellular glutathione. These effects were time and dose dependent. N-acytlcysteine as an antioxidant was found to inhibit sodium selenite-induced oxidative stress and apoptosis in NB4 cells.</p><p><b>CONCLUSION</b>Sodium selenite can induce apoptosis of NB4 cells and would possibly be used as an agent for the treatment of malignancy. The main mechanism of action might be related to oxidative stress induced by sodium selenite, thereby, leading to apoptosis as shown in NB4 cells.</p>
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Humanos , Antineoplásicos , Farmacología , Apoptosis , División Celular , Leucemia Promielocítica Aguda , Patología , Estrés Oxidativo , Especies Reactivas de Oxígeno , Metabolismo , Selenito de Sodio , Farmacología , Células Tumorales CultivadasRESUMEN
In order to explore the differences between the mechanisms of selenite-induced apoptosis and arsenic induced apoptosis in NB4 cells, growth inhibition was determined by MTT test, apoptosis determined by DNA electrophoresis and analysis of intracellular DNA contents, reactive oxygen species and reduced glutathione in the cell were measured by Lucigenin dependent chemoluminescent (CL) test and spectrophotometry, and mitochondrial transmembrane potential was measured by flow cytometry. The results showed that: 5 micro mol/L sodium selenite similar to 1 micro mol/L arsenic trioxide could induce the apoptosis of NB4 cells after treatment for 24 hours. Both could elevate the level of reactive oxygen species and intensify mitochondrial transmembrane potential collapse, accompanied with decrease of reduced glutathione centent. The effect of selenium selenite on these aspects was more significant than those of arsenic trioxide. Elevation of intracellular glutathione in N-acytlcysteine pretreated NB4 cells could enhance the selenite induced apoptosis and oxidative stress, but ameliorate the arsenic trioxide induced apoptosis and oxidative stress. It was concluded that sodium selenite and arsenic trioxide can induce the apoptosis of NB4 cells, but there are significant differences between the mechanisms of selenite-induced and arsenic-induced apoptosis in NB4 cells, particularly in the influence of intracellular glutathione content on the drug action.
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Humanos , Acetilcisteína , Farmacología , Apoptosis , Genética , Arsenicales , Farmacología , División Celular , ADN de Neoplasias , Genética , Metabolismo , Citometría de Flujo , Glutatión , Metabolismo , Membranas Intracelulares , Fisiología , Leucemia Promielocítica Aguda , Metabolismo , Patología , Potenciales de la Membrana , Mitocondrias , Fisiología , Óxidos , Farmacología , Especies Reactivas de Oxígeno , Metabolismo , Selenito de Sodio , Farmacología , Células Tumorales CultivadasRESUMEN
In order to evaluate the effect of sodium selenite on the activation of NFkappaB during selenite-induced apoptosis in NB4 cells, Western blot was used to measure the level of P65 in nuclear extraction of NB4 cells treated with sodium selenite to reflect the activation of NFkappaB; the apoptosis of NB4 cells was determined by morphological observation, DNA ladder electrophoresis and flow cytometry; and MTT test was used to measure the growth inhibition of cells. Results showed that sodium selenite (>/=5 micro mol/L) suppressed the cell growth, induced apoptosis and inhibited the activation of NF kappaB in a concentration- and time-dependency pattern. It was concluded that inhibition of NF kappaB might be one of the mechanisms in selenite-induced apoptosis in NB4 cells.
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Humanos , Apoptosis , División Celular , Relación Dosis-Respuesta a Droga , Activación Enzimática , FN-kappa B , Metabolismo , Selenito de Sodio , FarmacologíaRESUMEN
<p><b>OBJECTIVE</b>To study the effects of low dose sodium selenite combined with all-trans retinoic acid (ATRA) on apoptosis and differentiation of human acute promyelocytic leukemia (APL) NB4 cells.</p><p><b>METHODS</b>Apo-ptosis was detected by translocation of phosphatidylserine (PS) with a Annexin-V kit and DNA fragmentation by agarose gel electrophoresis analysis, cell differentiation was studied by flow cytometry of CD(11b) expression and NBT reduction assay.</p><p><b>RESULTS</b>Five micromol/L sodium selenite or 0.1 micromol/L ATRA alone could not induce apoptosis of NB4 cells within 48 hours. However, combination of the two drugs at the same doses as above could induce significant apoptosis in 48 hours characterized by increased PS translocation and DNA ladder. Sodium selenite at concentration of 2 micromol/L was not able to induce differentiation of NB4 cells, but when combined with 0.1 micromol/L ATRA, CD(11b) expression and NBT reduction were increased as compared with that of 0.1 micromol/L ATRA alone.</p><p><b>CONCLUSION</b>Low dose sodium selenite could enhance the effects of low dose ATRA in inducing apoptosis and differentiation of NB4 cells.</p>