Birth defects have become a public health concern.The hazardous environmental factors exposure to embryos could increase the risk of birth defects.Cadmium,a toxic environmental factor,can cross the placental barrier d...Birth defects have become a public health concern.The hazardous environmental factors exposure to embryos could increase the risk of birth defects.Cadmium,a toxic environmental factor,can cross the placental barrier during pregnancy.Pregnant woman may be subjected to cadmium before taking precautionary protective actions.However,the link between birth defects and cadmium remains obscure.Cadmium exposure can induce excessive apoptosis in neuroepithelium during embryonic development progresses.Cadmium exposure activated the p53 via enhancing the adenosine 5‘-monophosphate(AMP)-activated protein kinase(AMPK)and reactive oxygen species'(ROS)level.And cadmium decreases the level of Paired box 3(Pax3)and murine double minute 2(Mdm2),disrupting the process of p53 ubiquitylation.And p53 accumulation induced excessive apoptosis in neuroepithelium during embryonic development progresses.Excessive apoptosis led to the failure of neural tube closure.The study emphasizes that environmental materials may increase the health risk for embryos.Cadmium caused the failure of neural tube closure during early embryotic day.Pregnant women may be exposed by cadmium before taking precautionary protective actions,because of cadmium concentration-containing foods and environmental tobacco smoking.This suggests that prenatal cadmium exposure is a threatening risk factor for birth defects.展开更多
Background: The aim of this study was to assess the stress response and apoptosis on leucocytes, in patients under two different anesthetics techniques. Methods: Thirty patients ASA I-II were prospectively randomized ...Background: The aim of this study was to assess the stress response and apoptosis on leucocytes, in patients under two different anesthetics techniques. Methods: Thirty patients ASA I-II were prospectively randomized into two groups to receive either total intravenous anesthesia with propofol-remifentanil (TIVA Group, n = 15) or balanced inhalation anesthesia with sevoflurane-remifentanil (BAL Group, n = 15). The hemodynamic response: systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) at different time points: baseline, after intubation, after skin incision and at the end of surgery, was measured along with plasma levels of lactate, glucose, cortisol and leucocytes count. The biomarkers of apoptosis (Annexin V and Propidium Iodide) in neutrophils, monocytes and lymphocytes were evaluated at baseline, intraoperatively and two hours after surgery. Results: The study groups were comparable with respect to anthropometric data. No significant intergroup differences in SBP and DBP were revealed. The HR in the BAL group was lower after intubation (p = 0.007). In both groups, lactate, plasma glucose, cortisol and leucocytes count remained stable during surgery and two hours post-operatively. In the BAL group there were significant differences in Annexin V in neutrophils, baseline moment (p = 0.010). No significant differences were found in apoptosis markers (Annexin V and Propidium Iodide) in neutrophils, monocytes and lymphocytes, at different time points. Conclusion: Both TIVA and BAL were effective in suppressing the surgical stress, without inducing apoptosis in immune cells, in patients undergoing VCL.展开更多
Objective To investigate the peroxide effects of iodide excess on mitochondria in Fischer rat thyroid cell line(FRTL)in the early period.Methods After treatment with 0.0 mmol/L(control group)or 0.1 mmol/L potassium io...Objective To investigate the peroxide effects of iodide excess on mitochondria in Fischer rat thyroid cell line(FRTL)in the early period.Methods After treatment with 0.0 mmol/L(control group)or 0.1 mmol/L potassium iodide(KI)for 2,4 and 24 h,respectively,changes of mitochondrial superoxide formation were assayed by flow cytometry and fluorescence microscopy using mitochondria-targeted hydroethidine(Mito SOX).展开更多
基金supported by the National Natural Science Foundation of China(No.32172932)the Key Program of Natural Science Foundation of Heilongjiang Province of China(No.ZD2021C003)+2 种基金the China Agriculture Research System of MOF and MARA(No.CARS-35)the Distinguished Professor of Longjiang Scholars Support Project(No.T201908)the Heilongjiang Touyan Innovation Team Program。
文摘Birth defects have become a public health concern.The hazardous environmental factors exposure to embryos could increase the risk of birth defects.Cadmium,a toxic environmental factor,can cross the placental barrier during pregnancy.Pregnant woman may be subjected to cadmium before taking precautionary protective actions.However,the link between birth defects and cadmium remains obscure.Cadmium exposure can induce excessive apoptosis in neuroepithelium during embryonic development progresses.Cadmium exposure activated the p53 via enhancing the adenosine 5‘-monophosphate(AMP)-activated protein kinase(AMPK)and reactive oxygen species'(ROS)level.And cadmium decreases the level of Paired box 3(Pax3)and murine double minute 2(Mdm2),disrupting the process of p53 ubiquitylation.And p53 accumulation induced excessive apoptosis in neuroepithelium during embryonic development progresses.Excessive apoptosis led to the failure of neural tube closure.The study emphasizes that environmental materials may increase the health risk for embryos.Cadmium caused the failure of neural tube closure during early embryotic day.Pregnant women may be exposed by cadmium before taking precautionary protective actions,because of cadmium concentration-containing foods and environmental tobacco smoking.This suggests that prenatal cadmium exposure is a threatening risk factor for birth defects.
文摘Background: The aim of this study was to assess the stress response and apoptosis on leucocytes, in patients under two different anesthetics techniques. Methods: Thirty patients ASA I-II were prospectively randomized into two groups to receive either total intravenous anesthesia with propofol-remifentanil (TIVA Group, n = 15) or balanced inhalation anesthesia with sevoflurane-remifentanil (BAL Group, n = 15). The hemodynamic response: systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) at different time points: baseline, after intubation, after skin incision and at the end of surgery, was measured along with plasma levels of lactate, glucose, cortisol and leucocytes count. The biomarkers of apoptosis (Annexin V and Propidium Iodide) in neutrophils, monocytes and lymphocytes were evaluated at baseline, intraoperatively and two hours after surgery. Results: The study groups were comparable with respect to anthropometric data. No significant intergroup differences in SBP and DBP were revealed. The HR in the BAL group was lower after intubation (p = 0.007). In both groups, lactate, plasma glucose, cortisol and leucocytes count remained stable during surgery and two hours post-operatively. In the BAL group there were significant differences in Annexin V in neutrophils, baseline moment (p = 0.010). No significant differences were found in apoptosis markers (Annexin V and Propidium Iodide) in neutrophils, monocytes and lymphocytes, at different time points. Conclusion: Both TIVA and BAL were effective in suppressing the surgical stress, without inducing apoptosis in immune cells, in patients undergoing VCL.
文摘Objective To investigate the peroxide effects of iodide excess on mitochondria in Fischer rat thyroid cell line(FRTL)in the early period.Methods After treatment with 0.0 mmol/L(control group)or 0.1 mmol/L potassium iodide(KI)for 2,4 and 24 h,respectively,changes of mitochondrial superoxide formation were assayed by flow cytometry and fluorescence microscopy using mitochondria-targeted hydroethidine(Mito SOX).
