AIM: To report maternal and fetal adverse outcomes, in spite of appropriate treatment and regular follow up, in diabetic pregnant women with proliferative diabetic retinopathy. METHODS: Case series of four young pregn...AIM: To report maternal and fetal adverse outcomes, in spite of appropriate treatment and regular follow up, in diabetic pregnant women with proliferative diabetic retinopathy. METHODS: Case series of four young pregnant diabetics aged between 20 and 25 years with type 1 diabetes mellitus and proliferative diabetic retrinopathy. RESULTS: The maternal adverse outcomes were abortion in one patient, pre-eclampsia and preterm delivery in one patient, and renal failure requiring dialysis in one patient. The fetal adverse outcomes were neonatal death in one case and premature baby in another case. CONCLUSION: These cases highlight the fact that diabetic pregnant women should be closely followed up by the obstetricians and physicians when they have proliferative retinopathy. The proliferative diabetic retinopathy should be considered as a part of the assessment when counseling a diabetic woman in antenatal check up and also in the follow up visits during pregnancy.展开更多
Sensitive smell discrimination is based on structural plasticity of the olfactory bulb,which depends on migration and integration of newborn neurons from the subventricular zone.In this study,we examined the relations...Sensitive smell discrimination is based on structural plasticity of the olfactory bulb,which depends on migration and integration of newborn neurons from the subventricular zone.In this study,we examined the relationship between neural stem cell status in the subventricular zone and olfactory function in rats with diabetes mellitus.Streptozotocin was injected through the femoral vein to induce type 1 diabetes mellitus in Sprague-Dawley rats.Two months after injection,olfactory sensitivity was decreased in diabetic rats.Meanwhile,the number of Brd U-positive and Brd U+/DCX+double-labeled cells was lower in the subventricular zone of diabetic rats compared with agematched normal rats.Western blot results revealed downregulated expression of insulin receptorβ,phosphorylated glycogen synthase kinase 3β,and β-catenin in the subventricular zone of diabetic rats.Altogether,these results indicate that diabetes mellitus causes insulin deficiency,which negatively regulates glycogen synthase kinase 3β and enhances β-catenin degradation,with these changes inhibiting neural stem cell proliferation.Further,these signaling pathways affect proliferation and differentiation of neural stem cells in the subventricular zone.Dysfunction of subventricular zone neural stem cells causes a decline in olfactory bulb structural plasticity and impairs olfactory sensitivity in diabetic rats.展开更多
Objective This study aimed to investigate the susceptibility of mice with streptozotocin(STZ)-induced diabetes mellitus(TIDM) to the uptake of pentavalent inorganic arsenic(iAs^V) and the possible molecular mech...Objective This study aimed to investigate the susceptibility of mice with streptozotocin(STZ)-induced diabetes mellitus(TIDM) to the uptake of pentavalent inorganic arsenic(iAs^V) and the possible molecular mechanism. Methods TIDM was induced in mice by STZ. TIDM and normal mice were treated with 15.0 mg/kg Na2HAsO4·12H2O by intragastric administration. Then, the concentrations of arsenic in various tissues were measured by atomic fluorescence spectrometry. The gene expression levels of Pit1 and Pit2 were quantified by real-time RT-PCR, and their protein levels were detected by Western blotting in mouse heart, kidney, and liver tissues. Results The concentrations of arsenic in STZ-induced TIDM mouse tissues were higher at 2 h after intragastric administration of Na2HAsO4·12H2O. Compared with the levels in normal mice, PIT1 and PIT2, which play a role in the uptake of iAs^V, were upregulated in the livers and hearts of TIDM mice. PIT1 but not PIT2 was higher in TIDM mouse kidneys. The upregulation of Pit1 and Pit2 expression could be reversed by insulin treatment. Conclusion The increased uptake of iAs^V in TIDM mouse tissues may be associated with increased PIT1 and/or PIT2 expression.展开更多
文摘AIM: To report maternal and fetal adverse outcomes, in spite of appropriate treatment and regular follow up, in diabetic pregnant women with proliferative diabetic retinopathy. METHODS: Case series of four young pregnant diabetics aged between 20 and 25 years with type 1 diabetes mellitus and proliferative diabetic retrinopathy. RESULTS: The maternal adverse outcomes were abortion in one patient, pre-eclampsia and preterm delivery in one patient, and renal failure requiring dialysis in one patient. The fetal adverse outcomes were neonatal death in one case and premature baby in another case. CONCLUSION: These cases highlight the fact that diabetic pregnant women should be closely followed up by the obstetricians and physicians when they have proliferative retinopathy. The proliferative diabetic retinopathy should be considered as a part of the assessment when counseling a diabetic woman in antenatal check up and also in the follow up visits during pregnancy.
基金partly supported by the National Natural Science Foundation of China,No.81370448,81570725
文摘Sensitive smell discrimination is based on structural plasticity of the olfactory bulb,which depends on migration and integration of newborn neurons from the subventricular zone.In this study,we examined the relationship between neural stem cell status in the subventricular zone and olfactory function in rats with diabetes mellitus.Streptozotocin was injected through the femoral vein to induce type 1 diabetes mellitus in Sprague-Dawley rats.Two months after injection,olfactory sensitivity was decreased in diabetic rats.Meanwhile,the number of Brd U-positive and Brd U+/DCX+double-labeled cells was lower in the subventricular zone of diabetic rats compared with agematched normal rats.Western blot results revealed downregulated expression of insulin receptorβ,phosphorylated glycogen synthase kinase 3β,and β-catenin in the subventricular zone of diabetic rats.Altogether,these results indicate that diabetes mellitus causes insulin deficiency,which negatively regulates glycogen synthase kinase 3β and enhances β-catenin degradation,with these changes inhibiting neural stem cell proliferation.Further,these signaling pathways affect proliferation and differentiation of neural stem cells in the subventricular zone.Dysfunction of subventricular zone neural stem cells causes a decline in olfactory bulb structural plasticity and impairs olfactory sensitivity in diabetic rats.
基金supported by the National Natural Science Foundation of China[grant numbers 21277078,21407082]the Natural Science Foundation of Jiangsu Province[grant numbers BK20140426]+1 种基金the Natural Science Fund Project of Colleges in Jiangsu Province[grant numbers 16KJB330007]the National Undergraduate Innovation Experiment Project[grant numbers 201510304037Z]
文摘Objective This study aimed to investigate the susceptibility of mice with streptozotocin(STZ)-induced diabetes mellitus(TIDM) to the uptake of pentavalent inorganic arsenic(iAs^V) and the possible molecular mechanism. Methods TIDM was induced in mice by STZ. TIDM and normal mice were treated with 15.0 mg/kg Na2HAsO4·12H2O by intragastric administration. Then, the concentrations of arsenic in various tissues were measured by atomic fluorescence spectrometry. The gene expression levels of Pit1 and Pit2 were quantified by real-time RT-PCR, and their protein levels were detected by Western blotting in mouse heart, kidney, and liver tissues. Results The concentrations of arsenic in STZ-induced TIDM mouse tissues were higher at 2 h after intragastric administration of Na2HAsO4·12H2O. Compared with the levels in normal mice, PIT1 and PIT2, which play a role in the uptake of iAs^V, were upregulated in the livers and hearts of TIDM mice. PIT1 but not PIT2 was higher in TIDM mouse kidneys. The upregulation of Pit1 and Pit2 expression could be reversed by insulin treatment. Conclusion The increased uptake of iAs^V in TIDM mouse tissues may be associated with increased PIT1 and/or PIT2 expression.