A large amount of evidence has supported a clinical link between diabetes and inflammatory diseases,e.g.,cancer,dementia,and hypertension.In addition,it is also suggested that dysregulations related to Ca^(2+)signalin...A large amount of evidence has supported a clinical link between diabetes and inflammatory diseases,e.g.,cancer,dementia,and hypertension.In addition,it is also suggested that dysregulations related to Ca^(2+)signaling could link these diseases,in addition to 3'-5'-cyclic adenosine monophosphate(cAMP)signaling pathways.Thus,revealing this interplay between diabetes and inflammatory diseases may provide novel insights into the pathogenesis of these diseases.Publications involving signaling pathways related to Ca^(2+)and cAMP,inflammation,diabetes,dementia,cancer,and hypertension(alone or combined)were collected by searching PubMed and EMBASE.Both signaling pathways,Ca^(2+)and cAMP signaling,control the release of neurotransmitters and hormones,in addition to neurodegeneration,and tumor growth.Furthermore,there is a clear relationship between Ca^(2+)signaling,e.g.,increased Ca^(2+)signals,and inflammatory responses.cAMP also regulates pro-and anti-inflammatory responses.Due to the experience of our group in this field,this article discusses the role of Ca^(2+)and cAMP signaling in the correlation between diabetes and inflammatory diseases,including its pharmacological implications.As a novelty,this article also includes:(1)A timeline of the major events in Ca^(2+)/cAMP signaling;and(2)As coronavirus disease 2019(COVID-19)is an emerging and rapidly evolving situation,this article also discusses recent reports on the role of Ca^(2+)channel blockers for preventing Ca^(2+)signaling disruption due to COVID-19,including the correlation between COVID-19 and diabetes.展开更多
To evaluate the changes of 3', 5'-cyclic adenosine monophosphate (cAMP), thrombox-ane A2(TXA2) and prostacyclin (PGI2) in cerebrospinal fluid (CSF) in the asphyxiated newborn and explore their roles in hypoxic...To evaluate the changes of 3', 5'-cyclic adenosine monophosphate (cAMP), thrombox-ane A2(TXA2) and prostacyclin (PGI2) in cerebrospinal fluid (CSF) in the asphyxiated newborn and explore their roles in hypoxic-ischamic brain damage (HIBD). Thirty-six full term newborns were divided into 3 groups, including 12 with moderate-severe hypoxic-ischaemic encephalopathy (HIE), 13 with mild HIE, 11 without HIE (control group). The levels of cAMP, TXB2(TXA2 metabolite) and 6-keto-PGF1α(PGI2 metabolite) in CSF and plasma were measured 36-72 h after birth by RIA, and the concentrations were expressed as nM/L (cAMP), ng/L(TXB2 and 6-keto-PGF1α). The infants were followed-up at 6 and 12 month of age and Mental Development Index (MDI) and Psychomotor Development Index (FDD were measured using Bayley Scales of Infant Development (BSID). The CSF cAMP level in moderate-severe HIE group was 8. 60±2. 40, significantly lower than that of the mild HIE group (14. 83±2. 84) and the control group (24. 43±2. 39)(for both P<0. 01). The levels of TXB2 and 6-keto-PGF1α in CFS in the moderate-severe HIE group (206. 06±29. 74, 168. 47± 23. 02, respectively) were significantly higher than in the mild HIE group (83. 37±28. 57, 131. 42± 16. 57, respectively, P<0. 01) and the control group (41. 77±21. 58, 86. 23±13. 05, respectively, P<0. 01). The level changes of cAMP,TXB2 and 6-keto-PGF1α in plasma in all groups were similar to those in CSF, but no significant difference was found between mild HIE group and the control group (P>0. 05). The follow-up results showed that MDI and PDI of the moderate-severe HIE group were the lowest (84. 79±13. 34, 83. 50±13. 28, respectively), followed by mild HIE group (102.19±7. 02, 99. 94±9. 08, respectively) , with the control group being the highest (116. 63± 12.08, 116. 69±10. 87, respectively). Univariate analysis showed some significant difference (the moderate-severe HIE group vs. the mild HIE group or the control group, P<0. 01; the mild HIE group vs. the control group P<0. 05). The results suggested that the concentration of cAMP, TXA2 and T/K ratio in CSF after neonatal asphyxia might be sensitive markers in evaluating the severity of brain damage in early stage and predicting the future outcome.展开更多
文摘A large amount of evidence has supported a clinical link between diabetes and inflammatory diseases,e.g.,cancer,dementia,and hypertension.In addition,it is also suggested that dysregulations related to Ca^(2+)signaling could link these diseases,in addition to 3'-5'-cyclic adenosine monophosphate(cAMP)signaling pathways.Thus,revealing this interplay between diabetes and inflammatory diseases may provide novel insights into the pathogenesis of these diseases.Publications involving signaling pathways related to Ca^(2+)and cAMP,inflammation,diabetes,dementia,cancer,and hypertension(alone or combined)were collected by searching PubMed and EMBASE.Both signaling pathways,Ca^(2+)and cAMP signaling,control the release of neurotransmitters and hormones,in addition to neurodegeneration,and tumor growth.Furthermore,there is a clear relationship between Ca^(2+)signaling,e.g.,increased Ca^(2+)signals,and inflammatory responses.cAMP also regulates pro-and anti-inflammatory responses.Due to the experience of our group in this field,this article discusses the role of Ca^(2+)and cAMP signaling in the correlation between diabetes and inflammatory diseases,including its pharmacological implications.As a novelty,this article also includes:(1)A timeline of the major events in Ca^(2+)/cAMP signaling;and(2)As coronavirus disease 2019(COVID-19)is an emerging and rapidly evolving situation,this article also discusses recent reports on the role of Ca^(2+)channel blockers for preventing Ca^(2+)signaling disruption due to COVID-19,including the correlation between COVID-19 and diabetes.
文摘To evaluate the changes of 3', 5'-cyclic adenosine monophosphate (cAMP), thrombox-ane A2(TXA2) and prostacyclin (PGI2) in cerebrospinal fluid (CSF) in the asphyxiated newborn and explore their roles in hypoxic-ischamic brain damage (HIBD). Thirty-six full term newborns were divided into 3 groups, including 12 with moderate-severe hypoxic-ischaemic encephalopathy (HIE), 13 with mild HIE, 11 without HIE (control group). The levels of cAMP, TXB2(TXA2 metabolite) and 6-keto-PGF1α(PGI2 metabolite) in CSF and plasma were measured 36-72 h after birth by RIA, and the concentrations were expressed as nM/L (cAMP), ng/L(TXB2 and 6-keto-PGF1α). The infants were followed-up at 6 and 12 month of age and Mental Development Index (MDI) and Psychomotor Development Index (FDD were measured using Bayley Scales of Infant Development (BSID). The CSF cAMP level in moderate-severe HIE group was 8. 60±2. 40, significantly lower than that of the mild HIE group (14. 83±2. 84) and the control group (24. 43±2. 39)(for both P<0. 01). The levels of TXB2 and 6-keto-PGF1α in CFS in the moderate-severe HIE group (206. 06±29. 74, 168. 47± 23. 02, respectively) were significantly higher than in the mild HIE group (83. 37±28. 57, 131. 42± 16. 57, respectively, P<0. 01) and the control group (41. 77±21. 58, 86. 23±13. 05, respectively, P<0. 01). The level changes of cAMP,TXB2 and 6-keto-PGF1α in plasma in all groups were similar to those in CSF, but no significant difference was found between mild HIE group and the control group (P>0. 05). The follow-up results showed that MDI and PDI of the moderate-severe HIE group were the lowest (84. 79±13. 34, 83. 50±13. 28, respectively), followed by mild HIE group (102.19±7. 02, 99. 94±9. 08, respectively) , with the control group being the highest (116. 63± 12.08, 116. 69±10. 87, respectively). Univariate analysis showed some significant difference (the moderate-severe HIE group vs. the mild HIE group or the control group, P<0. 01; the mild HIE group vs. the control group P<0. 05). The results suggested that the concentration of cAMP, TXA2 and T/K ratio in CSF after neonatal asphyxia might be sensitive markers in evaluating the severity of brain damage in early stage and predicting the future outcome.
