1.Investigation of the Patient's Compliance with Medication of Our Hospital in 2003
Cheng PENG ; Hao SUN ; Zhaoli LUO ; Xingui MAO
China Pharmacy 1991;0(06):-
OBJECTIVE:To provide the reference for improvement in patient's compliance with medication and the quality of drug-therapy.METHODS:Patients' compliance with medication was investigated and the related items were statistically analyzed.RESULTS & CONCLUSION:Low awareness of the detailed content and significance of the drug-therapy existed among the patients.Pharmaceutical care must be improved and the function of pharmacists must be strengthened.
2.cPKCγ Deficiency Exacerbates Autophagy Impairment and Hyperphosphorylated Tau Buildup through the AMPK/mTOR Pathway in Mice with Type 1 Diabetes Mellitus.
Jiayin ZHENG ; Yue WANG ; Yue LIU ; Song HAN ; Ying ZHANG ; Yanlin LUO ; Yi YAN ; Junfa LI ; Li ZHAO
Neuroscience Bulletin 2022;38(10):1153-1169
Type 1 diabetes mellitus (T1DM)-induced cognitive dysfunction is common, but its underlying mechanisms are still poorly understood. In this study, we found that knockout of conventional protein kinase C (cPKC)γ significantly increased the phosphorylation of Tau at Ser214 and neurofibrillary tangles, but did not affect the activities of GSK-3β and PP2A in the hippocampal neurons of T1DM mice. cPKCγ deficiency significantly decreased the level of autophagy in the hippocampal neurons of T1DM mice. Activation of autophagy greatly alleviated the cognitive impairment induced by cPKCγ deficiency in T1DM mice. Moreover, cPKCγ deficiency reduced the AMPK phosphorylation levels and increased the phosphorylation levels of mTOR in vivo and in vitro. The high glucose-induced Tau phosphorylation at Ser214 was further increased by the autophagy inhibitor and was significantly decreased by an mTOR inhibitor. In conclusion, these results indicated that cPKCγ promotes autophagy through the AMPK/mTOR signaling pathway, thus reducing the level of phosphorylated Tau at Ser214 and neurofibrillary tangles.
AMP-Activated Protein Kinases/metabolism*
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Animals
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Autophagy
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Diabetes Mellitus, Type 1
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Glucose
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Glycogen Synthase Kinase 3 beta/metabolism*
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Mice
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Phosphorylation
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Protein Kinase C/metabolism*
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TOR Serine-Threonine Kinases/metabolism*
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tau Proteins/metabolism*