Absence of the β1 subunit of AMP‐activated protein kinase reduces myofibroblast infiltration of the kidneys in early diabetes

Activation of the heterotrimeric energy‐sensing kinase AMP‐activated protein kinase (AMPK) has been reported to improve experimental diabetic kidney disease. We examined the effect of type 1 diabetes in wild‐type (WT) mice and mice lacking the β1 subunit of AMPK (AMPK β1^?/? mice), which have reduced AMPK activity in kidneys and other organs. Diabetes was induced using streptozotocin (STZ) and the animals followed up for 4 weeks. Hyperglycaemia was more severe in diabetic AMPK β1^?/? mice, despite the absence of any difference in serum levels of insulin, adiponectin and leptin. There was no change in AMPK activity in the kidneys of diabetic WT mice by AMPK activity assay, or phosphorylation of either the αT172 activation site on the α catalytic subunit of AMPK or the AMPK‐specific phosphosite S79 on acetyl CoA carboxylase 1 (ACC1). Phosphorylation of the inhibitory αS485 site on the α subunit of AMPK was significantly increased in the WT diabetic mice compared to non‐diabetic controls. Despite increased plasma glucose levels in the diabetic AMPK β1^?/? mice, there were fewer myofibroblasts in the kidneys compared to diabetic WT mice, as evidenced by reduced α‐smooth muscle actin (α‐SMA) protein by Western blot, mRNA by qRT‐PCR and fewer α‐SMA‐positive cells by immunohistochemical staining. Albuminuria was also reduced in the AMPK β1^?/? mice. In contrast to previous studies, therefore, myofibroblasts were reduced in the kidneys of AMPK β1^?/? diabetic mice compared to diabetic WT mice, despite increased circulating glucose, suggesting that AMPK can worsen renal fibrosis in type 1 diabetes.     

Treatment of progressive macular hypomelanosis with narrow‐band ultraviolet B phototherapy

Treatment for progressive macular hypomelanosis (PMH) has been disappointing. Recently, Propionibacterium acnes had been postulated as the causative agent and narrow‐band ultraviolet B (NBUVB) had been shown to stimulate melanogenesis and has antibacterial properties. The aim of this study was to evaluate the effectiveness of NBUVB in the treatment of PMH. A retrospective analysis of PMH cases diagnosed and treated with NBUVB treatment from 1 January 2007 to 30 April 2009 at the National Skin Centre (NSC) was conducted. The diagnosis of PMH was clinical. Treatment with NBUVB (311 nm) was given twice to thrice weekly. The initial treatment dose was determined as 70% of the patients' individual 311 nm UVB minimal erythema dose. The dose was increased by 10–20% if previous treatment had caused no or slight erythema. Percentage repigmentation from baseline was assessed at each follow‐up. A total of six patients diagnosed with PMH were treated with NBUVB in NSC in the past 2 years. Three patients had good improvement and the remainder had moderate improvement. Recurrence did occur. No adverse events were documented. The success of NBUVB as a monotherapy provides a viable and relatively safe, albeit temporary relief, for these individuals.     

Catatonia in Dual Diagnosis: a Case Report

International Journal of Mental Health and Addiction - Catatonia is a syndrome resulting in both severe motor and speech disturbances. Catatonia in a dual diagnosis of cannabis dependence and...     

人参调控神经递质代谢的研究进展

人参具有大补元气、安神益智等功效，其主要有效成分为三萜皂苷、多糖和多肽等，可用于中枢神经系统疾病的治疗。人参化学成分及其活性代谢物对氨基酸类、单胺类和乙酰胆碱等神经递质的体内代谢过程等具有广泛的调节作用，其作用途径包含调节脑部代谢微环境、透过血脑屏障直接作用于神经元以及调节神经-内分泌网络等。在人参“安神益智”的理论指导下，结合人参化学成分和神经递质的体内代谢过程综述了人参调节大脑神经递质代谢的主要作用机制，以期为人参的深入研究提供依据。