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Contribution of polyol pathway to diabetes-induced oxidative stress.
Results indicate that similar to the situation in the lens, AR is also the major contributor to hyperglycemia-induced oxidative stress in the nerve, although increased flux of glucose through the polyol pathway leads to diabetic lesions in both the lenses and nerve, the mechanisms may be different. Expand
Endothelin-1 Overexpression Leads to Further Water Accumulation and Brain Edema after Middle Cerebral Artery Occlusion via Aquaporin 4 Expression in Astrocytic End-Feet
The current data suggest that astrocytic ET-1 has deleterious effects on water homeostasis, cerebral edema and BBB integrity, which contribute to more severe ischemic brain injury. Expand
Prenatal Immune Challenge Is an Environmental Risk Factor for Brain and Behavior Change Relevant to Schizophrenia: Evidence from MRI in a Mouse Model
The data indicate immune-associated environmental insults targeting early foetal development may have more extensive neurodevelopmental impact than identical insults in late prenatal life. Expand
Cdk5-mediated phosphorylation of endophilin B1 is required for induced autophagy in models of Parkinson's disease
It is shown that Cdk5-mediated phosphorylation of EndoB1 is essential for autophagy induction and neuronal loss in models of Parkinson’s disease. Expand
Osmotic Response Element-binding Protein (OREBP) Is an Essential Regulator of the Urine Concentrating Mechanism*
  • A. Lam, B. Ko, +4 authors S. Chung
  • Biology, Medicine
  • Journal of Biological Chemistry
  • 12 November 2004
Data indicate that in addition to vasopressin, OREBP is another essential regulator of the urine concentrating mechanism and develops progressive hydronephrosis soon after weaning, confirming the osmoprotective function of ORE BP implicated by the in vitro experiments. Expand
Chronic adiponectin deficiency leads to Alzheimer’s disease-like cognitive impairments and pathologies through AMPK inactivation and cerebral insulin resistance in aged mice
The results indicated that chronic APN deficiency inactivated AMPK causing insulin desensitization and elicited AD-like pathogenesis in aged mice which also developed significant cognitive impairments and psychiatric symptoms. Expand
Aldose reductase deficiency prevents diabetes-induced blood-retinal barrier breakdown, apoptosis, and glial reactivation in the retina of db/db mice.
Findings indicate that AR is responsible for the early events in the pathogenesis of diabetic retinopathy, leading to a cascade of retinal lesions, including blood-retinal barrier breakdown, loss of pericytes, neuro- retinal apoptosis, glial reactivation, and neovascularization. Expand
Berberine ameliorates β-amyloid pathology, gliosis, and cognitive impairment in an Alzheimer's disease transgenic mouse model
The results suggest that BBR provides neuroprotective effects in TgCRND8 mice through regulating APP processing and that further investigation of the BBR for therapeutic use in treating AD is warranted. Expand
Aldose Reductase–Deficient Mice Are Protected From Delayed Motor Nerve Conduction Velocity, Increased c-Jun NH2-Terminal Kinase Activation, Depletion of Reduced Glutathione, Increased Superoxide
Increased polyol pathway flux through AR is a major contributing factor in the early signs of diabetic neuropathy, possibly through depletion of glutathione, increased superoxide accumulation, increased JNK activation, and DNA damage. Expand