Hydrophilic acrylic intraocular lens optic opacification in a diabetic patient.

Purpose: To report clinicopathologic and ultrastructural feature of one opacified hydrophilic acrylic intraocular lens (IOL) explanted from a diabetic patient.

Methods: A 48-year-old man underwent trans pars plana vitrectomy and phacoemulsification with implantation of a hydrophilic acrylic lens OS in November 2008. The patient complained of a marked decrease in visual acuity in May 2009 as a result of a milky opalescence of the IOL.

Factors that Affect Medication Adherence in Elderly Patients with Diabetes Mellitus.

Background: This study was conducted to evaluate the factors affecting medication adherence in geriatric diabetic patients treated at private clinics and tertiary hospitals. We compared the factors affecting medication adherence between these two patient groups.

Methods: We included 108 diabetic patients older than 65 years treated at one tertiary hospital and 157 patients older than 65 years treated at two private clinics.

Clinical effects of conjunctiva-Müller muscle resection in anophthalmic ptosis.

Purpose: To evaluate the clinical effects of conjunctiva-Muller muscle resection through conjunctival incision in anophthalmic patients with mild ptosis.

Methods: Conjunctiva-Müller muscle resection was performed by one surgeon in 8 patients (8 eyes) who had received evisceration or enucleation and responded to 10% phenylephrine solution to correct ptosis. The average age of the patients was 35.

Activation of vascular protein kinase C-beta inhibits Akt-dependent endothelial nitric oxide synthase function in obesity-associated insulin resistance.

Activation of protein kinase C (PKC) in vascular tissue is associated with endothelial dysfunction and insulin resistance. However, the effect of vascular PKC activation on insulin-stimulated endothelial nitric oxide (NO) synthase (eNOS) regulation has not been characterized in obesity-associated insulin resistance. Diacylglycerol (DAG) concentration and PKC activity were increased in the aorta of Zucker fatty compared with Zucker lean rats.

Beta ig-h3 promotes renal proximal tubular epithelial cell adhesion, migration and proliferation through the interaction with alpha3beta1 integrin.

Betaig-h3 (betaig-h3) is a secretory protein composed of fasciclin I-like repeats containing sequences that allows binding of integrins and glycosaminoglycans in vivo. Expression of betaig-h3 is responsive to TGF-Beta and the protein is found to be associated with extracellular matrix (ECM) molecules, implicating betaig-h3 as an ECM adhesive protein of developmental processes. We previously observed predominant expression of betaig-h3 expression in the basement membrane of proximal tubules of kidney.

Elevation of urinary betaig-h3, transforming growth factor-beta-induced protein in patients with type 2 diabetes and nephropathy.

Transforming growth factor-beta (TGF-beta) is a pro-sclerotic growth factor implicated in the pathogenesis of diabetic nephropathy. betaig-h3 is an extracellular matrix protein which is induced in many cells by TGF-beta. This study examined urinary betaig-h3 excretion in diabetic patients with elevated urinary albumin excretion and the clinical application of urinary betaig-h3 as a marker of diabetic nephropathy.

Expression of TGF-beta-induced matrix protein betaig-h3 is up-regulated in the diabetic rat kidney and human proximal tubular epithelial cells treated with high glucose.

Background: betaig-h3 is an extracellular matrix protein whose expression in several cell types is greatly increased by transforming growth factor-beta (TGF-beta). TGF-beta is believed to be involved in the development of diabetic nephropathy and thus we have assessed the possibility that betaig-h3 may be a downstream molecule in this pathogenic process.

Methods: Immunoblotting and immunohistochemistry were done using an antibody against mouse betaig-h3 protein.

TGF-beta-induced protein beta ig-h3 is upregulated by high glucose in vascular smooth muscle cells.

TGF-beta-induced gene-h3 (beta ig-h3) is an adhesive molecule that interacts with integrins. Because TGF-beta plays an important role in diabetic complications and beta ig-h3 serves as a cell substrate, we hypothesized that diabetic conditions might increase beta ig-h3 synthesis in vascular smooth muscle cells (VSMCs), which may subsequently contribute to the pathogenesis of diabetic angiopathy. The concentrations of beta ig-h3 and TGF-beta were measured in conditioned media using an enzyme-linked immunosorbent assay.