Investigating an abnormal hump phenomenon in top gate a-InGaZnO thin-film transistors due to mobile sodium diffusion.

Top gate a-InGaZnO (IGZO) thin-film transistors (TFTs) annealed at high temperature show excellent initial current-voltage (I-V) characteristics. However, when they are exposed to positive gate bias for a long time, hump can occur in the subthreshold region. This abnormal hump is accelerated at a higher positive gate voltage and mitigate by a negative gate voltage. While the strength of the hump is irrelevant to a change in channel width, it relies significantly on channel length. This phenomenon might be due to mobile Na ions diffused from a glass substrate migrating toward the back and edge side of the IGZO semiconductor by a vertical gate electric field. When a layer of Al2O3 is formed between the IGZO semiconductor and the glass substrate, the hump phenomenon could be successfully solved by serving as a barrier for Na ions moving into the IGZO.

Molecular Ordering Behavior of Lyotropic Chromonic Liquid Crystals on a Polyimide Alignment Layer.

Coating-type polarizing films with a high dichroic ratio (DR) and polarization efficiency in the visible region were fabricated using a solution of ternary lyotropic chromonic liquid crystals (LCLCs). Optical characteristics of these anisotropic LCLC polarizing films were then determined. DR increased with increasing LCLC concentrations. Molecular ordering of these LCLCs on a rubbed polyimide (PI) layer increased because LCLC molecules' orientation was enhanced by the dielectric anisotropy effect from rubbing the surface of the PI. In addition, this study demonstrated how the interaction between liquid crystal aggregates and the PI surface with different LCLC solutions correlated with LCLC molecular orientations on the PI which is significantly dependent on whether the coating direction of the LCLC solution was parallel or perpendicular to the PI rubbing direction. It was found that the ordering direction at high LCLC concentrations was determined by shearing direction of the LCLC solution coating, whereas the ordering direction at low LCLC concentrations was governed by the dielectric anisotropy effect from the PI rubbing direction.

Long-term treatment of glucagon-like peptide-1 analog exendin-4 ameliorates diabetic nephropathy through improving metabolic anomalies in db/db mice.

Glucagon-like peptide-1 (GLP-1) is a gut incretin hormone and is a new clinically available class of agents for improving of insulin resistance in both animals and humans with type 2 diabetes. These studies aimed to determine whether long-term treatment with a long-acting GLP-1 analog, exendin-4, delayed the progression of diabetes. Male db/db mice and db/m mice at 8 wk of age were treated with exendin-4 for 8 wk, whereas the control db/db mice received only vehicle. Urinary albumin excretion was significantly decreased in db/db mice that were treated with 1 nmol/kg exendin-4 compared with those in db/db mice that were treated with 0.5 nmol/kg exendin-4 and control db/db mice (P < 0.005). Intraperitoneal glucose tolerance test was improved in db/db mice that were treated with 1 nmol/kg exendin-4 compared with other groups (P < 0.05). Despite this, fasting blood glucose, glycated hemoglobin, and creatinine concentrations were not significantly different among db/db mice. Renal histology studies further demonstrated that glomerular hypertrophy, mesangial matrix expansion, TGF-beta1 expression, and type IV collagen accumulation and associated glomerular lipid accumulation were significantly decreased in db/db mice that were treated with 1 nmol/kg exendin-4. Furthermore, there were fewer infiltrating inflammatory cells and apoptotic cells in the glomeruli of db/db mice that were treated with 1 nmol/kg exendin-4 compared with those in the other groups accompanied by an increase in the renal immunoreactivity of peroxisome proliferator-activated receptor alpha and GLP-1 receptor-positive cells and a decrease in 24-h urinary 8-hydroxy-deoxyguanosine levels (P < 0.01, respectively) along with decreases in lipid content. Taken together, exendin-4 treatment seems to ameliorate diabetic nephropathy together with improvement of the metabolic anomalies. These results suggest that exendin-4 could provide a therapeutic role in diabetic nephropathy that results from type 2 diabetes.

Accelerated diabetic nephropathy in mice lacking the peroxisome proliferator-activated receptor alpha.

Peroxisome proliferator-activated receptor (PPAR)alpha, a member of the ligand-activated nuclear receptor superfamily, plays an important role in lipid metabolism and glucose homeostasis and is highly expressed in the kidney. The present studies were aimed at determining the role of PPARalpha in the pathogenesis of diabetic nephropathy using PPARalpha-knockout mice and cultured murine mesangial cells. Diabetes was induced using a low-dose streptozotocin protocol in 8-week-old male 129 SvJ PPARalpha-knockout and wild-type mice. Diabetic PPARalpha-knockout and wild-type mice developed elevated fasting blood glucose (P < 0.001) and HbA1c levels (P < 0.001). Renal functional and histopathological changes in diabetic and nondiabetic PPARalpha-knockout and wild-type mice were evaluated after 16 weeks of hyperglycemia. PPARalpha immunostaining of the cortical tubules of diabetic wild-type mice was elevated by hyperglycemia. In diabetic PPARalpha-knockout mice, renal disease with accompanying albuminuria, glomerular sclerosis, and mesangial area expansion was more severe than in diabetic wild-type mice (P < 0.05) and was accompanied by increased levels of serum free fatty acids and triglycerides (P < 0.01). Furthermore, they exhibited increased renal immunostaining for type IV collagen and osteopontin, which was associated with increased macrophage infiltration and glomerular apoptosis. There were no significant differences in these indexes of renal disease between nondiabetic PPARalpha-knockout and wild-type mice and diabetic PPARalpha wild-type mice. In vitro studies demonstrated that high glucose levels markedly increased the expression of type IV collagen, transforming growth factor-beta1, and the number of leukocytes adherent to cultured mesangial cells. Adherence of leukocytes was inhibited by the PPARalpha agonist fenofibrate. Taken together, PPARalpha deficiency appears to aggravate the severity of diabetic nephropathy through an increase in extracellular matrix formation, inflammation, and circulating free fatty acid and triglyceride concentrations. PPARalpha agonists may serve as useful therapeutic agents for type 1 diabetic nephropathy.