A scanning Kelvin probe study of charge trapping in zone-cast pentacene thin film transistors.

We have used scanning Kelvin probe microscopy (SKPM) as a local probe to study charge trapping in zone-cast pentacene field effect transistors on both SiO(2) and benzocyclobutene (BCB) substrates. Annealing at 130 degrees C was found to reduce the threshold voltage, susceptibility to negative gate bias stress and trapping of positive charges within single pentacene grains. We conclude that oxygen is able to penetrate and disassociatively incorporate into crystalline pentacene, chemically creating electrically active defect states. Screening of a positive gate bias caused by electron injection from Au into pentacene was directly observed with SKPM. The rate of screening was found to change significantly after annealing of the film and depended on the choice of gate dielectric.

Does circulating erythropoietin reflect progression of IgA nephropathy? Comparison with urinary N-acetyl-beta-D-glucosaminidase.

BACKGROUND: Recent reports describe that erythropoietin (Epo) is produced by peritubular interstitial fibroblast-like cells in response to a hypoxic stimulus. We studied serum Epo levels as a possible marker of tubulointerstitial damage in the progression of IgA nephropathy (IgAN), in comparison with urinary (u-) levels of N-acetyl-beta-D-glucosaminidase (NAG), which is mainly derived from proximal tubular cells and is used as a marker of tubular damage. METHODS: Thirty-eight patients with IgA nephropathy (IgAN) with relatively preserved renal function (serum creatinine: sCr, 0.5-2.2 mg/dl) were examined. The severity of glomerulosclerosis and interstitial fibrosis of the renal biopsy tissue was expressed by semiquantitative grading scores. Clinical parameters including serum creatinine (sCr), blood pressures, and 24-h proteinuria levels were obtained at the renal biopsy. Epo was measured by a radioimmunoassay (RIA) of sera obtained in the morning and u-NAG was measured by colorimetric method of 24-h urine samples. RESULTS: The mean Epo level of the patients (17.7+/-6.3 mU/ml) was not different from the control level (19.3+/-3.7 mU/ml). There were no significant correlations between Epo levels and red blood cell (RBC) counts, haematocrit (Hct), or haemoglobin (Hb) levels. The mean u-NAG level of the patients (6.7+/-6.2 U/gCr) was significantly higher than the control level (1.9+/-0.5 U/gCr). There was an inverse quantitative correlation between Epo and u-NAG levels in the patients (P<0.02). The u-NAG levels showed quantitative positive correlations with sCr (P<0.001), u-proteins (P<0.001), systolic (SBP) (P<0.001), and diastolic blood pressures (DBP) (P<0.05). Conversely, Epo levels were inversely correlated with sCr, SBP and DBP (each P<0.05). The patients with higher u-proteins (>2.0 g/day) showed significantly decreased Epo levels (P<0.05) than those with lower u-proteins (<2.0 g/day). The both scores of glomerulosclerosis and interstitial fibrosis were positively correlated with the u-NAG levels (each P<0.001), but were not correlated with the Epo levels. CONCLUSIONS: The significant correlation between u-NAG and serum Epo levels suggests that tubular damage and interstitial cell dysfunction are associated each other in the progression of IgAN. Serum Epo levels bearing inverse correlations with sCr, blood pressure levels and heavy proteinuria seem to reflect clinical severity of IgAN, whereas u-NAG can be more useful progression marker of IgAN bearing correlations with both clinical and histological findings.

Effects of an anti-platelet drug (dilazep) in IgA nephropathy: comparison of clinical effects with renal biopsy findings.

To investigate renal biopsy findings arising in response to treatment with an anti-platelet drug in IgA nephropathy, 46 patients were treated with dilazep dihydrochloride (Dilazep), and a retrospective comparison was performed between the clinical effects and renal biopsy findings. After 6 months of treatment, 18 patients (39%) were judged to be improved if their proteinuria was ameliorated by a 25% or greater decrease with improved or persistent renal function. The group of improved patients exhibited mean decreased levels of urinary proteins in the range from 1.9 to 0.8 g/day after treatment (p < 0.01). By contrast, the unimproved group showed increased urinary proteins in the range from 1.2 to 2.0 g/day (p < 0.05). The improved group showed histological findings with fewer glomeruli exhibiting sclerosis and/or cellular crescents, with a lesser increase in mesangial matrix and with smaller tubulo-interstitial lesions than the unimproved group. By immunofluorescence, the improved group was found to have smaller amounts of glomerular IgA and IgG deposits. These findings suggest that an anti-proteinuric effect of Dilazep administration can be expected in patients with IgA nephropathy with relatively mild glomerulo-sclerotic lesions.

The effect of angiotensin II antagonist, Sar1-Ile8-angiotensin II, on furosemide-induced increase in plasma noradrenaline, renin activity and aldosterone in unanesthetized dogs.

In order to evaluate the role of the renin-angiotensin system and the sympathetic nervous system in the maintenance of blood pressure in the sodium-depleted state, the changes of plasma renin activity (PRA), plasma aldosterone concentration (PAC) and plasma noradrenaline (PNA) were examined in unanesthetized dogs after the administration of furosemide. Furthermore, the role of the renin-angiotensin system in the increased sympathetic nerve activity induced by furosemide was assessed by using Sar1-Ile8-angiotensin II, an angiotensin II antagonist. When a dose of 0.8 mg/kg of furosemide was injected intravenously, 3 times every 15 minutes, PRA and PNA were significantly increased with a concomitant increase in PAC. Sar1-Ile8-angiotensin II induced a significant increase in PAC and a slight increase in PRA, while no changes were found in PNA and the mean blood pressure. The increase in PNA induced by furosemide was inhibited dose-dependently by Sar1-Ile8-angiotensin II, through PRA and PAC were further increased. There results suggest that an administration of furosemide induced the increase in PNA and the increase in PNA by furosemide might by mediated by the renin-angiotensin system.