Effect of Porous Zirconia Coating on Human Gingival Fibroblasts and Its Mechanism.

Gingival fibroblasts play an important role in the constitution of soft tissue attachment. This study aims to investigate whether porous zirconia coating has a positive effect on promoting human gingival fibroblast attachment. The porous zirconia coating was loaded on zirconia surface by the dip coating method, surface morphology and composition were confirmed by scanning electron microscope and energy dispersive spectrometer; Tested the tensile bond strength by universal testing machine; Tested the surface roughness by roughness analyzer; Human gingival fibroblast proliferation, integrin ß1 and F-actin immunofluorescence staining explored the influence of porous zirconia on the adhesion and proliferation of human gingival fibroblast. Zirconia0.2 group showed spherical zirconia particles with diameters of 3-8 µm are distributed on the surface; The bonding strength of zirconia particle coating group reached 16.1±0.1 MPa, and the surface roughness was 0.715±0.091 µm; In comparison with control group (P < 0.01), the percentage of human gingival fibroblasts adhering to zirconia was markedly higher. In zirconia group, integrin-ß1 and F-actin fluoresced more obvious than in control group. Porous zirconia coating can form a porous structure on the surface and the porous structure can promote the attachment and proliferation of human gingival fibroblast, it will be more beneficial for soft tissue early sealing.

Expression of type-1 plasminogen activator inhibitor in the kidney of diabetic rat models.

INTRODUCTION: Intrarenal coagulation and fibrinolysis are thought to be involved in the pathogenesis of diabetic nephropathy. However, gene expression of fibrinolytic factors in diabetic nephropathy has not been clearly defined. Therefore we determined the gene expression of fibrinolytic factors in the kidneys of diabetic rats. MATERIALS AND METHODS: As a model of type1 diabetes male Sprague-Dawley rats were used. They were divided into three groups: control, streptozotocin (STZ)-induced diabetic, and insulin-treated diabetic. Otsuka Long-Evans Tokushima Fatty (OLETF) rats were used as a model of type 2 diabetes; and Long-Evans Tokushima Otsuka (LETO) rats, as the control. Renal gene expressions of type-1 plasminogen activator inhibitor (PAI-1), tissue-type PA (tPA), and urokinase-type PA (uPA) were examined by real-time PCR. Localization of PAI-1 mRNA was investigated by in situ hybridization. RESULTS: Renal PAI-1 mRNA levels (versus control) were increased by 60-80% in STZ-induced diabetic rats (10 days or 3 weeks post STZ injection); and insulin treatment reduced this increased expression to the control level. In OLETF rats (38 weeks old), the renal PAI-1 mRNA level was 2.5-fold higher than that in age-matched LETO rats. Both tPA and uPA mRNA levels were significantly lower than those in LETO rats. PAI-1 mRNA was observed in intraglomerular cells and tubular epithelial cells of both models. CONCLUSIONS: Renal PAI-1 gene expression is up-regulated in both type 1 and type 2 diabetic rats, and changes in gene expressions of fibrinolytic factors may play important roles in the development and pathogenesis of diabetic nephropathy.

Clinical profiles and outcomes of end-stage renal failure patients with late initiation of renal replacement therapy based on uremic symptoms under intensive renoprotective therapies.

AIM: This study describes the clinical profiles and outcomes of renal failure patients with late initiation of renal replacement therapies (RRT) based on uremic symptoms under intensive treatment prior to the start of RRT (IT). METHODS: Thirteen patients (male 10, female 3) with end-stage renal disease who preferred to wait for the initiation of RRT until uremic symptoms appeared regardless of serum creatinine (s-Cr) and 24-hour creatinine clearance (24-hour Ccr) were chosen. All patients received IT including a low-protein diet, antihypertensive drugs including enalapril, erythropoietin and others to prevent and manage uremic states until the initiation of RRT. Clinical findings at the initiation of RRT and the outcomes after the start of RRT were examined. RESULTS: RRT was initiated 23.6 +/- 16.9 months after IT without any complication in all patients when mild uremic symptoms appeared. Uremic symptoms, blood pressure, serum albumin, potassium, calcium and urinary Cr excretion were well controlled except inorganic phosphate, hemoglobin and cardiac size. 24-hour Ccr and s-Cr were 3.4 +/- 0.7 ml/min and 17.4 +/- 3.8 mg/dl at initiation of RRT. The outcomes of all the patients were all well during chronic RRT. CONCLUSION: Intensive treatment prior to the start of RRT can diminish uremic symptoms and complications so that RRT might be initiated safely and with fewer problems, even in the face of lower 24-hour Ccr and markedly higher s-Cr.