This study investigated the relation between periodontal condition and biting ability in a Chinese population using the pressure-detecting sheet. A total of 142 subjects residing in Nanchang, Jiangxi province, China, participated in the study. The examination included probing pocket depth (PD), clinical attachment level (CAL), bleeding on probing and coronal caries teeth. Biting abilities per person, biting force, biting pressure and occlusal contact area were measured using the sheet. Number of teeth present showed positive correlation with biting force and occlusal contact area, but were negatively correlated with biting pressure. No significant correlation was observed between the mean PD, percentage of pocket > or = 4 mm, bleeding index and any of biting abilities. The mean CAL showed a significantly negative correlation with biting force and occlusal contact area. Multiple stepwise regression analysis selected the number of teeth present, sex and age as the significant factors affecting the biting ability. However, no periodontal indices were picked up as the significantly contributing factor. There appears to be little effect of periodontal condition on biting ability. Ageing was selected as a contributing factor to reduction in the Chinese adults, but not in the Japanese population.

Proteinuria in passive Heymann nephritis (PHN) results from complement-mediated glomerular injury, since complement depletion with cobra venom factor (CVF) prevents proteinuria. However, there are no comprehensive morphological studies identifying the sites of injury leading to onset of proteinuria. To address this issue, we attempted to locate sites of injury involved in the onset of proteinuria in PHN. PHN was induced in intact Munich-Wistar rats (PHN-rats, examined at days 3, 5, and 7) and in complement-depleted rats (CVF treated, PHN-CVF-rats, examined at days 3 and 5). The distribution of endogenous albumin in the glomerular basement membrane (GBM) was studied in in situ drip-fixed glomeruli using immunogold immunocytochemistry, and glomerular anionic sites were visualized by polyethyleneimine staining. In addition, the ultrastructural localization of an epitope recognized by a proteinuria-inducing monoclonal antibody (called 5-1-6) directed against the slit diaphragm was examined. Significant proteinuria was seen in intact PHN-rats, starting at day 5. The intensity of gold labeling for endogenous albumin was significantly increased at the outermost site of the GBM (GBM interfacing foot process and the filtration slit, designated area O) at day 3 in both PHN-rats and PHN-CVF-rats in comparison to untreated controls. At day 5, labeling for albumin in area O was decreased in PHN-rats, but not in PHN-CVF-rats, where it was then higher; in PHN-rats, some areas between epithelial cells and subepithelial deposits were almost free of albumin labeling at day 7. There was no evidence of epithelial cell detachment in any group at day 5, but on day 7 limited focal detachment was seen exclusively in PHN-rats. In proteinuric rats, amorphous material that stained for albumin could be seen in the urinary space, without any exocytosis of labeling by glomerular epithelial cells. A significant reduction of intensity of staining for anionic sites was seen in parallel in both groups, but only in the regions of the lamina rara externa adjacent to subepithelial deposits. This local loss of charge might contribute to enhanced permeability to albumin in both PHN- and PHN-CVF-rats. Changes in the appearance of the filtration slits and in the density and distribution of antigen recognised by monoclonal antibody 5-1-6 were similar in PHN- and PHN-CVF-rats at day 5. Complement depletion prevented neither the reduction in anionic sites of the GBM nor the changes in the slit diaphragm observed. These data suggest that albumin leakage between the epithelial cell and the GBM (area O) could occur in PHN-rats, perhaps as a result of epithelial foot-process changes. This may be the final link in the chain of events responsible for the onset of proteinuria in PHN.

Plasma ghrelin level is influenced by Helicobacter pylori (H. pylori) status and the severity of gastric mucosal atrophy, and the ghrelin level is associated with nutrition status in hemodialysis patients. Here, we investigated the efficacy of H. pylori eradication therapy in improving nutrition status in relation to the ghrelin level in H. pylori-positive hemodialysis patients. Of H. pylori-positive patients receiving hemodialysis at 8 dialysis center, 21 patients underwent gastroduodenoscopy for evaluation of the severity of gastric atrophy, and nutrition markers and plasma ghrelin levels before and 1 year after H. pylori eradication therapy were evaluated. Serum cholinesterase level was significantly increased after H. pylori eradication compared with the level before eradication (303.2 ± 76.0 vs 287.3 ± 68.1 IU/L, p = 0.029). In particular, cholesterol (before, 196.6 ± 23.2 mg/dl; after, 206.1 ± 25.9 mg/dl, p = 0.042) and cholinesterase levels (before, 296.9 ± 70.8 IU/L; after, 316.4 ± 73.8 IU/L, p = 0.049) increased more strongly in patients with mild–moderate atrophy than those with severe atrophy, irrespective of improvement of plasma acyl-ghrelin and desacyl-ghrelin levels after eradication therapy. In conclusion, H. pylori eradication may improve nutrition status by increasing serum cholinesterase and cholesterol levels in hemodialysis patients, especially those with mild and moderate gastric mucosal atrophy.

The objective of this study was to review the use of intramedullary supracondylar (IMSC) nails for distal femoral fractures. We reviewed 24 fractures treated with second-generation IMSC nails. The fractures consisted of 18 type A1, one type A2, two type C1, one type C2, and two type C3 fractures. The relationships between clinical results and fracture type, approaches, and patient age were retrospectively reviewed. All fractures healed clinically and radiographically. Twenty-one patients maintained gait performance equivalent to that before injury. Average operating time was 108 min +/- 43 min. ROM in the knee of all patients was -5 degrees +/- 6 degrees in extension and 102 degrees +/- 38 degrees in flexion. Extension lag was influenced by surgical approach. The final knee arc was inversely correlated to patient age (R: 0.49, P<0.05). There were three varus/valgus deformities, two cases with loosening, and two with breakage of the distal locking screws, but no failure of the nail itself. Second-generation IMSC nailing for distal femur fractures was satisfactory in patients younger than 60 years of age.

Background: We have reported that vitamin D deficiency may be implicated in the pathogenesis of hypoalbuminemia observed in patients with end-stage renal disease, but the mechanism remains to be clarified. The aim of the present study was to determine whether supplementation with alfacalcidol might increase protein intake in hemodialyzed patients with hypoalbuminemia. Methods: Twelve patients with hypoalbuminemia under 3.5 g/dl undergoing maintenance hemodialysis and not taking active forms of vitamin D were orally supplemented with 0.5 µg of alfacalcidol daily for 8 weeks. Normalized protein catabolic rate (nPCR), an index of protein intake, and serum concentrations of albumin, interleukin-6 (IL-6), IL-1β, and soluble tumor necrosis factor-α receptor-II (sTNFR-II), an index of tumor necrosis factor-α activity, were determined before and after supplementation with alfacalcidol. Results: Supplementation with alfacalcidol increased nPCR from 0.96 ± 0.20 to 1.16 ± 0.15 g/kg/day (p < 0.005), thereby increasing serum albumin concentration from a baseline of 3.13 ± 0.35 to 3.32 ± 0.29 g/dl (p < 0.05). The baseline serum concentrations of sTNFR-II and IL-6 were markedly elevated, whereas those of IL-1β were under the detection limit. Supplementation with alfacalcidol significantly decreased serum concentration of sTNFR-II from 23.8 ± 4.38 to 19.7 ± 3.93 ng/ml (p < 0.001) but did not alter serum IL-6 concentration. Conclusion: Supplementation with alfacalcidol can increase protein intake and serum albumin concentration in hemodialyzed patients with hypoalbuminemia, probably through the suppressed tumor necrosis factor activity.