Cellular regulation of anti-nRNP antibody synthesis is different from that of anti-DNA antibody synthesis in patients with systemic lupus erythematosus

Summary The cellular regulation of anti-nuclear ribonucleoprotein (nRNP) antibody synthesis in patients with systemic lupus erythematosus (SLE) was examined and compared with that of anti-double-stranded DNA (dsDNA) antibodies. In vitro antibody production by lymphocytes from SLE patients with antibodies to either dsDNA or nRNP alone was measured using dsDNA-specific and nRNP-specific solid-phase radioimmunoassays (RIA). Lymphocytes of SLE patients with only anti-dsDNA antibodies and normal individuals failed to synthesize anti-nRNP antibody with or without nRNP stimulation. In contrast, lymphocytes from SLE patients with anti-nRNP antibody alone in their sera synthesized in vitro a large amount of anti-nRNP antibody with or without nRNP stimulation. Experiments with reconstituted autologous lymphocytes indicated that B cells and T cells were required for anti-nRNP antibody synthesis. As expected, helper function for antibody synthesis by autologous B cells resided in the T4-cell population and suppressor function in the T8-cell population. T8 cells from SLE patients with anti-nRNP antibody alone suppressed anti-nRNP antibody synthesis by autologous B cells irrespective of clinical activity. This is in contrast to anti-dsDNA antibody production, which was not suppressed by autologous T8 cells. These results indicate that the cellular regulation of anti-nRNP antibody synthesis in SLE is different from that of anti-dsDNA antibody syntheis. Increased anti-nRNP antibody synthesis may be due to increased T4-helper cell function rather than defective T8-suppressor function.     

Surface morphology smoothing of a 2 inch-diameter GaN homoepitaxial layer observed by X-ray diffraction topography

We investigated the surface morphology changes in a 2 inch-diameter, c-plane, free-standing GaN wafer using X-ray diffraction topography in a grazing-incidence geometry. We observed a decrease in the peak intensity and increase in the full width at half maximum of the GaN 11$\bar{2}$4 Bragg peak after the deposition of a homoepitaxial layer on the same GaN wafer. However, the lattice plane bending angles did not change after homoepitaxial layer deposition. Distorted-wave Born approximation calculations near the total external reflection condition revealed a decrease in the X-ray incidence angle of the 11$\bar{2}$4 Bragg peak after the homoepitaxial layer deposition. The decrease in both X-ray penetration and incidence angle induced broader and weaker diffraction peaks from the surface instead of the bulk GaN.

We investigated the surface morphology changes in a 2 inch-diameter, c-plane, free-standing GaN wafer using X-ray diffraction topography in a grazing-incidence geometry.     

Probucol and atorvastatin decrease urinary 8-hydroxy-2'-deoxyguanosine in patients with diabetes and hypercholesterolemia

To clarify whether probucol and statins suppress oxidative stress in diabetic patients, we studied the effects of probucol and the statin atorvastatin on urinary 8-hydroxy-2'deoxyguanosine (8-OHdG) levels in diabetics with hypercholesterolemia. A randomized, open study was performed on a total of 36 patients with type 2 diabetes and hypercholesterolemia. The patients were randomly assigned to a probucol group (500 mg/day, n = 18) or an atorvastatin group (10 mg/day, n = 18). During three months, total- and LDL-cholesterol decreased significantly in both groups. LDL-cholesterol was significantly lower in the atorvastatin group than probucol group. HDL-C decreased significantly in the probucol group and did not change in the atorvastatin group. 8-OHdG decreased significantly in both groups after 3 months; 12.4 +/- 7.5 to 8.1 +/- 4.2 ng/mg/Cr in the atorvastatin group (p < 0.05) and 12.3 +/- 8.8 to 6.8 +/- 2.6 ng/mg/Cr in the probucol group (p < 0.05), and these changes did not differ significantly between the two groups. But, in patients with high 8-OHdG levels (more than 10 ng/mg/Cr) before administration, urinary 8-OHdG decreased significantly from 19.5 +/- 4.9 to 9.2 +/- 3.4 ng/mg Cr (p < 0.01) in the atorvastatin group, and from 19.7 +/- 8.2 to 6.67 +/- 2.2 ng/mg Cr (p < 0.01) in the probucol group. Urinary 8-OHdG was significantly lower in the probucol group than in the atorvastatin group after the second and third months of administration (p < 0.05). These results suggest that while probucol and atorvastatin both reduce systemic oxidative stress, probucol might be the more useful in patients with strong oxidative stress.     

Short-term outcomes of local correction of stoma prolapse with a stapler device

Background

The aim of the present study was to classify the short-term outcomes of local correction of stoma prolapse with a stapler device.

Methods

The medical records of 11 patients undergoing local correction of stoma prolapse using a stapler device were retrospectively reviewed.

Results

No mortality or morbidity was observed after the surgery. Median operative time was 35 min (range 15–75 min), and blood loss was minimal. Median duration of follow-up was 12 months (range 6–55 months). One of the 11 patients had a recurrent stoma prolapse.

Conclusions

This technique can be a feasible, safe and minimally invasive correction procedure for stoma prolapse.     

Treatment with anti-TNF-α antibody infliximab reduces serum IL-15 levels in patients with rheumatoid arthritis

The aim of this study was to analyze the change of serum cytokines and pentosidine levels in patients with rheumatoid arthritis (RA) by infliximab treatment. Twenty-three patients with RA were studied for 30 weeks on the effects of infliximab treatment. Serum levels of IL-15, IL-16, IL-17, and granulocyte–macrophage colony-stimulating factor (GM-CSF) were measured with ELISA methods and pentosidine levels were determined using high-performance liquid chromatography, both at baseline and at 14 and 30 weeks after the initial treatment with infliximab. In addition, the patients also underwent physical and routine blood examinations. The higher levels of serum IL-15 in RA patients before treatment with infliximab significantly decreased at 14 and 30 weeks after the initial treatment with infliximab, but serum IL-16, IL-17, GM-CSF, and pentosidine levels did not decrease. The serum IL-17 and GM-CSF levels remained to be a limited detectable level at the pre- and posttreatment with infliximab. Infliximab treatment significantly lowered the serum levels of IL-15 in patients with RA. IL-15 is one of the crucial cytokines affected by infliximab.     

Oral administration of taurine improves experimental pancreatic fibrosis

Background and Aim: The mechanism of pancreatic fibrosis is unclear. Taurine is used in the clinical treatment of a wide variety of diseases, but its effect on improving pancreatic fibrosis is unknown. We examined whether a diet with added taurine improves pancreatic fibrosis induced by dibutyltin dichloride (DBTC) in an experimental chronic pancreatitis rat model. In addition, we examined the influence of taurine on pancreatic stellate cells. Methods: Pancreatic fibrosis was induced by DBTC. Rats were fed a taurine‐containing diet or a normal diet and were killed at 4 weeks. Pancreatic stellate cells were isolated from male Wistar rats. Cultured pancreatic stellate cells were incubated with or without taurine chloramine. Type I collagen and transforming growth factor‐β1 secretion was evaluated by ELISA, and matrix metalloproteinase activity was assessed by gelatin zymography. Interleukin‐6, interleukin‐2, and transforming growth factor‐β1 levels in the supernatants of pancreatic tissue homogenates were measured. Results: Pancreatic fibrosis induced by DBTC was improved remarkably by the oral administration of the taurine‐containing diet. Taurine chloramine decreased type I collagen, transforming growth factor‐β1, and matrix metalloproteinases 2 of the pancreatic stellate cell culture supernatant. Increased interleukin‐6 and decreased interleukin‐2 were found in the supernatants of the pancreatic tissue homogenates of DBTC‐induced pancreatitis rats compared with other groups. Conclusion: The oral administration of taurine improves pancreatic fibrosis. Taurine chloramine inhibits transforming growth factor‐β1 produced from activated pancreatic stellate cells and improves pancreatic fibrosis.     

Regulation of circulating immune complexes by complement receptor type 1 on erythrocytes in chronic viral liver diseases

BACKGROUND AND AIM: Complement receptor type 1 (CR1) is a transmembrane protein, and human erythrocyte CR1 (E-CR1) is involved in the transport of circulating immune complexes (IC) from the circulation to the reticuloendothelial system, including the liver and spleen. In chronic viral hepatitis, increased levels of IC containing viral particles and an association with various extrahepatic manifestations have been reported. However, regulatory mechanisms for IC levels are not fully understood. PATIENTS/SUBJECTS AND METHODS: We analysed IC, E-CR1, and quantitative polymorphism of the CR1 gene in 149 patients with chronic viral liver diseases and in 64 normal blood donors using an enzyme linked immunosorbent assay, radioimmunoassay, and polymerase chain reaction-restriction fragment length polymorphism, respectively. We also analysed the effect of CR1 gene polymorphism on IC binding to E-CR1 using molecular methods. RESULTS: E-CR1 levels in patients with chronic hepatitis and chronic viral liver diseases as a whole correlated inversely with increased levels of IC. Moreover, significantly high levels of IC were observed in patients with chronic hepatitis C (CH-C) who were homozygous for the E-CR1 low density allele. We also found low levels of E-CR1 in liver cirrhosis and CH-C but not in CH-B. Low levels of E-CR1 in CH-C were observed, even after considering the polymorphism of the CR1 gene. Finally, we demonstrated CR1 gene polymorphism dependent binding of hepatitis virus containing IC. CONCLUSIONS: Our results emphasise the important role of E-CR1 in clearance of IC from the circulation and the acquired, rather than inherited, decrease in E-CR1 in chronic viral liver diseases, especially of type C.