Increased expression of CD40 ligand by peripheral blood mononuclear cells in patients with systemic lupus erythematosus

AIM:To investigate expression and function of CD40 ligand by peripheral blood mononuclear cells (PBMCs) in patients with systemic lupus erythematosus (SLE).METHODS:Expression of CD40 ligand by PBMCs in patients with SLE and control were examined by flow cytometric analysis before and after stimulated by phytohemagglutinin(PHA)and depressed by Dexamethasone(Dex). The correlation between expression of CD40 ligand and SLE activity index(SLEDAI) was analysed in patients with SLE.RESULTS:The expression of CD40 ligand by PBMCs in patients with active SLE was higher than that in patients with inactive SLE and control. Though the expression of CD40 ligang by PBMCs could be stimulated by PHA in three groups, it was the highest in patients with active SLE. Dex depressed the expression of CD40 ligand by PBMCs significantly in patients with SLE, but not in control. There was high positive correlation between expression of CD40 ligand and SLEDAI in patients with active and inactive SLE.CONCLUSION:Increased expression of CD40L by PBMCs in patients with SLE may play an important role in pathogenesis of SLE.     

Expression and role of CD134 and NF-κB in renal tissue of lupus nephritis

AIM:To investigate the role of CD134 (OX40) and NF-κB in the pathogenesis of lupus nephritis (LN).METHODS:Renal in situ CD134 and NF-κB expression were examined in 40 biopsy specimens from LN patients by immunohistochemistry and microwave-based immunohistochemistry, respectively. The relationship between expression of CD134 and NF-κB was analyzed.RESULTS:The expression of glomerular and tubular CD134 and NF-κB in LN were higher than that in normal control, especially in class Ⅳ LN, where there was intense staining of endothelial cell, distal tubules, and interstitial mononuclear cell. The CD134 expression of glomerular and tubular was closely related to NF-κB expression, respectively (r=0.5542, P＜0.05;r=0.6279, P＜0.05). CONCLUSIONS:The abnormal expression of costimulatory molecule CD134 was well evidenced in LN. Strong expression of renal in situ NF-κB was likely mediated by CD134 signal pathway, which may play an important role in the pathogenesis of LN.     

Effects of FK506 on anti-glomerular basement membrane nephritis in rats

AIM:To investigate the effects of FK506 on anti-glomerular basement membrane(GBM) nephritis in rats. METHODS: Anti-GBM nephritis model was elaborated by rabbit anti-rat GBM antibody injection in SD rats in this study. The rats were divided into three groups: FK506 treated group(0.5 mg·kg^-1·d^-1, sc), untreated nephritis control group and normal control group. FK506 was administered daily six hours after injection of anti-GBM IgG. All the rats were observed urinary protein at the 4th day, the 14th day and the 21st day. At the same time, the kidney specimens were collected, and T cell transforming function was also monitored.RESULTS:Rats injected with rabbit anti-GBM Ab developed heavy proteinuria by 4 days, and serum creatinine and serum urea appeared which kept on the rising. Glmerular hypercellularity, crescents, and protein casts were observed in nephritic rats. By electron microscopy, the thickening of GBM and loss of foot processes were seen. T cell transforming function was higher than normal. But, all pathological changes obviously turned for the better in FK506 treated group. CONCLUSION:FK506 could inhibit the progression of rat anti-GBM nephritis.     

鸡肾型传染性支气管炎病毒的分离鉴定

从安徽省巢湖地区鸡群中出现的以肾肿大为主要特征的呼吸道疾病的病例中分离到1株病毒,易感雏鸡,病死鸡出现肾肿大、苍白呈花斑状、大量尿酸盐沉积;鸡胚连续盲传至第5代时开始出现死亡和侏儒胚.电镜观察可见80～120nm的病毒颗粒.分离病毒在鸡胚上可干扰新城疫病毒clone-30株的增殖.上述试验证实所分离的病毒为鸡肾型传染性支气管炎病毒,暂定名为NIBV-AH99.     

Impaired female fertility in tubulointerstitial antigen-like 1-deficient mice

Tubulointerstitial nephritis antigen-like 1 (Tinagl1, also known as adrenocortical zonation factor 1 [AZ-1] or lipocalin 7) is a matricellular protein. Previously, we demonstrated that Tinagl1 expression was restricted to extraembryonic regions during the postimplantation period and detected marked expression in mouse Reichert’s membranes. In uteri, Tinagl1 is markedly expressed in the decidual endometrium during the postimplantation period, suggesting that it plays a physical and physiological role in embryo development and/or decidualization of the uterine endometrium during pregnancy. In the present study, in order to determine the role of Tinagl1 during embryonic development and pregnancy, we generated Tinagl1-deficient mice. Although Tinagl1^–/– embryos were not lethal during development to term, homologous matings of Tinagl1^–/– females and Tinagl1^–/– males showed impaired fertility during pregnancy, including failure to carry pregnancy to term and perinatal lethality. To examine ovarian function, ovulation was induced with equine chorionic gonadotropin (eCG) and human chorionic gonadotropin (hCG); the number of ovulated oocytes did not differ between Tinagl1^–/– and Tinagl1^flox/flox. In vitro fertilization followed by embryo culture also demonstrated the normal developmental potential of Tinagl1-null embryos during the preimplantation period. Our results demonstrate that Tinagl1 deficiency affects female mice and results in subfertility phenotypes, and they suggest that although the potential of Tinagl1^–/– oocytes is normal, Tinagl1 is related to fertility in adult females but is not essential for either fertilization or preimplantation development in vitro.     

Persistent Hematuria as a Result of Chronic Renal Hypertension Secondary to Nephritis in a Stallion

A 13-year-old Lusitano stallion was referred to our institution with a history of severe hematuria for 8.5 months. The origin of the hematuria was determined to be the left kidney. The diagnostic workup failed to identify obstructive, infectious, or neoplastic conditions. The history and ultrasonographic examination suggested a chronic condition. The stallion was subjected to left nephrectomy because of the persistent hematuria and anemia. A histopathological examination detected lesions, which were compatible with chronic nephritis and vascular renal hypertension. It is hypothesized that changes in the normal parenchymal architecture produced a vascular aberration that led to renal hypertension, with subsequent blood extravasation and hematuria. The horse recovered completely after nephrectomy.     

Rapamycin markedly slows disease progression in a rat model of passive Heymann nephritis

AIM：To determine the effect of rapamycin on the progression of passive Heymann nephritis (PHN), and whether autophagy is involved in this process. METHODS：Male Sprague-Dawley rats (n=24) were randomly divided into 3 groups: control group, PHN group and rapamycin treatment group. The rat PHN model was induced by injection of anti-Fx1A serum through penile vein, and all rats were sacrificed on day 21. Automatic biochemical analyzer was used to detect 24 h urine protein, blood urea nitrogen and serum creatinine. Renal damage was observed through per-iodic acid-silver methenamine staining. The number of podocyte was estimated by Weibel-Gomez method. The glomerular deposition of C5b-9, the expression of caspase-3 and expression of autophagy marker LC3 in glomeruli were examined by immunofluorescence staining, immunohistochemical staining and Western blotting, respectively. RESULTS：Rapamycin significantly reduced proteinuria in the PHN rats (P<0.05), while the renal functions in 3 groups were normal, without significant difference. Although rapamycin limited weight gain in the rats, the health of the rats during drug treatment was not affected. Rapamycin retarded glomerular basement membrane thickening in the PHN rats. Rapamycin significantly reduced the podocyte deletion by preventing podocyte apoptosis. Rapamycin enhanced the level of autophagy of glomerular inherent cells. CONCLUSION：In the disease process of PHN, appropriate strength of autophagy plays a protective role. Rapamycin appropriately enhances autophagy and prevents podocyte apoptosis, thus reducing nephropathy and proteinuria. This may be one of the important mechanisms of rapamycin to slow down the progress of PHN.     

The role of TF-1 cell apoptosis-related gene 19 in systemic lupus erythematosus

AIM:To clarify the role of new apoptosis-related gene, TF-1 cell apoptosis-related gene 19(TFAR19), in the pathogenesis of systemic lupus erythematosis (SLE) and the relationship between TFAR19 and SLE.METHODS:DNA Ladder detection, Western blotting, immunological fluorescence method, ELISA and so on were used to test if ultraviolet B(UVB) could induce HaCaT cell apoptosis and TFAR19 expression.RESULTS:HaCaT cell apoptosis could be detected after 24 hours of 30 mj/cm² UVB irradiation. Also, we found that in active SLE patients, the TFAR19 antibody was increased, but not significant compared to the normal control.CONCLUSION:TFAR 19 is involved in the process of UVB induced ketatinocyte line HaCaT apoptosis and SLE pathogenesis.     

Effect of Natural Feed,Antibiotics, Tannin,Diphenyliodoniumchloride and Salicylic Acid Supplement on Plasma Uric Acid Concentration in Captive Willow Ptarmigan (Lagopus L. Lagopus)

Mortality due to nephritis and uric acid diathesis was observed during the fall and winter in captive willow ptarmigan. The present study examined how feed protein concentration influences feed and water consumption, plasma uric acid concentration, and mortality due to nephritis and uric acid diathesis in captive w^rillow ptarmigan. An increase in feed protein concentration from 14 to 24 % resulted in reduced feed consumption and increased plasma uric acid concentration. Mortality due to nephritis and uric acid diathesis was not influenced by variations in feed protein concentration, but an admixture of 14 % grass meal to the diet reduced the incidence markedly.