Objective To investigate the association of vascular calcification,fetuin A and Creaction protein (CRP),and explore the influence on cardiovascular events.Methods Sixty peritoneal dialysis (PD) patients were enrolled in this study.Carotid intima-media thickness (cIMT),fetuin A and CRP,along with the other serum related parameters were detected to find out their influence on vascular calcification in PD patients.The relationship between cIMT,fetuin A,CPR and cardiovascular events was analyzed in PD patients with 18 months followed-up.Results Of the 60 PD patients,carotid intima-media thickness (cIMT) was increased in 38 patients(63.3％).Compared with the non-increased cIMT patients,serum fetuin A concentration was significantly decreased(P ＜ 0.05),CRP(P＜0.01) and calcium × phosphate products(P＜0.05) were significantly increased in the highincreased cIMT group.Compared with the low-increased cIMT patients,fetuin A concentration was obviously lower(P ＜ 0.05) and calcium×phosphate products were obviously higher(P ＜ 0.05) in the highincreased cIMT group.Linear regression analysis discovered an obvious negative correlation between CRP and fetuin A(R2 =0.629,F=47.522,P ＜ 0.01),as well as fetuin A and calcium×phosphate products (R2=0.299,F=11.948,P=0.002).Multiple regression analysis indicated that fetuin A was independently negatively correlated with cIMT(B=-0.019,t =-6.042,P ＜ 0.01).At 18 months,there were 36 newly-happened cardiovascular events and among which 6 cases died.Logistic regression analysis found that increased cIMT was risk factor to cardiovascular events in PD patients(OR=3.691,95％CI 1.467-9.258,P=0.006).Conclusion Decreased fetuin A and increased calcium×phosphate products deteriorate carotid calcification in PD patients.Micro-inflammation of PD patients represented by high CRP levels may increase calcium×phosphate products by depressing the fetuin A level,and in the end will stimulate carotid calcification.Increased cIMT is a risk factor for cardiovascular events.

Objective To investigate the expressions of NBS1 mRNA and protein in the salivary gland of irradiated rats and explore the role of NBS1 in the repair of radiation injury of salivary gland epithelial cells.Methods Eighty rats were randomly divided into two groups for radiation and control (n =40 each).The rats were fractionally exposed to 3 Gy of 60Co γ-rays once in two days,leading to an accumulation dose of 3,6,9,12,15 Gy.The sham-irradiated controls were anesthetized in parallel but without irradiation.After 2-4 h of irradiation,the rats were sacrificed,IHC and RT-PCR were used to detect the expressions of NBS1 protein and mRNA in parotid and submandibular glands,and the ultra-structural changes in the glands were observed by a transmission electron microscopy.Results After irradiation,the salivary glands became atrophy and the parotid gland cells were damaged more serious than the submandibular gland cells.Compared with the controls,with the groups of dose,at 9,12,15 Gy in parotid gland (t =7.10,17.93,20.86,P ＜ 0.05),at 12,15 Gy in the submandibular gland (t =3.13,7.53,P ＜0.05),the expression of NBS1 mRNA was reduced.With the groups of dose at 9,12,15 Gy in paretid gland (t =4.29,17.91,91.29,P ＜ 0.05 ),the dose at 12,15 Gy in submandibular gland ( t =4.61,11.84,P＜0.05),the expression of NBS1 protein in serous cells,and the dose at 12,15 Gy in parotid gland ductal epithelial cell ( t =3.09,5.62,P ＜ 0.05) were reduced.But in the ductal epithelial cells as well as muoass cells in the submandibualr gland were steadily.Conclusions After irradiation,NBS1 at both protein and mRNA levels was dropped in the salivary gland of rats,which might contribute to the repair of radiation injury of salivary gland.

Objective To investigate T-bet mRNA expression on peripheral blood mononuclear cells (PBMCs) and its relations with allergen specific IgE (SIgE), eosinophile cationic protein (ECP) levels, and allergic symptom in patients with allergic rhinitis (AR). Methods The allergen, SIgE, and ECP in serum of patients with AR were detected by Unicap CAP system. Blood samples were taken from 15 healthy controls and 35 house dust mite allergic patients. PBMC was isolated by density gradient centrifugation and one part of them was cultured with mite allergen at a concentration of 50 μg/mL. PBMC was subjected to analysis of T-bet mRNA expression using semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR). Results The ratio of T-bet to β-actin mRNA levels was 0.418 ± 0. 101 in patients of AR and 0.706 ± 0.091 in healthy controls and the difference was significant (P ＜ 0.01). The expression intensity of T-bet mRNA was not related to varying severity of allergic symptom and ECP levels ( r = - 0.227, - 0.033, P ＞ 0.05). However, there was an inverse correlation between expression intensity of T-bet mRNA and SIgE concentration (r = -0.375, P ＜ 0.05). There was a positive correlation between SIgE and allergic symptom scores ( r = 0.426, P ＜ 0.05). After that PBMC was stimulated by mite allergen, the expression intensity of T-bet mRNA, ECP, and SIgE changed very little ( P ＞ 0.05). Conclusion Down-regulated expression of T-bet mRNA in mite-AR patients is not related to serum ECP and symptom scores but one of important links in the mechanism of imbalance of Th1/Th2 in the occurrence of AR. Specific allergen has no effect on T-bet mRNA, ECP, and SIgE of children and adults with AR in vitro. The level of SIgE objectively and directly indicates the severity of allergic symptom, but T-bet did not. T-bet may be one of indirect factors which affect the level of IgE.