Objective To study the relationship between periodontitis and chronic kidney disease (CKD) among Uygur adults of Xinjiang. Methods Data of 1650 Uygur adult residents (age＞18 years) in the Moyu county, Xinjiang were analyzed. The subjects were sampled randomly with stratify capacity from 15 villages among 364 villages. All the subjects received the questionnaire and the oral examination. The markers and risk factors of chronic renal injury were inspected. The subjects were categorized as periodontitis group and non-periodontitis group according to chronic periodontitis diagnostic criteria. The periodontitis group was further divided into mild, moderate and severe periodontitis. Results The data of 1415 subjects were completed. The prevalence of chronic periodontitis was 65.2% (95%CI:65.0-65.4). The prevalence of CKD was 5.2% (95%CI:5.1-5.3). Albuminuria was found in 4.2% (95%CI:4.1-4.3) of subjects. 1.3%(95%CI:1.3-1.4) of individuals had renal insufficiency. In periodontitis group, the prevalence of CKD was 6.4%, which was higher than that in non-periodontitis group 2.9% (χ2=7.841 ,P=0.005).Univariate regression analysis showed that severe periodontitis was risk factor of CKD (OR =3.2,95% CI:2.0-5.2). Multivariate logistic regression analysis showed that severe periodontitis was independently associated with CKD (OR = 1.9, 95%CI: 1.1-3.3). Conclusions In Uygur adults of rural area of Xinjiang, the prevalence of CKD is higher in periodontitis group as compared to non-periodontitis group. Severe periodontitis is an independent risk factor of CKD.

Objective To investigate the possible correlation between chronic periodontitis(CP)and chronic renal failure(CRF)by establishing chronic periodontitis and chronic renal failure model in SD rats. Methods Forty health male SD rats were divided into four groups: control group(A), CP group(B), CRF group(C), CP accompany with CRF group(D). Ten rats were sacrificed in every group at the end of week 8. The periodontal index, levels of serum Scr and BUN, the concentration of IL-1β and TNF-α were examined. The severity CP and CRF was quantified by histopathology. The date was statistically analyzed. Results Animal models were established successfully. Scr and BUN in group D, BUN were higher than that in group C[Scr(120.54±21.29)junol/L vs(93.63±18.82)u,mol/L, BUN(34.20±14.44)mmol/L vs(17.77±4.15)mmol/L, P<0.05]. The kidney change of inflammation was observed in group B, the grade of PAS and Masson in group C and D were higher than that in group A(P<0.01), and that in group D was higher than group C(P<0.05). Obvious inflammation of periodontal tissue was observed in group B and D. Attachment loss level(AL)in group D was higher than that in group B[(173.60± 16.75)μm vs(124.00±23.87)μm, P<0.05]. The level of IL-lβ and TNF-α in group B and C and D were higher than that in group A(P<0.05), and IL-lβ in group D was higher than that in group B and C(P<0.05), TNF-a in group D was higher than that in group B(P<0.05). 2×2 factorial design revealed that there were interactions between CP and CRF on the numerus of Scr and BUN and AL P<0.05), and the influence of each factor on that was significant(P<0.05), no interactions were noted between CP and CRF on IL-1β and TNF-α(P>0.05), but the influence of each factor on that was significant(P<0.05). Conclusions The SD rat models can appear chronic periodontitis and chronic renal failure at the same time. There is correlation between chronic periodontitis and chronic renal failure. Chronic periodontitis can aggravate chronic renal failure throngh the role of inflammation.

Objective To investigate the incidence and risk factors of acute kidney injury (AKI) in patients with multiple soft tissue contusion.Methods A total of 513 patients diagnosed as multiple soft tissue contusion in the First Affiliated Hospital of Xinjiang Medical University from January 1,2008 to January 1,2013 were retrospectively analyzed.Demographics,clinical data and laboratory examinations before and after AKI were collected and analyzed.Results The age of all subjects was 31.30 (12-78) years old with the male to female ratio of 2.1∶ 1.AKI occurred in 74 cases with an incidence rate of 14.4％.No AKI was observed in patients with assault injuries,while AKI was found in 27 cases (36.5％) with car accident injuries and 4 cases (5.4％) with other injuries.AKI showed in 1 case(1.4％) with damaged area under 1％,in 4 cases(5.4％) with damaged area ranged from 1％ to ＜ 3％,10 cases (13.5％) with damaged area ranged from 3％ to 5％ and 19 cases (25.7％) with damaged area over 5％ with significant difference among the groups (P ＜ 0.01).Incidence rate of AKI was significantly higher in patients with chronic kidney disease (CKD) than those without CKD (54.5％ vs 20.3％,P ＜ 0.01).Two of the AKI cases died,with a mortality rate of 2.7％.Multivariate logistic regression analysis showed that the followings were the independent risk factors for the occurrence of AKI in patients with multiple soft tissue injuries:age (OR =1.996),basic serum creatinine (OR =0.976),basic evaluated GFR (eGFR) (OR =0.964),serum potassium (OR =2.117),myoglobin (OR =0.950) and damaged area (OR =1.811).Conclusions Incidence rate of AKI is quite high in multiple soft tissue contusion.Age,basic serum creatinine,basic eGFR,serum potassium,myoglobin and damaged area are the independent risk factors for the occurrence of AKI in patients with multiple soft tissue injury.

Objective To analyse the relationship and mechanism between chronic periodontitis (CP) and IgA nephropathy (IgAN) by establishing animal model of chronic periodontitis and IgA nephropathy in SD rats.Methods Eighty health male SD rats were divided into four groups,control group (A,n=20),IgAN group (B,n=20),CP group (C,n=20),CP accompanied with IgAN group (D,n=20).CP model was established by ligating silk suture and besmeared pathogenic bacterium in rats dental cervix.Experimental IgAN model was established by lavage of bovine serum albumin (BSA) and injection of lipopolysaccharide (LPS) and carbon tetrachloride (CCl4).Ten rats were sacrificed in every group at the end of week 8 and 12.The blood,urine,kidney tissue samples were examined.The observation index included proteinuria,kidney and liver function,renal tissue pathology and periodontal tissue pathology.The data were statistically analysed.Results Animal models were established successfully.The levels of Scr and BUN in group A,B,C were not obvious difference,but that in group D was higher than the other third groups at 8 weeks (P ＜ 0.05).The levels of Scr and BUN in group D and group B were significantly higher than that in group A,meanwhile that in group D was significantly higher than that in group B at 12 weeks(P ＜ 0.05).The levels of 24 h urine protein in B,C,D groups were higher than that in group A at 8 weeks(P ＜ 0.05),but at 12 week,that in group D was higher than that in group B and C (P ＜ 0.05).At 8 weeks,glomeruli had little mesangial broadening and renal interstitium had mild hyperplasia of fibrous tissue in group B and D,and that in the group D significantly was heavier than that in group B.The focal varying degrees were glomerular mesangial proliferation hardening,glomerular mesangial broadening,focal segmental sclerosis,and diffuse or focal inflammatory cell infiltration in D group at the end of week 12.The score of PAS between group A and group C had no statistical significance.The scores of PAS in group B and D were higher than that in group A (P ＜ 0.01),and that in group D was higher than that in group B (P ＜ 0.01).Obvious inflammation of periodontal tissue was observed in group C and D,and modified sulcus bleeding index (MBI) were higher than that in group A and B,and MBI in group D was significantly higher than that in group C (P ＜ 0.01).Conclusions The model can be used to research the change of biochemistry and pathology and observe the relationship between chronic periodontitis and IgAN.This study shows that there is relationship between chronic periodontitis and IgAN.Chronic periodontitis maybe make more serious pathology damage in kidney by inflammation mechanism.

OBJECTIVE To investigate the effect of Turkish galls extract (TGE) on the expression of IgA in serum,urine and renal tissue of IgA nephropathy (IgAN) model rats.METHODS Fifty healthy male Sprague Dawley rats were randomly divided into normal control group,IgAN model group,and TGE 75,150 and 300 mg· kg-1 groups,10 rats per group.The model of IgAN rats was established with bovine serum albumin (BSA)+lipopolysaccharide (LPS)+carbon tetrachlorid (CCl4)for 12 weeks.From the 13th week,TGE was ig administrated once a day for 4 weeks.At the end of the 12th and 16th weeks,24 h urine protein was measured by BCA method.At the end of the 16th week,serum and urinary IgA levels were measured by enzyme linked immunosorbent assay(ELISA),serum creatinine(SCR) and blood urea nitrogen (BUN) were detected by an automatic biochemical analyzer,and the renal pathological changes were evaluated with an Oxford classification scoring system.The deposition of IgA immune complex in the kidney was observed by immunofluorescence assay.RESULTS At the end of 12th week,24 h urine protein increased in all IgAN groups (P＜0.05),compared with normal control group.At the end of 16th week,24 h urine protein,IgA content in serum and urine,SCr and BUN content in serum,score in Oxford classification of renal tissue and deposition of IgA immune complex in the kidney in IgAN model group were all higher than in normal control group (P＜0.05).Compared with IgAN model group,24 h urine protein,IgA content in serum and urine and SCr content in serum were decreased in all TGE groups (P＜0.05),and BUN content in serum and deposition of IgA immune complex in the kidney decreased in TGE 150 and 300 mg·kg-1 groups (P＜0.05).The score in Oxford classification of renal tissue was decreased in TGE 300 mg· kg-1 group only.CONCLUSION TGE has curative effect on IgAN model rats by reducing serum and urinary IgA and decreasing IgA immune complex deposition.

Objective To investigate the association of prevalence of periodontitis with metabolic syndrome (MS). Methods Data were analyzed from 1 650 Uygur rural residents in Moyu County. The subjects, aged over 18 years, were sampled randomly from 15 villages out of total 364 villages. Questionnaire, oral examination, and blood biochemical indicators were collected. The subjects were divided into groups with and without periodontitis based on chronic periodontitis diagnostic criteria, and the group with periodontitis was further divided into subgroups, each with mild, moderate, and severe periodontitis respectively. The diagnosis of MS was madeaccording to the definition of the International Diabetes Federation in 2005. Results Among 1 415 subjects whosedata were complete, there were 275 ( 19.4% ) subjects with MS and 934 (66.0%) subjects with periodontitis. The prevalence of MS was higher in the group with periodontitis than that without perionontitis (23.1% vs 12.3%, x2=23.9, P<0. 001 ). The prevalence of MS was increased with the grade of periodontitis, being 19.8%, 20.8%,27.6% in the mild, moderate, and severe periodontitis groups, respectively(x2= 31.9, P<0. 001 ). Multiple logistic regression analysis showed that the risk of MS increased with the grade of periodontitis, with OR 1. 6, 1.7,1.9, respectively, in the groups with mild, moderate, and severe periodontitis compared with that without perionontitis ( P<0.05 or P<0.01 ). Conclusions The prevalence of MS was related to periodontitis in the Uygur nationality and increased with the grade of periodontitis.

OBJECTIVETo investigate the association between pulmonary vascular remodeling and expression of hypoxia-inducible factor-1α (HIF-1α), endothelin-1 (ET-1) and inducible nitric oxide synthase (iNOS) in pulmonary vessels in neonatal rats with hypoxic pulmonary hypertension (HPH).

METHODSA neonatal rat model of HPH was established as an HPH group, and normal neonatal rats were enrolled as a control group. The mean pulmonary arterial pressure (mPAP) was measured. The percentage of medial thickness to outer diameter of the small pulmonary arteries (MT%) and the percentage of medial cross-section area to total cross-section area of the pulmonary small arteries (MA%) were measured as the indicators for pulmonary vascular remodeling. The immunohistochemical reaction intensities for HIF-1α, ET-1 and iNOS and their mRNA expression in lung tissues of neonatal rats were measured. Correlation analysis was performed to determine the relationship between pulmonary vascular remodeling and mRNA expression of HIF-1α, ET-1 and iNOS.

RESULTSThe mPAP of the HPH group kept increasing on days 3, 5, 7, 10, 14, and 21 of hypoxia, with a significant difference compared with the control group (P<0.05). The HPH group had significantly higher MT% and MA% than the control group from day 7 of hypoxia (P<0.05). HIF-1α protein expression increased significantly on days 3, 5, 7 and 10 days of hypoxia, and HIF-1α mRNA expression increased significantly on days 3, 5 and 7 days of hypoxia in the HPH group compared with the control group (P<0.05). ET-1 protein expression increased significantly on days 3, 5 and 7 days of hypoxia and ET-1 mRNA expression increased significantly on day 3 of hypoxia in the HPH group compared with the control group (P<0.05). Both iNOS protein and mRNA expression were significantly higher on days 3, 5 and 7 days of hypoxia than the control group (P<0.05). Both MT% and MA% were positively correlated with HIF-1α mRNA expression (r=0.835 and 0.850 respectively; P<0.05).

CONCLUSIONSPulmonary vascular remodeling is developed on day 7 of hypoxia in neonatal rats. HIF-1α, ET-1 and iNOS are all involved in the occurrence and development of HPH in neonatal rats.

Animals ; Animals, Newborn ; Endothelin-1 ; analysis ; physiology ; Hypertension, Pulmonary ; etiology ; metabolism ; pathology ; Hypoxia ; complications ; Hypoxia-Inducible Factor 1, alpha Subunit ; analysis ; physiology ; Immunohistochemistry ; Nitric Oxide Synthase Type II ; analysis ; physiology ; Pulmonary Artery ; chemistry ; pathology ; Rats ; Rats, Wistar

OBJECTIVETo investigate the effects of histone deacetylase 2 (HDAC2) expression on cell proliferation, apoptosis and migration of laryngeal squamous cell carcinoma (LSCC) Hep-2 cells.

METHODSHDAC2 siRNA and control siRNA were transfected into LSCC Hep-2 cells by lipofectamine 2000, and cells were divided into three experimental groups: untreated group, control siRNA group and HDAC2 siRNA transfection group. Western blotting was utilized to detect the expression of HDAC2 protein in Hep-2 cells. Cell proliferation and apoptosis were investigated by CCK-8 kit and flow cytometry, respectively. Boyden chamber was used to study cell migration. Expressions of cell apoptosis and cell migration related proteins were detected by Western blotting.

RESULTSHDAC2 siRNA significantly down-regulated the expression of HDAC2 protein in LSCC Hep-2 cells. Down-regulation of HDAC2 expression coincided with an inhibition of cell proliferation and migration along with an induced cell apoptosis of Hep-2 cells. Moreover, down-regulation of HDAC2 expression significantly increased the expressions of caspase-3 and caspase-9 proteins but decreased the expressions of matrix metalloproteinases (MMP)-2 and MMP-9 proteins.

CONCLUSIONSHDAC2 may play a pivotal role in the initiation and development of LSCC. Down-regulation of HDAC2 expression mediates cell apoptosis. Cell migration inhibition may be tightly associated with overexpression of caspase-3 and caspase-9 along with down-regulation of MMP-2 and MMP-9 expressions.

Apoptosis ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Caspase 3 ; metabolism ; Caspase 9 ; metabolism ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Down-Regulation ; Histone Deacetylase 2 ; genetics ; metabolism ; Humans ; Laryngeal Neoplasms ; metabolism ; pathology ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; RNA Interference ; RNA, Small Interfering ; genetics ; Transfection

AIM:To investigate the inhibitory effect of apolipoprotein A-I mimetic peptide D-4F on the scaven-ger receptor A1 ( SR-A1 ) in macrophage-derived foam cells induced by oxidized low-density lipoprotein ( ox-LDL ) . METHODS:RAW264.7 cells were pretreated with different concentrations (12.5, 25 and 50 mg/L) of D-4F or 50 mg/L inactive control peptide scrambled D-4F (sD-4F) for 1 h or endoplasmic reticulum stress (ERS) inhibitor 4-phenylbutyr-ic acid (5 mmol/L) for 30 min, followed by the treatment with 100 mg/L ox-LDL for 12 h.In addition, the cells were pre-treated with 50 mg/L D-4F or sD-4F for 1 h, and then stimulated with 2 mg/L tunicamycin (TM;an ERS inducer), for 4 h.The viability of the cells was measured by MTT assay, and the content of intracellular total cholesterol ( TC) was meas-ured by a tissue/cell TC assay.The protein and mRNA levels of SR-A1 and glucose-regulated protein 78 (GRP78) were analyzed by Western blotting and quantitative real-time PCR, respectively.The fluorescence intensity of DiI-ox-LDL in the cells was detected by a multifunctional microplate reader.RESULTS:D-4F significantly reduced ox-LDL-induced macro-phage injury and intracellular cholesterol accumulation, and attenuated the ox-LDL-induced expression of SRA1 and GRP78 in a dose-dependent manner.Additionally, D-4F significantly inhibited the TM-induced protein expression of SR-A1 and GRP78, and attenuated the uptake of ox-LDL by macrophages.CONCLUSION: D-4F reduces ox-LDL-induced macro-phage cholesterol accumulation and injury by inhibiting SR-A1 expression.The mechanism may be related to the inhibition of ERS signaling pathway mediated by GRP78.

OBJECTIVE Metastasis-associated in colon cancer-1 (MACC1) is an oncogene that has been newly identified. It promotes tumor proliferation and invasion via the MET pathway. Our study investigated the effects of Saikosaponin-b(SS-b) on the proliferation and apoptosis of HepG2 cells and its regulation on MACC1/c-Met/Akt signaling pathway. METHODS HepG2 cells were treated with SS-b (10-800 g·L-1) for 48 h in vitro. The CCK-8 assay was used to assess cell proliferation, and cell apoptosis was determined by Hoechst33258 staining, AnnexinⅤ/PI staining and caspase 3 assay. RT-PCR was used to examine the expression of MACC1, c- MET and hepatocyte growth factor (HGF) mRNA. MACC1 protein was detected by Western blot and immunohistochemistry. The protein expressions of p-c-MET, c-MET, p-AKT, AKT, p-BAD, BAD were measured by Western blot. RESULTS SS-b inhibited the growth of HepG2 cells in dose-dependent way and induced cell apoptosis significantly. HepG2 cells showed karyopyknosis, fragmentation and fluorescence highlight in SS-b treatment group. FCM results showed that apoptosis rate of HepG2 cells increased with SS- b concentration. The immunofluores?cence results showed that the MACC1 expression decreased significantly in HepG2 cells treated with SS-b. The expression levels of MACC1, c-MET and HGF mRNA in HepG2 cells were significantly inhibited by SS-b. SS-b also significantly decreased the protein expressions of MACC1, p-c-MET and p-AKT while increased the expression of p-BAD and caspase 3 in HepG2 cells(P<0.05). CONCLUSION SS-b inhibited the proliferation and induced the apoptosis of HepG2 cells by targeting the MACC1/c-Met/Akt signaling pathway.