Objective: To investigate the effect of PKG II (cGMP-dependent protein kinase II) on cell proliferation-related MAPK (mitogen-activated protein kinase)/ERK (extracellular signal-regulated kinase) downstream targets RSK1 (ribosomal S6 kinase 1) and proto-oncogenes c -Jun and c -Fos in gastric cancer SGC-7901 cells. Methods: Gastric cancer SGC-7901 cells were infected with Ad-LacZ and Ad- PKG II adenovirus, and then the PKG II was overexpressed in SGC-7901 cells. These cells were treated with PKG II specific activator - 8-pCPT-cGMP [8-(p-chlorophenylthio)-cyclic GMP], and then they were stimulated with EGF (epidermal growth factor). The proliferation of SGC-7901 cells was examined by MTT method, and the mRNAs expression levels of c-Jun and c-Fos and the protein expression levels of p-RSK1, c-Jun and c-Fos were examined by RT-PCR and Western blotting, respectively. The nuclear accumulation of p-RSK1 was observed under an immunofluorescence microscope. Results: EGF-induced increase of cell proliferation and the elevation of expressions of c-Jun and c-Fos mRNAs and proteins as well as p-RSK1 (Ser380-) protein in SGC-7901 cells which were infected with PKG II were significantly inhibited after treatment with 8-pCPT-cGMP. The phosphorylation of RSK1 (Ser380) was decreased, and the accumulation of p-RSK1 (Ser380) in nuclei of SGC-7901 cells was increased after stimulation with EGF, while it was decreased after treatment with 8-pCPT-cGMP. Conclusion: Activated PKG II can inhibits the proliferation of gastric cancer cells, phosphorylation of RSK1 (Ser380), nuclear accumulation of p-RSK1(Ser380) and the expressions of c -Jun and c -Fos genes which were induced by EGF. Copyright © 2012 by TUMOR.

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 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.

Female ; Fluoroscopy ; Humans ; Intubation, Intratracheal ; Male ; Middle Aged ; Tracheotomy ; methods

Adolescent ; Adult ; Aged ; Electrodes ; Epistaxis ; surgery ; Female ; Hemostasis, Endoscopic ; methods ; Humans ; Male ; Middle Aged ; Young Adult

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 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.

Background and Objective:Nitric oxide (NO) is involved in many physiologic and pathologic processes.As an important biologic mediator, NO has been the focus of cancer study for its function in tumorigenesis. Tumor progression.and death.This study investigated the effect of NO donor sodium nitroprusside(SNP)on the growth and proliferation of gastric cancer cell line AGS.Methods:The growth inhibition of AGS cells was analyzed by MTT assay.The cell cycle was measured using flow cytometry.The changes of mRNA expression of proliferating cell nuclear antigen (PCNA) and caspase-3 were examined by reverse transcriptase polymerase chain reaction (RT-PCR), and the protein expressions of PCNA and caspase.3 were analyzed by Western blot. Results:Dose-dependent SNP inhibited cell growth and proliferation.When the AGS cells were treated with SNP at 100,500,1000,1500,and 2000 μmol/L for 24 h.the growth inhibition rates were(2.02±2.96)%,(10.82±2.21)%,(18.95±3.35)%,(26.88±2.54)%,and(42.57±1.27)%,respectively(P<0.05).SNP altered the cell cycle in AGS cells.Compared with the control group,treatment with SNP at 100,500,1000,1500,and 2000 μmol/L for 24 h reduced the number of cells in the S phase by 2.29%,7.8%,11.34%,20.49%, and 23.6%,respectively, and enhanced the number of cells in the G_1/G_0 phases by 3.33%,9.3%,13.46%,21.37%,and 24.73%,respectively(P<0.05).With the increasing concentration and action time of SNP,the expressions of PCNA mRNA and protein decreased.The expression of caspase.3 mRNA remained unchanged,but procaspase-3 was activated.Conclusions:NO not only inhibits cell growth and proliferation, but also induces apoptosis in gastric cancer cells, and such effects of NO showed significant dosedependent activity.