Objective To analyze the prevalence and economic burden of diabetes in Guandu district of Kunming. Methods We used probability proportional to size (PPS) sampling method to select representative sample of 4595 residents aged 18 or over from this district. Each participant received face to face questionnaire interview and physical examination. We applied different methods to measure the direct,indirect and intangible costs of diabetes. Results In the study population, the overall prevalence of diabetes was 6.2%,and females had higher prevalence of diabetes than males (6.2%vs. 5.6%, <0.05) . The DALY/1000 population of diabetes was 3.52, among which males and females were 5.18 and 6.70, respectively. Mean unit direct costs, indirect costs and intangible costs of diabetes were 3464.49 Yuan,84.48 Yuan and 4 045.97 Yuan,respectively. The total economic burden of diabetes was 401.84 million Yuan. Intangible costs represented the largest component of economic burden of diabetes,followed by direct costs. Conclusion The huge economic burden of diabetes has become the cause for concern in Guandu district. Effective measures are needed to reduce the economic burden of diabetes.

Objective To explore the enhancement effects and mechanisms of IL-32β on human cervical carcinoma cells C33A to hypoxic/hypoglycemic condition.Methods After cultured in hypoxia/hypoglycemic circumstance and normal circumstance for 20 hours respectively, the mRNA and protein expression of IL-32β in C33A cells were detected by real time-polymerase chain reaction (RT-PCR) and Western blotting respectively.Trypan blue stain was used to detect C33A cells viability in hypoxia/hypoglycemic circumstance and adding 10, 100,500 ng/ml IL-32β circumstance.The xenografted tumor of nude mice was established by intraperitoneal injection, and their volumes were tested for a given time after injecting 0, 1.0 mg/kg IL-32β.siRNA was used to construct IL-32β knockdown cells and detect the expression of VEGF.Results Under the hypoxia/hypoglycemic circumstance, the expressions of IL-32β mRNA were (6.12 ± 0.03) times of the normal circumstance (F =43.16, P ＜ 0.05), the expressions of IL-32β protein were (2.23 ± 0.04) times of the normal circumstance (F =22.32, P ＜ 0.05).The C33A cells viability in hypoxia/hypoglycemic circumstance was (51.92 ± 3.41) ％, whereas, viability in 10 ng/ml IL-32β group was (55.23 ± 3.92) ％ (F =14.25, P ＜ 0.05), viability in 100 ng/ml IL-32β group was (62.52 ± 4.14) ％ (F =35.53, P ＜ 0.01), viability in 500 ng/ml IL-32β group was (69.14 ± 2.45) ％ (F =56.28, P ＜ 0.01).After 28 days, the volume of xenografted tumor of 0 mg/kg IL-32β group was (578 ± 64)mm3, and 1.0 mg/kg IL-32β group up to (1 402 ± 142) mm3 (F =27.84, P ＜ 0.01).In addition, compared with control group, the expression of VEGF in IL-32β knockdown C33A cells was significantly decreased (F =36.85, P ＜ 0.05).Conclusion IL-32β can enhance the resistance to hypoxic/hypoglycemic condition of C33A cells, which is associated with the increase of VEGF.

Objective To evaluate the clinical significance of combined measurement of antiperinuclear neutrophil cytoplasmic antibody(ANCA)and anti-saccharomyees cerevisia antibody(ASCA)for the diagnosis of inflammatory bowel disease(IBD)patients and difierentiation of Crohn's disease(CD)with ulcerative colitis(UC).Methods A total of 159 patients with IBD(97 UC,62 CD),167 patients with other non-IBD gastrointestinal conditions(NIBDC)and 25 healthy controls(HC)were recruited in our research.ASCA and ANCA were detected by enzyme-linked immunosorbent assay(ELISA)and indirect immunofluorescence assay.respectively.Results The prevalence of ASCA-IsA or IgG in CD group,UC group,NIBDC and HC were43.5%,14.4%,29.3%and 0,respectively.The prevalence of ASCA-IgA or IgG in CD group were higher than those in other groups(X2=16.76 or 4.12,P＜0.01 or＜0.05).The prevalence of ANCA in CD group.UC group,NIBDC and HC were 8.1%,56.7%,4.8%and 0,respectively.The prevalence of AMA in UC group were much higher than those in other groups(X2=38.08 or 90.47,P＜0.01).The sensitivity specificity and positive predictive value(PPV)in ASCA+/ANCA-were 40.3%.93.8% and 80.6%,respectively,and in ANCA+/ASCA-were 48.5%,98.4% and 97.9%,respectively.Condusions ASCA or ANCA testing alone are not sensitive enoulgh for diagnosing CD and UC,but their combination asses are specific for differential diagnosis between CD and UC.Combined testing of ASCA-IgA with IgG can improve the sensitivity in screening CD patients.The ASCA positive pattern in Chinese CD group are correlated with surgery.

Objective To evaluate the clinical outcomes of severely resorbed edentulous mandibles with tilted implants and fixed prostheses. Methods Ten patients with severely resorbed edentulous mandibles were en-rolled. Each patient received 4 implants,two posteriors placed tilted implants. Immediate loading of tilted implants were applied in all cases using a fixed provisional prosthesis. All patients were finalized 3-4 months with fixed pros-theses. Results 40/40 implants with initial torque(>35N.cm)were followed 1-1.5 years presenting 100%surviv-al. Conclusion The method of using tilted implants and fixed prostheses in the cases of severely resorbed edentu-lous mandibles can achieve an ideal short-term and medium-term effects.

Objective To investigate the differences in gene expression profiles of peripheral blood from patients with Keshan disease (KD) and the apoptosis mechanism in KD,to obtain diagnostic markers and establish diagnostic centroids plot for KD.Methods RNA was isolated from ten patients with KD diagnosed according to the clinical criteria for KD in China and ten health controls.The expression profiles were evaluated by Agilent 4 ×44K Whole Human Genome density oligonucleotide microarray analysis.The data were extracted by Agilent Feature Extraction Software t test,Pathway studio analysis and prediction analysis for microarray (PAM) were used to identify differently expressed genes,gene pathways,diagnostic markers and establish diagnostic centroids plot.Results Totally 1 570 up-regulated genes and 1 498 down-regulated genes were identified.Thirty-eight enrichment pathways were also identified,and the highest ranked by Pathway studio analysis was related to apoptosis.Six genes involved in apoptosis pathway were up-regulated in KD included ataxia telangiectasia mutated (ATM),cAMP-dependent protein kinase,protein kinase A (PKA),baculoviral IAP repeat-containing 2 (BIRC2),NLR family,apoptosis inhibitory protein (NAIP),BCL2-1ike 11 (Bim),BCL2-related protein A1 (BCL2A1) and down-regulated were 7 which included caspase 8 (CASP8),BCL2 binding component 3 (BBC3),BCL2--associated athanogene (BAG1),BCL2-associated X protein (BAX),BCL2-1ike 1 (BCL2L1),BCL2-related ovarian killer (BOK),and caspase 6 (CASP6).Forty-two diagnostic markers were obtained through PAM analysis.Conclusions Apoptosis related to genes and pathways might play an important role in the pathogenesis of KD.Forty-two markers could be used as molecular markers for the diagnosis of KD,which is important to the diagnosis of KD.

Objective To compare the efficacy and safety of tranexamic acid(TA)and norethisterone(NET)for the treatment of patients with ovulatory menorrhagia in China. Methods Onehundred and thirty one patients with proven ovulatory menorrhagia from gynecologic clinics of 5 teaching hospitals located in 4 different cities in China were enrolled during Jul 2004 to Dec 2006.Ameng them 128 completed the study.Patients were randomly divided into two therapeutic regimen groups:TA 1g thrice daily during menstrual cycle days(D)1-5,69 cases;or NET 5 mg twice daily on D19-26.59 cases.The drugs were administered for 2 consecutive cycles,then withdrawn and patients were followed-up for 1 more cycle.Data on menstrual blood loss [ estimated by pictorial blood assessment chart(PBAC)],length of menstrual periods,quality of life(QOL)evaluated by a 6 item health-related questionnaire were collectedbefore,during each cycle and were compared.Results Both treatments led to significant decreases of mean PBAC scores and shorter duration of menstrual periods,and improved the QOL ranking during the twotreatment cycles.The mean percentages of PBAC decrements in the TA first and second cycles were significantly greater than those in the NET corresponding cycles(35%VS 17%,P=0.004;4J4%VS 34%,P=0.04 respectively).The success rate of TA second cycle was higher than that of the NET second cycle (41%VS 24%,P=0.04).Improvement of QOL ranking in the TA first cycle was also significantly better than those in the NET first cycle ( P=0.03).The percentage of patients with at least 1 adverse event in TA group(19%)was significantly lower than that in NET group(35%,P=0.04).Patients'willingness tocontinue the treatment in the TA second and follow-up cycles(94%,79%respectively)were significantly higher than those in the corresponding cycles of NET groups(79%,59%respectively;P=0.01,P=0.02).Conclusion The regimen of TA 3 g daily during menstrual days 1-5 is a more effective and tolerable treatment than luteal phase norethisterone for patients with ovulatory menorrhagia.

OBJECTIVETo observe the effect of nano-Se-chondroitin sulfate on the growth and apoptosis of chondrocytes from patients with Kashin-Beck disease (KBD) exposed to T-2 toxin in vitro.

METHODSSamples of the articular cartilage were obtained from 6 patients with grade II/III KBD diagnosed in line with the National Clinical Diagnostic Criteria of KBD (WS/T 207-2010) for chondrocyte separation and culture in vitro. The separated chondrocytes were treated with synthesized nano-Se-chondroitin sulfate particles and T-2 toxin, alone or in combination, and the cell growth and apoptosis were observed using MTT assay, HE staining and flow cytometry.

RESULTSThe synthesized nano-Se-chondroitin sulfate, with a selenium entrapment ratio of 10.1%, spontaneously formed nanoparticles in distilled water with sizes ranging from 30 to 200 nm. Fourier-transform infrared spectroscopy suggested a possible covalent bond that bound Nano-Se and chondroitin sulfate. Within the concentration range of 50-200 ng/ml, nano-Se-chondroitin sulfate significantly inhibited T-2 toxin-induced apoptosis of the cultured chondrocytes and reduced the early apoptosis rate to (8.64∓1.57)% (P<0.05).

CONCLUSIONNano-Se-chondroitin sulfate can inhibit T-2 toxin-induced apoptosis of cultured chondrocytes from KBD patients in vitro, and serves as a promising candidate therapeutic agent for KBD.

Apoptosis ; drug effects ; Cells, Cultured ; Chondrocytes ; drug effects ; pathology ; Chondroitin Sulfates ; administration & dosage ; pharmacology ; Humans ; Kashin-Beck Disease ; pathology ; Middle Aged ; Nanostructures ; T-2 Toxin ; toxicity

BACKGROUNDTo study the apoptosis-inducing effect of Tanshinone and its molecular mechanism on human lung cancer cells.

METHODSHuman lung cancer cell line (SPC-A-1) was treated in vitro with 0.5 mg/L Tanshinone IIA for five days, and the cells treated with all trans retinoic acid (RA) or DDP as controls. Changes in cell morphology, apoptotic index and apoptosis related gene expression were detected by electron microscope, FCM and DNA-end-labeling.

RESULTSMany apoptotic cells were observed by light and electron microscopes. FCM examination showed that apoptotic index in Tanshinone group was much higher than that of DDP and control groups, but no difference was found statistically compared with RA group. The expression of p53, Fas and Bax genes in Tanshinone group was up-regulated markedly, but Bcl-2 was obviously down-regulated.

CONCLUSIONSTanshinone IIA can induce apoptosis in human lung cancer cell line (SPC-A-1) . Up-regulating expression of p53, Bax, Fas and down-regulating Bcl-2 expression might be its molecular mechanisms.

BACKGROUNDTo study the growth-inhibiting effect and its molecular mechanism of Tanshinone on human lung carcinoma cell line.

METHODSHuman lung adenocarcinoma cell line (SPC-A-1) was treated in vitro with 0.5μg/ml Tanshinone IIA for five days, and the cells treated with all trans retinoic acid (RA) and DDP as control. Changes in cell morphology, proliferation dynamics, cell cycle distribution and tumor-related gene expression were detected.

RESULTSThe cell growth and rate of clone formation of SPC-A-1 cells were markedly inhibited in Tanshinone group than RA group. Flow cytometry demonstrated that S phase cells decreased and G₀/G₁ phase cells increased in Tanshinone group. Expression of p53, p21 was up-regulated obviously but CDKN₂ was down-regulated markedly by Tanshinone IIA.

CONCLUSIONSTanshinone IIA can inhibit cell growth and clone formation in human lung cancer cell line (SPC-A-1) and its possible molecular mechanism may be inhibiting DNA synthesis by up-regulating p53, p21 and down-regulating CDKN₂.

Objective:To investigate the effects of fritinib on angiogenesis, tumor growth and inositol requiring enzyme 1 (IRE1) -apoptosis signal regulating kinase 1 (ASK1) -c-Jun N-terminal kinase (JNK) pathway in triple negative breast cancer.Methods:Triple negative breast cancer cells MDA-MB-231 were taken and divided into normal saline (NS) group, low-dose fritinib (LD) group, medium-dose fritinib (MD) group and high-dose fritinib (HD) group. NS group was added with 100 μmol/L normal saline. LD group, MD group and HD group were added with 25, 50 and 100 μmol/L fritinib, respectively. Cell proliferation was detected by MTT assay, cell apoptosis was detected by flow cytometry, the ability of cells to form mimicry vessels was observed by three-dimensional cell culture, and the related indexes of angiogenesis and IRE1-ASK1-JNK pathway were detected by Western blotting. Twenty triple-negative breast cancer rat models were divided into control group and experimental group by random number table method, with 10 rats in each group. The control group was given normal saline gavage and the experimental group was given 100 μmol/L fritinib gavage. The tumor growth of rats in the two groups was observed and recorded.Results:The 48 h cell proliferation rates of NS group, LD group, MD group and HD group were (85.44±5.58) %, (73.24±4.95) %, (61.53±4.07) % and (50.23±2.97) %, respectively ( F=4.01, P=0.002). Compared with the NS group, the cell proliferation rate in LD, MD and HD groups was significantly decreased in a dose-dependent manner (all P<0.05). The apoptosis rates of NS group, LD group, MD group and HD group were (3.41±0.39) %, (18.75±1.94) %, (24.97±2.58) % and (38.62±3.27) %, respectively ( F=18.99, P<0.001). Compared with the NS group, the apoptosis rate of LD, MD and HD groups was significantly increased in a dose-dependent manner (all P<0.05). The number of mimicry vessels in NS group, LD group, MD group and HD group was 19.58±2.11, 15.67±2.02, 11.57±1.73 and 5.20±1.23, respectively ( F=3.28, P=0.008). Compared with the NS group, the number of mimicry vessels in LD group, MD group and HD group was significantly reduced. The results were dose-dependent (all P<0.05). vascular endothelial growth factor (VEGF) protein expression in NS group, LD group, MD group and HD group was 2.36±0.21, 1.79±0.17, 1.48±0.14 and 0.94±0.10, respectively ( F=5.17, P<0.001). The expression of IRE1 protein was 1.18±0.12, 1.67±0.18, 2.03±0.24 and 2.39±0.28, respectively ( F=5.55, P<0.001). The expression of ASK1 protein was 1.09±0.11, 1.46±0.13, 1.81±0.18, 2.33±0.21 ( F=5.32, P<0.001), respectively. JNK protein expression was 1.01±0.09, 1.48±0.14, 1.86±0.21 and 2.28±0.24, respectively ( F=6.92, P<0.001). Compared with the NS group, VEGF protein expression in LD, MD and HD groups was significantly decreased, and the expressions of IRE1, ASK1 and JNK were significantly increased in a dose-dependent manner (all P<0.05). Compared with the control group, the tumor weight and volume of the experimental group were significantly decreased [ (0.55±0.10) g vs. (1.37±0.15) g, t=14.38, P<0.001; (77.39±3.21) mm 3vs. (118.26±5.34) mm 3, t=20.74, P<0.001], tumor inhibition rate was significantly increased [ (71.23±3.85) % vs. (32.56±3.08) %, t=24.80, P<0.001]. Conclusion:Fritinib has an inhibitory effect on the activity of triple negative breast cancer cells, which can significantly reduce their angiogenesis and inhibit tumor growth. Moreover, it is related to the activation of IRE1-ASK1-JNK pathway.