PurposeTo measure the areas and diameter lines of bronchi at acute exacerbation and at remission period in patients with chronic obstructive pulmonary disease (COPD) using CT, and to explore the correlation between the two periods and evaluate the comprehensive assessment in diagnosing COPD exacerbation.Materials and Methods Fifty-two COPD patients were scanned with 64-row spiral CT on chest and PFT at acute exacerbation and at remission period. The areas and diameter lines of apical segmental and the sub-segmental bronchi of the right upper lobe in the patients were measured at the two periods, including indicators such as wall thickness (WT), thickness-diameter ratio (TDR), wall area (WA), percentage of wall area (WA%). The differences of those indicators at the two periods were compared with such factors of COPD comprehensive assessment as forced expiratory volume at the first second% (FEV1%), percentage of forced expiratory volume in first second to forced vital capacity (FEV1/FVC), COPD assessment test (CAT), modified medical research council questionnaire (mMRC) for assessing the severity of breathlessness, 6-minute walking distance (6MWD). Results The patients had significant differences between acute exacerbation period and remission period in the indicators of COPD comprehensive assessment like FEV1%, FEV1/FVC, CAT, mMRC and 6MWD (t=-4.119,-2.583, 4.012, 3.321 and-3.892,P<0.05). Compared with those at remission period, the WT, TDR, WA and WA% of sub-segmental bronchi were all higher at acute exacerbation period (t=3.025, 2.341, 2.204 and 2.124, P<0.05); only TDR of segmental bronchi showed significant difference between the two periods (t=2.990,P<0.05). The correlation of sub-segmental bronchi with FEV1%, FEV1/FVC, CAT, mMRC and 6MWD was more significant than that of segmental bronchi with those indicators at the two periods.Conclusion The COPD comprehensive assessment can help diagnose COPD at acute exacerbation period; MSCT shows the remodeling of segmental and sub-segmental bronchi and the changes on the airway wall, and the quantitative measurement of sub-segmental bronchi has correlation with the differences of indicators in the comprehensive assessment; COPD comprehensive assessment seems to be more valuable than PFT in the estimation of COPD at acute exacerbation.

Objective:To explore the effect of fluoride exposure on the gene expression of phosphatidylinositol-3-kinase/protein kinase B/endothelial nitric oxide synthase (PI3K/Akt/eNOS) in rat aortic tissue, and to provide a theoretical basis for studying the mechanism of cardiovascular injury caused by endemic fluorosis.Methods:A total of 40 male Wistar rats were divided into 4 groups (10 rats in each group) via the random number table method according to body weight (80 - 100 g), namely control group (drinking distilled water), low-dose, medium-dose and high-dose groups [drinking distilled water containing 50, 100 and 150 mg/L sodium fluoride (NaF), respectively]. The rats were free to drink and eat. After feeding for 90 days, rats were sacrificed and the aortic tissue was taken. Three aortic tissue samples from the control group and the high-dose group were taken for mRNA sequencing, the differential genes were screened, and the differential genes were analyzed by GO function enrichment analysis and KEGG function enrichment analysis. At the same time, the mRNA expression levels of PI3K, Akt and eNOS in the aortic tissue of rats in each group were determined by real-time fluorescence quantitative PCR.Results:Compared with control group, there were 756 differential genes in high-dose group, including 654 up-regulated genes and 102 down-regulated genes. These differential genes were mainly related to biological processes such as muscle contraction, muscle regulation, muscle tissue development, striated muscle cell development, muscle cell differentiation, blood circulation regulation and striated muscle tissue development. They were mainly enriched in cyclic guanosine phosphate (cGMP-PKG) signaling pathway, relaxin signaling pathway and PI3K/Akt signaling pathway, etc. Compared with control group, the mRNA expression levels of PI3K and eNOS in aortic tissue of rats in low-dose, medium-dose and high-dose groups were significantly reduced ( P < 0.05); the mRNA expression level of Akt in low-dose group was significantly increased ( P < 0.05). Conclusion:Fluoride exposure has certain effects on the function and gene expression of rat aortic tissue, and PI3K/Akt/eNOS signaling pathway may play an important role in the process of fluoride induced aortic tissue injury in rats.

Osteoarthritis is a kind of joint disease with cartilage injury as the main pathological changes.There is no effective treatment for them.With the discovery,research and application of microRNA (miR),it also provides new hope for the treatment of osteoarthropathy.At present,the role of miR in the pathogenesis of cartilage injury has been fully recognized.In this paper,we reviewed the role of miR-140 in the development of osteoarthritis and its important target genes in recent years.

Objective To study the effect of T-2 toxin on proliferation and cell cycle of rat chondrocytes,in order to provide a new idea in molecular mechanism of T-2 toxin-induced chondrocyte damage.Methods Primary chondrocytes of neonatal Wistar rats were isolated and stained by toluidine blue staining and type Ⅱ collagen immunofluorescence staining.The effects of different concentrations of T-2 toxin [0 (control),1,5,10,20,50,100 μg/L)] on proliferation of chondrocytes for 24 h were detected by cell counting kit-8 (CCK-8) method,and control,1 (low dose),5 (medium dose),and 10 μg/L (high dose) T-2 toxin were selected for subsequent experiment;cell cycle changes were detected by flow cytometry;Real-time PCR and Western blotting were used to detect the effects of T-2 toxin on mRNA and protein expressions of proliferating cell nuclear antigen (PCNA) and Cyclin D1 in chondrocytes.Results With increase of T-2 toxin concentration (control,1,5,10,20,50,100 μg/L),the cell survival rates [(100.00 ± 0.00)％,(93.12 ± 1.66)％,(77.12 ± 1.11)％,(59.44 ± 4.09)％,(46.64 ± 3.86)％,(38.15 ± 3.37)％,(33.79 ± 0.99)％] were decreased,and the differences were statistically significant (F =139.21,P ＜0.05).The percentages of quiescent phase/pre-DNA synthesis phase (G0/G1 phase) ceils in 1,5,10 μg/L T-2 toxin groups [(22.03 ± 0.42)％,(30.54 ± 2.61)％,(36.01 ± 1.51)％] were significantly higher than that in control group [(13.79 ± 1.65)％,P ＜ 0.05];the percentages of DNA synthesis phase (S phase) cells [(60.27 ± 3.53)％,(53.88 ±4.38)％,(49.55 ± 2.49)％] were significantly lower than that in control group [(76.72 ± 4.24)％,P ＜ 0.05].The differences of mRNA levels of PCNA and Cyclin D1 between groups were statistically significant (F =46.80,17.97,P ＜ 0.05),and 5,10 μg/L T-2 toxin groups (0.77 ± 0.13,0.79 ± 0.08,0.60 ± 0.07,0.56 ± 0.05) were lower than the control group (0.99 ± 0.02,1.01 ± 0.01,P ＜ 0.05).The expressions of PCNA protein in 5,10 μg/L T-2 toxin groups (0.69 ± 0.03,0.49 ± 0.03) were lower than that in control group (0.92 ± 0.05,P ＜ 0.05);the expressions of Cyclin D1 protein in 1,5,10 μg/L T-2 toxin groups (0.80 ± 0.06,0.60 ± 0.07,0.33 ± 0.13) were lower than that in control group (0.95 ± 0.07,P ＜ 0.05).Conclusion T-2 toxin can inhibit the proliferation of chondrocytes,which may be worked through influencing the expression of cell cycle protein,causing cell cycle arrest,thereby inhibiting DNA synthesis.