Objective:To investigate the effects of sodium selenite on the cell apoptosis of K562 cells and to elucidate its molecular mechanisms.Methods:K562 cells were treated with various concentrations of sodium selenite at different time points,and then MTT assay was employed to evaluate the effects of sodium selenite on the proliferative inhibition of K562 cells.MTT assay was employed to evaluate the effects of sodium selenite on the proliferative inhibition of K562 cells.Electronmicroscopy,and TUNEL were performed to confirm the apoptosis of K562 cells,RT-PCR was employed to analyze the mRNA expression levels of Bcl-2 and Bax.Colorimetric method were used to measure the activities of caspase-3 of K562.Results:Sodium selenite could inhibit proliferation of K562 cells and induce them to undergo apoptosis.RT-PCR results showed that sodium selenite could decrease the mRNA expression level of Bcl-2 and increase the level of Bax of K562 cells which had been treated with sodium selenite for 48h significantly,and the activity of caspase-3 elevated remarkably too.Compared with the control group,the expression levels of Bcl-2,Bax and acivity of caspase-3 in 20?mol/L sodium selenite treatment group were markedly changed(P

Objective To optimize the extraction conditions for total flavonoids from Cibotium barometz by response surface meth-od(RSM). Methods According to the center combination of Box-Benhnken,using the RSM,the effects of ethanol concentration,the ratio of solid to liquid,the extraction time,and the extraction frequency were studied by central composite design. Results The opti-mal conditions of extraction were as follows:60％ethanol,the ratio of solid to liquid 1:40,refluxing and extracting twice,and 1.5 h for each time. Conclusion The actual extraction yield was 1.44％. The method of extraction has higher extraction efficiency than other methods and can provide a basis for the industrial production of the total flavonoids from S. barometz.

No abstract available.
Restraint, Physical*

We studied arterial oxygen desaturation, using a pulse oximeter, in 132 patients undergoing diagnostic upper gastrointestinal endoscopy to obtain predictive factors of the change. The baseline arterial oxygen saturation (SaO2) level was 98.8+/- 1.2%. During the procedure, oxygen desaturation (SaO2>95%) was found in 90.2% of the patients, Mild oxygen desaturation (95>SaO2>90%) was found in 9.8% of the patients, and there was no severe oxygen desaturation(SaO2<90%). Age(P=0.52), gender(P =0.48), smoking(P =0.71), body mass index(P =0.32), and endoscopy time(P = 0.68) was not related to the degree of oxygen desaturation. These results suggest that oxygen desaturation, which may rarely induce serious cardiopulmonary events, is not frequently observed during non-sedated diagnostic upper endoscopy.
Endoscopy ; Endoscopy, Gastrointestinal* ; Humans ; Oxygen*

OBJECTIVETo investigate the effect of Metformin on the proliferation and collagen synthesis of the human keloids fibroblasts as well as the effect on phosphorylation of Akt/FoxO1 signal transduction pathway.

METHODSFibroblasts of keloid were divided into control group treated with medium solution and experimental groups treated with different concentrations of Metformin. 48 h later CCK-8 assay was adopted to evaluate cell survival; Western blot was performed to detect the Akt and FoxO1 phosphorylation; and Hydroxyproline reagent kit was used to detect the collagen synthesis.

RESULTSWith different concentrations (30, 60, 90, 120 mmol/L) of Metformin, the absorbance of cultured keloid fibroblasts detected by CCK8 assay decreased by (13.30 ± 2.04)%, (22.64 ± 4.70)%, (54.00 ± 5.34)% and (63.12 ± 3.48)%. The growth of fibroblasts was suppressed by Metformin in a dose-dependent manner. It showed that the level of phoshpo-akt and phoshpo-foxOl in keloids fibroblasts in experimental groups was lower than that in the control group and the collagen synthesis were also decreased in experimental groups, all in a dose-dependent manner (P < 0.05, P < 0.01).

CONCLUSIONSMetformin can effectively inhibit the proliferation and collagen synthesis of the human keloids fibroblasts in vitro, which may be associated with the suppression of phosphorylation of Akt/FoxO1 signaling pathway

Cell Proliferation ; drug effects ; Collagen ; biosynthesis ; Dose-Response Relationship, Drug ; Fibroblasts ; cytology ; drug effects ; metabolism ; Forkhead Box Protein O1 ; Forkhead Transcription Factors ; metabolism ; Humans ; Keloid ; pathology ; Metformin ; pharmacology ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; metabolism ; Signal Transduction ; drug effects

Retrospective studies of duodenal polyps have shown a prevalence of 0.3-4.6% in patients referred to upper gastrointestinal endoscopy, and histologic classification have been inconsistent. A prospective consecutive study was carried out in 3,871 patients referred to diagnostic endoscopy, Sixteen patients had polyps in the first part of duodenum, for a prevalence 0.41%(0.28-0.53%, 95% confidence interval). Fourteen polyps were either inflammatory(thirteen polyps) or ectopic gastric mucosa(one polyp). Two hyperplasitc polyps were founded. All polyps were benign and sessile, and most of polyps(75%) were solitary.
Classification ; Duodenum ; Endoscopy* ; Endoscopy, Gastrointestinal ; Humans ; Polyps* ; Prevalence* ; Prospective Studies

OBJECTIVETo study the effect of nadroparin in the migration of breast cancer cells MDA-MB-231 and its action mechanism.

METHODThe MTT test was adopted to observe the effect of different concentrations of naringenin on the growth capacity of breast cancer cells MDA-MB-231. Wound healing and transwell experiment analysis were conducted to detect the effect of naringenin on the migration of breast cancer cells MDA-MB-231. Western blotting was adopted to investigate the effect of naringenin on protein expressions of MDA-MB-231 cell Integrin β3, β1 and matrix metalloproteinase MMP-2 and MMP-9. The computer virtual docking technique was used to evaluate the combining capacity of naringenin and Integrin β3 in vitro.

RESULTNaringenin inhibited the migration of MDA-MB-231 cells in a dose-dependent manner. In wound healing and transwell experiments, with the increase in the concentration of naringenin, the number of migrant MDA-MB-231 cells and the invasion capacity of breast cancer cells decreased. Naringenin could inhibit the protein expression of Integrin β3 in a dose-dependent manner, but with unobvious effect on expression of Integrin β1. Besides, naringenin could significantly inhibit the protein expressions of MMP-2 and MMP-9. The results of the computer virtual docking showed a negative value in the combining capacity between naringenin and Integrin β3, indicating the high affinity between them.

CONCLUSIONNaringenin can inhibit the growth capacity of breast cancer cells MDA-MB-231 and block the migration and invasion of breast cancer cells MDA-MB-231. Its mechanism is to down-regulate MMP-2 and MMP-9 expressions after combining with Integrin β3.

Breast Neoplasms ; drug therapy ; genetics ; metabolism ; pathology ; Cell Line, Tumor ; Cell Movement ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Female ; Flavanones ; pharmacology ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Integrins ; genetics ; metabolism ; Matrix Metalloproteinase 2 ; genetics ; metabolism ; Matrix Metalloproteinase 9 ; genetics ; metabolism ; Neoplasm Invasiveness

The DNA damage response is a cornerstone of genomic stability.The cell utilizes mutiple mechanisms including damage detection,cell cycle regulation,damage repair and apoptosis to keep cell homeostasis.The DNA damage response include several biochemical pathways:first,the recognition and repair of damaged DNA;second,the activation of DNA damage checkpoint,which arrests cell cycle progression so as to provides time for DNA repair and prevention of the transmission of genomic abnormalities to the daughter cells;third,apoptosis,which eliminates serious damaged cells.The double strand break(DSB) is believed to be one of the most severe types of DNA damage,and errors in DSB repair could result in genomic instability that might lead to malignancy.It has been reported recently that constitutive activation of the ATM-Chk2-p53 pathway and phosphorylation of histone H2AX acts as an inducible anti-cancer barrier in the early stages of human tumorigenesis.This ATM-regulated DNA damage response network maintains genomic integrity and delays or prevents cancer by eliciting growth arrest or cell death.In context with a recent report,the ATM-dependent DNA-damage cellular signaling has also been shown to be involved in the integration of human immunodeficiency virus type-1(HIV-1) into host genomes,and KU55933,a specific ATM inhibitor,attenuated the infection of HIV-1 into host cells.The regulation and mechanisms of the signaling pathways of DSB response,and its role in HIV-1 infection and malignancy genesis were reviewed.

Objective To investigate the effect of mycophenolate mofetil (MMF) and sildenafil on the systolic pulmonary arterial pressure (SPAP),right ventricular hypertrophy index (RVHI),pulmonary arterial and heart structural of pulmonary arterial hypertension (PAH) rat models.Methods The rat models of monocrotaline (MCT)-PAH were developed.Sprague-Dawley male rats were randomly assigned into the control group,the MCT group,the MMF (40 mg·kg-1·d-1) group,the sildenafil (20 mg·kg-1·d-1) group,and the MMF (40 mg·kg-1·d-1) + sildenafil (20 mg·kg-1·d-1) group.The SPAP and RVHI were measured,and the pulmonary arterial and heart structural changes were observed for all rats.Statistical analysis were performed by one-way ANOVA and rank-sum test.Results ① SPAP of the MMF group,the sildenafil group and the MMF + sildenafil group were (31±8),(37±8),(29±6) mmHg,while that of the MCT group was (53±7) mmHg,the difference was statistically significant (P＜0.01).The RVHIs in the MMF group,the sildenafil group and the MMF+sildenafil group were reduced [(0.365±0.038),(0.407±0.047),(0.325 ±0.459) respectively] when compared with the MCT group (0.543±0.080),the difference was statistically significant (P＜0.01).The SPAP between the MMF+sildenafil group and the sildenafil group was statistically significantly different (P＜0.05),and the RVHI difference between the MMF+ sildenafil group and the sildenafil group was statistically significant (P＜0.05).② The wall thic-kness/tubes diameter of the MMF group (0.355±0.074) and the MMF+sildenafil group (0.289±0.017) were reduced when compared with that of the MCT group [(0.466±0.006)],the difference was statistically significant (P＜0.05).The wall thickness/tubes diameter of the MMF group (0.355±0.074) were reduced compared with the sildenafil group (0.455±0.006),and the difference was statistically significant (P＜O.05).In addition,the wall thickness/tubes diameter of the MMF+ sildenafil group (0.289±0.017) was reduced when compared with that of the sildenafil group (0.455±0.006),and the difference was statistically significant (P＜ 0.05).Conclusion Both sildenafil and MMF can reduce the SPAP and RVHI of PAH rat models induced by MCT.MMF and sildenafil can reduce wall thickness as well.

Objective To evaluate the early diagnostic value of 1,3-β-D glucan(BG) and galactomannan(GM) test for invasive fungal infections(IFI)in intensive care unit(ICU) patients.Methods From 2013 to 2015,the concentration of serum BG and GM were detected in 452 cases of ICU patients,including 182 cases with diagnosis of IFI,46 cases with possible diagnosis of IFI and 224 cases of non-IFI.The diagnostic performance of BG,GM and combined test were analyzed.Results The sensitivity,specificity,positive predictive value(PPV) and negative predictive value(NPV)of BG test were 75.0%,80.4%,75.8%,79.6%.Those of GM test were 25.80%,85.7%,59.5% and 58.7%.The sensitivity and specificity of BG and GM combined test were 87.4% and 94.7% respectively.Conclusion BG and GM combined test could improve the diagnostic efficiency,reduce the false positive rate and false negative rete,which might be helpful for the early diagnosis of IFI in ICU patients.