Objective To investigate the drug resistance of clinical isolates in Pinggu area from 2011 to 2013,and guide clinical rational use of antibiotics.Methods Isolates from 2011 to 2013 in the hospital were collected and identified to species.Antibiotic susceptibility test were performed.For the infection with the same position and the same patient,only the first isolate was included. WHONET5.6 data analysis software was used for data auditing and inputing,the USA CLSI M100-S22 standard were refered to. Results Total of 5 794 strains of clinically isolated pathogenic bacteria were collected from 2011 to 2013,1 600 strains in 2011, 2 234 strains in 2012,1 960 strains In 2013.The detection rate of MRSA in each year from 2011 to 2013 were 63.50%,65.00%, 65.30% respectively.No vancomycin and linezolid-resistant Staphylococcus aureus was found.The resistance rate of Enterococcus to teicoplanin was <5%,to Linezolid <2.4% and to vancomycin <21.1%.The resistance rates of Escherichia coli and Klebsiella pneumoniae to imipenem and meropenem were both < 1.3%.The annual resistance rates of Acinetobacter bauman to imipenem were 34.6%,26.9%,29.3% respectively.Resistance rates of Pseudomonas aeruginosa to imipenem,meropenem,cefoperazone/shu-batan,piperacillin/tazobactam were lower than the national average.No polymyxin B resistance isolate was found.Stenotroph-omonas maltophilia were sensitive to ceftazidime and minocycline.Conclusion The antibiotic resistance rate data in Pinggu exhibits area specificity,which was different from the national antimicrobial resistance monitoring data in 2011.Detection rate of MRSA,re-sistance rate of enterococci to linezolid and vancomycin,Escherichia coli,Klebsiella pneumoniae,Enterobacter cloacae to imipenem, meropenem are increasing year by year.The resistance rates of Acinetobacter bauman and Pseudomonas aeruginosa are lower than the national average rate.

Objective To Investigate of drug resistance of Acinetobacter baumannii in Pinggu district from 2011 to 2015 ,and to guide clinical rational use of antibacterial drugs .Methods Retrospective analysis of drug resistance of Acinetobacter baumannii in clinical isolates were performed from 2011 - 2015 .Results From 2011 to 2015 1 744 strains of Acinetobacter baumannii were isola‐ted ,including respiratory specimens (96 .1% ) ,urine (1 .1% ) ,blood (0 .9% ) ,wound (0 .5% ) ,pus (0 .3% ) ,bile (0 .2% ) ,duct (0 .1% ) ,ortherl kinds of secretions (0 .7% ) .The rate of drug resistance to gentamicin ,tobramycin and Amikacin was under 45 .7% .Piperacillin /Tazobactam < 49 .0% ,ampicillin / Sulbactam < 52 .0% ,Imipenem < 50 .0% ,ceftazidime ,cefepime were clos‐en to 50 .0% .To Cefoperazone/Sulbactam ,it increased from 6 .1% to 57 .1% .While ,to Meropenem it increased from 34 .3% to 85 .7% .Conclusion From 2011 to 2015 ,Acinetobacter baumannii infection reduces year by year in our hospital .Pathogenic bacteria mainly comes from the respiratory tract ,urinary tract ,blood ,bile ,and other body fluids .The resistant rate is rising year by year ,to gentamicin ,tobramycin ,amikacin ,Piperacillin/Tazobactam ,Ampicillin/Sulbactam ,Ceftazidime and cefepime ,ciprofloxacin and Imi‐penem .The resistant rate marked increase ,to Cefoperazone/Sulbactam ,Meropenem ,Trimethoprim/Sulfamethoxazole .While ,it de‐creases year by year to minocycline ,tigecycline .

[Summary] Stress response is an organism ’ s mechanism of defense against various stimulations , involving nervous , endocrine , cardiovascular and immune systems .This review summarized the clinical research progress on effects of different anesthesia management on stress response and future trends of investigation .

AIM: To investigate the effect of urokinase plasminogen activator (uPA) on metastasis inhibition of gastric cancer SGC7901cells induced by parthenolide. METHODS: The changes of SGC7901 cells reproductive activity were analyzed by MTT. Light microscope was used to observe the cell morphological changes. The effects of parthenolide on migration and invasion capacity of SGC7901 cells were determined by using matrigel and transwell system. The expression of uPA was detected by Western blot and RT-PCR assays. RESULTS: Parthenolide inhibited the proliferation of SGC7901 cells in a time-and concentration -dependent manner ranging from 100 to 200 ?mol/L. Light microscopy showed the suppressing effect on growth of SGC7901 cells. After exposed to parthenolide, the migration and invasion capacity of SGC7901 cells were significantly decreased, the number of cells gradually decreased through the basement membrance. The Western blot assay showed that the expression of uPA protein declined gradually after exposed to parthenolide for various period of time. CONCLUSION: Parthenolide can inhibit the growth and metastasis activity of SGC7901 cells, and uPA played an important role in the latter process.

Objective To study the influence of artesunate (Akt) on the proliferation and apoptosis of human head and neck squamous cell carcinoma (HNSCC), and to explore its molecular mechanism thereof. Methods The HNSCC cell line,UM-SCC-10A cells, was cultured in vitro. The Inhibitory concentration 50 (IC50) was examined by MTT assay. The cell mor?phological changes were observed under inverted light micro-scope after being interfered by 0, 2.5, 5, 10, 20 and 40μmol/L Akt. Cell cycle changes and apoptosis were measured by flow cytometry. And the expression of cell cycle regulators and apop?totic associated protein were detected by Western blot assay. Results MTT assay demonstrated that Akt significantly inhib?ited the proliferation of UM-SCC-10A cells in dose-dependent manner. After UM-SCC-10A cells were treated with Akt for 48 h, IC50 was 15.01μmol/L. Morphological changes of cell apoptosis such as karyopyknosis and conglomeration were ob?served by Hoechst 33258 staining. Flow cytometry showed that the apoptosis was associated with cell cycle arrest during the G1 phase. Western blot analysis showed that p53 and p21 protein was up-regulated and Cyclin D protein was down-regulat?ed. Furthermore, results revealed that Bcl-2 associated X protein induced by a mitochondrial pathway, cytochrome C and caspase-3 were up-regulated, and Bcl-2 and procaspase-3 were down-regulated. The mitochondrial membrane potential was reduced. Conclusion Artesunate can induce apoptosis of UM-SCC-10A cells via a mitochondrial pathway, which was associated with cell cycle arrest in the G1 phase. As a result, artesunate has an obvious inhibitory effects on proliferation of UM-SCC-10A cells.

Humans ; Salivary Glands

Immobilization is a usual method to treat the injury of skeletal muscle system and plays an important role in rehabilitation of diseases. But immobilization also displays some negative effects, of all, muscle system is affected significantly. The mechanism is explored in the article from immobilization-induced skeletal muscle atrophy, the dropping of muscle power, reduction of vessels density in muscle and metabolic disturbance of muscle. The authors of the article advances that shortening the period of immobilization as possible and performing early rehabilitation are important to remove the negative influence of immobilization, but all treatments should obey the medical rules.

There are one third of synthesized proteins must be secreted to the cell surface or to the surrounding environment to acquire their native functional state. Most of them are exported by Sec translocase (secretion pathway). Sec translocase consists of a membrane embedded protein-conducting channel, termed SecYEG and a peripherally associated motor domain, the ATPase SecA. The SecDFyajC heterotrimeric membrane protein complex can facilitates protein translocation. SecB is a molecular chaperone that functions in the protein translocation pathway. SecM (secretion monitor) encoded by the 5' region of the secM-secA mRNA, which elongation arrest is required for upregulated expression of SecA. The signal sequence in the N terminus of the nascent peptide is first recognized by the signal recognition particle (SRP). SecB, the Sec-system-specific chaperone, channels the preprotein to the Sec translocation pathway and, ad- ditionally, actively targets the bound precursor to the translocase by its ability to bind SecA. The preprotein-bearing SecA then binds to the membrane, at a high-affinity SecA-binding site, SecYEG, which constitutes a channel for polypeptide movement. Continued translocation requires cycles of ATP hydrolysis bySecA, which is thought to occur in a step-wise fashion with a step of 20~30 amino acid residues.

Organic anion transporting polypeptides (OATP), a member of solute carrier (SLC) superfamily, is considered as an important transmembrane uptake transporters. OATP is involved in the transport of a variety of endo- and xenobiotics (bile acids, bilirubin, prostaglandin, thyroid hormones, steroid hormone conjugates), drugs and toxins in a Na+ and ATP independent manner. Multiple factors (eg. hormones, proinflammatory cytokines, drugs) can affect the distribution, expression and activity of OATPs, leading to an altered accumulation of OATP substrates and related food-drug and drug-drug interactions. Changes in the distribution and expression of OATPs in malignant tissues may be related to the pathological process of cancer, while the modulation epigenetic mechanism also contributes to its distribution patterns. This review describes the factors that can affect the expression or function of OATPs, which may provide a valuable reference for drug development and the clarification of pathogenesis.
Biological Transport ; Humans ; Neoplasms ; Organic Anion Transporters ; physiology ; Xenobiotics

Organic anion transporting polypeptides (OATP), a member of solute carrier (SLC) superfamily, is considered as an important transmembrane uptake transporters. OATP is involved in the transport of a variety of endo- and xenobiotics (bile acids, bilirubin, prostaglandin, thyroid hormones, steroid hormone conjugates), drugs and toxins in a Na+ and ATP independent manner. Multiple factors (eg. hormones, proinflammatory cytokines, drugs) can affect the distribution, expression and activity of OATPs, leading to an altered accumulation of OATP substrates and related food-drug and drug-drug interactions. Changes in the distribution and expression of OATPs in malignant tissues may be related to the pathological process of cancer, while the modulation epigenetic mechanism also contributes to its distribution patterns. This review describes the factors that can affect the expression or function of OATPs, which may provide a valuable reference for drug development and the clarification of pathogenesis.