Objective To investigate antimicrobial resistance characteristics and mechanisms of imipenem-resistant Pseudomonas aeruginosa (P .aeruginosa)isolated from clinical specimens.Methods Bacterial strains were identi-fied by BD Phoenix 100 automatic microbial analysis system,antimicrobial susceptibility testing was performed by Kirby-Bauer method;Carbapenemase genes (IMP ,VIM ,OXA,GES )and outer membrane protein gene oprD2 were detected by polymerase chain reaction.Results Resistant rates of imipenem-resistant P .aeruginosa strains to ami-kacin was the lowest (8.33%);resistant rates to gentamicin and tobramycin were<20%;resistant rates to the third and fourth generation cephalosporins,aztreonam,meropenem,compound sulfamethoxazole and minocycline were all>60%,and all strains were resistant to ampicillin/sulbactam.The positive rate of OXA-17 gene was 2.78%(n=1 ),deletion rate of oprD2 was 38.89%,the other drug-resistant genes were not detected.Conclusion Except aminoglycosides,resistance of imipenem-resistant P .aeruginosa to other antimicrobial agents is serious;resistance of P .aeruginosa to imipenem may be due to lacking of OprD2 and production of carbapenemases.

A reninoma is a renal juxtaglomerular cell apparatus tumor that produces excessive amounts of renin,resulting in secondary hyperaldosteronism,and associated hypertension and hypokalemia.It is a rare form of secondary hypertension and occurs mainly in young adult females.Common symptoms include headache,nocturia,polyuria,polydipsia,and fatigue.Imaging examination and selective renal vein sampling has been the traditional method of localizing the tumour.The diagnosis should be considered in all patients with hypertension and hypokalemia and no evidence of primary hyperaldosteronism and renal artery stenosis.Reninoma represents a surgically correctable cause of hypertension.

Objective The main economic qualities of natural triploid were evaluated and the result laid a foundation to culture new triploid variety of Dioscorea zingiberensis. Methods The ploidy level of series of D. zingiberensis from some areas of Yunnan Province were identified and the qualities of outputs per plantlet,propagation ratio,and diosgenin content etc. were measured. Results Five natural triploids were found and the qualities of the triploids all displayed diversity,output per plantlet 1 090.00—628.57 g,propagation ratio (ploidy) 72.43—29.43,dry substance ratio 36.95%—24.06%,and diosgenin content 4.40%—1.50%. The outputs of series 1 and series 3 exceed 1 000 g,the diosgenin content of series 2 reached to 4.40%,and series 3 displayed excellent quality of outputs per plantlet,propagation ratio,and diosgenin content. The synthetical index is maximum. Conclusion The series comprising good quality are obtained by the discovery of triploid and evaluation of qualities. The triploid variety is to be created with judgment and selection of progeny.

Animals ; Arbovirus Infections ; prevention & control ; virology ; Arboviruses ; growth & development ; Biomedical Research ; methods ; standards ; trends ; China ; Humans ; Insect Vectors ; virology

The syndrome of inappropriate antidiuretic hormone secretion ( SIADH ),characterized with dilutional hyponatremia,is the most frequent pathophysiology of euvolemic hyponatremia in hospital inpatients.Conventional therapies for SIADH include fluid resriction,saline infusion,and some pharmacologic adjustments of fluid balance.For various reasons,conventional therapies show poor efficiency.Vasopressin receptor antagonist,a new class of pharmacologic agent,can directly block vasopressin-mediated receptor activation and target underlying pathophysiology of SIADH.

Familial pancreatic cancer is a known hereditary cancer syndrome with autosomal dominant inheritance and accounts for about 3% of all pancreatic cancers. With the development of molecular genetics,several genes have been identified related with the familial pancreatic cancer, including breast cancer susceptibility gene 2, Palladin, cyclin-dependent kinase inhibitor 2A, et al. In particular, mutations in some of these genes have been defined as the hereditary basis of particular cancer syndromes. Molecular genetics surveillance for high risk populace can lead to the diagnosis of asymptomatic, early-stage pancreatic cancer or precancerous lesions.

Aged ; Diagnosis, Differential ; Humans ; Intermittent Claudication ; diagnosis ; etiology ; Male ; Middle Aged ; Nervous System Diseases ; complications ; diagnosis ; Vascular Diseases ; complications ; diagnosis

China ; Encephalitis Virus, Japanese ; genetics ; immunology ; isolation & purification ; Encephalitis, Japanese ; virology ; Humans ; Research ; trends

Animals ; China ; Culex ; Insect Vectors ; Longitudinal Studies

Objective: To study TLR4 expression in human prostate cancer PC3 cells and the related intracellular signaling mechanisms. Methods: Human prostate cancer PC3 cells were stimulated with TLR4-specific ligand lipopolysaccharide (LPS), then the cells and supernatants were collected 0, 2, 6, 12, 24, and 48 hours after LPS stimulation. TLR4 mRNA and protein expression was examined by reverse transcription-PCR and Western blotting analysis, respectively. The mRNA expression of TGF-β, VEGF, 1L-8, COX-2, and MMP3 was also measured by reverse transcription-PCR, and the levels of VEGF, IL-8 in the supernatants were examined by ELISA. To further study the related signaling pathway, MAPK and NF-κB signaling pathways were blocked by specific inhibitors in PC3 cells before LPS stimulations the cells were collected after 4 hours and the supernatants were collected after 24 hours; and the above mentioned factors were examined by reverse transcription-PCR and ELISA again. Results: TLR4 expression was up-regulated by LPS stimulation in human prostate cancer PC3 cells, which significantly increased mRNA expression of TGF-β, VEGF, IL-8, COX-2, and MMP3 and secretion of VEGF and IL-8 in the supernatants (P<0.05); further study showed that p38 MAPK and NF-κB signal pathways were involved in the process. Conclusion: TLR4 signaling promotes VEGF and IL-8 secretion through p38 MAPK and NF-κB signal pathways.