Environmental Microbiology is an important basic course of Environmental Engineering.Its characteristic is content broad,quick development and strong practicality,thus this curriculum's teaching has certain degree of difficulty.Some suggestions and concrete measures about teaching reform,which included curriculum's course content,teaching method,experiment teaching and assessment methods were proposed in this paper.

This paper explored the educational reform of dispensing Chinese drugherbs. The education reform included implementing the project of teaching methods, implementing modern experimental methods, cultivating comprehensive quality of students, training students' creative thinking, and stimulating the initiative of students. All these strategies could improve the quality of teaching and make students' comprehensive abilities meet the demand.

OBJECTIVE To study the clinical characteristics,prevention and treatment of nosocomial fungemia.METHODS Fifty four consecutive patients with nosocomial fungemia were studied in clinical retrospective manner.RESULTS Sixty fungal strains were isolated from blood.Candida was the predominant pathogenic organism(86.7%),6 cases had mixed infection causing by two fungal species(11.1%).Twenty two cases had concomitant bacteremia(40.7%).Overall mortality rate was 68.5%,directly related mortality rate in treatment group was significantly lower than that in nontreatment one(28.9% vs.88.9%,χ2=11.268，P＜0.01).Effective rate of amphotericin B was 68.8%,fluconazole 70.8%,combined treatment 80.0%.CONCLUSIONS Fungal infection has become prominently fatal cause of critically ill patients.Removing predisposing factors,monitoring fungal pathogen and effective antifungal therapy are important measures to reduce the incidence and mortality of fungal infection.Fluconazole and amphotericin B are effective drugs of treating deep fungal infection.

Adenoma, Acidophil ; metabolism ; Adult ; Angiomyolipoma ; genetics ; metabolism ; pathology ; Carcinoma, Renal Cell ; metabolism ; Codon ; Diagnosis, Differential ; Exons ; Female ; Follow-Up Studies ; Gene Deletion ; Genes, p53 ; Humans ; Kidney Neoplasms ; genetics ; metabolism ; pathology ; Male ; Melanoma-Specific Antigens ; metabolism ; Middle Aged ; Retrospective Studies ; Tumor Suppressor Protein p53 ; genetics ; metabolism

A strain was separeted from the Yueqing bay using pine pollen baiting.The vegetative thallus of the separated strain is oval and unincleate.It possesses a cell wall composed of many compact layers of closely pressed scales, which can be resolved where the cell wall is disrupted.The radiating branched extensions of the thallus, the ectoplasmic net, emerges from the sagenogenetosome.Asexual reproduction is by conversion of the vegetative thallus to many biflagellate zoospores, during which tetrads of cells are formed.It was identified with Schizochytrium sp.based on the features mentioned above.

Humans ; Musculoskeletal Diseases ; epidemiology ; prevention & control ; Occupational Diseases ; epidemiology ; prevention & control

OBJECTIVETo evaluate the effects of Yili dark bee propolis on the main cariogenic biofilm and mechanisms.

METHODSSusceptibilities to the ethanolic extract of propolis against Streptococcus mutans (S. mutans), Streptococcus sobrinus (S. sobrinus), Streptococcus sanguis (S. sanguis), Actinomyces viscosus (A. viscosus), and Actinomyces naeslundii (A. naeslundii) were analyzed by crystal violet stain method to determine the minimum biofilm eradication concentration (MBEC). The biofilm was initially cultivated for 24 h. Subsequently, the propolis groups with different concentration MBEC and initial pH 7.0 were cultured for 24 h. Moreover, the pH value was measured to evaluate the acid-producing ability of the tested plaque biofilm. The effects of propolis on the insoluble extracellular polysaccharide synthesis of S. mutans biofilm were evaluated by anthrone method.

RESULTSThe MBEC of Yili propolis on S. mutans, S. sobrinus, S. sanguis, A. viscosus, and A. naeslundii were 6.25, 1.56, 3.13, 0.78, and 0.78 mg.mL-1, respectively. Propolis could decrease the ΔpH of the tested plaque biofilm, and the differences between the control and propolis groups were statistically significant (P<0.05). At MBEC, propolis could reduce the ability of S. mutans in synthesizing insoluble extracellular polysaccharides.

CONCLUSIONYili propolis demonstrate remarkable eradicative effects on the cariogenic plaque biofilm, showing inhibition of the synthesis of biofilm-produced acids and insoluble extracellular polysaccharides.

Objective To determine the role of activated status of peroxisome proliferator-activated receptorγ/nuclear factor-κB ( PPAR-γ/NF-κB ) in coagulation disorders induced by sepsis. Methods Forty male Sprague-Dawley ( SD ) rats were randomly divided into four groups, n = 10 in each group: control group, lipopolysaccharide ( LPS ) challenged group, rosiglitazone ( ROSI, selective agonist of PPAR-γ) pretreatment group, and GW9662 ( PPAR-γ antagonist ) pretreatment group. The sepsis model was reproduced by injection of 6 mg/kg LPS via sublingual vein, and the rats in control group were injected with 2 mL/kg normal saline. The rats in ROSI pretreatment group were given 0.3 mg/kg ROSI by sublingual venous injection followed by injection of LPS 30 minutes later;and in GW9662 pretreatment group rats were given 0.3 mg/kg GW9662 by sublingual venous injection followed by 0.3 mg/kg ROSI 15 minutes later, followed by injection of LPS 30 minutes later. Blood was collected at 4 hours after LPS administration, and the expressions of PPAR-γ and NF-κBp65 in peripheral blood mononuclear cell ( PBMC ) were determined with immunocytocheminal technique and graph analysis. Plasma prothrombin time ( PT ), activated partial thromboplastin time ( APTT ), fibrinogen ( FIB ), and D-dimer were determined simultaneously. Results① PPAR-γ/NF-κB pathway: the expressions of PPAR-γ and NF-κBp65 were lowered in control group, and they were expressed in cytoplasm. In LPS challenged group the expression of PPAR-γ ( gray value ) was slightly increased but with no significant difference as compared with control group ( 111.01±4.06 vs. 98.46±5.99, P >0.05 ). In ROSI pretreatment group the expression of PPAR-γ( gray value ) was significantly higher than that in LPS challenged group ( 214.38±5.79 vs. 111.01±4.06, P<0.01 ), with dislocation into nuclei. In GW9662 pretreatment group the expression of PPAR-γ ( gray value ) was lowered but without significant difference compared with that of control group ( 44.21±2.64 vs. 98.46±5.99, P>0.05 ). In LPS challenged group the expression of NF-κBp65 ( gray value ) was significantly higher than that in control group ( 249.48±6.86 vs. 105.81±10.19, P < 0.01 ), and it was translocated into the nuclei. In ROSI pretreatment group the expression of NF-κBp65 ( gray value ) was significantly lower than that in LPS challenged group ( 102.47±8.05 vs. 249.48±6.86, P < 0.01 ), and it lied in cytoplasm. In GW9662 pretreatment group the expression of NF-κBp65 ( gray value ) showed no significant difference as compared with that of LPS challenged group ( 214.84±7.91 vs. 249.48±6.86, P>0.05 ).②Coagulation:compared with control group, PT and APTT were significantly prolonged, FIB was significantly decreased, and D-dimer was significantly increased in LPS challenged group [ PT ( s ):18.32±2.03 vs. 12.22±1.38, APTT ( s ):40.05±2.72 vs. 26.64±2.73, FIB ( g/L ): 1.65±0.51 vs. 3.60±0.37, D-dimer ( mg/L ): 2.58±0.73 vs. 0.37±0.06, all P < 0.01 ]. Compared with LPS challenged group, APTT and PT were significantly shortened, FIB was significantly increased, and D-dimer was significantly lowered in ROSI pretreatment group [ PT ( s ):13.93±1.67 vs. 18.32±2.03, APTT ( s ):30.29±0.86 vs. 40.05±2.72, FIB ( g/L ):3.18±0.69 vs 1.65±0.51, D-dimer ( mg/L ):0.40±0.12 vs. 2.58±0.73, all P<0.01 ]. All parameters in GW9662 pretreatment group showed no significant difference as compared with those of LPS challenged group. Conclusions PPAR-γagonist ROSI may ameliorate coagulation disorders in septic rats. PPAR-γ/NF-κB transduction pathway plays an important role in septic coagulopathy.

Objective To discuss the clinical value of electronic bronchoscopic intervention in treatment of tracheobronchial tuberculosis. Methods Clinical features of 45 patients with tracheal and bronchial tuberculosis which were confirmed by electronic bronchoscope and treated by bronchoscopic intervention were retrospectively analyzed from January 2007 to December 2013 in our hospital. Results The efficiency of bronchoscopic intervention is 88.9%, of which 28 cases achieved a significant effect (accounting for 62.2%). Conclusion Electronic bronchoscopic intervention is a preferred way in treatment of tracheobronchial tuberculosis.

Aim Tostudytheeffectsofferulicacid (FA) on doxorubicin (DOX) induced cellular injury inH9c2ratmyocardialcells.Methods H9c2cells were treated with 1μmol·L-1 DOX treated for 24 h to establish a myocardial injury model. 10, 20, 40μmol ·L-1 FA was added 2 h before DOX treatment. Cell viability was measured by cell counter kit ( CCK-8 ) . Morphological changes were observed by phase contrast microscope. LDH, CK, MDA, SOD levels were detec-ted by biochemical kits. Intracellular level of reactive oxygen species ( ROS) was examined by DCF-DA stai-ning with flow cytometry. Cellular apoptosis was detec-ted by AO-EB staining and DNA agarose gel electro-phoresis. The expression of caspase-3, Bax, Bcl-2 was evaluatedbyWesternblot.Results Exposureof H9c2 cells to DOX led to decrease in cell viability, in-crease in stress and apoptosis. FA pre-treatment im-proved cell viability in a dose-dependent manner, at-tenuated leakage of LDH and CK, and reversed mor-phological changes induced by DOX. FA suppressed DOX-induced oxidative stress as evidenced by reducing ROS and MDA generation and increasing SOD enzyme activity. FA depressed myocardial apoptosis by down-regulating pro-apoptotic protein caspase-3 and Bax, whereas up-regulating apoptosis inhibitory protein Bcl-2.Conclusions FAhasaprotectiveeffectonDOX-induced injury in H9c2 cells. This protection may re-sult from inhibition of myocardial oxidative stress and apoptosis.