Objective To discuss the relationship of cerebral infarction with hyperhomocysteinemia and the relationship between hyperhomocysteinemia and folic acid and Vitamine B12.Method We measured the concentrations of homocysteine with FIPA(fluorescence polarization immunoassay)and Vitamin B12 and folic acid with chemiluminescent competitive immunoassay in 40 cerebral infarction patients and 30 healthy controls.Results The concentration of homocysteine in study group was higher than the controls' (P< 0.01).Serum folic acid level in study group was lower than that in control group (P< 0.05).There is negative correlation between plasma homocysteine and serum folic acid(P< 0.05). Conclusions Hyperhomocysteinemia is an independent risk factor of atherosclerotic cerebral infarction.One reason of increased level of homocysteine in blood is that the deficiency of cofactors of enzymes involved in metabolism process.

Objective To investigate the clinical characteristics,distribution and drug sensitivity of pathogens causing intravenous catheter-related bloodstream infections (CRBSIs) in pediatric intensive care unit (PICU) so as to use antibiotics reasonably.Methods All patients with CRBSIs in PICU of Guangdong General Hospital from September 2009 to September 2014 were investigated and the drug resistance profiles of pathogens causing CRBSIs were also analyzed retrospectively.Results Between 2009 and 2014,there were totally 10 834 catheter days and 23 episodes of CRBSIs with an incidence of 2.1 infections per 1 000 catheter days.Catheter indwell time ＜ 7 days in 9 cases (39.1％),8 to 14 days in 10 cases (43.5％),14 to 21 days in 4 cases (17.4％).There were 13 strains (56.6％) of gram-positive bacteria,5 strains (21.7％) of gram-negative bacteria and 5 strains (21.7％) of fungi.The main pathogens causing CRBSIs were coagulase negative Staphylococci (7 strains,30.4％),Staphylococcus aureus (3 strains,13.0％),Candida albicans(3 strains,13.0％),Candida parapsilosis(2 strains,8.7％),and Enterobacter cloacae (2 strains,8.7 ％).The susceptibility to Vancomycin,Linezolid and Teicoplanin of coagulase negative Staphylococ cus such as S.epidermidis and to Imipenem,Piperacillin/Tazobactam,Cefoperazone/ Sulbactam and Amikacin of gram-positive bacteria arrived at 100.0％,respectively.The candida were 100％ susceptible to Amphotericin B,5-Flucytosine,Fluconazole and Voriconazole.Twenty-one cases (91.3％) received antibiotic treatment versus no antibiotic in 2 cases (8.7％).The average number of antibiotic kinds administered on the patients with fungal infection was 4.4,bacteria were 1.4.Ten cases (43.5％) treatment with 1 kind of antibiotic,4 cases (17.4％) with 2,4 cases (17.4％) with 3,5 cases (21.7％) with more than 3.Twenty-two cases (95.7％) cured and 1 case died (4.3％).Conclusions The major species of pathogen causing CRBSIs was coagulase negative staphylococci in PICU.It is critical for clinicians to guard against fungal infection because of prolonged catheter indwelling time and more antibiotics administered before indwelling catheter.It is effective way to prevent the CRBSIs by reasonably using antibiotics and shortening the time of catheter indwelling.Monitoring CRBSIs pathogenic bacteria distribution and drug susceptibility helps reasonable administration of antibiotics in the earlier time.

Objective To investigate the clinical outcomes of immunocompromised (IC) children with pediatric acute respiratory distress syndrome (PARDS) in pediatric intensive care unit (PICU).Methods Fifty-six PADRS children were enrolled and the data of clinical characteristics,immunological status,complications,treatments and outcomes were collected and analyzed by using univariate and multivariate regression models.Results There were 20 children in the immunocompromised group and 36 in the control group.Immunocompromised children were older and weighted greater than the control ones (P=0.003 and P＜0.01,respectively).Peripheral blood leukocyte,neutrophil and platelet counts were significantly lower in IC group compared with control group (P=0.060,P=0.006 and P=0.023,respectively).In addition,high-frequency oscillatory ventilation (HFOV) was used less frequently in the IC group (P=0.015).The PICU mortality of the IC group was significantly higher than that of control group (P=0.003).The proportion of IC patients and the incidence of ventilator-associated lung injury differed significantly between survivors and non-survivors (P=0.003 and P=0.046,respectively).After adjusting for other confounding factors by using multivariate logistic regression analysis,IC was associated with a higher mortality (OR=6.986,95％ CI:1.812-26.930,P=0.005).Survival analysis also indicated that IC children with ARDS had lower 28-day survival rate than the non-IC children (P=0.022).Conclusions IC children with PARDS have a higher PICU mortality than children with normal immune function.Immunocompromise is an important predictor of poor outcomes in children with PARDS.

Objective:To explore the effect of pediatric critical illness score (PCIS), pediatric risk of mortality Ⅲ score (PRISM Ⅲ), pediatric logistic organ dysfunction 2 (PELOD-2), pediatric sequential organ failure assessment (p-SOFA) score and Glasglow coma scale (GCS) in the prognosis evaluation of septic-associated encephalopathy (SAE).Methods:The data of children with SAE admitted to the Pediatric Intensive Care Unit (PICU), Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences from January 2010 to December 2020 were retrospectively analyzed. They were divided into the survival and death groups according to the clinical outcome on the 28th day after admission. The efficiency of PCIS, PRISM Ⅲ, PELOD-2, p-SOFA and GCS scores for predicting death were evaluated by the area under the ROC curve (AUC). The Hosmer-Lemeshow goodness-of-fit test assessed the calibration of each scoring system.Results:Up to 28 d after admission, 72 of 82 children with SAE survived and 10 died, with a mortality rate of 12.20%. Compared with the survival group, the death group had significantly lower GCS [7 (3, 12) vs. 12 (8, 14)] and PCIS scores [76 (64, 82) vs. 82 (78, 88)], and significantly higher PRISM Ⅲ [14 (12, 17) vs. 7 (3, 12)], PELOD-2 [8 (5, 13) vs. 4 (2, 7)] and p-SOFA scores [11 (5, 12) vs. 6 (3, 9)] ( P<0.05). The AUCs of PCIS, PRISM Ⅲ, PELOD-2, p-SOFA and GCS scores for predicting SAE prognosis were 0.773 ( P=0.012, AUC>0.7), 0.832 ( P=0.02, AUC>0.7), 0.767 ( P=0.014, AUC>0.7), 0.688 ( P=0.084, AUC<0.7), and 0.692 ( P=0.077,AUC<0.7), respectively. Hosmer-Lemeshow goodness-of-fit test showed that PCIS ( χ2=5.329, P=0.722) predicted the mortality and the actual mortality in the best fitting effect, while PRISM Ⅲ ( χ2=12.877, P=0.177), PELOD-2 ( χ2=8.487, P=0.205), p-SOFA ( χ2=9.048, P=0.338) and GCS ( χ2=3.780, P=0.848) had poor fitting effect. Conclusions:The PCIS, PRISM Ⅲ and PELOD-2 scores have good predictive ability assessing the prognosis of children with SAE, while the PCIS score can more accurately evaluate the fitting effect of SAE prognosis prediction.

The effects of tanshinone IIA on the proliferation of the human non-small cell lung cancer cell line A549 and its possible mechanism on the VEGF/VEGFR signal pathway were investigated. The exploration of the interaction between tanshinone IIA and its target proteins provides a feasible platform for studying the anticancer mechanism of active components of herbs. The CCK-8 assay was used to evaluate the proliferative activity of A549 cells treated with tanshinone IIA (2.5-80 μmol/L) for 24, 48 and 72 h, respectively. Flow cytometry was used for the detection of cell apoptosis and cell cycle perturbation. VEGF and VEGFR2 expression were studied by Western blotting. The binding mode of tanshinone IIA within the crystal structure of the VEGFR2 protein was evaluated with molecular docking analysis by use of the CDOCKER algorithm in Discovery Studio 2.1. The CCK-8 results showed that tanshinone IIA can significantly inhibit A549 cell proliferation in a dose- and time-dependent manner. Flow cytometry results showed that the apoptosis rate of tested group was higher than the vehicle control, and tanshinone IIA-treated cells accumulated at the S phase, which was higher than the vehicle control. Furthermore, the expression of VEGF and VEGFR2 was decreased in Western blot. Finally, molecular docking analysis revealed that tanshinone IIA could be stably docked into the kinase domain of VEGFR2 protein with its unique modes to form H-bonds with Cys917 and π-π stacking interactions with Val848. In conclusion, tanshinone IIA may suppress A549 proliferation, induce apoptosis and cell cycle arrest at the S phase. This drug may suppress angiogenesis by targeting the protein kinase domains of VEGF/VEGFR2.