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Objective To investigate the risk factors and prognostic factors of bloodstream infection in intensive care unit(ICU). Methods The data of patients with bloodstream infection in ICU of Harrison International Peace Hospital from October 2014 to October 2017 were retrospectively analyzed and 210 patients with negative blood culture were selected. The physiological and laboratory parameters were compared between patients with positive blood culture and those with negative blood culture. Multivariate logistic regression analysis was used to screen the risk factors of bloodstream infection. Overall, 189 patients with bloodstream infection were classified into survival group(n=121)and death group(n=68)according to the survival status within 30 days after blood culture. The risk factors related to 30-day patient outcome following bloodstream infection were analyzed. Results A total of 189 cases of bloodstream infection were identified in the ICU during the 3-year period, including 118 cases due to gram-negative bacilli, 65 cases caused by gram-positive cocci, and 6 cases due to fungi. Univariate analysis showed that prior use of carbapenem or third generation cephalosporins, central venous catheterization, length of hospital stay≥2 weeks, and mechanical ventilation were the risk factors of bloodstream infection(P<0.05). Multivariate logistic regression analysis showed that prior use of carbapenems or third-generation cephalosporins(OR=20.15), central venous catheterization(OR=25.34), and mechanical ventilation(OR=18.26)were independent risk factors for bloodstream infection in ICU patients. Univariate analysis showed that prior use of carbapenem or third generation cephalosporins, mixed infection or septic shock, multi-drug resistant bacterial infection, and high APACHE Ⅱ(acute physiological and chronic health evaluation system Ⅱ)score were significant risk factors for 30-day mortality following bloodstream infection(P<0.05). Multivariate logistic regression analysis showed mixed infection or septic shock(OR=15.30), multi-drug resistant bacterial infection(OR=10.75)and high APACHE Ⅱ score(OR=13.70)were independent risk factors for 30-day mortality following bloodstream infection. Conclusions Prior use of carbapenem or third generation cephalosporins, central venous catheterization and mechanical ventilation are independent risk factors for bloodstream infection in ICU patients. Mixed infection or septic shock, multi-drug resistant bacterial infection, and high APACHE Ⅱ score are independent risk factors for 30-day mortality following bloodstream infection.
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Objective To observe the mechanisms of autophagic eukaryotic cells in Acinetobacter microvilli removal and protein histological study on apoptosis induced by macrophages .Methods A model of Acinetobacter baumannii infection was established in 24 female OCR mice .The mice were randomly divided into control group (n= 12) and observation group (n= 12) .The control group was injected with normal saline ,and the observation group was injected with autophagy eukaryotic cells ,the histopathological changes of Acinetobacter and the induction of macrophage apoptosis were observed .Results There was no significant difference in the bacterial counts between the two groups of mice immediately after implantation (P>0 .05) ,the bacterial counts in the 24 and 48 h in the observation group was significantly lower than that in the control group (P<0 .05) .The lung tissue of mice in the ob-servation group injected after autophagy was normal ,the alveolar cavity was open ,no abnormal substances were found ,the alveolar wall was not obviously thickened ,and no inflammatory cell infiltration was found in the wall .The mice in the control group were in-jected with normal saline and lacked the ability to remove Acinetobacter ,resulting in a large number of inflammatory cell infiltra-tion ,vasodilatation ,and congestion in some mice .Conclusion Autophagic eukaryotic cells injected with Acinetobacter baumannii can increase the clearance rate ,induce apoptosis of macrophages and improve the quality of Acinetobacter baumannii .
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Objective To observe the mechanisms of autophagic eukaryotic cells in Acinetobacter microvilli removal and protein histological study on apoptosis induced by macrophages .Methods A model of Acinetobacter baumannii infection was established in 24 female OCR mice .The mice were randomly divided into control group (n= 12) and observation group (n= 12) .The control group was injected with normal saline ,and the observation group was injected with autophagy eukaryotic cells ,the histopathological changes of Acinetobacter and the induction of macrophage apoptosis were observed .Results There was no significant difference in the bacterial counts between the two groups of mice immediately after implantation (P>0 .05) ,the bacterial counts in the 24 and 48 h in the observation group was significantly lower than that in the control group (P<0 .05) .The lung tissue of mice in the ob-servation group injected after autophagy was normal ,the alveolar cavity was open ,no abnormal substances were found ,the alveolar wall was not obviously thickened ,and no inflammatory cell infiltration was found in the wall .The mice in the control group were in-jected with normal saline and lacked the ability to remove Acinetobacter ,resulting in a large number of inflammatory cell infiltra-tion ,vasodilatation ,and congestion in some mice .Conclusion Autophagic eukaryotic cells injected with Acinetobacter baumannii can increase the clearance rate ,induce apoptosis of macrophages and improve the quality of Acinetobacter baumannii .
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OBJECTIVE:To investigate the role of interferon to increase the sensibilization of MGMT positive glioma stem cel s to temozolomide in vitro. METHODS:Glioma cel lines, U251 and SKMG-4, were induced by suspended cloning bal formation method to harvest MGMT positive glioma stem cel s, U251G and SKMG-4G. Cel counting kit-8 assay was used to detect the kil ing effect of interferonα/βcombined with temozolomide on MGMT positive glioma stem cel s. RT-PCR and western blot assay were employed to determine the expression of MGMT and nuclear factorκB in MGMT positive glioma stem cel s. RESULTS AND CONCLUSION:Western blot results showed positive expression of MGMT in U251G and SKMG-4G cel s at protein levels. After intervention with interferonα/β, the mRNA expression of MGMT and nuclear factorκB in SKMG-4G and U251G cel s was reduced significantly, and then further decreased after temozolomide treatment. These findings indicate that interferonα/βcan remarkably strengthen the kil ing effect of temozolomide on MGMT positive glioma stem cel s.
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Lithium carbonate could be used to treat or prevent brain damage following traumatic injury and neurodegenerative diseases.It has been shown that its protective effect is related to protein kinase C (PKC) and extracellular signal-related kinase (ERK).It was demonstrated that PDBu,a PKC activator,inhibited amplitudes of delayed rectifier potassium current (It,) and produced a hyperpolarizing shift in the activation-voltage curve.The responses to PDBu were inhibited by lithium carbonate (50μmol/L).Further studies showed that when pretreated with MEK/ERK inhibitor U0126 (20 μmol/L),although PDBu significantly reduced IK,lithium did not reverse the effect of PDBu.Thus,the results suggested that PKC signaling cascades,along with MAPK (mitogen-activated protein kinase) pathway,were required in the phosphorylation of potassium channel,which was presented by regulation of potassium channel characteristic.AC-cAMP and their eross-talk with GC-cGMP pathway could also modulate the effect of lithium on PKC activation,which could be one of underlying mechanisms likely related to neuroprotective effect of lithium.
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Recent studies show that epileptic seizures result in mass free radical production and induce oxidative damage because of relative deficiency in anti-oxygen system.Mitochondrium is crucial to sustaining energy metabolism,regulating cell death,synthesising neurotransmitter and oxidating fatty acid.Mitochondrium is not only the place for free radical production,but also the target of oxidative damage.Mitochondrial oxidative stress and resultant dysfunction enhance epileptic susceptibility.Seizure-induced free radical can influence energy metabolism,destroy DNA construction and induce apoptosis in neurontoxic consequences in epilepsy.