Acute kidney injury following percutaneous coronary intervention （PCI） is associated with a worse outcome. However, the risk factors and outcomes of acute kidney injury （AKI） in patients after intracoronary stent ...Acute kidney injury following percutaneous coronary intervention （PCI） is associated with a worse outcome. However, the risk factors and outcomes of acute kidney injury （AKI） in patients after intracoronary stent implantation are still unknown. A retrospective case control study was done in 325 patients who underwent intracoronary stent implantation from January 2010 to March 2011 at the Drum Tower Hospital of Nanjing University School of Medicine. Those were excluded from the study if they had incomplete clinical data. The patients were divided into a normal group and a AKI group according to the standard of post-operation day 7 to identify AKI. The parameters of the patients included： 1） pre-operative ones： age, gender, hypertension, diabetes mellitus, cerebrovascular disease, left ventricular insufficiency, peripheral angiopathy, creatinine, urea nitrogen, estimated glomerular filtration rate （eGFR）, hyperuricemia, proteinuria, emergency operation, hydration, medications （ACEI/ARBs, statins）; 2） intraoperative ones： dose of contrast media, operative time, hypotension; and 3） postoperative one： hypotension. The parameters were analyzed with univariate analysis and multivariate logistical regression analysis. Of the 325 patients, 51（15.7%） developed AKI. Hospital day and in-hospital mortality were increased significantly in the AKI-group. Univariate analysis showed that age, pre-operative parameters （left ventricular insufficiency, peripheral angiopathy, creatinine, urea nitrogen, estimated glomerular filtration rate, hyperuricemia, proteinuria, hydration）, emergency operation, intraoperative parameters （operative time, hypotension） and postoperative hypotension were significantly different. However, multivariate logistic regression analysis revealed that increased age （OR=0.253, 95%CI=0.088-0.727）, pre-operative proteinuria （OR=5.351, 95%CI=2.128-13.459）, pre-operative left ventricular insufficiency （OR=8.704, 95%CI=3.170-23.898）, eGFR〈60 ml/min/1.73 m2 展开更多
BACKGROUND： Vibrio vulnifi cus inside the body could activate the NF-!B signaling pathwayand initiate the inflammatory cascade. The lung is one of the earliest organs affected by sepsisassociated with acute lung inju...BACKGROUND： Vibrio vulnifi cus inside the body could activate the NF-!B signaling pathwayand initiate the inflammatory cascade. The lung is one of the earliest organs affected by sepsisassociated with acute lung injury. High mobility group protein B1 （HMGB1） is an important late-actingpro-infl ammatory cytokine involving in the pathophysiology of sepsis. It is also involved in the injuryprocess in the lung, liver and intestine. There has been no report on the involvement of HMGB1 inVibrio vulnifi cus sepsis-induced lung injury.METHODS： Sixty rats were randomly divided into a normal control group （group A, n=10） anda Vibrio vulnificus sepsis group （group B, n=50）. Sepsis was induced in the rats by subcutaneousinjection of Vibrio vulnificus （concentration 6×108 cfu/mL, volume 0.1 mL/100g）） into the left lowerlimbs. The rats in group B were sacrifi ced separately 1, 6, 12, 24, and 48 hours after the infection.Their lungs were stored as specimens, lung water content was measured, and lung pathology wasobserved under a light microscope. The expressions of the HMGB1 gene and protein in the lungswere detected by RT-PCR and Western blot. Data were analyzed with one-way analysis of variance（ANOVA） and the LSD method for pair-wise comparison between the two groups. P〈0.05 wasconsidered statistically signifi cant.RESULTS： Compared to group A （0.652±0.177）, HMGB1 mRNA expression in the lungs ofgroup B was signifi cantly higher at 0 hour （1.161±0.358, P=0.013）, 24 hours （1.679±0.235, P=0.000）,and 48 hours （1.258±0.274, P=0.004） （P〈0.05）, and peaked at 24 hours. Compared to group A（0.594±0.190）, HMGB1 protein expression at 6 hours （1.408±0.567, P=0.026） after infection wassignificantly increased （P〈0. 05）, and peaked at 24 hours （2.415±1.064, P=0.000） after infection.Compared to group A （0.699±0.054）, lung water content was significantly increased at 6 hours（0.759±0.030, P=0.001）,12 hours （0.767±0.023, P=0.000）, 24 hours （0.771±0.04展开更多
BACKGROUND:Pulmonary fibrosis(PF)is one of the main causes of death in patients with paraquat(PQ)poisoning.This study aimed to evaluate the relationship between mitochondrial fi ssion and oxidative stress in PQ-induce...BACKGROUND:Pulmonary fibrosis(PF)is one of the main causes of death in patients with paraquat(PQ)poisoning.This study aimed to evaluate the relationship between mitochondrial fi ssion and oxidative stress in PQ-induced epithelial-mesenchymal transition(EMT)and PF.METHODS:C57BL/6 mice and MLE-12 cells were exposed to PQ to construct a PF model in vivo and in vitro.Histological changes in the lungs were examined by hematoxylin and eosin(H&E)staining.Mitochondrial morphology was detected by MitoTracker®Deep Red FM or transmission electron microscopy(TEM).Western blotting and immunofluorescence were used to determine the expression of protein.The migration ability of the cells was detected by the cell scratch test.Mitochondrial DNA(mtDNA)levels were assessed by real-time polymerase chain reaction(PCR).Enzyme-linked immunosorbent assay(ELISA)was applied to detect cytokine levels.Superoxide dismutase(SOD)activity and the levels of glutathione(GSH)and malondialdehyde(MDA)were detected by chemichromatometry.RESULTS:PQ exposure caused EMT and PF in vivo and in vitro.PQ destroyed mitochondrial structure and enhanced the expression of dynamin-related protein 1(Drp1),which were accompanied by oxidative stress.Inhibiting mitochondrial fission using mitochondrial division inhibitor-1(Mdivi-1),a selective inhibitor of Drp1,attenuated PQ-induced EMT and oxidative damage.Treatment with N-acetyl-L-cysteine(NAC),an antioxidant,reduced Drp1 expression,attenuated mitochondrial structure damage and inhibited PQ-induced EMT and PF.Both Mdivi-1 and NAC treatment markedly suppressed mtDNA release,the expression of Toll-like receptor 9(TLR9)and phosphorylation(P)-NF-κB p65 as well as cytokines(interleukin 6[IL-6],interleukin-1β[IL-1β],and tumor necrosis factor-α[TNF-α])production.CONCLUSION:Mutual promotion of mitochondrial fission and oxidative stress contributes to EMT in PQ-induced PF,which is associated with the mtDNA/TLR9/NF-κB pathway.展开更多
Emerged evidence has indicated that immunosuppression is involved in the occurrence and development of sepsis.To provide clinical practice recommendations on the immune function in sepsis,an expert consensus focusing ...Emerged evidence has indicated that immunosuppression is involved in the occurrence and development of sepsis.To provide clinical practice recommendations on the immune function in sepsis,an expert consensus focusing on the monitoring and treatment of sepsis-induced immunosuppression was developed.Literature related to the immune monitoring and treatment of sepsis were retrieved from PubMed,Web of Science,and Chinese National Knowledge Infrastructure to design items and expert opinions were collected through an online questionnaire.Then,the Delphi method was used to form consensus opinions,and RAND appropriateness method was developed to provide consistency evaluation and recommendation levels for consensus opinions.This consensus achieved satisfactory results through two rounds of questionnaire survey,with 2 statements rated as perfect consistency,13 as very good consistency,and 9 as good consistency.After summarizing the results,a total of 14 strong recommended opinions,8 weak recommended opinions and 2 non-recommended opinions were produced.Finally,a face-to-face discussion of the consensus opinions was performed through an online meeting,and all judges unanimously agreed on the content of this consensus.In summary,this expert consensus provides a preliminary guidance for the monitoring and treatment of immunosuppression in patients with sepsis.展开更多
Background：Mitofusin-2 （MFN2）,a well-known mitochondrial fusion protein,has been shown to participate in innate immunity,but its role in mediating adaptive immunity remains poorly characterized.In this study,we exp...Background：Mitofusin-2 （MFN2）,a well-known mitochondrial fusion protein,has been shown to participate in innate immunity,but its role in mediating adaptive immunity remains poorly characterized.In this study,we explored the potential role of MFN2 in mediating the immune function of T lymphocytes.Methods：We manipulated MFN2 gone expression in Jurkat cells via lentiviral transduction of MFN2 small interfering RNA （siRNA） or full-length MFN2.After transduction,the immune response and its underlying mechanism were determined in Jurkat cells.One-way analysis of variance and Student＇s t-test were performed to determine the statistical significance between the groups.Results：Overexpression of MFN2 enhanced the immune response of T lymphocytes by upregulating Ca2＋ （359.280 ± 10.130 vs.266.940 ± 10.170,P =0.000）,calcineurin （0.513 ± 0.014 vs.0.403 ± 0.020 nmol/L,P =0.024）,and nuclear factor of activated T cells （NFATs） activation （1.040 ± 0.086 vs.0.700 ± 0.115,P =0.005）,whereas depletion of MFN2 impaired the immune function ofT lymphocytes by downregulating Ca2＋ （141.140 ± 14.670 vs.267.060 ± 9.230,P =0.000）,calcineurin （0.054 ± 0.030 nmol/L vs.0.404 ± 0.063 nmol/L,P =0.000）,and NFAT activation （0.500 ± 0.025 vs.0.720 ± 0.061,P =0.012）.Furthermore,upregulated calcineurin partially reversed the negative effects ofMFN2 siRNA on T cell-mediated immunity evidenced by elevations in T cell proliferation （1.120 ± 0.048 vs.0.580 ± 0.078,P =0.040）,interleukin-2 （IL-2） production （473.300 ± 24.100 vs.175.330 ± 12.900 pg/ml,P =0.000）,and the interferon-γ/IL-4 ratio （3.080 ± 0.156 vs.0.953 ± 0.093,P =0.000）.Meanwhile,calcineurin activity inhibitor depleted the positive effects of overexpressed MFN2 on T cells function.Conclusions：Our findings suggest that MFN2 may regulate T cell immune functions primarily through the Ca2＋-calcineurin-NFAT pathway.MFN2 may represent a potential therapeutic target for T cell immune dysfunction-related diseases.展开更多
1.Introduction Sudden cardiac death(SCD)refers to sudden death due to a variety of cardiac causes.It is manifested as a sudden loss of consciousness,cardiac arrest,and respiratory arrest and generally shows early symp...1.Introduction Sudden cardiac death(SCD)refers to sudden death due to a variety of cardiac causes.It is manifested as a sudden loss of consciousness,cardiac arrest,and respiratory arrest and generally shows early symptoms that are atypical and not easily detected[1].According to a recent study,nearly 544000 patients suffer from SCD every year in China[2].展开更多
BACKGROUND:Due to the still sparse literature in China,the investigation of hyperoxemia management is required.Thus,we aim to conduct a retrospective study to provide more information about hyperoxemia management in i...BACKGROUND:Due to the still sparse literature in China,the investigation of hyperoxemia management is required.Thus,we aim to conduct a retrospective study to provide more information about hyperoxemia management in intensive care unit(ICU)patients.METHODS:We retrospectively screened the medical records of adult patients(age≥18 years)who required mechanical ventilation(MV)≥24 hours from January 1,2018,to December 31,2018.All arterial blood gas(ABG)tested during MV was retrieved,and MV settings were recorded.The median arterial partial pressure of oxygen(PaO2)>120 mmHg(1 mmHg=0.133 kPa)was defined as mild to moderate hyperoxemia,and PaO2>300 mmHg as extreme hyperoxemia.Intensivists’response to hyperoxemia was assessed based on the reduction of fraction of inspired oxygen(FiO2)within one hour after hyperoxemia was recorded.Multivariable logistic regression analysis was performed to determine the independent factors associated with the intensivists’response to hyperoxemia.RESULTS:A total of 592 patients were fi nally analyzed.The median Acute Physiology and Chronic Health Evaluation II(APACHE II)score was 21(15-26).The PaO2,arterial oxygen saturation(SaO2),FiO2,and positive end expiratory pressure(PEEP)were 96.4(74.0-126.0)mmHg,97.8%(95.2%-99.1%),0.4(0.4-0.5),and 5(3-6)cmH2O,respectively.Totally 174(29.39%)patients had PaO2>120 mmHg,and 19(3.21%)patients had extreme hyperoxemia at PaO2>300 mmHg.In cases of mild to moderate hyperoxemia with FiO2≤0.4,only 13(2.20%)patients had a decrease in FiO2 within one hour.The multivariable logistic regression analysis showed that a positive response was independently associated with FiO2(odds ratio[OR]1.09,95%confi dence interval[CI]1.06-1.12,P<0.001),PaO2(OR 1.01,95%CI 1.00-1.01,P=0.002),and working shifts(OR 5.09,95%CI 1.87-13.80,P=0.001).CONCLUSIONS:Hyperoxemia occurs frequently and is neglected in most cases,particularly when mild to moderate hyperoxemia,hyperoxemia with lower FiO2,hyperoxemia during night and middle-night shifts,or FiO2 less likely to be decreased展开更多
文摘Acute kidney injury following percutaneous coronary intervention （PCI） is associated with a worse outcome. However, the risk factors and outcomes of acute kidney injury （AKI） in patients after intracoronary stent implantation are still unknown. A retrospective case control study was done in 325 patients who underwent intracoronary stent implantation from January 2010 to March 2011 at the Drum Tower Hospital of Nanjing University School of Medicine. Those were excluded from the study if they had incomplete clinical data. The patients were divided into a normal group and a AKI group according to the standard of post-operation day 7 to identify AKI. The parameters of the patients included： 1） pre-operative ones： age, gender, hypertension, diabetes mellitus, cerebrovascular disease, left ventricular insufficiency, peripheral angiopathy, creatinine, urea nitrogen, estimated glomerular filtration rate （eGFR）, hyperuricemia, proteinuria, emergency operation, hydration, medications （ACEI/ARBs, statins）; 2） intraoperative ones： dose of contrast media, operative time, hypotension; and 3） postoperative one： hypotension. The parameters were analyzed with univariate analysis and multivariate logistical regression analysis. Of the 325 patients, 51（15.7%） developed AKI. Hospital day and in-hospital mortality were increased significantly in the AKI-group. Univariate analysis showed that age, pre-operative parameters （left ventricular insufficiency, peripheral angiopathy, creatinine, urea nitrogen, estimated glomerular filtration rate, hyperuricemia, proteinuria, hydration）, emergency operation, intraoperative parameters （operative time, hypotension） and postoperative hypotension were significantly different. However, multivariate logistic regression analysis revealed that increased age （OR=0.253, 95%CI=0.088-0.727）, pre-operative proteinuria （OR=5.351, 95%CI=2.128-13.459）, pre-operative left ventricular insufficiency （OR=8.704, 95%CI=3.170-23.898）, eGFR〈60 ml/min/1.73 m2
文摘BACKGROUND： Vibrio vulnifi cus inside the body could activate the NF-!B signaling pathwayand initiate the inflammatory cascade. The lung is one of the earliest organs affected by sepsisassociated with acute lung injury. High mobility group protein B1 （HMGB1） is an important late-actingpro-infl ammatory cytokine involving in the pathophysiology of sepsis. It is also involved in the injuryprocess in the lung, liver and intestine. There has been no report on the involvement of HMGB1 inVibrio vulnifi cus sepsis-induced lung injury.METHODS： Sixty rats were randomly divided into a normal control group （group A, n=10） anda Vibrio vulnificus sepsis group （group B, n=50）. Sepsis was induced in the rats by subcutaneousinjection of Vibrio vulnificus （concentration 6×108 cfu/mL, volume 0.1 mL/100g）） into the left lowerlimbs. The rats in group B were sacrifi ced separately 1, 6, 12, 24, and 48 hours after the infection.Their lungs were stored as specimens, lung water content was measured, and lung pathology wasobserved under a light microscope. The expressions of the HMGB1 gene and protein in the lungswere detected by RT-PCR and Western blot. Data were analyzed with one-way analysis of variance（ANOVA） and the LSD method for pair-wise comparison between the two groups. P〈0.05 wasconsidered statistically signifi cant.RESULTS： Compared to group A （0.652±0.177）, HMGB1 mRNA expression in the lungs ofgroup B was signifi cantly higher at 0 hour （1.161±0.358, P=0.013）, 24 hours （1.679±0.235, P=0.000）,and 48 hours （1.258±0.274, P=0.004） （P〈0.05）, and peaked at 24 hours. Compared to group A（0.594±0.190）, HMGB1 protein expression at 6 hours （1.408±0.567, P=0.026） after infection wassignificantly increased （P〈0. 05）, and peaked at 24 hours （2.415±1.064, P=0.000） after infection.Compared to group A （0.699±0.054）, lung water content was significantly increased at 6 hours（0.759±0.030, P=0.001）,12 hours （0.767±0.023, P=0.000）, 24 hours （0.771±0.04
基金supported by the Wenzhou Municipal Science and Technology Bureau(Y2020092)partly by the Key Specialty of Traditional Chinese Medicine of Zhejiang Province in the 13th Five-Year Plan period(Emergency Department).
文摘BACKGROUND:Pulmonary fibrosis(PF)is one of the main causes of death in patients with paraquat(PQ)poisoning.This study aimed to evaluate the relationship between mitochondrial fi ssion and oxidative stress in PQ-induced epithelial-mesenchymal transition(EMT)and PF.METHODS:C57BL/6 mice and MLE-12 cells were exposed to PQ to construct a PF model in vivo and in vitro.Histological changes in the lungs were examined by hematoxylin and eosin(H&E)staining.Mitochondrial morphology was detected by MitoTracker®Deep Red FM or transmission electron microscopy(TEM).Western blotting and immunofluorescence were used to determine the expression of protein.The migration ability of the cells was detected by the cell scratch test.Mitochondrial DNA(mtDNA)levels were assessed by real-time polymerase chain reaction(PCR).Enzyme-linked immunosorbent assay(ELISA)was applied to detect cytokine levels.Superoxide dismutase(SOD)activity and the levels of glutathione(GSH)and malondialdehyde(MDA)were detected by chemichromatometry.RESULTS:PQ exposure caused EMT and PF in vivo and in vitro.PQ destroyed mitochondrial structure and enhanced the expression of dynamin-related protein 1(Drp1),which were accompanied by oxidative stress.Inhibiting mitochondrial fission using mitochondrial division inhibitor-1(Mdivi-1),a selective inhibitor of Drp1,attenuated PQ-induced EMT and oxidative damage.Treatment with N-acetyl-L-cysteine(NAC),an antioxidant,reduced Drp1 expression,attenuated mitochondrial structure damage and inhibited PQ-induced EMT and PF.Both Mdivi-1 and NAC treatment markedly suppressed mtDNA release,the expression of Toll-like receptor 9(TLR9)and phosphorylation(P)-NF-κB p65 as well as cytokines(interleukin 6[IL-6],interleukin-1β[IL-1β],and tumor necrosis factor-α[TNF-α])production.CONCLUSION:Mutual promotion of mitochondrial fission and oxidative stress contributes to EMT in PQ-induced PF,which is associated with the mtDNA/TLR9/NF-κB pathway.
基金supported by grants from the National Natural Science Foundation of China(81730057,82130062)the Key Project of Military Medical Innovation Program of Chinese PLA(18CXZ026)+1 种基金the Guangdong Clinical Research Center for Critical Care Medicine(2020B1111170005)the Sun Yat?sen University Clinical Research Program 5010(2019002)。
文摘Emerged evidence has indicated that immunosuppression is involved in the occurrence and development of sepsis.To provide clinical practice recommendations on the immune function in sepsis,an expert consensus focusing on the monitoring and treatment of sepsis-induced immunosuppression was developed.Literature related to the immune monitoring and treatment of sepsis were retrieved from PubMed,Web of Science,and Chinese National Knowledge Infrastructure to design items and expert opinions were collected through an online questionnaire.Then,the Delphi method was used to form consensus opinions,and RAND appropriateness method was developed to provide consistency evaluation and recommendation levels for consensus opinions.This consensus achieved satisfactory results through two rounds of questionnaire survey,with 2 statements rated as perfect consistency,13 as very good consistency,and 9 as good consistency.After summarizing the results,a total of 14 strong recommended opinions,8 weak recommended opinions and 2 non-recommended opinions were produced.Finally,a face-to-face discussion of the consensus opinions was performed through an online meeting,and all judges unanimously agreed on the content of this consensus.In summary,this expert consensus provides a preliminary guidance for the monitoring and treatment of immunosuppression in patients with sepsis.
基金This study was supported by grants from the Natural Science Foundation of Zhejiang Province （No.LY13HI50006 and No. LY13H150004）, the National Natural Science Foundation （No. 81571937 and No. 81772112）, and the Key Construction Academic Subject （Medical Innovation） of Zhejiang Province （No. 11-CX26）.
文摘Background：Mitofusin-2 （MFN2）,a well-known mitochondrial fusion protein,has been shown to participate in innate immunity,but its role in mediating adaptive immunity remains poorly characterized.In this study,we explored the potential role of MFN2 in mediating the immune function of T lymphocytes.Methods：We manipulated MFN2 gone expression in Jurkat cells via lentiviral transduction of MFN2 small interfering RNA （siRNA） or full-length MFN2.After transduction,the immune response and its underlying mechanism were determined in Jurkat cells.One-way analysis of variance and Student＇s t-test were performed to determine the statistical significance between the groups.Results：Overexpression of MFN2 enhanced the immune response of T lymphocytes by upregulating Ca2＋ （359.280 ± 10.130 vs.266.940 ± 10.170,P =0.000）,calcineurin （0.513 ± 0.014 vs.0.403 ± 0.020 nmol/L,P =0.024）,and nuclear factor of activated T cells （NFATs） activation （1.040 ± 0.086 vs.0.700 ± 0.115,P =0.005）,whereas depletion of MFN2 impaired the immune function ofT lymphocytes by downregulating Ca2＋ （141.140 ± 14.670 vs.267.060 ± 9.230,P =0.000）,calcineurin （0.054 ± 0.030 nmol/L vs.0.404 ± 0.063 nmol/L,P =0.000）,and NFAT activation （0.500 ± 0.025 vs.0.720 ± 0.061,P =0.012）.Furthermore,upregulated calcineurin partially reversed the negative effects ofMFN2 siRNA on T cell-mediated immunity evidenced by elevations in T cell proliferation （1.120 ± 0.048 vs.0.580 ± 0.078,P =0.040）,interleukin-2 （IL-2） production （473.300 ± 24.100 vs.175.330 ± 12.900 pg/ml,P =0.000）,and the interferon-γ/IL-4 ratio （3.080 ± 0.156 vs.0.953 ± 0.093,P =0.000）.Meanwhile,calcineurin activity inhibitor depleted the positive effects of overexpressed MFN2 on T cells function.Conclusions：Our findings suggest that MFN2 may regulate T cell immune functions primarily through the Ca2＋-calcineurin-NFAT pathway.MFN2 may represent a potential therapeutic target for T cell immune dysfunction-related diseases.
基金Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences(No.2019-I2M-5-023)Hainan Provincial Science and Technology Major Project(No.ZDKJ201804)+2 种基金National Natural Science Foundation of China(No.81871611)National Natural Science Foundation of China(No.81760352)Project of Hainan Provincial Department of Education(No.Hnjg2019ZD-16)
文摘1.Introduction Sudden cardiac death(SCD)refers to sudden death due to a variety of cardiac causes.It is manifested as a sudden loss of consciousness,cardiac arrest,and respiratory arrest and generally shows early symptoms that are atypical and not easily detected[1].According to a recent study,nearly 544000 patients suffer from SCD every year in China[2].
文摘BACKGROUND:Due to the still sparse literature in China,the investigation of hyperoxemia management is required.Thus,we aim to conduct a retrospective study to provide more information about hyperoxemia management in intensive care unit(ICU)patients.METHODS:We retrospectively screened the medical records of adult patients(age≥18 years)who required mechanical ventilation(MV)≥24 hours from January 1,2018,to December 31,2018.All arterial blood gas(ABG)tested during MV was retrieved,and MV settings were recorded.The median arterial partial pressure of oxygen(PaO2)>120 mmHg(1 mmHg=0.133 kPa)was defined as mild to moderate hyperoxemia,and PaO2>300 mmHg as extreme hyperoxemia.Intensivists’response to hyperoxemia was assessed based on the reduction of fraction of inspired oxygen(FiO2)within one hour after hyperoxemia was recorded.Multivariable logistic regression analysis was performed to determine the independent factors associated with the intensivists’response to hyperoxemia.RESULTS:A total of 592 patients were fi nally analyzed.The median Acute Physiology and Chronic Health Evaluation II(APACHE II)score was 21(15-26).The PaO2,arterial oxygen saturation(SaO2),FiO2,and positive end expiratory pressure(PEEP)were 96.4(74.0-126.0)mmHg,97.8%(95.2%-99.1%),0.4(0.4-0.5),and 5(3-6)cmH2O,respectively.Totally 174(29.39%)patients had PaO2>120 mmHg,and 19(3.21%)patients had extreme hyperoxemia at PaO2>300 mmHg.In cases of mild to moderate hyperoxemia with FiO2≤0.4,only 13(2.20%)patients had a decrease in FiO2 within one hour.The multivariable logistic regression analysis showed that a positive response was independently associated with FiO2(odds ratio[OR]1.09,95%confi dence interval[CI]1.06-1.12,P<0.001),PaO2(OR 1.01,95%CI 1.00-1.01,P=0.002),and working shifts(OR 5.09,95%CI 1.87-13.80,P=0.001).CONCLUSIONS:Hyperoxemia occurs frequently and is neglected in most cases,particularly when mild to moderate hyperoxemia,hyperoxemia with lower FiO2,hyperoxemia during night and middle-night shifts,or FiO2 less likely to be decreased
