Objective: To investigate the mediating role of vaccine literacy between vaccine knowledge and vaccine hesitancy and the moderating role of parental education level, so as to provide references for adjusting vaccination strategies. Methods: From May to December 2024, a stratified random sampling method was used to select 10 community hospitals in Guiyang and Zunyi City, Guizhou Province. A total of 1 401 parents of children aged 0-6 years were surveyed regarding their socio demographic characteristics, vaccine knowledge, vaccine literacy, and vaccine hesitancy levels. Data were analyzed using common method bias tests, Spearman correlation analysis, mediation and moderation effects tests. Results: The mean score for vaccine knowledge, vaccine literacy and vaccine hesitancy were (2.96±1.11, 14.25±2.64, 39.12±4.93) among the 1 401 participants. Mediating effect analysis showed that both parental vaccine knowledge ( β =1.28, 95% CI =1.08-1.49) and vaccine literacy ( β =0.75, 95% CI =0.66-0.84) positively predicted vaccine hesitancy (both P <0.01). Meanwhile, vaccine literacy accounted for 28.1% of the total effect of mediation between knowledge and vaccine hesitancy. In the moderated effects analysis, education level positively predicted vaccine literacy ( β =0.40, 95% CI =0.24-0.57), and education level moderated the pathway of vaccine knowledge on vaccine hesitancy ( β = 0.28 , 95% CI =0.05-0.52) (both P <0.01). Conclusions Vaccine literacy partially mediates the relationship between vaccine knowledge and vaccine hesitancy. Parental education level positively moderates the prediction of vaccine knowledge on vaccine hesitancy score.

Objective:To investigate the changes of thyroid hormones and the flow velocity of superior thyroid artery in patients with Graves' disease and Hashimoto's thyrotoxicosis before and after treatment with methimazole.Methods:A case-control study was conducted to select 45 cases of Graves' disease and 45 cases of Hashimoto's thyroiditis from October 2021 to December 2022 in the Department of Endocrinology, North China University of Science and Technology Affiliated Hospital. The changes of thyroid hormone and blood flow velocity of superior thyroid artery in patients with Graves' disease and Hashimoto's thyroiditis before and after treatment with methimazole were analyzed. Measurement data satisfying normal distribution were expressed by xˉ±s, and the mean between two groups was compared by t test. Measurement data not satisfying normal distribution were expressed by M( Q1, Q3), and the median between two groups was compared by Wilcoxon rank sum test. χ 2 test was used to compare the constituent ratio of enumeration data among groups. Results:There was no significant difference in thyroid stimulating hormone (TSH) between the two groups before treatment, and there was no significant difference in TSH between the two groups after 1 month and 3 months of treatment (all P>0.05). The levels of free triiodothyronine (FT3) were (24.09±9.29) pmol/L and (17.41±9.36) pmol/L in Graves' disease group and Hashimoto's thyroiditis group respectively before treatment. FT4 were (60.23±20.82) and (43.47±21.71) pmol/L, respectively, and the peak stolie vloiy (PSV) were (69.53±5.70) and (52.65±4.64) cm/s, respectively in Graves' disease group and Hashimoto's thyroiditis group respectively before treatment. There were significant differences between the two groups ( t values wrere 3.39 and 3.74, Z=13.83, all P<0.001). The difference of FT3 between one month after treatment and before treatment was (-6.36±5.32) and (-12.64±9.08) pmol/L ( t=4.02, P<0.001) and the difference in FT3 between 3 months of treatment and before treatment was (-10.14±9.50) and (-17.80±11.17) pmol/L, respectively ( t=3.51, P<0.001) between the Graves disease group and the Hashimoto's thyroiditis group. The difference in FT4 between the Graves disease group and the Hashimoto's thyroiditis group after 1 month of treatment and before treatment was (-28.47±10.09) and (-20.57±14.48) pmol/L ( t=7.01, P<0.001), and the difference of FT4 was (-47.06±20.57) and (-30.17±20.54) pmol/L ( t=3.91, P<0.001) between the Graves disease group and the Hashimoto toxin group. The difference between one month after treatment and before treatment was (-13.10(-34.10,-2.60)) and (-10.50(-27.5,-0.20)) cm/s ( Z=2.63, P=0.009), respectively. The difference between 3 months and before treatment was (-31.40(-53.20,-12.70)) and (-19.90(-46.00,-4.70)cm/s ( Z=4.40, P<0.001)) between the Graves disease group and the Hashimoto's thyroiditis group, and the difference was statistically significant. Conclusion:Thyroid hormone levels were decreased after treatment with methimazole in patients with diffuse toxic goiter and Hashimoto toxemia, but the difference was not statistically significant. The PSV level of superior thyroid artery in patients with diffuse toxic goiter was significantly lower than that in patients with Hashimoto's thyrotoxicosis.

Objective:To investigate the efficacy and safety of tocilizumab in the treatment of critically ill children with acute necrotizing encephalopathy (ANE).Methods:It is a retrospective cohort study. The children with ANE admitted to the pediatric intensive care unit of 4 Chinese tertiary hospitals from December 2022 to November 2023 were divided into conventional treatment group and tocilizumab group, and the comparison between groups was performed by using Mann ‐ Whitney U test or Chi-square test. Results:Among 21 cases of severe ANE, there were 11 males with the onset age of 65 (27, 113) months. The duration from onset to PICU admission was 2 (1, 2) days. There were 13 cases of ultra-high fever (greater than 40 ℃), including 18 cases of convulsions, and 19 cases with a GCS score of less than 8 points. The causative agent was novel coronavirus Omicron in 7 cases and influenza A in 14 cases. All cases had central respiratory failure requiring mechanical ventilation. Of the 21 cases, 18 were shock, 15 were coagulopathy, 10 were kidney injury and 13 were liver dysfunction. Of these hospitalized patients, 8 children with ANE were treated with tocilizumab. Eight cases received continuous blood purification (CBP) treatment, 5 of them were combined with plasmapheresis. Serum cytokine levels were elevated in 21 children with ANE, including (interleukin, IL)-6 and IL-8 (61 (22, 1 513) and 68 (5, 296) ng/L). There were 14 cases (67%) deaths, including 11 cases in the conventional treatment group and 3 cases in the tocilizumab group. There was no significant difference in the mortality rate between the two groups ( P=0.056). Tocilizumab-related rash or other adverse events were not observed. Conclusions:The motality of critically ill ANE patients was high. The combination of Tocilizumab with conventional treatment did not reduce the motality of severe ANE patients, and no adverse reactions of tocilizumab were observed.

Objective:To investigate the neuroprotective effect of cerebroprotein hydrolysate (CH) -Ⅰ on cerebral ischemia-reperfusion injury in rats and its mechanism.Methods:Eighty adult healthy male SD rats were randomly divided into sham operation group, model group, CH-Ⅰ intervention group and cerebrolysin (CBL) positive control group. The model of ischemia-reperfusion injury was induced by temporarily occluding the left middle cerebral artery with suture-occluded method. The CH-Ⅰ and CBL groups intraperitoneally injected with CH-Ⅰ and CBL at 0, 3, 6 and 12 h after reperfusion at the dose of 20 mg/kg. The sham operation group and the model group were injected with the same volume of normal saline. At 24 h after reperfusion, the behavior changes of the rats were detected by the modified neurological severity score (mNSS). The volume of cerebral infarction was detected by TTC staining. The morphology and structure of neurons in ischemic cortex were observed by Nissl staining. The apoptosis of neurons in ischemic cortex was detected by TUNEL staining. The expression changes of phosphorylated extracellular signal-regulated kinase (pERK) 1/2, phosphorylated mitogen-activated protein kinase/extracellular signal-regulated kinase (pMEK) 1/2, phosphorylated cAMP response element binding protein (pCREB) and brain-derived neurotrophic factor (BDNF) in the ischemic cortex were detected by Western blot.Results:At 24 h after reperfusion, the mNSS score and cerebral infarct volume in the model group were significantly higher and larger than those in the sham group (all P<0.001). The mNSS scores and cerebral infarct volumes in the CH-Ⅰ and CBL groups were significantly reduced compared with those in the model group (all P<0.05), but there was no significant difference between the CH-Ⅰ group and the CBL group. Nissl and TUNEL staining showed that the degenerative cell index and apoptotic cell index in the CH-Ⅰ group were significantly lower than those in the model group (all P<0.01), but there were no significant difference between the CH-Ⅰ group and the CBL group. Western blot analysis showed that compared with the sham operation group, the pMEK1/2, pERK1/2 and pCREB expressions in ischemic cortex were significantly enhanced and the BDNF expression was significantly attenuated in the model group ( P<0.05). Compared with the model group, pMEK1/2, pERK1/2, and pCREB expressions in the CH-Ⅰ group were significantly decreased (all P<0.05), and the BDNF expression was significantly increased ( P<0.05). Conclution:CH-Ⅰ can reduce cerebral infarct volume and improve neurological function, and its mechanism may be associated with the inhibition of the MEK-ERK-CREB pathway as well as the enhancement of BDNF expression.

Objective:To investigate the tendency of bacterial distribution and drug resistance of clinically isolated pathogens in the pediatric intensive care unit (PICU), which provided references for the reasonable application of antibiotics.Methods:The distribution characteristics of all clinical isolates from PICU of Children′s Hospital of Shanghai Jiaotong University from January 2010 to December 2018 and their trend of drug resistance were retrospectively analyzed.Results:A total of 2 749 strains of bacteria were isolated, including 1 912 strains (69.6%) Gram-negative bacteria and 837 strains (30.4%) Gram-positive bacteria.The top 6 detected bacteria were Acinetobacter baumannii (749 stains, 27.2%), Klebsiella pneumoniae (289 stains, 10.5%), Staphylococcus aureus (214 stains, 7.8%), Stenotrophomonas maltophilia (207 stains, 7.5%), Escherichia coli (204 stains, 7.4%) and Pseudomonas aeruginosa (189 stains, 6.9%). Among them, the detective rate of Maltophilia Stenotrophomonasannually increased from 6 strains (2.8%) in 2010 to 39 strains (9.5%) in 2018.The resistance rates of Acinetobacter baumannii and Klebsiella pneumoniae to carbapenems increased year by year, which was up to 96.0% and 71.4% to Meropenem by 2018.Their resistance rates to the third-generation cephalosporins, aminoglycosides and sulfonamides were higher than 70.0%.The sensitivity rate to Tigecycline and Polymyxin was 100.0%.The detection rate of Methicillin-resistant Staphylococcus aureus (MRSA) significantly increased from 18.2% in 2010 to 50.0% in 2018 ( χ2=19.38, P=0.013). No Vancomycin-resistant strains were found. Conclusions:Gram-negative bacteria are the main clinical isolates of PICU.Acinetobacter baumannii, Klebsiella pneumoniae, and especially Pseudomonas maltophilus, have a significant growth trend in the detection rate. Acinetobacter baumannii and Klebsiella pneumoniae are highly resistant to carbapenems.MRSA annually grows, but it still maintains a high degree of sensitivity to Vancomycin.

Objective To investigate the efficacy of venous-arterial extracorporeal membrane oxygenation (VA-ECMO) in the treatment of refractory septic shock in children.Methods From January 2016 to December 2018,the clinical data of children with refractory septic shock (RSS) treated by VA-ECMO in Department of Critical Medicine Affiliated Children's Hospital of Shanghai Jiao Tong University were retrospectively analyzed.The patients with refractory septic shock (RSS) treated by VA-ECMO were compared with those with non-refractory septic shock (NRSS).Results There were 8 cases in the RSS-ECMO group and 6 cases in the NRSS-ECMO group.The sex,age,PRISM score,complication showed no significant difference in the two groups.The median time of ECMO in the RSS-ECMO group was 182 (141,216) h,and 5 patients were survived and were discharged from the hospital.The blood lactic acid and vasoactive drug index in the RSS-ECMO group was significantly higher than that in the NRSS-ECMO group (P＜0.05 or P＜0.01).The time of vasoactive drugs use and the ratio of combined continuous renal replacement therapy (CRRT) in the RSS-ECMO group were higher than those in the NRSS-ECMO group,but there was no significant difference (P ＞ 0.05).Atter ECMO establishment,the mean invasive arterial pressure increased significantly at 6 h,and lactic acid decreased significantly at 12 h after ECMO support.SCVO2 returned to normal at 24-h ECMO therapy.Conclusions The success rate of VA-ECMO treatment in children with refractory septic shock complicated with MODS is similar to that of children with non-refractory septic shock.The relationship between ECMO and hemodynamic indexes in sepsis should be further explored.

Objective: To investigate the effects of methylprednisolone on STAT3-ERK1/2 signaling pathway in lipopolysaccharide (LPS)-induced acute lung injury (ALI). Methods: The C57BL/6J male mice (8-week-old) were randomly(random number) divided into 4 groups: control group (control), LPS-induced endotoxemia model (LPS), only methylprednisolone (MP) administration group (MP), and intervention group with 2 mg/kg MP (LPS+MP) (n= 8 per group). The wet/dry (W/D) weight ratio of lung tissue, lung pathology by hematoxylin & eosin (HE) staining, serum and mRNA levels of TNF-α and IL-6 in lungs were determined. The protein levels of p-STAT3 and p-ERK1/2 in lungs were detected by Western blot. Statistical analyses were performed using One-way analysis of variance test to compare among multiple groups. Results: (1)MP treatment significantly decreased the lung W/D weight ratio compared with the LPS group[(3.01±0.84) vs(3.87±0.17), P = 0.038]; (2) The histopathological lesions of the lung were improved in the LPS+MP group compared with the LPS group accompanied with reduced inflammatory cell infiltration and attenuated the alveolar wall thickening; (3) The serum levels of TNF-α and IL-6 in the LPS+MP group was significantly decreased compared with the LPS group[(3.17±1.64) pg/mL vs (6.61±1.27) pg/mL, P = 0.003; (1.42±0.35) pg/mL vs (3.80±1.35) pg/mL, P = 0.008, respectively], and the mRNA levels of TNF-α and IL-6 in the LPS+MP group were significantly lower than those of the LPS group [(5.10±0.81) vs (12.2±5.05), P = 0.03; (1.62±1.00) vs (11.12±6.56), P=0.026; respectively]; (4) MP therapy significantly inhibited P-STAT3 and P-ERK1/2 protein levels [(0.26±0.05) vs (0.86±0.06), P < 0.001, (0.24±0.02) vs (1.34±0.32), P < 0.001]. Conclusions Methylprednisolone protects LPS-induced acute lung injury possibly via suppressing STAT3-ERK1/2 signaling pathway and reducing TNF-α and IL-6 expression.

Objective: To investigate the incidence and prognosis of hypophosphatemia in critically ill children treated with continuous blood purification (CBP). Methods: The medical records of the critically ill patients, who were treated with CBP, admitted to pediatric intensive care unit (PICU) of Shanghai Children's Hospital from May 2014 to April 2017 were retrospectively analyzed. The serum phosphorus levels were tested before CBP, at 48-72 h during CBP, at the end of CBP and on the next day after CBP finished. Phosphorus supplement was given to the children with severe hypophosphatemia. Results: A total of 85 patients met the inclusion criteria. The serum phosphorus levels at the 4 indicated time points were (1.4±0.5), (0.7±0.3), (0.8±0.3), (0.9±0.4) mmol/L, respectively (F=45.21, P<0.05). Among the children, 66 cases (78%) had hypophosphatemia during CBP. The incidences of moderate and severe hypophosphatemia were 32 (48%) and 9 (14%), respectively. There were 41 patients with CBP replacement rates of (35-49) ml/(kg·h), while 44 patients with CBP replacement rates of 50-70 ml/(kg·h). There were significant differences at 48-72 h during CBP, the end of CBP and on the next day after CBP ((0.8±0.4) vs. (0.5±0.2), (1.0±0.3) vs. (0.6±0.2), and (1.1±0.4) vs. (0.8±0.2) mmol/L; t=7.672, 4.060, 14.440, P<0.05). Atotal of 9 cases were treated with sodium glycerophosphate. Among the 85 children, 24 (28%) patients died while 61 (72%) survived. There were no significant differences between the two groups in serum phosphorus levels at the indicated time points ((1.4±0.5) vs. (1.4±0.5), (0.7±0.3) vs. (0.7±0.3), (0.7±0.3) vs. (0.8±0.3), and (1.0±0.3) vs. (0.9±0.3) mmol/L, respectively, P>0.05). Conclusions Hypophosphatemia is prone to occur during CBP, which probably related to the replacement rate. There was no significant relationship between hypophosphatemia and mortality in critically ill children after giving phosphorus supplementation.

Objective To investigate the effects of lipopolysaccharide (LPS) on the expressions of sodium taurocholate co-transporting polypeptide (Ntcp) and bile salt export pump (Bsep),as well as the liver function markers in the serum including total bilirubin (TBIL),total bile acids (TBA),alanine aminotransferase (ALT),aspartate aminotransferase (AST) in mice.Methods One hundred and twenty-eight C57BL/6 mice were intra-peritoneally injected with different doses of 5,10,20 or 40 mg/kg LPS (n =24),respectively.No treatment or treated with 0.9％ NaC1 in mice as controls.Serum TBIL,TBA,ALT and AST levels were measured at 24 h,48 h and 72 h after LPS injection in each group.The mRNA expressions of Ntcp and Bsep were detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR).The liver histological sections were stained with haematoxylin and eosin (H&E).Results The Ntcp and Bsep mRNA expressions in mice liver were significantly lower in livers of LPS-treated mice within 24-72 h compared with control group,and the lowest level was reached at 24 h in a dose-dependent manner.And the relative expressions of Ntcp mRNA and Bsep mRNA were (0.64 ± 0.02),(0.53 ± 0.14),(0.25±0.09),(0.15±0.07)and (0.74±0.12),(0.58±0.11),(0.41±0.09),(0.27 ± ± 0.11) in livers of mice injected with LPS in the different doses of 5,10,20,40 mg/kg,respectively.In addition,serum levels of TBIL,TBA,ALT,and AST were significantly increased in mice of LPS-treated group compared with control group,particularly within 24 h after LPS treatment.Serum levels of TBIL,TBA,ALT,and AST were significantly decreased in mice of 40 mg/kg LPS-treated 72 h group compared with 24 h group presenting them with (1.29 ± 0.25) μ mol/L vs.(1.71 ± 0.22) μ moL/L,(6.97 ± 0.98) μmol/Lvs.(8.96±1.01) μmol/L,(120.17±21.08) U/L vs.(179.22±16.57) U/L,(360.34 ±35.31) U/L vs.(510.97 ± 34.70) U/L,respectively.Furthermore,histological changes in liver depend on dose and the course of LPS treatment.Cytoplasm rarefaction and inflammatory cells infiltration were detected at 24 h after treatment with 5 or 10 mg/kg LPS.Acidophilic and vacuolar degeneration,neutrophils infiltration in the hepatic sinusoid and portal area,the proliferation of bile ductulus were observed at 48 h,72 h after treatment with 5 or 10 mg/kg LPS.In the 20 or 40 mg/kg LPS treatment groups,focal necrosis,infiltration with inflammatory cells,proliferation of bile ductulus and expansion of duct were observed at 24 h,48 h and 72 h after LPS treatment.Conclusions LPS decreases the mRNA expressions of Ntcp and Bsep in a dose dependent manner in mice,contributing to mechanism of liver injury induced by endotoxin.

Objective To investigate the effects and underlying mechanisms of methylprednisolone (MP) on liver injury induced by lipopolysaccharide (LPS).Methods Total of 48 C57BL/6 mice (8-week old) were randomly divided into the control group,LPS-induced endotoxemia model (1 h,2 h,4 h,8 h,24 h,48 h) and intervention group with MP therapy (n =6).Mice were intraperitoneally injected withLPS (20 mg/kg) for indicated time (1 h,2 h,4 h,8 h,24 h,48 h),and MP (20mg/kg) was intraperitonealinjected into micetointervene LPS-induced liver injury.Saline was used as control.Pathological changes of liver tissues were analyzed by hematoxylin & eosin (HE) staining.The serum levels of ALT,TBIL and TBA were determined,and the mRNA levels of TNF-α,IL-6,IL-1β and the protein levels of P62,LC3 Ⅱ/Ⅰ in livers were detected by real time-PCR and Western-blot.Results (1) MP therapy protects mice against LPS-induced liver injury at the dose of 20 mg (kg · d).The pathological sections showed that the structure of hepatic lobule,the hepatocyte vacuolar degeneration,eosinophilic degeneration were improved in LPS + MP/group compared with LPS group;(2) The serum levels of ALT,TBIL,TBA in LPS + MP group was significantly decreased compared with LPS 48 h group [(63.40 ±11.55) vs.(104.50±29.34) U/L,(0.37 ±0.08) vs.(0.52 ±0.12) μmol/L,(4.67 ±2.58) vs.(10.33 ± 2.34) μmol/L,P =0.009,P =0.032,P ＜ 0.01];(3) The mRNA levels of TNF-α,IL-6,IL-1β in LPS + MP group was significantly lower than that of LPS 48 h group [(4.18 ±0.81) vs.(10.09 ±4.73),(0.31 ±0.14) vs.(1.06 ±0.68),(0.17 ±0.05) vs.(1.22 ±0.50),respectively,all P ＜0.05];(4) LPS activated autophagy within 2h after LPS treatment.Then,autophagy was suppressed from 2h to 24h after LPS treatment indicated as the decreased expression of LC3 Ⅱ/Ⅰ.Interestingly,MP treatment significantly reversed LPS-suppressed autophagy showing that the protein level of LC3 Ⅱ/Ⅰ was significantly increased in LPS + MP group compared with LPS 48 h group.Conclusions MP therapy protects mice against LPS-induced liver injury and inflammation,partially due to activation of autophagy in livers.