Objective To observe the changing levels of serum sFas before and after intravenous i mmunoglobulin (IVIG) treatment of incomplete Kawasaki disease (IKD),to explore the roles of sFas in the pathogenesis of IKD and IVIG treatment mechanism.Methods Thirty eight cases of IKD children were selected as experimental group and 20 examples of the same age of children as the control group.The IKD children were treated by IVIG in combination with aspirin (ASP) ; and blood test was performed before treatment,3 days after treatment,and 14 days after treatment,respectively.Dual-resistant sandwich enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of serum sFas,plasma Fibrinogen (PT-D),d-dimer (D-D),and c-reactive protein (CRP).Results The levels of serum sFas,PT-D,D-D,and CRP were significantly higher than the control group for IKD children before treatment[(0.55 ± 0.14)ng/L vs (0.24 ±0.04) ng/L,(552.3 ± 147.2) mg/dl vs (277.3 ±82.5)mg/dl,(649.0 ±201.6) μg/L vs (315.4 ±91.8)μg/L,and(72.2 ±28.7)mg/L vs (7.2 ±2.9)mg/L; t' =12.41,9.11,8.64,13.82;All P ＜ 0.05] ;3 days after treatment,compared with those before treatment and control group,the sFas level of IKD children at the third day after treatment was significantly decreased compared to that before treatment and control groups,respectively [(0.43 ± 0.09) ng/L vs (0.55 ± 0.14) ng/L,(0.24 ± 0.04) ng/L,F =47.624,All P ＜0.05] ;For the level of sFas at the 14th day after treatment,no statistical significance was found between IKD children and the control group[(0.24 ±0.05) ng/L vs (0.24 ±0.04) ng/L,t =0.596,P ＞ 0.05].Conclusions The abnormally increased serum sFas level before IVIG treatment suggests that dysfunction of apoptosis be involved in the pathogenesis of the IKD.Intravenous immunoglobulin treatment may be involved in the apoptosis process.

Objectives To explore the change of interleukin-17 (IL-17) in Kawasaki disease (KD). Methods Fourty KD pediatric patients, among them 12 patients with echocardiographic abnormalities in acute phase, 25 age-matched non-KD patients were enrolled. The level of serum IL-17 was measured by enzyme linked immunosorbent assay in acute and convalescent phase of KD patients and non-KD patients. At the same time, C-reactive protein (CRP), globulin, albumin were detected. Results In acute phase of KD patients, the level of serum IL-17 were signiifcantly higher than that in convalescent phase of KD patients and non-KD patients (P<0.05). The level of serum IL-17 was no signiifcant differences in convalescent phase of KD patients and non-KD patients (P>0.05). In acute phase of KD patients with echocardiography abnormalities, the level of serum IL-17 was signiifcantly higher than that with non-echocardiography abnormalities (P<0.05). The level of serum IL-17 in acute phase of KD patients were positively correlated with CRP and globulin (r=0.750, 0.750, P<0.05), and negatively correlated with albumin (r=-0.779, P<0.05). Conclusions IL-17 may be involved in KD immune pathogenesis. Serum IL-17 is one of the activity index of KD, which associ-ated with cardiovascular damages.

Objective To study the expression levels of N-terminal pro-brain natriuretic peptide (NT-proBNP),serum albumin of Kawasaki' s disease (KD),incomplete Kawasaki' s disease (IKD),and children whose fever were unexplained and to explore the clinical significance of the levels of NT-proBNP and serum albumin in the early diagnosis of IKD.Methods The levels of NT-proBNP of 246 cases of KD (KD group),61 cases of IKD (IKD group) and 301 cases of children with unexplained fever (fever group)were measured by the enzyme-linked fluorescence analysis (ELFA) at the day of admission,meanwhile,the levels of albumin were tested in KD,and IKD children were underwent ECG and echocardiography.Based on the test results,patients were further divided into the group with cardiovascular damage and the group without cardiovascular damage.SPSS 19.0 was used for statistical analysis.The t test was used to compare the parameters between each group,the variance analysis and association analysis were carried out with Pearson's correlation analysis.The ROC curve analysis was done to identify the cardiovascular damage threshold.Results ① The level of plasma NT-proBNP of the KD group,the IKD group was significantly h igher than the fever group [(789.1±4.7) ng/L,(824.8±4.4) ng/L vs (92.5±2.3) ng/L,F=230.736,all P＜0.05];② The level of albumin of the KD group and the IKD group was significantly lower than that of the fever group [(33.9±2.8) g/L,(33.8±3.1) g/L vs (40.8±3.6) g/L,F=355.648,all P＜0.05]; ③ The levels of NT-proBNPs between the cardiovascular damage group and the groups without cardiovascular damage among the KD group,and those of the IKD groups were compared.In the KD group,the NT-proBNPs level of the two subgroups was (2948±3) g/L (n=103) vs (305±3) g/L,n=143; while in the IKD group,the NT-proBNPs of the two subgroups was (1454±4) g/L (n=38) vs (323±4) g/L (n=23).The dif-ferences were statistically significant (t=16.464,4.356,all P＜0.05).④ The plasma NT-proBNP level higher than 933.5 ng/L was identify as the indicator for cardiovascular damage in both KD and IKD children.Its sensi-tivity was 88.1％,and its specificity was 89％.⑤ When the level of NT-proBNP was higher than 250 ng/L,the sensitivity for diagnosis in the KD,the IKD was 80.9％,85.2％ respec-tively,and the specificity was 85.7％.When the level of NT-proBNP was higher than 250 ng/L and that of albumin was lower than 35 g/L,the sensitivity for diagnosis of KD,IKD was 67.5％,70.5％ respectively,the specificity was 99.7％.Conclusion The level of plasma NT-proBNP (＞250 ng/L) accompanied by decreased albumin (＜35 g/L) may be specific markers for early diagnosis of IKD.In addition,the level of NT-proBNP ≥933.5 ng/L can be used as a diagnostic threshold,which has good sensitivity and specificity for identifica-tion of cardiovascular damage in the KD and IKD in children.

Objective To study the protective effect of Panax notoginseng saponins(PNS)and its components Rg1 and Rb1 on oxygen-glucose deprivation/reoxygenation(OGD/Reox)-induced tight junction damage. Methods Anaerobic box were used to induce OGD in HUVEC cells for 6 h followed by reoxygenation for 24 h. Transepithelial/endothelial electrical resistance(TEER)and cell permeability were detected,immunefluorescence was used to observe the ZO-1 and claudin-5 protein expression. Results PNS 20,40 mg/L and ginsenoside Rb1 significantly inhibited the OGD/Reox-induced decreased tight junction resistance,and the increased cell permeability(P< 0.05). PNS 20,40 mg/L and ginsenoside Rb1 partly restored the inter-cellular tight junctions which were regularly arranged on the cell membrane, and the cells displayed cobble stone-like arrangement. Conclusions PNS ameliorates ischemia-induced vascular endothelial cell tight junction damage via MMP-9 and VEGF/VEGFR2 signaling pathway. Rb1 is one of the effective monomer components.

Objective:The emergence of polymyxin-resistant Klebsiella pneumoniae(KPN)in clinical settings necessitates an analysis of its antibiotic resistance characteristics,epidemiological features,and risk factors for its development.This study aims to provide insights for the prevention and control of polymyxin-resistant KPN infections. Methods:Thirty clinical isolates of polymyxin-resistant KPN were collected from the Third Xiangya Hospital of Central South University.Their antibiotic resistance profiles were analyzed.The presence of carbapenemase KPC,OXA-48,VIM,IMP,and NDM was detected using colloidal gold immunochromatography.Hypervirulent KPN was initially screened using the string test.Biofilm formation capacity was assessed using crystal violet staining.Combination drug susceptibility tests(polymyxin B with meropenem,tigecycline,cefoperazone/sulbactam)were conducted using the checkerboard method.Polymyxin-related resistance genes were detected by PCR.Multi-locus sequence typing(MLST)was performed for genotyping and phylogenetic tree construction.The study also involved collecting data from carbapenem-resistant(CR)-KPN polymyxin-resistant strains(23 strains,experimental group)and CR-KPN polymyxin-sensitive strains(57 strains,control group)to analyze potential risk factors for polymyxin-resistant KPN infection through univariate analysis and multivariate Logistic regression.The induction of resistance by continuous exposure to polymyxin B and colistin E was also tested. Results:Among the 30 polymyxin-resistant KPN isolates,28 were CR-KPN,all producing KPC enzyme.Four isolates were positive in the string test.Most isolates showed strong biofilm formation capabilities.Combination therapy showed additive or synergistic effects.All isolates carried the pmrA and phoP genes,while no mcr-1 or mcr-2 genes were detected.MLST results indicated that ST11 was the predominant type.The phylogenetic tree suggested that polymyxin-resistant KPN had not caused a hospital outbreak in the institution.The use of two or more different classes of antibiotics and the use of polymyxin were identified as independent risk factors for the development of polymyxin-resistant strains.Continuous use of polymyxin induced drug resistance. Conclusion:Polymyxin-resistant KPN is resistant to nearly all commonly used antibiotics,making polymyxin-based combination therapy a viable option.No plasmid-mediated polymyxin-resistant KPN has been isolated in the hospital.Polymyxin can induce resistance in KPN,highlighting the need for rational antibiotic use in clinical settings to delay the emergence of resistance.

BACKGROUND: Early fluid resuscitation is one of the fundamental treatments for acute pancreatitis (AP), but there is no consensus on the optimal fluid rate. This systematic review and meta-analysis aimed to compare the efficacy and safety of aggressive vs. controlled fluid resuscitation (CFR) in AP. METHODS: The Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, Embase, and Web of Science databases were searched up to September 30, 2022, for randomized controlled trials (RCTs) comparing aggressive with controlled rates of early fluid resuscitation in AP patients without organ failure on admission. The following keywords were used in the search strategy: "pancreatitis," "fluid therapy,""fluid resuscitation,"and "randomized controlled trial." There was no language restriction. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) framework was used to assess the certainty of evidence. Trial sequential analysis (TSA) was used to control the risk of random errors and assess the conclusions. RESULTS: A total of five RCTs, involving 481 participants, were included in this study. For primary outcomes, there was no significant difference in the development of severe AP (relative risk [RR]: 1.87, 95% confidence interval [CI] 0.95-3.68; P = 0.07; n = 437; moderate quality of evidence) or hypovolemia (RR: 0.98, 95% CI: 0.32-2.97; P = 0.97; n = 437; moderate quality of evidence) between the aggressive and CFR groups. A significantly higher risk of fluid overload (RR: 3.25, 95% CI: 1.53-6.93; P <0.01; n = 249; low quality of evidence) was observed in the aggressive fluid resuscitation (AFR) group than the controlled group. Additionally, the risk of intensive care unit admission ( P = 0.02) and the length of hospital stay ( P <0.01) as partial secondary outcomes were higher in the AFR group. TSA suggested that more studies were required to draw precise conclusions. CONCLUSION: For AP patients without organ failure on admission, CFR may be superior to AFR with respect to both efficacy and safety outcomes. REGISTRATION PROSPERO; https://www.crd.york.ac.uk/PROSPERO/ ; CRD 42022363945.
Humans ; Randomized Controlled Trials as Topic ; Fluid Therapy ; Hypovolemia ; Pancreatitis/therapy*