Objective:To investigate the effects of lipopolysaccharide (LPS)on the acute lung injury (ALI)and expressions of aquaporin 1 (AQP1)and aquaporin 5 (AQP5)in lung tissue of the rats. Methods:Forty-eight SPF grade male Wistar rats were randomly divided into control group and LPS group (n=24).The rats in LPS group were intravenously injected with LPS to induce ALI models,and the rats in control group were injected with saline. The rats were sacrificed at 2,6,12 and 24 h,and the samples were collected after the successful modeling.The pathological changes of lung tissue were observed with HE staining;the lung wet/dry weight (W/D)ratio and lung permeability index were detected;ELISA was used to detect the levels of TNF-αand MIP-1α.The expression levels of AQP1 and AQP5 protein and mRNA were measured by Western blotting,immunohistochemistry and Real-Time PCR methods. Results:Compared with control group, the TNF-α and MIP-1α levels in LPS group were significantly elevated at 2,6 and 12 h (P<0.05),and at 24 h they were gradually reduced to the normal level. The HE staining results showed the alveolar and interstitial edema at 2 h after LPS injection,obviously in 12 h. The lung W/D ratios and pulmonary permeability indexes at different time points in LPS group were significantly higher than those in control group (P<0.05),and they reached the peak at 12 h.The expression levels of AQP1 and AQP5 mRNA and protein in lung tissue of the rats at different time points in LPS group were significantly lower than those in control group (P<0.01 ). Conclusion:LPS can induce ALI in the rats and down-regulate the expressions of AQP1 and AQP5;LPS is involved in the formation of pulmonary edema.

Objective:To investigate the cytogenetic characteristics and influencing factors associated with first treatment response in primary childhood B-cell acute lymphoblastic leukemia (B-ALL).Methods:The data of 49 children with primary B-ALL who were admitted to the First Hospital of Xiamen University from April 2019 to September 2021 were retrospectively collected, and the clinical characteristics, cytogenetic and molecular biology findings and other clinical indicators before and after treatment were obtained. Genotyping, clinical risk stratification after the first induction chemotherapy and chemotherapy regimen development were performed according to the pediatric ALL treatment specification (2018 version). The relationship between different genotypes and clinical indicators in children with B-ALL was analyzed, and the correlation between clinical risk stratification and each indicator was analyzed by Spearman rank correlation analysis.Results:The median age of 49 children was 3.0 years old (interquartile range: 3.2 years old), 32 cases (65.3%) were male and 17 cases (34.7%) were female, with a male-to-female ratio of 1.88∶1. Thirty-five cases (71.4%) had gene mutations before treatment and 14 cases (28.6%) had no mutations. Among the 35 cases with mutations, E2A-PBX1 was found in 5 cases (10.2%), including 1 case with Philadelphia chromosome (Ph)-like; IKZF1 deletion was found in 8 cases (16.3%), including 4 cases with Ph-like, 1 case with Ph-positive, and 1 case with MLL rearrangement; MLL rearrangement was found in 3 cases (6.1%); Ph-like alone was found in 12 cases (24.5%); TEL-AML1 was found in 6 cases (12.2%), including 2 cases with Ph-like; 1 case (2.0%) with Ph-positive alone. The clinical risk stratification showed that 7 cases (14.3%) had high risk, 28 cases (57.1%) had intermediate risk, and 14 cases (28.6%) had low risk. The proportions of patients with high and intermediate clinical risk before induction chemotherapy [20.0% (7/35) vs. 0.0% (0/14), 62.9% (22/35) vs. 42.9% (6/14)] and the proportion of patients with altered mutation status on day 33 of induction chemotherapy [42.9% (15/35) vs. 0.0% (0/14)] were higher in patients with mutations before induction chemotherapy than those in patients without gene mutations before treatment (all P < 0.01). The gene mutation or not before treatment was not correlated with gender, white blood cell count at first diagnosis, hormone sensitivity, minimal residual disease (MRD) from the 15th to the 19th day of induction chemotherapy, and MRD on the 33rd day of induction chemotherapy (all P > 0.05). Clinical risk stratification of children was associated with white blood cell count at first diagnosis ( r = 0.392, P = 0.005), neutrophil count ( r = 0.453, P = 0.001), lymphocyte count ( r = 0.418, P = 0.001), monocyte count ( r = 0.359, P = 0.017), blood uric acid level ( r = 0.378, P = 0.007), and proportion of bone marrow naive lymphocyte count before treatment ( r = 0.316, P = 0.027) and from 15th to the 19th day of induction chemotherapy ( r = 0.399, P = 0.005) and the 33rd day of induction chemotherapy ( r = 0.408, P = 0.028), proportion of children with bone marrow MRD ≥ 0.000 1 on the 33rd day of induction chemotherapy ( χ2 = 15.42, P < 0.001), and proportion of children with gene mutations before treatment ( χ2 = 9.10, P = 0.005). Conclusions:High levels of leukocytes, neutrophils, lymphocytes, monocytes, naive lymphocytes, blood uric acid, and naive lymphocytes from the 15th to the 19th day and the 33rd day of chemotherapy, MRD on the 33rd day of chemotherapy and genotype in children with B-ALL may be associated with poor response to treatment. Clinical risk stratification is associated with gene mutation status, and gene mutation may be an important indicator of treatment response in children with B-ALL.

Objective:To investigate the expression and significance of the angiotensin Ⅱ and its receptors in lipopolysaccharide (LPS)-induced acute lung injury and acute kidney injury in rats.Methods:Forty eight Wistar rats were randomly divided into two groups: control group and endotoxin group (LPS group). LPS was injected through tail vein in LPS group, and the same amount of saline was injected through tail vein in control group.Samples were collected at 2 h, 6 h, 12 h and 24 h, respectively.The histopathology of lung and kidney was observed by HE staining.We detected lung wet/dry weight ratio, serum creatinine, urea nitrogen and Ang Ⅱ concentration in plasma, lung and kidney tissues by radioimmunoassay.Western blot and immunohistochemistry were used to detect the expression changes of AT1R and AT2R in lung and kidney tissue.Results:Compared with the control group, the pathology of lung and kidney tissue in LPS group showed different degrees of damage.The lung wet/dry weight ratio, serum creatinine and urea level in LPS group were significantly increased than that in control group( P<0.05). The Ang Ⅱ content in plasma increased significantly at 2 h and 6 h ( P<0.05), and the expression level of Ang Ⅱ in lung and kidney increased significantly at all time points ( P<0.05). The expression of AT1R in lung and kidney decreased significantly ( P<0.05), while the AT2R protein expression increased significantly ( P<0.05). Additionally the correlation analysis showed that the expression level of Ang Ⅱ and AT2R were positively correlated with lung and renal function, while the expression of AT1R was negatively correlated with lung and renal function. Conclusion:LPS results in the damage of lung and kidney function and the change of renin-angiotensin system.The changes of Ang Ⅱ and angiotension receptors were correlated with lung and kidney injury.Ang Ⅱ and angiotension receptors may be involved in LPS induced lung and kidney injury.