ObjectiveTo explore the risk factors of nosocomial infection in children with acute lymphoblastic leukemia during induction remission chemotherapy.MethodsThe children with acute lymphoblastic leukemia who were admitted to the Department of Pediatrics, Huai’an First Hospital Affiliated to Nanjing Medical University between December 2012 and December 2018 were divided into the infection group (including the severe infection subgroup and the non-severe infection subgroup) and the non-infection group according to whether nosocomial infection occurred during induction and remission chemotherapy. The clinical data of patients were collected. Univariate analysis and multivariate logistic regression were used to analyze the risk factors of nosocomial infection during induction remission chemotherapy in children with acute lymphoblastic leukemia.ResultsA total of 96 patients were included. There were 67 cases in the infection group (26 in the severe infection subgroup and 41 in the non-severe infection subgroup) and 29 cases in the non-infection group. Univariate analysis showed that the granulocyte deficiency time and the prevalence of skin and mucosal damage in the infection group were significantly higher than those in the non-infection group, and the infection group had significantly lower laminar bed use and serum albumin level than the non-infection group did (P< 0.05). Multivariate logistic regression analysis showed that prolonged agranulocytosis [odds ratio (OR)=23.075, 95% confidence interval (CI) (3.682, 144.617), P=0.001], skin and mucosal lesions [OR=12.376, 95%CI (1.211, 126.507), P=0.034], hypoalbuminemia [OR=5.249, 95%CI (1.246, 22.113), P=0.024] were independent risk factors for nosocomial infection during induction and remission of childhood acute lymphoblastic leukemia, while laminar bed [OR=0.268, 95%CI (0.084, 0.854), P=0.026] was the protective factor.ConclusionsLong-term agranulocytosis, skin and mucosal lesions, and hypoalbuminemia are independent risk factors for nosocomial infection in children with acute lymphoblastic leukemia during induction remission chemotherapy. Laminar flow bed is its protective factor.
Objective To investigate the possibility of gene therapy of osteolysis around artificial joint prosthesis by constructing the recombinant adenovirus which can silence tumor necrosis factor α (TNF-α). Methods The primer of small interfering RNA (siRNA) coding sequence of silent TNF-α was designed and amplified, and then RAPAD adenovirus packaging system was used to load the sequence to adenovirus, and the recombinant adenovirus Ad5-TNF-α-siRNA-CMVeGFP which lacked both E1 and E3 regions was constructed. Then 64 female BABL/C mice (weighing, 20-25 g) were randomly divided into 4 groups (n=16): blank control (group A), positive control (group B), simple adenovirus (group C), and treatment group (group D). The prosthetic-model was established in group A, and the prosthetic-loosening-model in groups B, C, and D. At 2 weeks after modeling, PBS solution was injected first, and then the same solution was injected 24 hours later in group A; titanium particle solution was injected, and then PBS solution, Ad5 E1-CMVeGFP (1 × 109 PFU/mL), and Ad5-TNF-α-siRNA-CMVeGFP (1 × 109 PFU/mL) were injected, respectively in groups B, C, and D 24 hours later, every 2 weeks over a 10-week period. The general condition of mice was observed after operation. The tissues were harvested for histological observation, and the expression of TNF-α was detected by Western blot at 12 weeks after operation. Results The positive clones were achieved by enzyme digestion and confirmed by DNA sequencing after loading the target genes into adenovirus vector, and then HEK293 cells were successfully transfected by recombinant adenovirus Ad5-TNF-α-siRNA-CMVeGFP. All mice survived to the completion of the experiment. Histological observation showed that there were few inflammatory cells and osteoclasts in group A, with a good bone formation; there were a large number of inflammatory cells and osteoclasts in groups B and C, with obvious bone destruction; inflammatory cells and osteoclasts in group D was less than those in groups B and C, with no obvious bone destruction. Significant difference was found in the limiting membrane thickness and the number of osteoclasts (group A lt; group D lt; group B lt; group C, P lt; 0.05). Western blot showed that the TNF-α expression levels were 0.235 ± 0.022, 0.561 ± 0.031, 0.731 ± 0.037, and 0.329 ± 0.025 in groups A, B, C, and D respectively, showing significant difference among 4 groups (P lt; 0.05). Conclusion The recombinant adenovirus for silencing TNF-α is successfully constructed, which can effectively inhibit osteolysis by silencing TNF-α expression in the tissues around prosthesis in mice.
Objective To observe the efficacy of hydrogel dressings in preventing and treating vein injury of rabbits so as to provide a experimental evidence for cl inical appl ication. Methods Twenty-four healthy large-eared Japanese rabbits (48 ears) were choosen, weighing (2.15 ± 0.15) kg, and divided into 3 groups randomly. The vein injury models were made byintravenously infusing 20% mannite (2.5 mL/kg). The sites of puncture were treated with hydrogel dressings (group A, n=8) and 25%MgSO4 (group B, n=8) 5 minutes after infusion. The sites of puncture were not treated as a blank control (group C, n=8). The tissue specimens were collected from the auricular veins at 24 hours after mannite infusion for histological observation by HE staining. The injury of the vessel wall, hemorrhage around the vessels, infiltration of inflammatory cells, and disturbance of circulation were observed to evaluate the injury degree of vein. Results There existed redness and congestion in the injured veins of each group. HE staining showed that in both groups A and B, the vessel wall was sl ightly injured and hemorrhage around the vessel was mild. There existed infiltration of inflammatory cells in the vessel wall and surrounding tissues. There also existed congestion and thrombus in the vessel lumen in these two groups. While in group C, the injury of vessel wall was severe, and schistic bleeding in the surrounding tissue of the vessel was existed. The severe congestion and thrombus in the vessel lumen was observed. There was no significant difference among three groups in the extent of vein wall injury and hemorrhage around the vessel (P gt; 0.05). The degree of infiltration of inflammatory cells and circulatory disturbance in both groups A and B were significantly less than that of group C (P lt; 0.05); but there was no significant difference between groups A and B (P gt; 0.05). Conclusion Hydrogel dressing is helpful to prevent vein injury of rabbits induced by mannite.