Abstract: Objective　To analyze the genotype of carbapenemase resistance genes and their genetic homology in multidrug-resistant Acinetobacter baumannii, and to provide a theoretical basis for guiding the rational use of antibiotics and controlling the prevalence of nosocomial infections. Methods A total of 83 multidrug-resistant Acinetobacter baumannii isolated from patients in the intensive care unit (ICU) and environmental specimens in the Sixth People's Hospital of Nantong from July 2020 to December 2021 were collected. The bacteria were identified and subjected to drug sensitivity tests using the BioMérieux DL96-Ⅱ automatic bacterial identification susceptibility system. The carbapenemase-related drug resistance gene types were detected using the polymerase chain reaction (PCR) method, and clones were analyzed by pulsed field gel electrophoresis (PFGE). Results The types of 83 ICU Acinetobacter baumannii specimens include sputum (43 strains), broncholavage fluid (20 strains), and surfaces of objects such as ventilators (20 strains). The resistance rates of all strains to imipenem, tetracycline, gentamicin, amikacin and ciprofloxacin were 100%, 32.5%, 38.6%, 41.0% and 77.1% respecitively, while the resistance rates to others such as ticarcillin and clavulanate were greater than 95%. All strains carried were detected to carry OXA-23 and OXA-51 genes, while OXA-24, OXA-58, IMP-1, VIM, IMP-4, SIM and NDM-1 resistance genes were all negative. PFGE homology analysis confirmed that 83 strains of Acinetobacter baumannii, with counts of 12, 18, 12, 13, 10, 6, 7, 5 respectively, mainly A, B, C, D, E clones, the rest were sporadic clones. Conclusions The carbapenem resistant Acinetobacter baumannii isolated from our ICU are widely drug-resistant to commonly used antimicrobial drugs, with B clone strain being the major prevalent strain. Carrying OXA-23 and OXA-51 genes may be an important reason for the resistance of Acinetobacter baumannii to carbapenem antibiotics in our ICU. Rational use of antimicrobial drugs, enhanced monitoring of bacterial resistance, and effective control of the generation and further spread of drug-resistant strains should be emphasized.

Radial-cephalic arteriovenous fistula (RCAVF) is considered the first choice for hemodialysis vascular access because of its high patency rate and less complications.But up to 50％ of the fistula can not mature.This is mainly due to persistent low blood flow or difficulty in cannulation can not lead to adequate hemodialysis.Inflow or outflow stenosis,anastomotic stenosis,exceedingly deep location of the vein,flow diversion into accessory veins are the common causes of impaired maturation.In addition,thrombosis is a common of stenosis.Preoperative assessment by physical examination and ultrasound examination of blood vessels,select the appropriate blood vessels for the fistula is of great significance.Choose the appropriate treatment for the cause of maturation disorders.Postoperative aspirin is widely used to prevent thrombosis and reduce the occurrence of stenosis;Surgery has the advantage of bypassing the damaged area but creating a new stoma;in recent years,endovascular technique because of its characteristics of minimally invasive in most of the time is the first choice.In this paper,the definition,etiology,diagnosis and treatment of fistula maturation disorder are reviewed.

For recently 30 years,with the progress of science,the development of intracavitary technology has been constantly improved and expanded.Reascularization technology makes the cure of vaso-occlusive disease a great leap.Because of its small trauma,repeatable,high security,near future curative effect,interventional therapy is distinctly superior to the traditional treatment such.Peripheral vascular lumen treatments including the balloon dilatation,stent-assisted angioplasty,catheter guided thrombolysis,and percutaneous mechanical thrombectomy,etc.Although angioplasty has become the best choice but the preferred treatment has limitations,such as for long and severe calcification of arteries occlusion surgery is difficult,immediate and long-term patency rate is low,the postoperative complications is frequent;Used for plaque ulcer and potentially thromboembolic disease,body highly risks of distal embolization;Inherent retraction force for postoperative lumen,intimal inflammation restenosis,stent thrombosis cause problems frequently.However,the percutaneous mechanical thrombectomy system is aimed at solving the clinical problems with good combination of engineering and technology research.The purpose of this paper is to expound the existing mechanical embolus removal system:SilverHawk/TurbjHawk aod Straub Rotarex thrombus,that is to elaborate its development status and clinical analysis.

Objective To establish spastic cerebral palsy model of macaque by partial resection of motor cortex and explore its evaluation method.Methods Four individuals of 3-month-old macaques were divided into healthy control group and operation model group according to random number table.Partial resection of the motor cortex was carried out in operation model group,in which precentral gyrus cortex from above the right lateral cerebral fissure to the inter-hemicerebral fissure,together with the posterior-superior frontal gyrus (about 0.3 to 0.5 cm in front of the anterior median sulcus) cortex were removed with the depth of about 0.5 to 0.6 cm.After the operation,the continuous camera shooting was used to record whether left limb motor dysfunction and abnormal posture existed or not.Muscle tension was assessed by manual examination of muscle tone with reference to the modified Ashworth scale.The quantitative indexes of the two groups were detected by using the gross motor and fine motor assessment scale.9.4T magnetic resonance imaging (MRI) was used to detect the brain imaging changes.Results After operation,the macaque in the operation model group immediately showed left hemiparesis,left upper limb abnormal lifting,left lower limb paralysis,left limb claudication,and eating mainly relied on the right side of the body.After 6 weeks of operation,left limb activity of the operation model group was significantly lower than that of the healthy control group,and the gross motor scores and fine motor scores were significantly lower than those of the healthy control group(Friedman test:χ2=33.939,P<0.05;χ2=37.526,P<0.05).The macaque in the operation model group showed some symptoms that abnormal posture mainly tilted to the left for the rest,sitting in a corner of the monkey cage,left arm was put on the cage to maintain postural balance,and movement was left slightly inclined,which had simulated the typical clinical manifestations of human spastic hemiplegic cerebral palsy.Muscle tension was checked by hand,and the left limb paralysis and muscle tension decreased after operation in the model group,and the left muscle tension increased gradually after 5 weeks,and gradually increased to score 4 points and the score remained 3 after 10 weeks.Brain MRI of 3 weeks postoperatively suggested scar tissue formation after right motor cortex resection,which supported the pathological changes of the hemiplegic cerebral palsy models.Conclusions Through the partial resection of the motor cortex,the model of spastic cerebral palsy was established successfully.The results of behavioral evaluation and MRI showed that the model was consis-tent with spastic hemiplegia.

Several human diseases have been associated with mitochondrial voltage-dependent anion channel-1 (VDAC1) due to its role in calcium ion transportation and apoptosis. Recent studies suggest that VDAC1 may interact with endothelium-dependent nitric oxide synthase (eNOS). Decreased VDAC1 expression may limit the physical interaction between VDAC1 and eNOS and thus impair nitric oxide production, leading to cardiovascular diseases, including pulmonary arterial hypertension (PAH). In this report, we conducted meta-analysis of genome-wide expression data to identify VDAC1 influenced genes implicated in PAH pathobiology. First, we identified the genes differentially expressed between wild-type and Vdac1 knockout mouse embryonic fibroblasts in hypoxic conditions. These genes were deemed to be influenced by VDAC1 deficiency. Gene ontology analysis indicates that the VDAC1 influenced genes are significantly associated with PAH pathobiology. Second, a molecular signature derived from the VDAC1 influenced genes was developed. We suggest that, VDAC1 has a protective role in PAH and the gene expression signature of VDAC1 influenced genes can be used to i) predict severity of pulmonary hypertension secondary to pulmonary diseases, ii) differentiate idiopathic pulmonary artery hypertension (IPAH) patients from controls, and iii) differentiate IPAH from connective tissue disease associated PAH.
Animals ; Anoxia ; Apoptosis ; Calcium ; Cardiovascular Diseases ; Connective Tissue Diseases ; Fibroblasts ; Gene Expression ; Gene Ontology ; Humans ; Hypertension ; Hypertension, Pulmonary* ; Ion Transport ; Lung Diseases ; Mice ; Mice, Knockout ; Nitric Oxide ; Nitric Oxide Synthase ; Pulmonary Artery ; Transcriptome

Objective:To investigate the damage and mechanism of artemisia annua pollen on tight junction of human nasal mucosa epithelial cells (HNEpC).Methods:HNEpC were cultured in vitro. Different concentrations of artemisia annua pollen (0, 20, 40, 80, 100, 160, 200 μg/ml) were used to intervene the cells for 24 h, and the cell proliferation activity was detected by the CCK-8 method. The expression and phosphorylation of p38MAPK signaling pathway were detected by Western Blot before and after the intervention of SB203580, a p38MAPK inhibitor in HNEpC. Immunofluorescence chemical staining, Western Blot and quantitative real-time PCR (qPCR) were used to observe the expression and distribution of tight junctions Occludin and Claudin-1. SPSS 21.1 software was used for statistical analysis.Results:CCK-8 results showed that, compared with the control group, the proliferation activity of HNEpC increased after 6 h intervention with different concentrations of artemisia annua pollen (all P<0.05). After 12 h of intervention, the proliferation activity of HNEpC in the 20, 40, 80, 100 and 160 μg/ml groups was not significantly changed (all P>0.05), while that in the 200 μg/ml group was decreased ( P<0.05). After the intervention for 24 h, the proliferation activity of cells in the 20 and 40 μg/ml groups was not significantly changed (all P>0.05), while that in the 80, 100, 160 and 200 μg/ml groups was decreased (all P<0.05). Immunofluorescence staining showed that the Occludin and Claudin-1 proteins in the normal control group were localized on the cell membrane and expressed more and formed a ring structure around the cell membrane. However, under the intervention of high concentration artemisia annua pollen, its expression level decreased, appeared broken, fuzzy, and nonuniform distribution. Western Blot and qPCR results showed that after 24 h of intervention, the expression levels of HNEpC Claudin-1 protein and its mRNA in the pollen groups (40, 80, 100, 160, 200 μg/ml) of artemisia annua decreased compared with those of those of the control group (mRNA expression levels were 0.567±0.214, 0.443±0.109, 0.462±0.160, 0.497±0.134, 0.388±0.076 compared with 1.001±0.067, respectively, all P<0.05). However, the mRNA of Occludin protein and its mRNA only decreased in the 200 μg/ml treatment group (mRNA expression level was 0.631±0.109 compared with 1.016±0.026, P<0.05), while all the other treatment groups increased (mRNA expression levels were 1.258±0.134, 1.827±0.103, 2.429±0.077, 1.707±0.085, 1.477±0.066 compared with 1.016±0.026, respectively, all P<0.05). Western Blot showed that p-p38MAPK expression increased after intervention with 100, 160, 200 μg/ml artemisia annua pollen for 24 h. SB203580 could inhibit the decreasing expression of Occludin caused by artemisinin pollen (mRNA expression was 1.255±0.179 compared with 0.631±0.109, P<0.05), but had no effect on Claudin-1 protein expression. Conclusion:Pollen from artemisia annua may activate p38MAPK signaling pathway and destroy the close connection of HNEpC.

Objective:To investigate the clinical effect of large medium thickness skin graft on the back and scalp replantation in the back donor area after complete resection of giant congenital melanoma nevus (GCMN) in children′s upper limbs.Methods:From April 2017 to may 2020, 16 pediatric patients with GCMN of upper limbs were treated in the First Affiliated Hospital of Air Force Military Medical University, including 9 males and 7 females, aged from 2 years to 7 months to 12 years. Giant melanoma nevus area 14 cm×11 cm-23 cm×20 cm, the wound after removing the skin of giant melanocytic nevus of the limb was covered with vaseline oil gauze for 2-3 days, and then a large medium thickness skin graft was cut on the back with a drum skin extractor for transplantation. The wound in the back skin donor area was replanted with a blade thick scalp.Results:The effect of excision of giant nevus of upper limb and skin grafting on the wound of back medium thickness donor area in 16 pediatric patients was satisfactory, and there were no serious complications such as skin necrosis and poor survival. Plasma swelling was formed under the skin graft of one child′s limb, which healed after opening and drainage and three dressing changes. Anti-scar and rehabilitation treatment was performed on the limb and donor site.The patients were followed up for 6-18 months. There was no obvious scar hyperplasia and contracture in the skin graft area and donor area. The skin color and elasticity of the back and limb skin graft area were close to the normal skin around the wound, and the activities of elbow joint, wrist joint and interphalangeal joint were not limited. The parents of the pediatric were satisfied with the function and appearance of the limb skin graft area and back skin donor area of giant nevus.Conclusions:The function and appearance of large medium thickness skin graft on the back after excision of congenital giant nevus of upper limb in pediatric are better; There is no obvious scar formation after scalp replantation in the back donor area, and the repair effect is better.

ObjectiveTo investigate the effect of 1，25（OH）₂D₃ on the level of peroxisome proliferator-activated receptor-γ （PPAR-γ） in the liver， the phenotype of hepatic macrophages， and liver inflammation in a rat model of nonalcoholic steatohepatitis （NASH）， as well as the mechanism of 1，25（OH）₂D₃ improving liver inflammation. MethodsAfter 1 week of adaptive feeding， 24 specific pathogen-free Wistar rats were randomly divided into normal group ［choline-supplemented L-amino acid-defined （CSAA） diet］， normal+1，25（OH）₂D₃ group ［CSAA diet+1，25（OH）₂D₃］， model group ［choline-deficient L-amino acid-defined diet （CDAA） diet］， and model+1，25（OH）₂D₃ group ［CDAA diet+1，25（OH）₂D₃］， with 6 rats in each group. The dose of 1，25（OH）₂D₃ was 5 μg/kg for intraperitoneal injection twice a week for 12 weeks. The serum levels of aspartate aminotransferase （AST） and alanine aminotransferase （ALT） were measured， liver histopathology was observed， and SAF score was assessed. M1 hepatic macrophages and M2 hepatic macrophages were measured to analyze in the change in the phenotype of hepatic macrophages， and ELISA was used to measure the levels of tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， interleukin-4 （IL-4）， and interleukin-10 （IL-10） in liver tissue， and qPCR was used to measure the mRNA level of PPAR-γ. The two-factor analysis of variance was use for comparison between groups， and the least significant difference t-test was used for further comparison； the Pearson method was used for correlation analysis. ResultsCompared with the normal group， the model rats with CDAA diet-induced NASH had significant increases in the serum levels of AST and ALT （P=0.019 and P<0.001）， the SAF score of liver histopathology （P<0.001）， the level of M1 hepatic macrophages （P<0.001）， and the ratio of M1 and M2 hepatic macrophages （P<0.001）， as well as a significant increase in the level of TNF-α （P<0.001） and a significant reduction in the level of IL-4 in liver tissue （P=0.025）. The 1，25（OH）₂D₃ group had significant reductions in the serum levels of ALT （P<0.001）， the SAF score of liver histopathology （P<0.001）， the level of M1 hepatic macrophages （P<0.001）， and the ratio of M1 and M2 hepatic macrophages （P=0.001）， the level of IL-1β （P<0.001） and a significant increase in the level of M2 hepatic macrophages （P=0.017）， the level of IL-10 （P=0.039）， the level of IL-4 （P<0.001）， the level of PPAR-γ （P=0.016）. There were significant interactions between CDAA diet-induced NASH model and 1，25（OH）₂D₃ in serum the levels of AST and ALT （P=0.007 and P=0.008）， the SAF scores of liver histopathology （P<0.001）， the level of M1 hepatic macrophages （P<0.001）， the level of M2 hepatic macrophages （P=0.008）， the ratio of M1 and M2 of hepatic macrophages （P=0.005）， the level of TNF-α （P<0.001）， the level of IL-10 （P=0.038）， the level of IL-4 （P<0.001） and the level of PPAR-γ （P=0.009）. The correlation analysis showed that PPAR-γ was negatively correlated with the ratio of M1 and M2 hepatic macrophages （r=-0.415， P=0.044） and was positively correlated with M2 hepatic macrophages （r=0.435， P=0.033）， IL-10 （r=0.433， P=0.035）， and IL-4 （r=0.532， P=0.007）. ConclusionThis study shows that 1，25（OH）₂D₃ improves liver inflammation in NASH by activating PPAR-γ to regulate the phenotypic transformation of hepatic macrophages.

Animals ; SARS-CoV-2 ; Antibodies, Neutralizing ; Macaca mulatta ; COVID-19/prevention & control* ; Antibodies, Viral ; Vaccines