Acquired Immunodeficiency Syndrome ; prevention & control ; Adult ; Burnout, Professional ; Chi-Square Distribution ; Female ; Humans ; Male ; Medical Staff ; Middle Aged ; Rural Population ; Surveys and Questionnaires ; Young Adult

Child ; Churg-Strauss Syndrome ; pathology ; Female ; Humans

Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Isocitrate Dehydrogenase ; genetics ; Leukemia, Myeloid, Acute ; genetics ; Male ; Mutation ; Nuclear Proteins ; genetics ; Prognosis ; Treatment Outcome

Objective To investigate celecoxib self-microemulsifying drug delivery system (CXB-SMEDDS) that was developed to increase the dissolution rate and oral bioavailability of celecoxib.Methods The formulation of CXB-SMEDDS was optimized by pseudo-ternary phase diagrams analysis.The appearance, morphology, particle size distribution and in vitro drug release behavior of CXB-SMEDDS were investigated after diluted by water.The bioavailability of CXB-SMEDDS was determined by oral administration to rats compared with CXB suspension.Results An optimized formulation was selected: Medium chain triglycerides as oil phase, Tween 20 as surfactant, Transcutol HP as cosurfactant.The ratio of oil phase, surfactant and cosurfactant was 2∶9∶9.Upon mixing with water, CXB-SMEDDS formed a clear and transparent microemulsion solution with homogeneous small spherical under transmission electron microscopy.For particle size of CXB-SMEDDS was found to be (57.6±14.2) nm.The in vitro dissolution test indicated a significant improvement in release characteristics of CXB.The AUC of CXB-SMEDDS and CXB suspension were (5.54±0.94) and (3.32±0.59) mg·L-1·h, respectively.The relative bioavailability was 166.9%.Conclusion The SMEDDS can significantly increase celecoxib dissolution in vitro and bioavailability in vivo.

Microbial is a renewable resource which can produce polysaccharide. Its unique physiological activities and broad applications are attracting increasing attention. In this article, the source and the fermenta- tion conditions of microbial polysaccharide was reviewed, with a view to provide a scientific basis for the production of the microbial polysaccharide.

Objective To explore the clinical modalities and diagnosis of respiratory failure due to laryngotracheal disorders in children,in order to reduce the misdiagnosis.Methods Fifteen patients(11 cases were male,4 cases were female) with respiratory failure in Intensive Care Unit, Tianjin Children′s Hospital from Jul.2006 to Jul.2009 were selected.Data including history,characteristics and results of spiral computerized tomography(CT) and reconstruction and magnetic resonance imaging(MRI) were reviewed.Results The major clinical manifestations indicated that 7 cases had laryngeal stridor,6 cases had recurrent pneumonia,5 cases had cyanosis after crying,and 12 patients were complicated with respiratory failure in 12 hours.Nine cases were recovered,3 cases were given up,and 3 cases died.All patients were performed with CT about laryngohypopharynx,and the results were cyst of root of tongue in 3 cases,trachea pressed by cyst of parapharyngeal space in 1 case.There were 11 cases examined by spiral CT and reconstruction,in which 6 cases were confirmed as tracheal stenosis,2 cases were left bifid tracheostoma,2 cases were pulmonary artery sling,and 1 case was diagnosed as tracheomalacia.Chest X-ray radiograph indicated that bronchopneumonia in 8 cases,bronchitis in 3 cases and negative in 4 cases.Echocardiograph examination was performed among 11 cases,in which 2 cases were pulmonary artery sling,2 cases were atrial septal defect,1 case was patent ductus arteriosus, and 6 cases were negative.Conclusions There is high morbidity of respiratory failure caused by laryngotracheal disorders in infants,but misdiagnosis ccures usually because of non-specific symptoms.If the infant must depend on mechanic ventilation for a long time and has airway obstruction,he should be examined early by using spiral CT.

Abstract: Objective　To explore the correlation between the levels of silent information regulator 1 (SIRT1) and forkhead box protein O3 (FOXO3) in peripheral blood mononuclear cells of patients with active pulmonary tuberculosis (APTB) and macrophage-related cytokines-inducible nitric oxide synthase (iNOS) and arginase-1 (Arg-1). Methods　A total of 64 APTB patients who were treated in Yubei Hospital, the First Affiliated Hospital of Chongqing Medical University from January 2020 to December 2021 were gathered as the APTB group, 59 people with latent tuberculosis infection (LTBI) were gathered as the LTBI group, and 62 healthy people were gathered as the control group. Quantitative real-time PCR (qPCR) method was performed to measure the levels of SIRT1 mRNA and FOXO3 mRNA in peripheral blood mononuclear cells. The enzyme-linked immunosorbent assay (ELISA) was performed to measure serum iNOS and Arg-1 levels; ROC curve was used to analyze the value of SIRT1 mRNA and FOXO3 mRNA levels in the differential diagnosis of LTBI and APTB; Pearson correlation was performed to analyze the correlation of SIRT1 mRNA and FOXO3 mRNA in peripheral blood mononuclear cells of APTB patients with serum iNOS and Arg-1 levels. Results　The levels of SIRT1 mRNA, FOXO3 mRNA and serum iNOS in peripheral blood mononuclear cells decreased in control group, LTBI group and APTB group, and the level of serum Arg-1 increased in turn (P<0.05). The AUCs of SIRT1 mRNA and FOXO3 mRNA in differential diagnosis of LTBI and APTB were 0.876 and 0.887, respectively, the sensitivity was 71.2% and 76.3%, and the specificity was 96.9% and 90.6% respectively. The levels of SIRT1 mRNA and FOXO3 mRNA in peripheral blood mononuclear cells of APTB patients were positively correlated (r=0.500, P<0.05), and they were positively correlated with serum iNOS and negatively correlated with serum Arg-1 (P<0.05). The SIRT1 mRNA, FOXO3 mRNA and serum iNOS in peripheral blood mononuclear cells of APTB patients after 6 months of treatment were higher than those before treatment, and serum Arg-1 was lower than before treatment (P<0.05). Conclusions　The levels of SIRT1 mRNA and FOXO3 mRNA in peripheral blood mononuclear cells of APTB patients are low, and they are positively correlated with macrophage-related cytokine iNOS and negatively correlated with Arg-1.

italic>γ-Aminobutyric acid (GABA) is a crucial inhibitory neurotransmitter found in various cells in the human body. While the GABAergic system is typically associated with the nervous system, recent research has revealed that immune cells and tumor cells also express components of this system. In the tumor microenvironment (TME), GABA is secreted to act extracellularly on other cells. GABA is metabolized via the GABA shunt and is involved in the tricarboxylic acid (TCA) cycle by generating succinate, which can provide energy for tumor cells. Activation of GABA receptors (GABARs) is a major pathway through which GABA participates in the regulation of antitumor immune responses. The activation of GABA type A receptors (GABA_ARs) can inhibit the activation and proliferation of T cells, elicit anti-inflammatory macrophages, and promote tumor cell growth and migration, while activation of GABA type B receptors (GABA_BRs) is generally considered to inhibit cancer cell migration and induce cancer cell apoptosis. In general, receptor activation inhibits immune cells, but the effect on tumor cells varies. Additionally, the downregulation of the expression levels of GABA transporters (GATs) is involved in tumor progression. Although antagonists of GABA metabolism and drugs that act on GABA receptors are considered therapeutic drugs for tumors, there have been few clinical studies conducted on them.

Objective To explore the relationship between coping style and family cohesion and adaptation among postoperative patients with breast cancer undergoing chemotherapy.Methods A cross-section survey was conducted among 300 postoperative patients with breast cancer undergoing chemotherapy,and Medical Coping Modes Scale and Family Cohesion and Adaptation Scale were used for evaluating.Results The average score of confronce in breast cancer patients was significandy higher than that in domestic norm [ ( 18.53 ± 1.44) vs ( 19.39 ± 3.04 ) ],and the average scores of resignation and avoidance were significantly lower than that in domestic norm [ ( 14.67 ± 1.10) vs ( 8.47 ± 3.58 ),( 16.38 ± 1.63 ) vs ( 14.45 ± 2.97 ) ;t =4.66,29.36,10.54,respectively;P ＜0.01 ].The mean scores of ideal and unsatisfied family cohesion of patients were significantly higher than that in domestic norm,and the mean scores of ideal and unsatisfied family adaptation were significantly lower than that in domestic norm( P ＜ 0.01 ).A significant correlation was found and family cohesion,unsatisfied family cohesion,real family adaptation,and unsatisfied family adaptation were correlated with the coping style( r =-0.14 -0.25,P ＜0.05 ).Conclusions The coping style of postoperative patients with breast cancer undergoing chemotherapy is correlated with their family cohesion and adaptation,so it is important to take action in the intervention to patients' family and.improve the coping style for patients.

Objective:To investigate the effect of metformin and arsenic trioxide on KG1a cells proliferation of acute myeloid leukemia and its possible mechanism.Methods:CCK-8 method was used to detect the killing effect of metformin,arsenic trioxide and combined application on KG1a cells.Annexin V-FITC/P1 Dual Stain Flow Cytometry was used to detect the effect of combined application on apoptosis of KG1 a cells.Western blot was used to detect the expression of intracellular apoptosis-,autophagy-related protein.Results:Metformin and arsenic trioxide alone or in combination could inhibit the proliferation of KG1 a cells and induce apoptosis of KG1 a cells,and the proliferation inhibition rate and apoptosis rate in the combined drug group were higher than those in the drug group alone(P＜0.05).The combination of drugs induced upregulation of Caspase 8 protein and P62 protein expression and was higher than that in the drug group alone(P＜0.05).Conclusion:Metformin can synergize with arsenic trioxide to kill KG1a cells,and its mechanism of action may be related to inducing apoptosis and enhancing autophagy.