Objective To investigate the effects of downregulating microRNA(miR)-550a-5p on the proliferation,migration and invasion of non-small cell lung cancer(NSCLC)and to explore its mo-lecular mechanisms.Methods The miR-550a-5p inhibitor and its negative control(inhibitor NC),as well as small interfering RNA targeting scavenger receptor class A member 3(si-SCARA3)and its negative control(si-NC)were individually or co-transfected into A549 cells.These cells were desig-nated as inhibitor NC group,miR-550a-5p inhibitor group,miR-550a-5p inhibitor+si-NC(co-trans-fection)group and miR-550a-5p inhibitor+si-SCARA3(co-transfection)group.Cell proliferation was assessed by CCK-8 assay;colony formation ability was evaluated using a plate cloning method;cell migration and invasion were detected by scratch assay and Transwell chamber assay,respectively;levels of matrix metalloproteinase(MMP)-2 and MMP-9 in the supernatant of A549 cells were measured by enzyme-linked immunosorbent assay(ELISA);apoptosis levels were determined by Annexin V/PI double staining.Results Compared with adjacent normal tissues,the expression level of miR-550a-5p was increased,while SCARA3 mRNA expression was decreased in NSCLC tissues(P＜0.05).Dual-luciferase reporter assays confirmed that miR-550a-5p directly targeted SCARA3.Compared with the inhibitor NC group,cell proliferation rate,colony formation number,migration and invasion ability of the miR-550a-5p inhibitor group decreased,apoptosis rate increased(P＜0.05).Compared with the inhibitor NC group,the expression levels of MMP-2 and MMP-9 in cell supernatant of the miR-550a-5p inhibitor group were decreased,and the expression levels of SCARA3 protein were increased(P＜0.05).Compared with the miR-550a-5p inhibitor group or the miR-550a-5p inhibitor+si-NC group,cell proliferation rate,clonal colony formation number,migration and invasion ability of the miR-550a-5p inhibitor+si-SCARA3 group were increased,and apoptosis rate was decreased(P＜0.05).Compared with the miR-550a-5p inhibitor group or the miR-550a-5p inhibitor+si-NC group,the miR-550a-5p inhibitor+si-SCARA3 group showed in-creased expression levels of MMP-2 and MMP-9 in the cell supernatant and decreased SCARA3 pro-tein expression levels(P＜0.05).Conclusion Downregulation of miR-550a-5p inhibits the prolif-eration,migration and invasion of NSCLC cells,and promotes apoptosis,possibly through upregulat-ing SC AR A3 expression.

Background Arsenic exposure is a common and important environmental and occupational hazardous factor in China, and arsenic-induced insulin resistance (IR) has attracted widespread attention as a negative health outcome to the population. Objective To explore part of the mechanism of hepatic IR induced by arsenic exposure based on the peroxisome proliferators-activated receptors γ (PPARγ)/ glucose transporter 4 (GLUT4) pathway, and to investigate potential effects of Ginkgo biloba extract (GBE) on hepatic IR induced by arsenic exposure and associated mechanism of action. Methods The target of drug action was predicted by network pharmacology and verified by in vivo and in vitro experiments. In vivo experiments: 48 SPF C57BL/6J male mice were divided into 4 groups, including control group, 50 mg·L⁻¹ NaAsO₂ model group (NaAsO₂), 50 mg·L⁻¹ NaAsO₂+10 mg·kg⁻¹ GBE intervene group (NaAsO₂+GBE), and 10 mg·kg⁻¹ GBE group (GBE), 12 mice in each group. The animals were given free access to purified water containing 50 mg·L⁻¹ NaAsO₂, or given intraperitoneal injection of normal saline containing 10 mg·kg⁻¹ GBE once per week. After 6 months of exposure, blood glucose detection, intraperitoneal glucose tolerance test (IPGTT), and insulin tolerance test (ITT) were performed. Serum and liver tissues were collected after the mice were neutralized, liver histopathological sections were obtained, serum insulin levels, liver tissue glycogen content, glucose content were detected by enzyme linked immunosorbent assay (ELISA), and the expression of PPARγ and GLUT4 proteins was detected by Western blot (WB). In vitro experiments: HepG2 cells were divided into 4 groups, including control group, 8 μmol·L⁻¹ NaAsO₂ group (NaAsO₂), 8 μmol·L⁻¹ NaAsO₂ + 200 mg·L⁻¹ GBE intervene group (NaAsO₂+GBE), and 200 mg·L⁻¹ GBE group (GBE). The levels of glycogen and glucose were detected by ELISA, and the expression of PPARγ and GLUT4 proteins was detected by WB. Results A strong binding effect between GBE and PPARγ was revealed by network pharmacology. In in vivo experiments, the NaAsO₂ group exhibited an elevated blood glucose compared to the control group, and the NaAsO₂+GBE group showed a decreased blood glucose compared to the NaAsO₂ group (P<0.01). The histopathological sections indicated severe liver structural damage in the arsenic exposure groups (NaAsO₂ group and NaAsO₂+GBE group), with varying staining intensity, partial liver cell necrosis, and diffuse red blood cell appearance. Both results of in vitro and in vivo experiments showed a decrease in glycogen synthesis and glucose uptake in the NaAsO₂ groups compared to the control groups, which was alleviated in the NaAsO₂+GBE group (P<0.01). The results of WB revealed inhibited PPARγ expression and reduced GLUT4 levels on the cell membrane, and all these changes were alleviated in the NaAsO₂+GBE group (P<0.01). Conclusion This study findings suggest that GBE antagonizes arsenic exposure-induced hepatic IR by regulating the PPARγ/GLUT4 pathway, indicating that GBE has a protective effect on arsenic exposure-induced hepatic IR, and PPARγ may be a potential therapeutic target for arsenic exposure-induced hepatic IR.

Objective:To analyze the differential expressions of proteins in aqueous humor in patients with exfoliation syndrome (XFS).Methods:A total of 20 patients were enrolled in the Department of Ophthalmology, People's Hospital of Hotan District from June 2020 to January 2021, including 10 patients with age-related cataract and 10 XFS patients combined with cataract, which were classified as cataract group and XFS group, respectively.A total of 50 to 100 μl aqueous humor was obtained in the middle of the anterior chamber through the intraoperative phacoemulsification channel.The proteins extracted from aqueous humor were analyzed by label-free quantitative proteomics technology.The cataract group was set as the control group, and the differentially expressed proteins (DEPs) in XFS group were screened according to P<0.05 and fold change >1.5.Gene ontology (GO) function analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathway analysis were used to explore the function and regulatory signaling pathways of DEPs in the XFS group.This study adhered to the Declaration of Helsinki.The study protocol was approved by the Ethics Committee of Tianjin Medical University Eye Hospital (No.2020KY[L]-21).Written informed consent was obtained from each subject. Results:In comparison with the cataract group, 25 DEPs were identified in the XFS group, primarily involved in cell adhesion, receptor, hydrolase, and molecular transport.Specifically, there were 14 down-regulated proteins including complement factor H-related protein 1 (CFHR1), endoplasmic reticulum chaperone BiP (HSPA5), biglycan (BGN), FRAS1-related extracellular matrix protein 2 (FREM2), hemoglobin subunit delta (HBD), hemoglobin subunit gamma-1 (HBG1), lysosomal thioesterase PPT2 (PPT2) etc., and 11 up-regulated proteins including latent-transforming growth factor beta-binding protein 2 (LTBP2), very low-density lipoprotein receptor (VLDLR), laminin subunit alpha-2 (LAMA2), coagulation factor Ⅸ (F9).Among them, FREM2 was the most significantly differentially expressed protein in XFS group with consistent expression levels across individual samples.GO analysis revealed that these DEPs mainly localized to the extracellular matrix of collagen, bound globin-hemoglobin complex, plasma lipoprotein particles and lysosomes.Molecular functions and biological processes showed that HBD and HBG1 were involved in cellular detoxification, PPT2 in hydrolase activity, and BGN and LTBP2 in glycosaminoglycan binding.KEGG signaling pathway analysis indicated that CFHR1 and F9 were associated with complement and coagulation cascade pathways, and FREM2 and LAMA2 were linked to the extracellular matrix interaction pathway.Conclusions:Disease progression of XFS may be associated with changes in extracellular matrix proteins, disruption of the blood-aqueous humor barrier, and potential inflammatory responses.The significant down-regulation of FREM2 protein may be a potential biomarker for XFS.

【Objective】 To monitor the positive rates of IgM and IgG antibodies and the changes in S/CO values over time in voluntary blood donors infected with SARS-CoV-2 after recovery, in order to provide theoretical basis and data support for ensuring clinical blood safety. 【Methods】 A total of 54 platelet donors who met the inclusion criteria were selected for this study, and 359 blood samples (plasma) from T1 to T7 (at 7 time points, spanning 14 to 15 weeks) were continuously monitored for SARS-CoV-2 IgM and IgG antibodies using fully automated chemi-luminescence method. 【Results】 Among 359 blood samples (plasma) from 54 donors, 349 were with valid test results.Eleven donors were tested positive for IgM, with a positive rate of 20.37%, and IgM antibody S/CO value gradually increased during T1-T3, but gradually decreased during T4-T7. Fifty-four donors were tested positive for IgG, with the positive rate of 100%, and the S/CO value of IgG antibody gradually decreased over time. During the period of T1 -T7, there was no significant difference in SARS-CoV-2 IgG antibody S/CO value between gender (male/female) or age group (18-39 years old /40-60 years old). 【Conclusion】 The positive rate of SARS-CoV-2 IgG antibody in platelet donors after recovery from SARS-CoV-2 infection was 100% during 2-14 weeks, and the IgG S/CO value gradually decreases over time. The long-term dynamic changes of SARS-CoV-2 serologically specific IgG and IgM antibodies in blood donors are worthy of further study.

【Objective】 To compare the current standards and explore the influencing factors for hemolysis rate of leukocyte-reduced red blood cells at the end of the preservation period, in order to formulate reasonable internal control indicators. 【Methods】 A retrospective analysis was performed on hemolysis rate of 427 samples of leukocyte-reduced red blood cells at the end of the preservation period in Nanning Blood Center from 2015 to 2022. Compared with the current standard for hemolysis rate at the end of the preservation period (GB 18469-2012 Quality Requirements for Whole Blood and Component Blood), the differences were analyzed, and the factors influncing the hemolysis rate were analyzed in terms of different blood donor groups. 【Results】 1) Among the 427 samples, the hemolysis rate of 418 (97.89%) did not exceed 0.4%, all lower than 0.8%; 2)the hemolysis rate of the male group was higher than that of the female group; 3) the hemolysis rate of the 18-29 years old group was lower than that of the 30-39 year old group and the 40-60 year old group, with statistically significant difference; 4) in terms of occupation, the hemolysis rate of students was the lowest, and the differences between groups were statistically significant; 5) no statistical significance was found in ethnicity and blood type. 【Conclusion】 Statistics indicated that gender, age, blood donation volume and occupation of blood donors were the influencing factors of hemolysis rate. The current standard is obviously higher in the qualified range of blood quality control in Nanning. It is advisable to formulate a reasonable quality control strategy with internal control index of hemolysis rate set <0.4%, which is conducive to making accurate evaluation of internal quality control and ensuring blood safety.

Clinical data of 62 cases of tracheobronchial foreign bodies with pulmonary atelectasis admitted in Second Affiliated Hospital and Yuying Children′s Hospital during January 2007 to December 2016 were retrospectively analyzed .There were 40 boys and 22 girls aged 9 months to 10 years, and the symptom onset ranged from 6 hours to 4 months prior to medical intervention .The foreign bodies were vegetables in 55 (88.71%), pieces of meat in 3 (4.84%) and chemical product in 4 cases (6.45%). Sixty patients recovered after medical intervention , 1 died preoperatively and 1 died of severe reexpansion pulmonary edema ( RPE) .The foreign bodies were successfully removed with rigid bronchoscopy in a single attempt in 47 children (77.05%), 1 child (1.64%) required two attempts to completely remove the foreign bodies;10 children ( 16.39%) were treated with fiberoptic bronchoscopy;3 children ( 4.92%) received thoracotomy , in which 1 child ( 1.64%) received a lobectomy due to pulmonary atelectasis and lung consolidation during operation .Conclusion Foreign bodies combined with pulmonary atelectasis in children are likely to be misdiagnosed , which led to severe adverse events . RPE is a serious postoperative complication of children receiving rigid bronchoscopy as a treatment , especially those diagnosed with tracheobronchial foreign bodies combined with pulmonary atelectasis .

AIM: To observe the effect of osthole on tricalcium phosphate (TCP) particles-induced calvarial osteolysis in vivo.METHODS:Male ICR mice were randomly divided into sham group , TCP group and osthole group .A mouse calvarial model of osteolysis was established by TCP particles .On the second postoperative day , osthole (20 mg/kg) was locally injected into the calvarium under the periosteum 3 times a week.Two weeks after osthole treatment , blood and calvaria were collected to determine the level of bone turnover markers such as alkaline phosphatase ( ALP) , osteocalcin and tartrate-resistant acid phosphatase ( TRACP) .The periosteum was performed to examine the release of tumor necrosis factor-α(TNF-α), interleukin-6 (IL-6) and IL-1βby ELISA.The calvaria was obtained for histological and molecular analyses.RESULTS:Data from HE and TRACP staining revealed that osthole prevented TCP particles-induced obvious increase in osteoclastogenesis and resorption area in the metaphysis of mouse calvaria .Osthole treatment increased ALP ac-tivity and osteocalcin level , and dncreased the activity of TRACP in the mouse serum compared with TCP group .Further-more, TCP particles-induced the releases of TNF-α, IL-6 and IL-1βwere significantly suppressed by osthole treatment .In addition, Western blot demonstrated that endoplasmic reticulum ( ER) stress markers such as glucose-regulated protein 78 (GRP78) and CAAT/enhancer binding protein homologous protein (CHOP) were significantly up-regulated in TCP parti-cles-implanted calvarial mice , indicating that TCP particles triggered an ER stress response in the mouse calvarial osteolysis model , which obviously attenuated by osthole .CONCLUSION:Osthole inhibits TCP particles-induced calvarial osteolysis in mice, which is mediated by inhibition of ER stress signaling pathway .