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Objective@#To analyze the ear, nose, and throat exam of some freshmen in the military college entrance examination in Shandong Province in 2020 and to facilitate adolescent targeted health promotion.@*Methods@#The 1 411 freshmen participating in the military college entrance examination in Jinan, Zibo and Weifang of Shandong Province were included. The ear, nose, and throat exam were performed by professionals using electric otoscope, 5 meter whispering test, and front rhinoscope.@*Results@#Nasal septal deviation and hypertrophy of inferior turbinate accounted for the highest proportion. Among 489 cases of nasal septum deviation, the detection rate of Jinan (15.97%) was significantly lower than that of Weifang (43.60%) and Zibo (46.53%) ( χ 2=63.32， P <0.05). For deviation of nasal septum, the detection rate in students with urban residence (31.53%) was significantly lower than that of rural students (39.03%) ( χ 2=4.11， P <0.05). Seventy two cases of inferior turbinate hyperplasia were detected, and the detection rate in Jinan (2.99%) was significantly lower than that in Weifang (6.51%) and Zibo (6.04%) ( χ 2=6.63， P <0.05). The detection rate of tonsil hypertrophy was significantly lower in boys (4.63%), students from urban area (3.94%), compared with that of girls(9.56%) and rural students (6.70%) ( χ 2=5.35，4.86， P <0.05). In pharyngeal examination, tonsil hyperplasia was the most common condition of enlarged tonsils ( n =214), which was significantly higher in Jinan(22.36%) than that of Weifang (11.71 %) and Zibo (10.74%) ( χ 2=22.39， P <0.05), and was significantly lower in boys (14.38%) and rural students (12.40%) than that in girls (22.79%) and urban students (17.24%) ( χ 2=4.70，4.65， P <0.05).@*Conclusion@#Nasal septum deviation and tonsil hypertrophy are the most prevalent upper airway diseases among freshmen participating in the military college entrance examination. Prevention and treatment of nasopharynx diseases should be emphasized.
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Objective@#To explore the synergistic effect of silibinin combined with crizotinib on anaplastic lymphoma kinase positive (ALK+ ) non-small cell lung cancer (NSCLC) cells and its mechanism.@*Methods@#H2228 and H3122 cells were treated with silibinin, crizotinib alone or in combination. Cell proliferation was measured by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and colony formation assay. Migration or invasion ability was tested by wound healing assay or transwell assay, respectively. Expressions of E-Cadherin and vimentin protein were examined by immunofluorescence staining. The protein expressions of ALK, p-ALK, E-Cadherin and Vimentin were detected by western blotting.The anti-cancer effect of silibinin combined with crizotinib in vivo was determined by subcutaneously injecting 2×106 H2228 cells into immunodeficient nude mice.@*Results@#The result of MTT assay showed that the cell viability of H2228 or H3122 treated with 100 μmol/L silibinin was (88.38±4.10)% or (72.27±3.62)%, respectively, marginally decreased compared with that of the control. The 50% inhibitory concentration (IC50) of H2228 cells treated with crizotinib alone or combined with 100 μmol/L silibinin was (917.10±7.75) nmol/L or (238.73±7.67) nmol/L, respectively. The IC50 of H3122 cells treated with crizotinib alone or combined with 100 μmol/L silibinin was (472.50±15.70) nmol/L or (206.10±12.01) nmol/L, respectively. The IC50s of H2228 and H3122 cells were significantly decreased by combined treatment of crizotinib and silibinin compared to crizotinib treatment alone (P<0.01). When compared with the control group, colony forming ratios of H2228 cells were (83.34±2.72)% in 100 μmol/L silibinin treatment group, (69.42±3.06)% in 400 nmol/L crizotinib treatment group and (27.32±1.42)% in combined treatment group. When compared with the control group, colony forming ratios of H3122 cells were (84.45±5.67)% in 100 μmol/L silibinin treatment group, (45.02±5.83)% in 400 nmol/L crizotinib treatment group and (17.43±3.83)% in combined treatment group. Silibinin combined with crizotinib treatment significantly inhibited the colony formation ability of H2228 and H3122 cells (P<0.01). Migration and invasion results showed that combined treatment of crizotinib and silibinin markedly inhibited the migration and invasion ability of H2228 cells (P<0.01). Western blot results indicated that treated with silibinin alone or in combination of crozitinib for 48 hours, the protein level of E-cadherin in H2228 cells was upregulated, while the expressions of p-ALK and vimentin were downregulated, without obvious alteration of ALK protein expression. In the xenograft model, the mean tumor weight was (9.40±2.58)g in crizotinib treatment group and (4.58±1.07)g in the combined treatment group. The inhibitory effect of tumor growth in vivo of combined treatment was significantly superior to that of crizotinib treatment alone (P<0.05).@*Conclusion@#Silibinin enhances the inhibitory effect of crizotinib on ALK positive NSCLC cells, which may be associated with suppression of ALK activity and mesenchymal-epithelial transition.
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OBJECTIVE To study the mechanisms of quinolones resistance in Escherichia coli.METHODS Forty E.coli clinical isolates were randomly collected from clinical specimens at the Tianjin First Central Hospital from Mar 2004 to Dec 2005.Then we detected the susceptibility to antibiotics in 40 clinical isolates of E.coli by MICs and K-B disk diffusion method.In order to investigate the mutations in the target genes,we amplified the QRDR of gyrA and parC by PCR.Later we analyzed the PCR products by single strand conformation polymorphism analysis(SSCP).In the meantime,the PCR products of marOR region were sequenced to detect the possible gene changes which contributed to the increasing expression of MarA and then lead to the Mar phenotype.RESULTS The alterations in gyrA were found in all quinolones-resistante strains.Asp87→Asn and Ala84→Pro were found besides the common amino acid alteration.The alterations in parC were found in thirty-six strains resistant to quinolones.There were no parC alterations in ECO24 which was nalidixic acid-resistant and ofloxacin/gatifloxacin-susceptible.ECO11 Which was resistant to quinolones only had no gene changes in marOR region.Six gene changes in marOR region were found in ECO5 which was resistant to mutiple antibodies.The alteration in 1879 bp changed the terminator.CONCLUSIONS The alterations in gyrA and parC are responsible for the resistant phenotypes in E.coli.That is,the alterations in the gyrA are primarily responsible for resistance to quinolones,and the alterations in the parC may play a complemental role in enhancing resistance to fluoroquinolones.Moreover,the randomly collected strains resistant to quinolones,have found some mutations in marOR.It may be play certain roles in multiple antibiotic resistance of E.coli.