RÉSUMÉ
The male patient of middle-age was admitted to Zhujiang Hospital, Southern Medical University on September 5, 2020, due to wear and rupture of the left foot hallux for more than 10 days, gradually developed swelling and blackening of the left foot and accompanied by drowsiness for 1day. Results from etiological examination of his wound secretions suggested the mixed infection of Wohlfahrtiimonas chitiniclastica and Enterococcus faecalis. The disease progressed rapidly and the patient still died of septic shock after anti-infective treatment. The infection of W. chitiniclastica is rare and has a great relationship with poor hygiene and chronic open wounds. It is necessary to use matrix-assisted laser desorption/ionization-time of flight mass spectrometry or 16S ribosomal RNA gene sequencing for strain identification. Moreover, it is recommended to use cephalosporins or carbapenems as first-line drugs due to the poor prognosis of patients with bloodstream infections.
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Aim To investigate the effects of daidzeinDD on the proliferation and apoptosis of non-small cell lung cancer cells,with a focus on the possible role of the p53 signaling pathway in this regard. Methods CCK-8 method and flow cytometry were used to detect the effects of soy isoflavone crude extract and DD on the viability and apoptosis of HELF and H1299 cells. Gene microarray was used to detect the changes in gene expression after treatment of H1299 cells with DD. GSEA and differential analysis were used to screen the major pathways and key genes. RT-qPCR and Western blot were performed to verify the differences in mRNA and protein expression of key genesp53 and CASP9 in the major pathways. After p53 inhibitor Pifithrin-α inhibited the expression of p53,the effect of DD on p53 mRNA and protein expression levels was examined,and the proliferative effect on H1299 cells was observed. Results Soy isoflavone crude extract and DD promoted proliferation and inhibited apoptosis of normal lung cells and inhibited proliferation and promoted apoptosis of lung cancer cells. p53 signaling pathway was significantly enriched in the DD-treated groupNES=1.78,P=0.000,and the expressions of p53 and CASP9 genes were found to be significantly up-regulated in the treated group. Compared with the control group,mRNA expression of CASP9 and p53 significantly increased in both HELF and H1299 cells treated with DDP<0.05,and p53 protein expression also increased in HELF cellsP<0.05. After inhibition of p53 expression,DD significantly increased the mRNA expression of p53 in H1299 and HELF cellsP<0.05 and also markedly increased the expression of p53 protein in H1299 cellsP<0.05,and it was observed that DD inhibited the proliferation of lung cancer cells. Conclusions DD inhibits the proliferation and promotes the apoptosis of lung cancer H1299 cells,and the mechanism mainly involves the p53 signaling pathway.
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<p><b>OBJECTIVE</b>To investigate the distribution of beta-2-AR +46 A-->G variant in Kazakans of Xinjiang and the relationship of the variant with low density lipoprotein-cholesterol (LDL-C) level in this population.</p><p><b>METHODS</b>The genotypes of beta-2-AR gene Arg16/Gly variant were detected by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique in 506 Kazakans with age from 30 to 69, and its distribution and relationship to LDL-C level were investigated.</p><p><b>RESULTS</b>(1) The frequencies of genotypes AA, AG, GG and alleles A, G of beta-2-AR +46 variant in this population were 0.310, 0.455, 0.235 and 0.538, 0.462 respectively, which were accorded with Hardy-Weinberg equilibrium. (2) The Gly16/Gly genotype had highest LDL-C level in the three genotypes, and were significantly higher than Arg16/Gly genotype (P < 0.05). (3) Comparing the effect of beta-2-AR gene +46 variant on serum lipid in males with females, we found that females with Gly16/Gly genotype had the highest level of serum LDL-C.</p><p><b>CONCLUSIONS</b>These data show that Gly16/Gly genotype of beta-2-AR gene +46 A-->G variant is associated with higher level of serum LDL-C in this population, especially in female.</p>
Sujet(s)
Adulte , Sujet âgé , Femelle , Humains , Mâle , Adulte d'âge moyen , Allèles , Asiatiques , Génétique , Cholestérol LDL , Sang , Génotype , Polymorphisme de restriction , Polymorphisme de nucléotide simple , Récepteurs bêta-2 adrénergiques , GénétiqueRÉSUMÉ
<p><b>OBJECTIVE</b>To investigate whether the variants A(-6)G and A(-20)C of angiotensinogen (AGT) gene are involved in the pathogenesis of essential hypertension in Kazakans.</p><p><b>METHODS</b>T his case control study recruited 125 subjects with hypertension and 74 normotensive subjects from Kazakans of Xinjiang. Genomic DNA from leukocytes was analyzed for genetic variants A(-6)G and A(-20)C in 5' upstream core promoter of AGT gene by polymerase chain reaction (PCR), single strand conformation polymorphism (SSCP), restriction fragment length polymorphism (RFLP) and automatic sequencing.</p><p><b>RESULTS</b>(1)There were only A(-6)G and A(-20)C variants in the -164 to +73 region of Kazakans' AGT gene. (2) The distributions of genotypes AA, AG, GG at locus -6 of AGT gene showed significant difference between the hypertensive group (0.39, 0.45, 0.16) and the normotensive group (0.49, 0.49, 0.02; Chi2=8.56, P=0.014). There were evident differences in the frequencies of the -6A and the -6G allele of the two groups (0.62, 0.38 and 0.73, 0.27; Chi2=5.35, P=0.021). (3) No significant difference was observed in the distribution of genotypes AA, AC, CC at locus -20 of AGT gene between the hypertensive group (0.69, 0.26, 0.05) and the normotensive group (0.65, 0.32, 0.03; Chi2=2.42, P=0.30). There was no distinct difference in the frequencies of the -20A allele and the -20C allele of the two groups (0.82, 0.18 and 0.82, 0.18; Chi2=0, P=0.99). (4) No significant difference was found at the levels of systolic and diastolic blood pressure between the groups corresponding to genotypes at the loci -6 and -20 of AGT gene.</p><p><b>CONCLUSION</b>The results suggest that the polymorphism of A(-6)G in 5' upstream core promoter of the AGT gene may be involved in the pathogenesis of essential hypertension in Kazakans, while the A(-20)C variant may not play an important role in the etiology of essential hypertension in Kazakans.</p>