ABSTRACT
Objective:To investigate the effect of different incubation time of aminolevulinic acid (ALA) on photodynamic inhibition of Propionibacterium acnes biofilms. Methods:Propionibacterium acnes biofilms were formed in 24-well plates with pre-placed cell slides and 96-well plates. The formation of the biofilm structure was observed by confocal laser scanning microscopy (CLSM) , and the growth activity of the biofilm was assessed by the tetrazolium salt XTT assay. The in vitro successfully constructed biofilm models were divided into 6 groups: negative control group receiving neither ALA treatment nor LED radiation, ALA group incubated with ALA alone for 30 minutes, LED group receiving LED radiation alone, ALA-PDT1 group, ALA-PDT2 group and ALA-PDT3 group incubated with ALA for 15, 30 and 60 minutes respectively followed by LED radiation. After the treatment, CLSM was performed to observe the biofilm structure, as well as to determine the dead/living bacteria ratio, and XTT assay to assess the growth activity of the biofilm. Differences among groups were analyzed using one-way analysis of variance and least significant difference- t test. Results:CLSM showed that the Propionibacterium acnes biofilm model was successfully constructed in vitro. The dead/living bacteria ratios were 0.90 ± 0.16, 1.75 ± 0.19, and 2.57 ± 0.32 in the ALA-PDT1 group, ALA-PDT2 group and ALA-PDT3 group respectively, which were significantly higher than the dead/living bacteria ratio in the negative control group (0.31 ± 0.01; t= 55.56, 138.62, 74.64, respectively, all P<0.001) ; the biofilm viability value was significantly lower in the ALA-PDT1 group, ALA-PDT2 group and ALA-PDT3 group (0.35 ± 0.02, 0.26 ± 0.02, 0.18 ± 0.01, respectively) than in the negative control group (0.43 ± 0.00; t= 35.66, 2.64, 110.96, respectively, all P < 0.001) . CLSM showed that the structure of the Propionibacterium acnes biofilm was destroyed under the action of ALA-PDT, and the destruction was aggravated with the prolongation of incubation time of ALA. Conclusion:The prolongation of incubation time of ALA can enhance the inhibitory effect of ALA-PDT on Propionibacterium acnes biofilms.
ABSTRACT
Objective:To explore the association of -592A/C and -1082A/G single nucleotide polymorphism in interleukin (IL)-10 gene with susceptibility to serofast in patients with syphilis.Methods:The SNPs of -592A/C and -1082A/g in the promoter region of IL-10 were detected by multiple single base extension (SNaP-shot) assay in 123 patients with syphilis(syphilis group), 118 patients with seronegative syphilis (seronegative syphilis group) and 120 healthy controls (healthy control group). The clinical characteristics, genotypes and allele frequencies of different subjects were compared.Results:There was no significant difference in age and gender between syphilis group, seronegative syphilis group and healthy control group ( P>0.05). There was no significant difference in the number of sexual partners, initial rapid plasma reagin test for syphilis (RPR) titer, stage, and Jihai reaction between the syphilis group and seronegative syphilis group ( P>0.05). There was no significant difference in the genotype and allele frequency of -592A/C and -1082A/G in the promoter region of IL-10 between the syphilis group, seronegative syphilis group and the control group ( P>0.05). Conclusions:There seems to be no evidence for association between -592A/C and -1082A/G single nucleotide polymorphism in IL-10 gene and susceptibility to serofast in patients with syphilis.
ABSTRACT
Guanosine triphosphate cyclohydrolase 1 (GTPCH1) is a protein encoded by the GCH1 gene,which catalyze GTP to tetrahydrofolinine (BH4) under physiological condition.BH4 is a coenzyme of aromatic amino acid hydroxylase and a cofactor of nitric oxide synthases.BH4 involves in the synthesis of various hormones and neurotransmitters and plays an important role in a series of pathophysiological processes in vivo.Recent studies showed that GTPCH1 is involved in the pathogenesis of neuropathic pain,doparesponsive dystonia,cancer and cardiovascular diseases.In this review,we will discuss the role of GTPCH1 in those diseases mentioned above.