Objective To investigate the infection of Mycoplasma in female urogenital system and the evolution of drug resistance. Methods Ureaplasma urealyticum (UU) and Mycoplasma hominis (MH) infections were examined by pathogen culture and fluorescence quantitative PCR in urogenital samples from 530 female patients in 2007, and drug sensitivity tests were performed in vitro. The results were compared with those in 2000. Results In 2000, there were 99 patients with Mycoplasma infections, in which 65 were of UU infections, 15 were of MH infections and 19 were of UU + MH infections. In 2007, there were 344 patients with Mycoplasma infections, in which 236 were of UU infections, 47 were of MH infections and 61 were of UU + MH infections. Patients aged 21～30 had the highest Mycoplasma infection rates both in 2000 (46.2%) and 2007 ( 50.5% ) ; while Mycoplasma infection rate in patients aged under 20 rose from 5.1% in 2000 to 12.8% in 2007 (χ2 = 4.682, P < 0.05). Both in 2000 and 2007, pathogens presented the highest drug resistance rates to tetracycline (TET) and erythromycin ( ERY ) which were all bore 80%. Compared with 2000, drug resistance rates to levofloxacin (LEV), azitromvcin (AZI) and ofloxacin (OFL) rose in 2007, and the differences were of statistical significance (P <0.05), while drug resistance rates to dmoxycycline (DOX), minocyclin (MIN) and josamycin (JOS) were still in the low level. Conclusions UU is the primary pathogen of infection in female urogenital system, and there is a tendency of Mycoplasma infection in younger age women. DOX, MIN and JOS can be the preferred medicines for Mycoplasma infections.

Hereditary gingival fibromatosis (HGF) is a rare inherited condition with fibromatoid hyperplasia of the gingival tissue that exhibits great genetic heterogeneity. Five distinct loci related to non-syndromic HGF have been identified; however, only two disease-causing genes, SOS1 and REST, inducing HGF have been identified at two loci, GINGF1 and GINGF5, respectively. Here, based on a family pedigree with 26 members, including nine patients with HGF, we identified double heterozygous pathogenic mutations in the ZNF513 (c.C748T, p.R250W) and KIF3C (c.G1229A, p.R410H) genes within the GINGF3 locus related to HGF. Functional studies demonstrated that the ZNF513 p.R250W and KIF3C p.R410H variants significantly increased the expression of ZNF513 and KIF3C in vitro and in vivo. ZNF513, a transcription factor, binds to KIF3C exon 1 and participates in the positive regulation of KIF3C expression in gingival fibroblasts. Furthermore, a knock-in mouse model confirmed that heterozygous or homozygous mutations within Zfp513 (p.R250W) or Kif3c (p.R412H) alone do not led to clear phenotypes with gingival fibromatosis, whereas the double mutations led to gingival hyperplasia phenotypes. In addition, we found that ZNF513 binds to the SOS1 promoter and plays an important positive role in regulating the expression of SOS1. Moreover, the KIF3C p.R410H mutation could activate the PI3K and KCNQ1 potassium channels. ZNF513 combined with KIF3C regulates gingival fibroblast proliferation, migration, and fibrosis response via the PI3K/AKT/mTOR and Ras/Raf/MEK/ERK pathways. In summary, these results demonstrate ZNF513 + KIF3C as an important genetic combination in HGF manifestation and suggest that ZNF513 mutation may be a major risk factor for HGF.
Animals ; Humans ; Mice ; Fibromatosis, Gingival/pathology* ; Gingiva ; Kinesins/genetics* ; Mutation/genetics* ; Phosphatidylinositol 3-Kinases/genetics*