Investigation of mixed species biofilm on corrosion of X65 steel in seawater environment.

Microbiologically influenced corrosion (MIC) is a complex process involving the cooperative effect of different bacterial species that coexist in the biofilm. Early studies focused on the MIC of single bacterial communities. However, in natural and industrial fields, biofilms are mostly composed of a variety of species. In this work, the effect of interspecific interaction on corrosion of X65 steel was investigated through the mixed culture of sulfate reducing bacteria (SRB) and iron oxidizing bacteria (IOB). Results demonstrated that the mixed microbial consortia created a cooperative effect to aggravate the local corrosion of X65 steel. Compared with the single species, the presence of IOB increased the growth activity of SRB cells and promoted the role of SRB in steel corrosion. The corrosion form on the surface of X65 steel gradually changed to annular pits induced by anaerobic SRB. The succession of dominant bacteria and the development of mixed species biofilm led to an increase in corrosion rate and local corrosion. The corrosion mechanism of X65 steel by mixed species biofilm at different stages was carefully elucidated.

Sequential activation of uterine epithelial IGF1R by stromal IGF1 and embryonic IGF2 directs normal uterine preparation for embryo implantation.

Embryo implantation in both humans and rodents is initiated by the attachment of a blastocyst to the uterine epithelium. For blastocyst attachment, the uterine epithelium needs to transform at both the structural and molecular levels first, and then initiate the interaction with trophectoderm. Any perturbation during this process will result in implantation failure or long-term adverse pregnancy outcomes. Endocrine steroid hormones, which function through nuclear receptors, combine with the local molecules produced by the uteri or embryo to facilitate implantation. The insulin-like growth factor (IGF) signaling has been reported to play a vital role during pregnancy. However, its physiological function during implantation remains elusive. This study revealed that mice with conditional deletion of Igf1r gene in uteri suffered from subfertility, mainly due to the disturbed uterine receptivity and abnormal embryo implantation. Mechanistically, we uncovered that in response to the nidatory estrogen on D4 of pregnancy, the epithelial IGF1R, stimulated by the stromal cell-produced IGF1, facilitated epithelial STAT3 activation to modulate the epithelial depolarity. Furthermore, embryonic derived IGF2 could activate both the epithelial ERK1/2 and STAT3 signaling through IGF1R, which was critical for the transcription of Cox2 and normal attachment reaction. In brief, our data revealed that epithelial IGF1R was sequentially activated by the uterine stromal IGF1 and embryonic IGF2 to guarantee normal epithelium differentiation during the implantation process.