DNB-001

The removal rate of some antibiotics in urban sewage by conventional treatment is low, which leads to an increase in antibiotic resistant bacteria in natural water environments. To reduce the ecological harm of antibiotics to the water in towns, a risk control technique for degradation of microantibiotics by the co-metabolism of antibiotic resistant denitrifying bacteria was proposed. Using sodium acetate as an electron donor and maintaining the concentration of ofloxacin (OFLX) at 1 μg·g^-1, gradually increasing the dominant growth of antibiotic degradation bacteria, denitrifying bacteria (DnB₁), trace antibiotics and sodium acetate, and denitrifying bacteria (DnB₂) with the presence of sodium acetate and nitrogen elements were cultured. The degradation effect of antibiotics through denitrification and the effects of antibiotics on denitrification of resistant denitrifying bacteria and the changes to the microbial community were investigated. The results showed that DnB₂ had a significant degradation effect on OFLX compared to DnB₁. The degradation to OFLX by DnB₁ and DnB₂ was 0.31 μg·g^-1 and 16.14 μg·g^-1, respectively. Increased OFLX concentration inhibited DnB₁ denitrification activity in the short term. The denitrification process of DnB₂ was less affected by OFLX. At the same time, high-throughput sequencing using the Illumina MiSeq platform was used. Based on the operational taxonomic unit information formed by the clustering of sequencing results, the diversity of each sample was compared and analyzed. The research results show that the relative abundance and diversity of the microbial community of DnB₁ are higher than those of DnB₂.

KR-31378 is a newly developed K(ATP)-channel opener. To investigate the ability of KR-31378 to protect retinal ganglion cells (RGC), experiments were conducted using two retinal ischemia models. Retinal ischemia was induced by transient high intraocular pressure (IOP) for acute ischemia and by three episcleral vein occlusion for chronic retinal ischemia. KR-31378 was injected intraperitoneally and administered orally in the acute and chronic ischemia models, respectively. Under the condition of chronic ischemia, RGC density in the KR-31378-treated group was statistically higher than that in the non-treated group, and IOP was reduced. In the acute retinal ischemia model, 90% of RGC were degenerated after one week in non-treated retina, but, RGC in KR-31378-treated retina were protected from ischemic damage in a dose-dependent manner and showed inhibited glial fibrillary acidic protein (GFAP) expression. Furthermore, the KR-31378 protective effect was inhibited by glibenclamide treatment in acute ischemia. These findings indicate that systemic KR-31378 treatment may protect against ischemic injury-induced ganglion cell loss in glaucoma.