Carbapenem-resistant Klebsiella pneumoniae (CRKP) was epidemic around the world and become a global threat to public health. The most important carbapenem-resistant mechanism is producing carbapenemases, especially Klebsiella pneumoniae carbapenemase (KPC), which is prevalent in the international clonal complex CC11. The high-risk multidrug-resistant CC11 is widespread worldwide, and KPC-producing and (New Delhi metallo) NDM-producing strains had been reported in this clonal complex before; moreover, cases with the CC11 strain faced more severe forms of drug resistance and treatment challenges than other clonal complexes. In this study, we identified an OXA-232-producing ST437 Klebsiella pneumoniae isolate in China, which belonged to CC11. The isolate was resistant to β-lactams, aminoglycosides, and fluoroquinolones but susceptible to fosfomycin, tigecycline, and colistin. The blaOXA-232 gene was located on a 6141 bp ColKP3-type nonconjugative plasmid, and the plasmid was transformed by chemical transformation successfully. This is the first report of OXA-232-producing ST437 K. pneumoniae in China, a new clone of high-risk multidrug-resistant CC11.

Purpose To investigate clinical characteristics of six cases of Eikenella corrodens infection in Ningbo First Hospital in China in recent 2 years. Methods We retrospectively analyze medical records of six cases of E. corrodens infection in Ningbo First Hospital from 2020 to 2021. And we describe the gender, age, clinical manifestations, antimicrobial administration, and treatment of the six patients. Results Five of the patients had deep infection and they were treated with surgical drainage or abscess resection plus antimicrobial administration. After treatment, five patients were discharged and recovered well, and another patient was transferred to another hospital for further treatment. All the six cases were in line with the reports on the clinical characteristics of patients infected with E. corrodens at home and abroad before 2021. Conclusion Eikenella corrodens is a part of the normal flora of human oropharynx, but it can migrate to other parts of the human body to cause severe invasive disease in humans. Although it is susceptible to most antimicrobials, it needs debridement in the treatment of deep infection.

c1q/TnF-α-related protein 9 (cTrP9) is downregulated in gestational diabetes mellitus (GdM) and may exert a protective effect against GdM, although its mechanism of action is yet to be elucidated. To investigate the specific role of cTrP9 in GdM, the human placental trophoblast cell line HTr8/SVneo was treated with high glucose (HG) to simulate the environment of GdM in vitro. The effects of cTrP9 on the HTr8/SVneo cells and endoplasmic reticulum (er) stress were analyzed before and after cTrP9 overexpression using reverse transcription-quantitative Pcr and western blotting. The results obtained demonstrated that cTrP9 alleviated er stress in the trophoblast cell line. after treating with the er-stress inducer tunicamycin, cell viability was investigated by performing cell counting Kit-8, Tunel and western blotting assays, which revealed that cTrP9 increased the activity of HTr8/SVneo cells induced by HG through the alleviation of er stress. Subsequently, eliSa and western blotting assay results demonstrated that cTrP9 inhibited HG-induced inflammation of the HTR8/SVneo cells by the reduction in ER stress. Finally, the detection of reactive oxygen species, nitric oxide (NO) synthase and NO levels confirmed that CTRP9 inhibited the oxidative stress of HTr8/SVneo cells induced by HG through the reduction of er stress. collectively, the results of the present study suggested that cTrP9 may decrease trophoblast cell damage caused by HG through the suppression of er stress, and therefore, cTrP9 may potentially be a therapeutic target in the treatment of GdM.