Patients with bloodstream infections (BSI) are associated with high mortality rates. Due to tigecycline has shown excellent in vitro activity against most pathogens, tigecycline is selected as one of the candidate drugs for the treatment of multidrug-resistant organisms infections. The purpose of this study was to evaluate the effectiveness and safety of the use of tigecycline for the treatment of patients with BSI. The PubMed and Embase databases were systematically searched, to identify published studies, and we searched clinical trial registries to identify completed unpublished studies, the results of which were obtained through the manufacturer. The primary outcome was mortality, and the secondary outcomes were the rate of clinical cure and microbiological success. 24 controlled studies were included in this systematic review. All-cause mortality was lower with tigecycline than with control antibiotic agents, but the difference was not significant (OR 0.85, [95% confidence interval (CI) 0.31–2.33; P = 0.745]). Clinical cure was significantly higher with tigecycline groups (OR 1.76, [95% CI 1.26–2.45; P = 0.001]). Eradication efficiency did not differ between tigecycline and control regimens, but the sample size for these comparisons was small. Subgroup analyses showed good clinical cure result in bacteremia patients with CAP. Tigecycline monotherapy was associated with a OR of 2.73 (95% CI 1.53–4.87) for mortality compared with tigecycline combination therapy (6 studies; 250 patients), without heterogeneity. Five studies reporting on 398 patients with Klebsiella pneumoniae carbapenemase-producing K. pneumoniae BSI showed significantly lower mortality in the tigecycline arm than in the control arm. The combined treatment with tigecycline may be considered the optimal option for severely ill patients with BSI.

We investigated the relationship between the outer membrane protein OprD₂ and carbapenem-resistance in 141 clinical isolates of Pseudomonas aeruginosa collected between January and December 2013 from the First Affiliated Hospital of Anhui Medical University in China. Agar dilution methods were employed to determine the minimum inhibitory concentration of meropenem (MEM) and imipenem (IMP) for P. aeruginosa. The gene encoding OprD₂ was amplified from141 P. aeruginosa isolates and analyzed by PCR and DNA sequencing. Differences between the effects of IMP^R and IMP^S groups on the resistance of the P. aeruginosa were observed by SDS-poly acrylamide gel electrophoresis (SDS-PAGE). Three resistance types were classified in the 141 carbapenem-resistant P. aeruginosa (CRPA) isolates tested, namely IMP^RMEM^R (66.7%), IMP^RMEM^S (32.6%), and IMP^RMEM^S (0.7%). DNA sequencing revealed significant diverse gene mutations in the OprD₂-encoding gene in these strains. Thirty-four strains had large fragment deletions in the OprD₂gene, in 6 strains the gene contained fragment inserts, and in 96 resistant strains, the gene featured small fragment deletions or multi-site mutations. Only 4 metallo-β-lactamase strains and 1 imipenem-sensitive (meropenem-resistant) strain showed a normal OprD₂ gene. Using SDS-PAGE to detect the outer membrane protein in 16 CRPA isolates, it was found that 10 IMP^RMEM^R strains and 5 IMP^RMEM^S strains had lost the OprD₂ protein, while the IMP^SMEM^R strain contained a normal 46-kDa protein. In conclusion, mutation or loss of the OprD₂-encoding gene caused the loss of OprD₂, which further led to carbapenem-resistance of P. aeruginosa. Our findings provide insights into the mechanism of carbapenem resistance in P. aeruginosa.

Liver cancer (LC), which is one of the most common types of cancer worldwide, is notorious for its high morbidity and mortality rates. Interleukin‑8 (IL‑8), an important member of the CXC chemokine family that was originally classified as a potent neutrophil chemoattractant, has been shown to serve an important role in inflammation, tumor growth, invasion and metastasis through interactions with its receptors. However, the expression and functional roles of IL‑8 and its receptors, CXC chemokine receptor (CXCR) 1 and CXCR2 in the progression of liver cancer remain to be fully elucidated. In the present study, it was shown that the mRNA levels of IL‑8, CXCR1 and CXCR2 were increased in peripheral blood mononuclear cells from patients with liver cancer compared with those from patients with cirrhosis or normal controls (P<0.05). Higher levels of CXCR1, CXCR2 and IL‑8 were associated with advanced tumor stage and increased risk of lymph node or distant metastasis. Immunohistochemistry showed that the IL‑8, CXCR1 and CXCR2 proteins were expressed in the cytoplasm of hepatoma cells at higher intensities than those of normal controls (P<0.05). The semi‑quantitative analysis revealed that the relative mean density of hepatic IL‑8, CXCR1 and CXCR2 staining in liver cancer was significantly increased compared with that in normal liver tissues (P<0.05). The analysis revealed that the mRNA expression of IL‑8 was positively associated with that of CXCR1 (r=0.618; P<0.05) and CXCR2 (r=0.569; P<0.05). The mRNA levels of CXCR1 and CXCR2 gradually increased with elevated expression of IL‑8 in liver cancer. Experiments were performed using human Huh‑7 and HepG2 cell lines, incubating cells with IL‑8 and conducting in vitro migration and invasion assays. The results showed that the wound healing activity and migration of Huh‑7 and HepG2 cells were increased by IL‑8. Pretreatment of the cells with anti‑CXCR1 or anti‑CXCR2 (5 µM) for 30 min markedly inhibited IL‑8‑directed cell migration. Taken together, these results indicated that IL‑8 promotes liver cancer cell migration via CXCR1 and CXCR2 and that targeting the CXCR1/2 may be a potential strategy for liver cancer treatment.

Background: Colistin has been considered as one of the most effective treatments in clinical infections, especially multidrug-resistant (MDR) bacteria-infected patients. The mcr-1 gene leads to polymyxin resistance in China. The present study investigated the prevalence of mcr-1 in a Chinese teaching hospital, and the molecular phenotypes of the positive strains were analyzed. Methods: A total of 1,112 Escherichia coli strains were collected from a Chinese University Hospital from January 2015 to January 2016. The mcr-1 gene was detected by PCR. All positive specimens were subjected to susceptibility testing, clinical analysis, phylogenetic analysis, DNA Southern blot hybridization, and gene sequencing. Results: Six (0.6%) strains of mcr-1-positive E. coli were susceptible to imipenem, meropenem, and tigecycline, except for one that presented moderate levels of tigecycline resistance. The six isolates were resistant to cefotaxime and cefepime and divided into six types of sequences. These positive strains carried a total of three plasmids: approximately 33, 61, and >92 kb plasmids. All patients were eventually cured using different types of antibiotics and discharged. Conclusion: The current study showed that the mcr-1 gene was responsible for the majority of colistin resistance in clinical isolates of E. coli. The gene can be transferred into plasmids containing other drug resistance genes by plasmid–DNA conjugation, which might cause severe consequences in drug-resistant strains. Thus, the widespread popularity of mcr-1 gene should be prevented.