It is currently unknown whether antibiotic monotherapy or combination therapy is a more effective treatment for patients with Pseudomonas aeruginosa bacteraemia. The present study consists of a systematic review and meta-analysis of cohort studies in associated studies. The treatment options of monotherapy and combination therapy have been compared, to determine which is more effective against P. aeruginosa bacteraemia. Several electronic bibliographic databases were systematically searched and clinical studies that compared combination therapy with monotherapy for P. aeruginosa bacteraemia were identified. Dersimonian and Laird's random-effects models were used to generate summary estimates of the effects and to assess their association according to different patient characteristics and research quality standards. A total of 17 studies were selected, 3 of which were prospective while the remaining 14 were retrospective. The studies involved a total of 2,504 patients. Significant differences between combination therapy and monotherapy treatment were not found when the data were combined (odds ratio (OR)=0.81, 95% confidence interval (CI)=0.61–1.08; P=0.035). The results demonstrated strength in a number of stratification and sensitivity analyses. The variables used included study type, treatment quality score and survival rate of subgroup analysis. To conduct cumulative meta-analysis, the number of years and samples were calculated. The OR value and 95% CI were stable and demonstrated good change trend. According to the size of the sample order following accumulation, OR values and 95% CI (0.89, 0.76–1.04) exhibited a narrow range. Neither combination therapy or monotherapy exhibited significant effects on the mortality of patients with P. aeruginosa bacteraemia. Future research is required and should include large, well-designed prospective cohorts, and grouped clinical studies.

The inflammatory response is closely associated with sepsis occurrence and progression. Damage to the function of the intestinal mucosal barrier is considered to be the ῾initiation factor᾿ for the development of multiple organ dysfunction syndrome, which is the most severe progression of sepsis. The aim of the present study was to investigate whether gadolinium chloride (GdCl 3 ) could alleviate the systemic inflammatory response and protect the function of the intestinal mucosal barrier in a rat model of sepsis. The mechanism underlying this protective effect was also explored. Sprague-Dawley rats were divided into four groups: Sham, sham + GdCl 3 , cecal ligation and puncture (CLP; a model of sepsis) and CLP + GdCl 3 . In each group, blood was collected from the abdominal aorta, and intestinal tissue was collected after 6, 12 and 24 h of successful modeling. Levels of tumor necrosis factor-α, interleukin (IL)-6 and IL-1β were determined using ELISA. Western blot analysis was used to determine levels of occludin, tight junction protein ZO-1 (ZO-1), myosin light chain kinase 3 (MLCK), NF-κB and caspase-3 in intestinal tissues. Hematoxylin-eosin staining was used to observe the degree of damage to intestinal tissue. The results indicated that in CLP sepsis model rats treated with GdCl 3 , the release of systemic and intestinal pro-inflammatory factors was reduced and tissue damage was alleviated when compared with untreated CLP rats. Additionally, the expression of occludin and ZO-1 was increased, while that of NF-κB, MLCK, and caspase-3 was reduced in the CLP + GdCl 3 rats compared with the CLP rats. GdCl 3 may alleviate systemic and intestinal inflammatory responses and reduce the expression of MLCK through inhibition of the activation of NF-kB. The results of the present study also indicated that GdCl 3 promoted the expression of occludin and ZO-1. GdCl 3 was also demonstrated to reduce cell apoptosis through the inhibition of caspase-3 expression.

Background: Tuberculosis (TB) is one of the most widespread and lethal infectious diseases worldwide. The emergence of drugresistant TB has hampered effective TB treatment and control. Prokaryotic ubiquitin-like Protein-Proteasome System (PPS) contributes to the survival of Mycobacterium tuberculosis in the host. However, whether PPS effects drug resistance of isoniazid monoresistant Mycobacterium tuberculosis (INH-MTB) is still unknown. Objectives: This study aimed at exploring the effect of PPS on drug resistance of INH-MTB strain. Methods: In this study, over-expression of strains and deletion of mutant strains were constructed using electroporation. The researchers identified these constructed strains by Quantitative Reverse Transcription Polymerase Chain Reaction (RT-qPCR) or PCR. The Minimum Inhibitory Concentration (MIC) of isoniazid in INH-MTB strain and its derivative PPS mutant strains were determined using the Resazurin micro-titre assay. Results: The MIC of isoniazid was 8 µg/mL higher in INH-MTB with Pup over-expression strain than that in INH-MTB. The MIC of isoniazid was 4.82 µg/mL, 4.98 µg/mL, 4.99 µg/mL, and 4.9 µg/mL lower in INH-MTB with deletion of Pup, Dop, PafA or Mpa strains than that in INH-MTB, respectively. The differences had statistical significance (P < 0.05). The MIC of isoniazid was 1.03 µg/mL higher in INH-MTB with PafA over-expression strain than that in INH-MTB. The MIC of isoniazid was 1.03 µg/mL and 0.68 µg/mL lower in INH-MTB with Dop, Mpa over-expression strains than that in INH-MTB, respectively. The differences had no statistical significance (P > 0.05). Conclusions: These results show that PPS effects the drug resistance of the INH-MTB strain.