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Klebsiella pneumoniae causes severe lung and bloodstream infections that are difficult to treat due to multidrug resistance. We hypothesized that antimicrobial resistance can be reversed by targeting chromosomal non-essential genes that are not responsible for acquired resistance but essential for resistant bacteria under therapeutic concentrations of antimicrobials. Conditional essentiality of individual genes to antimicrobial resistance was evaluated in an epidemic multidrug-resistant clone of K. pneumoniae (ST258). We constructed a high-density transposon mutant library of >430,000 unique Tn5 insertions and measured mutant depletion upon exposure to three clinically relevant antimicrobials (colistin, imipenem or ciprofloxacin) by Transposon Directed Insertion-site Sequencing (TraDIS). Using this high-throughput approach, we defined three sets of chromosomal non-essential genes essential for growth during exposure to colistin (n = 35), imipenem (n = 1) or ciprofloxacin (n = 1) in addition to known resistance determinants, collectively termed the “secondary resistome”. As proof of principle, we demonstrated that inactivation of a non-essential gene not previously found linked to colistin resistance (dedA) restored colistin susceptibility by reducing the minimum inhibitory concentration from 8 to 0.5 μg/ml, 4-fold below the susceptibility breakpoint (S ≤ 2 μg/ml). This finding suggests that the secondary resistome is a potential target for developing antimicrobial “helper” drugs that restore the efficacy of existing antimicrobials.
The secondary resistome of multidrug-resistant Klebsiella pneumoniae
Bimal Jana,a,1,2,* Amy K. Cain,3,†* William T. Doerrler,4 Christine J. Boinett,3,‡ Maria C. Fookes,3 Julian Parkhill,3 and Luca Guardabassib,1,2
Obesity-related cardiac lipid accumulation is associated with increased myocardial oxidative stress. The role of the antioxidant glutathione in cardiac lipotoxicity is unclear. Cystathionine β-synthase (Cbs) catalyzes the first step in the trans-sulfuration of homocysteine to cysteine, which is estimated to provide ∼50% of cysteine for hepatic glutathione biosynthesis. As cardiac glutathione is a reflection of the liver glutathione pool, we hypothesize that mice heterozygous for targeted disruption of Cbs (Cbs+/−) are more susceptible to obesity-related cardiolipotoxicity because of impaired liver glutathione synthesis. Cbs+/+ and Cbs+/− mice were fed a high fat diet (60% energy) from weaning for 13 weeks to induce obesity and had similar increases in body weight and body fat. This was accompanied by increased hepatic triglyceride but no differences in hepatic glutathione levels compared with mice fed chow. However, Cbs+/− mice with diet-induced obesity had greater glucose intolerance and lower total and reduced glutathione levels in the heart, accompanied by lower plasma cysteine levels compared with Cbs+/+ mice. Higher triglyceride concentrations, increased oxidative stress, and increased markers of apoptosis were also observed in heart from Cbs+/− mice with diet-induced obesity compared with Cbs+/+ mice. This study suggests a novel role for Cbs in maintaining the cardiac glutathione pool and protecting against cardiac lipid accumulation and oxidative stress during diet-induced obesity in mice.
Glutathione, Heart, Lipotoxicity, Metabolism, Obesity, Triglyceride, Cysteine
Altered Glutathione Homeostasis in Heart Augments Cardiac Lipotoxicity Associated with Diet-induced Obesity in Mice*
Sanjoy Ghosh,‡,1 Dian C. Sulistyoningrum,‡ Melissa B. Glier,‡ C. Bruce Verchere,‡ and Angela M. Devlin‡§,2
2011 Dec 9;
Nutritional status is an important factor in predicting the risk associated with surgery for cancer patients. This is especially true in colorectal cancer. Many nutritional assessments are used in clinical practice, but those assessments are rarely evaluated for their ability to predict postoperative outcome.
This is a retrospective, multi-institutional study of the ACS-NSQIP database, investigating preoperative nutrition status and its association with postoperative mortality and morbidity.
The prevalence of malnutrition is higher in colorectal cancer, when compared with other most common cancers. Among 42,483 colorectal cancer patients postoperative mortality was significantly associated with hypoalbuminemia (hazard ratio = 3.064, p < 0.001), body weight loss (hazard ratio = 1.229, p = 0.033) and body mass index of <18.5 kg/m2 (hazard ratio = 1.797, p < 0.001). Only hypoalbuminemia significantly predicted all postoperative complications, even in further multivariate logistic regression analyses (p < 0.001). Multiple regression analysis showed that the hypoalbuminemia group had the highest coefficient in significant association with length of total hospital stay (B = 3.585, p < 0.001) and overall complication (B = 0.119, p < 0.001). Conclusions In colorectal cancer, malnutrition significantly contributes to postoperative mortality, morbidity and length of total hospital stay. Hypoalbuminemia, with levels below 3.5 g/dl, serves as an excellent assessment tool and preoperative predictor of postoperative outcomes. Electronic supplementary material The online version of this article (doi:10.1186/s12937-015-0081-5) contains supplementary material, which is available to authorized users.
Preoperative malnutrition assessments as predictors of postoperative mortality and morbidity in colorectal cancer: an analysis of ACS-NSQIP
Wan-H Hu,1,2,3 Luis C. Cajas-Monson,1 Samuel Eisenstein,1,2 Lisa Parry,1,2 Bard Cosman,1,4 and Sonia Ramamoorthycorresponding author1,2