Ploidy is an important determinant of fluoroquinolone persister survival

1. Download : Download high-res image (209KB)
2. Download : Download full-size image

     

The influence of heart failure co-morbidity on high-sensitivity troponin T levels in COPD exacerbation in a prospective cohort study: data from the Akershus cardiac examination (ACE) 2 study

Context: Troponin (hs-TnT) levels predict mortality after acute exacerbation of COPD (AECOPD). Whether this is independent of heart failure (HF) is not established.

Material and methods: Prospectively included AECOPD patients adjudicated for acute HF categorized into three groups: (A) AECOPD, but acute HF the primary cause for hospitalization; (B) AECOPD the primary cause, but co-existing myocardial dysfunction and (C) AECOPD without myocardial dysfunction.

Results: About 103 AECOPD patients; 18% A, 27% B and 54% C. Hs-TnT level differed between the groups: (ng/l, median) A: 41, B: 25 and C: 15, p?=?0.03 for A versus B and p?=?0.005 for B versus C. During a median 826 days, 47% died. In Cox analysis, hs-TnT levels remained associated with mortality (hazard ratio per 10?ng/l 1.3, p?<?0.0001).

Conclusion: hs-TnT levels are influenced by myocardial dysfunction/HF in AECOPD, but provide independent prognostic information. The prognostic merit of hs-TnT cannot be attributed to HF alone.     

Metabolic engineering of Escherichia coli for 1-butanol production

Compared to ethanol, butanol offers many advantages as a substitute for gasoline because of higher energy content and higher hydrophobicity. Typically, 1-butanol is produced by Clostridium in a mixed-product fermentation. To facilitate strain improvement for specificity and productivity, we engineered a synthetic pathway in Escherichia coli and demonstrated the production of 1-butanol from this non-native user-friendly host. Alternative genes and competing pathway deletions were evaluated for 1-butanol production. Results show promise for using E. coli for 1-butanol production.     

Motivational state and reward content determine choice behavior under risk in mice

Risk is a ubiquitous feature of the environment for most organisms, who must often choose between a small and certain reward and a larger but less certain reward. To study choice behavior under risk in a genetically well characterized species, we trained mice (C57BL/6) on a discrete trial, concurrent-choice task in which they must choose between two levers. Pressing one lever (safe choice) is always followed by a small reward. Pressing the other lever (risky choice) is followed by a larger reward, but only on some of the trials. The overall payoff is the same on both levers. When mice were not food deprived, they were indifferent to risk, choosing both levers with equal probability regardless of the level of risk. In contrast, following food or water deprivation, mice earning 10% sucrose solution were risk-averse, though the addition of alcohol to the sucrose solution dose-dependently reduced risk aversion, even before the mice became intoxicated. Our results falsify the budget rule in optimal foraging theory often used to explain behavior under risk. Instead, they suggest that the overall demand or desired amount for a particular reward determines risk preference. Changes in motivational state or reward identity affect risk preference by changing demand. Any manipulation that increases the demand for a reward also increases risk aversion, by selectively increasing the frequency of safe choices without affecting frequency of risky choices.     

An integrated network analysis identifies how ArcAB enables metabolic oscillations in the nitric oxide detoxification network of Escherichia coli

The virulences of many pathogens depend on their abilities to detoxify the immune antimicrobial nitric oxide (NO?). The functions of bacterial NO? detoxification machinery depend on oxygen (O₂), with O₂ inhibiting some enzymes, whereas others use it as a substrate. Previously, Escherichia coli NO? detoxification was found to be highly attenuated under microaerobic conditions and metabolic oscillations were observed. The oscillations in [NO?] and [O₂] were found to result from the inhibitory action of NO? on aerobic respiration, the catalytic inactivation of NO? by Hmp (an NO? dioxygenase), and an imbalanced competition for O₂ between Hmp and cytochrome terminal oxidase activity. Here the authors investigated the role of the ArcAB two component system (TCS) in microaerobic NO? detoxification. The authors observed that wild‐type, ΔarcA , and ΔarcB had comparable initial NO? clearance times; however, the mutant cultures failed to exhibit [NO?] and [O₂] oscillations. Using an approach that employed experimentation and computational modeling, the authors found that the loss of oscillations in ΔarcA was due to insufficient induction of cytochrome bd ‐I expression. Collectively, these results establish ArcAB as a TCS that influences NO? detoxification in E. coli within the physiologically‐relevant microaerobic regime.