Alterations in tRNAs containing 2-methylthio-N6-(delta2-isopentenyl)-adenosine during growth of enteropathogenic Escherichia coli in the presence of iron-binding proteins.

Escherichia coli grown in chemically produced iron-deficient media have well characterized alterations in the chromatographic properties of tRNAs containing the modified nucleoside 2-methylthio-N6-(delta2-isopentenyl) adenosine. The present report shows that similar tRNA alterations occur in enteropathogenic E. coli inhibited by human milk and bovine colostrum, the inhibited bacteria containing 10% or less of the normal tRNA species. Adding sufficient iron to saturate the iron-binding capacity of the lactoferrin present in milk and colostrum reversed these changes which are probably due to a failure to methylthiolate the isopentenyladenosine. Although adding iron led to a rapid replacement of abnormal tRNA by the chromatographically normal species, and to a resumption of multiplication, the tRNA alterations are not directly related to the inhibition of growth. Strains of E. coli which grew normally in milk, colostrum and in defined media containing the iron-binding protein transferrin or ovotransferrin also contained about 90% of the abnormal species. Rapid conversion of abnormal tRNA to normal tRNA occurred on adding iron and in the absence of RNA synthesis. The tRNA changes are discussed in relation to their possible connection with both the adaptation of E. coli to growth under the iron-restricted conditions imposed by iron-binding proteins in tissue fluids and with bacterial pathogenicity.     

Maltose uptake in the Zea mays scutellum

Maltose transport in slices of the maize scutellum was demonstrated despite the presence of an active maltase situated at the cell surface. The maltase could be inhibited or destroyed by treatments (neutral pH during uptake, pretreatment in Tris buffer at pH 7·5, or in 0·01 N HCl) that allowed appreciable rates of maltose uptake to occur. Using Tris- and HCl-treated slices, it was found that at disaccharide concentrations of 50 and 100 mM, maltose and sucrose were taken up at very nearly the same rates. At sugar concentrations below 50 mM, sucrose was taken up at greater rates than maltose. The maltose content of the slices was directly proportional to the maltose concentration of the bathing solution, and about 4 hr were required for equilibration. From this, it is concluded that one way maltose enters the slices is by free or facilitated diffusion. However, endogenous maltose is utilized by the slices at rates that are much too low to account for the net rates of maltose uptake. Although the slices contain a high level of surface maltase activity, only a low level of endogenous maltase activity was found. This probably accounts for the slow utilization of endogenous maltose. Therefore, the existence of a specific maltose transport system is proposed; a system that contains a carrier saturable with maltose, but one that does not release free maltose into the cytoplasm.     

The relationship between sodium excretion and renin secretion by the perfused kidney.

The effect of altered tubular sodium reabsorption on renin secretion (RSR) was examined under conditions in which other factors influencing renin release could be controlled or excluded. To do this, isolated canine kidneys were perfused at constant pressure with blood circulating from donor animals. Volume expansion or hemorrhage of the donor dogs produced large changes in the animal's blood pressure, renal function, sodium excretion (UNaV), and RSR, but were without effect on renal hemodynamics, UNaV, or RSR in the perfused kidney. Hemodilution without volume expansion, resulted in hypotension, decreased UNaV and increased RSR in the donor dogs, and increased UNaV and suppressed RSR in the perfused kidney. These effects of hemodilution in the perfused kidney were partially reversed when plasma protein concentration was restored to control levels with hyperoncotic albumin, and, overall, there was a significant inverse relationship between electrolyte excretion and RSR. These results provide new evidence for the hypothesis that the rate at which sodium is delivered to the macula densa is an important determinant of the rate of renin secretion.     

The dicey dinner dilemma: Asymmetry in predator–prey risk‐taking,a broadly applicable alternative to the life‐dinner principle

Forty years ago, the ‘life‐dinner principle’ was proposed as an example of an asymmetry that may lead prey species to experience stronger selection than their predators, thus accounting for the high frequency with which prey escape alive from interaction with a predator. This principle remains an influential concept in the scientific literature, despite several works suggesting that the concept relies on many under‐appreciated assumptions and does not apply as generally as was initially proposed. Here, we present a novel model describing a very different asymmetry to that proposed in the life‐dinner principle, but one that could apply broadly. We argue that asymmetries between the relative costs and benefits to predators and prey of selecting a risky behaviour during an extended predator–prey encounter could lead to an enhanced likelihood of escape for the prey. Any resulting advantage to prey depends upon there being a behaviour or choice that introduces some inherent danger to both predator and prey if they adopt it, but which if the prey adopts the predator must match in order to have a chance of successful predation. We suggest that the circumstances indicated by our model could apply broadly across diverse taxa, including both risky spatial or behavioural choices.     

Aging aggravates ischemic stroke‐induced brain damage in mice with chronic peripheral infection

Ischemic stroke is confounded by conditions such as atherosclerosis, diabetes, and infection, all of which alter peripheral inflammatory processes with concomitant impact on stroke outcome. The majority of the stroke patients are elderly, but the impact of interactions between aging and inflammation on stroke remains unknown. We thus investigated the influence of age on the outcome of stroke in animals predisposed to systemic chronic infection. Th1‐polarized chronic systemic infection was induced in 18–22 month and 4‐month‐old C57BL/6j mice by administration of Trichuris muris (gut parasite). One month after infection, mice underwent permanent middle cerebral artery occlusion and infarct size, brain gliosis, and brain and plasma cytokine profiles were analyzed. Chronic infection increased the infarct size in aged but not in young mice at 24 h. Aged, ischemic mice showed altered plasma and brain cytokine responses, while the lesion size correlated with plasma prestroke levels of RANTES. Moreover, the old, infected mice exhibited significantly increased neutrophil recruitment and upregulation of both plasma interleukin‐17α and tumor necrosis factor‐α levels. Neither age nor infection status alone or in combination altered the ischemia‐induced brain microgliosis. Our results show that chronic peripheral infection in aged animals renders the brain more vulnerable to ischemic insults, possibly by increasing the invasion of neutrophils and altering the inflammation status in the blood and brain. Understanding the interactions between age and infections is crucial for developing a better therapeutic regimen for ischemic stroke and when modeling it as a disease of the elderly.     

Vegetation feedbacks of nutrient addition lead to a weaker carbon sink in an ombrotrophic bog

To study vegetation feedbacks of nutrient addition on carbon sequestration capacity, we investigated vegetation and ecosystem CO₂ exchange at Mer Bleue Bog, Canada in plots that had been fertilized with nitrogen (N) or with N plus phosphorus (P) and potassium (K) for 7–12 years. Gross photosynthesis, ecosystem respiration, and net CO₂ exchange were measured weekly during May–September 2011 using climate‐controlled chambers. A substrate‐induced respiration technique was used to determine the functional ability of the microbial community. The highest N and NPK additions were associated with 40% less net CO₂ uptake than the control. In the NPK additions, a diminished C sink potential was due to a 20–30% increase in ecosystem respiration, while gross photosynthesis rates did not change as greater vascular plant biomass compensated for the decrease in Sphagnum mosses. In the highest N‐only treatment, small reductions in gross photosynthesis and no change in ecosystem respiration led to the reduced C sink. Substrate‐induced microbial respiration was significantly higher in all levels of NPK additions compared with control. The temperature sensitivity of respiration in the plots was lower with increasing cumulative N load, suggesting more labile sources of respired CO₂. The weaker C sink potential could be explained by changes in nutrient availability, higher woody : foliar ratio, moss loss, and enhanced decomposition. Stronger responses to NPK fertilization than to N‐only fertilization for both shrub biomass production and decomposition suggest that the bog ecosystem is N‐P/K colimited rather than N‐limited. Negative effects of further N‐only deposition were indicated by delayed spring CO₂ uptake. In contrast to forests, increased wood formation and surface litter accumulation in bogs seem to reduce the C sink potential owing to the loss of peat‐forming Sphagnum.