This study examined potential mechanisms contributing to the inhibition of protein synthesis in skeletal muscle and heart after administration of tumor necrosis factor (TNF)-α. Rats had vascular catheters implanted, and TNF-α was infused continuously for 24 h. TNF-α decreased in vivo-determined rates of global protein synthesis in gastrocnemius (39%) and heart (25%). The TNF-α-induced decrease in protein synthesis in the gastrocnemius involved a reduction in the synthesis of both myofibrillar and sarcoplasmic proteins. To identify potential mechanisms responsible for regulating mRNA translation, we examined several eukaryotic initiation factors (eIFs) and elongation factors (eEFs). TNF-α decreased the activity of eIF-2B in muscle (39%) but not in heart. This diminished activity was not caused by a reduction in the content of eIF-2Bε or the content and phosphorylation state of eIF-2α. Skeletal muscle and heart from TNF-α-treated rats demonstrated 1) an increased binding of the translation repressor 4E-binding protein-1 (4E-BP1) with eIF-4E, 2) a decreased amount of eIF-4E associated with eIF-4G, and 3) a decreased content of the hyperphosphorylated γ-form of 4E-BP1. In contrast, the infusion of TNF-α did not alter the content of eEF-1α or eEF-2, or the phosphorylation state of eEF-2. In summary, these data suggest that TNF-α impairs skeletal muscle and heart protein synthesis, at least in part, by decreasing mRNA translational efficiency resulting from an impairment in translation initiation associated with alterations in eIF-4E availability.

The concept of vulnerability to spruce budworm refers to the probability of tree mortality resulting fromaagiven level of budworm attack. This paper reviews and analyses available information from the literature on stand vulnerability and timing of mortality during several budworm outbreaks. Timing of mortality during outbreaks appears to be fairly straightforward when considered in a general sense, with trees usually starting to die after four or five years of severe defoliation. Prediction of the total expected mortality in a given stand is more difficult, however, and attempts to relate mortality to stand characteristics have not shown strong relationships. Nevertheless, the data analysed suggest that for approximation purposes in a management sense, we can probably treat mortality during uncontrolled ,budworm outbreaks as a host-density dependent process. This is particularly so for fir in mature stands, where mortality approaches loo%', while fir in immature stands and spruce show lower, more variable mortality rates.Le concept de vulnerabilite 'a la tordeuse des bourgeons de ~'~pinette se rattache a la probabilite de mortalite des arbres resultant d'un niveau donne d'attaque de la tordeuse. Cet article passe en revue et analyse \'information disponible de la litterature specialisee sur la vulnerabilite et le synchronisme de la mortalit6 au cours de plusieurs invasions de la Tordeuse. Ce synchronisme de mortalite au cours des invasions semble Btre raisonnablement fidele lorsqu'on le considere dans son sens general, avec des arbres agonisant apres 4 ou 5 annees de defoliation grave. II est cependant plus difficile de predire la mortalite totale a laquelle s'attendre dans un peuplement donne, et les tentatives en vue de relier la mortalite aux caracteristiques du peuplement n'ont pas ete tr&s concluantes. Neanmoins, ,les donnees analysees sous-entendent que pour fins d'approximation, en termes de gestion, on peut probablement traiter la mortalit6 (durant les invasions incontrblees de la tordeuse) comme un Drocessus relie a la densite des hbtes. C'est le cas particulierement'pour le Sapin en peuplements matures, ou la mortalite approche les 100% alors que le Sapin en peuplements immatures et I'Epinette accusent des taux de mortalite plus faibles et plus variables.

This study examined the effect of ingesting caffeine (6 mg kg−1) on muscle carbohydrate and fat metabolism during steady‐state exercise in humans. Young male subjects (n= 10) performed 1 h of exercise (70 % maximal oxygen consumption (V̇O2,max)) on two occasions (after ingestion of placebo and caffeine) and leg metabolism was quantified by the combination of direct Fick measures and muscle biopsies. Following caffeine ingestion serum fatty acid and glycerol concentration increased (P≤ 0.05) at rest, suggesting enhanced adipose tissue lipolysis. In addition circulating adrenaline concentration was increased (P≤ 0.05) at rest following caffeine ingestion and this, as well as leg noradrenaline spillover, was elevated (P≤ 0.05) above placebo values during exercise. Caffeine resulted in a modest increase (P≤ 0.05) in leg vascular resistance, but no difference was found in leg blood flow. Arterial lactate and glucose concentrations were increased (P≤ 0.05) by caffeine, while the rise in plasma potassium was dampened (P≤ 0.05). There were no differences in respiratory exchange ratio or in leg glucose uptake, net muscle glycogenolysis, leg lactate release or muscle lactate, or glucose 6‐phosphate concentration. Similarly there were no differences between treatments in leg fatty acid uptake, glycerol release or muscle acetyl CoA concentration. These findings indicate that caffeine ingestion stimulated the sympathetic nervous system but did not alter the carbohydrate or fat metabolism in the monitored leg. Other tissues must have been involved in the changes in circulating potassium, fatty acids, glucose and lactate.