A COX-2 inhibitor reduces muscle soreness, but does not influence recovery and adaptation after eccentric exercise.

The aim of this study was to investigate the effect of a cyclooxygenase (COX)-2 inhibitor on the recovery of muscle function, inflammation, regeneration after, and adaptation to, unaccustomed eccentric exercise. Thirty-three young males and females participated in a double-blind, placebo-controlled experiment. Seventy unilateral, voluntary, maximal eccentric actions with the elbow flexors were performed twice (bouts 1 and 2) with the same arm, separated by 3 weeks.

Molecular pathogenesis of acromegaly.

Acromegaly is generally caused by growth hormone (GH) hypersecretion from a benign, monoclonal pituitary adenoma. As in other neoplastic conditions, pituitary tumor formation and dysregulated hormone secretion are most likely the ultimate result of a series of genetic alterations. A number of molecular and biochemical defects have been associated with pituitary tumorigenesis.

Pituitary tumor registry: a novel clinical resource.

Pituitary adenomas result in clinical sequelae and accelerated mortality due to central mass effects or pituitary hormone hypersecretion and/or insufficiency. The low annual incidence and prolonged natural history of these rare tumors has hindered efforts to evaluate long-term clinical outcomes. Care of these patients is often provided by larger tertiary specialist referral centers.

Long-acting lanreotide induces clinical and biochemical remission of acromegaly caused by disseminated growth hormone-releasing hormone-secreting carcinoid.

Ectopic GHRH-secreting tumors, such as carcinoid, rarely cause acromegaly. As protracted exposure to high levels of GH is associated with considerable morbidity and mortality, these patients require early and effective medical therapy to control hormonal hypersecretion. We employed a prolonged release somatostatin analog, lanreotide, to treat a patient with disseminated GHRH-producing carcinoid.