Turning and repositioning the critically ill patient with hemodynamic instability: a literature review and consensus recommendations.

In the critical care population, heart rate and rhythm, blood pressure, respiratory rate, and oxygen saturation are monitored continuously, providing immediate feedback regarding any changes in patient status. Hemodynamic instability is a term commonly used by clinicians to describe labile changes in cardiopulmonary status, although this term is poorly defined in the literature. The clinician's perception of hemodynamic instability may cause a delay or omission in turning, repositioning, and other interventions to advance patient mobility and may contribute to pressure ulcer formation. The intensive care unit's practice culture and individual clinician perceptions regarding hemodynamic instability may lead to staff not turning patients out of fear that they are "too unstable to turn." This article provides a discussion of the link between pressure ulcers and immobility, provides a review of current literature on progressive mobility and hemodynamic instability, and presents the results of a critical care consensus panel on safe and effective turning of critical care patients.

The hormonal herbicide, 2,4-dichlorophenoxyacetic acid, inhibits Xenopus oocyte maturation by targeting translational and post-translational mechanisms.

The widely used hormonal herbicide, 2,4-dichlorophenoxyacetic acid, blocks meiotic maturation in vitro and is thus a potential environmental endocrine disruptor with early reproductive effects. To test whether maturation inhibition was dependent on protein kinase A, an endogenous maturation inhibitor, oocytes were microinjected with PKI, a specific PKA inhibitor, and exposed to 2,4-D. Oocytes failed to mature, suggesting that 2,4-D is not dependent on PKA activity and likely acts on a downstream target, such as Mos. De novo synthesis of Mos, which is triggered by mRNA poly(A) elongation, was examined. Oocytes were microinjected with radiolabelled in vitro transcripts of Mos RNA and exposed to progesterone and 2,4-D. RNA analysis showed progesterone-induced polyadenylation as expected but none with 2,4-D. 2,4-D-activated MAPK was determined to be cytoplasmic in localization studies but poorly induced Rsk2 phosphorylation and activation. In addition to inhibition of the G2/M transition, 2,4-D caused abrupt reduction of H1 kinase activity in MII phase oocytes. Attempts to rescue maturation in oocytes transiently exposed to 2,4-D failed, suggesting that 2,4-D induces irreversible dysfunction of the meiotic signaling mechanism.