It is time to move from the nursing process to critical thinking

As we reflect on the concept of critical thinking in perioperative nursing practice, we should ask ourselves whether we think critically. If not, we must learn the principles of critical thinking and apply them in our clinical practice settings. Our perioperative nurse managers and directors must demonstrate critical thinking in leading other nurses in the delivery of quality, cost-effective, service-oriented patient care. They also must identify peers who use critical thinking skills to support and sustain them in their quest.     

Coordination in prehension. Information-based coupling of reaching and grasping

Research using the balanced placebo design seeks to differentiate the physiological and psychological effects of drinking alcohol. Questions regarding the validity of the design center about experimenter instructions, particularly in the antiplacebo cell at higher blood alcohol content (BAC) levels. This study tested the plausibility of two misattribution strategies designed to reduce the conflict between experimenter instructions and internal cues of drunkenness. Forty-two participants (BAC = .055) were told that they received no alcohol, with internal cues of drunkenness said to be produced by a (sham) second drug, a (placebo) tachistoscopic display, or no misattribution given. The placebo drug group reported less alcohol intoxication without reporting less physical impairment than the control or tachistoscopic groups. Doubt of instructions was expressed more frequently in the control group than in the placebo drug group. Mean time to first reported doubt of experimenter instructions was longer for the placebo drug group. A manipulation check designed to account for demand effects indicated that instituting the pharmacologic misattribution increased the success of the manipulation over the control group. Providing a credible attribution for internal symptoms of drunkenness makes experimenter's instructions more credible, improving the validity of the antiplacebo cell of the balanced placebo design.     

Phenotypic heterogeneity of mutational changes at a conserved nucleotide in 16 S ribosomal RNA

RNA sites that contain unpaired or mismatched nucleotides can be interaction sites for other macromolecules. C1054, a virtually universally conserved nucleotide in the 16 S (small subunit) ribosomal RNA of Escherichia coli, is part of a highly conserved bulge in helix 34, which has been located at the decoding site of the ribosome. This helix has been implicated in several translational events, including peptide chain termination and decoding accuracy. Here, we observed interesting differences in phenotype associated with the three base substitutions at, and the deletion of, nucleotide C1054. The phenotypes examined include suppression of nonsense codons on different media and at different temperatures, lethality conditioned by temperature and level of expression of the mutant rRNA, ribosome profiles upon centrifugation through sucrose density gradients, association of mutant 30 S subunits with 50 S subunits, and effects on the action of tRNA suppressor mutants. Some of our findings contradict previously reported properties of individual mutants. Particularly notable is our finding that the first reported 16 S rRNA suppressor of UGA mutations was not a C1054 deletion but rather the base substitution C1054A. After constructing deltaC1054 by site-directed mutagenesis, we observed, among other differences, that it does not suppress any of the trpA mutations previously reported to be suppressed by the original UGA suppressor. In general, our results are consistent with the suggestion that the termination codon readthrough effects of mutations at nucleotide 1054 are the result of defects in peptide chain termination rather than of decreases in general translational accuracy. The phenotypic heterogeneity associated with different mutations at this one nucleotide position may be related to the mechanisms of involvement of this nucleotide, the two-nucleotide bulge, and/or helix 34 in particular translational events. In particular, previous indications from other laboratories of conformational changes associated with this region are consistent with differential effects of 1054 mutations on RNA-RNA or RNA-protein interactions. Finally, the association of a variety of phenotypes with different changes at the same nucleotide may eventually shed light on speculations about the coevolution of parts of ribosomal RNA with other translational macromolecules.     

A putative heterotrimeric G protein inhibits the fusion of COPI-coated vesicles. Segregation of heterotrimeric G proteins from COPI-coated vesicles

Heterotrimeric G proteins have been implicated in the regulation of intracellular protein transport, but their mechanism of action remains unclear. In vivo, secretion of chromogranin B, tagged with the green fluorescent protein, was inhibited by the addition of a general activator of trimeric G proteins (AlF4-) to stably transfected Vero cells and resulted in an accumulation of the tagged protein in the Golgi apparatus. In an in vitro assay that reconstitutes intra-Golgi protein transport, we find that a membrane-bound and AlF4--sensitive factor is involved in the fusion reaction. To determine whether this effect is mediated by a heterotrimeric G protein localized to COPI-coated transport vesicles, we determined the presence of G proteins on these vesicles and found that they were segregated relative to the donor membranes. Because G proteins do not have an obvious sorting, retention, or retrieval signal, we considered the possibility that other interactions might be responsible for this segregation. In agreement with this, we found that trimeric G proteins from isolated Golgi membranes were partially insoluble in Triton X-100. Identification of the proteins that interact with the heterotrimeric G proteins in the Golgi-derived detergent-insoluble complex might help to reveal the regulation of protein secretion mediated by heterotrimeric G proteins.