The Australasian triage scale: examining emergency department nurses' performance using computer and paper scenarios

Study objective: The purpose of this study is to examine emergency nurses' performance using triage scenarios characterized by type of patient population (adult versus pediatric) and mode of delivery (paper versus computer). Methods:   A combination of paper-based (script alone) and computer-based (script plus still photographs) triage scenarios were used. Of the 28 scenarios used, half were written and half were computer based. Within each subgroup, there were 7 adult and 7 pediatric scenarios. Participants were asked to allocate an Australasian Triage Scale category for each triage scenario. Results: One hundred sixty-seven participants completed a total of 2,349 adult scenarios, and 161 participants completed 2,265 pediatric scenarios. Sixty-one percent of the triage decisions made by the nurses were “expected” triage decisions, 18% were “undertriage,” decisions, and 21% were “overtriage” decisions. Nurse triage allocation decisions for the scenarios containing still photographs delivered by computer demonstrated a higher average agreement percentage of 66.2% (κ=0.56; &tau;b=0.77; P<.0001) compared with the average agreement percentage of 55.4% (κ=0.42; &tau;b=0.75; P<.0001) using paper-based (text-only) scenarios. Conclusion: The mode of delivery appeared to have an effect on the nurses' triage performance. It is unclear whether the use of simple still photographs used in the computer mode of delivery resulted in a higher incidence of expected triage decisions and, thus, improved performance. The use of cues such as photographs and video footage to enhance the fidelity of triage scenarios may be useful not only for the education of triage nurses but also the conduct of research into triage decisionmaking. However, further exploration and research in this area are warranted.

Blind separation of cyclostationary signals from instantaneous mixtures

This paper presents a new approach for blind separation of unknown cyclostationary signals from instantaneous mixtures. The proposed method can perfectly separate the mixed source signals so long as they have either different cyclic frequencies or clock phases. This is a weaker condition than those required by the algorithms. The separation criterion is to diagonalize a polynomial matrix whose coefficient matrices consist of the correlation and cyclic correlation matrices, at time delay &tau;=0, of multiple measurements.

Increase in S6K1 phosphorylation in human skeletal muscle following resistance exercise occurs mainly in type II muscle fibres

To investigate the in vivo effects of resistance exercise on translational control in human skeletal muscle, we determined the phosphorylation of AMP-activated kinase (AMPK), eukaryotic initiation factor 4E-binding protein (4E-BP1), p70/p85-S6 protein kinase (S6K1), and ribosomal S6 protein (S6). Furthermore, we investigated whether changes in the phosphorylation of S6K1 are muscle fiber type specific. Eight male subjects performed a single high-intensity resistance exercise session. Muscle biopsies were collected before and immediately after exercise and after 30 and 120 min of postexercise recovery. The phosphorylation statuses of AMPK, 4E-BP1, S6K1, and S6 were determined by Western blotting with phospho-specific and pan antibodies. To determine fiber type-specific changes in the phosphorylation status of S6K1, immunofluorescence microscopy was applied. AMPK phosphorylation was increased approximately threefold immediately after resistance exercise, whereas 4E-BP1 phosphorylation was reduced to 27 ± 6% of preexercise values. Phosphorylation of S6K1 at Thr421/Ser424 was increased 2- to 2.5-fold during recovery but did not induce a significant change in S6 phosphorylation. Phosphorylation of S6K1 was more pronounced in the type II vs. type I muscle fibers. Before exercise, phosphorylated S6K1 was predominantly located in the nuclei. After 2 h of postexercise recovery, phospho-S6K1 was primarily located in the cytosol of type II muscle fibers. We conclude that resistance exercise effectively increases the phosphorylation of S6K1 on Thr421/Ser424, which is not associated with a substantial increase in S6 phosphorylation in a fasted state.

STAT3 signaling is activated in human skeletal muscle following acute resistance exercise

The transcription factor signal transducer and activator of transcription 3 (STAT3) has been identified as a mediator of cytokine signaling and implicated in hypertrophy; however, the importance of this pathway following resistance exercise in human skeletal muscle has not been investigated. In the present study, the phosphorylation and nuclear localization of STAT3, together with STAT3-regulated genes, were measured in the early recovery period following intense resistance exercise. Muscle biopsy samples from healthy subjects (7 males, 23.0 + 0.9 yr) were harvested before and again at 2, 4, and 24 h into recovery following a single bout of maximal leg extension exercise (3 sets, 12 repetitions). Rapid and transient activation of phosphorylated (tyrosine 705) STAT3 was observed at 2 h postexercise. STAT3 phosphorylation paralleled the transient localization of STAT3 to the nucleus, which also peaked at 2 h postexercise. Downstream transcriptional events regulated by STAT3 activation peaked at 2 h postexercise, including early responsive genes c-FOS (800-fold), JUNB (38-fold), and c-MYC (140-fold) at 2 h postexercise. A delayed peak in VEGF (4-fold) was measured 4 h postexercise. Finally, genes associated with modulating STAT3 signaling were also increased following exercise, including the negative regulator SOCS3 (60-fold). Thus, following a single bout of intense resistance exercise, a rapid phosphorylation and nuclear translocation of STAT3 are evident in human skeletal muscle. These data suggest that STAT3 signaling is an important common element and may contribute to the remodeling and adaptation of skeletal muscle following resistance exercise.

Muscle atrophy and hypertrophy signaling in patients with chronic obstructive pulmonary disease

Rationale: The molecular mechanisms of muscle atrophy in chronic obstructive pulmonary disease (COPD) are poorly understood. In wasted animals, muscle mass is regulated by several AKT-related signaling pathways.
Objectives: To measure the protein expression of AKT, forkhead box class O (FoxO)-1 and -3, atrogin-1, the phosphophrylated form of AKT, p70^S6K glycogen synthase kinase-3ß (GSK-3ß), eukaryotic translation initiation factor 4E binding protein-1 (4E-BP1), and the mRNA expression of atrogin-1, muscle ring finger (MuRF) protein 1, and FoxO-1 and -3 in the quadriceps of 12 patients with COPD with muscle atrophy and 10 healthy control subjects. Five patients with COPD with preserved muscle mass were subsequently recruited and were compared with six patients with low muscle mass.
Methods: Protein contents and mRNA expression were measured by Western blot and quantitative polymerase chain reaction, respectively.
Measurements and Main Results: The levels of atrogin-1 and MuRF1 mRNA, and of phosphorylated AKT and 4E-BP1 and FoxO-1 proteins, were increased in patients with COPD with muscle atrophy compared with healthy control subjects, whereas atrogin-1, p70^S6K, GSK-3ß, and FoxO-3 protein levels were similar. Patients with COPD with muscle atrophy showed an increased expression of p70^S6K, GSK-3ß, and 4E-BP1 compared with patients with COPD with preserved muscle mass.
Conclusions: An increase in atrogin-1 and MuRF1 mRNA and FoxO-1 protein content was observed in the quadriceps of patients with COPD. The transcriptional regulation of atrogin-1 and MuRF1 may occur via FoxO-1, but independently of AKT. The overexpression of the muscle hypertrophic signaling pathways found in patients with COPD with muscle atrophy could represent an attempt to restore muscle mass.

Tenocyte responses to mechanical loading in vivo : A role for local insulin-like growth factor 1 signaling in early tendinosis in rats

Objective
To investigate tenocyte regulatory events during the development of overuse supraspinatus tendinosis in rats.

Methods
Supraspinatus tendinosis was induced by running rats downhill at 1 km/hour for 1 hour a day. Tendons were harvested at 4, 8, 12, and 16 weeks and processed for brightfield, polarized light, or transmission electron microscopy. The development of tendinosis was assessed semiquantitatively using a modified Bonar histopathologic scale. Apoptosis and proliferation were examined using antibodies against fragmented DNA or proliferating cell nuclear antigen, respectively. Insulin-like growth factor 1 (IGF-1) expression was determined by computer-assisted quantification of immunohistochemical reaction. Local IGF-1 signaling was probed using antibodies to phosphorylated insulin receptor substrate 1 (IRS-1) and ERK-1/2.

Results
Tendinosis was present after 12 weeks of downhill running and was characterized by tenocyte rounding and proliferation as well as by glycosaminoglycan accumulation and collagen fragmentation. The proliferation index was elevated in CD90+ tenocytes in association with tendinosis and correlated with increased local IGF-1 expression by tenocytes and phosphorylation of IRS-1 and ERK-1/2. Both apoptosis and cellular inflammation were absent at all time points.

Conclusion
In this animal model, early tendinosis was associated with local stimulation of tenocytes rather than with extrinsic inflammation or apoptosis. Our data suggest a role for IGF-1 in the load-induced tenocyte responses during the pathogenesis of overuse tendon disorders.

Does interpersonal psychotherapy improve clinical care for adolescents with depression attending a rural child and adolescent mental health service? Study protocol for a cluster randomised feasibility trial

Background: Depression amongst adolescents is a costly societal problem. Little research documents the effectiveness of public mental health services in mapping this problem. Further, it is not clear whether usual care in such services can be improved via clinician training in a relevant evidence based intervention. One such intervention, found to be effective and easily learned amongst novice clinicians, is Interpersonal Psychotherapy (IPT). The study described in the current paper has two main objectives. First, it aims to investigate the impact on clinical care of implementing Interpersonal Psychotherapy for Adolescents for the treatment of adolescent depression within a rural mental health service compared with Treatment as Usual (TAU). The second objective is to record the process and challenges (i.e. feasibility, acceptability, sustainability) associated with implementing and evaluating an evidence-based intervention within a community service. This paper outlines the study rationale and design for this community based research trial.

Methods/design: The study involves a cluster randomisation trial to be conducted within a Child and Adolescent Mental Health Service in rural Australia. All clinicians in the service will be invited to participate.  Participating clinicians will be randomised via block design at each of four sites to (a) training and delivery of IPT, or (b) TAU. The primary measure of impact on care will be a clinically significant change in depressive  symptomatology, with secondary outcomes involving treatment satisfaction and changes in other symptomatology. Participating adolescents with significant depressive symptomatology, aged 12 to 18 years, will complete assessment measures at Weeks 0, 12 and 24 of treatment. They will also complete a depression inventory once a month during that period. This study aims to recruit 60 adolescent participants and their parent/guardian/s. A power analysis is not indicated as an intra-class correlation coefficient will be calculated and used to inform sample size calculations for subsequent large-scale trials. Qualitative data regarding process implementation will be collected quarterly from focus groups with participating clinicians over 18 months, plus phone interviews with participating adolescents and parent/guardians at 12 weeks and 24 weeks of treatment. The focus group qualitative data will be analysed using a Fourth Generation Evaluation methodology that includes a constant comparative cyclic analysis method.

Discussion: This study protocol will be informative for researchers and clinicians interested in considering, designing and/or conducting cluster randomised trials within community practice such as mental health services.

High temporal resolution observations of the pulsar microstructure at 102 MHz

We report observations of the microstructure of 7 pulsars at 102 MHz with a time resolution of up to 1 μs. We have detected fine pulse structure with a μs time-scale for all seven pulsars. We observe that interstellar scattering does not broaden the μs time-scale pulsar microstructure, and find structure of a time-scale much shorter than the interstellar scatter broadening. In addition to the previously known structure with time-scale &tau;_μ of tens of μs, we have detected structures with characteristic time-scale of a few μs, nearly equal to the reciprocal of the analysis bandwidth. This suggests that even shorter micropulses may exist.
Micropulses usually cluster in groups, each of duration tens to hundreds of μs, which may be identified as microstructure observed previously with smaller time resolution.
In addition to the previously known quasi-periodicity of hundreds of milliseconds, we reveal a structures with characteristic period of tens of μs. We observe structures with short quasi-periodicity to have a limited bandwidth. The characteristic period P_μ of these structures in PSR B0950+08 does not have a common value for different frequency regions in the same single pulse.
Scattering was revealed as a train of quasi-periodic micropulses with an exponentially damped envelope. The scatter-broadening and decorrelation bandwidth were measured. We report two time-scales of decorrelation bandwidth of pulsar PSR B0950+08 and propose two branches of Δν_d(ν) dependence.
The dispersion measure of PSR B0950+08 as DM= 2.9686 ± 0.0001 pc cm⁻³ has been determined.

Altering dietary nutrient intake that reduces glycogen content leads to phosphorylation of nuclear p38 MAP kinase in human skeletal muscle: association with IL-6 gene transcription during contraction

To determine the effect of glycogen availability and contraction on intracellular signaling and IL-6 gene transcription, eight males performed 60 min of exercise on two occasions: either with prior ingestion of a normal (Con) or low carbohydrate (LCHO) diet that reduced pre-exercise muscle glycogen content. Muscle biopsies were obtained and analyzed for IL-6 mRNA. In addition, nuclear proteins were isolated from the samples and analyzed for the mitogen- activated protein kinases (MAPK) c-jun amino-terminal kinase (JNK) 1 and 2 and p38 MAPK. Nuclear fractions were also analyzed for the phosphorylated forms of JNK (p-JNK) and p38 MAPK (p-p38 MAPK) and the abundance of the nuclear transcription factors nuclear factor of activated T cells (NFAT) and nuclear factor kappa-β (NF-κβ). No differences were observed in the protein abundance of total JNK 1/2, p38 MAPK, NFAT, or NF-κβ before exercise, but the nuclear abundance of p-p38 MAPK was higher (P<0.05) in LCHO. Contraction resulted in an increase (P<0.05) in nuclear p-JNK 1/2, but there were no differences when comparing CON with LCHO. The fold increase in IL-6 mRNA with contraction was potentiated (P<0.05) in LCHO. A correlation between pre-exercise nuclear phosphorylated p38 MAPK and contraction-induced fold increase in IL-6 mRNA was performed, revealing a highly significant correlation (r=0.96; P<0.01). We next incubated L6 myotubes in ionomycin (a compound known to induce IL-6 mRNA) with or without the pyridinylimidazole p38 MAPK inhibitor SB203580. Treatments did not affect total nuclear p38 MAPK, but ionomycin increased (P<0.05) both nuclear p-p38 MAPK and IL-6 mRNA. The addition of SB203580 to ionomycin decreased (P<0.05) nuclear p-p38 MAPK and totally abolished (P<0.05) the ionomycin- induced increase in IL-6 mRNA. These data suggest that reduced carbohydrate intake that results in low intramuscular glycogen leads to phosphorylation of p38 MAPK at the nucleus. Furthermore, phosphorylation of p38 MAPK in the nucleus appears to be an upstream target for IL-6, providing new insights into the regulation of IL-6 gene transcription.