[Effects of ASPAN's evidence-based clinical practice guidelines for promotion of hypothermia of patients with total knee replacement arthroplasty].

PURPOSE: In this study an examination was done of the effects of the American Society of PeriAnesthesia Nurses (ASPAN) Evidence-Based Clinical Practice Guidelines on body temperature, shivering, thermal discomfort, and time to achieve normothermia in patients undergoing total knee replacement arthroplasty (TKRA) under spinal anesthesia. METHODS: This study was an experimental study with a randomized controlled trial design. Participants (n=60) were patients who underwent TKRA between December 2011 and March 2012. Experimental group (n=30) received active and passive warming measures as described in the ASPAN's guidelines. Control group (n=30) received traditional care. Body temperature, shivering, thermal discomfort, time to achieve normothermia were measured in both groups at 30 minute intervals. RESULTS: Experimental group had slightly higher body temperature compared to control group (p=.002). Thermal discomfort was higher in the experimental group before surgery but higher in the control group after surgery (p=.034). It decreased after surgery (p=.041) in both groups. Time to achieve normothermia was shorter in the experimental group (p=.010). CONCLUSION: ASPAN's guidelines provide guidance on measuring patient body temperature at regular intervals and on individualized and differentiated hypothermia management which can be very useful in nursing care, particularly in protecting patient safety and improving quality of nursing.

[The effects of pre-operative visual information and parental presence intervention on anxiety, delirium, and pain of post-operative pediatric patients in PACU].

PURPOSE: The purpose of this study was to test whether pre-operative visual information and parental presence had positive effects on anxiety, delirium, and pain in pediatric patients who awoke from general anesthesia in a post-surgical stage. METHODS: This study used a non equivalent control-group post test design (n=76). Independent variables were provision of pre-operative visual information and parental presence for post-surgical pediatric patients in PACU (post anesthesia care unit). Dependent variables were anxiety, delirium, and pain in the pediatric patients measured three times at 10 minute intervals after extubation in the PACU. Measurements included Numerical Rating Scale for assessing state anxiety, Pediatric Anesthesia Emergence Delirium Scale by Sikich & Lerman (2004) for delirium, and Objective Pain Scale by Broadman, Rice & Hannallah (1988) for pain. RESULTS: Experimental group showed significantly decreased state anxiety at time points-10, 20, and 30 minutes after extubation. Delirium was significantly lower at 10 minutes and 30 minutes after extubation in the experimental group. Pain was significantly lower at 10 minutes after extubation in the experimental group. CONCLUSION: The results of this study suggest that this intervention can be a safe pre-operative nursing intervention for post-surgical pediatric patients at PACU.

Comparison of Escherichia coli uropathogenic genes (kps, usp and ireA) and enteroaggregative genes (aggR and aap) via multiplex polymerase chain reaction from suprapubic urine specimens of young children with fever.

OBJECTIVE: Escherichia coli is the most frequently identified microbiological agent in childhood urinary tract infections (UTIs). However, the pathogenic role of this organism in young children remains to be clearly elucidated. So far, no studies have been conducted in which multiplex polymerase chain reaction (PCR) has been applied to determine the association between childhood UTIs and E. coli and urovirulent genes. MATERIAL AND METHODS: Altogether, 330 suprapubic urine specimens from febrile young children were cultured. In 33 of the cases, E. coli was identified; among these cases, 18 had a UTI (>10(4)-10(5) cfu/ml), four had a suspected UTI (>10(2)-10(3) cfu/ml) and 11 did not have UTIs (10(2) cfu/ml). Using multiplex PCR, three uropathogenic E. coli (UPEC) genes and two enteroaggregative E. coli (EAEC) genes were detected. RESULTS: In the UTI-UPEC cases, the kps gene was detected in 18 of 22 cases (82%) and the usp gene in 16 of 22 cases (73%). Among the 18 cases of children with UTIs characterized by 10(4)-10(5) E. coli cfu/ml, urinary tract abnormalities were identified via dimercaptosuccinic acid scans in seven of 18 cases (39%) and via voiding cystourethrograms in four of the 18 cases (22%). CONCLUSIONS: The UPEC kps and usp genes were clearly associated with childhood UTIs, and may also be associated with kidney or urinary tract dysfunctions in young children. Escherichia coli colony count numbers in excess of 10(4)-10(5) cfu/ml in the suprapubic urine were considered to be strong evidence of UTI in infants.

Mechanisms involved in prostaglandin E2-mediated neuroprotection against TNF-alpha: possible involvement of multiple signal transduction and beta-catenin/T-cell factor.

Cerebrospinal fluid prostaglandin E2 (PGE2) and tumor necrosis factor-alpha (TNF-alpha) levels are elevated in patients with Alzheimer's disease (AD), which suggests that they are involved in neurodegeneration. We previously reported that TNF-alpha derived from human macrophages, in response to beta-amyloid or amyloidogenic C-terminal peptide, is a main mediator of inflammatory neurotoxicity. In a continuation of this work, the present study investigated the direct effect of PGE2, one of the major prostaglandins produced in the brain, on cell viability in SH-SY5Y neuronal cells treated with TNF-alpha. PGE2 did not promote neurotoxicity, but rather had a strong protective effect against TNF-alpha by ameliorating TNF-alpha-induced apoptosis and also by rescuing the intracellular level of beta-catenin, a key transducer of the Wnt signaling pathway. PGE2-mediated stabilization of beta-catenin was accompanied by T-cell factor/lymphoid enhancer factor (Tcf/Lef)-mediated transcriptional activation, which was followed by an increase in the cyclinD1 level. Pharmacological studies provided further evidence supporting the notion that PGE2-mediated neuroprotection against TNF-alpha involves the stimulation of Tcf/Lef signaling through EP1-, EP2-, and EP4-mediated increases of beta-catenin in SH-SY5Y cells. In addition, this PGE2 effect appears to be dependent on the activation of protein kinase A, phosphatidylinositol 3-kinase, phospholipase C, and to a lesser extent protein kinase C. Thus, the molecular mechanism governing the inhibitory effect of PGE2 against TNF-alpha may involve the activation and cross talk of multiple signal transduction and play an important role in regulating the survival of neurons during the neurotoxic inflammatory response associated with neurodegenerative diseases including AD.

Cyclic AMP inhibition of tumor necrosis factor alpha production induced by amyloidogenic C-terminal peptide of Alzheimer's amyloid precursor protein in macrophages: involvement of multiple intracellular pathways and cyclic AMP response element binding protein.

In the present study, we focused on the molecular events involved in tumor necrosis factor-alpha (TNF-alpha) production in response to the amyloidogenic 105-amino acid carboxyl-terminal fragment (CT105) of amyloid precursor protein, a candidate alternative toxic element in Alzheimer's disease pathology, and the mechanisms by which cyclic AMP regulates the relating inflammatory signal cascades. CT105 at nanomolar concentrations strongly activated multiple signaling pathways involving tyrosine kinase-dependent extracellular signal-regulated kinase and p38 mitogen-activated protein kinases. Moreover, phosphatidylinositol 3-kinase/Akt signal was required for excess TNF-alpha production in human macrophages derived from THP-1 cells. Interferon-gamma significantly potentiated the induction of the CT105-mediated signal cascade. These multiple signaling pathways in turn converged, at least in part, at the nuclear transcription factor known as cAMP response element binding protein (CREB), which acts on the TNF-alpha gene promoter through the cAMP response element. The cell-permeable cAMP analog dibutyryl cAMP partially and almost simultaneously suppressed all of these CT105-induced signaling pathways through excessive CREB phosphorylation, which led to decreased CREB DNA binding activity and reduced TNF-alpha expression. Furthermore, dibutyryl cAMP decreased the interaction of the p65 nuclear factor-kappa B with CREB binding protein, thus further inhibiting CT105-mediated TNF-alpha expression. Collectively, the detailed molecular mechanisms of amyloidogenic CT-induced TNF-alpha production as negatively regulated by cAMP may advance the possibility of targeted treatment in Alzheimer's disease.