Transition to the neonatal nurse practitioner role: making the change from the side to the head of the bed

Role transition is never easy, but is complicated by the experienced neonatal nurse's frustration with reverting to a student role and becoming a novice practitioner, sometimes after years of developing a reputation as an expert nurse. This article discusses this transition, focusing on the skills needed to move successfully from nurse to nurse practitioner. Common to all advanced practice transitions are stages similar to those Benner identifies in her novice-to-expert theory of nursing practice. Feelings of frustration and inadequacy are common during the first year as an NNP. Studies focusing on role transition and role development suggest that a strong nursing identity is important for success in the NNP practice environment. Strategies to enhance the transition are discussed.     

Temporally jittered speech produces performance intensity, phonetically balanced rollover in young normal-hearing listeners

This study investigates whether temporally jittered stimuli will produce performance-intensity, phonetically balanced (PI-PB) rollover in young adults with normal hearing. Although not yet explicitly stated in the literature, there is clinical and theoretical evidence to suggest that PI-PB rollover, such as that found in cases of acoustic neuroma, is caused by neural dyssynchrony in the auditory system. Sixteen participants were tested with intact and temporally jittered word lists in quiet at 40, 55, 65, and uncomfortable listening level -5 dB HL. The results show significant rollover in the jittered but not the intact conditions. The results are consistent with the existing evidence that suggests that neural PI-PB rollover is caused by decreased neural synchrony and support the claim that temporal jitter simulates neural dyssynchrony. Furthermore, these results are consistent with the hypothesis that synchrony coding plays an important role in the perception of high-level speech.     

Altered modulation of soluble guanylate cyclase in lymphocytes from patients with liver disease

Studies of animal models suggest that the activation of soluble guanylate cyclase by nitric oxide is altered in liver disease. We studied 77 patients with liver disease and 17 controls, to investigate whether the activation of soluble guanylate cyclase is altered in lymphocytes from patients with liver disease. The basal content of guanosine 3',5'-cyclic monophosphate (cGMP) in lymphocytes was decreased both in patients with liver cirrhosis (by 52%) and in patients with chronic hepatitis (by 62%). Activation of soluble guanylate cyclase by nitric oxide was higher in lymphocytes from patients with cirrhosis (3100+/-1000% of basal) or with hepatitis (5200+/-2500% of basal) than in lymphocytes from controls (1200+/-500% of basal). cGMP in plasma was increased in patients with liver disease. Successful (but not unsuccessful) treatment with interferon of patients with hepatitis due to virus C reversed all the above alterations. Altered modulation of soluble guanylate cyclase by nitric oxide in liver disease may play a role in the hemodynamic alterations found in these patients.     

A sulphated fucan from the Laminaria abyssalis inhibits the human T cell lymphotropic virus type 1-induced syncytium formation in HeLa cells

This work evaluated the effect of a sulphated fucan extracted from the Laminaria abyssalis marine algae on the human T cell lymphotropic virus type 1 (HTLV-1)-induced syncytium formation. The experiments were carried out in HeLa cells cocultured with a HTLV-1-infected T cell line (C91/PL cells) in the presence of the sulphated polysaccharide at concentration below that corresponding to the ED50. The sulphated fucan inhibited almost 100% of the syncytium formation at concentration of 100 microg/mI and was still active (>95%) at a concentration of 25 microg/ml. It was also observed that the best inhibition occurred when the compound was added in the first 2 h of the cell-to-cell contact. This is the first report showing that a purified sulphated polysaccharide, extracted from marine algae, is able to inhibit the cell-to-cell contact essential for the spreading of the HTLV-1.     

Acid suppression therapy may not alter malignant progression in Barrett's metaplasia showing p53 protein accumulation

OBJECTIVES: Several previous studies have shown that malignant progression in Barrett's metaplasia (BM) occurs even in patients treated with fundoplication or acid suppression therapy (AST). The aim of this study was to test the hypothesis that AST may not alter malignant progression in BM if key genes involved in DNA repair and cell cycle control, particularly p53, are defective. METHODS: Initial and follow-up biopsies from 21 patients with BM treated with AST and observed for 1-13 yr were entered in the study. All biopsies were graded for dysplasia and evaluated for p53 protein accumulation and oxidative DNA damage by immunohiostochemistry, using antibodies to p53 and to 8-hydroxydeoxyguanosine, respectively. DNA ploidy was determined using image analysis. Statistical analysis was performed using Kaplan-Meier curves, log rank test, and multivariate regression. RESULTS: Patients with p53 positive initial biopsies were more likely to have progression in dysplasia grade (p = 0.022) and DNA ploidy status (p = 0.023) than those with p53 negative biopsies. In eight patients AST resulted in significant reduction in oxidative DNA damage in the five patients with p53-negative initial biopsies, but not the three with p53 positive ones (p = 0.0007). CONCLUSIONS: We conclude that failure of AST to alter malignant progression in BM may be due, at least in part, to defects in DNA repair and cell cycle control resulting from p53 gene mutation, present before AST treatment. Although AST may be effective in preventing further DNA damage, it is unlikely to alter progression in genetically unstable cells.