Translation and validation of the Nursing Outcomes Classification labels and definitions for acute care nursing in Iceland

BACKGROUND: The Nursing Outcomes Classification (NOC), second edition, consists of 260 patient outcomes with definitions. This has been translated into five languages, but has not been clinically validated outside the United States of America (USA). AIM: The aim of this paper is to describe the translation of the labels and definitions from the NOC, second edition from English to Icelandic and validation for acute-care nursing in Iceland. METHOD: A survey that has been designed to identify nurses' perception of the percentage of patients' for whom each NOC outcome is relevant in clinical nursing practice was used for clinical validation in this study. The translation procedure involved source to target language translation, parallel comparison, pilot test and field test. Validation included test-retest to measure the reliability for each of the 260 outcome variables. Data collected from 140 clinical nurses from 54 departments within 13 nursing specialties at Landspitali University-Hospital in Iceland, in November 2001, were analysed to establish construct validity by confirmatory factor analysis. Internal consistency was calculated. RESULTS: Translation was successful. Test-retest showed that 181 of the 260 NOC outcomes were significant (P < 0.05) and moderately or highly correlated (r > 0.50) (Pearson's correlation). The confirmatory factor analysis showed that 22 of the 29 NOC classes had only one factor at the loading criteria > or =0.30. Of the 260 outcomes, 244 had loading on one factor (> or =0.30) within its class. Internal consistency was >0.80 (Cronbach's alpha). LIMITATIONS: Low response rate was a limitation. The indicators of each NOC outcome were not addressed. CONCLUSION: The Icelandic version of the NOC survey is a comprehensive tool that can be applied to nursing in acute-care for research purposes as well as to prepare for the implementation of NOC in clinical information systems.     

In vivo mapping of temporospatial changes in manganese enhancement in rat brain during epileptogenesis

Mesial temporal lobe epilepsy is associated with structural and functional abnormalities, such as hippocampal sclerosis and axonal reorganization. The temporal evolution of these changes remains to be determined, and there is a need for in vivo imaging techniques that can uncover the epileptogenic processes at an early stage. Manganese-enhanced magnetic resonance imaging may be useful in this regard. The aim of this study was to analyze the temporospatial changes in manganese enhancement in rat brain during the development of epilepsy subsequent to systemic kainate application (10 mg/kg i.p.). MnCl(2) was given systemically on day 2 (early), day 15 (latent), and 11 weeks (chronic phase) after the initial status epilepticus. Twenty-four hours after MnCl(2) injection T1-weighted 3D MRI was performed followed by analysis of manganese enhancement. In the medial temporal lobes, there was a pronounced decrease in manganese enhancement in CA1, CA3, dentate gyrus, entorhinal cortex and lateral amygdala in the early phase. In the latent and chronic phases, recovery of the manganese enhancement was observed in all these structures except CA1. A significant increase in manganese enhancement was detected in the entorhinal cortex and the amygdala in the chronic phase. In the latter phase, the structurally intact cerebellum showed significantly decreased manganese enhancement. The highly differentiated changes in manganese enhancement are likely to represent the net outcome of a number of pathological and pathophysiological events, including cell loss and changes in neuronal activity. Our findings are not consistent with the idea that manganese enhancement primarily reflects changes in glial cells.     

Association of prolactin and its receptor gene regions with familial breast cancer

CONTEXT: The contribution of prolactin (PRL) through its receptor (PRLR) to the pathogenesis and progression of human mammary tumors has received recent attention. OBJECTIVE: We investigated whether genetic variation in the PRL and PRLR genes is associated with the risk of breast cancer (BC). DESIGN: We conducted a case-control study with a total of seven single nucleotide polymorphisms (SNPs). SETTING: The study was conducted at an academic research laboratory and university clinics. PATIENTS AND OTHER PARTICIPANTS: A total of 441 German familial, unrelated BC cases and 552 controls matched by age, ethnicity, and geographical region participated in the study. INTERVENTION(S): There were no interventions. MAIN OUTCOME MEASURES(S): SNP genotype and haplotype distributions and haplotype interactions were correlated with the risk of BC. RESULTS: Two SNPs (rs1341239 and rs12210179) within the PRL promoter regions were significantly associated with increased risk in homozygotes for the variant alleles [odds ratio (OR), 1.67 and 95% confidence interval (CI), 1.11-2.50; and OR, 2.09 and 95% CI, 1.23-3.52, respectively]. The PRL haplotype containing the variant alleles of the promoter SNPs increased significantly the risk of BC (OR 1.42, 95%CI 1.07-1.90). A PRLR haplotype was associated with a significant decrease in BC risk (OR 0.69, 95% CI 0.54-0.89). An increasing number of PRL and PRLR risk haplotypes led to a significant trend of increasing risk for BC (chi(2) = 12.15; P = 0.007). CONCLUSIONS: Genetic variation in the PRL and PRLR genes was shown to influence BC risk. Additional studies are needed to further clarify the role of the PRL and PRLR genes in the risk of BC.     

Oral factor Xa inhibitors for thromboprophylaxis in major orthopedic surgery: a review

Venous thromboembolism (VTE), which includes deep vein thrombosis and pulmonary embolism, is a major cause of morbidity and mortality in patients undergoing major orthopedic surgery. Routine thromboprophylaxis has been the standard of care over the last 20 years. Currently available options for the prevention of VTE in major orthopedic surgery include low molecular weight heparins, vitamin K antagonists, and, more recently, the synthetic pentasaccharide fondaparinux. Although effective, all these drugs have several limitations and new oral antithrombotics offering predictable, effective and safe anticoagulation are strongly needed. This overview focuses on the most advanced oral direct inhibitors to factor Xa rivaroxaban, apixaban, LY517717 and YM150; specifically, the results of phase II and III studies and the designs of ongoing clinical trials in patients undergoing elective hip and knee replacement are reviewed.     

Acute Kidney Injury Following Aortic Valve Replacement in Patients Without Chronic Kidney Disease

BackgroundThe data on acute kidney injury (AKI) in patients without chronic kidney disease (CKD) after transcatheter aortic valve replacement (TAVR) are limited. The study sought to compare the incidence of AKI and its impact on 5-year mortality after TAVR and surgical aortic valve replacement (SAVR) in patients without CKD.MethodsThis registry included data from 6463 consecutive patients who underwent TAVR or SAVR. CKD was defined as estimated glomerular filtration rate <60 mL/min/1.73 m². AKI was defined according to the Kidney Disease Improving Global Outcomes criteria. For sensitivity analysis, propensity-score matching between TAVR and SAVR was performed.ResultsThe study included 4555 consecutive patients (TAVR, n = 1215 and SAVR, n = 3340) without CKD. Propensity-score matching identified 542 pairs. Patients who underwent TAVR had a significantly lower incidence of AKI in comparison to those who underwent SAVR (unmatched 4.7% vs 16.4%, P < 0.001, multivariable analysis: odds ratio, 0.29, 95% confidence interval [CI], 0.20-0.41; matched 5.9% vs 19.0%, P < 0.001). Patients with AKI had significantly increased 5-year mortality compared with those without AKI (unmatched 36.0% vs 19.1%, log-rank P < 0.001; matched 36.3% vs 24.0%, log-rank P < 0.001). The adjusted hazard ratios for 5-year mortality were 1.58 (95% CI, 1.20-2.08) for AKI grade 1, 3.27 (95% CI, 2.09-5.06) for grade 2, and 4.82 (95% CI, 2.93-8.04) for grade 3.ConclusionsTAVR in patients without CKD was associated with a significantly less frequent incidence of AKI compared with SAVR. AKI significantly increased the risk of 5-year mortality after either TAVR or SAVR, and increasing severity of AKI was incrementally associated with 5-year mortality.     

Effect of Calcium Nitrate on the Properties of Portland–Limestone Cement-Based Concrete Cured at Low Temperature

The effect of calcium nitrate (CN) dosages from 0 to 3% (of cement mass) on the properties of fresh cement paste rheology and hardening processes and on the strength of hardened concrete with two types of limestone-blended composite cements (CEM II A-LL 42.5 R and 42.5 N) at different initial (two-day) curing temperatures (−10 °C to +20 °C) is presented. The rheology results showed that a CN dosage up to 1.5% works as a plasticizing admixture, while higher amounts demonstrate the effect of increasing viscosity. At higher CN content, the viscosity growth in normal early strength (N type) cement pastes is much slower than in high early strength (R type) cement pastes. For both cement-type pastes, shortening the initial and final setting times is more effective when using 3% at +5 °C and 0 °C. At these temperatures, the use of 3% CN reduces the initial setting time for high early strength paste by 7.4 and 5.4 times and for normal early strength cement paste by 3.5 and 3.4 times when compared to a CN-free cement paste. The most efficient use of CN is achieved at −5 °C for compressive strength enlargement; a 1% CN dosage ensures the compressive strength of samples at a −5 °C initial curing temperature, with high early strength cement exceeding 3.5 MPa but being less than the required 3.5 MPa in samples with normal early strength cement.     

Integron-containing IncU R plasmids pRAS1 and pAr-32 from the fish pathogen Aeromonas salmonicida

A 45-kb R plasmid, pRAS1, that confers resistance to tetracyclines, trimethoprim, and sulfonamides was isolated in 1989 from an atypical strain of the fish pathogen Aeromonas salmonicida. This plasmid could be transferred by conjugation to Escherichia coli with a high degree of efficiency (frequency, 0.48). The following year pRAS1 was isolated from A. salmonicida subsp. salmonicida in the same area. Incompatibility group U plasmid pRAS1 contained a drug resistance-determining region of 12 kb consisting of a class 1 integron similar to In4 of Tn1696 but with a dfrA16 gene cassette inserted. Close to IS6100 at the right end of Tn4 was a truncated Tn1721. Restriction enzyme analysis showed that R plasmid pAr-32, isolated from A. salmonicida in Japan in 1970, had the same backbone structure as pRAS1, while the drug resistance-determining region contained a complex class 1 integron with an aadA2 cassette; the chloramphenicol resistance gene catA2, as in In6 of pSa; and a duplicate of the 3' conserved segment of the integron.     

Development and aging of cortical thickness correspond to genetic organization patterns

There is a growing realization that early life influences have lasting impact on brain function and structure. Recent research has demonstrated that genetic relationships in adults can be used to parcellate the cortex into regions of maximal shared genetic influence, and a major hypothesis is that genetically programmed neurodevelopmental events cause a lasting impact on the organization of the cerebral cortex observable decades later. Here we tested how developmental and lifespan changes in cortical thickness fit the underlying genetic organizational principles of cortical thickness in a longitudinal sample of 974 participants between 4.1 and 88.5 y of age with a total of 1,633 scans, including 773 scans from children below 12 y. Genetic clustering of cortical thickness was based on an independent dataset of 406 adult twins. Developmental and adult age-related changes in cortical thickness followed closely the genetic organization of the cerebral cortex, with change rates varying as a function of genetic similarity between regions. Cortical regions with overlapping genetic architecture showed correlated developmental and adult age change trajectories and vice versa for regions with low genetic overlap. Thus, effects of genes on regional variations in cortical thickness in middle age can be traced to regional differences in neurodevelopmental change rates and extrapolated to further adult aging-related cortical thinning. This finding suggests that genetic factors contribute to cortical changes through life and calls for a lifespan perspective in research aimed at identifying the genetic and environmental determinants of cortical development and aging.There is a growing realization that events during development impact brain and cognition throughout the entire lifespan (1). For instance, the major portion of the relationship between cortical thickness and IQ in old age can be explained by childhood IQ (2), and genotype may explain a substantial part of the lifetime stability in intelligence (3). Effects of genes on the organization of the cortex have been shown in adults (4–6), but it is unknown whether and how regional differences in cortical development correspond to these regional genetic subdivisions.Although consensus has not been reached for the exact trajectories, cortical thickness as measured by MRI appears to decrease in childhood (7–12). The exact foundation for this thinning is not known, as MRI provides merely representations of the underlying neurobiology, and available histological data cannot with certainty be used to guide interpretations of MRI results. Although speculative, apparent thickness decrease may be grounded in factors such as synaptic pruning and intracortical myelination, although the link between established synaptic processes (13–15) and cortical thickness has not been empirically confirmed. After childhood, cortical thinning continues throughout the remainder of the lifespan, speculated to reflect neuronal shrinkage and reductions in number of spines and synapses (16), although similar to development, we lack data to support a direct connection between cortical thinning and specific neurobiological events.It has been demonstrated that genetic correlations between thickness in different surface locations can be used to parcellate the adult cortex into regions of maximal shared genetic influence (4). This result can be interpreted according to the hypothesis that genetically programmed neurodevelopmental events cause lasting impact on the organization of the cerebral cortex detectable decades later (4–6). Here we tested how developmental and lifespan changes fit the genetic organization of cortical thickness in a large longitudinal sample with 1,633 scans from 974 participants between 4.1 and 88.5 y of age, including 773 scans from children below 12 y Genetically based subdivisions of cortical thickness from an independent dataset of 406 twins (4) were applied to the data, yielding 12 separate regions under maximum control of shared genetic influences. We hypothesized that thickness in cortical regions with overlapping genetic architecture would show similar developmental and adult age change trajectories and dissimilar trajectories for regions with low genetic overlap.     

Cancer risk in patients with type 2 diabetes mellitus and their relatives

Epidemiological studies indicate that risks of certain cancers are increased in individuals hospitalized for type 2 diabetes mellitus (T2DM), which may not be representative of the entire population of T2DM patients as most of them are treated in primary health cares. To examine the subsequent cancer risk in individuals with T2DM from hospitals and primary health cares, and in their siblings and spouses, standardized incidence ratios (SIRs) were used to assess systematically risks of 35 cancer sites/types in individuals with T2DM using a nationwide Swedish database covering the period 1964 through 2010. Increased SIRs were recorded for 24 cancer sites/types in individuals with T2DM. The highest SIRs were for pancreatic cancer and liver cancer (2.98 and 2.43, respectively). A decreased SIR was noted for prostate cancer. Five cancers showed increased SIRs during the whole follow‐up period: colon, liver, pancreatic, endometrial and kidney cancers. T2DM patients in inpatient, outpatient and primary health care showed similar risk patterns. The overall SIRs for cancer in the siblings and spouses of individuals with T2DM were 0.97 and 1.01, respectively. The insulin users showed an overall increased risk of cancer. This study showed increased risks of 24 cancers in individuals with T2DM, but not in their siblings or spouses, suggesting that the profound metabolic disturbances of the underlying disease may explain the observed increases. Further studies examining the endogenous and exogenous factors underlying these associations are needed.     

Incidence and survival in non-hereditary amyloidosis in Sweden

Background

Energy from liquids is one of the most important factors that could impact on the high prevalence of children and adolescents obesity around the world. There are few data on the liquid consumption in Brazil. The aim of this study is to evaluate the volume and quality of liquids consumed by Brazilian children and adolescents and to determine the proportion of their daily energy intake composed of liquids.

Methods

A multicenter study was conducted in five Brazilian cities; the study included 831 participants between 3 and 17 years of age. A four-day dietary record specific to fluids was completed for each individual, and the volume of and Kcal from liquid intake were evaluated. The average number of Kcal in each beverage was determined based on label information, and the daily energy intake data from liquids were compared with the recommendations of the National Health Surveillance Agency (Agência Nacional de Vigilancia Sanitária?C ANVISA), the Brazilian food regulation authority, according to each subject??s age.

Results

As the children aged, the volume of carbonated beverages that they consumed increased significantly, and their milk intake decreased significantly. For children between the ages of 3 and 10, milk and dairy products contributed the greatest daily number of Kcal from liquids. Sugar sweetened beverages which included carbonated beverages, nectars and artificial beverages, accounted for 37% and 45% of the total Kcal from liquid intake in the 3- to 6-year-old and 7- to 10- year-old groups, respectively. Among adolescents (participants 11- to 17- years old), most of the energy intake from liquids came from carbonated beverages, which accounted for an average of 207 kcal/day in this group (42% of their total energy intake from liquids). Health professionals should be attentive to the excessive consumption of sugar sweetened beverages in children and adolescents. The movement toward healthier dietary patterns at the individual and population levels may help to improve programs for preventing overweight and obesity in children and adolescents.

Conclusion

From childhood to adolescence the daily volume of liquid ingested increased reaching a total of 2.0 liters on average. Of this volume, the daily volume of milk ingested decreased while the carbonated drinks, sweetened, nectars and artificial beverages increased significantly. The proportion of water remained constant in about 1/3 of the total volume. From 3 to 17 years of age the energy intake from carbonated beverages increased by about 20%. The carbonated drinks on average corresponded to a tenth of the daily requirements of energy of adolescents.