Quality improvement in clinical documentation: does clinical governance work?

INTRODUCTION: The quality of nursing documentation is still a challenge in the nursing profession and, thus, in the health care industry. One major quality improvement program is clinical governance, whose mission is to continuously improve the quality of patient care and overcome service quality problems. The aim of this study was to identify whether clinical governance improves the quality of nursing documentation. METHODS: A quasi-experimental method was used to show nursing documentation quality improvement after a 2-year clinical governance implementation. Two hundred twenty random nursing documents were assessed structurally and by content using a valid and reliable researcher made checklist. RESULTS: There were no differences between a nurse's demographic data before and after 2 years (P>0.05) and the nursing documentation score did not improve after a 2-year clinical governance program. CONCLUSION: Although some efforts were made to improve nursing documentation through clinical governance, these were not sufficient and more attempts are needed

Teletraffic Performance of GSM900/DCS1800 in Street Microcells

Radio planners often refer to the buildings in cities as "urban clutter," a nuisance they must accomrnodate. A more appropriate attitude for personal communication systems is to utilize the electromagnetic shielding offered by buildings to form microcells

Laboratory-based and office-based Globorisk scores to predict 10-year risk of cardiovascular diseases among Iranians: results from the Fasa PERSIAN cohort.

BACKGROUND: Globorisk is a novel risk prediction model for predicting cardiovascular disease (CVD). Globorisk is a country-specific risk prediction model that determines CVD risk for all countries. This model has two versions; laboratory-based and office-based. This study aimed to determine the agreement between laboratory-based and office-based models in a large sample of the general population. METHODS: Baseline data from the Fasa cohort study was used for the current study. In total, 6810 participants ≥ 40 years without any history of cardiovascular disease or stroke were included in the study. To determine the laboratory-based risk model, factors include age, sex, current smoking status, history of diabetes, systolic blood pressure (SBP), and total cholesterol. To estimate the office-based risk model, factors were age, sex, current smoking status, SBP, and body mass index (BMI). Kappa statistics was used to distinguish the agreement between grouped scores in these two models. Additionally, correlation coefficients and scatter plots were used to determine the linear correlation between the two models. RESULTS: In this study 46.53% of the participants were men. The mean age (SD) of participants was 51.08 (7.88) years. Agreements between the two models were moderate and substantial in all women and all men, respectively. The agreement between the two CVD risk groups was 90.15% (kappa = 0.717) in all men, 92.94% (kappa = 0.571) among men aged  60 years (r = 0.94). Among all women, there was a very strong positive correlation (r = 0.87), and the strong positive correlation remained among  60 years old (r = 0.76). CONCLUSION: The Globorisk office-based model which is easier to use as it does not require blood testing can determine the risk groups in this population. The Globorisk office-based model may be used for CVD risk screening in low-middle income countries where resources are limited

Circulatory proteins relate cardiovascular disease to cognitive performance: a Mendelian randomisation study

Background and objectives: Mechanistic research suggests synergistic effects of cardiovascular disease (CVD) and dementia pathologies on cognitive decline. Interventions targeting proteins relevant to shared mechanisms underlying CVD and dementia could also be used for the prevention of cognitive impairment. Methods: We applied Mendelian randomisation (MR) and colocalization analysis to investigate the causal relationships of 90 CVD-related proteins measured by the Olink CVD I panel with cognitive traits. Genetic instruments for circulatory protein concentrations were obtained using a meta-analysis of genome-wide association studies (GWAS) from the SCALLOP consortium (N = 17,747) based on three sets of criteria: 1) protein quantitative trait loci (pQTL); 2) cis-pQTL (pQTL within ±500 kb from the coding gene); and 3) brain-specific cis-expression QTL (cis-eQTL) which accounts for coding gene expression based on GTEx8. Genetic associations of cognitive performance were obtained from GWAS for either: 1) general cognitive function constructed using Principal Component Analysis (N = 300,486); or, 2) g Factor constructed using genomic structural equation modelling (N = 11,263–331,679). Findings for candidate causal proteins were replicated using a separate protein GWAS in Icelanders (N = 35,559). Results: A higher concentration of genetically predicted circulatory myeloperoxidase (MPO) was nominally associated with better cognitive performance (p < 0.05) using different selection criteria for genetic instruments. Particularly, brain-specific cis-eQTL predicted MPO, which accounts for protein-coding gene expression in brain tissues, was associated with general cognitive function (βWald = 0.22, PWald = 2.4 × 10−4). The posterior probability for colocalization (PP.H4) of MPO pQTL with the g Factor was 0.577. Findings for MPO were replicated using the Icelandic GWAS. Although we did not find evidence for colocalization, we found that higher genetically predicted concentrations of cathepsin D and CD40 were associated with better cognitive performance and a higher genetically predicted concentration of CSF-1 was associated with poorer cognitive performance. Conclusion: We conclude that these proteins are involved in shared pathways between CVD and those for cognitive reserve or affecting cognitive decline, suggesting therapeutic targets able to reduce genetic risks conferred by cardiovascular disease

Visual Tracking: An Experimental Survey

There is a large variety of trackers, which have been proposed in the literature during the last two decades with some mixed success. Object tracking in realistic scenarios is difficult problem, therefore it remains a most active area of research in Computer Vision. A good tracker should perform well in a large number of videos involving illumination changes, occlusion, clutter, camera motion, low contrast, specularities and at least six more aspects. However, the performance of proposed trackers have been evaluated typically on less than ten videos, or on the special purpose datasets. In this paper, we aim to evaluate trackers systematically and experimentally on 315 video fragments covering above aspects. We selected a set of nineteen trackers to include a wide variety of algorithms often cited in literature, supplemented with trackers appearing in 2010 and 2011 for which the code was publicly available. We demonstrate that trackers can be evaluated objectively by survival curves, Kaplan Meier statistics, and Grubs testing. We find that in the evaluation practice the F-score is as effective as the object tracking accuracy (OTA) score. The analysis under a large variety of circumstances provides objective insight into the strengths and weaknesses of trackers

Associations of genetically predicted vitamin B12 status across the pohenome

Variation in vitamin B12 levels has been associated with a range of diseases across the life-course, the causal nature of which remains elusive. We aimed to interrogate genetically predicted vitamin B12 status in relation to a plethora of clinical outcomes available in the UK Biobank. Genome-wide association study (GWAS) summary data obtained from a Danish and Icelandic cohort of 45,576 individuals were used to identify 8 genetic variants associated with vitamin B12 levels, serving as genetic instruments for vitamin B12 status in subsequent analyses. We conducted a Mendelian randomisation (MR)-phenome-wide association study (PheWAS) of vitamin B12 status with 945 distinct phenotypes in 439,738 individuals from the UK Biobank using these 8 genetic instruments to proxy alterations in vitamin B12 status. We used external GWAS summary statistics for replication of significant findings. Correction for multiple testing was taken into consideration using a 5% false discovery rate (FDR) threshold. MR analysis identified an association between higher genetically predicted vitamin B12 status and lower risk of vitamin B deficiency (including all B vitamin deficiencies), serving as a positive control outcome. We further identified associations between higher genetically predicted vitamin B12 status and a reduced risk of megaloblastic anaemia (OR = 0.35, 95% CI: 0.20–0.50) and pernicious anaemia (0.29, 0.19–0.45), which was supported in replication analyses. Our study highlights that higher genetically predicted vitamin B12 status is potentially protective of risk of vitamin B12 deficiency associated with pernicious anaemia diagnosis, and reduces risk of megaloblastic anaemia. The potential use of genetically predicted vitamin B12 status in disease diagnosis, progression and management remains to be investigated

Iron Status and Risk of Stroke.

Background and Purpose- Both iron deficiency and excess have been associated with stroke risk in observational studies. However, such associations may be attributable to confounding from environmental factors. This study uses the Mendelian randomization technique to overcome these limitations by investigating the association between genetic variants related to iron status and stroke risk. Methods- A study of 48 972 subjects performed by the Genetics of Iron Status consortium identified genetic variants with concordant relations to 4 biomarkers of iron status (serum iron, transferrin saturation, ferritin, and transferrin) that supported their use as instruments for overall iron status. Genetic estimates from the MEGASTROKE consortium were used to investigate the association between the same genetic variants and stroke risk. The 2-sample ratio method Mendelian randomization approach was used for the main analysis, with the MR-Egger and weighted median techniques used in sensitivity analyses. Results- The main results, reported as odds ratio (OR) of stroke per SD unit increase in genetically determined iron status biomarker, showed a detrimental effect of increased iron status on stroke risk (serum iron OR, 1.07; 95% CI, 1.01-1.14; [log-transformed] ferritin OR, 1.18; 95% CI, 1.02-1.36; and transferrin saturation OR, 1.06; 95% CI, 1.01-1.11). A higher transferrin, indicative of lower iron status, was also associated with decreased stroke risk (OR, 0.92; 95% CI, 0.86-0.99). Examining ischemic stroke subtypes, we found the detrimental effect of iron status to be driven by cardioembolic stroke. These results were supported in statistical sensitivity analyses more robust to the inclusion of pleiotropic variants. Conclusions- This study provides Mendelian randomization evidence that higher iron status is associated with increased stroke risk and, in particular, cardioembolic stroke. Further work is required to investigate the underlying mechanism and whether this can be targeted in preventative strategies

Genetically determined blood pressure, antihypertensive drug classes and risk of stroke subtypes

Objective: We employed Mendelian Randomization to explore whether the effects of blood pressure (BP) and BP lowering through different antihypertensive drug classes on stroke risk vary by stroke etiology. Methods: We selected genetic variants associated with systolic and diastolic BP and BP-lowering variants in genes encoding antihypertensive drug targets from a GWAS on 757,601 individuals. Applying two-sample Mendelian randomization, we examined associations with any stroke (67,162 cases; 454,450 controls), ischemic stroke and its subtypes (large artery, cardioembolic, small vessel stroke), intracerebral hemorrhage (ICH, deep and lobar), and the related small vessel disease phenotype of WMH. Results: Genetic predisposition to higher systolic and diastolic BP was associated with higher risk of any stroke, ischemic stroke, and ICH. We found associations between genetically determined BP and all ischemic stroke subtypes with a higher risk of large artery and small vessel stroke compared to cardioembolic stroke, as well as associations with deep, but not lobar ICH. Genetic proxies for calcium channel blockers, but not beta blockers, were associated with lower risk of any stroke and ischemic stroke. Proxies for CCBs showed particularly strong associations with small vessel stroke and the related radiological phenotype of WMH. Conclusions: This study supports a causal role of hypertension in all major stroke subtypes except lobar ICH. We find differences in the effects of BP and BP lowering through antihypertensive drug classes between stroke subtypes and identify calcium channel blockade as a promising strategy for preventing manifestations of cerebral small vessel disease