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Articles by A. Evans
Total Records ( 3 ) for A. Evans
  T. P. Lodise , J. Graves , A. Evans , E. Graffunder , M . Helmecke , B. M. Lomaestro and K. Stellrecht
  There is growing concern that vancomycin has diminished activity for methicillin-resistant Staphylococcus aureus (MRSA) infections, with vancomycin MICs at the high end of the CLSI susceptibility range. Despite this growing concern, there are limited clinical data to support this notion. To better elucidate this, a retrospective cohort study was conducted among patients with MRSA bloodstream infections who were treated with vancomycin between January 2005 and May 2007. The inclusion criteria were as follows: at least 18 years old, nonneutropenic, with an MRSA culture that met the CDC criteria for bloodstream infection, had received vancomycin therapy within 48 h of the index blood culture, and survived >24 h after vancomycin administration. Failure was defined as 30-day mortality, bacteremia ≥10 days on vancomycin therapy, or a recurrence of MRSA bacteremia within 60 days of vancomycin discontinuation. Classification and regression tree (CART) analysis identified the vancomycin MIC breakpoint associated with an increased probability of failure. During the study period, 92 patients met the inclusion criteria. The vancomycin MIC breakpoint derived by CART analysis was ≥1.5 mg/liter. The 66 patients with vancomycin MICs of ≥1.5 mg/liter had a 2.4-fold increase in failure compared to patients with MICs of ≤1.0 mg/liter (36.4% and 15.4%, respectively; P = 0.049). In the Poisson regression, a vancomycin MIC of ≥1.5 mg/liter was independently associated with failure (adjusted risk ratio, 2.6; 95% confidence interval, 1.3 to 5.4; P = 0.01). These data strongly suggest that patients with MRSA bloodstream infections with vancomycin MICs of ≥1.5 mg/liter respond poorly to vancomycin. Alternative anti-MRSA therapies should be considered for these patients.
  Y He , A Dagher , Z Chen , A Charil , A Zijdenbos , K Worsley and A. Evans
 

White matter tracts, which play a crucial role in the coordination of information flow between different regions of grey matter, are particularly vulnerable to multiple sclerosis. Many studies have shown that the white matter lesions in multiple sclerosis are associated with focal abnormalities of grey matter, but little is known about the alterations in the coordinated patterns of cortical morphology among regions in the disease. Here, we used cortical thickness measurements from structural magnetic resonance imaging to investigate the relationship between the white matter lesion load and the topological efficiency of structural cortical networks in multiple sclerosis. Network efficiency was defined using a ‘small-world’ network model that quantifies the effectiveness of information transfer within brain networks. In this study, we first classified patients (n = 330) into six subgroups according to their total white matter lesion loads, and identified structural brain networks for each multiple sclerosis group by thresholding the corresponding inter-regional cortical thickness correlation matrix, followed by a network efficiency analysis with graph theoretical approaches. The structural cortical networks in multiple sclerosis demonstrated efficient small-world architecture regardless of the lesion load, an organization that maximizes the information processing at a relatively low wiring cost. However, we found that the overall small-world network efficiency in multiple sclerosis was significantly disrupted in a manner proportional to the extent of total white matter lesions. Moreover, regional efficiency was also significantly decreased in specific brain regions, including the insula and precentral gyrus as well as regions of prefrontal and temporal association cortices. Finally, we showed that the lesions also altered many cortical thickness correlations in the frontal, temporal and parietal lobes. Our results suggest that the white matter lesions in multiple sclerosis might be associated with aberrant neuronal connectivity among widely distributed brain regions, and provide structural (morphological) evidence for the notion of multiple sclerosis as a disconnection syndrome.

  M. S Wright , D. K Wilson , S Griffin and A. Evans
 

This study obtained qualitative data to assess how parental role modeling and parental social support influence physical activity in underserved (minority, low-income) adolescents. Fifty-two adolescents (22 males, 30 females; ages 10–14 years, 85% African-American) participated in a focus group (6–10 per group, same gender). Focus groups were audiotaped, transcribed and coded by independent raters. Inter-rater reliabilities indicated adequate agreement [inter-rater reliability (r) = 0.84]. Themes were identified for parental role modeling and parental social support. Regarding parental role modeling, adolescents reported that parents engaged in a variety of different types of physical activities with their children such as walking, cycling and playing basketball; however, activity was infrequent. Sex differences were noted in parental social support indicating that female adolescents reported receiving more emotional and negative support for physical activity (being required to play outside with a sibling), while boys reported receiving more tangible types of support for physical activity. Adolescents also generated ideas on how to increase parental social support and in particular tangible support was highlighted as important by both males and females. This study suggests that future interventions should focus on improving parental engagement and tangible support that involve direct participation from parents in physical activities with their adolescents.

 
 
 
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