Summary Objectives We aimed to determine whether implementation of a structured multi-disciplinary EEG monitoring pathway improved the timeliness of anti-seizure medication administration in response to electrographic seizures in encephalopathic critically ill children. Methods A multidisciplinary team developed a pathway to standardize EEG monitoring and seizure management in encephalopathic critically ill children, aiming to decrease the time from electrographic seizure onset to anti-seizure medication administration. Data was collected to inform the team of improvement opportunities which were then provided by an institutional pathway, staff education, and streamlined communication. Measurements were obtained prior to and after pathway implementation to assess for improvement. Results We collected data on 41 patients before and 21 after pathway implementation. There were no differences between the baseline and pathway groups in demographic characteristics, acute encephalopathy etiologies, or anti-seizure medications utilized. The median duration from seizure onset to anti-seizure medication administration was shorter for patients treated with the pathway (64 minutes [50, 101]) compared to patients treated prior to pathway implementation (139 minutes [71, 189]) (p=0.0006). The interval from seizure onset to anti-seizure medication order was shorter for the pathway group (31 minutes [20, 49]) than the baseline group (71 minutes [33, 131]) (p=0.003). The interval from anti-seizure medication order to administration was shorter for the pathway group (30 minutes [19, 40]) than the baseline group (40 minutes [17, 68]) (p=0.047). Seizure termination was more likely to occur following initial anti-seizure medication administration in the pathway than baseline group (67% vs. 27%, p=0.002). Significance Implementation of the pathway resulted in a significant reduction in the duration between electrographic seizure onset and anti-seizure medication administration, and a significant increase in the rate of electrographic seizure termination following an initial anti-seizure medication. Further study is needed to determine whether these changes are associated with improved outcomes.

No abstract

An experiment was conducted to test the hypothesis that mindful attention to change regarding heart rate (HR) would result in greater control over HR. Experimental groups monitored the changing or stable nature of HR, respectively. All participants' HR slowed during the decrease phase. Participants whose attention was directed to the stable nature of HR performed the worst on the increase phase of the HR control task. These results suggest that mindfulness, instantiated here as attention to variability, is a means to increasing control.

No abstract

No abstract

RationaleAquaporin-5 (AQP5) can cause mucus overproduction and lower lung function. Genetic variants in the AQP5 gene might be associated with rate of lung function decline in chronic obstructive pulmonary disease (COPD).MethodsFive single nucleotide polymorphisms (SNPs) in AQP5 were genotyped in 429 European American individuals with COPD randomly selected from the NHLBI Lung Health Study. Mean annual decline in FEV1 % predicted, assessed over five years, was calculated as a linear regression slope, adjusting for potential covariates and stratified by smoking status. Constructs containing the wildtype allele and risk allele of the coding SNP N228K were generated using site-directed mutagenesis, and transfected into HBE-16 (human bronchial epithelial cell line). AQP5 abundance and localization were assessed by immunoblots and confocal immunofluoresence under control, shear stress and cigarette smoke extract (CSE 10%) exposed conditions to test for differential expression or localization.ResultsAmong continuous smokers, three of the five SNPs tested showed significant associations (0.02>P>0.004) with rate of lung function decline; no associations were observed among the group of intermittent or former smokers. Haplotype tests revealed multiple association signals (0.012>P>0.0008) consistent with the single-SNP results. In HBE16 cells, shear stress and CSE led to a decrease in AQP5 abundance in the wild-type, but not in the N228K AQP5 plasmid.ConclusionsPolymorphisms in AQP5 were associated with rate of lung function decline in continuous smokers with COPD. A missense mutation modulates AQP-5 expression in response to cigarette smoke extract and shear stress. These results suggest that AQP5 may be an important candidate gene for COPD.

To enable future studies on host resistance factors and therapy, inbred and outbred mouse strains were tested for susceptibility to vaginal candidiasis. Groups of mice were given 0.5 mg estradiol 3 days before and 4 days after intravaginal challenge with a suspension of Candida albicans. On day 1 after challenge, a swab was used to quantitate infection in all groups and to assure equivalent infection levels. On day 6, this was repeated and the experiment was terminated. BALB/c, the reference strain in repeated experiments, was susceptible, showing persistent infection with levels of cfu at day 6 falling within a range between a twofold decrease and a fourfold increase in relation to day 1 levels. CD-1 outbred mice were markedly resistant, with day 6 cfu levels showing a 74- to 87-fold decrease with respect to day 1 levels, whereas other outbred strains (CF-1, SW, ICR) were susceptible. A BALB/c substrain (ByJ) was also susceptible. With exception of CBA/J, which showed modest resistance, all inbred strains were similarly susceptible, including DBA/2, AKR/J, C3H/HeN, A/J and C57BL/6. The differences between CD-1 and BALB/c mice were also seen with a second C. albicans isolate. Our results show susceptibility to vaginal candidiasis is independent of the major histocompatibility locus H2 haplotype and any effect ascribable to use of particular commercial mouse suppliers. Differences among mouse strains in susceptibility to C. albicans, as seen in previous studies involving nonvaginal challenge routes, are not reflected in this vaginal candidiasis model; in general, such resistance patterns appear specific to the route of challenge administration. The resistance seen in mouse strain CD-1 is of particular interest in that CD-1 is known to be resistant to endocrine disruption by estrogen. Our results suggest this estrogen insensitivity may have broad-ranging effects on processes other than gametogenesis, including vaginal susceptibility to candidiasis.

No abstract