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BACKGROUND: Sports nutrition is an impactful component to sports performance. The purpose of the current study was to investigate the sports nutrition knowledge of National Collegiate Athletic Association collegiate athletes and assess self-reported perceived requirements for energy and macronutrient intake. A secondary aim was to evaluate the awareness of physical and emotional perceptions associated with mindful eating. METHODS: Participants included NCAA Division I (DI, n = 45), II (DII, n = 31), and III (DIII, n = 47) athletes. Athletes completed a validated questionnaire designed to assess sports nutrition knowledge and were asked questions about their perceived dietary energy and macronutrient requirements. Daily energy intake values were calculated using a recommended relative energy intake value of 40, 50, and 60 kcal/kg/day for low, moderate, and high activity levels, respectively. Carbohydrate recommendations were calculated using 4, 6, and 8 g/kg/day, protein recommendations were calculated using relative intakes of 1.4, 1.6, and 1.8 g/kg/day, and fat recommendations were calculated from a relative percentage of total predicted daily energy requirements, equating to 15, 25, and 30% of daily energy. Additionally, athletes completed a questionnaire to assess mindfulness regarding eating habits. RESULTS: Overall, athletes answered 45.5 ± 13.5% of questions correctly on the nutrition questionnaire with significant differences observed between male (48.6 ± 13.6%) and female athletes (43.6 ± 13.2%; p = 0.044), as well as significant differences observed between DI athlete scores (38.8 ± 14.1%) and DII athletes (47.7 ± 11.4%; p = 0.002), and DI athletes and DIII athletes (51.71 ± 11.83%; p = <0.001). All athletes significantly (p < 0.001) underestimated daily energy intake requirements (female, 2,112 ± 575 kcal/day; male, 3,283 ± 538 kcal/day). The mindfulness eating habits total score was significantly higher in male athletes (65.1 ± 6.5) compared to female athletes (60.9 ± 9.5; p = 0.009). CONCLUSIONS: Division I, II, and III collegiate athletes have poor sports nutrition knowledge, with Division I athletes having exhibited lower scores compared to Division II and III athletes on the sports nutrition knowledge questionnaire. Athletes from all levels of collegiate sports underestimated their energy and macronutrient requirements. Differences in mindful eating habits among female and male athletes were also evident.

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CLINICAL SCENARIO: Sport-related injuries are a common occurrence within the athletic population and every athlete responds differently. The cognitive, emotional, and behavioral responses associated with injuries ultimately impact the injury rehabilitation process and return to play. Specifically, self-efficacy significantly impacts the rehabilitation process and psychological techniques to improve self-efficacy are crucial in the recovery process. Imagery is one of these beneficial techniques. CLINICAL QUESTION: Does the use of imagery during injury rehabilitation improve self-efficacy of rehabilitation capabilities compared with rehabilitation alone in athletes with a sport-related injury? SUMMARY OF KEY FINDINGS: The current literature was searched to identify the effects of imagery use to improve self-efficacy of rehabilitation capabilities, and 2 studies were selected: a mixed methods ecologically valid design and randomized controlled trial. Both studies investigated the relationship between imagery and self-efficacy and found positive results for imagery use in rehabilitation. Additionally, one of the studies specifically assessed rehabilitation satisfaction and found positive results. CLINICAL BOTTOM LINE: The use of imagery should be considered as a clinical option for increasing self-efficacy during injury rehabilitation. STRENGTH OF RECOMMENDATION: Based on the Oxford Centre for Evidence-Based Medicine strength of recommendation, there is a grade B of recommendation to support the use of imagery to improve self-efficacy of rehabilitation capabilities during an injury rehabilitation program.

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BACKGROUND AND PURPOSE: Perfusion MR imaging measures of relative CBV can distinguish recurrent tumor from posttreatment radiation effects in high-grade gliomas. Currently, relative CBV measurement requires normalization based on user-defined reference tissues. A recently proposed method of relative CBV standardization eliminates the need for user input. This study compares the predictive performance of relative CBV standardization against relative CBV normalization for quantifying recurrent tumor burden in high-grade gliomas relative to posttreatment radiation effects. MATERIALS AND METHODS: We recruited 38 previously treated patients with high-grade gliomas (World Health Organization grades III or IV) undergoing surgical re-resection for new contrast-enhancing lesions concerning for recurrent tumor versus posttreatment radiation effects. We recovered 112 image-localized biopsies and quantified the percentage of histologic tumor content versus posttreatment radiation effects for each sample. We measured spatially matched normalized and standardized relative CBV metrics (mean, median) and fractional tumor burden for each biopsy. We compared relative CBV performance to predict tumor content, including the Pearson correlation (r), against histologic tumor content (0%-100%) and the receiver operating characteristic area under the curve for predicting high-versus-low tumor content using binary histologic cutoffs (≥50%; ≥80% tumor). RESULTS: Across relative CBV metrics, fractional tumor burden showed the highest correlations with tumor content (0%-100%) for normalized (r = 0.63, P < .001) and standardized (r = 0.66, P < .001) values. With binary cutoffs (ie, ≥50%; ≥80% tumor), predictive accuracies were similar for both standardized and normalized metrics and across relative CBV metrics. Median relative CBV achieved the highest area under the curve (normalized = 0.87, standardized = 0.86) for predicting ≥50% tumor, while fractional tumor burden achieved the highest area under the curve (normalized = 0.77, standardized = 0.80) for predicting ≥80% tumor. CONCLUSIONS: Standardization of relative CBV achieves similar performance compared with normalized relative CBV and offers an important step toward workflow optimization and consensus methodology.

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BACKGROUND AND PURPOSE: MR imaging-based modeling of tumor cell density can substantially improve targeted treatment of glioblastoma. Unfortunately, interpatient variability limits the predictive ability of many modeling approaches. We present a transfer learning method that generates individualized patient models, grounded in the wealth of population data, while also detecting and adjusting for interpatient variabilities based on each patient's own histologic data. MATERIALS AND METHODS: We recruited patients with primary glioblastoma undergoing image-guided biopsies and preoperative imaging, including contrast-enhanced MR imaging, dynamic susceptibility contrast MR imaging, and diffusion tensor imaging. We calculated relative cerebral blood volume from DSC-MR imaging and mean diffusivity and fractional anisotropy from DTI. Following image coregistration, we assessed tumor cell density for each biopsy and identified corresponding localized MR imaging measurements. We then explored a range of univariate and multivariate predictive models of tumor cell density based on MR imaging measurements in a generalized one-model-fits-all approach. We then implemented both univariate and multivariate individualized transfer learning predictive models, which harness the available population-level data but allow individual variability in their predictions. Finally, we compared Pearson correlation coefficients and mean absolute error between the individualized transfer learning and generalized one-model-fits-all models. RESULTS: Tumor cell density significantly correlated with relative CBV (r = 0.33, P < .001), and T1-weighted postcontrast (r = 0.36, P < .001) on univariate analysis after correcting for multiple comparisons. With single-variable modeling (using relative CBV), transfer learning increased predictive performance (r = 0.53, mean absolute error = 15.19%) compared with one-model-fits-all (r = 0.27, mean absolute error = 17.79%). With multivariate modeling, transfer learning further improved performance (r = 0.88, mean absolute error = 5.66%) compared with one-model-fits-all (r = 0.39, mean absolute error = 16.55%). CONCLUSIONS: Transfer learning significantly improves predictive modeling performance for quantifying tumor cell density in glioblastoma.

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Dietary management of 418 adult patients with galactosaemia (from 39 centres/12 countries) was compared. All centres advised lactose restriction, 6 restricted galactose from galactosides ± fruits and vegetables and 12 offal. 38% (n=15) relaxed diet by: 1) allowing traces of lactose in manufactured foods (n=13) or 2) giving fruits, vegetables and galactosides (n=2). Only 15% (n=6) calculated dietary galactose. 32% of patients were lost to dietetic follow-up. In adult galactosaemia, there is limited diet relaxation.

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Despite initial and often dramatic responses of epidermal growth factor receptor (EGFR)-addicted lung tumors to the EGFR-specific tyrosine kinase inhibitors (TKIs), gefitinib and erlotinib, nearly all develop resistance and relapse. To explore novel mechanisms mediating acquired resistance, we employed non-small-cell lung cancer (NSCLC) cell lines bearing activating mutations in EGFR and rendered them resistant to EGFR-specific TKIs through chronic adaptation in tissue culture. In addition to previously observed resistance mechanisms including EGFR-T790M 'gate-keeper' mutations and MET amplification, a subset of the seven chronically adapted NSCLC cell lines including HCC4006, HCC2279 and H1650 cells exhibited marked induction of fibroblast growth factor (FGF) 2 and FGF receptor 1 (FGFR1) mRNA and protein. Also, adaptation to EGFR-specific TKIs was accompanied by an epithelial to mesenchymal transition (EMT) as assessed by changes in CDH1, VIM, ZEB1 and ZEB2 expression and altered growth properties in Matrigel. In adapted cell lines exhibiting increased FGF2 and FGFR1 expression, measures of growth and signaling, but not EMT, were blocked by FGFR-specific TKIs, an FGF-ligand trap and FGFR1 silencing with RNAi. In parental HCC4006 cells, cell growth was strongly inhibited by gefitinib, although drug-resistant clones progress within 10 days. Combined treatment with gefitinib and AZD4547, an FGFR-specific TKI, prevented the outgrowth of drug-resistant clones. Thus, induction of FGF2 and FGFR1 following chronic adaptation to EGFR-specific TKIs provides a novel autocrine receptor tyrosine kinase-driven bypass pathway in a subset of lung cancer cell lines that are initially sensitive to EGFR-specific TKIs. The findings support FGFR-specific TKIs as potentially valuable additions to existing targeted therapeutic strategies with EGFR-specific TKIs to prevent or delay acquired resistance in EGFR-driven NSCLC.

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BACKGROUND/AIM: A mainstay of laboratory research into new therapies for sepsis has been the cecal ligation and puncture (CLP) model in rodents. Previous data indicate that the number of punctures made in the cecum and needle size utilized are primary determinants of mortality. Despite this, variability exists in mortality from this model, even when needle size is held constant. The aim of the present study was to evaluate the influence of the length of cecum ligated, independent of needle size, as a determinant of mortality. MATERIALS AND METHODS: We evaluated this by ligating various cecal lengths in male Sprague-Dawley rats. A double puncture was then made with a 20-gauge needle, and mortality was analyzed. Plasma TNF-alpha and IL-6 expression was assessed at 6 h. Animals received no antibiotics, were not fasted, and fluid resuscitation was administered. RESULTS: We determined that mortality does not begin to occur until a distance of >5% of cecal length is ligated. Further, our findings indicate that in this model, 90-100% mortality occurs 4 days following CLP when a distance of >30% is ligated. TNF-alpha and IL-6 expression is markedly increased with increasing length of cecum ligated. CONCLUSIONS: Our data demonstrate that the length of cecum ligated is a major determinant of mortality in the CLP model of sepsis. These findings indicate that investigators must rigorously control the distance of the cecum ligated in order to generate consistent mortality and inflammation data when utilizing the CLP model in rats. Further, the mortality from this model can be adjusted to fit the individual needs of a particular experiment.

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Single nucleotide polymorphisms (SNP) in the human IL-6, IL-10, TNFalpha and TNFbeta genes have been associated with gene function and susceptibility to disease. In this study, primers containing mismatches at 1-3 nucleotide positions were designed to incorporate a new restriction site recognized by endonucleases AlwNI, BcgI, BglI, BsaBI, BslI, BstXI, EcoNI or XcmI for genotyping SNPs in the IL-6 gene (position - 174), IL-10 gene (positions -592 and -1082), TNFalpha gene (positions -238, - 308 and -863) and TNFbeta gene (position + 249) by mismatched polymerase chain reaction and restriction fragment length polymorphism (PCR/RFLP). Our results show that appropriately designed BslI-based mismatched PCR/RFLP assays can be successfully used to determine the genotypes for approximately 40% of SNPs. The mismatched PCR strategy can be coupled with multiplex-amplification to enable simple and rapid determination of several SNP genotypes in a single reaction.

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Myotonic dystrophy (DM), an autosomal dominant neuromuscular disease, is associated with expansion of a polymorphic (CTG)n repeat in the 3'-untranslated region of the DM protein kinase (DMPK) gene. The repeat expansion results in decreased levels of DMPK mRNA and protein, but the mechanism for this decreased expression is unknown. Loss of a nuclease-hypersensitive site in the region of the repeat expansion has been observed in muscle and skin fibroblasts from DM patients, indicating a change in local chromatin structure. This change in chromatin structure has been proposed as a mechanism whereby the expression of DMPK and neighboring genes, sine oculis homeobox (Drosophila) homolog 5 (SIX5) and dystrophia myotonica-containing WD repeat motif (DMWD), might be affected. We have developed a polymerase chain reaction (PCR)-based method to assay the chromatin sensitivity of the region adjacent to the repeat expansion in somatic cell hybrids carrying either normal or affected DMPK alleles and show that hybrids carrying expanded alleles exhibit decreased sensitivity to PvuII digestion in this region. Semiquantitative multiplex reverse transcriptase PCR (RT/PCR) assays of gene expression from the chromosomes carrying the expanded alleles showed marked reduction of DMPK mRNA, partial inhibition of SIX5 expression from a congenital DM chromosome, and no reduction of DMWD mRNA. Nested RT/PCR analysis of DMPK mRNA from somatic cell hybrids carrying the repeat expansions revealed that most of the DMPK transcripts expressed from the expanded alleles lacked exons 13 and 14, whereas full-length transcripts were expressed predominantly from the normal alleles. These results suggest that the CTG repeat expansion leads to a decrease in DMPK mRNA levels by affecting splicing at the 3' end of the DMPK pre-mRNA transcript.

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Emergency department (ED) staff caring for patients contaminated with toxic chemicals are at risk for developing toxicity from secondary contamination. This report describes three cases of occupational illnesses associated with organophosphate toxicity caused by exposure to a contaminated patient and underscores the importance of using personal protection equipment (PPE) and establishing and following decontamination procedures in EDs and other areas of acute care hospitals.

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In Case 1, a nurse describes a scenario in which a patient's functional and legal families disagree about who has the right to make consent decisions. Case 2 reveals the situation's legal and ethical implications for nurses and how they can facilitate a resolution.

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OBJECTIVE: Many children with human immunodeficiency virus (HIV) infection are surviving long enough to reach school age. This study describes issues related to school attendance and disclosure of HIV infection in a population of HIV-infected children. METHODS: A statewide pediatric HIV surveillance system was used to collect data on school-age (>/=5 years old) HIV-infected children. In addition, HIV clinic nurses familiar with the child's history participated in a cross-sectional survey that collected information on school-related issues during the 1993-1994 school year. RESULTS: Of the 92 school-age children, only 3 were too ill to attend school. Another 5 children were home-schooled. Of the 84 who attended school outside the home, 25% had severe symptoms of HIV infection (Centers for Disease Control and Prevention [CDC] clinical category C). Absence from school ranged from less than 2 weeks during the year for half of the children (51%) to more than 8 weeks for 9 children (12%). Twenty-nine percent of the children received medication in school, usually administered by the school nurse. Over two thirds of the 50 children ages 5 to 10 years had not been told that they had HIV infection. Only 1 of the 20 children more than 10 years of age was not aware of her HIV infection. For 53% of the children attending school, no school personnel had been informed of the child's HIV infection. Administration of HIV medications at school, age of child, and treatment at one particular HIV clinic were associated with the parents' decision to inform school personnel. In the 47% of cases where the school had been informed, school nurses were most frequently notified, followed by principals and teachers. CONCLUSION: Only 3% of school-age children were too ill to attend school, and almost all were enrolled in public schools. The number of HIV-infected children reaching school age will continue to grow, and public schools will bear the responsibility for educating these children. Health care providers will increasingly be called upon for guidance by both educators and families to assure that HIV-infected children receive the best education possible.

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This article describes a case in which the health-care team initiated treatments assuming that the information provided by the patient was true. Following the onset of complications requiring additional consents and leading to a long-term relationship with family members, there was serious conflict between what was discovered to be a functional family unit and a legal family unit. The patient's wishes were uncertain and not legally supported. After being declared competent for consent, the patient still failed to clearly communicate his wishes to those affected. The case is followed by an ethical analysis.

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To test the hypothesis that apoptosis is involved in human brain neurodegenerative disorders, we investigated whether DNA fragmentation occurs in Alzheimer's disease (AD). Huntington's disease (HD) and Parkinson's disease, as well as in temporal lobe epilepsy, using neurologically normal post-mortem human brain tissue as a control. Using in situ end labelling of DNA, we found evidence of DNA fragmentation in cells in temporal cortex and hippocampus from patients with AD and in striatum from those with HD. In contrast, only scattered DNA fragmentation positive cells were detected in the pial surfaces of some of the neurologically normal human brains. Thus, cells in the HD striatum and AD temporal cortex exhibited DNA fragmentation, suggesting that apoptosis may be involved in these disorders.

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It has been suggested that the increased transient expression of immediate-early gene transcription factors seen in nerve cells following an afterdischarge may initiate longer lasting or permanent changes in gene expression which underly the development of kindling. Since the development of kindling is sensitive to pharmacological blockade of the N-methyl-D-aspartate receptor, we tested whether the increased expression of the immediate-early genes c-fos, jun-B, c-jun, krox-20, and krox-24 following a kindling afterdischarge was also sensitive to N-methyl-D-aspartate receptor blockade by MK-801. In this report we demonstrate that all five immediate-early genes are induced by an amygdala afterdischarge. N-methyl-D-aspartate receptor blockade by a dose of MK-801 that significantly retards the development of amygdala kindling failed to attenuate immediate-early gene expression. These results suggest that although expression of these five immediate-early genes occurs after an amygdala afterdischarge their expression is not involved in the N-methyl-D-aspartate receptor-mediated component of amygdala kindling.

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In ovarian follicles of Drosophila, changes in external osmolarity affect the steady-state potentials of oocytes more than those of nurse cells. Thus the osmolarity of the incubation medium affects the occurrence and the direction of an electrical gradient across the connecting intercellular bridges. At 255 mOsm nurse cell Em averaged 2.5 mV negative to oocyte Em (P < 0.001). At 275 and at 300 mOsm there was no significant difference between oocyte and nurse cell. At 400 mOsm nurse cell Em averaged 1.1 mV positive to oocyte Em (P = 0.007). The osmolarity of adult Drosophila hemolymph was measured by a variation of freezing point depression and averaged 251 +/- 9 (SE) mOsm. The measured osmolarity and measured ionic concentrations of adult Drosophila hemolymph were used to develop an incubation medium, which was used to incubate developing ovarian follicles. Electrical measurements made in this saline, which mimics in vivo conditions, confirmed reports of a nurse cell-oocyte electrical gradient, with nurse cell Em significantly more negative than oocyte Em. Microinjections of the negatively charged dye Lucifer yellow CH showed that this charged molecule accumulated in the oocyte at the in vivo osmolarity, and in the nurse cells at highly elevated osmotic levels.

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Neurons undergoing delayed neuronal death produced by hypoxia-ischaemia (HI) or status epilepticus (SE) showed a massive expression of c-Jun in their nuclei 24 h after the insult. With SE there was also a weaker induction of c-Fos and Jun B in dying neurons. SE induced in the presence of the NMDA antagonist MK-801 produced no delayed c-Jun expression in the hippocampus and nerve cell death did not occur in this region, although there was a delayed c-jun expression in the amygdala/piriform region, and cell death occurred in this area. Activation of central muscarinic receptors with pilocarpine, or block of D2 dopamine receptors with haloperidol, treatments which do not cause neuronal damage, strongly induced Fos and Jun B in hippocampal and striatal neurons, but only induced c-Jun very weakly. Thus, c-Jun may participate in the genetic cascade of events that produce programmed cell death in neurons.

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The Safe Medical Device Act places a legal responsibility on health care practitioners to assess and report malfunctioning medical equipment. As a result of this law, the Food and Drug Administration (FDA) will for the first time have direct regulatory authority over hospitals. Today's complex and technological critical care setting requires that the nurse understand the legal and professional responsibilities imposed by this Act.

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