Assessment of Dietary Intake and Eating Attitudes in Recreational and Competitive Adolescent Rock Climbers: A Pilot Study

The dietary intake and eating attitudes of adolescent climbers has not previously been studied. To fill this knowledge gap, we administered three surveys to 22 rock climbers (13 males, 9 females, age 14.2 ± 1.9 years): climbing ability, three-day dietary recall, and Eating Attitude Test-26 (EAT-26). The majority (82%) of climbers did not meet their target energy intake (target = 2,471 ± 493 kcal·day−1; actual = 1,963 ± 581 kcal·day−1) (p = 0.003) and 86% of climbers consumed below their target carbohydrate intake (target = 283 ± 67 g·day−1; actual intake = 226 ± 72 g·day−1) (p = 0.009). Average dietary protein intake was 95 ± 51 g·day−1, with the majority of climbers meeting their target intake of 88 ± 21 g (p = 0.580). Seventy-three percent of climbers consumed below their target dietary fat intake (target = 90 ± 21 g·day−1; actual = 69 ± 20 g·day−1) (p = 0.001). Average EAT-26 scores were 5.3 ± 4.1, indicating minimal risk of disordered eating attitudes/behaviors. There were no significant differences in boulderers vs. top rope climbers for energy/macronutrient intake, BMI, and EAT-26 score. There were no associations between energy intake and EAT-26 score (R2 = 0.245, p = 0.271) or climbing ability and EAT-26 score (R2 = p = 0.217). These data suggest that, with the exception of dietary protein intake, adolescent climbers fail to meet target dietary intakes, and exhibit minimal risk of disordered eating

Clusters in Various Cosmological Models: Abundance and Evolution

The combination of measurements of the local abundance of rich clusters of galaxies and its evolution to higher redshift offers the possibility of a direct measurement of $\Omega_0$ with little contribution from other cosmological parameters. We investigate the significance of recent claims that this evolution indicates that $\Omega_0$ must be small. The most recent cluster velocity dispersion function from a compilation including the ESO Northern Abell Cluster Survey (ENACS) results in a significantly higher normalization for models, corresponding to $\sigma_8\approx 0.6$ for $\Omega_0=1$, compared to the Eke, Cole, & Frenk result of $\sigma_8=0.52\pm 0.04$. Using the ENACS data for a $z=0$ calibration results in strong evolution in the abundance of clusters, and we find that the velocity dispersion function is consistent with $\Omega_0=1$. The results are dependent upon the choice and analysis of low-redshift and high-redshift data, so at present, the data is not good enough to determine $\Omega_0$ unambiguously.Comment: 4 pages Latex using sprocl.sty, 1 figure. To appear in Proceedings of 12th Potsdam Cosmology Workshop, "Large-Scale Structure: Tracks and Traces" Sept. 15-19, 199

Past Tense Formation in Williams Syndrome

It has been claimed that in the language systems of people with Williams syndrome (WS), syntax is intact but lexical memory is impaired. Evidence has come from past tense elicitation tasks with a small number of participants where individuals with WS are said to have a specific deficit in forming irregular past tenses. However, typically developing children also show poorer performance on irregulars than regulars in these tasks, and one of the central features of WS language development is that it is delayed. We compared the performance of 21 participants with WS on two past tense elicitation tasks with that of four typically developing control groups, at ages 6, 8, 10, and adult. When verbal mental age was controlled for, participants in the WS group displayed no selective deficit in irregular past tense performance. However, there was evidence for lower levels of generalisation to novel strings. This is consistent with the hypothesis that the WS language system is delayed because it has developed under different constraints, constraints that perhaps include atypical phonological representations. The results are discussed in relation to dual-mechanism and connectionist computational models of language development, and to the possible differential weight given to phonology versus semantics in WS development

Phreddie\u27s great adventure

Phreddie\u27s great adventur

Performance of lateral flow device and galactomannan for the detection of Aspergillus species in bronchoalveolar fluid of patients at risk for invasive pulmonary aspergillosis

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/111755/1/myc12327.pd

Epidural Hematoma Following Cervical Spine Surgery.

STUDY DESIGN: A multicentered retrospective case series. OBJECTIVE: To determine the incidence and circumstances surrounding the development of a symptomatic postoperative epidural hematoma in the cervical spine. METHODS: Patients who underwent cervical spine surgery between January 1, 2005, and December 31, 2011, at 23 institutions were reviewed, and all patients who developed an epidural hematoma were identified. RESULTS: A total of 16 582 cervical spine surgeries were identified, and 15 patients developed a postoperative epidural hematoma, for a total incidence of 0.090%. Substantial variation between institutions was noted, with 11 sites reporting no epidural hematomas, and 1 site reporting an incidence of 0.76%. All patients initially presented with a neurologic deficit. Nine patients had complete resolution of the neurologic deficit after hematoma evacuation; however 2 of the 3 patients (66%) who had a delay in the diagnosis of the epidural hematoma had residual neurologic deficits compared to only 4 of the 12 patients (33%) who had no delay in the diagnosis or treatment (P = .53). Additionally, the patients who experienced a postoperative epidural hematoma did not experience any significant improvement in health-related quality-of-life metrics as a result of the index procedure at final follow-up evaluation. CONCLUSION: This is the largest series to date to analyze the incidence of an epidural hematoma following cervical spine surgery, and this study suggest that an epidural hematoma occurs in approximately 1 out of 1000 cervical spine surgeries. Prompt diagnosis and treatment may improve the chance of making a complete neurologic recovery, but patients who develop this complication do not show improvements in the health-related quality-of-life measurements

C5 Palsy After Cervical Spine Surgery: A Multicenter Retrospective Review of 59 Cases.

STUDY DESIGN: A multicenter, retrospective review of C5 palsy after cervical spine surgery. OBJECTIVE: Postoperative C5 palsy is a known complication of cervical decompressive spinal surgery. The goal of this study was to review the incidence, patient characteristics, and outcome of C5 palsy in patients undergoing cervical spine surgery. METHODS: We conducted a multicenter, retrospective review of 13 946 patients across 21 centers who received cervical spine surgery (levels C2 to C7) between January 1, 2005, and December 31, 2011, inclusive. P values were calculated using 2-sample t test for continuous variables and χ(2) tests or Fisher exact tests for categorical variables. RESULTS: Of the 13 946 cases reviewed, 59 patients experienced a postoperative C5 palsy. The incidence rate across the 21 sites ranged from 0% to 2.5%. At most recent follow-up, 32 patients reported complete resolution of symptoms (54.2%), 15 had symptoms resolve with residual effects (25.4%), 10 patients did not recover (17.0%), and 2 were lost to follow-up (3.4%). CONCLUSION: C5 palsy occurred in all surgical approaches and across a variety of diagnoses. The majority of patients had full recovery or recovery with residual effects. This study represents the largest series of North American patients reviewed to date

Activating WASP mutations associated with X-linked neutropenia result in enhanced actin polymerization, altered cytoskeletal responses, and genomic instability in lymphocytes

X-linked neutropenia (XLN) is caused by activating mutations in the Wiskott-Aldrich syndrome protein (WASP) that result in aberrant autoinhibition. Although patients with XLN appear to have only defects in myeloid lineages, we hypothesized that activating mutations of WASP are likely to affect the immune system more broadly. We generated mouse models to assess the role of activating WASP mutations associated with XLN (XLN-WASP) in lymphocytes. XLN-WASP is expressed stably in B and T cells and induces a marked increase in polymerized actin. XLN-WASP–expressing B and T cells migrate toward chemokines but fail to adhere normally. In marked contrast to WASP-deficient cells, XLN-WASP–expressing T cells proliferate normally in response to cell-surface receptor activation. However, XLN-WASP–expressing B cells fail to proliferate and secrete lower amounts of antibodies. Moreover, XLN-WASP expression in lymphocytes results in modestly increased apoptosis associated with increased genomic instability. These data indicate that there are unique requirements for the presence and activation status of WASP in B and T cells and that WASP-activating mutations interfere with lymphocyte cell survival and genomic stability

Clinical and biochemical characterization of four patients with mutations in ECHS1

Short-chain enoyl-CoA hydratase (SCEH, encoded by ECHS1) catalyzes hydration of 2-trans-enoyl-CoAs to 3(S)-hydroxy-acyl-CoAs. SCEH has a broad substrate specificity and is believed to play an important role in mitochondrial fatty acid oxidation and in the metabolism of branched-chain amino acids. Recently, the first patients with SCEH deficiency have been reported revealing only a defect in valine catabolism. We investigated the role of SCEH in fatty acid and branched-chain amino acid metabolism in four newly identified patients. In addition, because of the Leigh-like presentation, we studied enzymes involved in bioenergetics. Metabolite, enzymatic, protein and genetic analyses were performed in four patients, including two siblings. Palmitate loading studies in fibroblasts were performed to study mitochondrial β-oxidation. In addition, enoyl-CoA hydratase activity was measured with crotonyl-CoA, methacrylyl-CoA, tiglyl-CoA and 3-methylcrotonyl-CoA both in fibroblasts and liver to further study the role of SCEH in different metabolic pathways. Analyses of pyruvate dehydrogenase and respiratory chain complexes were performed in multiple tissues of two patients. All patients were either homozygous or compound heterozygous for mutations in the ECHS1 gene, had markedly reduced SCEH enzymatic activity and protein level in fibroblasts. All patients presented with lactic acidosis. The first two patients presented with vacuolating leukoencephalopathy and basal ganglia abnormalities. The third patient showed a slow neurodegenerative condition with global brain atrophy and the fourth patient showed Leigh-like lesions with a single episode of metabolic acidosis. Clinical picture and metabolite analysis were not consistent with a mitochondrial fatty acid oxidation disorder, which was supported by the normal palmitate loading test in fibroblasts. Patient fibroblasts displayed deficient hydratase activity with different substrates tested. Pyruvate dehydrogenase activity was markedly reduced in particular in muscle from the most severely affected patients, which was caused by reduced expression of E2 protein, whereas E2 mRNA was increased. Despite its activity towards substrates from different metabolic pathways, SCEH appears to be only crucial in valine metabolism, but not in isoleucine metabolism, and only of limited importance for mitochondrial fatty acid oxidation. In severely affected patients SCEH deficiency can cause a secondary pyruvate dehydrogenase deficiency contributing to the clinical presentatio