Measured and predicted resting energy expenditure in wheelchair rugby athletes

Objective: Report measured resting energy expenditure (REE) in wheelchair rugby athletes and evaluate agreement between REE and the prediction models of Chun, Cunningham, Harris-Benedict, Mifflin, Nightingale and Gorgey, and Owen.

Design: Cohort-based validation study.

Setting. Paralympic team training camp.

Participants: Fourteen internationally competitive athletes who play wheelchair rugby, 13 of whom had cervical spinal cord injuries (SCI).

Outcome Measures: A portable metabolic analyzer was used to measure REE following an overnight fast and dual-energy X-ray absorptiometry (DXA) was used to assess lean body mass for the prediction equations.

Results: REE in the current sample was 1735?±?257?kcal?×?day^?1 ranging from 1324 to 2068?kcal?×?day^{?1 Bhambhani Y. Physiology of wheelchair racing in athletes with spinal cord injury. Sports Med 2002;32(1):23–51.[Crossref], [PubMed], [Web of Science ®] , [Google Scholar]}. Bland–Altman analyses revealed negative mean bias but similar limits of agreement between measured REE and scores predicted by Chun, Cunningham, Mifflin, Nightingale and Gorgey, and Owen models in elite athletes who play wheelchair rugby.

Conclusion: Prediction models regressed on persons with and without SCI under-predicted REE of competitive wheelchair rugby athletes. This outcome may be explained by the higher REE/fat-free mass (FFM) ratio of current athletes compared to less active samples. Findings from the current study will help practitioners to determine nutrient intake needs on training days of varied intensity.     

Does a tensioning device pinned to the tibia improve knee anterior–posterior load‐displacement compared to manual tensioning of the graft following anterior cruciate ligament reconstruction? A cadaveric study of two tibial fixation devices

Devices that are pinned to the tibia to tension an anterior cruciate ligament (ACL) graft produce joint reaction loads that in turn can affect the maintenance of graft initial tension after tibial fixation and hence knee anterior-posterior (AP) load-displacement. However, the effect of these devices on AP load-displacement is unknown. Our objectives were to determine whether tensioning by device versus tensioning by hand causes differences in AP load-displacement and intraarticular graft tension for two commonly used tibial fixation devices: a bioresorbable interference screw and a WasherLoc. AP load-displacement and intraarticular graft tension were measured in 20 cadaveric knees using a custom arthrometer. An initial tension of 110 N was applied to a double-looped tendon graft with the knee at extension using a tensioning device pinned to the tibia and a simulated method of tensioning by hand. After inserting the tibial fixation device, the 134 N anterior limit (i.e., anterior position of the tibia with respect to the femur with a 134 N anterior force applied to the tibia) and 0 N posterior limit (i.e., AP position of the tibia relative to the femur with a 0 N force applied to the tibia) were measured with the knee in 25 degrees flexion. Intraarticular graft tension was measured at extension. These limits and intraarticular graft tension were also measured after cyclically loading the knee 300 times. Compared to a simulated method of tensioning by hand, tensioning with a device pinned to the tibia did not decrease the 134 N anterior limit and did not cause posterior tibial translation. However, intraarticular graft tension was maintained better with a tensioning device pinned to the tibia for the Washerloc, but not the interference screw. For two commonly used tibial fixation devices, a tensioning device pinned to the tibia does not improve AP load-displacement at 25 degrees flexion over tensioning by hand when the graft is tensioned at full extension, but does improve the maintenance of intraarticular graft tension for the Washerloc.     

Differential distribution of growth associated protein (GAP-43) in the motor nuclei of the adult rat conus medullaris

GAP-43 is normally produced by neurons during developmental growth and axonal regeneration, but it is also expressed in specific regions of the normal adult nervous system. We studied the protein expression of GAP-43 within the conus medullaris portion of the spinal cord in adult male rats. Immunohistochemistry for choline acetyltransferase (ChAT) was first performed to identify specific efferent autonomic and motor nuclei in lumbosacral segments of the spinal cord. Adjacent sections were then processed for GAP-43 immunoreactivity (IR). We show GAP-43 IR in the superficial portion of the dorsal horn, the intermediolateral nucleus, and the dorsal commissural tract. We also demonstrate a differential distribution of GAP-43 IR between different motor nuclei of the conus medullaris. Using densitometry, the most prominent GAP-43 IR was detected in the dorsolateral and dorsomedial motor nuclei, which represent the human Onufs nucleus homologue. Confocal microscopy of double immunofluorescent labeling for ChAT and GAP-43 demonstrate GAP-43 IR in the neuropil of the autonomic and motor nuclei, and many of the GAP-43 IR arbors are in close apposition with the efferent cholinergic neurons. We note that the efferent neurons of both the autonomic and somatic nuclei, which are ultimately responsible for the integrated normal control of the lower urinary tract, bowel and sexual functions, are heavily innervated by GAP-43 enriched projections. We speculate that these functionally related neurons retain a physiological GAP-43-associated synaptic plasticity throughout adult life.     

Interpersonal callousness, hyperactivity/impulsivity, inattention, and conduct problems as precursors to delinquency persistence in boys: a comparison of three grade-based cohorts.

Boys who exhibit interpersonal callousness (IC), hyperactivity/impulsivity (HI), inattention (IN), and conduct problems (CP) may be at risk for exhibiting persistent delinquent behavior. However, few studies have established the distinctiveness of these constructs or examined their relative contributions to the prediction of delinquent behavior across different developmental periods. This study explores these issues using boys from the youngest (1st grade, N = 849), middle (4th grade, N = 868), and oldest (7th grade, N = 856) cohorts of the Pittsburgh Youth Study. Confirmatory factor analysis indicates that the 4 constructs are related, yet independent, from childhood to adolescence. After controlling for the overlap among the constructs, CP significantly predicted delinquency persistence in the youngest cohort, whereas CP and IN predicted delinquency persistence in the middle cohort. IC uniquely predicted delinquency persistence for the oldest cohort. The results suggest that the saliency of specific predictors of delinquent behavior may change from childhood to adolescence.     

Supported planar bilayers in studies on immune cell adhesion and communication

Supported planar bilayers have been used extensively in immunology to study molecular interactions at interfaces as a model for cell-cell interaction. Examples include Fc receptor-mediated adhesion and signaling and formation of the immunological synapse between T cells and antigen-presenting cells. The advantage of the supported planar bilayer system is control of the bilayer composition and the optical advantages of imaging the cell-bilayer or bilayer-bilayer interface by various types of trans-, epi- and total internal reflection illumination. Supported planar bilayers are simple to form by liposome fusion and recent advances in micro- and nanotechnology greatly extend the power of supported bilayers to address key questions in immunology and cell biology.     

Myricetin as a Promising Molecule for the Treatment of Post-Ischemic Brain Neurodegeneration

The available drug therapy for post-ischemic neurodegeneration of the brain is symptomatic. This review provides an evaluation of possible dietary therapy for post-ischemic neurodegeneration with myricetin. The purpose of this review was to provide a comprehensive overview of what scientists have done regarding the benefits of myricetin in post-ischemic neurodegeneration. The data in this article contribute to a better understanding of the potential benefits of myricetin in the treatment of post-ischemic brain neurodegeneration, and inform physicians, scientists and patients, as well as their caregivers, about treatment options. Due to the pleiotropic properties of myricetin, including anti-amyloid, anti-phosphorylation of tau protein, anti-inflammatory, anti-oxidant and autophagous, as well as increasing acetylcholine, myricetin is a promising candidate for treatment after ischemia brain neurodegeneration with full-blown dementia. In this way, it may gain interest as a potential substance for the prophylaxis of the development of post-ischemic brain neurodegeneration. It is a safe substance, commercially available, inexpensive and registered as a pro-health product in the US and Europe. Taken together, the evidence available in the review on the therapeutic potential of myricetin provides helpful insight into the potential clinical utility of myricetin in treating neurodegenerative disorders with full-blown dementia. Therefore, myricetin may be a promising complementary agent in the future against the development of post-ischemic brain neurodegeneration. Indeed, there is a scientific rationale for the use of myricetin in the prevention and treatment of brain neurodegeneration caused by ischemia.     

Microtubules and mitosis]

The mitotic chromosome movements are discussed in relation with recent studies on tubulins, their assembly and disassembly, and the associated proteins. The role of contractile proteins in the mitotic spindle is considered, and also that of the calcium regulating protein (CDR) which has been demonstrated recently in the mitotic spindle. The study of more "primitive" mitoses underlines the differences between polar and chromosomal MT. The linear growth of the first, and the sliding movements of MT from opposing poles, explain the growth in length of the mitotic figure and the separation of chromosomes. The complex relations between various types of MT and the possibility of biochemical varieties of tubulins, are discussed.     

Variations in Prkdc and susceptibility to benzene-induced toxicity in mice.

Benzene, a carcinogen that induces chromosomal breaks, is strongly associated with leukemias in humans. Possible genetic determinants of benzene susceptibility include proteins involved in repair of benzene-induced DNA damage. The catalytic subunit of DNA-dependent protein kinase (DNA-PKcs), encoded by Prkdc, is one such protein. DNA-PKcs is involved in the nonhomologous end-joining (NHEJ) pathway of DNA double-strand break (DSB) repair. Here we compared the toxic effects of benzene on mice (C57BL/6 and 129/Sv) homozygous for the wild-type Prkdc allele and mice (129/SvJ) homozygous for a Prkdc functional polymorphism that leads to diminished DNA-PK activity and enhanced apoptosis in response to radiation-induced damage. Male and female mice were exposed to 0, 10, 50, or 100 ppm benzene for 6 h/d, 5 d/week for 2 weeks. Male mice were more susceptible to benzene toxicity compared with females. Hematotoxicity was evident in all male mice but was not seen in female mice. We observed similar, large increases in both micronucleated erythrocyte populations in all male mice. Female mice had smaller but significant increases in micronucleated cells. The p53-dependent response was induced in all strains and genders of mice following benzene exposure, as indicated by an increase in p21 mRNA levels in bone marrow that frequently corresponded with cell cycle arrest in G2/M. Prkdc does not appear to be a significant genetic susceptibility factor for acute benzene toxicity. Moreover, the role of NHEJ, mediated by DNA-PK, in restoring genomic integrity following benzene-induced DSB remains equivocal.