Accuracy assessment of methods for determining hip movement in seated cycling

The goal of this research was to examine the accuracy of three methods used to indicate the hip joint center (HJC) in seated steady-state cycling. Two of the methods have been used in previous studies of cycling biomechanics and included tracking a marker placed over the superior aspect of the greater trochanter, a location that estimates the center of rotation of the hip joint, and assuming that the hip is fixed. The third method was new and utilized an anthropometric relationship to determine the hip joint location from a marker placed over the anterior-superior iliac spine. To perform a comparative analysis of errors inherent in the three methods, a standard method which located the true hip joint center was developed. The standard method involved establishing a pelvis-fixed coordinate system using a triad of video markers attached to an intracortical pin. Three-dimensional motion analysis quantified the true hip joint center position coordinates. To provide data for the comparative analysis, the intracortical pin was anchored to a single subject who pedaled at nine cadence-workrate combinations while data for all four methods were simultaneously recorded. At all cadence-workrate combinations the new method was more accurate than the trochanter method with movement errors lower by a factor of 2 in the vertical direction and a factor of 3 in the horizontal direction. Relative to the errors introduced by the fixed hip assumption, the new method was also generally more accurate by at least a factor of 2 in the horizontal direction and had comparable accuracy in the vertical direction. For computed kinetic quantities, the new method most accurately indicated hip joint force power but the fixed hip method most accurately indicated the work produced by the hip joint force over the crank cycle.     

FOS is induced by singing in distinct neuronal populations in a motor network

The acute and subacute effects of intracerebroventricularly (ICV) administered nerve growth factor (NGF) or brain-derived neurotrophic factor (BDNF) on locomotor activity were evaluated in awake adult rats. Immediately after ICV injection through an implanted cannula, locomotor activity was measured by a computerized system using infrared photocells, which allowed us to record locomotion, motility, and rearing simultaneously. A single dose of 5 microg mouse beta-NGF produced significant increases in horizontal ambulatory components of locomotor activity (locomotion and motility), but not vertical movement (rearing) 30-45 min after ICV administration. These increases lasted for at least 3-4 h. Systemic injection of 2.0 mg/kg mecamylamine, a central nicotinic receptor antagonist, inhibited the hyperactivity induced by NGF. Systemic injection of 0.5 mg/kg scopolamine, a muscarinic receptor antagonist, did not interfere with the NGF effects. Thus, while scopolamine induced marked increases in all three measures of behavior in both NGF and cytochrome-c-treated animals, locomotion and motility remained significantly higher in the NGF group. Immunohistochemistry demonstrated that NGF diffused readily from the ventricular space into brain parenchyma on the injected side and could be visualized 1 h after ICV injection. These results suggest that ICV administration of NGF increases locomotor activity by inducing acetylcholine release, and that nicotinic receptors are involved in the hyperactivity induced by NGF. ICV administration of 5 microg recombinant human BDNF had no significant effect on locomotor activity during the 0- to 4-h period after ICV injection. However, it produced significant decreases in locomotion, motility, and rearing 24-26 h later. Hence ICV administration of BDNF has entirely different effects on animal behavior from those evoked by NGF. While NGF elicits increases in ambulatory behavior within hours, BDNF causes delayed decreases in ambulatory behavior.     

Bovine IgG2a antibodies to Haemophilus somnus and allotype expression

AIMS/BACKGROUND: To characterise clinically a large kindred segregating retinitis pigmentosa and sensorineural hearing impairment in an autosomal dominant pattern and perform genetic linkage studies in this family. Extensive linkage analysis in this family had previously excluded the majority of loci shown to be involved in the aetiologies of RP, some other forms of inherited retinal degeneration, and inherited deafness. METHODS: Members of the family were subjected to detailed ophthalmic and audiological assessment. In addition, some family members underwent skeletal muscle biopsy, electromyography, and electrocardiography. Linkage analysis using anonymous microsatellite markers was performed on DNA samples from all living members of the pedigree. RESULTS: Patients in this kindred have a retinopathy typical of retinitis pigmentosa in addition to a hearing impairment. Those members of the pedigree examined demonstrated a subclinical myopathy, as evidence by abnormal skeletal muscle histology, electromyography, and electrocardiography. LOD scores of Zmax = 3.75 (theta = 0.10), Zmax = 3.41 (theta = 0.10), and Zmax = 3.25 (theta = 0.15) respectively were obtained with the markers D9S118, D9S121, and ASS, located on chromosome 9q34-qter, suggesting that the causative gene in this family may lie on the long arm (q) of chromosome 9. CONCLUSIONS: These data indicate that the gene responsible for the phenotype in this kindred is located on chromosome 9 q. These data, together with evidence that a murine deafness gene is located in a syntenic area of the mouse genome, should direct the research community to consider this area as a candidate region for retinopathy and/or deafness genes.     

The gene encoding human glutathione synthetase (GSS) maps to the long arm of chromosome 20 at band 11.2

Two forms of glutathione synthetase deficiency have been described. While one form is mild, causing hemolytic anemia, the other more severe form causes 5-oxo-prolinuria with secondary neurological involvement. Despite the existence of two deficiency phenotypes, Southern blots hybridized with a glutathione synthetase cDNA suggest that there is a single glutathione synthetase gene in the human genome. Analysis of somatic cell hybrids showed the human glutathione synthetase gene (GSS) to be located on chromosome 20, and this assignment has been refined to subband 20q11.2 using in situ hybridization.     

The diversity gain of transmit diversity in wireless systems withRayleigh fading

In this paper, we study the ability of transmit diversity to provide diversity benefit to a receiver in a Rayleigh fading environment. With transmit diversity, multiple antennas transmit delayed versions of a signal to create frequency-selective fading at a single antenna at the receiver, which uses equalization to obtain diversity gain against fading. We use Monte Carlo simulation to study transmit diversity for the case of independent Rayleigh fading from each transmit antenna to the receive antenna and maximum likelihood sequence estimation for equalization at the receiver. Our results show that transmit diversity with M transmit antennas provides a diversity gain within 0.1 dB of that with M receive antennas for any number of antennas. Thus, we can obtain the same diversity benefit at the remotes and base stations using multiple base-station antennas only