Abstract Not Available.

Intramuscular EMG of the lateral pterygoid muscles, surface EMG of the temporalis and masseter muscles, electrogoniometry and force measurements of the TMJ were synchronously used to investigate the biomechanical role of the two portions of the lateral pterygoid muscle in relation to internal derangement (ID) of the temporomandibular joint (TMJ). This study dealt with the EMG analysis of five static conditions: resting, resisted protraction, maximum voluntary contraction (MVC) in opening, in molar and incisor clenching of TMJ ID and control subjects. The analysis of variance results of the integrated linear envelop (LE) EMG showed no significant differences between the two groups. The integrated LE EMG of the SLP was significantly lower in the TMJ group during molar clenching (104$\mu$V $\pm$ 60.0 over 159$\mu$V $\pm$ 68.8 for a p =.020). The SLP seemed to have lost its discal stabilizing function during clenching. The integrated LE EMG signals of the ILP were significantly higher in the TMJ ID group during rest, resisted protraction and incisor clenching (p =.029, p =.046, p =.031 respectively). The ILP muscle has probably adapted to control the inner joint instability while continuing its own actions. The results of the isometric forces showed that TMJ ID subjects exhibited significantly lower molar bite forces (297.1N over 419N, p =.042) confirming that they have less muscle strength and tissue tolerance than subjects with healthy masticatory muscle system. Incisor bite forces, however, showed a tendency to be higher in the TMJ ID group (233N over 180.5N, p =.168), possibly resulting from the training of a protracted bite and/or hyperactivity of the ILP associated with ID. Therefore a neuromuscular adaptation could be occurring in TMJ ID masticatory system affecting muscular actions and forces. (Abstract shortened by UMI.)

This study determined whether lifts rated as acceptable by the 1991 NIOSH equation calculations elicited myoelectric amplitudes of the erector spinae musculature (ES) within acceptable muscular load limits for continuous repetitive lifting tasks. Ten male subjects had surface electrodes placed bilaterally along the spine at levels T9, L1 and L3, 4 cm, 9 cm nd 3 cm lateral to the midline, respectively. Each subject performed eight trials of five lifting conditions that were used to examine the horizontal factor (HF) and asymmetrical factor (AF) of the 1991 NIOSH equation. All lifts were ordered randomly and initiated and terminated in a standing position. The lifting motion was unconstrained and incorporated a "flatback", free-style lifting technique. EMG data were collected and linear envelopes (LE) were ensemble averaged across subject trials for each condition and normalized to a maximum voluntary contraction (MVC). Subject LE EMGs were ensemble averaged to generate condition LE EMG averages and subsequently converted to amplitude probability distribution functions (APDF). Percent MVC values from the APDF curves were compared to muscular load limits. A three-way, repeated measures, mixed model analysis of variance determined significant main effects for conditions, electrode placements and probability levels of the APDFs. There was general agreement between the 1991 NIOSH equation and muscular load limits. Bilateral T9 ES often exceeded "static" muscular loads and right L3 often exceeded "static" and "median" muscular loads. There was a significant (p 0.01) difference for each main effect. The APDF EMG analysis was more sensitive to differentiating between conditions than the 1991 NIOSH equation. Phasic and amplitude EMG analysis of the ES for occupational lifting tasks could be best represented by the musculature at L3, 3 cm lateral to the midline.

Research on the mechanisms by which the brain codes, understands, and remembers reward has focused on sites lying along the medial forebrain bundle (MFB). Regions more anterior to the MFB, such as the medial prefrontal cortex (MPFC) and caudate-putamen (CPu), have received little attention in this regard. Consequently, the first experiment was to determine the distribution of sites in the MPFC and CPu that support intracranial self-stimulation. Overall, 255 MPFC and 187 CPu individual sites were evaluated in 67 animals using moveable electrodes; only 11% of the examined areas showed reliable self-stimulation, which was in most cases accompanied by overt seizures. Most positive sites were clustered in the ventromedial aspects of the MPFC and CPu. Charge values obtained for both regions were widely distributed and ranged from 0.68 to 1.63 $\mu$C across sites, values in line with those reported for MFB sites. One of the problems encountered in this study was the slow acquisition of MPFC self-stimulation. In order to overcome this obstacle, some subjects were implanted with two electrodes, one aimed at the MPFC, and the other at the CPu, ventral tegmental area, or lateral hypothalamus. Once stable thresholds were obtained at the extra MPFC sites, self-stimulation was then evaluated at the MPFC site. Only animals with CPu placements showed transference of this behaviour to the MPFC, suggesting that these two regions might form part of the same reward substrate, a view that has anatomical and electrophysiological support. The next step was to estimate the excitability cycles that characterize MPFC and CPu reward fibers. Using the behavioural adaptation of the refractory period test, the range of recovery from refractoriness was determined to span from 0.8 to 5.4 ms for the CPu and 1.4 to 7.9 ms for the MPFC. These values tend to be longer than the ones typically obtained at MFB self-stimulation sites. One interpretation of the overlap in these estimates is that these regions constitute two separate locations along the same axonal bundle. This hypothesis was investigated in the third experiment using the behavioural collision technique. Nine ipsilateral pairs of CPu and MPFC sites were evaluated for axonal connectivity, four of which showed a pattern consistent with the interpretation that at least a subset of fibers course between the MPFC and CPu. The conduction velocity estimates of these were calculated to be between 0.2 and 1.8 m/s, values that are much less than the estimates reported for the MFB and consistent with the activation of thin, unmyelinated axons. The anatomical relationship between the MPFC and CPu is characterized by direct corticostriatal projections, some of which use glutamate as a neurotransmitter. There is also some evidence that dopaminergic fibers make direct contact with these descending neurons. The behavioural estimates of refractoriness and the conduction velocities obtained here closely match those found electrophysiologically for dopaminergic and glutamatergic fibers. Given this background, a model of a possible neuronal interaction between the MPFC and CPu reward regions is proposed to account for the findings reported here, suggesting the involvement of these neurotransmitter systems in mediating the rewarding effects of MPFC and CPu stimulation.

Abstract not available.

Abstract not available.

Abstract not available.

I have conducted sequence analysis of a zebrafish cDNA that encodes the protein DNA (5-cytosine) methyltransferase. I show that during development transcription of this zebrafish DNA methyltransferase gene is most high at blastula where it is ubiquitously expressed. At 24 hours of development, highest expression is observed in the brain, neural tube, eyes, and differentiating somites. To further assess the role of DNA methylation during development, I treated zebrafish embryos with 5-aza-cytidine (5-azaC), a nucleotide analog known to induce cellular differentiation and DNA hypomethylation in mammalian cell cultures. Treatments with 5-azaC during blastula and early gastrula caused a perturbation of the body axis resulting in loss of tail, and loss or abnormal development of the somites. Histological sections and in situ hybridization revealed whole or partial loss of a differentiated notochord and mid-line muscle in treated embryos. There was loss of expression of no tail in the notochord and eng in muscle-pioneer cells at 24 hours. When examined during gastrulation, 5-azaC treated embryos has a shortened and thickened axial mesoderm. DNA analysis on 5-azaC-treated embryos indicated an overall decrease in DNA methylation when compared to untreated controls. Embryos treated with 6-aza-cytidine, a cytidine analog not known to affect DNA methylation, showed neither abnormal development nor hypomethylation. Our findings suggest that normal DNA methylation is required for proper differentiation of dorsal mesoderm and pattern development of the dorsal-ventral body axis.

No description available.

No description available.