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Neurobiologists address neural structure, development, and function at the level of "macrocircuits" (how different brain compartments are interconnected; what overall pattern of activity they produce) and at the level of "microcircuits" (how connectivity and physiology of individual neurons and their processes within a compartment determine the functional output of this compartment). Work in our lab aims at reconstructing the developing Drosophila brain at both levels. Macrocircuits can be approached conveniently by reconstructing the pattern of brain lineages, which form groups of neurons whose projections form cohesive fascicles interconnecting the compartments of the larval and adult brain. The reconstruction of microcircuits requires serial section electron microscopy, due to the small size of terminal neuronal processes and their synaptic contacts. Because of the amount of labor that traditionally comes with this approach, very little is known about microcircuitry in brains across the animal kingdom. Many of the problems of serial electron microscopy reconstruction are now solvable with digital image recording and specialized software for both image acquisition and postprocessing. In this chapter, we introduce our efforts to reconstruct the small Drosophila larval brain and discuss our results in light of the published data on neuropile ultrastructure in other animal taxa.

This study investigated the relationship between cognitive impairment and physical function in acute stroke patients without communication disorders. Sixteen stroke patients were assessed for cognitive status, sitting balance and gait ability on admission to an acute hospital. Eleven were subsequently assessed at discharge from the acute facility and at six weeks post-stroke. Cognitive status as measured at admission was not correlated with physical function at admission, discharge or at six weeks post-stroke. Nevertheless, cognitive status at admission was positively correlated with cognition at discharge (rho= 0.76) and 6 weeks post-stroke (rho=0.69). Cognition was not found to be related to sitting balance or gait performance at any of the tests. Sitting balance at 48 hours post-stroke was correlated with sitting balance at discharge (rho=0.68). Moreover gait performance at admission (on average 48 hours post-stroke) was correlated with gait at discharge and 6 weeks post-stroke. Although cognition, sitting balance and gait performance all improved during the first six weeks post-stroke, no relationships were found between cognitive impairment and either balance or gait at 48 hours post-stroke, hospital discharge or at 6 weeks post-stroke. Thus, in this small sample, no evidence was provided that poor cognition was associated with poor physical recovery.

One-hundred-and-twenty healthy volunteers (ranging in age from 10 to 25 years), completed a questionnaire concerning the type and amount of regular activity and history of low back pain. There were 41 who participated in at least 6 hours of dance per week and 79 non-dancers. Computer-based analysis of videotape records examined sagittal standing posture and thoracolumbar flexion-extension mobility On average, dancers undertook 19 h/wk more regular activity (p = 0.0001), were lighter by 7 kg (p = 0.001), had straighter standing postures (p < 0.001) and greater thoracic and lumbar sagittal excursions (by 23° and 9°, respectively) (p < 0.01). One or more episodes of back pain of at least two days duration was experienced by 24% of all subjects in the past year, and 18% recalled at least one episode of back pain in earlier years. Dancers experienced significantly more back pain in the last year, and in earlier years, compared to non-dancers (37% versus 18% and 24% versus 14%, respectively), but the relative incidence of back pain expressed as hours of activity per incident was less for dancers (1:20 hours) than non-dancers (1:5 hours). The non-dancers who experienced pain had more flexed lumbar spine standing postures (p = 0.01), and a direct correlation between lumbar spine excursion and severity of the worst pain episode over the previous year (p = 0.02).

It has previously been shown that the mitochondrial DNA (mtDNA) of Saccharomyces cerevisiae becomes thermosensitive due to the inactivation of the mitochondrial DNA helicase gene, PIF1. A suppressor of this thermosensitive phenotype was isolated from a wild-type plasmid library by transforming a pif1 null strain to growth on glycerol at the non-permissive temperature. This suppressor is a nuclear gene encoding a 135 amino acid protein that is itself essential for mtDNA replication; cells lacking this gene are totally devoid of mtDNA. We therefore named this gene RIM1 for replication in mitochondria. The primary structure of the RIM1 protein is homologous to the single-stranded DNA binding protein (SSB) from Escherichia coli and to the mitochondrial SSB from Xenopus laevis. The mature RIM1 gene product has been purified from yeast extracts using a DNA unwinding assay dependent upon the DNA helicase activity of SV40 T-antigen. Direct amino acid sequencing of the protein reveals that RIM1 is a previously uncharacterized SSB. Antibodies against this purified protein localize RIM1 to mitochondria. The SSB encoded by RIM1 is therefore an essential component of the yeast mtDNA replication apparatus.