NOREC, an improved disaster communications network for Alaska.
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Biomedical subjects
Publications and source records attributed to J K Johnson.
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Progressive declines in memory function accompany normal aging, mild cognitive impairment (MCI), and Alzheimer's disease (AD). Neuropathological studies suggest that damage to neurons providing connections between cortical areas may contribute to memory impairments in AD. Because AD develops slowly, similar neuropathological changes, to a lesser degree, may be present in MCI and some asymptomatic elderly subjects. In this study we tested the hypothesis that corticocortical interactions between sensory regions are impaired in aging, MCI, and AD, as compared with young subjects. When sensory cortical evoked potentials are elicited by pairs of stimuli the amplitudes of potentials to the second stimulus are attenuated. Corticocortical interactions were assessed by presenting stimulus pairs in different modalities (auditory/visual). There were significant group differences in the degree that a visual stimulus attenuated subsequent auditory potentials (young > healthy elderly > MCI > AD). Control experiments indicated equivalent amplitude reductions for all groups to the second stimulus for stimulus pairs having the same modality. These findings are compatible with progressive declines in corticocortical processing in aging, MCI, and AD.
The objective of this study was to determine when the retina, lateral geniculate nucleus (LGN), and striate cortex first send out axons, and first connect with each other, during embryonic development in the ferret. Specifically, we were interested in the timing relationship between axon outgrowth and known temporal patterns of neurogenesis in the LGN and striate cortex. Ferrets (Mustela putorius furo) were selected for study because of their immature developmental state in late gestation and relatively large litters. We examined axon outgrowth from the retina, and anlagen of presumptive LGN and striate cortex between embryonic day 21-30 (E21-E30) using in situ inoculations of two fluorescent lipophilic dyes, DiI and DiA. DiI inoculations were made into the cortex and contralateral thalamus, and DiA inoculations were made into the contralateral eye. Retinal axon termination zones in the diencephalon following the DiA inoculations were used to validate the location of the LGN. Visual cortex and LGN neurogenesis begins at E20 in ferrets. No axon outgrowth could be documented from retina or anlagen of striate cortex and LGN until E24. At E24 some retinal axons reach and cross the chiasm, cortical axons extend some distance within the cortical radiations, and thalamic axons are within the internal capsule. Retinogeniculate, geniculocortical, and corticogeniculate axons extend to their target structures by E27, as evidenced by retrograde labeling in cells of origin. These data suggest that in the ferret retina, and developing LGN and striate cortex, (1) axon outgrowth from each visual area begins within 24-h of each other, after neurogenesis has begun at the source but before it is complete in the target; (2) axons may be generated before parent cell bodies have completed migration; and (3) arriving axons are in a position to influence target structures almost from their inception.
Three dogs treated for systemic blastomycosis with intravenous amphotericin B (one case) or amphotericin B lipid complex (two cases) developed mild to severe calcinosis cutis two to six weeks after the initiation of treatment. Abnormalities in serum calcium and phosphorus during treatment for blastomycosis or at the time of diagnosis of calcinosis cutis were slight or absent. The calcification was not associated with lesions of cutaneous blastomycosis. Calcification was limited to the skin in two cases and may have also involved the kidneys in one. The calcinosis cutis resolved completely in all three dogs with no (two cases) or only palliative (one case) therapy.
This study compared ampicillin/sulbactam plus probenecid with ceftriaxone for treatment of uncomplicated gonorrhea. Of the 297 men and women who were enrolled and randomized to receive either ampicillin/sulbactam (1.0 g/0.5 g) with probenecid (1 g) or ceftriaxone (0.25 g), 274 patients were evaluable. Both ampicillin/sulbactam and ceftriaxone were administered by intramuscular injections. Patients were gonococcal contacts, had positive culture results for Neisseria gonorrhoeae, or had clinical evidence of gonorrhea. Specimens for gonococcal cultures were collected from the cervix (female patients), urethra, rectum, and pharynx at pretreatment and test-of-cure visits. The presence of N. gonorrhoeae and a test-of-cure visit were required for drug efficacy analysis. Of the 274 evaluable patients, 195 (71.2%) had positive culture results for N. gonorrhoeae. Cure was achieved in 93 (94.9%) of 98 patients receiving ampicillin/sulbactam with probenecid and in 96 (99.0%) of 97 patients receiving ceftriaxone. Penicillinase-producing N. gonorrhoeae strains were found in 21 (10.8%) patients; these were eradicated by either ampicillin/sulbactam with probenecid (N = 9) or ceftriaxone (N = 12). Overall, the two drug regimens were very well tolerated and no serious adverse effects were noted. Ampicillin/sulbactam with probenecid may be useful as single-dose therapy in patients with uncomplicated genitorectal gonorrhea.
3,4-diaminopyridine was evaluated for its ability to improve muscle strength, respiratory function and electromyographic compound muscle action potentials in human botulism. In a double blind, placebo controlled study, 3,4-diaminopyridine failed to improve these parameters in a 31-year old patient with severe food-borne type A botulism. The addition of an anti-cholinesterase medication to the 3,4-diaminopyridine did not add any benefit. Lack of clinical improvement from 3,4-diaminopyridine in this patient differed from some reports of benefit in animals experimentally poisoned with type A botulinum toxin.
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Medication of broilers with arprinocid [9-(2-chloro-6-fluorophenylmethyl)-9H-purine-6-amine] gave protection against the effects of coccidiosis in both battery and floor-pen trials. In battery trials, efficacy was tested on single-species inoculations of Eimeria acervulina, E. mivati, E. necatrix, E. maxima, E. Brunetti, and E. tenella. Two strains of each species recently recovered from the field, were tested separately. In floor-pen trials, all six species, both field and laboratory strains, were used as a mixed infection. In batteries, 60 and 70 ppm essentially eliminated coccidiosis-induced mortality and weight depression. Effects of 50 ppm on weight gain were variable. The effectiveness of different medication levels varied between strains within a species. In floor-pen trials, 40, 60, or 80 ppm was effective in controlling mortality and weight depression, and increasing feel-conversion ratios. All levels were significantly as effective as monensin in protecting against coccidiosis. With severe exposure to coccidia, 60 and 80 ppm gave significantly lower lesion socres than did 40 ppm of arprinocid or 120 ppm monensin.
The suprachiasmatic nucleus (SCN) receives a direct photic projection from the retina, the retinohypothalamic tract (RHT), and an indirect photic projection from the intergeniculate leaflet of the thalamus, the geniculohypothalamic tract (GHT). The primary neurochemical signal in the GHT appears to be neuropeptide Y (NPY), and several lines of evidence indicate that NPY may be involved in determining the response of the SCN to light. The purpose of the present study was (i) to localize NPY binding sites in the hamster SCN and to compare the distribution of these binding sites with the terminal field of the RHT and (ii) to determine if SCN levels of NPY binding change during the day. RHT fibers, defined using the carbocyanine dye DiI, were localized primarily within the ventrolateral region of the SCN. The distribution of NPY receptors, as visualized by 125I-peptide YY (PYY) binding, overlapped the projection field of the RHT. Specific binding of 125I-PYY was significantly greater in the ventrolateral SCN than in the medial SCN. To determine whether NPY binding changes during the day, the levels of 125I-PYY in the SCN were determined 4 h before the onset of darkness, 1 h before the onset of darkness and 2 h after the onset of darkness in hamsters housed in a 14:10 light-dark cycle. The levels of binding at 4 and 1 h before dark onset were significantly lower than 2 h after the onset of darkness. In contrast, no significant differences were observed in 125I-PYY binding over these same sampling intervals in either the medial preoptic area or the lateral hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)