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Biomedical subjects

S Gibson

Publications and source records attributed to S Gibson.

At least 163 records · Page 9Linked to original sources

Susceptibility of nonhuman primate species to infection by simian rotavirus SA-11.

Enzyme-linked immunosorbent assay examination of sera from three nonhuman primate species demonstrated the presence of antibody reacting with simian rotavirus SA-11 and calf rotavirus C486. The occurrence of this antibody in sera from adult, wild-caught animals suggests natural rotovirus infection. The occurrence of antibody was highest in the chimpanzee and declined, respectively, in the rhesus macaque and in the squirrel monkey. Inoculation of three infant rhesus macaques, a nursery-reared chimpanzee, and a cesarian-derived nursery-reared baboon with SA-11 virus resulted in enteric infection, with virus excretion beginning 48 to 72 hours after oral administration of the virus. Clinical disease, as manifested by diarrhea, was observed only in the chimpanzee. Inoculation of ten squirrel monkeys, from 30 to 191 days old, induced infection only in the monkey inoculated at 30 days of age. This monkey became ill within 48 hours after viral administration and was euthanatized. Necropsy demonstrated a generalized infection, with virus recovered from lung, liver, kidney, spleen, and intestine. The remaining nine inoculated squirrel monkeys failed to develop enteric infection and did not respond with antibody to SA-11 virus.

Animals↗

Training for practice.

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Education, Nursing, Continuing↗

L-Arabinose-ornithine-Irgasan medium for differentiating Serratia species.

A semisolid medium (designated Serratia differentiation medium) containing L-arabinose, ornithine, and selective inhibitor was used to differentiate three clinically encountered Serratia species. The inhibitor, Irgasan DP-300, was incorporated to eliminate false-positive reactions from most remaining Enterobacteriaceae. The suspected Serratia colony was inoculated as a stab into the medium. Serratia marcescens was indicated by a change in color from olive to purple following 18 h of incubation, whereas S. rubidaea (not listed in Bergey's Manual of Determinative Bacteriology) was indicated by a change to bright yellow. S. liquefaciens (described in Bergey's Manual of Determinative Bacteriology [8th ed., 1974] as Enterobacter liquefaciens) produced a small purple band at the top of the medium and a yellow or yellow-green butt. Absence of growth and color change following incubation indicates that the suspected colony is a non-Serratia. Thirty-six Serratia strains and 97 other Enterobacteriaceae and Pseudomonadaceae strains were tested. Two strains of the non-Serratia Enterobacteriaceae (one each of Citrobacter freundii and Proteus morganii) and two strains of Pseudomonas aeruginosa produced a color change in the medium. All of the Serratia strains tested were correctly identified using this medium, while 96% of the other species tested were inhibited.

Arabinose↗

Automated microbiological detection/identification system.

An automated, computerized system, the AutoMicrobic System, has been developed for the detection, enumeration, and identification of bacteria and yeasts in clinical specimens. The biological basis for the system resides in lyophilized, highly selective and specific media enclosed in wells of a disposable plastic cuvette; introduction of a suitable specimen rehydrates and inoculates the media in the wells. An automated optical system monitors, and the computer interprets, changes in the media, with enumeration and identification results automatically obtained in 13 h. Sixteen different selective media were developed and tested with a variety of seeded (simulated) and clinical specimens. The AutoMicrobic System has been extensively tested with urine specimens, using a urine test kit (Identi-Pak) that contains selective media for Escherichia coli, Proteus species, Pseudomonas aeruginosa, Klebsiella-Enterobacter species, Serratia species, Citrobacter freundii, group D enterococci, Staphylococcus aureus, and yeasts (Candida species and Torulopsis glabrata). The system has been tested with 3,370 seeded urine specimens and 1,486 clinical urines. Agreement with simultaneous conventional (manual) cultures, at levels of 70,000 colony-forming units per ml (or more), was 92% or better for seeded specimens; clinical specimens yielded results of 93% or better for all organisms except P. aeruginosa, where agreement was 86%. System expansion in progress includes antibiotic susceptibility testing and compatibility with most types of clinical specimens.

Bacteria↗

Cerebrospinal fluid levels of beta endorphin in painful and painless diabetic polyneuropathy.

beta endorphin (beta-EP) is an important modulator of central pain pathways. To examine whether changes in central production of beta-EP contribute to the pathogenesis of diabetic neuropathic pain, we compared the cerebrospinal fluid (CSF) levels of beta-EP and its precursor proopiomelanocortin (POMC) between 15 diabetic patients with chronic painful diabetic polyneuropathy, eight patients with severe painless diabetic neuropathy, and ten nondiabetic controls. Both peptides were measured by specific monoclonal antibody-based two-site immunoradiometric assays (IRMAs). In the diabetic patients with painful neuropathy, mean +/- SD CSF beta-EP concentrations (5.7 +/- 2.2 pmol/L) were comparable to those of the diabetic patients with painless neuropathy (6.0 +/- 2.3 pmol/L) and did not correlate with the severity of neuropathic pain. CSF beta-EP, but not POMC, concentrations were lower in the diabetic neuropathic patients overall (5.8 +/- 1.9 pmol/L) compared to the control subjects (7.6 +/- 2.2 pmol/L) (p < 0.05). CSF POMC showed no intergroup differences. However, POMC levels were 80-fold higher than those of beta-EP and should always be considered when interpreting immunoreactive beta-EP or other derivative peptide levels in CSF. We conclude that CSF beta-EP levels appear to be reduced in diabetic polyneuropathy but they do not relate to the presence of neuropathic pain. This might explain why opioid analgesics are of little, if any, help in alleviating diabetic neuropathic pain.

Cohort Studies↗