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Biomedical subjects

S K Tait

Publications and source records attributed to S K Tait.

5 recordsLinked to original sources
PubMed1984

Asymptomatic neonatal colonisation by Clostridium difficile.

In a prospective survey of infants born in a single maternity unit, asymptomatic faecal colonisation by Clostridium difficile occurred in 31 (47%) of 66 babies who provided a faecal sample during week one of life and at age 14 and 28 days, and in 46 (30.7%) of the total of 150 babies for whom at least one faecal sample was obtained during the month of study. There was no evidence for acquisition of the organism from the mother during delivery and colonisation was unrelated to the means of delivery, infant sex, means of feeding, duration of hospital stay, or antibiotic treatment. New colonisation occurred throughout the month of the study and further evidence for environmental acquisition was obtained by the finding of a similar strain of C difficile in 7 babies from one ward together with positive environmental cultures. Colonisation was frequently transient and occasionally intermittent; most infants kept the same strain during their period of carriage. Twenty two (47.8%) babies colonised by C difficile had low titres of cytopathic faecal toxin but none had symptomatic diarrhoea or features of necrotizing enterocolitis. The in vitro toxigenic potential of 57 toxigenic isolates from 36 babies was low and 12 babies carried non-toxigenic strains. Transient colonisation by C difficile in early life is almost certainly more common than is generally recognized and the neonate provides an important reservoir of potential infection.

Bacterial Toxins↗
PubMed1983

Effect of parasympathetic denervation on acetylcholine levels in the rat parotid gland. Is there an extraneuronal pool of acetylcholine?

Parasympathetic denervation of the rat parotid gland by avulsion of the auriculotemporal nerve caused a marked and lasting decrease in gland weight. Parasympathectomy did not change the levels of choline in the gland but decreased by 60% the levels of acetylcholine (ACh) ten days after surgery and 65% at 28 days. It is puzzling that relatively high levels of ACh remained after parasympathetic denervation. The presence of additional cholinergic nerves that innervate the gland, or pass through it en route to other structures may account for some of the remaining ACh. Also, Schwann cells from denervated nerves might have contributed to some of the ACh. The existence of an extraneuronal source of ACh is considered.

Acetylcholine↗
PubMed1983

Effects of oral phosphatidylcholine on mouse brain choline and acetylcholine.

Oral phosphatidylcholine (PC) in a dose of 250 mg/kg choline equivalent, was given 1, 2, 4, 8, 12, and 24 hr prior to brain assay to groups of fasted mice. The animals were then killed by focused microwave irradiation to the head and brain choline (Ch) and acetylcholine (ACh) assayed by chemical demethylation using gas chromatography-nitrogen phosphorous (GC-NP) detection. Mouse brain Ch levels increased significantly at 4 (P less than .001) and 8 (P less than .01) hr after PC administration. However, there was no change in mouse brain ACh. When this experiment was repeated in a second series of animals at 1, 3, 6, and 12 hr pretreatment with PC, only the 6 hr pretreatment showed a significant increase in brain Ch (P less than .01). The effects of PC administration to alter the known ACh depleting effects of scopolamine were also determined by giving PC orally 4 hr before and scopolamine, 0.1, 0.32, and 1 mg/kg, one hr before microwave irradiation. The known depleting effects of scopolamine pretreatment on brain ACh were confirmed (P less than .001). A large dose (1 mg/kg) of scopolamine also caused a decrease in brain Ch (P less than .001). Pretreatment with PC reversed the depletion of brain Ch induced by scopolamine but had no effect on depleted brain ACh. The results indicate that, although mouse brain Ch can be increased by oral PC, there is no effect on mouse brain ACh.

Acetylcholine↗
PubMed1979

Urinary neurotransmitter metabolites in drug-free chronic schizophrenic patients measured by gas chromatography selected positive ion monitoring.

The free urinary metabolites, homovanillic, indoleacetic and 5-hydroxyindoleacetic acid were measured in 24 h urines obtained from seven highly selected drug-free chronic schizophrenic patients and seven mentally normal control subjects on a low amine diet. Gas chromatography selected ion monitoring of silylated extracts was used to assay each metabolite using its own deuterated form as an internal standard. In the electron impact mode the positive ion fragments used to quantitate the amount of each metabolite in the urine were, respectively, m/z 209/211 for homovanillic acid, 319/321 for indoleacetic acid and 290/292 for 5-hydroxyindoleacetic acid. It was found essential that each compound be assayed using its own deuterated derivative as the internal standard. When expressed per mg creatinine, the homovanillic and 5-hydroxyindoleacetic acid levels of the chronic schizophrenic patients were in the normal range, but indoleacetic acid was slightly and statistically significantly higher, p = 0.01.

Acids↗