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Biomedical subjects

G Tobin

Publications and source records attributed to G Tobin.

At least 91 records · Page 5Linked to original sources
PubMed1983

Vasoactive intestinal peptide evoked secretion of fluid and protein from rat salivary glands and the development of supersensitivity.

Vasoactive intestinal peptide (VIP) injected intravenously was found to induce a flow of saliva from both the parotid and the submaxillary gland in the rat. The secretion was slow in onset. The amount of saliva secreted from the parotid gland was less than that from the submaxillary gland. Parotid saliva was very viscous. VIP-evoked parotid saliva was more protein rich than both submaxillary saliva and saliva secreted in response to other sialagogue drugs including the beta-adrenergic receptor agonist isoprenaline. The effect of VIP was direct; it occurred after removal of the adrenals, after degeneration of intraglandular nerves and in the presence of autonomic blockers. A supersensitivity to VIP was demonstrable. In the parotid and the submaxillary glands the secretory response to VIP was enlarged following parasympathetic denervation and decentralization, respectively, while after sympathetic denervation supersensitivity was only found to develop in the submaxillary gland.

Adrenalectomy↗
PubMed1983

Atropine-resistant secretion of parotid saliva on stimulation of the auriculo-temporal nerve.

Non-adrenergic non-cholinergic parasympathetic secretory responses in parotid glands of rats have been demonstrated by electrical stimulation of the auriculo-temporal nerve after appropriate blocking drugs and compared with secretion in the absence of these drugs. After atropine +/- adrenergic blocking drugs secretion was greatly reduced but some secretion was always evident at frequencies of 5 Hz and higher. The time taken for secretion to appear was greatly increased and this may relate to an absence of accompanying myoepithelial contraction. Continuous stimulation always produced greater flows of saliva than intermittent bursts of stimulation at higher frequencies both in the absence and in the presence of blocking drugs. Thus it is likely in vivo that secretion is induced by relatively steady nerve-impulse traffic at moderate frequencies rather than by bursts of high frequency stimulation. Possible transmitters contributing to the atropine-resistant secretion are considered.

Adrenergic alpha-Antagonists↗
PubMed1983

The effects of supplementation of the diet with highly palatable foods upon energy balance in the rat.

Full energy balance studies have been performed for 9 weeks on four groups of four adult female rats housed in a continuously running indirect calorimeter; for four weeks two of the groups received highly palatable foods in addition to a standard pelleted diet. A further sixteen groups, of which eight received the palatable foods, provided additional carcass composition data. All practicable precautions were taken to measure energy exchange accurately. Comparison of 'start-to-finish' apparent energy balance with carcass composition changes showed a systematic error of approx. +3% of energy throughput. This was most probably caused by losses of energy in food and excreta, which led to over-estimation of energy intake. Variations among individual balance periods added a standard error of approx. +/- 1%: the source of error here was probably imperfect matching of animals analysed at intermediate stages. The rats offered the palatable foods increased their metabolizable energy (m.e.) intake by 106 kJ/day, 51% of the control groups' intake, in the first week of supplementation. Over the whole 4 weeks of supplementation the increase was 64 kJ/day, or 31%. Withdrawal of the palatable foods led to an immediate fall in intake to about two-thirds of control level, and a return to control level over the next 2-3 weeks. Energy expenditure rose more slowly than intake, reaching a fairly steady level ca. 5 days after introduction of the palatable foods. Expenditure was then ca. 22 kJ/day above control level; an increase of 12% above control expenditure or, allowing for systematic and random errors, 33-37% of the additional m.e. intake. Expenditure returned to control level over the 2 weeks after ceasing supplementation. The experimental groups gained weight at a declining rate throughout the period of supplementation. The gain in live body weight at the end was ca. 32 g, but this comprised a carcass weight gain of 37 g and a loss of 5 g gastrointestinal tract contents. The carcass weight gain comprised 27 g fat (i.e. ca. 70% of the weight gained), 9 g lean tissue and 1 g additional water. The gain of carcass energy was 1100 kJ. There was a small increase in body length, an increase in liver weight, and an increase in the weight of the interscapular brown adipose tissue pad. Regression analysis showed that the increase in the weight of the interscapular brown adipose tissue pad reflected the increase in total body fat.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1982

A clinical trial of levamisole in primary biliary cirrhosis.

A small pilot study of levamisole in primary biliary cirrhosis failed to demonstrate any improvement in liver function and immunological abnormalities even in 'early' cases. This may be due to the fact that the defect in the immune system lies in its afferent arm. At present, levamisole, which is potentially toxic, cannot be recommended in conventional doses for the treatment of this disease.

Clinical Trials as Topic↗
PubMed1981

Unstable angina: natural history and determinants of prognosis.

One hundred one patients with unstable angina were treated conservatively without the routine use of beta receptor blocking agents, calcium antagonist drugs, anticoagulant agents or nitrates. Only two patients underwent arteriography and coronary arterial bypass surgery during hospitalization and one patient during the 1st year of follow-up study. The 28 day mortality rate was 4 percent and the total 1 year cardiac mortality rate 10 percent. Two patients died from carcinoma. The incidence rate of nonfatal myocardial infarction was 9 percent during the first 28 days and a further 3 percent for the 1st year. These results compare favorably with the immediate and 1 year prognosis reported from other studies using different treatment procedures, including modern intensive drug treatment and coronary arterial bypass surgery. Various factors studied during the acute stage of unstable angina were assessed in an effort to predict the immediate and long-term outcome. Only persistence of pain after admission to the hospital was found a significant indicator of an adverse prognosis. Modern medical treatment of unstable angina with beta receptor blocking agents, calcium antagonist drugs, anticoagulant agents, nitrates and antiarrhythmic agents is critically examined. The paucity of proper randomized controlled studies confirming the value of medication is underlined. There is little evidence to show that aggressive or intensive medical or surgical treatment is superior to a conservative approach to management in the coronary care unit. This approach includes bed rest until the pain has resolved, symptomatic drug treatment only, the minimal use of invasive investigations and careful risk factor intervention.

Adrenergic beta-Antagonists↗
PubMed1979

Carotid or jugular amino acid infusions and food intake in the cockerel.

1. Infusions of histidine into the carotid arteries of cockerels receiving a histidine-limiting, imbalanced diet caused an increase in food intake, whereas similar infusions into the jugular veins did not. 2. Infusions of lysine into the carotid arteries or jugular veins of young cockerels receiving a balanced, low-protein diet caused decreases in food intake. There was evidence of a more marked effect of carotid infusion. 3. The mechanisms of food intake regulation by amino acids in mammals are applicable to birds and excesses of single amino acids do seem to affect food intake directly.

Animals↗
PubMed1977

Experiments with beta-chain variants of the hemoglobin of Mus musculus.

Starch gel electrophoretic and ultracentrifuge methods failed to demonstrate any differences between the hemoglobins of mice of the Shanghai and HBBP/Cag strains and crosses among these strains. The apparent identity of these hemoglobins is thought to stem from the contribution of Asian mice to the British mouse fancy from which the laboratory strains have Hbb-p in part descend. Maleate buffer of pH 7 or above can be used to prevent the formation of disulfide-bridged dimers of mouse hemoblobins. However, the minor electrophoretic bands of Hbb-p and Hbb-d react with approximately twice as much maleate as the major bands of each of these hemoglobins, although the minor bands like the major contain only one free cysteine group per beta chain. This can be explained by the alkylation of the epsilon-amino of lysine residue beta76, but some evidence for the alkylation of histidine in the minor band of Hbb-p is also presented.

Animals↗