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Biomedical subjects

A Bennett

Publications and source records attributed to A Bennett.

At least 199 records · Page 11Linked to original sources
PubMed1980

Prostaglandin-like material extracted from squamous carcinomas of the head and neck.

Tumour-associated prostaglandin-like material, assessed by bioassay, has been examined in 37 patients with primary and metastatic squamous carcinomas of the head and neck, previously treated by radiotherapy and chemotherapy followed by radical surgery. High amounts of prostaglandin-like material were extracted from tumours excised within 3 months of radiotherapy and chemotherapy. These amounts correlated with necrosis, inflammation and fibrosis, but not with tumour site, size or degree of differentiation. Most of the prostaglandins formed by these treated tumours thus seem to be associated with host stromal and inflammatory cells, rather than the neoplastic cells. The possible roles of prostaglandins in facilitating the spread of squamous carcinomas are discussed.

Adult↗
PubMed1980

Weight therapy as part of rehabilitation.

Working with those who are overweight has received little attention or publicity, even though most practitioners have at some time tried to help a client deal with obesity. This review of findings related to 101 cases describes a weight loss program for the disabled at a rehabilitation center and outlines principles that have relevance for any worker whose clients have weight-related problems.

Adolescent↗
PubMed1980

Antagonism of prostanoid-induced contractions of rat gastric fundus muscle by SC-19220, sodium meclofenamate, indomethacin or trimethoquinol.

1 The effects of SC-19220, sodium meclofenamate, indomethacin or trimethoquinol were studied on contractions of the rat stomach longitudinal muscle to prostaglandin D2 (PGD2), PGE2, PGF2 alpha, PGH2, epoxymethano PGH2 analogues, PGI2, 6-keto-PGF1 alpha, 6,15-diketo-PGF1 alpha and thromboxane B2. All the drugs reduced contractions to all the prostanoids, but the degree of reduction differed widely. Selectivity of blockade was assessed by comparison with acetylcholine (ACh). 2 With SC-19220 5 micrograms/ml the effect on thromboxane B2, PGD2 or PGH2 and its epoxymethano analogues was not significantly different from the small effect on ACh, but the other prostanoids were blocked to greater extents. 3 The effect of the cyclo-oxygenase inhibitor sodium meclofenamate, 1 or 2 micrograms/ml, on 6,15-diketo-PGF1 alpha or thromboxane B2 was similar to the small antagonism of ACh, whereas the other prostanoids were blocked to greater extents. Indomethacin, 1 microgram/ml, also reduced contractions to the prostanoids, but antagonism of the PGH2 epoxymethano analogues was considerably less than with meclofenamate. 4 The beta-adrenoceptor stimulant trimethoquinol, 50 ng/ml, was the most potent prostanoid antagonist tested; all the prostanoids except PGE2 were antagonized more than ACh.

Acetylcholine↗
PubMed1980

Antagonism by fenamates of prostaglandin action in guinea-pig and human alimentary muscle.

1 Low concentrations of meclofenamate, flufenamate or mefenamate had little effect on contractions in response to acetylcholine in any tissue studied. 2 Sodium meclofenamate potently antagonized contractions of guinea-pig ileum longitudinal muscle to prostaglandin E2 (PGE2), PGF2 alpha or PGD2. 3 In guinea-pig colonic longitudinal muscle, contractions to PGE2 were reduced by sodium meclofenamate, but contractions of the longitudinal or circular muscle to PGF2 alpha or PGD2 were less effectively inhibited. 4 In human gastrointestinal longitudinal muscle, sodium meclofenamate or flufenamate potently inhibited contractions to PGF2 alpha, but not to PGE2. 5 Sodium mefenamate or mefenamic acid, even in high concentrations, had little effect on contractions to PGF2 alpha, but tended to inhibit PGE2-induced contractions of human gastrointestinal longitudinal muscle. 6 The therapeutic advantages of prostaglandin synthesis inhibitors which also antagonize responses to certain prostaglandins are discussed.

Animals↗
PubMed1980

Decrease in aspirin-induced gastric mucosal damage in rats by oral administration of the cytotoxic drugs melphalan and methotrexate.

Gastric mucosal damage by aspirin and chemotherapeutic drugs was studied in Wistar rats. Aspirin 60 mg given by stomach tube caused substantial gastric mucosal damage as judged by visual examination of the stomachs removed four hours later. Melphalan and methotrexate given daily for four days had no significant macroscopic effect on the gastric mucosa, but reduced the damage caused by aspirin. This protective effect my involve a stimulation of prostaglandin synthesis by the stomach, increased mucus secretion, and/or inhibition of acid secretion.

Animals↗
PubMed1980

Regional differences in the responses to prostanoids of circular muscle from guinea-pig isolated intestine.

The effects of prostaglandins (PGs) D2, E2, F2 alpha, an epoxymethano analogue of PGH2 (U-46619), prostacyclin (PGI2), 6-keto-PGF1 alpha and thromboxane (TX) B2 were tested on spirally-cut strips of guinea-pig isolated ileum or colon. In the ileum no prostanoid exerted a marked effect on the resting tissue, but PGD2, PGE2 or PGI2 1 ug ml-1 inhibited submaximal contraction to KC1. U-46619 1 ug ml-1 either inhibited or increased contractions in KC1, but PGF2 alpha, 6-keto-PGF1 alpha or TXB2 1 ug ml-1 had no significant effect. PGE2 relaxed colonic strips whereas the other prostanoids caused contraction, except for TXB2 which had no effect. The PG antagonist SC-19220 blocked colonic contractions to the prostanoids, and the residual inhibitory effect of PGD2, U-46619 or PGI2 was demonstrated by the reduction of submaximal contractions to acetylcholine. Our results suggest that prostanoid receptors mediating inhibitory responses of circular muscle predominate in the ileum, whereas in the colon both excitatory and inhibitory prostanoid receptors occur.

Animals↗