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Biomedical subjects

P Furness

Publications and source records attributed to P Furness.

36 records · Page 2Linked to original sources
PubMed1992

Thromboxane receptor antagonism combined with thromboxane synthase inhibition. 4. 8-[[(4-Chlorophenyl)sulfonyl]amino]-4-(3-(3-pyridinyl) propyl)octanoic acid and analogs.

The title compound (10a) and its analogs were synthesized and found to possess two activities, the inhibition of the biosynthesis of thromboxane A2 and antagonism of its receptors. The in vitro and in vivo profile of these compounds as thromboxane receptor antagonists (TxRAs) and thromboxane synthase inhibitors (TxSIs) is described. 10a and its analogs displayed very potent TxRA activity in human washed platelets (IC50 approximately 10(-7)-10(-9) M) and dog saphenous vein (pA2 approximately 9) and also potent TxSI activity (IC50 approximately 10(-9) M). The good bioavailability and the long duration of action of some of these compounds was demonstrated using ex vivo measurement of the TxRA activity upon oral administration to guinea pigs. Compounds 10a, 20, and 33 potently inhibited arachidonic acid induced bronchoconstriction in guinea pigs.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Thromboxane receptor antagonism combined with thromboxane synthase inhibition. 1. (+/-)-(3-pyridinylbicycloheptyl)alkanoic acids.

The design, synthesis, and in vitro pharmacology of a new class of compounds exerting both thromboxane receptor antagonist and thromboxane synthase inhibitory activities is described. [(3-Pyridinyl)bicycloheptyl] alkanoic acid 9 and its analogues, designed with the help of molecular modeling, were synthesized and found to be inhibitors of thromboxane A2 (TxA2) biosynthesis in a human platelet microsomal preparation. The compounds were also found to antagonize both platelet and vascular TxA2 receptors. The compounds inhibited the U 46619 induced aggregation of human washed platelets and platelet-rich plasma and the U 46619 induced contraction of the dog saphenous vein.

Blood Platelets↗
PubMed1991

Changes in amplitude and latency of the P300 component of the auditory evoked potential with sedative and anaesthetic concentrations of nitrous oxide.

The P300 component of the auditory evoked response was recorded from six subjects whilst they listened via headphones to a series of clicks which were interrupted unpredictably by a tone burst. They were instructed to press a button as quickly as possible after hearing the tone whilst breathing first air and then a series of increasing concentrations of nitrous oxide. Both the amplitude and the latency of the P300 changed in a dose-dependent manner with nitrous oxide, as did minimum reaction time. At nitrous oxide concentrations which prevented recall of any events that occurred whilst breathing the gas, four subjects continued to respond to the tone by pressing the button. In three subjects, the P300 wave was still detectable with a nitrous oxide concentration at which the task was no longer performed. These results show that there is retention of the ability to perform a reaction time task when there is a complete loss of recall of the task. There may be some recognition of an auditory stimulus, as manifest by a P300 wave, albeit reduced greatly in amplitude, in the absence of a motor response to it. The P300, therefore, merits investigation as a tool for studying conscious awareness under anaesthesia.

Anesthesia Recovery Period↗
PubMed1988

Structure-activity profile of a series of novel triazoloquinazoline adenosine antagonists.

During a search for benzodiazepine receptor modulators, a highly potent adenosine antagonist (CGS 15943) was discovered. The compound was defined as a resonance-stabilized hybrid of the canonical structures 9-chloro-2-(2-furyl)[1,2,4]triazolo[1,5-c]quinazolin-5-amine (2a) and 9-chloro-2-(2-furyl)-5,6-dihydro[1,2,4]triazolo[1,5-c]-quinazolin- 5-imine (2b). Spectroscopic evidence and chemical reactivity in polar media favor the amine form 2a as the major contributor of the two canonical structures. The synthesis of 2 and some of its analogues and the structure-activity relationships in four biological test systems are described. Replacement of the 9-chloro group by hydrogen, hydroxyl, or methoxyl gave compounds with comparable binding potency at the A1 and A2 receptors but much less activity as antagonists of 2-chloroadenosine in guinea pig tracheal strips. Alkylation of the 5-amino group caused, in general, a loss of binding activity, particularly at the A2 receptor, as well as complete loss of activity in the tracheal model. Modification of the 2-furyl group caused a pronounced loss of activity in all of the test systems.

Adenosine↗
PubMed1977

Long-lasting increases in the tremor of human hand muscles following brief, strong effort.

1. Long-lasting (up to 4 h) increases in finger tremor were produced by intense brief effort to contract the muscle. 2. Similar increases resulted from intense effort which did not contract the muscle because the motor nerve was blocked. 3. Comparable contractions induced electrically failed to give rise to increased tremor. 4. Power spectral analysis (1-15 HZ) revealed that all frequencies of tremor were approximately equally increased. 5. It is concluded that these long-lasting increases in tremor are of central nervous origin.

Action Potentials↗
PubMedDate not supplied

Iga nephropathy, antineutrophil cytoplasmic antibodies and crescentic glomerulonephritis in a patient with the Hermansky-Pudlak syndrome.

Hermansky-Pudlak syndrome is an uncommon cause of renal dysfunction. Because of the risk of bleeding in this condition, few patients have undergone a renal biopsy. Renal dysfunction has been attributed to the deposition of ceroid pigment in the tubules and interstitial fibrosis. We report a case with renal biopsy findings of ceroid deposition and interstitial fibrosis, but also of mesangial IgA deposition, crescentic glomerulonephritis, and an interstitial lymphocytic infiltrate. Furthermore, perinuclear antineutrophil cytoplasmic antibodies of the IgG subclass were detected in a blood sample. It is well known that ceroid pigment in this syndrome accumulates in monocytes, macrophages and T lymphocytes and it has been suggested that this may affect their function. We suggest that this novel combination of renal changes might be explained on the basis of alterations in immune mechanisms in the Hermansky-Pudlak syndrome.

Adult↗