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Biomedical subjects

J R O'BRIEN

Publications and source records attributed to J R O'BRIEN.

At least 19 recordsLinked to original sources
PubMed1964

CLINICAL TRIALS WITH AGENTS CURRENTLY USED IN THE MANAGEMENT OF VAGINITIS.

Results of treatment of 151 cases of vaginitis in patients attending a leukorrhea clinic were studied. The incidence of each type of vaginitis is recorded. Analysis of results of treatment with six compounds currently used in the therapy of vaginitis indicated that acetarsol or pimaricin compounds, with their broader spectra of activity, appeared to be most useful, prior to establishment of a definite diagnosis by means of cultures. Chlordantoin is an effective antifungal agent and is associated with a high percentage of "culture cures". Resistant cases should be investigated for diabetes mellitus, and many are aided by a low carbohydrate diet. Metronidazole was used only for resistant cases of trichomoniasis, with a cure rate of over 80% when both partners were treated simultaneously. Triple-sulfa vaginal cream was effective in over 80% of patients with nonspecific vaginitis; no cases of resistant bacterial infections were encountered. Dienestrol cream was effective in relieving the symptoms of atrophic vaginitis.

Anti-Bacterial Agents↗
PubMed1964

NICKERSON'S MEDIUM IN THE DIAGNOSIS OF VAGINAL MONILIASIS.

One thousand one hundred and ninety-four cultures for vaginal moniliasis were performed on 1034 patients, using Nickerson's medium, to confirm the simplicity of the procedure and to demonstrate the inaccuracy of clinical impressions when compared to culture results. The error in the diagnosis of vaginal moniliasis on clinical impression and the wet-smear technique was as great as 60% when compared to the results of culture. The method employing this medium is easily adapted to routine office use, and offers an accurate and convenient means of diagnosis. The overall incidence of vaginal moniliasis in the variety of clinical groups studied was 21.3%.

Candidiasis, Vulvovaginal↗
PubMed1964

A COMPARISON OF PLATELET AGGREGATION PRODUCED BY SEVEN COMPOUNDS AND A COMPARISON OF THEIR INHIBITORS.

The aggregating effects of adenosine diphosphate, thrombin, 5-hydroxytryptamine, tryptamine, adrenaline and noradrenaline, and tri-ethyl tin have been carefully compared. The first three compounds in some circumstances produce remarkably similar effects although there are important differences. The kinetics of aggregation induced by adrenaline (and noradrenaline) are quite different and the tri-ethyl tin effects are different again. Anti-serotonins specifically inhibit 5-hydroxytryptamine and the anti-adrenaline drug phentolamine specifically inhibits the effects of the catecholamines. Experiments presented suggest but do not prove that aggregation produced by all these compounds is accompanied by the liberation of diphosphate from the platelets and that platelet triphosphate may be converted to diphosphate. How these different compounds all produce this effect is discussed. Either the presence of diphosphate or the action of a triphosphatase might be the immediate cause of aggregation if there is a single final common cause. The anti-adrenaline phentolamine prolongs the bleeding time, so adrenaline or noradrenaline may be involved in platelet phenomena in haemostasis.

Adenine Nucleotides↗
PubMed1961

The adhesiveness of native platelets and its prevention.

THE FOLLOWING METHODS WERE USED TO MEASURE THE ADHESION TO VARIOUS SURFACES OF PLATELETS IN WHOLE BLOOD OR PLASMA: 1, two measurements gave an estimate in vivo of platelet adhesion to cut human capillaries; 2, platelets adhering to damaged cells in vitro were counted directly; 3, a highly reproducible method for estimating platelet adhesion to glass was devised; 4, the manner in which platelets adhere to each other (aggregation) was also studied. Platelet adhesion to all these surfaces was found to be dependent upon calcium and independent of all clotting factors except that platelet aggregation is probably dependent upon thrombin. A number of drugs-mostly antimalarials, antihistaminics, and local anaesthetics-in suitable concentration inhibited adhesion. They probably form a fixed, orientated layer on glass and possibly on cells and make these surfaces unattractive to a platelet. They also stick reversibly to live cells (including platelets) altering their permeability, and they may make platelets less adhesive. Consequently the possibility of using antiadhesive drugs therapeutically to inhibit thrombus formation was considered.

Adhesiveness↗
PubMed1960

The effect of heparin on the early stages of blood coagulation.

From experiments reported it is concluded that heparin combines with and inactivates Christman factor (C.F.) to form reversibly a heparin-C.F. complex. Apart from the effect of heparin on C.F. and on thrombin, heparin in moderate concentrations was not shown to inactivate any other coagulation factors."Available" heparin is defined as heparin in such a state that it can delay some clotting systems. Heparin was rendered "unavailable" or inactive by plasma C.F. and especially by serum C.F., by platelet protein (but not intact platelets), and by platelet-like activity of serum (P.L.A.S.). These three proteins uniquely among all the plasma and serum proteins inactivate heparin. If an appropriate concentration of heparin is added to whole blood the clotting time is prolonged, due presumably to the inactivation of C.F. by heparin: "available" heparin disappears during clotting and none is found in the serum. The interactions summarized above probably account for these findings. The disappearance of available heparin would also account for the normal thrombin generation and prothrombin consumption observed when heparinized blood clots. Some properties of P.L.A.S. are reported and its possible role in normal coagulation is considered. Heparin is known to become attached preferentially to one protein rather than another. Some plasma and serum fractions can be arranged in order of their increasing affinity for heparin thus: beta Lipoproteins<thrombin clotting system<C.F.<platelet protein<protamine sulphate.

Blood Coagulation↗