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Biomedical subjects

E J Walaszek

Publications and source records attributed to E J Walaszek.

At least 19 recordsLinked to original sources

A computer-assisted teaching system in pharmacology for health professionals.

In this report the authors describe experiences with a computer-assisted teaching system in teaching pharmacology to medical students and other health professionals. The system is composed of both computer-assisted instruction and computer-managed instruction. The "Keller Plan" philosophy was adopted, and the pharmacology course was organized into modules. Students were required to meet minimum proficiency requirements in each module and have multiple chances to reach this or higher levels. The advantages of this system are numerous. The department can provide both scheduled and independent study courses in basic pharmacology to students of different educational levels. Students can progress through a course at various speeds; that is, achievement is constant, but time is variable. Both the students and instructors are provided with frequent and rapid feedback. Most importantly, students with low aptitudes achieve significantly higher scores on the pharmacology portion of the examination of the National Board of Medical Examiners.

Computer-Assisted Instruction↗

Acetal phosphatidic acids: novel platelet aggregating agents.

1 Palmitaldehyde, olealdehyde and linolealdehyde acetal phosphatidic acids induced rapid shape change and dose-dependent biphasic aggregation of human platelets in platelet-rich plasma; aggregation was reversible at low doses and irreversible at high doses of the acetal phosphatidic acids. The palmitaldehyde congener elicited monophasic dose-dependent aggregation of sheep platelets in platelet-rich plasma.2 The threshold concentration for palmitaldehyde acetal phosphatidic acid (PGAP)-induced platelet aggregation was 2.5-5 muM for human platelets and 0.25-0.5 muM for sheep platelets. PGAP was 4-5 times as potent versus human platelets as the olealdehyde and linolealdehyde acetal phosphatidic acids, which were equipotent.3 PGAP-induced irreversible aggregation of [(14)C]-5-hydroxytryptamine ([(14)C]-5-HT)-labelled human platelets in platelet-rich plasma was accompanied by release of 44.0+/-2.4% (s.e.) of the platelet [(14)C]-5-HT; reversible aggregation was not associated with release. In contrast, PGAP-induced release of [(14)C]-5-HT-labelled sheep platelets was dose-dependent.4 The adenosine diphosphate (ADP) antagonist, 2-methylthio-AMP, and the cyclo-oxygenase inhibitor, aspirin, abolished PGAP-induced second phase aggregation and release in human platelets but did not affect the first, reversible, phase of aggregation. Both the first and second phases of PGAP-induced aggregation were abolished by chlorpromazine, by the phospholipase A(2) inhibitor, mepacrine, and by nmolar concentrations of prostaglandin E(1) (PGE(1)); these agents abolished the second, but not the first phase of ADP-induced aggregation.5 The related phospholipids, lecithin, lysolecithin and phosphatidic acid, at <100 muM, neither induced aggregation of human platelets in platelet-rich plasma, nor modified PGAP-induced aggregation; 1-palmityl lysophosphatidic acid elicited aggregation of human platelets at a threshold concentration of 100 muM.6 It is concluded that the acetal phosphatidic acids induce platelet aggregation per se by direct action at the platelet membrane, and that the acetal function is of primary importance in their potent platelet-stimulating activity. Moreover, as the acetal phosphatidic acids are the major components of the smooth muscle-contracting acidic phospholipid tissue extract ;Darmstoff' (Vogt, 1949), their potent platelet-aggregating properties may be of physiological or pathological significance.

Adenosine Diphosphate↗

2,3-Dihydroxyphenethanolamine as an adrenergic agent.

In an attempt to further define the role of the m-hydroxy group in adrenergic agents, 2,3-dihydroxyphenethanolamine hydrobromide and N-isopropyl-2,3-dihydroxyphenethanolamine hydrobromide were prepared. These agents are less active than norepinephrine in alpha- and beta-adrenergic in vitro tests. The synthesis and conclusions from the tests are discussed.

Animals↗

Sex differences in reflex tachycardia induced by hypotensive drugs in unanesthetized rats.

Possible sex differences in autonomic regulation of the heart were studied by injecting standard hypotensive doses of histamine or bradykinin to induce reflex tachycardia in awake rats. Although depressor responses to both drugs were unaltered, the tachycardia was greatly reduced by beta-adrenergic blockade with propranolol and abolished almost completely after combined blockade with propranolol and atropine. These findings indicate that the tachycardia was mostly due to increased sympathetic stimulation wiht a minor contribution from parasympathetic withdrawal. With large doses of bradykinin, direct myocardial stimulation also seemed likely, since some residual tachycardia remained even after combined blockade. Reflex tachycardia was generally more pronounced in male than in female rats. Because males had lower base-line heart rates and more tachycardia that was resistant to beta-adrenergic blockade than females, autonomic regulation was concluded to be predominantly parasympathetic in males and sympathetic in females. Whereas the exact cause of these variations in chronotropic regulation is unknown, it was considered possible that differences in sex hormones may have affected sensitivity of some component of the reflex arc.

Animals↗

Uptake of histamine by rabbit hypothalamic slices.

The accumulation of [-14C] histamine into slices of rabbit hypothalamus was studied. All areas of hypothalamus took up histamine against a concentration gradient. The highest accumulation was into the infundibular area and the lowest into the mamillary body. The uptake did not correlate with the level of endogenous histamine. The uptake continued for at least two hours and a maximum tissue/medium ratio of about 5.6 was reached. The major part of radioactivity was chromatographically shown to be histamine. The uptake was temperature dependent and required sodium. It was not significantly inhibited by compound 48/80, but it could be inhibited with desipramine and 5-hydroxytryptamine. Therefore, the uptake of histamine shares many characteristics of the uptake of monoamines by brain slices, even if the rate of uptake appeared to be slower.

Animals↗