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Biomedical subjects

P G Iatridis

Publications and source records attributed to P G Iatridis.

At least 19 recordsLinked to original sources

Integration of pharmacology into a problem-based learning curriculum for medical students.

The purpose of this study is threefold: (1) to describe a method of integration of pharmacology subject matter with other disciplines, in a problem-based learning (PBL) curriculum employed at the Northwest Center for Medical Education (NWCME), Indiana University School of Medicine; (2) to present various evaluation methods employed to assess students' learning of pharmacology knowledge; and (3) to compare the academic performance of students who underwent a traditional curriculum versus the PBL curriculum in terms of class evaluations and the standard national board medical licensure examinations. The PBL curriculum is designed for the first 2 years of medical education and consists of six sequential steps: steps 1 and 2 deal with biochemistry and anatomy respectively; steps 3, 4 and 5 deal with physiology, neuroscience and general pathology/microbiology respectively; and step 6 is a multidisciplinary step, which integrates basic science subjects with clinical medicine, emphasizing the mechanism of disease in an organ-system approach. In the PBL curriculum students start learning pharmacology within 6 months of admission. The content and process of pharmacology are spread across the first and in the second year. The pharmacology content is divided into three segments, each of which is integrated with other basic science subjects that have maximum mutual relevance. The three segments are as follows: the general and systemic pharmacology (50%) was included in step 3; the neuropharmacology and toxicology (35%) part was included in step 4; the third segment consisted of antimicrobial agents, anticancer and antiinflammatory agents (15%) and was included in step 5. The class evaluation of student performance in the PBL curriculum consisted of two elements, the content examinations and the process evaluations, which include the tutorial and the triple-jump evaluations of problem-solving skills. In order to assess the overall academic performance of the PBL curriculum and traditional curriculum groups, three classes of students who took the PBLC were compared with three classes of students who underwent a TC for performance in terms of class grades and scores of National Board examinations (NBMEI and/or USMLE I). The PBL curriculum students performed as well as or better than the TC students as measured by the NMBEI and/or USMLE I. The gain in pharmacology knowledge of PBL students is accompanied by the presence of a positive experience that learning pharmacology is enjoyable. Our experience suggests that the segmental integration approach of instruction coupled with a system of content (internal and external examinations) and process (tutorial and triple-jump) evaluations, as outlined in this paper is a contextualized learning method that offers an effective way of imparting pharmacology knowledge to medical students.

Education, Medical, Undergraduate

Structure-function relationship of 3-phosphoglycerate analogues with platelet aggregation and thromboxane A2 formation.

We have studied the effects of 2,3-diphosphoglycerate (2,3-DPG), 3-phosphoglycerate (3-PG), 3-phosphoglyceraldehyde (3-PGA), 2-phosphoglycerate (2-PG) and beta-glycerol phosphate (beta-GP) on platelet aggregation and on thromboxane B2 (TXB2) formation. The results show that 2,3-DPG, 3-PG, and 3-PGA inhibited platelet aggregation and TXB2 formation induced by norepinephrine, ADP, epinephrine, and collagen; but they also induced platelet aggregation and TXB2 formation in the presence of subthreshold concentrations of Na arachidonate. 2-PG and beta-GP were inactive. The results also show that there is a structure-function relationship between 2,3-DPG, 3-PG, and 3-PGA with platelet aggregation phenomena and prostaglandin synthesis.

2,3-Diphosphoglycerate

The combined effects of 2,3-DPG and Na-arachidonate on platelet aggregation and on TXA2 formation.

We have investigated the effects of 2,3-DPG on platelet aggregation in the presence of suboptimal concentrations of Na-Arachidonate by using the two cuvette transfer experiments of Hamberg, Svensson and Samuelsson (3). The results show that 2,3-DPG enhanced or induced platelet aggregation in the presence of suboptimal concentrations of Na-Arachidonate. Imidazole, a TXA2 synthetase inhibitor, and Lasix, when added inhibited 2,3-DPG effects on platelet aggregation, suggesting that 2,3-DPG may act either on cyclooxygenase or on TXA2 synthetase of prostaglandin synthesis. A specific RIA assay showed that 2,3-DPG when added to suboptimal concentrations of Na-Arachidonate enhanced the formation of TXB2, a stable metabolite of TXA2. We have concluded that during intravascular hemolysis 2,3-DPG release may be a key component in preventing and/or inducing thrombosis.

2,3-Diphosphoglycerate

The role of HF cofactor in the Hageman factor-dependent fibrinolytic mechanism.

In 1969, Ogston et al. reported that the normal activation of fibrinolysis by surface contact requires, in addition to Hageman factor and plasminogen, a HF cofactor which is present in the euglobulin fraction and other factor(s) present in the supernatant. It has also been suggested that the glass-treated plasma is deficient in HF cofactor, In our laboratory the glass-treated plasma was found not to be deficient in HF or in a streptokinase-activated proactivator or in plasminogen. The glass-treated plasma was found deficient in prekallikrein in kininogen and in clotting factors XI, IX, VIII and V. The results presented indicate that HF cofactor activity is not different from that of kallikrein and that HF cofactor does not act as a plasminogen proactivator. Furthermore, the results indicate that the "other factors' present in the supernatant are not involved in contact-activated fibrinolysis.

Blood Coagulation Factors

Thrombin-induced vasodilation in the hindlimb (dog).

The objective of this study is to test the hypothesis that the vasodilation produced by intra-arterial injection of thrombin to the hindlimb of a dog may be caused by the secondary release or production of some vasodilating substance. The vasodilator response to thrombin was compared with the vasodilator response to acetylcholine, isoproterenol, histamine and serotonin before and after blockade with atropine, propranolol, phenergan or methyl-D-lysergic acid butanolamide (UML-491), respectively. Though the appropriate blocking agent blocked the vasodilator response to the respective drug, the thrombin-induced vasodilation was not blocked. These data support the hypothesis that thrombin-induced vasodilation is a response to the thrombin moiety.

Acetylcholine

Vasodilator effect of thrombins prepared from normal or deficient human or canine plasmas.

Thrombins prepared from plasmas deficient in various clotting factors are capable of inducing vasodilator response to the hindlimb of the dog and this response proved to be similar to that produced by thrombins prepared from normal plasmas. Thus the vascular effect of thrombin is not mediated by any other clotting factor which might be present in small amounts in the thrombin preparations. Thrombin prepared from canine normal plasma exerted a more potent vasodilator response, indicating a species specificity for the vascular response to thrombin. Since the vasodilating effect of thrombin is not mediated by (i) a nervous mechanism, (ii) any known vasodilating substance or (iii) any other clotting factor, it is concluded that the thrombin moiety possesses vasodilating properties.

Animals

Stimulation of human platelet aggregation by phospholipase-A and a saline "extract" of a polyurethane.

A saline extract of polyurethane (SPU) induces enzymatic conversion of arachidonic acid (either exogenous or released through the action of exogenous phospholipase-A) by activating a hitherto undiscovered labile enzyme, synthetase-alpha which is not blocked by aspirin. Addition of SPU, plus arachidonic acid or SPU plus phospholipase-A to platelet-rich plasma (PRP) triggers a biphasic platelet aggregation. Incubation of SPU with PRP results in activation and exhaustion of synthetase-alpha; this renders platelets refractory to the various aggregating agents.

Aspirin

2,3-diphosphoglycerate: a physiological inhibitor of platelet aggregation.

2,3-Diphosphoglycerate (2,3-DPG) may inhibit the platelet release reaction and the irreversible aggregation of human blood platelets induced by adenosine diphosphate, epinephrine, or norepinephrine. The effects of 2,3-DPG on platelet aggregation were more pronounced in cases with low hematocrit (less than 30 percent). Dipyridamole and vincaminor potentiated the antiaggregating effect of 2,3-DPG. Erythocytes (10-3 to 10-4 per microliter) exhibited a similar antiaggregating effect, especially when secured from anemic patients.

Adenosine Diphosphate