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Biomedical subjects

J Turk

Publications and source records attributed to J Turk.

At least 181 records · Page 10Linked to original sources
PubMed1984

The influence of a therapeutic dose of nitroglycerin on invasive and non-invasive parameters of left ventricular performance in coronary heart disease.

To assess the influence of a therapeutic dose of 0.5 mg sublingual nitroglycerin (NTG) on left ventricular performance, 32 patients with coronary heart disease were studied. After routine coronary angiography the patients underwent cinearteriography and phonomechanocardiography before and four minutes after NTG administration. After NTG, end-diastolic pressure and systolic aortic pressure fell significantly, while heart rate, ejection fraction and dp/dt increased. After NTG, a significant prolongation of the pre-ejection period index (PEPI) and isovolumetric relaxation time (IVRT), increase in the PEP/LVET ratio and decrease of the "a" wave of the apexcardiogram were found. The usual therapeutic sublingual NTG dose causes profound haemodynamic changes which are due to decreased preload and afterload and altered contractility induced by NTG.

Cardiac Output↗
PubMed1983

Iodination of arachidonic acid mediated by eosinophil peroxidase, myeloperoxidase and lactoperoxidase. Identification and comparison of products.

Arachidonic acid undergoes iodination in the presence of hydrogen peroxide, iodide, and either eosinophil peroxidase, myeloperoxidase or lactoperoxidase. The profile of products generated by each of the three peroxidases is similar as determined by reversed-phase high-performance liquid chromatography. Structural analysis of the products indicate that: 1, each of the four double bonds in arachidonic acid is susceptible to iodination; 2, arachidonic acid can be multiply iodinated; and 3, the carboxylate moiety does not participate in the formation of all products. The isomeric composition of the isolated products indicates that peroxidase-mediated iodination of arachidonate is not stereoselective.

Animals↗
PubMed1983

Identification of lipoxygenase products from arachidonic acid metabolism in stimulated murine eosinophils.

The presence of arachidonic acid lipoxygenase pathways in murine eosinophils was demonstrated by the isolation and identification of several lipoxygenase products from incubations of these cells. The most abundant arachidonate metabolite from murine eosinophils stimulated with ionophore A23187 and exogenous arachidonic acid was 12-S-hydroxyeicosatetraenoic acid (12-S-HETE), and the next most abundant was 15-HETE. Two families of leukotrienes were also recovered from these incubations. One family comprised the hydrolysis products of leukotriene A4, and the other included products derived from the 14,15-oxido analog of leukotriene A4 (14,15-leukotriene A4). Two double oxygenation products of arachidonate were also identified. These compounds were a 5,15-dihydroxyeicosatetraenoic acid (5,15-diHETE) and a 5,12-dihydroxyeicosatetraenoic acid (5,12-diHETE). Eosinophil stimulation promoter is a murine lymphokine which enhances the migration of eosinophils. When murine eosinophils were incubated with eosinophil stimulation promoter in concentrations sufficient to produce a migration response, a 2-3-fold increase in the production of 12-HETE was observed compared to unstimulated cells. Coupled with the recent demonstration that arachidonic acid lipoxygenase inhibitors suppress the migration response to eosinophil stimulation promoter and that 12-HETE induces a migration response, this observation provides further evidence in support of the hypothesis that eosinophil stimulation promoter stimulation of eosinophils results in the generation of lipoxygenase products which modulate the migratory activity of the cells.

Animals↗
PubMed1983

Intervention with epinephrine in hypotension associated with mastocytosis.

The occurrence of the episodes of vasodilatory hypotension can be a life-threatening manifestation of systemic mastocytosis. This article describes the reversal by epinephrine of episodes of severe hypotension in two hospitalized patients with mastocytosis. Recognition of the efficacy of epinephrine in hypotension associated with mastocytosis can be important when other methods fail to restore hemodynamic stability.

Aged↗
PubMed1982

Formation of a novel dihydroxy acid from arachidonic acid by lipoxygenase-catalyzed double oxygenation in rat mononuclear cells and human leukocytes.

Elicited rat peritoneal mononuclear cells converted arachidonic acid to a new dihydroxy acid, 5(S), 15(S)-dihydroxy-6,13-trans-8,11-cis-eicosatetraenoic acid (5,15-DiHETE). In this system, the amount of 5,15-DiHETE formed was about 20% that of leukotriene B4. The structure of the compound was determined by ultraviolet and mass spectrometric analysis, and comparison to a reference compound prepared by incubation of synthetic 5(R,S)-hydroxy- or hydroperoxy-6-trans-8,11,14-cis-eicosatetraenoic acid (5(R,S)-HETE or HPETE) with soybean lipoxygenase (linoleate:oxygen oxidoreductase, EC 1.13.11.12). Cell incubations performed under an atmosphere of 18O2 demonstrated that both hydroxyl groups in the cell product derived from molecular oxygen and that the oxygen atoms were from different oxygen molecules. Steric analysis indicated that each hydroxyl group had the S-configuration. The structural data thus indicate that 5,15-DiHETE is formed by an enzymatic double oxygenation of arachidonic acid catalyzed by both C-5 and C-15 lipoxygenases. Incubations with with [3H 8]5 (S)-HETE and [3H8]15(S)-HETE revealed that both compounds could be converted to the product. When [3H8]5(S), 15(S)-DiHPETE was added to cells, the majority of the substrate was reduced to 5,15-DiHETE. Leukocytes obtained from three human donors with peripheral blood eosinophilia also synthesized 5,15-DiHETE. Formation of the compound occurred in both eosinophils and neutrophils from these donors.

Animals↗
PubMed1982

Arachidonic acid 15-lipoxygenase products from human eosinophils.

A series of six derivatives of arachidonic acid containing a conjugated triene system and hydroxyl groups at C-15 and at C-8 or C-14 (15-series leukotrienes) was isolated from eosinophil-rich human leukocyte preparations. Among classes of leukocytes in these preparations, eosinophils were the dominant source of the 15-series leukotrienes. The most abundant arachidonate metabolite recovered from human eosinophils was 15(S)-hydroxy-5,8,11-cis-13-trans-eicosatetraenoic acid. This compound was synthesized by a lipoxygenase enzyme and is a reduction product of the precursor to the 15-series leukotrienes (15(S)-hydroperoxy-5,8,11-cis-13-trans-eicosatetraenoic acid).

Arachidonate Lipoxygenases↗
PubMed1982

ST-T segment changes in patients with essential hypertension.

The cause of ischaemic ST-T segment changes in essential hypertension (EH) was investigated. The ECG was compared to coronary arteriograms and autopsy findings. In group A (n = 75) without ventricular hypertrophy (LVH) pathologic ST-T changes were found in 39 patients. All of these had a coronary artery disease (CAD). In group B (n = 50) with LVH a pathologic ST-T segment was observed in 20 patients; 16 of these had a CAD. The association between pathologic ST-T segments and CAD was significant in both groups. It is concluded that among patients with EH, changes in the ST-T segment are almost always due to the CAD, regardless of the presence LVH.

Adult↗
PubMed1982

Arachidonic acid metabolism of the murine eosinophil. II. Involvement of the lipoxygenase pathway in the response to the lymphokine eosinophil stimulation promoter.

Eosinophil stimulation promoter (ESP) is a murine lymphokine that enhances the migration of eosinophils. Exogenous arachidonic acid between 0.5 and 2 micrograms/ml potentiated the activity of ESP on murine eosinophil migration, whereas such concentrations did not affect migration in the absence of ESP. Among the lipoxygenase products identified from an enriched population of murine eosinophils, leukotriene B4 (optimal activity at 100 ng/ml) and 12-HETE (optimal activity at 2 micrograms/ml) stimulated migration of these cells. Another lipoxygenase product from these cells 15-HETE inhibited ESP-induced migration; between 5 and 10 micrograms/ml 15-HETE decreased by one-half both stimulated migration and 12-HETE biosynthesis. Structurally diverse drugs at concentrations that inhibited HETE biosynthesis inhibited ESP-induced migration. The concentrations that decreased migration activity by one-half were 5 microM NDGA, 10 microM ETYA, and 150 microM BW755C. Aspirin and indomethacin at concentrations reported to inhibit prostaglandin biosynthesis did not substantially inhibit ESP activity, but concentrations of indomethacin above 20 microM caused concentration-dependent inhibition of migration. The selective lipoxygenases inhibitor 134,7,10,13-eicosatetraynoic acid was more potent than ETYA in inhibition of ESP-induced migration, and the selective cyclooxygenase inhibitor 6,9,12-octadecatriynoic acid did not effect inhibition. These results are consistent with the hypothesis that stimulation of eosinophils by the lymphokine ESP involves the generation of lipoxygenase products from arachidonic acid, which positively and negatively regulate the migratory activities of these cells.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1979

A mechanism for the hydroperoxide-mediated inactivation of prostacyclin synthetase.

Hydroxyl radical generation was demonstrated during heme-catalyzed decomposition of 15-hydroperoxy arachidonic acid. The hydroperoxide-mediated inactivation of prostacyclin synthetase seems to be related to the generation of this highly reactive species. A relationship between hydroperoxides and the hydroxyl radical may be important in the modulation of prostacyclin synthesis in diseased states.

Animals↗
PubMed1978

Variation in delayed hypersensitivity in onchocerciasis.

Soluble antigen preparations were made from Onchocerca volvulus adults recovered from subcutaneous nodules, and from Necator americanus third-stage larvae. Intradermal skin tests were carried out on a total of 100 individuals clinically classified as having either the generalized form of onchocerciasis (86 cases, or the localized sowda form (14 cases). 91 of the people studied produced immediate reactions to the onchocercal antigen, but only those with sowda showed delayed reactions, though one person with generalized disease showed a doubtful delayed reaction. Reactions to N. americanus antigen, both immediate and delayed, were seen in both forms of the disease. The lack of delayed skin reaction in the generalized form of onchocerciasis is discussed, and a comparison is made with other diseases. Preliminary evidence for the existence of a true spectrum of clinical and immunological forms of onchocerciasis is suggested by one case in this study.

Adolescent↗
PubMed1978

Fluorescent derivatives of prostaglandins and thromboxanes for liquid chromatography.

Fluorescent esters of the prostaglandins D2, E2, F2alpha, and 6-keto-F1alpha and of thromboxane B2 have been prepared using the reagent 4-bromomethyl-7-methoxycoumarin. All of these derivatives can be separated in a single run either by thin-layer or high-performance liquid chromatography (TLC or HPLC). As little as 20 ng of PGE2 can be detected after derivatization and HPLC analysis. Identification of thromboxane B2 produced by human platelets and of 6-keto-PG F1alpha produced by bovine aortic microsomes has been achieved with this method.

Animals↗
PubMed1975

alpha-Methyl substrates of carboxypeptidase A. A steric probe of the active site.

Although optical resolution of alpha-methylphenylalanine (alpha-Me-Phe) has been achieved by the action of carboxypeptidase A on the N-trifluoroacetyl derivative of the amino acid (TFA-alpha-Me-Phe), it is improbable that an alpha-methyl substrate could bind in the same orientation as glycyl-L-tyrosine, due to steric interaction of the alpha-methyl group with an atom in the imidazole ring of zinc ligand His-196. The kinetic parameters for TFA-alpha-Me-Phe and for an ester substrate bearing an alpha-methyl group (beta-hippuryl-alpha-methylphenyllactic acid, HMPL) have been determined and compared to those for the appropriate nonmethylated control substrates. Both TFA-alpha-Me-Phe and HMPL appear to be bound nearly as well as are their respective controls, and HMPL is hydrolyzed nearly as rapidly as its control. TFA-alpha-Me-Phe, however, is hydrolyzed only about one-fiftieth as rapidly as is the nonmethylated substrate. These findings are consistent with the possibilities that: (1) the proposed substrate-induced conformational shift of Tyr-248 is hindered when the methylated substrates are bound; (2) the orientation in which alpha-methyl substrates are bound precludes optimal positioning of Tyr-248 and the scissile bond even after the rotation of Tyr-248 has occurred; (3) amides and esters are bound in different orientations, and in the amide orientation an alpha-methyl group is so directed as to interfere with the approach of Glu-270 to the scissile bond.

Binding Sites↗
PubMed1975

Alkylating analogs of bradykinin.

Three analogs of bradykinin have been synthesized which bear a bromoacetyl function on the alpha-amino group or on an anilinic amino group at position 5 or 8. It was hoped that one or more of these analogs might act as an irreversible bradykinin antagonist or as a long-acting converting enzyme inhibitor. Although none of the analogs exhibited the desired pharmacological properties, the methods described for the synthesis and characterization of peptides bearing anilinic bromoacetyl groups are of potential utility in the development of antagonists of other tyrosine--or phenylalanine--containing peptides.

Amino Acid Sequence↗