T-lymphocyte clones from leprosy skin lesions.
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Biomedical subjects
Publications and source records attributed to C L Cooper.
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We have investigated the contribution of Ca++ and calmodulin to the action of norepinephrine (NE) on prostaglandin (PG) synthesis and vascular tone in the Tyrode's perfused rat kidney. Lowering the Ca++ concentration (0.6 mM) reduced and raising the Ca++ concentration (5.4 mM) enhanced the renal vasoconstriction and PG output elicited by NE. Calcium channel blockers diltiazem or nimodipine inhibited the vasoconstriction and PG output caused by NE. Ca++-free Tyrode's solution containing ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid abolished NE-induced vasoconstriction and reduced PG output by 25 to 38%. Addition of intracellular Ca++ antagonists 8-(diethylamino) octyl 3,4,5 trimethoxybenzoate, dantrolene or ryanodine to Ca++-free Tyrode's solution inhibited NE-induced PG output. Calmodulin inhibitors trifluoperazine, N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide or calmidazolium diminished PG output and the renal vasoconstriction elicited by NE in the presence and absence of Ca++. Mepacrine and indomethacin inhibited NE-induced renal vasoconstriction and PG output. Arachidonic acid-induced PG output was abolished by indomethacin but was unaltered by mepacrine, Ca++ antagonists or calmodulin inhibitors. We conclude that NE produces renal vasoconstriction by a mechanism that depends primarily on extracellular Ca++ and calmodulin, whereas NE-induced PG output depends on both extra- and intracellular Ca++ and calmodulin.
Within the context of a larger study on psychosocial stress, it was desirable to measure pilot performance. A variety of reasons dictated reliance upon self-reported performance. Since no suitable alternative was available, a measure of self-reported performance was devised by the authors. It is a 15-item inventory that measures performance as the summation of the 15 items weighted for their contribution to performance. The reported is not just for its intrinsic interest but to highlight the methods of construction, which could be applied to any similar vehicle.
Several prognostic indices for predicting various aspects of coronary artery disease were significantly improved by the inclusion of psychosocial factors. 218 patients with valvular heart disease who had undergone routine coronary arteriography before valve replacement were studied in terms of cigarettes smoked, family history of ischaemic heart disease, HDL:cholesterol ratio, angina, sex, blood pressure and four psychosocial characteristics (i.e. social support, work stress, life events and Type A behavior). It was found that the psychosocial factors improved the preoperative predictive power of significant coronary artery disease on four criteria: previous history of hypertension, previous history of myocardial infarction, signs of peripheral vascular disease and ECG evidence of myocardial infarction.
This study assessed the mental well-being and job satisfaction of a random sample of 318 tax officers in England, Scotland, Wales and Northern Ireland. It was found that tax officers were less satisfied with their jobs, and showed signs of mental stress in contrast with other normative groups. Using multivariate analysis, it was found that 'autocratic management style' was a strong predictor of job dissatisfaction, while 'qualitative and quantitative work overload' was the major source of lack of mental well-being.
The sources of occupational and domestic stress, together with life events and coping strategies, were assessed in terms of their influence on job dissatisfaction, mental health, and performance among a group of 442 commercial airline pilots. It was found that self-perceived poor performance was associated with job-related factors such as fatigue and anxiety about required courses, performance checks, and insufficient flying time, particularly among older pilots. Job dissatisfaction was predicted by lack of career opportunities, poor organizational climate and morale, and lack of autonomy at work, together with some domestic stressors (e.g., family health). Overall mental ill-health was found to be associated with lack of autonomy at work, fatigue, and flying patterns, together with an inability to relax and a lack of social support.
We have studied the effect of angiotensin II and bradykinin on prostaglandin output and vascular tone during extracellular calcium depletion and administration of calcium antagonists and calmodulin inhibitors to elucidate the mechanism of action in the isolated rat kidney perfused with Tyrode's solution. Administration of angiotensin II (0.028-0.28 nmol) or bradykinin (0.28-2.8 nmol) enhanced the output of prostaglandin E2 and 6-keto-prostaglandin F1 alpha in a dose-dependent manner. Angiotensin II, but not bradykinin, produced renal vasoconstriction. Omission of calcium from the medium or infusion of calcium entry blockers, diltiazem (60 microM), or nimodipine (47 microM), failed to alter prostaglandin output elicited by angiotensin II or bradykinin; however, the effect of angiotensin II to produce renal vasoconstriction was inhibited. If calcium was omitted from the medium, the intracellular calcium antagonists, 8-(diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride (23 microM), dantrolene sodium (31 microM), or ryanodine (2 microM), attenuated prostaglandin output caused by angiotensin II but not bradykinin. Calmodulin inhibitors, trifluoperazine (2 microM), napthalene sulfonamide hydrochloride (2 microM), or calmidazolium (2 microM), diminished prostaglandin output elicited by angiotensin II, but not that caused by bradykinin. Trifluoperazine, but not naphthalene sulfonamide or calmidazolium, attenuated the renal vasoconstrictor effect of angiotensin II. Prostaglandin output induced by angiotensin II and bradykinin were inhibited by mepacrine and indomethacin, whereas, the prostaglandin output caused by exogenous arachidonic acid (33 nmol) was abolished by indomethacin but was unaltered by mepacrine, calcium antagonists, and calmodulin inhibitors. From these data, we conclude that angiotensin II produces renal vasoconstriction by a mechanism dependent on extracellular calcium but not calmodulin, whereas angiotensin II-induced prostaglandin output depends on intracellular calcium and calmodulin. In contrast, bradykinin appears to stimulate prostaglandin synthesis by a calcium/calmodulin-independent mechanism.
The authors have investigated the effect of norepinephrine (NE) and selective alpha-1, alpha-2 and beta adrenergic receptor agonists and antagonists on prostaglandin (PG) output and vascular tone to determine the type of adrenergic receptor involved in these biological actions of NE in the isolated rat kidney perfused at a constant flow rate with Tyrode's solution. Renal arterial administration of NE (0.32-3.2 nmol) and the selective alpha-1 adrenergic receptor agonists phenylephrine (3-29.5 nmol), cirazoline (0.5-4.6 nmol) and amidephrine (4.1-41 nmol) produced dose-related increases in PG output and perfusion pressure. Administration of the selective alpha-2 adrenergic receptor agonists B-HT 933 (2-20 nmol) and guanabenz (1.7-17 nmol) into the kidney produced only small increases in PG output and perfusion pressure, whereas another selective alpha-2 adrenergic receptor agonist xylazine (1-20 nmol) failed to increase perfusion pressure or PG output. Infusion of the beta adrenergic receptor agonist isoproterenol reduced perfusion pressure, but failed to increase the output of PGs. The selective alpha-1 adrenergic receptor antagonist prazosin (2.7 X 10(-6) M) inhibited PG output and renal vasoconstriction elicited by phenylephrine, cirazoline and amidephrine, but not that caused by B-HT 933 and guanabenz. In contrast, the selective alpha-2 adrenergic receptor antagonist rauwolscine (1.3 X 10(-6) M) inhibited the small rise in PG output and perfusion pressure elicited by B-HT 933 and guanabenz, but not that caused by NE, phenylephrine, cirazoline or amidephrine. The beta adrenergic receptor antagonist propranolol (3.86 X 10(-6) M) did not alter PG output or renal vasoconstriction produced by NE or alpha-1 and alpha-2 adrenergic receptor agonists.(ABSTRACT TRUNCATED AT 250 WORDS)
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The purpose of this study was to assess the impact of the pilot's job on the personal and life satisfaction of his wife. A representative sample of 282 wives of commercial airline pilots was investigated to empirically determine which sources of stress and demographic characteristics would predict life dissatisfaction. It was found, using multiple regression analysis, that life dissatisfaction was significantly predicted by "domestic role overload," and "the job's impact on social life," particularly for wives whose husbands worked for smaller airlines. In addition, the wives were concerned about the "fear of husband's job loss."
This paper looks at a number of potential occupational stressors found to predict job dissatisfaction and ill health (both mental and physical) in a variety of different occupational settings. Factors intrinsic to the nature of the job, role ambiguity and conflict, poor relationships at work, lack of career development, inadequate organisation structure/climate, and problems associated with the interface between work and homelife are the focal points of attention. Many of these sources of occupational stress are prevalent in the field of aviation, and may be exacerbated by the move toward deregulation and increasing commercial competition within the industry.
Recent psychological thinking has expressed dissatisfaction with life events/life changes research. The cornerstone of such research in aviation studies is the work of Alkov. We adapted Alkov's approach and used it to see if we could extend our understanding of the mechanisms involved in the life events/accident and incident relationship. Alkov's 22-item questionnaire was expanded and administered by post as part of a much larger study. Replies were received from 442 commercial pilots working for British companies. Multivariate analysis revealed that the pilots merely regarded the 22 items as comprising three trends--Emotional Losses, Pilot Characteristics, and Emotional Gains. The overall conclusion proposes that, while Alkov's approach is interesting, expansion of it reveals that background contextual factors should be examined. Additionally, pilots' perception of the effects of life events on accident/incident potential is made on relatively broad discriminations, rather than on finely tuned judgements.
This article attempts to review the research literature relating the possible psychosocial precursors to cancer. It explores the evidence linking personality predispositions and adverse life events to cancer, providing an indication of where future research should be pursued.
The relationship between the effects of glucocorticoids on renal vascular reactivity and prostaglandin synthesis elicited by noradrenaline (NA), angiotensin II (AII), arginine vasopressin (AVP) and bradykinin (Bk) was investigated in the isolated kidney of the rat perfused with Tyrode solution. Administration of NA 0.3-3.0 nmol, AII 0.028-0.28 nmol, AVP 0.027-0.27 nmol and Bk 0.28-2.8 nmol enhanced in a dose-dependent manner the renal output of immunoreactive prostaglandin E2 (PGE2) and 6-keto-PGF1 alpha. NA, AII and AVP, but not Bk, produced renal vasoconstriction and increased perfusion pressure. In the presence of dexamethasone (2.6 X 10(-5)M) or corticosterone (2.9 X 10(-5) M), the effects of NA and AII, in enhancing prostaglandin synthesis and producing renal vasoconstriction, were reduced. In contrast, stimulation of prostaglandin synthesis by Bk and AVP and the renal vasoconstriction produced by AVP were not altered by the glucocorticoids. Dexamethasone or corticosterone did not alter the output of prostaglandins elicited by A-23187 or arachidonic acid (AA). Addition of mepacrine (2.1 X 10(-5)M) to the perfusion fluid reduced the renal output of prostaglandins elicited by the vasoactive hormones and by A-23187, but not by AA; the vasoconstrictor response to NA and AII, but not to AVP was reduced. In kidneys in which prostaglandin synthesis was inhibited by indomethacin (2.8 X 10(-6)M), administration of dexamethasone also reduced the renal vasoconstrictor effect of NA and AII. These data indicate that in Tyrode-perfused rat kidney the glucocorticoids dexamethasone and corticosterone exert a differential effect on the renal vascular reactivity to vasoactive hormones, and that their inhibitory effect on NA and AII-induced renal vasoconstriction appears to be unrelated to prostaglandin synthesis.
A description of a patient with a germ cell tumor of the anterior mediastinum is presented along with a review of the pertinent medical literature.
The membrane localization and properties of the Rhodopseudomonas sphaeroides sn-glycerol-3-phosphate acyltransferase have been examined utilizing enzymatically prepared acyl-acyl carrier protein (acyl-ACP) substrates as acyl donors for sn-glycerol-3-phosphate acylation. Studies conducted with membranes prepared from chemotrophically and phototrophically grown cells show that sn-glycerol-3-phosphate acyltransferase activity is predominantly (greater than 80%) associated with the cell's cytoplasmic membrane. Enzyme activity associated with the intracytoplasmic membranes present in phototrophically grown R. sphaeroides was within the range attributable to cytoplasmic membrane contamination of this membrane fraction. Enzyme activity was optimal at 40 degrees C and pH 7.0 to 7.5, and required the presence of magnesium. No enzyme activity was observed with any of the long-chain acyl-CoA substrates examined. Vaccenoyl-ACP was the preferred acyl-ACP substrate and vaccenoyl-ACP and palmitoyl-ACP were independently utilized to produce lysophosphatidic and phosphatidic acids. With either vaccenoyl-ACP or palmitoyl-ACP as sole acyl donor substrate, the lysophosphatidic acid formed was primarily 1-acylglycerol-3-phosphate and the Km(app) for sn-glycerol-3-phosphate utilization was 96 microM. The implications of these results to the mode and regulation of phospholipid synthesis in R. sphaeroides are discussed.
We have investigated the mechanism of action of arginine vasopressin (AVP) on vascular tone and renal output of prostaglandins (PGs) by examining the effect of Ca++ depletion, Ca++ antagonists and calmodulin inhibitors in the isolated Tyrode perfused rat kidney. Administration of AVP (0.027-0.27 nmol) into the kidney produced a dose-related renal vasoconstriction and an increase in the output of PGE2 and 6-keto-PGF1 alpha, the stable hydrolysis product of PGI2. Omission of Ca++ (1.8 mM) or addition of Ca++ channel blockers, diltiazem (6.0 X 10(-5) M) or nimodipine (4.7 X 10(-5) M), to the perfusion fluid attenuated the renal vasoconstriction, but not the output of PGs elicited by AVP. Infusion of intracellular Ca++ antagonists, Dantrium (3.1 X 10(-5) M), TMB-8 (2.3 X 10(-6) M) or ryanodine (2 X 10(-6) M) or calmodulin inhibitors, trifluoperazine (2 X 10(-6) M) or W-7 (2 X 10(-6) M), abolished the rise in renal output of PGs produced by AVP during Ca++ depletion. Calmodulin inhibitors, which inhibited the AVP-induced release of PGs in the presence of Ca++, failed to alter the renal vasoconstrictor effect of the peptide. Administration of d(CH2)5Tyr(Me)AVP, a selective antagonist of pressor actions of AVP, abolished the renal vasoconstrictor response and release of PGs elicited by AVP. In contrast, d(CH2)5-D-ValVAVP, an antagonist of antidiuretic and to a lesser extent of pressor actions of AVP, failed to alter the renal vasoconstrictor response but attenuated the output of PGs produced by AVP. AVP antagonists did not alter the effect of angiotensin II (0.096 nmol) to cause renal vasoconstriction and enhance PG output.(ABSTRACT TRUNCATED AT 250 WORDS)
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