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Biomedical subjects

J Neumann

Publications and source records attributed to J Neumann.

At least 37 records · Page 2Linked to original sources
PubMed1990

Immunological tolerance in human transplantation. The possible existence of a maternal effect.

We analyzed data from 93 patients who received a kidney graft from their parents; 55 were transplanted with a kidney from their mothers (Mat.) and thirty-eight from their fathers (Pat.) The Pat. group has shown a better graft and patient survival as well as long-term renal function when compared with the Mat. group. This pattern was more evident with time. Long-term graft function assessed by creatinine levels also showed differences between the groups, favoring the Pat. group. The results are interesting since recent reports have claimed a tolerance developed by the individual to noninherited HLA antigens of their mother.

Adolescent↗
PubMed1990

[Assessment of health status and current life style of patients with malignant neoplasms].

A review is given on the results of a study investigating the state of health and the psycho-social situation of 211 patients who underwent follow-up for malign neoplasm in the oncological Health Center of Magdeburg. In the course of a conversation the patients were questioned about social and other factors specific for their disease. For evaluating the psychic situation the questionnaire of Höck and Hess was used. The results of the study allowed to conclude that more than 50% of the patients showed psychoreactive disorders. Depending from age and sex as well as the diagnosis marked differences concerning the frequences of psychic peculiarities and the evaluation of the state of health were revealed. The results demonstrate that in addition to specific oncological knowledge the consideration of social and psychic factors is necessary for an optimum follow-up in order to recognize and prevent disorders in this field.

Adaptation, Psychological↗
PubMed1990

Differential antagonism by 1,3-dipropylxanthine-8-cyclopentylxanthine and 9-chloro-2-(2-furanyl)-5,6-dihydro-1,2,4-triazolo(1,5-c)quinazolin-5-im ine of the effects of adenosine derivatives in the presence of isoprenaline on contractile response and cyclic AMP content in cardiomyocytes. Evidence for the coexistence of A1- and A2-adenosine receptors on cardiomyocytes.

The antagonism by the A1-adenosine receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) and the A2-adenosine receptor antagonist [9-chloro-2-(2-furanyl)-5,6-dihydro-1,2,4-triazolo (1,5-c)quinazolin-5-imine] (CGS 15943A) of the effects of the A1-adenosine receptor agonist (-)-N6-phenylisopropyladenosine (R-PIA) and the A2-adenosine receptor agonist 5'-N-ethyl-carboxamideadenosine (NECA) in the presence of isoprenaline on contractile response and cyclic AMP (cAMP) content in cardiomyocytes from guinea pig cardiac ventricles were studied. In electrically driven (1 Hz) guinea pig ventricular cardiomyocytes R-PIA concentration-dependently (0.0001-100 microM) reduced the stimulatory effects of isoprenaline (0.01 microM) on contractile response and on cAMP content. The A1-adenosine receptor antagonist DPCPX (0.3 microM) antagonized the effects of R-PIA on contractile reponse and on cAMP content, whereas the A2-adenosine receptor antagonist CGS 15943A (0.01 microM) was ineffective. NECA (0.0001-100 microM) reduced the effects of isoprenaline (0.01 microM) on contractile response to about the same extent as R-PIA. However, NECA did not change cAMP content. DPCPX (0.3 microM) antagonized the effects of NECA on contractile response and evoked a cAMP-increasing effect of NECA, which was 38% of the isoprenaline value at most. In contrast, CGS 15943A did not affect the reduction of contractile response induced by NECA, whereas CGS 15943A revealed a cAMP-decreasing effect of NECA (0.1-10 microM). This study provides functional evidence that both, cAMP-decreasing A1- and cAMP-increasing A2-adenosine receptors are present on ventricular cardiomyocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1989

[Pancytopenia during low-dose oral methotrexate therapy of psoriatic arthritis].

Pancytopenia and interstitial pneumonia occurred in a 70-year-old woman with psoriatic arthritis and compensated renal insufficiency while she was being treated with low doses of the folic-acid antagonist methotrexate (5 mg weekly). Despite the administration of platelets, red blood cells, antibiotics, acyclovir and folinic acid (100 mg daily), the pneumonia progressed, and the patient died of global respiratory failure.

Administration, Oral↗
PubMed1989

Effects of adenosine analogues on force and cAMP in the heart. Influence of adenosine deaminase.

The effects of the adenosine receptor agonists (-)-N6-phenylisopropyladenosine (PIA) and 5'-N-ethylcarboxamideadenosine (NECA) on the force of contraction, adenylate cyclase activity and cAMP content in the presence of isoprenaline (Iso) were studied in ventricular preparations of the guinea-pig heart. Only in the presence of adenosine deaminase (ADA) and 50 mM sodium chloride, i.e. under 'optimal' conditions, did PIA and NECA reduce the Iso-stimulated adenylate cyclase activity in broken cell preparations, with a maximal effect of about 25%. In electrically driven (1 Hz) papillary muscles from guinea-pigs, both compounds concentration dependently reduced the Iso-stimulated force of contraction maximally by about 50% in the presence of ADA (1 microgram/ml). cAMP was measured in the same preparations. Low concentrations (0.1-1 microM) of PIA reduced the cyclic AMP content while higher concentrations increased the cyclic AMP content. The negative inotropic effect of NECA was accompanied by a concentration-dependent increase in the cyclic AMP content. We conclude that the negative inotropic effect of PIA in the presence of Iso is only in part due to a decrease in the cyclic AMP content resulting from inhibition of adenylate cyclase activity. Such an effect was only detected in the presence of ADA so that endogenous adenosine can obviously mask small effects of PIA on adenylate cyclase activity or the cyclic AMP content. In addition, the negative inotropic effect of NECA in the presence of isoprenaline was not accompanied by a reduction but an increase in the cyclic AMP content.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1989

Effects of adenosine analogues on contractile response and cAMP content in guinea-pig isolated ventricular myocytes.

In the present study the effects of adenosine analogues were investigated on cAMP content and contractile response in guinea-pig ventricular myocytes. The adenosine analogues (-)-N6-phenylisopropyladenosine (R-PIA), 5'-N-ethylcarboxamideadenosine (NECA) and (+)-N6-phenylisopropyladenosine (S-PIA) in the presence of 0.01 mumol/l isoprenaline reduced contractile response concentration-dependently. R-PIA and NECA were about equipotent (IC25: 0.01 mumol/l and 0.039 mumol/l respectively), while S-PIA was less potent (IC25: 0.6 mumol/l). Isoprenaline stimulated cAMP content was reduced by R-PIA (IC25: 0.004 mumol/l) and with lower potency by S-PIA (IC25: 0.15 mumol/l), but the extent of reduction of cAMP by R-PIA and S-PIA (to 55% and 64% respectively) was less than the reduction of contractile response (to 26% and 55% respectively). This suggests that the effects of R- and S-PIA on contractile response are only in part due to a reduction in cAMP content. In addition, NECA did not decrease cAMP content but decreased contractile response to the same extent as R-PIA. Similar results were obtained in the presence of the phosphodiesterase inhibitor Ro 20-1724. Time course studies revealed that the effects of R-PIA (1 mumol/l) on cAMP content and contractile response coincided reaching steady state after 5 min and remained stable thereafter. The effects of NECA (1 mumol/l) on contractility also reached steady state within 5 min, whereas it did not change cAMP content. It is concluded that the reduction of contractility by adenosine analogues in the presence of isoprenaline can only in part be explained by a reduction of cAMP content.(ABSTRACT TRUNCATED AT 250 WORDS)

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1989

On the mechanism of positive inotropic effects of alpha-adrenoceptor agonists.

The positive inotropic effect of the alpha 1-adrenoceptor agonist phenylephrine is accompanied by an increase in the presumed second messengers inositol 1,4,5-trisphosphate (1,4,5-IP3) and inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP4). Both 1,4,5-IP3 and 1,3,4,5-IP4 sensitize myocardial contractile proteins in chemically skinned fibers. In addition to the Ca++ releasing effect of 1,4,5-IP3 from the sarcoplasmic reticulum the Ca++-sensitizing effect of the inositol phosphates may play a role in alpha 1-adrenergic positive inotropism. In isolated heart muscle preparations from patients with endstage heart failure (due to dilated cardiomyopathy) beta-adrenergic as well as alpha 1-adrenergic effects are reduced compared to preparations from healthy hearts. The reduced beta-adrenergic effects can in part be explained by an increased content of signal transducing G1-proteins. It is tempting to investigate whether other G proteins are also altered in severe congestive heart failure.

Adrenergic alpha-Agonists↗
PubMed1989

Basal and isoprenaline-stimulated cAMP content in failing versus nonfailing human cardiac preparations.

We measured force of contraction and cAMP content in human isolated electrically driven right ventricular trabeculae carneae with and without the addition of isoprenaline (0.2 microM). Basal cAMP content was approximately 200% higher in preparations from nonfailing hearts than from hearts with end-stage myocardial failure. Isoprenaline was less effective in increasing force of contraction in failing (by approximately 100%) than in nonfailing cardiac preparations (by approximately 500%). With isoprenaline, cAMP content was approximately 50% lower in failing than in nonfailing preparations. We conclude that the reduced increase in force of contraction of failing human cardiac preparations with isoprenaline added may be causally related to an inadequately increased cAMP content.

Cyclic AMP↗
PubMed1989

Phosphodiesterase inhibition and positive inotropic effects.

Many newly developed positive inotropic agents are phosphodiesterase inhibitors. In the heart at least four phosphodiesterases (PDE I-IV) have been isolated. Depending on the species investigated, the positive inotropic effects of the PDE inhibitors appear to be correlated to the inhibition of a soluble or particulate PDE III or to a particulate PDE bound to the sarcoplasmic reticulum. In human ventricular tissue isolated from hearts with end-stage heart failure due to idiopathic dilated cardiomyopathy the positive inotropic effect of phosphodiesterase inhibitors is greatly reduced compared to healthy controls. This cannot be explained by an impaired sensitivity of the PDEs because the PDEs were similarly inhibited by PDE inhibitors in both healthy and diseased hearts. However, because the reduced positive inotropic effect is accompanied by a reduced increase in cellular cAMP concentration, an impaired formation of cAMP by the adenylate cyclase is probably involved. The impaired adenylate cyclase activity can result from an increased inhibitory GTP-binding protein (Gi-protein) recently observed in failing hearts.

Animals↗
PubMed1989

Association of human immunodeficiency virus (HIV) p24 antigenemia with decrease in CD4+ lymphocytes and onset of acquired immunodeficiency syndrome during the early phase of HIV infection.

Human immunodeficiency virus (HIV) p24 antigenemia was assessed in a longitudinal study of 52 homosexual men who developed serum antibody to HIV. Antibody seroconversion to HIV as defined by a positive HIV enzyme immunoassay (EIA) confirmed by Western (immuno-) blot was associated with three major patterns of HIV antigenemia. In the first pattern, a transient antigenemia was noted 6 (six subjects) and 12 (one subject) months prior to detection of antibody by HIV EIA and Western blot in 7 (13.5%) of the 52 men. Use of an EIA employing a recombinant envelope protein (ENV9) was able to detect antibody in four of these seven men at the time of this early antigenemia. In the second pattern, HIV p24 antigenemia occurred in 8 (15.4%) of the 52 subjects within the first 12 months after HIV antibody seroconversion. No p24 antigen was detected in the 37 (71.1%) remaining subjects. CD4+ cell numbers were lower in antigen-positive men before and after antibody seroconversion. Development of acquired immunodeficiency syndrome (AIDS) or AIDS-related complex was strongly associated with evidence of persistent p24 antigenemia during the early, postseroconversion period. HIV p24 antigenemia may be of value in determining appropriate cohorts for drug therapy trials for subjects with early-phase HIV infection.

AIDS-Related Complex↗
PubMed1989

[A historico-social approach to the medical scientific theory of Ludwik Fleck (1896-1961)].

Ludwik Fleck has shown in his discussion of the logical empirism of the Vienna Circle that his concept of reality presupposes an unproven logico-structural correspondence between the world and the formal logical structure of language, i.e. between reality and thought. Upon this questionable foundation he proceeds to develop his own position concerning the theory of medical science. He claims that scientific knowledge is at no time exempt from cultural, historical and social conditions, of which scientific knowledge itself is a function. These conditions find expression in the style of thought of a particular epoch ("Denkstil") as well as in the interaction of the participating scientists ("Denkkollektiv"). Flecks merits for having explicated the conditionality of the process of scientific knowledge over against positivistic thought have been honourably elaborated in many studies. The present study offers an analysis of the manner in which the Fleck position attempts to serve as an explanation of change in the content and style of thought in history. It will be made clear that these changes and developments can only be explained as the result of the interaction and competition among the collectives of scientists and thinkers. Fleck deprives his socio-historical position of its logical foundation by radicalizing these conditions in such a manner that they become fundamental determinants of human thought generally and for the individual scientist particularly. As a consequence, from the perspective in which the thought of the individual is thus determined, he can neither establish a convincing theory for changes in thought in history nor for the human relations obtaining within the collective of scientists and thinkers.

Austria↗
PubMed1988

Increase in myocardial Gi-proteins in heart failure.

The contractile response and myocardial content of Gi-proteins were examined in cardiac preparations from explanted hearts of four different patients with end-stage heart failure. Three patients had idiopathic dilated cardiomyopathy and one patient had inflammatory heart disease. Preparations from patients with idiopathic dilated cardiomyopathy showed reduced contractile response to the cAMP-increasing agent isoprenaline and an increase in myocardial Gi-proteins, compared with preparations from non-failing hearts. Therefore it is conceivable that an increase in myocardial Gi-proteins is causally related to heart failure due to idiopathic dilated cardiomyopathy. In the preparation from the patient with inflammatory heart disease the contractile response to isoprenaline was not reduced and likewise content of Gi-proteins was not changed.

Cardiomyopathy, Dilated↗
PubMed1988

The effects of roxatidine acetate (HOE-760) on 24-hour intragastric acidity in healthy volunteers: comparison with ranitidine and placebo.

In a series of double-blind randomized studies in normal volunteers using continuous intragastric pH monitoring, the effects of different dosage regimens of roxatidine, a new H2-receptor antagonist, were compared with placebo and ranitidine. Roxatidine acetate, 75 mg twice daily, decreased median 24 h gastric acidity from pH 1.6 to 3.2 and median nocturnal acidity from 1.5 to 3.0. Roxatidine acetate, 150 mg at bedtime, raised median 24 pH of the same 17 subjects to 2.4 and nocturnal pH to 5.9. In another series of experiments, 150 mg roxatidine acetate at bedtime was as effective as ranitidine 300 mg nocte raising median nocturnal pH (14 volunteers) from 1.4 to 6.65 compared to 6.7, respectively. However, when drugs were taken after the evening meal (post cenam nocte, pcn) roxatidine acetate 150 mg was less potent than ranitidine 300 mg with median night-time pH rising from 1.3 to 3.2 and 4.0, respectively, in 28 volunteers. Roxatidine acetate 300 mg pcn raised the pH to 4.9 suggesting that roxatidine is 1-2 times as potent as ranitidine, on a milligram-for-milligram basis.

Adolescent↗
PubMed1988

Adenosine inhibits the positive inotropic effect of 3-isobutyl-1-methylxanthine in papillary muscles without effect on cyclic AMP or cyclic GMP.

1 Adenosine and the adenosine receptor agonist (-)-N6-phenylisopropyladenosine (PIA) produced a small positive and negative inotropic effect, respectively, in isolated electrically driven papillary muscles of guinea-pigs. 2 Adenosine (100 mumol l-1) had no effect on cyclic AMP or cyclic GMP content. PIA (100 mumol l-1) slightly increased cyclic AMP. 3 In the presence of 3-isobutyl-1-methylxanthine (IBMX; 60 mumol l-1), which increased force of contraction 2 fold, adenosine and PIA exerted strong negative inotropic effects. PIA was more potent than adenosine (mean IC25 2.1 and 168 mumol -1, respectively). 4 In contrast, the nucleosides did not affect the increase in force of contraction produced by elevating extracellular Ca2+ concentration. 5 The IBMX-antagonistic effects of adenosine and PIA were not accompanied by modification of the IBMX-induced increase in cyclic AMP and cyclic GMP. 6 The effects of adenosine and PIA on force of contraction were accompanied by a partial reversal of the IBMX-induced increase in the maximal rate of depolarization of slow action potentials. 7 It is concluded that adenosine and PIA are able to attenuate the positive inotropic effect of a phosphodiesterase inhibitor. This effect is unlikely to be due to a reduction of the IBMX-induced increase in cyclic AMP content. It is conceivably due to an inhibition of the stimulant action of cyclic AMP on slow Ca2+ channels leading to the reduction of the slow inward current which in turn reduces force of contraction.

1-Methyl-3-isobutylxanthine↗