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Biomedical subjects

G Baumann

Publications and source records attributed to G Baumann.

At least 181 records · Page 10Linked to original sources
PubMed1996

[Interventional pneumology: procedures for pulmonary hemorrhage and tumor-induced superior vena cava syndrome].

Interventional pneumology includes both bronchological and vascular methods of diagnostic and therapy, especially in case of pneumological emergency, such as pulmonary hemorrhage and superior vena cava syndrome. In massive pulmonary hemorrhage bronchological diagnosis is needed to determine the location and activity of the bleeding, as well as angiography of bronchial arteries, and of pulmonary arteries, respectively. Bronchus occlusion by aid of balloon catheter or double lumen tube are intermediate methods to bridge over till defenitive surgery or embolisation of bronchial or pulmonal arteries as complementary methods in patients with pulmonary hemorrhage. In patients suffering from superior vena cava syndrome caused by neoplasms venous angioplasty and Wallstent implantation provide immediate clinical improvement.

Angioplasty, Balloon↗
PubMed1996

[Percutaneous "high risk" angioplasty with prophylactic cardiopulmonary support. High risk PTCA with mechanical circulatory support].

With improved technology and development of several mechanical assist devices, the indications of percutaneous transluminal coronary revascularization have been extended. In 39 patients (30 men, mean age = 60.1 +/- 8.1 years) with angina pectoris or heart failure, with poor operative risk-benefit ratio and ejection fraction < 35% and/or target vessel supplying > 50% of the viable myocardium, we performed assisted percutaneous transluminal coronary revascularization. Intraortic balloon counterpulsation (n = 16), extracorporal circulation (n = 21), or hemopump (n = 2) were used for mechanical support. Complete 6-week follow up was possible in 27 patients. An improvement of left-ventricular function (patients with EF < or = 35% demonstrated an improvement: 27 +/- 7 vs 36 +/- 10%, p < 0.05), heart failure (patients with EF < or = 35% demonstrated an improvement of maximal oxygen uptake: 14 +/- 4 vs 17 +/- 4 ml/kg/min; p < 0.05) and a marked improvement of angina (23/38 demonstrated CCS-improvement of at least one class) was found. Hospital mortality was as low as 2.6%. Major postinterventional complications included nonfatal myocardial infarction (n = 2), fatal retroperitoneal bleeding (n = 1), pulmonary edema (n = 1), nonfatal ventricular fibrillation (n = 1), cerebrovascular event without residual (n = 1), and deep vein thrombosis (n = 4). In conclusion, assisted percutaneous revascularization was successful in a high risk subset of patients with increased surgical risk and/or poor ventricular function.

Aged↗
PubMed1996

[Pharmacotherapy of severe heart failure with inodilators--new approaches].

Severe congestive heart failure and cardiogenic shock don't resemble a homogeneous clinical picture, but a syndrome that is based on very different etiologies. What all the etiologies have in common is the inadequate peripheral O2-supply to essential organs with or without signs of severe pulmonary congestion up to pulmonary edema. For prognosis and therapy is a fast diagnostical clarification of the causes crucial. The therapeutical procedure for the various etiologies may be diametrically opposed. For the therapy is it also dicisive to distinguish between acute myocardial failure, e.g. acute myocardial infarction, and the development of myocardial failure from a longer existing consistent congestive heart failure (cardiomyopathy). Whenever possible, next to symptomatically therapy of cardiogenic shock the basic conditions of the disease should be cured (e.g., PTCA, lysis with acute myocardial infarction, lysis in acute pulmonary embolism). In myogenic cardiogenic shock the use of positive-inotropic substances with and without simultaneous vasodilatory effects, if necessary in combination with other vasodilators, may be life-saving. Up until now there still doesn't exist an alternative to the catecholamines in the acute phase, initially they should be used as a first-line-therapy to stabilize the hemodynamics. The insertion of a Swan-Ganz-catheter for invasive therapy-monitoring, especially for the regulation of the therapy is a "condition sine qua non" for every patient with unstable hemodynamics. Because of the prompt beta-receptor-down-regulation during shock, caused by endogenous catecholamines, successful therapy with exogenous catecholamines is limited (adrenaline, dopamine, dobutamine), on account of the acceleration and intensification of the beta-receptor-down-regulation process. Possible beta-receptor independent alternatives are beta 2-agonists (dopexamine), PDE-III-inhibitors (amrinone, milrinone, enoximone) as well as H2-receptor agonists (impromidine, arpromidine) and finally the calcium-sensitisers (pimobendane). First results give rise to optimism to effectively reduce the mortality of congestive heart failure. The combination of these new pharmacological possibilities with interventional transcutaneous applicable assist-systems (aortic counterpulsationpump IABP, hemopump, transcutaneous heart-lung-machine) as well as the transitory application of an artificial heart (Novacor) can possibly increase the success of these therapeutic strategies. So far there are no convincing results shown in the world literature.

Adrenergic beta-Agonists↗
PubMed1995

Crystal structure of the SH2 domain from the adaptor protein SHC: a model for peptide binding based on X-ray and NMR data.

Src homology 2 domains (SH2) are protein molecules found within a wide variety of cytoplasmic signalling molecules that bind with high affinity to phosphotyrosyl (pY)-containing protein sequences. We report here for crystal structure of the SH2 domain from the adaptor protein SHC (Shc), which has been refined by restrained least-squares methods to an R-factor of 17.3% to 2.7 A. The overall Shc architecture is essentially similar to that determined in other SH2 domains but it shows significant differences in a number of loops, thus providing a molecular surface with no obvious secondary pocket. Based on the knowledge of the crystal structure of the protein a model for a low affinity Shc-bound peptide has been generated from nuclear magnetic resonance data in solution using transferred nuclear Overhauser enhancements as intramolecular distance restraints. The model shows that the tyrosine moiety binds Shc in a rather similar way to that observed for other SH2-peptide complexes, but that the residue in position +3 does not seem to make specific contact with the protein. An intermolecular crystallographic interaction occurs between the pY-binding site and the C-terminal residues of a symmetry-related molecule. This crystal packing interaction suggests how inhibitory regulation could play a role in SHC activity.

Amino Acid Sequence↗
PubMed1995

[Venous angioplasty and Wallstent implantation in emergency treatment of superior vena cava syndrome caused by tumor].

HISTORY AND CLINICAL FINDINGS: A 58-year-old man was hospitalized because of threatened asphyxia resulting from massive obstruction to neck vein flow and increased venous markings over the ventral and dorsal thorax. The previous year he had received radiotherapy (total of 55.8 Gy) for squamous cell carcinoma in the right upper lobe of the lung (primary stage T2 N2 M0). The signs of venous congestion had developed over several months. TESTS: Emergency phlebography demonstrated obstruction to superior vena cava (SVC) flow by tumour compression. TREATMENT AND COURSE: It was possible to pass the SVC obstruction with a hydrophilic guide-wire and then perform a balloon angioplasty, followed later by implantation of two intraluminal expandable stents ("Wallstent"). The dyspnoea quickly improved after the successful recanalization. The day after the intervention palliative radiotherapy of the SVC obstruction was begun. But increased venous markings over the thorax recurred, but without dyspnoea, after 4 1/2 months free of signs of venous congestion. Repeat phlebography again demonstrated complete obstruction of the SVC by the tumour. Recanalization by balloon angioplasty was again achieved. CONCLUSIONS: This case underlines the value of percutaneous balloon angioplasty with stent implantation as supplementary treatment in the late stages of SVC obstruction by tumour.

Angioplasty, Balloon↗
PubMed1995

The crystal structures of the SH2 domain of p56lck complexed with two phosphonopeptides suggest a gated peptide binding site.

Src homology-2 (SH2) domains are protein modules found within a wide variety of cytoplasmic signalling molecules that bind with high affinity to phosphotyrosyl-containing protein sequences. In order to develop SH2 inhibitors that contain phosphotyrosyl analogues resistant to cellular phosphatases, we have solved the crystal structures of the SH2 domain of p56lck in separate complexes with two high-affinity p-(phosphonomethyl)phenylalanine-containing peptides. The structures have been determined at 2.3 A and 2.25 A, and refined to crystallographic R-factors of 19.2% and 18.5%, respectively. The conformation of the SH2 domain of p56lck is essentially similar to that observed in Src and Lck complexed with a phosphotyrosine-containing peptide except in some loops and especially in the loop that connects the second and third beta-strands. This loop, which was involved in hydrogen-bond interactions with the phosphotyrosine moiety, has moved away in the phosphonopeptide complexes as a rigid body by about 7 A on two hinges leaving the tyrosine phosphate mimetic moiety accessible to the solvent. Some intramolecular hydrogen bonds with other residues of the third and fourth beta-strands stabilize an open conformation of the lid, suggesting a flap mechanism for peptide binding.

Amino Acid Sequence↗
PubMed1995

Modulation of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 on human coronary smooth muscle cells by cytokines.

Adhesion molecules have been demonstrated immunohistochemically on smooth muscle cells in atherosclerotic plaques. In endothelial cells cytokines are potent modulators of adhesion molecule expression. We therefore investigated the effects of cytokines on adhesion molecule expression on cultured human coronary and pulmonary smooth muscle cells by cell ELISA and confocal microscopy. Human coronary and pulmonary smooth muscle cells expressed ICAM-1 and VCAM-1 but not E-selectin. ICAM-1 expression was upregulated by TNF alpha, Il-1 beta and IFN-gamma. VCAM-1 expression was increased by TNF alpha and weakly by Il-1 beta, IFN-gamma had no effect on VCAM-1 expression. Cytokine effects on ICAM-1 and VCAM-1 were based on de novo synthesis. These results demonstrate that cytokines regulate ICAM-1 and VCAM-1 expression on human coronary and pulmonary smooth muscle cells. These effects may play an important role in the immune mechanisms in atherosclerosis.

Cells, Cultured↗
PubMed1995

Effects of prostaglandin E1, prostaglandin E0 and SPM 206 on isolated human coronary arteries.

The effects of PGE1, PGE0 and the stable PGE1-analogue SPM 206 on human epicardial coronary arteries were studied in vitro. The tension of the isolated arterial rings was measured isometrically. After precontraction, concentration-response curves with the compounds were performed. PGE1 and SPM 206 elicited concentration-dependent relaxations which are counteracted by a contractile action in higher concentrations. In PGE0, the contractile action occurred even in lower concentrations. This contraction was antagonized by the selective thromboxane A2 antagonist SQ 29,548, resulting in an equipotent relaxation for all three compounds.

Alprostadil↗
PubMed1995

Pituitary adenylate cyclase activating peptides are endothelium-independent dilators of human and porcine coronary arteries.

The PACAPs have been shown to be potent vasodilators in different animal species. Data in humans are still lacking. Therefore we investigated the effects of PACAP 38, PACAP 27 and VIP on isolated human and porcine coronary arteries (HCA and PCA). Our data show, that the PACAPs are endothelium-independent vasorelaxants, which in HCA are slightly more potent than VIP. The N-terminal shortened peptides PACAP 6-38 and PACAP 6-27 also show relatively potent vasorelaxant effects, acting as partial agonists. Glibenclamide, a selective inhibitor of ATP-sensitive potassium channels, partially reverses the effects of the PACAPs, indicating an involvement of these channels in the mechanism of action.

Animals↗
PubMed1995

Dynamic three-dimensional transesophageal echocardiography using a computed tomographic imaging probe--clinical potential and limitation.

Dynamic three-dimensional echocardiography is a new diagnostic tool for spatial visualisation of cardiac anatomy and volumetric assessment. A computer-controlled probe acquires parallel tomographic slices, from which dynamic three-dimensional images of the heart can be reconstructed. Thirty adult patients with valvular heart diseases, congenital heart diseases, intracardiac masses, heart failure and other cardiac lesions, underwent conventional two-dimensional (n = 30), three-dimensional echocardiography (n = 30) and thermodilution (n = 17). The feasibility, usefulness and possibility of simulating a surgical view of intracardiac anatomy and exact volumetry were determined. The two different morphologic images were compared qualitatively. For quantitative analysis volumetry was performed using standard thermodilution technique and dynamic three-dimensional echocardiography. In more than 80% of the patients additional morphologic information was gained and a strong correlation (r = 0.75-0.95) between two volumetry assessments was found. Based on this findings, dynamic three-dimensional echocardiography is an additional and valuable approach in the perioperative and intensive care management in this group of patients.

Adult↗
PubMed1995

Analysis of alternans in late potentials. Correlations between epicardial and body surface recordings.

The methodical performance of the signal-averaged electrocardiogram is strongly influenced by the beat-to-beat reproducibility of late potentials (LPs). Especially at higher heart rates, epicardial recordings from infarct regions show progressive beat-to-beat prolongations with alternating conduction block. To analyze the influence of beat-to-beat-alternans of LPs on the signal-averaging process, epicardial and body surface recordings were studied at different heart rates and extrastimulation. Epicardial and body surface recordings were obtained from dogs with 4-day postligation of the left anterior descending coronary artery (Harris model). Body surface potentials were averaged in different modes to a final noise level of 0.3 microV (rms) and digitally bandpass filtered (40-250 Hz). Modulation of the heart rate was performed by atrial or His-bundle pacing and by atrial premature extrastimulation. Pacing up to heart rates close to 180 beats/min produced no significant changes in the duration of LPs in epicardial and averaged body surface recordings; however, at higher pacing rates, considerable prolongation of LPs with different patterns in the epicardial leads was observed. In these cases, averaging of all beats revealed only a slight prolongation of LPs, as seen from the body surface. Selective averaging of beats with prolonged epicardial LPs showed the prolongation or absence of LPs, as seen in the epicardial recordings. Similar observations were made using an atrial extrastimulation technique, whereby the average of the premature beats was compared to the average of all normal sinus beats. Selective beat averaging of body surface potentials can unmask the prolongation of LPs due to atrial pacing or extrastimulation, as seen in recordings from the infarcted epicardium. The evidence of this modulation of LPs may improve the positive predictive value of the signal-averaged electrocardiogram.

Action Potentials↗
PubMed1995

Growth hormone binding to a circulating receptor fragment--the concept of receptor shedding and receptor splicing.

Recent advances in the understanding of circulating growth hormone binding proteins (GHBP) are reviewed. The high affinity GHBP represents the ectodomain of the GH receptor (GHR); it is either cleaved from membrane-bound GHRs (man, rabbit) or derived from an alternatively spliced GHR mRNA (rodents). Another circulating GHBP, of low affinity and not GHR-related, is only partially characterized. The GHBPs complex about half of the GH in human plasma. They act as a buffer regulating free and bound GH, prolong GH half-life, and modulate GH bioactivity through competition with GHRs for ligand. The plasma levels of both GHBPs are developmentally upregulated during childhood and remain relatively constant thereafter. Different species vary in their regulation of GHBP, with sexual dimorphism and large pregnancy-related changes in some but not all species. A variety of conditions associated with altered GH responsivity (resistance or hypersensitivity) are attended by altered levels of the high affinity GHBP. Generally, GH resistance is characterized by decreased GHBP levels, and the converse is true in GH hypersensitivity such as in obesity. It has been postulated that the plasma GHBP level reflects tissue concentrations of the GHR, but this remains to be proven. The high affinity GHBP appears to be positively, though imperfectly, linked to GH action. Soluble receptor isoforms analogous to the GHBP have been demonstrated for several members of the cytokine receptor family to which the GHR belongs. The ultimate biological role of these circulating receptor ectodomains remains to be fully defined.

Adult↗
PubMed1995

Tyrosine-phosphorylated forms of Ig beta, CD22, TCR zeta and HOSS are major ligands for tandem SH2 domains of Syk.

The protein tyrosine kinase Syk plays an important role in signal transduction from the B cell antigen receptor and possibly also from the TCR. We have examined the binding specificity of Syk-derived SH2 domains in vitro and found that the tandem SH2 domains have two major ligands in activated Ramos B cells as well as in activated Jurkat T cells. The SH2-binding proteins in Ramos B cells were identified as the tyrosine-phosphorylated forms of the Ig alpha beta heterodimer and of CD22. Binding to the Ig alpha beta heterodimer seems to occur predominantly via Ig beta, indicating that the two receptor components might couple to distinct signaling pathways. In Jurkat T cells one of the SH2-binding proteins represents the tyrosine-phosphorylated TCR zeta chain. The identity of the second SH2 ligand, called HOSS, is not known. HOSS is discussed as a putative member of the receptor family characterized by the immunoreceptor tyrosine-based activation motif.

Antigens, CD↗
PubMed1995

Heterogeneity of left ventricular regional wall thickening following dobutamine infusion in normal human subjects.

BACKGROUND: Pathophysiological data and pragmatic clinical experience with stress echocardiography suggest that inotropic stimulation with simultaneous changes in heart rate and loading conditions can affect the function of various myocardial regions asymmetrically, inducing heterogeneity in wall motion and thickening, possibly mimicking 'ischaemic' regional hypokinesis or lack of hyperkinesis during stress. OBJECTIVES: To describe, in a quantitative fashion, the physiological contractile response of different left ventricular regions following dobutamine infusion. METHODS: Two hundred and twenty-three in-hospital patients undergoing dobutamine stress echocardiography and coronary angiography were initially considered. Of these 223 patients, 18 had angiographically normal coronary arteries, normal resting function, negative ergonovine and exercise stress tests, and negative dobutamine stress echocardiograms; of the 18, only in 11 patients (six females, age = 56 +/- 10 years) was it possible to obtain quantitative measurements of the middle segments of the inferior, anterior, lateral, and septal walls. Two-dimensional echocardiographic measurements of wall thickness were obtained at the end-diastolic (onset of Q wave) and end-systolic phases, both at baseline (rest) and at the peak of the dobutamine infusion (40 micrograms.min-1.kg-1 plus atropine). RESULTS: Dobutamine increased heart rate (rest = 69 +/- 9 vs dobutamine = 138 +/- 13 beats.min-1; P < 0.01), whereas systolic blood pressure did not change significantly (rest = 136 +/- 15 vs dobutamine = 150 +/- 25 mmHg, P = ns). During stress, % systolic thickening decreased in the inferior wall (rest = 73 +/- 24 vs dobutamine +/- 50 +/- 9%; P < 0.01), whereas it tended to increase to a variable extent in the other regions, i.e. septal (rest = 46 +/- 17 vs dobutamine = 68 +/- 13%, P < 0.01), anterior (rest 62 +/- 19 vs dobutamine = 69 +/- 11%, P = ns), and lateral wall (rest = 48 +/- 16 vs dobutamine = 61 +/- 18%, P = ns). The decrease in % systolic thickening of the inferior wall was inversely correlated with the increase in end-diastolic wall thickness (r = -0.75; P < 0.01), but neither with heart rate (r = 0.15; P = ns) nor with systolic blood pressure changes (r = 0.05; P = ns). CONCLUSIONS: Heterogeneity of left ventricular wall thickening can be induced or magnified by dobutamine infusion even in subjects without coronary artery disease, with the inferior wall showing a lack of hyperkinesis, up to relative hypokinesis, in comparison with other myocardial regions. Caution in aggressive dobutamine stress echocardiography reading, especially in the inferior wall, might be warranted.

Adult↗
PubMed1995

Enhanced migratory activity of vascular smooth muscle cells with high expression of platelet-derived growth factor A and B.

UNLABELLED: Proliferation and migration of vascular smooth muscle cells (SMCs) are major events in atherogenesis. It is known that platelet-derived growth factor (PDGF) stimulates both of these processes in a paracrine fashion, whereas autocrine stimulation has been shown only for proliferation. The aim of this study was to investigate the influence of PDGF expression in SMCs on migratory activity of these cells. SMCs were cultivated from the vascular tissue of 23 patients. Cellular motility was analyzed by a computer-assisted motion analysis system; 54 images per sample, obtained during an observation period of eighteen hours, were analyzed. PDGF-A and PDGF-B mRNA levels were determined by quantitative polymerase chain reaction (PCR) following reverse transcription. To quantitate mRNA content of SMCs, the authors coamplified cDNA copies of mRNA from cells and from a synthetic reference RNA in the same reaction vessel. Cells derived from atherosclerotic lesions produced a 1.6-fold increase of PDGF-A (P < 0.05) and a 5-fold increase of PDGF-B mRNA (P < 0.05) as compared with those from normal vessels. The migratory velocity (range 11.1-49.2 microns/hr) was independent of PDGF-A and PDGF-B mRNA expression. A significant correlation between levels of PDGF-A mRNA and PDGF-B mRNA and the degree of directional changes of SMCs on the covered track (klinokinesis) was found (P < 0.05). CONCLUSION: PDGF-A and PDGF-B mRNA expression is significantly correlated with positive klinokinesis without affecting migratory velocity. This finding reflects enhanced migratory activity of SMCs. Besides its known mitogenic effects, the authors present evidence that PDGF may act as an autocrine motogen* in SMCs.

Adolescent↗
PubMed1995

Growth hormone-binding protein in human lymph.

The high affinity GH-binding protein (GHBP) is a soluble circulating ectodomain of the GH receptor (GHR). In humans, it is thought to be released from the plasma membrane-bound GHR by proteolysis at or near the transmembrane domain. GHBP modulates GH action by 1) intravascular complex formation, and 2) competing with the GHR for ligand in tissues (interstitial complex formation). Little is known about the tissue source(s) of GHBP, the local regulation of GHBP generation, or its concentration in the interstitium. To begin addressing these questions, we studied GHBP levels in peripheral lymph, whose composition approximates that of interstitial fluid. Lymph was collected in 13 healthy adult men from cannulated lymphatic vessels in the calf. Venous and arterial blood samples were collected from the femoral vein and radial artery contemporaneously with lymph collection. Potential GHBP production by endothelial or blood cells was assessed by examining conditioned medium from in vitro cell cultures. GHBP activity was measured by standardized GH binding/column chromatography assay. GHBP was consistently and significantly lower in lymph (mean +/- SD, 4.6 +/- 1.2% GH bound/200 microL) than in venous (14.1 +/- 3.0%) or arterial (14.9 +/- 3.6%) plasma. Conditioned medium from endothelial or blood cell cultures did not contain detectable GHBP. We conclude that the level of GHBP in peripheral lymph is substantially lower than that in the peripheral circulation, and that components of the vasculature are not important sources of GHBP. These findings suggests that 1) the main tissue sources of GHBP in man are the central organs (especially liver); and 2) transcapillary diffusion of GHBP into the interstitial space is restricted.

Adult↗