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T Böhm

Publications and source records attributed to T Böhm.

35 records · Page 2Linked to original sources
PubMed1996

[Calcium antagonists and ischemic heart disease].

The authors give a short account about the significance, basic rules in regulation of intracellular (cytosolic) calcium homeostasis, distribution of calcium channels in different organs and characteristics of L channels in cardiovascular system. The different types of calcium channel blockers (dihydropyridines, phenylalkilamines, benzothiazepines), their similarities, dissimilarities (cardio, -vascular selectivity) are discussed. Differences in calcium homeostasis, in sympathetic innervation between vascular smooth- and heart muscle in briefly disputed. The basic role of endothel cell dysfunction in development of ischemic heart disease, the possible mechanisms (potential anti-remodeling, antifissuring, antiischemic, cardioprotective, sympaticolytic effects) of different calcium antagonists in the treatment of patients with ischemic heart disease are reviewed. Potential adverse effects of calcium channel blockers (proischemic, proarrhythmic, procongestive, prohaemorrhagic effects) are also mentioned. Finally the up-date preventive and therapeutic indications of different calcium channel blockers in the clinical management of patients with stable, unstable angina pectoris, silent myocardial ischemia, vasospastic angina, acute myocardial infarction is shortly reported.

Angina, Unstable↗
PubMed1996

Activation of S-phase-promoting CDKs in late G1 defines a "point of no return" after which Cdc6 synthesis cannot promote DNA replication in yeast.

In eukaryotic cells, DNA replication is confined to a discrete period of the cell cycle and does not usually recur until after anaphase. In the budding yeast Saccharomyces cerevisiae, assembly of pre-replication complexes (pre-RCs) at future origins as cells exit mitosis (or later during G1 is necessary for subsequent initiation of DNA replication triggered by activation in late G1 of Cdc28/Cdk1 kinases associated with B-type cyclins Clb1-Clb6. The absence of pre-RCs during G2 and M phases could explain why origins of DNA replication fire only once during the cell cycle, even though S-phase-promoting Cdks remain active from the beginning of S phase through the end of M phase. Formation of pre-RCs and their maintenance during G1 depend on the synthesis and activity of an unstable protein encoded by CDC6. We find that Cdc6 synthesis can only promote DNA replication in a restricted window of the cell cycle: between destruction of Clbs after anaphase and activation of Clb5/ and Clb6/Cdk1 in late G1. The latter corresponds to a "point of no return," after which Cdc6 synthesis can no longer promote DNA replication. Cdc6 protein can be made throughout the cell cycle and, in certain circumstances, can accumulate within the nuclei of G2 and M phase cells without inducing re-replication. Thus, control over Cdc6 degradation and/or nuclear localization is not crucial for preventing origin re-firing. Our data are consistent with the notion that cells can no longer incorporate de novo synthesized Cdc6 into pre-RCs once C1b/Cdk1 kinases have been activated. We show that Cdc6p associates with Clb/Cdk1 kinases from late G1 until late anaphase, which might be important for inhibiting pre-RC assembly during S, G2, and M phases. Inhibition of pre-RC assembly by the same kinases that trigger initiation explains how origins are prevented from re-firing until Clb kinases are destroyed after anaphase.

Anaphase↗
PubMed1996

Isolation and characterization of tissue-type plasminogen activator- binding proteoglycans from human umbilical vein endothelial cells.

We analyzed the tissue-type plasminogen activator (TPA)-binding proteoglycans (PGs) on human umbilical vein endothelial cells (HUVECs), which were metabolically labeled with [35S]NA2SO4. Cell extracts were then prepared and subjected to affinity chromatography on diisopropyl fluorophosphate (DFP)-inactivated TPA-Sepharose 4B. Approximately 6% of the incorporated 35S radioactivity bound to DFP-treated TPA-Sepharose 4B and was eluted with 2 mol/L NaCl. In addition to NaCl, heparin, arginine, and lysine but not glycine, epsilon-amino-n-caproic acid or aspartic acid inhibited this binding and eluted the bound 35S radioactivity. Urea-containing polyacrylamide gel electrophoresis of the eluted material consistently revealed two main signals of 35S radioactivity (one with an M(r) between 600,000 and 750,000 [PGA] and the other with an M(r) between 120,000 and 180,000 [PGC]). Occasionally a less intense signal with an M(r) between 340,000 and 440,000 (PGB) was seen. Heparitinase treatment markedly decreased the intensities of both 35S signals (PGA and PGB), and chondroitinases AC and ABC abolished the 35S signal of PGC, indicating that most of the HUVEC-incorporated radioactivity with an affinity for TPA could be attributed to heparan sulfate- and chondroitin sulfate-like structures. Reductive elimination, which was performed to separate the possible glycosaminoglycan moieties from the core proteins, confirmed the PG-like nature of this material and again revealed heparan sulfate and chondroitin sulfate as the major glycosaminoglycan components. We therefore conclude that HUVECs synthesize TPA-binding, heparan sulfate- and chondroitin sulfate-containing PGs. In vivo, similar PGs may play a role in TPA binding to endothelial cells and thereby possibly influence TPA activity and/or provide an intravascular storage pool of TPA.

Cells, Cultured↗
PubMed1995

Roles and regulation of Cln-Cdc28 kinases at the start of the cell cycle of Saccharomyces cerevisiae.

In budding yeast G1 cells increase in cell mass until they reach a critical cell size, at which point (called Start) they enter S phase, bud and duplicate their spindle pole bodies. Activation of the Cdc28 protein kinase by G1-specific cyclins Cln1, Cln2 or Cln3 is necessary for all three Start events. Transcriptional activation of CLN1 and CLN2 by SBF and MBF transcription factors also requires an active Cln-Cdc28 kinase and it has therefore been proposed that the sudden accumulation of CLN1 and CLN2 transcripts during late G1 occurs via a positive feedback loop. We report that whereas Cln1 and Cln2 are required for the punctual execution of most, if not all, other Start-related events, they are not required for the punctual activation of SBF- or MBF-driven transcription. Cln3, on the other hand, is essential. By turning off cyclin B proteolysis and turning on proteolysis of the cyclin B-Cdc28 inhibitor p40SIC1, Cln1 and Cln2 kinases activate cyclin B-Cdc28 kinases and thereby trigger S phase. Thus the accumulation of Cln1 and Cln2 kinases which starts the yeast cell cycle is set in motion by prior activation of SBF- and MBF-mediated transcription by Cln3-Cdc28 kinase. This dissection of regulatory events during late G1 demands a rethinking of Start as a single process that causes cells to be committed to the mitotic cell cycle.

CDC28 Protein Kinase, S cerevisiae↗
PubMed1994

The B-type cyclin kinase inhibitor p40SIC1 controls the G1 to S transition in S. cerevisiae.

When yeast cells reach a critical size, they initiate bud formation, spindle pole body duplication, and DNA replication almost simultaneously. All three events depend on activation of Cdc28 protein kinase by the G1 cyclins Cln1, -2, and -3. We show that DNA replication also requires activation of Cdc28 by B-type (Clb) cyclins. A sextuple clb1-6 mutant arrests as multibudded G1 cells that resemble cells lacking the Cdc34 ubiquitin-conjugating enzyme. cdc34 mutants cannot enter S phase because they fail to destroy p40SIC1, which is a potent inhibitor of Clb but not Cln forms of the Cdc28 kinase. In wild-type cells, p40SIC1 protein appears at the end of mitosis and disappears shortly before S phase. Proteolysis of a cyclin-specific inhibitor of Cdc28 is therefore an essential aspect of the G1 to S phase transition.

Anaphase-Promoting Complex-Cyclosome↗
PubMed1992

Platelet PGI2-receptor behaviour change after treatment with acetylsalicylic acid in healthy volunteers.

After treatment of human platelet membrane fractions with different concentrations of acetylsalicylic acid (ASA) the Iloprost binding capacity (Bmax) and also the dissociation constant (Kd) of the high-affinity PGI2-receptor increased significantly (p less than 0.01, low-affinity receptor only an increase of Bmax, p less than 0.01), whereas only a significant (p less than 0.05) increase of the Kd of the high-affinity receptor was observed for intact platelets.

Adolescent↗
PubMed1992

Turning points and change in psychoanalysis.

The turning point is defined as the sudden change of quality that plays the part of a forerunner or prerequisite to the slow structural change in psychoanalytic treatment. Turning points have two common elements, confrontation and surprise, that lead to the centre of the turning point experience -- the feeling of having an inner life--which leads up to the interpretive working through process that corresponds to structural change. To restore or create the feeling of having an inner life runs parallel to restoring the psychoanalytic process from acting-out temptations. Harold Stewart's agents of change are discussed as having the characteristics of turning points and clinical vignettes are described to show the main points. Finally, the countertransference aspect of allowing turning points to happen is discussed.

Countertransference↗
PubMed1990

Properties of a potassium-selective ion channel in human melanoma cells.

Currents through ion channels were measured from cells of a human melanin-producing melanoma cell line (IRG 1) with the patch clamp technique. In these cells the most frequently observed channel is a potassium channel. The channel activates slowly at depolarizing voltage steps but does not inactivate. Single channel potassium currents can be measured in cell-attached patches at the resting potential of melanoma cells. The channel has a conductance of approximately 10 pS. As measured from the reversal potentials of single channel currents, the permeability ratio for sodium and potassium, PNa/PK, is between 0.03 and 0.04. Open probability is increased at positive potentials. Mean open times are prolonged at voltage steps to more positive potentials. Closed time histograms are fitted by two exponentials. The slow shut time is decreased at positive potentials. In whole cell measurements, cell conductance measured between -20 and + 70 mV was reduced by 10 mM tetraethylammonium chloride from 6.4 +/- 1.2 nS (n = 4) to 0.8 +/- 0.3 nS (n = 3). Application of isoproterenol decreases the probability of the channel being open without any change in the single channel conductance. A possible role of the 10 pS potassium channel in the growth of melanoma cells is discussed.

Cyclic AMP↗
PubMed1987

Human acute unclassified leukemia with a unique t(4;17) chromosomal translocation expresses T lymphoid and myeloid surface antigens after in vitro culture.

Bilineage differentiation along both the T lymphoid and the myeloid lineage while in in vivo diffusion chamber (DC) and in vitro suspension culture was observed in a case of acute unclassified leukemia (null-AL) and t(4;17). Prior to culture, the blast cells were TdT and la positive but did not express any lineage-specific antigenic markers. Furthermore, the immunoglobulin heavy chain and T cell receptor beta-chain genes were in germline configuration. Cytogenetically, all metaphases had the unique translocation t(4;17) (q25;q23) prior to and after culture, supporting the leukemic origin of the cells. During both DC culture and suspension culture with and without tetradecanoyl-phorbol-acetate (TPA), a substantial increase in the absolute and relative number of cells expressing both myeloid and T lymphoid antigenic markers occurred. Double-fluorescence analysis demonstrated the expression of antigenic markers of both lineages on the same population of cells, and electron microscopy revealed the induction of myeloperoxidase after both DC and suspension culture. Immunoglobulin heavy chain and T cell receptor beta-chain genes remained in germline configuration after treatment with TPA, when analyzed with JH and CT beta probes, respectively. These findings indicate that this case represents a null-AL with dual-lineage capabilities, which has probably arisen from the malignant transformation of a bipotential stem cell of lymphoid and myeloid progeny.

Antigens, Neoplasm↗
PubMedDate not supplied

Risk of bacteremia induced by transesophageal echocardiography: analysis of 100 consecutive procedures.

The incidence of bacteremia induced by transesophageal echocardiography (TEE) and, consequently, the need for an antibiotic prophylaxis before TEE is still controversial. Therefore, we studied the incidence of bacteremia associated with TEE prospectively in 100 consecutive patients without clinical or laboratory signs of bacterial infection. Blood samples were drawn immediately before and at 0, 5, and 15 minutes after TEE. In addition, swabs were taken from the pharyngeal region before TEE and from the distal part of the TEE-probe before and after TEE. All blood cultures taken before TEE remained sterile. After TEE, three positive blood cultures were found in two patients: the first patient had two different species of coagulase-negative staphylococci in cultures taken at 0 minutes (Staphylococcus capitis) and 15 minutes (Staphylococcus cohnii) after TEE, whereas the sample taken after 5 minutes remained sterile. In the second patient, Propionibacterium species appeared after 7 days of processing in a culture taken immediately after TEE, but not in the samples taken after 5 and 15 minutes. None of the three microorganisms found in the blood were simultaneously isolated in pharyngeal specimens or TEE-probe specimens of the same patient. Thus positive blood cultures in both patients were considered contaminated. This study demonstrates that TEE, when performed by an experienced investigator, is not associated with an increased risk of bacteremia. Accordingly, it is justified to perform TEE examinations (also in high-risk patients) without antibiotic prophylaxis.

Adult↗