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Biomedical subjects

B Müller

Publications and source records attributed to B Müller.

At least 397 records · Page 22Linked to original sources
PubMed1988

[Transient erythroblastopenia in childhood].

Clinical and laboratory findings in 9 patients with transient erythroblastopenia of childhood (TEC) are presented and compared with the literature. TEC mainly affects infants presenting with normochromic, normocytic anemia and reticulocytopenia. Liver, spleen and lymph nodes are not enlarged. As a rule the white blood cell count is normal and the platelet count elevated. Bone marrow examination reveals absence of erythropoiesis. TEC is a self-limiting disorder which needs no therapeutic measures other than transfusion where necessary.

Anemia↗
PubMed1988

Comparative analysis of genes encoding methyl coenzyme M reductase in methanogenic bacteria.

The sequence of the gene cluster encoding the methyl coenzyme M reductase (MCR) in Methanococcus voltae was determined. It contains five open reading frames (ORF), three of which encode the known enzyme subunits. Putative ribosome binding sites were found in front of all ORFs. They differ in their degrees of complementarity to the 3' end of the 16 S rRNA, which is discussed in terms of different translation efficiencies of the respective genes. The codon usage bias is different in the subunit encoding genes compared with the two other ORFs in the cluster and two other known genes of Mc. voltae. This is interpreted in terms of increased translational accuracy of the highly expressed MCR subunit genes. The derived polypeptide sequences encoded by the five ORFs of the MCR cluster were compared to those of the respective genes in Methanobacterium thermoautotrophicum Marburg and Methanosarcina barkeri. Conserved regions were detected in the enzyme subunits, which are candidates for factor binding domains. Conserved hydrophobic sequences found in the alpha and beta subunits are discussed with respect to the membrane association of the enzyme.

Amino Acid Sequence↗
PubMed1988

Influence of a beta-adrenergic agonist on septic shock-induced alterations of phosphatidylcholine metabolism in rat lung.

Changes in surfactant function play an important part in the pathogenesis of adult respiratory distress syndrome (ARDS). Since beta-adrenergic agonists have been shown to exert a decisive influence on surfactant secretion, we studied the effect of fenoterol on lung phospholipid metabolism under conditions of experimental sepsis. Fenoterol administered to live rats increased the incorporation of choline into lung tissue by 80% in normal, by 35% in septic animals. It had no comparable effect on palmitate incorporation. It increased the activity of choline kinase in control animals, but had no additional effect on animals with increased values due to sepsis. Phosphotransferase activity diminished during sepsis was stimulated, and phospholipase activity reduced. Fenoterol restored phosphatidylcholine to normal levels in lung tissue and bronchoalveolar lavage and prevented lysophosphatidylcholine generation. Fenoterol also increased the amount of palmitate in phosphatidylcholine from bronchoalveolar lavage in septic animals. The results imply that a beta-adrenergic agonist influences the conditions of lung phospholipid metabolism altered by sepsis towards normal.

Animals↗
PubMed1988

To extract or not to extract in secretin radioimmunoassay?

The importance of an ethanol extraction procedure in the radioimmunoassay of plasma secretin was investigated. The extraction step led to a higher assay sensitivity of 0.35 fmol/ml, compared to 5.93 fmol/ml using unextracted samples. The rise of plasma secretin after infusion of a low dose of secretin (1 pmol.kg-1.h-1) in 10 healthy humans was only detected after sample extraction. Higher doses (3 and 9 pmol.kg-1.h-1) resulted in increments of plasma IRS (immunoreactive secretin), which could be recorded both with and without sample extraction. After a steak meal 7 of 10 subjects showed a significant increase of plasma secretin assaying extracted plasma samples. The secretin release occurred in spikes. The mean increase of plasma IRS in this group was 0.6 fmol/ml, the mean maximal secretin release above basal was 2.3 fmol/ml. Without sample extraction, plasma secretin was not significantly changed. We conclude that plasma samples should be extracted in order to detect physiological postprandial secretin release.

Animals↗
PubMed1988

Changes in the pituitary-thyroid axis accompanying major affective disorders.

The reports tries to show the intercorrelations between the TRH-test and the peripheric thyroid function during the course of affective disorders. The sample comprised 22 manic (15 follow-up) and 24 depressive (13 follow-up) patients. As parameters serum thyroxine, triiodothyronine, T3-uptake, FT4-index, T3/T4-ratio, TSH basal and 30 min after 200 micrograms TRH i.v. were determined. In a smaller group of patients reverse-T3 was measured, too. During acute mania and depression there is an increase of thyroxine. We observed a stronger conversion of T4 to rT3 with less inactivation of T4 to T3 in mania than in depression. Both groups show attenuated TSH response to TRH stimulation in florid psychoses. Comprehensing all results we come to the conclusion that the changes in the pituitary-thyroid axis accompanying affective psychoses start from the thyroidea and not from the anterior pituitary gland.

Adolescent↗
PubMed1988

Potential therapeutic mechanisms of stable prostacyclin (PGI2)-mimetics in severe peripheral vascular disease.

In 2 randomized, double-blind studies, 109 diabetic patients with trophic lesions and 101 non-diabetics suffering from peripheral vascular disease (PVD) stage IV (Fontaine) received daily 6-hour i.v. infusions of iloprost (less than or equal to 2ng/kg/min) or of placebo over 28 days. Iloprost treatment was superior to placebo, showing ulcer healing in more than 60% of patients compared to less than 25% in the control group. The beneficial effects were sustained during a 1 year follow-up period. Platelet activation, adhesion, aggregation and release reaction on atherosclerotic lesions, impaired microvascular perfusion, loss of microvascular barrier function, increased white blood cell - vessel wall interaction and hemorheological disturbances are all believed to play a role in PVD. Stable PGI2-mimetics inhibit platelet activation by all endogenous mediators as well as platelet release of mitogenic factors (PDGF).

Animals↗
PubMed1988

Adherence of leucocytes to electrically damaged venules in vivo. Effects of iloprost, PGE1, indomethacin, forskolin, BW 755 C, sulotroban, hirudin, and thrombocytopenia.

Increased adherence of leucocytes to the vessel wall is thought to be a key event in potentially deleterious leucocyte-vessel wall interactions in a variety of diseases associated with microvasculatory dysfunction. As measured by videomicroscopy in mesenteric venules (phi 40 +/- 8 microns) of anaesthetized rats, an injury caused by one short electrical stimulus to the venule wall led to a prolonged increase of marginated (sticking and rolling) leucocytes from 228/mm2 to 797/mm2 without affecting red cell velocity and shear rate. Iloprost (0.1 micrograms/kg/min i.v.), PGE1 (2.0 micrograms/kg/min i.a.), BW 755 C (40 mg/kg s.c.), forskolin (0.3 mg/kg i.v.), and hirudin (500 IU/kg + 200 IU/kg/h i.v.) all significantly attenuated injury-induced leucocyte margination. Indomethacin (10 mg/kg s.c.) had no effect and sulotroban (0.5 mg/kg/min) showed borderline efficacy. Platelet depletion by rat antiplatelet serum completely inhibited increased leucocyte margination. PGI2 mimetics, drugs interfering with lipoxygenase metabolism, and thrombin inhibitors may therefore be useful to prevent exaggerated leucocyte-vessel wall interactions.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1988

Pharmacological profile of a new potent 5-hydroxytryptamine (5-HT2) alpha 1-receptor antagonist.

In in vitro binding studies ZK 33.839 (4-(3-[3-(4-(4-fluorobenzoyl)-1-piperidinyl)-propoxy]-4-methoxyphenyl)- 2-pyrrolidone) showed highly specific binding affinity for 5-hydroxytryptamine (5-HT2) and alpha 1-receptors. With 2.0 nmol/l and 5.2 nmol/l both Ki-values occur in the same concentration range. The pharmacodynamic profile of ZK 33.839 has been investigated under in vitro and in vivo conditions. In human platelets, in rat vascular smooth muscle and in guinea pig tracheal smooth muscle 5-HT-induced proaggregatory and contractile effects were inhibited dose-dependently with IC50-values ranging from 1.85 x 10(-8) mol/l to 9 x 10(-9) mol/l. 5-HT-induced amplification of the response of rabbit femoral artery to different vasoconstrictors (angiotensin II, histamine, norepinephrine, and prostaglandin F2 alpha) and 5-HT-mediated increase of microvascular permeability in hamster cheek pouch preparation were also inhibited by ZK 33.839. ZK 33.839 was found to be a potent alpha 1-receptor antagonist, the pA2-value in rat aortic strips determined against phenylephrine was 9.16. In blood-perfused hindquarters of anaesthetized rats, pretreated with reserpine, pressor dose-response curves to norepinephrine and 5-HT were shifted to a higher dose range. ZK 33.839 lowered blood pressure in conscious Dahl-S-rats and in anaesthetized rabbits. Decrease of blood pressure was due to a decrease of peripheral vascular resistance. Cardiac output and heart rate were not significantly altered. ZK 33.839 is a potential antihypertensive compound which combines vasodilatatory effects due to selective alpha 1-receptor antagonistic action and platelet antiaggregatory, antivasospastic, and vasoprotective properties due to selective 5-HT2-receptor blockade.

Adrenergic alpha-Agonists↗
PubMed1988

[Comparison of the pharmacokinetics of iron in pregnant and nonpregnant women after oral administration of Vitaferro].

In this paper we represent results concerning pharmacokinetics and bioavailability of iron after the oral application of Vitaferro to women in the second half of pregnancy suffering or not from anaemia in comparison to nonpregnant women. The significance of different parameters used to proof an iron deficiency is discussed. In all pregnant probands the bioavailability of Vitaferro is about twice as high as in nonpregnant women. Also the parameters of elimination refer to an enhanced retention of iron during pregnancy. We conclude from our investigations that an iron deficiency may be diagnosed well by the determination of haemoglobin values, iron concentration in serum, binding capacity and resorption of iron. During pregnancy the preparation Vitaferro is well resorbed and does not cause incompatibilities. Thus it is suitable for the treatment of anaemia during pregnancy.

Administration, Oral↗
PubMed1988

Ultrastructure of skeletal muscle in rheumatoid myositis.

Muscle biopsies from 8 cases of rheumatoid myositis (5 females and 3 males) were studied by electron microscopy. All muscle fibers studied showed either necrosis or atrophy, the latter varying from slight to severe. Mononuclear cell infiltration was present in all cases, with 4 types of cells observed (lymphocytes, plasma cells, macrophages and mast cells). The capillary endothelium showed proliferation of organelles, occlusion of lumina, and thickening of the basement membrane. The pathogenesis of muscle damage in rheumatoid myositis is discussed.

Arthritis, Rheumatoid↗