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Biomedical subjects

S Braun

Publications and source records attributed to S Braun.

At least 307 records · Page 17Linked to original sources

Verification of impedance measurements by a volumetric and electromechanical model.

A dynamic model of the middle ear and mastoid cavity will be presented. A variety of precisely controlled volumetric changes were simulated by the model, singularly or in conjunction with pressure changes, mass and friction effects at the level of the drum. The contributions of each factor alone and in controlled combinations to the acoustic impedance were serially tested and recorded. The validity of static compliance and tympanometry in volumetric middle ear and mastoid estimates is questioned. The model demonstrated dependability of impedance tympanometric techniques in measuring intratympanic air fluid contents and pressure changes. The model provided objective evidence on the capability of impedance techniques to differentiate mechanical traction on the drum from traction brought about by negative pressures. Clinical applications of these findings will be discussed.

Acoustic Impedance Tests↗

Metabolism of phosphate and calcium after severe accidental trauma.

Hypophosphatemia is a common finding during the first 4-5 days after severe accidental trauma. We demonstrated that hypophosphatemia after trauma is caused by a definite decrease in renal phosphate threshold (TmPO4/GFR), that is the theoretical plasma phosphate concentration at which all of the filtered phosphate is reabsorbed by the renal tubules and renal excretion of phosphate is close to zero. We speculated that the decrease in renal phosphate threshold could be due to an increased activity of PTH which in turn could be the result of ionized hypocalcemia. In 7 patients with severe and in 8 patients with moderate trauma, however, we found ionized calcium and PTH levels to be within normal limits. Total plasma calcium was below normal (1.90-2.00 mmol/l) up to 20 days after trauma, probably due to a decreased plasma albumin concentration (25-30 g/l). We conclude, that ionized hypocalcemia and consecutive stimulation of PTH is not the cause of decreased renal phosphate threshold after severe accidental trauma.

Adolescent↗

The interaction of Mn2+ with turkey erythrocyte adenylate cyclase.

Mn2+ at concentrations below 0.1 mM supports the activation of turkey erythrocyte adenylate cyclase (ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1) by beta-agonists or NaF, similarly to Mg2+ at 5.0 mM. At higher concentrations, Mn2+ is strongly inhibitory, as is Mg2+ above 6 mM. Also, Mn2+ with GTP, but in the absence of beta-agonist, is very potent in reversing the Gpp(NH)p permanently active state to the basal state. beta-Receptor (R) to guanyl nucleotide regulatory protein (N) coupling still occurs at inhibitory Mn2+ concentrations, since the intrinsic kinetic parameters which characterize the R to N coupling interrelationship are unaffected by Mn2+ at a wide concentration range. It is suggested that the inhibitory effect of Mn2+ is due to the impairment of the guanyl nucleotide regulatory protein (N) to the catalytic subunit (C) interaction.

Adenylyl Cyclase Inhibitors↗

[Atrial myxoma. Report of eight surgical cases, four with electron microscopy study (author's transl)].

From 1970 to 1979 we studied and operated on 8 patients with atrial myxoma, 7 females and 1 male, 24 to 58 years of age. Symptoms had been present for 4 to 24 months prior to surgery. Five patients were functional class IV (NYHA), 2 class III and one class I. All patients were studied by catheterization and angiography. The diagnosis was suspected from physical findings in 3 patients and was not made before surgery in 2 cases. The tumor was located at the left atrium in 6 patients and the right atrium in 2. Electron microscopy performed in 4 cases revealed the typical findings of myxomatous tissue. Adequate resection under extracorporeal circulation was possible in all subjects. One female who was in severe congestive heart failure died shortly after operation. The survivors did well, remaining functional class I, one to nine years after surgery.

Adult↗

Kinetics of interaction between beta-receptors, GTP protein, and the catalytic unit of turkey erythrocyte adenylate cyclase.

The kinetics of turkey erythrocyte membrane adenylate cyclase activation by beta-agonists and guanyl-5'-yl imidodiphosphate is explored as a function of the concentration of the GTP regulatory protein and of the catalytic unit. It was found that the overall kinetics of activation is first order and is independent of the concentration of the GTP regulatory unit N, the catalytic unit C, and of hormone over a very wide concentration range. It was established that the rate-limiting step does not involve GDP dissociation from the inactive N unit or the association between activated N' and C. Also, it was found that guanyl-5'-yl imidodiphosphate binding occurs in a random fashion and is not hormone dependent. These results enable us to exclude models of the sequential type in which N in its inactive form is bound to receptor R, is released in an active form N' upon hormone activation, and then binds to C, activating the latter. An acceptable model that accounts for all of the data conforms to the original formulation of "collision coupling" in which N is tightly associated to C at all times.

Adenylyl Cyclases↗

Combined hMG/hCG treatment in subfertile men with idiopathic normogonadotrophic oligozoospermia.

Forty-eight patients with idiopathic normogonadotrophic oligozoospermia were treated with hMG plus hCG over a period of 3 months. Total sperm output increased by an average of 15.3 million spermatozoa per ejaculate and a similar significant increase was seen in the percentage of motile spermatozoa. Sixteen of the 48 men increased their sperm output by 25 million or more. Follow-up information was available in 33 patients. Ten pregnancies were reported within one year after initiation of treatment. Six of 12 responders impregnated their wives, whereas only 4 pregnancies were reported in a group of 21 non-responders. Endocrinological investigations showed no differences in mean basal levels of LH and FSH, or in the gonadotrophin response to a 100 micrograms GnRH stimulation between responders and non-responders. However, mean basal plasma testosterone concentration was significantly lower in the responder group than in the non-responders. Responsiveness to gonadotrophin treatment tended to be better in patients with basal plasma testosterone concentration lower than 4.5 ng/ml. Combined hMG/hCG treatment in subfertile men with idiopathic oligozoospermia seems to be efficient in only a small proportion of cases.

Adult↗

Effects of tiapamil on myocardial performance in coronary artery disease.

Tiapamil has been extensively investigated for treatment of cardiac arrhythmias. Concern persists, however, that, as a calcium antagonist, it may seriously depress myocardial function. To investigate this possibility, 20 patients were given tiapamil intravenously and studied by radionuclide ventriculography. Tiapamil markedly lowered arterial pressure. Left ventricular ejection fraction increased from 54 +/- 3.3 to 57 +/- 3.3%. No significant change in heart rate was noted. Tiapamil did not increase the extent of left ventricular asynergy. The potent vasodilator properties of tiapamil compensate for any intrinsic decrease in left ventricular contractibility, and therefore overall cardiac function is not worsened by the drug in patients with normal or moderately reduced resting ventricular ejection fractions.

Blood Pressure↗

Antiarrhythmic effects of tiapamil on exercise-induced arrhythmias in patients with coronary artery disease.

57 patients were admitted to the study, 3-6 weeks after acute myocardial infarction. They received either placebo or 1 mg/kg tiapamil intravenously according to a randomized, double-blind procedure. The study had two objectives: (a) to assess the effect of tiapamil on work tolerance and exercise-induced myocardial ischemia: (b) to demonstrate possible antiarrhythmic effects against exercise-induced arrhythmias. The duration of exercise and physical work capacity increased slightly in both groups, these effects, however, not reaching statistical significance. On the other hand, the number of exercise-induced extrasystoles did not change significantly under placebo but decreased from 30.9 to 14.8 beats/min after tiapamil (p less than 0.01). No side effects were observed. While the hemodynamic effects of tiapamil in patients with coronary artery disease are yet to be elucidated, our findings confirm the efficacy of this calcium antagonist against exercise-induced ventricular premature beats in patients with coronary artery disease.

Adult↗

Mechanism of control of the turkey erythrocyte beta-adrenoceptor dependent adenylate cyclase by guanyl nucleotides: a minimum model.

Treatment of native turkey erythrocyte membranes with GMP and epinephrine produces a highly active but metastable form of adenylate cyclase which decays slowly to basal native state. The decay process is greatly facilitated by GTP and GDP beta S1, and is further enhanced by 1-epinephrine. This decay process is prevented reversibly by GMP. GppNHp, like GMP, prevents the decay process first reversibly, but with time stabilizes the highly active state in a persistently active state. The expression of the catalytic activity of the enzyme in the metastable state can also be inhibited reversibly by GTP, GDP beta S and GMP at all times during the decay process. The GppNHp stabilized form is not susceptible to nucleotide inhibition. Thus, two forms of the guanyl nucleotide unit are postulated to exist: an "open" and a "closed" form. In the presence of hormone and GTP, the enzyme shuttles between these two forms continuously. GMP and GppNHp favor the complete conversion to the "open" form in the presence of beta-agonist. Evidence is also presented for the existence of two GTP dependent processes which exhibit different apparent affinities towards the nucleotide: A high affinity GTP binding process is essential for the fruitful coupling between receptor and enzyme, and a low affinity GTPase site which is responsible for the termination of the hormonal signal.

Adenylyl Cyclases↗

Activation of adenylate cyclase from purified platelet membranes by prostaglandin E1 and its inhibition by L-epinephrine: mechanistic effects.

Activation and inhibition of adenylate cyclase in purified human platelet membranes by hormones and guanyl nucleotides was studied. The rate constant of enzyme activation (kon) was measured using the GTP analog guanylimidodiphosphate (Gpp(NH)p), and the rate constant of enzyme deactivation (koff) was determined using the guanosine diphosphate analog guanosine 5'-0-(2-thio)-diphosphate (GDP beta S). PGE1 which was found previously (15) to accelerate kon has been found to accelerate also koff, from 0.1 sec-1 (6 min-1) to 0.2 sec-1 (12 min-1). The alpha 2-adrenergic inhibitory hormone 1-epinephrine did not alter kon, whether measured in the absence or presence of GTP, and also did not alter koff, whether measured under basal or PGE1-dependent GTP-ase activity at any concentration of GTP tested. These results suggest that the alpha 2-adrenergic receptor exerts its inhibitory effect on adenylate cyclase by a mechanism which does not involve its direct interaction with the GTP regulatory protein that is associated with the stimulatory hormone. These results support the view that the inhibitor involves the interaction of the inhibitory receptor with a GTP binding unit separate from the one mediating hormonal stimulation. This regulatory unit attenuates the adenylate cyclase activity either by interacting directly with the catalytic moiety or by modulating the interaction of the stimulatory GTP regulatory protein with the catalytic moiety.

Adenylyl Cyclase Inhibitors↗