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Biomedical subjects

A Hermann

Publications and source records attributed to A Hermann.

At least 19 recordsLinked to original sources
PubMed1992

Sarcoplasmic calcium-binding protein-immunoreactive material in the central nervous system of the snail, Helix pomatia.

In Helix pomatia a 10 kDa sarcoplasmic calcium binding protein I (SCP I)-immunoreactive material was localized immunologically in neurons of the central nervous system, including the electrically silent serotonergic metacerebral giant neuron. Antisera against sarcoplasmic calcium binding protein II (SCP II) stained a 20 kDa protein in individual muscle cells of the epineurium. SCP- and parvalbumin (PV)-immunoreactive material were not co-localized.

Animals↗
PubMed1992

Quantification of Ile-Ser-Bradykinin degradation in human serum and ascites.

A leucine aminopeptidase (LAP) and a carboxypeptidase (CP) activity in human serum and malignant ascites degrade Ile-Ser-Bradykinin (ISB = T-Kinin) in two catalytic steps to desArg9Bradykinin. The catalytic activity in serum is always higher than in ascites. In serum the carboxypeptidase activity is higher than the LAP activity whereas in ascites the two activities are not different.

Amino Acid Sequence↗
PubMed1992

Calcium-binding proteins in chemoreceptors of Xenopus laevis.

Calcium-binding proteins were investigated immunohistochemically in chemo-receptors of the olfactory epithelium and taste buds of the clawed frog, Xenopus laevis. Calmodulin-, S-100- and calbindin-immunoreactive material were found in sensory cells of the olfactory epithelium; however, parvalbumin-like material was absent in these cells. Taste buds of the palate showed calmodulin-, S-100- and parvalbumin-immunoreactive material in sensory cells, while calbindin-immunoreactive material in supporting cells. Merkel cells, surrounding the base of the taste buds in a ring-like manner, exhibited calmodulin- and S-100-immunoreactive material.

Animals↗
PubMed1992

In vivo fate and scavenger receptor recognition of oxidized lipoprotein[a] isoforms in rats.

High levels of Lp[a] in blood form an independent risk factor for atherosclerosis. Oxidative modification of Lp[a] may be involved in the suggested atherogenic action of Lp[a]. After Cu(2+)-mediated oxidative modification of the 440 kDa and 610 kDa apo[a] isoforms of lipoprotein[a] (Ox-Lp[a]), the in vivo fate was investigated in rats. Ox-Lp[a], when injected into rats, was rapidly removed from the blood circulation by the liver, in which the intrahepatic fate is dependent on the degree of oxidation of the isoforms. Upon oxidation to a slightly increased negative charge of Lp[a], the high molecular weight form of Lp[a] is recognized more efficiently by the Kupffer cells than by the endothelial cells. When the liver uptake of Ox-Lp[a] is blocked by preinjection of polyinosinic acid (poly I), the association of Ox-Lp[a] with the rat heart is increased 20-fold. In vitro studies show that the association and degradation of 125I-labeled Ox-Lp[a] with liver endothelial and Kupffer cells was inhibited by oxidized LDL (Ox-LDL), poly I, or Ox-Lp[a] itself by 60-90%, while only a partial competition was found with acetylated-LDL (up to 25%). In conclusion, after oxidative modification of Lp[a], there is recognition of Ox-Lp[a] by specific oxidized-lipoprotein receptors on liver endothelial and Kupffer cells; the relative importance at low degrees of oxidation of Lp[a] is dependent on the molecular weight of the apo[a] isoforms. Under conditions in which liver uptake is not adequate, the deposition of Ox-Lp[a] in the heart may be of potential pathological importance.

Animals↗
PubMed1992

Dissociation-enhanced lanthanide fluorescence immunoassay of lipoprotein(a) in serum.

Lipoprotein(a), a human serum lipoprotein structurally related to low-density lipoprotein (LDL), contains in addition to apolipoprotein B (apo B) apolipoprotein(a) [apo(a)], a glycoprotein with a strong homology to plasminogen. Lp(a) is a risk factor for coronary heart disease and ischemic cerebrovascular disease. Several immunological techniques are used to quantify Lp(a) in human serum, including radioimmunoassays, rocket immunoelectrophoresis, and enzyme-linked immunosorbent assays. Only the last method is suitable for large-scale clinical studies. We describe another solid-phase immunoassay, based on the dissociation-enhanced lanthanide fluorescence system Delfia (Wallac Oy), and outline the technical details. A polyclonal antiserum directed against Lp(a) was used as the capture antibody. Two kinds of detection antibodies were applied, a polyclonal antiserum against apo B and the polyclonal antiserum against Lp(a). The results agree excellently with the values estimated by rocket immunoelectrophoresis. This assay is easily established, measures Lp(a) in a wide concentration range, and is suitable for screening large populations.

Enzyme-Linked Immunosorbent Assay↗
PubMed1991

Calcium-binding proteins in Aplysia neurons.

1. Calcium (Ca)-binding proteins of neuronal ganglia and of single, identified neurons of the marine mollusk, Aplysia californica, were investigated. Using transblot/45Ca overlays two proteins, at Mr 45,000 and Mr 23,000, with a high Ca-binding ability were found. 2. Western blot analysis revealed that the protein at Mr 45,000 could be separated by 2D-PAGE into proteins with Mr 40,000 and Mr 43,000. The protein at Mr 40,000 immunocross-reacted with antisera directed against parvalbumin and rat calbindin D-28K, indicating a novel Ca-binding protein sharing common antigenic determinants for both proteins. 3. The protein at Mr 23,000 could be separated into a group of proteins with Mr 13,000-20,000 which showed a high degree of similarity to sarcoplasmatic calcium-binding proteins (SCP). 4. We further investigated the protein pattern of single, identified neurons of different electrical activity (bursting, beating, and silent) by 2D-PAGE. Major differences were found in the range of low Mr and low pI, where Ca-binding proteins are generally located. A protein at high concentrations characteristic for silent cells migrated at a position similar to crayfish SCP. 5. The results show that various Ca-binding proteins are characteristic for neurons in the Aplysia nervous system and support the idea that they may effect the electrical behavior of nerve cells.

Action Potentials↗
PubMed1990

[Peroneal weakness].

The 22 year old male patient was admitted because of right sided peroneal nerve palsy two months after transient foot drop on the left side. Both pareses developed under a strict dietary regime leading to a weight loss of about 30 kg within 3 months. Slimmers' paralysis of peroneal nerve was diagnosed after exclusion of polyneuropathy or trauma as possible causes. Complete remission followed after a less restrictive diet.

Adult↗
PubMed1989

[Hypertension].

This 40 year old man had been treated adequately for arterial hypertension over the last 10 years. Within one year this arterial tension rose continuously in spite of treatment. A low blood-potassium value found on routine chemical analysis prompted an investigation on secondary causes for hypertension. The results of a peripheral renin-study were typical for secondary aldosteronism. An abdominal aortography and selective angiography of the renal arteries visualized an intrarenal arterial aneurysm with stenoses as causative factor of the renovascular hypertension. Antihypertensive treatment with an ACE-blocker permitted to normalize the blood-pressure values subsequently.

Adult↗
PubMed1988

Prism adaptation in Parkinson's disease.

Prism adaptation is impaired by lesions in the basal ganglia in non-human primates, suggesting that this area is involved in this form of visuomotor learning. We investigated the ability of patients with Parkinson's disease to prism adapt. Patients and controls wore prisms which deflected vision laterally by 11 degrees. After baseline testing with a localisation task that permitted no feedback about performance accuracy, prism adaptation was tested at 4 minute intervals over a 28 minute trial. All subjects erred initially, reaching too far to the left of the target, but a separate pointing task encouraged adaptation and reaching error decreased at a similar rate in Parkinsonians and controls. Immediately after the prisms were removed, all subjects reached to the right of the target. This negative after effect was present in controls but not patients when assessed 4 minutes later, suggesting that the patients could not maintain the new sensorimotor relationship imposed by the prisms after their removal. This is similar to performance on visuospatial and executive tasks in Parkinsonians, where ongoing behaviour cannot be modulated without external guidance.

Adaptation, Ocular↗
PubMed1987

Differential effects of pentylenetetrazole on ion currents of Aplysia neurones.

The effect of the convulsant drug pentylenetetrazole (PTZ) on separated membrane current components has been studied in identified voltage-clamped Aplysia neurones. External PTZ blocks the voltage-dependent Na+, Ca2+ currents and the delayed rectifier current (INa, ICa and IK,V, respectively). The amplitude of the Ca2+-activated K+ current (IK,Ca) is increased. The amplitude of the fast inactivating K+ current (IA) is transiently increased at low concentrations of PTZ but is depressed at higher concentrations or after long-lasting application of the drug. The effect of PTZ on leakage current (IL) seems to depend on the cell type. In some cells (R-15, L-7, LP-1) IL is decreased while it is increased in other cells (L-11, BL-1, BR-1). PTZ accelerates the inactivation of IK,V and IA and shifts the current-voltage relation of ICa to negative voltages by 5-8 mV. Pressure injection of PTZ into the neurone did not affect IK,V or IK,Ca. Thus PTZ seems to act on the outside of the plasma membrane. The effect of external PTZ on INa, ICa, IK,V and IL is also observed if the internal Ca2+ activity is buffered with EGTA suggesting that an increase in the internal Ca2+ activity is not involved. At -40 mV PTZ induces a tetrodotoxin-insensitive inward current carried by Na+ ions. PTZ transforms the beating pacemaker cell L-11 into a bursting pacemaker and the bursting pacemaker cell R-15 exhibits 'square-wave'-like oscillations of the membrane potential.

Action Potentials↗
PubMed1987

Action and location of neuropeptide tyrosine (Y) on hippocampal neurons of the rat in slice preparations.

The action of bath applied NPY (1-1,000 nM) was investigated on hippocampal slices of the rat with extra- and intracellular recording. Neuropeptide Y (NPY) at 10-1,000 nM caused a concentration-dependent, long-lasting reduction of excitatory postsynaptic potentials (EPSPs) in the hippocampal subfield CA1 and the area dentata, and an even stronger reduction of population spikes. Paired pulse experiments with low intensity, stimulation-evoked PSPs showed a marked increase in facilitation in the presence of NPY, indicating a presynaptic action. Spontaneous burst firing of CA1 pyramidal cells in low calcium, high magnesium medium was reduced, indicating a partially postsynaptic inhibitory action of NPY on their dendrites. Intracellular recording from CA1 somata during NPY administration revealed a reduction of the amplitudes of excitatory-inhibitory postsynaptic potential (EPSP-IPSP) sequences in the absence of changes in membrane potential and conductance. Accommodation of firing during long depolarizing pulses and afterhyperpolarizations were unchanged. The innervation pattern of NPY immunoreactive fibers in the same regions was studied in slices adjacent to the ones used for electrophysiology by using antisera against NPY and light and electron microscopy. There is a dense innervation of CA1 by NPY-immunoreactive axons and terminals, particularly in the stratum moleculare. NPY-immunoreactive neurons are present in the stratum oriens and pyramidale. The NPY labeled axons of the stratum moleculare participate in numerous synaptic contacts with the smaller dendritic elements in this layer, many of which belong to pyramidal neurons. These observations provide evidence for a dendritic NPY-immunoreactive innervation of CA1 neurons, which is in keeping with the electrophysiological effects of NPY on pyramidal neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Fluctuations of the Ca2+-activated K+ current in Aplysia neurones.

Fluctuations of the Ca2+-activated K+ current were measured in identified Aplysia neurones under voltage clamp conditions. The amplitude of IK,Ca was manipulated by ionophoretic injections of Ca2+. At small amplitudes of Ca2+-activated outward currents the variance of the Ca2+-activated current fluctuations increases linearly with the mean outward current. The single-channel conductance estimated from the variance of the fluctuations and the mean outward current is 11 +/- 3 pS at -30 mV. Power spectra of the Ca2+-activated K+ current can be fitted by the sum of two Lorentzian components with corner frequencies of about 10 Hz and 120 Hz.

Animals↗
PubMed1987

Charybdotoxin selectively blocks small Ca-activated K channels in Aplysia neurons.

The action of charybdotoxin (ChTX), a peptide component isolated from the venom of the scorpion Leiurus quinquestriatus, was investigated on membrane currents of identified neurons from the marine mollusk, Aplysia californica. Macroscopic current recordings showed that the external application of ChTX blocks the Ca-activated K current in a dose- and voltage-dependent manner. The apparent dissociation constant is 30 nM at V = -30 mV and increases e-fold for a +50- to +70-mV change in membrane potential, which indicates that the toxin molecule is sensitive to approximately 35% of the transmembrane electric field. The toxin is bound to the receptor with a 1:1 stoichiometry and its effect is reversible after washout. The toxin also suppresses the membrane leakage conductance and a resting K conductance activated by internal Ca ions. The toxin has no significant effect on the inward Na or Ca currents, the transient K current, or the delayed rectifier K current. Records from Ca-activated K channels revealed a single channel conductance of 35 +/- 5 pS at V = 0 mV in asymmetrical K solution. The channel open probability increased with the internal Ca concentration and with membrane voltage. The K channels were blocked by submillimolar concentrations of tetraethylammonium ions and by nanomolar concentrations of ChTX, but were not blocked by 4-aminopyridine if applied externally on outside-out patches. From the effects of ChTX on K current and on bursting pacemaker activity, it is concluded that the termination of bursts is in part controlled by a Ca-activated K conductance.

Action Potentials↗
PubMed1986

Source localization in intracavitary 60Co therapy with semiconductor and TL detectors.

Thermoluminescence and p-type semiconductor detectors were used for localization of the source in intracavitary (modified Stockholm method) treatment. The results were compared with X-ray films, and especially good agreement was obtained if the detectors were positioned on both sides of the patients. The measurements performed on Stage III to IV carcinoma cervix uteri patients indicate that the intracavitary source can deviate to both sides with equal probability. The magnitude of the deviation is described by a Gaussian distribution with an expected value of zero and S.D. of 8mm.

Brachytherapy↗
PubMed1985

Effects of caffeine on hippocampal pyramidal cells in vitro.

The effects of caffeine on the electrophysiological properties of CA1 pyramidal neurones were investigated in the rat hippocampal slice preparation in vitro. A concentration-dependent increase in both the extracellularly recorded excitatory postsynaptic potential (e.p.s.p.) and the population spike resulting from stimulation of the stratum radiatum could be evoked by caffeine with a threshold concentration of 10 microM. Intracellular recordings demonstrate a caffeine-evoked decrease in resting membrane potential, an increase in input resistance, a reduction of the long afterhyperpolarization (a.h.p.) and a decrease in accommodation. The interaction between caffeine and adenosine was investigated on the extracellularly recorded e.p.s.p. The maximal response evoked by caffeine was increased in the presence of adenosine and the adenosine concentration-response curve was shifted to the right in a parallel fashion in the presence of caffeine. It is suggested that the effects of caffeine on hippocampal neurones may be mediated by a decrease of one or more potassium conductance(s), and that adenosine and caffeine may compete for the same electrophysiologically active receptor site on these cells.

Adenosine↗
PubMed1984

Asymmetric lipid fluidity in human erythrocyte membrane: new spin-label evidence.

We have synthesized spin-labeled analogues of phosphatidylcholine, phosphatidylserine, and phosphatidylethanolamine with a short beta chain (C5) bearing a doxyl group at the fourth position. When added to an erythrocyte suspension, the labels immediately incorporate in the membrane. The orientation of the spin-labels was assessed in the bilayer (i) by addition in the medium of a nonpermeant reducer (ascorbate at 5 degrees C) or (ii) by following spontaneous reduction at 37 degrees C due to the endogenous reducing agents present in the cytosol. Both techniques prove that the spin-labels are originally incorporated in the outer leaflet and redistribute differently after incubation. After a 5-h incubation at 5 degrees C, the phosphatidylcholine derivative remained in the outer layer, while the phosphatidylethanolamine and phosphatidylserine derivatives were found principally in the inner leaflet. During the incubation, a small fraction of the spin-labels is hydrolyzed, particularly the phosphatidylserine derivative, presumably by an endogenous phospholipase A2. Because the hydrolyzed spin-labeled fatty acids are rejected in the aqueous phase, the spectra of the intact membrane-bound phospholipids can be obtained by an adequate spectral subtraction. The ESR spectrum corresponding to a probe in the outer leaflet indicates a more restricted motion than that associated with probes in the inner leaflet. Additional experiments have been carried out to prove that the difference in viscosity, which is likely to be due to anisotropic cholesterol distribution, is not attributable to modification of the cell morphology.(ABSTRACT TRUNCATED AT 250 WORDS)

Electron Spin Resonance Spectroscopy↗
PubMed1984

Action of quinidine on ionic currents of molluscan pacemaker neurons.

The effects of quinidine on the fast, the delayed, and the Ca2+-activated K+ outward currents, as well as on Na+ and Ca2+ inward currents, were studied at the soma membrane from neurons of the marine mollusk Aplysia californica. External quinidine blocks these current components but to different degrees. Its main effect is on the voltage-dependent, delayed K+ current, and it resembles the block produced by quaternary ammonium ions (Armstrong, C. M., 1975, Membranes, Lipid Bilayers and Biological Membranes: Dynamic Properties, 3:325-358). The apparent dissociation constant is 28 microM at V = +20 mV. The blocking action is voltage and time dependent and increases during maintained depolarization. The data are consistent with the block occurring approximately 70-80% through the membrane electric field. Internal injection of quinidine has an effect similar to that obtained after external application, but its time course of action is faster. External quinidine may therefore have to pass into or through the membrane to reach a blocking site. The Ca2+-activated K+ current is blocked by external quinidine at concentrations 20-50-fold higher compared with the delayed outward K+ current. In addition, it prolongs the time course of decay of the Ca2+-activated K+ current. Na+ and Ca2+ inward currents are also blocked by external quinidine, but again at higher concentrations. The effects of quinidine on membrane currents can be seen from its effect on action potentials and the conversion of repetitive "beating" discharge activity to "bursting" pacemaker activity.

Animals↗