Biomedical subjects

C Hauptmann

Publications and source records attributed to C Hauptmann.

6 recordsLinked to original sources

PubMed2005

Effectively desynchronizing deep brain stimulation based on a coordinated delayed feedback stimulation via several sites: a computational study.

In detailed simulations we present a coordinated delayed feedback stimulation as a particularly robust and mild technique for desynchronization. We feed back the measured and band-pass filtered local filed potential via several or multiple sites with different delays, respectively. This yields a resounding desynchronization in a naturally demand-controlled way. Our novel approach is superior to previously developed techniques: It is robust against variations of system parameters, e.g., the mean firing rate. It does not require time-consuming calibration. It also prevents intermittent resynchronization typically caused by all methods employing repetitive administration of shocks. We suggest our novel technique to be used for deep brain stimulation in patients suffering from neurological diseases with pathological synchronization, such as Parkinsonian tremor, essential tremor or epilepsy.

Brain↗

PubMed2003

Information capacity and pattern formation in a tent map network featuring statistical periodicity.

We provide quantitative support to the observation that lattices of coupled maps are "efficient" information coding devices. It has been suggested recently that lattices of coupled maps may provide a model of information coding in the nervous system because of their ability to create structured and stimulus-dependent activity patterns which have the potential to be used for storing information. In this paper, we give an upper bound to the effective number of patterns that can be used to store information in the lattice by evaluating numerically its information capacity or information rate as a function of the coupling strength between the maps. We also estimate the time taken by the lattice to establish a limiting activity pattern.

Journal Article↗

PubMed2003

Stimulus-dependent onset latency of inhibitory recurrent activity.

This paper gives an explanation for the experimentally observed onset latencies of the inhibitory responses that vary from a few milliseconds to hundreds of milliseconds in systems where the conduction delays are only several milliseconds in the feedback pathways. To do this we use a simple mathematical model. The model consists of two delay differential equations (DDE) where the nonlinear relation between the postsynaptic potential and the firing frequency of the neuron population arises from the stoichiometry of the transmitter-receptor kinetics. The parameters of the model refer to the hippocampal feedback system, and the modeling results are compared with corresponding experiments.

Excitatory Postsynaptic Potentials↗

PubMed2001

Epileptiform activity in a neocortical network: a mathematical model.

A simple mathematical model describing the generation and propagation of epileptiform activity in a cerebral cortical network is presented. The model consists of a system of nonlinear delay differential equations. Physiological properties are taken into account as nonlinear transmission of signals at the synapse, temporal and spatial summation of incoming signals at the soma, active membrane characteristics, and dendritic and axonal propagation times. The influence of the connectivity and the temporal parameters on the oscillatory properties of the model is studied. The computer simulations are in agreement with experimental observations in cortical networks: whereas a weak excitatory or strong inhibitory synaptic connection strength produces a stationary status with short-lasting responses to external stimuli, increases in excitation or decreases in inhibition induce spontaneous and stimulus-evoked rhythmic discharges. Synaptic burst-like activity is observed only for an intermediate range of excitatory and inhibitory connection strengths and external inputs. The form and duration of the bursts can also be controlled by the temporal parameters. The results demonstrate that relatively simple mathematical equations are sufficient to model some of the network properties underlying the generation and propagation of epileptiform activity.

Epilepsy↗

PubMed1992

[Procollagen III propeptide. Values in the course of pediatric celiac disease].

OBJECTIVES: An explanation for an incomplete catch-up growth in children with coeliac disease has not yet been found. The marker of growth procollagen-III-propeptide could possible provide a better understanding of the actual regulation of growth in the situation. METHODS: The investigation was made in children with established coeliac disease (n = 30). A commercial radioimmunoassay was used for the measurement of PC-III-P. RESULTS: A close relationship (r = 0.75; P < 0.0001) was found between height velocity and PC-III-P in serum of coeliac children. There was also a good correlation (r = 0.54; P < 0.001; n = 72) with serum levels of alcaline phosphatase. Only weak correlations were found to insulin-like growth factor I (r = 0.33; P < 0.05; n = 62), to urinary calcium (r = 0.27; P < 0.05; n = 62), and to the maturation of bones (r = 0.25; P < 0.05; n = 54). In accordance with the good correlation between height velocity and PC-III-P normal results were found in normal growing children with coeliac disease. Reduced serum levels of PC-III-P were found in coeliac children who failed to show a complete catch-up growth while on a gluten-free diet. CONCLUSIONS: Gluen challenge, as required for the confirmation of the diagnosis, led to a significant further decrease of the values of PC-III-P. Parallel investigations for IgA endomysium antibodies in serum suggest that besides dietary errors additional factors may impede growth, or in other words that disorders of growth regulation persist in some patients with coeliac disease even under treatment. This assumption will have to be tested by further investigations.

Body Height↗

PubMed1976

[The ultrastructure of human pituitary adenomas (author's transl)].

34 pituitary adenomas were examined by light and electron microscopical methods. Slices of tumor tissue fixed in formaldehyde or Bouin's solution, respectively, and embeded in paraffin were stained by hematoxylin-eosin, Goldner's method (including Orang G), periodic acid Schiff (PAS) reaction, and in some cases by Herlant's tetrachrom. The ultrastructure was studied using tumor tissue fixed in glutaraldehyde within 1 hour after removal. The adenomas were classified by their light microscopical characteristics as chromophilic or chromophobe tumors. Employing the PAS reaction and Goldner's staining method, 27 adenomas were found to give intense or weak staining reactions. By electron microscopical investigation , all the adenomas studied were seen to contain secretory granules more or less densely packed within the cytoplasm. The number of these granules was strongly correlated with the intensity of the tinctorial properties of the tumor tissue. Out of 11 acidophilic adenomas, 10 were observed consisting of typical STH cells. 4 acromegalic patients were found to possess heavily or poorly granulated STH cell adenomas (two patients in each of these groups). One patient with a clinical history of liver cirrhosis and gynecomastia was observed bearing an acidophilic (and erythrosinophilic) adenomatous hyperplasia of prolactin cells, 13 tumors consisted of cells exhibiting almost weak amphophilic staining properties and secretory granules of 100-250nm diameter, thus resembling cells which have been reported to produced ACTH. One of the patients suffering from these adenomas, showed the clinical signs of M. Cushing. By ultrastructural criterions, 3 adenomas with PAS-positive tumor cells were considered to be composed of gonadotropic cells. Only 7 adenomas were observed which did not give any chromophilic reaction. These tumors consisted of extreme poorly granulated cells which could not be significantly associated with one of the pituitary hormones by their morphological properties. In respect of the abundance of mitochondria, 4 out of the adenomas were designated as oncocytic tumors.

Acromegaly↗