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J Ulrich

Publications and source records attributed to J Ulrich.

At least 91 records · Page 5Linked to original sources
PubMed1989

Computer-assisted morphometry of synaptic plasticity during aging and dementia.

A computer assisted morphometric study has been carried out on synaptic membranes in the dentate gyrus supragranular layer and cerebellar glomerulus from adult, old and demented patients. Numerical (Nv) and surface (Sv) densities as well as average area (S) of the synaptic contact zones were calculated directly on electron microscopic negatives by means of an ASBA (Wild Leitz, AG) image analyzer properly programmed. The results showed a decrease of Nv in both the CNS areas investigated during aging and, to a higher extent, in senile dementia. S was found to be significantly increased in old and demented CNS as compared with adult values. In the old hippocampus Sv was decreased by 40% whereas no significant difference was present between old and adult cerebellum; in senile dementia this parameter underwent a significant decrease in both areas investigated. We interpret the present findings in terms of morphological remodelling capability of the synaptic junctional zones during aging and disease.

Aged↗
PubMed1989

Quantitative morphology of the zinc-iodide-osmium (ZIO) stained synaptic vesicles.

A computer assisted morphometric method has been elaborated to quantify synaptic vesicles evidenced by means of the Zinc-Iodide-Osmium (ZIO) staining procedure in nerve endings of a very discrete area of the cerebellar granular layer: the glomerulus. The following parameters were calculated directly on electron microscopic negatives of 4.67 microns 2 of surface terminal area: number of vesicles per unit area (Na), and per unit volume (Nv), volume density (Vv), average diameter (d) and average volume of the single vesicle (V). Ultrastructural changes taking place at nerve endings also cover synaptic vesicles, thus quantitative studies regarding vesicle population at synaptic regions can be correlated to functional changes occurring in the process of chemical transmission and reflect the plasticity of synaptic junctional zones. Although this histochemical staining method generally is referred to as unspecific, after comparing our data with the available literature reports, we propose that ZIO-positive vesicles could have a physiological significance. These ZIO-positive organelles could take part in the intraterminal homeostatic control of Ca++ ions.

Animals↗
PubMed1988

[Clinical aspects and functional diagnostic findings of Takayasu disease].

Aetiopathogenesis, clinical picture, laboratorical and functional diagnostic methods of ten patients suffering from Takayasu's arteritis out of 1164 patients suspicious of cerebrovascular insufficiency are described. The combined use of Dopplersonography, ophthalmodynamometry and ophthalmodynamography permit in all cases the assessment of vascular pathology in supraaortic arteries. The specific diagnosis was made in connection which clinical, anamnestical and paraclinical findings. There are some characteristic functional diagnostic results in Takayasu's arteritis. The noninvasive diagnostic methods are useful tools to estimate the progredience of this disease in his chronical course.

Adolescent↗
PubMed1988

Differential modification of muscarinic cholinergic receptors in the hippocampus of patients with Alzheimer's disease: an autoradiographic study.

We have used quantitative light microscopic autoradiographic techniques to analyze changes in muscarinic cholinergic receptors in the hippocampus in Alzheimer type dementia (ATD). The density and distribution of muscarinic cholinergic receptors has been correlated with the density of neurons, neuritic plaques and neurofibrillary tangles in the CA1 subfield of the hippocampus of control and ATD patients. The number of pyramidal cells per mm2 in the CA1 sector was significantly decreased in ATD cases as compared to controls, although there were large variations among cases. The most marked reductions in cell counts were observed in patients with a history of profound dementia. The densities of muscarinic receptors, as well as the proportions of M1 and M2 subtypes, in the CA1 sector and dentate gyrus were not significantly different between ATD and old non-demented patients. Neuritic plaques, even in high numbers, did not affect the density of muscarinic receptors; moreover, the densities of receptors over the neuritic plaques did not differ from the surrounding neuropil. However, in some ATD cases there was a marked decrease in the concentration of these receptors in the CA1 sector and subiculum, with no change in the proportions of muscarinic receptor sybtypes. These patients exhibited frequent extracellular remnants of neurofibrillary tangles (ghost tangles), but scarce neuritic plaques, and were those showing severe losses of pyramidal cells. There was a significant positive correlation between the total concentration of muscarinic receptors in the CA1 and the density of pyramidal cells, suggesting that decreases in receptor concentration result from a severe neuronal loss. We observed that the ratio of muscarinic receptors per pyramidal cell was significantly increased in ATD patients. This might indicate a possible up-regulatory mechanism for muscarinic receptors in the population of remaining neurons in ATD However, decreases of receptor numbers following severe neuronal fall out suggest that compensatory mechanisms are no longer possible in such cases. The question is raised whether these differences between cases reflect different diseases or different stages of the same disease.

Aged↗
PubMed1988

Effects of aluminium chloride on cultured cells from rat brain hemispheres.

Neurofilamentous tangles have been induced by aluminium chloride in rat brain neurons cultivated on astroglial feeder layers. Monoclonal antibodies to neurofilaments were found to stain these aluminium-induced tangles. Immunostaining of these structures with anti-paired helical filament serum was always negative, though good staining of neuronal perikarya was achieved. This observation supports the hypothesis that aluminium-induced tangles are made up of neurofilament proteins. These tangles appear to be distinct immunochemically from Alzheimer-paired helical filaments.

Aluminum↗
PubMed1988

Progressive supranuclear palsy: extensive neuropil threads in addition to neurofibrillary tangles. Very similar antigenicity of subcortical neuronal pathology in progressive supranuclear palsy and Alzheimer's disease.

Light microscopic immunohistochemical investigations were performed on neurofibrillary tangles (NFT) in four histologically confirmed cases of Alzheimer's disease (AD) and in five patients with a progressive supranuclear palsy (PSP). The antibody panel included antisera to the neuronal microtubule-associated protein, tau, and to isolated paired helical filaments (PHF), as well as mouse monoclonal antibodies (MAbs) to phosphorylated epitopes on high and medium molecular weight neurofilament subunits (RT97 and BF10, respectively). Paraffin sections were also impregnated with the Gallyas silver method, which specifically stains tangles and cortical neuropil threads in AD, but does not stain normal neurofilaments. All tangles in PSP and AD showed consistent immunostaining with antibodies to tau protein and isolated PHF, regardless of their localization. MAbs RT97 and BF10, however, did not stain or only weakly stained, subcortical tangles in PSP and AD, whereas most cortical NFT in AD were intensely immunostained. All tangles in PSP were as heavily impregnated with Gallyas as they were in AD. Furthermore there were extensive networks of Gallyas-positive, tau- and PHF-immunoreactive neurites in subcortical gray areas containing NFT, and bundles of positive axons in white matter tracts interconnecting subcortical nuclei of PSP. Our studies indicate a much more extensive disruption of fibrillar proteins in PSP subcortical neurons than previously reported. They furthermore indicate a very similar antigenic profile of NFT in PSP and AD, as far as subcortical neurons are concerned.

Aged↗
PubMed1988

Working capacity after myocardial infarction.

The study presents data regarding the functional assessment and prognosis of acute myocardial infarction survivors resident in Prague 4 and an industrial region in north Bohemia. No demonstrable differences between the incidence of myocardial infarction in various professions were found. Acute myocardial infarction occurred in 0.52-0.73% of the total number of workers enrolled in the study. Rehabilitation programmes succeeded in significantly increasing working tolerance, overall performance, and in decreasing the heart rate/blood pressure index within the first six months after acute myocardial infarction. In patients resuming their original jobs, all these parameters were substantially more favourable than in those not seeking re-employment. Prognosis was assessed in 1072 patients. The 10-year mortality was 52.1%. Of the survivors, 30% of patients returned to work, and 24% and 46% remained in partial and full-time retirement, respectively.

Adult↗
PubMed1988

Anatomical re-evaluation of lumbar dura mater with regard to postspinal headache. Effect of dural puncture.

The effects of puncture of fresh cadaver dura with 20-, 22-, 26- and 29-gauge needles were observed. A 'tin-lid' phenomenon, manifested with all needle sizes, was capable of sealing the resultant hole. The larger the needle, the larger the hole, while rotation of the needle bevel 90 degrees to the fibres altered the shape of the hole. Holes made in thicker parts of the dura tended to retract more rapidly than those in thinner areas.

Anesthesia, Spinal↗
PubMed1988

Quantitative morphology of synaptic plasticity in the aging brain.

Quantitation of synaptic ultrastructural changes is of great importance in neurobiology, since merely qualitative alterations, if not extreme, are not readily detectable. In the present paper we discuss our previous and present findings on the number (numerical density: Nv), size (average length of the synaptic profiles: L) and surface contact area (surface density: Sv) of the synaptic junctions in aging rodent and human brains. We found that number and size of the synapses are in a close inverse relationship so as to maintain the total surface contact are among the nerve cells constant. These three parameters are closely related to each other, their quantitation may thus represent a reliable index of the morphological aspects of synaptic plasticity, i.e. the modification of ultrastructure occurring at synaptic membranes after transient changes in synaptic activity. During aging, the morphological plasticity of synapses appears to be seriously impaired: the number of synapses and the total surface contact area among the nerve cells are markedly reduced. However, old nerve cells seem to retain the ability to modify their synaptic endings and to partially compensate for the reduced surface density of the contact zones by expanding the average size of the persisting junctions. Our recent studies on synaptic plasticity in human brains from old and demented subjects showed that while the size of the synaptic contacts remains constant, the numerical and surface densities undergo a further decrease in demented brains relative to that in normal aging.

Adult↗
PubMed1987

Alzheimer dementia and Pick's disease: neurofibrillary tangles and Pick bodies are associated with identical phosphorylated neurofilament epitopes.

Sections of formaldehyde-fixed paraffin-embedded cortical and hippocampal brain tissue from five cases with senile dementia of Alzheimer type (SDAT) and five cases with Pick's disease (PD) were immunostained with the monoclonal antibodies (mabs) 147, RT 97, BF 10 and 8D8 with and without pretreatment with alkaline phosphatase (AP) or trypsin (Tr). The mabs 147, RT 97 and BF 10 had previously been demonstrated to bind exclusively to phosphorylated epitopes of neurofilament proteins, while mab 8D8 is shown in this report to bind mainly, but not exclusively, to phosphorylated neurofilament epitopes. The mabs RT 97, BF 10 and 8D8, but not 147 stain most, if not all, Pick bodies (PB) and Alzheimer neurofibrillary tangles (NFT). When sections are pretreated with AP or Tr the immunostaining with mab BF 10 is very resistent in both PB and NFT. This resistance of PB and NFT is in contrast to the reduced staining of axons and of swollen cells in PD by the same enzymatic pretreatment. Immunostaining with mab RT 97 of PB and NFT is reduced moderately by AP and considerably by Tr. Only when stained with mab 8D8 is there a discrepancy between PB and NFT in their reaction to the pretreatment with AP: NFT staining with mab 8D8 is not affected, while that of PB is abolished. Thus, in spite of their different ultrastructure, PB and NFT are very similar immunocytochemically and in the accessibility of their phosphorylated epitopes to enzymatic treatment.

Alzheimer Disease↗
PubMed1987

A special type of senile plaque, possibly an initial stage.

It is customary to distinguish "primitive", "classic" and "compact" ("burned out") senile plaques in Alzheimer's disease and senile dementia of the Alzheimer type (SDAT). Primitive plaques are characterized by altered neurites without accumulation of amyloid, classic plaques by an amyloid core surrounded by altered neurites and compact plaques by amyloid without pathological neurites. Here we describe a further type of plaque in which no amyloid or obviously altered neurites could be found by light microscopy with appropriate stains. This type of plaque was found mainly in the lateral entorhinal region and could be recognized by a slightly more intense staining and an altered texture of the neuropil in a spherical area having the same size as an early or mature plaque (100-150 microns in diameter). In non-serial paraffin sections (3-4 microns thick), a dark, silver-positive cell measuring 10-12 microns in diameter was found in the center of 49 out of 400 such plaques (about 12%), which is the expected frequency if one assumes that every plaque contains such a cell and measures itself about 125 microns. In fact, the reconstruction of 15 plaques (from four different patients) by means of serial sections demonstrated the presence of a central cell in each of them suggesting that this cell is an essential component of this plaque type. The central cell did not react with antibodies against cells of the mononuclear phagocyte lineage, such as alpha-1-antichymotrypsin, alpha-1-antitrypsin, leucocyte common antigen and lysozyme.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Granular cell tumors: evidence for heterogeneous tumor cell differentiation. An immunocytochemical study.

Eighteen granular cell tumors from various sites were examined with antisera directed against protein S-100, neuron specific enolase (NSE), alpha-1-antichymotrypsin, and alpha-1-antitrypsin, glial fibrillary acidic protein (GFAP), lysozyme, factor VIII-related antigen, myoglobin and vimentin, as well as with a monoclonal antibody (lu-5) directed against a panepithelial marker. The immunocytochemical reaction pattern of the tumors was heterogeneous. The brain and pituitary tumors and one thyroid tumor reacted for alpha-1-antichymotrypsin and alpha-1-antitrypsin, but not for S-100 protein and NSE. However, tumors from other sites showed immunoreactions for S-100 protein and NSE and some also for vimentin. Reactions for alpha-1-antichymotrypsin and alpha-1-antitrypsin were not observed. All other reactions were similarly negative. We conclude that the morphologically homogeneous group of granular cell tumors is biologically heterogeneous.

Cell Differentiation↗
PubMed1987

Cytoskeletal immunohistochemistry of Alzheimer's dementia and related diseases. A study with monoclonal antibodies.

Mabs directed against phosphorylated epitopes on the heavy and medium neurofilament protein were used to immunostain histological sections from brains of patients without neurological disease and patients suffering from SDAT, Pick's disease, Parkinson's disease, progressive supranuclear palsy and encephalomalacias of the white matter inducing chromatolysis in the overlying cortex. In normal brains only axons but never perikarya were stained. In the pathological brains, however, swollen neurons with chromatolysis and swollen cells in Pick's disease, NFT in SDAT, Pick bodies in Pick's disease, the centers of Lewy bodies in Parkinson's disease and some tangles in progressive supranuclear palsy were stained. These changes are perikaryal alterations. The results are discussed in relation to the formation of NFT in SDAT, i.e. the PHF as seen by electron microscopy. It is concluded that in spite of the reliable staining of NFT with some of our mabs, with sera directed against PHF, MAPs and other cytoskeletal proteins there is no absolutely specific immunoreaction for PHF. The most similar pattern to that observed in NFTs of SDAT is seen in the Pick bodies of Pick's disease, although these do not consist of PHF when looked at with the electron microscope, and although they behave differently from NFT in some 'conventional' histological stains. From this nonspecificity of the immunoreaction and from the presence of multiple cytoskeletal epitopes in NFT it is concluded that NFT (i.e. PHF) are probably not derived from one particular cytoskeletal element but are reassembled from proteolytic breakdown fragments of several of these elements. In this regard the similarities and dissimilarities with the alterations of Pick's disease might be specially relevant and deserve further studies, especially as the clinical features of SDAT and Pick's disease can be very similar.

Alzheimer Disease↗