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Biomedical subjects

W Schlote

Publications and source records attributed to W Schlote.

At least 37 records · Page 2Linked to original sources
PubMed1996

[Consensus report: tissue handling in suspected Creutzfeldt-Jakob disease and other spongiform encephalopathies (prion diseases) in the human. European Union Biomed-1 Concerted Action].

Despite many sensational and intimidating reports in the mass media, transmissible spongiform encephalopathies (prion diseases) are not contagious in the usual sense. Successful transmission requires both specific material (an affected individual's tissue, from or adjacent to CNS) and specific modes (mainly penetrating contact with the recipient). Nevertheless, specific safety precautions are mandatory to avoid accidental transmission and to decontaminate any infectivity. The autopsy is essential for definite diagnosis of these disorders. Recommendations are given here for safe performance of the autopsy, for neuropathology service and appropriate decontamination; they are based on the current literature and on precautions taken in most laboratories experienced in handling tissue from transmissible spongiform encephalopathies. In essence, special care must be taken to avoid penetrating wounds, possible contamination should be kept to a minimum, and potentially infectious material must be adequately decontaminated by specific means. The full English text of this Consensus Report was published in Brain Pathology 5: 319-322 (1995).

Autopsy↗
PubMed1995

Localisation and association of pathomorphological changes at the brainstem in Alzheimer's disease.

The brainstems of ten patients with Alzheimer's disease were examined with specific silver impregnations for beta-amyloid deposits, neurofibrillary tangles, neuropil threads and neuritic plaques. The results show a selective and focal involvement of brainstem nuclei, which are diffusely connected to the cortex or are neuronally connected with other damaged subcortical and cortical regions. Therefore, it is concluded that neuronal connectivity plays an important role in the pathogenesis of Alzheimer's disease lesions. This may be due to the intraneuronal transport of beta-amyloid precursor protein. There was a local association between neurofibrillary tangles and neuropil threads, but not between beta-amyloid structures on the one hand and neurofibrillary structures on the other hand. Neuritic plaques were rarely found.

Aged↗
PubMed1995

Ultrastructural differences of hippocampal lipofuscin in human development.

The lipofuscin of pyramidal cells in each hippocampal subfield of each of seven human autopsy cases without brain disease at the age of 3-12 months (infants) and of 17-23 years (young adults) was comparatively investigated at the electron microscopic level. In infant pyramidal neurons of the hippocampal subfields CA 1, CA 2, CA 3 and CA 4 O-2, very small lipofuscin particles were observed. The lipofuscin composition showed a slightly larger granular component compared to the vacuolar component with one or two small lipid droplets. No obvious ultrastructural variability of lipofuscin granules was observed. The CA 1 lipofuscin in young adults consists of larger particles than in infants, but no obvious difference in the composition of granular and vacuolar components from the infant lipofuscin was seen. The amount of lipofuscin in CA 1 strongly increased in young adults compared to infants and appeared in a perinuclear distribution. In young adults, in contrast to the infant group, the amount of lipofuscin in the subfields CA 2, CA 3 and CA 4 was significantly higher than in CA 1. In CA 2, CA 3 and CA 4 pyramidal neurons, the vacuolar component was significantly larger than the granular component. The similarity of infant hippocampal lipofuscin patterns in all subfields is discussed as a state of immaturity. To explain the observed differences between the CA 1 and the other subfields during neuronal development, as shown in the young adult group, several factors are discussed: the effects of cell specific metabolism, cellular functional activity, cytoprotective mechanisms and effects of efferent and afferent pathways connected with the subfields.

Adolescent↗
PubMed1995

Human diseases with defects in oxidative phosphorylation. 1. Decreased amounts of assembled oxidative phosphorylation complexes in mitochondrial encephalomyopathies.

The amount of oxidative phosphorylation enzymes in mitochondrial encephalomyopathy patients has been studied by two-dimensional electrophoresis (blue native PAGE/Tricine-SDS-PAGE). Only 20 mg muscle was required to identify and analyse complexes I, III, IV, and V after Coomassie staining. In most cases reduced amounts of the involved complex(es) correlated well with decreased enzyme activities. The reliability of the method was reflected by the constant mutual ratio of the complexes found in all controls. Deviations from normal ratios were found to be more sensitive indicators for a defect than the absolute quantities, which varied considerably within the control group both in the enzymic and in the electrophoretic analysis. The effect of the mitochondrial tRNA(Leu(UUR)) mutation in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes on the amount of oxidative phosphorylation complexes was demonstrated for the first time directly on the protein level. In patients without known DNA mutations, specific defects of single complexes were identified. The new technique is a sensitive method for the identification of oxidative phosphorylation defects, complementary to enzymic measurements.

Adult↗
PubMed1995

Selective quantitative analysis of the intensity of immunohistochemical reactions.

The present study reports a new method for the densitometric measurement of the intensity of immunohistochemical reactions. This method is based on a programm for the Kontron VIDAS image analysis system and has been designed for the measurement of small differences in the relative intensity of immunohistochemical reactions. Immunohistochemistry was performed with the avidin-biotin-peroxidase complex and diaminobenzidine-HCl and H2O2 for enzyme visualization. Several methods for shade correction and image processing were elaborated. The study was carried out on gerbil Purkinje cells using monoclonal antibodies raised against calbindin D28k. Prerequesites of correct measurement were standardized preparation, i.e., identical thickness of the paraffin sections, identical performance of immunohistochemistry, and avoidance of any counterstaining. The evaluation of small intensity differences of immunohistochemical reactions was found to be feasible either by substractive shade correction and standardized normalization or by shade correction by division by a reference image and standardized thresholding. Small differences in antigen concentration were not detectable without additional image processing.

Animals↗
PubMed1995

Neuron-specific enolase in gerbil brain and serum after transient cerebral ischemia.

BACKGROUND AND PURPOSE: The sensitivity and validity of serum neuron-specific enolase as a marker of brain injury were tested after global cerebral ischemia. METHODS: Sixty-nine Mongolian gerbils were perfusion fixed after variable reperfusion after 5-minute (group 1) or 15-minute (group 2) bilateral carotid occlusion. Neuron-specific enolase was analyzed by an enzyme immunoassay in serum of control, sham-operated, and ischemic animals before euthanasia and in nonischemic gerbil brains. Brains were processed for histology, immunohistochemistry, and morphometric evaluation of ischemic neuronal damage. RESULTS: After cerebral ischemia, loss of neuronal immunoreactivity was closely associated with increased neuron-specific enolase serum levels, which were significantly elevated by 24 hours (group 1) or by 4 hours (group 2) of reperfusion (P < .001). Response of serum levels depended on the duration of preceding ischemia, and maximum concentrations were approximately 3-fold (group 1) or 20-fold (group 2) those of nonischemic control. Morphological damage became apparent 48 hours (group 1) or 12 hours (group 2) after ischemia, as indicated by histological and morphometric data. CONCLUSIONS: Significantly elevated neuron-specific enolase serum levels could be demonstrated as a consequence of ischemia-induced cytoplasmic loss of neuron-specific enolase in central nervous system neurons, corresponded quantitatively to the severity of cerebral ischemia, and were detectable before irreversible neuronal injury. Therefore, analysis of serum neuron-specific enolase is suggested to be both a valuable diagnostic tool in clinical management of the initial stages of global cerebral ischemia and a prognostic parameter during the postischemic course.

Animals↗
PubMed1994

Histologic aspects from ruptured and nonruptured aneurysms.

We performed light microscopic examinations on 76 aneurysms from 72 patients (multiple aneurysms in four patients). The slides were stained with HE, Elastica-van-Gieson, Goldner and Prussian blue for iron. Based on morphological findings we were able to differentiate 4 groups of aneurysms. Aneurysmal walls frequently showed complete fibrosis or intimal hyperplasia. One third of the patients had prodromal signs such as headache or neurological deficits before the first subarachnoidal haemorrhage. These aneurysmal walls also had atherosclerotic changes in most cases. Haemodynamic stress as a causal factor seemed to be very important in aneurysmal wall formation. Four patients presented with giant aneurysms with thick fibrotic walls and intimal hyperplasia. 11 aneurysms had never bled. Their walls showed likewise atherosclerotic changes, intimal hyperplasia and sometimes haemosiderin deposits indicating earlier, local, clinically silent bleeding. In aneurysms after one or multiple bleedings, granulocytes and lymphocytes and partly organized thrombi could be found displaying varying degrees of reparative processes. There is a slight positive correlation between the degree of potential reparative processes and the time intervals between bleeding and histological investigation. Therefore obviously, local reparative processes stabilizing the aneurysmal wall may take place in aneurysms even after bleeding.

Adult↗
PubMed1993

Miniplaques and shapeless cerebral amyloid deposits in a case of Gerstmann-Sträussler-Scheinker's syndrome.

Multicentric plaques of typical pathomorphology have been described in two members of the well-documented German family "Sch" with Gerstmann-Sträussler-Scheinker's syndrome (GSS). The case of a third affected member with a clinical course of 10 years is now reported. In addition to multicentric plaques, small granules of prion protein (PrP) with stellate ultrastructure (miniplaques) were found in the tractus perforans and alveus of the hippocampal area. At the ultrastructural level, shapeless amyloid deposits of irregularly arranged bundles of amyloid fibrils were also observed in the same region. All amyloid precipitates apparent at the light microscopic level immunostained for PrP. These observations widen the known spectrum of amyloid plaque morphology in GSS. The multicentric plaque should still, however, be considered the diagnostic hallmark of this disease.

Amyloid↗
PubMed1993

Early ultrastructural studies on local acid phosphatase activity in rat sciatic nerve after nerve crush.

Rat sciatic nerve was crushed at mid thigh level. 30 minutes up to 24 hours after the lesion, the nerve was excised, fixed, stained for acid phosphatase activity, and embedded in araldite. The nerve was cut lengthwise over a distance of 6 mm proximally and distally to the lesion and examined by electron microscopy. Not more than 30 minutes after damage fundamental changes were found to take place, with little difference between the proximal and the distal "stump". Changes affect the axon itself, the axolemma and the Schwann cell. In the axoplasm, structures not existent in normal axons became visible during the first hour. Acid phosphatase activity appeared in the endoplasmatic reticulum, vesicles and cisterns, along the axolemma, and in the Schwann cell. Enzyme filled vesicles were released from the Schwann cell into the axoplasm. Mitochondria were found in increasing numbers in the axoplasm next to the lesion, being mainly small and round in shape and prominent where various organelles and enzymes had accumulated. It is concluded that the axon itself is capable of enzyme activation and organelle production, and that there is a complex interaction between the Schwann cell and the axoplasm after nerve crush.

Acid Phosphatase↗
PubMed1992

Pituitary adenomas: tumor cell growth by cluster formation. Pattern analysis based on immunohistochemistry.

The topographical distribution of adrenocorticotropic hormone, growth hormone and prolactin was studied in nine multihormonal pituitary adenomas and two normal adenohypophyses using quantitative immunohistochemical methods. For each pituitary hormone paraffin sections stained by antihormone antibodies were scanned with a light microscope equipped with a projection and scanning device. The number of immunoreactive cells of each square in the grid was counted and transformed into pseudocolors. In this way, the distribution of each hormone was documented. A chi-square test was applied to these distribution patterns to prove randomness. A nonrandom distribution of immunoreactive cells was observed in all pituitary adenomas and normal pituitary glands. Cluster formations of immunoreactive cells were found for each hormone. The clusters were surrounded by halo-like areas of decreasing number of immunoreactive cells from center to periphery. The cluster-halo type of immunoreactive cells was found not only in the adenomas but also in the normal pituitary gland. This may be explained by the similarity of biological processes during cell proliferation either in normal development or in adenoma formation. It can be concluded from our studies that pituitary adenomas in most cases develop by multicentric but not diffuse proliferation of cell clones of different endocrine activity.

Adenoma↗
PubMed1992

Delayed neuronal death and delayed neuronal recovery in the human brain following global ischemia.

The understanding of delayed hippocampal death as a therapeutic window for post-ischemic treatment of the brain has led to numerous investigations focusing upon underlying cellular mechanisms and pharmacological potentials in gerbils and rats. Nevertheless, studies on the occurrence of delayed neuronal death in the human brain have been singular and dealt with only small files of patients. To complement these limited data, in the present study 26 adult patients with a history of a single cardiac arrest were included. Following successful resuscitation, individual survival ranged from less than 1 h to 186 days (mean = 11 days). The severity of the resultant ischemic injury in hippocampus CA1, among Purkinje cells, or in frontal neocortex, respectively, was quantified by direct counting of necrotic neurons. Additionally, hippocampal specimens were immunostained for neuron-specific enolase. The data obtained demonstrate the occurrence of delayed neuronal death in human hippocampus and, in a minor form, in cerebellar Purkinje cells. This is in contrasts to the immediate manifestation of ischemic neuronal necrosis in the neocortex. Unlike previous findings in experimental animals and in humans, the delay of CA1 cell death could be defined as lasting about 7 days following cardiac arrest. Moreover, the immunohistochemical results indicate delayed neuronal recovery in CA1, which in the time course reciprocally corresponds to delayed manifestation of hippocampal neuronal death. Interpretation of the results must consider the lack of information about the exact individual duration of cardiac arrest and resuscitation, as well as missing data concerning pre-ischemic physiological variables.

Adult↗
PubMed1992

Malignant rhabdoid tumor: primary intracranial manifestation in an adult.

Clinical, histopathological, and ultrastructural features of an extended intracranial malignant neoplasm are presented. Following incomplete extirpation of a large epidural tumor at the temporal base of the skull, the 21-year-old male patient suffered from several local recurrences and died at the age of 27. The neoplasm was defined by its histopathological and ultrastructural characteristics and by the pattern of its antigenicity as a malignant rhabdoid tumor (MRT). Considering previous publications on MRT, this case may be the first of primary intracranial MRT appearing in an adult.

Adult↗
PubMed1992

Desmoplastic supratentorial neuroepithelial tumours of infancy.

The clinicopathological features of two infants with desmoplastic supratentorial neuroepithelial tumours are described. The cases were similar to the 26 cases reported previously as desmoplastic infantile ganglioglioma and superficial cerebral astrocytoma attached to dura. Neuronal differentiation was absent on routine stains, but was immunohistochemically established. We review the literature and suggest classifying this clinicopathological entity by using a general designation such as desmoplastic supratentorial neuroepithelial tumours of infancy, a term which indicates the variability in the amount and lines of differentiation.

Astrocytoma↗
PubMed1992

Immunocytochemical characterization of cytomegalovirus (CMV) infected giant cells in perinatal acquired human immunodeficiency virus (HIV) infection.

In a pediatric case of necrotizing CMV myelitis after perinatal HIV infection characteristic cytomegalic cells, which could not be attached to a particular cell line by cell morphology, were studied after immunostaining with monoclonal and polyclonal antibodies raised against GFAP, S100 protein, NSE, synaptophysin, factor VIII, vimentin, macrophages, leukocytes, CMV, HSV I + II, toxoplasma, and HIV 1 gp41. Astrocytes, oligodendrocytes, neurons, ependymal and endothelial cells, macrophages, and Schwann cells stained positively with CMV antiserum. With regard to their immunological features the majority of cytomegalic cells ("owl eye cells") was identified as astrocytes, and in decreasing frequency, the remainder was characterized as macrophages, mesenchymal, and endothelial cells. It is concluded that CMV giant cells represent one phase of virus induced cell transformation, not only one single, but numerous cell types are exposed to after CMV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1992

[Cerebral resuscitation].

The present paper illustrates the physiological basis of brain function as well as the pathophysiological and neurochemical cascades during cerebral ischemia and subsequent reperfusion. It is emphasized that brain resuscitation preferably focuses upon those cerebral functions or structures, respectively, which are not definitely damaged until the early period of recirculation. Finally, current experimental considerations and already clinically established concepts in treatment of ischemic brain injury are pointed out. Their principles of action and their therapeutical value in cerebral resuscitation following cardiocirculatory arrest are discussed.

Cerebrovascular Circulation↗
PubMed1991

Global cerebral ischemia and subsequent selective hypothermia. A neuropathological and morphometrical study on ischemic neuronal damage in cat.

A new method of external selective brain cooling is described, showing its effectiveness in reducing neuronal damage following global cerebral ischemia in cat. The cooling apparatus consists of a specially fitted kind of water jacket in which the animal's head was laid. In a preliminary study it was verified that the device effectively reduces brain temperature without the risk of cardiac arrhythmias due to lowering of core temperature. In the main study cardiac arrest was induced in 23 adult cats, followed after 15 min by cardiopulmonary resuscitation (CPR). Eight cats could not be revived; of the 15 remaining animals, 7 were assigned to the control group (normothermia) and 8 to the treatment group (cerebral hypothermia). The latter received external brain cooling for 30 min, starting as soon as CPR was begun. Four hours after cardiac arrest all animals were transcardiacally perfused with glutardialdehyde. The brains were stored in fixative and subsequently processed for histopathological and morphometrical evaluation by light microscopy. Analysis of the resulting data showed that animals in the treatment group had a significantly higher percentage of undamaged neurons than animals in the control group, both in the cingulate gyrus (38% vs 10%) and in the parietal cortex (39% vs 14%). The treatment group also had more undamaged neurons in the hippocampus and fewer severely damaged neurons in all three regions, but these differences, though suggestive, were not statistically significant.

Analysis of Variance↗
PubMed1991

Neuronal autophagy in experimental scrapie.

In this study we report the formation of giant autophagic vacuoles (AV) in neurons in experimental scrapie in hamsters. Autophagy is an important step in the cellular turnover of proteins and organelles. It is known to occur in neurons under physiological as under pathological conditions. Giant AV, however, are seen very rarely only in pathological states. In our model AV are much more numerous after intracerebral (i.c.) transmission of the scrapie agent than after the transmission via the intraperitoneal route which points to a correlation between the intensity of the process and the period of incubation. As the appearance of the AV in our model is correlated chronologically with that of scrapie-associated fibrils, at least after i.c. transmission, the process may be related to a disturbance of cellular protein metabolism and, thus, to the processing of prion protein.

Animals↗