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Biomedical subjects

A Probst

Publications and source records attributed to A Probst.

245 records · Page 14Linked to original sources
PubMedDate not supplied

Computed tomographic anatomy of the canine pancreas.

Barium sulfate was administered into the coeliac artery of 5 canine cadavers to allow for contrast computed tomography of the pancreas. Contiguous, 2-mm-thick slices were acquired. Multiplanar and three-dimensional reformatting were performed to clarify the anatomic relationship. After imaging, the cadavers were frozen, cross sections obtained, and plastinated. These were compared to the computed tomography images. Five plain and contrast enhanced computed tomographic series of normal live controls were acquired and evaluated retrospectively. In the study of the canine cadavers the pancreas became opacified and appeared homogenous with irregular contour. In normal live controls, acquiring an image at the end of expiration allowed a detailed view of the pancreatic parenchyma in the non-alterated pancreas, but pancreatic and bile ducts could not be seen. Adjacent to the hepatic hilus the pancreatic body appeared as a dorsoventrally flattened structure bordering on the ventral surface of the portal vein, both in cadavers and normal live controls. The right lobe extended caudodorsally to the right abdominal wall and aligned with the cranial part of the duodenum. The left lobe was adjacent to the gastric body in all dogs although it was separated from the gastric fundus by the dorsal extremity of the spleen in normal live controls. Neither kidney was suitable as an anatomic marker for localization of the pancreas, unlike traditional references in textbooks. We recommended using the portal vein to localize the pancreatic body, the descending duodenum for the right lobe, and the dorsal extremity of the spleen as well as the gastric fundus for the left lobe.

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Frontotemporal lobar degeneration. An update on clinical, pathological and genetic findings.

Frontotemporal lobar degeneration is the second most common form of cortical dementia in the presenium after Alzheimer's disease. Clinically, based on consensus guidelines, three distinct disease entities can be distinguished: frontotemporal dementia, semantic dementia and progressive nonfluent aphasia. Dementia of frontal type and motor neuron disease inclusion dementia are the most frequent neuropathological subtypes of frontotemporal lobar degeneration. By using immunohistochemistry, the latter is characterized by the presence of filamentous ubiquitin-reactive but tau-negative inclusions in nerve cell bodies and neurites. In contrast, Pick's disease and familial frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) are both characterized by abundant filamentous nerve cell inclusions made up of the microtubule-associated protein tau. The recent discovery of more than 15 different mutations in the tau gene in FTDP-17 brought the tau protein to the centre stage. These findings had a major impact on our understanding of neurodegenerative disorders characterized by tau filamentous inclusions in neurones and/or glial cells which are grouped under the generic term of tauopathies. However, as exciting these new molecular insights are, it would be inappropriate to lump frontotemporal lobar degeneration as tauopathies. Recent neuropathological and genetic data strongly suggest that there is more than one genetic background for frontotemporal lobar degeneration.

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PubMedDate not supplied

Cellular mechanisms of bone repair.

The extent of callus formation about a bone fracture depends on the rigidity of fracture fixation. The mechanism that converts the mechanical stimulus into the biologic response is unknown. On the basis of existing literature, an attempt has been made to define a model that explains this mechanobiologic transduction. Once integrity of the bone has been disrupted, a sequence of biochemical and cellular events commences that induces inflammatory reactions. Messengers (e.g., metabolites of the clotting or complement system, eicosanoids, or growth factors) are released or activated. They control the migration, proliferation, and protein synthesis of cells that are essential for angiogenesis and connective tissue formation. The key component in this inflammatory sequence seems to be the macrophage. Growth factors (e.g., released by macrophages) stimulate endothelial cells to form capillaries and mesenchymal cells to synthesize their matrix. In mechanically neutral areas, the fracture cavity is revascularized and osteoblasts proliferate and form bone. In mechanically instable fracture areas, spreading capillaries are disrupted by shear forces. In these areas, therefore, the milieu becomes hypoxic again. This milieu seems to support the differentiation of chondrocytes that stabilize the fracture by cartilage formation. If the strength of repair tissue is surpassed, the disrupture of the repair tissue triggers the mechanisms of inflammation again and additional cells immigrate and proliferate. Their protein synthesis increases repair callus. The increase of callus formation, however, stops when the tissue is capable of resisting motion. Links to the callus formation in osteitis are shown.

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The elusive nature of cerebellar somatostatin receptors: studies in rat, monkey and human cerebellum.

The pharmacological profile and localization of somatostatin (SRIF) receptors were determined in rat, monkey and human cerebellum. In rat cerebellar cortex, low sst1/sst4, intermediate sst2 and very high sst3 receptor mRNA levels were found. sst1 mRNA was also expressed in the deep cerebellar nuclei. [125I]Tyr3-octreotide binding sites in cerebellar membranes correlated with recombinant sst2, but not with sst5 or sst3 receptors and were found in the molecular layer of the cerebellum. [125I]CGP 23996 (in Na(+)-buffer) binding in rat cerebellum correlated with sst1 or sst4, but not with sst2, sst3 or sst5 receptor binding. Similar data were obtained in rhesus monkey cerebellum. mRNAs for all five receptors were found in the granule cell layer of the human cerebellum and/or in the dentate nucleus. [125I]Tyr3-octreotide binding was strong in the molecular layer and correlated with that of recombinant sst2 receptors, but not with sst3 or sst5 receptors. [125I]CGP 23996 (in Mg(++)-buffer) binding was heterogeneous (about 75%, to sst2 and 25% to sst1 and/or sst4 receptors). The molecular and granular layers were equally and the dentate nucleus strongly labeled. Thus, SRIF receptors of the sst2, sst1 and/or sst4 subtype are presnt in the rat, monkey and human cerebellum. In the latter two species, the sst2 type appears to be predominant. Surprisingly, the high expression of sst3 receptor mRNA is not supported by radioligand binding data in any of the species studied. The reason for this discrepancy remains to be elucidated.

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PubMedDate not supplied

Pharmacokinetics and tissue distribution of the renin inhibitor N-(2-(R)-benzyl-3-tert-butyl-sulfonyl-propionyl)-His-ChacVal-n-butylami ne in marmosets.

The fate of CGP 38 560 [N-(2-(R)-benzyl-3-tert-butyl-sulfonyl-propionyl)-His-ChacVal-n-bu tylamine], a potent renin inhibitor, has been studied in marmosets. [3H]CGP 38 560 is rapidly cleared from the plasma. The elimination process is biphasic, with a t1/2 of 4.8 +/- 1.0 min (mean +/- SD) in the first phase and 26.6 +/- 8.4 min (mean +/- SD) in the second. The kinetics of elimination from plasma are similar when measured both in a radio-inhibitor binding assay and radiometrically using 3H-labeled substance. The drug is mainly eliminated in the bile, almost 73.8% of the i.v. administered dose being excreted within the first 60 min. It is detectable in bile in both unchanged (8.6%) and metabolized form. HPLC analysis of bile extracts showed at least five tritiated peaks representing constituents capable of binding human renin (A, B, C, D, and E). These fractions were isolated, purified, and analyzed by mass spectrometry. Peak E corresponded to unchanged CGP 38 560. Metabolites A, B, C, and D are more polar than the parent compound, as indicated by their retention times upon HPLC analysis. The metabolic pathways inferable from the respective molecular weights are hydroxylation, oxygenation, and, in one case, cleavage of the n-butylamino group located at the COOH-terminal. From comparisons of the pharmacokinetic parameters after iv (0.1 mg/kg) and oral (10 mg/kg) administration, it can be estimated that the bioavailability of CGP 38 560 in the marmoset is 0.3%.(ABSTRACT TRUNCATED AT 250 WORDS)

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Amyloid angiopathy combined with granulomatous angiitis of the central nervous system: report on two patients.

We report here two cases of isolated angiitis of the central nervous system associated with congophilic angiopathy. The clinical history lasted 9 months in the first patient (65 years old) and 9 years in the second patient (59 years old). It was characterized by progressive intellectual deterioration, increased protein content of the CSF and evidence of focal brain lesions in the CT scan. One patient showed chronic intracranial hypertension. Vascular lesions were limited to the brain and were characterized by granulomatous and necrotizing angiitis of the small leptomeningeal and intracortical vessels. Amyloid deposits were present in large amounts along vascular segments showing vasculitis, in foreign body giant cells, in plaque-like structures surrounding diseased perforating arterioles, along cortical microvessels and in many neuritic plaques. Close proximity and topographic overlap of vasculitis and amyloid changes suggest a possible pathogenetic relationship.

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Ganglioglioma of the brain stem: neurological dysfunction of 16-year duration.

An autopsy case of a brain stem ganglioglioma in a 38-year-old male patient with neurological dysfunction of 16-year duration is reported. Immunohistochemical investigation of the tumor was performed using a panel of antibodies against neurofilament protein (NFP), synaptophysin (SY 38), beta-tubulin (TUJ1), neuron specific enolase (NSE), and glial fibrillary acidic protein (GFAP). The value of these markers in the establishment of the diagnosis, as well as the general features, the prognosis and the therapeutic approach of the gangliogliomas are discussed.

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Rapidly progressing dementia with filopodia-like cytoskeletal neuritic anomalies, but without Alzheimer changes.

An unusual case of dementia is reported. The patient was a woman who died at the age of 69 years and 6 months after a two years history of organic dementia. Possibly the disease was familial. Examination of the brain at autopsy revealed no atrophy. In routine histology the brain seemed to be normal. However, when the sections were stained with highly sensitive techniques such as an antibody to phosphorylated Tau (PHF-1), widespread neuritic pathology was discovered. Probably both, axons and dendrites were involved. Only few perikarya were reactive with the antibody. In some of them, morphologic alterations were reminiscent of Pick's disease.

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Subependymoma of the third ventricle after partial resection of a craniopharyngioma and repeated postoperative irradiation.

We present the case of a 28-year-old man who underwent craniotomy and subsequent radiotherapy for a suprasellar craniopharyngioma at the age of 8 years. The patient suffered from a severe pituitary deficiency until his death. The cause of death was a bronchopneumonia. At necropsy epithelial tissue characteristic of craniopharyngioma was no longer found, but instead a subependymoma of the third ventricle. Up to now most reported primary central nervous system tumors associated with subependymomas were ependymomas. However, in 1 case very similar to ours a subependymoma was associated with a craniopharyngioma. Furthermore, only rare examples of subependymomas of the third ventricle have been reported. The growth of a subependymoma might have been induced by intense reactive gliosis as a response of the adjacent brain tissue to the craniopharyngioma. However, in view of the repeated post-operative irradiation in our case the possibility of radiation-induced glioma has also to be considered.

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PubMedDate not supplied

[Senile subcortical neurofibrillary degeneration with the presence of twisted tubules and straight filaments. Atypical form of progressive supranuclear paralysis].

A case with wide-spread subcortical neurofibrillary changes, cell loss and gliosis in a 81 year old man is described. The most affected areas were both pallida, Luys subthalamic bodies, the substantia nigra and the denate nuclei of the cerebellum. The cerebral cortex contained only a few senile plaques. We interpreted this case as a variety of progressive supranuclear palsy despite the lack of the typical supranuclear ophtalmoplegia and of superior colliculi involvement. In the subthalamic body and in the substantia nigra fibrillary tangles were investigated ultrastructurally and found to consist of two kinds of fibrillary material: straight fine filaments of 100 A and twisted tubules with an average diameter of 200 A. We did not see 150 A straight filaments like those found in some cases of progressive supranuclear palsy. The possible significancy of each kind of neuro-fibrillary tangles and of their simultaneous occurrence in the subcortex of this case is discussed.

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