Salt preference in desalivate rats.
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Animals↗
Biomedical subjects
G F Walter
Publications and source records attributed to G F Walter.
[Accidental saline poisoning in newborn infants. Morphologic findings and pathogenetic discussion].
In the nursery of an Austrian hospital, five newborns accidentally received 10% natrium chloride solution by infusion or oral feeding. Because of wrong labelling by the hospital pharmacy the solution was taken for 10% glucose. In all five newborns, bradycardia, edemas, cyanosis and cramps occurred. In all cases, autopsy revealed a fatal haemorrhagic encephalopathy and more or less extended haemorrhages of the lungs, the kidneys and the liver. There was no suppurative pneumonia and no arteritis. The intracerebral bleedings, thromboses and necroses may be provoked by tissue shrinking caused by hypernatraemic dehydration. The cerebral lesions again cause hyperosmolarity leading to death in most cases. Peritoneal dialysis which may be life-saving in some cases, unfortunately has not been performed in the present cases.
Accidents↗
[The intermediate form of maple syrup disease].
A severely retarded and tetraspastic child died at the age of four years upon a respiratory infection with acidosis, disturbances of serum electrolytes and lactic aciduria. Brain autopsy showed a spongy degeneration and led to suspect an inborn error of amino-acid metabolism. These findings corresponded with the results of computer-tomography and were supported by post mortem amino-acid analysis. An intermediate variant of leucinosis was detected in an younger sister at the age of five months after cerebral convulsions and opisthotonic posture. The activity of the branched chain ketoacid decarboxylase in fibroblasts was reduced to 3-4% of normal. A protein restricted diet allowed a nearly normal cerebral development and improvement of computer-tomographic results. The similarity of clinical and biochemical data in both children indicate that a maple syrup urine disease was most likely the underlying disease in the older sister. Later performed electron-microscopical examinations of the older sister indicate that spongy degeneration of the central nervous system in leucinoisis is caused by a spongy myelinopathy, which is different from the alterations found in Canavan's disease, what could be pointed out for the first time.
Amino Acids, Branched-Chain↗
Case report. Ultrastructural changes of muscles during attacks of adynamia episodica hereditaria.
In an ultrastructural study of biopsies of quadriceps femoris muscle from two patients during attacks of adynamia episodica hereditaria. Marked pinocytosis along the sarcolemma and an interfibrillary oedema were observed, together with a 'bamboo-like' shape of the myofibrils. Other non-specific abnormalities were also found.
Female↗
Histochemical and ultrastructural analysis of the mitochondrial changes in a familial mitochondrial myopathy.
Two familial cases of progressive external ophthalmoplegia with involvement of pharyngeal and distal muscles are presented. 'Ragged-red' fibres were found in both cases. Excessive amounts of RNA, as evidenced by the acridine orange-induced fluorescence, were noted in many muscle fibres, mostly in the 'ragged-red' fibres. At the ultrastructural level, numerous mitochondrial changes with paracrystalline formations were noted. Those formations were observed in three forms and three-dimensional reconstruction is proposed which suggests that the paracrystalline formations consist of undulating parallel leaflets joined along the top of the undulations. Small transverse bridges between neighbouring cristae and between cristae and paracrystalline formations are also emphasized. All those mitochondrial abnormalities are thought to represent the morphological expression of a biochemical deficiency in the inner membrane. They are interpreted thus: firstly, the biochemical defect leads to a multiplication of the mitochondria with increase in their volume and proliferation of the cristae in order to improve energy production; secondly, bridges between the modified inner membranes induce attachment of the neighbouring cristae and result in paracrystalline formations.
Adenosine Triphosphate↗
Leigh's disease--several nosological entities with an identical histopathological complex?
Although Leigh's disease corresponds to a quite distinct histopathological complex, clinical and biochemical findings may be very divergent. By the description of classical and borderline cases and by the comparison with cases from the literature, it is suggested that Leigh's disease encompasses several nosological entities related to different disorders of the energy metabolism. They produce an identical histopathological complex. New evidence for a cerebral mitochondriopathy is also given.
Adult↗
Dysontogenetic brain tumours--proposal for an improved classification.
The International World Health Organisation (WHO) classification of central nervous system tumours does not give an extensive classification of germ cell tumours and other malformative tumours and tumour-like lesions. In the same way, no consistent classification of dysontogenetic brain tumours can be found in the classical handbooks. For an eventual new edition of the WHO classification, it is proposed to reconsider and improve the classification of these tumours, based on their ontogenetic relations.
Brain↗
Different rates of neuronal degeneration: an exquisite variation of the 'Cascade' hypothesis.
This morphometric, quantitative and correlative multivariate study of the hippocampal formation in human brains from two distinct normal aging populations provides an additional support to the notion that neuritic plaques (NP) are an earlier stage of the pathological process underlying neurofibrillary tangle (NFT) formation. It is shown that the rate of transformation of NP-affected neurons into NFT-bearing neurons may vary remarkably between distinct populations. In addition, it is put forward that different rates of neuronal degeneration may be one of the explanations for the existence of conflicting hypotheses regarding pathogenesis of NP and NFT and the relationships of these important histological markers to psychical deterioration.
Adult↗
Doxorubicin-induced cell death in highly invasive human gliomas.
Glioblastoma is the most invasive form of primary brain tumors, and is often refractory to chemotherapy. Herein, we provide evidence that two highly invasive human glioma cell lines U-87 MG and U-373 MG, entered apoptosis after 48 hours following 24 h growth arrest induced by Doxorubicin (10 micrograms/2 x 10(5) cells/ml). Apoptosis depended solely on the level of intracellular drug accumulation, and it was not related to a functional p53 tumor suppressor factor. The multidrug resistance gene 1 (mdr-1) encoded P-glycoprotein (P-gp) was weakly expressed in these cells upon exposure to Doxorubicin, and exerted no influence on the extent of cellular drug efflux. Drug efflux occurred only in U-373 MG glioma cells subsequent to physical damage of the membrane upon exposure to Doxorubicin. Pretreatment of tumor cells with 10 micrograms/ml Doxorubicin precluded tumor formation on the chorioallantoic membrane (CAM) of embryonated hen eggs. Single-dose application of 0.4 microgram Doxorubicin on CAM/U-87 MG and CAM/U-373 MG tumor transplants inhibited tumor invasion in CAM tissue by 40 to 50%. These data suggest that highly invasive glioblastomas can be driven to apoptosis following growth arrest induced by Doxorubicin, providing that intracellular drug accumulation suffices cytotoxic levels.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Pathology of Jakob-Creutzfeldt disease.
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Brain↗
Extracerebral subdural manifestation of Chester-Erdheim disease associated with a giant adenoma of the pituitary.
Chester-Erdheim disease is a rare non-Langerhans histiocytosis, affecting within the CNS mainly the neurohypophyseal unit, the retrobulbar space and the parenchyma of cerebellum, cerebrum and brainstem. Here we present a case of a 55-year-old woman who developed an exophthalmus, edema and dyspnea, finally leading to death 4 months post admission to the hospital. A cMRI showed a retrobulbar fibrosis, a tumor in the sella turcica, and further tumor formation expanding from the pons to the spinal cord, but without involvement of the dural sheet. Autopsy revealed multiple tumors attached to the pituitary gland, the tentorium, and the brainstem as well as a diffuse thickening of the dura. Histologically, the tumor tissue consisted of densely packed lipid-laden foamy macrophages positive for CD68 and intervening fibrillary cords. Interestingly, tumor cells did not infiltrate/affect the parenchyma but showed a strictly extracerebral/ subdural location. In addition, sections of the pituitary tumor revealed a chromophobe giant adenoma of the pituitary gland. As to our knowledge this is the first detailed description of an exceptional case of intracranial CED presenting with strictly extracerebral/subdural tumor masses accompanied by a giant adenoma of the pituitary gland.
Adenoma, Chromophobe↗
Expression of MMP-2, MMP-7, MMP-9, MMP-10 and MMP-11 in human astrocytic and oligodendroglial gliomas.
The members of the matrix metalloproteinase family (MMP) have the ability to degrade macromolecules of the extracellular matrix and are responsible for tumor invasion and infiltration, limiting the effectiveness of the neurosurgical resection of brain tumors. Among the glial brain tumors, astrocytomas and oligodendrogliomas are the most important tumor entities and require a different therapeutic approach. To determine the pattern of MMP expression in astrocytic and oligodendroglial tumors, sections of astrocytic and oligodendroglial differentiated glioblastomas (WHO grade IV), as well as of anaplastic oligodendrogliomas (WHO grade III) and anaplastic gemistocytic astrocytomas (WHO grade III) were immunostained for MMP-2, MMP-7, MMP-9, MMP-10 and MMP-11. MMP-7, MMP-10 and MMP-11 were strongly expressed by neoplastic gemistocytic astrocytes while oligodendrocytic tumor regions showed only a low immunoreaction. In contrast, MMP-2 and MMP-9 mainly immunolabeled vascular structures. These data indicated that MMP-7, MMP-10 and MMP-11 contribute to the worse prognosis of astrocytic tumors when compared to oligodendrogliomas, while MMP-2 and MMP-9 might play an important role in neo-angiogenesis and tumor vascularization.
Astrocytoma↗
Primary malignant histiocytosis of the brain: a clinical, radiological and morphological study with cytological and immunohistochemical demonstration of atypical histiocytes.
Clinical, radiological and morphological findings in the case of a 79-year-old patient with a primary malignant histiocytosis of the brain are reported. The tumor was exclusively situated in the brain as proven by autopsy and was spreading on the inside of the lateral ventricles. The demonstration of atypical histiocytic cells in the CSF and the immunohistochemical demonstration of lysozyme, alpha 1-antitrypsin and alpha 1-antichymotrypsin which are typical for histiocytes, underline the histiocytic origin of the tumor.
Aged↗
Predominantly cerebral manifestation in Urbach-Wiethe's syndrome (lipoid proteinosis cutis et mucosae): a clinical and pathomorphological study.
The neurological and psychiatric manifestations in a case of Urbach-Wiethe's disease are reported. The present case is characterized by the predominance of cerebral symptoms: ataxia, psychomotoric seizures, paranoic hallucinatory psychosis and attacks of rage. At autopsy, deposits of amyloid-like material in the walls of the brain vessels could be observed. This finding, together with the mucocutaneous alterations, confirmed the diagnosis of the rare disease know as "lipoid proteinosis cutis et mucosae".
Adult↗
Brain edema in acute arterial hypertension III: fluorescence microscopic results.
Evans blue fluorescence micrographs were investigated from cat brain preparations 5 minutes after angiotensin-induced acute arterial hypertension and intravenous Evans-Blue injection to detect the main localization of Evans-Blue extravasation on the cerebral vasculature. The typical finding was pericapillary and perivenular fluorescence in the cortical grey matter, concentrated in the cytoplasm of neurons. Very intensive staining in the near vicinity of leaking vessels was additionally caused by diffuse fluorescence. The results support the hypothesis that acute arterial hypertension causes critical increase of cerebral venular pressure and venular congestion by overwhelming of cerebral venous outflow-capacity, followed by blood-brain barrier disturbance mainly at the capillaryvenular level.
Angiotensin II↗
[Ultrastructural study of a medullomyoblastoma (author's transl)].
A third case in between twelve reported cases of medullo-myyoblastoma was investigated by electron microscopy. The muscle cells seemed to originate of proliferated endothelial cells. Because of the derivation from two blastodermic layers the tumour was considered a teratoid.
Cerebellar Neoplasms↗