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Biomedical subjects

M Toga

Publications and source records attributed to M Toga.

At least 73 records · Page 4Linked to original sources
PubMed1982

Corticolipotropin immunoreactivity in silent chromophobe adenomas: a light and electron microscopic study.

Twenty silent human pituitary adenomas were morphologically studied. Immunoperoxidase methods showed numerous adrenocorticotropic hormone-immunoreactive tumor cells in 14 cases by light microscopy and in one additional case by electron microscopy. Three of these cases were positive for beta-endorphin and one for beta-lipotropin by electron microscopy. These immunoreactions were found in undifferentiated tumors as well as in oncocytic adenomas, and could not be related to the presence of basophils by light microscopy. The peptides so detected in silent adenomas may have no biological activity and may correspond to common precursor molecule subunits.

Adenoma, Chromophobe↗
PubMed1982

Immunohistochemical and immunoelectron-microscopic study of pituitary adenomas associated with Cushing's disease. A report of 13 cases.

Thirteen pituitary adenomas were removed from patients with Cushing's disease by the transphenoidal route. All cases demonstrated a typical histochemical and ultrastructural pattern. Immunocytochemical study by means of the immunoperoxidase technique and light or electron microscopy demonstrated 1-24/1-39 adrenocorticotropic hormone (ACTH) in all cases, lipotropin/melanotropin (beta-LPH/beta-MSH) in 10 cases, beta-endorphin in 8 cases, and an absence of calcitonin in all cases. In addition, in 2 cases tumor tissue contained a few antiprolactin immunoreactive cells. These ACTH, beta-LPH, and beta-endorphin immunoreactivities may reflect either the peptides themselves or their precursors or intermediate products. The authors also suggest a possible intermediate-lobe-like processing of beta-LPH leading to beta-endorphin production, which may act on PRL cells. In addition, no positive arguments for the existence of a common precursor for calcitonin and ACTH could be provided from this study.

Adenoma↗
PubMed1982

[Enteropathy due to clofazimine treatment. A case report with an ultrastructural study].

The authors report a case of enteropathy due to clofazimine treatment for prurigo nodularis. The drug usually restricted to the treatment of leprosy has sometime been given to patients suffering from skin diseases because of its assumed anti-inflammatory effects. When high dosage of clofazimine treatment is carried on during a long period, and drug accumulates in the tissues and precipitates as a solid. This crystal storage in the lamina propria of the jejunal mucosa and in the mesenteric lymph nodes accounts for an enteropathy, sometime severe but slowly regressing after drug withdrawal. The electron microscopic study shows the prints of these crystals in autophagic vacuoles of histiocytes.

Clofazimine↗
PubMed1981

Experimental hexachlorophene encephalopathy in mice and baboons: light and electron microscopic study.

An experimental study on acute Hexachlorophene (HCP) neurotoxicity is reported in mice and baboons: - by light microscopy, a severe spongiform lesion of the central nervous system is localized in the white matter without myelin breakdown or cellular reaction; - by electron microscopy, the myelin alteration is characterized by the presence of vacuolation of "splitting" in the intralamellar spaces of compact sheaths; myelinated axons are occasionally involved. The changes described are discussed according to various reports on HCP neurotoxicity in humans and experimental animals. The effects of this chemical agent on the central nervous system is related to the percentage of HCP in talcum powder or solution for topical use. The toxicity of very low dosage level is demonstrated in baboons. Therefore HCP use cannot be recommended for young infants.

Administration, Topical↗
PubMed1981

Germinomas of the brain. Light and electron microscopic study. A report of seven cases.

The authors report seven cases of intracerebral germinomas studied on autopsy and/or biopsy material. Electron microscopy was done in five cases. Tumors were located on the middle line of the brain (pineal area, suprasellar region, third ventricle). Light microscopic features were stereotyped with PAS + round tumor cells and inflammatory mononuclear cells. By electron microscopy, fenestrated nucleoli, glycogen storage and annulate lamellae were always found, as well as a striking macrophagic activity of histiocytes. This immune reaction is supposed to contribute to the relatively favorable prognosis of these original brain tumors.

Adolescent↗
PubMed1981

Polysaccharide (amylopectin-like) storage myopathy histochemical ultrastructural and biochemical studies.

A case of an adult polysaccharide myopathy is reported in a patient with progressive muscular atrophy and weakness of limb girdles. Histochemistry and electron microscopy showed in some muscle fibers, a storage material composed of amylopectin-like filaments. Biochemical results were normal and no enzyme deficiency was found. This case is compared with three other published cases. Pathological conditions with amylopectin or amylopectin-like storage material are reviewed.

Amylopectin↗
PubMed1981

Subsequent morphological changes in periodic paralysis. A study of seven cases.

Muscle biopsies were studied in seven patients with various types of periodic paralysis. A sequence for the histopathological feature is suggested: 1. Histology may be normal early in the disease. 2. Vacuolation is found during the active phase characterized by frequent attacks. 3. Tubular aggregates appear later when the frequency of the attacks decreases. 4. Degenerative changes are correlated with the presence of permanent myopathic weakness.

Adolescent↗
PubMed1981

Anatomical study of experimental kuru in the Rhesus monkey.

The authors report the morphology and topography of CNS lesions in experimental kuru (third passage) in the rhesus monkey. The main lesions encountered are spongiosis of the neuropile with neuronal vacuolization, moderate astrocytic gliosis, and slight neuronal depopulation. In all cases, lesions predominated in the grey matter of the cerebral hemispheres (cortex, neostriatum). Lesions were minimal in cerebellum and brain stem. The authors compare their results with these observed species of Primates (chimpanzee, spider monkey, marmoset, squirrel monkey).

Animals↗
PubMed1981

Hexachlorophene and the central nervous system. Toxic effects in mice and baboons.

A study on hexachlorophene encephalopathy in mice and baboons is reported. By light microscopy, a severe spongiform lesion of the central nervous system (CNS) was localized in the white matter, without myelin breakdown or cellular reaction. By electron microscopy, the myelin alteration was characterized by wide intralamellar spaces or "splitting" developed in the intraperiod line of compact sheaths. The acute changes described were induced by administration of the drug by the digestive or cutaneous routes at various dosage levels in an aqueous solution or in talcum powder. The toxic effects depended on the age of the animals, the survival times and the concentrations of hexachlorophene, i.e., 6%, 3%, and 0.5%. The findings are compared with previous reports on the neurotoxicity of hexachlorophene and other chemicals in human and experimental animals. Hexachlorophene cannot be recommended for use in young infants because of its neurotoxicity in very low doses as demonstrated in the present report.

Age Factors↗
PubMed1981

Prostaglandins and steroidogenesis in isolated bovine adrenal cells. Effects of ACTH, prostaglandin-synthesis inhibitors, prostaglandins and prostaglandin analogs.

In bovine adrenal cortex cells, dispersed without preferential loss of cells, we investigated (1) whether endogenous prostaglandins (PGs) are involved in ACTH-induced adrenal steroidogenesis, and (2) the steroidogenic effects of PGs and PG analogs. Free cells produced considerable amounts of PGE2, whereas only minute quantities of PGF2 alpha and PGA1 were synthesized. PGE2 synthesis, however, was not significantly increased when ACTH elicited a steroidogenic response in free cells. High concentrations of PG-synthesis inhibitors such as indomethacin affected both PG synthesis and steroidogenesis, whereas intermediate concentrations (10(-6) M) inhibited production of both PGE2 and aldosterone even after cAMP and cortisol response to ACTH had returned to normal values. It is concluded that endogenous PGE2 is not a link in the acute mechanism of action of trophic hormones in which cAMP is involved. Of the prostanoid structures, PGs of the E series were the most potent stimulating agents of cortisol production, although less active than ACTH. On the other hand, PGA1 induced an ACTH-like aldosterone synthesis. PGE2 was less active, and other prostanoid structures were without effect on aldosterone production. It is suggested that in pathological circumstances, PGA1 regulates aldosterone production and PGE2 increases both aldosterone and cortisol production.

Adrenal Cortex↗
PubMed1981

Melanocytic involvement in giant axonal neuropathy.

The skin of a patient with giant axonal neuropathy was studied by light and electron microscopy. Enlarged melanocytes protruded into the papillary dermis. An increased number of microfilaments (100 A), which accumulated in rounded or irregular clusters was the main pathological feature. Melanosomes and melanisation were normal. A similar increase of microfilaments was seen in axons and Schwann cells of peripheral nerves, fibroblasts and endothelial cells. This suggests that this metabolic, probably inborn and genetic disorder, does not only affect the nervous system but also the whole microfilament system (cytoskeleton).

Axons↗
PubMed1981

[Primary brain lymphomas. Anatomoclinical, ultrastructural and immunocytochemical study about 23 cases (author's transl)].

Twenty-three cases of primary brain lymphomas were morphologically studied. Electron microscopy was done in twelve cases and immunoperoxidase reactions for light chains of immunoglobulins in ten cases. The patients were fourteen males and nine females. Except two children, the mean age was 50 years. Clinical features and pre-operative investigations lacked any specificity. Post-operative radiotherapy could be performed in thirteen patients, eleven of them being still alive with a follow-up varying from 2,5 months to 4,5 years. All the other patients persued fulminating course (max: 4,5 months). Tumors were preferentially located in frontal and temporal lobes. On gross examination, well limited tumors were more frequent than ill-defined or purely infiltrating tumors. Microscopically, all the lymphomas were of the diffuse type. Perivascular clusters of lymphoma cells, meningeal and parenchymal infiltrates and sub-ependymal sprouts were found in the peritumoral areas. The lymphomas were cytologically characterized according to the modified Kiel classification (Lennert et al, 1975) using light and electron microscopic data. So were identified thirteen lymphoblastic lymphomas (with one convoluted-cell type), one centroblastic lymphoma, eight immunoblastic lymphomas (two with plasmacytic differentiation). Light chains of human immunoglobulins were immunocytologically demonstrated in six of twelve tumors tested, all the positive cases corresponding to immunoblastic lymphomas. A unique case of primary meningeal Hodgkin's disease was found. These results were compared with the rare previous reports associating these different morphological investigations.

Adolescent↗
PubMed1980

The retina in Lafora disease: light and electron microscopy.

Lafora bodies are described in the retina of a 16 year old female who died five years after the onset of a typical familial progressive myoclonus epilepsy which was diagnosed as Lafora disease by brain biopsy and by autopsy findings. The patient was the offspring of consanguinous parents who had three affected siblings out of nine. The fine structure and distribution of Lafora bodies, which represent a specific non-lysosomal cell storage disorder, is reported for the first time in the human retina. The nature of the abnormal material in the Lafora bodies, which are identical to those present in the brain, heart and liver tissues in the same patient and in her brother, is discussed according to their iodide spectrum. In this respect, Lafora disease might be related to the inborn errors of carbohydrate metabolism and its relationship with Type IV Glycogenosis (Anderson's disease) must be verified by further investigations.

Adolescent↗