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Biomedical subjects

M Wolman

Publications and source records attributed to M Wolman.

At least 19 recordsLinked to original sources
PubMed2000

Morality of the privacy of genetic information: possible improvements of procedures.

Genetic screening has opened up new paths for progress in preventive and curative medicine, and will probably progressively increase its positive contribution in the future. Rules and regulations have been established attempting to protect the donors' rights and to avoid damage to the donor and to others. Present day regulations seem unable to prevent the occurrence of serious problems and possible dangers. These are: 1. Ownership of genetic information and right to determine to whom it is divulged. 2. Direct emotional damage to individuals (mainly young persons expecting late-onset catastrophes) by having the information. 3. Damage caused by unsought for findings. 4. Restriction of transfer of information to the stated aim. 5. Right to release information important for public safety. The aim of this article is to propose that the donor's ownership of the information be abolished and that a board should decide to whom the genetic information should be given. An alternative solution is to leave the decisions regarding to whom genetic information should be divulged in the hands of the donor and his physician, controlled by an institutional review board.

Computer Security↗
PubMed1994

Histochemical study of the blue autofluorescence of collagen in oral irritation fibroma: effects of age of patients and of the duration of lesions.

The intensity of the autofluorescence of collagen was measured in 27 irritation fibromata of the buccal mucosa and 13 of the lip. The intensity of fluorescence correlated positively with the duration of the lesion. The fluorescence intensity also increased with the patients' age. The present observations show that in irritation fibromata of buccal and lip mucosae, the intensity of blue autofluorescence of the collagen increases with duration of the lesions and with the age of patients.

Adolescent↗
PubMed1993

Lipid pigments.

Explore the source record for details and available documents.

Aging↗
PubMed1993

Pathological changes in organs of rats chronically exposed to hypoxia. Development of pulmonary lipidosis.

Rats were exposed to chronic normobaric hypoxia of progressively increasing severity; down to 8% or 7% oxygen concentrations. In addition to loss of weight, pathology revealed congestion, haemorrhages, hypertrophy of the heart involving mainly the right ventricle, thickening of arteries, ischaemic changes in the myocardium and extramedullary haematopoiesis in the spleen. Changes not described up until now were: 1) sheets of foam cells in the pulmonary alveoli; 2) foamy and solid storing cells in the spleen; 3) mucoid changes in the atrioventricular valve leaflets; 4) hyperplasia of the juxtaglomerular apparatus; 5) atrophy of the adrenal glomerulosa and hyperplasia of medulla; 6) atrophy of the perifollicular B-cell zone in the spleen; and 7) lipid pigment deposition in various organs. The findings indicate that severe chronic hypoxia induces a significant pulmonary lipidosis similar to that caused by amphiphilic cationic drugs, presumably by inhibiting hydrolytic enzyme activities. The observations are of importance in human hypoxic conditions and open the possibility of their rational treatment.

Adrenal Glands↗
PubMed1992

The pituitary-thyroid axis effects on ocular and orbital tissues: a histological, histochemical, and morphometric study.

This work tests the notion that the effect of thyroid hormone on orbital and ocular tissues is mediated through its action on their lysosomal enzymes. Hyperthyroidism was produced in guinea pigs by thyroxin and TSH; hypothyroidism was induced by thiouracil. After treatment for 10 to 21 days, several ocular and orbital tissues were taken for histological, morphometrical, and histochemical examinations. High acid phosphatase activity was demonstrated in extraocular muscles, optic nerve and the retinal pigment epithelium of thyroxine- and TSH-treated animals. The findings fit the notion that the effects of thyroid hormones are mediated through lysosomes also in ocular and orbital tissues.

Adipose Tissue↗
PubMed1991

Connective tissue nevi collagens. Study with picrosirius red and polarizing microscopy.

Biopsy specimens of five connective tissue nevi were examined under crossed polars after staining with Picrosirius red. One biopsy specimen was from a solitary nevus, another from a Shagreen patch. The other three specimens were of erupted nevi. In all cases, thick (as well as thin) collagen fibers appeared green to yellow. In contrast, thick fibers of normal human dermis appeared orange to red. The findings indicate that the collagen of collagenous connective tissue nevi is less well packed than normal collagen. Examination of the polarization colors of Picrosirius red-stained sections is a useful procedure for diagnosing collagenous connective tissue nevi.

Adult↗
PubMed1991

Reappraisal of the role of macrophages in the pathogenesis of atherosclerosis.

New Zealand rabbits were fed an atherogenic diet, 8 with and 8 without twice weekly intravenous injections of GdCl2. The injections caused a reduction in the phagocytic activity of the reticuloendothelial system by one fourth to one half. No significant differences were found between the two groups in the planimetric extent of atheromata in the aortae. GdCl2 treatment inhibited the deposition of sudanophilic lipids in depth of the arterial wall. The findings indicate that macrophages are the primary foam cells and their uptake of lipoproteins is essential for the deposition of lipids in myocytes. Lipid-laden myocytes and ground substance mucopolysaccharides represent sinks in which lipids are removed from the flow and accumulate locally.

Animals↗
PubMed1989

Are the polarization colors of picrosirius red-stained collagen determined only by the diameter of the fibers?

Polarization colors of various purified collagens were studied in fibers of similar thickness. Three different soluble collagens of type I, insoluble collagen type I, lathyritic collagen type I, two p-N-collagens type I, pepsin extract collagen type II, two soluble collagens type III, p-N-collagen type III, and soluble collagen type V were submitted to a routine histopathologic procedure of fixation, preparation of 5-microns-thick sections, staining with Picrosirius red and examination under crossed polars. Polarization colors were determined for thin fibers (0.8 micron or less) an thick fibers, (1.6-2.4 microns). Most thin fibers of collagens and p-N-collagens showed green to yellowish-green polarization colors with no marked differences between the various samples. Thick fibers of all p-N-collagens, lathyritic and normal 0.15 M NaCl-soluble collagens showed green to greenish-yellow polarization colors, while in all other collagens, polarization colors of longer wavelengths (from yellowish-orange to red) were observed. These data suggested that fiber thickness was not the only factor involved in determining the polarization colors of Picrosirius red-stained collagens. Tightly packed and presumably, better aligned collagen molecules showed polarization colors of longer wavelengths. Thus, packing of collagen molecules and not only fiber thickness plays a role in the pattern of polarization colors of Picrosirius red-stained collagens.

Animals↗
PubMed1989

A histochemical principle bearing on correctness of diagnosis in storage diseases.

A principle is proposed which may help pathologists avoid errors in diagnosis of storage diseases. Tissues from patients in whom a tentative diagnosis of a metabolic disorder has been made often store a number of metabolites in the cells. The presence of these metabolites can occur in single-enzyme or activator defects as a result of the following causes: (a) deposition of metabolites situated near the main substrate of the defective enzyme in the catabolic path, and compounds which were changed after they were deposited; (b) presence of multiple substrates for this enzyme; (c) co-deposition of molecules bound to the main substrates; (d) existence of multiple substrates for a single defective activator molecule. In contrast to these causes, variability in processes not associated with a single-enzyme or activator deficiency may be due to the following: (e) inhibition of multiple hydrolases by drugs or metabolites; (f) localization of substrates and hydrolases in different compartments; (g) multiple enzyme deficiencies; (h) concentration of metabolites beyond the catabolic capacity of cells. According to the proposed principle, diagnosis of storage disease resulting from a single enzyme deficiency can be negated if a wide-range histochemical test shows that the main substrate of a deficient enzyme is not present in some primary storage cells. The validity of the principle and possible pitfalls are discussed.

Enzymes↗