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Biomedical subjects

M M Silver

Publications and source records attributed to M M Silver.

At least 73 records · Page 4Linked to original sources
PubMed1986

Renal and systemic kappa light chain deposits and their plasma cell origin identified by immunoelectron microscopy.

Kappa light chain determinants were identified by immunoelectron microscopy in nodular glomerulosclerotic lesions and systemic interstitial deposits from a man who died several years after the onset of proteinuric renal failure treated by hemodialysis. He developed adrenal and hepatic failure preterminally but not overt malignant myeloma. Specific labeling was most concentrated over the inner aspect of glomerular basement membrane and the mesangium, which suggested that the protein was nonfiltrable. Tubular basement membrane labeling was densest over the outer aspect, which suggested that the protein perfused from the interstitium rather than from the tubular lumen. We identified the source of the protein as a population of plasma cells present within bone marrow and renal interstitium; these showed specific immunogold labeling for kappa light chain protein over organelles concerned with protein synthesis, secretion, and storage. This appears to be the first identification of light chain determinants in human interstitial para-amyloid deposits with the use of immunogold ultrastructural techniques in tissues prepared for electron microscopy by standard methods and stored as epoxy resin blocks.

Adrenal Glands↗
PubMed1986

Chronic ileal obstruction in adults due to peri-ileal vitelline vascular remnants.

Two young adults had distal ileal obstruction at sites where a fold of mesentery extended from its posterior leaf to the antimesenteric border of the bowel. No Meckel's diverticulum or mesoumbilical band was present in either case. Clinical, gross and microscopic findings suggested that the mesenteric fold represented a remnant of vitelline vessel that persisted in the peri-ileal portion of its course. Chronic ileal obstruction was apparently due to disordered peristalsis caused by the fold tethering the adjoining posterior bowel wall. In one patient, a chronic ulcer at the site of obstruction was interpreted as being an additional complication of the congenital lesion.

Adult↗
PubMed1985

Hyperinsulinemia in myotonic dystrophy: identity of the maternal factor causing the neonatal myotonic dystrophy syndrome.

An environmental factor acting on the fetus is thought to cause a neonatal syndrome characterized by marked muscular hypotonia, lack of respiratory drive and feeding difficulties, in some infants born to mothers with myotonic dystrophy. Mortality is high, especially amongst those babies born prematurely, but muscle strength and tone improve rapidly in survivors. Nevertheless, most survivors have physical deformities and mental retardation and are thought to develop myotonic dystrophy later. We propose that alterations in maternal insulin secretion (usual in myotonic dystrophy subjects) alter fetal blood glucose and amino acid levels and retard growth and maturation of fetal skeletal muscle. This leads to severe muscular hypotonia in affected infants. Also, we suggest that infants who die during the perinatal period may not have inherited the defective autosomal dominant gene that causes myotonic dystrophy.

Female↗
PubMed1985

Immunoelectron microscopic labeling of immunoglobulin in plasma cells after osmium fixation and epoxy embedding.

Previous studies have found that immunoglobulin cannot be immunolabeled in tissues prepared for electron microscopy by usual methods. To test this conclusion, we used a protein A-gold postembedding immunolabeling method on tissues that were fixed in glutaraldehyde, post-fixed in osmium tetroxide, and embedded in epoxy resin; sections were pretreated with sodium metaperiodate. A variety of common fixation protocols were also used and the most suitable conditions for immunolabeling were determined. This technique permitted the ultrastructural localization of immunoglobulin light chains in optimally preserved and contrasted plasma cells from human tonsil, lymph nodes, plasmacytomas, and a renal biopsy. We were able to demonstrate multiple antigens in the same tissue and label antigens in tissues that had been stored for many years in epoxy resin. The technique allows quantitation of the gold label over plasma cell organelles and therefore gives information about the immunoglobulin secretory pathway in these cells. We found that the protein A-gold procedure compares favorably in technical ease with the immunoperoxidase, avidin-biotin peroxidase, and immunoglobulin-colloidal gold immunolabeling methods, and has added advantages in allowing precise localization and quantitation of the labeled antigen.

Epoxy Compounds↗
PubMed1985

Laryngeal atresia, pleurodesis, and diaphragmatic hypertrophy in a newborn infant with findings relevant to fetal lung development.

A rare congenital malformation, cartilaginous subglottic laryngeal atresia, was found associated with developmental growth disturbances in the lungs (hypoplasia), diaphragm (hypertrophy), and pleural cavities (pleurodesis) in a newborn premature male infant who died immediately after birth. Because of coexistent esophageal atresia, tracheoesophageal fistula, and anal atresia, the lower respiratory tract and gastrointestinal canal together formed a closed system throughout fetal life. A mechanism whereby diaphragmatic hypertrophy and mesenchymal obliteration of the pleural cavities may have evolved during uterine development is suggested. Since pulmonary hypoplasia was also present, an explanation of this unique constellation of development abnormalities has a bearing on normal lung development.

Abnormalities, Multiple↗
PubMed1984

Morphologic and morphometric analyses of muscle in the neonatal myotonic dystrophy syndrome.

Autopsy studies of three premature siblings who died soon after birth with the neonatal myotonic dystrophy syndrome revealed pulmonary hypoplasia and congenital pleural effusions. Neither of these findings has been described previously in this condition. New ultrastructural findings include focal diaphragmatic myofiber degeneration and necrosis, which were attributed to over-stretching of the fetal diaphragm. In addition, abnormally small stores of free and intravesicular glycogen were observed in skeletal muscle fibers. The morphometric features of control fetal and neonatal skeletal muscle were recorded for comparison with muscle fiber measurements in the three infants. Fiber diameters in the latter were much smaller than expected for body weights. The morphologic and morphometric findings support the concept that fetal muscle maturation is severely retarded in this syndrome.

Brain↗
PubMed1983

Juvenile xanthogranuloma.

Three infants with juvenile xanthogranuloma are described. Of the two with ocular involvement, one responded to topical corticosteroid and mydriatic therapy and the other to irradiation. The third had skin lesions alone. In the first case new histologic findings were made: lipid vacuoles were observed, by light and electron microscopy, in smooth muscle cells of erector pili and in Schwann cells of small nerves. These findings, along with the detection of lipid vacuoles in mast cells, support the concept that the condition results from local tissue injury that evokes a histioxanthomatous response. Treatment of juvenile xanthogranuloma should be tailored to the individual case and ranges from no active intervention (when there are skin lesions alone or ocular involvement limited to the eyelid or the epibulbar tissue) to a combination of corticosteroid therapy, irradiation and surgery (when there are iris lesions, which rarely resolve spontaneously and may have serious complications). A trial of topical corticosteroid therapy alone in uncomplicated cases is suggested since it was curative in one of the cases presented here.

Conjunctiva↗
PubMed1983

Segmental myofiber necrosis in myotonic dystrophy - An immunoperoxidase study of immunoglobulins in skeletal muscle.

Because serum immunoglobulin G levels are low in patients with myotonic dystrophy, it was hypothesized that it might be catabolized within abnormal muscle fibers. Accordingly, immunohistochemical stains for immunoglobulins were performed on muscle sections derived at biopsy or autopsy from patients with myotonic dystrophy, other forms of muscular dystrophy, nondystrophic muscle disease, or normal muscle. Positive staining for immunoglobulins was found only in necrotic segments of myofibers (in 7 of 19 dystrophic and 6 of 27 nondystrophic subjects), and it is believed that the staining was due to nonspecific diffusion. However, staining reactions distinguished between incipient necrosis and artifactual contraction bands and allowed us to study segmental myofiber necrosis, comparing its frequency in the various muscle diseases. Segmental myofiber necrosis was present in 4 of 16 cases of myotonic dystrophy. The relevance of this finding to the clinical and morphologic features of myotonic dystrophy is discussed.

Adolescent↗
PubMed1982

Monocyte IgG-Fc receptors in myotonic dystrophy.

Myotonic dystrophy (MyD), an autosomal dominant neuromuscular disease with multisystem abnormalities, is associated with hypercatabolism of IgG. The hypercatabolism is not related to structural abnormalities of the IgG molecule in MyD but appears to be due to a derangement of the serum IgG concentration-fractional catabolic rate relationship. Since the catabolic pattern of IgG is governed by the Fc portion of the molecule, the possibility of Fc receptor dysfunction in MyD has been explored. We have observed that although MyD patients have normal numbers of Fc receptor bearing leucocytes in their peripheral blood, MyD monocytes express significantly (P less than 0.02) greater numbers of Fc receptors (47.9 +/- 21.2 X 10(3) receptors/monocyte) than do monocytes of healthy subjects (29.1 +/- 9.6 X 10(3) receptors/monocyte). The mean affinity constants of the Fc receptors was lower in the MyD group (1.5 +/- 0.7 X 10(8)/M) than the normal control group (2.4 +/- 0.9 X 10(8)/M) but this difference was not statistically significant. MyD monocytes showed a propensity to shed Fc receptors in culture at 37 degrees C whereas no significant shedding was observed with control monocytes. Thus MyD monocytes may shed Fc receptors at physiological temperatures but at the same time express more receptors per cell than normal monocytes. This suggests that MyD monocytes may have an abnormally high turn-over of Fc receptors.

Cells, Cultured↗
PubMed1981

The morphology of the human newborn ductus arteriosus: a reappraisal of its structure and closure with special reference to prostaglandin E1 therapy.

The ductus arteriosus was examined in 103 fetuses and infants to define the normal structure, development, and morphologic features of the functional and anatomic phases of ductal closure. New contributions include ultrastructural observations and the light microscopic definition of the junctional regions of the ductus with the pulmonary artery and aorta. Observations relating to ductal closure include hyperemia of the ductal vasa vasorum, the presence of longitudinal muscle bands in the inner media, necrosis of the inner ductal wall, and organization of intraluminal thrombi. We found that a ductus arteriosus that fails to close normally is liable to show morphologic lesions, including intimal fibrinous deposits, medial hemorrhages, and dissecting aneurysms. The findings were used comparatively to investigate whether prostaglandin E1 infusion, given to maintain ductal patency in 7 infants with ductus dependent congenital heart disease, was associated with specific morphologic features. We could not delineate specific changes attributable to its use.

Age Factors↗
PubMed1980

Calcification in porcine xenograft valves in children.

Calcification developed in the degenerating collagen of the cusps of three porcine xenograft heart valves implanted in children for less than 4 years. The morphologic features and effects of this calcification are presented. Calcification of porcine xenografts seems to occur more frequently and at an earlier stage after insertion in children than in adults. Host factors, possibly related to calcium homeostasis, may promote calcification; hence, these valves may not be appropriate for use in children.

Adolescent↗
PubMed1980

Oncocytic cardiomyopathy in an infant with oncocytosis in exocrine and endocrine glands.

An 11 week old female infant with congenitally malformed eyes died from intractable cardiac arrhythmia. The heart showed extensive oncocytic transformation of myocytes, and this distinctive cardiomyopathy affected the conduction system. Oncocytes were found also in endocrine (pituitary, thyroid) and exocrine (submandibular, sublingual, minor salivary) glands. There is morphologic evidence that the lesions were caused early in gestation, possibly by a viral infection such as rubella.

Cardiomyopathies↗
PubMed1980

Primary hydronephrosis. Assessment of diuretic renography, pelvis perfusion pressure, operative findings, and renal and ureteral histology.

Hydronephrosis generally implies ureteropelvic junction obstruction, but may be mimicked by a variety of other disorders. The authors have attempted to determine the relative diagnostic value of diuretic renography and the pelvis perfusion test in children with hydronephrosis by correlating the results with operative findings, renal and ureteral histology, and postoperative results.

Child↗