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Biomedical subjects

J R Manaligod

Publications and source records attributed to J R Manaligod.

At least 37 records · Page 2Linked to original sources
PubMed1984

Lymphangiosarcoma in chronic lymphedema that followed dissection of the groin in surgical management of a malignant melanoma.

A 41-year-old white man who had a malignant melanoma in the left lumbar area was treated by wide excision and dissection of the ipsilateral inguinal lymph nodes. Progression and irreversible lymphedema of the left lower extremity developed. Fourteen years after the surgery, numerous purplish plaques and nodules developed on the left leg and thigh. Histologic examination by conventional and electron microscopy yielded the diagnosis of angiosarcoma. The patient died 18 months after the diagnosis was made.

Chronic Disease↗
PubMed1983

Myeloid bodies in drug-induced acute tubular necrosis.

A growing list of drugs, metals, and chemicals has been implicated as the cause of functional and structural damage specifically to the proximal tubular epithelium. Renal biopsies were obtained from three patients who had developed nephrotoxic agent-related acute renal failure. Two of the patients had received gentamicin and viomycin; the third patient had heavy exposure to chromium. All three biopsies showed acute tubular necrosis (ATN) on light microscopy. Electron microscopy revealed that the proximal tubular cells and, to a lesser degree, the distal tubular cells, contained abundant, variably sized myeloid bodies. In our previous experimental study of viomycin-induced ATN in rats, similar ultrastructural findings of a gradual increase in the number of myeloid bodies in the proximal tubular cells were also observed. The constant presence of myeloid bodies in the tubular epithelial cells following drug-induced tubular necrosis suggests that they may represent lysosomal isolation of drug-bound cytoplasmic structures, as a cellular mechanism to degrade toxic substances and, therefore, may serve as an ultrastructural marker of cellular drug uptake and drug disposition.

Acute Kidney Injury↗
PubMed1982

Inclusion body myositis. A corticosteroid-resistant idiopathic inflammatory myopathy.

In seven patients with slowly progressive muscle weakness, inclusion body myositis (IBM) was diagnosed on biopsy. None had stigmata of collagen-vascular disease or malignancy. Serum creatine kinase levels were mildly or moderately increased. The six patients treated with prednisone did not improve. Needle electromyography showed a "myopathic" pattern in all patients, but four also had diffuse neurogenic changes with normal nerve conductions. Histologic study of muscle showed a mixture of small rounded fibers varying in size, atrophic angulated fibers forming small groups, and hypertrophic fibers. Variable amounts of inflammation, necrosis, and regeneration were seen in all specimens. All showed numerous intracytoplasmic vacuoles lined with purple-blue granules. Electron microscopy showed membranous whorls and masses of abnormal filaments measuring 14 to 18 nm in diameter. Although IBM seems to be a distinct type of inflammatory myopathy, its etiology and pathogenesis are not clear.

Adult↗
PubMed1982

Desmoplastic malignant melanoma: a study by conventional and electron microscopy.

A 61-year-old white man presented himself with a mass that had recurred on the chin. Conventional microscopy of sections from this mass showed atypical spindle cells surrounded by abundant collagen and resembled fibrosarcoma. Stains for melanin revealed pigment in the cytoplasms of the atypical spindle cells. Study of sections by electron microscopy demonstrated round, oval, and spindle-shaped cells having desmosomes and containing abundant melanosomes in varying stages of maturation. On the basis of both conventional microscopy and electron microscopy, the diagnosis was desmoplastic malignant melanoma. An unusual finding by electron microscopy was the presence of tubuloreticular intracytoplasmic inclusions in the neoplastic melanocytes.

Chin↗
PubMed1981

Lysosomal glycogen storage disease with normal acid maltase.

Two unrelated 16-year-old boys had mental retardation, cardiomegaly, and proximal myopathy. One also had hepatomegaly. Histochemistry and electronmicroscopy of muscle biopsies showed lysosomal glycogen storage resembling acid maltase deficiency. Biochemical studies of skeletal muscle showed increased content of glycogen of normal structure; acid alpha-glucosidase activity in both urine and muscle was normal. Other enzymes of glycogen metabolism were also normal. The cause of this apparently generalized glycogenosis with no demonstrable enzyme defect is unknown.

Acid Phosphatase↗
PubMed1981

Fatal infantile glycogen storage disease: deficiency of phosphofructokinase and phosphorylase b kinase.

A girl with congenital limb weakness, mental retardation, and corneal ulceration died with respiratory insufficiency at age 4 years. Histochemistry of muscle biopsy showed only nonspecific myopathy, but electronmicroscopy revealed subsarcolemmal and intramyofibrillar accumulation of glycogen. Biochemical studies showed increased glycogen content of muscle with lack of phosphofructokinase. Phosphorylase b kinase activity was about 30% of normal. The relationship of the double enzyme deficiency to this unusual clinical picture is unclear.

Biopsy↗
PubMed1980

Angiosarcoma arising in a plexiform neurofibroma: a case report.

A left cervical mass developed in a 14-year-old white boy with stigmata of von Recklinghausen's disease. Excision biopsy examination showed a plexiform neurofibroma with angiosarcoma. Ultrastructural studies confirmed the endothelial nature of the malignant cells.

Adolescent↗
PubMed1980

Mesangiolysis of isolated renal glomeruli with the formation of lobular sacs or cysts.

60% trichloracetic acid (TCA) will dissolve the cells and mesangial matrix of isolated renal glomeruli before it dissolves the basement membranes (BM). With the removal of the mesangial cells and matrix, the paramesangial BM stands out in sharp relief. It is thicker than that of the capillary loops and is provided with prominent ridges and spurs. These thick collars of BM now border the narrow channels left after the removal of the mesangium. The channels communicate with the capillary lumens. They widen asynchronously with the continued action of the TCA leading at first to more axial cavitation of the lobules of the glomerulus and finally to the conversion of these lobules into sacs or cysts. This is brought about by the unfolding of the capillaries within the investing sheath of BM which is common to the capillary loops and the widened stalks and intercapillary axial portions of the mesangium.

Animals↗
PubMed1976

Morphologic studies in a patient with homocystinuria due to 5, 10-methylenetetrahydrofolate reductase deficiency.

Biochemical and morphologic studies on a patient with homocystinuria due to a deficiency of 5, 10-methylenetetrahydrofolate reductase (EC. 1.1.1.68) were performed. The concentrations of homocystine in the patient's plasma and urine were 2.97 mumol/dl and 44.67 mumol/24 hr, respectively. Activities of 5, 10-methylenetetrahydrofolate reductase (expressed as nanomoles of formaldehyde formed per hr per mg of protein) in cultured skin fibroblasts and liver tissue were 0.53 (control: 5.14) and 0.00 (control: 13.80), respectively. The major abnormalities were found in the arterial bed, consisting of intimal hyperplasia, fragmentation, and disruption of elastic lamellae and subcellular changes in the endothelial cells. Extensive thrombosis was observed. The brain and the liver also showed widespread pathologic changes. In the former, neuronal loss and cellular damage were prominent and extensive. Diffuse demyelination with moderate astrocytosis was found; but demyelination was out of proportion to the vascular changes. Hirano bodies in the cortical neurons and crystalline and lamellar bodies in the Purkinje cells were observed. In the liver, there were fatty change and mild to moderate portal fibrosis. Bizarre, giant mitochondria and membrane-bound multivesicular bodies were found. Mild pathologic changes were also observed in the striated muscles and the kidneys. Focal fragmentation, disruption, and smearing of the Z discs and disorganization of the myofilaments were found in the skeletal muscles. The kidneys showed shrunken glomeruli, thickened basement membranes, and swelling of epithelial as well as endothelial cells.

Aorta↗
PubMed1975

Leukemic urate nephropathy.

The tubules appear to be the primary sites of injury in renal failure and urate nephropathy associated with leukemia. Tubular injury is not always associated with precipitation and phagocytosis of crystals, except in the collecting tubules where cellular changes are invariably caused by intraluminal crystallization of urates. The electron microscopical observations in this communication may apply to the urate nephropathy associated with hyperuricemia of various causes.

Basement Membrane↗