The universal occurrence of weakness of skeletal musculature on disuse, however produced, and the paucity of published reports on the fine structural changes in human disuse atrophy, prompted the present investigation. The quadriceps muscle of a leg immobilized in plaster cast (for fracture) and of the opposite non-immobilized limb was biopsied in four adult males, after periods of immobilization from 50 to 75 days. These 8 muscle specimens were examined for histopathological changes, and muscle fibre diameters were measured by micrometry from paraffin sections. The histograms revealed a larger proportion of small fibres (less than 20 micron) and a smaller proportion of large fibres (greater than 40 micron) in the immobilized limb compared to the opposite. Thus, light microscopy showed only atrophic changes. This was confirmed by electronmicroscopy, where atrophy of few to several muscle fibres was seen in the form of loss of myofibrils, collapse and folding of the basement membrane and prominence of glycogen or muscle nuclei. The atrophic change was more severe in the immobilized limbs, but it was also noticeable in all the non-immobilized limbs. Degenerative changes, especially disorganization and breakdown of myofibrils, and fragmentation of plasma membrane, were also seen in occasional atrophied muscle fibres, again more frequently in the immobilized limb. Lipofuscin was often found accumulated in muscle fibres and occasionally in endothelial cells of intramuscular blood vessels; the latter showed prominent pinocytotic vesicles or thickened basement membrane. It is concluded that both atrophy and degeneration of fibres of proximal muscles can occur as non-specific consequences of disuse of the limb in man, that degeneration is a latter and more severe change, that muscles even of the non-immobilized leg are subjected to disuse atrophy during bed-rest, and that the proximal muscles in man seem to have a natural susceptibility to atrophy and degeneration in any muscular disorders.

Adult↗

PubMedDate not supplied

Effect of prolonged anticonvulsant medication in epileptic patients: serum lipids, vitamins B6, B12, and folic acid, proteins, and fine structure of liver.

Twenty-seven epileptic patients, most from low socioeconomic groups and aged 15-54 years, were studied for effects of prolonged anticonvulsant medication. They had received the usual doses of phenobarbitone and diphenylhydantoin (PHT) regularly for 3-32 years, with control of seizures, and had not taken any B-vitamins in the year before investigation. Besides reduced serum and cerebrospinal fluid (CSF) folate levels, significantly increased levels of total vitamin B6 in CSF and serum and of vitamin B12 in serum were found in patients as compared with normal healthy subjects. The bone marrow was normoblastic, and significant elevation of serum triglycerides and/or cholesterol was observed in patients. The total protein level was only slightly reduced as compared with that of controls, but there was significant increase in beta-lipoprotein fraction on gel electrophoresis. Plasma proteins concerned with vitamins and lipid transport showed no remarkable change, and no abnormal protein was detected. Although there was no clinical hepatic involvement, liver biopsy performed in 9 of 27 patients revealed fine structural changes in hepatocytes suggestive of varying degrees of drug-induced changes. A ramifying network of short, smooth, endoplasmic cisternae with depleted rough endoplasmic reticulum (RER), distended sinusoids with Kupffer cells, dark shrunken hepatocytes with reduced mitochondria, and increased lipofuscin were observed. This suggested an adaptive response of the liver, a reversible change, possibly related to the increased serum lipids in the same patients.

Adolescent↗

PubMedDate not supplied

Fine structure of A: autonomic nerve fibers and terminals in human myocardium; and B: myocardial changes in congenital heart disease.

In a histological and fine structural study of right atrial biopsy specimens from 31 patients with rheumatic heart disease (RHD), aged 7 to 46 years, and 11 patients with congenital heart disease (CHD), aged 3 to 36 years, nerve fibers or endings were seen by electron microscopy in 11 specimens. There was concurrence of ordinary axons along with terminals bearing pale cholinergic or dark adrenergic synaptic vesicles. Smaller and denser cholinergic vesicles suggested proliferation followed by exhaustion of such nerve endings. The closest proximity of nerve terminal to muscle fiber was about 100 nm. In one RHD specimen a "specific terminal cell" was present between a nerve ending and muscle fiber; in another a possible neuromuscular contact was developing at the surface of a regenerating small muscle fiber with a few myofilaments. Unmyelinated axons amidst increased subendocardial and subepicardial collagen, with prominent fibroblasts and depleted muscle fibers, were seen more frequently in specimens of CHD. Loss of myofibrils and accumulation of mitochondria, with infrequent formation of lipofuscin bodies, characterized degenerating muscle fibers in CHD also, although to a lesser degree than in RHD (reported earlier, 1985). The myocardial blood vessels in CHD tended to have pale swollen endothelial cells and narrowed lumen. The most severely affected cases of CHD were those with (1) a very wide atrial septal defect (ASD), (2) ventricular septal defect (VSD) with vegetations near the defect, (3) infundibular pulmonary stenosis, and (4) Fallot's tetralogy.

Adolescent↗

PubMedDate not supplied

Peripheral neuropathology of leprosy--a brief historical review: 1882-1991.

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Animals↗

PubMedDate not supplied

Culture and phagocytic characteristics of Schwann cells in vitro. A possible model substrate for cultivation of M. leprae.

Tissue cultures of five acoustic and four spinal schwannomas demonstrated good growth and migration of Schwann cells within two to four days. Two types of cells corresponding to Antoni type A tissue and Antoni type B tissue were clearly recognized. Both these cell types showed avid phagocytosis when the cultures were inoculated with mycobacteria, either ICRC bacilli or M. leprae. The phagocytic index was 95% at the end of two hours. The Schwann cells grown in vitro also showed intense acid phosphatase reaction with Gomori's stain, suggesting lysosomal activity. Neither this nor any phagocytosis was evidenced by fetal fibroblasts cultured similarly. Cells from two spinal neurofibromas grew and migrated slowly in vitro and were mainly fibroblasts.

Cells, Cultured↗