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Biomedical subjects

G Sobue

Publications and source records attributed to G Sobue.

At least 343 records · Page 19Linked to original sources
PubMed1985

Chronic experimental allergic neuritis (EAN) in juvenile guinea pigs: immunological comparison with acute EAN in adult guinea pigs.

In order to approach the mechanism of chronic or relapsing course in human chronic inflammatory demyelinating polyradiculoneuropathy, we established a chronic model of experimental allergic neuritis (EAN) in juvenile guinea pigs, and investigated the underlying cellular immune phenomenon in comparison with acute EAN in adult animals of the same strain. Two-week-old Hartley guinea pigs, sensitized with bovine peripheral nerve homogenate, developed chronic or relapsing EAN, whereas all adult animals developed acute monophasic EAN. Morphological examination of both the chronic and acute forms revealed scattered demyelination and mononuclear cell infiltrates which were essentially restricted to the peripheral nervous system, and indistinguishable from each other. Both the in vitro lymphocyte mitogenic response and in vivo skin testing revealed a significantly lower response to neuritogenic antigens (P2 protein and peripheral nerve myelin) in juvenile chronic EAN than in adult acute EAN throughout their respective courses. In addition, we showed, by means of assessing peripheral blood lymphocyte number and its subpopulations, that normal 2-week-old Hartley guinea pigs have not fully developed immunologically. These observations suggested that there was some immunological incompetence especially in cellular immunity in 2-week-old juvenile guinea pigs and that this might be one possible factor leading to chronic EAN.

Acute Disease↗
PubMed1985

Tissue culture studies of Schwann cell proliferation and differentiation.

Neonatal rat sciatic nerve Schwann cells in monolayer culture are stimulated to proliferate and to express a lipid and a protein characteristic of myelin by agents which raise intracellular cyclic adenosine 3',5'-monophosphate. Both glial growth factor and axolemmal fragments increase the rate of mitosis of cultured rat and human Schwann cells. Rat Schwann cell mitosis is enhanced by a soluble factor produced by concanavalin A-stimulated blood mononuclear cells and inhibited by lead salts. Schwann-like cells cultured from human dermal and plexiform neurofibromas resemble normal human Schwann cells in phenotype and response to mitogens.

Animals↗
PubMed1985

Adhesion of axolemmal fragments to Schwann cells: a signal- and target-specific process closely linked to axolemmal induction of Schwann cell mitosis.

Radioiodinated rat CNS axolemmal fragments adhered to cultured rat Schwann cells by a time-, temperature-, and concentration-dependent process independent of extracellular ionized calcium. Adhesion showed target and signal specificity; axolemmal fragments adhered to endoneurial or dermal fibroblasts to a much lesser extent than to Schwann cells, and plasma membrane fragments from skeletal muscle, erythrocytes, or PNS myelin adhered to Schwann cells to a lesser extent than did axolemmal fragments. Brief trypsinization removed 94 to 97% of bound radioactivity from Schwann cells previously incubated with 125I-axolemmal fragments for up to 24 hr, indicating that adhesion was largely a surface phenomenon rather than the result of rapid internalization of axolemmal fragments by the Schwann cells. When adhesion was compared to the axolemmal mitogenic response of Schwann cells, the concentration of axolemmal fragments yielding half-maximal adhesion was the same as the concentration producing half-maximal stimulation of Schwann cell mitosis. Trypsin digestion, homogenization, or heating of axolemmal fragments before application to cultured Schwann cells diminished adhesion and axolemmal fragment-induced stimulation of Schwann cell mitosis in a parallel fashion. Whereas adhesion of axolemmal fragments to the surfaces of the cultured Schwann cells reached completion within 4 hr in this assay system, induction of Schwann cell mitosis by the fragments required contact with Schwann cells for a minimum of 6 to 8 hr and reached a maximum when the axolemmal fragments had adhered to the Schwann cells for 24 hr or more.

Animals↗
PubMed1984

Astroglial proliferation and phenotype are modulated by neuronal plasma membrane.

The rate of proliferation of rat astroglia cultured in a serum-free medium, estimated by tritiated thymidine radioautography, was diminished by more than 50% by addition of rat central nervous system axolemmal fragments to the culture medium. Addition of the axolemmal fragments also induced a phenotypic alteration of the cultured astroglia, from cells of irregular shape containing a fine meshwork of intracytoplasmic glial fibrils to star-shaped cells with thicker, cable-like glial fibrils.

Animals↗
PubMed1984

Schwann cell galactocerebroside induced by derivatives of adenosine 3',5'-monophosphate.

Indirect immunofluorescence was used to show the presence of galactocerebroside (galC), a lipid found in myelin, on the surface of about half of the Schwann cells isolated from neonatal rat sciatic nerves and cultured for 1 day without neurons. By day 4 in vitro, the Schwann cells had all lost their surface galC. Three days after beginning treatment with 10(-3) molar 8-bromo-adenosine 3',5'-monophosphate (8-bromo cyclic AMP) or N6,O2'-dibutyryl adenosine 3',5'-monophosphate (dibutyryl cyclic AMP), galC reappeared on the Schwann cells, and 2 days later 48 percent of the cultured Schwann cells showed surface galC. Tritium from tritiated D-galactose was incorporated into galC by the 8-bromo cyclic AMP-and dibutyryl cyclic AMP-treated cultures at a rate 15 times the control rate.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1984

Axolemma is a mitogen for human Schwann cells.

The mechanisms responsible for the induction of Schwann cell proliferation in peripheral nerves undergoing wallerian degeneration and segmental demyelination are not understood. To determine whether contact with axolemma stimulates mitosis of human Schwann cells, cultured Schwann cells from spinal roots obtained postmortem and from sural nerve biopsy specimens were incubated with axolemmal fractions prepared from human spinal cord or from adult rat central nervous system. Schwann cell proliferation was estimated by autoradiographic assay of tritiated thymidine incorporation. Schwann cell labeling indices after exposure to human or rat axolemmal fractions ranged from 26.7 to 59.9%; labeling indices of Schwann cells cultured without axolemmal fraction were 9.8 to 22.4%. The stimulation index, or ratio of Schwann cell labeling index with axolemmal fraction to that without axolemmal fraction, ranged from 1.97 to 3.40. This study demonstrates that both human and rat axolemma are capable of stimulating human Schwann cell replication in vitro.

Adolescent↗
PubMed1983

Specific and potent mitogenic effect of axolemmal fraction on Schwann cells from rat sciatic nerves in serum-containing and defined media.

Using cultures of Schwann cells from neonatal rat sciatic nerves, we examined the mitogenic activity of an axolemmal fraction from adult rat CNS. Axolemmal fraction proved a potent mitogen, stimulating [3H]thymidine incorporation into Schwann cell DNA 13.5-fold over control values when axolemmal fraction equivalent to 16 micrograms of protein per culture microwell or more was added. Half maximal stimulation was obtained with addition of axolemmal fraction equivalent to 4 micrograms of protein. The concentration-dependence and magnitude of the mitogenic response of the cultured cells were nearly identical whether they were maintained in vitro for 1 day or for 2 weeks prior to addition of the axolemmal fraction. A study of the time-course of the effect of axolemmal fraction on Schwann cell mitosis showed that maximal [3H]thymidine incorporation took place during the fifth day after addition of axolemmal fraction. Axolemmal fraction also produced stimulation of [3H]thymidine incorporation into Schwann cells, seeded and cultured in a serum-free defined medium. Though the concentration-dependence of the mitogenic effect in the absence of serum was similar to that in a serum-containing medium, maximal stimulation in the defined medium was only 2.8-fold. The mitogenic activity of axolemmal fraction was rapidly and almost totally inactivated by sonication or homogenization, and was partially lost after exposure to heat. The mitogenic activities of plasma membrane fragments from rat skeletal muscle or rat erythrocytes, and of mitochondrial fragments (the major contaminant of the axolemmal fraction) were one-tenth that of axolemmal fraction or less. In contrast to glial growth factor prepared from bovine pituitaries (GGF-BP), which stimulates proliferation of both fibroblasts and Schwann cells, axolemmal fraction induced proliferation of Schwann cells but not of endoneurial fibroblasts; cultures treated with axolemmal fraction demonstrated a 3-fold increase in Schwann cell population in 10 days without detectable increase in number of fibroblasts. Also in contrast to GGF-BP, the mitogenic effect of which is considerably enhanced by simultaneous addition of cholera toxin to the medium, cholera toxin had no effect on the Schwann cell proliferative response to axolemmal fraction.

Animals↗
PubMed1983

Sensory ataxia. A residual disability of Guillain-Barré syndrome.

Four patients had idiopathic acute polyradiculoneuritis (Guillain-Barré syndrome) with sensory ataxia as the most prominent symptom. Sensory ataxia remained as a residue even three to five years after onset, despite good recovery of muscle weakness in five to 14 months. Sural nerve biopsy specimens disclosed a severe loss of large myelinated fibers and a high incidence of active axonal degeneration.

Adult↗
PubMed1983

Amyotrophic lateral sclerosis. Lack of central chromatolytic response of motor neurocytons corresponding to active axonal degeneration.

Ventral spinal roots and anterior horn cells in the lateral nuclear group of the fourth lumbar segment from 21 patients with amyotrophic lateral sclerosis (ALS) and 23 control patients were morphometrically analyzed. The number of large myelinated fibers was remarkably decreased, while small myelinated fibers were well preserved. The population of large myelinated fibers significantly correlated with the population of anterior horn cells. Numerous axonal degenerations were observed in the ventral spinal roots of patients with ALS, even in patients with severe loss of neurons and axons. In spite of this high frequency of active axonal degeneration, the incidence of central chromatolysis of anterior horn cells remained at the control level.

Adult↗
PubMed1983

Degenerating compartment and functioning compartment of motor neurons in ALS: possible process of motor neuron loss.

Using a morphometric method, we studied ventral spinal roots and anterior horn neurons of the fourth lumbar segment in 17 patients with ALS. Both populations of large myelinated fibers and anterior horn cells had significantly high correlations to muscle strength in the legs and duration of symptoms. However, active axonal degeneration was consistently present in terms of either large myelinated fibers or anterior horn cells.

Aged↗
PubMed1982

The role of macrophages in demyelination in experimental allergic neuritis.

The role of macrophages and serum factors in demyelination in experimental allergic neuritis (EAN) was examined by a simple in vitro method. Cultivated rabbit peritoneal macrophages, preincubated with serum obtained from rabbit EAN produced by sensitization with bovine spinal nerve roots, could agglutinate and phagocytize purified bovine or rabbit peripheral nerve myelin. Sera from normal animals or from controls given adjuvant alone could not. Adhesion and phagocytosis were inhibited if EAN sera were absorbed with peripheral nerve myelin. Rabbit red blood cells were not phagocytized by macrophages exposed to EAN serum. Concomitant to these observations, three lysosomal acid hydrolases: acid proteinase, acid phosphatase and beta-glucuronidase, were assayed with respect to their topographical and chronological distribution. In the group examined at clinical onset, increases in the specific activities were 1.5-3.0-fold in the spinal roots and 1.0-1.5-fold in the sciatic nerves compared with control. The degree of increase in total activities per whole root or sciatic nerve was much higher for specific activities. The topographical distribution of the increase closely corresponded to the histological distribution of EAN lesions. These observations suggested that the increased lysosomal activity originated from lysosomal-rich infiltrating cells. These observations strongly indicated the significant role of macrophages activated by EAN serum in the demyelination of EAN.

Acid Phosphatase↗
PubMed1982

Xeroderma pigmentosum: neurological, neurophysiological and morphological studies.

In 3 cases of xeroderma pigmentosum showing signs of peripheral neuropathy, electrophysiological studies were made. In one of them, a sural nerve biopsy was performed. MCV obtained from the lower limbs were moderately reduced in all cases, and SCV could be obtained in only 1 case from the median nerve. Auditory brain stem responses were not obtainable in all cases. Sural nerve biopsy revealed a marked decrease of myelinated fibers and also suggested severe damage in both myelinated and unmyelinated fibers. Teased fiber study showed myelin ovoids and indicated axonal degeneration. Sensory nerves including the acoustic nerve may suffer damage earlier than the motor nerve. In all cases CT scans revealed brain atrophy and thickening of the skull.

Adolescent↗