Biomedical subjects
Publications and source records attributed to T Saida.
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Alterations of nodal and paranodal axolemma of the rat sciatic nerve were investigated in antigalactocerebroside serum-induced demyelination. A ferric ion-ferrocyanide (FeFCN) stain that appears to stain the regions with a high sodium channel density in nerve fibers was applied. When acute conduction block was initiated 20 to 180 minutes after the antiserum injection, myelin terminal loops began to be detached from the paranodal axolemma and reaction product of FeFCN stain originally localized at the nodes decreased in density and extended to the paranodal axolemma. By the time that complete conduction block was established, 5 hours after the injection, FeFCN stain was barely detectable around the nodal area. The loss of staining was associated with detachment and vesiculovacuolar degeneration of the paranodal myelin. This rapid deterioration and disappearance of normal cytochemical characteristics of the axolemma in the presence of only modest paranodal demyelination could be a morphological correlate of the loss of excitability of the axon membrane.
A double-blind crossover trial was conducted of thyrotropin releasing hormone treatment in six patients with amyotrophic lateral sclerosis. Patients received 4 mg of thyrotropin releasing hormone intramuscularly daily during the two-week treatment period. Although three patients reported subjective improvement, objective evaluation failed to demonstrate therapeutic effectiveness of thyrotropin releasing hormone in this dosage.
A 42-year-old man had a metastatic melanoma in the brain, but no obvious primary melanoma could be detected. A halo nevus-like depigmented lesion was found on the left side of the patient's back. The histopathologic features of the depigmented lesion were compatible with those of a spontaneously regressed primary lesion of malignant melanoma. Enhanced immune responses to autologous and homologous melanoma cells were not detected when investigated in the late disease stage. Subsequently, the patient died of disseminated melanoma.
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A novel benzophenone derivative, 2-(2-benzoyl-4-chlorophenoxy)-N-methylpropionamide (Ch-13), induced phenotypic differentiation linked to the inhibition of cell proliferation in human thymic acute lymphoblastic leukemia cell line HPB-ALL cells. The Ch-13-induced morphological changes consist of a decrease in cell size, nucleolar disappearance, and an alteration in the chromatin distribution, resembling large or atypical lymphocytes. Treatment with Ch-13 brought about a remarkable reduction in OKT6-, OKT4/Leu3a-, and OKT9-positive cells. At the optimal differentiation-inducing dose (5 X 10(-5)M), Ch-13 inhibited the cell proliferation, de novo DNA synthesis, and specific antibody-induced cell surface antigen capping.
Experimental allergic neuritis (EAN) was induced in 2 groups of inbred Lewis rats by sensitization with P2 protein and peripheral nervous system (PNS) myelin, both purified from bovine intradural roots. Light- and electronmicroscopic study of P2-induced EAN revealed demyelinative lesions in spinal ganglia and root nerves and less frequently in peripheral nerves and root entry zones. Both small and large myelinated fibers were demyelinated, contradictory to the reported selective binding of anti-P2 antibodies to myelin of large fibers. The early lesions were characterised by perivenular lymphocytic infiltration, and subsequent "dissolution" of myelin sheath was associated with invasive of phagocytic cells. The distribution of demyelinative lesions and patterns of demyelination resembled those of PNS myelin-induced EAN except that the disease was milder and dissolution of myelin and intramyelinic edema were more frequently found in P2-induced EAN. The abundance of demyelination in P2-induced EAN strikes contrast to the scarcity of myelin change in experimental allergic encephalomyelitis (EAE) induced by myelin basic protein immunization.
The case of a 54-year-old man with primary malignant melanoma of the esophagus is described. The results of morphologic examination are presented, and the histogenesis of the tumor and the classification of melanomas are briefly discussed. Histologic examination suggested that this was a case of primary malignant melanoma of the esophagus arising from melanosis of the esophageal mucosa. Like melanomas from the oral mucosa, vagina, anus, and vulva, the tumor had lentiginous radial components.
An indole alkaloid, teleocidin, induced phenotypic differentiation in the thymic ALL cell line HPB-ALL. Within 30 min of seeding in the presence of teleocidin, the cells formed a smooth round shape. Upon 5-day exposure to teleocidin, most of the cells became smaller and reminiscent of large or atypical lymphocytes. A thymic antigen stained with monoclonal antibody OKT6 was remarkably reduced while Leu2a-positive cells were increased in the treated cells. Upon teleocidin-induced phenotypic differentiation, the growth rate of cells was inhibited, their ability to incorporate DNA via [3H]-labelled precursors was reduced, their ability to bind sRBC rosettes was increased. These changes were paralleled to that induced by 12-o-tetradecanoyl-phorbol-13-acetate.
A case of multiple trichilemmal cysts is presented. After trauma, a large tumor developed on one of the cysts. The histologic features of this tumor were similar to those of proliferating trichilemmal cyst, but some of the tumor cells showed definite nuclear atypicality. The malignant potential of this tumor was confirmed by later development of metastases to the regional lymph nodes.
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The in vivo demyelinating capacity of sera from 27 patients with Guillain-Barré syndrome (GBS) and 47 other individuals was studied by intraneural injection into rat sciatic nerves. The morphological features of the nerves in cross section taken just proximal to the site of needle insertion was assessed 48 hours after injection and the extent of demyelination was quantitated. All 27 GBS serum samples were obtained in the first three weeks of clinical disease. Of these, 11 (41%) produced demyelination. Demyelinative activity of GBS sera correlated only with severity of clinical disease (p less than 0.01). The extent of demyelination after intraneural injection of human sera was less intense on average than that produced by sera from animals with experimental allergic neuritis. Three of 40 (7.5%) sera obtained from normal subjects and patients with other neurological diseases also caused in vivo demyelination, although the activity was weaker and occurred less often than with GBS serum.
Intraneural injection of antisera from rabbits with high antigalactocerebroside antibody levels into rat sciatic nerve produced acute nerve conduction block. This was first apparent in some motor axons between 30 and 60 minutes after injection and progressed to completion within 2 to 4 hours. Concurrent morphological evidence of demyelination was present, but structural changes at the time of onset of block were mild and were restricted to the myelin and Schwann cell, particularly at the paranodal areas and Schmidt-Lanterman clefts. It is suggested that paranodal lesions could account for the observed conduction block.
This report described a new method for the microanalysis of sphingolipids and its application for the characterization of cerebrosides and sulfatides in multiple sclerosis brain and rat sciatic nerves undergoing Wallerian degeneration. Tissue was extracted with isopropanol/hexane (20:78), and the total lipids obtained were subjected to benzoylation-desulfation. A portion of this was directly analyzed by silica-column high performance liquid chromatography for the determination of nonhydroxycerebroside, hydroxycerebroside, nonhydroxysulfatide, and hydroxysulfatide. Another portion was fractionated by thin-layer chromatography, and the spots corresponding to the sphingolipid derivatives were eluted. The material from each spot was analyzed by reverse phase high performance liquid chromatography for its homolog composition. With this new procedure the concentrations and homolog compositions of cerebrosides and sulfatides were measured in plaque, periplaque, and normal-appearing white matter from brains of multiple sclerosis patients and Wallerian degenerated rat sciatic nerves distal to the nerve transection. One piece of plaque studied contained only 1.86, 2.76, 0.60, and 0.45 nmol of nonhydroxycerebroside, hydroxycerebroside, nonhydroxysulfatide and hydroxysulfatide/mg of protein, respectively. These concentrations are less than 1% of those found in normal white matter. Periplaques were found to contain concentrations of these sphingolipids between those of plaque and normal white matter. The levels of these sphingolipids in degenerative nerves were 10-20% below normal the third day after the nerve was severed and about 70% below normal after 10 days. The rate of decrease lessened from ten days to 55 days. The homolog compositions of these sphingolipids in both multiple sclerosis brain and degenerating nerves were similar to those in the control. The implications of these findings and the advantages of this new analytical method are discussed.
1. We have observed conduction in single rat spinal ventral root nerve fibres following acute topical application of anti-galactocerebroside serum.2. Conduction of nerve impulses was initially slowed and subsequently blocked at the site of serum exposure.3. Conduction block occurred within as little as 1 hr in more slowly conducting (20-30 m/sec) myelinated fibres but occurred later in fibres conducting more rapidly.4. Conduction block was preceded by a rise in internodal conduction time from the normal 20 musec to about 200 musec.5. At nodes exposed to serum, conduction block was invariably associated with greatly decreased depolarization; this was contrasted with nodes exposed to local anaesthetic or tetrodotoxin where conduction block occurred despite nodal depolarization well beyond threshold potential.6. Nodal capacitance and resistance were estimated from simultaneous recordings of membrane current and extracellular potential at blocked nodes exposed to local anaesthetic or tetrodotoxin (normal nodes) and at blocked nodes exposed to anti-galactocerebroside serum.7. For normal fibres of internodal length 0.8-1.1 mm, an upper limit estimate for average nodal capacitance was 2.6 +/- 0.3 pF and a lower limit estimate for average nodal resistance was 55 +/- 10 MOmega. There was an order of magnitude increase in the capacitance of nodes at which conduction block occurred following exposure to anti-galactocerebroside serum.8. We conclude that the early conduction block caused by anti-galactocerebroside serum is due to paranodal demyelination and that acute paranodal demyelination is sufficient to cause conduction block.
12-O-Tetradecanoylphorbol-13-acetate (TPA), a potent tumor promoter, induced phenotypic differentiation in the human thymic acute lymphocytic leukemia cell line, HPB-ALL. Within 30 min of seeding in the presence of TPA, the cells formed a smooth round shape. After a 7-day exposure to TPA, most of the cells became smaller and reminiscent of large or atypical lymphocytes. Electron microscopic analysis evidenced morphological differentiation in TPA-treated HPB-ALL cells. Thymic antigens stained with monoclonal antibody OKT6 were dramatically reduced while Leu2a-positive cells were increased in the TPA-treated HPB-ALL cells. However, OKT3-positive cells did not appear in these TPA-treated cells for up to 7 days. Upon TPA-induced phenotypic differentiation, the growth rate of cells was significantly inhibited, their ability to incorporate DNA and RNA via 3H-labeled precursors was reduced, their ability to bind sheep red blood cell rosettes was significantly increased, and the proportion of terminal deoxynucleotidyl transferase-positive cells was decreased.