Establishment of an attenuated ML-17 strain of Japanese encephalitis virus.
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Biomedical subjects
Publications and source records attributed to I Yoshida.
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A highly specific enzyme immunoassay for determining hCG was established by using beta-D-galactosidase as label. In order to increase the specificity of the assay, an antiserum against whole hCG was purified on a column of hCG beta carboxyl-terminal peptide (residues 123-145) covalently linked to Sepharose 4B. The antibody (N101S) thus prepared showed a weak cross-reactivity with human LH in an assay using hCG-enzyme conjugate, but the slight cross-reactivity was virtually avoided when an hCG beta carboxyl-terminal peptide was used as a peptide in the enzyme conjugate. N101S antibody was compared with antiserum (B1B) directed against a carboxyl-terminal peptide (123-145). In hCG measurement N101S gave about 30 times higher sensitivity than B1B, although the former antibody was less sensitive to carboxyl-terminal peptides of hCG beta. The enzyme immunoassay using a combination of N101S antibody and a carboxyl-terminal peptide (130-145)-enzyme conjugate was able to detect as little as 0.25 mIU of hCG without the interference of LH. The performance and validity of this assay were comparable to those of conventional radioimmunoassay.
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A 41-year-old Japanese male with a new type of primary familial amyloidosis was reported. The patient developed vitreous opacities, and later, disturbances in the gastrointestinal and nervous systems. At autopsy, amyloid was observed in the vitreous and the retinal vessels. There were extensive cerebral infarcts and heavy meningo-vascular amyloid deposition. Although the postmortem study revealed slight peripheral nerve degeneration in the lower extremities secondary to amyloid deposition, there was no clinical evidence of polyneuropathy.
The mechanism for regulating interferon production was investigated in relation to accentuation of production in serum-free human diploid cells (strain WI-38) treated with N2,O2-dibutyryl guanosine 3',5'-cyclic monophosphate (db-cyclic GMP). Interferon production in serum-free WI-38 cell cultures in response to Newcastle disease virus (NDV) was greatly reduced. In these cells, there was decreased incorporation of 5-3H-uridine into the acid-insoluble fraction, but unimpaired incorporation of U-14C-L-leucine, as compared with serum-containing cultures. When serum-free cell cultures were treated with 0.2 mM-db-cyclic GMP, incorporation of both 5-3H-uridine and U-14C-L-leucine was increased and there was an 8-fold enhancement in the yield of interferon in response to NDV. Induction of db-cyclic GMP-treated cells by NDV in the presence of cycloheximide and actinomycin D suggests that db-cyclic GMP enhances transcription of the interferon gene, and thereby augments interferon production.
Interferon production by Newcastle disease virus in human diploid (WI-38) cells was greatly reduced in the absence of serum. Pretreatment of the serum-free cells with insulin in excess of 1.2 IU/ml for 2 h before induction considerably increased the amount of interferon produced. No enhancement of interferon production was seen when the cells were exposed to insulin 2 h after induction or later. The insulin's effect persisted for at least 6 h after its removal, but not for 24 h. A possible mechanism of insulin action is discussed.
Mice infected with Mycobacterium tuberculosis BCG were more resistant than normal mice to ectromelia virus infection. It is suggested that enhanced interferon production in peritoneal exudate cells and spleen cells of BCG-infected mice plays an important role in this resistance.
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Peripheral neuropathy was not found even six to ten years after the onset of visual symptoms in a family with primary amyloidosis, except in the propositus at the terminal stage. The propositus had mainly ocular and CNS involvement. An ocular manifestation, the vitreous opacity, was the only involvement in the family members, in spite of the long clinical course. This family may have a different type of familial primary amyloidosis from that previously reported.
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In 51 normal young female subjects, stimulation by name calling or by intermittent photic stimulation was given during sleep. At different intervals after the stimulation, the subject was awakened and asked if she could recall it. If alpha activity had not been elicited by the stimulus, there was no recall. If the time occupied by alpha activity evoked by the stimulation was more than 30 sec, the stimulus could be recalled after a long period of sleep. When the evoked alpha activity lasted for less than 30 sec and the subject slept again, the longer the evoked alpha activity, the longer the sleeping time span with the memory retention of the preceding stimulation. With equal durations of evoked alpha activity, retention of the stimulus was better when the sleep following was REM stage than when it was NREM stage (stage 2). The results might be explained by the assumption that process of consolidation takes place most rapidly during wakefulness and is inhibited during sleep but to a lesser degree during REM stage than during NREM stage (stage 2).
Erthrocytes collected from monkey species including grivet, rhesus, and cynomolgus monkeys were stabilized by fixation with glutaraldehyde of a low concentration and were freeze-dried in vacuo. These freeze-dried erythrocytes were compared with fresh erythrocytes for measles viral hemagglutination and hemagglutination inhibition and could be used in both tests instead of fresh erythrocytes. They maintained their initial appearance and sensitivity to measles viral hemagglutinins after storage at 4 degrees C for 4 months more.
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Over a period from spring to fall in 1974, a disease with delayed growth, anemia, abnormal feathers, and leg paralysis as main symptoms broke out in flocks of chickens inoculated with Marek's disease vaccine. A virus was isolated from affected birds in the field and the same lot of Marek's disease vaccine as inoculated into these birds. It had a common antigenicity to the T strain of reticuloendotheliosis virus (REV) and could not be discriminated from this strain on the basis of morphology or property. When chicks were inoculated with it, they presented essentially the same symptoms as the birds affected in the field. Since the disease was reproduced in this manner, it was presumed to have been caused by REV contained in the vaccine as contaminant. The virus persisted in the body for long time and also induced horizontal infection.