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Biomedical subjects

Y Yoshikawa

Publications and source records attributed to Y Yoshikawa.

At least 343 records · Page 19Linked to original sources
PubMed1986

Effect of complement depletion by cobra venom factor on fowlpox virus infection in chickens and chicken embryos.

The course of infection with an attenuated strain of fowlpox virus (FPV), which is known to induce antibody-independent activation of complement via the alternative pathway, was investigated in 1- to 3-day-old chickens and 14-day-old chicken embryos by treatment with cobra venom factor (CVF). CVF was found to inhibit complement activity transiently via the alternative pathway but not via the classical pathway. In chickens treated with CVF, virus growth in the skin was enhanced, and pock lesions tended to disseminate, leading to fatal infection in some birds. Histologically, an acute inflammation at an early stage of infection (within 3 days) was inhibited, and virus content in the pock lesion was increased. In chicken embryos with immature immune capacities, CVF treatment caused changes in pock morphology from clear pocks to diffuse ones, an increase in virus content in the pock, and inhibition of cell infiltration. Thus, FPV infection was aggravated in both CVF-treated chickens and chicken embryos. These results are discussed in relation to roles of complement in the elimination of virus at an early stage of FPV infection.

Animals↗
PubMed1986

Characteristics of fresh isolates of wild measles virus.

Characteristics of fresh isolates of wild measles virus were studied by immunofluorescence using monoclonal antibodies, SDS-polyacrylamide gel electrophoresis, and electron microscopy. By the immunofluorescence test, hemagglutinin, nucleocapsid-associated phosphorylated, and fusion proteins were found only in the cytoplasm of cells infected with the virus at a low passage level. Nucleocapsid (NP) and membrane (M) proteins were found in both the cytoplasm and nuclei. Since the M protein is present only in the cytoplasm of cells infected with the laboratory strain of measles virus, this intranuclear M protein may be specific to the wild virus. At an increased passage level, the intranuclear M protein became undetectable, but the NP protein was still present in the nuclei. SDS-polyacrylamide and electron microscopy showed that wild measles viruses were shown to have characteristics similar to those of laboratory strains.

Animals↗
PubMed1985

Requirement of methionine for the replication of canine distemper virus in Vero cells.

The replication of canine distemper virus (CDV) in Vero cells was found to require certain amino acids such as arginine, methionine and valine. The deprivation of methionine caused the most marked reduction in virus yield. In cells cultured in medium deprived of methionine, the early processes of viral replication such as adsorption, penetration and uncoating of virus occurred at normal rates, but the syntheses of viral RNA and protein were markedly reduced. The addition of S-adenosylmethionine to methionine-free medium resulted in the growth of CDV to the level obtained in cells with complete medium. Moreover, cycloleucine, which is known to reduce the methylation of mRNA by inhibiting the synthesis of S-adenosylmethionine, also inhibited the growth of CDV, and the addition of methionine or S-adenosylmethionine reversed the inhibitory effect of cycloleucine. The possibility of an inhibition of methylation of mRNA in methionine-deprived cells is discussed.

Animals↗
PubMed1985

Growth of defective subacute sclerosing panencephalitis viruses in human neural cells and their neurovirulence in mice.

A defective subacute sclerosing panencephalitis (SSPE) virus which had been passaged in human embryonic lung cells was transferred to cultures of three neural cell types: neuroblastoma, oligodendroglioma and glioblastoma. The growth characteristics of the virus in these cells were essentially similar to those in non-neural cells. On the other hand, a marked difference in neurovirulence was noticed for the virus grown in neural cells when examined by intracerebral inoculation into mice. The virus passaged in neuroblastoma and oligodendroglioma cells showed high neurovirulence, inducing an acute encephalitis, whereas the virus passaged in human embryonic lung cells and that in glioblastoma cells did not show neurovirulence. These results suggest that the virus recovered its neurovirulence after passage in certain human neural cells.

Animals↗
PubMed1985

Isolation and characterization of canine distemper virus-specific RNA.

Ten species of virus-specific RNA were detected in Vero cells infected with the FXNO strain of canine distemper virus (CDV). The largest RNA was the genome-sized RNA and the nine smaller species were polyadenylated RNAs. Similar results were obtained for nine other strains of CDV. The molecular weights of these ten RNAs were determined to be 4.61 X 10(6), 2.46 X 10(6), 1.52 X 10(6), 1.32 X 10(6), 1.19 X 10(6), 1.07 X 10(6), 0.77 X 10(6), 0.65 X 10(6), 0.58 X 10(6), and 0.48 X 10(6). By in vitro translation of the polyadenylated RNAs in a rabbit reticulocyte lysate system, three different proteins which probably correspond to H, NP, and M were synthesized from the fraction containing RNAs 7, 8, 9, and 10.

Animals↗
PubMed1985

Ontogeny of the third component of complement of Japanese quails.

Ontogeny of quail complement was examined in terms of serum C3 level, cytolytic activity of total complement, functional activity of C3 via the classical pathway (CCP) and an alternative route (ACP), and the distribution of C3-bearing cells. In serum, C3 was detected from 7-day-old embryos by rocket immunoelectrophoresis. Thereafter, its concentration increased rapidly and reached the adult level at 4-5 weeks of age. Total activities of serum complement via CCP and ACP, both of which were assayed by cell lysis, were detected first in 10-day-old embryos, and increased sharply after hatching, reaching the maximum level at 5 weeks of age. Deposition of C3 on the cell surface via CCP and ACP was also clearly demonstrated from 10-day-old embryos by haemagglutination and immunofluorescence techniques, respectively. By an immunofluorescence technique using anti-quail C3 monospecific serum, cells belonging to the reticuloendothelial system were indicated to serve major sites for the synthesis of C3 during ontogenesis.

Aging↗
PubMed1985

Role of macrophages in atherosclerosis. Sequential observations of cholesterol-induced rabbit aortic lesion by the immunoperoxidase technique using monoclonal antimacrophage antibody.

To elucidate the role of macrophages in atherosclerosis, sequential observations were carried out on cholesterol-induced aortic lesions of the rabbit with the immunoperoxidase technique by use of monoclonal antimacrophage antibody. Animals on cholesterol diets for 8 weeks or longer showed increased accumulations of lipid-filled macrophages in the intima. At a very early stage, when no grossly visible alterations were observed, macrophages were seen clinging to the endothelial surface with apparent penetration of the endothelium. A single line of three or four vacuolated macrophages were found in otherwise normal subendothelial spaces. In flat lesions consisting of a few layers of foam cells, lipid-laden macrophages were the cells that predominated. In advanced plaque lesions, negatively staining, most presumably, smooth muscle foam cells became noticeable and increased in number. At this stage, macrophage foam cells predominated in the superficial layer of the lesion, whereas negatively staining foam cells were prevalent in deeper areas. Macrophages were also spotted within areas of necrosis, and they were occasionally observed near the necrotic core of the atheroma. During 24 to 74 weeks after termination of the cholesterol diet, the number of cells with specific macrophage staining markedly diminished. The results support the concept that circulating monocytes are the prime source of foam cells in the initial phase of atherogenesis. It seems likely that the major role of macrophages in atherogenesis is to remove lipids from areas of lesion formation. The failure of macrophages to perform their scavenger role successfully may be a major factor in the accumulation of lipid-rich debris in advanced lesions. Relative paucity of macrophages may also be an important factor explaining why regression of atherosclerosis occurs rarely in the rabbits.

Animals↗
PubMed1985

Encephalitis induced in non-human primates by canine distemper virus adapted to human neural cells.

The Onderstepoort strain of canine distemper virus (CDV) adapted to human oligodendroglioma, neuroblastoma and glioblastoma cells, was intracerebrally inoculated into cynomolgus monkeys. All the three viruses caused periventricular encephalitis involving the brain stem. When the neurovirulence of these viruses were compared in terms of clinical signs and histopathological changes, the oligodendroglioma-adapted virus showed the neurovirulence of the highest degree inducing degeneration of axons and glial cells. Chronic encephalitis was also observed. The neuroblastoma-adapted virus induced predominantly nerve-cell degeneration although clinically this virus showed slightly lower degree of neurovirulence than the oligodendroglioma-adapted viruses. The glioblastoma-adapted virus showed clinically much lower neurovirulence than the other two viruses; all monkeys infected with this virus survived and produced high level of antibody in most cases. Histopathologically degeneration of axons and glial cells was characteristics although the incidence was less frequent than the oligodendroglioma-adapted virus. Predominant involvement of nerve cells by neuroblastoma-adapted virus and predominant involvement of axon and glial cells by oligodendroglioma-adapted virus and by glioblastoma-adapted virus suggest that in vitro tropism of the virus to neural cells is partially reflected on tropism of the virus in the CNS.

Animals↗
PubMed1984

Granulomatous glomerulonephritis in Wegener's granulomatosis.

Review of the kidneys in 24 autopsy cases of Wegener's granulomatosis revealed a significant granulomatous glomerular lesion in eight of the cases. To gain a better understanding of this peculiar lesion, focusing on its pathogenesis, we attempted a thorough investigation on both glomerular and vascular lesions of the kidneys. Semiquantitative analysis of the glomerular lesions indicated that existence of a severe glomerular damage probably constitutes a necessary condition in the development of granulomatous glomerulonephritis, because the granulomatous glomerular lesion was typically seen in company with a widely distributed glomerular lesion represented by thrombotic and necrotic occlusion of capillary tufts and crescent formation. Necrotizing vasculitis in the kidney was always encountered, especially in small branches of renal arteries and vasa recta. A serial section study of the two most typical cases indicated that granulomatous inflammation apparently originated in hilar arteriolitis , which extended along the pericapsular space and developed into diffusely circumferential periglomerular inflammation. We conclude that two factors are jointly at work, one inside and the other outside of the glomerulus in the pathogenesis of granulomatous glomerulonephritis: there is a thrombotic and necrotic lesion of the glomerular tuft, on the one hand and pericapsulitis originating in hilar arteriolitis on the other.

Adolescent↗
PubMed1984

Renal amyloidosis with crescents.

An unusual case of renal amyloidosis associated with extensive crescents is reported. Light and electron microscopic examination revealed that deposits of amyloid were almost invariably involved in the locations in which proliferations of epithelial cells in the capsular spaces had merged with the glomerular tufts. Gaps or fractures of the capillary walls were present at such sites, in which amyloid fibrils were mingled with thrombic material containing fibrin. It is highly conceivable that the gaps apparently induced by amyloid deposition, with leakage of fibrin-fibrinogen into the capsular space, play a crucial role in the development of the extracapillary proliferation.

Aged↗
PubMed1984

Growth of measles and subacute sclerosing panencephalitis viruses in human neural cell lines.

Growth of cell-free subacute sclerosing panencephalitis (SSPE) virus was compared with that of measles virus in three human neural cell lines; neuroblastoma, oligodendroglioma, and glioblastoma. The Edmonston strain of measles virus replicated in these neural cells as efficiently as in Vero cells. In contrast, the growth of the Mantooth strain of SSPE virus was suppressed moderately in neuroblastoma cells and markedly in oligodendroglioma and glioblastoma cells in spite of the induction of apparent cytopathic effects in these cells. Virus adsorption, defective interfering particles, interferon, and temperature sensitivity were not responsible for this low yield of SSPE virus in neural cell lines. Synthesis of viral proteins of SSPE virus was slower than that of measles virus in oligodendroglioma and glioblastoma cells. These results suggest that the slow rate of synthesis of viral proteins may be relevant to the low yield of SSPE virus in neural cells.

Cell Line↗
PubMed1984

Effect of papaverine treatment on replication of measles virus in human neural and nonneural cells.

The replication of measles virus in human neural and nonneural cell lines in terms of growth and cytopathic effect was affected by treatment of the cells with papaverine, which increases endogenous cyclic AMP. Suppression of virus growth was most prominent in neuroblastoma cells, followed by that in epidermoid carcinoma and glioblastoma cells, whereas the suppressive effect was relatively weak in oligodendroglioma cells. The papaverine-induced suppression of virus growth in neuroblastoma cells was studied in detail. The suppression that occurred was dependent on the dose of papaverine and was reversible. By treatment with 10 microM papaverine, virus-cell interactions were modified as follows: (i) early replication steps such as adsorption, penetration, and uncoating of the virus were not affected; (ii) synthesis of viral RNAs, including genomic RNA and mRNA, was inhibited; (iii) translation of viral proteins from mRNA was not blocked; and (iv) glycosylation and transport of viral glycoproteins to the cell membrane were not inhibited, but phosphorylation was blocked. The significance of suppressed virus replication in neural cells is discussed in relation to the persistence mechanisms of measles virus in the central nervous system.

Animals↗