PubMed Health⌕ Search

Biomedical subjects

J Calafat

Publications and source records attributed to J Calafat.

105 records · Page 6Linked to original sources
PubMed1970

Genetic transmission of viruses that incite mammary tumor in mice.

Electron microscopy, immunofluorescence, and bioassay demonstrated the presence of a mammary tumor inciting virus in untreated mice of three different inbred strains, and in irradiated or urethan-treated mice of two other mouse strains, indicating the ubiquitous nature of this group of viruses. In general these viruses are transmitted vertically by the gametes of the mouse strain in which they naturally occur. The virus is present in every cell, although often in an incomplete form. If a mammary tumor inciting virus is introduced into a different mouse strain, only milkborne transmission will take place, after which the virus is found in a limited number of tissues. It has been speculated that mammary tumor inciting viruses are transmitted as genetic factors of the host strain to which they belong. There is some evidence that a repressor, produced by a regulator gene, controls the rate of release of such a genetically transferred virus. Repression can be abrogated by a carcinogenic treatment. The repressor would also cause resistance to a superinfecting mammary tumor inciting virus by interference with its replication.

Animals↗
PubMedDate not supplied

Virus-induced central positional nystagmus in mice.

Geotropic direction-changing nystagmus in lateral body positions was observed in 4-week-old BALB/c mice after intracerebral injection with a temperature-sensitive mutant of mouse hepatitis virus. The positional nystagmus was detected already 2 days after infection and it lasted half a year at least. The nystagmic responses of the semicircular canals were also evaluated before and after infection. They were unaltered during the disease, which was clinically manifested by general weakness, ataxia and tremor. Histopathological examination 2 weeks after infection revealed demyelination in various parts of the CNS.

Animals↗
PubMedDate not supplied

YKL-40, a mammalian member of the chitinase family, is a matrix protein of specific granules in human neutrophils.

YKL-40, also called human cartilage glycoprotein-39 (HC gp-39), is a member of family 18 glycosyl hydrolases. YKL-40 is secreted by chondrocytes, synovial cells, and macrophages, and recently it has been reported that YKL-40 has a role as an autoantigen in rheumatoid arthritis (RA). The function of YKL-40 is unknown, but the pattern of its expression in normal and disease states suggests that it could function in remodeling or degradation of the extracellular matrix. High levels of YKL-40 are found in synovial fluid from patients with active RA. Neutrophils are abundant in synovial fluid of patients with RA, and the cells are assumed to play a role in joint destruction in that disorder. Therefore, we examined whether neutrophils are a source of YKL-40. YKL-40 was found to colocalize and comobilize with lactoferrin (the most abundant protein of specific granules) but not with gelatinase in subcellular fractionation studies on stimulated and unstimulated neutrophils. Double-labeling immunoelectron microscopy confirmed the colocalization of YKL-40 and lactoferrin in specific granules of neutrophils. Immunohistochemistry on bone marrow cells showed that neutrophil precursors begin to synthesize YKL-40 at the myelocyte-metamyelocyte stage, the stage of maturation at which other specific granule proteins are formed. Assuming that YKL-40 has a role as an autoantigen in RA by inducing T cell-mediated autoimmune response, YKL-40 released from neutrophils in the inflamed joint could be essential for this response. In RA and other inflammatory diseases, YKL-40 released from specific granules of neutrophils may be involved in tissue remodeling or degradation.

Adipokines↗