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Biomedical subjects

J B Hudson

Publications and source records attributed to J B Hudson.

At least 73 records · Page 4Linked to original sources
PubMed1985

Transmission electron microscopy of urinary sediment in human acute renal failure.

Urinary sediments from 31 patients with acute tubular necrosis (ATN) were studied using transmission electron microscopy (TEM). Variable quantities of renal tubule cells (RTCs), characterized by abundant cytoplasmic organelles, were a consistent finding in these sediments. TEM analyses of well-preserved RTCs permitted identification of their nephron segment(s) of origin. On the basis of the severity of ultrastructural changes observed, the sediments were divided into three types. Type I (N = 11) and II (N = 8) consisted of homogeneous populations of severely and mildly affected RTCs, respectively, while Type III (N = 12) sediments were composed of a heterogeneous population of variably affected cells. A correlation was found between the sediment type and the severity of the clinical illness. Of the 11 patients with Type I sediments, only two survived and they required chronic dialysis support. In contrast, seven of eight patients exhibiting Type II sediments survived, with only one requiring temporary dialysis therapy. Patients with Type III sediments had an intermediate course, with six of seven survivors regaining sufficient renal function to remain off dialysis over a 3-month period of observation. Our study suggests that TEM of urinary sediment can provide a useful non-invasive means of studying patients with ATN.

Acute Kidney Injury↗
PubMed1982

Murine cytomegalovirus-induced immunosuppression.

The mechanism of murine cytomegalovirus-induced immunosuppression was investigated by examining the roles played by lymphocytes and adherent cells derived from spleens of infected SWR/J mice. As few as 100 infected cells per spleen were correlated with complete abrogation of mitogen responses at 4 and 5 days after infection. In a series of cell mixing experiments it was shown that the deficiency in infected spleens was due partly to the adherent cells, which apparently secreted an immunosuppressive factor, and partly to the infected lymphocytes, which upon exposure to this factor could no longer respond to concanavalin A presented to them by normal adherent cells.

Animals↗
PubMed1981

Murine cytomegalovirus infection in the spleen and its relationship to immunosuppression.

An attempt was made to correlate murine cytomegalovirus-induced immuno-suppression with the presence of virus-infected cells in the spleen. For this purpose, SWR/J mice were infected with murine cytomegalovirus, and spleens were removed periodically and assayed for the presence of infectious centers in different cell populations and for their capacity to respond to mitogens. The maximal degree of immunosuppression correlated with the peak in adherent cell infectious centers. This was followed by a rapid rise in the number of cells per spleen (splenomegaly), a more gradual return to normal responsiveness to mitogens, and a rapid disappearance of infectious centers. These results add more support to the hypothesis that murine cytomegalovirus-induced immunosuppression is caused indirectly by infection of adherent spleen cells.

Animals↗
PubMed1980

Minor base sequence differences between the genomes of two strains of murine cytomegalovirus differing in virulence.

Two strains of murine cytomegalovirus (MCMV), differing in virulence towards mice, were compared for possible genetic differences. The two strains behaved identically in cell cultures, although the virulent strain gave higher yields of infectious virus in salivary glands. The viral DNAs displayed identical reassociation kinetics, but minor differences in their base sequences were revealed by restriction endonuclease profiles. The endonuclease profile of the "virulent" strain was conserved during serial high multiplicity infection in vitro.

Animals↗
PubMed1980

Immunosuppressive effect of murine cytomegalovirus.

Murine cytomegalovirus suppressed the ability of spleen cells to respond to mitogens in vitro. The degree of suppression was proportional to the multiplicity of infection. This effect could not be explained by cytolysis of lymphocytes, an alteration in the kinetics of the response to mitogen, or a direct competition between virions and mitogen molecules for cell-surface receptors. Nor was it due to simple contact between cell and virus, since ultraviolet-inactivated murine cytomegalovirus failed to suppress the response to mitogens. Reconstitution experiments were performed which involved mixing various combinations of infected and uninfected macrophages and lymphocytes. Under these conditions, it was found that the infected macrophages and lymphocytes. Under these conditions, it was found that the infected macrophages had an impaired capacity to mediate the response ot T lymphocytes to concanavalin A. This suggests that murine cytomegalovirus may cause immunosuppression indirectly by interfering with macrophage function.

Animals↗