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Biomedical subjects

J B Hudson

Publications and source records attributed to J B Hudson.

At least 109 records · Page 6Linked to original sources
PubMed1977

Transformation of cultured rat adrenocortical cells by Kirsten murine sarcoma virus (Ki-MSV).

Two-week-old primary cultures of normal adult rat adrenal cortex were exposed to Kirsten murine sarcoma virus (KiMSV). Within a week, the adrenal cells, which are normally fusiform and aligned in parallel, became pleomorphic and piled up extensively. Saturation density increased from 5-10 x 10(4) to 5-10 x 10(5) cells/cm2, population doubling time during exponential growth decreased from 36-40 to 16h, acid production increased and the growth rate became independent of a reduction in serum concentration from 10% to 1%. Inoculation of 2 x 10(6) of these transformed cells into immuno-depressed rats produced rapidly growing tumors within 1 week. Histologically, the tumors were pleomorphic carcinomas with areas ranging from anaplasia to near-normal, highly differentiated adrenocortical tissue. In addition to histologic evidence of differentiation, metabolic studies using 14C-prognenolone showed that the transformed cells were capable of 20alpha reduction and delta5,3beta dehydrogenation, both characteristic of normal steroid-secreting tissues. The transformed adrenocortical cells produced infectious C-type virus as indicated by electron microscopy, 3H-uridine incorporation, and focus formation in NRK (normal rat kidney) cultures. The neutralization pattern of this virus resembled that of authentic Ki-MSV. The transformation of adrenocortical cells by K-MSV demonstrates the capacity of this agent to induce carcinomas in differentiated cells after short-term culture, and widens the range of tissues known to be susceptible to K-MSV to include a secretory epithelium of mesodermal origin.

Adrenal Cortex↗
PubMed1977

Murine cytomegalovirus infection in a non-permissive line of mouse fibroblasts.

A line of murine cytomegalovirus (MCMV)-resistant cells was derived from mouse embryo cultures. The virus penetrated the nuclei of these resistant cells efficiently and a small amount of viral gene transcription occurred, although no viral DNA synthesis was detected. Synthesis of cellular DNA, RNA and protein continued unabated, and the infected cells grew at the same rate as uninfected cells. The block in virus replication in these cells appears to be between early transcription and viral DNA synthesis.

Animals↗
PubMed1977

Cell cycle dependency of murine cytomegalovirus replication in synchronized 3T3 cells.

Synchronized murine 3T3 cells have been used to investigate the possible dependency of murine cytomegalovirus replication upon the cell cycle. The normal latent period of 12 h characteristic of asynchronous 3T3 cells was protracted to more than 24 h after an early G1 infection in synchronous cells. In this case viral progeny were not detected until after the initiation of the host S-phase. Cells maintained in the G1 phase did not replicate virus. This failure could not be explained by a decrease in virus penetration but was apparently due to a requirement for an event associated with the host S-phase. Thymidine-induced inhibition of cell cycle traverse also blocked virus replication. Viral DNA synthesis did not initiate until after the initiation of host DNA. In contrast, herpes simplex virus type 1 replicated in 3T3 cells independently of the cell cycle.

Animals↗
PubMed1977

Immune complex glomerulonephritis associated with Klebsiella pneumoniae infection.

The kidneys of three patients who died of pneumonia due to Klebsiella pneumoniae were studied at autopsy by light and immunofluoerescent microscopy. One had no clinical evidence of renal disease; two had only microscopic hematuria and mild proteinuria. Light microscopy revealed focal proliferative glomerulonephritis in all three cases. Also in all three, immunofluorescent microscopy revealed a granular deposition of capsular polysaccharide antigens of Klebsiella pneumoniae in association with immunoglobulins and complement components in the mesangium and along the glomerular basement membrane. Furthermore, the glomerular bound immunoglobulins were eluted and demonstrated to contain antibodies specific to a capsular polysaccharide antigen of Klebsiella pneumoniae isolated from each patient. These findings may illustrate that the capsular polysaccharides of Klebsiella pneumoniae are antigenic, and that the immune complex deposition in the kidney during infection with this agent can be associated with renal morphological changes. Whether or not clinical evidence of nephritis occurs may depend on the characteristics of the infection and the host factors.

Aged↗
PubMed1976

Lesions produced by human herpesviruses 1 and 2. Morphologic features in rabbit corneal epithelium.

The morphologic features of corneal lesions produced in rabbits by human herpesviruses, types 1 and 2 (HH1 and HH2), were studied using light and electron microscopic techniques. Also, healing lesions produced by the HH1 virus and treated by idoxuridine were similarly investigated. Scanning electron micrographs showed that although the morphology of HH1 and HH2 lesions was similar in most respects. HH2 lesions typically were raised, whereas the edges of HH1 lesions were not elevated above the corneal surface. In both HH1 and HH2 lesions, infected epithelial cells first separated from neighboring cells, then became globular, and finally were removed, leaving a central excavation. During healing of HH1 lesions, normal epithelial cells invaded the central crater from all sides to cover damaged cells and reconstitute the epithelial surface.

Animals↗
PubMed1976

Ultrastructural study of lesions induced in rabbit cornea by Herpes Simplex virus types 1 and 2.

Herpes simplex virus types 1 and 2 were used to infect rabbit corneas (without abrasion), and the resulting lesions were compared by light and electron microscopy. The type 1-induced lesion developed more quickly; the infected epithelial cells underwent a progression of defined morphological changes leading to organelle destruction, cell rounding, and death. Virus particles were abundant in the nuclei and cytoplasm of all types of cell in the epithelium, in intercellular spaces, and on the basement membrane. Occasionally, virus was seen to replicate within stromal fibroblasts. In contrast, type 2, although causing similar changes in the epithelial cells, was relatively inefficient in the production of mature virions. Thus type 2 nucleocapsids were synthesized within nuclei in numbers comparable to those of types 1, but intact cytoplasmic virions were uncommon, apparently because of degradation of type 2 virions in cytoplasmic vesicles or tubules. Extracellular type 2 particles were rarely seen. This finding offers an explanation for the relatively slow development of the type 2-induced lesion, but not for its greater severity. All epithelial cells appeared to be capable of supporting replication of either type of virus.

Animals↗