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Biomedical subjects

J L Li

Publications and source records attributed to J L Li.

152 records · Page 9Linked to original sources
PubMed1978

Replication of Epstein-Barr virus DNA in epithelial cells in vivo.

Epstein-Barr virus (EBV)-specific complementary RNA (cRNA) was hybridized in situ to oropharyngeal epithelial cells taken from patients with infectious mononucleosis. Cells from patients shedding virus in the throat hybridized signifnicant quantities of cRNA, whereas cells from EBV-negative sources did not. The degree of hybridization indicated a large EBV genome number per infected epithelial cell and suggested that these cells were the source of virus found in the throat. This finding may explain the presence of the EBV genome in the malignant epithelial cells of nasopharyngeal carcinoma.

Autoradiography↗
PubMed1975

Demonstration of oncogenic potential of mammalian cells transformed by DNA-containing viruses following photodynamic inactivation.

The oncogenic properties of hamster embryo cells transformed by herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) and SV40 virus following photodynamic inactivation using neutral red were determined by subcutaneous inoculation into newborn Syrian hamsters. Cells transformed by all three viruses produced palpable tumors after different latent periods. Histopathological examination showed that HSV-2 tumors were fibrosarcomas and metastases were often seen in the lungs. HSV-2 primary tumors were reinoculated subcutaneously into weanling hamsters; they developed palpable tumors within 2 weeks. HSV-specific antigens were detected in the cytoplasm and/or on the surface of both the HSV-1 and HSV-2 tumor-cell cultures by the indirect immunofluorescence technique. The same method revealed SV40 tumor antigen in the nuclei of the SV40 tumor cells. Sera from HSV or SV40 tumor-bearing hamsters gave positive reactions when tested against HSV-infected hamster cells or SV40-infected monkey cells, respectively. These results demonstrate that herpes simplex virus and SV40, whose infectivity was lost following photodynamic inactivation, retained the virus genetic information necessary for transformation of normal cells to an oncogenic phenotype.

Animals↗
PubMedDate not supplied

Centrifugal innervation modulates visual activity of tectal cells in pigeons.

Centrifugal modulation of visual responsiveness of tectal cells by the isthmo-optic nucleus (ION) through the retina was studied in homing pigeons. Visual activity evoked by computer-generated stimuli was reduced by an average of 59% in tectal cells whose receptive fields (RFs) either overlapped with, or were close to, those of isthmo-optic cells whose activity was blocked by the injection of lidocaine through micropipettes. Activity usually recovered to 87% of pre-drug controls in 8-17 min (average 12.3 min) after stopping lidocaine injections. Those tectal cells whose RFs were far from those of ION cells did not show clear-cut changes in their visual responsiveness to isthmo-optic lidocaine application. The spatial relationship between receptive fields of tectal and isthmo-optic cells, saline controls, as well as the specificity, reproducibility and reversibility of effects of ION-injected lidocaine on tectal activity, show that this chemical action is pharmacological, not toxicological. Neuronal circuitry underlying centrifugal modulation of tectal activity by isthmo-optic cells is discussed.

Action Potentials↗