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Biomedical subjects

J E Shaw

Publications and source records attributed to J E Shaw.

At least 127 records · Page 7Linked to original sources

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↗

Synthesis of Epstein-Barr virus DNA in vitro: effects of phosphonoacetic acid, N-ethylmaleimide, and ATP.

Nuclei from superinfected Raji cells synthesized Epstein-Barr Virus (EBV) DNA in vitro in the absence of cell DNA synthesis. The synthesis of EBV DNA in vitro was inhibited by phosphonoacetic acid and N-ethylmaleimide, and maximum synthesis was achieved in the absence of an ATP-regenerating system. Nuclei from mock-infected cells required an ATP-regenerating system for maximum DNA synthesis.

Acetates↗

Transformation of cells by herpes simplex virus--fact or fantasy?

The replication of herpes simplex virus types 1 and 2 is defective in XC cells. One lesion is the failure of viral proteins to be transported to the cell nucleus. The resistance of XC cells to the toxic effects of herpes simplex virus is apparently not due directly to the presence of RNA tumor virus in these cells. Other cell lines transformed by RNA tumor viruses exhibited no comparable resistance. The nature of the association between HSV and cell for a number of generations after first selecting "transformants" is not yet established; on prolonged subculture, much of the original HSV information fails to be expressed. Not more than approximately to 0.1 viral genomes per cell remains permanently associated with the host DNA. The "transformants" retain the capacity to synthesize HSV-specific polypeptides, as determined by radioimmunoprecipitation. The "transformants" have a number of characteristics which distinguish them from parental cells, and such characteristics in the light of the immunological data suggest that XC cells exposed to HSV can permanently retain HSV-specific information.

Antigens, Viral↗

Iodination of herpesvirus nucleic acids.

A simple method is described for the iodination of herpes simplex virus (HSV) DNA. The procedure involved synthesis of 125-I-labeled 5-iodo-dCTP which was subsequently used as a precursor for the in vitro repair synthesis of HSV DNA. Synthesis of 5-iodo-dCTP and purification from oxidation and reduction reagents, buffer salts, unreacted dCTP and Na125-I was accomplished in a single chromatographic step. It was possible to prepare 125-I-labeled HSV DNA in vitro with specific activities exceeding 10-8 counts/min/mu-g. The DNA prepared by this method reassociated with DNA extracted from HSV-infected HEp-2 cells but not with HEp-2 cell DNA. Iodinated HSV DNA was susceptible to S-1-endonuclease digestion once denatured but was resistant to digestion in the native form. This method was used to synthesize 125-I-labeled ribo-CTP (5-iodo-CTP) which was used to prepare cytomegalovirus-specific complementary RNA. The method should be of value in the preparation of viral probes and for use in autoradiography of viral nucleic acids.

Autoradiography↗

Response of the isolated perfused stomach of the dog to electrical vagal stimulation.

The left vagal trunk of blood-perfused, isolated, canine stomach was continously stimulated electrically for periods of 30 min at 7 v and 5-msec duration; the frequency of stimulation was varied without interruption from 0.5 to 10 Hz. Plasma immunoreactive gastrin (IRG), total gastric blood flow (GBF), and gastric acid output (GAO) were monitored continuously. When the vagus was stimulated, gastrin concentrations and GBF increased rapidly, while GAO rose at a slower rate. Two Hertz appeared to be the optimal stimulus frequency for increasing plasma IGR levels, while 10 Hz was most effective for increasing GBF. Increasing the frequency from 0 to 0.5 Hz produced the maximum observed change in GAO; additional increments to 2 or 10 Hz produced no consistent additional increase in GAO. The results indicate that plasma IRG concentration and GBF increase in response to various frequencies of vagal stimulation. Vagal stimulation increases the output of immunoreactive gastrin, as well as acid, from the isolated canine stomach.

Animals↗

Early inhibition of cellular DNA synthesis by high multiplicities of infectious and UV-inactivated Reovirus.

Inhibition of cellular DNA synthesis began 6 to 8 h after reovirus infection at a multiplicity of infection of 10 PFU per cell. However, as the multiplicity of infection was increased to a maximum of 10(3) PFU/cell, inhibition of DNA synthesis began earlier after infection (2-4 h postinfection), and the initial rate of inhibition increased. The enhanced inhibition of DNA replication at high virus multiplicities appeared to be selective since RNA synthesis was not detectably altered as late as 9 h postinfection and inhibition of protein synthesis did not begin until 7 to 9 h after infection. Early inhibition of DNA synthesis did not appear to be related to changes in thymidine pool characteristics, thymidine kinase activity, or detectable degradation of cellular DNA. Even though the particle-to-PFU ratio was increased by ultraviolet light inactivation of virus, the ability to induce early inhibition of DNA synthesis was not diminished.

Animals↗