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Biomedical subjects

J Hay

Publications and source records attributed to J Hay.

At least 235 records · Page 13Linked to original sources
PubMed1980

Linkage disequilibria between HLA-B and the rarer properdin factor B alleles, BfF1 and BfS1.

Phenotypic association and highly significant linkage disequilibria have been demonstrated for HLA-B18 and BfF1 and HLA-Bw50 and BfS1 alleles among Caucasians from Australia and the United States (San Francisco Bay area). The HLA-B18, BfF1 association appears to be associated with HLA-Aw30. It is possible that BfS1 arose as a mutation, after the evolutionary splitting of HLA-Bw21, on an HLA-Bw50 haplotype, and that BfF1 arose on an HLA-Aw30, B18 haplotype.

Alleles↗
PubMed1980

Behavioural abnormalities in Toxoplasma-infected mice.

Observational methods, using video recordings and computer-assisted data analysis, were used to investigete the behaviour of Toxoplasma-infected mice. Infection had a selective effect, increasing the amount of general movement but decreasing the amounts of rearing and digging. In addition infection affected the pattern of bouts of behaviour, increasing the number of shorter bouts, and this was found to underlie a variety of specific behavioural changes. The results indicate that Toxoplasma infection probably affects the animal's response to its environment and the stimulation arising from it, and may even affect endogenous regulatory processes in the brain.

Animals↗
PubMed1980

Teachers in general practice: a comparative study.

Thirty-nine randomly selected general practitioners in the Cambridgeshire Health Area were surveyed in an attempt to determine whether there were prior differences between those practitioners who choose to become involved with undergraduate medical students and those who choose not to. Teachers were found to have graduated more recently, subscribe to more journals and were more likely to use medical libraries than non-teachers. All the solo practitioners in the study and two of the four practitioners in two-man groups belonged to a subgroup of non-teachers who had never had students and did not want students in the future. This subfroup also subscribed to fewer journals than the other groups, bought fewer textbooks and used medical libraries less. The only prior differences between teachers and non-teacher that have been demonstrated are year of graduation and type of practice. Other differences could well be attributed to the influence of the students themselves. Studies are needed to clarify this issue, especially as it realates to continuing medical education.

Education, Medical, Continuing↗
PubMed1980

Liver disease and the e antigen in HBsAg carriers with chronic renal failure.

This study was undertaken to assess the frequency of development and the stages of evolution of chronic liver disease in patients with renal failure who are chronic carriers of hepatitis B surface antigen. Cirrhosis or chronic active hepatitis developed in five of 21 patients and could not be predicted by the initial histological appearance or by HLA-A and B typing but was associated with the e antigen in four of the five patients. However, the antigen was not a consistent indicator of a poor prognosis, as the four other e antigen positive patients did not develop chronic liver disease during the period of the study. Transmission of hepatitis B to spouses occurred in four cases, was fatal in one instance, and was associated with e antigen in three of the four. Determination of e antigen status in renal unit patients who are carriers of hepatitis B surface antigen may be of value to the patient and his home environment.

Acute Disease↗
PubMed1980

Specific viral antigens in rat cells transformed by herpes simplex virus type 2 and in rat tumors induced by inoculation of transformed cells.

A rat cell line, RE1, oncogenically transformed by a herpes simplex virus type 2 ts mutant (ts 1), has been demonstrated to contain herpes simplex virus type 2-specific thymidine kinase activity, as have two of four tumors induced in rats by inoculation of these transformed cells. A high proportion of sera from tumor-bearing rats (5 of 11) have detectable antibody against herpes simplex virus thymidine kinase, and there is a correlation between enzyme activity in a tumor and antibody in "tumor sera." A proportion of tumor sera possess neutralizing activity for herpes simplex virus infectivity. Immunfluorescence studies indicate that the transformed cells express antigens which are probably induced early in herpes simplex virus type 2-productive infection.

Animals↗
PubMed1979

Mutant of herpes simplex virus type 2 with temperature-sensitive lesions affecting virion thermostability and DNase activity: identification of the lethal mutation and physical mapping of the nuc-lesion.

We had previously shown that a temperature-sensitive (ts) mutant of herpes simplex virus type 2 strain HG52, ts13, induced a heat-labile DNase activity in infected cells (B. Francke, H. Moss, M. C. Timbury, and J. Hay, J. Virol. 26:209-213, 1978). Earlier work indicated that the mutant also possessed temperature-sensitive infectivity (I. W. Halliburton and M. C. Timbury, J. Gen. Virol. 30:207-221, 1976). In this study temperature-stable revertants of ts13 have been isolated; examination of them revealed that ts13 is a double mutant, with genetically distinct temperature-sensitive lesions affecting nuclease activity and particle stability. The lethal mutation, in the cell system studied, is the latter. Revertants, which all maintain the nuclease lesion, grew well at a high temperature. Physical mapping of the nuclease lesion placed it between 0.12 and 0.21 (fractional length) on the virus genome, quite distant from the lethal mutation at 0.64 to 0.70.

Animals↗
PubMed1978

Synthesis of herpes simplex virus DNA in preparations of chromatin from infected cell nuclei.

Chromatin prepared from cells infected with Herpes simplex virus type 1 or type 2 can synthesize both virus and cell DNA in vitro. The rate of synthesis is comparable to that of isolated whole nuclei. Incorporation is limited, and both cell and virus DNA synthesis are sensitive to the presence of virus-specific antiserum and phosphonoacetate. In chromatin from cells infected with a phosphonoacetate resistant virus mutant, both types of DNA synthesis are resistant to the presence of the inhibitor.

Cell Line↗
PubMed1978

Alkaline DNase activity in cells infected with a temperature-sensitive mutant of herpes simplex virus type 2.

BHK cells infected with the temperature-sensitive mutant ts13 of herpes simplex virus type 2 at a nonpermissive temperature lack the alkaline nuclease activity, which is induced by the mutant at a permissive temperature and by wild-type virus at either temperature. For ts13, enzyme activity could be induced by a temperature shift to permissive conditions, but not in the presence of cycloheximide. After a shift from permissive to nonpermissive conditions in the presence of cycloheximide, the activity was stable in wild-type, but not in mutant-infected, cells. After extensive purification, the wild-type nuclease was fourfold more heat stable in the presence of substrate than was the mutant enzyme. Mixtures of both purified enzymes showed the predicted intermediate stabilities. The results strongly suggest that the enzyme is virus coded and that the mutant possesses a lesion in the structural gene of the enzyme.

Cell Line↗
PubMed1978

The absence of Trypanosoma congolense from the lymph of an infected sheep.

The lymph draining the prefemoral lymph node of a sheep infected with Trypanosoma congolense was examined over a period of 10 days. Only six trypanosomes were detected in 1500 ml of this fluid during this time, in spite of the animal having about 65,000 organisms/ml in its blood. It is concluded that the suggestion that T congolense is a strict plasma parasite is essentially proven for this specific situation.

Animals↗
PubMed1976

Mutants of herpes simplex virus types 1 and 2 that are resistant to phosphonoacetic acid induce altered DNA polymerase activities in infected cells.

Three mutants of herpes simplex virus (HSV) have been isolated which form plaques in the presence of 100 mug/ml phosphonoacetic acid (PPA). All three mutants (3 from HSV-1 strain 17 syn+, 14 from HSV-1 strain 17 syn, and 19 from HSV-2) induce viral DNA synthesis and viral DNA polymerase activity, and these are much less sensitive to PPA than the wild-type virus. The results support the hypothesis that PPA interacts directly with the viral DNA polymerase protein, at least part of which is virus coded.

Acetates↗
PubMed1976

Herpesvirus proteins: DNA polymerase and pyrimidine deoxynucleoside kinase activities in temperature-sensitive mutants of herpes simplex virus type 2.

Eleven temperature-sensitive mutants of herpes simplex virus type 2 strain HG52 were examined for ability to induce DNA polymerase activity in BHK 21/C13 cells. All mutants induced DNA polymerase at a permissive temperature, (31 degrees C) and all DNA-positive mutants at a non-permissive temperature (38 degrees C). Three DNA-negative mutants induced no DNA polymerase (ts 6, ts 9) or very little DNA polymerase (ts 11), at a non-permissive temperature, while ts 1, also DNA negative, induced a little more DNA polymerase than wild-type, often at both temperatures. The DNA polymerase induced by ts 6 at 31 degrees C was temperature-sensitive in vivo, but only slightly so in vitro. These results were confirmed immunologically and suggest that HSV-2 codes for at least part of a DNA polymerase activity, necessary for infection, and that full expression of this enzyme involves at least three viral genes.

Antigens, Viral↗
PubMed1976

Herpesvirus proteins: induction of nucleoside phosphotransferase activity after herpes simplex virus infection.

After herpes simplex virus infection of hamster kidney cells there is an induction of nucleoside phosphotransferase activity which can utilize AMP as phosphate donor. The activity is immunologically specific for the infected cell and is induced concomitantly with the virus-coded pyrimidine deoxynucleoside kinase activity. Phosphotransferase activity is not induced in cells lacking both thymidine and deoxycytidine kinase activity.

Adenosine Monophosphate↗