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Biomedical subjects

J Holliday

Publications and source records attributed to J Holliday.

At least 37 records · Page 2Linked to original sources
PubMed1987

An evaluation and follow-up investigation of a behavioural group treatment programme for obesity.

This paper describes an evaluation and 2-year follow-up of a comprehensive behavioural group obesity programme. The sample was made up of three groups totalling 31 patients who were referred to the Weight Reduction Advice Service at Prince of Wales Hospital, Randwick. Patients were thoroughly screened prior to treatment and completed psychological questionnaires before and after treatment. The programme consisted of weekly, 1.5- to 2-hour sessions of formal treatment. An additional 2 sessions were held fortnightly. Treatment was conducted by a clinical psychologist, two dietitians and a physiotherapist. Outcome results for the end of treatment and at 2 years follow-up are presented. The implications of the results for the treatment of obesity are discussed.

Adult↗
PubMed1985

Induction of a deoxyuridine triphosphate nucleotidohydrolase activity in Epstein-Barr virus-infected cells.

Superinfection of Raji cells with Epstein-Barr virus (EBV) or chemical induction of HR-1 cells with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) results in the induction of a deoxyuridine triphosphate nucleotidohydrolase (dUTPase) which is not observed in mock-treated cells or TPA-treated EBV genome-negative BJAB cells. The EBV-induced dUTPase could be distinguished from the host dUTPase based upon differences in their migration in polyacrylamide gels and sensitivity to the 5-mercurithioguanosine derivitive of dUTP. The expression of the EBV-specified dUTPase is prevented by phosphonoacetic acid indicating that its expression is dependent upon EBV-DNA replication.

Antiviral Agents↗
PubMed1983

Functional mapping of the Epstein-Barr virus genome: identification of sites coding for the restricted early antigen, the diffuse early antigen, and the nuclear antigen.

Attempts were made to functionally map antigenic expression of the Epstein-Barr virus (EBV) to specific regions on the EBV genome, using the B95-8 strain. Experiments were performed to map the expression of early antigen (EA), both restricted and diffuse (R and D, respectively), and the EBV nuclear antigen (EBNA), using intact B95-8 DNA, cloned BamHI fragments or Charon 4A fragments. DNA preparations were microinjected into two EBV genome-negative epithelial tumor cell lines. Expression of EBV antigens was monitored using precharacterized human sera, as well as monoclonal antibodies to EA-R and EA-D. The data suggest that EA-R maps to the BamHI H fragment, and EA-D maps to the Charon 4A fragment 7. A previous report that BamHI K is associated with the expression of a nuclear neoantigen tentatively identified as EBNA (W.P. Summers, E.A. Grogan, D. Shedd, M. Robert, C.R. Liu, and G. Miller, Proc. Nat. Acad. Sci. USA 79, 5688-5692, 1982) was also confirmed.

Antibodies, Monoclonal↗
PubMed1982

A survey of haematological values in Sydney.

A survey of haematological values in Sydney was conducted in conjunction with the Sydney Coronary Heart Disease Prevention Programme. The sample consisted of 4374 'self-referred' Sydney inhabitants between 11-90 yr of age. Comparison of the haemoglobin concentrations with those obtained in 2 previous Australian surveys suggested that the haemoglobin values in Australia have not varied in the last 25 yr.

Adolescent↗
PubMed1976

Murine leukaemia virus group-specific antigen in tumor-resistant tetraparental AKR reversible CBA/H-T6 chimaeras.

Various facts are now known about the relative lymphoma resistance of a group of tetraparental AKR reversible CBA/H-T6 chimaeras derived by early embryo aggregation. Firstly, their tumour resistance is not due to the lack of the lymphomaprone AKR cells. Secondly, results showing titres of MuLV-gs antigen comparable with, and occasionally in excess of, those in the AKR suggest that the tumour resistance of the chimaeras is unlikely to be due to a lack of oncogenic leukaemia virus. However, in marked contrast to the AKR, antibody-viral antigen renal complexes in the chimaeras were minimal. Lack of viral antigens could not explain the relative lack of renal complexes. Absence of the corresponding anti-viral antibody is the most likely explanation and this has to be attributed to the CBA component of the tetraparental AKR reversible CBA/H-T6 chimaeras. We suggest that with tolerance to the leukaemia virus being maintained and in the absence of anti-viral antigenic complexes, tumour-specific sites can be recognized and thus tumours are eliminated. This hypothesis remains to be proven.

AKR murine leukemia virus↗
PubMed1975

Failure to detect antibody against Gross virus in tetraparental AKR reversible CBA mouse chimaeras.

In spite of early acquisition upon the germ line, tolerance to the Gross (gs) virus is short-lived in the AKR. From about the age of 3 months anti-gs antibodies occur and these complex with the corresponding viral antigens. Such complexes are best seen in the glomeruli by means of immunofluorescence. In marked contrast to the AKR, renal complexes were minimal in a group of AKR reversible CBA/H-T6 chimaeras derived by early embryo aggregation. This was particularly surprising since large numbers of type C murine leukaemia virus-like particles were identified in the chimaeras and the tissues were found to be saturated with gs antigen. The lack of renal antigen-antibody complexes was the first suggestion that anti-gs antibody might not be present in the chimaeras and renal elution studies here support this assumption. In contrast to the AKR where "split " renal eluates have been shown to have anti-gs activity, no activity was demonstrated in eluates from any of the chimaras. Tolerance to the oncogenic Gross virus in the chimaeras has to be attributed to the CBA parental strain component and since this component is also held responsible for the tumour resistance of these chimaeras, both phenomena could well be related. In this context it would appear that in the absence of masking by antibody viral antigenic complexes, tumour specific sites can be recognized in the chimaeras and unlike the AKR "normal" tumour immunity can be effected. This hypothesis is currently bei-ng tested.

AKR murine leukemia virus↗
PubMed1975

Murine leukaemia virus expression in the AKR following thymectomy.

Thymectomy effectively prevents the development of spontaneous lymphoma in the AKR but how this effect is achieved remains to be determined. One possible mechanism, namely suppression of genomic expression of the oncogenic murine leukaemia virus now seems unlikely since levels of the group specific MuLV antigen were in comparision with their sham operated controls unaltered in both neonatally and adult thymectomized AKR.

Age Factors↗
PubMed1975

Investigation of NZB mice born to BALB/c immunized against NZB allotype.

Allotype suppression is held to be an example of T-cell suppressor function. Failure of generalized suppressor T-cell function is considered to be responsible for the chronic and progressive disease of the NZB. The possible association of allotype suppression and autoimmune disease has been investigated here in a group of NZB mice, transplanted and born from BALB/c recipients whilst producing anti-NZB allotype. In this situation it was anticipated that if allotype suppression should fail this would coincide with the development of autoimmune disease; both processes reflecting failure of T-cell suppressor function. However, in spite of the fact that allotype suppression was not achieved, certain observations seem important. The fact that NZB born the BALB/c were in no way different from normally derived NZB confirms that the cause of the NZB disease is established prior to the stage of implantation. Maternal influence at or beyond this stage appears of little consequence in terms of effecting the development or progression of the NZB disease. The failure to induce allotype suppression in the NZB is important. In this context this strain appears to be no different from the majority of other strains that have been tested as homozygotes. The suppression obtained with (BALB/c X SJL/J)F1 hybrids in which chronic suppression has been achieved therefore seems to represent an exceptional situation and this suggests that it is perhaps unwise to base general assumptions as to the universal adaptability of T-cell control mechanisms upon unusual findings. It must be remembered that only homozygotes were examined here. Earlier attempts to induce allotype suppression in homozygotes also failed, even in the SJL/J. Since allotype suppression has only been demonstrated in heterozygote mice there is a distinct possibility that this phenomenon never occurs in the homozygote situation. The significance of this possibility is discussed.

Age Factors↗