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J C Long

Publications and source records attributed to J C Long.

88 records · Page 5Linked to original sources
PubMed1974

An antigen in Hodgkin's disease tissue cultures: radioiodine-labeled antibody studies.

An antiserum was prepared in rabbits against an antigen obtained by density gradient sedimentation of centrifuged medium from monolayer cultures of spleens involved by Hodgkin's disease. The antiserum was tested by isotopic antibody techniques with cells from each of eight cultures derived from spleens involved by Hodgkin's disease, four cultures derived from normal adult spleen, and one culture each of fetal spleen and thymus. By an indirect radioiodine-labeled antibody assay, anti-Hodgkin's disease globulin reacted with an antigen on the surface of cells from the Hodgkin's disease cultures, the quantity of which was related to the number of target cells and the amount of antibody used. This Hodgkin's disease tissue-culture antigen did not react with a rabbit antiserum against fractionated medium from a normal spleen culture, nor against noncultured Hodgkin's disease tumor tissue. The tumor specificity of the Hodgkin's disease tissue-culture antigen was assessed by a direct technique using (125)I-labeled anti-Hodgkin's disease globulin absorbed with either cultured Hodgkin's disease cells or with cultured normal cells. By this method the quantity of antigen on cells from Hodgkin's disease cultures was 15- to 30-fold greater than that on cells from normal cultures. The Hodgkin's disease tissue-culture antigen is intimately associated with the propagation of the tumor in monolayer cultures, but its identity has not been established: it could be a viral component, a tumor or fetal antigen, or a normal tissue constituent.

Animals↗
PubMed1973

A tumor antigen in tissue cultures derived from patients with Hodgkin's disease.

Pellets obtained from supernatant fluids of monolayer cultures of cells from patients with Hodgkin's disease were fractionated by isopycnic density sedimentation. Material in a peak of specific gravity 1.15-1.21 g/ml from two Hodgkin's disease cultures was used to immunize rabbits, and the antisera obtained in this manner were reacted by agar-gel diffusion and immunoelectrophoresis with antigens from the purified peaks and the unfractionated pellets of centrifuged culture medium from all the cultures. The antisera reacted with material from 9 of 10 lines derived from spleens of patients with Hodgkin's disease, 2 of 8 cell lines from histologically negative spleens from patients with Hodgkin's disease and with 3 of 6 lymphoma cell lines not diagnosed as Hodgkin's disease. The antisera did not react with 12 cell cultures prepared from normal adult and fetal spleen and thymus. The antigen from cultures from patients with Hodgkin's disease was not found in material sedimenting at lower specific gravities; it resisted Tweenether solubilization, and migrated as a single band by immunoelectrophoresis. The antigen was not found in disrupted, noncultured tumor cells from patients with Hodgkin's disease, and an antiserum against noncultured, minced tumor tissue did not react with the Hodgkin's disease tissue-culture material. No immunological relationship was found between the tissue culture antigen and Epstein-Barr, RD-114, or Rauscher murine leukemia viruses. The Hodgkin's disease antigen may be a tumorrelated antigen or a component of an oncogenic virus.

Animals↗
PubMedDate not supplied

Mu opioid receptor gene variants: lack of association with alcohol dependence.

The mu opioid receptor is implicated in the reward, tolerance and withdrawal effects of alcohol and other drugs of abuse. This hypothesis is supported by the effects of alcohol on beta-endorphin release, of mu opioid receptor agonists and antagonists on alcohol consumption, and by the activation of the dopaminergic reward system by both alcohol and opiates. In addition, the murine mu opioid receptor locus, Oprm, is implicated as the major quantitative trait locus (QTL) affecting the different levels of morphine consumption between two inbred mouse strains that also exhibit differences in alcohol and cocaine consumption. Detection of genetic variation affecting OPRM1 expression or mu opioid receptor function would be an important step towards understanding the origins of inter-individual variation in response to mu opioid receptor ligands and in diseases of substance dependence. We directly sequenced the human mu opioid receptor locus, OPRM1, to detect natural variation that might affect function and/or be associated with psychiatric phenotypes related to opioid function. Four DNA sequence variants were found: three non-synonymous substitutions (Ala6Val [rare], Asn40Asp, [0.10-0.16], Ser147Cys [rare]) and one intronic variant (IVS2+691G/C [0.55-0.63]). OPRM1 alleles, genotypes and haplotypes from three psychiatrically characterized population samples (US Caucasian [USC, n=100], Finnish Caucasian [FC, n=324] and Southwestern American Indian [SAI, n=367]), were used to perform association and sib-pair linkage analyses with alcohol and drug dependence diagnoses. No significant association of OPRM1 genetic variation to phenotype was observed. This analysis has 80% power to detect a small to moderate effect of OPRM1 variation on alcohol dependence and 100% power to detect effects of the magnitude of the ALDH2*2 variant. While these data do not support a role of the mu opioid receptor in susceptibility to alcohol dependence, the potential relationship between OPRM1 genetic variation and response to endogenous opioids and exogenous opiates can now be investigated.

Adult↗