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L E Porter

Publications and source records attributed to L E Porter.

24 records · Page 2Linked to original sources
PubMed1983

Characterization and quantitation of human hepatic estrogen receptor.

Because the liver is an estrogen-sensitive organ and such sensitivity necessitates the presence of an hepatic estrogen receptor, we assayed whole human liver cytosol for the presence of estrogen receptor. Scatchard plot analysis of specific [3H]diethylstilbestrol binding to whole human liver cytosol from both sexes demonstrated hormone binding that is of high affinity (Kd = 10(-10)M) and low capacity (1-10 fmol/mg cytosol protein), and that is saturable and specific for steroidal and nonsteroidal estrogens, but not for other steroids. The protein can be further characterized as an estrogen receptor by its binding to heparin-Sepharose. In addition, gel filtration chromatography of [3H]estrogen-labeled cytosol on Sephadex G-100 indicates that potentially contaminating proteins, such as albumin and sex-steroid-binding globulin, do not bind [3H]estrogen in whole cytosol. We conclude that human liver from both sexes has estrogen receptor and that the presence of estrogen receptor in human liver explains the sensitivity of the human liver to estrogen.

Chromatography, Affinity↗
PubMed1981

Effect of ethanol feeding upon levels of a male-specific hepatic estrogen-binding protein: a possible mechanism for feminization.

Male, but not female, rat liver cytosol contains an estrogen-binding protein with unique properties: rapid binding of estradiol, high binding capacity, moderate affinity for estradiol, and specificity for steroidal estrogens and weak androgens, but not for nonsteroidal estrogens or other steroids. The estradiol-binding activity of this protein is reduced in cytosol from livers of alcohol-fed rats as compared to that from their isocalorically fed controls. The properties of this male-specific hepatic estrogen-binding protein suggest a role for this protein in the regulation of estrogen levels in the male animal. Moreover, the reduction in activity of this unique protein in the liver of alcohol-fed animals may explain, at least in part, the feminization commonly seen in chronic alcoholic men.

Animals↗
PubMedDate not supplied

T cell activation and retargeting using staphylococcal enterotoxin B and bispecific antibody: an effective in vivo antitumor strategy.

The aim of this work was to test for cure and immunity in a micrometastatic tumor model using in vivo T cell activation with staphylococcal enterotoxin B (SEB) and retargeting with antitumor x anti-CD3 F(ab')2 bispecific antibodies (bsAb). All studies were performed in C3H/HeN mice using syngeneic tumor cell lines. For survival studies, mice were injected intravenously on day 0 with CL62 (a p97-transfected clone of the K1735 murine melanoma tumor). Day-3 treatments included saline (control), SEB (50 gamma g intraperitoneal) with or without bsAb (5 micrograms i.v.). Cured mice, surviving beyond 60 days, were rechallenged with subcutaneous CL62, K1735, or a nonmelanoma control, AG104. SEB activation studies were performed with pulmonary tumor-infiltrating lymphocytes isolated from 10-day established CL62 tumors. Maximal tumor-infiltrating lymphocyte cytotoxicity was demonstrated 24 h following SEB injection, therefore bsAb treatments were administered 24 h after SEB. When survival was examined at 60 days, there were significantly more survivors in the group receiving SEB plus bsAb (70%) compared to the group receiving SEB alone (30%), and the controls (0%) (P = 0.02 and P < 0.01, respectively). Mice cured of CL62 using SEB alone or with bsAb demonstrated equal immunity to CL62, however, mice treated with SEB plus bsAb were more often immune to the p97-parental cell line, K1735(P = 0.001). Ag104 consistently grew in all mice. Results of these studies demonstrate that SEB plus bsAb can be effective, not only in curing tumors but also in providing protective immunity against targeted and non-targeted tumor antigens.

Animals↗