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Biomedical subjects

J G Kenimer

Publications and source records attributed to J G Kenimer.

29 records · Page 2Linked to original sources
PubMed1983

Modulation of synapse formation by cyclic adenosine monophosphate.

Synapses between neuroblastoma-hybrid cells and myotubes exhibit a high degree of plasticity. Increase of cyclic adenosine monophosphate (AMP) levels of the hybrid cells for several days results in the appearance of functional voltage-sensitive Ca2+ channels, which are required for evoked secretion of acetylcholine. The results show that cyclic AMP regulates synaptogenesis by regulating the expression of voltage-sensitive Ca2+ channels, and suggest that cyclic AMP affects posttranslational modifications of some glycoproteins and cellular levels of certain proteins.

Animals↗
PubMed1983

Monoclonal antibodies as probes of tetanus toxin structure and function.

Monoclonal antibodies specific for fragment B, fragment C, and light chain of tetanus toxin were prepared by fusion of P3X63Ag8 BALB/c myeloma cells with spleen cells from BALB/c mice immunized with tetanus toxoid or fragment B. Hybridoma colonies were assayed for antibody production by an enzyme-linked immunosorbent assay. Fourteen positive clones were identified, cloned by limiting dilution, and injected intraperitoneally into mice to obtain ascites fluids. Thirteen of the monoclonal antibodies were of the immunoglobulin G1 subclass and one was immunoglobulin G2. Two of the antibodies were directed against sites on fragment C, nine were directed against the light chain, and three were directed against the portion of fragment B which does not comprise the light chain of tetanus toxin. At least one antibody in each group exhibited significant toxin neutralization activity. However, only one of these neutralizing antibodies strongly inhibited the binding of 125I-tetanus toxin to ganglioside-coated plates. These data indicate that interference with receptor recognition is not the only means of neutralizing tetanus toxin. Monoclonal antitoxins as potential therapeutic and prophylactic reagents are discussed.

Animals↗
PubMed1983

Induction of estrogen and progesterone receptors and decidualization in the hamster uterus by cholera toxin.

Cholera toxin (CT) injected ip on day 1 (day of ovulation) of the 4-day hamster estrous cycle, when circulatory progesterone is high and estrogen low, induced a massive uterine decidual reaction, a progesterone-dependent growth normally triggered by the implanting blastocyst. However, CT injected ip on day 3, when circulatory estrogen is high and progesterone low, did not induce a decidual reaction but, instead, intensified the effects of estrogen (stromal edema and stimulation of the mucosa). These cycle day effects were reproduced in one uterine horn injected intraluminally with CT, but not in the other horn of the same animal given solvent alone as a control. The intrauterine injection of CT had no effect on the concentration of serum estrogen or progesterone. The decidual reaction resulting from intrauterine injection of CT on day 1 was accompanied by increases in estrogen receptor (femtomoles per mg DNA) in both cytoplasm and nucleus. In long term ovariectomized hamsters, an ip or intrauterine injection of CT induced only histological effects of estrogen (stromal edema and mucosal mitosis) without affecting circulatory estrogen. These estrogenic effects were accompanied by increases in receptors for estrogen and progesterone in both cytoplasm and nucleus. CT injected ip into ovariectomized hamsters primed with estrogen intensified the stromal edema and mucosal mitosis and resulted in progesterone and estrogen receptor levels equal to or greater than those after the administration of CT or estrogen alone. When progesterone was included in the priming (estrogen + progesterone + CT), all receptor levels were decreased, and a massive decidual reaction resulted. Thus, the induction of estrogen receptor by CT may have been the primary event that triggered the decidual reaction. Whether CT-induced estrogen receptor is mediated by cAMP, a known mediator of CT, remains to be determined.

Animals↗
PubMed1982

Desensitization of PGE1 receptors in neuroblastoma-glioma hybrid cells.

Prostaglandin E1 receptor sites were measured in homogenates of NG108-15 neuroblastoma-glioma hybrid cells after exposure of intact cells to PGE1. Scatchard analysis of competitive binding studies showed that incubation of NG108-15 cells in the presence of 2.5 microM PGE1 for 16 h resulted in a loss of PGE1 receptors and an increase in the dissociation constant of the remaining receptors. Thus, cells challenged with PGE1 not only lose adenylate cyclase activity, but also lose PGE1 receptors and decreased the affinity of the remaining receptors for PGE1.

Adenosine Triphosphate↗
PubMed1976

Failure of triiodothyronine to prevent propylthiouracil-induced hypothyroidism and goiter in fetal sheep.

Administration of propylthiouracil (PTU) to pregnant, third trimester sheep led to decreasing serum thyroxine and increasing serum thyroid-stimulating hormone in both mothers and fetuses. Hypothyroidism appeared more pronounced in the fetuses than in the ewes, and goiter formation was observed in all fetuses exposed to PTU. Concomitant administration of triiodothyronine failed to protect the fetuses from the effects of PTU.

Animals↗
PubMed1975

Purification and properties of rat liver adenine phosphoribosyltransferase.

The adenine phosphoribosyltransferase (AMP: pyrophosphate phosphoribosyltransferase, EC 2.4.2.7) of rat liver was purified to a specific activity of 1.1 mumol of AMP formed per min per mg. The enzyme activity is associated with an apparently homogenous protein as shown by isoelectrofocusing, acrylamide gel electrophoresis, and N-terminal amino acids analysis (phenylalanine). The molecular weight of the enzyme was estimated to be approx. 20 000 by acrylamide gel electrophoresis in the presence of sodium dodecylsulfate and by sucrose density gradient zone sedimentation. The rat liver enzyme exhibited initial burst synthesis of AMP when 1-pyrophosphorylribose 5-phosphate was added. The 1-pyrophosphorylribose 5-phosphate initial-burst activity copurifies with the adenine phosphoribosyltransferase activity. A PH optimum of 10.0 was demonstrable for the adenine phosphoribosyltransferase. The initial-burst and steady-state phases of AMP synthesis catalyzed by highly purified rat liver adenine phosphoribosyltransferase have been partially characterized by the use of ligands which bind to sulfhydryl groups. Studies utilizing p-chloromercuribenzoate and HgCl2 as inhibitors of AMP sulfhydryl during the initial-burst and steady-state phases have revealed that sulfhydryl groups with different rates of ligand binding are present in the enzyme. The initial-burst phase was thereby delineated from the steady-state phase by use of these mercurial ligands. This delineation was also accomplished by titration with the Mg-2+ chelator, EDTA. The inhibitory effects of mercurials and EDTA were reversed by beta-mercaptoethanol and excess Mg-2+, respectively. Quantitative binding studies with 5,5'-dithiobis(2-nitrobenzoic acid) and p-chloromercuribenzoate yielded values of 3.65 and 3.6 mol of sulfhydryl per mol of enzyme, respectively. 3.3 mol of cysteic acid per mol of performic acid-oxidized enzyme were found by amino acid analysis.

Adenine Phosphoribosyltransferase↗
PubMed1975

The thyrotropin in hydatidiform moles is human chorionic gonadotropin.

Thyrotropic activity (TSH), measured by the McKenzie mouse bioassay, has been correlated with human chorionic gonadotropin (hCG) activity, measured by radioimmunoassay, in serum and tissue samples from 11 patients with hydatidiform mole and in partially and highly purified preparations of urinary hCG. Serum samples, taken at various times before and after removal of the moles, gave a ratio of 0.42 plus or minus 0.24 muU TSH/U hCG (mean plus or minus SD) (N)=43). In all cases where hCG activity fell below 150-175 U/ml (n=49), thyroid stimulating activity was undetectable (smaller than 40 muU/ml). We extracted lyophylized molar tissue by a modification of the Bates alcohol-saline method and purified the resultant extract by a combination of gel chromatography, affinity chromatography using Concanavalin A coupled to Sepharose, and isoelectrofocusing. Following extraction, an approximately 20-fold purification was achieved without significant alteration of the ratio of the two activities. Using results from all phases of purification the ratio of muU TSH/U hCG was 0.51 plus or minus 0.35(n = 23). Both activities were in the same position on disc gel electrophoresis. Activity ratios were less constant when partially purified preparations of urinary hCG were assayed for both thyrotropic and hCG activities. The presence of an hCG immunoreactive species, presumably hCG-beta subunit, which contains no thyrotropic activity but has an approximately 10-fold greater activity on a weight basis than intact hCG, may be a partial explanation for this observation. Isoelectrofocusing of a urinary hCG preparation showed that all hCG immunoreactive species with pl's between 3. 5 and 5.0 contained thyrotropic activity in proportion to their hCG content. Seven highly purified hCG preparations had thyrotropic activity with a ratio of 0.48 plus or minus 0.18 muU TSH/U hCG. These results indicate that hCG has intrinsic thyrotropic activity. On a molecular basis it is calculated that hCG contains approximately 1/4000 the thyrotropic activity of human pituitary TSH. In conditions of grossly elevated serum hCG levels, such as hydatidiform mole, this thyrotropic activity can be sufficient to produce hyperthyroidism.

Biological Assay↗
PubMed1975

The thyrotoxicosis of hydatidiform mole.

In 14 women with hydatidiform mole, 9 were hyperthyroid. Serum thyroxine (T4) levels varied between 18 and 34 mug/100 ml, and serum triiodothyronine (T3) levels between 300 and 800 ng/100 ml in the hyperthyroid patients. Bioassayable thyroid-stimulating hormone (molar TSH) was found in high concentrations in the serum of 13 patients in whom preoperative serum was available. There was a close correlation between the serum levels of human chorionic gonadotrophin, molar TSH, and T3. Intravenous sodium iodide caused a fall in serum T3 and, to a lesser extent, in T4 in hyperthyroid patients but not in a euthyroid patient. Removal of molar tissue caused a dramatic fall in the serum levels of T3, T4, molar TSH, and human chorionic gonadotrophin. The close correlation between the serum concentrations of molar TSH and human chorionic gonadotrophin lend support to the suggestion that the human chorionic gonadotrophin molecule itself, when present in large amounts, stimulates thyroid function significantly.

Chorionic Gonadotropin↗