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Biomedical subjects

R Quarto

Publications and source records attributed to R Quarto.

47 records · Page 3Linked to original sources
PubMed1986

Parathyroid mitogenic activity in plasma from patients with familial multiple endocrine neoplasia type 1.

Hyperplasia of the parathyroid glands is a central feature of familial multiple endocrine neoplasia type 1. We used cultured bovine parathyroid cells to test for mitogenic activity in plasma from patients with this disorder. Normal plasma stimulated [3H]thymidine incorporation, on the average, to the same extent as it was stimulated in a plasma-free control culture. This contrasted with the results of the tests with plasma from patients with familial multiple endocrine neoplasia type 1, in which parathyroid mitogenic activity increased 2400 percent over the control value (P less than 0.001). Plasma from these patients also stimulated the proliferation of bovine parathyroid cells in culture, whereas plasma from normal subjects inhibited it. Parathyroid mitogenic activity in plasma from the patients with familial multiple endocrine neoplasia type 1 was greater than that in plasma from patients with various other disorders, including sporadic primary hyperparathyroidism (with adenoma, hyperplasia, or cancer of the parathyroid), sporadic primary hypergastrinemia, sporadic pituitary tumor, familial hypocalciuric hypercalcemia, and multiple endocrine neoplasia type 2 (P less than 0.05). Parathyroid mitogenic activity in the plasma of patients with familial multiple endocrine neoplasia type 1 persisted for up to four years after total parathyroidectomy. The plasma also had far more mitogenic activity in cultures of parathyroid cells than did optimal concentrations of known growth factors or of any parathyroid secretagogue. This mitogenic activity had an apparent molecular weight of 50,000 to 55,000. We conclude that primary hyperparathyroidism in familial multiple endocrine neoplasia type 1 may have a humoral cause.

Adenoma↗
PubMed1986

The receptor for immunoglobulin E: examination for kinase activity and as a substrate for kinases.

Purified receptor-immunoglobulin E (IgE) complexes incubated with [gamma-32P]-ATP incorporated phosphorus into tyrosines on the beta and gamma chains of the receptor. The activity had the typical characteristics of a tyrosine kinase. Immunoprecipitation of the complexes with anti-IgE left the activity in the supernatant, demonstrating that the receptor itself was not the kinase. The receptor was also phosphorylated when membranes or intact cells were incubated with radioactive ATP or phosphate, respectively, but in each case the subunits or amino acid residues that were modified were distinctive.

Animals↗
PubMed1986

Antibodies cytotoxic to bovine parathyroid cells in autoimmune hypoparathyroidism.

We utilized a recently developed long-term serum-free culture system for bovine parathyroid cells to detect antibodies in seven patients with autoimmune hypoparathyroidism (AHP). Antibodies were tested by indirect immunofluorescence methods and by cytotoxicity utilizing the chromium (51Cr) release technique. Seven AHP sera caused specific lysis [57 +/- 6% release of 51Cr vs. 5 +/- 1% for 56 controls (15 normal subjects and 41 patients with diverse other conditions associated with immune dysfunction)]. The least effect of any of the AHP sera on cell lysis exceeded the greatest effect of any of the control sera. Absorption of AHP sera (two cases) with bovine pituitary, thyroid, liver, or kidney cells did not affect lysis, but absorption with adrenal or parathyroid cells caused a marked decrease in specific lysis. Cytotoxicity determined by 51Cr release increased with antiserum concentration and time of incubation. Cytotoxicity was dependent on complement. Replicating parathyroid cells provide a uniform reproducible detection method for anti-parathyroid antibodies in AHP. The autoantibodies in AHP appear to be specific for tissue (parathyroid and adrenal cortex) but not for species.

Adrenal Cortex↗
PubMed1986

The receptor for immunoglobulin E as a membrane protein.

Mast cells and related cells have a surface glycoprotein that avidly binds monomeric immunoglobulin E (IgE). This protein is more complex than originally thought, its analysis having been complicated by its lability in mild detergents. The properties of this receptor, especially with respect to its interaction with lipids and detergents, is reviewed and the implications for the study of other membrane protein systems are discussed.

Detergents↗
PubMed1985

Noncovalently and covalently bound lipid on the receptor for immunoglobulin E.

We describe experiments which indicate that lipids interact with the receptor for immunoglobulin E (IgE) in several ways. Evidence for loosely bound lipid comes from observations on the special conditions that are required in order to oxidatively iodinate the alpha chain of the receptor in IgE-receptor complexes. Evidence for tightly, but still noncovalently, bound lipids comes from studies on the lipids required to inhibit dissociation of the subunits of the receptor in micellar detergent. Finally, biosynthetic studies indicate that the subunits of the receptor contain ester-linked fatty acids. The latter modification appears to take place on receptors that have already been inserted into the plasma membrane.

Animals↗
PubMed1985

Coordinate synthesis and degradation of the alpha-, beta- and gamma-subunits of the receptor for immunoglobulin E.

The surface receptor for immunoglobulin E (IgE) on rat basophilic leukemia cells and their normal counterparts has been postulated to consist of four polypeptide chains: a 45-kDa alpha-chain which binds IgE, a 33-kDa beta-component and two disulfide-linked, 9-10-kDa gamma-polypeptides. The instability of this complex in mild detergents makes it possible that, in vivo also, the structure may not be stable and that there is an independent assembly or exchange of the chains. We studied this question using surface-labeling and biosynthetic labeling techniques and found that the chains turn over coordinately and do not independently exchange. The results provide further support for the proposal that the alpha beta gamma 2 complex is the unit receptor for IgE.

Animals↗
PubMedDate not supplied

In vivo and in vitro effects of insulin-like growth factor-I (IGF-I) on femoral mRNA expression in old rats.

The in vivo response of bone to IGF-I infusion in a marrow ablation model and the effect of IGF-I on bone marrow stromal cells in vitro was evaluated. IGF-I (25 ng/day), infused directly into femur, stimulated the expression of alkaline phosphatase, procollagen alpha 1 (I) and osteopontin mRNA, while osteocalcin mRNA was not affected. The dose dependency to IGF-I was bi-phasic, with stimulation at 25 and 50 ng but not at 150 ng/day. The effect of IGF-I was observed in the aged but not in the adult rat femur. However, the elevated mRNA levels in old bones with IGF-I treatment were still below those observed in adult bones. The effect of IGF-I was also examined in cultured stromal cells. IGF-I (50 ng/ml) stimulates the expression of alkaline phosphatase, procollagen alpha 1 (I), osteopontin and osteocalcin mRNA in stromal cells from both adult and old rats. These results suggest that the lack of response of adult bone to IGF-I in vivo was not due to the impaired response of the stromal cells to IGF-I. Differences in the responses of stromal cells from adult and old animals were noted. In the presence of serum (10%), stromal cells from adult rats were stimulated to synthesize DNA at lower levels of IGF-I than stromal cells from old animals. Our results show that IGF-I can stimulate mRNA expression of osteoblast markers in vivo in aged rats in a marrow ablation model and enhance DNA synthesis and gene expression in cultured marrow stromal cells from old rats. Thus, it is possible that exogenous IGF-I could be beneficial in treating age-associated osteopenia.

Aging↗
PubMedDate not supplied

Microenvironment and stem properties of bone marrow-derived mesenchymal cells.

Adult stem cells are self-renewing, pluripotent, and able to repopulate the tissue in which they reside. Cells endowed with these properties have been isolated from several tissues and an increasing number of reports provide evidence of their ability, following transplantation, to engraft host tissues other than those of their origin. In this setting, interest in the well-documented capacity of bone marrow stromal cells to undergo multilineage differentiation is growing. Neural and cardiomyogenic lineages have recently been proposed as additional differentiative pathways of these cells. However, culture conditions and inductive molecules can alter the behavior of bone marrow stromal cells and the microenvironment is critical for proper in vivo delivery. The maintenance of their stem properties and the possibility of reprogramming their commitment is a field of primary interest given the potential use of these cells in regenerative medicine. We discuss here how the microenvironmental cues, and the growth factors that physiologically govern commitment and subsequent differentiation, influence the properties of bone marrow stromal cells and modulate their engraftment into host tissues.

Bone Marrow Cells↗
PubMedDate not supplied

Bone marrow stromal damage after chemo/radiotherapy: occurrence, consequences and possibilities of treatment.

High dose chemotherapy (CT) followed by bone marrow transplant (BMT) is increasingly used for the treatment of both hematological and solid neoplasms, but an understanding of its late consequences on the marrow microenvironment is still only at its beginning. It is in fact known that marrow stroma is damaged by high-dose cytotoxic therapy and by radiation exposure. However little is known on the extent of this damage and on the self-repair ability of the stroma. The damage of the stromal microenvironment affects the long-term stem cell engraftment and the maintenance of hemopoietic functions. Furthermore, marrow stroma also represents a progenitor compartment for endosteal osteoblasts, and therefore its damage implies alterations of bone metabolism. Indeed, osteoporosis has recently been recognized as a consequence, of BMT, but only a few studies have been performed to establish the functional status of the stromal compartment after treatment with cytotoxic drugs with or without total body irradiation (TBI) and its role in post-BMT sequelae.

Animals↗