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Biomedical subjects

M Maya

Publications and source records attributed to M Maya.

At least 19 recordsLinked to original sources
PubMed2001

Characterization of plasma acylcarnitines in patients under valproate monotherapy using ESI-MS/MS.

OBJECTIVES: The effect of administration of the antiepileptic drug valproate (VPA), on the composition of the plasma acylcarnitine profile (including free carnitine) was investigated. DESIGN AND METHODS: Plasma samples were obtained from 18 individuals (13 males:5 females; 15-65 y) on long-term treatment with VPA (resulting in plasma levels of 14.6-135.0 mg/L; therapeutic conc.: 40-100 mg/L). Acylcarnitines (AC) in plasma were quantified by electrospray tandem mass spectrometry (ESI-MS/MS). RESULTS: VPA was found to increase the levels (mean +/- SD, microM) of 3-hydroxy-isovalerylcarnitine (0.10 +/- 0.04; controls: 0.02-0.06), C14:2 acylcarnitine (0.11 +/- 0.05; controls: 0.02-0.08), propylglutarylcarnitine (0.06 +/- 0.05; controls: 0.00-0.04), and C18-0H-acylcarnitine (0.09 +/- 0.05; controls: 0.00-0.04). The free carnitine (C) (42.2 +/- 9.0; controls: 22.3-54.9) and the total carnitine (52.3 +/- 10.1; controls: 26.5-73.6) were not significantly altered by VPA. Other AC (C2-C18, monounsaturated and hydroxylated) were all within the control range and especially no increase of C8 (valproyl) carnitine was observed. A positive correlation was found between the ratios [AC] / [C] (p < 0.05) or [long-chain AC (C10-C18)] / [C] (p < 0.09) with the plasma VPA concentration. CONCLUSIONS: The unequivocal increase in 3-hydroxy-isovalerylcarnitine is consistent with the increase of 3-hydroxy-isovaleric acid observed in urine of VPA treated patients. This finding suggests an interaction mechanism of VPA with specific enzymes, namely involved in leucine metabolism. Adult patients under VPA monotherapy do not suffer from carnitine deficiency; the effect of the accumulating acylcarnitines is ill-defined.

Adolescent↗
PubMed1994

Regulation of rat thyroxine-binding globulin and transthyretin: studies in thyroidectomized and hypophysectomized rats given tri-iodothyronine or/and growth hormone.

We have investigated the role of the thyroid compared with the hypophysis in the regulation of the two saturable thyroid hormone carriers of rat serum, thyroxine-binding globulin (TBG) and transthyretin (TTR). We examined, at serum and hepatic mRNA level, the responses of TBG and TTR to thyroidectomy (Tx), hypophysectomy (Hx) and replacement treatments with tri-iodothyronine (T3) or/and GH, both hormones which are depleted when the thyroid or hypophysis are removed. The studies were performed on male rats at the age of 8 weeks, when the developmentally regulated TBG becomes undetectable after its transient postnatal rise, while the nondevelopmentally regulated TTR presents its normal, age-independent level of expression. Tx-induced TBG re-expression was completely reversed by T3 replacement and unresponsive to GH replacement. TTR in the serum, on the other hand, was not affected by Tx or T3 replacement, moderately reduced by Tx in terms of the amount of mRNA, and markedly reduced by GH replacement. GH treatment, moreover, inhibited the expression of TTR in euthyroid controls. Hx, like Tx, induced TBG re-expression, an effect efficiently antagonized by T3 replacement. However, TBG synthesis was higher in Hx than in Tx rats and less effectively antagonized by T3 replacement. Most unexpectedly, GH induced a dramatic further increase in TBG synthesis, and the TBG synthesized in the GH-replaced Hx rats was entirely resistant to down-regulation by T3 replacement. TTR was markedly decreased at both serum and hepatic levels by Hx, unaffected by T3 and further decreased by GH replacement.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

A senescence up-regulated protein: the rat thyroxine-binding globulin (TBG).

Thyroxine-binding globulin (TBG), the major carrier of thyroid hormones in human serum, was thought to be absent in most species, including rodents. We demonstrated recently that in fact the rat possesses a TBG gene, virtually non-expressed in young adults, but actively transcribed during post-natal development. We now find that the TBG gene is also increasingly re-expressed during senescence. Evidence is presented suggesting that physiologically decreased thyroid hormone levels, characteristic of neonates and of ageing rats, might constitute a common factor inducing up-regulation of TBG in both developmental and ageing processes. Rat TBG is to our knowledge the first biochemical 'positive' (i.e. increasing) marker of non-pathological senescence, expressed at both biosynthetic and bloodstream levels.

Aging↗
PubMed1991

Acquired immunodeficiency syndrome-associated lymphomas: clinical, pathologic, immunologic, and viral characteristics of 111 cases.

The incidence of lymphomas in individuals infected with the human immunodeficiency virus has increased progressively since the beginning of the acquired immunodeficiency syndrome (AIDS) epidemic. The present series includes 111 patients, all diagnosed and studied at one hospital in New York City. There were 108 men and three women; the average age was 39 years and male homosexuality was the predominant risk factor. The materials examined originated from 138 surgical specimens and 24 autopsies. There were 11 cases of Hodgkin's lymphoma and 100 cases of non-Hodgkin's lymphomas (NHL), a proportion strongly skewed in favor of the latter. Hodgkin's lymphoma in AIDS patients was characterized by advanced clinical stage, high histologic grade, and frequent bone marrow involvement. Non-Hodgkin's lymphoma in AIDS patients, in contrast to the general population, originated predominantly in extranodal locations (61 cases) versus locations in which the lymph nodes were the site of the primary tumors (39 cases). In the digestive tract, the unusual oral and anal primary locations were often noted and were possibly related to specific risk factors. There were 15 cases of NHL of the central nervous system, an incidence 14 times greater than that recorded in the general population. The majority of NHLs were of high histologic grade, Burkitt's and large cell immunoblastic, representing most of the cerebral and gastrointestinal tumors. All NHLs were of B-cell immunophenotype. Lymphadenopathies with the histologic features of human immunodeficiency virus infection, particularly of the late stage (type C), often preceded NHL. Probing for Epstein-Barr virus genome was more frequently positive in Hodgkin's lymphoma than in NHL. Immunologic evaluations showed severely depressed T cell counts and CD4 to CD8 cell ratios as well as markedly increased levels of antilymphocyte antibodies. Reflecting the background of profound immune deficiency, the AIDS-associated lymphomas were characterized by high aggressiveness, early tendency to generalization, frequent post-treatment relapse, and short periods of survival.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Characterization of a major development-regulated serum thyroxine-binding globulin in the euthyroid mouse.

We confirm our finding of a major development-regulated thyroxine-binding globulin (TBG) in the serum of the euthyroid mouse and investigate a number of its binding, structural and regulatory properties. Between 16 days foetal and 60 days postnatal life, the thyroxine (T4)- and tri-iodothyronine (T3)-binding activities of the sera show a striking ontogenic pattern: the binding is 2-3 times higher in foetuses than in mothers, then further increases after birth, reaching between 3 and 5 days maximum values which are 7-8 times higher than the adult ones. This pattern is not correlated with the ontogenesis of the acknowledged specific (transthyretin, TTR) and non-specific (albumin, alpha 1-foetoprotein) thyroid-hormone carriers of the mouse sera. PAGE studies demonstrate that the protein responsible for the elevated binding of the perinatal period is an alpha 1-globulin, with a migration similar to that of human and rat TBGs. Scatchard analysis is consistent with the notions that the T4-binding sites of TBG have high association constants, about two orders of magnitude above the T4 sites of TTR (10(9) M-1 as against 10(7) M-1) and low capacities (37 and 4 nmol/g of serum proteins in pups and adults respectively). Isoelectric focusing (i.e.f.) demonstrates that mouse TBG is a microheterogeneous protein separable, as a function of the pH gradient, in up to 10-12 isoforms, Marked shifts of the relative abundance of isoforms in the course of development are evidenced. The modulation of the TBG binding activity by non-esterified fatty acids (NEFA) and the control of its synthesis by the thyroid status are also reported. Mono- and poly-unsaturated NEFAs are strong inhibitors of the TBG, although they affect TTR less readily. On the other hand, the biosynthesis and/or secretion of TBG, but not of TTR, is under thyroid-hormone control, experimental hypothyroidism inducing a marked increase of the serum TBG. The TBG of mouse behaves as a highly significant parameter of development, pointing to a likely important function of the protein in the process of maturation. Our finding of major TBGs in both euthyroid rats and mice suggests that TBG is more widely spread than was thought until now, but difficult to detect in certain species outside definite maturation stages.

Aging↗
PubMed1990

Persistent lymphadenopathies in people at high risk for HIV infection. Clinicopathologic correlations and long-term follow-up in 79 cases.

Clinicopathologic correlations were explored in 79 patients at high risk for human immunodeficiency virus (HIV) infection who had lymph node biopsy for persistent lymphadenopathies and were followed for intervals of up to 7.2 years. Three histologic patterns, follicular hyperplasia with cytolysis (A), follicular involution with hypervascularity (C), and a combination of the previous two (B), were recognized. Ninety lymph node biopsies (79 primary and 11 sequential) were classified into the three histologic patterns and the results correlated with the immunologic data and clinical course. Of 31 patients who showed a pattern A at the initial biopsy, the condition of 58% remained stationary and 42% progressed to acquired immune deficiency syndrome (AIDS); of 31 patients who had initial B pattern, the condition of 36% remained stationary and 64% progressed to AIDS; and of 17 patients who initially had histologic pattern C, the condition of 6% remained stationary and 94% progressed to AIDS. Forty-one patients died during this follow-up, representing 32% of those who had a pattern A, 52% of those who had a pattern B, and 88% of those who had a pattern C at the initial lymph node biopsy. Medial survival times were 54.4 months for pattern A, 35.6 months for pattern B, and 8.4 months for pattern C. Sequential biopsies showed persistence of the same pattern or changes generally in the direction of pattern A to pattern C over variable amounts of time. Lymphocyte evaluation expressed by total counts of T4 cells, T8 cells, T4/T8 cell ratios, and anti-lymphocyte antibody levels expressed by increases in counts of surface immunoglobulin-positive lymphocytes showed positive correlations with lymph node histologic patterns. All three parameters proved to be useful prognostic indicators for the course of the HIV infection. The pathogenetic significance of lymph node histologic patterns, although not clearly understood, suggests the relation of follicular hyperplasia (pattern A) to acute viral lymphadenitis and of follicular involution with hypervascularity (pattern C) to cellular immune deficiency.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Effect of adrenalectomy at different pregnancy stages on maternal and fetal serum corticosteroid binding globulin and corticosterone in the rat.

The response of pregnant rat corticosteroid binding globulin to maternal adrenalectomy was studied as a function of the stage of pregnancy. Non-pregnant or pregnant rats were deprived of their adrenal glands during 4 days. In non-pregnant animals, adrenalectomy led to undetectable corticosterone levels and to the doubling of corticosteroid binding globulin. In pregnant rats adrenalectomized at 12 days and studied at 16 days, the serum corticosterone was likewise undetectable and the corticosteroid binding globulin was doubled as compared with pregnant rats of the corresponding age. In contrast, adrenalectomy from day 14 to 18 or from day 16 to 20 did not deplete the maternal serum corticosterone and the corticosteroid binding globulin remained unchanged. Under these conditions neither fetal corticosteroid binding globulin nor fetal corticosterone were modified. However, when the pregnant rats adrenalectomized from day 16 to 20 also received an injection of 30 mg of metyrapone on days 19 and 20 in order to inhibit fetal adrenal secretion, the maternal response was again a depletion of serum corticosterone together with an increase in corticosteroid binding globulin. Under these conditions, the fetus also reacted by a fall of corticosterone and a rise of corticosteroid binding globulin. Our results suggest that the maternal response of corticosteroid binding globulin to adrenalectomy depends on the pregnancy stage inasmuch as it may be influenced by a supply of corticosterone from the fetus during late pregnancy. Moreover, they show that in this late period, fetal corticosteroid binding globulin is regulated independently.

Adrenal Glands↗
PubMed1990

Immunological quantitation of rat and mouse thyroxine-binding globulins. Ontogenesis and sex-dependence of the circulating levels of the thyroxine-binding globulins.

We describe the preparation of monospecific antisera against a thyroxine-binding globulin partially purified from immature rat sera by affinity chromatography on thyroxine-Sepharose. The antisera are used for the rocket immunoelectrophoresis assay of rat thyroxine-binding globulin and also, owing to their partial cross-reactivity with mouse thyroxine-binding globulin, for the quantitation of this serum binding protein in the mouse. The thyroxine-binding globulin is measured in developing rats and in sexually mature male and female rats and mice. The results of the ontogenetic study confirm the postnatal surge of serum thyroxine-binding globulin levels, formerly demonstrated with binding techniques. They allow further to define the correlations, dependent on age, of the immunoquantitated thyroxine-binding globulin and transthyretin levels with the abilities of the sera to bind thyroxine. In sexually mature rats and mice we demonstrate an opposite sex-dependence of thyroxine-binding globulin levels, characterized by increased levels of the protein in the female rats versus increased levels of the protein in the male mice. This is the first report of immunological quantitation of rat and mouse thyroxine-binding globulins.

Aging↗
PubMed1990

[Specificity of hatchet flaps in the laterofacial region].

The hatchet flap, well known for the repair after skin resection of the nasal pyramid, is adapted, in a cutaneo-aponeurotic form, to the laterofacial region. The authors describe the principle of the technique which they illustrate by several clinical cases. Its simplicity, its harmonious adaptation and its reliability led them to consider that it has a place in the therapeutic arsenal for skin repair after resection of jugal and temporo-jugal lesions.

Aged↗
PubMed1989

Thyroxine-binding globulin and thyroxine-binding prealbumin in hypothyroid and hyperthyroid developing rats.

We present evidence based on equilibrium and non-equilibrium binding studies, as well as on immunological techniques, that of the two rat specific thyroid-hormone-binding proteins, i.e., thyroxine-binding globulin (TBG) and thyroxine-binding prealbumin (TBPA), TBG but not TBPA is regulated by the thyroid hormones (TH). Hypothyroidism, induced from the day of birth by daily treatment with propylthiouracil (PTU-rats), leads to dramatic and sustained increases of the TH-binding abilities of the sera measured at equilibrium, whereas hyperthyroidism, induced by treatment with thyroxine (T4-rats), leads to the decrease of these abilities. Polyacrylamide gel electrophoresis and isoelectrofocalisation of radioiodinated T4-labelled sera, together with immunoassay of TBPA, demonstrate that both effects are due to TBG, the levels of which rise in PTU-rats and decline in T4-rats, while TBPA levels do not respond to either depletion or excess of the thyroid hormones. TBG rather than TBPA appears as the key thyroid-hormone-binding protein of the rat, inasmuch as it alone expresses a regulatory function of the thyroid hormones at protein synthesis level.

Aging↗
PubMed1989

Binding activities of thyroxine binding globulin versus thyroxine binding prealbumin in rat sera: differential modulation by thyroid hormone ligands, oleic acid and pharmacological drugs.

We use gel equilibration and electrophoretic techniques to compare the binding properties of thyroxine binding globulin and thyroxine binding prealbumin in rat sera. The evidence indicates that TBG bears the serum lowest capacity highest affinity sites for thyroxine (T4) and triiodothyronine (T3) (Ka1 greater than or equal to 10(9) M-1) as well as weaker saturable T3 sites (Ka2 approximately 10(8) M-1). TBPA bears for T4 only Ka2 approximately 10(8) M-1 sites and for T3 only Ka approximately 10(6) M-1 sites. Consistent with these parameters are the specific responses of TBG and TBPA binding activities to varying serum concentrations of T4, T3, oleic acid, the drugs diphenylhydantoin or salicylate. The primary attack of these compounds is aimed at TBG. Small T4, oleate or DPH doses chase the TBG-bound T4 to TBPA, high doses of T4 or oleate but not of DPH inhibiting the T4 binding to both proteins. In the T3-serum interactions, all tested compounds displace the TBG-bound hormone without chasing it to TBPA. The high reactivity of TBG sites designates the protein as crucially involved in modulating the free vs bound serum levels of T4 and T3 against physiological or pathological variations of binding competitors.

Animals↗
PubMed1989

Inflammatory competence of fetal rat: acute-phase plasma protein response of the fetus treated by turpentine in utero.

Using crossed immunoelectrophoresis, immunoelectrodiffusion, autoradiography, and equilibrium binding techniques, we demonstrate that the rat fetus, directly challenged in utero at 18 days by a single subcutaneous turpentine injection, presents a complex acute-phase plasma inflammatory response. A number of fetal serum proteins, 48 h after the injection, increase in concentration by factors of about 2-5. These positive acute-phase reactants (APR) are alpha 1-acute-phase globulin (alpha 1-AP), alpha 2-macroglobulin (alpha 2-M), alpha 1-acid glycoprotein (alpha 1-AG), haptoglobin (Hp), and hemopexin (Hpx). A number of proteins decrease, behaving like negative APRs. These are albumin, alpha 1-fetoprotein (AFP), transferrin, GHR-P63, thyroxine-binding prealbumin (TBPA), and transcortin (CBG). The marked fall in concentration of two of the high-affinity hormone-binding proteins of the fetal rat, i.e., the estrophilic AFP and TBPA, induce significant decreases (by 25-40%) of the estrogen- and thyroxine-binding abilities of the fetal serum. While the plasma inflammatory response of the fetus is qualitatively similar to that of the adult, the fetal reactions are, as a rule, quantitatively weaker. The characteristics of the plasma inflammatory response of the fetus are discussed in relation to the highly dynamic state of its development.

Acute-Phase Proteins↗
PubMed1989

[A thyroxine-binding globulin of major biological significance in the serum of mice: demonstration and ontogenesis].

We demonstrate in the mouse serum a hitherto unrecognized major thyroxine binding globulin (TBG), analogous to human TBG or to the recently discovered rat TBG. Our demonstration is based on equilibrium dialysis, electrophoresis, immunoelectrodiffusion and autoradiography techniques. Mouse TBG displays a remarkable ontogenic pattern, with 2-3 times higher activity in foetal than in maternal serum, and a further dramatic increase after birth. Between 1 and 5 days, the T4 binding to serum reaches peak levels 7-10 times more elevated than those measured in normal or pregnant adults. We also present for the first time the ontogenesis of the thyroxine binding prealbumin (TBPA), considered until now as the only specific T4 carrier of the murine species. We show that throughout development it is the TBG, not the TBPA, which crucially governs the level of the T4-serum interactions.

Aging↗
PubMed1987

A thyroxine binding globulin (TBG)-like protein in the sera of developing and adult rats.

We report evidence based on equilibrium binding, electrophoretic, autoradiographic studies, that the rat possesses a major high affinity thyroid hormone binding protein, with an electrophoretic mobility and binding properties similar to those of the human thyroxine binding globulin (TBG). We show that in the sera of postnatal developing animals, the thyroxine and the triiodothyronine binding activities increase up to 10 times over adult or foetal levels, due to a high transient post-natal surge of the rat TBG. In the adult serum, the TBG persists in decreased amounts: it then yields the predominant role as thyroxine carrier to the thyroid binding prealbumin, but retains the major role as binder of triiodothyronine i.e. of the biologically active thyroid hormone.

Age Factors↗