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Biomedical subjects

E Orti

Publications and source records attributed to E Orti.

At least 19 recordsLinked to original sources
PubMed2000

pi conjugation across the tetrathiafulvalene core: synthesis of extended tetrathiafulvalene derivatives and theoretical analysis of their unusual electrochemical properties

A series of extended tetrathiafulvalene (TTF) derivatives bearing one or two 1,4-dithiafulven-6-yl substitutents has been prepared. The new compounds present remarkable electrochemical singularities compared with other TTF derivatives, which are strongly affected by the nature of the substitution on the lateral heterocycle(s). This unusual electrochemical behaviour follows a square-scheme sequence and is attributed to structural changes upon oxidation of the pi-donating molecules. Digital simulations of the electrochemical data have been used to reach the values of the kinetic and thermodynamic constants involved in the square scheme. Theoretical calculations establish an important contribution of a highly delocalised resonant form involving a tetravalent sulphur in oxidised species, which could justify the occurrence of an electrochemical behaviour distinct from that of TTF. Finally, third-order susceptibilities chi 3 of two of these systems, for which electron-donating and electron-withdrawing substituents coexist and are conjugated through the TTF pi system, are given.

Journal Article↗
PubMed1999

Antispasmodic action of propinox on the isolated human gallbladder: possible mechanism of action.

Propinox is an antispasmodic drug frequently used in the treatment of disorders of the gastrointestinal tract, the uterus and the gallbladder, but little is known about its relaxing activity in gallbladder tissue. The main objective of this study was to determine the antispasmodic activity of propinox, compared to other antispasmodics, in the gallbladder and to assess its binding affinity to receptor sites which may be involved in its mechanism of action. Antispasmodic activity of propinox, (-) scopolamine-n-butyl bromide, atropine and verapamil was determined in human gallbladders to reduce the risk of interspecies variability. Inhibitory activities (ED50) of carbachol-induced contraction were: atropine 5.03 x 10(-8) M > propinox 1.25 x 10(-7) M > verapamil 6.63 x 10(-6) M > (-) scopolamine-n-butyl bromide 5.4 x 10(-5) M. pD'2 for propinox was 6.94, indicating non competitive inhibition of carbachol action. Radioligand binding studies were performed to determine if the antispasmodic action of the drug involved binding to muscarinic receptors or calciumantagonist sites. The inhibition constant (Ki) of propinox for muscarinic receptors of guinea pig ileum smooth muscle, which contains a mixed M2-M3 receptor population, was 1.6 x 10(-6) M. Ki for brain muscarinic receptors (M1) was 1.0 x 10(-4) M, for cardiac receptors (M2) 1.2 x 10(-6) M and from salivary gland receptors (M3) 1.5 x 10(-6) M. For binding to the dihidropiridine calcium antagonist binding sites, Ki were: 4.9 x 10(-5) M for propinox and 2.2 x 10(-7) M for verapamil. For the phenylalkylamine binding sites Ki were: 5.0 x 10(-6) M for propinox and 3.5 x 10(-8) M for verapamil. For the benzothiacepine binding sites, Ki for propinox was 5.2 x 10(-6) M. The following may be concluded: 1.--The antispasmodic activity of propinox in isolated human gallbladder was comparatively less potent than that of atropine and more potent than those of verapamil and (-) scopolamine-n-butyl bromide. 2.--Propinox showed binding to muscarinic and calcium receptors that can be related to its antispasmodic activity; suggesting that the drug is an antispasmodic with anticholinergic and musculotropic activity. 3.--The dual mechanism of action, anticholinergic and calcium-blocking, would induce synergism of pharmacodynamic effects and minimize adverse events of pure antimuscarinic drugs or calcium antagonists.

Animals↗
PubMed1995

Hormone-induced hyperphosphorylation of specific phosphorylated sites in the mouse glucocorticoid receptor.

The glucocorticoid receptor (GR) is phosphorylated in its basal state, and rapidly undergoes hormone-induced hyperphosphorylation after binding glucocorticoids. Previously, we have identified seven phosphorylated sites in the mouse GR. Most of the sites are located in the regions of the N-terminal domain that are necessary for maximum transcriptional activity and reduce nonspecific binding to DNA. Using WCL2 cells, which overexpress mouse GRs, we now quantitate hormone-induced hyperphosphorylation at each of these sites. Addition of triamcinolone acetonide to WCL2 cells results in significant hyperphosphorylation at the majority of the sites. The hyperphosphorylation ratio, i.e. the 32P incorporation into GRs from hormone-treated cells divided by 32P incorporation into GRs from untreated cells, was above 1.0 for all sites but serine 150 and threonine 159. Serine 220 displays marked hormone dependence, with a ratio of 3. For most sites the ratio was about 1.5. Hormone-induced hyperphosphorylation not only increases the charge at selected phosphorylated sites but also provides a substantial increase in the overall negative charge around the region of the N-terminal domain that is involved in transactivation.

Animals↗
PubMed1994

[Schoenlein-Henoch purpura associated with spiramycin and with important digestive manifestations].

Schönlein-Henoch purpura is a vasculitis due to hypersensitivity characteristic of the infancy that affects preferably small vessels. The etiology is unknown, although it has been related to allergic reactions to drugs, infections, vaccines and insecta bites. An adult with a Schönlein-Henoch purpura after receiving spiramicin is presented, beginning with epigastric pain and vomiting and the purpura appearing subsequently.

Aged↗
PubMed1990

Segmental tuberculosis of the colon diagnosed by colonoscopy.

We describe the case of a woman with rectorrhagia and rectal tenesmus. Colonoscopy revealed a 3-4 cm-long ulcerated lesion with a reduced colon lumen 35 cm from the anus, and multiple biopsies were obtained from the ulcerated region, but histopathology was non-specific. Biopsy culture was positive for M. tuberculosis. Anti-tuberculous chemotherapy was initiated on the diagnosis of segmental tuberculosis of the colon. Subsequent evolution was favorable, both clinically and endoscopically. Emphasis is placed on the importance of colonoscopy and biopsy in the diagnosis of tuberculosis of the colon.

Aged↗
PubMed1990

[Complicated hepatic hydatid cyst and acute pancreatitis. Value of ERCP and treatment with endoscopic sphincterotomy].

We present the case of a 29 year-old cholecystectomized woman with hepatic hydatid cysts who was admitted for acute pancreatitis. Echography and abdominal CAT revealed three thydatid cysts-the one in the right liver lobe being complicated-as well as pancreatitis. Endoscopic retrograde cholangiopancreatography (ERCP) confirmed the suspected diagnosis of intrabiliary hydatid cyst rupture. An endoscopic sphincterotomy was performed, posterior evolution being asymptomatic, thus permitting the postponing of surgery.

Adult↗
PubMed1990

[Physical exercise and gastric acid secretion].

The effects of physical exercise on the basal acid secretion of the stomach has been investigated in 10 healthy individuals and 16 hypersecretors with duodenal ulcer. The gastric basal secretion was collected during 3 hours; during the first hour the patient was at rest, during the second he realized a training exercise, according to Roskamm's formula, and in the third was at rest. While normal subjects showed a significative reduction of the acid secretion during the period of exercise, in the hypersecretory patients with ulcer the acid secretion increased significantly during exercise, from 4.25 +/- 1.52 mEq/h to 7.79 +/- 3.49 mEq/h; these figures reverted to normal values (5.45 +/- 2.21) during the recovery period. We comment the potential mechanisms of these differences in both groups of patients.

Adult↗
PubMed1989

Hypertrophic pyloric stenosis in the adult.

In view of the low incidence of hypertrophic pyloric stenosis, we present a case of this pathology in a male aged 74. Stenosis was of the diffuse type, associated with gastric ulcer and chronic atrophic gastritis. The patient was admitted to our Service with upper digestive tract hemorrhage after deterioration of the ulcer.

Aged↗
PubMed1986

Evidence of high affinity, stereoselective binding sites for [3H]-aldosterone in the spinal cord.

Cytosol from the spinal cord (SC) of adrenalectomized rats was incubated with a range of [3H]-aldosterone (ALDO) concentrations and the results analyzed according to Scatchard. High affinity (Kd less than or equal to 1 nM) as well as low affinity (Kd 30-195 nM) sites were measured; the low affinity site was abolished by co-incubation with the pure antiglucocorticoid RU 28362. [3H]-ALDO in concentrations shown to bind to the high affinity site only, was completely displaced by the spirolactone, RU 26752, but not by RU 28362; however, the latter compound competed for 40% of the sites when incubated with a higher (10 nM) concentration of [3H]-ALDO, binding approximately one-half to each receptor type. The high affinity site was distributed uniformly in four sections of the SC, with significantly lower levels in the region corresponding to the filum terminale and horse tail and slightly higher in the cervical and lumbar enlargements. The high affinity site acquired increased affinity for DNA-cellulose after heat-induced transformation, with reduced capacity to bind to DEAE-cellulose. These results suggest that the SC contains, in addition to glucocorticoid receptors, binding molecules of high affinity and stereoselectivity for mineralocorticoids, and that, under appropriate conditions, present increased affinity for DNA acceptor sites.

Aldosterone↗
PubMed1985

Properties and distribution of glucocorticoid-binding sites in cytosol of the spinal cord.

We have examined the spinal cord for the presence of glucocorticoid-binding sites. For this purpose, cytosol from the spinal cord of adrenalectomized rats was incubated with (3H)-dexamethasone. Maximal binding was obtained after 20 h of incubation at 0 degree C in the presence of 20 mM molybdate, whereas at 20 degrees C the maximum was at 2 h. Using a range of (3H)-dexamethasone concentrations (0.2-30 nM), low capacity (161 +/- 23 fmol/mg protein) and high affinity (Kd 3.2 +/- 0.3 nM) sites were measured. Binding sites decreased by 25% and Kd increased 2.5-fold after incubation with a pure glucocorticoid (RU 26988). Relative binding affinities of several competitors of 10 nM (3H)-dexamethasone were: triamcinolone acetonide 108, dexamethasone 100, RU 26988 54, corticosterone 18, progesterone 17, aldosterone 7, estradiol and testosterone less than 1. Sedimentation coefficients in glycerol gradients containing molybdate were in the range of those published for glucocorticoid receptors (9.6-9.8 S). Binding of (3H)-dexamethasone was decreased by omitting a SH-protective agent from the buffer or by addition of SH-blocking reagents such as N-ethylmaleimide and p-chloromercuribenzoate. Using rats of different ages, it was found that binding sites were much lower in spinal cord from 2- to 8-day-old rats than in rats of 13-20 days and adults. Regional distribution studies using cytosol from spinal cords dissected between vertebrae C1-C2, C3-C7, T1-T8, T9-L3 and L4-L6 revealed that binding sites were higher in regions containing the cervical (C3-C7) and lumbar (T9-L3) enlargements, with respect to L4-L6.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1984

Regulation of adenosine-3',5'-monophosphate levels in rat anterior pituitary by adrenal corticoids.

The effect of adrenal cortical hormones on basal and prostaglandin-E2 (PGE2)-stimulated levels of cAMP was studied in incubated rat anterior pituitaries. It was found that oral administration of dexamethasone (DEX) at the concentration of 10 micrograms/mL of drinking saline to adrenalectomized (ADX) rats for four days decreases basal and PGE2-stimulated cAMP levels in the pituitary but not in the hypothalamus. Furthermore, a time-course study demonstrated that acute intraperitoneally (IP) DEX treatment had no effect; whereas, after one day of oral DEX, PGE2-stimulated levels, but not basal, were already reduced. The effect of DEX was also obtained with two natural rat adrenal hormones like corticosterone and deoxycorticosterone, whereas, progesterone and testosterone, which share with the corticoids a ring A-unsaturated-three-ketone structure but are devoid of corticoid activity, did not modify at physiological doses the levels of cAMP. More physiological validation of these results was given by experimental procedures that modified endogenous adrenal secretion. Thus, reduction of plasma corticoids by ADX significantly increased basal and PGE2-stimulated cAMP levels in the pituitary, whereas, increments of plasma corticosterone produced by ACTH had the reverse effect in intact rats. It is suggested that adrenal gland regulation of cAMP may reflect involvement of the nucleotide in the mechanism of action of corticoids at the pituitary level.

Adrenal Cortex Hormones↗
PubMed1983

Autologous mixed lymphocyte reaction in man. VI. Deficiency of autologous mixed lymphocyte reaction in type I (insulin-dependent) diabetes mellitus.

Autologous mixed lymphocyte reaction (AMLR) was examined in the peripheral blood from 20 patients with type I (insulin-dependent) diabetes mellitus. Six of 20 patients demonstrated deficient AMLR when compared to the range for simultaneously studied age and sex matched healthy controls. The kinetics of AMLR with regard to duration of the peak proliferative response was similar to controls, the peak response being on day 6. In allogeneic MLR. T cells from patients responded normally. However, non-T cells from patients were poor stimulators against responder T cells from healthy controls. This study demonstrates a deficiency of AMLR in a subset of patients with type I diabetes that further supports an abnormal immune regulation and might be an important mechanism in the pathogenesis and autoimmune manifestations of type I diabetes.

Adolescent↗
PubMed1982

Deficiency of suppressor T-cells in insulin-dependent diabetes mellitus: an analysis with monoclonal antibodies.

Peripheral blood from 25 patients with insulin-dependent diabetes mellitus was examined for any alteration in the proportions and or functions of immunoregulatory T-cell subsets, defined with monoclonal antibodies. Ten of 25 (40%) patients demonstrated deficiency of OKT8+ (suppressor/cytotoxic) T-cells. Eight of these 10 patients had abnormally high ratios of OKT4+/OKT8+ T-cells. Nine of 10 patients with abnormally low proportion of OKT8+ T-cells had deficient concanavalin A-induced suppressor cell activity against the proliferative response of autologous or allogeneic lymphocytes to phytohemagglutinin. No correlation was observed between the deficiency of suppressor T-cells and the control of diabetes. Therefore, it is likely that the deficiency of suppressor cells is related to insulin-dependent diabetes mellitus itself and not to the metabolic changes that are associated with diabetes mellitus. This study demonstrates both quantitative and qualitative deficiency of suppressor T-cells in at least some patients with insulin-dependent diabetes, that might play an important role in the pathogenesis and autoimmune manifestations of a proportion of patients with insulin-dependent diabetes mellitus.

Adolescent↗
PubMed1982

Regulation of glucocorticoid receptors in brain by corticosterone treatment of adrenalectomized rats.

Binding of (3H)-corticosterone in cytosol of hippocampus and hypothalamus has been measured in adrenalectomized (ADX) rats in the presence or absence of corticosterone replacement therapy (suspended shortly before receptor analysis). Corticosterone pellet implantation into female rats or oral corticosterone administration in salinized drinking water given to males for 3 weeks reduced (3H)-corticosterone binding by half in the hippocampus. This reduction was observed whether corticosterone or dexamethasone was employed as competitor to determine nonspecific binding, thus eliminating transcortin as the cause of the corticosterone effect on binding. Scatchard analysis of binding data revealed that the reduction was mostly due to decreased number of receptors. Animals pretreated with corticosterone had a reduction in thymus weight, indicating further the biological effectiveness of the treatment. Further, serum corticosterone in ADX rats pretreated with corticosterone (but with therapy suspended for 24 h) was very low and similar to that of untreated ADX rats. Uptake studies after injection of (3H)-corticosterone intravenously into ADX rats showed that the injected hormone was absent from blood and brain tissues 1 day later, ruling out (in addition to the measurement of serum corticosterone) that the reduction in binding was due to occupation of receptor sites by exogenous corticosterone remaining after withdrawal from therapy. It is suggested that down-regulation of glucocorticoid receptors in brain follows the chronic corticosterone administration. These data are discussed in relation with evidence for down-regulation of other classes of steroid receptors in several tissues, and the consequence that changes in receptor binding in brain may have on the feedback mechanism of corticoids at the central level.

Adrenalectomy↗