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Biomedical subjects

F Martínez

Publications and source records attributed to F Martínez.

At least 19 recordsLinked to original sources
PubMed1997

Indomethacin and piroxicam inhibit Na+-adenosine transport in rat renal brush-border membranes.

The effects of the cyclooxygenase inhibitors, indomethacin and piroxicam, were evaluated on Na+-dependent [3H]adenosine transport in rat renal brush-border membranes of the outer renal cortex of the rat. Adenosine co-transport (1-10 microM) was estimated in the presence of 0.001-10 microM indomethacin and piroxicam. Both drugs inhibited the Na+-dependent transport in a dose-dependent manner with IC50 of 3.5 microM and 0.1 microM, respectively. The Na+-independent transport was not modified. Preincubations carried out on the vesicles with 10-50 microM arachidonic acid increased transport in a dose-dependent manner up to 1.7 times. Whereas 50 pM to 5 microM prostaglandin E2 in the presence of indomethacin did not change carrier activity, 5 microM prostaglandin E2 increased the Na+-dependent transport 1.5 times. Other prostanoid synthesis pathways were investigated with 10 microM nordihydroguaiaretic acid (lipoxygenase inhibitor), and 17-octadecynoic acid and clotrimazole (leukotriene and cytochrome P450 inhibitors). Our results demonstrated that the Na+-dependent adenosine transport in brush-border membranes was inhibited by indomethacin and piroxicam, suggesting that cyclooxygenase activity might modulate this co-transport.

Adenosine↗
PubMed1997

Comparison of the role of cervical and intrauterine insemination techniques on the incidence of multiple pregnancy after artificial insemination with donor sperm.

PURPOSE: Our purpose was to investigate the role of the insemination technique used in an artificial insemination program with donor sperm (AID) in multiple pregnancy rates. METHODS: We carried out a retrospective nonrandom analysis of 300 pregnancies corresponding to 300 cycles in women from our Artificial Insemination Donor Sperm Program. All cycles were stimulated with gonadotropins. Single and multiple pregnancy cycles and intracervical and intrauterine pregnant cycles were compared. RESULTS: Intracervical insemination was performed in 173 cycles (58%), and intrauterine insemination in 127 (42%). Two hundred twenty-three pregnancies were single (74%), and 77 multiple (26%). In multiple pregnancy cycles, initial dose and mean total daily dose of gonadotropins, plasma estradiol levels, and number of follicles > or = 14 mm were significantly higher compared to those in single pregnancy cycles. Multiple pregnancy rte was significantly higher among pregnancies after intrauterine insemination (32%) than after intracervical insemination (21%). CONCLUSIONS: The intrauterine technique of insemination in AID-stimulated cycles with gonadotropins is related to multiple pregnancy risk.

Adult↗
PubMed1997

Sodium-dependent adenosine transport is diminished in brush border membrane vesicles from hypothyroid rat kidney.

Studies of the uptake of [3H]adenosine ([3H]ADO) were performed using brush border membrane vesicles (BBMV) from normal (N) and hypothyroid (Tx) rat kidneys, to test if decreased Na+ reabsorption in hypothyroidism might be associated with abnormalities in ADO transport. [3H]ADO uptake (1-10 micromol) for both conditions was measured in the presence of Na+ (10-150 mmol/l); the effects of dipyridamole (10 micromol/l) and 1, 3-dipropyl-8-(2-amino-4-chlorophenyl)xanthine (PACPX, 10 micromol/l) were also studied. Na+-stimulated ADO uptake was decreased in Tx BBMV. Michaelis-Menten constants showed a decreased ADO carrier affinity (Km 2.46 +/- 0.14 in N, vs Km 4.46 +/- 0.88 micromol/l in Tx, P<0.05), with no change in the number of carriers (Vmax 295 +/- 25 in N, vs 229.2 +/- 56 pmol.min-1.mg protein in Tx). Na+ affinity remained unchanged (K Na+ 11.5 +/- 3.5 in N, vs K Na+ 12.72 +/- 0.7 mmol/l in Tx). Inhibition of Na+-dependent ADO transport was 50% in N as opposed to 58% in Tx with dipyridamole, and 72% in N versus 47% in Tx with PACPX. These results suggest that decreased Na+-dependent ADO cotransport contributes to the diminished tubular reabsorption that occurs in hypothyroidism.

Adenosine↗
PubMed1997

Mutational analysis of the MPZ, PMP22 and Cx32 genes in patients of Spanish ancestry with Charcot-Marie-Tooth disease and hereditary neuropathy with liability to pressure palsies.

Charcot-Marie-Tooth disease (CMT) and hereditary neuropathy with liability to pressure palsies (HNPP) are two inherited peripheral neuropathies. The most prevalent mutations are a reciprocal 1.5-Mb duplication and 1.5-Mb deletion, respectively, at the CMT1A/HNPP locus on chromosome 17p11.2. Point mutations in the coding region of the myelin genes, peripheral myelin protein 22 (PMP22), myelin protein zero (MPZ) or connexin 32 (Cx32) have been reported in CMT patients, including CMT type 1 (CMT1), CMT type 2 (CMT2) and Déjérine-Sottas neuropathy (DS) patients, and only in the coding region of PMP22 in HNPP families lacking a deletion. We have investigated point and small mutations in the MPZ, PMP22 and Cx32 genes in a series of patients of Spanish ancestry: 47 CMT patients without duplications, and 5 HNPP patients without deletions. We found 15 different mutations in 16 CMT patients (34%). Nine different mutations in ten patients were detected in the Cx32 gene, this being the most frequently involved gene in this series, whereas five mutations involved the MPZ gene and only one the PMP22 gene. Six out of nine nucleotide substitutions in the Cx32 gene involved two codons encoding arginine at positions 164 and 183, suggesting that these two codons may constitute two Cx32 regions prone to mutate in the Spanish population. Analysis of HNPP patients revealed a 5' splicing mutation in intron 1 of the PMP22 gene in a family with autosomal dominance, which confirms allelic heterogeneity in HNPP. Ectopic mRNA analysis on leukocytes suggests that this mutation might behave as a null allele.

Charcot-Marie-Tooth Disease↗
PubMed1997

Structural and functional changes in mitochondria associated with trophoblast differentiation: methods to isolate enriched preparations of syncytiotrophoblast mitochondria.

The syncytiotrophoblast of the human placenta is derived from the fusion of cytotrophoblast cells. The syncytiotrophoblast and cytotrophoblast cells have different functional properties. Here, we document that syncytiotrophoblast mitochondria have a distinct phenotype that differs from that of the mitochondria ofcytotrophoblast cells. Syncytiotrophoblast mitochondria are small and have a dense matrix and vesicular cristae. They contain the machinery to convert cholesterol into pregnenolone. The larger cytotrophoblast mitochondria have lamellar cristae and do not have detectable P450scc. These observations imply that trophoblast mitochondria undergo morphological and functional changes as cytotrophoblast cells differentiate into syncytiotrophoblast. Structural changes in mitochondria and accumulation of P450scc were induced in a clonal line of BeWo choriocarcinoma cells by treatment with 8-Br-cAMP, which promotes formation of syncytial structures in these cultures. We conclude that the terminal differentiation program of trophoblast cells includes major changes in the architecture and function of mitochondria. Based on the unique features of syncytiotrophoblast mitochondria, we developed a method to prepare highly enriched syncytiotrophoblast mitochondria from term placenta using differential centrifugation and density gradient centrifugation.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1996

Cerebrospinal fluid tyrosine and 3,4-dihydroxyphenylacetic acid levels in migraine patients.

We studied biochemical parameters related with central dopaminergic neurotransmission in migraine patients during crisis. We determined tyrosine and 3,4-dihydroxyphenylacetic acid (DOPAC) levels in cerebrospinal fluid (CSF) of 47 patients, 29 suffering migraine without aura and 18 suffering migraine with aura, comparing them with 27 control subjects. Tyrosine levels did not differ significantly between patients and controls. The CSF concentration of DOPAC was 0.73 +/- 0.55 ng/ml in the control population, 3.84 +/- 2.08 ng/ml in patients with migraine without aura and 3.30 +/- 1.49 ng/ml in patients suffering migraine with aura. The concentration of DOPAC correlated positively with the intensity of headache. These results suggest that patients with migraine have a central dopaminergic hyperfunction, probably related to a coexisting central dysfunction of noradrenergic neurotransmission.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Evidence for a common origin of most Friedreich ataxia chromosomes in the Spanish population.

Haplotype analysis is a powerful approach to understand the spectrum of mutations accounting for a disease in a homogeneous population. We show that haplotype variation for 10 markers linked to the Friedreich ataxia locus (FRDA) argues in favor of an important mutation homogeneity in the Spanish population, and positions the FRDA locus in the region where it has been recently isolated. We also report the finding of a new single nucleotide polymorphism called FAD1. The new marker shows a very strong linkage disequilibrium with Friedreich ataxia (FA) in both the Spanish and French populations. suggesting the existence of an ancient and widespread FRDA mutations. Inclusion of FAD1 in the extended haplotype analysis has allowed to postulate that this main FRDA mutation could account for 50-90% of the disease chromosomes. The results indicate that FA, despite clinical heterogeneity, could have originated from a few initial mutations.

Adaptor Proteins, Signal Transducing↗
PubMed1995

Modulation of the release of adenosine by glucose and chemical hypoxia in cultured renal cells (MDCK line).

The effect of changes in the external concentrations of glucose on the release of adenosine of cultured renal cells (MDCK line) was studied. Adenosine release was markedly increased by the addition of glucose (5.5 mM) to monolayers of MDCK cells deprived of glucose for 24 hours. Addition of glucose to either the apical or basolateral side of the monolayer elicited a marked release of adenosine at the contralateral compartment. Removal of sodium in the external media blunted the response to glucose. Methylglucose that is transported into the cell but not metabolized also markedly increased adenosine release. Deoxyglucose that induces chemical hypoxia stimulated the release of adenosine. These results suggest that variations in extracellular glucose might be a physiological modulator of the cell regulation of adenosine.

Adenosine↗
PubMed1995

Localization of a gene for X-linked nonspecific mental retardation (MRX24) in Xp22.2-p22.3.

Nonspecific X-linked mental retardation (MRX) includes several distinct genetic entities in which mental retardation is not associated with additional distinguishing physical changes. We report linkage data in a Spanish family with MRX, using polymorphic DNA markers distributed over the X chromosome. Two-point linkage analysis demonstrated close linkage between the MRX locus and DXS85 in Xp22.3 with a peak lod score of 2.28 at a theta = 0.00. Analysis of multiple informative meioses suggested a localization of the MRX locus (MRX24) between DXS278 and DXS207. Multipoint linkage analysis resulted in a maximum LOD score of 2.45 at 3 cM proximal to DXS85, and allowed us to reject a localization of the MRX24 gene in all other regions from Xp21-Xqter. These findings localize the MRX24 gene in the chromosomal region Xp22.2-p22.3.

Chromosome Mapping↗
PubMed1995

An autosomal dominant retinitis pigmentosa family with close linkage to D7S480 on 7q.

Retinitis pigmentosa is the most prevalent inherited disorder of the retina. It can be autosomal dominant (adRP), autosomal recessive (arRP) or X-linked (XLRP). A form of adRP mapping to chromosome 7q was reported in a large Spanish pedigree. We have typed DNA from the members of another Spanish family for polymorphic markers from the known candidate genes. Positive lod scores were obtained only for the markers located on 7q31-35, giving a maximum lod score of 2.98 (3.01 by multipoint analysis) at theta = 0.00 for D7S480. A brief clinical evaluation is given.

Chromosome Mapping↗
PubMed1995

The effect of osmolarity on human placental mitochondria function.

Human placental explants survive large changes in osmolarity, but the mechanism for this property is unknown. The goal of this work was to examine the effect of osmolarity on human placental mitochondria. Mitochondria from human term placenta were isolated by differential centrifugation, and incubated in the presence of different concentrations of sucrose or KCl, to modify the osmolarity of the media. Rat liver mitochondria were used as control. The parameters studied were: respiration rate, adenine nucleotide hydrolysis, calcium transport, membrane potential, and mitochondrial morphology. Stimulation of the mitochondrial respiration rate and an increase in Ca2+ transport was observed in the presence of K+. With sucrose, Ca2+ transport showed a complex kinetic behavior, whereas the respiratory control was slightly diminished. Although the ATPase activity was enhanced in the absence of a respiratory substrate, no change in ATP hydrolysis due to osmolarity was observed. ADP hydrolysis was inhibited by a high K+ concentration, but not by sucrose. The membrane potential was not modified by osmolarity, even in the absence of sucrose or K+ in the medium. Mitochondria isolated with KCl showed aggregation, whereas dispersed mitochondria were observed with sucrose. This study showed that sucrose-induced changes in osmolarity, does not modify metabolic and transport properties of human placental mitochondria, whereas KCl-induced osmolarity changes does affect these functions.

Adenosine Triphosphatases↗
PubMed1995

Treatment with various antibiotics of experimental endocarditis caused by penicillin-resistant Streptococcus sanguis.

BACKGROUND: Streptococcus sanguis currently accounts for one-half of viridans streptococci. Treatment has become complicated due to the increase in resistance to penicillin and cephalosporins. The aim of the study was to assess the efficacy of various antibiotics as monotherapy and in association with gentamicin, in a experimental model of infective endocarditis in rabbits. The effects were compared with a control group and a group given classical penicillin-gentamicin treatment. MATERIAL AND METHODS: Infective endocarditis was induced in 180 rabbits with a clinical isolate of Streptococcus sanguis. Treatment was started 48 h after infection, and lasted 5 days. The animals were divided into nine groups of 20 rabbits: G1, untreated controls; G2, penicillin-gentamicin; G3, clindamycin-gentamicin; G4, imipenem; G5, imipenem-gentamicin; G6, teicoplanin; G7, teicoplanin-gentamicin; G8, vancomycin and G9, vancomycin-gentamicin. Response to therapy was evaluated by mortality curves, as negative blood cultures, concentration of S. sanguis in aortic vegetations and rate of sterilization of vegetations. RESULTS: Vegetation weight was significantly lower in treated groups than in controls; lower weights were found in G5, 6, and 9. G9 sterilized 75% of the vegetations. Death occurred in 25% of the control group and in 4.76% of G6 and 7. Blood cultures became negative most rapidly in G9. CONCLUSIONS: Combined treatment with vancomycin-gentamicin may be highly efficacious in patients with endocarditis caused by penicillin-resistant Streptococcus sanguis. Other combinations, such as imipenem-gentamicin and teicoplanin-gentamicin, may be also advantageous.

Animals↗