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A Nieto

Publications and source records attributed to A Nieto.

At least 55 records · Page 3Linked to original sources
PubMed2001

Avidity analysis of the human immune response to a chitin binding protein of Toxoplasma gondii.

A 30-33 kDa electroeluted fraction of T. gondii tachyzoites improved discrimination between acute and chronic phase sera when used instead of the whole tachyzoite extract in an avidity-ELISA. In order to identify the components of these fractions, crude tachyzoite antigen was fractionated by anionic exchange chromatography. The 30-33 kDa antigen cluster eluted in the not-bound fraction could account for a large proportion of the antibody response against the 30-33 kDa electroeluted fraction. According to the N-terminal sequence data, this antigen fraction is composed mainly of SAG1 and another protein with high homology to chitin binding proteins from plants.

Animals↗
PubMed2001

Lack of association between NRAMP1 gene polymorphisms and Trypanosoma cruzi infection.

Genetic analysis in mice and humans have established the key role of the human natural resistance-associated macrophage protein 1 (NRAMP1) in resistance to intracellular infections. In the present study we investigated whether four NRAMP1 polymorphisms (5'(GT)n, -236 C-->T, D543N, and 3'UTR deletion) were important in determining the susceptibility to Trypanosoma cruzi infections as well as in the development of chagasic cardiac disease. Genotyping for these variants was assessed in 83 seropositive (asymptomatic, n=51, cardiomyopathic, n=32) and 85 seronegative individuals from a Peruvian population where T. cruzi is endemic. No statistically significant differences either between patients and controls or between asymptomatic and cardiomyopathic individuals were observed with respect to NRAMP1 variants. Our data suggest that the NRAMP1 genetic polymorphism analysed do not play a major role in the pathogenesis of T. cruzi infection in this Peruvian sample.

Adolescent↗
PubMed2001

Chemokine receptor CCR5 polymorphisms and Chagas' disease cardiomyopathy.

In this study we investigated the possible role of two CCR5 gene polymorphisms, CCR5Delta32 deletion and CCR5 59029 A-->G promoter point mutation, in determining the susceptibility to Trypanosoma cruzi infection as well as in the development of chagasic heart disease. These CCR5 polymorphisms were assessed in 85 seropositive (asymptomatic, n=53; cardiomyopathic, n=32) and 87 seronegative individuals. The extremely low frequency (0.009) of the CCR5Delta32 allele in our population did not allow us to analyse its possible influence on T. cruzi infection. We found no differences in the distribution of CCR5 59029 promoter genotype or phenotype frequencies between total chagasic patients and controls. However, we observed that the CCR5 59029-A/G genotype was significantly increased in asymptomatic with respect to cardiomyopathic patients (P=0.02; OR=0.33, 95% CI 0.10-0.94). In addition, the presence of the CCR5 59029-G allele was also increased in asymptomatics when compared with cardiomyopathics (P=0.02; OR=0.35, 95% CI 0.12-0.96). Our data suggest that the CCR5 59029 promoter polymorphism may be involved in a differential susceptibility to chagasic cardiomyopathy.

Adolescent↗
PubMed2001

Increased tissue concentrations of arachidonic acid in umbilical artery and placenta in fetal growth retardation.

OBJECTIVE: To compare the fatty acid phospholipid composition of the umbilical artery and the placenta in cases of fetal growth retardation (FGR) and of normal growth, as well as in symmetric and asymmetric FGR. DESIGN: Case-control study. SETTING: University hospital. POPULATION: Thirty-nine FGR cases (12 asymmetric, 27 symmetric) and 78 cases with normal growth. MAIN OUTCOME MEASURES: Thin layer gas-liquid capillary chromatography of phospholipid fatty acids in umbilical artery and placental cotyledons. Newborns were classified as FGR if their weight was under the 10th percentile for our center. FGR was defined as symmetric if the ponderal index was >2.32, and as asymmetric if it was <2.32. RESULTS: In FGR, arachidonic acid was significantly increased both in placenta (24.05%+/-2.78 vs 22.46%+/-2.93) and in umbilical artery (16.76%+/-2.40 vs 15.58%+/-3.67). Indeed this increase was significantly higher in asymmetric than in symmetric FGR (25.70+/-2.32 vs 23.32+/-2.68 in placenta and 18.06+/-1.46 vs 16.14 +/-2.53 in umbilical artery). On the other hand, in the placenta there were a number of differences in the metabolic ratios analyzed when comparing symmetric and asymmetric FGR, indicating a lower DHA availability and a higher n-6 fatty acid elongation and desaturation in asymmetric FGR. CONCLUSION: FGR is characterized by an increase in arachidonic acid both in the placenta and umbilical artery phospolipids, probably reflecting a different mobilization from tissue stores. It is speculated that the different arterial composition could be partially responsible for the increased cardiovascular risk of FGR in adulthood. On the other hand the metabolic status of the placenta concerning polyunsaturated fatty acids was very different in symmetric and asymmetric FGR, suggesting a different pathogenesis.

Adult↗
PubMed2001

Mortality trends from oral cancer in Andalusia, Spain, 1975-1998.

Morbidity and mortality rates from oral cancer appear to be on the rise among developed countries throughout the world during the last decades. The object of the present study was to investigate the recent changes in the mortality from oral cancer in the more than seven million inhabitants of Andalusia, Spain. Data on the number of deaths by oral cancer from 1975 to 1998 were obtained from annual publications by the Statistics Institute. Crude, age-standardized, truncated, cumulative and age-specific rates of mortality were calculated by gender as well as potential years of life lost rates. Poisson regression models were fitted in order to quantify the influence of age and year of death on the mortality rates by gender.Age-adjusted mortality rates increased from 2.79 in 1975-79 to 3.41 in 1995-98 in males and from 0.39 to 0.45 in females during the same period. Increases were more marked when comparing the truncated age-adjusted rates. Relative risks increased with age from 2.35 to 23.12 in 55 to 64-y-old and 85-y-old males respectively, and from 2.91 to 21.50 in 55 to 64-y-old and 85-y-old females respectively, when comparing with the 35-54-y-old age group. There was an interaction between age at death and year of death in males but not in females. Mortality from oral cancer increased in males in Andalusia over the study period, simultaneous to an important change in the pattern of occurrence by age. There was a cohort effect in males and females across the studied time interval.

Adult↗
PubMed2001

Modulation of the cellular immune response by a carbohydrate rich fraction from Echinococcus granulosus protoscoleces in infected or immunized Balb/c mice.

Infection of Balb/c mice with Echinococcus granulosus protoscoleces constitutes the model for secondary hydatid infection. The immune response of Balb/c mice infected with E. granulosus is characterized by secretion of antibodies specific for carbohydrate epitopes and production of type-2 cytokines. A role for glycoconjugates in the induction of type-2 responses has been suggested in other host--parasite systems. Although glycoconjugates are immunogenic in E. granulosus infection, the role of these molecules in the establishment of the type-2 response has never been analysed. In this study, a carbohydrate rich fraction (E4+) from E. granulosus protoscoleces was obtained using the monoclonal antibody E492/G1 specific for the moiety Galalpha(1,4)Gal which is widely represented in protoscoleces and other E. granulosus antigenic preparations. The results showed that E4+ was immunogenic in Balb/c mice evoking an antibody response mainly directed against carbohydrate epitopes. In addition, splenocytes from E4+-immunized mice showed suppressed proliferative responses to Con A and E4+ induced IL-10 secretion by E4+-primed and naive splenocytes. The fraction E4+ also was immunogenic in infected mice during early infection. In this case also, splenocytes from infected mice as well as peritoneal cells from infected or naive mice, when stimulated in vitro with E4+, secreted IL-10. Collectively, these results suggest that E4+ may be involved in immunosuppression phenomena and, by stimulating IL-10 secretion, may contribute to the induction and sustaining of the type-2 cytokine response established in early experimental infection.

Animals↗
PubMed2001

PA subunit from influenza virus polymerase complex interacts with a cellular protein with homology to a family of transcriptional activators.

The PA subunit of the influenza virus polymerase complex is a phosphoprotein that induces proteolytic degradation of coexpressed proteins. Point mutants with reduced proteolysis induction reconstitute viral ribonucleoproteins defective in replication but not in transcriptional activity. To look for cellular factors that could associate with PA protein, we have carried out a yeast two-hybrid screen. Using a human kidney cDNA library, we identified two different interacting clones. One of them was identified as the human homologue of a previously described cDNA clone from Gallus gallus called CLE. The human gene encodes a protein of 36 kDa (hCLE) and is expressed ubiquitously in all human organs tested. The interaction of PA and hCLE was also observed with purified proteins in vitro by using pull-down and pep-spot experiments. Mapping of the interaction showed that hCLE interacts with PA subunit at two regions (positions 493 to 512 and 557 to 574) in the PA protein sequence. Immunofluorescence studies showed that the hCLE protein localizes in both the nucleus and the cytosol, although with a predominantly cytosolic distribution. hCLE was found associated with active, highly purified virus ribonucleoproteins reconstituted in vivo from cloned cDNAs, suggesting that PA-hCLE interaction is functionally relevant. Searches in the databases showed that hCLE has 38% sequence homology to the central region of the yeast factor Cdc68, which modulates transcription by interaction with transactivators. Similar homologies were found with the other members of the Cdc68 homologue family of transcriptional activators, including the human FACT protein.

Amino Acid Sequence↗
PubMed2001

The cost of asthma treatment in Spain and rationalizing the expense.

According to Weiss et al. [12], the main providers of asthma care in the United States in 1992 were general and family medicine + internal medicine (46%), pediatrics (19%), allergy (25%), pulmonary medicine (5%), and others (5%). In an overall climate of a shift of referral from primary care to the specialties, specialists will have to provide evidence that their intervention in the control of patients provides truly better clinical and economical outcomes than that of general practitioners. In order to support this hypothesis, we estimated: (1) the development of the costs of medication for asthma in a population of 40 million people (Spain) and (2) the correlation between these costs and the intervention of a specialized attendance. In Spain the annual costs incurring from allergic diseases are estimated to be approximately 1,500 million Euros and, the cost due to asthma alone is about 900-1,200 million Euros. There are two main ways to explain the size of these figures. First, the prevalence of allergic diseases is rising year by year. Second, the relevance of allergology in the control of asthma is often greatly reduced. This has resulted in a reduction in the etiological diagnosis and treatment with specific immunotherapy (SIT). However, SIT is the only specific causal treatment of allergic asthma that is able to modify the natural history of disease or disease progression. So, it is possible to hypothesize that this reduction in a proper etiological diagnosis and treatment could be a cause (among others) of increasing costs.

Anti-Asthmatic Agents↗
PubMed2000

Mutational analysis in a cohort of 224 tuberous sclerosis patients indicates increased severity of TSC2, compared with TSC1, disease in multiple organs.

Tuberous sclerosis (TSC) is a relatively common hamartoma syndrome caused by mutations in either of two genes, TSC1 and TSC2. Here we report comprehensive mutation analysis in 224 index patients with TSC and correlate mutation findings with clinical features. Denaturing high-performance liquid chromatography, long-range polymerase chain reaction (PCR), and quantitative PCR were used for mutation detection. Mutations were identified in 186 (83%) of 224 of cases, comprising 138 small TSC2 mutations, 20 large TSC2 mutations, and 28 small TSC1 mutations. A standardized clinical assessment instrument covering 16 TSC manifestations was used. Sporadic patients with TSC1 mutations had, on average, milder disease in comparison with patients with TSC2 mutations, despite being of similar age. They had a lower frequency of seizures and moderate-to-severe mental retardation, fewer subependymal nodules and cortical tubers, less-severe kidney involvement, no retinal hamartomas, and less-severe facial angiofibroma. Patients in whom no mutation was found also had disease that was milder, on average, than that in patients with TSC2 mutations and was somewhat distinct from patients with TSC1 mutations. Although there was overlap in the spectrum of many clinical features of patients with TSC1 versus TSC2 mutations, some features (grade 2-4 kidney cysts or angiomyolipomas, forehead plaques, retinal hamartomas, and liver angiomyolipomas) were very rare or not seen at all in TSC1 patients. Thus both germline and somatic mutations appear to be less common in TSC1 than in TSC2. The reduced severity of disease in patients without defined mutations suggests that many of these patients are mosaic for a TSC2 mutation and/or have TSC because of mutations in an as-yet-unidentified locus with a relatively mild clinical phenotype.

Adolescent↗
PubMed2000

Molecular characterization of P-29, a metacestode-specific component of Echinococcus granulosus which is immunologically related to, but distinct from, antigen 5.

In this work the characterization of P-29, a novel 29 kDa antigen from Echinococcus granulosus is reported. E. granulosus was identified while looking for parasite antigens distinct from those present in hydatid cyst fluid. A monoclonal antibody (mAb 47H.PS) prepared against protoscolex components revealed that P-29 is localized to the tegument and rostellum of protoscoleces, and to the germinal layer of the cyst, but it is absent in hydatid cyst fluid or adult worm extracts. Several internal fragments of P-29 showed sequence identity to the amino acid sequence encoded by Eg6, a partial gene sequence reported to code for an epitope of antigen 5 (Ag5), one of the major diagnostic antigens of the parasite. We confirmed that Eg6 encodes a sub-fragment of P-29 by mapping the epitope of mAb 47H.PS, and isolating the full length P-29 cDNA. Since Eg6 had been, postulated to encode a fragment of Ag5, we specifically studied the relationship of P-29 and Ag5 by: (i) examining the cross-reactivity displayed by different mAbs; (ii) comparison of their peptide finger prints; and (iii) a comparative study of their diagnostic value. Our results prove unequivocally that P-29 and Ag5 are immunologically related, but different proteins, raising several questions on the current knowledge of Ag5.

Amino Acid Sequence↗
PubMed2000

Involvement of Fcgamma receptor IIIA genotypes in susceptibility to rheumatoid arthritis.

OBJECTIVE: To investigate a possible association of Fcgamma receptor IIIA (FcgammaRIIIA) gene polymorphism at position 158 with susceptibility to, and the outcome of, rheumatoid arthritis (RA). METHODS: One hundred seventeen RA patients and 142 unrelated healthy control subjects from the same geographic area were studied. Genotyping for FcgammaRIIIA-158V/F was performed by a method based on polymerase chain reaction (PCR) and restriction fragment length polymorphism analysis using amplification-created restriction sites. HLA-DRB1 typing by PCR-sequence-specific oligonucleotide hybridization (reverse hybridization) was also performed. RESULTS: Allele and genotype distributions in healthy controls were similar to those reported in other populations. The overall distribution of genotypes in the patients was significantly different from that in the controls (P = 0.023, by chi-square test from 3 x 2 contingency table). An overrepresentation of the FcgammaRIIIA-158FF genotype in the patients was observed (for 158FF versus non-158FF P = 0.01, odds ratio [OR] 1.98, 95% confidence interval [95% CI] 1.16-3.4). However, the FcgammaRIIIA-158VF genotype was increased in controls (for 158VF versus non-158VF P = 0.021, OR 0.54, 95% CI 0.32-0.92). No associations were found with any of a series of clinical parameters. Analysis of FcgammaRIIIA-158FF along with shared epitope showed that the presence of both factors increased the susceptibility to RA (P = 0.0009, OR 3.6, 95% CI 1.63-8.01); however, they probably do not interact to produce this effect. CONCLUSION: These results indicate that the FcgammaRIIIA-158 genotypes confer differential susceptibility to RA in our study population. Further studies to elucidate the role of this polymorphism in the pathogenesis of RA and other autoimmune diseases are warranted.

Adult↗
PubMed2000

Intestinal toxicity of ketoprofen-trometamol vs its enantiomers in rat. Role of oxidative stress.

OBJECTIVE: Gastrointestinal damage and bleeding are the major side effects of non-steroidal anti-inflammatory drugs (NSAID), however the mechanisms of this ulcerogenic action are not fully understood. It has recently been proposed that neutrophil-and oxygen radical-dependent microvascular injuries may be important prime events that lead to mucosal injury. In addition, other factors like bile flow, intact bacterial flora or feeding conditions may contribute to the formation of lesions. Ketoprofen is a NSAID that exists as a pair of R(-) and S (+) enantiomers; like other 2-arylpropionic acids, its anti-inflammatory effects resides almost exclusively in the S (+) isomer. The present study was undertaken to explore the role of oxidative stress in the pathogenesis of intestinal injury induced by oral administration of racemic ketoprofen and its enantiomers given as their water soluble tromethamine salts. MATERIAL AND METHODS: Evaluation of intestinal damage and activities of oxidative stress related enzymes such as myeloperoxidase (MPO), xanthine-oxidase (XO) and superoxide dismutase (SOD) were studied in an experimental animal model using refed rats. RESULTS: After the oral treatment followed by a refeeding period of 24 h, ketoprofen (100, 50, 25 mg/Kg b.w.) dose-dependently caused longitudinal ulcers on the mesenteric side of the middle and lower intestine lumen. The intestinal toxicity caused by S(+)-ketoprofen was significantly lower than the effect observed after racemate and R(-) enantiomer treatments (P <0.001), though the bioinversion of R(-)-ketoprofen to S(+)-enantiomer that occurs in the rat has to be considered. XO activity was unaffected by the studied drugs. Enhanced enteropathy by the racemate and its R (-)-enantiomer was correlated with a significant increase of MPO activity as an index of neutrophil infiltration, and a decrease in SOD activity (p<0.05 Vs control). S(+)-ketoprofen did not significantly change these parameters. CONCLUSIONS: These results suggest that reactive oxygen metabolites can contribute significantly to the development of intestinal lesions, and that R(-)-ketoprofen present in racemic preparations can enhance the toxic intestinal effects of S (+)-enantiomer via modification of neutrophil migration and oxidative stress.

Administration, Oral↗
PubMed2000

Latex sensitization in children with spina bifida: follow-up comparative study after two years.

BACKGROUND: Previous findings suggest that sensitization to latex in children with spina bifida is a dynamic process. OBJECTIVE: To study if changes appear in the sensitization status after withdrawal of latex. METHODS: We studied a consecutive sample of 68 children with spina bifida, by means of latex skin prick tests and quantification of serum latex-specific IgE on two separate occasions two years apart. RESULTS: Forty-four (65%) were classified as nonsensitized, 6 (9%) showed indeterminate results, and 18 (26%) were sensitized to latex, six of whom had clinical reactions to latex. They were instructed to avoid latex. In a second evaluation, 2 years later, 38 (56%) were classified as nonsensitized, 3 (4%) as indeterminate, and 27 (40%) as sensitized to latex, 11 of whom had presented latex symptoms. This meant 22% of spina bifida children demonstrated progressive sensitization, in spite of having adopted a latex-free environment at our hospital. It illustrates the progressive character of latex sensitization in these patients. CONCLUSION: Latex avoidance measures both in the medical and home settings must be stressed. We recommend that children with spina bifida should be periodically evaluated regarding latex sensitization.

Adolescent↗
PubMed2000

HLA haplotypes are associated with differential susceptibility to Trypanosoma cruzi infection.

We explored a possible role of HLA class II genes in determining the susceptibility to Trypanosoma cruzi infection as well as in the development of chagasic heart disease in a rural mestizo population from Arequipa (Southern Peru). HLA-DRB1 and DQB1 polymorphisms were determined in 85 seropositive (asymptomatic, n=52; cardiomyopathic, n=33) and 87 seronegative individuals. We observed that the DRB1*14-DQB1*0301 haplotype correlates with not having T. cruzi infection in a highly endemic area (OR= 0.26 (0.124.63); Pc=0.01). This protective association is a dominant trait. We found no differences in the allelic or haplotypic distributions we examined between asymptomatic and cardiomyopathic patients in this population. Our data offer indirect but compelling evidence that polymorphism in HLA region is involved in a differential susceptibility to T. cruzi chronic infection.

Adolescent↗
PubMed2000

HLA class I and class II allele distribution in the Peruvian population.

The distribution of HLA-A, -B, -C, -DRB1 and -DQB1 alleles in the Peruvian population was studied and compared with those of other populations in order to provide further information about their anthropological origin. Our data are consistent with the Mestizo character of this population. In terms of genetic distance Peruvians are closest to Bolivians, which is in agreement with the geographical location and the cultural and anthropological background of the two human groups. Several HLA-B alleles originally described in genetically isolated Amerindian tribes are also present in the sample studied here. This fact and the reported finding of these alleles in several Amerindian groups suggests that they were present in the first wave of humans that populated South America (Paleoindians) before they split to give rise to the different South American tribes.

Asian People↗
PubMed2000

IL-6 promoter polymorphisms in rheumatoid arthritis.

We investigated the possible association between the IL-6 promoter polymorphisms, at positions -622 and -174, and susceptiblity to, and/or outcome of, rheumatoid arthritis (RA). A total of 163 patients with RA and 157 healthy controls were genotyped for IL-6 using a PCR-RFLP method. The -622 and -174 alleles were in complete linkage disequilibrium. No difference was observed in the distribution of IL-6 promoter genotype or allele frequencies between RA patients and controls. However, a significant difference in the mean age at disease onset between IL-6 genotypes was observed. The present data appear to rule out an important role of IL-6 promoter polymorphisms in the susceptibility to RA. However, IL-6 genotypes may contribute to the pathogenesis of the disease by influencing the age at disease onset.

Adult↗
PubMed2000

The search of latex sensitization in spina bifida: diagnostic approach.

BACKGROUND: Sensitization to latex has become a major problem in children with spina bifida. Life-threatening reactions may occur in these patients, therefore the search of latex sensitization must be an active task in all of these children. OBJECTIVE: To design an approach for the diagnosis of latex sensitization in children with spina bifida. METHODS: We studied 100 consecutive unselected patients. Skin prick tests with a commercial latex extract were performed, latex-specific serum immunoglobulin (Ig) E was determined by CAP test, and risk factors were studied. Originally, patients with an area of latex skin test > 50% of the area of histamine and/or CAP class > or = 3 were considered sensitized to latex. Diagnostic tests were also performed in a control group of 51 atopic and nonatopic children. RESULTS: After performing a receiver-operating characteristics curve for both tests we recommend skin tests > 25% of the area of histamine (sensitivity - SEN = 79%, specificity - SPE = 100%, positive predictive value - PPV = 100%, negative predictive value - NPV = 90%), or CAP class > or = 2 (SEN = 88%, SPE = 100%, PPV = 100%, NPV = 94%) as diagnostic cut-off points. The anamnesis had a SEN of 44% for diagnosis, and a SPE of 100%. Latex sensitization was associated with more than 5 operations (OR = 8, 95% CI = 3-21.3), a personal history of atopy (OR = 11.5, 95% CI = 2.3-57.1), and serum total IgE > or = 2 z-units (OR = 4, 95% CI = 1. 6-10). CONCLUSION: For the routine evaluation of children with spina bifida, we propose a diagnostic algorithm with skin prick tests as a first step and CAP second.

Child↗