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Biomedical subjects

C Monteiro

Publications and source records attributed to C Monteiro.

At least 37 records · Page 2Linked to original sources

Mechanisms underlying degeneration of cryopreserved vascular homografts.

OBJECTIVE: To analyze the mechanism(s) underlying homograft degeneration, we designed an experimental model in which the behavior of cryopreserved autografts and homografts, as well as fresh autografts, implanted in the same animal was compared. METHODS: A cryopreserved homograft was implanted in the aorta of 14 sheep. The excised aortic autologous segment was then subjected to cryopreservation, and 1 to 8 weeks later it was implanted 1 to 2 cm below the cryopreserved homograft. The intermediate segment of the native aorta, the fresh autograft, was dissected at this point. Animals were put to death at different times and the implanted segments were harvested together with a portion of native aorta. Histologic and immunohistochemical analyses, as well as cell viability assessments, were then performed on the explanted segments. Similar studies were also conducted on fragments of cryopreserved autografts and homografts before implantation. RESULTS: With the exception of a partial loss of the endothelium, cryopreserved specimens retained cell viability and morphologic integrity before implantation. Explanted cryopreserved homografts showed profound changes affecting all strata, as well as a decline in cell viability. Lymphocyte infiltrates were found up to 12 months after implantation. Endothelium was always absent in cryopreserved homografts. However, a reendothelialization of the cryopreserved autografts was observed. After an initial period of neuronal degeneration, reenervation of the cryopreserved autograft segment occurred 6 to 12 months after the operation. Findings regarding the fresh autografts were similar to those of the cryopreserved autografts. CONCLUSION: Our results suggest that the immunologic reaction rather than the cryopreservation process is responsible for the degenerative process occurring in cryopreserved homografts.

Animals↗

Genetic and environmental factors regulating blood pressure in childhood: prospective study from 0 to 3 years.

OBJECTIVES: Blood pressure (BP) regulation depends on the interaction between multiple environmental and genetic factors. Of these, BP sensitivity to dietary sodium intake has been one that has been investigated in adults but not in children. The aim of the present study was to investigate, prospectively, the BP profile in relation to different genetic and hormonal factors, in the first 3 years of life. POPULATION AND METHODS: Thirty-nine children born at term following normal pregnancies, with uncomplicated neonatal periods, were randomly selected to take part in the study. BP, weight and length were evaluated every 3 months from birth to 3 years. At the age of 12 months, haptoglobin phenotypes and plasma active renin concentration were determined as well as random urine evaluation of aldosterone, cAMP, dopamine and digoxin-like immunoreactive substances (DLIS). Family history of cardio-vascular diseases was also recorded. RESULTS: Systolic BP (SBP) demonstrated a gradual increase until the age of 6 months with little variation up to 36 months. Tracking of SBP values was also observed from the first year as infants with high values (above the 75 percentile) maintained this tendency up to, at least, the age of 36 months. The comparison between SBP and diastolic BP (DBP) according haptoglobin phenotypes demonstrated that SBP was systematically higher in allele 1, with apparently an increasing tendency with age, although the differences did not have statistical significance. The comparative study between haptoglobin phenotypes, with correction for the covariates fractional excretion of sodium and potassium, showed that allele 1 carriers had significantly lower plasma renin and urine aldosterone and cAMP concentrations than allele 2, but dopamine excretion was found to be higher in allele 1 than in allele 2. There were no differences among variables relating to family history of cardiovascular disease. CONCLUSIONS: There was an early tracking process of BP values from the first 6 months of life which persists through, at least, to the age of 36 months. Differences in sodium handling between haptoglobin 1 and 2 phenotypes were already present in early childhood, although no significant repercussion in BP values could be demonstrated in the 3-year duration of this study.

Age Factors↗

Glutathione S-transferase mu polymorphism and susceptibility to lung cancer in the Portuguese population.

Epidemiological studies have led to the suggestion that a genetic basis may exist in the individual variation in predisposition to cancer. Interindividual differences in human toxicological response to carcinogenic exposure have been attributed to heritable polymorphisms in metabolism, namely glutathione S-transferases (GSTs) coding for enzymes that are known to be detoxifiers of carcinogens. Within the human GST mu class, there is a specific isozyme that is frequently lacking. To check whether or not this association exists in the Portuguese population with lung cancer, we used polymerase chain reaction (PCR)-based genotyping to examine GSTM1 polymorphism (nulled and non-nulled) in 84 individuals as a control healthy population and a group of 98 lung cancer patients. In this study we were able to find a frequency of the GSTM1 phenotype among our healthy control subjects consistent with earlier genotyping studies in other Caucasoid populations. For the group of individuals with lung cancer as a whole, or in subsets of histological subtypes, our data for the Portuguese population did not show a positive correlation between the null allele and this neoplasm. In contrast, we found a slight increase in the frequency of the wild-type allele in our lung cancer group.

Carcinoma, Small Cell↗

APC intragenic haplotypes in familial adenomatous polyposis.

Genetic epidemiological studies are useful for the knowledge of the association of markers and genes involved in diseases. In the present work, we studied the frequency of four adenomatous polyposis coli intragenic RFLP markers often used in risk evaluation in a population of 10 familial adenomatous polyposis patients from 10 unrelated Portuguese familial adenomatous polyposis families not sharing the same mutation, and in a population of 55 unrelated healthy Portuguese volunteers. We compared the frequency obtained to normal and affected populations and to results already reported in other populations. We observed allelic frequencies for the Portuguese population that agree with the published ones. The intragenic polymorphisms show strong gametic disequilibrium suggesting little recombination between them. We observed haplotype frequencies significantly different in patients and controls. The gametic disequilibrium may be due to a common founder for a proportion of apparently unrelated probands.

Adenomatous Polyposis Coli↗

Damage to UV-sensitive cells by short UV in photographic flashes.

Light emitted by electronic photographic flash units is shown to damage bacteria and human skin fibroblasts deficient in repair systems, with survival curves very similar to those produced by 254 nm short UV. The lesions induced by these flashes are as photorepairable by the photolyase enzyme as those induced by 254 nm UV and result in equivalent survival rates. Biological dosimetry performed with microorganisms highly sensitive to UV (Escherichia coli K12 AB2480, deficient in excision and recombinational-dependent repair systems and Bacillus subtilis UVSSP spores, deficient in excision and in a specific spore repair process) revealed that each 1 ms flash of light from the photographic unit used in this work contained the equivalent of 0.25 J m-2 of 254 nm UV, when measured at a distance of 7.0 cm. This dose of UV was found to be lethal to both repair-deficient E. coli bacteria and repair-deficient human skin fibroblasts obtained from xeroderma pigmentosum donors, as well as mutagenic in B/r wild-type and HCR-mutant bacteria.

Bacillus subtilis↗

Presymptomatic diagnosis in Portuguese FAP families using intragenic RFLPs and (CA)n flanking markers by fluorescence based semiautomated DNA analysis.

Owing to the large size of the APC gene, responsible for familial adenomatous polyposis, direct screening for individual mutations is not a practical approach. In the present study we establish the methodology of fluorescence based semi-automated DNA analysis to perform presymptomatic diagnosis of members at risk from 11 Portuguese FAP families with three (CA)n markers flanking the APC gene, MBC, CB26, and YN5.64, and four intragenic RFLPs. Haplotypes were constructed on the basis of individual genotypes and their segregation through generations were followed. The study was informative for 12% of subjects using only intragenic RFLPs and increased to 90% when we used the three (CA)n flanking markers. We report two of the 11 families under study in our laboratory and show recombinant events leading to a precise localisation of the CB26 marker between D5S82 and the APC gene. In one family there was a loss of (CA) units of one allele of the CB26 marker from an unaffected mother to her son.

Adenomatous Polyposis Coli↗

Histologic and genetic assessment of explanted allograft valves.

A possible way of analyzing the immune response triggered by the allograft and the cellular viability is to compare immunocompetent and immunosuppressed patients, such as those having valve replacement and heart transplantation, respectively. These groups differ in immunosuppression therapy, preparation methods, valve hemodynamics. In the present study, we investigated polymerase chain reaction-amplified DNA flanking hypervariable (CA)n regions obtained from valve leaflets taken from patients having valve replacement or heart transplantation and performed a histologic analyses of the cells. In addition, we assessed an autograft valve to compare the hemodynamic effects on the cellular composition of the valve leaflet. We conclude that leaflet cellularity of the heart transplantation and autograft patients is superior to that of the valve replacement patients. These differences were consistent with the occurrence of an immune response in the valve replacement group, which was prevented or abrogated by immunosuppressive therapy administered to the heart transplantation group. However, it cannot be excluded that preparation procedures have a long-term effect on the extracellular matrix, leading to deterioration of cell adhesion and homing conditions.

Adult↗

The allograft valve in heart transplantation and valve replacement. Genetic assessment of the origin of the cells by means of deoxyribonucleic acid profiles.

Assessment of the cellular origin of allograft valves is essential in comprehending their biologic behavior and in improving preparation methods. In this study we retrospectively analyzed 10 allografts obtained from patients who underwent valve replacement or heart transplantation. Histologic evaluation and deoxyribonucleic acid amplification by polymerase chain reaction technology with fluorescence labeled primers was performed on different parts of the valve leaflets. Automated analyses of the obtained amplimers showed in the heart transplantation group the presence of receptor cells interspersed with native donor cells in three cases. Preliminary results for the valve replacement group are inconclusive as yet.

Adult↗

On the mechanisms of genotoxicity and metabolism of quercetin.

Quercetin has been the subject of numerous studies on its genetic toxicity and carcinogenicity. Despite its well-proven genetic damaging activity for various genetic end-points (reverse mutations, induction of SOS functions, induction of sister chromatid exchanges, chromosomal aberrations and micronuclei), the mechanisms of genetic damage by quercetin remain, by and large, unknown. The present study aims to further extend the observations on the possible active oxygen species mediated DNA-damaging activity of quercetin and the role of cytochrome P450-dependent metabolism on the genotoxicity of quercetin. The results reported in this work show that quercetin can produce the OH. radical, as assessed by deoxyribose degradation in the presence of Fe3+/EDTA (ethylenediaminetetraacetic acid), and that it induces strand breakage in isolated plasmidic DNA (pUC18). The data support the hypothesis that the production of OH. is mediated by H2O2. The results with genetically engineered V79 cells expressing rat cytochromes 1A1, 1A2 and 2B1 failed to demonstrate metabolism of quercetin, as indicated by the fact that neither an enhancement nor a decrease in the genotoxicity of quercetin was observed. Results obtained on the pH dependence of the induction of chromosomal aberrations by quercetin in V79 cells show that, as the pH value of the medium is increased to 8.0, there is a significant increase in the number of aberrant cells, as expected if oxygen radicals are responsible for the formation of chromosomal aberrations.

Animals↗

Helicobacter pylori detection: a quality and cost analysis.

Histopathologic interpretation of hematoxylin and eosin (H&E)-stained endoscopic biopsies is a common method for identifying Helicobacter pylori. Few studies report the accuracy of this method, and none have compared costs of other diagnostic methods. In the clinical setting of a community hospital using standard diagnostic techniques, the purpose of this study were to determine 1) the comparative sensitivities and specificities of the H&E stain, the Warthin-Starry silver stain, the Giemsa stain, and the CLOtest; 2) the sensitivity and specificity of an "experienced" pathologist in identifying H. pylori by H&E stains, compared with a rotating pathology faculty; and 3) the time to diagnosis (turnaround time) and current patient charges for each diagnostic method. Bacterial identification by the silver stain (or a combination of other tests which were likely to compensate for false-positive and false-negative silver stains) were used as the diagnostic standard in evaluating 94 consecutive cases with the following results: The H&E stain interpreted by the rotating pathology staff was the least sensitive method and one of the least specific tests that were studied. The silver and Giemsa stains were equally sensitive in identifying H. pylori; the silver stain was more specific. The CLOtest was less sensitive than the silver and Giemsa stains, but was equally specific. CLOtest was similar in sensitivity to the H&E stain examined by the "experienced" pathologist, but was more specific. An experienced pathologist was significantly more sensitive than the rotating pathologists in evaluating H&E-stained slides. Therefore, if H&E stains are used to identify H. pylori, which is a common practice, it may be advantageous to use an experienced pathologist. The CLOtest was a simple, rapid, and cost effective substitute for H&E stains in the identification of H. pylori.

Biopsy↗

The worldwide magnitude of protein-energy malnutrition: an overview from the WHO Global Database on Child Growth.

Using the WHO Global Database on Child Growth, which covers 87% of the total population of under-5-year-olds in developing countries, we describe the worldwide distribution of protein-energy malnutrition, based on nationally representative cross-sectional data gathered between 1980 and 1992 in 79 developing countries in Africa, Asia, Latin America, and Oceania. The findings confirm that more than a third of the world's children are affected. For all the indicators (wasting, stunting, and underweight) the most favourable situation--low or moderate prevalences--occurs in Latin America; in Asia most countries have high or very high prevalences; and in Africa a combination of both these circumstances is found. A total 80% of the children affected live in Asia--mainly in southern Asia--15% in Africa, and 5% in Latin America. Approximately, 43% of children (230 million) in developing countries are stunted. Efforts to accelerate significantly economic development will be unsuccessful until optimal child growth and development are ensured for the majority.

Africa↗

Systemic lupus erythematosus in a child receiving long-term interferon therapy.

Systemic lupus erythematosus (SLE) developed in a 10 1/2-year-old white boy with juvenile laryngeal papillomatosis who had been treated with interferon alfa-n1 for 7 years. His age, gender, and fast recovery after discontinuation of interferon therapy and institution of appropriate treatment for SLE are compatible with a diagnosis of drug-induced SLE. Autoimmune disorders may occur as a complication of interferon therapy.

Autoimmune Diseases↗

Tracheal agenesis.

Tracheal agenesis is a rare congenital anomaly. We report a case and review the cases previously reported. Clinical features that might indicate tracheal agenesis include antenatal polyhydramnios, severe respiratory distress, absence of an audible cry, failure to advance an endotracheal tube beyond the larynx, a palpable distal trachea, clinical improvement after esophageal intubation, and roentgenographic absence of a tracheal air column with an abnormal position of the carina. For immediate management of the affected infant, we recommend intubation of the esophagus with an endotracheal tube to provide an air passage, and determination of the level of the defect by careful use of contrast material and roentgenography. Infants having type I tracheal agenesis may benefit from immediate tracheostomy.

Bronchial Fistula↗

Linkage of hereditary motor and sensory neuropathy type I to the pericentromeric region of chromosome 17.

Vance et al. have reported linkage of hereditary motor and sensory neuropathy type I (HMSN I) to the pericentromeric region of chromosome 17. We have studied eight families with HMSN I (also called the hypertrophic form of Charcot-Marie-Tooth disease) for linkage of the disease locus to polymorphic loci in the centromeric region of chromosome 17. Linkage has been confirmed for D17S58 (EW301) with a maximum lod score of 5.89 at theta = 0.08 and for D17S71 (pA10-41) with a maximum lod score of 3.22 at theta = 0.08. EW301 is on 17p, 5.5 centimorgans from the centromere. Two families, previously reported as being linked to the Duffy blood group locus on chromosome 1, were included in this study, and one now provides positive lod scores for chromosome 17 markers. There was no evidence of heterogeneity.

Charcot-Marie-Tooth Disease↗

The frequency and origin of the sickle cell mutation in the district of Coruche/Portugal.

The frequency of the beta S mutation in the district of Coruche/Portugal is estimated to be about 4% from analysis of a group of 181 school children and their teachers in an area in which malaria has been endemic until recently. Several white Portuguese patients with sickle cell disease (six homozygous SS and one S beta degree thalassaemia) were found in a group of 309 further patients who were known and followed up by local medical practitioners. These patients had clinical and haematological features similar to patients of African origin, although their growth and sexual development appeared to be normal. The analysis of an array of polymorphic restriction sites within the beta S globin gene cluster (beta S haplotype) showed patterns that are known to occur in Africa. The frequencies of the three main African beta S haplotypes termed Senegal, Bantu, and Benin reflect the extent of Portuguese naval explorations. It is concluded that the sickle cell gene in Portugal has probably been imported from Africa and has been amplified in comparison with other genes characteristic for African races because of the selective advantage of AS heterozygotes in an area endemic for malaria.

Adolescent↗

Oxidative stress in trisomy 21. A possible role in cataractogenesis.

Previous studies have suggested that free radicals and related species play a role in lens damage. The molecules involved may include proteins, lipids and DNA. Focal cortical changes and cortical liquefaction have been reported in patients with Down's syndrome over the age of 15 years. There is evidence supporting the hypothesis that trisomy 21 patients have an increase in free radical reactions and lipoperoxidation susceptibility. This could be due to an increase in the H2O2 generation catalysed by CuZn SOD although the activity of other gene products coded for on chromosome 21 cannot be excluded. Thiobarbituric acid reactive products were measured in human erythrocytes of nine DS patients and nine age-matched controls. There was a significant increase in the first group (21.0 +/- 2.3 nmol MDA/g Hb vs 16.4 +/- 2.9 nmol MDA/g Hb; p less than or equal to 0.01). In plasma, however, TBA products and antioxidant levels (ascorbic acid, tocopherol and uric acid) were not significantly different. Further studies should be carried out, namely through the use of more specific and sensitive methods, to assess the possible association between oxidative stress and cortical lens damage in DS patients.

Adolescent↗