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Biomedical subjects

M Rios

Publications and source records attributed to M Rios.

At least 37 records · Page 2Linked to original sources
PubMed2000

Cell typing the sensitized transfusion-dependent patient.

Extended red cell typing is required for the management of transfusion-dependent patients to confirm the identity of suspected alloantibodies or determine the specificity of potential additional antibodies that may be formed in the future. Typing may be complicated by the presence of circulating allogeneic cells or a positive direct antiglobulin test. Phenotyping such individuals by hemagglutination is dependent on the separation of a reticulocyte-enriched fraction by differential centrifugation. Flow cytometric typing of reticulocytes is also possible. The effectiveness of these techniques is limited in those who are heavily transfused or have low reticulocyte counts. Heavily transfused patients with sickle cell anemia may be typed, however, following hypotonic lysis of allogeneic cells. In patients with a positive direct antiglobulin test, sensitized cells are usually typed with either direct agglutinating antisera and/or IgG antisera following elution of the autoantibody. Inactivation of some antigens during the elution process or the lack of some antisera specificities limit such typing. By designing appropriate oligonucleotide primers, polymerase chain reaction (PCR) amplification of target gene sequences for most blood group systems and the identification of a large number of their allelic specificities is now possible. Peripheral blood leukocytes can be used as the DNA source. Restriction fragment length polymorphism determination is widely adopted for the identification of allelic specificity of the amplified target sequence. Alternate strategies, including allele-specific PCR, are often employed if the genetic basis of the polymorphism is more complex than a single nucleotide substitution, or if it does not create or ablate a restriction endonuclease cleavage site. These techniques may permit genotyping of sensitized transfusion-dependent patients, and can improve transfusion safety and efficacy.

Blood Group Antigens↗
PubMed1999

Geographic diversity of adult t-cell leukemia/lymphoma in Brazil. The Brazilian ATLL Study Group.

We describe 195 cases of adult T-cell leukemia/lymphoma (ATLL) reported to the national registry of T-cell malignancies in Brazil between 1994 and 1998. We compared the effect of demographic differences and clinical features of 150 consecutive ATLL cases in different regions of this diverse country. At diagnosis, the predominant clinical sub-type was the acute type (60%), followed by lymphoma (22%), chronic (10%) and smoldering (8%) types. Although we expected that different sub-types would be present in different regions, on the basis of immunogenetic factors determined by ethnicity, we did not demonstrate these differences. There were no significant differences among ATLL subtypes by age or gender. No ethnic group predominated in the total population of patients, but significant differences were noted when examining ethnic distribution by region. Reflecting the general population distribution, white patients were seen more often in São Paulo and black patients in Bahia, than in other regions. In most regions, cases were equally distributed between blacks and mulattos, except in Pernambuco, where blacks were less frequent. The main clinical features were lymphadenopathy, skin lesions, hypercalcemia and hepatomegaly. Fourteen patients (9%) suffered from HTLV-I-associated myelopathy (HAM/TSP), either at diagnosis or during follow-up of ATLL. All cases but one had antibodies to HTLV-I, with concordant results with ELISA, WB and PCR analyses. For the antibody-negative case, pol and tax gene sequences were present in tumor cells when subjected to PCR analyses. The prognosis was generally poor, suggesting that the disease in Brazil behaves in similar fashion regardless of ethnic or geographical differences.

Adolescent↗
PubMed1999

An inverse correlation of HTLV-I viral load in CSF and intrathecal synthesis of HTLV-I antibodies in TSP/HAM.

The authors measured human T-cell lymphotrophic virus type I (HTLV-I) proviral load and intrathecal synthesis of antibodies to HTLV-I in CSF of 13 Brazilian patients with tropical spastic paraparesis/ HTLV-I-associated myelopathy (HAM). The authors also measured HTLV-I proviral load in peripheral blood mononuclear cells of five of these patients and found that it was 10- to 100-fold higher than that in CSF cells. The combination of HTLV-I proviral load and intrathecal synthesis of antibodies to HTLV-I appears to be a useful marker of disease progression. Patients with high viral load and no intrathecal synthesis of antibodies to HTLV-I had more rapidly progressing, serious clinical disease.

Adult↗
PubMed1999

Catecholamine synthesis is mediated by tyrosinase in the absence of tyrosine hydroxylase.

Catecholamine neurotransmitters are synthesized by hydroxylation of tyrosine to L-dihydroxyphenylalanine (L-Dopa) by tyrosine hydroxylase (TH). The elimination of TH in both pigmented and albino mice described here, like pigmented TH-null mice reported previously (Kobayashi et al., 1995; Zhou et al., 1995), demonstrates the unequivocal requirement for catecholamines during embryonic development. Although the lack of TH is fatal, TH-null embryos can be rescued by administration of catecholamine precursors to pregnant dams. Once born, TH-null pups can survive without further treatment until weaning. Given the relatively rapid half-life of catecholamines, we expected to find none in postnatal TH-null pups. Despite the fact that the TH-null pups lack TH and have not been supplemented with catecholamine precursers, catecholamines are readily detected in our pigmented line of TH-null mice by glyoxylic acid-induced histofluorescence at postnatal day 7 (P7) and P15 and quantitatively at P15 in sympathetically innervated peripheral organs, in sympathetic ganglia, in adrenal glands, and in brains. Between 2 and 22% of wild-type catecholamine concentrations are found in these tissues in mutant pigmented mice. To ascertain the source of the catecholamine, we examined postnatal TH-null albino mice that lack tyrosinase, another enzyme that converts tyrosine to L-Dopa but does so during melanin synthesis. In contrast to the pigmented TH-null mice, catecholamine histofluorescence is undetectable in postnatal albino mutants, and the catecholamine content of TH-null pups lacking tyrosinase is 18% or less than that of TH-null mice with tyrosinase. Thus, these extraordinary circumstances reveal that tyrosinase serves as an alternative pathway to supply catecholamines.

Adrenal Glands↗
PubMed1999

Direct Evidence of Nociceptive Input to Human Anterior Cingulate Gyrus and Parasylvian Cortex.

Many lines of evidence implicate the anterior cingulate cortex (ACC, Brodmann's area 24) and parasylvian cortex in pain perception. Clinical studies demonstrate alterations in pain and temperature sensation after lesions of these structures. Imaging studies reveal increased blood flow in ACC and parasylvian cortex, both ipsilateral and contralateral to painful stimuli. Additionally, painful stimuli evoke potentials that seem to arise from these cortical structures. Short-duration cutaneous stimulation with a CO(2) laser evokes pain-related potentials (LEPs) with a vertex maximum and an initial negative peak followed by a positive wave. The cutaneous laser stimulus evokes a pure pain sensation due to selective activation of cutaneous nociceptors. Electrical source modeling has suggested that the vertex maximum of the scalp LEP arises, in part, from generators in the cingulate gyrus and parasylvian cortex. Thus, imaging and electrophysiologic studies suggest that these cortical structures are activated by painful stimuli. However, these studies incorporate multiple assumptions and therefore do not establish the presence of nociceptive inputs to ACC and parasylvian cortex. We review our recent reports of intracranial potentials evoked by painful stimuli. These studies provide direct evidence of nociceptive inputs to the human ACC and parasylvian cortex.

Journal Article↗
PubMed1999

Prevalence of childhood overweight in Northwestern Spain: a comparative study of two periods with a ten year interval.

OBJECTIVE: To determine the prevalence of overweight children and its modifications over a period of 10 y and whether changes in overweight prevalence is similar in the inland and coastal areas in our country. DESIGN: Cross-sectional study in two stages, the initial survey being in 1985 and the second in 1995. SUBJECTS: 1131 children (827 and 304 from coastal and inland areas respectively) in the initial survey, and 903 children (695 and 208 from coastal and inland areas) in the second survey, of both sexes, aged from 6 to 15 y were selected by a random process from the total school population in the Province of Pontevedra, North-western Spain. MEASUREMENTS: Overweight was defined in terms of body mass index (BMI), using Spanish standards. Children having BMI at or above the 85th percentile were classed as overweight and at or above the 95th percentile as very overweight. RESULTS: Overall prevalence of overweight and very overweight were significantly higher in the second survey than in the first, 18.1% vs 11.7%, P<0.05 for overweight prevalence and 6.8% vs 2.7%, P<0.05 for very overweight prevalence respectively. When we compared modifications in overweight prevalence over the period 10 y between the inland and coastal areas of our country, increase prevalence was observed in the inland area 9.8% vs 19.7%, P<0.05 for initial and secondary surveys respectively, whereas in the coastal area overweight prevalence remains stable, 20.2% vs 17.6%, P>0.05. CONCLUSION: An increased prevalence of overweight children of both sexes in over a period of 10 y was observed, however, this increase was particularly caused by an increased prevalence in the inland area whereas in coastal area it remained stable. We speculate that differences in overweight prevalence between both areas might be due to differences in physical activity associated with different degrees in technological development between inland and coastal areas.

Adolescent↗
PubMed1999

Clonal diversity of Chilean isolates of enterohemorrhagic Escherichia coli from patients with hemolytic-uremic syndrome, asymptomatic subjects, animal reservoirs, and food products.

To determine clonal relationship among Chilean enterohemorrhagic Escherichia coli (EHEC) strains from different sources (clinical infections, animal reservoirs, and food), 54 EHEC isolates (44 of E. coli O157, 5 of E. coli O111, and 5 of E. coli O26) were characterized for virulence genes by colony blot hybridization and by pulsed-field gel electrophoresis (PFGE). By colony blotting, 12 different genotypes were identified among the 44 E. coli O157 isolates analyzed, of which the genetic profile stx1+ stx2+ hly+ eae+ was the most prevalent. All human O157 strains that were associated with sporadic cases of hemolytic-uremic syndrome (HUS) carried both the stx1 and stx2 toxin-encoding genes and were eaeA positive. Only 9 of 13 isolates from human controls were stx1+ stx2+, and 8 carried the eaeA gene. Comparison of profiles obtained by PFGE of XbaI-digested genomic DNA showed a great diversity among the E. coli O157 isolates, with 37 different profiles among 39 isolates analyzed. Cluster analysis of PFGE profiles showed a wide distribution of clinical isolates obtained from HUS cases and asymptomatic individuals and a clonal relationship among O157 isolates obtained from HUS cases and pigs. Analysis of virulence genes showed that a correlation exists among strains with the genotype stx1+ stx2+ eae+ and pathogenic potential. A larger difference in the PFGE restriction patterns was observed among the EHEC strains of serogroups O26 and O111. These results indicate that several different EHEC clones circulate in Chile and suggest that pigs are an important animal reservoir for human infections by EHEC. Guidelines have been proposed for better practices in the slaughter of animals in Chile.

Animals↗
PubMed1999

Applications of molecular genotyping to immunohaematology.

The genes encoding 20 of the 23 blood group systems have been cloned and sequenced. This has allowed the determination of the molecular basis of many blood group antigens and phenotypes. In this review we outline the basis of the genetic code, summarise molecular events that give rise to polymorphic antigens and to blood group phenotypes, and describe how polymerase chain reaction-based techniques can be applied in the clinical setting.

Blood Group Antigens↗
PubMed1998

A novel mutation in the coding sequence of the FY*B allele of the Duffy chemokine receptor gene is associated with an altered erythrocyte phenotype.

The Duffy blood group system is of clinical and biological significance. Antibodies to Duffy antigens are responsible for some cases of transfusion incompatibility and newborn hemolytic disease. The Duffy protein is a receptor for the Plasmodium vivax erythrocyte-binding protein and is also a receptor for various chemokines (thus renamed Duffy Antigen Receptor for Chemokines [DARC]). The two Duffy polymorphic antigens, Fya and Fyb (coded by the FY*A and FY*B alleles), are present on erythrocyte membranes. The Fy(a-b-) phenotype is the predominant one in populations of black people and also occurs in other populations, including some non-Ashkenazi Jewish groups. The Fy(a-b-) phenotype has been associated with a mutation in the FY*B promoter at the GATA box that abolishes the expression of erythrocyte Duffy protein. We describe here a novel mutation, present in the FY*B coding sequence (271C --> T), that is associated with some Fy(b-) phenotypes among non-Ashkenazi Jews and among Brazilian blacks. The mutation is present in Fy(b-) individuals, who have wild-type FY*B GATA and carry the previously described 304G --> A substitution. The 271C --> T and 304G --> A can be identified by restriction enzyme-generated restriction fragment length polymorphisms. The 271C --> T substitution represents a considerable change in chemical nature (Arg91 --> Cys), one which may affect the antigenic determinants of DARC, and thus be of clinical significance. The mutation may have implications for some physiological roles of DARC and be of interest in malaria research and in studies of population genetics.

Agglutination Tests↗
PubMed1998

Increased activity of lecithin:cholesterol acyltransferase during short-term oral estrogen progestin replacement therapy in a group of postmenopausal women.

The aim of the study was to assess the short-term effect of estrogen-progestin therapy on the plasma level of lecithin: cholesterol acyltransferase ([LCAT] EC 2.3.1.43), a key enzyme in the cholesterol reverse-transport process. The trial included 21 women with at least 6 months of menopause, which was confirmed by anamnesis, physical evaluation, and follicle-stimulating hormone (FSH) determination. Women receiving pharmacological treatment or who had any kind of endocrine disorder were excluded. In addition, we evaluated and confirmed normal Papanicolaou and mammography tests in all 21 women included in the trial. They received conjugated equine estrogen 0.625 mg daily, plus cyclic medroxyprogesterone acetate (5 mg daily) for 12 days each month. Plasma levels of LCAT, cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides, apoB, and apoAI were evaluated before and after 1 and 3 months of therapy. Pretherapy and posttherapy results were analyzed statistically by Wilcoxon's rank-sum test for paired samples. No significant changes were observed either for body mass index or for blood pressure. A significant increase in plasma LCAT activity was found at the first and third month posttherapy (P < .005). In addition, after 3 months of therapy, HDL-C significantly increased (P < .005), in contrast to the significant decrease detected in total cholesterol (P < .025), LDL-C (P < .005), cholesterol to HDL-C and LDL-C/HDL-C ratios (P < .005). Triglyceride levels did not show significant modification. In conclusion, our results indicate that short-term estrogen-progestin therapy produces a significant increase in plasma LCAT activity, as well as beneficial changes in the lipid profile, in postmenopausal women.

Adult↗
PubMed1998

High prevalence of abnormal glucose tolerance and metabolic disturbances in first degree relatives of NIDDM patients. A study in Catalonia, a mediterranean community.

Our study aimed to analyse clinical and metabolic characteristics of first degree relatives of patients with non-insulin-dependent diabetes mellitus (NIDDM) in Catalonia. Two hundred and five subjects (39.8 +/- 14.2 year-old, 61% women) were included in the study. An oral glucose tolerance test (OGTT) was performed, obtaining basal plasma glucose and insulin, in order to calculate, %B (HOMA beta cell function) and %S (HOMA insulin sensitivity). A 30.7% of subjects showed an abnormal glucose tolerance, either as impaired glucose tolerance (IGT) (20.5%) or as NIDDM (10.2%). Glycaemia after the OGTT (120 min) was independently determined by fasting glycaemia and age (R2 = 0.50; P < 0.001). As expected, subjects with normal glucose tolerance (NGT) were significantly younger than IGT and NIDDM subjects. The relatives with IGT and NIDDM display more features of syndrome-X when compared to NGT. Likewise, NGT relatives were less insulin sensitive and their basal insulin levels were higher when compared with a control group of subjects without familial history of NIDDM (log %S, 3.6 +/- 0.4 vs. 3.9 +/- 0.4; P = 0.000; log-insulin 2.4 +/- 0.4 vs. 2.1 +/- 0.6 mU/l; P < 0.02). In comparison with the general population, of any age group, NIDDM and IGT were more common in those subjects with a family history of NIDDM. Interestingly, the rates, of abnormal glucose tolerance in the 55-64 and > 64 year groups in the general population were similar to those seen in relatives two decades younger. Our study not only confirms a high prevalence of impaired glucose tolerance (IGT and NIDDM) in subjects with a family history of NIDDM, but also that these abnormalities can be detected at a very early age. Globally, this piece of information corroborates that special attention and precocious detection programs should be addressed to relatives of NIDDM patients.

Adult↗
PubMed1998

Defective human T-cell lymphotropic virus type I (HTLV-I) provirus in 10 Chilean seronegative patients with tropical spastic paraparesis or HTLV-I-associated myelopathy.

We studied the presence of tax and ltr genes from human T-cell lymphotropic virus type I (HTLV-I) provirus in the peripheral blood mononuclear cells from 15 seronegative patients with tropical spastic paraparesis or HTLV-I-associated myelopathy by PCR. Only a region of the tax gene from 10 patients was amplified. The nucleotide homologies of six Chilean isolates to the ATK-1 clone ranged between 98.7 and 99.4%.

Adult↗
PubMed1998

Painful stimuli evoke potentials recorded over the human anterior cingulate gyrus.

Clinical studies of cingulotomy patients and imaging studies predict that the human cingulate gyrus might display pain-related activity. We now report potentials evoked by painful cutaneous stimulation with a CO2 laser (LEP) and recorded from subdural electrodes over the medial wall of the hemisphere. In response to facial laser stimulation on both sides, a negative (latency 211-242 ms) and then a positive wave (325-352 ms) were recorded from the cortex of right medial wall and from the falcine dura overlying the left medial wall. Medial wall LEPs were similar to scalp LEPs and were largest over the anterior cingulate and superior frontal gyri just anterior to motor cortex contralateral to the side of stimulation. These results demonstrate that there is significant direct nociceptive input to the human anterior cingulate gyrus (Brodmann's area 24).

Adult↗
PubMed1998

Painful stimuli evoke potentials recorded from the parasylvian cortex in humans.

Cutaneous stimulation of the face and hand with a CO2 laser in three awake patients evoked potentials (LEPs) recorded from the dominant left parasylvian cortex. These were recorded by means of a subdural grid of electrodes implanted for evaluation of epilepsy. Stimulation of the contralateral face resulted in waveforms consisting of a negative potential (N2, 162 +/- 5 ms; mean +/- SE) followed by a positive potential (P2, 340 +/- 18 ms). Both waves occurred at longer latency after hand than after facial stimulation. N2 and P2 potentials recorded from the grid correspond well in morphology to those recorded from the scalp in four additional patients tested with the same stimulation paradigm. The N2 waves recorded from the subdural grid occurred at significantly shorter latencies than did those recorded from the scalp (184 +/- 6 ms), but the P2 waves at the grid occurred at significantly longer latencies than did those recorded at the scalp (281 +/- 13 ms). The amplitudes of the potentials recorded from the grid were maximal over the parietal operculum both for contralateral stimulation of the face or hand and for ipsilateral stimulation of the face. Potentials also were recorded in this area after stimulation of the ipsilateral hand. The cortical distributions of these potentials suggest that their generators are located in the parietal operculum or in the insula, or in both, consistent with previous PET, magnetoencephalographic, and scalp LEP source analyses. These previous analyses provide indirect evidence of nociceptive input to parasylvian cortex because the interpretation of each analysis incorporates multiple assumptions. The present results are the first direct evidence of nociceptive input to the human parasylvian cortex.

Adult↗
PubMed1997

HTLV-I and HTLV-II infections in hematologic disorder patients, cancer patients, and healthy individuals from Rio de Janeiro, Brazil.

To clarify the seroprevalence of human T-cell lymphotropic virus type I (HTLV-I) among hematologic and cancer patients in the State of Rio de Janeiro, Brazil, we investigated sera from 2430 individuals from the following groups: 152 patients with T-cell diseases, 250 with B-cell disorders, 67 with myeloid leukemia, 41 with Hodgkin's disease, 351 with a history of multiple blood transfusions, 235 patients with solid tumors of different types, and 109 family members of HTLV-I-infected patients. Antibodies to HTLV-I were screened by enzyme-linked immunosorbent assay or particle agglutination assays (or both). Repeatedly reactive samples were tested by Western blot and polymerase chain reaction assay to differentiate HTLV-I from HTLV-II. We found an increased seroprevalence rate of HTLV-I among those with lymphoid malignancies, mainly in T-cell diseases (28.9%), and these results were important in characterizing 44 cases of adult T-cell leukemia/lymphoma. We confirmed the presence of HTLV-I and HTLV-II infections in blood donors (0.4% and 0.1%, respectively), in patients exposed to multiple blood transfusions (10.2% and 0.8%, respectively), and in 30 (27.5%) of 109 family members of HTLV-I- or HTLV-II-infected patients. We also confirmed the high rate occurrence of adult T-cell leukemia/lymphoma among lymphoproliferative disorders in Rio de Janeiro, Brazil.

Adolescent↗