Laura Rocha

Childhood obesity prevalence is rising and new therapeutical approaches are needed. Metformin is likely beneficial in obese and/or insulin-resistant children/adolescents, but its role in this setting is still unclear. We aimed to evaluate the effectiveness, in terms of weight loss and insulin resistance, and safety of metformin in nondiabetic overweight/obese children and adolescents. We retrospectively reviewed clinical records of 78 nondiabetic obese/overweight [body mass index (BMI)≥85th/95th percentile for age and sex] children and adolescents. Anthropometric and metabolic outcomes of 39 patients treated with metformin (mean daily dose: 1.3±0.5 g) were analyzed and compared to lifestyle intervention alone at different follow-up times (12 and 24 months). The mean age of the 78 patients was 13.3 years, 41 were females and mean BMI and BMI-SDS were 32.8 kg/m2 and 3.1, respectively. There was a decrease in mean BMI-SDS within each treatment group in all periods, except at 24 months ...

ABSTRACT Background: Obesity in children has been increasing dramatically, with a significant increase in cardiovascular and metabolic diseases risk. The role of thyroid dysfunction has been extensively analyzed in obese adults, but to a limited extent in children. Aims: To estimate the prevalence of hyperthyrotropinemia in obese children and to analyze the influence of BMI–SDS and TSH in other metabolic variables. Methods: Retrospective study with data from the first evaluation of obese children in our clinic. Demographic, anthropometric and metabolic variables were studied. Descriptive analysis consisted of frequencies distribution for qualitative variables and mean±S.D. for continuous variables. For the association between BMI–SDS, thyroid function and other metabolic variables multiple linear regression models were used. A P value ≤0.05 was considered for statistical significance. Results: We obtained data from 348 children with mean age of 11.7±3.1 years and mean BMI–SDS of 2.9±0.7. The prevalence of hyperthyrotropinemia was 8.9% and of homeostasis model assessment-insulin resistance (HOMA-IR) elevation was 69.3%. Children with hyperthyrotropinemia revealed fT3 and HOMA-IR significantly higher than those with normal serum values. BMI–SDS was positively correlated with TSH and fT4 but not with fT3, when controlled for sex, age and pubertal stage. BMI–SDS and TSH were positively and independently correlated with HOMA-IR, but not with the lipids. Conclusions: The prevalence of hyperthyrotropinemia was similar to that reported in other studies and appeared to be influenced by metabolic factors other than fT3 or TRH. Children with hyperthyrotropinemia had significantly higher fT3 and HOMA-IR. BMI–SDS was positively correlated with TSH, fT4 and HOMA-IR. TSH and BMI–SDS were positively and independently correlated with HOMA-IR, which suggests that hyperthyrotropinemia might exacerbate insulin resistance in obese children.

The most prevalent physiological effects of ANG II, the main product of the renin-angiotensin system, are mediated by the AT1 receptor, a rhodopsin-like AGPCR. Numerous studies of the cardiovascular effects of synthetic peptide analogs allowed a detailed mapping of ANG II's structural requirements for receptor binding and activation, which were complemented by site-directed mutagenesis studies on the AT1 receptor to investigate the role of its structure in ligand binding, signal transduction, phosphorylation, binding to arrestins, internalization, desensitization, tachyphylaxis, and other properties. The knowledge of the high-resolution structure of rhodopsin allowed homology modeling of the AT1 receptor. The models thus built and mutagenesis data indicate that physiological (agonist binding) or constitutive (mutated receptor) activation may involve different degrees of expansion of the receptor's central cavity. Residues in ANG II structure seem to control these conformational changes and to dictate the type of cytosolic event elicited during the activation. 1) Agonist aromatic residues (Phe8 and Tyr4) favor the coupling to G protein, and 2) absence of these residues can favor a mechanism leading directly to receptor internalization via phosphorylation by specific kinases of the receptor's COOH-terminal Ser and Thr residues, arrestin binding, and clathrin-dependent coated-pit vesicles. On the other hand, the NH2-terminal residues of the agonists ANG II and [Sar1]-ANG II were found to bind by two distinct modes to the AT1 receptor extracellular site flanked by the COOH-terminal segments of the EC-3 loop and the NH2-terminal domain. Since the [Sar1]-ligand is the most potent molecule to trigger tachyphylaxis in AT1 receptors, it was suggested that its corresponding binding mode might be associated with this special condition of receptors.

At the rat motor endplate, pre-synaptic facilitatory adenosine A2A and muscarinic M1 receptors are mutually exclusive. We investigated whether these receptors share a common intracellular signalling pathway. Suppression of McN-A-343-induced M1 facilitation of [3H]ACh release was partially recovered when CGS21680C (an A2A agonist) was combined with the cyclic AMP antagonist Rp-cAMPS. Forskolin, rolipram and 8-bromo-cyclic AMP mimicked CGS21680C blockade of M1 facilitation. Both Rp-cAMPs and nifedipine reduced augmentation of [3H]ACh release by McN-A-343 and CGS21680C. Activation of M1 and A2A receptors enhanced Ca2+ recruitment through nifedipine-sensitive channels. Nifedipine inhibition revealed by McN-A-343 was prevented by chelerythrine (a PKC inhibitor) and Rp-cAMPS, suggesting that Ca(v)1 (L-type) channels phosphorylation by PKA and PKC is required. Rp-cAMPS inhibited [3H]ACh release in the presence of phorbol 12-myristate 13-acetate, but PKC inhibition by chelerythrine had no effect on release in the presence of 8-bromo-cyclic AMP. This suggests that the involvement of PKA may be secondary to M1-induced PKC activation. In conclusion, competition of M1 and A2A receptors to facilitate ACh release from motoneurons may occur by signal convergence to a common pathway involving PKA activation and Ca2+ influx through Ca(v)1 (L-type) channels.

The harmonisation of food composition databases (FCDB) has been a recognised need among users, producers and stakeholders of food composition data (FCD). To reach harmonisation of FCDBs among the national compiler partners, the European Food Information Resource (EuroFIR) Network of Excellence set up a series of guidelines and quality requirements, together with recommendations to implement quality management systems (QMS) in FCDBs. The Portuguese National Institute of Health (INSA) is the national FCDB compiler in Portugal and is also a EuroFIR partner. INSA's QMS complies with ISO/IEC (International Organization for Standardisation/International Electrotechnical Commission) 17025 requirements. The purpose of this work is to report on the strategy used and progress made for extending INSA's QMS to the Portuguese FCDB in alignment with EuroFIR guidelines. A stepwise approach was used to extend INSA's QMS to the Portuguese FCDB. The approach included selection of reference standards and guides and the collection of relevant quality documents directly or indirectly related to the compilation process; selection of the adequate quality requirements; assessment of adequacy and level of requirement implementation in the current INSA's QMS; implementation of the selected requirements; and EuroFIR's preassessment 'pilot' auditing. The strategy used to design and implement the extension of INSA's QMS to the Portuguese FCDB is reported in this paper. The QMS elements have been established by consensus. ISO/IEC 17025 management requirements (except 4.5) and 5.2 technical requirements, as well as all EuroFIR requirements (including technical guidelines, FCD compilation flowchart and standard operating procedures), have been selected for implementation. The results indicate that the quality management requirements of ISO/IEC 17025 in place in INSA fit the needs for document control, audits, contract review, non-conformity work and corrective actions, and users' (customers') comments, complaints and satisfaction, with minor adaptation. Implementation of the FCDB QMS proved to be a way of reducing the subjectivity of the compilation process and fully documenting it, and also facilitates training of new compilers. Furthermore, it has strengthened cooperation and trust among FCDB actors, as all of them were called to be involved in the process. On the basis of our practical results, we can conclude that ISO/IEC 17025 management requirements are an adequate reference for the implementation of INSA's FCDB QMS with the advantages of being well known to all members of staff and also being a common quality language among laboratories producing FCD. Combining quality systems and food composition activities endows the FCDB compilation process with flexibility, consistency and transparency, and facilitates its monitoring and assessment, providing the basis for strengthening confidence among users, data producers and compilers.

To evaluate the relationships between depression and ageing, nutrition, and selected haematologic variables. A cross-sectional study was performed in elderly institutionalized patients (n=100) of all nursing homes in the Brazilian city of Uberlandia, with determination of the Geriatric Depression Scale (GDS) and the Mini-Nutritional Assessment (MNA) scores, and selected haematologic variables. GDS had a significant negative dependence with the MNA for the entire institutionalized population. The prevalence of depression was higher among females, but significant correlations existed between GDS scores and erythrocytes counts, haemoglobin levels, or haematocrit values for the males only. However, a borderline correlation existed between GDS and the mean corpuscular volume (MCV) values in the females. Depression was associated with worsening of nutritional status and the degree of anemia of the entire elderly population and the male, but not the female subjects. The borderline correlation observed between the GDS and MCV for the female subjects suggests that the nutritional deficiencies responsible for the MCV increase are a cause, and not an effect, of depression.

The mechanisms underlying improvement of neuromuscular transmission deficits by glucocorticoids are still a matter of debate despite these compounds have been used for decades in the treatment of autoimmune myasthenic syndromes. Besides their immunosuppressive action, corticosteroids may directly facilitate transmitter release during high-frequency motor nerve activity. This effect coincides with the predominant adenosine A2A receptor tonus, which coordinates the interplay with other receptors (e.g. muscarinic) on motor nerve endings to sustain acetylcholine (ACh) release that is required to overcome tetanic neuromuscular depression in myasthenics. Using myographic recordings, measurements of evoked [(3)H]ACh release and real-time video microscopy with the FM4-64 fluorescent dye, results show that tonic activation of facilitatory A2A receptors by endogenous adenosine accumulated during 50 Hz bursts delivered to the rat phrenic nerve is essential for methylprednisolone (0.3 mM)-induced transmitter release facilitation, because its effect was prevented by the A2A receptor antagonist, ZM 241385 (10 nM). Concurrent activation of the positive feedback loop operated by pirenzepine-sensitive muscarinic M1 autoreceptors may also play a role, whereas the corticosteroid action is restrained by the activation of co-expressed inhibitory M2 and A1 receptors blocked by methoctramine (0.1 μM) and DPCPX (2.5 nM), respectively. Inhibition of FM4-64 loading (endocytosis) by methylprednisolone following a brief tetanic stimulus (50 Hz for 5 s) suggests that it may negatively modulate synaptic vesicle turnover, thus increasing the release probability of newly recycled vesicles. Interestingly, bulk endocytosis was rehabilitated when methylprednisolone was co-applied with ZM241385. Data suggest that amplification of neuromuscular transmission by methylprednisolone may involve activation of presynaptic facilitatory adenosine A2A receptors by endogenous adenosine leading to synaptic vesicle redistribution.

In Brazil, resolution 196/96 and its amendments regulate the preservation of rights, respect and dignity of human beings involved in research. To analyze the adequacy of Free Communications (FC) presented during the XVIII Congresso Pernambucano de Cardiologia to resolution 196/96. During a cross-sectional study, interviews were carried out with the authors of the FC presented at the Congress and the abstracts of the studies were assessed in order to identify the need for previous approval by a Research Ethics Committee (REC). A total of 90 FC were presented and, in most of them (86.8%), medical files were the most commonly used source of data. Only 23.1% of the FC were submitted to the assessment of a REC and 15.4% of them used a Free and Informed Consent Form (FICF). Among the authors whose studies were not assessed by a REC, 65.6% stated that this conduct was not necessary and 18% of them were unaware of the need to submit the study to such assessment. The written authorization given by the institution where the FC were carried out was not obtained in 56.6% of the studies. Most of the authors (80.0%) stated that they had never read Resolution 196/96. The proportion of FC submitted to a REC was significantly higher among authors that had read Resolution 196/96 (p = 0.005). The FC design influenced the non-submission of the studies to a REC (p < 0.001). Most of the FC that were authorized by the institution where they were carried out were submitted to a REC (p < 0.001). Most of the FC presented at the Congress did not follow the Brazilian regulations concerning the ethics in research.

AMP dephosphorylation via ecto-5′-nucleotidase/CD73 is the rate limiting step to generate extracellular adenosine (ADO) from released adenine nucleotides. ADO, viaA2Areceptors (A2ARs), is a potent modulator of neuromuscular and immunological responses. The pivotal role of ecto-5′-nucleotidase/CD73, in controlling extracellular ADO formation, prompted us to investigate its role in a rat model of experimental autoimmune myasthenia gravis (EAMG). Results show that CD4+CD25+FoxP3+regulatory T cells express lower amounts of ecto-5′-nucleotidase/CD73 as compared to controls. Reduction of endogenous ADO formation might explain why proliferation of CD4+T cells failed upon blockingA2Areceptors activation with ZM241385 or adenosine deaminase in EAMG animals. Deficits in ADO also contribute to neuromuscular transmission failure in EAMG rats. Rehabilitation ofA2AR-mediated immune suppression and facilitation of transmitter release were observed by incubating the cells with the nucleoside precur...

Dengue virus (DENV; Genus Flavivirus, Family Flaviviridae) has been circulating in Brazil since at least the mid-1980s and continues to be responsible for sporadic cases of Dengue fever and Dengue hemorrhagic fever throughout this country. Here, we describe the full genomes of two new Brazilian DENV-serotype 1 (DENV-1) variants and analyze these together with all other available American DENV-1 full-genome sequences. Besides confirming the existence of various country-specific DENV-1 founder effects that have produced a high degree of geographical structure in the American DENV-1 population, we also identify that one of the new viruses is one of only three detectable intra-American DENV-1 recombinants. Although such obvious evidence of genetic exchange among epidemiologically unlinked Latin American DENV-1 sequences is relatively rare, we find that at the population-scale there exists substantial evidence of pervasive recombination that most likely occurs between viruses that are so genetically similar that it is not possible to reliably distinguish and characterize individual recombination events.

Motor nerve terminals possess multiple voltage-sensitive calcium channels operating acetylcholine (ACh) release. In this study, we investigated whether facilitation of neuromuscular transmission by adenosine generated during neuronal firing was operated by Ca(2+) influx via 'prevalent' P-type or via the recruitment of 'silent' L-type channels. The release of [(3)H]ACh from rat phrenic nerve endings decreased upon increasing the stimulation frequency of the trains (750 pulses) from 5 Hz (83 +/- 4 x 10(3) disintegrations per minute per gram (d.p.m. g(-1)); n = 11) to 50 Hz (30 +/- 3 x 10(3) d.p.m. g(-1); n = 5). The P-type Ca(2+) channel blocker, omega-agatoxin IVA (100 nm) reduced (by 40 +/- 10%; n = 6) the release of [(3)H]ACh evoked by 50-Hz trains, while nifedipine (1 microM, an L-type blocker) was inactive. Tetanic depression was overcome (88 +/- 6 x 10(3) d.p.m. g(-1); n = 12) by stimulating the phrenic nerve with 50-Hz bursts (five bursts of 150 pulses, 20 s interburst interval). In these conditions, omega-agatoxin IVA (100 nM) failed to affect transmitter release, but nifedipine (1 microM) decreased [(3)H]ACh release by 21 +/- 7% (n = 4). Inactivation of endogenous adenosine with adenosine deaminase (ADA, 0.5 U ml(-1)) reduced (by 54 +/- 8%, n = 5) the release of [(3)H]ACh evoked with 50-Hz bursts. This effect was opposite to the excitatory actions of adenosine (0.5 mm), S-(p-nitrobenzyl)-6-thioinosine (5 microM, an adenosine uptake blocker) and CGS 21680C (3 nM, a selective A(2A) receptor agonist); as the A(1) receptor agonist R-N(6)-phenylisopropyl adenosine (R-PIA, 300 nM) failed to affect the release of [(3)H]ACh, the results indicate that adenosine generated during 50-Hz bursts exerts an A(2A)-receptor-mediated tonus. The effects of ADA (0.5 U ml(-1)) and CGS 21680C (3 nm) were prevented by nifedipine (1 microM). Blocking tonic A(2A) receptor activation, with ADA (0.5 U ml(-1)) or 3,7-dimethyl-1-propargyl xanthine (10 microM, an A(2A) antagonist), recovered omega-agatoxin IVA (100 nM) inhibition and caused the loss of function of nifedipine (1 microM). Data indicate that, in addition to the predominant P-type Ca(2+) current triggering ACh release during brief tetanic trains, motoneurones possess L-type channels that may be recruited to facilitate transmitter release during high-frequency bursts. The fine-tuning control of Ca(2+) influx through P- or L-type channels is likely to be mediated by endogenous adenosine. Therefore, tonic activation of presynaptic A(2A) receptors operating Ca(2+) influx via L-type channels may contribute to overcome tetanic depression during neuronal firing.

The aim of this study was to verify the promoting effect of carbamide peroxide on dimethylbenzanthracene (DMBA)-induced carcinogenesis in the hamster buccal pouch, in order to reduce the period of latency for tumor formation. Sixteen hamsters were randomized into two groups of eight animals each. The hamsters of the group I had their right buccal pouches treated with 0.5% DMBA and 10% carbamide peroxide teeth bleaching gel for 55 days. The animals of the group II had their right pouches treated only with DMBA. After, six animals of each group had their pouches prepared for light microscopy. Histomorphometry was performed to assess the presence of keratinization, nuclear polymorphism, pattern of invasion, number of blood vessels, and inflammatory infiltrate in the tumor front. Furthermore, the newly formed lesions were graded according the Bryne's grading system. The remaining animals had the vascular system of the pouches casted by Mercox and qualitatively analyzed by scanning electron microscopy. Histopathological analysis of the buccal pouches treated with DMBA and carbamide peroxide exhibited formation of squamous cell carcinoma well-differentiated with a high degree of malignancy in all pouches. The development of this neoplasm was associated with a significant increase in the number of blood vessels, presence of keratin pearls, and inflammatory infiltrate. The pouches of the group II showed inflammation, epithelial hyperplasia, dysplasia, and squamous cell carcinoma in only three right pouches. The analysis of the electron micrographs of the pouches chemically inducted with DBMA and carbamide peroxide reveled formation of a new vascular network characteristic of squamous cell carcinoma. The protocol presented here, using DMBA associated with carbamide peroxide, shortens the period of latency to produce squamous cell carcinoma in the hamster buccal pouch, decreasing the time and costs of the experiments.

The word angiogenesis indicates the formation of new vascular segments from existing vessels such as capillaries and venules. Blood vessel formation in tumors is the result of rapid, disorganized vascular growth through two distinct mechanisms: sprouting and intussusceptive angiogenesis. The objective of this study was to elucidate the morphological aspects of these two vascular growth mechanisms in oral squamous cell carcinoma induced in hamster buccal pouch. Eight Syrian golden hamsters had their right buccal pouch treated with DMBA 0.5% and 10% carbamide peroxide for 90 days in order to produce squamous cell carcinoma in this site. Next, buccal pouches of the animals were submitted to the vascular corrosion technique and then analyzed by scanning electron microscopy. The vascular figures of sprouts were observed in the entire vascular network of the buccal pouches, as opposed to the intussusceptive angiogenesis that was predominantly observed in the sub-epithelial network. It was possible to differentiate the figures of sprouts from artifacts by the analysis of the blind ending of these structures. Intussusceptive angiogenesis was identified by the presence of holes trespassing the lumen of the capillaries. Vascular expansion occurred through intussusceptive angiogenesis in two ways: by the fusion of the pillars to form a new capillary and, by increasing the girth of the pillar to form meshes. The method of corrosion associated with scanning electron microscopy proved to be an excellent tool to study the two types of angiogenesis in oral squamous cell carcinoma in the hamster buccal pouch.

At the rat motor endplate, pre-synaptic facilitatory adenosine A2A and muscarinic M1 receptors are mutually exclusive. We investigated whether these receptors share a common intracellular signalling pathway. Suppression of McN-A-343-induced M1 facilitation of [3H]ACh release was partially recovered when CGS21680C (an A2A agonist) was combined with the cyclic AMP antagonist Rp-cAMPS. Forskolin, rolipram and 8-bromo-cyclic AMP mimicked CGS21680C blockade of M1 facilitation. Both Rp-cAMPs and nifedipine reduced augmentation of [3H]ACh release by McN-A-343 and CGS21680C. Activation of M1 and A2A receptors enhanced Ca2+ recruitment through nifedipine-sensitive channels. Nifedipine inhibition revealed by McN-A-343 was prevented by chelerythrine (a PKC inhibitor) and Rp-cAMPS, suggesting that Ca(v)1 (L-type) channels phosphorylation by PKA and PKC is required. Rp-cAMPS inhibited [3H]ACh release in the presence of phorbol 12-myristate 13-acetate, but PKC inhibition by chelerythrine had no effect on release in the presence of 8-bromo-cyclic AMP. This suggests that the involvement of PKA may be secondary to M1-induced PKC activation. In conclusion, competition of M1 and A2A receptors to facilitate ACh release from motoneurons may occur by signal convergence to a common pathway involving PKA activation and Ca2+ influx through Ca(v)1 (L-type) channels.

The effects of anti-angiogenic therapies in guiding tumor angioarchitecture prompted us to examine the modifications in the vascular network of the oral squamous cell carcinoma (SCC) produced by the multitargeted tyrosine kinase inhibitor sunitinib malate. Twelve Syrian hamsters had their right buccal pouches submitted to tumor induction with dimethylbenzanthracene and carbamide peroxide for 55 days. The animals were then divided into two groups of six animals each; group I was treated with sunitinib malate and group II (control) was remained untreated. After 4 weeks, the hamsters had their vascular networks casted by Mercox® resin and analyzed by scanning electron microscopy. The qualitative study of the vascular network of the control tumor-bearing pouches showed images of intussusception and sprouting angiogenesis, flattened blood vessels, abrupt variations in their diameter, and a tortuous course. The samples treated with sunitinib exhibited a qualitative reduction of the signs of vascular proliferation. In addition, these casts presented an attenuation of the morphological features observed in the untreated tumor-bearing pouches. Quantitative analysis demonstrated that the pouches treated with sunitinib did not show a decrease (P > 0.05) in the vascular diameter and intervessel distances when compared with the control group. The results of the present study suggest that sunitinib may act on the vascular network of oral SCC, normalizing the blood vessels. However, further experiments should be performed in order to determine a judicious dose of this anti-angiogenic therapy.

Page 1. Determination of elements in kidney, serum and urine of Wistar rats with Acute Renal Insufficiency using NAA Laura C. Oliveira • Cibele B. Zamboni • Edson A. Pessoa • Fernanda T. Borges Received: 6 June 2011 © Akadémiai Kiadó, Budapest, Hungary 2011 ...

To investigate whether a sensorimotor deficit of the upper limb following a brachial plexus injury (BPI) affects the upright balance. Eleven patients with a unilateral BPI and 11 healthy subjects were recruited. The balance assessment included the Berg Balance Scale (BBS), the number of feet touches on the ground while performing a 60 s single-leg stance and posturographic assessment (eyes open and feet placed hip-width apart during a single 60 s trial). The body weight distribution (BWD) between the legs was estimated from the center of pressure (COP) lateral position. The COP variability was quantified in the anterior-posterior and lateral directions. BPI patients presented lower BBS scores (p = 0.048) and a higher frequency of feet touches during the single-leg stance (p = 0.042) compared with those of the healthy subjects. An asymmetric BWD toward the side opposite the affected arm was shown by 73% of BPI patients. Finally, higher COP variability was observed in BPI patients compared with healthy subjects for anterior-posterior (p = 0.020), but not for lateral direction (p = 0.818). This study demonstrates that upper limb sensorimotor deficits following BPI affect body balance, serving as a warning for the clinical community about the need to prevent and treat the secondary outcomes of this condition.

FUNDAMENTO: No Brasil, a resolução 196/96 e suas complementares regulamentam a preservação dos direitos, do respeito e da dignidade dos seres humanos envolvidos em pesquisas. OBJETIVO: Analisar a adequação dos temas livres (TLs) apresentados durante o XVIII Congresso Pernambucano de Cardiologia à resolução 196/96. MÉTODOS: Estudo de Corte Transversal. Foram realizadas entrevistas com autores dos TLs apresentados. Os resumos dos trabalhos foram analisados no sentido de identificar a necessidade de prévia aprovação por um Comitê de Ética em Pesquisa (CEP). RESULTADOS: Foram apresentados 90 TLs. A fonte de dados mais utilizada foram prontuários médicos (86,8%). Apenas 23,1% dos TLs foram submetidos à avaliação por um CEP e em 15,4% foi utilizado Termo de Consentimento Livre e Esclarecido (TCLE). Entre os autores cujos trabalhos não foram avaliados por um CEP, 65,6% afirmaram que esta não era uma conduta necessária e 18,0% deles desconheciam a necessidade de realizar tal avaliação. A autorização escrita do responsável pela instituição onde os TLs foram realizados não foi obtida em 56,6% das pesquisas. A maioria (80,0%) dos autores afirmou nunca ter lido a resolução 196/96. A proporção dos TLs submetidos a um CEP foi significativamente maior entre autores que haviam lido a resolução 196/96 (p = 0,005). O desenho dos TLs influenciou a não submissão dos trabalhos a um CEP (p < 0,001). A maioria dos TLs que foram autorizados pelo responsável da instituição onde foram realizados foi submetida a um CEP (p < 0,001). CONCLUSÃO: A maioria dos TLs apresentados não se adequou às regulamentações brasileiras em ética em pesquisa.

Neutron Activation Analysis (NAA) technique has been used to determine elements concentrations in urine of rats Wistar (control group) and rats Wistar with Acute Renal Failure (ARF). These data contribute for applications in health area related to biochemical analyses using urine to monitor the dialyze treatment.

ABSTRACT In this study the neutron activation analysis (NAA) technique was applied to determine Ca and Mg in whole blood from inhabitants of Brazil for the purpose of establishing concentration ranges indicative of sex and age. The initiative to perform these measurements is related to the increase in heart disease. According to recent statistics from WHO, the average is one death due to heart attack in Brazil, every five minutes. The measures were performed considering lifestyle factors (non-smokers, non-drinkers and no history of toxicological exposure) of Brazilian inhabitants. A healthy group constituted of male (n = 94) and female (n = 84) blood donors, ages between 18 and 70 years and above 50 kg, was selected from the blood banks and hematological laboratories of Brazil. The influence of sex was also investigated considering several age ranges (18–29, 30–40, 41–50, >50 years). The results show significant differences when a comparison is made by sex and age and may be useful to identify or prevent clinical diseases. These results emphasize the need to perform periodic evaluation of Ca and Mg in blood.