Transsynaptic Tracing from Peripheral Targets with Pseudorabies Virus Followed by Cholera Toxin and Biotinylated Dextran Amines Double Labeling.

Transsynaptic tracing has become a powerful tool used to analyze central efferents that regulate peripheral targets through multi-synaptic circuits. This approach has been most extensively used in the brain by utilizing the swine pathogen pseudorabies virus (PRV)(1). PRV does not infect great apes, including humans, so it is most commonly used in studies on small mammals, especially rodents. The pseudorabies strain PRV152 expresses the enhanced green fluorescent protein (eGFP) reporter gene and only crosses functional synapses retrogradely through the hierarchical sequence of synaptic connections away from the infection site(2,3). Other PRV strains have distinct microbiological properties and may be transported in both directions (PRV-Becker and PRV-Kaplan)(4,5). This protocol will deal exclusively with PRV152. By delivering the virus at a peripheral site, such as muscle, it is possible to limit the entry of the virus into the brain through a specific set of neurons. The resulting pattern of eGFP signal throughout the brain then resolves the neurons that are connected to the initially infected cells. As the distributed nature of transsynaptic tracing with pseudorabies virus makes interpreting specific connections within an identified network difficult, we present a sensitive and reliable method employing biotinylated dextran amines (BDA) and cholera toxin subunit b (CTb) for confirming the connections between cells identified using PRV152. Immunochemical detection of BDA and CTb with peroxidase and DAB (3, 3'-diaminobenzidine) was chosen because they are effective at revealing cellular processes including distal dendrites(6-11).

AINT/ERIC/TACC: an expanding family of proteins with C-terminal coiled coil domains:an expanding family of proteins with C-terminal coiled coil domains

The AINT/ERIC/TACC genes encode novel proteins with a coiled coil domain at their C-terminus. The founding member of this expanding family of genes, transforming acidic coiled coil 1 (TACC1), was isolated from a BAC contig spanning the breast cancer amplicon-1 on 8p11. Transfection of cells in vitro with TACC1 resulted in anchorage-independent growth consistent with a more "neoplastic" phenotype. Database searches employing the human TACC1 sequence revealed other novel genes, TACC2 and TACC3, with substantial sequence homology particularly in the C-terminal regions encoding the coiled coil domains. TACC2, located at 10q26, is similar to anti-zuai-1 (AZU-1), a candidate breast tumour suppressor gene, and ECTACC, an endothelial cell TACC which is upregulated by erythropoietin (Epo). The murine homologue of TACC3, murine erythropoietin-induced cDNA (mERIC-1) was also found to be upregulated by Epo in the Friend virus anaemia (FVA) model by differential display-PCR. Human ERIC-1, located at 4p16.3, has been cloned and encodes an 838-amino acid protein whose N- and C-terminal regions are highly homologous to the shorter 558-amino acid murine protein, mERIC-1. In contrast, the central portions of these proteins differ markedly. The murine protein contains four 24 amino acid imperfect repeats. ARNT interacting protein (AINT), a protein expressed during embryonic development in the mouse, binds through its coiled coil region to the aryl hydrocarbon nuclear translocator protein (ARNT) and has a central portion that contains seven of the 24 amino acid repeats found in mERIC-1. Thus mERIC-1 and AINT appear to be developmentally regulated alternative transcripts of the gene. Most members of the TACC family discovered so far contain a novel nine amino acid putative phosphorylation site with the pattern [R/K]-X(3)-[E]-X(3)-Y. Genes with sequence homology to the AINT/ERIC/TACC family in other species include maskin in Xenopus, D-TACC in Drosophila and TACC4 in the rabbit. Maskin contains a peptide sequence conserved among eIF-4E binding proteins that is involved in oocyte development. D-TACC cooperates with another conserved microtubule-associated protein Msps to stabilise spindle poles during cell division. The diversity of function already attributed to this protein family, including both transforming and tumour suppressor properties, should ensure that a new and interesting narrative is about to unfold.

Burkholderia multivorans survival and trafficking within macrophages

Cystic fibrosis (CF) patients are at great risk of opportunistic lung infection, particularly by members of the Burkholderia cepacia complex (Bcc). This group of bacteria can cause damage to the lung tissue of infected patients and are very difficult to eradicate due to their high levels of antibiotic resistance. Though the highly virulent B. cenocepacia has been the focus of virulence research for the past decade, B. multivorans is emerging as the most prevalent Bcc species infecting CF patients in North America. Despite several studies detailing the intramacrophage trafficking and survival of B. cenocepacia, no such data exists for B. multivorans. Our results demonstrated that clinical CF isolates, C5568 and C0514, and an environmental B. multivorans isolate, ATCC17616, were able to replicate and survive within murine macrophages in a manner similar to B. cenocepacia K56-2. These strains were also able to survive but were unable to replicate within human THP-1 macrophages. Differences in macrophage uptake were observed among all three B. multivorans strains; these variances were attributed to major differences in O-antigen production. Unlike B. cenocepacia-containing vacuoles, which delay phagosomal maturation in murine macrophages by 6 h, all B. multivorans containing vacuoles co-localized with late endosome/lysosomal marker LAMP-1 and the lysosomal marker dextran within 2 h of uptake. Together, these results indicate that while both Bcc species are able to survive and replicate within macrophages, they utilize different intramacrophage survival strategies. To observe differences in virulence the strains were compared using the Galleria mellonella model. When compared to the B. multivorans strains tested, B. cenocepacia K56-2 is highly virulent in this model and killed all worms within 24 h when injected at 107 CFU. B. multivorans clinical isolates C5568 and C0514 were significantly more virulent than the soil isolate ATCC17616, which was avirulent, even when worms were injected with 107 CFU. These results suggest strain differences in the virulence of B. multivorans isolates.

No major schizophrenia locus detected on chromosome 1q in a large multicenter sample

Reports of substantial evidence for genetic linkage of schizophrenia to chromosome 1q were evaluated by genotyping 16 DNA markers across 107 centimorgans of this chromosome in a multicenter sample of 779 informative schizophrenia pedigrees. No significant evidence was observed for such linkage, nor for heterogeneity in allele sharing among the eight individual samples. Separate analyses of European-origin families, recessive models of inheritance, and families with larger numbers of affected cases also failed to produce significant evidence for linkage. If schizophrenia susceptibility genes are present on chromosome 1q, their population-wide genetic effects are likely to be small.

Purple sweet potato colour - a potential therapy for galactosemia?

Galactosemia is an inherited metabolic disease in which galactose is not properly metabolised. There are various theories to explain the molecular pathology, and recent experimental evidence strongly suggests that oxidative stress plays a key role. High galactose diets are damaging to experimental animals and oxidative stress also plays a role in this toxicity which can be alleviated by purple sweet potato colour (PSPC). This plant extract is rich in acetylated anthocyanins which have been shown to quench free radical production. The objective of this Commentary is to advance the hypothesis that PSPC, or compounds therefrom, may be a viable basis for a novel therapy for galactosemia.

AgriSense: Multichannel disposable sensors for animal health disease diagnostics

Rapid and sensitive detection of viral infections associated with Bovine Respiratory Disease (BRD) in live animals is recognized as key to minimizing the impact of this disease. ELISA-based testing is limited as it typically relies on the detection of a single viral antibody subtype within an individual test sample and testing is relatively slow and expensive. We have recently initiated a new project entitled AgriSense to develop a novel low-cost and label-free, integrated bimodal electronic biosensor system for BRD. The biosensor system will consist of an integrated multichannel thin-film-transistor biosensor and an electrochemical impedance spectroscopy biosensor, interfaced with PDMS-based microfluidic sample delivery channels. By using both sensors in tandem, nonspecific binding biomolecules must have the same mass to charge ratio as the target analyte to elicit equivalent responses from both sensors. The system will target simultaneous multiplexed sensing of the four primary viral agents involved in the development of BRD: bovine herpesvirus-1 (BHV-1), bovine parainfluenza virus-3 (BPIV-3), bovine respiratory syncytial virus (BRSV), and bovine viral diarrhea (BVD). Optimized experimental conditions derived through model antigen-antibody studies will be applied to the detection of serological markers of BRD-related infections based on IgG interaction with a panel of sensor-immobilized viral proteins. This rapid, “cowside” multiplex sensor capability presents a major step forward in disease diagnosis, helping to ensure the integrity of the agri-food supply chain by reducing the risk of disease spread during animal movement and transport.

Prevalence of germ-line mutations in p16, p19ARF, and CDK4 in familial melanoma:analysis of a clinic-based population

Five to ten percent of individuals with melanoma have another affected family member, suggesting familial predisposition. Germ-line mutations in the cyclin-dependent kinase (CDK) inhibitor p16 have been reported in a subset of melanoma pedigrees, but their prevalence is unknown in more common cases of familial melanoma that do not involve large families with multiple affected members. We screened for germ-line mutations in p16 and in two other candidate melanoma genes, p19ARF and CDK4, in 33 consecutive patients treated for melanoma; these patients had at least one affected first or second degree relative (28 independent families). Five independent, definitive p16 mutations were detected (18%, 95% confidence interval: 6%, 37%), including one nonsense, one disease-associated missense, and three small deletions. No mutations were detected in CDK4. Disease-associated mutations in p19ARF, whose transcript is derived in part from an alternative codon reading frame of p16, were only detected in patients who also had mutations inactivating p16. We conclude that germ-line p16 mutations are present in a significant fraction of individuals who have melanoma and a positive family history.

LDL-cholesterol concentrations: a genome-wide association study.

BACKGROUND: LDL cholesterol has a causal role in the development of cardiovascular disease. Improved understanding of the biological mechanisms that underlie the metabolism and regulation of LDL cholesterol might help to identify novel therapeutic targets. We therefore did a genome-wide association study of LDL-cholesterol concentrations. METHODS: We used genome-wide association data from up to 11,685 participants with measures of circulating LDL-cholesterol concentrations across five studies, including data for 293 461 autosomal single nucleotide polymorphisms (SNPs) with a minor allele frequency of 5% or more that passed our quality control criteria. We also used data from a second genome-wide array in up to 4337 participants from three of these five studies, with data for 290,140 SNPs. We did replication studies in two independent populations consisting of up to 4979 participants. Statistical approaches, including meta-analysis and linkage disequilibrium plots, were used to refine association signals; we analysed pooled data from all seven populations to determine the effect of each SNP on variations in circulating LDL-cholesterol concentrations. FINDINGS: In our initial scan, we found two SNPs (rs599839 [p=1.7x10(-15)] and rs4970834 [p=3.0x10(-11)]) that showed genome-wide statistical association with LDL cholesterol at chromosomal locus 1p13.3. The second genome screen found a third statistically associated SNP at the same locus (rs646776 [p=4.3x10(-9)]). Meta-analysis of data from all studies showed an association of SNPs rs599839 (combined p=1.2x10(-33)) and rs646776 (p=4.8x10(-20)) with LDL-cholesterol concentrations. SNPs rs599839 and rs646776 both explained around 1% of the variation in circulating LDL-cholesterol concentrations and were associated with about 15% of an SD change in LDL cholesterol per allele, assuming an SD of 1 mmol/L. INTERPRETATION: We found evidence for a novel locus for LDL cholesterol on chromosome 1p13.3. These results potentially provide insight into the biological mechanisms that underlie the regulation of LDL cholesterol and might help in the discovery of novel therapeutic targets for cardiovascular disease.

Las capacidades ético-discursivas como capacidades para el reconocimiento recíproco: bases de un modelo de desarrollo humano

I defend three discourse ethical capabilities for human development: 1) Capability for selfunderstanding; 2) Capability to ground judgements in a dialogue with the affected; 3) Capability to carry out, with others, the justice projects agreed by common consent. Here I interpret them as capabilities for “reciprocal recognition.” I claim that the forms of selfrelation of the subject, defined by Axel Honneth, complement the capability for selfunderstanding. Honneth also offers an idea of justice that reviews the second mentioned capability. But I question the concept of “struggle” in Honneth from the perspective of the third capability, showing the advantages of co-responsibility. Then, I show that the three capabilities can be specified in indicators in each one of the spheres of the society where important ethical issues are confronted, and I give the example of what happens within the business sector. Finally, I defend a procedure to measure such indicators with concrete data. This procedure will allow us to evaluate the ethical level of a society evaluating the “ethical capabilities” of their citizens.

GREBP, un nouveau facteur de transcription contrôlant l’expression de la guanylate cyclase A, récepteur de l’ANP, via l’élément de réponse au cGMP

La découverte du système des peptides natriurétiques (NP), au début des années 80, fut une découverte majeure qui révéla le rôle endocrinien du cœur. Les connaissances sur la relaxation vasculaire, la diurèse et la natriurèse provoquées par ce système ont évolué vers un niveau de complexité insoupçonné à cette époque. Nous savons à présent que les NP sont impliqués dans plusieurs autres mécanismes dont la prolifération cellulaire, l’apoptose, l’inhibition du système rénine-angiotensine-aldostérone (RAAS) et le métabolisme des adipocytes. Le métabolisme des lipides est maintenant devenu une cible de choix dans la lutte contre l’obésité. Cette condition aux proportions pandémiques est un facteur de risque majeur dans l’apparition de l’hypertension et du syndrome métabolique (MetS). La compréhension des mécanismes et des défauts de la voie des NP pourrait avoir un impact positif sur le contrôle du MetS et de l’hypertension. L’expression du récepteur des peptides natriuretiques de type 1 (NPR1/GCA) est contrôlée par plusieurs agents incluant son propre ligand, le peptide natriurétique de l’oreillette (ANP). La découverte d’une boucle de retro-inhibition, dans les années 90, a été un événement majeur dans le domaine des NP. En effet, suite à une stimulation à l’ANP, le NPR1/GCA peut inhiber l’activité transcriptionnelle de son propre gène par un mécanisme dépendant du cGMP. Notre groupe a identifié un élément cis-régulateur responsable de cette sensibilité au cGMP et mon projet consistait à identifier la ou les protéine(s) liant cet élément de réponse au cGMP (cGMP-RE). Nous avons identifié un clone liant le cGMP-RE en utilisant la technique du simple hybride chez la levure et une banque d’ADN complémentaire (ADNc) de rein humain. Ce clone provient d’un ADNc de 1083-bp dont le gène est localisé sur le chromosome 1 humain (1p33.36) et codant pour une protéine dont la fonction était inconnue jusqu’ici. Nous avons nommé cette nouvelle protéine GREBP en raison de sa fonction de cGMP Response Element Binding Protein. Des essais de liaison à l’ADN ont montré que cette protéine possède une affinité 18 fois plus élevée pour le cGMP-RE que le contrôle, tandis que des expériences de retard sur gel (EMSA) ont confirmé la spécificité des interactions protéine-ADN. De plus, l’immuno-précipitation de la chromatine (ChIP) a prouvé que GREBP lie le cGMP-RE dans des conditions physiologiques. La liaison de GREBP au cGMP-RE inhibe l’expression du gène rapporteur luciférase sous contrôle du promoteur de npr1/gca. L’inhibition de GREBP à l’aide d’ARN interférant active le promoteur de npr1/gca. Dans les cellules NCI-H295R, l’ANP stimule l’expression de grebp de 60% après seulement 3 heures et inhibe l’expression de npr1/gca de 30%. GREBP est une protéine nucléaire surtout exprimée dans le cœur et ayant le facteur eIF3F comme partenaire. Les variations nucléotidiques du gène sont plus fréquentes chez les patients hypertendus que chez des patients normotendus ou hypertendus souffrant de MetS. Nous rapportons ici l’existence d’un gène spécifique à l’humain qui agit comme répresseur transcriptionnel de npr1/gca et potentiellement impliqué dans le développement de l’hypertension.

Études des mécanismes d’induction de l’immunosuppression par le virus Herpès Humain 6

HHV-6 is a ubiquitous human herpesvirus. Most individuals become infected at the age of 2 years. Primary infection by the virus causes a self-limiting febrile illness called exanthem subitum or roseola. In adults, primary infection may cause mononucleosis-like illnesses. The infection usually remains latent in healthy individuals, but often reactivates in immunocompromised individuals, for example, transplant patients and AIDS patients. The virus has also been associated with cancers and lymphoproliferative disorders. The virus encodes two proteins that interact with p53. However, little is known concerning the impact of the virus on cell cycle progression in human cells. The investigations reported in the thesis were focused on this issue. We show here that that HHV-6 infection delays the cell cycle progression in human T cell line HSB-2, as well as in primary human T cells and causes their accumulation in S and G2/M phase. By degrading the viral DNA in the virus-infected cells, we show that the infected cells accumulate in the G2/M and not in the S phase. We observed an increase in the kinase activity of cdc2 in virus-infected cells despite lower levels of its catalytic partners, cyclin A and cyclin B. We show here that the viral early antigen p41 associates with, and increases the kinase activity of, CDK1. Our studies have shown that there is a drastic reduction of p21 protein, despite the virus-induced stabilization and activation of p53 suggesting that p53 may be transcriptionally inactivated in the virus-infected cells. This decrease of p21 in infected cells was partially restored by proteasome inhibitors. These results suggest that HHV-6 causes perturbations in the normal progression of cell cycle in human T cells. Autophagy is a physiological cell process during which old cellular constituents and long-lived proteins in cells are degraded. This process is regulated in a cell cycle-dependent manner. We show here that infection with HHV-6 induces autophagy in HSB-2 cells. This was shown by the induction of LC-3 II as well as by the appearance of autophagic vacuoles in the virus-infected cells. However, we found that the virus inhibits fusion between autophagic vacuoles and lysosomes formed in infected cells, thus evading the autophagic response of infected host cells. Finally we tried to investigate replication of the virus in human cells in the absence of P53; a tumor suppressor gene which is also known as "the guardian of the genome ". During these investigations, we found that that inhibition of p53 gene expression mediated by siRNA as well as its inhibition by pharmacological inhibitors leads to massive cell death in human T cell line HSB-2 that carries a wild-type p53. We show that this death also occurs in another cell line CEM, which carries a transcriptionally mutated p53. Interestingly, the cell death could be prevented by pharmacological inhibitors of autophagy and necroptosis. Taken together, our results provide important novel insights concerning the impact of HHV-6 on cell cycle regulation and autophagy as well as of basal level p53 in cell survival.

Profilage Moléculaire de la Scoliose Idiopathique de l’Adolescent

La scoliose idiopathique de l’adolescent (SIA) est la déformation la plus fréquente en orthopédie pédiatrique. C'est une maladie qui génère des déformations complexes du rachis, du thorax et du bassin affectant plus sévèrement et majoritairement les filles à la puberté. Malgré de nombreuses années de recherches approfondies dans le domaine de la SIA, la cause n'a toujours pas été résolue. OBJECTIFS : Il a été démontré qu’il existe une dysfonction de la signalisation de la mélatonine par les protéines G inhibitrices (Gi) dans les ostéoblastes isolés de patients atteints de SIA. Ceci a conduit à une stratification des patients en trois groupes fonctionnels. Le but de ce projet de maîtrise est d’établir les profils d’expression moléculaire correspondant à chacun des groupes fonctionnels. Les objectifs spécifiques sont d’identifier les gènes responsables de l’initiation de la SIA et du défaut différentiel observé dans la signalisation des récepteurs couplés aux protéines Gi. MÉTHODES : Des ARNs ont été préparés à partir d’ostéoblastes isolés de patients atteints de SIA sélectionnés pour chaque groupe fonctionnel et comparés aux ARNs obtenus d’ostéoblastes de sujets sains. En plus, des cellules sanguines (PBMCs) isolées d’une paire de jumelles monozygotes discordantes pour la scoliose ont été étudiées pour comparer leur profil d’expression génétique. Nous avons utilisé des biopuces à ADN contenant un ensemble de 54,000 sondes permettant l’analyse du niveau d’expression de plus de 47,000 transcrits représentant 30,000 gènes humains bien caractérisés (Affymetrix, GeneChip® Human gene 1.0 ST array). Les gènes retenus ont par la suite été validés par qPCR sur un plus grand nombre de patients afin de tester la spécificité des profils d’expression pour chaque groupe de patients à partir des cellules osseuses dérivées lors de la chirurgie. RÉSULTATS: Le profilage moléculaire proposé permettra d’établir les fondements moléculaires de la SIA selon le test fonctionnel développé par le Dr Moreau et son équipe et d’identifier de nouveaux gènes associés à la SIA. Ce projet a permis de mettre en évidence des gènes possiblement impliqués dans le défaut de signalisation associé aux protéines Gi communs aux trois groupes, ainsi que des gènes spécifiques à certains groupes, pouvant contribuer au développement de certaines co-morbidités et/ou au risque d’aggravation des déformations rachidiennes. L’étude préliminaire des jumelles monozygotes discordantes pour la scoliose a mis en évidence un nombre limité de gènes possiblement associés au défaut de signalisation observé chez la jumelle scoliotique, gènes dont l’expression pourrait être influencée par des modifications d’ordre épigénétique liées à l’environnement. CONCLUSION: Les données obtenues par des approches de transcriptomiques dans le cadre de ce projet soutiennent notre méthode de stratification fonctionnelle des patients SIA et ont conduit à l’identification de nouveaux gènes associés à la SIA. Ces résultats jettent un éclairage nouveau sur la SIA et contribuent à une meilleure compréhension des mécanismes et facteurs impliqués dans l’étiologie de la SIA. À cet égard, nos résultats permettront éventuellement d’identifier des cibles thérapeutiques potentielles et des traitements personnalisés compte tenu des profils moléculaires distincts observés pour chaque groupe de patients.

Herpesviruses including novel gammaherpesviruses are widespread among phocid seal species in Canada.

Little is known about herpesviruses in Canadian pinnipeds. We measured prevalence of antibodies to herpesviruses in the sera from Canadian phocid seals by an indirect enzyme-linked immunosorbent assay. Wild harbor seals (Phoca vitulina) and captive harbor seals were positive for antibodies to Phocid herpesvirus 1 (PhoHV-1) at prevalences of 91% and 100%, respectively. Sera from wild hooded seals (Cystophora cristata), harp seals (Pagophilus groenlandica), and grey seals (Halichoerus grypus) were positive for antibodies to PhoHV-1 antigenically related herpesvirus antigens at 73%, 79%, and 96%, respectively. We isolated new herpesviruses in cell culture from two hunter-harvested ringed seals (Pusa hispida) in poor body condition from Ulukhaktok, Northwest Territories, Canada; one lethargic hooded seal from the St. Lawrence Estuary, Québec, Canada; and one captive, asymptomatic harp seal from the Magdalen Islands, Québec. Partial sequencing of the herpesvirus DNA polymerase gene revealed that all four virus isolates were closely related to PhoHV-2, a member of the Gammaherpesvirinae subfamily, with nucleotide similarity ranging between 92.8% and 95.3%. The new seal herpesviruses were genetically related to other known pinniped herpesviruses, such as PhoHV-1, Otariid herpesvirus 3, Hawaiian monk (Monachus schauinslandi) seal herpesvirus, and Phocid herpesvirus 5 with 47–48%, 55%, 77%, and 70–77% nucleotide similarities, respectively. The harp seal herpesvirus and both ringed seal herpesviruses were almost identical to each other, whereas the hooded seal herpesvirus was genetically different from the three others (92.8% nucleotide similarity), indicating detection of at least two novel seal herpesviruses. These findings are the first isolation, partial genome sequencing, and identification of seal gammaherpesviruses in three species of Canadian phocid seals; two species of which were suspected of exposure to one or more antigenically related herpesviruses based on serologic analyses.

El liderazgo organizacional: una aproximación desde la perspectiva etológica

La presente investigación plantea la necesidad fundamental de generar un proceso de análisis, tendiente a proponer dinámicas organizativas humanas, desde un enfoque etológico. La etología aparece entonces como un estudio sistemático del comportamiento animal, sus formas de asociación, su disparidad, pero sobre todo, su accionar orgánico en la búsqueda de un comportamiento colectivo que propenda por el bien común. En esta medida el liderazgo surge como una posibilidad clara de fomentar relaciones humanas centradas en las diferentes vertientes relacionales; cultura, comunicación, comunidad, axiología, y finalmente etología. Así mismo, se examinan las diferentes estrategias que el liderazgo como posibilidad de cambio dentro de las organizaciones, puede ser fundamentado mediante procesos de comparación etológica, y así generar propuestas que configuren un quehacer organizacional desde la solidaridad, el liderazgo, y el desenvolvimiento interno y externo de las organizaciones.

Percentiles de grasa corporal por bioimpedancia eléctrica en niños y adolescentes de Bogotá, Colombia: Estudio FUPRECOL

Objetivo: Recientemente, se han propuesto varios dispositivos de impedancia bioeléctrica (BIA) para la estimación rápida de la grasa corporal. Sin embargo, no han sido publicadas referencias de grasa corporal para niños y adolescentes en población Colombiana. El objetivo de este estudio fue establecer percentiles de grasa corporal por BIA en niños y adolescentes de Bogotá, Colombia de entre 9 y 17.9 años, pertenecientes al estudio FUPRECOL. Métodos: Estudio descriptivo y transversal, realizado en 2.526 niños y 3.324 adolescentes de entre 9 y 17.9 años de edad, pertenecientes a instituciones educativas oficiales de Bogotá, Colombia. El porcentaje de grasa corporal fue medido con Tanita® Analizador de Composición Corporal (Modelo BF-689), según edad y sexo. Se tomaron medidas de peso, talla, circunferencia de cintura, circunferencia de cadera y estado de maduración sexual por auto-reporte. Se calcularon los percentiles (P3, P10, P25, P50, P75, P90 y P97) y curvas centiles por el método LMS según sexo y edad y se realizó una comparación entre los valores de la CC observados con estándares internacionales. Resultados: Se presentan valores de porcentaje de grasa corporal y las curvas de percentiles. En la mayoría de los grupos etáreos la grasa corporal de las chicas fue mayor a la de los chicos. Sujetos cuyo porcentaje de grasa corporal estaba por encima del percentil 90 de la distribución estándar normal se consideró que tenían un elevado riesgo cardiovascular (chicos desde 23,4-28,3 y chicas desde 31,0-34,1). En general, nuestros porcentajes de grasa corporal fueron inferiores a los valores de Turquía, Alemania, Grecia, España y Reino Unido. Conclusiones: Se presentan percentiles del porcentaje de grasa por BIA según edad y sexo que podrán ser usados de referencia en la evaluación del estado nutricional y en la predicción del riesgo cardiovascular desde edades tempranas.