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1.
Orv Hetil ; 161(4): 151-160, 2020 Jan.
Artículo en Húngaro | MEDLINE | ID: mdl-31955583

RESUMEN

Introduction: The prevalence of overweight and obesity is increasing worldwide, which affects not only adults, but children and adolescents as well. Moreover, this condition may lead to several comorbidities, such as elevated or even high blood pressure. Aim: Aim of this study was to assess the prevalence of overweight- and obesity-related elevated and high blood pressure in a population aged 3-18 years in Hungary. Method: Between 2005 and 2018, altogether 8624 (boys = 4719) individuals were enrolled to this study. Normal weight, overweight and obese groups were created on the basis of body mass index. The diagnosis of elevated (systolic and/or diastolic blood pressure is between 90th and 95th percentile) and high blood pressure (systolic and/or diastolic blood pressure is over 95th percentile) was based on detailed examination (laboratory tests, abdominal ultrasonography, paediatric cardiology and 24-hours ambulatory blood pressure monitoring). Results: In this study, the prevalence of overweight and obesity was 23.5% overall, 26.4% in boys and 20% in girls. The prevalence of elevated blood pressure was 9.8% in overweight patients, while it was 4.6% in the obese group. The prevalence of high blood pressure was 8.3% (odds ratio: 1.1%, 95% CI) among overweight subjects, while it was 26.7% (odds ratio: 3.6, 95% CI) in the obese group. Conclusion: To the best of our knowledge, this is the first Hungarian population-based study on the prevalence of overweight- and obesity-related elevated and high blood pressure assessed in a large contemporary cohort of children and adolescents. The cardiovascular risk is increased in this patient group. Hence, it is essential to set up a proper primary prevention strategy. Orv Hetil. 2020; 161(4): 151-160.


Asunto(s)
Hipertensión/epidemiología , Obesidad Pediátrica/epidemiología , Adolescente , Niño , Preescolar , Femenino , Humanos , Hungría/epidemiología , Masculino , Prevalencia
2.
Sci Data ; 7(1): 26, 2020 01 21.
Artículo en Inglés | MEDLINE | ID: mdl-31964867

RESUMEN

This database is the first large dataset of haemodynamic changes of normal-weight pupils during a field exercise test. Here, we present a dataset for anthropometric and hemodynamic parameters measured both during relaxation and after exercise containing 1,173,342 data segments from 65,345 acquisition points of 10,894 normal weight subjects, covering an age range of 6-18 years collected in a course of 12 years. Data acquisition was carried out under standardised measuring conditions and specifications. Hemodynamic parameters were measured in the normal-weight population with a new and simple Fit-Test which could facilitate new projects worldwide to study and compare cardiovascular fitness.

3.
Neurol Sci ; 41(1): 125-129, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-31478152

RESUMEN

OBJECTIVE: The prevalence of xeroderma pigmentosum (XP) is quite low in Europe, which may result in a delay in determining the appropriate diagnosis. Furthermore, some subtypes of XP, including XPA, may manifest themselves with quite severe neurological symptoms in addition to the characteristic dermatological lesions. Accordingly, the aim of the current study is to highlight the predominant neurological aspects of XPA, as well as mild-to-moderate dermatological signs in a Hungarian family with 5 affected siblings. CASE REPORTS: The symptoms of the Caucasian male proband started to develop at 13-14 years of age with predominantly cerebellar, hippocampal, and brainstem alterations. His elder sister and three younger brothers all presented similar, but less expressed neurological signs. The diagnostic work-up, including clinical exome sequencing, revealed 2 novel compound heterozygous mutations (p.Gln146_Tyr148delinsHis, p.Arg258TyrfsTer5) in the XPA gene. Surprisingly, only mild-to-moderate dermatological alterations were observed, and less severe characteristic ophthalmological and auditory signs were detected. CONCLUSIONS: In summary, we present the first family with genetically confirmed XPA in the Central-Eastern region of Europe, clearly supporting the notion that disturbed function of the C-terminal region of the XPA protein contributes to the development of age-dependent neurologically predominant signs. This case series may help clinicians recognize this rare disorder.

4.
Sci Rep ; 9(1): 16569, 2019 Nov 12.
Artículo en Inglés | MEDLINE | ID: mdl-31719606

RESUMEN

Hun, Avar and conquering Hungarian nomadic groups arrived to the Carpathian Basin from the Eurasian Steppes and significantly influenced its political and ethnical landscape, however their origin remains largely unknown. In order to shed light on the genetic affinity of above groups we have determined Y chromosomal haplogroups and autosomal loci, suitable to predict biogeographic ancestry, from 49 individuals, supposed to represent the power/military elit. Haplogroups from the Hun-age are consistent with Xiongnu ancestry of European Huns. Most of the Avar-age individuals carry east Eurasian Y haplogroups typical for modern north-eastern Siberian and Buryat populations and their autosomal loci indicate mostly un-admixed Asian characteristics. In contrast the conquering Hungarians seem to be a recently assembled population incorporating un-admixed European, Asian as well as admixed components. Their heterogeneous paternal and maternal lineages indicate similar supposed phylogeographic origin of males and females, derived from Central-Inner Asian and European Pontic Steppe sources.

5.
Ideggyogy Sz ; 72(7-8): 273-277, 2019 Jul 30.
Artículo en Inglés | MEDLINE | ID: mdl-31517460

RESUMEN

Cerebral cavernous malformations (CCMs) represent a relatively rare and heterogeneous clinical entity with mutations identified in three genes. Both sporadic and familial forms have been reported. We present a young female patient with episodic paresthesia and headaches, but without acute neurological deficits. Her mother had a hemorrhaged cavernoma surgically removed 21 years ago. Cranial magnetic resonance imaging revealed multiple cavernous malformations in the size of a few millimeters and the ophthalmologic exam detected retinal blood vessel tortuosity in the proband. Targeted exome sequencing analysis identified a nonsense mutation in exon 16 of the KRIT1 gene, which resulted in a premature stop codon and a truncated protein underlying the abnormal development of cerebral and retinal blood vessels. This mutation with pathogenic significance has been reported before. Our case points to the importance of a thorough clinical and molecular work up despite the uncertain neurological complaints, since life style recommendations, imaging monitoring and genetic counseling may have major significance in the long term health of the patient.


Asunto(s)
Hemangioma Cavernoso del Sistema Nervioso Central/diagnóstico , Proteína KRIT1/genética , Vasos Retinianos/diagnóstico por imagen , Femenino , Cefalea/etiología , Hemangioma Cavernoso del Sistema Nervioso Central/diagnóstico por imagen , Hemangioma Cavernoso del Sistema Nervioso Central/genética , Humanos , Imagen por Resonancia Magnética , Mutación , Parestesia/etiología , Linaje , Eliminación de Secuencia/genética
6.
J Appl Genet ; 60(2): 151-162, 2019 May.
Artículo en Inglés | MEDLINE | ID: mdl-30706430

RESUMEN

Autosomal recessive primary microcephaly (MCPH) is a group of rare neurodevelopmental diseases with severe microcephaly at birth. One type of the disorder, MCPH2, is caused by biallelic mutations in the WDR62 gene, which encodes the WD repeat-containing protein 62. Patients with WDR62 mutation may have a wide range of malformations of cortical development in addition to congenital microcephaly. We describe two patients, a boy and a girl, with severe congenital microcephaly, global developmental delay, epilepsy, and failure to thrive. MRI showed hemispherical asymmetry, diffuse pachygyria, thick gray matter, indistinct gray-white matter junction, and corpus callosum and white matter hypoplasia. Whole exome sequencing revealed the same novel homozygous missense mutation, c.668T>C, p.Phe223Ser in exon 6 of the WDR62 gene. The healthy parents were heterozygous for this mutation. The mutation affects a highly conserved region in one of the WD repeats of the WDR62 protein. Haplotype analysis showed genetic relatedness between the families of the patients. Our findings expand the spectrum of mutations randomly distributed in the WDR62 gene. A review is also provided of the brain malformations described in WDR62 mutations in association with congenital microcephaly.


Asunto(s)
Discapacidades del Desarrollo/genética , Microcefalia/genética , Proteínas del Tejido Nervioso/genética , Discapacidades del Desarrollo/diagnóstico por imagen , Discapacidades del Desarrollo/fisiopatología , Femenino , Sustancia Gris/diagnóstico por imagen , Sustancia Gris/patología , Haplotipos , Homocigoto , Humanos , Masculino , Microcefalia/diagnóstico por imagen , Microcefalia/fisiopatología , Mutación Missense/genética , Linaje , Sustancia Blanca/diagnóstico por imagen , Sustancia Blanca/patología
7.
Sci Data ; 6: 190010, 2019 02 05.
Artículo en Inglés | MEDLINE | ID: mdl-30720799

RESUMEN

Suicide is one of the leading causes of mortality worldwide; it causes the death of more than one million patients each year. Suicide is a complex, multifactorial phenotype with environmental and genetic factors contributing to the risk of the forthcoming suicide. These factors first generally lead to mental disorders, such as depression, schizophrenia and bipolar disorder, which then become the direct cause of suicide. Here we present a high quality dataset (including processed BAM and VCF files) gained from the high-throughput whole-exome Illumina sequencing of 23 suicide victims - all of whom had suffered from major depressive disorder - and 21 control patients to a depth of at least 40-fold coverage in both cohorts. We identified ~130,000 variants per sample and altogether 442,270 unique variants in the cohort of 44 samples. To our best knowledge, this is the first whole-exome sequencing dataset from suicide victims. We expect that this dataset provides useful information for genomic studies of suicide and depression, and also for the analysis of the Hungarian population.


Asunto(s)
Trastorno Depresivo Mayor/genética , Suicidio , Secuenciación del Exoma Completo , Estudios de Cohortes , Genoma Humano , Secuenciación de Nucleótidos de Alto Rendimiento , Humanos , Hungría/epidemiología
9.
BMC Genomics ; 19(1): 778, 2018 Oct 29.
Artículo en Inglés | MEDLINE | ID: mdl-30373510

RESUMEN

BACKGROUND: Understanding the underlying genetic structure of human populations is of fundamental interest to both biological and social sciences. Advances in high-throughput genotyping technology have markedly improved our understanding of global patterns of human genetic variation. The most widely used methods for collecting variant information at the DNA-level include whole genome sequencing, which remains costly, and the more economical solution of array-based techniques, as these are capable of simultaneously genotyping a pre-selected set of variable DNA sites in the human genome. The largest publicly accessible set of human genomic sequence data available today originates from exome sequencing that comprises around 1.2% of the whole genome (approximately 30 million base pairs). RESULTS: To unbiasedly compare the effect of SNP selection strategies in population genetic analysis we subsampled the variants of the same highly curated 1 K Genome dataset to mimic genome, exome sequencing and array data in order to eliminate the effect of different chemistry and error profiles of these different approaches. Next we compared the application of the exome dataset to the array-based dataset and to the gold standard whole genome dataset using the same population genetic analysis methods. CONCLUSIONS: Our results draw attention to some of the inherent problems that arise from using pre-selected SNP sets for population genetic analysis. Additionally, we demonstrate that exome sequencing provides a better alternative to the array-based methods for population genetic analysis. In this study, we propose a strategy for unbiased variant collection from exome data and offer a bioinformatics protocol for proper data processing.


Asunto(s)
Genética de Población , Genoma Humano , Genómica , Bases de Datos Genéticas , Evolución Molecular , Marcadores Genéticos , Variación Genética , Genómica/métodos , Humanos , Polimorfismo de Nucleótido Simple , Secuenciación del Exoma Completo
10.
PLoS One ; 13(10): e0205920, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-30335830

RESUMEN

It has been widely accepted that the Finno-Ugric Hungarian language, originated from proto Uralic people, was brought into the Carpathian Basin by the conquering Hungarians. From the middle of the 19th century this view prevailed against the deep-rooted Hungarian Hun tradition, maintained in folk memory as well as in Hungarian and foreign written medieval sources, which claimed that Hungarians were kinsfolk of the Huns. In order to shed light on the genetic origin of the Conquerors we sequenced 102 mitogenomes from early Conqueror cemeteries and compared them to sequences of all available databases. We applied novel population genetic algorithms, named Shared Haplogroup Distance and MITOMIX, to reveal past admixture of maternal lineages. Our results show that the Conquerors assembled from various nomadic groups of the Eurasian steppe. Population genetic results indicate that they had closest connection to the Onogur-Bulgar ancestors of Volga Tatars. Phylogenetic results reveal that more than one third of the Conqueror maternal lineages were derived from Central-Inner Asia and their most probable ultimate sources were the Asian Scythians and Asian Huns, giving support to the Hungarian Hun tradition. The rest of the lineages most likely originated from the Bronze Age Potapovka-Poltavka-Srubnaya cultures of the Pontic-Caspian steppe. Available data imply that the Conquerors did not have a major contribution to the gene pool of the Carpathian Basin.


Asunto(s)
Grupo de Ascendencia Continental Asiática/genética , Genoma Mitocondrial , Filogenia , Cementerios , Pool de Genes , Genética de Población , Geografía , Migración Humana , Humanos , Hungría , Cráneo/anatomía & histología
11.
J Hum Genet ; 63(11): 1189-1193, 2018 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-30181650

RESUMEN

Heterozygous disruptions in FOXP1 are responsible for developmental delay, intellectual disability and speech deficit. Heterozygous germline PTCH1 disease-causing variants cause Gorlin syndrome. We describe a girl with extreme megalencephaly, developmental delay and severe intellectual disability. Dysmorphic features included prominent forehead, frontal hair upsweep, flat, wide nasal bridge, low-set, abnormally modelled ears and post-axial cutaneous appendages on the hands. Brain MRI showed partial agenesis of the corpus callosum and widely separated leaves of the septum pellucidum. Exome sequencing of a gene set representing a total of 4813 genes with known relationships to human diseases revealed an already known heterozygous de novo nonsense disease-causing variant in FOXP1 (c.1573C>T, p.Arg525Ter) and a heterozygous novel de novo frameshift nonsense variant in PTCH1 (c.2834delGinsAGATGTTGTGGACCC, p.Arg945GlnfsTer22). The composite phenotype of the patient seems to be the result of two monogenic diseases, although more severe than described in conditions due to disease-causing variants in either gene.


Asunto(s)
Agenesia del Cuerpo Calloso/genética , Factores de Transcripción Forkhead/genética , Discapacidad Intelectual/genética , Megalencefalia/genética , Mutación , Receptor Patched-1/genética , Proteínas Represoras/genética , Agenesia del Cuerpo Calloso/patología , Niño , Femenino , Humanos , Discapacidad Intelectual/patología , Megalencefalia/patología
12.
Pediatr Nephrol ; 33(10): 1713-1721, 2018 10.
Artículo en Inglés | MEDLINE | ID: mdl-29956005

RESUMEN

BACKGROUND: Autosomal recessive polycystic kidney disease (ARPKD) is genetically one of the least heterogeneous ciliopathies, resulting primarily from mutations of PKHD1. Nevertheless, 13-20% of patients diagnosed with ARPKD are found not to carry PKHD1 mutations by sequencing. Here, we assess whether PKHD1 copy number variations or second locus mutations explain these cases. METHODS: Thirty-six unrelated patients with the clinical diagnosis of ARPKD were screened for PKHD1 point mutations and copy number variations. Patients without biallelic mutations were re-evaluated and screened for second locus mutations targeted by the phenotype, followed, if negative, by clinical exome sequencing. RESULTS: Twenty-eight patients (78%) carried PKHD1 point mutations, three of whom on only one allele. Two of the three patients harbored in trans either a duplication of exons 33-35 or a large deletion involving exons 1-55. All eight patients without PKHD1 mutations (22%) harbored mutations in other genes (PKD1 (n = 2), HNF1B (n = 3), NPHP1, TMEM67, PKD1/TSC2). Perinatal respiratory failure, a kidney length > +4SD and early-onset hypertension increase the likelihood of PKHD1-associated ARPKD. A patient compound heterozygous for a second and a last exon truncating PKHD1 mutation (p.Gly4013Alafs*25) presented with a moderate phenotype, indicating that fibrocystin is partially functional in the absence of its C-terminal 62 amino acids. CONCLUSIONS: We found all ARPKD cases without PKHD1 point mutations to be phenocopies, and none to be explained by biallelic PKHD1 copy number variations. Screening for copy number variations is recommended in patients with a heterozygous point mutation.


Asunto(s)
Variaciones en el Número de Copia de ADN , Heterocigoto , Fenotipo , Riñón Poliquístico Autosómico Recesivo/genética , Receptores de Superficie Celular/genética , Adolescente , Alelos , Niño , Preescolar , Análisis Mutacional de ADN , Exones/genética , Femenino , Pruebas Genéticas , Humanos , Lactante , Recién Nacido , Masculino , Mutación Puntual , Riñón Poliquístico Autosómico Recesivo/diagnóstico , Índice de Severidad de la Enfermedad
14.
Pediatr Nephrol ; 33(3): 439-446, 2018 03.
Artículo en Inglés | MEDLINE | ID: mdl-29032433

RESUMEN

BACKGROUND: A 7-month-old male infant was admitted because he was suffering from nephrotic syndrome, along with encephalomyopathy, hypertrophic cardiomyopathy, clinically suspected deafness and retinitis pigmentosa, and an elevated serum lactate level. METHODS: Coenzyme Q10 supplementation was started because of the clinical suspicion of primary CoQ10 deficiency. Despite intensive efforts, he passed away 4 weeks after admission. RESULTS: The results of genetic tests, available postmortem, explored two hitherto undescribed mutations in the PDSS2 gene. Both were located within the polyprenyl synthetase domain. Clinical exome sequencing revealed a heterozygous missense mutation in exon 3, and our in-house joint-analysis algorithm detected a heterozygous large 2923-bp deletion that affected the 5 prime end of exon 8. Other causative defects in the CoQ10 and infantile nephrosis-related genes examined were not found. A postmortem histological, immunohistochemical, and electron microscopic evaluation of the glomeruli revealed collapsing-sclerosing lesions consistent with diffuse mesangial sclerosis. The extrarenal alterations included hypertrophic cardiomyopathy and diffuse alveolar damage. A histological evaluation of the central nervous system and skeletal muscles did not demonstrate any obvious abnormality. CONCLUSIONS: Until now, the clinical features and the mutational status of 6 patients with a PDSS2 gene defect have been reported in the English literature. Here, we describe for the first time detailed kidney morphology features in a patient with nephrotic syndrome carrying mutations in the PDSS2 gene.


Asunto(s)
Transferasas Alquil y Aril/genética , Ataxia/genética , Riñón/patología , Enfermedades Mitocondriales/genética , Debilidad Muscular/genética , Síndrome Nefrótico/genética , Esclerosis/genética , Ubiquinona/deficiencia , Ataxia/complicaciones , Autopsia , Resultado Fatal , Pruebas Genéticas/métodos , Humanos , Lactante , Masculino , Enfermedades Mitocondriales/complicaciones , Debilidad Muscular/complicaciones , Mutación , Síndrome Nefrótico/complicaciones , Síndrome Nefrótico/etiología , Esclerosis/complicaciones , Ubiquinona/análogos & derivados , Ubiquinona/genética , Ubiquinona/uso terapéutico
15.
Sci Rep ; 7(1): 7106, 2017 08 02.
Artículo en Inglés | MEDLINE | ID: mdl-28769055

RESUMEN

We carried out whole-exome ultra-high throughput sequencing in brain samples of suicide victims who had suffered from major depressive disorder and control subjects who had died from other causes. This study aimed to reveal the selective accumulation of rare variants in the coding and the UTR sequences within the genes of suicide victims. We also analysed the potential effect of STR and CNV variations, as well as the infection of the brain with neurovirulent viruses in this behavioural disorder. As a result, we have identified several candidate genes, among others three calcium channel genes that may potentially contribute to completed suicide. We also explored the potential implication of the TGF-ß signalling pathway in the pathogenesis of suicidal behaviour. To our best knowledge, this is the first study that uses whole-exome sequencing for the investigation of suicide.


Asunto(s)
Trastorno Depresivo Mayor/genética , Trastorno Depresivo Mayor/psicología , Estudios de Asociación Genética , Suicidio , Secuenciación del Exoma Completo , Alelos , Mapeo Cromosómico , Variaciones en el Número de Copia de ADN , ADN Viral , Exones , Femenino , Redes Reguladoras de Genes , Genes Ligados a X , Variación Genética , Humanos , Mutación con Pérdida de Función , Masculino , Repeticiones de Microsatélite , Modelos Biológicos
17.
PLoS One ; 12(4): e0174886, 2017.
Artículo en Inglés | MEDLINE | ID: mdl-28422985

RESUMEN

As part of the effort to create a high resolution representative sequence database of the medieval Hungarian conquerors we have resequenced the entire mtDNA genome of 24 published ancient samples with Next Generation Sequencing, whose haplotypes had been previously determined with traditional PCR based methods. We show that PCR based methods are prone to erroneous haplotype or haplogroup determination due to ambiguous sequence reads, and many of the resequenced samples had been classified inaccurately. The SNaPshot method applied with published ancient DNA authenticity criteria is the most straightforward and cheapest PCR based approach for testing a large number of coding region SNP-s, which greatly facilitates correct haplogroup determination.


Asunto(s)
ADN Antiguo/análisis , ADN Mitocondrial/genética , Haplotipos , Secuenciación de Nucleótidos de Alto Rendimiento/métodos , Tipificación Molecular/métodos , Paleontología , Huesos/química , ADN Mitocondrial/historia , Fósiles , Historia Medieval , Humanos , Hungría , Reacción en Cadena de la Polimerasa , Polimorfismo de Nucleótido Simple , Análisis de Secuencia de ADN
18.
PLoS One ; 11(3): e0149241, 2016.
Artículo en Inglés | MEDLINE | ID: mdl-26934356

RESUMEN

Alport syndrome (AS) is an inherited type IV collagen nephropathies characterized by microscopic hematuria during early childhood, the development of proteinuria and progression to end-stage renal disease. Since choosing the right therapy, even before the onset of proteinuria, can delay the onset of end-stage renal failure and improve life expectancy, the earliest possible differential diagnosis is desired. Practically, this means the identification of mutation(s) in COL4A3-A4-A5 genes. We used an efficient, next generation sequencing based workflow for simultaneous analysis of all three COL4A genes in three individuals and fourteen families involved by AS or showing different level of Alport-related symptoms. We successfully identified mutations in all investigated cases, including 14 unpublished mutations in our Hungarian cohort. We present an easy to use unified clinical/diagnostic terminology and workflow not only for X-linked but for autosomal AS, but also for Alport-related diseases. In families where a diagnosis has been established by molecular genetic analysis, the renal biopsy may be rendered unnecessary.


Asunto(s)
Autoantígenos/genética , Colágeno Tipo IV/genética , Mutación , Nefritis Hereditaria/genética , Adulto , Preescolar , Diagnóstico Diferencial , Femenino , Secuenciación de Nucleótidos de Alto Rendimiento , Humanos , Masculino , Persona de Mediana Edad , Nefritis Hereditaria/diagnóstico , Linaje , Flujo de Trabajo
20.
PLoS Genet ; 10(2): e1004166, 2014 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-24586196

RESUMEN

During muscle development, myosin and actin containing filaments assemble into the highly organized sarcomeric structure critical for muscle function. Although sarcomerogenesis clearly involves the de novo formation of actin filaments, this process remained poorly understood. Here we show that mouse and Drosophila members of the DAAM formin family are sarcomere-associated actin assembly factors enriched at the Z-disc and M-band. Analysis of dDAAM mutants revealed a pivotal role in myofibrillogenesis of larval somatic muscles, indirect flight muscles and the heart. We found that loss of dDAAM function results in multiple defects in sarcomere development including thin and thick filament disorganization, Z-disc and M-band formation, and a near complete absence of the myofibrillar lattice. Collectively, our data suggest that dDAAM is required for the initial assembly of thin filaments, and subsequently it promotes filament elongation by assembling short actin polymers that anneal to the pointed end of the growing filaments, and by antagonizing the capping protein Tropomodulin.


Asunto(s)
Citoesqueleto de Actina/genética , Proteínas Adaptadoras Transductoras de Señales/genética , Proteínas de Drosophila/genética , Desarrollo de Músculos/genética , Sarcómeros/genética , Citoesqueleto de Actina/metabolismo , Actinas/metabolismo , Proteínas Adaptadoras Transductoras de Señales/metabolismo , Animales , Diferenciación Celular , Proteínas de Drosophila/metabolismo , Drosophila melanogaster/crecimiento & desarrollo , Regulación del Desarrollo de la Expresión Génica , Ratones , Desarrollo de Músculos/fisiología , Miocardio/metabolismo , Miofibrillas/genética , Miofibrillas/metabolismo , Miosinas/genética , Sarcómeros/fisiología , Sarcómeros/ultraestructura
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