RESUMO
Genetic regulatory networks are the key to understanding biochemical systems. One condition of the genetic regulatory network under different living environments can be modeled as a synchronous Boolean network. The attractors of these Boolean networks will help biologists to identify determinant and stable factors. Existing methods identify attractors based on a random initial state or the entire state simultaneously. They cannot identify the fixed length attractors directly. The complexity of including time increases exponentially with respect to the attractor number and length of attractors. This study used the bounded model checking to quickly locate fixed length attractors. Based on the SAT solver, we propose a new algorithm for efficiently computing the fixed length attractors, which is more suitable for large Boolean networks and numerous attractors' networks. After comparison using the tool BooleNet, empirical experiments involving biochemical systems demonstrated the feasibility and efficiency of our approach.
Assuntos
Algoritmos , Fenômenos Bioquímicos/genética , Redes Reguladoras de Genes/genética , Computação Matemática , Simulação por Computador , Modelos GenéticosRESUMO
Self-organized systems, genetic regulatory systems and other living systems can be modeled as synchronous Boolean networks with stable states, which are also called state-cycle attractors (SCAs). This paper summarizes three classes of SCAs and presents a new efficient binary decision diagram based algorithm to find all SCAs of synchronous Boolean networks. After comparison with the tool BooleNet, empirical experiments with biochemical systems demonstrated the feasibility and efficiency of our approach.
Assuntos
Modelos Genéticos , Algoritmos , Animais , Redes Reguladoras de Genes , SoftwareRESUMO
Disorders of the motor neurons may affect both the upper and lower neurons, primarily the lower motor neurons as in the spinal muscular atrophies are primarily the upper motor neurons as in the familial spastic paraplegias. Amyotrophic lateral sclerosis is a degenerative disorder of the motor neuron that results in paralysis and wasting of voluntary muscles. Large motor neurons in the cerebral cortex, brain stem and spinal cord degenerate or are lost. Hyaline inclusions may be seen in the cytoplasm of surviving motor neurons. Acute axonal degeneration of peripheral motor fibers occurs at all levels, including the distal axon. Subclinical involvement of the spinecerebellar tracts, posterior column and Clarke's column as well as loss of large neurons in the dorsal root ganglia and neurons of oculomotor nuclei has been reported. The average duration of life onset of symptoms of amyotrophic lateral sclerosis is three years and ninety per cent of patients died within 5 years. The basic mechanism of disease in amyotrophic lateral sclerosis remains unknown. There is no known treatment that will prevent, reverse or otherwise alter the course of the disease. Autosomal dominant and autosomal recessive forms of amyotrophic lateral sclerosis are genetic models of amyotrophic lateral sclerosis which may provide insight into the disease mechanism of sporadic amyotrophic lateral sclerosis, five to ten percent of adult cases of amyotrophic lateral sclerosis with early onset of symptoms and a more benign course. It is conceivable that both genetic and sporadic forms of amyotrophic lateral sclerosis result from failure of the same or similar neuronal mechanism triggered by defective genes and by an environment agent in sporadic amyotrophic lateral sclerosis.
Assuntos
Esclerose Lateral Amiotrófica/genética , Esclerose Lateral Amiotrófica/classificação , Esclerose Lateral Amiotrófica/fisiopatologia , Animais , Ligação Genética/genética , HumanosAssuntos
Hipotireoidismo Congênito , Proteínas de Ligação ao GTP/deficiência , Pseudo-Hipoparatireoidismo/genética , Adulto , Pré-Escolar , Feminino , Humanos , Hipotireoidismo/genética , Hipotireoidismo/metabolismo , Lactente , Masculino , Hormônio Paratireóideo/metabolismo , Linhagem , Pseudo-Hipoparatireoidismo/metabolismo , Pseudopseudo-Hipoparatireoidismo/genéticaRESUMO
Foremost in the differential diagnosis of hypertension is the identification of surgically correctable lesions. Increased plasma renin activity in a hypertensive patient suggests the presence of a renovascular or renal etiology. We have recently seen two adolescent patients whose hyperreninemia was cuased by a pheochromocytoma. Secondary hyperaldosteronism was an associated finding.
Assuntos
Neoplasias das Glândulas Suprarrenais/complicações , Hiperaldosteronismo/etiologia , Feocromocitoma/complicações , Renina/sangue , Adolescente , Neoplasias das Glândulas Suprarrenais/sangue , Feminino , Humanos , Hipertensão Renal/sangue , Hipertensão Renal/etiologia , Masculino , Feocromocitoma/sangueRESUMO
Two children, ages 13 2/12 and 6 6/12 years, with osteogenesis imperfecta were treated with salmon calcitonin. During the course of therapy the older child developed calcitonin dose-related hypomagnesemia on two occasions. The younger child, coincident with otitis media and vomiting, developed hypomagnesemia, hypophosphatemia, hyponatremia, and hypokalemia. Since rib biopsies obtained before and after one year of treatment with salmon calcitonin failed to demonstrate any histologic changes, therapy was discontinued because of the induced metabolic consequences of calcitonin therapy.