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inglés al portugués: Internal Medicine Textbook Detailed field: Medicina (general)
Texto de origen - inglés Abducens nerve
The sixth cranial nerve innervates the lateral rectus muscle. A palsy produces horizontal diplopia, worse on gaze to the side fo the lesion. A nuclear lesion has different consequences, because the abducens nucleus contain interneurons that project via the longitudinal fasciculus to the medial rectus subnucleus of the contralateral oculomotor complex. Therefore, an abducens nuclear lesion produces a complete lateral gaze palsy, from weakness of both the ipsilateral lateral rectus and the contralateral medial rectus. Foville's syndrome following dorsal pontine injury includes lateral gaze palsy, ipsilateral facial palsy, and contralateral hemiparesis incurred by damage to descending corticospinal fibers. Millard-Gubler's syndrome, from ventral pontine injury is similar, except for the eye findings. There is lateral rectus weakness only, instead of gaze palsy, because the abducens fascicle is injured rather than the nucleus. Infarct, tumor hemorrhage, vascular malformation, and multiple sclerosis are the most common etiologies of brainstem abducens palsy.
After leaving the ventral pons, the abducens nerve runs forward along the clivus to pierce the dura at the petrous apex, where it enters the cavernous sinus. Along its subarachnoid course it is susceptible to meningitis, tumor (meningioma, chordoma, carcinomatous meningitis), subarachnoid hemorrhage, trauma and compression by aneurysm or dolichoectatic vessels. At the petrous apex, mastoiditis can produce deafness, pain, and ipsilateral abducens palsy (Gradenigo's syndrome). In the cavernous sinus, the nerve can be affected by cavernous aneurysm, carotid cavernous fistula, tumor (pituitary adenoma, meningioma, nasopharyngeal carcinoma), herpes infection and Tolosa-Hunt syndrome.
Traducción - portugués Nervo abducente
O sexto nervo craniano inerva o músculo reto lateral. A paralisia do nervo produz diplopia que piora quando o paciente olha para o lado da lesão; nas lesões nucleares, porém, os sinais e sintomas são diferentes, pois o núcleo abducente contém interneurônios que cursam pelo fascículo longitudinal medial até o subnúcleo do reto medial, no complexo oculomotor contralateral. Por isso, lesões nucleares do abducente enfraquecem tanto o reto lateral ipsolateral como o reto medial contralateral, paralisando completamente o movimento conjugado lateral.
Lesões dorsais da ponte causam a síndrome de Foville, cujos sintomas são paralisia do movimento conjugado lateral, paralisia facial ipsolateral e hemiparesia contralateral, esta última causada por danos às fibras corticospinais descendentes; lesões pontinas ventrais causam a síndrome de Millard-Gubler, que é idêntica, exceto pelos achados oculares: há fraqueza apenas do reto lateral, sem paralisia do movimento conjugado, pois a lesão atinge o fascículo abducente e não o núcleo. As etiologias mais comuns de paralisia do abducente ao nível do tronco cerebral são infarto, tumor, hemorragia, malformação vascular e esclerose múltipla.
Após deixar a ponte ventral, o nervo abducente avança anteriormente ao longo do clivus, penetra na dura ao nível do ápice petroso, chegando ao seio cavernoso. Em seu trajeto subaracnóide, é suscetível a meningite, tumores (meningioma, cordoma, meningite carcinomatosa), hemorragia subaracnóide, trauma e compressão por aneurismas ou vasos dolicoectásicos. As mastoidites do ápice petroso podem causar surdez, dor e paralisia ipsolateral do abducente (síndrome de Gradenigo); no seio cavernoso, o nervo pode ser atingido por aneurismas carotídeos, fístulas carotídeo-cavernosas, tumores (adenoma hipofisário, meningioma, carcinoma nasofaríngeo), infecções herpéticas e síndrome de Tolosa-Hunt.
inglés al portugués: Molecular Biology Paper
Texto de origen - inglés DNA double-strand breaks (DSBs) are a common form of DNA damage and DSB rejoining is a fundamental mechanism of genome protection. Breaks arise through direct action of ionizing radiation or some chemicals, and indirectly as a product of blocked replication forks. The ability to repair DSBs and to ensure that repair is performed with appropriate fidelity is a fundamental part of genome protection. Repair of DSBs is of cardinal importance to prevent chromosomal fragmentation, translocations and deletions. In the somatic cells the genomic instability resulting from persistent or incorrectly repaired DSBs can lead to carcinogenesis through activation of oncogenes, inactivation of tumour-suppressor genes or loss of heterozygosity, while in the germline they can lead to inborn defects (1,2). It has been shown that there are three major pathways to repair DSBs in eukaryotes, i.e., homologous recombination (HR), single-strand annealing (SSA) and non-homologous end-joining (NHEJ), outlined in Fig. 1 and the participating proteins listed in Fig. 2 (1-3). NHEJ pathway plays an important role in DNA repair in mammalian cells as some rodent mutant cell lines defective in NHEJ are extremely sensitive to ionizing radiation.
Traducción - portugués As quebras de fita dupla de DNA (DSB — double-strand break) são um tipo comum de dano ao DNA, e a reconexão de DSB é um mecanismo fundamental para proteger o genoma. As quebras podem surgir tanto por ação direta de radiação ionizante ou de algumas substâncias químicas como indiretamente, devido ao bloqueio de forquilhas de replicação. A capacidade de reparar DSBs e de garantir que os reparos tenham a fidelidade apropriada é uma parte fundamental da proteção do genoma. O reparo de DSBs é de essencial importância na prevenção contra fragmentação, translocações e deleções de cromossomos. A instabilidade causada por DSBs persistentes ou reparadas incorretamente pode levar à carcinogênese em células somáticas (por meio da ativação de oncogenes, inativação de genes supressores de tumor ou perda da heterozigosidade) e a defeitos congênitos em células germinativas (1,2). Demonstrou-se que as principais vias de reparo de DSBs em eucariotos são três: recombinação homóloga (HR — homologous recombination), hibridização de fita única (SSA — single-strand annealing) e reunião de pontas não-homólogas (NHEJ — non-homologous end-joining). A Figura 1 mostra as vias de reparo e a Figura 2 apresenta uma lista das proteínas participantes (1 3). A via de reparo NHEJ desempenha importante papel no reparo do DNA de células mamíferas, pois algumas linhagens celulares mutantes de roedores com NHEJ defeituosa são extremamente sensíveis à radiação ionizante.
inglés al portugués (Associação Brasileira de Tradutores, verified) portugués al inglés (Associação Brasileira de Tradutores, verified) inglés al portugués (American Translators Association, verified) francés al portugués (Ministère de l'Éducation Nationale)
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