Rastreamento familiar do fator V de Leiden: a importância da deteccão de portadores heterozigotos / Familiar tracking of factor V Leiden: the importance of detection in heterozygous carriers

O fator de Leiden é uma mutacão genética que predispõe seus portadores ao tromboembolismo venoso. O objetivo do estudo foi investigar a distribuicão dos alelos em 21 membros da família de três pacientes portadores de trombose com a presenca da mutacão do fator V de Leiden. A deteccão da mutacão no gene do fator V foi realizada entre portadores da mutacão no estado heterozigoto. Este estudo foi realizado no Centro de Hematologia e Hemoterapia do Ceará - Hemoce. Observou-se a presenca da mutacão no estado heterozigoto na família 1 (83,3 por cento), na família 2 (40 por cento) e na família 3 (50 por cento). No total de 24 membros (pacientes e familiares) analisados, 50 por cento (12/24) apresentaram a mutacão, todos no estado heterozigoto, 66,7 por cento (8/12) não apresentaram trombose. A deteccão do fator V de Leiden em pacientes portadores de eventos trombóticos é recomendado para esclarecimento das causas e para efetuar o rastreamento em membros de sua família, ainda sem o aparecimento de eventos trombóticos, de forma a avaliar os riscos associados e assim determinar um acompanhamento médico preventivo.

Role of the septal area in feeding behavior elicited by electrical stimulation of the lateral hypothalamus of the rat.

1. The present study was undertaken to investigate the influence of the septal area on neural mechanisms involved in feeding behavior elicited by electrical stimulation of the lateral hypothalamic area of the rat. 2. Electrolytic damage to medial and lateral septal nuclei induced a significant increase (18.29 +/- 1.69 to 25.05 +/- 2.31 g, P less than 0.05, N = 14) in food intake elicited by hypothalamic stimulation. The threshold current for stimulus-induced eating decreased by 20% after septal lesion. 3. A significant decrease in food ingestion was observed after electrical stimulation of the septal nuclei, either preceding (27.47 +/- 1.57 to 19.30 +/- 2.06 g, P less than 0.05, N = 13) or simultaneous (26.20 +/- 1.60 to 12.10 +/- 2.40 g, P less than 0.05, N = 11) with hypothalamic stimulation. 4. The results indicate an inhibitory effect of the septum on the lateral hypothalamic area and also suggest that the functional state of the lateral hypothalamus, which is responsible for the feeding behavior, depends on the activity pattern of the septal area.

Role of the septal area in feeding behavior elicited by electrical stimulation of the lateral hipothalamus of the rat

The present study was undertaken to investigate the influence of the septal area on neural mechanisms involved in feeding behavior elicited by electrical stimulation of the lateral hypothalamic area of the rat. Electrolytic damage to medial and lateral septal nuclei induced a significant increase (18.29 + or - 1.69 to 25.05 + or - 2.31 g, P<0.05, N = 14) in food intake elicited by hypothalamic stimulation. The threshold current for stimulus-induced eating decreased by 20% after septal lesion. A significant decrease in food ingestion was observed after electrical stimulation of the septal nuclei, either preceding (27.47 + or - 1.57 to 19.30 + or - 2.06 g P <0.05, N = 13) or simultaneous (26.20 + or - 1.60 to 12.10 + or - 2.40 g, P<0.05, N = 11) with hypothalamic stimulation. The results indicate an inhibitory effect of the septum on the lateral hypothalamic area and also suggest that the functional state of the lateral hypothalamus, which is responsible for the feeding behavior, depends on the activity pattern of the septal area

Feeding behavior elicited by electrical stimulation of the lateral hypothalamic area in the rat: role of the adrenergic pathways and receptors.

To study the role played by neurotransmitters and their receptor mechanisms in the control of feeding behavior elicited by electrical stimulation, drugs that affect neurotransmission were injected via cannula electrodes into the lateral hypothalamic area. Pretreatment with noradrenaline (0.5 and 1.0 nmol) significantly increased the effect of hypothalamic stimulation on feeding, whereas injection of 1.0, 2.0 and 4.0 nmol of adrenaline or dopamine was ineffective. Phentolamine (40.0, 80.0 and 100.0 nmol) and propranolol (40.0, 80.0 and 120.0 nmol) induced a decrease in food intake, suggesting the involvement of both alpha and beta receptors in this mechanism. However, isoprenaline (20.0 nmol) also reduced food intake. Reduction of food intake by propranolol was probably related to the action of the local anesthetic. Alphamethyl-p-tyrosine (203.0 nmol), reserpine (32.8 nmol) and 6-hydroxydopamine (200.0 nmol) inhibited the feeding behavior elicited by electrical stimulation of the lateral hypothalamic area. These results suggest that electrical stimulation of the lateral hypothalamic area elicits feeding behavior by releasing noradrenaline. Alpha-adrenergic receptors seem to play a facilitatory role in feeding behavior.

Effect of electrical and chemical stimulation of the lateral hypothalamus on taste preferences.

Bipolar stainless steel electrodes or stainless steel cannulas were implanted stereotaxically into the lateral hypothalamus of rats. Drinking was elicited by electrical or chemical (carbachol or angiotensin II) stimulation of animals, which were offered water and solutions of sodium chloride, saccharin, acetic acid and quinine. During electrical stimulation, ingestion of water and of all the solutions increased significantly. The same rats ingested significantly more sodium chloride and saccharin solution after 23 h water deprivation and electrical stimulation of the lateral hypothalamus. Carbachol administered into the lateral hypothalamus induced ingestion of saccharin solution and water but not of sodium chloride. Angiotensin II injected into the lateral hypothalamus did not induce drinking in most of the rats and those which drank preferred sodium chloride, saccharin and water. Several of the rats which did not respond to angiotensin II injection into the lateral hypothalamus, 72 h after angiotensin II responded to injection of carbachol by drinking the saccharin solution. The results of electrical stimulation suggest that the lateral hypothalamus consists of neurons involved in the ingestion of primary taste solutions. Depending on the functional state of the organism, lateral hypothalamic stimulation modifies ingestion of other taste substances but not of salt, as indicated by water deprivation. Chemical stimulation indicates that the neurotransmitter responsible for salt intake is not cholinergic and that the cholinergic neurons evoke preference for sweet taste and water. It appears that angiotensin II is involved in salt intake, as well as in producing preference for sweet taste and water.