Cultivo do milho irrigado.

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In vitro cultured progenitors and precursors of cardiac cell lineages from human normal and post-ischemic hearts.

The demonstration of the presence of dividing primitive cells in damaged hearts has sparked increased interest about myocardium regenerative processes. We examined the rate and the differentiation of in vitro cultured resident cardiac primitive cells obtained from pathological and normal human hearts in order to evaluate the activation of progenitors and precursors of cardiac cell lineages in post-ischemic human hearts. The precursors and progenitors of cardiomyocyte, smooth muscle and endothelial lineage were identified by immunocytochemistry and the expression of characteristic markers was studied by western blot and RT-PCR.The amount of proteins characteristic for cardiac cells (alpha-SA and MHC, VEGFR-2 and FVIII, SMA for the precursors of cardiomyocytes, endothelial and smooth muscle cells, respectively) inclines toward an increase in both alpha-SA and MHC. The increased levels of FVIII and VEGFR2 are statistically significant, suggesting an important re-activation of neoangiogenesis. At the same time, the augmented expression of mRNA for Nkx 2.5, the trascriptional factor for cardiomyocyte differentiation, confirms the persistence of differentiative processes in terminally injured hearts. Our study would appear to confirm the activation of human heart regeneration potential in pathological conditions and the ability of its primitive cells to maintain their proliferative capability in vitro. The cardiac cell isolation method we used could be useful in the future for studying modifications to the microenvironment that positively influence cardiac primitive cell differentiation or inhibit, or retard, the pathological remodeling and functional degradation of the heart

Remoção de torrões de lotes de sementes de soja para prevenir a disseminação do nematoide de cisto.

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Bickerstaff's Encephalitis, Guillain-barré Syndrome And Idiopathic Intracranial Hypertension: Are They Related Conditions?

[No abstract available]663 B744746Hughes, R.A., Cornblath, D.R., Guillain-Barré syndrome. (2005) Lancet, 366, pp. 1653-1666Overell, J.R., Willison, H.J., Recent developments in Miller Fisher syndrome and related disorders (2005) Curr Opin Neurol, 18, pp. 562-566Odaka, M., Yuki, N., Yamada, M., Bickerstaff's brainstem encephalitis: Clinical features of 62 cases and a subgroup associated with Guillain-Barré syndrome (2003) Brain, 126, pp. 2279-2290Ball, A.K., Clarke, C.E., Idiopathic intracranial hypertension (2006) Lancet Neurol, 5, pp. 433-442Walker, R.W., Idiopathic intracranial hypertension: Any light on the mechanism of the raised pressure? (2001) J Neurol Neurosurg Psychiatry, 71, pp. 1-5Weiss, G.B., Bajwa, Z.H., Mehler, M.F., Co-occurrence of pseudotumor cerebri and Guillain-Barré syndrome in an adult (1991) Neurology, 41, pp. 603-604Ropper, A.H., Marmarou, A., Mechanism of pseudotumor in Guillain-Barré syndrome (1984) Arch Neurol, 41, pp. 259-261Pulitanò, S., Viola, L., Genovese, O., Miller-Fisher syndrome mimicking intracranial hypertension following head trauma (2005) Childs Nerv Syst, 21, pp. 473-476Fisher, M., An unusual variant of acute idiopathic polyneuritis (syndrome of ophthalmoplegia, ataxia and areflexia) (1956) N Engl J Med, 255, pp. 57-65Bickerstaff, E.R., Brain-stem encephalitisfurther observations on a grave syndrome with benign prognosis (1957) Br Med J, 1, pp. 1384-1387Al-Din, A.N., The nosological position of the ophthalmoplegia, ataxia and areflexia syndrome: "the spectrum hypothesis (1987) Acta Neurol Scand, 75, pp. 287-294Chiba, A., Kusunoki, S., Obata, H., Serum anti-GQ1b IgG antibody is associated with ophthalmoplegia in Miller Fisher syndrome and Guillain-Barré syndrome: Clinical and immunohistochemical studies (1993) Neurology, 43, pp. 1911-1917Nagaoka, U., Kato, T., Kurita, K., Cranial nerve enhancement on three-dimensional MRI in Miller Fisher syndrome (1996) Neurology, 47, pp. 1601-1602Kornberg, A.J., Pestronk, A., Blume, G.M., Selective staining of the cerebellar molecular layer by serum IgG in Miller Fisher and related syndromes (1996) Neurology, 47, pp. 1317-1320Lo, Y.L., Chan, L.L., Pan, A., Ratnagopal, P., Acute ophthalmoparesis in the anti-GQ1b antibody syndrome: Electrophysiological evidence of neuromuscular transmission defect in the orbicularis oculi (2004) J Neurol Neurosurg Psychiatry, 75, pp. 436-440Yuki, N., Koga, M., Bacterial infections in Guillain-Barré and Fisher syndromes (2006) Curr Opin Neurol, 19, pp. 451-457Kwon, H.M., Hong, Y.H., Sung, J.J., A case of Bickerstaff's brainstem encephalitisthe evidence of cerebellum involvement by SPM analysis using PET (2006) Clin Neurol Neurosurg, 108, pp. 418-420Urushitani, M., Udaka, F., Kameyama, M., Miller Fisher-Guillain-Barré overlap syndrome with enhancing lesions in the spinocerebellar tracts (1995) J Neurol Neurosurg Psychiatry, 58, pp. 241-243Ogawara, K., Kuwabara, S., Yuki, N., Fisher syndrome or Bickerstaff brainstem encephalitis? Anti-GQ1b IgG antibody syndrome involving both the peripheral and central nervous systems (2002) Muscle Nerve, 26, pp. 845-849Overell, J.R., Hsieh, S.T., Odaka, M., Treatment for Fisher syndrome, Bickerstaff's brainstem encephalitis and related disorders (2007) Cochrane Database Syst Rev, 1. , CD00476