[Admission to hospital for subarachnoid hemorrhage].
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Biomedical subjects
Publications and source records attributed to F Rubio.
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The wheat root high-affinity K+ transporter HKT1 functions as a sodium-coupled potassium co-uptake transporter. At toxic millimolar levels of sodium (Na+), HKT1 mediates low-affinity Na+ uptake while potassium (K+) uptake is blocked. In roots, low-affinity Na+ uptake and inhibition of K+ uptake contribute to Na+ toxicity. In the present study, the selectivity among alkali cations of HKT1 expressed in Xenopus oocytes and yeast was investigated under various ionic conditions at steady state. The data show that HKT1 is highly selective for uptake of the two physiologically significant alkali cations, K+ and Na+ over Rb+, Cs+ and Li+. In addition, Rb+ and Cs+, and an excess of extracellular K+ over Na+, are shown to partially reduce or block HKT1-mediated K(+)-Na+ uptake. Furthermore, K+, Rb+ and Cs+ also effectively reduce outward currents mediated by HKT1, thereby causing depolarizations. In yeast, HKT1 can produce high-affinity Rb+ uptake at approximately 15-fold lower rates than for K+. Rb+ influx in yeast can be mediated by the ability of the yeast plasma membrane proton pump to balance the >or= 35-fold lower HKT1 conductance for Rb+. A model for HKT1 activity is presented involving a high-affinity K+ binding site and a high-affinity Na+ binding site, and competitive interactions of K+, Na+ and other alkali cations for binding to these two sites. Possible implications of the presented results for physiological K+ and Na+ uptake in plants are discussed.
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We present the preliminary results of six months cerebrovascular pathology follow-up carried out at the Sant Boi Local Hospital as from when a Neurological Unit was set up within the Internal Medecine Service. For this purpose we drew up a prospective study based on questionnaires. A total of 69 neurological patients (2.45% of all those hospitalized) were studied, 62.3% of whom suffered acute stroke. Diagnostic and therapeutic activities were analyzed with regards to the afore mentioned pathology, as well as various data of an epidermiological nature. Lastly we present the experimental multidisciplinary approach to acute stroke as performed during hospitalization by the Internal Medecine Service, Convalescence Unit and an Interdepartmental Socio-Sanitary Functional Unit.
Sodium (Na+) at high millimolar concentrations in soils is toxic to most higher plants and severely reduces agricultural production worldwide. However, the molecular mechanisms for plant Na+ uptake remain unknown. Here, the wheat root high-affinity potassium (K+) uptake transporter HKT1 was shown to function as a high-affinity K(+)-Na+ cotransporter. High-affinity K+ uptake was activated by micromolar Na+ concentrations; moreover, high-affinity Na+ uptake was activated by K+ (half-activation constant, 2.8 microM K+). However, at physiologically detrimental concentrations of Na+, K+ accumulation mediated by HKT1 was blocked and low-affinity Na+ uptake occurred (Michaelis constant, approximately 16 mM Na+), which correlated to Na+ toxicity in plants. Point mutations in the sixth putative transmembrane domain of HKT1 that increase Na+ tolerance were isolated with the use of yeast as a screening system. Na+ uptake and Na+ inhibition of K+ accumulation indicate a possible role for HKT1 in physiological Na+ toxicity in plants.
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NaCl-sensitive yeast mutants were isolated to identify genes essential for NaCl tolerance. Complementation of a mutant highly sensitive to Na+ and Li+ led to the isolation of the CNB1 gene. This gene encodes the regulatory subunit (CNB) of the Ca2+/calmodulin-dependent protein phosphatase calcineurin. Cells deficient in CNB accumulated Li+ due to reduced expression of ENA1, a gene encoding a P-type ATPase involved in Na+ and Li+ efflux. In addition, the K+ transport system of cnb1 delta cells was not converted to the high affinity state that facilitates better discrimination of K+ over Na+. Thus the cnb1 delta strain resembled a trk1 mutant. These results indicate that adaptation to NaCl stress in Saccharomyces cerevisiae requires a signal transduction pathway involving Ca2+ and protein phosphorylation-dephosphorylation. In this pathway, calcineurin would coordinate gene expression and activity of ion transporters to facilitate ion homeostasis.
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Primary meningeal lymphomas are an infrequent disease representing 1% of the primary cerebral lymphomas. Progressive paraparesia constitutes the most frequent presentation with progressive infiltration of the cranial nerves being an usual initial manifestation. The case of a primary meningeal lymphoma is presented in a 76 years old patient in whom the form of presentation involved progressive infiltration of cranial nerves. Repeated lumbar punctions demonstrated infiltration of cranial nerves. Repeated lumbar punctions demonstrated inflammatory changes with high protein levels and low sugar levels in cerebrospinal fluid and pleocytosis. No malignant cells were observed upon cytologic study of the LCR. The importance of the determination of tumor markers in LCR and the use of MR with gadolinium in the early diagnosis of this entity is commented upon.
The ENA2 gene encoding a P-type ATPase involved in Na+ and Li+ effluxes in Saccharomyces cerevisiae has been isolated. The putative protein encoded by ENA2 differs only in thirteen amino acids from the protein encoded by ENA1/PMR2. However, ENA2 has a very low level of expression and for this reason did not confer significant Li+ tolerance on a Li+ sensitive strain. ENA1 and ENA2 are the first two units of a tandem array of four highly homologous genes with probably homologous functions.
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Antiphospholipid antibodies (APA) have been described not only in systemic lupus erythematosus but also in several inflammatory diseases of the connective tissue, some infections, neoplasms, in pregnancy and even in apparently healthy individuals. Arterial and venous thrombosis are some of the clinical manifestations most frequently associated with APA. Two patients with ankylosing spondylitis with antiphospholipid antibodies are presented. The first patient developed a infarct in the pons as a complication at 34 years of age, with high titres of anticardiolipin antibodies as the only factor predisposing a cerebral vascular accident. The second patient had deep vein thrombosis with the presence of circulating anticoagulant. These are the first cases of antiphospholipid syndrome associated to ankylosing spondylitis in the literature.
Peduncular hallucinations are generally associated with lesions of the midbrain. We describe a 68-year-old man who developed left hemiparesis, paraesthesias on the left side and vivid visual hallucinations, suggesting peduncular hallucinosis. MRI demonstrated a right posterior thalamic infarct as the sole lesion.
According to the diagnostic criteria currently in use, the so-called "unilateral" forms of the moyamoya disease, or rather those in which the disorders of the disease itself--such as occlusion of the internal supraclinoid carotid artery or its terminal branches and development of abnormal collateral circulation in the region of the basal ganglia--are only found in one hemisphere and should be considered as "probable" forms of the disease with a much lower incidence than the bilateral or "defined" forms of the same. One patient with a primary intraventricular hemorrhage (PIVH) in whom an occlusion of the right internal carotid artery was angiographically demonstrated and in whom collateral type moyamoya circulation was found as was the presence of an aneurysm in the right coroid territory is presented. The association of PIVH, unilateral moyamoya disease and aneurysm is infrequent in the literature, with the origin of the bleeding, in some cases, having been attributed to rupture of the aneurysm. Since angiographic control was not available in the patient presented it cannot be excluded that the aneurysm was really a pseudoaneurysm therefore being a consequence, rather than a cause, of the arterial rupture. Thus one of the other mechanisms proposed must be invoked to explain the pathogenesis of the PIVH: rupture of a perforating artery or of a microaneurysm located in the subependimary periventricular region. The treatment recommended for these case of PIVH associated to aneurysm is chirurgical if persistence is demonstrated in successive arteriographies.
We report the case of a 25-year old man with vestibulocochlear and ocular impairment compatible with Cogan's syndrome. Later on, severe headache developed. CT scan showed an ischaemic lesion in the right frontal lobe. Magnetic resonance imaging demonstrated multiple bilateral nodular lesions on T2-weighted sequences. These were unmodified at a second MRI examination performed six months later. Under corticosteroids, the neurological and ophthalmic symptoms disappeared, but the patient remained deaf. We believe that this patient had vasculitis involving the brain, with infarcts. To our knowledge, no case of Cogan's syndrome with cerebral magnetic resonance imaging has yet been reported.