81 research outputs found

    Etnopaleontonímia balear. Recull de noms populars de fòssils de les illes Balears

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    En aquest treball es recopilen, estudien i interpreten, des d'una perspectiva etnopaleontològica, les aportacions i influències exercides pels fòssils en relació al patrimoni lingüístic (noms populars) de l'àmbit geogràfic de les Illes Balears.Ethnopalaeotoponymy in the Balearic Islands. A collection of popular fossil names used in the the Balearic Islands In this paper we bring together, study and interpret, from an ethnopaleontological perspective, the contribution and influence of fossils in relation to the linguistic heritage (popular names) of the geographical area of the Balearic Islands

    Fiebre botonosa mediterránea. Una enfermedad frecuente en Mallorca

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    Unidades deposicionales del Neógeno menorquín

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    En el Neógeno de Menorca se han diferenciado cinco Unidades deposicionales integradas en dos secuencias. La secuencia inferior comprende una Unidad Basal y una Unidad Detrítica, que registran un ciclo transgresivo - regresivo contemporáneo de una fase diastrófica. Se atribuye al Mioceno inferior y se correlaciona con los depósitos de la misma edad existentes en Mallorca. La secuencia superior comprende tres Unidades. La Unidad Inferior de Barras, discordante sobre la secuencia inferior y sobre el basamento, registra un rápido episodio transgresivo, seguido de una ligera regresión; comprende facies de plataforma progradante hacia el Sur y se atribuye al Tortoniense. Una importante ruptura sedimentaria marca el inicio de la Unidad Arrecifal, que comprende facies de plataforma "off-shore", talud y pared arrecifal y "lagoon"; se atribuye al Tortoniense superior-Messiniense y se correlaciona con el Complejo Arrecifal definido por Esteban (1979). La Unidad Superior de Barras se adosa y/o recubre tanto los taludes de la Unidad Arrecifal como las megalaminas de progradación de la Unidad Inferior de Barras; sus facies corresponden a barras de plataforma y presentan una posición cronoestratigráfica incierta, pudiéndose atribuir tanto al Complejo Terminal messiniense, como incluso al Plioceno.Five depositional units, arranged in two sequences, have been recognized in the Neogene at the island Menorca. The Lower Sequence comprises the "Unidad Basal" (Basal Unit) and the "Unidad Detrítica" (Detritic Unit). This sequence displays a transgressive-regresive cycle coeval with a diastrophic phase. It is a ascribed to Lower Miocene and has been correlated with deposits of the same age at Mallorca. The Upper Sequence comprises three units. The "Unidad Inferior de Barras" (Lower Bar Unit) lies unconformable over the Lower Sequence and over the basement. This unit records a fast transgressive episode followed by a slight regression. The "Unidad Inferior de Barras" comprises facies of a southprograding shelf ascribed to Tortonian. A significant sedimentary break underlines the beginning of the "Unidad Arrecifal" (Reef Unit). This unit comprises offshore shelf facies, reef-talus, reef-wall and lagoon facies. The unit is ascribed to Upper Tortonian-Messinian and is correlated with the Reef Complex defined by ESTEBAN (1979). The "Unidad Superior de Barras" (Upper Bar Unit) is leant against or recoveririg both the talusses of the "Unidad Arrecifal" and the mega-fore:,ets of the prograding "Unidad Inferior de Barras". The facies ccrrespond to shelf bars, displaying an uncertain cronostratigraphic position. They can be attributed to the Messinian Terminal Con-plex or even to the Pliocene

    Neuronal effects of Sugammadex in combination with Rocuronium or Vecuronium.

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    Rocuronium (ROC) and Vecuronium (VEC) are the most currently used steroidal non-depolarizing neuromuscular blocking (MNB) agents. Sugammadex (SUG) rapidly reverses steroidal NMB agents after anaesthesia. The present study was conducted in order to evaluate neuronal effects of SUG alone and in combination with both ROC and VEC. Using MTT, CASP-3 activity and Western-blot we determined the toxicity of SUG, ROC or VEC in neurons in primary culture. SUG induces apoptosis/necrosis in neurons in primary culture and increases cytochrome C (CytC), apoptosis-inducing factor (AIF), Smac/Diablo and Caspase 3 (CASP-3) protein expression. Our results also demonstrated that both ROC and VEC prevent these SUG effects. The protective role of both ROC and VEC could be explained by the fact that SUG encapsulates NMB drugs. In BBB impaired conditions it would be desirable to control SUG doses to prevent the excess of free SUG in plasma that may induce neuronal damage. A balance between SUG, ROC or VEC would be necessary to prevent the risk of cell damag

    Sugammadex, a neuromuscular blockade reversal agent, causes neuronal apoptosis in primary cultures.

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    Sugammadex, a γ-cyclodextrin that encapsulates selectively steroidal neuromuscular blocking agents, such as rocuronium or vecuronium, has changed the face of clinical neuromuscular pharmacology. Sugammadex allows a rapid reversal of muscle paralysis. Sugammadex appears to be safe and well tolerated. Its blood-brain barrier penetration is poor (< 3% in rats), and thus no relevant central nervous toxicity is expected. However the blood brain barrier permeability can be altered under different conditions (i.e. neurodegenerative diseases, trauma, ischemia, infections, or immature nervous system). Using MTT, confocal microscopy, caspase-3 activity, cholesterol quantification and Western-blot we determine toxicity of Sugammadex in neurons in primary culture. Here we show that clinically relevant sugammadex concentrations cause apoptotic/necrosis neuron death in primary cultures. Studies on the underlying mechanism revealed that sugammadex-induced activation of mitochondria- dependent apoptosis associates with depletion of neuronal cholesterol levels. Furthermore SUG increase CytC, AIF, Smac/Diablo and CASP-3 protein expression in cells in culture. Potential association of SUG-induced alteration in cholesterol homeostasis with oxidative stress and apoptosis activation occurs. Furthermore, resistance/sensitivity to oxidative stress differs between neuronal cell types

    Determination of neuronal antibodies in suspected and definite Creutzfeldt-Jakob disease

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    IMPORTANCE Creutzfeldt-Jakob disease (CJD) and autoimmune encephalitis with antibodies against neuronal surface antigens (NSA-abs) may present with similar clinical features. Establishing the correct diagnosis has practical implications in the management of care for these patients. OBJECTIVE To determine the frequency of NSA-abs in the cerebrospinal fluid of patients with suspected CJD and in patients with pathologically confirmed (ie, definite) CJD. DESIGN, SETTING, AND PARTICIPANTS A mixed prospective (suspected) and retrospective (definite) CJD cohort study was conducted in a reference center for detection of NSA-abs. The population included 346 patients with suspected CJD and 49 patients with definite CJD. MAIN OUTCOMES AND MEASURES Analysis of NSA-abs in cerebrospinal fluid with brain immunohistochemistry optimized for cell-surface antigens was performed. Positive cases in the suspected CJD group were further studied for antigen specificity using cell-based assays. All definite CJD cases were comprehensively tested for NSA-abs, with cell-based assays used for leucine-rich glioma-inactivated 1 (LGI1), contactin-associated protein-like 2 (CASPR2), N-methyl-D-aspartate (NMDA), and glycine (GlY) receptors. RESULTS Neuronal surface antigens were detected in 6 of 346 patients (1.7%) with rapid neurologic deterioration suggestive of CJD. None of these 6 patients fulfilled the diagnostic criteria for probable or possible CJD. The target antigens included CASPR2, LGI1, NMDAR, aquaporin 4, Tr (DNER [δ/notch-like epidermal growth factor-related receptor]), and an unknown protein. Four of the patients developed rapidly progressive dementia, and the other 2 patients had cerebellar ataxia or seizures that were initially considered to be myoclonus without cognitive decline. The patient with Tr-abs had a positive 14-3-3 test result. Small cell lung carcinoma was diagnosed in the patient with antibodies against an unknown antigen. All patients improved or stabilized after appropriate treatment. None of the 49 patients with definite CJD had NSA-abs. CONCLUSIONS AND RELEVANCE A low, but clinically relevant, number of patients with suspected CJD had potentially treatable disorders associated with NSA-abs. In contrast, none of 49 patients with definite CJD had NSA-abs, including NMDAR-abs, GlyR-abs, LGI1-abs, or CASPR2-abs. These findings suggest that cerebrospinal fluid NSA-abs analysis should be included in the diagnostic workup of patients with rapidly progressive central nervous system syndromes, particularly when they do not fulfill the diagnostic criteria of probable or possible CJD

    WIN 55,212-2, agonist of cannabinoid receptors, prevents amyloid β1-42 effects on astrocytes in primary culture

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    Alzheimer´s disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to many human diseases, including AD. However, studies on the effects of cannabinoids on astrocytes functions are scarce. In primary cultured astrocytes we studied cellular viability using MTT assay. Inflammatory and oxidative stress mediators were determined by ELISA and Westernblot techniques both in the presence and absence of Aβ1-42 peptide. Effects of WIN 55,212-2 (a synthetic cannabinoid) on cell viability, inflammatory mediators and oxidative stress were also determined. Aβ1-42 diminished astrocytes viability, increased TNF-α and IL-1β levels and p-65, COX-2 and iNOS protein expression while decreased PPAR-γ and antioxidant enzyme Cu/Zn SOD. WIN 55,212-2 pretreatment prevents all effects elicited by Aβ1-42. Furthermore, cannabinoid WIN 55,212-2 also increased cell viability and PPAR-γ expression in control astrocytes. In conclusion cannabinoid WIN 55,212-2 increases cell viability and anti-inflammatory response in cultured astrocytes. Moreover, WIN 55,212-2 increases expression of anti-oxidant Cu/Zn SOD and is able to prevent inflammation induced by Aβ1-42 in cultured astrocytes. Further studies would be needed to assess the possible beneficial effects of cannabinoids in Alzheimer's disease patients

    Epilepsy surgery in drug resistant temporal lobe epilepsy associated with neuronal antibodies

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    We assessed the outcome of patients with drug resistant epilepsy and neuronal antibodies who underwent epilepsy surgery. Retrospective study, information collected with a questionnaire sent to epilepsy surgery centers. Thirteen patients identified, with antibodies to GAD (8), Ma2 (2), Hu (1), LGI1 (1) or CASPR2 (1). Mean age at seizure onset: 23 years. Five patients had an encephalitic phase. Three had testicular tumors and five had autoimmune diseases. All had drug resistant temporal lobe epilepsy (median: 20 seizures/month). MRI showed unilateral temporal lobe abnormalities (mainly hippocampal sclerosis) in 9 patients, bilateral abnormalities in 3, and was normal in 1. Surgical procedures included anteromesial temporal lobectomy (10 patients), selective amygdalohippocampectomy (1), temporal pole resection (1) and radiofrequency ablation of mesial structures (1). Perivascular lymphocytic infiltrates were seen in 7/12 patients. One year outcome available in all patients, at 3 years in 9. At last visit 5/13 patients (38.5%) (with Ma2, Hu, LGI1, and 2 GAD antibodies) were in Engel's classes I or II. Epilepsy surgery may be an option for patients with drug resistant seizures associated with neuronal antibodies. Outcome seems to be worse than that expected in other etiologies, even in the presence of unilateral HS. Intracranial EEG may be required in some patients
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