1,530 research outputs found

    Opere del conte Algarotti.

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    Includes index in vol. 7.Added t.p. in vol. 1, engraved by Giuseppe Patrini. Engraved portrait medallion of the author on t.p. in vol. 1, small woodcut title-vignettes on title pages in vol. 2-10.Mode of access: Internet

    Pragmatic aspects of grammaticalization: scilicet in Early Latin comedy

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    This study aims to describe the grammaticalization path of scilicet in the Latin comedy of Plautus and Terence. Adopting the theoretical framework of the Functional Discourse Grammar (Hengeveld & Mackenzie 2008), the analysis of the occurrences of scilicet in the Early Latin comedy allows us to identify four different readings of the same lexical item: (i) as a main verb of the sentence meaning ‘it is obvious’, which governs both past and future infinitival clauses; (ii) as a focalizer meaning ‘certainly’, which singles out and highlights a specific constituent of the sentence; (iii) as an epistemic modal adverb meaning ‘certainly’, which encodes the speaker’s commitment to the truth of the propositional content (‘subjectification’); (iv) at the discourse level, as both an illocutionary modifier, which reinforces the directive force of the sentence, and a discourse marker meaning ‘yes, of course’, which encodes the speaker’s affirmative answer to previous directives or questions of the addressee (‘intersubjectification’). In the latter case scilicet acquires a pragmatic-textual value that guarantees the fluidity and cohesion of the discourse act. The distribution of the different functions of scilicet in Plautus and Terence allow us to hypothesize an ‘evolutionary’ continuum in a diachronic perspective, which involves a grammaticalization process from the original impersonal verb to the epistemic modal adverb, and then to the discursive-pragmatic marker

    Effects of aging on the mechanical threshold of rat skeletal muscle fibers

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    Mechanical threshold was measured 'in vitro' in extensor digitorum longus (EDL) muscle fibers from rats of 3-4 and 29 months of age, by means of a two microelectrode 'point' voltage clamp. The potential needed for evoking a barly visible contraction was determined using depolarizing command pulses of 5-500 ms duration. At each pulse duration, the EDL fibers from aged rats contracted at a significantly more negative potential than did those from the younger adult rats. Accordingly, the strength duration curve of the aged EDL was significantly shifted towards more negative potentials compared to that for adult rats. The rheobase voltages estimated from the fit of such curves were -62.6 ± 0.81 mV and -57.1 ± 0.87 mV in aged and adult EDL fibers, respectively. The data suggest that changes in excitation-contraction coupling the prolongation of contractile times observed during aging in mammalian skeletal muscle. These results are consistent with the known reduction in rate and extent of Ca++ uptake by sarcoplasmic reticulum in aged rats

    The effect of diphenylamine-2-carboxylate on C1- channel conductance and on excitability characteristics of rat skeletal muscle

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    The effect of diphenylamine-2-carboxylate (DPC), a blocker of the Cl- conductance pathway in Cl- transporting epithelia, has been evaluated in-vitro on the electrophysiological variables of rat extensor digitorum longus muscle fibres. DPC (5-240 μM) caused a dose-related increase of membrane resistance which was attributed entirely to a fall in Cl- channel conductance (IC50, 120 μM), since potassium conductance was not affected by the treatment. DPC also modified fibre excitability. A significant dose-dependent increase was observed in the latency of the action potential and in the excitability of the membrane. DPC was less potent on striated fibres than anthracene-9-carboxylic acid, another specific blocker of C1- channel conductance. Moreover DPC was less potent on skeletal muscle than on C1- transporting epithelia. Morphological differences in the Cl- channels or of the drug binding sites may account for the differences between tissues

    Taurine: the appeal of a safe amino acid for skeletal muscle disorders.

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    Taurine is a natural amino acid present as free form in many mammalian tissues and in particular in skeletal muscle. Taurine exerts many physiological functions, including membrane stabilization, osmoregulation and cytoprotective effects, antioxidant and anti-inflammatory actions as well as modulation of intracellular calcium concentration and ion channel function. In addition taurine may control muscle metabolism and gene expression, through yet unclear mechanisms. This review summarizes the effects of taurine on specific muscle targets and pathways as well as its therapeutic potential to restore skeletal muscle function and performance in various pathological conditions. Evidences support the link between alteration of intracellular taurine level in skeletal muscle and different pathophysiological conditions, such as disuse-induced muscle atrophy, muscular dystrophy and/or senescence, reinforcing the interest towards its exogenous supplementation. In addition, taurine treatment can be beneficial to reduce sarcolemmal hyper-excitability in myotonia-related syndromes. Although further studies are necessary to fill the gaps between animals and humans, the benefit of the amino acid appears to be due to its multiple actions on cellular functions while toxicity seems relatively low. Human clinical trials using taurine in various pathologies such as diabetes, cardiovascular and neurological disorders have been performed and may represent a guide-line for designing specific studies in patients of neuromuscular diseases

    EFFECTS OF TAURINE DEPLETION ON EXCITATION-CONTRACTION COUPLING AND CL- CONDUCTANCES OF RAT SKELETAL MUSCLE.

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    The pharmacological action of taurine on skeletal muscle is to stabilize sarcolemma by increasing macroscopic conductance to Cl- (GCl), whereas a proposed physiological role for the amino acid is to modulate excitation-contraction coupling mechanism via Ca2+ availability. To get insight in the physiological role of taurine in skeletal muscle, the effects of its depletion were evaluated on voltage threshold for mechanical activation and GCl with the two intracellular microelectrode method in 'point' voltage clamp mode and current clamp mode, respectively. The experiments were performed on extensor digitorum longus muscle fibers from rats depleted of taurine by a chronic 4 week treatment with guanidinoethane sulfonate, a known inhibitor of taurine transporter. The treatment significantly modified the mechanical threshold of striated fibers; i.e. at each pulse duration they needed significantly less depolarization to contract and the fitted rheobase voltage was more negative by 10 mV with respect to untreated muscle fibers. In parallel, the treatment with guanidinoethane sulfonate produced a significant 40% lowering of GCl. In vitro application of 60 mM of taurine to such depleted muscles almost completely restored the mechanical threshold and increased GCl even above the value of untreated control. However, in vitro application of 60 mM of either taurine or guanidinoethane sulfonate to untreated control muscles did not cause any change of the mechanical threshold but increased GCl by 40% and 21%, respectively. Furthermore, 100 microM of the S-(-) enantiomer of 2-(p-chlorophenoxy)propionic acid almost fully blocked GCl but did not produce any change in the mechanical threshold of normal muscle fibers. The present results show that the large amount of intracellular taurine plays a role in the excitation-contraction coupling mechanism of striated muscle fibers. This action is independent from any effect involving muscle Cl- channels, but it is likely mediated by the proposed ability of taurine to modulate Ca2+ availability through the interaction with the Ca2+ transporters present on sarcoplasmic reticulum
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