2,231 research outputs found

    Dependent plural pronouns with Skolemized choice functions

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    The present paper discusses two interesting phenomena concerning phi-features on plural pronouns: (i) plural pronouns that denote atomic individuals (‘dependent plural pronouns’), and (ii) plural pronouns with more than one binder (‘partial binding’). A novel account of these two phenomena is proposed, according to which all occurrences of phi-features are both semantically and morphologically relevant. For such a ‘uniformly semantic account’ of phi-features, dependent plural pronouns constitute a theoretical challenge, while partial binding is more or less straightforwardly accounted for. In order to make sense of the semantic effects of the phi-features on dependent plural pronouns, the following idea is pursued: the phi-features on a dependent plural pronoun reflect the range of values that the pronoun takes, rather than the particular value it denotes at a time. This idea is implemented in a compositional semantics by making use of (Skolemized) choice functions. An appealing feature of the present account is that, unlike its predecessors, it accounts for dependent plural pronouns without c-commanding antecedents in essentially the same way as for those with c-commanding antecedents. It is also shown how this account of dependent plural pronouns can straightforwardly be augmented with set indices to account for partial binding

    Electric foot-shock stress drives TNF-alpha production in the liver of IL-6-deficient mice

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    Objectives: Accumulating evidence has shown that interleukin-6 (IL-6) has pleiotropic effects on a variety of biological functions, including its antiapoptotic potential during liver injury. Our previous work demonstrated that restraint stress-induced elevation of plasma IL-6 negatively regulates plasma tumor necrosis factor-alpha (TNF-alpha). Herein, we further clarified the mechanism underlying the above finding and investigated the effect of IL-6 on liver apoptosis triggered by stress. Methods: Male C57BL/6J and IL-6-deficient C57BL/SV129 mice were exposed to 1 h of electric foot-shock stress. Thereafter, the serum, liver and spleen TNF-alpha levels were measured at several time points. Serum alanine aminotransferase (ALT), liver caspase-3 and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling ( TUNEL) activities were analyzed to evaluate the severity of liver injury and apoptosis. Results: The liver, but not the spleen, of the IL-6-deficient mice exhibited a significant increase in TNF-alpha level after stress in parallel with serum TNF-alpha elevation, whereas no such TNF-alpha responses were found in the wild animals. No significant differences in stress-induced elevation of serum ALT levels, liver caspase-3 activities and the number of TUNEL-positive hepatocytes were found between the wild and IL-6-deficient mice. Conclusions: Taken together, these results indicate that IL-6 may play a critical role in suppressing TNF-alpha production in the liver, thereby decreasing the blood TNF-alpha level. In contrast, IL-6 secretion was shown to have no protective effect on stress-triggered liver injury. Copyright (C) 2004 S. Karger AG, Basel

    De re readings of nested which-phrases in embedded questions

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    Presupposed ignorance and exhaustification: how scalar implicatures and presuppositions interact

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    We investigate the interactions between scalar implicatures and presuppositions in sentences containing both a scalar item and presupposition trigger. We first critically discuss Gajewski and Sharvit’s previous approach. We then closely examine two ways of integrating an exhaustivity-based theory of scalar implicatures with a trivalent approach to presuppositions. The empirical side of our discussion focuses on two novel observations: (i) the interactions between prosody and monotonicity, and (ii) what we call presupposed ignorance. In order to account for these observations, our final proposal relies on two mechanisms of scalar strengthening, the Presupposed Ignorance Principle and an exhaustivity operator which lets the presuppositions of negated alternatives project

    Japanese nominal conjunction only has the split reading

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    The hepatic sympathetic nerve plays a critical role in preventing Fas induced liver injury in mice

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    Background: Although previous studies have shown that the hepatic sympathetic nerve controls various physiological functions in the liver, the role of this nerve in liver injury has yet to be clarified.Aims: The purpose of this study was to elucidate the role of this nerve, based on our newly developed technique for selectively removing the activities of the hepatic sympathetic nerve.Subjects and methods: Male C57BL/6 mice were operated on for hepatic sympathetic denervation. Thereafter, mice were intravenously administered 0.25 or 0.35 mg/g weight of the Fas agonist antibody, Jo-2, after which mortality by fulminant hepatitis was evaluated. Apoptosis in the liver was also examined by both terminal deoxynucleotidyl transferase mediated dUTP nick end labelling and caspase-3 assay.Results: Mortality in sympathectomised mice was significantly higher than that in sham operated mice following administration of Jo-2. This result was also supported by apoptosis data in which sympathectomised livers exhibited a significant elevation in the number of apoptotic hepatocytes and caspase-3 activity after Jo-2 treatment compared with sham operated livers. Moreover, pretreatment with norepinephrine dose dependently inhibited the hepatic sympathectomy induced increase in mortality after Jo-2 injection. Antiapoptotic protein levels of FLICE inhibitory protein, Bcl-xL, and Bcl-2 in the liver were significantly lower in sympathectomised mice at one and two hours following Jo-2 treatment than in sham operated animals. In addition, interleukin 6 supplementation dose dependently suppressed the hepatic sympathectomy induced increase in mortality after Jo-2 treatment.Conclusions: These results suggest that norepinephrine released from the hepatic sympathetic nerve plays a critical role in protecting the liver from Fas mediated fulminant hepatitis, possibly via mechanisms including antiapoptotic proteins and interleukin 6

    Social disruption stress exacerbates alpha-galactosylceramide-induced hepatitis in mice

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    Objective: Psychosocial stress has been suggested as a possible aggravating factor in liver diseases, however, the underlying mechanism has yet to be clarified. Recently, our research revealed that electric foot-shock stress aggravated NK1.1 Ag+ T cell-dependent a-galactosylceramide (alpha-GalCer)-induced hepatitis in mice via a mechanism mediated by endogenous glucocorticoids. In this study, we examined whether or not such aggravation could be applied to a psychosocially stressful situation, e.g. social disruption stress. Methods: Male wildtype C57BL/6 (B6) or B6 hepatitis virus type B surface antigen transgenic (HBs-tg) mice, a hepatitis B virus carrier mouse model, were exposed 3 times in 1 week to social disruption stress in which an 8-month-old aggressive male intruder was placed into their home cage (5 mice per group) for 2 h. Twelve hours after the final exposure to the stress, the wild-type and HBs-tg mice were intravenously injected with alpha-GalCer. Results:The stress-exposed wild-type mice exhibited significantly reduced thymus weight loss compared with the control animals. Moreover, this stress regimen led to a significant increase in serum alanine aminotransferase levels in both the wild-type and the HBs-tg mice, although the increase in the HBs-tg mice was higher than that in the wild-type mice. Conclusion: These findings demonstrated that, similar to electric foot-shock stress, social disruption stress exacerbated alpha-GalCer-induced hepatitis. Copyright (C) 2005 S. Karger AG, Basel

    Varieties of intensification

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    This paper is a commentary on Beltrama and Bochnak (2015), who propose a uniform semantics for different uses of cross-categorial intensifiers -issimo in Italian and šému in Washo as universal quantifiers over contexts. Two concerns of their uniform semantics are raised, (i) unexpected restrictions on intensification, and (ii) non-truth-conditional intensification. It is argued that a uniform semantics like Beltrama and Bochnak’s is unachievable, and suggested that the multitude of uses commonly observed with intensifiers should be captured in terms of semantic similarity, rather than semantic identit
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