Aspects of Passives in Capeverdean (Santiago’s variety)

The present dissertation intends to study passives in Capeverdean. I argue that Capeverdean have eventive passives with specific morphology, postverbal morphemes, -du and -da, which affix to the verb to form passives and interact with the TMA morphemes available in the language in the same way as in the active voice. I also show that Capeverdean only allows short passives. However, this study demonstrates that the by-phrase, although not expressed phonologically, is implicit and can be tracked through instrumentals and Agent-oriented adverbs. In order to account for this specific property of Capeverdean passives, I assume the existence of a Voice head which introduces the external argument in all finite sentences in Capeverdean, except in unaccusatives, following proposals from Marantz (1984), Kratzer (1996), Sailor & Ahn (2010), Pratas (2014). I also assume that this Voice head is subject to a Doubly Filled Comp Filter, similar to what is proposed in Koopman (1997), which determines that either heads or specifiers can be overt, never both. In the case of passives, I propose that external argument is in Spec,Voice and the passive morphology is lexicalized in Voice0 and that while Spec,Voice is silent, Voice0 is not. This configuration can be explained if it is assumed, following Costa & Martins (2004), that in Capeverdean passives Voice0 is a strong functional head, thus requiring visibility at PF. This restriction, combined with the Doubly Filled Comp filter, imposes that Spec,Voice is silent.

Molecular targeting of proteins by homocysteine: implications in familial and clinical hypercholesterolemia

Cardiovascular diseases (CVDs) are one of the leading causes of death and disability worldwide and one of its underlying causes is hypercholesterolemia. Hypercholesterolemia can have genetic (familial hypercholesterolemia, FH) and non-genetic causes (clinical hypercholesterolemia, CH), the first much more severe, with occurrence of premature atherosclerosis. While the pathophysiological role of homocysteine (Hcy) on CVD is still controversial, molecular targeting of protein by S and N-homocysteinylation offers a new paradigm to be considered in the vascular pathogenesis of hypercholesterolemia. On this regard, the present study aims to give new insights on protein targeting by Hcy in both CH and FH conditions. A total of 187 subjects were included: 65 normolipidemic and 122 hypercholesterolemic. Total (tHcy) and free (fHcy) fractions were quantified in serum samples after validation of an HPLCFD method, to assess S-homocysteinylation. Also, the lactonase (LACase) activity of paraoxonase-1 (PON1) was quantified by a colorimetric assay, as a surrogate of N-homocysteinylation. tHcy does not differ among groups. Nevertheless, fHcy declines in the hypercholesterolemic groups, with more evidence to the FH population. Consequently, there seems to be an increase of Shomocysteinylation, regardless of lipid lowering therapy (LLT). Also, despite of LLT use, LACase activity is lower in FH, thus the risk for protein N-homocysteinylation seems to be higher. Moreover, the decrease in LACase/ApoA1 and LACase/HDL ratios in FH, shows that HDL is dysfunctional in this population, despite its normal concentration values. Data supports that the pathophysiological role of Hcy on hypercholesterolemia may reside in its ability to post-translationally modify proteins. This role is particularly evident in FH condition. In the future, it will be interesting to identify which target proteins are modified and thus involved in vascular pathology progression.