In this article we examine the allomorphic variation found in Pennsylvania Dutch plurality. In spite of over 250 years of variable contact with English, Pennsylvania Dutch plural allomorphy has remained largely distinct from English, except for a number of loan words and borrowings from English. Adopting a One Feature-One Head (OFOH) Architecture that interprets licit syntactic objects as spans, we argue that plurality is distributed across different root-types, resulting in stored lexical-trees (L-spans) in the bilingual mental lexicon. We expand the traditional feature inventory to be ‘mixed,’ consisting of both semantically-grounded features as well as ‘pure’ morphological features. A key claim of our analysis is that the s-exponent in Pennsylvania Dutch shares a syntactic representation for native and English-origin roots, although it is distinct from a ‘monolingual’ English representation. Finally, we highlight how our treatment of plurality in Pennsylvania Dutch, and allomorphic variation more generally, makes predictions about the nature of bilingual morphosyntactic representations.

Languages like Afrikaans are sometimes said to feature a class of adpositions that can be described as "intransitive" (e.g. binne "inside", bo "upstairs", agter "in the back", buite "outside", onder "downstairs" voor "in the front"). It is argued that such elements in fact instantiate a "hybrid" category -the locative noun category -which is not missing a Ground external argument but is actually lexicalising the nominal structure associated with that Ground argument itself. Such locative nouns pattern with R-pronouns and home-class nouns and therefore probably share a similar internal structure with these better-studied elements of language.

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Background: Background:Sickle cell disease (SCD) is caused by a point mutation in the beta globin gene. SCD is characterized by chronic hemolytic anemia, vaso-occlusive events leading to tissue ischemia and progressive organ failure. A chronic inflammatory state is part of the pathophysiology of SCD. Patients with SCD have extremely variable phenotypes, from a mild disease to severe complications including early age death.The spleen is commonly injured in SCD. Early splenic dysfunction and progressive spleen atrophy are common. Splenomegaly and hypersplenism, can also occur with loss of the crucial splenic function. Acute, life-threatening spleen-related complications in SCD are well studied. The implications of the spleen status including asplenia and splenomegaly/ hypersplenism in vaso-occlusive crisis and long-term complications in SCD remain to be determined.