abstract: The dichotomy between @entity161 and @entity13521 is, as E. Kraepelin suspected, flawed; no unequivocal separation can be achieved. There are no categories of @entity716 , but only continua of variation. However, the definition of nuclear symptoms by K. Schneider reveals the fundamental characteristics of the core syndrome--it is independent of the environment and constant in incidence across populations that have been separated for thousands of years. The associated genetic variation must be as old as @entity1 and represent a component of diversity that crosses the population as a whole. The fecundity disadvantage that accompanies the syndrome requires a balance in a substantial and universal advantage; this advantage, it is proposed, is the speciation characteristic of language; language and @entity716 have a common evolutionary origin. Language, it is suggested, originated in a critical change on the sex chromosomes (the 'speciation event'--the genetic change that defined the species) occurring in East Africa between 100 and 250 thousand years ago that allowed the two hemispheres to develop with a degree of independence. Language can be understood as bi-hemispheric with one component function--a linear output sequence--confined to the dominant hemisphere--and a second--parallel distributed sampling occurring mainly in the non-dominant hemisphere. This mechanism provides an account of the generativity of language. The significance of nuclear symptoms is that these reflect a breakdown of bi-hemispheric coordination of language, perhaps specifically of the process of 'indexicalisation' (the distinction between 'I' and 'you') of self- versus other-generated references. Nuclear symptoms can be described as 'language at the end of its tether'; the phenomena and population characteristics of the nuclear syndrome of @entity161 thus yield clues to the origin of the species.

title: Is @entity161 the price that XXXX pays for language?

entities_list: @entity1 :: ('9606', 'Species') :: ['Homo sapiens']

entities_list: @entity161 :: ('MESH:D012559', 'Disease') :: ['schizophrenia']

entities_list: @entity716 :: ('MESH:D011605', 'Disease') :: ['psychosis']

entities_list: @entity13521 :: ('MESH:C564108', 'Disease') :: ['manic-depressive illness']

answer: @entity1 :: (9606,Species) :: ['Homo sapiens']


abstract: The Wnts are a family of glycoproteins that regulate cell proliferation, fate decisions, and differentiation. In our study, we examined the contribution of Wnts to the development of ventral midbrain (VM) dopaminergic (DA) neurons. Our results show that @entity12401 is expressed in DA precursor cells and that @entity12401 signaling takes place in these cells, as assessed in TOPGAL [Tcf optimal-promoter beta-galactosidase] reporter @entity19 . We also found that @entity6034 , -3a, and -5a expression is differentially regulated during development and that partially purified Wnts distinctively regulate VM development. @entity6035 promoted the proliferation of precursor cells expressing the orphan nuclear receptor-related factor 1 ( @entity55236 ) but did not increase the number of @entity669 hydroxylase-positive neurons. Instead, @entity68934 increased the number of @entity35 midbrain DA neurons in @entity35 embryonic day 14.5 precursor cultures by two distinct mechanisms. @entity6034 predominantly increased the proliferation of @entity55236 + precursors, up-regulated cyclins D1 and D3, and down-regulated @entity5447 and @entity25033 mRNAs. In contrast, @entity28407 primarily increased the proportion of @entity55236 + precursors that acquired a neuronal DA phenotype and up-regulated the expression of @entity66464 and c-ret mRNA. Moreover, the soluble @entity462 -rich domain of Frizzled-8 (a Wnt inhibitor) blocked endogenous Wnts and the effects of @entity6034 a on proliferation and the acquisition of a DA phenotype in precursor cultures. These findings indicate that Wnts are key regulators of proliferation and differentiation of DA precursors during VM neurogenesis and that different Wnts have specific and unique activity profiles.

title: Differential regulation of midbrain dopaminergic neuron development by @entity6034 , XXXX , and @entity28407 .

entities_list: @entity462 :: ('MESH:D003545', 'Chemical') :: ['cysteine']

entities_list: @entity669 :: ('CHEBI:18186', 'Chemical') :: ['tyrosine']

answer: @entity6035 :: (303181(Tax:10116),Gene) :: ['Wnt-3a']