| 1. |
- Bylund, Emanuel, 1979-, et al.
(författare)
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Does bilingualism come with linguistic costs? A meta-analytic review of the bilingual lexical deficit
- 2023
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Ingår i: Psychonomic Bulletin & Review. - : Springer Science and Business Media LLC. - 1069-9384 .- 1531-5320. ; 30:3, s. 897-913
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Forskningsöversikt (refereegranskat)abstract
- A series of recent studies have shown that the once-assumed cognitive advantage of bilingualism finds little support in the evidence available to date. Surprisingly, however, the view that bilingualism incurs linguistic costs (the so-called lexical deficit) has not yet been subjected to the same degree of scrutiny, despite its centrality for our understanding of the human capacity for language. The current study implemented a comprehensive meta-analysis to address this gap. By analyzing 478 effect sizes from 130 studies on expressive vocabulary, we found that observed lexical deficits could not be attributed to bilingualism: Simultaneous bilinguals (who acquired both languages from birth) did not exhibit any lexical deficit, nor did sequential bilinguals (who acquired one language from birth and a second language after that) when tested in their mother tongue. Instead, systematic evidence for a lexical deficit was found among sequential bilinguals when tested in their second language, and more so for late than for early second language learners. This result suggests that a lexical deficit may be a phenomenon of second language acquisition rather than bilingualism per se.
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| 2. |
- Lundqvist, Martin H., et al.
(författare)
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Is the Brain a Key Player in Glucose Regulation and Development of Type 2 Diabetes?
- 2019
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Ingår i: Frontiers in Physiology. - : FRONTIERS MEDIA SA. - 1664-042X. ; 10
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Forskningsöversikt (refereegranskat)abstract
- Ever since Claude Bernards discovery in the mid 19th-century that a lesion in the floor of the third ventricle in dogs led to altered systemic glucose levels, a role of the CNS in whole-body glucose regulation has been acknowledged. However, this finding was later overshadowed by the isolation of pancreatic hormones in the 20th century. Since then, the understanding of glucose homeostasis and pathology has primarily evolved around peripheral mechanism. Due to scientific advances over these last few decades, however, increasing attention has been given to the possibility of the brain as a key player in glucose regulation and the pathogenesis of metabolic disorders such as type 2 diabetes. Studies of animals have enabled detailed neuroanatomical mapping of CNS structures involved in glucose regulation and key neuronal circuits and intracellular pathways have been identified. Furthermore, the development of neuroimaging techniques has provided methods to measure changes of activity in specific CNS regions upon diverse metabolic challenges in humans. In this narrative review, we discuss the available evidence on the topic. We conclude that there is much evidence in favor of active CNS involvement in glucose homeostasis but the relative importance of central vs. peripheral mechanisms remains to be elucidated. An increased understanding of this field may lead to new CNS-focusing pharmacologic strategies in the treatment of type 2 diabetes.
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| 3. |
- Webb, Dominic-Luc, et al.
(författare)
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Bariatric surgery - time to replace with GLP-1?
- 2017
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Ingår i: Scandinavian Journal of Gastroenterology. - : Taylor & Francis. - 0036-5521 .- 1502-7708. ; 52:6-7, s. 635-640
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Forskningsöversikt (refereegranskat)abstract
- Obesity with a body mass index (BMI) over 30kg/m(2) represents a significant risk for increased morbidity and mortality, with reduced life expectancy of about 10 years. Until now, surgical treatment has been the only effective longterm intervention. The currently standardized method of bariatric surgery, gastric bypass, means that many gastrointestinal peptide hormones are activated, yielding net reductions in appetite and food intake. Among the most important gut peptide hormones in this perspective is glucagon-like peptide-1 (GLP-1), which rises sharply after gastric bypass. Consistent with outcomes of this surgery, GLP-1 suppresses appetite and reduces food intake. This implies that GLP-1 has the potential to achieve a similar therapeutic outcome as gastric bypass. GLP-1 analogs, which are used for the treatment of type 2 diabetes mellitus, also lead to significant weight loss. Altered hormonal profiles after gastric bypass therefore indicate a logical connection between gut peptide hormone levels, weight loss and glucose homeostasis. Furthermore, combinations of GLP-1 with other gut hormones such as peptide YY (PYY) and cholecystokinin (CCK) may be able to reinforce GLP-1 driven reduction in appetite and food intake. Pharmacological intenvention in obesity by use of GLP-1 analogs (exenatide, liraglutide, albiglutide, dulaglutide, lixisenatide, taspoglutide) and inhibitors of dipeptidyl peptidase-IV (DPP-IV) degradation that inactivate GLP-1 (sitagliptin, vildagliptin), leading to reduced appetite and weight with positive effects on metabolic control, are realistically achievable. This may be regarded as a low-risk therapeutic alternative to surgery for reducing obesity-related risk factors in the obese with lower BMIs.
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