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Health promotion
Published in Théodore H. MacDonald, Rethinking Health Promotion, 2012
All of this raises terribly serious issues about the importance of community validation of what may, on the surface, appear as scientifically neutral psychology. Among psychologists themselves, who may not be aware of the wider health promotion implications, there will be some who are quite prepared to apply their discipline to individuals in third-world countries in the spirit of neutrality described above (Reeler 1991; Tembo 1991; Foster and Louw-Potgieter 1991), while others declare that the cultural conditions and the distortion imposed on these conditions by disadvantageous trading relations with industrialised nations render it impossible to use traditional ‘psychological science’ in the third world in the way in which it is used in the first (Akin-Ojundeji 1991; Antaki 1989; Harris 1990; Jahoda 1983; Omari 1983; Smith 1991/2; Sinha 1983).
The Jackson Laboratory Mouse Mutant Resource
Published in John P. Sundberg, Handbook of Mouse Mutations with Skin and Hair Abnormalities, 2020
Other mutants, while not exact models, provide tools for studying specific biological systems. Many model systems that do not mimic human diseases can be used to study basic metabolic or developmental processes. We have a group of mutations affecting different cells of the cerebellum or different stages in cerebellar development: staggerer (sg) and weaver (wv) affect granule cells, nervous (nr) and Purkinje cell degeneration (pcd) affect Purkinje cells, and reeler (rl) interferes with normal neuron migration. Research by neurologists using this collection of cerebellar mutants has led to a better understanding of the development of the cerebellum and the functional relationship among cerebellar cells.6–9 Another important group of mutations are those with white spotting accompanied by a deficiency or absence of enteric ganglion cells of the colon, similar to human Hirschsprung’s disease. These include two recessive mutations—piebald lethal (sl) and lethal spotting (ls)10 — and a dominant gene — dominant megacolon (Dom).11 The osteopetrotic mutations — osteopetrosis (op), osteosclerosis (oc), microphthalmia (mi), and grey lethal (gl) — have been the key to studying the method of correction for marble bone disease of children.12 Spina bifida and neural tube anomalies, all too common birth defects among children, are being studied using curly tail (ct)u and homozygous splotch (Sp/Sp) and looptail (Lp/Lp) embryos.14 A group of mutations affecting the kidney — congenital polycystic kidneys (cpk), congenital progressive hydronephrosis (cph), and kidney disease (kd) — is providing new insight into renal development and function as well as mouse models for human polycystic kidney disease.10
Continuum modeling for neuronal lamination during cerebral morphogenesis considering cell migration and tissue growth
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2021
Hironori Takeda, Yoshitaka Kameo, Taiji Adachi
The neuronal migration during cerebral morphogenesis is regulated by extracellular signaling molecules including reelin (Marin et al. 2010; Valiente and Marin 2010; Chai et al. 2016). Reelin, which is secreted from the neurons in the MZ (D'Arcangelo et al. 1995), is thought to act as a chemoattractant in neuronal migration (D'Arcangelo and Curran 1998; Caffrey et al. 2014). In reeler mutants, which have reelin-deficient cerebrums, the neuronal lamination is inverted, forming in an outside-in manner, through inhibition of the neuronal migration (Sheppard and Pearlman 1997). To address the mechanisms governing the formation of inside-out lamination, it is necessary to clarify how neuronal migration is regulated by signaling molecules.
Unravelling the genetic architecture of autosomal recessive epilepsy in the genomic era
Published in Journal of Neurogenetics, 2018
Jeffrey D. Calhoun, Gemma L. Carvill
Lissencephaly, or smooth brain, can be conceptualized on the opposite end of the spectrum to polymicrogyria, as this malformation presents with reduced or absent folds in the cerebral cortex. The famous reeler mouse led to discovery of RELN, encoding Reelin; later RELN variants in a small number of families with lissencephaly with AR inheritance were identified (D'Arcangelo et al., 1995; Hong et al., 2000). Disrupted RELN function causes neuronal migration defects due to altered cell adhesion (Dulabon et al., 2000).
Reelin promotes oligodendrocyte precursors migration via the Wnt/β-catenin signaling pathway
Published in Neurological Research, 2021
Yaping Liu, Yuanyuan Wang, Wen Yuan, Fuxing Dong, Fei Zhen, Jing Liu, Lihua Yang, Xuebin Qu, Ruiqin Yao
Studies have found that Reelin plays an important role in the migration of nerve cells [38]. In reeler mice, nerve cells do not migrate to the designated location, but ectopic Reelin injection can compensate for this phenomenon [39]. In this study, we found that OPCs activity and proliferation did not change after Reelin treatment, but OPCs migration ability was greatly increased, indicating that Reelin plays a role in promoting OPCs migration in vitro.