Stress and Health Outcomes in Midwestern Latinx Youth: The Moderating Role of Ethnic Pride.

Background: Stress has been linked to numerous health outcomes, including internalizing and externalizing behaviors, self-esteem, and physical health. Culture has also been linked to stress and health. This study examined the links between stress and health, and the potential moderating role of Latinx ethnic pride (LEP).

The oligodendrocyte-myelin glycoprotein gene is highly expressed during the late stages of myelination in the rat central nervous system.

Oligodendrocyte-myelin glycoprotein (OMgp) is expressed on the surface of oligodendrocytes and neurones and is thought to inhibit axonal regeneration after brain injury in adult, like Nogo and myelin-associated glycoprotein (MAG). We previously observed that the OMgp gene locus on chromosome 17 could be associated with autism, a developmental disorder. The aim of the present study was to characterise the developmental expression of OMgp mRNA in the central nervous system.

Oligodendrocyte myelin glycoprotein growth inhibition function requires its conserved leucine-rich repeat domain, not its glycosylphosphatidyl-inositol anchor.

The oligodendrocyte myelin glycoprotein (OMgp) inhibits neurite outgrowth and axonal regeneration after brain injury, but its normal function remains unknown. Several observations suggest its implication in cell growth regulation. Here we report an analysis of the domain requirement in OMgp proliferation inhibitory function.

Molecular analysis of the oligodendrocyte myelin glycoprotein gene in autistic disorder.

We previously observed in four autistic patients a new allele (GXAlu 5) of the GXAlu microsatellite marker located in intron 27b of the neurofibromatosis type 1 (NF1) gene (17q11.2). This large intron contains the OMGP gene, coding for the oligodendrocyte myelin glycoprotein expressed by neurons and oligodendrocytes.

SMN1 gene study in three families in which ALS and spinal muscular atrophy co-exist.

Spinal muscular atrophy (SMA) is caused by SMN1 gene deletions or mutations, and ALS is the most frequent motor neuron condition in adults. The authors describe three families in which ALS and SMA coexist. The authors found that no SOD1 mutation was found within these families; all three ALS cases had at least two SMN1 copies; and an abnormal SMN1 gene locus did not explain the co-occurrence of these two motor neuron disorders in these families.