OFF-LOADING PRESSURE RELIEF WITH FOAM CUT OUT CUSHIONS: EXPERIENCES FROM RANCHO LOS AMIGOS NATIONAL REHABILITATION CENTER.

This paper explores the efficacy of the cushion fitting technique using foam cut out cushions for off-loading bony prominences in the sitting position, with a particular focus on reducing the high risk of developing pressure injuries among aging wheelchair users. This technique, historically employed at Rancho Los Amigos National Rehabilitation Center, has shown promising results in reducing pressure injuries for patients with spinal cord injuries. However, its widespread adoption remains limited. This manuscript aims to raise awareness about foam cut out cushions, its historical context, and its contemporary relevance by presenting customized solutions for individual patients with specific deformities. Key clinical points are highlighted, emphasizing the importance of skilled clinicians in the fitting process and the need to consider foam cut out cushions alongside other preventive measures. Case examples illustrate successful outcomes, demonstrating improved pelvic stability, posture, and off-loading of bony prominences. By promoting foam cut out cushions as a valuable cushioning option, this manuscript equips clinicians with knowledge to utilize this technique effectively.

Combined expression trait correlations and expression quantitative trait locus mapping.

Coordinated regulation of gene expression levels across a series of experimental conditions provides valuable information about the functions of correlated transcripts. The consideration of gene expression correlation over a time or tissue dimension has proved valuable in predicting gene function. Here, we consider correlations over a genetic dimension. In addition to identifying coregulated genes, the genetic dimension also supplies us with information about the genomic locations of putative regulatory loci. We calculated correlations among approximately 45,000 expression traits derived from 60 individuals in an F2 sample segregating for obesity and diabetes. By combining the correlation results with linkage mapping information, we were able to identify regulatory networks, make functional predictions for uncharacterized genes, and characterize novel members of known pathways. We found evidence of coordinate regulation of 174 G protein-coupled receptor protein signaling pathway expression traits. Of the 174 traits, 50 had their major LOD peak within 10 cM of a locus on Chromosome 2, and 81 others had a secondary peak in this region. We also characterized a Riken cDNA clone that showed strong correlation with stearoyl-CoA desaturase 1 expression. Experimental validation confirmed that this clone is involved in the regulation of lipid metabolism. We conclude that trait correlation combined with linkage mapping can reveal regulatory networks that would otherwise be missed if we studied only mRNA traits with statistically significant linkages in this small cross. The combined analysis is more sensitive compared with linkage mapping alone.

Distinguishing covariation from causation in diabetes: a lesson from the protein disulfide isomerase mRNA abundance trait.

Protein disulfide isomerase (Pdi) is reported to be an insulin-regulated gene whose expression level is increased in the livers of rats with streptozotocin-induced diabetes. We found that Pdi mRNA is approximately 20-fold more abundant in the diabetes-susceptible BTBR mouse strain relative to the diabetes-resistant C56BL/6 (B6) strain. A genetic analysis was carried out to determine whether there is a causal relationship between elevated Pdi expression and diabetes phenotype in BTBR-ob/ob mice. We mapped Pdi mRNA abundance as a quantitative trait in 108 (B6 x BTBR)F(2)-ob/ob mice segregating for diabetes. We detected a single linkage at the telomeric end of chromosome 11, where the Pdi gene itself resides (logarithm of odds score >30.0). No linkage was detected for the Pdi mRNA trait in the regions where we have previously identified quantitative trait loci for diabetes traits. Sequencing of the Pdi promoter and cDNA revealed several single nucleotide polymorphisms between these two mouse strains. We conclude that in our experimental model, elevated Pdi expression is cis regulated and is not linked to diabetes susceptibility. Genetic analysis is a powerful tool for distinguishing covariation from causation in expression array studies of disease traits.