Artificial Shading Can Adversely Affect Heat-tolerant Lettuce Growth and Taste, with Concomitant Changes in Gene Expression

Shading has been used to produce high-quality lettuce (Lactuca sativa) in locations where production conditions are not optimal for this cool-season crop. To learn what additional benefits shading provides if heat-tolerant cultivars are used and to understand the effects of shading on growth, sensory quality, chemical content, and transcriptome profile on heat-tolerant lettuce, we grew two romaine lettuce cultivars with and without shading using 50% black shadecloth in 2018 and 2019. Shading reduced plant leaf temperatures, lettuce head fresh weights, glucose and total sugars content, and sweetness, but not bitterness, whereas it increased lettuce chlorophyll b content compared with unshaded controls. Transcriptome analyses identified genes predominantly involved in chlorophyll biosynthesis, photosynthesis, and carbohydrate metabolism as upregulated in unshaded controls compared with shaded treatments. For the tested cultivars, which were bred to withstand high growing temperatures, it may be preferable to grow them under unshaded conditions to avoid increased infrastructure costs and obtain lettuce deemed sweeter than if shaded.

Keloid-Specific Gene Expression Profiling for Accurate Diagnostic and Therapeutic Applications

Scars are a heterogeneous disease including normotrophic scars, hypertrophic scars, and keloids. Of these lesions, keloids are a distinct subtype from any other type of scar. Clinically, it causes pain, itching, or tenderness, causing life discomfort and characteristically irreversible. Despite various treatment modalities, restoring keloids to normal tissues is difficult, and frequent recurrences have been reported. Therefore, it is essential to identify keloid-specific genes for accurate diagnosis and treatment of keloids. In an effort to find out keloid-specific genes, several studies compared keloids with scar-free normal skin, which leading general scar-related genes to be chosen rather than keloid-specific genes. To select for highly accurate keloid-specific genes and pathways, we compared the transcriptome profile of keloids with those of normotrophic scars and hypertrophic scars, which acquired from formalin-fixed paraffin-embedded human skin samples using high-throughput RNA-sequencing techniques. Differential expression analyses and over-representation analyses revealed that genes related to nervous system process were upregulated in keloids, whereas genes related with immune responses were downregulated in keloids. Additionally, the extracellular matrix related processes were highlighted in both hypertrophic scars and keloids. Finally, we highlight potential keloid-specific biomarkers and expression changes that can be employed for future therapeutics of keloids.

An interferon-related signature characterizes the whole blood transcriptome profile of insulin-resistant individuals—the CODAM study

Background Worldwide, the prevalence of obesity and insulin resistance has grown dramatically. Gene expression profiling in blood represents a powerful means to explore disease pathogenesis, but the potential impact of inter-individual differences in a cell-type profile is not always taken into account. The objective of this project was to investigate the whole blood transcriptome profile of insulin-resistant as compared to insulin-sensitive individuals independent of inter-individual differences in white blood cell profile. Results We report a 3% higher relative amount of monocytes in the insulin-resistant individuals. Furthermore, independent of their white blood cell profile, insulin-resistant participants had (i) higher expression of interferon-stimulated genes and (ii) lower expression of genes involved in cellular differentiation and remodeling of the actin cytoskeleton. Conclusions We present an approach to investigate the whole blood transcriptome of insulin-resistant individuals, independent of their DNA methylation-derived white blood cell profile. An interferon-related signature characterizes the whole blood transcriptome profile of the insulin-resistant individuals, independent of their white blood cell profile. The observed signature indicates increased systemic inflammation possibly due to an innate immune response and whole-body insulin resistance, which can be a cause or a consequence of insulin resistance. Altered gene expression in specific organs may be reflected in whole blood; hence, our results may reflect obesity and/or insulin resistance-related organ dysfunction in the insulin-resistant individuals.