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This Week in PNAS: Aug 1, 2017

For a study slated to appear in the early, online edition of the Proceedings of the National Academy of Sciences this week, researchers at the University of Illinois at Urbana-Champaign describe deep evolutionary conservation across genes implicated in autism spectrum disorder. The team began in somewhat unconventional places — honeybee colonies — to try to get a better handle on ASD contributors. The team used RNA sequencing to assess brain gene expression in bees selected from seven genetically distinct colonies, focusing on differentially expressed genes in 11 honeybees that did not respond to social stimuli such as queen bee larvae in a typical manner. The search led to signatures that included the bee versions of genes linked to ASD, the authors note, pointing to "deep conservation for genes associated with a human social pathology and individual differences in insect social behavior."

A team from Australia, the US, and Switzerland compares three different SNP-based methods for estimating inbreeding depression — the decline in survival, fertility, and other fitness measures in the offspring of related parents — to come up with an approach to correct for biases in inbreeding depression estimates related to linkage disequilibrium heterogeneity. After establishing this bias correction method, which tied in linkage disequilibrium and minor allele frequency stratification data, the researchers applied the so-called LDMS to more than two dozen traits in around 140,000 UK Biobank participants. "Out results illustrate that a careful choice of the measure of inbreeding combined with LDMS stratification improves both detection and quantification of [inbreeding depression] using SNP data."

Finally, investigators from Stanford University report on a blood serum cytokine signature that appears to coincide with presence and severity of myalgic encephalomyelitis or chronic fatigue syndrome, dubbed ME/CFS for short. Using a Luminex 51-multiplex array, the team tracked serum cytokine levels in 192 individuals with ME/CFS and 392 unaffected control individuals. Generally speaking, it saw enhanced serum levels of TGF-beta in those with ME/CFS, for example, while affected individuals had lower-than-usual serum resistin levels. The group notes that still more cytokines appeared to correspond with disease severity in the ME/CFS group, including cytokines contributing to pro-inflammatory processes.