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A paper in press in the Journal of Bioterrorism & Biodefense has reignited the debate about the decade-old US anthrax investigation. According to The New York Times, "the new paper raises the prospect — for the first time in a serious scientific forum — that the Army biodefense expert identified by the FBI as the perpetrator, Bruce E. Ivins, had help in obtaining his germ weapons or conceivably was innocent of the crime" he was accused of — mailing letters tainted with dried anthrax spores to politicians and members of the media. The National Academy of Sciences' Alice Gast tells the Times that the potential value of the chemical signatures identified in this new paper had not been fully explored until now. "It just wasn't pursued as vigorously as the microbiology," Gast says. "In interviews, the three authors said their analysis suggested the FBI might have pursued the wrong suspect, and that the case should be reopened," the Times says, adding that "their position may embolden calls for a national commission to investigate the first major bioterrorist attack in American history." This week, the PBS news magazine Frontline — along with ProPublica and the McClatchy Company — digs into the Amerithrax investigation, calling it "the country's most notorious act of bioterrorism."

The Scan

Self-Reported Hearing Loss in Older Adults Begins Very Early in Life, Study Says

A JAMA Otolaryngology — Head & Neck Surgery study says polygenic risk scores associated with hearing loss in older adults is also associated with hearing decline in younger groups.

Genome-Wide Analysis Sheds Light on Genetics of ADHD

A genome-wide association study meta-analysis of attention-deficit hyperactivity disorder appearing in Nature Genetics links 76 genes to risk of having the disorder.

MicroRNA Cotargeting Linked to Lupus

A mouse-based study appearing in BMC Biology implicates two microRNAs with overlapping target sites in lupus.

Enzyme Involved in Lipid Metabolism Linked to Mutational Signatures

In Nature Genetics, a Wellcome Sanger Institute-led team found that APOBEC1 may contribute to the development of the SBS2 and SBS13 mutational signatures in the small intestine.