null genotype underpins recurrence of meningiomas.

Introduction: Meningiomas are the most common primary central nervous system (CNS) tumor in adults, comprising one-third of all primary adult CNS tumors. Although several recent publications have identified molecular alterations in meningioma including characteristic mutations, copy number alterations, and gene expression signatures, our understanding of the drivers of meningioma recurrence is limited.

Objective: To identify gene expression signatures of 1p22qNF2 meningioma recurrence, with concurrent biallelic inactivation of and loss of chr1p that are heterogenous but enriched for recurrent meningiomas.

Aroclor speciation by unsupervised exploratory analysis of congener proportions in multivariate space: A southern California bight sediment and fish study.

Polychlorinated biphenyl (PCB) congeners, sold commercially as different mixtures under the trade name Aroclor in the USA, pose ecological and public health hazards. In the environment, they are monitored as Aroclors for potential source tracking and more accurately as congeners to understand the extent of PCB contamination in total. Because of the subjectivity with which Aroclors are currently identified in samples, striving towards clarity is a focus for analytical chemists.

Alterations in large-scale resting-state network nodes following transcranial focused ultrasound of deep brain structures.

Background: Low-intensity transcranial focused ultrasound (tFUS) is a brain stimulation approach that holds promise for the treatment of brain-based disorders. Studies in humans have shown that tFUS can successfully modulate perfusion in focal sonication targets, including the amygdala; however, limited research has explored how tFUS impacts large-scale neural networks.

Objective: The aim of the current study was to address this gap and examine changes in resting-state connectivity between large-scale network nodes using a randomized, double-blind, within-subjects crossover study design.

Spontaneous mutation in 2310061I04Rik results in reduced expression of mitochondrial genes and impaired brain myelination.

Here, we describe a spontaneous mouse mutant with a deletion in a predicted gene 2310061I04Rik (Rik) of unknown function located on chromosome 17. A 59 base pair long deletion occurred in the first intron of the Rik gene and disrupted its expression. Riknull mice were born healthy and appeared anatomically normal up to two weeks of age.