Alarm substances are airborne chemical signals, released by an individual into the environment, which communicate emotional stress between conspecifics. Here we tested whether humans, like other mammals, are able to detect emotional stress in others by chemosensory cues. Sweat samples collected from individuals undergoing an acute emotional stressor, with exercise as a control, were pooled and presented to a separate group of participants (blind to condition) during four experiments. In an fMRI experiment and its replication, we showed that scanned participants showed amygdala activation in response to samples obtained from donors undergoing an emotional, but not physical, stressor. An odor-discrimination experiment suggested the effect was primarily due to emotional, and not odor, differences between the two stimuli. A fourth experiment investigated behavioral effects, demonstrating that stress samples sharpened emotion-perception of ambiguous facial stimuli. Together, our findings suggest human chemosensory signaling of emotional stress, with neurobiological and behavioral effects.

We use genome-wide nucleosome maps to study sequence specificity of intrinsic histone-DNA interactions. In contrast with previous approaches, we employ an analogy between a classical one-dimensional fluid of finite-size particles in an arbitrary external potential and arrays of DNA-bound histone octamers. We derive an analytical solution to infer free energies of nucleosome formation directly from nucleosome occupancies measured in high-throughput experiments. The sequence-specific part of free energies is then captured by fitting them to a sum of energies assigned to individual nucleotide motifs. We have developed hierarchical models of increasing complexity and spatial resolution, establishing that nucleosome occupancies can be explained by systematic differences in mono-and dinucleotide content between nucleosomal and linker DNA sequences, with periodic dinucleotide distributions and longer sequence motifs playing a minor role. Furthermore, similar sequence signatures are exhibited by control experiments in which nucleosome-free genomic DNA is either sonicated or digested with micrococcal nuclease, making it possible that current predictions based on high-throughput nucleosomepositioning maps are biased by experimental artifacts.chromatin structure | histone-DNA interactions | nucleosome positioning | biophysical models I n eukaryotes, 75%-90% of genomic DNA is packaged into histone-DNA complexes called nucleosomes, with adjacent nucleosomes separated by stretches of linker DNA (1). Each nucleosome consists of 147 base pairs (bp) of DNA wrapped around a histone octamer in a left-handed superhelix (2). Arrays of nucleosomes fold into filamentous chromatin fibers which constitute building blocks for higher-order structures (3). DNA wrapped in a nucleosome is occluded from interacting with other DNA-binding proteins such as transcription factors, RNA polymerase, and DNA repair complexes (2). On the other hand, histone tail domains act as substrates for posttranslational modifications, providing binding sites for chromatin-associated proteins which facilitate transitions between active and silent chromatin states (4).Several distinct factors affect nucleosome positions in living cells. First of all, intrinsic histone-DNA interactions are sequence-specific: for example, polyðdA∶dTÞ tracts are well known to disfavor nucleosome formation (5, 6). In addition, nucleosome-depleted regions can be generated through the action of ATP-dependent chromatin remodeling enzymes (7) and histone acetylases (8). Finally, non-histone DNA-binding factors can alter nucleosome positions through binding their cognate sites and either displacing nucleosomes or hindering their subsequent formation (9, 10).The nucleosome code hypothesis states that DNA sequence is the primary determinant of nucleosome positions in living cells (11). This hypothesis is often contrasted with the idea of statistical positioning which asserts that most nucleosomes are ordered into regular arrays simply by steric exclusion (12, 13). In this view the nucleosoma...

SUMMARY Oncocytomas are predominantly benign neoplasms possessing pathogenic mitochondrial mutations and accumulation of respiration-defective mitochondria, characteristics of unknown significance. Using exome and transcriptome sequencing, we identified two main subtypes of renal oncocytoma. Type 1 is diploid with CCND1 rearrangements, whereas type 2 is aneuploid with recurrent loss of chromosome 1, X or Y, and/or 14 and 21, which may proceed to more aggressive eosinophilic chromophobe renal cell carcinoma (ChRCC). Oncocytomas activate 5′ adenosine monophosphate-activated protein kinase (AMPK) and Tp53 (p53) and display disruption of Golgi and autophagy/lysosome trafficking, events attributed to defective mitochondrial function. This suggests that the genetic defects in mitochondria activate a metabolic checkpoint, producing autophagy impairment and mitochondrial accumulation that limit tumor progression, revealing a novel tumor-suppressive mechanism for mitochondrial inhibition with metformin. Alleviation of this metabolic checkpoint in type 2 by p53 mutations may allow progression to eosinophilic ChRCC, indicating that they represent higher risk.

We analyze the indirect exchange interaction between two two-state systems, e.g., spins 1/2, subject to a common finite-temperature environment modeled by bosonic modes. The environmental modes, e.g., phonons or cavity photons, are also a source of quantum noise. We analyze the coherent vs noise-induced features of the two-spin dynamics and predict that for low enough temperatures the induced interaction is coherent over time scales sufficient to create entanglement. A nonperturbative approach is utilized to obtain an exact solution for the onset of the induced interaction, whereas for large times, a Markovian scheme is used. We identify the time scales for which the spins develop entanglement for various spatial separations. For large enough times, the initially created entanglement is erased by quantum noise. Estimates for the interaction and the level of quantum noise for localized impurity electron spins in Si-Ge type semiconductors are given.