Neuro-functional modeling of near-death experiences in contexts of altered states of consciousness.

Near-death experiences (NDEs) including out-of-body experiences (OBEs) have been fascinating phenomena of perception both for affected persons and for communities in science and medicine. Modern progress in the recording of changing brain functions during the time between clinical death and brain death opened the perspective to address and understand the generation of NDEs in brain states of altered consciousness. Changes of consciousness can experimentally be induced in well-controlled clinical or laboratory settings.

Awareness and consciousness in humans and animals - neural and behavioral correlates in an evolutionary perspective.

Awareness or consciousness in the context of stimulus perception can directly be assessed in well controlled test situations with humans via the persons' reports about their subjective experiences with the stimuli. Since we have no direct access to subjective experiences in animals, their possible awareness or consciousness in stimulus perception tasks has often been inferred from behavior and cognitive abilities previously observed in aware and conscious humans. Here, we analyze published human data primarily on event-related potentials and brain-wave generation during perception and responding to sensory stimuli and extract neural markers (mainly latencies of evoked-potential peaks and of gamma-wave occurrence) indicating that a person became aware or conscious of the perceived stimulus.

Integrated annotation and analysis of in situ hybridization images using the ImAnno system: application to the ear and sensory organs of the fetal mouse.

An in situ hybridization (ISH) study was performed on 2000 murine genes representing around 10% of the protein-coding genes present in the mouse genome using data generated by the EURExpress consortium. This study was carried out in 25 tissues of late gestation embryos (E14.5), with a special emphasis on the developing ear and on five distinct developing sensory organs, including the cochlea, the vestibular receptors, the sensory retina, the olfactory organ, and the vibrissae follicles.

A SIRT7-dependent acetylation switch of GABPβ1 controls mitochondrial function.

Mitochondrial activity is controlled by proteins encoded by both nuclear and mitochondrial DNA. Here, we identify Sirt7 as a crucial regulator of mitochondrial homeostasis. Sirt7 deficiency in mice induces multisystemic mitochondrial dysfunction, which is reflected by increased blood lactate levels, reduced exercise performance, cardiac dysfunction, hepatic microvesicular steatosis, and age-related hearing loss.

Retinoic acid deficiency impairs the vestibular function.

The retinaldehyde dehydrogenase 3 (Raldh3) gene encodes a major retinoic acid synthesizing enzyme and is highly expressed in the inner ear during embryogenesis. We found that mice deficient in Raldh3 bear severe impairment in vestibular functions. These mutant mice exhibited spontaneous circling/tilted behaviors and performed poorly in several vestibular-motor function tests.