Nightmares are intense, emotionally negative mental experiences that usually occur during late-night sleep and result in abrupt awakenings. Questionnaire-based studies have shown that nightmares are related to impaired sleep quality; however, the polysomnographic profile of nightmare subjects has been only scarcely investigated. We investigated the sleep architecture of 17 individuals with frequent nightmares and 23 control subjects based on polysomnographic recordings of a second night spent in the laboratory after an adaptation night. Nightmare subjects in comparison with control subjects were characterized by impaired sleep architecture, as reflected by reduced sleep efficiency, increased wakefulness, a reduced amount of slow wave sleep, and increased nocturnal awakenings, especially from Stage 2 sleep. While these differences were independent of the effects of waking psychopathology, nightmare subjects also exhibited longer durations of REM sleep that was mediated by heightened negative affect. Our results support that nightmares are related to altered sleep architecture, showing impaired sleep continuity and emotion-related increase in REM propensity.

One of the most important omissions in recent evolutionary theory concerns how eukaryotes could emerge and evolve. According to the currently accepted views, the first eukaryotic cell possessed a nucleus, an endomembrane system, and a cytoskeleton but had an inefficient prokaryotic-like metabolism. In contrast, one of the most ancient eukaryotes, the metamonada Giardia lamblia, was found to have formerly possessed mitochondria. In sharp contrast with the traditional views, this paper suggests, based on the energetic aspect of genome organization, that the emergence of eukaryotes was promoted by the establishment of an efficient energy-converting organelle, such as the mitochondrion. Mitochondria were acquired by the endosymbiosis of ancient alpha-purple photosynthetic Gram-negative eubacteria that reorganized the prokaryotic metabolism of the archaebacterial-like ancestral host cells. The presence of an ATP pool in the cytoplasm provided by this cell organelle allowed a major increase in genome size. This evolutionary change, the remarkable increase both in genome size and complexity, explains the origin of the eukaryotic cell itself. The loss of cell wall and the appearance of multicellularity can also be explained by the acquisition of mitochondria. All bacteria use chemiosmotic mechanisms to harness energy; therefore the periplasm bounded by the cell wall is an essential part of prokaryotic cells. Following the establishment of mitochondria, the original plasma membrane-bound metabolism of prokaryotes, as well as the funcion of the periplasm providing a compartment for the formation of different ion gradients, has been transferred into the inner mitochondrial membrane and intermembrane space. After the loss of the essential function of periplasm, the bacterial cell wall could also be lost, which enabled the naked cells to establish direct connections among themselves. The relatively late emergence of mitochondria may be the reason why multicellularity evolved so slowly.

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Lovastatin inhibited the growth of Candida albicans in a fungistatic way. Although it triggers apoptosis in a great variety of eukaryotic cells, including many tumour cell lines, lovastatin failed to provoke apoptotic events in this human pathogen. The fungistatic behaviour of this statin might arise from its negative influence on membrane fluidity. Because yeast-->pseudomycelium and hyphae morphogenetic transitions took place under exposure to lovastatin morphogenetic switch and apoptotic cell death must be regulated independently in C. albicans.