Experimental demonstration of quantum effects in the operation of microscopic heat engines

The heat engine, a machine that extracts useful work from thermal sources, is one of the basic theoretical constructs and fundamental applications of classical thermodynamics. The classical description of a heat engine does not include coherence in its microscopic degrees of freedom. By contrast, a quantum heat engine might possess coherence between its internal states. Although the Carnot efficiency cannot be surpassed, and coherence can be performance degrading in certain conditions, it was recently predicted that even when using only thermal resources, internal coherence can enable a quantum heat engine to produce more power than any classical heat engine using the same resources. Such a power boost therefore constitutes a quantum thermodynamic signature. It has also been shown that the presence of coherence results in the thermodynamic equivalence of different quantum heat engine types, an effect with no classical counterpart. Microscopic heat machines have been recently implemented with trapped ions, and proposals for heat machines using superconducting circuits and optomechanics have been made. When operated with standard thermal baths, however, the machines implemented so far have not demonstrated any inherently quantum feature in their thermodynamic quantities. Here we implement two types of quantum heat engines by use of an ensemble of nitrogen-vacancy centres in diamond, and experimentally demonstrate both the coherence power boost and the equivalence of different heat-engine types. This constitutes the first observation of quantum thermodynamic signatures in heat machines

A hippocampal circuit linking dorsal CA2 to ventral CA1 critical for social memory dynamics

Recent results suggest that social memory requires the dorsal hippocampal CA2 region as well as a subset of ventral CA1 neurons. However, it is unclear whether dorsal CA2 and ventral CA1 represent parallel or sequential circuits. Moreover, because evidence implicating CA2 in social memory comes largely from long-term inactivation experiments, the dynamic role of CA2 in social memory remains unclear. Here, we use pharmacogenetics and optogenetics in mice to acutely and reversibly silence dorsal CA2 and its projections to ventral hippocampus. We show that dorsal CA2 activity is critical for encoding, consolidation, and recall phases of social memory. Moreover, dorsal CA2 contributes to social memory by providing strong excitatory input to the same subregion of ventral CA1 that contains the subset of neurons implicated in social memory. Thus, our studies provide new insights into a dorsal CA2 to ventral CA1 circuit whose dynamic activity is necessary for social memory.We thank David H. Brann and the other members of the Siegelbaum laboratory for helpful discussions and João Cerqueira for critical input. This work was supported by R01 MH104602 and R01 MH106629 from the NIH (S.A.S.), by PD/BD/113700/2015 from the Portuguese Foundation for Science and Technology (T.M.) and by the European Molecular Biology Organization (A.O.)

OXPHOS Supercomplexes as a Hallmark of the Mitochondrial Phenotype of Adipogenic Differentiated Human MSCs

Mitochondria are essential organelles with multiple functions, especially in energy metabolism. Recently, an increasing number of data has highlighted the role of mitochondria for cellular differentiation processes. Metabolic differences between stem cells and mature derivatives require an adaptation of mitochondrial function during differentiation. In this study we investigated alterations of the mitochondrial phenotype of human mesenchymal stem cells undergoing adipogenic differentiation. Maturation of adipocytes is accompanied by mitochondrial biogenesis and an increase of oxidative metabolism. Adaptation of the mt phenotype during differentiation is reflected by changes in the distribution of the mitochondrial network as well as marked alterations of gene expression and organization of the oxidative phosphorylation system (OXPHOS). Distinct differences in the supramolecular organization forms of cytochrome c oxidase (COX) were detected using 2D blue native (BN)-PAGE analysis. Most remarkably we observed a significant increase in the abundance of OXPHOS supercomplexes in mitochondria, emphasizing the change of the mitochondrial phenotype during adipogenic differentiation

Transcriptome Kinetics of Circulating Neutrophils during Human Experimental Endotoxemia

Polymorphonuclear cells (neutrophils) play an important role in the systemic inflammatory response syndrome and the development of sepsis. These cells are essential for the defense against microorganisms, but may also cause tissue damage. Therefore, neutrophil numbers and activity are considered to be tightly regulated. Previous studies have investigated gene transcription during experimental endotoxemia in whole blood and peripheral blood mononuclear cells. However, the gene transcription response of the circulating pool of neutrophils to systemic inflammatory stimulation in vivo is currently unclear. We examined neutrophil gene transcription kinetics in healthy human subjects (n = 4) administered a single dose of endotoxin (LPS, 2 ng/kg iv). In addition, freshly isolated neutrophils were stimulated ex vivo with LPS, TNFα, G-CSF and GM-CSF to identify stimulus-specific gene transcription responses. Whole transcriptome microarray analysis of circulating neutrophils at 2, 4 and 6 hours after LPS infusion revealed activation of inflammatory networks which are involved in signaling of TNFα and IL-1α and IL-1β. The transcriptome profile of inflammatory activated neutrophils in vivo reflects extended survival and regulation of inflammatory responses. These changes in neutrophil transcriptome suggest a combination of early activation of circulating neutrophils by TNFα and G-CSF and a mobilization of young neutrophils from the bone marrow

Mitochondria in neutrophil apoptosis

Central in the regulation of the short life span of neutrophils are their mitochondria. These organelles hardly contribute to the energy status of neutrophils but play a vital role in the apoptotic process. Not only do the mitochondria contain cytotoxic proteins that are released during apoptosis and contribute to caspase activation, but they also act as sensors of the metabolic and redox state of the cell and as scavengers of free Ca2+. The balance of the expression and activity of the proapoptotic and antiapoptotic members of the Bcl-2 family of proteins determines the life span of neutrophils, because these proteins are essential for the formation of a permeability transition pore in the mitochondria and also seem to control the release of Ca2+ from the endoplasmic reticulum and thereby mitochondrial energy metabolis

The expression pattern of genes related to melanogenesis and endogenous opioids in psoriasis

The melanocortin system is a major regulator of stress responses in the skin and is responsible for the induction of melanin synthesis through activation of melanogenesis enzymes. The expression of both melanocortin system genes and melanogenesis enzyme genes is altered in psoriasis, and the focus here was on twelve genes related to the signal transduction between them. Additionally, five endogenous opioid system genes that are involved in cutaneous inflammation were examined. Quantitative real-time-PCR was utilized to measure mRNA expression in punch biopsies from lesional and non-lesional skin of psoriasis patients and from the skin of healthy control subjects. Most of the genes related to melanogenesis were down-regulated in patients (CREB1, MITF, LEF1, USF1, MAPK14, ICAM1, PIK3CB, RPS6KB1, KIT, and ATRN). Conversely, an up-regulation occurred in the case of opioids (PENK, PDYN, and PNOC). The suppression of genes related to melanogenesis is in agreement with the reported reduction in pigmentation signaling in psoriatic skin and potentially results from the pro-inflammatory environment. The increase in endogenous opioids can be associated with their involvement in inflammatory dysregulation in psoriasis

Specific disruption of hippocampal mossy fiber synapses in a mouse model of familial Alzheimer's disease

10.1371/journal.pone.0084349PLoS ONE91e8434