Strongly correlated excitonic insulator in atomic double layers.

Excitonic insulators (EIs) arise from the formation of bound electron-hole pairs (excitons)1,2 in semiconductors and provide a solid-state platform for quantum many-boson physics3-8. Strong exciton-exciton repulsion is expected to stabilize condensed superfluid and crystalline phases by suppressing both density and phase fluctuations8-11. Although spectroscopic signatures of EIs have been reported6,12-14, conclusive evidence for strongly correlated EI states has remained elusive. Here we demonstrate a strongly correlated two-dimensional (2D) EI ground state formed in transition metal dichalcogenide (TMD) semiconductor double layers. A quasi-equilibrium spatially indirect exciton fluid is created when the bias voltage applied between the two electrically isolated TMD layers is tuned to a range that populates bound electron-hole pairs, but not free electrons or holes15-17. Capacitance measurements show that the fluid is exciton-compressible but charge-incompressible-direct thermodynamic evidence of the EI. The fluid is also strongly correlated with a dimensionless exciton coupling constant exceeding 10. We construct an exciton phase diagram that reveals both the Mott transition and interaction-stabilized quasi-condensation. Our experiment paves the path for realizing exotic quantum phases of excitons8, as well as multi-terminal exciton circuitry for applications18-20.

Hypotensive hemorrhage increases calcium uptake capacity and Bcl-XL content of liver mitochondria.

We tested the hypothesis that the response of mitochondrial uptake of calcium and content of Bcl proteins to reversible hemorrhagic shock increases the vulnerability for hepatocellular death. Pentobarbital-anesthetized rats were bled to a mean arterial pressure of 30 to 40 mmHg for 1 h. A subset was then resuscitated (isotonic sodium chloride solution, three times shed volume). Liver mitochondria were isolated at the end of hemorrhage and 1.5 h after the onset of resuscitation. Resuscitation accelerated mitochondrial respiration in the presence of adenosine diphosphate (state 3) above control (P<0.01). The respiratory control ratio ([RCR] state 3/state 4) was calculated using the respiratory rate in the presence of carboxyatractyloside (state 4). The RCR was depressed at the end of hemorrhage and recovered completely in response to resuscitation (P<0.05). The mitochondrial capacity for calcium uptake increased at the end of hemorrhage and remained greater than control (P<0.01) after resuscitation when plasma ornithine carbamoyltransferase (an index of hepatocellular injury) was greater than control (P<0.05). At this time, the capacity for calcium uptake was correlated with plasma ornithine carbamoyltransferase (r=0.819, P<0.01). Mitochondrial content of Bcl-xL, an antiapoptotic protein, was increased at the end of hemorrhage (P<0.03) with no further change after resuscitation and no change in mitochondrial Bak, a proapoptotic protein. Thus, mitochondrial mechanisms are triggered early during reversible hypovolemia that may limit the intensity of intracellular calcium signaling and its potential to cause cellular injury and death.