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Quantum gravity in an AdS spacetime is described by an SU (N ) Yang-Mills theory on a sphere, a bounded many-body system. We argue that in the high temperature phase the theory is intrinsically non-perturbative in the large N limit. At any nonzero value of the 't Hooft coupling λ, an exponentially large (in N 2 ) number of free theory states of wide energy range (of order N ) mix under the interaction. As a result the planar perturbation theory breaks down. We argue that an arrow of time emerges and the dual string configuration should be interpreted as a stringy black hole.

Solid-phase microextraction (SPME) is a promising technique for determining organic contaminants within biotic systems. Existing in vivo SPME-kinetic calibration (SPME-KC) approaches are unwieldy due to the necessity of predetermining a distribution coefficient for the analyte of interest in the tissue and the preloading of a calibrating compound to the fiber. In this study, a rapid and convenient SPME alternative calibration method for in vivo analysis, termed SPME-sampling rate (SPME-SR) calibration, was developed and validated under both laboratory and field conditions to eliminate such presampling requirements. Briefly, the SPME probe is inserted into tissue, in this study fish dorsal-epaxial muscle, for 20 min allowing the concentrations of target analytes in the fish muscle to be determined by the extracted amount of analyte and the predetermined sampling rates. Atrazine, carbamazepine, and fluoxetine were detected nonlethally in the low ppb levels within fish muscle, with both laboratory and field-derived results obtained by in vivo SPME-KC comparable (within a factor of 1.27) to those obtained by lethal sampling followed by tissue liquid extraction. The technique described in this study represents an important advance which broadens the application of SPME in vivo sampling technology.

BackgroundDiabetes mellitus (DM) is associated with mitochondrial oxidative stress. We have shown that myocardial oxidative stress leads to diastolic dysfunction in a hypertensive mouse model. Therefore, we hypothesized that diabetes mellitus could cause diastolic dysfunction through mitochondrial oxidative stress and that a mitochondria‐targeted antioxidant (MitoTEMPO) could prevent diastolic dysfunction in a diabetic mouse model.Methods and ResultsC57BL/6J mice were fed either 60 kcal % fat diet (high‐fat diet [HFD]) or normal chow (control) for 8 weeks with or without concurrent MitoTEMPO administration, followed by in vivo assessment of diastolic function and ex vivo studies. HFD mice developed impaired glucose tolerance compared with the control (serum glucose=495±45 mg/dL versus 236±30 mg/dL at 60 minutes after intraperitoneal glucose injection, P<0.05). Myocardial tagged cardiac magnetic resonance imaging showed significantly reduced diastolic circumferential strain (Ecc) rate in the HFD mice compared with controls (5.0±0.3 1/s versus 7.4±0.5 1/s, P<0.05), indicating diastolic dysfunction in the HFD mice. Systolic function was comparable in both groups (left ventricular ejection fraction=66.4±1.4% versus 66.7±1.2%, P>0.05). MitoTEMPO‐treated HFD mice showed significant reduction in mitochondria reactive oxygen species, S‐glutathionylation of cardiac myosin binding protein C, and diastolic dysfunction, comparable to the control. The fasting insulin levels of MitoTEMPO‐treated HFD mice were also comparable to the controls (P>0.05).ConclusionsMitoTEMPO treatment prevented insulin resistance and diastolic dysfunction, suggesting that mitochondrial oxidative stress may be involved in the pathophysiology of both conditions.