Coarse-grained entropy and causal holographic information in AdS/CFT

We propose bulk duals for certain coarse-grained entropies of boundary regions. The `one-point entropy' is defined in the conformal field theory by maximizing the entropy in a domain of dependence while fixing the one-point functions. We conjecture that this is dual to the area of the edge of the region causally accessible to the domain of dependence (i.e. the `causal holographic information' of Hubeny and Rangamani). The `future one-point entropy' is defined by generalizing this conjecture to future domains of dependence and their corresponding bulk regions. We show that the future one-point entropy obeys a nontrivial second law. If our conjecture is true, this answers the question "What is the field theory dual of Hawking's area theorem?"Comment: 43 pages, 9 figures. v3: minor changes suggested by referee v2: added a few additional reference

A proof of the generalized second law for rapidly changing fields and arbitrary horizon slices

The generalized second law is proven for semiclassical quantum fields falling across a causal horizon, minimally coupled to general relativity. The proof is much more general than previous proofs in that it permits the quantum fields to be rapidly changing with time, and shows that entropy increases when comparing any slice of the horizon to any earlier slice. The proof requires the existence of an algebra of observables restricted to the horizon, satisfying certain axioms (Determinism, Ultralocality, Local Lorentz Invariance, and Stability). These axioms are explicitly verified in the case of free fields of various spins, as well as 1+1 conformal field theories. The validity of the axioms for other interacting theories is discussed.Comment: 44 pages, 1 fig. v3: clarified Sec. 2; signs, factors/notation corrected in Eq. 75-80, 105-107; reflects published version. v4: clearer axioms in Sec. 2.3, fixed compensating factor of 2 errors in Eq. 54,74 etc., and other errors. Results unaffected. v5: fixed typos. v6: replaced faulty 1+1 CFT argument, added note on recent progres

Overcoming status quo bias in the human brain

Humans often accept the status quo when faced with conflicting choice alternatives. However, it is unknown how neural pathways connecting cognition with action modulate this status quo acceptance. Here we developed a visual detection task in which subjects tended to favor the default when making difficult, but not easy, decisions. This bias was suboptimal in that more errors were made when the default was accepted. A selective increase in subthalamic nucleus (STN) activity was found when the status quo was rejected in the face of heightened decision difficulty. Analysis of effective connectivity showed that inferior frontal cortex, a region more active for difficult decisions, exerted an enhanced modulatory influence on the STN during switches away from the status quo. These data suggest that the neural circuits required to initiate controlled, nondefault actions are similar to those previously shown to mediate outright response suppression. We conclude that specific prefrontal-basal ganglia dynamics are involved in rejecting the default, a mechanism that may be important in a range of difficult choice scenarios

Evaluation of Vascular Control Mechanisms Utilizing Video Microscopy of Isolated Resistance Arteries of Rats

This protocol describes the use of in vitro television microscopy to evaluate vascular function in isolated cerebral resistance arteries (and other vessels), and describes techniques for evaluating tissue perfusion using Laser Doppler Flowmetry (LDF) and microvessel density utilizing fluorescently labeled Griffonia simplicifolia (GS1) lectin. Current methods for studying isolated resistance arteries at transmural pressures encountered in vivo and in the absence of parenchymal cell influences provide a critical link between in vivo studies and information gained from molecular reductionist approaches that provide limited insight into integrative responses at the whole animal level. LDF and techniques to selectively identify arterioles and capillaries with fluorescently-labeled GS1 lectin provide practical solutions to enable investigators to extend the knowledge gained from studies of isolated resistance arteries. This paper describes the application of these techniques to gain fundamental knowledge of vascular physiology and pathology in the rat as a general experimental model, and in a variety of specialized genetically engineered designer rat strains that can provide important insight into the influence of specific genes on important vascular phenotypes. Utilizing these valuable experimental approaches in rat strains developed by selective breeding strategies and new technologies for producing gene knockout models in the rat, will expand the rigor of scientific premises developed in knockout mouse models and extend that knowledge to a more relevant animal model, with a well understood physiological background and suitability for physiological studies because of its larger size

Tailoring an intervention to the context and system redesign related to the intervention: A case study of implementing shared medical appointments for diabetes

<p>Abstract</p> <p>Background</p> <p>Incorporating shared medical appointments (SMAs) or group visits into clinical practice to improve care and increase efficiency has become a popular intervention, but the processes to implement and sustain them have not been well described. The purpose of this study was to describe the process of implementation of SMAs in the local context of a primary care clinic over time.</p> <p>Methods</p> <p>The setting was a primary care clinic of an urban academic medical center of the Veterans Health Administration. We performed an in-depth case analysis utilizing both an innovations framework and a nested systems framework approach. This analysis helped organize and summarize implementation and sustainability issues, specifically: the pre-SMA local context; the processes of tailoring and implementation of the intervention; and the evolution and sustainability of the intervention and its context.</p> <p>Results</p> <p>Both the improvement intervention and the local context co-adapted and evolved during implementation, ensuring sustainability. The most important promoting factors were the formation of a core team committed to quality and improvement, and the clinic leadership that was supported strongly by the team members. Tailoring had to also take into account key innovation-hindering factors, including limited resources (such as space), potential to alter longstanding patient-provider relationships, and organizational silos (disconnected groups) with core team members reporting to different supervisors.</p> <p>Conclusion</p> <p>Although interventions must be designed to meet the needs of the sites in which they are implemented, specific guidance tailored to the practice environment was lacking. SMAs require complex changes that impact on care routines, collaborations, and various organizational levels. Although the SMA was not envisioned originally as a form of system redesign that would alter the context in which it was implemented, it became clear that tailoring the intervention alone would not ensure sustainability, and therefore adjustments to the system were required. The innovation necessitated reconfiguring some aspects of the primary care clinic itself and other services from which the patients and the team were derived. In addition, the relationships among different parts of the system were altered.</p

Observation of soft magnetorotons in bilayer quantum Hall ferromagnets

Inelastic light scattering measurements of low-lying collective excitations of electron double layers in the quantum Hall state at total filling nu_T=1 reveal a deep magnetoroton in the dispersion of charge-density excitations across the tunneling gap. The roton softens and sharpens markedly when the phase boundary for transitions to highly correlated compressible states is approached. The findings are interpreted with Hartree-Fock evaluations that link soft magnetorotons to enhanced excitonic Coulomb interactions and to quantum phase transitions in the ferromagnetic bilayers.Comment: ReVTeX4, 4 pages, 4 EPS figure

Lung Injury Pathways: Adenosine Receptor 2B Signaling Limits Development of Ischemic Bronchiolitis Obliterans Organizing Pneumonia

Purpose/Aim of the Study: Adenosine signaling was studied in bronchiolitis obliterans organizing pneumonia (BOOP) resulting from unilateral lung ischemia. Materials and Methods: Ischemia was achieved by either left main pulmonary artery or complete hilar ligation. Sprague–Dawley (SD) rats, Dahl salt sensitive (SS) rats and SS mutant rat strains containing a mutation in the A2B adenosine receptor gene (Adora2b) were studied. Adenosine concentrations were measured in bronchoalveolar lavage (BAL) by HPLC. A2A (A2AAR) and A2B adenosine receptor (A2BAR) mRNA and protein were quantified. Results: Twenty-four hours after unilateral PA ligation, BAL adenosine concentrations from ischemic lungs were increased relative to contralateral lungs in SD rats. A2BAR mRNA and protein concentrations were increased after PA ligation while miR27a, a negatively regulating microRNA, was decreased in ischemic lungs. A2AAR mRNA and protein concentrations remained unchanged following ischemia. A2BAR protein was increased in PA ligated lungs of SS rats after 7 days, and 4 h after complete hilar ligation in SD rats. SS-Adora2b mutants showed a greater extent of BOOP relative to SS rats, and greater inflammatory changes. Conclusion: Increased A2BAR and adenosine following unilateral lung ischemia as well as more BOOP in A2BAR mutant rats implicate a protective role for A2BAR signaling in countering ischemic lung injury

Effect of Combination Folic Acid, Vitamin B6 , and Vitamin B12 Supplementation on Fracture Risk in Women: A Randomized, Controlled Trial.

Epidemiologic studies have demonstrated an association of elevated plasma homocysteine levels with greater bone resorption and fracture risk. Vitamins B12 , B6 , and folic acid are cofactors in homocysteine metabolism, and supplementation with B vitamins is effective in lowering homocysteine levels in humans. However, randomized trials of supplemental B vitamins for reduction of fracture risk have been limited. Therefore, we performed an ancillary study to the Women's Antioxidant and Folic Acid Cardiovascular Study (WAFACS), a large randomized trial of women with preexisting cardiovascular disease or three or more coronary risk factors, to test whether a daily B vitamin intervention including folic acid (2.5 mg/day), vitamin B6 (50 mg/day), and vitamin B12 (1 mg/day) reduces nonspine fracture risk over 7.3 years of treatment and follow-up. Among 4810 women, we confirmed 349 nonspine fracture cases by centralized review of medical records. In a substudy of 300 women (150 in treatment group and 150 controls) with paired plasma samples at randomization and follow-up (7.3 years later), we measured two bone turnover markers, including C-terminal cross-linking telopeptide of type I collagen (CTX) and intact type I procollagen N-propeptide (P1NP). In Cox proportional hazards models based on intention-to-treat, we found no significant effects of B vitamin supplementation on nonspine fracture risk (relative hazard = 1.08; 95% confidence interval, 0.88 to 1.34). In a nested case-cohort analysis, there were no significant effects of B vitamins on fracture risk among women with elevated plasma homocysteine levels, or low levels of vitamins B12 or B6 , or folate at baseline. Furthermore, treatment with B vitamins had no effect on change in markers of bone turnover. We found no evidence that daily supplementation with B vitamins reduces fracture risk or rates of bone metabolism in middle-aged and older women at high risk of cardiovascular disease. © 2017 American Society for Bone and Mineral Research

Posttransplant lymphoproliferative disorders in neuronal xenotransplanted macaques

Posttransplant lymphoproliferative disorders (PTLDs) are a heterogeneous group of lymphoid proliferations that occur in the setting of depressed T-cell function due to immunosuppressive therapy used following solid organ transplantation, hematopoietic stem cell transplantation, and also xenotransplantation. In the present study, 28 immunosuppressed parkinsonian Macaca fascicularis were intracerebrally injected with wild-type or CTLA4-Ig transgenic porcine xenografts to identify a suitable strategy to enable long-term cell survival, maturation, and differentiation. Nine of 28 (32%) immunosuppressed primates developed masses compatible with PTLD, located mainly in the gastrointestinal tract and/or nasal cavity. The masses were classified as monomorphic PTLD according to the World Health Organization classification. Immunohistochemistry and polymerase chain reaction (PCR) analyses revealed that the PTLDs were associated with macaca lymphocryptovirus as confirmed by double-labeling immunohistochemistry for CD20 and Epstein-Barr nuclear antigen 2 (EBNA-2), where the viral protein was located within the CD20+ neoplastic B cells. In sera from 3 distinct phases of the experimental life of the primates, testing by quantitative PCR revealed a progression of the viral load that paralleled the PTLD progression and no evidence of zoonotic transmission of porcine lymphotropic herpesvirus through xenoneuronal grafts. These data suggest that monitoring the variation of macaca lymphocryptovirus DNA in primates could be used as a possible early diagnostic tool for PTLD progression, allowing preemptive treatment such as immunosuppression therapy reduction