Universality of Phases in QCD and QCD-like Theories

We argue that the whole or the part of the phase diagrams of QCD and QCD-like theories should be universal in the large-N_c limit through the orbifold equivalence. The whole phase diagrams, including the chiral phase transitions and the BEC-BCS crossover regions, are identical between SU(N_c) QCD at finite isospin chemical potential and SO(2N_c) and Sp(2N_c) gauge theories at finite baryon chemical potential. Outside the BEC-BCS crossover region in these theories, the phase diagrams are also identical to that of SU(N_c) QCD at finite baryon chemical potential. We give examples of the universality in some solvable cases: (i) QCD and QCD-like theories at asymptotically high density where the controlled weak-coupling calculations are possible, (ii) chiral random matrix theories of different universality classes, which are solvable large-N (large volume) matrix models of QCD. Our results strongly suggest that the chiral phase transition and the QCD critical point at finite baryon chemical potential can be studied using sign-free theories, such as QCD at finite isospin chemical potential, in lattice simulations.Comment: v1: 35 pages, 6 figures; v2: 37 pages, 6 figures, minor improvements, conclusion unchanged; v3: version published in JHE

Pliocene-Quaternary crustal melting in central and northern Tibet and insights into crustal flow

There is considerable controversy over the nature of geophysically recognized low-velocity-high-conductivity zones (LV-HCZs) within the Tibetan crust, and their role in models for the development of the Tibetan Plateau. Here we report petrological and geochemical data on magmas erupted 4.7-0.3 Myr ago in central and northern Tibet, demonstrating that they were generated by partial melting of crustal rocks at temperatures of 700-1,050°C and pressures of 0.5-1.5 GPa. Thus Pliocene-Quaternary melting of crustal rocks occurred at depths of 15-50 km in areas where the LV-HCZs have been recognized. This provides new petrological evidence that the LV-HCZs are sources of partial melt. It is inferred that crustal melting played a key role in triggering crustal weakening and outward crustal flow in the expansion of the Tibetan Plateau

RAF Kinase Activity Regulates Neuroepithelial Cell Proliferation and Neuronal Progenitor Cell Differentiation during Early Inner Ear Development

Background: Early inner ear development requires the strict regulation of cell proliferation, survival, migration and differentiation, coordinated by the concerted action of extrinsic and intrinsic factors. Deregulation of these processes is associated with embryonic malformations and deafness. We have shown that insulin-like growth factor I (IGF-I) plays a key role in embryonic and postnatal otic development by triggering the activation of intracellular lipid and protein kinases. RAF kinases are serine/threonine kinases that regulate the highly conserved RAS-RAF-MEK-ERK signaling cascade involved in transducing the signals from extracellular growth factors to the nucleus. However, the regulation of RAF kinase activity by growth factors during development is complex and still not fully understood. Methodology/Principal Findings: By using a combination of qRT-PCR, Western blotting, immunohistochemistry and in situ hybridization, we show that C-RAF and B-RAF are expressed during the early development of the chicken inner ear in specific spatiotemporal patterns. Moreover, later in development B-RAF expression is associated to hair cells in the sensory patches. Experiments in ex vivo cultures of otic vesicle explants demonstrate that the influence of IGF-I on proliferation but not survival depends on RAF kinase activating the MEK-ERK phosphorylation cascade. With the specific RAF inhibitor Sorafenib, we show that blocking RAF activity in organotypic cultures increases apoptosis and diminishes the rate of cell proliferation in the otic epithelia, as well as severely impairing neurogenesis of the acoustic-vestibular ganglion (AVG) and neuron maturation. Conclusions/Significance: We conclude that RAF kinase activity is essential to establish the balance between cell proliferation and death in neuroepithelial otic precursors, and for otic neuron differentiation and axonal growth at the AVG

Predictors of Hepatitis Knowledge Improvement Among Methadone Maintained Clients Enrolled in a Hepatitis Intervention Program

This randomized, controlled study (n = 256) was conducted to compare three interventions designed to promote hepatitis A virus (HAV) and hepatitis B virus (HBV) vaccination completion, among clients undergoing methadone maintenance treatment (MMT) in Los Angeles and Santa Monica. The participants were randomized into three groups: Motivational Interviewing-Single Session (MI-Single), Motivational Interviewing-Group (MI-Group), or Nurse-Led Hepatitis Health Promotion (HHP). All three treatment groups received the 3-series HAV/HBV vaccine. The MI sessions were provided by trained therapists, the Nurse-Led HHP sessions were delivered by a research nurse. The main outcome variable of interest was improvement in HBV and HCV knowledge, measured by a 6-item HBV and a 7-item HCV knowledge and attitude tool that was administered at baseline and at 6-month follow-up. The study results showed that there was a significant increase in HBV- and HCV-related knowledge across all three groups (p < 0.0001). There were no significant differences found with respect to knowledge acquisition among the groups. Irrespective of treatment group, gender (P = 0.008), study site (P < 0.0001) and whether a participant was abused as a child (P = 0.017) were all found to be predictors of HCV knowledge improvement; only recruitment site (P < 0.0001) was found to be a predictor of HBV knowledge. The authors concluded that, although MI-Single, MI-Group and Nurse-Led HHP are all effective in promoting HBV and HCV knowledge acquisition among MMT clients, Nurse-Led HHP may be the method of choice for this population as it may be easier to integrate and with additional investigation may prove to be more cost efficient

Monazite trumps zircon: applying SHRIMP U–Pb geochronology to systematically evaluate emplacement ages of leucocratic, low-temperature granites in a complex Precambrian orogen

Although zircon is the most widely used geochronometer to determine the crystallisation ages of granites, it can be unreliable for low-temperature melts because they may not crystallise new zircon. For leucocratic granites U–Pb zircon dates, therefore, may reflect the ages of the source rocks rather than the igneous crystallisation age. In the Proterozoic Capricorn Orogen of Western Australia, leucocratic granites are associated with several pulses of intracontinental magmatism spanning ~800 million years. In several instances, SHRIMP U–Pb zircon dating of these leucocratic granites either yielded ages that were inconclusive (e.g., multiple concordant ages) or incompatible with other geochronological data. To overcome this we used SHRIMP U–Th–Pb monazite geochronology to obtain igneous crystallisation ages that are consistent with the geological and geochronological framework of the orogen. The U–Th–Pb monazite geochronology has resolved the time interval over which two granitic supersuites were emplaced; a Paleoproterozoic supersuite thought to span ~80 million years was emplaced in less than half that time (1688–1659 Ma) and a small Meso- to Neoproterozoic supersuite considered to have been intruded over ~70 million years was instead assembled over ~130 million years and outlasted associated regional metamorphism by ~100 million years. Both findings have consequences for the duration of associated orogenic events and any estimates for magma generation rates. The monazite geochronology has contributed to a more reliable tectonic history for a complex, long-lived orogen. Our results emphasise the benefit of monazite as a geochronometer for leucocratic granites derived by low-temperature crustal melting and are relevant to other orogens worldwide

Global Self-Organization of the Cellular Metabolic Structure

Background: Over many years, it has been assumed that enzymes work either in an isolated way, or organized in small catalytic groups. Several studies performed using "metabolic networks models'' are helping to understand the degree of functional complexity that characterizes enzymatic dynamic systems. In a previous work, we used "dissipative metabolic networks'' (DMNs) to show that enzymes can present a self-organized global functional structure, in which several sets of enzymes are always in an active state, whereas the rest of molecular catalytic sets exhibit dynamics of on-off changing states. We suggested that this kind of global metabolic dynamics might be a genuine and universal functional configuration of the cellular metabolic structure, common to all living cells. Later, a different group has shown experimentally that this kind of functional structure does, indeed, exist in several microorganisms. Methodology/Principal Findings: Here we have analyzed around 2.500.000 different DMNs in order to investigate the underlying mechanism of this dynamic global configuration. The numerical analyses that we have performed show that this global configuration is an emergent property inherent to the cellular metabolic dynamics. Concretely, we have found that the existence of a high number of enzymatic subsystems belonging to the DMNs is the fundamental element for the spontaneous emergence of a functional reactive structure characterized by a metabolic core formed by several sets of enzymes always in an active state. Conclusions/Significance: This self-organized dynamic structure seems to be an intrinsic characteristic of metabolism, common to all living cellular organisms. To better understand cellular functionality, it will be crucial to structurally characterize these enzymatic self-organized global structures.Supported by the Spanish Ministry of Science and Education Grants MTM2005-01504, MTM2004-04665, partly with FEDER funds, and by the Basque Government, Grant IT252-07

Oncogenic role of EAPII in lung cancer development and its activation of the MAPK–ERK pathway

Cancer progression involves multiple complex and interdependent steps, including progressive proliferation, angiogenesis and metastases. The complexity of these processes requires a comprehensive elucidation of the integrated signaling networks for better understanding. EAPII interacts with multiple cancer-related proteins, but its biological significance in cancer development remains unknown. In this report we identified the elevated level of EAPII protein in non-small-cell lung carcinoma (NSCLC) patients and NSCLC cell lines in culture. The oncogenic role of EAPII in lung cancer development was demonstrated using NSCLC cells with genetic manipulations that influence EAPII expression: EAPII overexpression increases proliferation of NSCLC cells with an accelerated transition of cell cycle and facilitates xenograft tumor growth in vivo; EAPII knockdown results in apoptosis of NSCLC cells and reduces xenograft tumor formation. To further explore the mechanism of EAPII's oncogenic role in lung cancer development and to elucidate the potential signaling pathway(s) that EAPII may impact, we employed antibody array to investigate the alternation of the major signaling pathways in NSCLC cells with altered EAPII level. We found that EAPII overexpression significantly activated Raf1 and ERK1/2, but not c-Jun N-terminal kinase and p38 pathways. Consistently, the protein and mRNA levels of MYC and cyclin D1, which are targets of the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK–ERK) pathway, are significantly increased by EAPII overexpression. Taken together, we demonstrated that EAPII is an oncogenic factor and the activation of MAPK–ERK signaling pathway by EAPII may contribute to lung cancer development

Synthetic biology: Understanding biological design from synthetic circuits

An important aim of synthetic biology is to uncover the design principles of natural biological systems through the rational design of gene and protein circuits. Here, we highlight how the process of engineering biological systems — from synthetic promoters to the control of cell–cell interactions — has contributed to our understanding of how endogenous systems are put together and function. Synthetic biological devices allow us to grasp intuitively the ranges of behaviour generated by simple biological circuits, such as linear cascades and interlocking feedback loops, as well as to exert control over natural processes, such as gene expression and population dynamics