Multi-particle structure in the Z_n-chiral Potts models

We calculate the lowest translationally invariant levels of the Z_3- and Z_4-symmetrical chiral Potts quantum chains, using numerical diagonalization of the hamiltonian for N <= 12 and N <= 10 sites, respectively, and extrapolating N to infinity. In the high-temperature massive phase we find that the pattern of the low-lying zero momentum levels can be explained assuming the existence of n-1 particles carrying Z_n-charges Q = 1, ... , n-1 (mass m_Q), and their scattering states. In the superintegrable case the masses of the n-1 particles become proportional to their respective charges: m_Q = Q m_1. Exponential convergence in N is observed for the single particle gaps, while power convergence is seen for the scattering levels. We also verify that qualitatively the same pattern appears for the self-dual and integrable cases. For general Z_n we show that the energy-momentum relations of the particles show a parity non-conservation asymmetry which for very high temperatures is exclusive due to the presence of a macroscopic momentum P_m=(1-2Q/n)/\phi, where \phi is the chiral angle and Q is the Z_n-charge of the respective particle.Comment: 22 pages (LaTeX) plus 5 figures (included as PostScript), BONN-HE-92-3

The Deconfinement Phase Transition in One-Flavour QCD

We present a study of the deconfinement phase transition of one-flavour QCD, using the multiboson algorithm. The mass of the Wilson fermions relevant for this study is moderately large and the non-hermitian multiboson method is a superior simulation algorithm. Finite size scaling is studied on lattices of size $8^3\times 4$, $12^3\times 4$ and $16^3\times 4$. The behaviours of the peak of the Polyakov loop susceptibility, the deconfinement ratio and the distribution of the norm of the Polyakov loop are all characteristic of a first-order phase transition for heavy quarks. As the quark mass decreases, the first-order transition gets weaker and turns into a crossover. To investigate finite size scaling on larger spatial lattices we use an effective action in the same universality class as QCD. This effective action is constructed by replacing the fermionic determinant with the Polyakov loop identified as the most relevant Z(3) symmetry breaking term. Higher-order effects are incorporated in an effective Z(3)-breaking field, $h$, which couples to the Polyakov loop. Finite size scaling determines the value of $h$ where the first order transition ends. Our analysis at the end - point, $h_{ep}$, indicates that the effective model and thus QCD is consistent with the universality class of the three dimensional Ising model. Matching the field strength at the end point, $h_{ep}$, to the $\kappa$ values used in the dynamical quark simulations we estimate the end point, $\kappa_{ep}$, of the first-order phase transition. We find $\kappa_{ep}\sim 0.08$ which corresponds to a quark mass of about 1.4 GeV .Comment: LaTex, 25 pages, 18 figure

SHANK3 controls maturation of social reward circuits in the VTA.

Haploinsufficiency of SHANK3, encoding the synapse scaffolding protein SHANK3, leads to a highly penetrant form of autism spectrum disorder. How SHANK3 insufficiency affects specific neural circuits and how this is related to specific symptoms remains elusive. Here we used shRNA to model Shank3 insufficiency in the ventral tegmental area of mice. We identified dopamine (DA) and GABA cell-type-specific changes in excitatory synapse transmission that converge to reduce DA neuron activity and generate behavioral deficits, including impaired social preference. Administration of a positive allosteric modulator of the type 1 metabotropic glutamate receptors mGluR1 during the first postnatal week restored DA neuron excitatory synapse transmission and partially rescued the social preference defects, while optogenetic DA neuron stimulation was sufficient to enhance social preference. Collectively, these data reveal the contribution of impaired ventral tegmental area function to social behaviors and identify mGluR1 modulation during postnatal development as a potential treatment strategy

Greater maintenance of bone mineral content in male than female athletes and in sprinting and jumping than endurance athletes: a longitudinal study of bone strength in elite masters athletes.

We investigated longitudinal changes in tibia bone strength in master power (jumping and sprinting) and endurance (distance) athletes of both sexes. Bone mass but not cross-sectional moment of inertia was better maintained in power than endurance athletes over time, particularly in men and independent of changes in performance. OBJECTIVE:Assessment of effects of sex and athletic discipline (lower limb power events, e.g. sprint running and jumping versus endurance running events) on longitudinal changes in bone strength in masters athletes. METHODS:We examined tibia and fibula bone properties at distal (4% distal-proximal tibia length) and proximal (66% length) sites using peripheral quantitative computed tomography (pQCT) in seventy-one track and field masters athletes (30 male, 41 female, age at baseline 57.0 ± 12.2 years) in a longitudinal cohort study that included at least two testing sessions over a mean period of 4.2 ± 3.1 years. Effects of time, as well as time × sex and time × discipline interactions on bone parameters and calf muscle cross-sectional area (CSA), were examined. RESULTS:Effects of time were sex and discipline-dependent, even following adjustment for enrolment age, sex and changes in muscle CSA and athletic performance. Male sex and participation in power events was associated with better maintenance of tibia bone mineral content (BMC, an indicator of bone compressive strength) at 4% and 66% sites. In contrast, there was no strong evidence of sex or discipline effects on cross-sectional moment of inertia (CSMI, an indicator of bone bending and torsional strength-P > 0.3 for interactions). Similar sex and discipline-specific changes were also observed in the fibula. CONCLUSIONS:Results suggest that male athletes and those participating in lower limb power-based rather than endurance-based disciplines have better maintenance of bone compressive but not bending and torsional strength

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

Insulin induces long-term depression of ventral tegmental area dopamine neurons via endocannabinoids.

The prevalence of obesity has markedly increased over the past few decades. Exploration of how hunger and satiety signals influence the reward system can help us understand non-homeostatic feeding. Insulin may act in the ventral tegmental area (VTA), a critical site for reward-seeking behavior, to suppress feeding. However, the neural mechanisms underlying insulin effects in the VTA remain unknown. We demonstrate that insulin, a circulating catabolic peptide that inhibits feeding, can induce long-term depression (LTD) of mouse excitatory synapses onto VTA dopamine neurons. This effect requires endocannabinoid-mediated presynaptic inhibition of glutamate release. Furthermore, after a sweetened high-fat meal, which elevates endogenous insulin, insulin-induced LTD is occluded. Finally, insulin in the VTA reduces food anticipatory behavior in mice and conditioned place preference for food in rats. Taken together, these results suggest that insulin in the VTA suppresses excitatory synaptic transmission and reduces anticipatory activity and preference for food-related cues