The Phoenix Project: Master Constraint Programme for Loop Quantum Gravity

The Hamiltonian constraint remains the major unsolved problem in Loop Quantum Gravity (LQG). Seven years ago a mathematically consistent candidate Hamiltonian constraint has been proposed but there are still several unsettled questions which concern the algebra of commutators among smeared Hamiltonian constraints which must be faced in order to make progress. In this paper we propose a solution to this set of problems based on the so-called {\bf Master Constraint} which combines the smeared Hamiltonian constraints for all smearing functions into a single constraint. If certain mathematical conditions, which still have to be proved, hold, then not only the problems with the commutator algebra could disappear, also chances are good that one can control the solution space and the (quantum) Dirac observables of LQG. Even a decision on whether the theory has the correct classical limit and a connection with the path integral (or spin foam) formulation could be in reach. While these are exciting possibilities, we should warn the reader from the outset that, since the proposal is, to the best of our knowledge, completely new and has been barely tested in solvable models, there might be caveats which we are presently unaware of and render the whole {\bf Master Constraint Programme} obsolete. Thus, this paper should really be viewed as a proposal only, rather than a presentation of hard results, which however we intend to supply in future submissions.Comment: LATEX, uses AMSTE

Long-term denervation in humans causes degeneration of both contractile and excitation-contraction coupling apparatus, which is reversible by functional electrical stimulation (FES): a role for myofiber regeneration?

J Neuropathol Exp Neurol. 2004 Sep;63(9):919-31. Long-term denervation in humans causes degeneration of both contractile and excitation-contraction coupling apparatus, which is reversible by functional electrical stimulation (FES): a role for myofiber regeneration? Kern H, Boncompagni S, Rossini K, Mayr W, Fan\uf2 G, Zanin ME, Podhorska-Okolow M, Protasi F, Carraro U. Source From Ludwig Boltzmann Institute of Electrostimulation and Physical Rehabilitation, Department of Physical Medicine, Wilhelminenspital, Vienna, Austria. Abstract Over the last 30 years there has been considerable interest in the use of functional electrical stimulation (FES) to restore movement to the limbs of paralyzed patients. Spinal cord injury causes a rapid loss in both muscle mass and contractile force. The atrophy is especially severe when the injury involves lower motoneurons because many months after spinal cord injury, atrophy is complicated by fibrosis and fat substitution. In this study we describe the effects of long-term lower motoneuron denervation of human muscle and present the structural results of muscle trained using FES. By means of an antibody for embryonic myosin, we demonstrate that many regenerative events continue to spontaneously occur in human long-term denervated and degenerated muscle (DDM). In addition, using electron microscopy, we describe i) the overall structure of fibers and myofibrils in long-term denervated and degenerated muscle, including the effects of FES, and ii) the structure and localization of calcium release units, or triads; the structures reputed to activate muscle contraction during excitation-contraction coupling (ECC). Both apparatus undergo disarrangement and re-organization following long-term denervation and FES, respectively. The poor excitability of human long-term DDM fibers, which extends to the first periods of FES training, may be explained in terms of the spatial disorder of the ECC apparatus. Its disorganization and re-organization following long-term denervation and FES, respectively, may play a key role in the parallel disarrangement and re-organization of the myofibrils that characterize denervation and FES training. The present structural studies demonstrate that the protocol used during FES training is effective in reverting long-term denervation atrophy and dystrophy. The mean fiber diameter in FES biopsies is 42.2 +/- 14.8 SD (p < 0.0001 vs DDM 14.9 +/- 6.0 SD); the mean percentile of myofiber area of the biopsy is 94.3 +/- 5.7 SD (p < 0.0001 vs DDM 25.7 +/- 23.7 SD); the mean percentile fat area is 2.1 +/- 2.4 SD (p < 0.001 vs DDM 12.8 +/- 12.1 SD); and the mean percentile connective tissue area is 3.6 +/- 4.6 SD (p < 0.001 vs DDM 61.6 +/- 20.1 SD). In DDM biopsies more than 50% of myofibers have diameter smaller than 10 microm, while the FES-trained subjects have more that 50% of myofibers larger than 30 microm. The recovery of muscle mass seems to be the result of both a size increase of the surviving fibers and the regeneration of new myofibers. PMID: 15453091 [PubMed - indexed for MEDLINE

Apoptosis of skeletal and cardiac muscles and physical exercise

Aging (Milano). 1997 Feb-Apr;9(1-2):19-34. Apoptosis of skeletal and cardiac muscles and physical exercise. Carraro U, Franceschi C. Source C.N.R. Unit for Muscle Biology and Physiopathology, Department of Biomedical Sciences, University of Padova, Italy. Abstract Besides the well-known reciprocal influences of skeletal muscle and heart during and after physical exercise, a new perspective is emerging on the short- and long-term effects of exercise-induced damage, in particular the pathogenic role of inappropriate apoptosis in skeletal and cardiac muscle. Cells from multicellular organisms self-destruct when they are no longer needed, or have become damaged; they do this by activating a genetically controlled cell suicide machinery that leads to programmed cell death (PCD), or apoptosis. Apoptosis is a specific form of programmed cell death that plays an important role in development, growth regulation and disease. Skeletal muscles in adult animals are fully differentiated syncytial cells. Apoptosis, which is known to be present in tissues that modulate their cellular homeostasis under the influence of growth and/or hormonal factors, has been recently described in early stages of myocardial infarct, and in dystrophic skeletal muscle. The role and the cellular and molecular aspects of muscle cell death and apoptosis are far from clear, particularly following several types of muscle damage (genetic defects, exercise-induced damage, oxidative stress, etc.). It can be predicted that apoptosis plays a major role in regulating myoblast proliferation during muscle regeneration, and in the progression of dystrophinopathies. A particularly important area has recently developed concerning cardiac muscle and reperfusion injury after ischemia; in this case as well, a major role of apoptosis is emerging. PMID: 9177583 [PubMed - indexed for MEDLINE