A probabilistic analysis of the multiknapsack value function

The optimal solution value of the multiknapsack problem as a function of the knapsack capacities is studied under the assumption that the profit and weight coefficients are generated by an appropriate random mechanism. A strong asymptotic characterization is obtained, that yiclds a closed form expression for certain special cases

Statistical mechanics of the multi-constraint continuous knapsack problem

We apply the replica analysis established by Gardner to the multi-constraint continuous knapsack problem,which is one of the linear programming problems and a most fundamental problem in the field of operations research (OR). For a large problem size, we analyse the space of solution and its volume, and estimate the optimal number of items to go into the knapsack as a function of the number of constraints. We study the stability of the replica symmetric (RS) solution and find that the RS calculation cannot estimate the optimal number of items in knapsack correctly if many constraints are required.In order to obtain a consistent solution in the RS region,we try the zero entropy approximation for this continuous solution space and get a stable solution within the RS ansatz.On the other hand, in replica symmetry breaking (RSB) region, the one step RSB solution is found by Parisi's scheme. It turns out that this problem is closely related to the problem of optimal storage capacity and of generalization by maximum stability rule of a spherical perceptron.Comment: Latex 13 pages using IOP style file, 5 figure

A probabalistic analysis of the multiknapsack value function

"September 1984.

Stochastic integer programming

No abstract

Growth hormone secretagogues modulate inflammation and fibrosis in mdx mouse model of Duchenne muscular dystrophy

Introduction: Growth hormone secretagogues (GHSs) exert multiple actions, being able to activate GHS-receptor 1a, control inflammation and metabolism, to enhance GH/insulin-like growth factor-1 (IGF-1)-mediated myogenesis, and to inhibit angiotensin-converting enzyme. These mechanisms are of interest for potentially targeting multiple steps of pathogenic cascade in Duchenne muscular dystrophy (DMD). Methods: Here, we aimed to provide preclinical evidence for potential benefits of GHSs in DMD, via a multidisciplinary in vivo and ex vivo comparison in mdx mice, of two ad hoc synthesized compounds (EP80317 and JMV2894), with a wide but different profile. 4-week-old mdx mice were treated for 8 weeks with EP80317 or JMV2894 (320 μg/kg/d, s.c.). Results: In vivo, both GHSs increased mice forelimb force (recovery score, RS towards WT: 20% for EP80317 and 32% for JMV2894 at week 8). In parallel, GHSs also reduced diaphragm (DIA) and gastrocnemius (GC) ultrasound echodensity, a fibrosis-related parameter (RS: ranging between 26% and 75%). Ex vivo, both drugs ameliorated DIA isometric force and calcium-related indices (e.g., RS: 40% for tetanic force). Histological analysis highlighted a relevant reduction of fibrosis in GC and DIA muscles of treated mice, paralleled by a decrease in gene expression of TGF-β1 and Col1a1. Also, decreased levels of pro-inflammatory genes (IL-6, CD68), accompanied by an increment in Sirt-1, PGC-1α and MEF2c expression, were observed in response to treatments, suggesting an overall improvement of myofiber metabolism. No detectable transcript levels of GHS receptor-1a, nor an increase of circulating IGF-1 were found, suggesting the presence of a novel receptor-independent mechanism in skeletal muscle. Preliminary docking studies revealed a potential binding capability of JMV2894 on metalloproteases involved in extracellular matrix remodeling and cytokine production, such as ADAMTS-5 and MMP-9, overactivated in DMD. Discussion: Our results support the interest of GHSs as modulators of pathology progression in mdx mice, disclosing a direct anti-fibrotic action that may prove beneficial to contrast pathological remodeling