Portfolio optimization in the Kenyan stock market: a comparison between mean-variance optimization and threshold accepting

A Dissertation submitted in partial fulfillment of the requirements for the Master of Science in Mathematical Finance (MSc.MF) at Strathmore UniversityThe Mean-Variance Optimization (MVO) model has been used in asset allocation problems since the inception of Modern Portfolio Theory in 1952. Several improvements and alternatives to MVO have been suggested and used since then. These include adding constraints to the traditional MVO model, using alternative risk measures and use of non risk-reward models. This study seeks to compare this risk-reward model against the Threshold Accepting model, which is a general optimization model, in portfolio selection in the Kenyan stock market to establish optimal stock portfolios to be held by investors in The Nairobi Securities Exchange (NSE). A comparison is done between the two models by measuring their performance using the following performance ratios: Sharpe Ratio, Sortino Ratio and Information Ratio using 29 stocks in the NSE from 1998 - 2016. Using portfolio performance ratios, it is concluded that the Threshold Accepting (TA) model outperforms the Mean-Variance Optimization model but the latter is observed as a more consistent model. The TA model has portfolios with generally more superior returns relative to the risk taken for the full period; however, this is not consistent over varying time estimates. This observation implies that attention should be given to the TA model rather than the classical MVO approach with the aim of improving optimal portfolio selection

MOESM2 of The structural and functional contributions of β-glucosidase-producing microbial communities to cellulose degradation in composting

Additional file 2: Figure S2. Differences in the abundance and expression of family 1 β-glucosidase genes from bacteria (GH1) in the natural compost and the inoculated compost

MOESM4 of The structural and functional contributions of β-glucosidase-producing microbial communities to cellulose degradation in composting

Additional file 4. Additional Materials and Methods

Discovery of 4‑[(2<i>R</i>,4<i>R</i>)‑4-({[1-(2,2-Difluoro-1,3-benzodioxol-5-yl)cyclopropyl]­carbonyl}­amino)-7-(difluoro­methoxy)-3,4-dihydro‑2<i>H</i>‑chromen-2-yl]benzoic Acid (ABBV/GLPG-2222), a Potent Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Corrector for the Treatment of Cystic Fibrosis

Cystic fibrosis (CF) is a multiorgan disease of the lungs, sinuses, pancreas, and gastrointestinal tract that is caused by a dysfunction or deficiency of the cystic fibrosis transmembrane conductance regulator (CFTR) protein, an epithelial anion channel that regulates salt and water balance in the tissues in which it is expressed. To effectively treat the most prevalent patient population (F508del mutation), two biomolecular modulators are required: correctors to increase CFTR levels at the cell surface, and potentiators to allow the effective opening of the CFTR channel. Despite approved potentiator and potentiator/corrector combination therapies, there remains a high need to develop more potent and efficacious correctors. Herein, we disclose the discovery of a highly potent series of CFTR correctors and the structure–activity relationship (SAR) studies that guided the discovery of ABBV/GLPG-2222 (<b>22</b>), which is currently in clinical trials in patients harboring the F508del CFTR mutation on at least one allele

Discovery of 4‑[(2<i>R</i>,4<i>R</i>)‑4-({[1-(2,2-Difluoro-1,3-benzodioxol-5-yl)cyclopropyl]­carbonyl}­amino)-7-(difluoro­methoxy)-3,4-dihydro‑2<i>H</i>‑chromen-2-yl]benzoic Acid (ABBV/GLPG-2222), a Potent Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Corrector for the Treatment of Cystic Fibrosis

Cystic fibrosis (CF) is a multiorgan disease of the lungs, sinuses, pancreas, and gastrointestinal tract that is caused by a dysfunction or deficiency of the cystic fibrosis transmembrane conductance regulator (CFTR) protein, an epithelial anion channel that regulates salt and water balance in the tissues in which it is expressed. To effectively treat the most prevalent patient population (F508del mutation), two biomolecular modulators are required: correctors to increase CFTR levels at the cell surface, and potentiators to allow the effective opening of the CFTR channel. Despite approved potentiator and potentiator/corrector combination therapies, there remains a high need to develop more potent and efficacious correctors. Herein, we disclose the discovery of a highly potent series of CFTR correctors and the structure–activity relationship (SAR) studies that guided the discovery of ABBV/GLPG-2222 (<b>22</b>), which is currently in clinical trials in patients harboring the F508del CFTR mutation on at least one allele