Public health challenges in the political economy of conflict: the case of Syria

Recent uprisings in the Arab world and a full‐scale war in Syria are widely viewed as popular demand for political voice against repressive regimes. However, growing economic inequalities and serious economic dysfunction played a role as trigger for conflict than is commonly accepted. Tunisia, Egypt and Syria all implemented policies of liberalization over the past two decades, leading to the worsening of living standards for the majority. The various forms of liberalization played a significant role in embedding social division and discontent whose outcomes affected other countries of the region with the onset of market reforms in nascent welfare states. Egypt, for example, was viewed by the World Bank as an economic ‘best performer’, despite regular riots over food prices, job losses and land expropriation for tourism. Tunisia was praised by donors just prior to the uprising (in 2010), for ‘weathering well’ the global economic downturn through ‘sound macroeconomic management’. In Syria, the market economy made its mark over the 90s, but macroeconomic adjustment policies were implemented in a bilateral agreement with the European Union and approved by the International Monetary Fund in 2003. The economic stabilization programme that followed had limited concern for social impacts such as jobs losses, price rises and national debt, which ultimately caused immense hardship for the population at large, acting as a trigger for the initial uprising in 2011, prior to its transformation into a fully blown conflict. This article focuses on reforms implemented in the health sector and sets these in the context of the current political economy of Syria. It suggests that a protective approach to public health services during and in the aftermath of conflict may increase the possibilities of reconstruction and reconciliation between warring sides. Copyright © 2015 John Wiley & Sons, Ltd.     

Postprandial Effect of a High-Fat Meal on Endotoxemia in Arab Women with and without Insulin-Resistance-Related Diseases

This study determined the effects of a high-fat meal on circulating endotoxin and cardiometabolic indices in adult Arab women. The cohort consisted of 92 consenting Saudi women (18 non-diabetic (ND)) control subjects; Age 24.4 ± 7.9 year; body mass index (BMI) 22.2 ± 2.2 Kg/m²), 24 overweight/obese (referred to as overweight-plus (overweight⁺)) subjects (Age 32.0 ± 7.8 year; BMI 28.5 ± 1.5 Kg/m²) and 50 type 2 diabetes mellitus (T2DM) patients (Age 41.5 ± 6.2 year; BMI 35.2 ± 7.7 Kg/m²). All were given a high-fat meal (standardized meal: 75 g fat, 5 g carbohydrate, 6 g protein) after an overnight fast of 12–14 h. Anthropometrics were obtained and fasting blood glucose, lipids, and endotoxin were serially measured for four consecutive postprandial hours. Endotoxin levels were significantly elevated prior to a high-fat meal in the overweight⁺ and T2DM than the controls (p < 0.05). Furthermore, the postprandial cardiometabolic changes led to a more detrimental risk profile in T2DM subjects than other groups, with serial changes most notable in glucose, triglycerides, high density lipoprotein-cholesterol (HDL-cholesterol), and insulin levels (p-values < 0.05). The same single meal given to subjects with different metabolic states had varying impacts on cardiometabolic health. Endotoxemia is exacerbated by a high-fat meal in Arab subjects with T2DM, accompanied by a parallel increase in cardiometabolic risk profile, suggesting disparity in disease pathogenesis of those with or without T2DM through the altered cardiometabolic risk profile rather than variance in metabolic endotoxinaemia with a high-fat meal.     

Proportion and predictors of Hypogonadism Recovery in Men with Macroprolactinomas treated with dopamine agonists

Pituitary - Hypogonadism is the most common form of hypopituitarism in men with macroprolactinoma. However, evidence on factors related to hypogonadism recovery is limited. We estimated the...     

Mutations in K-Ras linked to levels of osteoprotegerin and sensitivity to TRAIL-induced cell death in pancreatic ductal adenocarcinoma cells

Osteoprotegerin (OPG) is a soluble receptor expressed in the serum of patients with diabetes, arthritis and pancreatic cancer. While OPG has been considered a tumor survival factor for bone metastasizing breast and prostate cancers, the role of OPG in pancreatic cancer, which itself rarely metastasizes to bone, is not known. Pancreatic ductal adenocarcinoma (PDAC) cell lines were found to secrete OPG and the level of OPG production correlated with sensitivity to TRAIL-induced apoptosis. Silencing OPG sensitized cells to TRAIL-induced apoptosis. Interestingly, a positive correlation was noted between OPG production level and K-Ras mutation status. Earlier studies implicated K-Ras in conferring resistance to TRAIL-induced apoptosis in pancreatic cells and this study demonstrates that K-Ras mediated TRAIL resistance in pancreatic cancer cells occurs due to increased OPG production. Silencing K-Ras in pancreatic cancer cells decreased OPG levels and increased sensitivity to TRAIL-induced apoptosis. These observations indicate that OPG can play a role in both cell survival and in PDAC cell sensitivity to TRAIL-induced apoptosis, which may contribute to metastasis. Targeted inhibition of OPG binding to TRAIL may represent a therapeutic approach in the treatment of pancreatic cancer.     

Instability and translocation through nanopores of DNA interacting with single-layer materials

In this study, we use classical applied mathematical modelling to employ the 6–12 Lennard-Jones potential function along with the continuous approximation to investigate the interaction energies between a double-stranded deoxyribonucleic acid (dsDNA) molecule and two-dimensional nanomaterials, namely graphene (GRA), hexagonal boron nitride (h-BN), molybdenum disulphide (MoS₂), and tungsten disulphide (WS₂). Assuming that the dsDNA molecule has a perpendicular distance Δ above the nano-sheet surface, we calculated the molecular interaction energy and determined the relation between the location of the minimum energy and Δ. We also investigated the interaction of a dsDNA molecule with the surface of each nano-sheet in the presence of a circular hole simulating a nanopore. The radius of the nanopore that results in the minimum energy was determined. Our results show that the adsorption energies of the dsDNA molecule with GRA, h-BN, MoS₂, and WS₂ nano-sheets corresponding to the perpendicular distance Δ = 20 Å are approximately 70, 82, 28, and 26 (kcal mol⁻¹), respectively, and we observed that the dsDNA molecule moves through nanopores of radii greater than 12.2 Å.

Using classical applied mathematical modelling to employ the 6–12 Lennard-Jones potential function along with the continuous approximation to investigate the interaction energy between dsDNA and 2D-nanomaterials, namely GRA, h-BN, MoS₂ and WS₂ sheets.