The effects of ownership structure, sub-optimal cash holdings and investment inefficiency on dividend policy: evidence from Indonesia

We investigate how a firm's decision to hold excessive cash or to overinvest could influence its dividend payout policy in Indonesia. Additionally, we examine the association between corporate ownership structure and cash dividends. Using a data set of Indonesian listed firms for the period from 1995 to 2014, we find that excessive cash holding (overinvestment) positively (negatively) affects a firm's likelihood of paying dividends. Also, we find that family, foreign, state and institutional ownership have significantly negative links with dividends, which suggests the signals of expropriation of firms' wealth by major shareholders. These findings strongly support the expropriation hypothesis that commonly applies to firms with higher level of concentration or to firms in a weak legal environment by which the rights of minority interests are put at risk by large shareholders

Areca nut chewing and dependency syndrome: Is the dependence comparable to smoking? a cross sectional study

<p>Abstract</p> <p>Background</p> <p>Areca nut is the seed of fruit oriental palm known as <it>Areca catechu</it>. Many adverse effects of nut chewing have been well documented in the medical literature. As these nuts are mixed with some other substances like tobacco and flavouring agents, it has been hypothesized that it might also cause some dependency symptoms among its users. Therefore, the objective of this study was to investigate dependency syndrome among areca nut users with and without tobacco additives and compare it with dependency associated with cigarette smoking among the male Pakistani population.</p> <p>Methods</p> <p>This was an observational cross sectional study carried out on healthy individuals, who were users of any one of the three products (areca nut only, areca nut with tobacco additives, cigarette smokers). Participants were selected by convenience sampling of people coming to hospital to seek a free oral check up. Information was collected about the socio-demographic profile, pattern of use and symptoms of dependency using the DSM-IV criteria for substance dependence. We carried out multiple logistic regressions to investigate association between socio-demographic profile, pattern of substance use and dependency syndrome.</p> <p>Results</p> <p>We carried out final analysis on 851 individuals, of which 36.8% (n = 314) were areca nut users, 28.4% (n = 242) were the chewers of areca with tobacco additives and 34.7% (n = 295) were regular cigarette smokers. Multivariate analyses showed that individuals using areca nut with tobacco additives were significantly more likely to have dependency syndrome (OR = 2.17, 95% CI 1.39-3.40) while cigarette smokers were eight times more likely to have dependency syndrome as compared to areca nut only users.</p> <p>Conclusions</p> <p>Areca nut use with and without tobacco additives was significantly associated with dependency syndrome. In comparison to exclusive areca nut users, the smokers were eight times more likely to develop dependence while areca nut users with tobacco additives were also significantly more likely to suffer from the dependence.</p

Immune-Mediated Inflammation May Contribute to the Pathogenesis of Cardiovascular Disease in Mucopolysaccharidosis Type I.

BackgroundCardiovascular disease, a progressive manifestation of α-L-iduronidase deficiency or mucopolysaccharidosis type I, continues in patients both untreated and treated with hematopoietic stem cell transplantation or intravenous enzyme replacement. Few studies have examined the effects of α-L-iduronidase deficiency and subsequent glycosaminoglycan storage upon arterial gene expression to understand the pathogenesis of cardiovascular disease.MethodsGene expression in carotid artery, ascending, and descending aortas from four non-tolerized, non-enzyme treated 19 month-old mucopolysaccharidosis type I dogs was compared with expression in corresponding vascular segments from three normal, age-matched dogs. Data were analyzed using R and whole genome network correlation analysis, a bias-free method of categorizing expression level and significance into discrete modules. Genes were further categorized based on module-trait relationships. Expression of clusterin, a protein implicated in other etiologies of cardiovascular disease, was assessed in canine and murine mucopolysaccharidosis type I aortas via Western blot and in situ immunohistochemistry.ResultsGene families with more than two-fold, significant increased expression involved lysosomal function, proteasome function, and immune regulation. Significantly downregulated genes were related to cellular adhesion, cytoskeletal elements, and calcium regulation. Clusterin gene overexpression (9-fold) and protein overexpression (1.3 to 1.62-fold) was confirmed and located specifically in arterial plaques of mucopolysaccharidosis-affected dogs and mice.ConclusionsOverexpression of lysosomal and proteasomal-related genes are expected responses to cellular stress induced by lysosomal storage in mucopolysaccharidosis type I. Upregulation of immunity-related genes implicates the potential involvement of glycosaminoglycan-induced inflammation in the pathogenesis of mucopolysaccharidosis-related arterial disease, for which clusterin represents a potential biomarker

Disease causing mutations in inverted formin 2 regulate its binding to G-actin, F-actin capping protein (CapZ α-1) and profilin 2

Focal segmental glomerulosclerosis (FSGS) is a devastating form of nephrotic syndrome which ultimately leads to end stage renal failure (ESRF). Mutations in inverted formin 2 (INF2), a member of the formin family of actin-regulating proteins, have recently been associated with a familial cause of nephrotic syndrome characterized by FSGS. INF2 is a unique formin that can both polymerize and depolymerize actin filaments. How mutations in INF2 lead to disease is unknown. In the present study, we show that three mutations associated with FSGS, E184K, S186P and R218Q, reduce INF2 auto-inhibition and increase association with monomeric actin. Furthermore using a combination of GFP–INF2 expression in human podocytes and GFP-Trap purification coupled with MS we demonstrate that INF2 interacts with profilin 2 and the F-actin capping protein, CapZ α-1. These interactions are increased by the presence of the disease causing mutations. Since both these proteins are involved in the dynamic turnover and restructuring of the actin cytoskeleton these changes strengthen the evidence that aberrant regulation of actin dynamics underlies the pathogenesis of disease

GlomSpheres as a 3D co-culture spheroid model of the kidney glomerulus for rapid drug-screening

The glomerulus is the filtration unit of the kidney. Injury to any component of this specialised structure leads to impaired filtration and eventually fibrosis and chronic kidney disease. Current two and three dimensional (2D and 3D) models that attempt to recreate structure and interplay between glomerular cells are imperfect. Most 2D models are simplistic and unrepresentative, and 3D organoid approaches are currently difficult to reproduce at scale and do not fit well with current industrial drug-screening approaches. Here we report a rapidly generated and highly reproducible 3D co-culture spheroid model (GlomSpheres), better demonstrating the specialised physical and molecular structure of a glomerulus. Co-cultured using a magnetic spheroid formation approach, conditionally immortalised (CI) human podocytes and glomerular endothelial cells (GEnCs) deposited mature, organized isoforms of collagen IV and Laminin. We demonstrate a dramatic upregulation of key podocyte (podocin, nephrin and podocalyxin) and GEnC (pecam-1) markers. Electron microscopy revealed podocyte foot process interdigitation and endothelial vessel formation. Incubation with pro-fibrotic agents (TGF-β1, Adriamycin) induced extracellular matrix (ECM) dysregulation and podocyte loss, which were attenuated by the anti-fibrotic agent Nintedanib. Incubation with plasma from patients with kidney disease induced acute podocyte loss and ECM dysregulation relative to patient matched remission plasma, and Nintedanib reduced podocyte loss. Finally, we developed a rapid imaging approach to demonstrate the model’s usefulness in higher throughput pharmaceutical screening. GlomSpheres therefore represent a robust, scalable, replacement for 2D in vitro glomerular disease models

Evaluation of the protective effect of Paeonia emodi Wall on rat model of Parkinson’s disease induced by 6 hydroxy dopamine

Background: Generation of reactive oxygen species together with paucity of antioxidant defense is considered as an important cause for dopaminergic neuronal death. Review of literature indicates that none of the drugs so far studied for preventing the PD were found to be promising for use. Therefore, the present study was planned to evaluate the neuroprotective effect of Paeonia emodi Wall (PEW) in 6-hydroxy dopamine induced Parkinson’s disease (PD) model.Methods: The study was conducted on Wistar rats where Parkinson’s disease was induced by producing the striatal 6-hydroxy dopamine lesions. The test animals received ethanolic extract of PEW at dose of 200 and 300mg/kg for 28 days. Circling behavior, spontaneous locomotor activity, muscular coordination and akinesia were studied. Antioxidant levels were assessed by biochemical estimation and histopathology was carried out for dopaminergic neuronal loss.Results: PEW ethanolic extract showed significant dose dependent recovery in number of circlings, line crossing, muscular coordination and akinesia. A significant increase in MDA levels and decreased GSH level in PEW treated groups was observed in test groups as compared to control group (p<0.05). Normal architecture was retained only in PEW 300mg/Kg (p<0.05). L-Dopa did not showed effect on biochemical and histological parameters.Conclusions: The ethanolic extract of PEW showed neuroprotective activity against 6-hydroxy dopamine induced Parkinson’s disease in rats in both 200 and 300mg/kg doses. The protective action of PEW in PD can be because of its ability to reduce the oxidative stress