Assessing payment instrument alternatives using cognitive mapping and the choquet integral

Technological advances have increased the diversity of payment instruments and transaction channels, heightening consumers' expectations for services in this regard. Coupled with an increasing competitiveness of the banking industry, this has emphasized the great importance of understanding consumers' choices of payment instruments. In order to meet their customers' expectations, banks have to understand what determines their choices of payment instruments. This study aims to uncover these determinants of payment instrument choice, through the use of cognitive mapping to structure the decision problem, and its combination with the Choquet integral to identify the overall preferred payment instrument from the user perspective. The results show that direct debits and electronic cards constitute the preferred payment instruments, and automated teller machines (ATMs) and point-of-sale (POS) the overall preferred transaction channels. Understanding consumers' choices of payment instrument, the factors underlying them and their interactions can contribute to better planning by banks at the distribution channel level. Strengths, limitations and managerial implications of our proposal are also discussed.info:eu-repo/semantics/publishedVersio

A cognition-driven risk evaluation framework for consumer loans

Credit to personal consumption is an important activity of the financial system and crucial to the socio-economic development of a country. It is important, therefore, that the methods and techniques used to evaluate consumer credit risk be as efficient and informative as possible, in order to strengthen decisions to approve or reject credit and promote sustainable economic growth. This study aims to create a multiple criteria expert system which integrates cognitive maps and the measuring attractiveness by a categorical based evaluation technique (MACBETH) to create a complementary framework for consumer credit risk assessment. The results show that this integrated approach allows the evaluation process of consumer credit risk to be more informed and transparent, providing value for the evaluation processes of this type of credit application as a result of the privileged contact established with a panel of credit analysts. Limitations and managerial implications are also discussed.info:eu-repo/semantics/publishedVersio

Palmitate-Induced β-Cell Dysfunction Is Associated with Excessive NO Production and Is Reversed by Thiazolidinedione-Mediated Inhibition of GPR40 Transduction Mechanisms

BACKGROUND: Type 2 diabetes often displays hyperlipidemia. We examined palmitate effects on pancreatic islet function in relation to FFA receptor GPR40, NO generation, insulin release, and the PPARgamma agonistic thiazolidinedione, rosiglitazone. PRINCIPAL FINDINGS: Rosiglitazone suppressed acute palmitate-stimulated GPR40-transduced PI hydrolysis in HEK293 cells and insulin release from MIN6c cells and mouse islets. Culturing islets 24 h with palmitate at 5 mmol/l glucose induced beta-cell iNOS expression as revealed by confocal microscopy and increased the activities of ncNOS and iNOS associated with suppression of glucose-stimulated insulin response. Rosiglitazone reversed these effects. The expression of iNOS after high-glucose culturing was unaffected by rosiglitazone. Downregulation of GPR40 by antisense treatment abrogated GPR40 expression and suppressed palmitate-induced iNOS activity and insulin release. CONCLUSION: We conclude that, in addition to mediating acute FFA-stimulated insulin release, GPR40 is an important regulator of iNOS expression and dysfunctional insulin release during long-term exposure to FFA. The adverse effects of palmitate were counteracted by rosiglitazone at GPR40, suggesting that thiazolidinediones are beneficial for beta-cell function in hyperlipidemic type 2 diabetes

Excessive Islet NO Generation in Type 2 Diabetic GK Rats Coincides with Abnormal Hormone Secretion and Is Counteracted by GLP-1

BACKGROUND: A distinctive feature of type 2 diabetes is inability of insulin-secreting beta-cells to properly respond to elevated glucose eventually leading to beta-cell failure. We have hypothesized that an abnormally increased NO production in the pancreatic islets might be an important factor in the pathogenesis of beta-cell dysfunction. PRINCIPAL FINDINGS: We show now that islets of type 2 spontaneous diabetes in GK rats display excessive NO generation associated with abnormal iNOS expression in insulin and glucagon cells, increased ncNOS activity, impaired glucose-stimulated insulin release, glucagon hypersecretion, and impaired glucose-induced glucagon suppression. Pharmacological blockade of islet NO production by the NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) greatly improved hormone secretion from GK islets suggesting islet NOS activity being an important target to inactivate for amelioration of islet cell function. The incretin hormone GLP-1, which is used in clinical practice suppressed iNOS and ncNOS expression and activity with almost full restoration of insulin release and partial restoration of glucagon release. GLP-1 suppression of iNOS expression was reversed by PKA inhibition but unaffected by the proteasome inhibitor MG132. Injection of glucose plus GLP-1 in the diabetic rats showed that GLP-1 amplified the insulin response but induced a transient increase and then a poor depression of glucagon. CONCLUSION: The results suggest that abnormally increased NO production within islet cells is a significant player in the pathogenesis of type 2 diabetes being counteracted by GLP-1 through PKA-dependent, nonproteasomal mechanisms

Nutrient limitations to bacterial and fungal growth during cellulose decomposition in tropical forest soils

Nutrients constrain the soil carbon cycle in tropical forests, but we lack knowledge on how these constraints vary within the soil microbial community. Here, we used in situ fertilization in a montane tropical forest and in two lowland tropical forests on contrasting soil types to test the principal hypothesis that there are different nutrient constraints to different groups of microorganisms during the decomposition of cellulose. We also tested the hypotheses that decomposers shift from nitrogen to phosphorus constraints from montane to lowland forests, respectively, and are further constrained by potassium and sodium deficiency in the western Amazon. Cellulose and nutrients (nitrogen, phosphorus, potassium, sodium, and combined) were added to soils in situ, and microbial growth on cellulose (phospholipid fatty acids and ergosterol) and respiration were measured. Microbial growth on cellulose after single nutrient additions was highest following nitrogen addition for fungi, suggesting nitrogen as the primary limiting nutrient for cellulose decomposition. This was observed at all sites, with no clear shift in nutrient constraints to decomposition between lowland and montane sites. We also observed positive respiration and fungal growth responses to sodium and potassium addition at one of the lowland sites. However, when phosphorus was added, and especially when added in combination with other nutrients, bacterial growth was highest, suggesting that bacteria out-compete fungi for nitrogen where phosphorus is abundant. In summary, nitrogen constrains fungal growth and cellulose decomposition in both lowland and montane tropical forest soils, but additional nutrients may also be of critical importance in determining the balance between fungal and bacterial decomposition of cellulose

GPR40 is expressed in glucagon producing cells and affects glucagon secretion.

The free fatty acid receptor, GPR40, has been coupled with insulin secretion via its expression in pancreatic beta-cells. However, the role of GPR40 in the release of glucagon has not been studied and previous attempts to identify the receptor in alpha-cells have been unfruitful. Using double-staining for glucagon and GPR40 expression, we demonstrate that the two are expressed in the same cells in the periphery of mouse islets. In-R1-G9 hamster glucagonoma cells respond dose-dependently to linoleic acid stimulation by elevated phosphatidyl inositol hydrolysis and glucagon release and the cells become increasingly responsive to fatty acid stimulation when overexpressing GPR40. Isolated mouse islets also secrete glucagon in response to linoleic acid, a response that was abolished by antisense treatment against GPR40. This study demonstrates that GPR40 is present and active in pancreatic alpha-cells and puts further emphasis on the importance of this nutrient sensing receptor in islet function. (c) 2006 Elsevier Inc. All rights reserved

Дослідження впливу соціальних медіа на поведінку споживачів покоління Y

Members from different generations create challenges for marketing specialists due to their unique behaviour specifics and in the context of constant technology development, these challenges become only harder. In the current marketing situation, there is a new challenge – outreach and interest for generation Y consumers. A question arises – which means to apply and which of them would be effective. It is a new field of research both for scientists and marketing practitioners. The article analyses the members of generation Y because in their case there are most prominent scientific discovery inquiries on their behaviour and marketing management decisions. By evaluating that, the aim of the article is to create a model of the influence of social media for generation Y consumer purchase decisions. The need to offer a new model has appeared due to the changes in the current world that are changing the habits and features of the society, constantly improving technologies are changing the lifestyle, values and needs of people. The marketing decisions that were applied before are not presenting the desired results in the current market. Previous research allows identifying the specifics of generation Y, however, due to constantly changing technology environment it is not clearly known how this generation makes the decisions to purchase something. When wishing to find the right way to sell products and services to this generation, it is necessary to understand it and to find ways to communicate with it. When creating social media content and creating added value to the customers, it is vital to understand the complexity of the external and internal factors that determine their choice to buy. To achieve the goal of this article, the theoretical part presents a complex analysis of factors that determine consumer behaviour in social media, applications of generation theory for making marketing decisions; characteristics of generation Y were identified. In this research, marketing factors that influence the consumer’s decision to buy were analysed, their effects and application in the purchase process of generation Y consumers were evaluated.Ця стаття узагальнює аргументи та контраргументи в межах наукової дискусії з питання впливу соціальних медіа на поведінку споживачів покоління Y. Систематизація літературних джерел та підходів до вивчення поведінки споживачів засвідчила, що в умовах розвитку інформаційних технологій та соціальних мереж суттєвих змін зазнають соціальні процеси у споживчій поведінці людей, особливо це стосується покоління Y. Актуальність вирішення даної наукової проблеми полягає в тому, що купівельний процес та споживча поведінка покоління Y залежить від зміни у сучасному світі, які впливають на звички та особливості суспільства, цінності та потреби людей. Авторами наголошено, що одним із основних каналів спілкування покоління Y є соціальні мережі. Основною метою проведеного дослідження є вивчення особливостей поведінки споживачів покоління Y та впливу соціальних медіа на їх рішення щодо придбання товарів або послуг. Дослідження питання впливу соціальних медіа на поведінку споживачів покоління Y в статті здійснено в наступній логічній послідовності: створення контенту на Youtube каналі для оцінки ефективності інструментів соціальних медіа; встановлення факторів, які визначають залучення покоління Y до соціальних медіа; проведення онлайн-опитування споживачів покоління Y для оцінки відповідності виявлених факторів. Контент Youtube каналу складається з інформації про транспортні засоби, їх обслуговування, ремонт та інші пов'язані теми. Методичним інструментарієм встановлення факторів, які визначають причини залучення покоління Y до соціальних медіа стали метод кейсів та опитування. До процесу опитування було залучено 359 осіб, 271 з яких були предсавниками покоління Y, народжених у період 1981-2000 роки, періодом дослідження обрано термін з 12 червня по 17 грудня 2018 року. Результати проведеного дослідження дозволили авторам виділити основні маркетингові фактори, що впливають на рішення споживача, оцінено їх вплив на купівельний процес споживачів покоління Y

Metformin ameliorates dysfunctional traits of glibenclamide- and glucose-induced insulin secretion by suppression of imposed overactivity of the islet nitric oxide synthase-no system

Metformin lowers diabetic blood glucose primarily by reducing hepatic gluconeogenesis and increasing peripheral glucose uptake. However, possible effects by metformin on beta-cell function are incompletely understood. We speculated that metformin might positively influence insulin secretion through impacting the beta-cell nitric oxide synthase (NOS)-NO system, a negative modulator of glucose-stimulated insulin release. In short-time incubations with isolated murine islets either glibenclamide or high glucose augmented insulin release associated with increased NO production from both neural and inducible NOS. Metformin addition suppressed the augmented NO generation coinciding with amplified insulin release. Islet culturing with glibenclamide or high glucose revealed pronounced fluorescence of inducible NOS in the beta-cells being abolished by metformin co-culturing. These findings were reflected in medium nitrite-nitrate levels. A glucose challenge following islet culturing with glibenclamide or high glucose revealed markedly impaired insulin response. Metformin coculturing restored this response. Culturing murine islets and human islets from controls and type 2 diabetics with high glucose or high glucose + glibenclamide induced a pronounced decrease of cell viability being remarkably restored by metformin co-culturing. We show here, that imposed overactivity of the beta-cell NOS-NO system by glibenclamide or high glucose leads to insulin secretory dysfunction and reduced cell viability and also, importantly, that these effects are relieved by metformin inhibiting beta-cell NO overproduction from both neural and inducible NOS thus ameliorating a concealed negative influence by NO induced by sulfonylurea treatment and/or high glucose levels. This double-edged effect of glibenclamide on the beta-cellsuggests sulfonylurea monotherapy in type 2 diabetes being avoided

Abnormally decreased NO and augmented CO production in islets of the leptin-deficient ob/ob mouse might contribute to explain hyperinsulinemia and islet survival in leptin-resistant type 2 obese diabetes.

The role of the gaseous messengers NO and CO for β-cell function and survival is controversial. We examined this issue in the hyperglycemic-hyperinsulinemic ob/ob mouse, an animal model of type 2 obese diabetes, by studying islets from obese vs lean mice regarding glucose-stimulated insulin release in relation to islet NO and CO production and the influence of modulating peptide hormones. Glucose-stimulated increase in ncNOS-activity in incubated lean islets was converted to a decrease in ob/ob islets associated with markedly increased insulin release. Both types of islet displayed iNOS activity appearing after ~60min in high-glucose. In ob/ob islets the insulinotropic peptides glucagon, GLP-1 and GIP suppressed NOS activities and amplified glucose-stimulated insulin release. The insulinostatic peptide leptin induced the opposite effects. Suppression of islet CO production inhibited, while stimulation amplified glucose-stimulated insulin release. Nonincubated isolated islets from young and adult obese mice displayed very low ncNOS and negligible iNOS activity. In contrast, production of CO, a NOS inhibitor, was impressively raised. Glucose injections induced strong activities of islet NOS isoforms in lean but not in obese mice and confocal microscopy revealed iNOS expression only in lean islets. Islets from ob/ob mice existing in a hyperglycemic in vivo milieu maintain elevated insulin secretion and protection from glucotoxicity through a general suppression of islet NOS activities achieved by leptin deficiency, high CO production and insulinotropic cyclic-AMP-generating hormones. Such a beneficial effect on islet function and survival might have its clinical counterpart in human leptin-resistant type 2 obese diabetes with hyperinsulinemia