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Purpose: What is the impact of financial literacy on the lending activity of banks? Based on the results of the S&P Global FinLit Survey for an extensive sample of countries, this paper aims to provide the first global test for the impact of country-level financial literacy on the lending activity of commercial banks. Design/methodology/approach: The authors use data on financial literacy by country from the S&P Global FinLit Survey that was completed in 2014 and lending activity and macroeconomic control variables data from the World Bank from 2015 to 2017 to estimate the cross-sectional effect of financial literacy on the importance of loans and of non-performing loans, using different estimation methods. Findings: The results show that, first, financial literacy favors lending activity, contributing to enhance the importance of credit in the economy. Second, financial literacy prevents bad loans from building up, thus reducing credit risk and favoring the quality of the credit portfolio of banks. These results are robust to several controls for macroeconomic conditions and the quality of institutions. They are also robust to different estimation methods. Research limitations/implications: The evidence of the positive (negative) impact of population financial literacy on the quantity (poor quality) of loans suggests that the efforts to enhance the financial literacy of the population contribute to the sustainable development of the financial sector and economic growth. Originality/value: The paper extends to an international and country-level the available evidence of the consequences of the existence (or lack of) of financial literacy for the lending activity of commercial banks, focusing on the amount of credit granted and the quality of such credit. Thus, the paper provides an exploratory analysis of the impact of country-level financial literacy on the lending activities of commercial banks. [ABSTRACT FROM AUTHOR]

The worldwide incidence of bone disorders is raising, mainly due to aging population. The lack of effective treatments is pushing the development of synthetic bone substitutes (SBSs). Most ceramic-based SBSs commercially available display limited handling properties. Attempting to solve these issues and achieve wider acceptance by the clinicians, granular ceramics have been associated with hydrogels (HGs) to produce injectable/moldable SBSs. Dextrin, a lowmolecular- weight carbohydrate, was used to develop a fully resorbable and injectable HG. It was first oxidized with sodium periodate and then cross-linked with adipic acid dihydrazide. The in vivo biocompatibility and safety of the dextrin-based HG was assessed by subacute systemic toxicity and skin sensitization tests, using rodent models. The results showed that the HG did not induce any systemic toxic effect, skin reaction, or genotoxicity, neither impaired the bone repair/regeneration process. Then, the HG was successfully combined with granular bone substitute, registered as Bonelike (250–500 μm) to obtain a moldable/injectable SBS, which was implanted in tibial fractures in goats for 3 and 6 weeks. The obtained results showed that HG allowed the stabilization of the granules into the defect, ensuring effective handling, and molding properties of the formulation, as well as an efficient cohesion of the granules. [ABSTRACT FROM AUTHOR]

The surface concentration of CBD−FITC conjugates, adsorbed on cellulose fibers, was determined by image analysis. The program consists of two scripts, the first dedicated to the elaboration of the calibration curve. The emission of fluorescent light, detected by image analysis, is correlated with the concentration of CBD solutions. This calibration is then used (second script) to determine the concentration of CBDs adsorbed on cellulosic fibers. This method allows the direct estimation of the surface concentration of adsorbed CBDs, which usually is not accurately calculated from depletion studies, since the surface area is hardly known. By observing different spots in the surface of the fibers, site-specific information is obtained. It was verified that the physically heterogeneous fibers exhibit different amounts of adsorbed CBDs. [ABSTRACT FROM AUTHOR]

Abstract  A method for the gram-scale production of cellulose-binding domains (CBD) through the proteolytic digestion of a commercial enzymatic preparation (Celluclast) was developed. The CBD obtained, isolated from Trichoderma reesei cellobiohydrolase I, is highly pure and heavily glycosylated. The purified peptide has a molecular weight of 8.43 kDa, comprising the binding module, a part of the linker, and about 30% glycosidic moiety. Its properties may thus be different from recombinant ones expressed in bacteria. CBD-fluorescein isothiocyanate conjugates were used to study the CBD-cellulose interaction. The presence of fluorescent peptides adsorbed on crystalline and amorphous cellulose fibers suggests that amorphous regions have a higher concentration of binding sites. The adsorption is reversible, but desorption is a very slow process. [ABSTRACT FROM AUTHOR]

Phosphatidylinositol 3-kinase (PI3K) promotes cell survival and communication by activating its downstream effector Akt kinase. Here we show that PS1, a protein involved in familial Alzheimer's disease (FAD), promotes cell survival by activating the PI3K/Akt cell survival signaling. This function of PS1 is unaffected by ?-secretase inhibitors. Pharmacological and genetic evidence indicates that PS1 acts upstream of Akt, at or before PI3K kinase. PS1 forms complexes with the p85 subunit of PI3K and promotes cadherin/PI3K association. Furthermore, conditions that inhibit this association prevent the PS1-induced PI3K/Akt activation, indicating that PS1 stimulates PI3K/Akt signaling by promoting cadherin/PI3K association. By activating PI3K/Akt signaling, PS1 promotes phosphorylation/inactivation of glycogen synthase kinase-3 (GSK-3), suppresses GSK-3-dependent phosphorylation of tau at residues overphosphorylated in AD and prevents apoptosis of confluent cells. PS1 FAD mutations inhibit the PS1-dependent PI3K/Akt activation, thus promoting GSK-3 activity and tau overphosphorylation at AD-related residues. Our data raise the possibility that PS1 may prevent development of AD pathology by activating the PI3K/Akt signaling pathway. In contrast, FAD mutations may promote AD pathology by inhibiting this pathway. [ABSTRACT FROM AUTHOR]