Co-patents’ commercialization: evidence from China

Co-patents are outcomes of R&D collaboration, which has been proven with higher-quality. Does this mean that high-quality patents should also extend their advantage to the technology market? Based on the transaction cost theory, we use the China National Intellectual Property Administration (CNIPA) database and logit model to explore the effect of co-ownership on firms’ patent commercialization and the factors of co-patents that affect their commercialization. Our findings illustrate that co-ownership has a negative impact on patent commercialization. In addition, the co-owner’s nature, country, and co-patent’s industry influence the commercialization of co-patents. Firstly, a company and a university or research institution’s co-owned co-patents are less likely to be commercialization than a company and a company coowned co-patents. Secondly, multi-countries co-owned co-patents are less likely to be commercialization than a single-country coowned co-patents. Thirdly, co-patents in high technology (hightech) industries are less likely to be commercialization than copatents in non-high-tech industries. This paper supports policymakers in implementing policies to promote the co-patents’ commercialization. Meanwhile, our paper suggests that to pursue the economic value of the R&D collaborative intellectual property fruits, R&D collaborative intellectual property fruits are not be encouraged to be applied as the co-patents.European Union (EU) TIN2016-75850-

Deletion of Glucose Transporter GLUT8 in Mice Increases Locomotor Activity

Transport of glucose into neuronal cells is predominantly mediated by the glucose transporters GLUT1 and GLUT3. In addition, GLUT8 is expressed in some regions of the brain. By in situ hybridization we detected GLUT8-mRNA in hippocampus, thalamus, and cortex. However, its cellular and physiological function is still unknown. Thus, GLUT8 knockout (Slc2a8−/−) mice were used for a screening approach in the modified hole board (mHB) behavioral test to analyze the role of GLUT8 in the central nervous system. Slc2a8−/− mice showed increased mean velocity, total distance traveled and performed more turns in the mHB test. This hyperactivity of Slc2a8−/− mice was confirmed by monitoring locomotor activity in the home cage and voluntary activity in a running wheel. In addition, Slc2a8−/− mice showed increased arousal as indicated by elevated defecation, reduced latency to the first defecation and a tendency to altered grooming. Furthermore, the mHB test gave evidence that Slc2a8−/− mice exhibit a reduced risk assessment because they performed less rearings in an unprotected area and showed significantly reduced latency to stretched body posture. Our data suggest that behavioral alterations of Slc2a8−/− mice are due to dysfunctions in neuronal processes presumably as a consequence of defects in the glucose metabolism

Transport characteristics of guanidino compounds at the blood-brain barrier and blood-cerebrospinal fluid barrier: relevance to neural disorders

Guanidino compounds (GCs), such as creatine, phosphocreatine, guanidinoacetic acid, creatinine, methylguanidine, guanidinosuccinic acid, γ-guanidinobutyric acid, β-guanidinopropionic acid, guanidinoethane sulfonic acid and α-guanidinoglutaric acid, are present in the mammalian brain. Although creatine and phosphocreatine play important roles in energy homeostasis in the brain, accumulation of GCs may induce epileptic discharges and convulsions. This review focuses on how physiologically important and/or neurotoxic GCs are distributed in the brain under physiological and pathological conditions. Transporters for GCs at the blood-brain barrier (BBB) and the blood-cerebrospinal fluid (CSF) barrier (BCSFB) have emerged as substantial contributors to GCs distribution in the brain. Creatine transporter (CRT/solute carrier (SLC) 6A8) expressed at the BBB regulates creatine concentration in the brain, and represents a major pathway for supply of creatine from the circulating blood to the brain. CRT may be a key factor facilitating blood-to-brain guanidinoacetate transport in patients deficient in S-adenosylmethionine:guanidinoacetate N-methyltransferase, the creatine biosynthetic enzyme, resulting in cerebral accumulation of guanidinoacetate. CRT, taurine transporter (TauT/SLC6A6) and organic cation transporter (OCT3/SLC22A3) expressed at the BCSFB are involved in guanidinoacetic acid or creatinine efflux transport from CSF. Interestingly, BBB efflux transport of GCs, including guanidinoacetate and creatinine, is negligible, though the BBB has a variety of efflux transport systems for synthetic precursors of GCs, such as amino acids and neurotransmitters. Instead, the BCSFB functions as a major cerebral clearance system for GCs. In conclusion, transport of GCs at the BBB and BCSFB appears to be the key determinant of the cerebral levels of GCs, and changes in the transport characteristics may cause the abnormal distribution of GCs in the brain seen in patients with certain neurological disorders

EU copyright law ::a commentary /

"This significantly revised and updated second edition builds upon the authoritative foundations of the first edition. It addresses the rapid development of EU copyright law in relation to the advancement of new technologies, the need for a borderless digital market and the considerable number of EU legal instruments enacted as a result. Alongside full legislative analysis and article-by-article commentary, the Commentary illustrates the underlying basic principles of free movement and non-discrimination. It provides insights into the influence of copyright on other areas of EU policy, including telecoms and bilateral trade agreements. This unique Commentary describes and analyses each EU directive in turn and discusses anticipated future challenges, utilising a clear structure to enable the reader to navigate the Commentary effectively. Written by a team of leading experts in the field, this Commentary combines theory and practice to tackle the role of copyright in society and the economy, making this a key resource for academics, researchers, practitioners and policymakers in copyright and comparative law"-

EU copyright law ::a commentary /

"'Comprehensive and up-to-date, this collection of contributions on EU copyright law signals the emergence of a truly European body of legal commentary on copyright law. The authors, many of them very distinguished, hail from 9 different Member States. As a result, the book contains a wealth of references not only to EU authorities but also to national laws and decisions. Moreover, in addition to covering general principles of European copyright, and analyzing each copyright Directive, the book examines future prospects for copyright in the EU.'--Jane Ginsburg, Columbia Law School, US. This authoritative reference work presents comprehensive article-by-article commentary on each of the EU Directives in the field of copyright, as well as analysis of the underlying basic concepts and principles such as free movement and non-discrimination. Published as part of the Elgar Commentaries series, this unique book describes and analyses each EU directive in turn, taking into account all recent legislative amendments and pending initiatives in the context of the EU Digital Agenda, as well as the case law of the Court of Justice of the European Union. With a clear structure allowing readers to navigate quickly to a specific point, the book not only sets out the law, but boldly discusses challenges for the future that will underpin copyright in the years to come. It also presents ongoing discussions in WIPO and assesses the role of copyright in society and economy both from an EU and an international perspective. EU Copyright Law is a seminal commentary work from a team of leading experts in the field combining aspects of theory and practice and placing copyright in perspective. It will be an indispensable reference tool for academics, researchers, practitioners and policymakers in copyright law and comparative law."--Back cover