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-

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

Taalontwikkeling en taalstoornissen: Theorie, diagnostiek en behandeling

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