1,721,557 research outputs found
Privacy Accountability and Penalties for IoT Firms.
No full textInternet of things (IoT) business partnership are formed by technological partners and traditional manufacturers. IoT sensors and devices capture data from manufacturers' products. Data enforce product/service innovation thanks to data sharing among companies. However, data sharing among firms increases the risk of data breaches. The latter is due to two phenomena: information linkage and privacy interdependency. Data Protection Authorities (DPA) protect data users' rights and fine firms if there is an infringement of privacy laws. DPA sanction the responsible for the infringement of privacy laws. We present two different business scenarios: the first occurs when each firm is a data owner; the second occurs when only the manufacturer is the data owner. For both scenarios, we present two fair penalty schemes that suggest the following: total amount of the fine; and how to share the fine among participants. Penalties critically vary at how innovation networks are structured in IoT industries. Our penalties provide incentives to data sharing since they redistribute firms' responsibility against data breaches. Our penalties may mitigate the risk on the manufacturer if is the unique responsible for data handling
Targeting of Epidermal Growth Factor Receptor and Protein Kinase A : Molecular basis and therapeutic applications.
No full textA novel approach in the treatment of cancer: targeting the epidermal growth factor receptor.
No full text
Pollution responsibility allocation in supply networks: A game-theoretic approach and a case study
No full textA unified cooperative model for environmental costs in supply chains: the Shapley value for the linear case.
No full text8-Chloro-cAMP inhibits transforming growth factor alpha transformation of mammary epithelial cells by restoration of the normal mRNA patterns for cAMP-dependent protein kinase regulatory subunit isoforms which show disruption upon transformation
Full text linkDifferential regulation of the regulatory subunits of cAMP-dependent protein kinase isozymes correlates with the growth inhibitory effect of site-selective 8-Cl-cAMP demonstrated in cancer cell lines (Ally, S., Tortora, G., Clair, T., Grieco, D., Merlo, G., Katsaros, D., Ogreid, D., Døskeland, S.O., Jahnsen, T., and Cho-Chung, Y.S. (1988) Proc. Natl. Acad. Sci. U. S. A. 85, 6319-6322). Such selective modulation of protein kinase isozyme regulatory subunits was also found in the 8-Cl-cAMP-induced inhibition of both transformation and transforming growth factor alpha (TGF alpha) production in Ki-ras-transformed rat kidney fibroblasts (Tortora, G., Ciardiello, F., Ally, S., Clair, T., Salomon, D. S., and Cho-Chung, Y. S. (1989) FEBS Lett. 242, 363-367). In this work, we have demonstrated that 8-Cl-cAMP antagonizes the TGF alpha effect in TGF alpha-transformed mouse mammary epithelial cells (NOG-8TFC17) at the level of gene expression for cAMP receptor protein isoforms, RI and RII (the regulatory subunits of protein kinase isozymes). Northern blot analysis demonstrated that in the transformed NOG-8TFC17 cells, compared with the nontransformed counterpart NOG-8 cells, the mRNA levels for the RI alpha cAMP receptor protein markedly increased, whereas the mRNA levels for the RII alpha and RII beta cAMP receptor proteins decreased. 8-Cl-cAMP, which induced growth inhibition and phenotypic reversion in NOG-8TFC17 cells, caused an inverse change in the mRNA patterns of the cAMP receptor proteins; RI alpha cAMP receptor mRNA sharply decreased to levels comparable with that of the nontransformed NOG-8 cells, whereas RII beta mRNA increased to a level even greater than that in the NOG-8 cells. In addition, one mRNA species of RII alpha increased, whereas the other RII alpha mRNA species decreased during the treatment. The mRNA level for the catalytic subunit of protein kinase, however, did not change during 8-Cl-cAMP treatment. In addition, 8-Cl-cAMP brought about a reduction in both TGF alpha mRNA and protein levels. These coordinated changes in the expression of the cAMP receptor proteins and TGF alpha were not observed during cis-hydroxyprolineor TGF beta-induced growth inhibition of the NOG-8TFC17 cells. Thus, the antagonistic effect of 8-Cl-cAMP toward TGF alpha-induced transformation involves modulation of the expression of a specific set of cellular genes
- …
