LARGE BENTHIC FORAMINIFERA PFENDERICONUS GLOBULUS SIREL & DECEVILER IN SIREL ET AL., 2020 (PRIABONIAN OF TURKEY): A JUNIOR SYNONYM OF PFENDERICONUS MINDANAOENSIS MATSUMARU, 2017 (THANETIAN? OF THE PHILIPPINE ARCHIPELAGO)

Pfendericonus mindanaoensis Matsumaru, 2017 from the Thanetian? of the Philippine Archipelago and Pfendericonus globulus Sirel & Deceviler (in Sirel et al. 2020) from the Priabonian of Turkey display the same internal structure, similar dimensions and both are characterized by possessing wedge-like adult chambers. These species are thus considered synonymous and therefore based on priority date of publication, P. globulus should be considered a subjective junior synonym of P. mindanaoensis.

Actavis Group PTC EHF v ICOS Corporation

H1 Patents – European Patents – Pharmaceuticals – Tadalafil – Dosing regimens – Revocation – Obviousness – Obvious to try – Fair expectation of success – Relevant factors – Dose ranging studies – Routine tests – Whether permissible to take into account information not available at priority date – The “patent bargain” – The “problem-and-solution” approach – Role of the appellate court – Appeal to Supreme Court

13. Patents III

All books in this flagship series contain carefully selected substantial extracts from key cases, legislation, and academic debate, providing able students with a stand-alone resource. This chapter discusses patent infringement, exceptions to infringement, and entitlement. Assessment of whether a patent has been infringed involves a three-stage process. First, the patent claims must be construed to see whether the defendant’s activities fall within the scope of the monopoly. Second, identify the infringing acts that the defendant is alleged to have carried out. Third, consider the applicability of exceptions to infringement. The chapter then focuses on three key exceptions to infringement within the Patents Act 1977: acts done for experimental purposes (‘experimental use’); acts done for private and non-commercial purposes (‘private use’); and the right to continue use begun before the priority date (‘prior use’). Finally, it considers persons entitled to the grant of a patent.

Obtaining a Granted Patent

The Patent Cooperation Treaty (PCT) is a special agreement under Article 19 of the Paris Convention and is open only to states that are members of the Convention. Its main purpose is to make the patent application process simpler and cheaper by having a single set of formal requirements, and a single search and publication procedure, and by postponing translation requirements until thirty months from the priority date. This chapter first discusses the procedure for filing an international application, that is, a PCT application. It then explains the International Preliminary Report on Patentability (IPRP)—a preliminary, non-binding opinion by the international preliminary examining authority (IPEA) on the novelty, inventive step, and industrial applicability of the claimed invention.

Filing a Patent Application

This chapter first addresses questions such as whether a patent application should be filed at all, and if so, when and where to file. As a general rule, if an invention appears patentable and may be of some commercial interest, a priority application should be filed. The applicant then has one year under the Paris Convention before significant amounts of time and money must be invested in filing in other countries. If the decision is made to file in other countries, or even to proceed to obtain a patent in the home country, the first filing gives a priority date that can be relied upon later. In other words, when in doubt, file an application. The remainder of the chapter discusses non-convention filings, European patent applications, international applications, registrations and patents of importation, and petty patents.

Empirical assessment of the time course of innovation in biomedical engineering: first results of a comparative approach

The pathway from the flash of a technological invention until its use as a medical device in every day care is tedious and burdensome. But the often postulated acceleration has to balance the speed of innovation and the indispensable product safety by an improved understanding of the innovation cycle. While several studies investigated the time course of pharmaceutical innovation, a comparable empirical analysis of medical devices is lacking. Thus we evaluated the time between the patent priority date and the corresponding receipt of the CE mark as a function of a medical device risk class in 61 cases. The statistical analysis yielded a time increment (trend) from medical devices in risk category I (median = 5.8 years) compared to risk category III (median = 10.4 years), which is close to literature reported values for drug development (9–12 years). The difference between products in risk classes I and II did not reach significance. To investigate the underlying facts, a text-mining approach especially to resolve the ambiguity of, e.g. patents, CE Marks etc. is suggested for increasing the sample size.

Prior Designs

Article 4 of the Regulation provides that ‘a design shall be protected by a Community design to the extent that it is new and has individual character’. Both novelty and individual character are assessed against designs made available to the public prior to the relevant date (the date of disclosure in the European Union for unregistered Community designs and the application or priority date for RCDs).

Sympathetic Neuropathy Of The Hematopoietic Stem Cell Niche Is Essential For Myeloproliferative Neoplasms

Myeloproliferative neoplasms (MPNs) are originated by mutations in a hematopoietic stem cell (HSC), frequently in the Janus kinase 2 (JAK2) gene. Different outcomes of this common event and limited efficacy of JAK2 inhibitors suggest the contribution of other factors. Additional HSC mutations and HSC-niche interaction might influence MPN progression, characterized by sequential expansion of HSCs, blood cells and megakaryocytes. Ensuing bone marrow (BM) fibrosis and osteosclerosis, which are contributed by osteoblastic lineage cells in a BCR/ABL CML model (Schepers et al Cell Stem Cell 2013), impede normal hematopoiesis. We have previously shown that BM nestin+ mesenchymal stem cells (MSCs) innervated by sympathetic nerve fibers regulate HSCs (Méndez-Ferrer et al Nature 2008 & 2010). Here we demonstrate that damage to this regulatory network is required for MPN manifestation. Nestin+ MSCs and NESTIN mRNA expression were rapidly reduced in the BM of MPN patients and mice expressing the human JAK2-V617F mutation. This reduction was not due to nestin+ MSC differentiation into fibroblasts or osteoblasts, as shown by 25-week lineage-tracing studies using Nes-CreERT2;RCE-loxP mice, but instead caused by early MSC apoptosis. In turn, nestin+ cell reduction stimulated MPN progression; selective nestin+ cell depletion using Nes-CreERT2;iDTA mice increased peripheral white and red blood cells, megakaryocytic invasion of spleen germinal centers and BM osteosclerosis. Our recent results indicate that the neural crest contributes during development to BM MSCs with specialized HSC niche function and that postnatal murine BM Nestin-GFP+ cells do not only contain MSCs but also Schwann cell precursor-like cells (Isern et al, ISSCR Annual Meeting 2013). BM Nestin-GFP+ cells from MPN mice showed reduced expression of HSC maintenance and mesenchymal genes, and increased expression of genes related to axon guidance and Schwann cell differentiation. Principal component analyses of independent biological samples further showed that control BM nestin+ cells clustered together with MSCs, whereas MPN BM nestin+ cells resembled Schwann cell precursors. These data suggested alterations to the neural component of the BM HSC niche in MPN. Indeed, BM sympathetic nerve fibers and Schwann cells, closely associated but different from Nestin-GFP+ cells, were rapidly reduced in the BM of diseased animals. Symptomatic MPN mice were treated with selective β3-adrenergic agonists to compensate for the loss of sympathetic stimulation of nestin+ MSCs. Treatment with BRL37344 or the recently FDA approved drug Mirabegron prevented MPN-associated neutrophilia and thrombocytosis, while it did not affect peripheral blood counts of wild-type mice. While vehicle-injected animals showed severe BM fibrosis, long-term BRL37344 treatment led to virtual absence of focal reticulin deposits or excessive fibroblasts. To further confirm the contribution of BM neural damage to MPN pathogenesis, diseased mice were treated with a neuroprotective agent. Sympathetic nerve-ensheathing Schwann cells were strongly reduced in the BM of vehicle-injected animals but preserved in 4-methylcatechol-treated mice. Like in BRL37344-treated animals, this was associated with prevention of very early MPN events, including neutrophilia and BM overproduction of the pro-inflammatory cytokine interleukin-1β. Since MPN is originated by a mutant HSC, we reasoned that sympathetic neuropathy might contribute to MPN pathogenesis through early disruption of the HSC niche. The chemokine Cxcl12 regulates HSC migration and proliferation. At early MPN stage, HSC expansion and mobilization correlated with decreased BM Cxcl12 expression and protein levels. Concomitantly, BM nestin+ MSC number and their Cxcl12 expression were significantly reduced. BRL37344 treatment completely restored the number of BM nestin+ cells and improved Cxcl12 BM levels. Treatment with 4-methylcatechol or BRL37344 prevented the early expansion of mutant hematopoietic progenitors, whereas long-term BRL37344 treatment efficiently reduced mutant hematopoietic progenitor numbers in BM and peripheral blood. These results demonstrate that damage of the niche, induced by the mutated HSCs, critically contributes to JAK2-V617F+ MPN pathogenesis. They also unravel HSC niche-forming MSCs and their neural regulation as promising novel therapeutic targets in MPN. Disclosures: Arranz: Centro Nacional de Investigaciones Cardiovasculares (CNIC): National patent application number 201330677 entitled “Neuroprotective/neurocompensatory therapy for the treatment of myeloproliferative diseases”, with priority date May 10, 2013, National patent application number 201330677 entitled “Neuroprotective/neurocompensatory therapy for the treatment of myeloproliferative diseases”, with priority date May 10, 2013 Patents & Royalties. Off Label Use: Beta-3-adrenergic agonists (e.g. FDA-approved Mirabegron) and neuroprotective drugs for the treatment of myeloprolifeative diseases. Isern:Centro Nacional de Investigaciones Cardiovasculares (CNIC): National patent application number 201330677 entitled “Neuroprotective/neurocompensatory therapy for the treatment of myeloproliferative diseases”, with priority date May 10, 2013, National patent application number 201330677 entitled “Neuroprotective/neurocompensatory therapy for the treatment of myeloproliferative diseases”, with priority date May 10, 2013 Patents & Royalties. Méndez-Ferrer:Centro Nacional de Investigaciones Cardiovasculares (CNIC): National patent application number 201330677 entitled “Neuroprotective/neurocompensatory therapy for the treatment of myeloproliferative diseases”, with priority date May 10, 2013, National patent application number 201330677 entitled “Neuroprotective/neurocompensatory therapy for the treatment of myeloproliferative diseases”, with priority date May 10, 2013 Patents & Royalties.