Accountability in patenting of federally funded research

Bayh-Dole allows academic grantees to patent federally-funded research for purposes of promoting the commercialization of this research. To ensure commercialization goals are achieved, the Act requires grantees to report to funding agencies not only the existence of federally-funded patents but also utilization efforts they and their licensees/assignees are making. Although reporting is a cornerstone of accountability under Bayh-Dole, information about grantee compliance with reporting requirements is incomplete and dated. In fact, the last significant study of the question dates back to the late 1990s and analyzes only 633 patents. Since that time, concerns have emerged that federally-funded university patents are being asserted improperly against independent commercializers or even assigned to so-called “patent trolls.” This article provides fresh evidence indicating substantial under-reporting of the existence of federal funding in over 30,000 academic biomedical patents issued between 1980 to 2007. The article finds substantial under-reporting of federal funding even in the case of patents on FDA-approved drugs, which should presumably receive significant attention from universities. Grantees’ failure to report federal funding suggests similar, or even more significant, noncompliance with requirements to report utilization information. However, compliance with reporting requirements on utilization cannot be assessed because of secrecy associated with relevant government databases. Accordingly, the article makes a fresh argument that the Commerce Department, which has the requisite regulatory authority, work with funding agencies, to improve transparency. Greater transparency would not only motivate grantees to improve reporting but would also allow assessment of whether grantee patent management is actually achieving Bayh-Dole\u27s utilization goals

University Software Ownership and Litigation: A First Examination

Software patents and university-owned patents represent two of the most controversial intellectual property developments of the last twenty-five years. Despite this reality, and concerns that universities act as “patent trolls” when they assert software patents in litigation against successful commercializers, no scholar has systematically examined the ownership and litigation of university software patents. In this Article, we present the first such examination. Our empirical research reveals that software patents represent a significant and growing proportion of university patent holdings. Additionally, the most important determinant of the number of software patents a university owns is not its research and development (“R&D”) expenditures (whether computer science-related or otherwise) but, rather, its tendency to seek patents in other areas. In other words, universities appear to take a “one size fits all” approach to patenting their inventions. This one size fits all approach is problematic given the empirical evidence that software is likely to follow a different commercialization path than other types of invention. Thus, it is perhaps not surprising that we see a number of lawsuits in which university software patents have been used not for purposes of fostering commercialization, but instead, to extract rents in apparent holdup litigation. The Article concludes by examining whether this trend is likely to continue in the future, particularly given a 2006 Supreme Court decision that appears to diminish the holdup threat by recognizing the possibility of liability rules in patent suits, as well as recent case law that may call into question certain types of software patents

Antiangiogenic Therapies for Advanced Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) is a significant cause of death worldwide. HCC is a highly vascular tumor, and proangiogenic cytokines such as vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and fibroblast growth factor may play crucial roles in this disease. Sorafenib, a multikinase inhibitor that blocks VEGF and PDGF signaling, was the first systemic therapy to demonstrate improved survival in patients with advanced HCC. Several other drugs targeting VEGF are in development. Because of the anticipation of eventual resistance to anti-VEGF therapies, drugs that also target alternative proangiogenic pathways are being investigated. Recent clinical and preclinical data along with ongoing studies are reviewed

Unique challenges accompany thick-shell CdSe/nCdS (n \u3e 10) nanocrystal synthesis

Thick-shell CdSe/nCdS (n \u3e10) nanocrystals were recently reported that show remarkably suppressed fluorescence intermittency or blinking at the single-particle level as well as slow rates of Auger decay. Unfortunately, whereas CdSe/nCdS nanocrystal synthesis is well-developed up to n \u3c 6 CdS monolayers (MLs), reproducible syntheses for n \u3e 10 MLs are less understood. Known procedures sometimes result in homogeneous CdS nucleation instead of heterogeneous, epitaxial CdS nucleation on CdSe, leading to broad and multimodal particle size distributions. Critically, obtained core/shell sizes are often below those desired. This article describes synthetic conditions specific to thick-shell growth (n\u3e 10 and n\u3e 20 MLs) on both small (sub2 nm) and large (\u3e4.5 nm) CdSe cores. We find added secondary amine and low concentration of CdSe cores and molecular precursors give desired core/shell sizes. Amine-induced, partial etching of CdSe cores results in apparent shell-thicknesses slightly beyond those desired, especially for very-thick shells (n \u3e20 MLs). Thermal ripening and fast precursor injection lead to undesired homogeneous CdS nucleation and incomplete shell growth. Core/shells derived from small CdSe (1.9 nm) have longer PL lifetimes and more pronounced blinking at single-particle level compared with those derived from large CdSe (4.7 nm). We expect our new synthetic approach will lead to a larger throughput of these materials, increasing their availability for fundamental studies and applications

CDK inhibitors reduce cell proliferation and reverse hypoxia-induced metastasis of neuroblastoma tumours in a chick embryo model

Neuroblastoma is a paediatric cancer with a poor prognosis. This is in part due to widespread metastasis at time of presentation, which is refractory to current treatment modalities. New therapeutic agents that can control not only tumour growth but also metastasis are urgently needed. The differentiation therapy, retinoic acid, is currently used in clinic, leading to terminal differentiation of neuroblastoma cells thus reducing tumour growth in the primary tumour as well as at metastatic sites. However, retinoic acid only works in a subset of patients. We investigated the potential of CDK inhibitors, Palbociclib and RO-3306, on neuroblastoma cell differentiation, tumour progression and metastasis by utilising a 3R compliant cost effective preclinical chick embryo model. In both SK-N-AS and BE(2)C cell lines, when engrafted on the chorioallantoic membrane of chick embryos, we observed a reduction of tumour cell proliferation as well as a reduction in hypoxia preconditioning-driven metastasis by 60%. In addition, the expression of a panel of genes with known roles in metastasis, which increased upon hypoxia-preconditioning, was largely reduced by a CDK1 inhibitor. These results provide a promising alternative to currently existing therapies and might aid the development of new treatment protocols for retinoic acid-resistant patients

Author Correction: Intensified summer monsoon and the urbanization of Indus Civilization in northwest India.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper.NERC (NE/H011463/1

Is Bayh-Dole Good for Developing Countries? Lessons from the US Experience

The US Bayh-Dole Act encourages university patenting of inventions arising from publicly funded research. Lessons from three decades of US experience serve as a cautionary tale for those countries that may choose to emulate Bayh-Dole