Formulas for fair, reasonable and non-discriminatory royalty determination

This paper takes an axiomatic approach to determining “Fair, Reasonable, and Non-Discriminatory” (“FRAND”) royalties for intellectual property (“IP”) rights. Drawing on the extensive game theory literature on “surplus sharing/cost sharing” problems, I describe specific formulas for determining license fees that can be derived from basic fairness principles. In particular, I describe the Shapley Value, the Proportional Sharing Rule and the Nucleolus. The Proportional Sharing Rule has the advantage that it is the only rule that is invariant to mergers and splitting of the IP owners. I also explain why, at times, there may be no acceptable to solution. Further, I contrast these rules with the Efficient Component Pricing Rule (“ECPR”) suggested by Baumol and Swanson. Unlike, the ECPR, the rules identified in this paper can uniquely determine license fees when there is more than one owner of essential IP, and also incorporate various notions of fairness and equity.FRAND, Royalty Rates, Intellectual Property

Sequential auction and auction design

Often an auction designer has the option of selling, or purchasing, those lots available in one auction or a sequence of auctions. In addition, bidder opportunities will not be static, in part due to arrival of information, but also because bidders can face deadlines for making decisions. This paper examines the optimal decision about how to divide what is available over time.sequential auctions

Sequential auction and auction design

Often an auction designer has the option of selling, or purchasing, those lots available in one auction or a sequence of auctions. In addition, bidder opportunities will not be static, in part due to arrival of information, but also because bidders can face deadlines for making decisions. This paper examines the optimal decision about how to divide what is available over time

Formulas for fair, reasonable and non-discriminatory royalty determination

This paper takes an axiomatic approach to determining “Fair, Reasonable, and Non-Discriminatory” (“FRAND”) royalties for intellectual property (“IP”) rights. Drawing on the extensive game theory literature on “surplus sharing/cost sharing” problems, I describe specific formulas for determining license fees that can be derived from basic fairness principles. In particular, I describe the Shapley Value, the Proportional Sharing Rule and the Nucleolus. The Proportional Sharing Rule has the advantage that it is the only rule that is invariant to mergers and splitting of the IP owners. I also explain why, at times, there may be no acceptable to solution. Further, I contrast these rules with the Efficient Component Pricing Rule (“ECPR”) suggested by Baumol and Swanson. Unlike, the ECPR, the rules identified in this paper can uniquely determine license fees when there is more than one owner of essential IP, and also incorporate various notions of fairness and equity

Resale price maintenance post Leegin: A model of rpm incentives

The prominent Babies R Us decision (McDonough et al., v. Toys R US, Inc., 2009) was the first to explore the economic consequences of resale price maintenance after the Supreme Court’s Leegin Decision. Previously, litigation concerned the presence or absence of an agreement; but that changed with the new jurisprudence which instead emphasized the restraint’s direct anti-competitive effects. While the district court’s decision in the Babies R Us case rested on the factual circumstances of the case, it did not have before it an economic model through which those facts could be integrated. This paper offers such a mode, the predicates of which are drawn from the case. The conclusions that are drawn from the model are fully consistent with the court’s decisio

Resale price maintenance post Leegin: A model of rpm incentives

The prominent Babies R Us decision (McDonough et al., v. Toys R US, Inc., 2009) was the first to explore the economic consequences of resale price maintenance after the Supreme Court’s Leegin Decision. Previously, litigation concerned the presence or absence of an agreement; but that changed with the new jurisprudence which instead emphasized the restraint’s direct anti-competitive effects. While the district court’s decision in the Babies R Us case rested on the factual circumstances of the case, it did not have before it an economic model through which those facts could be integrated. This paper offers such a mode, the predicates of which are drawn from the case. The conclusions that are drawn from the model are fully consistent with the court’s decisio

Cytosolic calcium and protein kinase C reduce complement-mediated glomerular epithelial injury

Cytosolic calcium and protein kinase C reduce complement-mediated glomerular epithelial injury. In rat membranous nephropathy, proteinuria is due to formation of the C5b-9 membrane attack complex of complement (C), and is associated with morphological evidence of glomerular epithelial cell (GEC) injury. Analogous morphological changes are induced by C5b-9 in cultured GEC. In addition, in cultured GEC C5b-9 induces Ca2+ influx, as well as Ca2+ mobilization and increased 1,2-diacylglycerol due to the activation of phospholipase C. In this study we investigated how this GEC activation pattern might influence C-mecliated GEC injury. We demonstrate that the C5b-9-induced increase in cytosolic Ca2+ concentration ([Ca2+]i) did not impair ATP generation by mitochondria, suggesting that it does not contribute to cytotoxicity. Moreover, this increase in [Ca2+]i protected GEC from C-mediated cytolysis. However, a large increase in [Ca2+]i (produced by the Ca2+ ionophore A23187) impaired ATP generation and aggravated C-mediated cytotoxicity, suggesting that intact mitochondrial activity is necessary for GEC to withstand C attack. Activation of protein kinase C (PKC) by phorbol myristate acetate (PMA) also decreased C-mediated cytolysis. Conversely, C lysis was enhanced in GEC that had been pretreated for 18 hours with a high dose of PMA to deplete PKC, and following PKC inhibition with H-7. Therefore, PKC activation, possibly resulting from C5b-9-induced increase in 1,2-diacylglycerol, triggered mechanisms that protected GEC from C-mediated injury. Thus, as a consequence of C5b-9-induced phospholipase activation, the amount of C-induced GEC injury is diminished

Glomerular epithelial cell products stimulate mesangial cell proliferation in culture

Glomerular epithelial cell products stimulate mesangial cell proliferation in culture. Glomerular epithelial cells (GEC) and mesangial cells (MC) are both involved in glomerular diseases. To elucidate potential interactions between these glomerular cell types, we examined whether products of GEC affect the proliferative activity of MC. We found that cultured rat GEC secrete soluble factors into the supernate (GEC-CM) that induce proliferation of quiescent rat MC. The mitogenic activity was trypsin sensitive and partially heat-labile. Biochemical analysis of GEC-CM by gel filtration HPLC, reverse phase HPLC, and isoelectric focusing revealed at least three mitogenic fractions as well as inhibitory activity present in GEC-CM. Competitive binding assays with 125I-labeled PDGF did not show significant amounts of PDGF in GEC-CM. The biochemical features of the GEC-derived MC growth factors are distinct from IL-6, PDGF, bFGF, and endothelin, previously described GEC-derived MC growth factors. Additionally, significant contributions of known growth factors such as IL-1, IL-2, IL-3, IL-4, IL-5, TNFα, TGFβ, and GM-CSF are unlikely. The results indicate that GEC produce several biochemically-distinct MC growth regulators. While these epithelial cell-derived mitogens for MC require further characterization, they may play an important role in the regulation of MC replication, such as during embryogenesis and glomerular disease

Altered glomerular permeability induced by F(ab′)2 and Fab′ antibodies to rat renal tubular epithelial antigen

Altered glomerular permeability induced by F(ab′)2 and Fab′ antibodies to rat renal tubular epithelial antigen. Rats injected with F(ab′)2 and Fab′ antibody fragments directed against an antigen in the rat proximal tubular epithelial brushborder (Fx1A) developed immediate proteinuria [F(ab′)2 43.2 ± 6.7, N = 6; Fab′ 9.5 ± 2.8, N = 5; normal 1.6 ± 0.9 mg/day, N = 20]), that subsided after 3 to 5 days' duration. This reaction is in contrast to one exhibited by rats given intact IgG anti-Fx1A; the rats that did not develop immediate proteinuria (2.2 ± 0.3 mg/day, N = 5), and the glomerular binding of125I-antibody fragments was significantly less than that of intact IgG [F(ab′)2 0.11 ± 0.01; Fab′ 0.03 ± 0.01; IgG 0.17 ± 0.01% administered equimolar dose] at 24 hr. No proteinuria resulted from equimolar doses of nonantibody F(ab′)2 and Fab′. Less than 8% of the proteinuria induced by antibody fragments represented injected material, and 30 to 38% was albumin. Immunofluorescence revealed faint and diffuse glomerular capillary wall deposits of F(ab′)2 and Fab′ and tubular brushborder staining. Subepithelial, electrondense deposits and focal, podocyte effacement were seen by electron microscopy in rats given the F(ab′)2 antibody. Light microscopy and colloidal iron-staining were normal. In our study antibody fragments appear to interact directly with components of the outer, glomerular capillary wall to alter permeability in the absence of recognized mediators such as complement and inflammatory cells.Modification de la perméabilité glomérulaire déterminée par anticorps chez des rats anti-épithélium tubulaire F(ab′)2 et Fab′. Les rats été injectés avec des fragments F(ab′)2 et Fab′ contra anticorps de la bordure en brosse de l'épithélium tubulaire proximal de rat (Fx1A) ont immédiatement une protéinurie [F(ab′)2 43,2 ± 6,7, N = 6; Fab′ 9,5 ± 2,8, N = 5; normaux 1,6 ± 0,9 mg/d, N = 20] qui persiste pendant 3 à 5 jours. Cela réaction est différent de ce qui est observé chez les rats qui reçoivent l'IgG anti-Fx1A intacte; les rats quelles n'ont pas de protéinurie immédiate (2,2 ± 0,3 mg/d, N = 5) quoiqu'à 24 heures la liaison glomérulaire de fragments125I de l'anticorps soit significativement plus faible que celle de I'IgG intacte [F(ab′)2 0,11 ± 0,01; Fab′ 0,03 ± 0,01; IgG 0,17 ± 0,01 en % de la dose équimolaire administrée]. Aucune protéinurie n'a été la conséquence de l'administration équimolaire de F(ab′)2 et Fab′ non-anticorps. Moins de 8% de la protéinurie déterminée par les fragments d'anticorps représentent du matériel injecté et 30 à 38% est de l'albumine. L'immunofluorescence a montré des dépôts faibles et diffus, sur les parois des capillaires giomérulaires, de F(ab′)2 et Fab′ et le marquage de la bordure en brosse. En électronique, des dépôts denses sous-épithéliaux et l'effacement local des podocytes ont été observés chez les rats qui avaient reçu l'anticorps F(ab′)2. La microscopie optique et la coloration par le fer colloïdal n'ont pas montré d'anomalies. Dans notre étude les fragments d'anticorps semblent avoir paroi externe du capillaire glomérulaire et avoir modifié la perméabilité en l'absence de médiateurs connus tels le complément ou les cellules inflammatoires

Effect of diet, age and sex on the renal response to immune injury in the rat

Effect of diet, age and sex on the glomerular response to immune injury in the rat. We investigated the effect of three factors, namely dietary protein intake, age and sex, on the susceptibility of the renal glomerulus to the binding of antiglomerular basement membrane antibody (anti-GBM) in the early (heterologous) phase of anti-GBM nephritis, and the consequent reduction in glomerular filtration rate (GFR) as measured by inulin clearance (CIn). The effect of diet was examined in ≈ 8 week-old female Munich-Wistar rats fed a 40% high (HP) or a 6% low (LP) protein diet, and that of sex and age in male and female rats, 6 week or 10 month old. Following an intravenous dose (3 to 20 µg/g body wt) of radiolabeled nephritogenic anti-GBM, assessment of glomerular function was followed by quantitation of anti-GBM binding (values corrected for GBM surface area) in isolated glomeruli. At a given plasma level of antibody, the degree of binding of anti-GBM was slightly but significantly higher in HP than LP-fed rats; the decrease in GFR was significantly more pronounced in HP than LP-fed animals. The amount of anti-GBM binding was significantly greater in adult than young animals; however, the consequent decrease in GFR was more pronounced in the young than adult animals. Sex dependency was not discernible in anti-GBM binding or reduction in GFR. In all of the above experimental groups, the degree of anti-GBM binding was closely correlated with the plasma level of anti-GBM, but not with effective renal plasma flow rate, measured by PAH clearance. Separate groups of rats were subjected to experimental manipulation of single nephron GFR, glomerular capillary hydraulic pressure and glomerular plasma flow rate, by partial aortic constriction and saralasin administration. This set of experiments, using a tracer amount of non-nephritogenic anti-GBM, revealed that glomerular anti-GBM binding is independent of any of the above parameters. The studies indicate that dietary protein intake and age, but not sex, are among the factors determining the susceptibility of the glomerulus to acute immune injury. Since the binding of anti-GBM is determined by the affinity property of the glomerulus per se, and not by the prevailing hemodynamic pattern, the observed dependence of susceptibility to functional impairment on age and protein intake appears to also reflect a property of the glomerulus, which is influenced by age and the degree of dietary protein intake