Products Liability: Imposing Strict Products Liability on the Trademark Licensor

Connelly v. Uniroyal, Inc., 75 ill. 2d 393, 389 N.E.2d 155 (1979). The recent case of Connelly v. Uniroyal, Inc. presents an interesting combination of two separate areas of the law: trademark and strict products liability. These two areas, while differing in the scope of protection offered, have evolved from one basic policy, that is, a deep concern for the welfare of the purchasing public. The former protects the consumer economically by theoretically assuring that the purchaser will, in fact, be buying what he intends to buy. The latter protects the consumer by holding a manufacturer strictly liable for injuries caused by its defective product. Both are based on warranty theory, and each is supported by the rationale that enforcement of the law will encourage the manufacture of better products. There are, however, some differences. Strict products liability accomplishes its objectives directly, by allowing the injured consumer to bring suit against the manufacturer and others in the distributive chain. Trademark law has developed a more circuitous route to achieve its purposes. Protection is not given directly to the consumer but to the trademark owner who, in order to prevent public deception, can bring an infringement action against those who copy or imitate his mark. Thus the mark owner becomes the “vicarious avenger” of the public’s injury. At least in theory, the consumer should be able to continue to rely on the trademark as a symbol of the quality he has come to expect from products bearing the mark because of the mark owner’s self-interest in protecting the goodwill that he has established in his business via the mark

Emphysematous Pyelonephritis and Pneumo-Vena Cava

West J Emerg Med. 2010;11(5):518-519

Crisaborole Ointment Improves Quality of Life of Patients with Mild to Moderate Atopic Dermatitis and Their Families.

IntroductionThe impact of crisaborole ointment, a nonsteroidal phosphodiesterase 4 inhibitor for the treatment of mild to moderate atopic dermatitis (AD), on quality of life (QoL) was assessed in two identically designed phase 3 studies (AD-301: NCT02118766; AD-302: NCT02118792, both at http://www.clinicaltrials.gov ).MethodsIn both studies, patients aged ≥ 2 years with mild to moderate AD per the Investigator's Static Global Assessment were randomly assigned 2:1 to receive crisaborole or vehicle twice daily for 28 days. QoL was assessed using the Children's Dermatology Life Quality Index (CDLQI) (2-15 years), the Dermatology Life Quality Index (DLQI) (≥ 16 years), and the Dermatitis Family Impact Questionnaire (DFI) (parents/caregivers/family of patients aged 2-17 years). Established QoL score severity bands provided clinical context.ResultsGreater mean improvement in QoL was observed in crisaborole-treated patients than in vehicle-treated patients at day 29 [mean change from baseline (∆BL), CDLQI: - 4.6 vs. - 3.0; P < 0.001; DLQI: - 5.2 vs. - 3.5; P = 0.015]. At baseline, more than half the patients had a "moderate effect" or higher of AD on QoL. At day 29, there was a trend toward more crisaborole- than vehicle-treated patients having "small effect" to "no effect", The QoL of parents/caregivers/family improved more for crisaborole-treated than for vehicle-treated patients (∆BL, DFI: - 3.7 vs. - 2.7; P = 0.003).ConclusionCrisaborole treatment results in clinically meaningful improvement in QoL for patients and their parents/caregivers/families.Trial registrationAD-301: http://www.clinicaltrials.gov , NCT02118766; AD-302: http://www.clinicaltrials.gov , NCT02118792.FundingAnacor Pharmaceuticals, Inc., a wholly owned subsidiary of Pfizer Inc., New York, NY

Multiparty Non-Interactive Key Exchange and More From Isogenies on Elliptic Curves

We describe a framework for constructing an efficient non-interactive key exchange (NIKE) protocol for n parties for any n >= 2. Our approach is based on the problem of computing isogenies between isogenous elliptic curves, which is believed to be difficult. We do not obtain a working protocol because of a missing step that is currently an open mathematical problem. What we need to complete our protocol is an efficient algorithm that takes as input an abelian variety presented as a product of isogenous elliptic curves, and outputs an isomorphism invariant of the abelian variety. Our framework builds a cryptographic invariant map, which is a new primitive closely related to a cryptographic multilinear map, but whose range does not necessarily have a group structure. Nevertheless, we show that a cryptographic invariant map can be used to build several cryptographic primitives, including NIKE, that were previously constructed from multilinear maps and indistinguishability obfuscation

Multiparty Non-Interactive Key Exchange and More From Isogenies on Elliptic Curves

We describe a framework for constructing an efficient non-interactive key exchange (NIKE) protocol for n parties for any n ≥ 2. Our approach is based on the problem of computing isogenies between isogenous elliptic curves, which is believed to be difficult. We do not obtain a working protocol because of a missing step that is currently an open mathematical problem. What we need to complete our protocol is an efficient algorithm that takes as input an abelian variety presented as a product of isogenous elliptic curves, and outputs an isomorphism invariant of the abelian variety. Our framework builds a cryptographic invariant map, which is a new primitive closely related to a cryptographic multilinear map, but whose range does not necessarily have a group structure. Nevertheless, we show that a cryptographic invariant map can be used to build several cryptographic primitives, including NIKE, that were previously constructed from multilinear maps and indistinguishability obfuscation

IBD genetic risk profile in healthy first-degree relatives of Crohn's disease patients

BACKGROUND: Family history provides important information on risk of developing inflammatory bowel disease [IBD], and genetic profiling of first-degree relatives [FDR] of Crohn's disease [CD]- affected individuals might provide additional information. We aimed to delineate the genetic contribution to the increased IBD susceptibility observed in FDR. METHODS: N = 976 Caucasian, healthy, non-related FDR; n = 4997 independent CD; and n = 5000 healthy controls [HC]; were studied. Genotyping for 158 IBD-associated single nucleotide polymorphisms [SNPs] was performed using the Illumina Immunochip. Risk allele frequency [RAF] differences between FDR and HC cohorts were correlated with those between CD and HC cohorts. CD and IBD genetic risk scores [GRS] were calculated and compared between HC, FDR, and CD cohorts. RESULTS: IBD-associated SNP RAF differences in FDR and HC cohorts were strongly correlated with those in CD and HC cohorts, correlation coefficient 0.63 (95% confidence interval [CI] 0.53 - 0.72), p = 9.90 x 10(-19). There was a significant increase in CD-GRS [mean] comparing HC, FDR, and CD cohorts: 0.0244, 0.0250, and 0.0257 respectively [p < 1.00 x 10(-7) for each comparison]. There was no significant difference in the IBD-GRS between HC and FDR cohorts [p = 0.81]; however, IBD-GRS was significantly higher in CD compared with FDR and HC cohorts [p < 1.00 x 10(-10) for each comparison]. CONCLUSION: FDR of CD-affected individuals are enriched with IBD risk alleles compared with HC. Cumulative CD-specific genetic risk is increased in FDR compared with HC. Prospective studies are required to determine if genotyping would facilitate better risk stratification of FDR

Oral leukoplakia and risk of progression to oral cancer: A population-based cohort study

BACKGROUND: The optimal clinical management of oral precancer remains uncertain. We investigated the natural history of oral leukoplakia, the most common oral precancerous lesion, to estimate the relative and absolute risks of progression to cancer, the predictive accuracy of a clinician\u27s decision to biopsy a leukoplakia vis-à-vis progression, and histopathologic predictors of progression. METHODS: We conducted a retrospective cohort study (1996-2012) of patients with oral leukoplakia (n = 4886), identified using electronic medical records within Kaiser Permanente Northern California. Among patients with leukoplakia who received a biopsy (n = 1888), we conducted a case-cohort study to investigate histopathologic predictors of progression. Analyses included indirect standardization and unweighted or weighted Cox regression. RESULTS: Compared with the overall Kaiser Permanente Northern California population, oral cancer incidence was substantially elevated in oral leukoplakia patients (standardized incidence ratio = 40.8, 95% confidence interval [CI] = 34.8 to 47.6; n = 161 cancers over 22 582 person-years). Biopsied leukoplakias had a higher oral cancer risk compared with those that were not biopsied (adjusted hazard ratio = 2.38, 95% CI = 1.73 to 3.28). However, to identify a prevalent or incident oral cancer, the biopsy decision had low sensitivity (59.6%), low specificity (62.1%), and moderate positive-predictive value (5.1%). Risk of progression to oral cancer statistically significantly increased with the grade of dysplasia; 5-year competing risk-adjusted absolute risks were: leukoplakia overall = 3.3%, 95% CI = 2.7% to 3.9%; no dysplasia = 2.2%, 95% CI = 1.5% to 3.1%; mild-dysplasia = 11.9%, 95% CI = 7.1% to 18.1%; moderate-dysplasia = 8.7%, 95% CI = 3.2% to 17.9%; and severe dysplasia = 32.2%, 95% CI = 8.1%-60.0%. Yet 39.6% of cancers arose from biopsied leukoplakias without dysplasia. CONCLUSIONS: The modest accuracy of the decision to biopsy a leukoplakia vis-à-vis presence or eventual development of oral cancer highlights the need for routine biopsy of all leukoplakias regardless of visual or clinical impression. Leukoplakia patients, particularly those with dysplasia, need to be closely monitored for signs of early cancer

Ulcerative colitis-risk loci on chromosomes 1p36 and 12q15 found by genome-wide association study.

Ulcerative colitis is a chronic inflammatory disease of the colon that presents as diarrhea and gastrointestinal bleeding. We performed a genome-wide association study using DNA samples from 1,052 individuals with ulcerative colitis and preexisting data from 2,571 controls, all of European ancestry. In an analysis that controlled for gender and population structure, ulcerative colitis loci attaining genome-wide significance and subsequent replication in two independent populations were identified on chromosomes 1p36 (rs6426833, combined P = 5.1 x 10(-13), combined odds ratio OR = 0.73) and 12q15 (rs1558744, combined P = 2.5 x 10(-12), combined OR = 1.35). In addition, combined genome-wide significant evidence for association was found in a region spanning BTNL2 to HLA-DQB1 on chromosome 6p21 (rs2395185, combined P = 1.0 x 10(-16), combined OR = 0.66) and at the IL23R locus on chromosome 1p31 (rs11209026, combined P = 1.3 x 10(-8), combined OR = 0.56; rs10889677, combined P = 1.3 x 10(-8), combined OR = 1.29)