English Trade Mark Law in the Eighteenth Century: Blanchard v Hill Revisited - Another 'Case of Monopolies'?

The decision of Lord Hardwicke LC in Blanchard v Hill in 1742 is the earliest reported case on the equitable jurisdiction to grant injunctive relief against trade mark piracy. The ambiguous manner in which the case was reported led to the decision being interpreted as either the basis of equitable jurisdiction or a denial of jurisdiction. This article seeks to establish the background to the case, what actually happened, and the immediate impact of the decision. The scene is set, however, in a parallel symbolic universe – heraldry – because in 1740, the officers of arms were confronted with a trade mark case.

Revisited: the inertia tensor as a proprioceptive invariant in humans

A multitude of tasks that we perform on a daily basis require precise information about the orientation of our limbs with respect to the environment and the objects located within it. Recent studies have suggested that the inertia tensor, a physical property whose values are time- and co-ordinate-indepenclent, may be an important informational invariant used by the proprioceptive system to control the movements of our limbs (Pagano et al., Ecol. Psychol. 8 (1996) 43; Pagano and Turvey, Percept. Psychophys. 52 (1992) 617; Pagano and Turvey, J. Exp. Psychol. Hum. Percept. Perform. 21 (1995) 1070). We tested this hypothesis by recording the angular errors made by subjects when pointing to virtual targets in the dark. Close examination of the pointing errors made did not show any significant effects of the inertia tensor modifications on pointing accuracy. The kinematics of the pointing movements did not indicate that any on-line adjustments were being made to compensate for the inertia tensor changes. The implications of these findings with respect to the functioning of the proprioceptive system are discussed.

Familial idiopathic methemoglobinemia revisited: original cases reveal 2 novel mutations in NADH cytochrome b5 reductase

In 1943, the first description of familial idiopathic methemoglobinemia in the United Kingdom was reported in 2 members of one family. Five years later, Quentin Gibson (then of Queen's University, Belfast, Ireland) correctly identified the pathway involved in the reduction of methemoglobin in the family, thereby describing the first hereditary trait involving a specific enzyme deficiency. Recessive congenital methemoglobinemia (RCM) is caused by a deficiency of reduced nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase. One of the original propositi with the type 1 disorder has now been traced. He was found to be a compound heterozygote harboring 2 previously undescribed mutations in exon 9, a point mutation Gly873Ala predicting a Gly291Asp substitution, and a 3-bp in-frame deletion of codon 255 (GAG), predicting loss of glutamic acid. A brother and a surviving sister are heterozygous; each bears one of the mutations. Thirty-three different mutations have now been recorded for RCM. The original authors' optimism that RCM would provide material for future genetic studies has been amply justified.