Structure,scale and emergence

In this paper I consider the structures that chemists and physicists attribute at the molecular scale to substances and materials of various kinds, and how they relate to structures and processes at other scales. I argue that the structure of a substance is the set of properties and relations which are preserved across all the conditions in which it can be said to exist. In short, structure is abstraction. On the basis of this view, and using concrete examples, I argue that structures, and therefore the chemical substances and other materials to which they are essential, are emergent. Firstly, structures themselves are scale-dependent because they can only exist within certain physical conditions, and a single substance may have different structures at different scales (of length, time and energy). Secondly, the distinctness of both substances and structures is a scale-dependent relationship: above a certain point, two distinct possibilities may become one. Thirdly, the necessary conditions for composition, for both substances and molecular species, are scale-dependent. To know whether a group of nuclei and electrons form a molecule it is not enough to consider energy alone: one also has to know about their environment and the lifetime over which the group robustly hangs together.     

The complete structure of ryanodine

Zusammenfassung Die Struktur des Ryanodins und die Natur der Ryanodin-Anhydroryanodin-Umlagerung wird diskutiert.     

Trends in A8 migration to the UK during the recession

A substantial proportion of contemporary migration flows to the UK are made by nationals from countries which have recently joined the EU. The nature of A8 migration during the recession is examined in this paper, mainly using data from the Worker Registration Scheme. The recession has seen a decline in new A8 migrants entering the UK labour market, but the decline has been sectorally uneven, with demand for migrant labour being most persistent in the agricultural sector, raising questions about why this part of the UK economy is so different.     

The structure of beta-lactoglobulin and its similarity to plasma retinol-binding protein

Since its first isolation, bovine beta-lactoglobulin (BLG) has been an enigma: although it is abundant in the whey fraction of milk, its function is still not clear. The results of the many physicochemical studies on the protein need a structural interpretation. We report here the structure of the orthorhombic crystal form of cow BLG at pH 7.6, at a resolution of 2.8 A. It has an unusual protein fold, composed of two slabs of antiparallel beta-sheet, which shows a remarkable similarity to plasma retinol-binding protein. A possible binding site for retinol in BLG has been identified by model-building. This suggests a role for BLG in vitamin A transport and we have discovered specific receptors for the BLG-retinol complex in the intestine of neonate calves.     

Substantial confusion

In this paper I defend, against Eric Scerri’s objections, the following theses: (i) that Lavoisier and Mendeleev shared a ‘core conception’ of chemical element, and (ii) that this core conception underwrites referential continuity in the names of particular elements.     

A synthetic attractant for the male spruce budworm mothChoristoneura fumiferana (Clem.)

Zusammenfassung Die besondere Eigenschaft desn-Octadekanitrils als Lockstoff für die männliche MotteChoristoneura fumiferana (Clem.) wurde festgestellt.     

A subset of NSAIDs lower amyloidogenic Abeta42 independently of cyclooxygenase activity.

Epidemiological studies have documented a reduced prevalence of Alzheimer's disease among users of nonsteroidal anti-inflammatory drugs (NSAIDs). It has been proposed that NSAIDs exert their beneficial effects in part by reducing neurotoxic inflammatory responses in the brain, although this mechanism has not been proved. Here we report that the NSAIDs ibuprofen, indomethacin and sulindac sulphide preferentially decrease the highly amyloidogenic Abeta42 peptide (the 42-residue isoform of the amyloid-beta peptide) produced from a variety of cultured cells by as much as 80%. This effect was not seen in all NSAIDs and seems not to be mediated by inhibition of cyclooxygenase (COX) activity, the principal pharmacological target of NSAIDs. Furthermore, short-term administration of ibuprofen to mice that produce mutant beta-amyloid precursor protein (APP) lowered their brain levels of Abeta42. In cultured cells, the decrease in Abeta42 secretion was accompanied by an increase in the Abeta(1-38) isoform, indicating that NSAIDs subtly alter gamma-secretase activity without significantly perturbing other APP processing pathways or Notch cleavage. Our findings suggest that NSAIDs directly affect amyloid pathology in the brain by reducing Abeta42 peptide levels independently of COX activity and that this Abeta42-lowering activity could be optimized to selectively target the pathogenic Abeta42 species.