'Trusting the numbers': mineral prospecting, raising finance and the governance of knowledge

Mineral prospecting and raising finance for ‘junior’ mining firms has historically been regarded as a speculative activity. For the regulators of securities markets upon which ‘junior’ mining companies seek to raise capital, a perennial problem has been handling not only the indeterminacy of scientific claims, but also the social basis of epistemic practices. This paper examines the production of a system of public warrant and associated knowledge practices intended to enable investors to differentiate between ‘destructive’ and ‘productive’ varieties of financial speculation. It traces the use of the notion of ‘disclosure’ in constructing and legitimizing the ‘juniors’ market in Canada. It argues that though the work of ‘economics’ may be necessary in the construction of markets, it is by no means sufficient. Attention must also be given to the ways in which legal models of ‘the free-market’ can be translated and constantly re-worked across the sites and spaces of regulatory practice, animating the geographies of markets.

'Trusting the numbers': mineral prospecting, raising finance and the governance of knowledge

Mineral prospecting and raising finance for ‘junior’ mining firms has historically been regarded as a speculative activity. For the regulators of securities markets upon which ‘junior’ mining companies seek to raise capital, a perennial problem has been handling not only the indeterminacy of scientific claims, but also the social basis of epistemic practices. This paper examines the production of a system of public warrant and associated knowledge practices intended to enable investors to differentiate between ‘destructive’ and ‘productive’ varieties of financial speculation. It traces the use of the notion of ‘disclosure’ in constructing and legitimizing the ‘juniors’ market in Canada. It argues that though the work of ‘economics’ may be necessary in the construction of markets, it is by no means sufficient. Attention must also be given to the ways in which legal models of ‘the free-market’ can be translated and constantly re-worked across the sites and spaces of regulatory practice, animating the geographies of markets.

Worked to Death? A census-based longitudinal study of the relationship between the numbers of hours spent working and mortality risk

Background There has been an increasing interest in the health effects of long
working hours, but little empirical evidence to substantiate early
10 case series suggesting an increased mortality risk. The aim of the
current study is to quantify the mortality risk associated with long
working hours and to see if this varies by employment relations and
conditions of occupation.
Methods A census-based longitudinal study of 414 949 people aged 20-59/64
15 years, working at least 35 h/week, subdivided into four occupational
classes (managerial/professional, intermediate, own account workers,
workers in routine occupations) with linkage to deaths records
over the following 8.7 years. Cox proportional hazards models were
used to examine all-cause and cause-specific mortality risk.
20 Results Overall 9.4% of the cohort worked 55 or more h/week, but this
proportion was greater in the senior management and professional
occupations and in those who were self-employed. Analysis of 4447
male and 1143 female deaths showed that hours worked were
associated with an increased risk of all-cause mortality only for
25 men working for more than 55 or more h/week in routine/semiroutine
occupations [adjusted hazard ratios (adjHR) 1.31: 95%
confidence intervals (CIs) 1.11, 1.55)] compared with their peers
working 35–40 h/week. Their equivalent risk of death from cardiovascular
disease was (adjHR 1.49: 95% CIs 1.10, 2.00).
30 Conclusions These findings substantiate and add to the earlier studies indicating
the deleterious impact of long working hours but also suggest that
the effects are moderated by employment relations or conditions of
occupation. The policy implications of these findings are discussed.

BIIL 284 reduces neutrophil numbers but increases P. aeruginosa bacteremia and inflammation in mouse lungs

BACKGROUND: A clinical study to investigate the leukotriene B(4) (LTB(4))-receptor antagonist BIIL 284 in cystic fibrosis (CF) patients was prematurely terminated due to a significantly increased risk of adverse pulmonary events. We aimed to establish the effect of BIIL284 in models of Pseudomonas aeruginosa lung infection, thereby contributing to a better understanding of what could have led to adverse pulmonary events in CF patients.

METHODS: P. aeruginosa DNA in the blood of CF patients during and after acute pulmonary exacerbations and in stable patients with non-CF bronchiectasis (NCFB) and healthy individuals was assessed by PCR. The effect of BIIL 284 treatment was tested in an agar bead murine model of P. aeruginosa lung infection. Bacterial count and inflammation were evaluated in lung and other organs.

RESULTS: Most CF patients (98%) and all patients with NCFB and healthy individuals had negative P. aeruginosa DNA in their blood. Similarly, the P. aeruginosa-infected mice showed bacterial counts in the lung but not in the blood or spleen. BIIL 284 treatment decreased pulmonary neutrophils and increased P. aeruginosa numbers in mouse lungs leading to significantly higher bacteremia rates and lung inflammation compared to placebo treated animals.

CONCLUSIONS: Decreased airway neutrophils induced lung proliferation and severe bacteremia in a murine model of P. aeruginosa lung infection. These data suggest that caution should be taken when administering anti-inflammatory compounds to patients with bacterial infections.