Notes from Some Small Countries: A Study of the 'New Punitiveness' in Ireland, Scotland and New Zealand

In recent years there has been a remarkable surge of interest in the concept of punitiveness in theoretical criminology. Accounts serve to emphasise rupture over continuity, drawing attention to the increased focus on managerialism, risk and expressive penal policies in countries such as England and the US. Criticisms of these accounts have drawn attention to the weak empirical base for such assertions and the continued relevance of local cultural, historical and political conditions in mediating the effect of more punitive trends. In light of the relative neglect of smaller jurisdictions in this literature it was decided to locate these debates in three small common law jurisdictions, namely, Ireland, Scotland and New Zealand over the period 1976-2006 with a view to assessing the empirical evidence for penal change. This was done using a broader definition of punitiveness than normally employed incorporating indices relating to the ‘front end’ (eg police powers) as well as the ‘back end’ (eg prison and probation) of the criminal justice system. Data were collected on the three case studies using a multi-method approach involving examination of extensive quantitative data, interviews with key criminal justice stakeholders and documentary analysis. The data provide some support for the ‘new punitiveness’ thesis in these countries through a pattern of increased legislative activity aimed at controlling violent and sexual offenders and significant increases in the lengths of sentences imposed. However, analysis of qualitative data and a larger number of variables reveals distinctly different patterns of punitiveness over the thirty year period in the three countries. It is argued that the study holds important lessons for comparative criminology into the ‘new punitiveness’. There is a need for qualitative as well as quantitative data; for multiple rather than singular indices across a wide range of areas (juvenile justice, prison conditions, etc); and for ‘front end’ as well as ‘back end’ indices.

Predictors and dynamics of postpartum relapses in women with multiple sclerosis

Several studies have shown that pregnancy reduces multiple sclerosis (MS) relapses, which increase in the early postpartum period. Postpartum relapse risk has been predicted by pre-pregnancy disease activity in some studies.

Second Equal Treatment Act for the commercial sector

This book analyses one of the first pieces of legislation promoted by Angela Merkel, who started her political career as a minister for women's equality under Helmut Kohl. The name of the Act, Second Equal Treatment Act, allured to the Equal Treatment Act of the 1950s which implemented the barest minimum requirements to make the German constitution's demand to guarantee equal rights for women more than a hollow formula. However, this Act, while abolishing blatant discrimination of women through statute in fields such as family law, did nothing to further substantive equality. In 1990, when Germany was reunited, women from Eastern Germany had a first hand experience what the absence of such furtherance meant under capitalism. Used to being at nor risk to fall into poverty just because they divorced, or decided to become a mother without male protection, to being in full employment and not at the mercy of payments by their husbands, women from Eastern Germany were dismissed in large numbers, and found themselves sent back to the kitchen. The first minister for women affairs from their ranks made the "2nd Equality Act", but this act did little more than the minimum required by the EEC legislation. Again, substantive equality was not addressed through German Federal legislation. This was left to some of the German states - whose competences were limited to the public services. Most of those states which did create positive action measures for women employed in the public services were governed not by Christian Democrats - but this was the theme of another book.

A multivariate analysis of beta diversity across organisms and environments

We examined variability in hierarchical beta diversity across ecosystems, geographical gradients, and organism groups using multivariate spatial mixed modeling analysis of two independent data sets. The larger data set comprised reported ratios of regional species richness (RSR) to local species richness (LSR) and the second data set consisted of RSR: LSR ratios derived from nested species-area relationships. There was a negative, albeit relatively weak, relationship between beta diversity and latitude. We found only relatively subtle differences in beta diversity among the realms, yet beta diversity was lower in marine systems than in terrestrial or freshwater realms. Beta diversity varied significantly among organisms' major characteristics such as body mass, trophic position, and dispersal type in the larger data set. Organisms that disperse via seeds had highest beta diversity, and passively dispersed organisms showed the lowest beta diversity. Furthermore, autotrophs had lower beta diversity than organisms higher up the food web; omnivores and carnivores had consistently higher beta diversity. This is evidence that beta diversity is simultaneously controlled by extrinsic factors related to geography and environment, and by intrinsic factors related to organism characteristics.

PIAS1 is increased in human prostate cancer and enhances proliferation through inhibition of p21

Prostate cancer development and progression are associated with alterations in expression and function of elements of cytokine networks, some of which can activate multiple signaling pathways. Protein inhibitor of activated signal transducers and activators of transcription (PIAS)1, a regulator of cytokine signaling, may be implicated in the modulation of cellular events during carcinogenesis. This study was designed to investigate the functional significance of PIAS1 in models of human prostate cancer. We demonstrate for the first time that PIAS1 protein expression is significantly higher in malignant areas of clinical prostate cancer specimens than in normal tissues, thus suggesting a growth-promoting role for PIAS1. Expression of PIAS1 was observed in the majority of tested prostate cancer cell lines. In addition, we investigated the mechanism by which PIAS1 might promote prostate cancer and found that down-regulation of PIAS1 leads to decreased proliferation and colony formation ability of prostate cancer cell lines. This decrease correlates with cell cycle arrest in the G0/G1 phase, which is mediated by increased expression of p21(CIP1/WAF1). Furthermore, PIAS1 overexpression positively influences cell cycle progression and thereby stimulates proliferation, which can be mechanistically explained by a decrease in the levels of cellular p21. Taken together, our data reveal an important new role for PIAS1 in the regulation of cell proliferation in prostate cancer.

STAT3 regulated ARF expression suppresses prostate cancer metastasis

Prostate cancer (PCa) is the most prevalent cancer in men. Hyperactive STAT3 is thought to be oncogenic in PCa. However, targeting of the IL-6/STAT3 axis in PCa patients has failed to provide therapeutic benefit. Here we show that genetic inactivation of Stat3 or IL-6 signalling in a Pten-deficient PCa mouse model accelerates cancer progression leading to metastasis. Mechanistically, we identify p19(ARF) as a direct Stat3 target. Loss of Stat3 signalling disrupts the ARF-Mdm2-p53 tumour suppressor axis bypassing senescence. Strikingly, we also identify STAT3 and CDKN2A mutations in primary human PCa. STAT3 and CDKN2A deletions co-occurred with high frequency in PCa metastases. In accordance, loss of STAT3 and p14(ARF) expression in patient tumours correlates with increased risk of disease recurrence and metastatic PCa. Thus, STAT3 and ARF may be prognostic markers to stratify high from low risk PCa patients. Our findings challenge the current discussion on therapeutic benefit or risk of IL-6/STAT3 inhibition.