Falling Incapacity Benefit claims in a former industrial city: policy impacts or labour market improvement?

This article provides an in-depth study of Incapacity Benefit (IB) claims in a major city and of the factors behind their changing level. It relates to the regime prior to the introduction of the Employment and Support Allowance (ESA) in 2008. Glasgow has had one of the highest levels of IB in Britain with a peak of almost one fifth of the working age population on IB or Severe Disablement Allowance (SDA). However, over the past decade the number of IB claimants in Glasgow, as in other high claiming areas, has fallen at a faster rate than elsewhere, and Glasgow now has twice the national proportion of working-age people on IB/SDA rather than its peak of three times. The rise in IB in Glasgow can be attributed primarily to deindustrialisation; between 1971 and 1991, over 100,000 manufacturing jobs were lost in the city. Policy response was belated. Lack of local statistics on IB led to a lengthy delay in official recognition of the scale of the issue, and targeted programmes to divert or return IB claimants to work did not begin on any scale until around 2004. Evidence presented in the article suggests that the reduction in claims, which has mainly occurred since about 2003, has been due more to a strengthening labour market than to national policy changes or local programmes. This gives strong support to the view that excess IB claims are a form of disguised unemployment. Further detailed evaluation of ongoing programmes is required to develop the evidence base for this complex area. However, the study casts some doubt on the need for the post-2006 round of IB reforms in high-claim areas, since rapid decline in the number of claimants was already occurring in these areas. The article also indicates the importance of close joint working between national and local agencies, and further development of local level statistics on IB claimants

Endangered Archaeology in the Middle East and North Africa: Introducing the EAMENA Project

This project uses satellite imagery and historic aerial photographs to discover and interpret archaeological sites. It has created an open access database of archaeological records that provides basic information so that the sites can be better under- stood and preserved in the future. The threats to sites in the Middle East and North Africa are increasing and creating a record of previously unrecorded sites using this methodology may be our the last chance before they are destroyed

Endangered Archaeology in the Middle East and North Africa: Introducing the EAMENA Project

This project uses satellite imagery and historic aerial photographs to discover and interpret archaeological sites. It has created an open access database of archaeological records that provides basic information so that the sites can be better under- stood and preserved in the future. The threats to sites in the Middle East and North Africa are increasing and creating a record of previously unrecorded sites using this methodology may be our the last chance before they are destroyed

Impaired Mitochondrial Microbicidal Responses in Chronic Obstructive Pulmonary Disease Macrophages

RATIONALE: Chronic obstructive pulmonary disease (COPD) is characterized by impaired clearance of pulmonary bacteria. OBJECTIVES: The effect of COPD on alveolar macrophage (AM) microbicidal responses was investigated. METHODS: Alveolar macrophages (AMs) were obtained from bronchoalveolar lavage from healthy donors or COPD patients and challenged with opsonized serotype 14 Streptococcus pneumoniae. Cells were assessed for apoptosis, bactericidal activity and mitochondrial reactive oxygen species (mROS) production. A transgenic mouse line, in which the CD68 promoter ensures macrophage specific expression of human Mcl-1 (CD68.hMcl-1), was used to model the molecular aspects of COPD. MEASUREMENTS AND MAIN RESULTS: COPD AM had elevated levels of Mcl-1, an anti-apoptotic Bcl-2 family member, with selective reduction of delayed intracellular bacterial killing. CD68.hMcl-1 AM phenocopied the microbicidal defect since transgenic mice demonstrated impaired clearance of pulmonary bacteria and increased neutrophilic inflammation. Murine bone marrow-derived macrophages (BMDM) and human monocyte-derived macrophages (MDM) generated mitochondrial reactive oxygen species (mROS) in response to pneumococci, which co-localized with bacteria and phagolysosomes to enhance bacterial killing. The Mcl-1 transgene increased oxygen consumption rates and mROS expression in mock-infected BMDM but reduced caspase-dependent mROS production after pneumococcal challenge. COPD AM also increased basal mROS expression, but failed to increase production after pneumococcal challenge, in keeping with reduced intracellular bacterial killing. The defect in COPD AM intracellular killing was associated with a reduced ratio of mROS /superoxide dismutase 2. CONCLUSIONS: Upregulation of Mcl-1 and chronic adaption to oxidative stress alters mitochondrial metabolism and microbicidal function, reducing the delayed phase of intracellular bacterial clearance in COPD

Structures of the CCR5 N Terminus and of a Tyrosine-Sulfated Antibody with HIV-1 gp120 and CD4

The CCR5 co-receptor binds to the HIV-l gp120 envelope glycoprotein and facilitates HIV-l entry into cells. Its N terminus is tyrosine-sulfated, as are many antibodies that react with the co-receptor binding site on gp120. We applied nuclear magnetic resonance and crystallographic techniques to analyze the structure of the CCR5 N terminus and that of the tyrosine-sulfated antibody 412d in complex with gp120 and CD4. The conformations of tyrosine-sulfated regions of CCR5 (α-helix) and 412d (extendedloop) are surprisingly different. Nonetheless, a critical sulfotyrosine on CCR5 and on 412d induces similar structural rearrangements in gp120. These results now provide a framework for understanding HIV-l interactions with the CCR5 N terminus during viral entry and define a conserved site on gp120, whose recognition of sulfotyrosine engenders posttranslational mimicry by the immune system

The Impossibility of a Perfectly Competitive Labor Market

Using the institutional theory of transaction cost, I demonstrate that the assumptions of the competitive labor market model are internally contradictory and lead to the conclusion that on purely theoretical grounds a perfectly competitive labor market is a logical impossibility. By extension, the familiar diagram of wage determination by supply and demand is also a logical impossibility and the neoclassical labor demand curve is not a well-defined construct. The reason is that the perfectly competitive market model presumes zero transaction cost and with zero transaction cost all labor is hired as independent contractors, implying multi-person firms, the employment relationship, and labor market disappear. With positive transaction cost, on the other hand, employment contracts are incomplete and the labor supply curve to the firm is upward sloping, again causing the labor demand curve to be ill-defined. As a result, theory suggests that wage rates are always and everywhere an amalgam of an administered and bargained price. Working Paper 06-0

Targeted Isolation of Antibodies Directed against Major Sites of SIV Env Vulnerability

The simian immunodeficiency virus (SIV) challenge model of lentiviral infection is often used as a model to human immunodeficiency virus type 1 (HIV-1) for studying vaccine mediated and immune correlates of protection. However, knowledge of the structure of the SIV envelope (Env) glycoprotein is limited, as is knowledge of binding specificity, function and potential efficacy of SIV antibody responses. In this study we describe the use of a competitive probe binding sort strategy as well as scaffolded probes for targeted isolation of SIV Env-specific monoclonal antibodies (mAbs). We isolated nearly 70 SIV-specific mAbs directed against major sites of SIV Env vulnerability analogous to broadly neutralizing antibody (bnAb) targets of HIV-1, namely, the CD4 binding site (CD4bs), CD4-induced (CD4i)-site, peptide epitopes in variable loops 1, 2 and 3 (V1, V2, V3) and potentially glycan targets of SIV Env. The range of SIV mAbs isolated includes those exhibiting varying degrees of neutralization breadth and potency as well as others that demonstrated binding but not neutralization. Several SIV mAbs displayed broad and potent neutralization of a diverse panel of 20 SIV viral isolates with some also neutralizing HIV-27312A. This extensive panel of SIV mAbs will facilitate more effective use of the SIV non-human primate (NHP) model for understanding the variables in development of a HIV vaccine or immunotherapy