Survival rates of captive-bred Asian Houbara Chlamydotis macqueenii in a hunted migratory population

Asian Houbara Chlamydotis macqueenii numbers are declining owing to unsustainable levels of hunting and poaching, with the main conservation response being population reinforcement through the release of captive-bred birds. We assessed the contribution of captive breeding to the species’ conservation by examining the fates of 65 captive-bred birds fitted with satellite transmitters and released during spring (March–May) and autumn (August) into breeding habitat in Uzbekistan. Of the released birds, 58.5% survived to October, the month favoured by Emirati hunters in Uzbekistan, but only 10.8% of those released survived the winter to return as sub-adults next spring. To mitigate and compensate the loss of wild adults to hunting, the number of released birds needs to be an order of magnitude higher than hunting quotas (with a release of between 1640-1920 required for a hypothetical quota of 200), indicating that releases may be costly and do not remove the need for a biologically determined sustainable hunting quota

The incidence of all stroke and stroke subtype in the United Kingdom, 1985 to 2008: a systematic review

<p>Abstract</p> <p>Background</p> <p>There is considerable geographic variation in stroke mortality around the United Kingdom (UK). Whether this is due to geographical differences in incidence or case-fatality is unclear. We conducted a systematic review of high-quality studies documenting the incidence of any stroke and stroke subtypes, between 1985 and 2008 in the UK. We aimed to study geographic and temporal trends in relation to equivalent mortality trends.</p> <p>Methods</p> <p>MEDLINE and EMBASE were searched, reference lists inspected and authors of included papers were contacted. All rates were standardised to the European Standard Population for those over 45, and between 45 and 74 years. Stroke mortality rates for the included areas were then calculated to produce rate ratios of stroke mortality to incidence for each location.</p> <p>Results</p> <p>Five papers were included in this review. Geographic variation was narrow but incidence appeared to largely mirror mortality rates for all stroke. For men over 45, incidence (and confidence intervals) per 100,000 ranged from 124 (109-141) in South London, to 185 (164-208) in Scotland. For men, premature (45-74 years) stroke incidence per 100,000 ranged from 79 (67-94) in the North West, to 112 (95-132) in Scotland. Stroke subtype data was more geographically restricted, but did suggest there is no sizeable variation in incidence by subtype around the country. Only one paper, based in South London, had data on temporal trends. This showed that there has been a decline in stroke incidence since the mid 1990 s. This could not be compared to any other locations in this review.</p> <p>Conclusions</p> <p>Geographic variations in stroke incidence appear to mirror variations in mortality rates. This suggests policies to reduce inequalities in stroke mortality should be directed at risk factor profiles rather than treatment after a first incident event. More high quality stroke incidence data from around the UK are needed before this can be confirmed.</p

Captive breeding and the conservation of the threatened houbara bustards

Translocation of captive-bred individuals to reinforce wild populations may be an important conservation approach for some species, but can be detrimental when employed to boost exploited wild populations, particularly where repeated long-term reinforcement aims to compensate for repeated unregulated offtake. We review evidence that captive breeding alters multiple physiological, life-history and temperamental traits through founder effects, genetic drift and unintended adaption to captivity; degrades learnt behaviours; and compromises biogeography, population structure and viability through introgression. We highlight these risks for the globally threatened African houbara Chlamydotis undulata and Asian houbara C. macqueenii, 2 bustard species hunted throughout much of their ranges and now subject to multiple large-scale captive-breeding programmes and translocations. In eastern Morocco, annual releases of captive-bred African houbara are 2–3 times higher than original wild numbers, but no investigation of their potentially deleterious effects has, to our knowledge, been published, although most wild populations may now have been replaced by captive-bred domestic stock, which are reportedly not self-sustaining. Despite multiple decades of reinforcement, we are not aware of any analysis of the contribution of captive breeding to African houbara population dynamics, or of the genomic consequences. Asian houbara release programmes may also be promoting rather than preventing declines, and need to contextualise themselves through rigorous analyses of wild population numbers, demographic rates and threats, maintenance of phylogeographic concordance of released with supplemented populations, profiling of traits crucial to survival and the measurement and modelling of the impacts of reinforcement on physiological and behavioural fitness of wild populations

The cAMP-specific phosphodiesterase PDE4A5 is cleaved downstream of its SH3 interaction domain by caspase-3 : consequences for altered intracellular distribution

The unique N-terminal region of the cAMP-specific phosphodiesterase PDE4A5, which confers an ability to bind to certain protein SH3 domains, is cleaved during apoptosis in both Rat-1 fibroblasts and PC12 cells. Cleavage was abolished by the caspase-3-selective inhibitor, z-DEVD-CHO but not the caspase-1 selective inhibitor, z-YVAD-CHO. Caspase-3 treatment of PDE4A5, expressed either transiently in COS cells or generated in vitro by coupled transcription translation, generated a similar cleavage product of 100 kDa compared with the native 110-kDa PDE4A5. This product could be detected immunochemically with an antibody raised to a C-terminal PDE4A5 peptide but not an antibody raised to the N terminus of PDE4A5, indicating that caspase-3 caused N-terminal cleavage of PDE4A5. Deletion of the putative caspase-3 cleavage site, (69)DAVD(72), in PDE4A5, or generation of either the D72A or the D69A mutants, ablated the ability of caspase-3 to cause cleavage. The N-terminal truncate PDE4A5-DeltaP3 was engineered to mimic the caspase-cleaved product of PDE4A5. This showed altered catalytic activity and, unlike PDE4A5, was unable to interact with the SH3 domain of the tyrosyl kinase, LYN. Although both PDE4A5 and PDE4A5-DeltaP3 were localized at cell cortical regions (ruffles), the distinct perinuclear association noted for both PDE4A5 and LYN was not seen for PDE4A5-DeltaP3. Staurosporine-induced apoptosis caused a marked redistribution of PDE4A5 but not PDE4A8 in stably transfected Rat-1 cells. The PDE4-selective inhibitor, rolipram together with the adenylyl cyclase activator forskolin, caused a synergistic increase in the apoptosis of Rat-1 cells. Overexpression of PDE4A5 in Rat-1 cells protected against staurosporine-induced apoptosis in contrast to overexpression of PDE4A8, which potentiated apoptosis. PDE4A5 may be the sole PDE4 family member to provide a substrate for caspase-3 cleavage and this action serves to remove the SH3 binding domain that is unique to this isoform within the PDE4A family and to alter its intracellular targeting

Regulation of Stem Cell Pluripotency and Differentiation Involves a Mutual Regulatory Circuit of the Nanog, OCT4, and SOX2 Pluripotency Transcription Factors With Polycomb Repressive Complexes and Stem Cell microRNAs

Coordinated transcription factor networks have emerged as the master regulatory mechanisms of stem cell pluripotency and differentiation. Many stem cell-specific transcription factors, including the pluripotency transcription factors, OCT4, NANOG, and SOX2 function in combinatorial complexes to regulate the expression of loci, which are involved in embryonic stem (ES) cell pluripotency and cellular differentiation. This review will address how these pathways form a reciprocal regulatory circuit whereby the equilibrium between stem cell self-renewal, proliferation, and differentiation is in perpetual balance. We will discuss how distinct epigenetic repressive pathways involving polycomb complexes, DNA methylation, and microRNAs cooperate to reduce transcriptional noise and to prevent stochastic and aberrant induction of differentiation. We will provide a brief overview of how these networks cooperate to modulate differentiation along hematopoietic and neuronal lineages. Finally, we will describe how aberrant functioning of components of the stem cell regulatory network may contribute to malignant transformation of adult stem cells and the establishment of a "cancer stem cell" phenotype and thereby underlie multiple types of human malignancies

The androgen receptor and stem cell pathways in prostate and bladder cancers (Review)

Bladder cancer is three times more common in men than in women. However, the physiological basis of the male predominance of bladder cancer remains poorly understood. A higher than expected association of prostate and bladder cancers has also been reported which may indicate a common mechanism of carcinogenesis. Consistent with this, androgens and the androgen receptor (AR) play essential roles in prostate carcinogenesis and are believed to play a role in bladder carcinogenesis. There is also evidence implicating cancer stem cells in prostate and bladder cancers. Indeed putative prostate and bladder cancer stem cells share some common molecular features. We highlight key proteins (CD49f, CD133, PTEN, CD44) which are implicated in both prostate and bladder cancers and are enriched in putative prostate and bladder cancer stem cells. We examine published chromatin immuno-precipitation studies analyzing the genome-wide distribution of the AR to identify AR association with, and by inference potential AR-regulation of, these loci. We discuss recent evidence indicating a role for the AR in the splicing of the key urological stem cell protein CD44. We propose a model whereby aberrant AR regulation of these putative stem cell proteins contributes to malignant transformation of prostate and bladder cells. For these reasons we propose that the relationship between androgens and cancer stem cell associated proteins warrants further investigation