Falling "fortresses": Unlocking Governance Entanglements and Shifting Knowledge Paradigms to Counter Climate Change Threats in Biodiversity Conservation.

Biodiversity conservation is facing unprecedented challenges at the intersection of rapidly changing climates, widespread ecosystem degradation under the influence of global warming and resultant human tragedies over livelihood, habitation, adaptation and coping needs. These challenges are more acute across biodiversity hotspots in the Global South. This study disentangles the complex interplay to propose alternative paradigms of governance and policy thinking necessary for sustainable biodiversity conservation. Climate change impacts are exposing critical deficiencies of 'scientific forest management' pursued for over a century. For example, recurrent disasters and ecological shifts are increasingly obfuscating cognitive and physical boundaries between the reserve forest and human habitations; putting additional stress on livelihoods which in turn escalate pressures on the forest commons and fuel further conflicts between conservation governance and local communities. Instead of assisting in adaptation, the existing conservation governance mechanisms are producing further conflicts between humans and non-humans; livelihoods and conservation; disaster management and development. Conducted in the Sundarbans Biosphere Reserve -world's largest mangrove forest ecosystem and a climate change hotspot located along the Bay of Bengal across India and Bangladesh -the study finds an urgent need of rethinking and recalibrating biodiversity conservation in the times of climate change. However, institutional and market-based approaches such as promoting ecotourism or mangrove plantations may have little impact in this regard, the study finds. Instead, integrating cultural ecosystem services and co-producing knowledge will be critical to tackle the entanglements of climate change and its impacts on local lives, livelihoods and biodiversity conservation.

Increased expression of B-lymphocyte chemoattractant, but not pro-inflammatory cytokines, in muscle tissue in rhesus chronic Lyme borreliosis.

Inflammation in skeletal muscle is a consistent feature of Lyme borreliosis, both in the human disease and experimental models. This study had two goals: to evaluate the expression of selected pro-inflammatory and chemokine genes in skeletal muscle in the Rhesus model of Lyme disease, and to identify unexpected cytokine genes involved in Lyme myositis. Two different techniques for measuring cytokine messenger RNA (mRNA) levels were used to achieve these goals: gene expression microarrays and. real-time RT-PCR (Taqman). Muscle from necropsies and biopsies were used, and were obtained from both infected and uninfected non-human primates (NHPs). Although many cytokines were found expressed in muscle tissue, pro-inflammatory cytokines commonly associated with inflammation were not consistently upregulated in infected muscles relative to uninfected muscles. However, B-lymphocyte chemoattractant (BLC), a chemokine implicated in the trafficking of B-cells into tissue, was increased in expression. This study is the first to extensively characterize cytokine gene expression in chronically inflamed tissue in Lyme borreliosis.

Exposure to low dose of gamma radiation enhances the excision repair in Saccharomyces cerevisiae.

The effect of low doses of ionizing and nonionizing radiation on the radiation response of yeast Saccharomyces cerevisiae toward ionizing and nonionizing radiation was studied. The wild-type strain D273-10B on exposure to 54 Gy gamma radiation (resulting in about 10% cell killing) showed enhanced resistance to subsequent exposure to UV radiation. This induced UV resistance increased with the incubation time between the initial gamma radiation stress and the UV irradiation. Exposure to low doses of UV light on the other hand showed no change in gamma or UV radiation response of this strain. The strains carrying a mutation at rad52 behaved in a way similar to the wild type, but with slightly reduced induced response. In contrast to this, the rad3 mutants, defective in excision repair, showed no induced UV resistance. Removal of UV-induced pyrimidine dimers in wild-type yeast DNA after UV irradiation was examined by analyzing the sites recognized by UV endonuclease from Micrococcus luteus. The samples that were exposed to low doses of gamma radiation before UV irradiation were able to repair the pyrimidine dimers more efficiently than the samples in which low gamma irradiation was omitted. The nature of enhanced repair was studied by scoring the frequency of induced gene conversion and reverse mutation at trp and ilv loci respectively in strain D7, which showed similar enhanced UV resistance induced by low-dose gamma irradiation. The induced repair was found to be essentially error-free. These results suggest that irradiation of strain D273-10B with low doses of gamma radiation enhances its capability for excision repair of UV-induced pyrimidine dimers.