ice might be also partially contributed by the similar mechanisms of premature ageing like phenotype, however, the exact molecular evidences need to be further provided. To exclude the contribution of non cell autonomous effects in skin tumor phenotypes observed in the full knockout mice, future studies should include the conditional deletion of this gene from the skin. In summary, we demonstrate for the first time that JWA deficiency enhances DNA GSK-126 site damage in epidermal cells induced by DMBA, however, suppresses TPA-induced MEK-ERK activation, cell proliferation, and formation of skin papillomas. These data has potential clinical implications for targeting JWA in chemoprevention and therapy of skin tumors. or total amounts of JNK and p38 were detected by Western blotting. ” Each experiment was performed in triplicate. “8549627 Malaria infects 200 to 300 
million people globally and kills approximately 900,000 every year. Current anti-malaria drugs, such as quinine and artemisinin derivatives can effectively clear malaria parasites in blood, however a significant numbers of severe malaria patients including CM patients die or develop severe sequelae regardless of treatment. It is not clear which factors exacerbate mortality among this subset of CM patients, therefore important questions remain to be answered concerning the mechanism of malaria pathogenesis and development of effective therapies. Existing anti-malaria therapy focus on clearance of parasites from blood. This strategy does not prevent secondary deleterious effects such as neurological disorders and cognitive problems caused by parasite derived factors. Recent studies have demonstrated that many pathological changes result from malaria-induced secondary effects which involve various signaling molecules and pathways in the host, indicating that malaria pathogenesis is highly complex and multifactorial,. Recently, it has been shown that increased level of free Heme produced during malaria infection induces inflammation that damages host vascular endothelium which is responsible for induction of fatal cerebral pathogenesis as well as acute lung injury /ARDS. Heme oxygenase is the rate-limiting step enzyme in the degradation of Heme groups to biliverdin, carbon monoxide and iron. Up-regulation of HO-1 protects against cellular stress including oxidative stress, heavy metal toxicity, UV radiation, and inflammation, thus preventing deleterious effects of Heme and mediating anti-inflammatory and anti-apoptotic functions. HO-1 induced by reactive oxygen species and nitric oxide, has recently been shown to STAT3 Activation in Severe Malaria be involved in regulation of angiogenesis. HO-1 may facilitate the repair of injured tissues through inhibition of infiltrating inflammatory cells. Severe malaria is associated with perturbation of inflammatory cytokines, chemokines, antiinflammatory cytokines and angiopoietic factors. Chemokine CXCL10 is a cytokine belonging to the CXC chemokine family. CXCL10 binds CXCR3 receptor to induce chemotaxis, apoptosis, cell growth and angiostasis. It is expressed early in mice infected with P. berghei ANKA as well as in human CM. Studies conducted in India and Ghana have identified CXCL10 as a serological marker highly linked with increased risk of fatal P. falciparum-mediated CM mortality in humans. Following our report of a role of CXCL10 in fatal human CM, several groups utilized gene knockout mice in ECM to confirm and demonstrate the role of CXCL10/CXCR3 inter