In this task, you are given a abstract of article and corresponding title of an article. Your task is to generate label "yes" if title is right for article, otherwise generate "no".

[Q]: Abstract: The Saccharomyces cerevisiae Pif1 helicase is the prototypical member of the Pif1 DNA helicase family, which is conserved from bacteria to humans. Here we show that exceptionally potent G-quadruplex unwinding is conserved among Pif1 helicases. Moreover, Pif1 helicases from organisms separated by more than 3 billion years of evolution suppressed DNA damage at G-quadruplex motifs in yeast. The G-quadruplex-induced damage generated in the absence of Pif1 helicases led to new genetic and epigenetic changes. Furthermore, when expressed in yeast, human PIF1 suppressed both G-quadruplex-associated DNA damage and telomere lengthening.. Title: Pif1 family helicases suppress genome instability at G-quadruplex motifs
[A]: yes

[Q]: Abstract: BACKGROUND Saphenous vein graft (VG) failure occurs more frequently compared with arterial grafts, and graft thrombosis represents the main cause of early occlusion. Because CD40-CD40L pathway CD40 represents a culprit link between local inflammation and coagulation cascade, we investigate the role of CD40 and its soluble ligand (sCD40L) in the immediate in vitro response of VG to arterial pressures, and the potential effects of Simvastatin (Merck Sharp&Dohme, White-house Station, NJ) supplementation.
METHODS Samples of saphenous vein and of internal mammary artery (IMA) were obtained from sixteen patients without history of statin therapy. Segments underwent pulsatile pressure distension and culture with or without supplementation of Simvastatin. CD40 and sCD40L were assessed in tissue lysate and in culture supernatant, respectively. sCD40L serum concentrations were also measured.
RESULTS During the course of the experiment, the CD40 expression was significantly lower in IMA samples compared with both distended and not distended VG. Pressure distension up-regulated the production of CD40 in VG segments after 24 and 48 h. Statin supplementation significantly reduced the expression of CD40 in both venous (P < 0.001) and arterial samples (P < 0.001). This effect of Simvastatin was not affected by the treatment with L-NAME, but it was reversed by the addition of mevalonic acid. Mean sCD40L content in culture supernatants increased over time, suggesting that not only platelets but also the vessel wall is a source of CD40 and sCD40L.
CONCLUSIONS Simvastatin treatment modulates endothelial CD40-sCD40L in both venous and arterial grafts, and therefore may represent a useful tool in the pharmacological prevention of graft failure.. Title: Simvastatin reduces CD40 expression in an experimental model of early arterialization of saphenous vein graft.
[A]: yes

[Q]: Abstract: Epidermal Langerhans cells (LCs) play a key role in immune defense mechanisms and in numerous immunological disorders. In this report, we show that percutaneous infection of C57BL/6 mice with the helminth parasite Schistosoma mansoni leads to the activation of LCs but, surprisingly, to their retention in the epidermis. Moreover, using an experimental model of LC migration induced by tumor necrosis factor (TNF)-, we show that parasites transiently impair the departure of LCs from the epidermis and their subsequent accumulation as dendritic cells in the draining lymph nodes. The inhibitory effect is mediated by soluble lipophilic factors released by the parasites and not by host-derived antiinflammatory cytokines, such as interleukin-10. We find that prostaglandin (PG)D2, but not the other major eicosanoids produced by the parasites, specifically impedes the TNF-triggered migration of LCs through the adenylate cyclasecoupled PGD2 receptor (DP receptor). Moreover, the potent DP receptor antagonist BW A868C restores LC migration in infected mice. Finally, in a model of contact allergen-induced LC migration, we show that activation of the DP receptor not only inhibits LC emigration but also dramatically reduces the contact hypersensitivity responses after challenge. Taken together, we propose that the inhibition of LC migration could represent an additional stratagem for the schistosomes to escape the host immune system and that PGD2 may play a key role in the control of cutaneous immune responses.. Title: Role of the Parasite-Derived Prostaglandin D2 in the Inhibition of Epidermal Langerhans Cell Migration during Schistosomiasis Infection
[A]:
yes