On the validity of the Einstein’s Relation and the Fick I Law on the nanoscale: On the validity of the Einstein’s Relation and the Fick I Law on thenanoscale

The classical Einstein’s relation for the Brownian migration has a mesoscopic character and it deteriorates when e.g. diffusion in solids is considered in the nanoscale (i.e. if the diffusion distance is comparable with the atomic spacing). This behaviour is strongly related to the well-known diffusion paradox, predicting infinitely fast diffusion kinetics at short times (distances). Indeed, according to the Fick I law the gradient is infinite if there is a discontinuity in the density at the beginning (which is the case in typical interdiffusion measurements). In this paper these questions and a possible resolution of the above paradox will be discussed on the basis of results obtained in our Laboratory

Halting viruses in scale-free networks

The vanishing epidemic threshold for viruses spreading on scale-free networks indicate that traditional methods, aiming to decrease a virus' spreading rate cannot succeed in eradicating an epidemic. We demonstrate that policies that discriminate between the nodes, curing mostly the highly connected nodes, can restore a finite epidemic threshold and potentially eradicate a virus. We find that the more biased a policy is towards the hubs, the more chance it has to bring the epidemic threshold above the virus' spreading rate. Furthermore, such biased policies are more cost effective, requiring less cures to eradicate the virus

Microthrombotic renal involvement in an SLE patient with concomitant catastrophic antiphospholipid syndrome: the beneficial effect of rituximab treatment

LBK

JAK-STAT inhibition impairs K-RAS-driven lung adenocarcinoma progression

Oncogenic KRAS has been difficult to target and currently there is no KRASbased targeted therapy available for patients suffering from KRASdriven lung adenocarcinoma (AC). Alternatively, targeting KRASdownstream effectors, KRAScooperating signaling pathways or cancer hallmarks, such as tumorpromoting inflammation, has been shown to be a promising therapeutic strategy. Since the JAKSTAT pathway is considered to be a central player in inflammationmediated tumorigenesis, we investigated here the implication of JAKSTAT signaling and the therapeutic potential of JAK1/2 inhibition in KRASdriven lung AC. Our data showed that JAK1 and JAK2 are activated in human lung AC and that increased activation of JAKSTAT signaling correlated with disease progression and KRAS activity in human lung AC. Accordingly, administration of the JAK1/2 selective tyrosine kinase inhibitor ruxolitinib reduced proliferation of tumor cells and effectively reduced tumor progression in immunodeficient and immunocompetent mouse models of KRASdriven lung AC. Notably, JAK1/2 inhibition led to the establishment of an antitumorigenic tumor microenvironment, characterized by decreased levels of tumorpromoting chemokines and cytokines and reduced numbers of infiltrating myeloid derived suppressor cells, thereby impairing tumor growth. Taken together, we identified JAK1/2 inhibition as promising therapy for KRASdriven lung AC.(VLID)510233