Mn0.8Zn0.2Fe2O4 nanoparticulates spinel ferrites:An approach to enhance the antenna field strength for improved magnitude versus offset（MVO）

Electromagnetic signals in deep reservoir are very weak so that it is difficult to predict about the presence of hydrocarbon in seabed logging(SBL) environment.In the present work,Mn0.8Zn0.2Fe2O4 nanoferrites were prepared by a sol–gel technique at different sintering temperatures of450 °C,650 °C and 850 °C to increase the strength of electromagnetic(EM) antenna.XRD,FESEM,Raman spectroscopy and HRTEM were used to analyze the phase,surface morphology and size of the nanoferrites.Magnetic properties of the nanoferrites were also measured using an impedance network analyzer.However,nanoferrites sintered at 850 °C with initial permeability of 200 and Q factor of 50 were used as magnetic feeders with the EM antenna.Lab scale experiments were performed to investigate the effect of magnetic field strength in scale tank.SPSS and MATLAB softwares were also used to confirm the oil presence in scale tank.It was observed that the magnitude of the EM waves for the antenna was increased up to 233%.Finally,the correlation values also show 208% increase in the magnetic field strength with the presence of the oil.Therefore,antenna with Mn0.8Zn0.2Fe2O4 nanoferrites based magnetic feeders can be used for deep water and deep target hydrocarbon exploration.     

Specificity in Toll-like receptor signalling through distinct effector functions of TRAF3 and TRAF6

Toll-like receptors (TLRs) are activated by pathogen-associated molecular patterns to induce innate immune responses and production of pro-inflammatory cytokines, interferons and anti-inflammatory cytokines. TLRs activate downstream effectors through adaptors that contain Toll/interleukin-1 receptor (TIR) domains, but the mechanisms accounting for diversification of TLR effector functions are unclear. To dissect biochemically TLR signalling, we established a system for isolating signalling complexes assembled by dimerized adaptors. Using MyD88 as a prototypical adaptor, we identified TNF receptor-associated factor 3 (TRAF3) as a new component of TIR signalling complexes that is recruited along with TRAF6. Using myeloid cells from TRAF3- and TRAF6-deficient mice, we show that TRAF3 is essential for the induction of type I interferons (IFN) and the anti-inflammatory cytokine interleukin-10 (IL-10), but is dispensable for expression of pro-inflammatory cytokines. In fact, TRAF3-deficient cells overproduce pro-inflammatory cytokines owing to defective IL-10 production. Despite their structural similarity, the functions of TRAF3 and TRAF6 are largely distinct. TRAF3 is also recruited to the adaptor TRIF (Toll/IL-1 receptor domain-containing adaptor-inducing IFN-beta) and is required for marshalling the protein kinase TBK1 (also called NAK) into TIR signalling complexes, thereby explaining its unique role in activation of the IFN response.     

Speech sounds learned by sleeping newborns

It is not yet clear whether humans are able to learn while they are sleeping. Here we show that full-term human newborns can be taught to discriminate between similar vowel sounds when they are fast asleep. It is possible that such sleep training soon after birth could find application in clinical or educational situations.