Електрофізичні властивості системи політетрафторетилен – вуглецеві нанотрубки

Проведено дослідження комплексної діелектричної проникності та електропровідності в надвисокочастотному діапазоні (9 ГГц) і на низьких частотах (0,1; 1 та 10 кГц) двох систем політетрафторетилен – багатошарові вуглецеві нанотрубки з вихідними та диспергованими у водному середовищі . Введення диспергованих нанотрубок в полімер знижує поріг перколяції з 4,5 % до 2,6 % (мас.) за рахунок рівномірного розподілу наповнювача у полімері, що призводить до зростання міжфазної поверхні взаємодії полімер – вуглецеві нанотрубки, яка проявляється в збільшенні значень дійсної та уявної складової комплексної діелектричної проникності.Проведены исследования комплексной диэлектрической проницаемости и электропроводности в сверхвысокочастотном диапазоне (9 ГГц) и на низких частотах (0,1; 1; 10 кГц) двух систем политетрафторэтилен–многослойные углеродные нанотрубки с исходными и диспергированными у водной среде. Введение диспергированных нанотрубок в полимер снижает порог перколяции с 4,5% до 2,6 % (масс.) за счет равномерного распределения наполнителя в полимере, что приводит к возрастанию межфазной поверхности взаимодействия полимер – углеродные нанотрубки, которая проявляется в увеличении значений действительной и мнимой составляющей комплексной диэлектрической проницаемости.Complex dielectric permeability and conductivity of two systems, namely polytetrafluorethylene – intact carbon nanotubes and polytetrafluorethylene – carbon nanotubes dispersed in aqueous media, has been studied in super high-frequency range (9 GHz) and at low frequencies (0,1; 1 and 10 kHz). Doping of the polymer with the dispersed nanotubes decreases percolation threshold (limit ) from 4,5 wt. % to 2,6 wt. % due to uniform distribution of the filler in the polymer. This results to increase of interface interaction polymer - carbon nanotubes that is demonstrated by increase of value of real and imaginary component of complex dielectric permeability

The receptor binding domain of the new middle east respiratory syndrome coronavirus maps to a 231-residue region in the spike protein that efficiently elicits neutralizing antibodies

The spike (S) protein of the recently emerged human Middle East respiratory syndromecoronavirus (MERS-CoV) mediates infection by binding to the cellular receptor dipeptidyl peptidase 4 (DPP4). Here we mapped the receptor binding domain in the S protein to a 231-amino-acid fragment (residues 358 to 588) by evaluating the interaction of spike truncation variants with receptor-expressing cells and soluble DPP4. Antibodies to this domain-mch less so those to the preceding N-terminal region-efficiently neutralize MERS-CoV infection

Inhibition of middle east respiratory syndrome coronavirus infection by anti-CD26 monoclonal antibody

We identified the domains of CD26 involved in the binding of Middle East respiratory syndrome coronavirus (MERS-CoV) using distinct clones of anti-CD26 monoclonal antibodies (MAbs). One clone, named 2F9, almost completely inhibited viral entry. The humanized anti-CD26 MAb YS110 also significantly inhibited infection. These findings indicate that both 2F9 and YS110 are potential therapeutic agents for MERS-CoV infection. YS110, in particular, is a good candidate for immediate testing as a therapeutic modality for MERS

Dipeptidyl peptidase 4 is a functional receptor for the emerging human coronavirus-EMC

Most human coronaviruses cause mild upper respiratory tract disease but may be associated with more severe pulmonary disease in immunocompromised individuals. However, SARS coronavirus caused severe lower respiratory disease with nearly 10% mortality and evidence of systemic spread. Recently, another coronavirus (human coronavirus-Erasmus Medical Center (hCoV-EMC)) was identified in patients with severe and sometimes lethal lower respiratory tract infection. Viral genome analysis revealed close relatedness to coronaviruses found in bats. Here we identify dipeptidyl peptidase 4 (DPP4; also known as CD26) as a functional receptor for hCoV-EMC. DPP4 specifically co-purified with the receptor-binding S1 domain of the hCoV-EMC spike protein from lysates of susceptible Huh-7 cells. Antibodies directed against DPP4 inhibited hCoV-EMC infection of primary human bronchial epithelial cells and Huh-7 cells. Expression of human and bat (Pipistrellus pipistrellus) DPP4 in non-susceptible COS-7 cells enabled infection by hCoV-EMC. The use of the evolutionarily conserved DPP4 protein from different species as a functional receptor provides clues about the host range potential of hCoV-EMC. In addition, it will contribute critically to our understanding of the pathogenesis and epidemiology of this emerging human coronavirus, and may facilitate the development of intervention strategies

Dipeptidyl peptidase 4 is a functional receptor for the emerging human coronavirus-EMC

Most human coronaviruses cause mild upper respiratory tract disease but may be associated with more severe pulmonary disease in immunocompromised individuals. However, SARS coronavirus caused severe lower respiratory disease with nearly 10% mortality and evidence of systemic spread. Recently, another coronavirus (human coronavirus-Erasmus Medical Center (hCoV-EMC)) was identified in patients with severe and sometimes lethal lower respiratory tract infection. Viral genome analysis revealed close relatedness to coronaviruses found in bats. Here we identify dipeptidyl peptidase 4 (DPP4; also known as CD26) as a functional receptor for hCoV-EMC. DPP4 specifically co-purified with the receptor-binding S1 domain of the hCoV-EMC spike protein from lysates of susceptible Huh-7 cells. Antibodies directed against DPP4 inhibited hCoV-EMC infection of primary human bronchial epithelial cells and Huh-7 cells. Expression of human and bat (Pipistrellus pipistrellus) DPP4 in non-susceptible COS-7 cells enabled infection by hCoV-EMC. The use of the evolutionarily conserved DPP4 protein from different species as a functional receptor provides clues about the host range potential of hCoV-EMC. In addition, it will contribute critically to our understanding of the pathogenesis and epidemiology of this emerging human coronavirus, and may facilitate the development of intervention strategies