Diffúzió és szegregáció nanoszerkezetekben = Diffusion and segregation in nanonstructures

Szimulációkból, majd kísérletileg is megmutattuk, hogy ha a diffúziós együttható erősen függ a koncentrációtól, akkor az eredetileg éles határfelület lineárisan (nem parabolikusan, ahogyan azt a klasszikus Fick I. egyenletből várnánk) tolódik el nanoskálán fázisszeparálódó (Ni-Au) rendszerben, sőt eredetileg elmosódott határfelület kiélesedhet még ideális (korlátlan kölcsönös oldhatóságú) szilárd rendszerekben is (pl. Mo-V rendszer). Szimulációkból ugyancsak megmutattuk, hogy a kiélesedés akkor is végbemegy, ha a diffúziós feszültségek hatását figyelembe vesszük. Megmutattuk, hogy a nanoskálán végtelen gyors kinetikát jósoló jól ismert diffúziós paradoxon feloldható: egy kezdeti éles koncentrációprofil esetén a határfelület véges diffúziós permeabilitása határozza meg az áramot, amely kezdetben jó közelítéssel állandó és ez lineáris kinetikához vezethet. A fenti eredmények a nanoskálájú szilárdtest reakciók értelmezésében fontosak lehetnek. Az irodalomban korábban közölt, túl egyszerűsített, egyenletnél általánosabbat adtunk meg a szegregáció által stabilizált szemcseméret hőmérsékletfüggésére és ennek érvényességét a rendelkezésre álló adatokból igazoltuk. | It has been shown, both from simulation and experiments, that - if the diffusion coefficient has strong composition dependence - an initially sharp interface shifts linearly (not by a parabolic law, expected from the classical Fick I. equation) on nanoscale, and an initially diffuse interface can become sharper even in ideal (mutually completely soluble) systems (e.g. Mo/V system). It was also obtained from simulations that this sharpening takes place even if the effect of stresses, of diffusional origin, is taken into account. We have shown that the well-known diffusion paradox, predicting infinitely fast kinetics at the nanoscale, can be resolved: for an initially abrupt composition profile the flux crossing the interface is determined by the finite diffusion permeability of the interface. This is, in a good approximation, is constant at the beginning and this leads to a linear kinetics. These results can be important in the interpretation of solid state reaction on the nanoscale. General (more general than the oversimplified one published in the literature recently) relation between the segregation stabilized grain size and the temperature was derived and its validity is confirmed on the basis of available experimental data

On Linear Codes with Random Multiplier Vectors and the Maximum Trace Dimension Property

Let $C$ be a linear code of length $n$ and dimension $k$ over the finite field $\mathbb{F}_{q^m}$. The trace code $\mathrm{Tr}(C)$ is a linear code of the same length $n$ over the subfield $\mathbb{F}_q$. The obvious upper bound for the dimension of the trace code over $\mathbb{F}_q$ is $mk$. If equality holds, then we say that $C$ has maximum trace dimension. The problem of finding the true dimension of trace codes and their duals is relevant for the size of the public key of various code-based cryptographic protocols. Let $C_{\mathbf{a}}$ denote the code obtained from $C$ and a multiplier vector $\mathbf{a}\in (\mathbb{F}_{q^m})^n$. In this paper, we give a lower bound for the probability that a random multiplier vector produces a code $C_{\mathbf{a}}$ of maximum trace dimension. We give an interpretation of the bound for the class of algebraic geometry codes in terms of the degree of the defining divisor. The bound explains the experimental fact that random alternant codes have minimal dimension. Our bound holds whenever $n\geq m(k+h)$, where $h\geq 0$ is the Singleton defect of $C$. For the extremal case $n=m(h+k)$, numerical experiments reveal a closed connection between the probability of having maximum trace dimension and the probability that a random matrix has full rank

Altered agonist sensitivity of a mutant V2 receptor suggests a novel therapeutic strategy for nephrogenic diabetes insipidus.

Loss of function mutations of the type 2 vasopressin receptor (V2R) in kidney can lead to nephrogenic diabetes insipidus (NDI). We studied a previously described, but uncharacterized mutation of V2R (N321K missense mutation) of an NDI patient. The properties of the mutant receptor were evaluated. We constructed a highly sensitive Epac based BRET (bioluminescence resonance energy transfer) biosensor to perform real-time cAMP measurements after agonist stimulation of transiently transfected HEK293 cells with V2Rs. beta-arrestin binding of the activated receptors was examined with luciferase-tagged beta-arrestin and mVenus-tagged V2Rs using BRET technique. Cell surface expressions of HA-tagged receptors were determined with flow cytometry using anti-HA-Alexa488 antibodies. Cellular localization examinations were implemented with fluorescent tagged receptors visualized with confocal laser-scanning microscopy. The effect of various vasopressin analogues on V1R was tested on mouse arteries by wire myography. N321K mutant V2R showed normal cell surface expression but the potency of AVP for cAMP generation was low, while the clinically used desmopressin (dDAVP) was not efficient. The beta-arrestin binding and internalization properties of the mutant receptor were also different compared to the wild type. Function of the mutant receptor can be rescued with administration of V2R receptor agonist dVDAVP, which had no detectable side effects on V1R in the effective cAMP generating concentrations. Based on the findings we could propose a therapeutical strategy for NDI patients carrying the N321K mutation, since our in vivo experiments suggest that dVDAVP could rescue the function of the N321K-V2R without significant side effect on V1R

What have we learned from two-pore potassium channels? Their molecular configuration and function in the human heart

Two-pore domain potassium channels (K2P) control excitability, stabilize the resting membrane potential below firing threshold, and accelerate repolarisation in different cells. Until now, fifteen different genes for the six K2P channel subfamily were cloned. The pore-forming part is translated from two genes and they are built up from a dimer of two two-unit transmembrane domains functioning with a wide spectrum of physiological profiles. K2P ion channels were discovered in the last two decades and gave novel opportunity to recognize the complex molecular mechanism of the potassium ion flux, and may lead to the design of individual drug targeting in the future. In this review, we summarise the structure, function, channelopathies and pharmacological silhouette of the two-pore potassium channels in the human tissues. In addition, we present the computer model of the partially reconstructed wild type K2P1/TWIK1 lacking the intracellular C and N terminal loop

Spontaneous emission of radiation by metallic electrons in the presence of electromagnetic fields of surface plasmon oscillations

The spontaneous emission of radiation of metallic electrons embedded in a high-intensity enhanced surface plasmon field is considered analytically. The electrons are described by exact dressed quantum states which contain the interaction with the plasmon field non-perturbatively. Considerable deviations from the pertubative behaviour have been found in the intensity dependence of the emitted fundamental and the second harmonic signals, even at moderate incoming laser intensities. The theoretical predictions deduced from the formalism are in good qualitative agreement with the experimental results.Comment: 23 pages, 6 figure

Vezetőképesség moduláció ZnO nanoszálakon bioreceptorokkal = Conductivity Modulation of ZnO Nanowires by Bioreceptors (CoMoNano)

Kimutattuk, hogy az egyszerű és alacsony hőmérsékletű nedves kémiai eljárásban a vizes cinknitrát/hexametiltetramin oldat koncentrációjának csökkentésével csökken a növesztett ZnO nanoszálak vastagsága. Újszerű módszert dolgoztunk ki a nanoszál növesztésére, amelyben a ZnO magrétegre leválasztott Stöber szilika nanogömbök monorétegével nemcsak vékony de hosszabb nanoszálak is növeszthetőek. Kimutattuk, hogy az ilyen szálnak jobb az UV fénnyel történő modulálhatósági hatásfoka. Megmutattuk, hogy rendezett, lokalizált nanoszálak növeszthetők a magrétegre felvitt PMMA fedőrétegben kialakított nukleációablakokon keresztül. Az így növesztett nanoszálak rendezettsége, minősége inkább az alkalmazott magréteg kristályi minőségétől függ, semmint a felületi durvaságától. Eljárást dolgoztunk ki az IC planár technológiába jobban integrálható horizontális nanoszálak növesztésére. A kontaktusokról induló és oxidon tovább növő szálak lehetővé teszik az eszköz térvezérlésű tranzisztorként hátsó gate általi vezérelhetőségét, amivel növelhető a szál modulálhatósági hatásfokát, modulálási sebességét. Demonstráltuk a horizontális szálak modulálhatóságát UV fényre (kb. öt nagyságrend változás ) illetve az IgG fehérjére Z domén receptorokkal. A modulálás már nagyon kis IgG (25 nM) koncentrációnál megfigyelhető, de a koncentráció növekedésével telítési jelleget mutat. Ennek valószínűleg a szálon szabadon maradt receptorok csökkenő száma lehet az oka. | We have shown that in the chemical bath deposition the thickness of the grown ZnO nanowires (NWs) is reduced with decreasing concentration of the aqueous zinc nitrate and hexamethylentetramine. A novel route has been developed using a monolayer of silica nanospheres deposited on ZnO seedlayer to grow thin but much longer NWs than usual. Such NWs were observed to have better UV modulation property than those formed without nanosphere layer. We demonstrated that the selective growth of NWs could be well realized via the nucleation windows pre-formed in the PMMA cap-layer over the seed layer. The crystal quality and alignment of such NWs was determined by the dispersion in the crystallographic orientation of the seed layer while the role of its surface roughness was negligible. Method to grow horizontal NWs which is integrable into IC planar technology has been developed. Being nucleated from the electrodes then grown along oxide surface, the NWs can be gated by a back electrode as a field effect transistor, thus their modulation efficiency, speed can be further achieved. Modulation of the horizontal NWs has been demonstrated for UV illumination (five order of magnitude change) and IgG with Z domain receptors. The modulation effect of IgG can be observed even at very low concentration (25 nM), which showed a saturation tendency with increasing IgG concentration, probably due to the limitation of the available binding sites of the Z domains on the NW surface for the IgGs

Mutation in the V2 vasopressin receptor gene, AVPR2, causes nephrogenic syndrome of inappropriate diuresis

Nephrogenic syndrome of inappropriate antidiuresis (NSIAD) is a recently discovered rare disease caused by gain-of-function mutations of the V2 vasopressin receptor gene, AVPR2. To date, mutations of Phe229 and Arg137 have been identified as gain-of-function in the V2 vasopressin receptor (V2R). These receptor mutations lead to hyponatremia, which may lead to clinical symptoms in infants. Here we present a newly identified I130N substitution in exon 2 of the V2R gene in a family, causing NSIAD. This I130N mutation resulted in constitutive activity of the V2R with constitutive cyclic adenosine monophosphate (cAMP) generation in HEK293 cells. This basal activity could be blocked by the inverse agonist tolvaptan and arginine-vasopressin stimulation enhanced the cAMP production of I130N-V2R. The mutation causes a biased receptor conformation as the basal cAMP generation activity of I130N does not lead to interaction with β-arrestin. The constitutive activity of the mutant receptor caused constitutive dynamin-dependent and β-arrestin-independent internalization. The inhibition of basal internalization using dominant-negative dynamin resulted in an increased cell surface expression. In contrast to the constitutive internalization, agonist-induced endocytosis was β-arrestin dependent. Thus, tolvaptan could be used for treatment of hyponatremia in patients with NSIAD who carry the I130N-V2R mutation.Kidney International advance online publication, 1 July 2015; doi:10.1038/ki.2015.181. © 2015 International Society of Nephrolog