Электрохимическое осаждение контактных материалов в постростовой технологии фотоэлектрических преобразователей

Investigations and modeling of ohmic contacts electrochemical deposition process in postgrowth technology of photovoltaic converters fabrication have been carried out. The technology of Ag/Au contact system galvanic deposition at vertical and horizontal position of heterostructure and anode in the electrolyte has been developed. The increase of contact system deposition uniformity up to ∼ 95% at the thickness of contact bus-bars ∼ 5 µm on the heterostructure area with 4 inch diameter has been archived.

Utilizing ultra-wideband with wireless telecommunications applications microstrip

<p>The small aspect, as well as low margins of the microstrip chip amplifier (MPA) is being used in a contact system. For the last few times within the last year's research, the majority of work with MPA has been centered towards designing the portable antenna design. Wireless networking systems may be fitted with a new ultrawideband digital monopoly antenna. Throughout this exponentially changing environment, and dual multi-standard antennas play a crucial role in the implementation of cell towers. This paper presents the nature of an ultra-wideband (UWB)-based antenna array for the shape of a substratum, feeding strategies or openings.</p>

Polyphosphate-induced Thrombosis in Mice is Factor XII-Dependent and is Attenuated by Histidine-rich Glycoprotein

Histidine-rich glycoprotein (HRG) is an abundant plasma protein that binds factor (F) XIIa and inhibits FXII autoactivation and FXIIa-mediated activation of FXI. Polyphosphate (polyP), a potent procoagulant released from activated platelets, may serve as a physiological activator of the contact system. Previously, we showed that HRG binds DNA and neutralizes its procoagulant activity. Consequently, we set out to determine whether the capacity of HRG to bind polyanions enables it to regulate polyP-induced thrombosis. In a plate-based assay, immobilized polyP bound HRG, FXII, and FXIIa in a zinc-dependent manner. Basal and polyP-induced thrombin generation were greater in plasma from HRG-deficient mice than in plasma from wild-type mice. Intraperitoneal injection of polyP shortened the activated partial thromboplastin time, enhanced thrombin generation, increased thrombin-antithrombin (TAT) levels, reduced lung perfusion, and promoted pulmonary fibrin deposition to a greater extent in HRG-deficient mice than in wild-type mice, effects that were abrogated with FXII knockdown. Therefore, HRG attenuates the procoagulant and prothrombotic effects of polyP in a FXII dependent manner by modulating the contact system.

A novel murine in vivo model for acute hereditary angioedema attacks

Hereditary Angioedema (HAE) is a rare genetic disease generally caused by deficiency or mutations in the C1-inhibitor gene, SERPING1, a member of the Serpin family. HAE results in acute attacks of edema, vasodilation, GI pain and hypotension. C1INH is a key inhibitor of enzymes controlling complement activation, fibrinolysis and the contact system. In HAE patients, contact system activation leads to uncontrolled production of bradykinin, the vasodilator responsible for the characteristic symptoms of HAE. In this study, we present the first physiological in vivo model to mimic acute HAE attacks. We evaluate hypotension, one of the many hallmark symptoms of acute HAE attacks using Serping1 deficient mice (serping1−/−) and implanted telemetry. Attacks were induced by IV injection of a silica nanoparticle (SiNP) suspension. Blood pressure was measured in real time, in conscious and untethered mice using implanted telemetry. SiNP injection induced a rapid, reversible decrease in blood pressure, in the presence of angiotensin converting enzyme (ACE) inhibition. We also demonstrate that an HAE therapeutic, ecallantide, can prevent HAE attacks in this model. The in vivo murine model described here can facilitate the understanding of acute HAE attacks, support drug development and ultimately contribute to improved patient care.