Галльский пласт в современном немецком литературном языке: структурно-системный и функционально-динамический аспекты

Диссертационное исследование Меремкуловой Татьяны Игоревны выполнено в русле контактной лингвистики, стремительно развивающейся ветви исторического языкознания, и посвящено определению структурно-системных и функционально-динамических характеристик заимствованных лексических единиц галльского пласта в системе современного немецкого литературного языка и в синхронной немецкой литературной речи.The dissertation research of Meremkulova Tatyana Igorevna is carried out in the mainstream of the contact linguistics, the rapidly developing branch of historical linguistics, and is devoted to the determination of structural-systemic and functional-dynamic characteristics of the borrowed lexical units of the Gallic layer in the system of modern German literary language and in synchronous German literary speech

The effect of the nitric oxide synthase inhibitor N-nitro-L-arginine-methyl ester on neuropeptide-induced vasodilation and protein extravasation in human skin

Endogenous neuropeptides released from nociceptors can induce vasodilation and enhanced protein extravasation (neurogenic inflammation). The role of nitric oxide (NO) in the induction of neurogenic inflammation is controversial. In this study, dermal microdialysis was used in awake humans (n = 39) to deliver substance P (SP; 10-7 and 10-6M) or calcitonin gene-related peptide (CGRP; 5 × 10-7M and 2 × 10-6M). Neuropeptide-induced local and axon reflex erythema was assessed by laser Doppler imaging. Total protein concentration in the dialysate was measured to quantify local protein extravasation. The responses were assessed in the absence and the presence of the nitric oxide synthase inhibitor, N-nitro-L-arginine-methyl ester (L-NAME) added to the perfusate at concentrations of 5, 10 or 20 mM. L-NAME (5 mM) applied via the dialysis catheters reduced local blood flow by approximately 30%. In addition, L-NAME inhibited SP-induced vasodilation by about 40% for 10-7M SP and 30% for 10-6M SP (n = 11, p &lt; 0.01). In contrast, CGRP-induced vasodilation was only marginally inhibited by L-NAME. SP, but not CGRP, provoked a dose-dependent increase in protein extravasation. L-NAME (5 mM) inhibited this increase by up to 40% for both SP concentrations used (n = 11, p &lt; 0.01). Higher concentrations of L-NAME did not further reduce SP- or CGRP-induced vasodilation or SP-induced protein extravasation. Exogenously applied SP induces vasodilation and protein extravasation, which is partly NO mediated, whereas CGRP-induced vasodilation appears to be NO independent.<br/