Оценка языка-пиджина руссенорск глазами современного лингвиста<br>(Assessment of the pidgin Russenorsk (RN) seen with the eyes of a contemporary linguist)

The first linguistic description of RN was published by Olaf Broch in German in 1927 in Archiv für slavishe Philologie and in the same year also in Norwegian, at the request of the editor of the Norwegian philological journal Maal og Minne. In 1930 he published the RN texts which were known then and which he had used as a basis for the description of 1927. Broch's interest in RN was concentrated on a pure description of this phenomenon, by him characterized as "a kind of language [...] a mixture of different constituents like the ones we know from different parts of the world under more or less the same conditions». We have passed through a period of comparing RN to other pidgins, establishing RN as a grammatical system with simple morphology, with a syntax that is far from being without rules, but its syntactical possibilities are restricted, as in other pidgins. The history of RN shows that as long as RN was the only means of communication between Norwegians and Russians in Northern Norway the assessment was positive, but when Norwegian merchants started learning Russian proper, RN lost its status as "the fourth language" in Northern Norway, and was characterized in the same derogatory way as colonial pidgins. RN, however, differs from them, in having a special status as a dual-sourced pidgin, while most Atlantic and Pacific pidgin, creoloid and post-creoloid languages have a single main source.This seems to stimulate to more extensive studies into the features of the pidgin and contact languages of the Arctic and the northern regions. Such investigations can hopefully lead to important modifications and necessary redefinitions of the theoretical models employed in pidgin and creole studies

How do normal faults grow?

Normal faults grow via synchronous increase in displacement and length (‘propagating fault model’, also known as the ‘isolated fault model’), or by rapid length establishment and subsequent displacement accrual (constant-length fault model). We here use time-series displacement (D) and length (L) data from natural and experimental faults to elucidate growth styles and D-L trajectories throughout fault life, and to assess the applicability of the two fault models. We show that the growth of most faults is characterized by two stages, with the first defined by fault lengthening (20-30% of fault lifespan) and the second by displacement accrual (70-80% of fault lifespan). Although broadly adhering to the constant-length model, fault growth throughout the lengthening stage, during which significant displacement (10-60% of the total end-of-life fault displacement) may also accumulate, is achieved through rapid tip propagation, relay breaching, and segment linkage, characteristics perhaps most intuitively thought to reflect growth in accordance with the propagating model. The subsequent growth stage is dominated by displacement accrual with limited lateral tip propagation, a phenomenon best described by the constant-length model. We also show that, despite being used primarily in support of the propagating model, global displacement-length (D-L) datasets are equally compatible with the constant-length model

Cytokine pattern in patients with ST-elevation myocardial infarction treated with the interleukin-6 receptor antagonist tocilizumab

Background Tocilizumab improves myocardial salvage index (MSI) in patients with ST-elevation myocardial infarction (STEMI), but its mechanisms of action are unclear. Here, we explored how cytokines were affected by tocilizumab and their correlations with neutrophils, C-reactive protein (CRP), troponin T, MSI and infarct size.Methods STEMI patients were randomised to receive a single dose of 280 mg tocilizumab (n=101) or placebo (n=98) before percutaneous coronary intervention. Blood samples were collected before infusion of tocilizumab or placebo at baseline, during follow-up at 24–36, 72–168 hours, 3 and 6 months. 27 cytokines were analysed using a multiplex cytokine assay. Cardiac MRI was performed during hospitalisation and 6 months.Results Repeated measures analysis of variance showed significant (p&lt;0.001) between-group difference in changes for IL-6, IL-8 and IL-1ra due to an increase in the tocilizumab group during hospitalisation. IL-6 and IL-8 correlated to neutrophils in the placebo group (r=0.73, 0.68, respectively), which was attenuated in the tocilizumab group (r=0.28, 0.27, respectively). A similar pattern was seen for MSI and IL-6 and IL-8 in the placebo group (r=−0.29, –0.25, respectively) in patients presenting ≤3 hours from symptom onset, which was attenuated in the tocilizumab group (r=−0.09,–0.14, respectively).Conclusions Tocilizumab increases IL-6, IL-8 and IL-1ra in STEMI. IL-6 and IL-8 show correlations to neutrophils/CRP and markers of cardiac injury in the placebo group that was attenuated in the tocilizumab group. This may suggest a beneficial effect of tocilizumab on the ischaemia-reperfusion injury in STEMI patients.Trial registration number NCT03004703

Randomized Trial of Interleukin-6 Receptor Inhibition in Patients With Acute ST-Segment Elevation Myocardial Infarction

Background - Prompt myocardial revascularization with percutaneous coronary intervention (PCI) reduces infarct size and improves outcomes in patients with ST-segment elevation myocardial infarction (STEMI). However, as much as 50% of the loss of viable myocardium may be attributed to the reperfusion injury and the associated inflammatory response. Objectives - This study sought to evaluate the effect of the interleukin-6 receptor inhibitor tocilizumab on myocardial salvage in acute STEMI. Methods - The ASSAIL-MI trial was a randomized, double-blind, placebo-controlled trial conducted at 3 high-volume PCI centers in Norway. Patients admitted with STEMI within 6 h of symptom onset were eligible. Consenting patients were randomized in a 1:1 fashion to promptly receive a single infusion of 280 mg tocilizumab or placebo. The primary endpoint was the myocardial salvage index as measured by magnetic resonance imaging after 3 to 7 days. Results - We randomized 101 patients to tocilizumab and 98 patients to placebo. The myocardial salvage index was larger in the tocilizumab group than in the placebo group (adjusted between-group difference 5.6 [95% confidence interval: 0.2 to 11.3] percentage points, p = 0.04). Microvascular obstruction was less extensive in the tocilizumab arm, but there was no significant difference in the final infarct size between the tocilizumab arm and the placebo arm (7.2% vs. 9.1% of myocardial volume, p = 0.08). Adverse events were evenly distributed across the treatment groups. Conclusions - Tocilizumab increased myocardial salvage in patients with acute STEMI. (ASSessing the effect of Anti-IL-6 treatment in Myocardial Infarction [ASSAIL-MI]; NCT03004703

Interleukin-6 inhibition in ST-elevation myocardial infarction: Immune cell profile in the randomised ASSAIL-MI trial

Background We recently showed that interleukin (IL)-6 inhibition by tocilizumab improves myocardial salvage in ST-elevation myocardial infarction (STEMI). However, the mechanisms for this effect are not clear. Methods In this exploratory sub-study of the ASSAIL-MI trial, we examined leukocyte differential counts and their relation to myocardial salvage and peak troponin T (TnT) in STEMI patients randomised to tocilizumab (n = 101) or placebo (n = 98). We performed RNA-sequencing on whole blood (n = 40) and T cells (n = 20). B and T cell subpopulations were examined by flow cytometry (n = 69). Findings (i) STEMI patients had higher neutrophil counts at hospitalisation compared with stable angina patients. (ii) After percutaneous coronary intervention there was a gradual decline in neutrophils, which was significantly more pronounced in the tocilizumab group. (iii) The decrease in neutrophils in the tocilizumab group was associated with improved myocardial salvage and lower peak TnT. (iv) RNA-sequencing suggested that neutrophil function was also attenuated by tocilizumab. (v) B and T cell sub-populations changed only minimally after STEMI with minor effects of tocilizumab, supported as well by RNA-sequencing analyses of T cells. (vi) However, a low CD8+ count was associated with improved myocardial salvage in patients admitted to the hospital > 3 h after symptom onset. Interpretation Tocilizumab induced a rapid reduction in neutrophils and seemed to attenuate neutrophil function in STEMI patients potentially related to the beneficial effects of tocilizumab on myocardial salvage. Funding South-Eastern Norway Regional Health Authority (Nos. 2019067, 2017084), the Central Norway Regional Health Authority and Norwegian Research Council (No. 283867)