Стилистический эффект разговорной речи и его составляющие

В обучении русскому языку как иностранному на современном этапе большое внимание уделяется особенностям русской разговорной речи. Это обусловлено целым рядом причин, среди которых, на наш взгляд, можно выделить следующие: во-первых, разговорная речь всегда отличается активностью проникновения во все сферы жизнедеятельности людей и функционирует как в повседневном общении, так и в различных сферах (литературе, кино, политике и т.д.). Во-вторых, разговорная речь носит многожанровый характер, что зачастую затрудняет ее понимание иностранными студентами. В-третьих, в разговорную речь помимо слов нейтрального стиля все активнее стала проникать арготическая лексика. Именно в связи с этим особый интерес у нас вызывает разговорный стиль речи в преломлении на инофонную аудиторию

Polyclonal CD8⁺ T Cell Effector Capacity by ERK1/2 Signaling Ability.

†<p>IQR = Interquartile Range.</p>††<p>GMF = Geometric Mean Fluorescence Intensity.</p

Study Participant Characteristics.

†<p>IQR = Interquartile Range.</p>††<p>ART = Antiretroviral Treatment.</p

p-ERK1/2-refractory CD8⁺ T cells exhibit low per cell effector function in response to HIV-1 Gag stimulation.

<p>(A–E) Response of total CD8⁺ T cells to 12 hours HIV-1 Gag peptides and 20 minutes PMA+I. (<b>A</b>) Gating for CD8⁺ p-ERK1/2-refractory versus responsive T cell subsets. (B) Frequency of p-ERK1/2-refractory cells. (C) Gating for IFN-γ (dashed gate) and perforin expression (solid gate) within p-ERK1/2 subsets. (D) IFN-γ expression by ERK1/2 signaling response. Left graph displays frequency of IFN-γ⁺ cells contained within the parent population. Right graph, the IFN-γ geometric mean fluorescence intensity (GMF) of IFN-γ⁺ cells (E) Perforin expression by ERK1/2 signaling response. Left graph, frequency of perforin⁺ cells. Right graph, perforin GMF of perforin⁺ cells. (F–J) Response of highly activated (CD38⁺HLA-DR⁺) CD8⁺ T cells. (F) Gating for p-ERK1/2-refractory versus responsive subsets. (G) Frequency of p-ERK1/2-refractory cells within the CD38⁺HLA-DR⁺ compartment. (H) Gating for IFN-γ and perforin expression within activated p-ERK1/2 subsets. (I) IFN-γ expression by ERK1/2 signaling response: Left graph, frequency of IFN-γ⁺ cells. Right graph, IFN-γ GMF of IFN-γ⁺ cells. (J) Perforin expression by ERK1/2 signaling response. Left graph, frequency of perforin⁺ cells. Right graph, perforin GMF in perforin⁺ cells. (K–L) CD8⁺ T cells, (K) Gating for IFN-γ⁺CD107α⁺ expression and frequency of IFN-γ⁺CD107α⁺ cells within p-ERK1/2 subsets. (M) CD107α expression within IFN-γ⁺ cells by ERK1/2 signaling response: Left graph, frequency of CD107α⁺ cells. Right graph, CD107α GMF of CD107α⁺ cells. Significance Not Significant (NS) p>0.01, Marginal (M) p<0.01, *p<0.05, **p<0.005, ***p<0.0005. (A,C,F,H,K, n = 1; D,E,I,J, n = 30; L,M, n = 14).</p

p-ERK1/2-refractory CD8⁺ T cells are distinct from classical exhaustion, remain stable over time and predict HIV-1 viral load.

<p>(A–D) CD8⁺ T cells following 20 minutes PMA+I<b>.</b> (A) Panels from left to right: ERK1/2 phosphorylation in total CD8⁺ T cells. Gating for PD1 expression. Gating for p-ERK1/2-refractory versus responsive subsets within the PD1⁺ compartment. (B) Frequency of p-ERK1/2-refractory cells within the PD1⁺ compartment. (C) Panels from left to right: The ERK1/2 phosphorylation response in total CD8⁺ T cells, Gating for Tim-3 expression in total CD8⁺ T cells. Gating for Tim-3 expression in total CD8⁺ T cells. (D) Frequency of p-ERK1/2-refractory cells contained within the Tim-3⁺ compartment. (E–F) Smoothed moving average plots displaying the frequency of p-ERK1/2-refractory (E) and CD38⁺HLADR⁺ (F) CD8⁺ T cells from HIV-1-infected treatment-naïve adults followed longitudinally over the first 2.5 years of infection. (G) Lowess plots displaying average viral load over time in patients stratified by high or low p-ERK1/2-refractory measurement at study entry. Open squares with black line represents individuals with a first clinical visit % p-ERK1/2-refractory CD8⁺ T cell measurement above the median frequency. Closed triangles with grey line represents individuals below the median frequency. Individuals with a high p-ER1/2-refractory measurement during early infection maintain significantly higher viral loads over time. (A,C n = 1; B n = 11; D, n = 20; E–F, n = 27 with 2–4 time points per individual, G, n = 74).</p

p-ERK1/2-Refractory CD8⁺ T cells exhibit low per cell effector function in response to polyclonal stimulation.

<p>(A–E) Response of total CD8+ T cells to140 minutes PMA+I. (<b>A</b>) Gating for CD8⁺ p-ERK1/2-refractory versus responsive T cell subsets. (B) Frequency of p-ERK1/2-refractory cells. (C) Gating for IFN-γ (dashed gates) and perforin (solid gates) expression within p-ERK1/2 subsets. (D) IFN-γ expression by ERK1/2 signaling response. Left graph displays frequency of IFN-γ⁺ cells contained within the parent population. Right graph, the IFN-γ geometric mean fluorescence intensity (GMF) of IFN-γ⁺ cells (E) Perforin expression by ERK1/2 signaling response. Left graph, frequency of perforin⁺ cells. Right graph, perforin GMF of perforin⁺ cells. (F–G) Response of highly activated (CD38+HLA-DR+) CD8+ T cells. (F) Gating for p-ERK1/2-refractory versus responsive subsets. (G) Frequency of p-ERK1/2-refractory cells within the CD38+HLA-DR+ compartment. (H) Gating for IFN-γ and perforin expression within activated p-ERK1/2 subsets. (I) IFN-γ expression by ERK1/2 signaling response: Left graph, frequency of IFN-γ⁺ cells. Right graph, IFN-γ GMF of IFN-γ⁺ cells. (J) Perforin expression by ERK1/2 signaling response. Left graph, frequency of perforin⁺ cells. Right graph, perforin GMF in perforin⁺ cells. Significance Not Significant (NS) p>0.01, Marginal (M) p<0.01, *p<0.05, **p<0.005, ***p<0.0005. (A,C,F,H, n = 1; D,E,I,J, n = 19).</p

Characteristics of HIV-positive men who have sex with men (MSM) in San Francisco in the Options cohort at the time of first ACASI, 2009–2010.

<p>Characteristics of HIV-positive men who have sex with men (MSM) in San Francisco in the Options cohort at the time of first ACASI, 2009–2010.</p

Estimated mean number of sexual partners per prior 3-month period and 95% confidence intervals [CI] for each sexual behavior variable of interest among MSM in Options/San Francisco, 2009–2010.

∧<p>Number of participants who contribute to each time point varies because this was not a strictly longitudinal cohort study. All participants started contributing data in 2009, and were at various times since diagnosis when they completed their ACASIs.</p>∧∧<p>PDP = potentially discordant partners (HIV-negative or unknown-status partners).</p>*<p>UAI = unprotected anal intercourse.</p>**<p>uIAI = unprotected insertive anal intercourse.</p>***<p>For participants with plasma viral load <500 copies/ml, number of PDP with whom uIAI occurred was set to 0.</p

Mean number of partners of various types per 3 months since HIV diagnosis among HIV-positive MSM in San Francisco, 2009–2010.

<p>An immediate drop in the total number of male partners in the first year of infection was followed by increases in number of partners over the following 3–4 years. The trend was similar for potentially serodiscordand partners (PDPs) although they comprised only 1/3 to 1/2 of total partnerships. However, unprotected anal intercourse (UAI) with PDPs occurred in far fewer partnerships throughout the follow-up period. Partnerships in which the HIV-positive participant was the insertive partner during unprotected anal intercourse (uIAI) accounted for fewer than 10% of all partnerships and in very few of those partnerships did the participant have sufficient plasma viral load (VL >500 copies/ml) to present a significant transmission risk.</p

Direction of exposure and T cell IFN-γ response correlations.

<p>IFN-γ T cell responses from the viremic partner (VP) group were plotted against the corresponding average number of unprotected receptive (A) or insertive (B) anal exposures to a partner's HIV-1. Significant correlations (denoted by *) were determined by two-tailed nonparametric spearmans correlation, spearman r (r), and linear regression analysis was plotted as straight lines.</p