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

CD8⁺ T cells lacking CD96 produce perforin and IFNγ following stimulation with PMA/ionomycin.

<p>FACS sorted CD96⁺ and CD96^neg were stimulated with PMA/ionomycin and assessed for A) IFNγ and B) perforin production in an ELISPOT assay. Bars represent the mean value ± SD of three independent experiments and show spot forming units (SFU) per 5000 cells. Statistical analysis was performed using Student’s T test *p < 0.05.</p

CD96 T cell expression in HIV-1-infected subjects is down-regulated compared to healthy controls (HC).

<p>PBMCs from elite controllers (EC, n = 20), viremic non-controllers (NC, n = 20) and healthy controls (HC, n = 40) were surface stained for CD96 expression. A) Representative histograms (dark grey = fluorescence minus one (FMO) control, solid black line = NC, light grey = EC, dotted black line = HC) and dot plots. B) Percentage of CD8⁺ T cells expressing CD96. C) Mean fluorescence intensity (MFI) of CD96 on CD8⁺ T cells. D) Percentage of naïve and different CD8⁺ T cell memory populations (TCM = central memory T cell, TEM = effector memory T cell, TEMRA = terminally differentiated effector memory T cell) expressing CD96. E) CD96 MFI on CD8⁺ T cells within each memory subset. The bars represent the mean and error bars represent the range from minimum to maximum value. Statistical analysis was performed using Kruskal Wallis tests with Dunn’s post-test *p < 0.05, **p < 0.01, ***p < 0.001.</p

CD96 expression is down-modulated by LPS stimulation and up-regulated by TCR engagement.

<p>A) Percentage of CD38⁺ HLA-DR⁺ CD8⁺ T cells as a measure of immune activation. B) Association of CD96 MFI on CD8⁺ T cells and percentage of CD38⁺ HLA-DR⁺ CD8⁺ T cells (n = 40). C) Percentage of CD96 expression and D) CD96 MFI on CD8⁺ T cell following stimulation with either LPS, PHA, IL-12/18 and anti-CD3/CD28 for 24 hrs compared to unstimulated cells. Statistical analysis was performed using Student’s T test *p < 0.05, **p < 0.01, ***p < 0.001. Correlations were determined by two-tailed non-parametric Spearman correlations.</p

Effect of antiretroviral drugs on LINE-1 retrotransposition frequency.

<p>A. The LINE-1 retrotransposition reporter plasmid 99gfpLRE3 encodes the full-length, retrotransposition competent LRE3 LINE-1 element under the control of its natural promoter. An eGFP retrotransposition reporter cassette was inserted into the LRE3 3′ UTR. The cassette encodes eGFP under the control of a CMV promoter, in inverse orientation relative to the LRE3 sequence. The eGFP coding sequence is interrupted by an intron inserted in the same transcriptional orientation as LRE3. Transcription from the CMV promoter does can not yield a spliced eGFP sequence. Transcription from the LINE-1 promoter does not lead to eGFP expression, as the eGFP coding sequence is inverted in the resulting mRNA. However, retrotransposition of this RNA, and integration into the genome, allows a sense eGFP mRNA to be transcribed from the CMV promoter. Thus in cells transfected with 99gfpLRE3, eGFP expression acts as a reporter for the completion of a successful retrotransposition event. The 99gfpJM111 plasmid is analogous to 99gfpLRE3, but incorporates point mutations in ORF1 which render its LINE-1 element retrotransposition incompetent. 99gfpJM111 was therefore employed as a negative control in all assays. Both the 99gfpLRE3 and 99gfpJM111 plasmids also encode puromycin resistance markers allowing for selection of transfected cells. B–D. HeLa cells were incubated in triplicate with five-fold serial dilutions of antiretroviral drugs, and transfected with the LINE-1 retrotransposition reporter plasmid 99gfpLRE3. Transfectants were selected with puromycin. Five days post-transfection, cells were stained with the viability dye 7-AAD, and analyzed by FACS. Retrotransposition frequency was determined by excluding 7-AAD-positive events, and then gating on the eGFP-positive population. Shown is representative data from one of three independent experiments. B. In the absence of drugs, a distinct eGFP-positive population of viable cells, representing cells that have undergone LINE-1-LRE3 retrotransposition events, is clearly distinguishable. Shown is one of six replicates of no drug control. C. In the presence of elevated concentrations of nRTIs, the eGFP-positive population is greatly diminished in frequency, indicating suppression of retrotransposition. Shown is one of three replicates of 25 µM stavudine treatment. D. LINE-1 retrotransposition, as reported by eGFP expression, is inhibited by nRTIs in a dose dependent manner, while nevirapine has no effect. Shown are the mean frequencies of eGFP-positive cells amongst the viable 7-AAD-negative subsets, as determined in triplicate, with standard errors represented by error bars. Dashed horizontal lines indicate 50% and 90% inhibition levels.</p

The absolute number and CD96 MFI of CD96⁺CD8⁺ T cells correlates with CD4⁺ T cell counts.

<p>Association of A) CD96 MFI on CD8⁺ T cells (n = 37) and B) the number of CD96⁺CD8⁺ T cells with CD4⁺ T cell counts (n = 36). Correlations were determined by two-tailed non-parametric Spearman correlations.</p

MAIT cells are reduced in frequency and functionally impaired in human T lymphotropic virus type 1 infection: Potential clinical implications

<div><p>HTLV-1 infection is associated with several inflammatory disorders, including the neurodegenerative condition HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). It is unclear why a minority of infected subjects develop HAM/TSP. The cellular immune response has been implicated in the development of inflammatory alterations in these patients; however the pathogenic mechanisms for disease progression remain unclear. Furthermore, HTLV-1-infected individuals have an increase incidence of <i>Mycobacterium tuberculosis</i> (Mtb) infection, suggesting that immunological defect are associated with HTLV-1 infection. Evidence suggests an important role for Mucosal-associated invariant T (MAIT) cells in the early control of Mtb infection. Chronic viral infections like HIV and HCV have been associated with decreased frequency and functionality of MAIT cells. We hypothesized that HTLV-1 infection is associated with similar perturbations in MAIT cells. We investigated MAIT cell frequency, phenotype, and function by flow cytometry in a cohort of 10 asymptomatic and 10 HAM/TSP HTLV-1 infected patients. We found that MAIT cells from HTLV-1-infected subjects were reduced and showed high co-expression of the activation markers CD38 and HLA-DR but normal levels of CCR6 and CD127. MAIT cells had a lower expression of the transcription factor PLZF in HAM/TSP patients. Unlike Tax-specific CD8+T cells, which are hyperfunctional, MAIT cells from HTLV-1-infected subjects had a poor IFNγ response following antigen stimulation. MAIT cell perturbations in HTLV-1 infection were not associated with HTLV-1 proviral load and MAIT cells were not infected by HTLV-1 <i>in vivo</i>. Rather, MAIT cells loss was associated with immune activation. Overall, our results do not support a role for MAIT cells in HAM/TSP pathogenesis but reduced numbers of MAIT cells, together with their poor functionality, could contribute to the increased susceptibility of HTLV-1-infected individuals to other infectious agents.</p></div

MAIT cells are reduced in HTLV-1 infection.

<p>Representative flow plots showing gating strategy and MAIT cell frequency in healthy controls and HTLV-infected individuals (A). Frequency of MAIT cells in healthy controls (n = 12) and HLTV-1 patients (n = 20) (B). Frequency of MAIT cells in asymptomatic (n = 10) and HAM/TSP (n = 10) HTLV-1 patients (C). ** indicates p < 0.001. The lines and whiskers represent the median and interquartile range respectively.</p

Schema of CD4∶CD8 ratio in HIV infection.

<p>Uncontrolled HIV infection results in depletion of CD4+ T cells with concomitant increase in CD8+ T cells, mostly of an effector phenotype. This process is largely driven by high levels of T cell activation. With introduction of antiretroviral therapy, there is a decrease in T cell activation and a resulting drop in activation and proliferation of CD8+ T cells. There is also some recovery of CD4+ T cells. However, an inverted CD4∶CD8 ratio persists due to persistently expanded CD8+ T cell population.</p

MAIT cells are activated in HTLV-1 infection.

<p>Co-expression of CD38 and HLA-DR by CD4 T cells in healthy controls (n = 12) and HLTV-1 patients (n = 20) (A). Co-expression of CD38 and HLA-DR by CD4 T cells in asymptomatic (n = 10) and HAM/TSP (n = 10) HTLV-1 patients (B). Co-expression of CD38 and HLA-DR by CD8 T cells in healthy controls and HLTV-1 patients (C). Co-expression of CD38 and HLA-DR by CD4 T cells in asymptomatic and HAM/TSP HTLV-1 patients (D). Co-expression of CD38 and HLA-DR by MAIT cells in healthy controls and HLTV-1 patients (E). Co-expression of CD38 and HLA-DR by MAIT cells in asymptomatic and HAM/TSP HTLV-1 patients (F). * indicates p <b>≤</b> 0.05, ** indicates p < 0.01, and *** indicates p < 0.001. The lines and whiskers represent the median and interquartile range respectively.</p