Разработка и исследование конструкции привода управляемого задерживающего устройства шароструйно-эжекторного бурового снаряда

В работе рассмотрены принципы шароструйного бурения, а так же устройство шаростуйно-эжекторного снаряда. Предложены варианты модернизации данного снаряда.In this paper, the principles of pellet impact drilling, as well as the construction of a pellet-ejector projectile, are considered. Variants of modernization of this projectile are offered

Examples of paired T2*-T1 non-concordance.

<p>Panel A: T2* and T1 map in a healthy volunteer. Panel B: T1 map and T2* map of two patients with normal T2* but low T1. Colour scale for T1 map is on top, for T2* map is at the bottom of the picture. Please note the blue shift of the myocardium in the T1 maps represented in panel B, compared to the healthy volunteer. Similarly, some pink areas may be spotted in the corresponding T2* maps, absent in the healthy volunteer. Nevertheless, dark blood T2* analysis performed with CMR Tools Thalassemia plug in gave normal results in both patients.</p

Myocardial T2*—T1 mapping relationship in Thalassemia major.

<p>(B): log-log linear regression lines for T2*—T1 (here Dark Blood T2*—MOLLI) in three different T2* intervals (T2* <20ms, T2* = 20-30ms and T2* >30ms)<b>–</b>for >30ms, the regression line is not drawn as the p value is 0.38 (weak relationship). (A): On the Y-axis are represented the r2 values of the relationship between T2* and T1 (both after log transformation). Data are obtained for a 30 samples moving window, with steps of 1 sample at a time, smoothed by a low-pass filter of order 3. Afterward, a new equispaced series was generated by linear interpolation. The point, corresponding to T2* = 28.7ms, was the local maximum found by setting the first derivative equal to 0, immediately before a large variation of the determination coefficient. A rounded value of T2* = 30ms has then been used to delimit a T2* range of 20-30ms, with suspect mild iron accumulation.</p

T2* vs T1 in Thalassemia major patients.

<p>The dashed lines highlight the cut off points for T2* (here Dark Blood, conventionally 20ms) and T1 (MOLLI, 916ms, as calculated from the healthy volunteer cohort). Dots localised in the grey quadrants represents discordance. All subjects with a discordant classification (n = 62, 38% of the cohort) fall into the lower right panel, i.e. they are characterized by normal T2*(iron not present), low T1 (iron present). Thus, apparently, T2* fails to identify 2 out of every 3 patients with cardiac iron overload.</p

Examples of paired T1 mapping and corresponding T2* map.

<p>Panel A: T1 mapping, with colour scale bar on top. Panel B: T2* map, with colour scale bar below. In both panels, from left to right, data from a normal volunteer, a patient with mild iron overload, a patient with moderate iron overload and a patient with severe iron overload, are separately shown. Colour scale for T1 map is on top, for T2* map is at the bottom of the picture. Low T1, corresponding to iron, is represented in blue in the T1 maps, and low T2* is represented in pink-to-blue.</p

Baseline patient characteristics.

<p>Baseline patient characteristics.</p

Affinity-purified maternal CHB serum antibodies co-localize with α_1G.

<p>(<b>A</b>) Cardiomyocytes from ventricle of human fetal hearts, gestational week 20.6, were dissociated, immunofluorescence stained, and visualized with confocal microscopy. Cardiomyocytes are stained for Cav3.1 (α_1G) (Red), for the cardiomyocyte marker anti-Troponin-T (Green), and nuclei visualized with DAPI (Blue). Secondary antibodies alone gave no stain. Inset image demonstrates expression on the surface in a cross section image. Images shown are representative of various cardiomyocyte samples; similar staining patterns were obtained in four replicate experiments. Secondary antibodies, anti-rabbit-IgG-Cy3 (Red) and anti-mouse-IgG-Alexa488 (green) alone give no stain (data not shown). Note that DAPI stains the nuclei of cardiomyocytes and of other cells present in the samples, such as fibroblasts. Scale bar represents 12 µm. (<b>B</b>) Dissociated and non-permeabilized cardiomyocytes from ventricle of 20.6 week human fetal hearts, immunofluoresence stained for α_1G affinity-purified serum (red), and α_1G (green). Co-localization of staining (yellow) was assessed with confocal microscopy. Scale bar represents 12 µm.</p

T-type calcium channel α_1G is expressed in the AV node of human fetal hearts.

<p>(<b>A</b>) Masson's trichrome staining of 21-week human fetal heart demonstrates morphology of the AVJ region with light pink staining of the spindle-like cells in the AV node (AVN) and the AV bundle (AVB), green staining corresponding to collagen fibres. (<b>B</b>) α_1G staining (Red) is present in AVJ and AV bundle regions which are distinguishable by positive NF-160 staining (Green). Scale bars represent 100 µm (A) and 150 µm (B).</p

Expression analysis, and CHB maternal sera immune reactivity towards α_1G.

<p>(<b>A</b>) Although both α_1G and α_1H are expressed in human fetal hearts, real time PCR demonstrates that transcripts from <i>CACNA1G</i> (α_1G) are 2.2- to 4-fold higher in the AVJ than in the apex tissue (between 18–22.6 weeks gestation), whereas <i>CACNA1H</i> expression levels are between 0.7- and 1.1-fold in the AVJ compared to the apex. (<b>B</b>) Combining the data from 3 hearts (18.0 weeks-22.6 weeks), shows that <i>CACNA1G</i> expression in the AVJ is significantly higher than <i>CACNA1H</i> in the AVJ (p<0.05). (<b>C</b>) Western blot with human fetal heart lysate (20.4 weeks) demonstrates α_1G expression by a Cav3.1 commercial antibody (lane 1), that is blocked by the peptide immunogen of this antibody (aa1–22 of rat α_1G) (lane 2). CHB sera (anti-Ro and anti-La titer >100 IU) also binds to α_1G (lane 3); this reactivity is blocked by the α_1G p305 peptide (lane 4). Sera from mothers with anti-Ro/La antibodies (anti-Ro = 60 IU and anti-La titer >100 IU) giving birth to normal babies do not have immune reactivity to the α_1G protein (lane 5), and a commercial α_1H antibody confirms that the band seen is not α_1H. (<b>D</b>) α_1G isolated from human fetal heart (AV junction, ventricle, and apex) was immunoprecipitated with a Cav3.1 antibody, and the immunoblot was probed with human sera. Immunoblot was subsequently stripped and re-probed with a second Cav3.1 antibody towards a different epitope, demonstrating presence and specificity of the IP towards α_1G. Note that CHB sera is defined as anti-Ro^/La positive sera from pregnancies affected by CHB. Normal sera are from pregnancies with a healthy outcome and not affected by CHB.</p

Maternal sera antibody profile screening of α_1G peptides.

<p>Maternal sera from one CHB⁺ pregnancy (<b>A, C, E</b>) and one CHB⁻ pregnancy (<b>B, D, F</b>) were tested in ELISA against 15aa long overlapping peptides derived from extracellular regions of α_1G: T-type aa130–380 (<b>A, B</b>); aa774–963 (<b>C, D</b>); and, aa1308–1536 (<b>E, F</b>). Reactivity above threshold (HC: Average+3×St. Dev; set at 0.59, 0.64, 0.48 respectively for A/B, C/D, and E/F) was observed in the CHB⁺ but not CHB⁻ serum to α_1G peptides p305 (aa305–319, light grey bar) and p315 (aa315–323, dark grey bar) was observed in the CHB⁺ but not the CHB⁻ serum. Above threshold reactivity was also observed among peptides in the region spanning aa1308–1536.</p