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Abstract: Stearns‐Noechel model was utilized as a primary reference to study color matching principles of digital rotor spun yarn. Three primary colored (red, yellow and blue) cotton fibers were used to spin blended yarns. Spectral reflectance of the two‐component and three‐component samples was measured with data color spectrophotometer. For these samples, the Stearns‐Noechel model parameter M was determined. Four methods were employed to calculate the M value to improve accuracy of the model, 1.Classical method, named as M1; 2.Optimizing the M1 value obtained by the classical method considering the wavelength factor, named as M2; 3.Simplified M2 according to the linear correlation with the wavelength, named as M3; 4. Simplified M2 according to the segmentation correlation with the wavelength, named as M4. The study shows that average color difference of the two‐component decreases from 2.7 to 1.48, and for three‐component samples from 3.32 to 1.66, by using M2 instead of M1. While calculated using M3, the color difference of the two types of samples will be 1.73 and 2.19, correspondingly. This cannot meet color matching needs. As for M4, the average color difference of the two categories will be 1.54 and 1.91, better than the result obtained using M1 and M3, worse than M2. [ABSTRACT FROM AUTHOR]

Donors of nitroxyl (HNO), the reduced congener of nitric oxide (NO), exert positive cardiac inotropy/lusitropy in vivo and in vitro, due in part to their enhancement of Ca2+ cycling into and out of the sarcoplasmic reticulum. Here we tested whether the cardiac action of HNO further involves changes in myofilament–calcium interaction. Intact rat trabeculae from the right ventricle were mounted between a force transducer and a motor arm, superfused with Krebs–Henseleit (K-H) solution (pH 7.4, room temperature) and loaded iontophoretically with fura-2 to determine [Ca2+]i. Sarcomere length was set at 2.2–2.3 μm. HNO donated by Angeli's salt (AS; Na2N2O3) dose-dependently increased both twitch force and [Ca2+]i transients (from 50 to 1000 μm). Force increased more than [Ca2+]i transients, especially at higher doses (332 ± 33% versus 221 ± 27%, P < 0.01 at 1000 μm). AS/HNO (250 μm) increased developed force without changing Ca2+ transients at any given [Ca2+]o (0.5–2.0 mm). During steady-state activation, AS/HNO (250 μm) increased maximal Ca2+-activated force ( Fmax, 106.8 ± 4.3 versus 86.7 ± 4.2 mN mm−2, n= 7–8, P < 0.01) without affecting Ca2+ required for 50% activation (Ca50, 0.44 ± 0.04 versus 0.52 ± 0.04 μm, not significant) or the Hill coefficient (4.75 ± 0.67 versus 5.02 ± 1.1, not significant). AS/HNO did not alter myofibrillar Mg-ATPase activity, supporting an effect on the myofilaments themselves. The thiol reducing agent dithiothreitol (DTT, 5.0 mm) both prevented and reversed HNO action, confirming AS/HNO redox sensitivity. Lastly, NO (from DEA/NO) did not mimic AS/HNO cardiac effects. Thus, in addition to reported changes in Ca2+ cycling, HNO also acts as a cardiac Ca2+ sensitizer, augmenting maximal force without altering actomyosin ATPase activity. This is likely to be due to modulation of myofilament proteins that harbour reactive thiolate groups that are targets of HNO. [ABSTRACT FROM AUTHOR]

Rotationally accelerated shot peening (RASP) is an innovative surface nanocrystallization technique, which can effectively produce gradient nanostructured layers on bulk metallic materials. In current work, the microstructural evolution and mechanical properties of the RASP‐processed 316L stainless steels are systematically explored. The results show that deformation twinning plays a significant role in fabricating nano‐grains. At the depth of ≈200 µm, unidirectional parallel mechanical twins are observed as the dominated deformation activity in each grain. With the decrease of depth (to ≈100 µm), twin‐twin intersections occur under a higher strain rate, which divide coarse grains into finer blocks. Eventually, nano‐grains form via grain rotation and grain boundary sliding at the topmost surface. Deformation twinning is still acted as an operative grain refinement mechanism in the nano‐grains. Importantly, the strength of the treated 316L stainless steel is improved while the ductility is decent. The improved strength is obtained from grain refinement, a high density of dislocations, deformation twins, and strain‐induced martensitic phase. For the good ductility, it is ascribed to the existence of slightly deformed coarse grains, ultrafine/nano‐twins and strain gradient. Rotationally accelerated shot peening (RASP) is used to produce gradient nanostructured layers on 316L stainless steel surfaces. The microstructural evolution and enhanced mechanical properties of the processed samples are systematically explored, which is expected to expand the application of the 316L stainless steel as a structural material. [ABSTRACT FROM AUTHOR]

Background Cardiac failure is the primary cause of death in most patients with pulmonary arterial hypertension (PH). As pleiotropic cytokines, human resistin (Hresistin) and its rodent homolog, resistin-like molecule α, are mechanistically critical to pulmonary vascular remodeling in PH. However, it is still unclear whether activation of these resistin-like molecules can directly cause PH-associated cardiac dysfunction and remodeling. Methods and Results In this study, we detected Hresistin protein in right ventricular (RV) tissue of patients with PH and elevated resistin-like molecule expression in RV tissues of rodents with RV hypertrophy and failure. In a humanized mouse model, cardiac-specific Hresistin overexpression was sufficient to cause cardiac dysfunction and remodeling. Dilated hearts exhibited reduced force development and decreased intracellular Ca 2+ transients. In the RV tissues overexpressing Hresistin, the impaired contractility was associated with the suppression of protein kinase A and AMP-activated protein kinase. Mechanistically, Hresistin activation triggered the inflammation mediated by signaling of the key damage-associated molecular pattern molecule high-mobility group box 1, and subsequently induced pro-proliferative Ki67 in RV tissues of the transgenic mice. Intriguingly, an anti-Hresistin human antibody that we generated protected the myocardium from hypertrophy and failure in the rodent PH models. Conclusions Our data indicate that Hresistin is expressed in heart tissues and plays a role in the development of RV dysfunction and maladaptive remodeling through its immunoregulatory activities. Targeting this signaling to modulate cardiac inflammation may offer a promising strategy to treat PH-associated RV hypertrophy and failure in humans.