Unlike optical waves, acoustic waves in fluids are described by scalar pressure fields, and therefore are considered spinless. Here, we demonstrate
Unveiling spins of physical systems usually gives people a fundamental understanding of the geometrical properties of waves from classical to quantum aspects. A great variety of research has shown that transverse waves can possess nontrivial spins and spin-related properties naturally. However, until now, we still lack essential physical insights about the spin nature of longitudinal waves. Here, demonstrated by elastic waves, we uncover spins for longitudinal waves and the mixed longitudinal-transverse waves that play essential roles in spin-momentum locking. Based on this spin perspective, several abnormal phenomena beyond pure transverse waves are attributed to the hybrid spin induced by mixed longitudinal-transverse waves. The unique hybrid spin reveals the complex spin essence in elastic waves and advances our understanding about their fundamental geometrical properties. We also show that these spin-dependent phenomena can be exploited to control the wave propagation, such as nonsymmetric elastic wave excitation by spin pairs, a unidirectional Rayleigh wave, and spin-selected elastic wave routing. These findings are generally applicable for wave cases with longitudinal and transverse components.
The prognosis for hepatocellular carcinoma (HCC) remains dismal in terms of overall survival (OS), and its molecular pathogenesis has not been completely defined. Here, we report that expression of deubiquitylase ubiquitin-specific protease 7 (USP7) is higher in human HCC tissues than in matched peritumoral tissues. Ectopic USP7 expression promotes growth of HCC cells in vivo and in vitro. Mechanistically, USP7 overexpression fosters HCC cell growth by forming a complex with and stabilizing thyroid hormone receptor-interacting protein 12 (TRIP12), which induces constitutive p14 ARF ubiquitination. Clinically, USP7 overexpression is significantly correlated with a malignant phenotype, including larger tumor size, multiple tumor, poor differentiation, elevated alpha-fetoprotein, and microvascular invasion. Moreover, overexpression of USP7 and/or TRIP12 correlates with shorter OS and higher cumulative recurrence rates of HCC. Conclusion: USP7 stabilizes TRIP12 by deubiquitination, thus constitutively inactivating p14 ARF and promoting HCC progression. This represents a novel marker for predicting prognosis and a potential therapeutic target for HCC. (HEPATOLOGY 2015;61:1603-1614 H epatocellular carcinoma (HCC) ranks as the fifth-most common cancer and the third cause of cancer-related mortality worldwide, mainly owing to its high rate of metastasis and recurrence.1 The recent identification of several oncogenes and tumor-suppressor genes has significantly deepened the understanding of the invasion and metastasis of HCC. 2 However, the effects of tumor progressionrelated genes often depend on the level of their protein products as well as their post-translational Abbreviations: 2D-LC-MS/MS, two-dimensional liquid chromatography coupled with tandem mass
Indices of dopamine transmission were measured in the postmortem striatum of DYT1 dystonia brains. A significant increase in the striatal 3,4-dihydroxyphenylacetic acid/dopamine ratio was found. Quantitative autoradiography revealed no differences in the density of dopamine transporter or vesicular monoamine transporter-2 binding; however, there was a trend toward a reduction in D(1) receptor and D(2) receptor binding. One brain with DYT1 parkinsonism was similarly evaluated and marked reductions in striatal dopamine, 3,4-dihydroxyphenylacetic acid, and homovanillic acid content as well as the density of binding of all four dopaminergic ligands were measured.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.