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Topological materials is one of the hottest topics in condensed matter physics because of its exotic properties such as robust metallic boundary states, Fermi arcs, and the spin‐momentum‐locking helicity. The topologically protected conducting boundary states spanning the whole bandgap are expected to serve as robust and wide‐range‐energy transition states facilitating catalytic reactions. Recently, some topological materials have been found to be high‐performance catalysts, which might open an emerging research field. Herein, an overview of topological materials is given and then recent progress in topological material catalysts (TMCs) is presented. As it is a new field, more detailed and accurate mechanisms behind the high performance of TMCs are urgently needed. Combining theoretical and experimental studies is a promising way to resolve these puzzles. Heterostructures, dopants, and defects have the chance to tune the catalytic activity of TMCs while retaining topological surface states (TSSs). Also, more TMCs are needed to be discovered, and more catalytic reactions are to be investigated for TMCs in the future. [ABSTRACT FROM AUTHOR]

Controlling light at the nanoscale by exploiting ultra‐confined polaritons—hybrid light and matter waves—in various van der Waals (vdW) materials empowers unique opportunities for many nanophotonic on‐chip technologies. So far, mainstream approaches have relied on interfacial techniques (e.g., refractive optics, meta‐optics, and moire engineering) to manipulate the polariton wavefront. Here, it is proposed that orbital angular momentum (OAM) of incident light can offer a new degree of freedom to structure vdW polaritons. With vortex excitations, a new class of accelerating polariton waves is observed—Airy‐like hyperbolic phonon polaritons (PhPs) in high‐symmetry orthorhombic vdW crystal α‐MoO3. In analogous to the well‐known Airy beams in free space, such Airy‐like PhPs also exhibit self‐accelerating, nonspreading, and self‐healing characteristics. Interestingly, the helical phase gradient of the vortex beam leads to asymmetry excitation of polaritons, as a result, the Airy‐like PhPs possess asymmetric propagation features even with a symmetric mode, analogous to the asymmetry hyperbolic shear polaritons in low‐symmetry crystals. The finding highlights the potential of OAM to manipulate polaritons in vdW materials, which can be further extended into a variety of applications such as active structured polaritonic devices. [ABSTRACT FROM AUTHOR]

Excessive bone resorption by osteoclasts (OCs) plays an important role in lytic bone diseases, such as osteoporosis. Although the pharmacological treatment of osteoporosis has been extensively developed, alternative treatments are still needed. Deguelin, a rotenoid isolated from several plant species, is a strong antitumor agent; however, its effect on OCs remains unclear. To the best of our knowledge, this is the first study to report that deguelin inhibits the receptor activator of nuclear factor‐κB (NF‐κB) ligand (RANKL)‐induced osteoclastogenesis, messenger RNA expression of osteoclastic‐specific genes, and osteoclastic bone resorption, in primary bone marrow‐derived macrophages. At the molecular level, deguelin markedly blocked RANKL‐induced osteoclastogenesis by attenuating the phosphorylation of NF‐κB p65 and inhibiting p65 nuclear translocation. In addition, deguelin suppressed the downstream expression of nuclear factor of activated T‐cell cytoplasmic 1, which is a crucial transcription factor in OC differentiation. Consistent with the in vitro results, deguelin inhibited lipopolysaccharide‐induced bone resorption by suppressing osteoclastogenesis. Taken together, our findings reveal that deguelin has antiosteoclastic effects in vitro and in vivo and possesses potential as a new therapeutic option for osteolytic bone diseases. Deguelin suppresses osteoclast formation and function in vitro. Deguelin impairs the receptor activator of nuclear factor‐κB (NF‐κB) ligand (RANKL)‐induced NF‐κB signaling pathway. Deguelin suppresses osteolysis in vivo. Deguelin may be used for treating osteoclast‐related diseases. [ABSTRACT FROM AUTHOR]

Summary Based on the global method, an approach is proposed to consider the effect of anchor reinforcement on slope stability, where equilibrium conditions are formulated in terms of the whole slip body. Anchor pre‐tension is assumed to be undertaken by the whole slip body instead of individual slices, causing internal force within slope more realistic. Meanwhile, the optimization model for locating the critical slip surface is of weak nonlinearity and easy to solve using the conventional optimization procedures. The effects of anchoring orientation and position are thoroughly investigated, and interesting results are obtained. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the Gynecology Imaging Reporting and Data System (GI-RADS) for diagnosis of malignant adnexal masses in a Chinese population.Methods: A retrospective study was conducted of patients who underwent evaluation of suspected adnexal masses at a hospital in Tianjin, China, between January 1, 2015, and January 31, 2016. Ultrasonographic diagnosis was based on the GI-RADS classification-a standardized summary of imaging data that estimates the risk of malignancy-and compared with the final pathological diagnosis.Results: Among 242 patients, thick wall, solid papillary projection, solid area, central blood flow, ascites, and GI-RADS classification were associated with malignancy (P<0.05 for all variables). The 263 masses evaluated were classified as GI-RADS 2 (functional cyst; n=65), GI-RADS 3 (benign neoplasm; n=68), GI-RADS 4 (one or two morphological findings suggestive of malignancy; n=101), and GI-RADS 5 (≥3 morphological findings suggestive of malignancy; n=28). Four malignant cases with false-negative findings were misclassified as GI-RADS 3, whereas 24 benign cases with false-positive findings were misclassified as GI-RADS 4. The sensitivity, specificity, false-positive rate, false-negative rate, accuracy, and Youden index of the GI-RADS classification were 96.4%, 84.3%, 18.5%, 3.0%, 89.3%, and 80.7%, respectively.Conclusion: The GI-RADS classification performed well in the diagnosis of malignant adnexal masses. [ABSTRACT FROM AUTHOR]

A bipolar junction transistor (BJT)‐based CMOS temperature sensor exploiting the piecewise BJT process spread compensation property of the base recombination current is proposed to reduce the process variations of the base–emitter voltage (Vbe). The weighted combinations of different on‐chip resistors are explored to minimise their associated process spread. Fabricated in standard 0.18‐μm CMOS, the chip prototype occupies an active area of 0.036 mm2 and draws 3 μA from a 1.2 V supply, with a measured maximum inter‐/intra‐die variation in Vbe of <1.5 mV from −40 to 125°C from two batches. Using the measured Vbe, ΔVbe and the first‐batch‐only calibration parameters, the chip prototype demonstrates an untrimmed batch‐to‐batch inaccuracy of ± 1.5°C (3σ) within the same temperature range (24 samples from 2 batches). [ABSTRACT FROM AUTHOR]

Loss of strength in human and animal models of aging can be partially attributed to a well-recognized decrease in muscle mass; however, starting at middle-age, the normalized force (force/muscle cross-sectional area) in the knee extensors and single muscle fibers declines in a curvilinear manner. Strength is lost faster than muscle mass and is a more consistent risk factor for disability and death. Reduced expression of the voltage sensor Ca2+ channel α1 subunit (Cav1.1) with aging leads to excitation-contraction uncoupling, which accounts for a significant fraction of the decrease in skeletal muscle function. We recently reported that in addition to its classical cytoplasmic location, fast skeletal muscle troponin T3 (TnT3) is fragmented in aging mice, and both full-length TnT3 (FL-TnT3) and its carboxyl-terminal (CT-TnT3) fragment shuttle to the nucleus. Here, we demonstrate that it regulates transcription of Cacna1s, the gene encoding Cav1.1. Knocking down TnT3 in vivo downregulated Cav1.1. TnT3 downregulation or overexpression decreased or increased, respectively, Cacna1s promoter activity , and the effect was ablated by truncating the TnT3 nuclear localization sequence. Further, we mapped the Cacna1s promoter region and established the consensus sequence for TnT3 binding to Cacna1s promoter. Systemic administration of BDA-410, a specific calpain inhibitor, prevented TnT3 fragmentation, and Cacna1s and Cav1.1 downregulation and improved muscle force generation in sedentary old mice. [ABSTRACT FROM AUTHOR]

The Paleoproterozoic was an important stage in the evolution of life and the environment during Earth's history. Understanding astronomical rhythms and solar system behavior in the Paleoproterozoic is often challenging. In this study, ∼190 m high‐resolution magnetic susceptibility (MS) and ∼30 m high‐resolution Ba/Al data are used to conduct cyclostratigraphic analyses of the Chuanlinggou Formation in the Yanliao Rift, North China Craton. Spectral analysis indicates significant peaks at wavelengths of 12.1–7.7, 2.8–1.6, 0.58–0.33, and 0.29–0.22 m, which matches well with the astronomical cycles predicted by Waltham for ∼1,640 Ma. A 9.9‐Myr astronomical time scale is constructed by tuning the MS series to the 405‐kyr‐long eccentricity cycle. The geological records show ∼1.56‐Myr very long eccentricity period and ∼1.0‐Myr very long obliquity period (close to 3(s4 − s3) − 2(g4 − g3) = 0) in the Paleoproterozoic. The sea‐level change curve predicted by dynamic noise models reveals a significant ∼1.0‐Myr period, indicating that sea level fluctuation may have been driven by the very long obliquity period. Bayesian inversion is used to further estimate the evolution of the ancient Earth‐Moon orbital parameters, constraining a precession rate of 87.14 ± 0.25 arcsec/year and an Earth‐Moon distance of 341,530 ± 390 km for the Paleoproterozoic Changcheng System. These results indicate that astronomical orbital forcing may have played an important role in climate and sea‐level changes in the Precambrian, increasing the understanding of the fundamentals of global sea level fluctuations, orbitally driven mechanisms and the chaotic behavior of the Precambrian solar system. Plain Language Summary: Orbital parameters and long‐term behavior have changed during geological history. For the first time, we found new resonance states between Mars and Earth (i.e., a very long eccentricity period of ∼1.56 Myr and a very long obliquity period of ∼1.0 Myr) from the geological records of the Paleoproterozoic Changcheng System in the Yanliao Rift of the North China Craton. The reconstructed sea‐level change curve shows a significant ∼1.0‐Myr period, indicating that sea level fluctuations may have been driven by the very long obliquity period in the Precambrian. The orbital parameters in the Paleoproterozoic are recovered using Ba/Al ratios, and the calculated precession constant is 87.14 ± 0.25 arcsec/year. The Earth‐Moon distance was 341,530 ± 390 km, and the length of day (LOD) was 18.06 ± 0.05 hr, which indicates that lunar recession may have been slower in deep time. These results increase the understanding of astronomical rhythms and the chaotic behavior of the solar system in the Precambrian. Key Points: A new Earth‐Mars resonance state (3(s4 − s3) − 2(g4 − g3) = 0) is revealed from the Precambrian geological recordsThe ∼1.0‐Myr very long obliquity period significantly affected sea level fluctuations under the Mesoproterozoic greenhouse climate [ABSTRACT FROM AUTHOR]

SUMMARY: Auxin is indispensable to the fertilization‐induced coordinated development of the embryo, endosperm, and seed coat. However, little attention has been given to the distribution pattern, maintenance mechanism, and function of auxin throughout the process of seed development. In the present study, we found that auxin response signals display a dynamic distribution pattern during Arabidopsis seed development. Shortly after fertilization, strong auxin response signals were observed at the funiculus, chalaza, and micropylar integument where the embryo attaches. Later, additional signals appeared at the middle layer of the inner integument (ii1′) above the chalaza and the whole inner layer of the outer integument (oi1). These signals peaked when the seed was mature, then declined upon desiccation and disappeared in the dried seed. Auxin biosynthesis genes, including ASB1, TAA1, YUC1, YUC4, YUC8, and YUC9, contributed to the accumulation of auxin in the funiculus and seed coat. Auxin efflux carrier PIN3 and influx carrier AUX1 also contributed to the polar auxin distribution in the seed coat. PIN3 was expressed in the ii1 (innermost layer of the inner integument) and oi1 layers of the integument and showed polar localization. AUX1 was expressed in both layers of the outer integument and the endosperm and displayed a uniform localization. Further research demonstrated that the accumulation of auxin in the seed coat regulates seed size. Transgenic plants that specifically express the YUC8 gene in the oi2 or ii1 seed coat produced larger seeds. These results provide useful tools for cultivating high‐yielding crops. Significance Statement: The present study revealed the dynamic auxin distribution pattern and its establishment and maintenance mechanism throughout seed development in Arabidopsis thaliana and further demonstrated that the accumulation of auxin in the seed coat regulates seed size. [ABSTRACT FROM AUTHOR]

Due to the extremely intrinsic heterogeneity among glioma patients, the outcomes of these patients are tremendously different. Therefore, the exploitation of novel biomarker classification of glioma is vitally important for deep insight into the essence and predicting the prognosis of glioma. We aim to analyze the correlation between TP73 mRNA expression, DNA methylated alteration and the prognosis of WHO grade II/III glioma, utilizing bioinformatics to evaluate its significance as a risk‐factor in predicting the prognosis of these glioma patients. The analysis found that TP73 expression was positively correlated with the grade of glioma, and showed a strong correlation with glioma molecular classification, which revealed significantly higher TP73 expression in IDH‐wildtype than in IDH‐mutant subtype of WHO grade II/III glioma. Cox regression analysis indicated that high expression of TP73 shared an independent high‐risk factor impacting the prognosis of WHO grade II/III glioma. We discovered 8 DNA promoter methylation sites with prognostic significance, which were negatively associated with TP73 expression, and positively associated with beneficial overall survival (OS) and progression‐free survival (PFS). Integrating with four independent glioma datasets, subsequent Meta‐analysis verified that low expression of TP73 was closely related to favorable OS, especially in IDH‐mutant subtype. Moreover, we found that 1p/19qCodel/TP73low subgroup shared the most favorable OS, 1p/19qNon−codel/TP73high subgroup suffered the worst OS. Meanwhile, the enrichment analysis of TP73‐related differential mRNAs demonstrated that TP73 aberration in WHO grade II/III glioma might be closely related to cell cycle and P53 signaling pathways. Finally, TP73 expression of 53 glioma specimens was measured by qRT‐PCR, which was consistent with the previous analytical result, and TP73 high‐expression subgroup suffered worse PFS than TP73 low‐expression subgroup. In summary, our funding supports that TP73 gene can perform as a reliable biomarker to evaluate the survival outcome of patients diagnosed with WHO grade II/III glioma. [ABSTRACT FROM AUTHOR]

Summary: Acute pancreatitis (AP), an inflammatory disorder of the pancreas with a high hospitalization rate, frequently leads to systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). However, therapeutic targets for effective treatment and early intervention of AP are still urgently required to be identified. Here, we have observed that the expression of pancreatic lincRNA‐EPS, a long intergenic non‐coding RNA, is dynamically changed during both caerulein‐induced AP (Cer‐AP) and sodium taurocholate‐induced severe AP (NaTc‐SAP). The expression pattern of lincRNA‐EPS is negatively correlated with the typical inflammatory genes such as IL‐6, IL‐1β, CXCL1, and CXCL2. Further studies indicate that knockout of lincRNA‐EPS aggravates the pathological symptoms of AP including more induction of serum amylase and lipase, severe edema, inflammatory cells infiltration and acinar necrosis in both experimental AP mouse models. Besides these intrapancreatic effects, lincRNA‐EPS also protects against tissue damages in the extra‐pancreatic organs such as lung, liver, and gut in the NaTc‐SAP mouse model. In addition, we have observed more serum pro‐inflammatory cytokines TNF‐α and IL‐6 in the lincRNA‐EPS‐/‐ NaTc‐SAP mice and more extracellular HMGB1 around injured acinar cells in the pancreas from lincRNA‐EPS‐/‐ NaTc‐SAP mice, compared with their respective controls. Pharmacological inhibition of NF‐κB activity by BAY11‐7082 significantly abolishes the suppressive effect of lincRNA‐EPS on TLR4 ligand‐induced inflammatory genes in macrophages. Our study has described a protective role of lincRNA‐EPS in alleviating AP and SAP, outlined a novel pathway that lincRNA‐EPS suppresses HMGB1‐NF‐κB‐dependent inflammatory response in pancreatic macrophages and provided a potential therapeutic target for SAP. [ABSTRACT FROM AUTHOR]

Osteolytic diseases are characterized by an increase in the number and/or activity of bone‐resorbing osteoclasts. Identification of natural compounds that can suppress osteoclast formation and function is crucial for the prevention and treatment of osteolytic diseases. Vitexin, a naturally‐derived flavonoid extracted from various medicinal plant species, demonstrates a broad range of pharmacological properties including anticancer and anti‐inflammatory effects. Here in this study, we showed that vitexin exerts antiosteoclastogenic effects by directly inhibiting receptor activator of nuclear factor‐κB ligand (RANKL)‐induced osteoclast formation and bone resorption in vitro and protected against lipopolysaccharide (LPS)‐induced inflammatory osteolysis in vivo. Vitexin suppressed the early activation of ERK and p38 MAPK pathways in response to RANKL thereby attenuating the downstream induction of c‐Fos and NFATc1, and abrogating the expression of osteoclast marker genes. Collectively, these results provide evidence for the therapeutic application of vitexin in the treatment of osteoclast‐mediated bone lytic diseases. [ABSTRACT FROM AUTHOR]

Osteoclasts (OCs) are multinuclear giant cells responsible for bone resorption, and an excessive bone resorption by OCs plays an important role in osteoporosis. Commonly used drugs for the treatment of osteoporosis have severe side effects. As such, identification of alternative treatments is essential. Garcinol, a polyisoprenylated benzophenone extracted from the fruit of Garcinia indica, has shown a strong antitumor effect through the nuclear factor‐κB (NF‐κB) and mitogen‐associated protein kinases (MAPK) signaling pathways. However, the role of garcinol in the osteoclastogenesis is still unclear. Here, we demonstrated that garcinol can inhibit the receptor activator of NF‐κB ligand (RANKL)‐induced osteoclastogenesis, osteoclastogenesis‐related gene expression, the f‐actin ring, and resorption pit formation. In addition, garcinol abrogated RANKL‐induced osteoclastogenesis by attenuating the degradation of the MAPK, NF‐κB, and PI3K‐AKT signaling pathway as well as downstream factors c‐jun, c‐fos, and NFATC1. In vivo, suppression of osteoclastogenesis by garcinol was evidenced by marked inhibition of lipopolysaccharide‐induced bone resorption. In conclusion, our data demonstrated that garcinol inhibited the RANKL‐induced osteoclastogenesis by suppressing the MAPK, NF‐κB, and PI3K‐AKT signaling pathways and thus has potential as a novel therapeutic option for osteolytic bone diseases. Garcinol suppresses osteoclast (OCs) formation and function in vitro. Garcinol impairs the receptor activator for the nuclear factor‐κB ligand (RANKL)‐induced mitogen‐associated protein kinases (MAPK), nuclear factor‐κB (NF‐κB), and AKT signaling pathway. Garcinol suppresses osteolysis in vivo. Garcinol may be a new therapeutic option for osteolytic bone diseases [ABSTRACT FROM AUTHOR]

Aim: Symptoms of autonomic failure are frequently the presentation of advanced age and neurodegenerative diseases that impair adaptation to common physiologic stressors. The aim of this work was to examine the interaction between the sympathetic and motor nervous system, the involvement of the sympathetic nervous system (SNS) in neuromuscular junction (NMJ) presynaptic motor function, the stability of postsynaptic molecular organization, and the skeletal muscle composition and function. Methods: Since muscle weakness is a symptom of diseases characterized by autonomic dysfunction, we studied the impact of regional sympathetic ablation on muscle motor innervation by using transcriptome analysis, retrograde tracing of the sympathetic outflow to the skeletal muscle, confocal and electron microscopy, NMJ transmission by electrophysiological methods, protein analysis, and state of the art microsurgical techniques, in C57BL6, MuRF1KO and Thy‐1 mice. Results: We found that the SNS regulates motor nerve synaptic vesicle release, skeletal muscle transcriptome, muscle force generated by motor nerve activity, axonal neurofilament phosphorylation, myelin thickness, and myofibre subtype composition and CSA. The SNS also modulates the levels of postsynaptic membrane acetylcholine receptor by regulating the Gαi2‐Hdac4‐Myogenin‐MuRF1pathway, which is prevented by the overexpression of the guanine nucleotide‐binding protein Gαi2 (Q205L), a constitutively active mutant G protein subunit. Conclusion: The SNS regulates NMJ transmission, maintains optimal Gαi2 expression, and prevents any increase in Hdac4, myogenin, MuRF1, and miR‐206. SNS ablation leads to upregulation of MuRF1, muscle atrophy, and downregulation of postsynaptic AChR. Our findings are relevant to clinical conditions characterized by progressive decline of sympathetic innervation, such as neurodegenerative diseases and aging. [ABSTRACT FROM AUTHOR]