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Traditionally, the ampacity of an overhead transmission line (OHTL) is a static value obtained based on adverse weather conditions, which constrains the transmission capacity. With the continuous growth of power system load, it is increasingly necessary to dynamically adjust the ampacity based on weather conditions. To this end, this paper models the heat balance relationship of the OHTL based on a BP neural network using Bayesian optimization (BO-BP). On this basis, an OHTL ampacity prediction method considering the model error is proposed. First, a two-stage current-stepping ampacity prediction model is established to obtain the initial ampacity prediction results. Then, the risk control strategy of ampacity prediction considering the model error is proposed to correct the ampacity based on the quartile of the model error to reduce the risk of the conductor overheating caused by the model error. Finally, a simulation is carried out based on the operation data of a 220-kV transmission line. The simulation results show that the accuracy of the BO-BP model is improved by more than 20% compared with the traditional heat balance equation. The proposed ampacity prediction method can improve the transmission capacity by more than 150% compared with the original static ampacity.

We generalize a real-space Chern number formula for gapped free fermions to higher orders. Using the generalized formula, we prove recent proposals for extracting thermal and electric Hall conductance from the ground state via the entanglement Hamiltonian in the special case of non-interacting fermions, providing a concrete example of the connection between entanglement and topology in quantum phases of matter.

Spinal cord injury (SCI) is a high incident rate of central nervous system disease that usually causes paralysis below the injured level. The occurrence of chronic inflammation with the axonal regeneration difficulties are the underlying barriers for the recovery of SCI patients. Current studies have paid attention to controlling the instigative and developmental process of neuro-inflammation. Ethyl pyruvate, as a derivative of pyruvate, has strong anti-inflammatory and neuroprotective functions. Herein, we reviewed the recent studies of ethyl pyruvate and high mobility group box-1 (HMGB1). We think HMGB1 that is one of the main nuclear protein mediators to cause an inflammatory response. This protein induces astrocytic activation, and promotes glial scar formation. Interestingly, ethyl pyruvate has potent inhibitory effects on HMGB1 protein, as it inhibits chronic inflammatory response by modulating the HMGB1/TLR4/NF-κB signaling pathway. This paper discusses the potential mechanism of ethyl pyruvate in inhibiting chronic inflammation after SCI. Ethyl pyruvate can be a prospective therapeutic agent for SCI.

Froth flotation is a commonly utilized beneficiation technique for effectively separating apatite from other gangue minerals, such as calcite. It is difficult to achieve good separation with fatty acid collectors due to their similar interactions with apatite and calcite. In this work, sodium N-lauroyl sarcosinate (SNLS) was used as the collector for the selective separation of calcite from apatite without a depressant. The experiments revealed that SNLS had a much better selectivity and a stronger affinity with calcite compared to apatite, with little effect on the flotation of apatite observed at a pH of 10. Fourier transform infrared (FTIR) analyses were conducted to explain the selective collector process of SNLS. The mechanism experiments demonstrate that SNLS can chemically bond to apatite and calcite minerals to produce Ca-NLS chelates. The active O atoms of the amide and carboxyl groups of SNLS accomplish this. Calcite has a greater Ca-reactivity than apatite, and as a result, the adsorption quantity on the calcite surface is greater than that on the apatite surface. FTIR analyses indicate that SNLS exhibits a greater affinity for the calcite surface than for apatite, a finding that is supported by first-principle density functional theory (DFT) calculations showing a higher adsorption energy of SNLS on the calcite surface. DFT calculations showed that SNLS forms stronger O-Ca bonds on the calcite surface and is less hindered by H2O. This work shows that the surfactant sodium N-lauroylsarcosinate (SNLS) can be an ideal collector for the flotation of phosphate minerals.

The complexity of central nervous system diseases together with their intricate pathogenesis complicate the establishment of effective treatment strategies. Presently, the superiority of adipose-derived mesenchymal stem cells (ADSCs) on neuronal injuries has attracted significant attention. Similarly, extracellular vesicles (EVs) are potential interventional agents that could identify and treat nerve injuries. Herein, we reviewed the potential effects of ADSCs and EVs on amyotrophic lateral sclerosis (ALS) injured nerves, and expound on their practical application in the clinic setting. This article predominantly focused on the therapeutic role of ADSCs concerning the pathogenesis of ALS, the protective and reparative effects of EVs on nerve injury, as well as the impact following the combined usage of ADSCs and EVs in ALS.

BackgroundDrug-resistance is a major obstacle to the treatment of breast cancer. Circular RNA (circRNA) circ-MMP11 has been reported to be promoting the progression of breast cancer. This study is designed to explore the role and mechanism of circ-MMP11 in lapatinib resistance in breast cancer.MethodsCirc-MMP11, microRNA-153-3p (miR-153-3p), and Anillin (ANLN) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability, number of colonies, apoptosis, migration, and invasion were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation, flow cytometry, and transwell assays, respectively. Exosomes were exerted and detected by differential centrifugation and a transmission electron microscope. The protein levels of CD63, CD9, and ANLN were assessed by western blot assay. The binding relationship between miR-153-3p and circ-MMP11 or ANLN was predicted by circinteractome or starbase, and then verified by a dual-luciferase reporter assay and RNA pull-down assay. The biological role of circ-MMP11 on breast cancer tumor growth and drug resistance was detected by the xenograft tumor model in vivo.ResultsCirc-MMP11 and ANLN were highly expressed, and miR-153-3p was decreased in LR breast cancer tissues and cells. Circ-MMP11 could be transported by exosomes. Furthermore, circ-MMP11 knockdown promoted lapatinib sensitivity by repressing cell viability, colony number, migration, invasion, and boosting apoptosis in LR breast cancer cells. Circ-MMP11 deficiency improved the drug sensitivity of breast cancer in vivo. Mechanically, circ-MMP11 could regulate ANLN expression through sponging miR-153-3p.ConclusionCirc-MMP11 could be transferred by exosomes in breast cancer cells. And circ-MMP11 functioned as a sponge of miR-153-3p to regulate ANLN expression, thereby promoting lapatinib resistance in breast cancer cells, providing therapeutic targets for the treatment of breast cancer.

Thalidomide was first marketed in 1957 but soon withdrawn because of its notorious teratogenicity. Studies on the mechanism of action of thalidomide revealed the pleiotropic properties of this class of drugs, including their anti-inflammatory, antiangiogenic and immunomodulatory activities. Based on their notable activities, thalidomide and its analogues, lenalidomide and pomalidomide, have been repurposed to treat erythema nodosum leprosum, multiple myeloma and other haematological malignancies. Thalidomide analogues were recently found to hijack CRL4CRBN ubiquitin ligase to target a number of cellular proteins for ubiquitination and proteasomal degradation. Thalidomide-mediated degradation of SALL4 and p63, transcription factors essential for embryonic development, very likely plays a critical role in thalidomide embryopathy. In this review, we provide a brief retrospective summary of thalidomide-induced teratogenesis, the mechanism of thalidomide activity, and the latest advances in the molecular mechanism of thalidomide-induced birth malformations.

Background/Aims: Resistance to trastuzumab remains a common challenge to HER-2 positive breast cancer. Up until now, the underlying mechanism of trastuzumab resistance is still unclear. tRNA-derived small non-coding RNAs, a new class of small non-coding RNA (sncRNAs), have been observed to play an important role in cancer progression. However, the relationship between tRNA-derived fragments and trastuzumab resistance is still unknown. Methods: We detected the levels of tRNA-derived fragments expression in normal breast epithelial cell lines, trastuzumab-sensitive and -resistant breast cancer cell lines using high-throughput sequencing. qRT-PCR was conducted to validate the differentially expressed fragments in serums from trastuzumab-sensitive and -resistant patients. A receiver operating characteristic (ROC) curve analysis was performed to evaluate the power of specific tRNA-derived fragments. Progression-free survival (PFS) was analyzed using Cox-regression. Results: Our sequence results showed that tRNA-derived fragments were differentially expressed in the HBL-100, SKBR3, and JIMT-1 cell lines. tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN were found significantly upregulated in trastuzumab-resistant patients compared to sensitive individuals, and the ROC analysis showed that tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN were correlated with trastuzumab resistance. In a multivariate analysis, higher levels of tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN expression were associated with significantly shorter PFS in patients with metastatic HER-2 positive breast cancer. Conclusion: Our results suggest that tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN play important roles in trastuzumab resistance. Patients with high levels of tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN expression benefitted less from trastuzumab-based therapy than those that express lower-levels of these molecules. tRF-30-JZOYJE22RR33 and tRF-27-ZDXPHO53KSN may be potential biomarkers and intervention targets in the clinical treatment of trastuzumab-resistant breast cancer.

Abstract Background X-linked lymphoproliferative syndrome type 1 (XLP1) is an X-linked recessive genetic disorder with a strong resemblance to hemophagocytic lymphohistiocytosis (HLH). Causative mutations for XLP1 have been identified in SH2D1A, located on chromosome Xq25. Case presentation We report a case of an 18-month-old male with a novel nonsense mutation in SH2D1A. The patient presented the typical phenotype of HLH, including splenomegaly and hemophagocytosis in the bone marrow. Thus, he was initially diagnosed with HLH based on HLH-2004 guidelines. High-throughput amplicon sequencing was performed to detect mutations in the most commonly reported causative genes of HLH, i.e., PRF1, UNC13D, STX11, STXBP2, SH2D1A, and XIAP. A likely pathogenic nonsense mutation was detected in SH2D1A (NM_002351.4:c.300T>A). The mutation was inherited from the patient’s mother, and an X-linked recessive mode of inheritance was confirmed by a two-generation pedigree analysis based on Sanger sequencing results. Conclusions The nonsense mutation in SH2D1A (NM_002351.4:c.300T>A) was reported for the first time in a case of XLP1 and was considered to be likely pathogenic based on the truncation of the mRNA sequence. This finding expands the spectrum of known XLP-related mutations in Chinese patients and indicates the utility of amplicon sequencing for XLP and HLH diagnosis.

Abstract Background Fusion genes generated from chromosomal translocation play an important role in hematological malignancies. Detection of fusion genes currently employ use of either conventional RT-PCR methods or fluorescent in situ hybridization (FISH), where both methods involve tedious methodologies and require prior characterization of chromosomal translocation events as determined by cytogenetic analysis. In this study, we describe a real-time quantitative reverse transcription PCR (qRT-PCR)-based multi-fusion gene screening method with the capacity to detect 22 fusion genes commonly found in leukemia. This method does not require pre-characterization of gene translocation events, thereby facilitating immediate diagnosis and therapeutic management. Methods We performed fluorescent qRT-PCR (F-qRT-PCR) using a commercially-available multi-fusion gene detection kit on a patient cohort of 345 individuals comprising 108 cases diagnosed with acute myeloid leukemia (AML) for initial evaluation; remaining patients within the cohort were assayed for confirmatory diagnosis. Results obtained by F-qRT-PCR were compared alongside patient analysis by cytogenetic characterization. Results Gene translocations detected by F-qRT-PCR in AML cases were diagnosed in 69.4% of the patient cohort, which was comparatively similar to 68.5% as diagnosed by cytogenetic analysis, thereby demonstrating 99.1% concordance. Overall gene fusion was detected in 53.7% of the overall patient population by F-qRT-PCR, 52.9% by cytogenetic prediction in leukemia, and 9.1% in non-leukemia patients by both methods. The overall concordance rate was calculated to be 99.0%. Fusion genes were detected by F-qRT-PCR in 97.3% of patients with CML, followed by 69.4% with AML, 33.3% with acute lymphoblastic leukemia (ALL), 9.1% with myelodysplastic syndromes (MDS), and 0% with chronic lymphocytic leukemia (CLL). Conclusions We describe the use of a F-qRT-PCR-based multi-fusion gene screening method as an efficient one-step diagnostic procedure as an effective alternative to lengthy conventional diagnostic procedures requiring both cytogenetic analysis followed by targeted quantitative reverse transcription (qRT-PCR) methods, thus allowing timely patient management.

Abstract Background Long noncoding RNAs (lncRNAs) have emerged as critical regulators in a variety of human cancers, including gastric cancer (GC). However, the function and mechanisms responsible for these molecules in GC are not fully understood. In our previous study, we found that GC associated lncRNA HOXA11-AS is significantly upregulated in GC tissues. Over-expressed HOXA11-AS promotes GC cells proliferation and invasion through scaffolding the chromatin modification factors PRC2, LSD1 and DNMT1. Methods HOXA11-AS expression levels in GC cells was detected by quantitative real-time PCR (qPCR). HOXA11-AS siRNAs and overexpression vector were transfected into GC cells to down-regulate or up-regulate HOXA11-AS expression. In vitro and in vivo assays were performed to investigate the functional role of HOXA11-AS in GC cells cell cycle progression, invasion and metastasis. RIP and ChIP assays were used to determine the mechanism of HOXA11-AS’s regulation of underlying targets. Results We found that knockdown of HOXA11-AS induced GC cells G0/G1 phase arrest and suppressed GC cells migration, invasion and metastasis in vivo. Moreover, mechanistic investigation showed that HOXA11-AS could interact with WDR5 and promote β-catenin transcription, bind with EZH2 and repress P21 transcription, and induce KLF2 mRNA degradation via interacting with STAU1. Conclusions Taken together, these findings show that HOXA11-AS not only could promote GC cells migration and invasion in vitro, but also promotes GC cells metastasis in vivo, at least in part, by regulating β-catenin and KLF2.

In this paper and its upcoming sequel, we study nonequilibrium dynamics in driven (1+1)-dimensional conformal field theories (CFTs) with periodic, quasiperiodic, and random driving. We study a soluble family of drives in which the Hamiltonian only involves the energy-momentum density spatially modulated at a single wavelength. The resulting time evolution is then captured by a Möbius coordinate transformation. In this paper, we establish the general framework and focus on the first two classes. In periodically driven CFTs, we generalize earlier work and study the generic features of entanglement and energy evolution in different phases, i.e., the heating and nonheating phases and the phase transition between them. In quasiperiodically driven CFTs, we mainly focus on the case of driving with a Fibonacci sequence. We find that (i) the nonheating phases form a Cantor set of measure zero; (ii) in the heating phase, the Lyapunov exponents (which characterize the growth rate of the entanglement entropy and energy) exhibit self-similarity, and can be arbitrarily small; (iii) the heating phase exhibits periodicity in the location of spatial structures at the Fibonacci times; (iv) one can find exactly the nonheating fixed point, where the entanglement entropy and energy oscillate at the Fibonacci numbers, but grow logarithmically and polynomially at the non-Fibonacci numbers; (v) for certain choices of driving Hamiltonians, the nonheating phases of the Fibonacci driving CFT can be mapped to the energy spectrum of electrons propagating in a Fibonacci quasicrystal. In addition, another quasiperiodically driven CFT with an Aubry-André–type sequence is also studied. We compare the CFT results to lattice calculations and find remarkable agreement.

In this work, we study non-equilibrium dynamics in Floquet conformal field theories (CFTs) in 1+1D, in which the driving Hamiltonian involves the energy-momentum density spatially modulated by an arbitrary smooth function. This generalizes earlier work which was restricted to the sine-square deformed type of Floquet Hamiltonians, operating within a $\mathfrak{sl}_2$ sub-algebra. Here we show remarkably that the problem remains soluble in this generalized case which involves the full Virasoro algebra, based on a geometrical approach. It is found that the phase diagram is determined by the stroboscopic trajectories of operator evolution. The presence/absence of spatial fixed points in the operator evolution indicates that the driven CFT is in a heating/non-heating phase, in which the entanglement entropy grows/oscillates in time. Additionally, the heating regime is further subdivided into a multitude of phases, with different entanglement patterns and spatial distribution of energy-momentum density, which are characterized by the number of spatial fixed points. Phase transitions between these different heating phases can be achieved simply by changing the duration of application of the driving Hamiltonian. We demonstrate the general features with concrete CFT examples and compare the results to lattice calculations and find remarkable agreement.

We study the energy and entanglement dynamics of (1+1)D conformal field theories (CFTs) under a Floquet drive with the sine-square deformed (SSD) Hamiltonian. Previous work has shown that this model supports both a nonheating and a heating phase. Here, we analytically establish several robust and “superuniversal” features of the heating phase which rely on conformal invariance but not on the details of the CFT involved. First, we show the energy density is concentrated in two peaks in real space, a chiral and an antichiral peak, which leads to an exponential growth in the total energy. The peak locations are set by fixed points of the Möbius transformation. Second, all of the quantum entanglement is shared between these two peaks. In each driving period, a number of Bell pairs are generated, with one member pumped to the chiral peak and the other member pumped to the antichiral peak. These Bell pairs are localized, accumulate at these two peaks, and can serve as a source of quantum entanglement. Third, in both the heating and nonheating phases, we find that the total energy is related to the half system entanglement entropy by a simple relation E(t)∝cexp[(6/c)S(t)] with c being the central charge. In addition, we show that the nonheating phase, in which the energy and entanglement oscillate in time, is unstable to small fluctuations of the driving frequency in contrast to the heating phase. Finally, we point out an analogy to the periodically driven harmonic oscillator which allows us to understand global features of the phases and introduce a quasiparticle picture to explain the spatial structure, which can be generalized to setups beyond the SSD construction.

The idea of the out-of-time-order correlator (OTOC) has recently emerged in the study of both condensed matter systems and gravitational systems. It not only plays a key role in investigating the holographic duality between a strongly interacting quantum system and a gravitational system, it also diagnoses the chaotic behavior of many-body quantum systems and characterizes information scrambling. Based on OTOCs, three different concepts—quantum chaos, holographic duality, and information scrambling—are found to be intimately related to each other. Despite its theoretical importance, the experimental measurement of the OTOC is quite challenging, and thus far there is no experimental measurement of the OTOC for local operators. Here, we report the measurement of OTOCs of local operators for an Ising spin chain on a nuclear magnetic resonance quantum simulator. We observe that the OTOC behaves differently in the integrable and nonintegrable cases. Based on the recent discovered relationship between OTOCs and the growth of entanglement entropy in the many-body system, we extract the entanglement entropy from the measured OTOCs, which clearly shows that the information entropy oscillates in time for integrable models and scrambles for nonintgrable models. With the measured OTOCs, we also obtain the experimental result of the butterfly velocity, which measures the speed of correlation propagation. Our experiment paves a way for experimentally studying quantum chaos, holographic duality, and information scrambling in many-body quantum systems with quantum simulators.

Chromosomal aberrations are useful in assessing treatment options and clinical outcomes of acute myeloid leukemia (AML) patients. However, 40 ∼ 50% of the AML patients showed no chromosomal abnormalities, i.e., with normal cytogenetics aka the CN-AML patients. Testing of molecular aberrations such as FLT3 or NPM1 can help to define clinical outcomes in the CN-AML patients but with various successes. Goal of this study was to test the possibility of Wilms' tumor 1 (WT1) gene overexpression as an additional molecular biomarker. A total of 103 CN-AML patients, among which 28% had overexpressed WT1, were studied over a period of 38 months. Patient's response to induction chemotherapy as measured by the complete remission (CR) rate, disease-free survival (DFS) and overall survival (OS) were measured. Our data suggested that WT1 overexpression correlated negatively with the CR rate, DFS and OS. Consistent with previous reports, CN-AML patients can be divided into three different risk subgroups based on the status of known molecular abnormalities, i.e., the favorable (NPM1(mt)/no FLT3(ITD)), the unfavorable (FLT3(ITD)) and the intermediate risk subgroups. The WT1 overexpression significantly reduced the CR, DFS and OS in both the favorable and unfavorable groups. As the results, patients with normal WT1 gene expression in the favorable risk group showed the best clinical outcomes and all survived with complete remission and disease-free survival over the 37 month study period; in contrast, patients with WT1 overexpression in the unfavorable risk group displayed the worst clinical outcomes. WT1 overexpression by itself is an independent and negative indicator for predicting CR rate, DFS and OS of the CN-AML patients; moreover, it increases the statistical power of predicting the same clinical outcomes when it is combined with the NPM1(mt) or the FLT3(ITD) genotypes that are the good or poor prognostic markers of CN-AML.

Abstract Introduction Atopic dermatitis (AD) is a chronic immuno-inflammatory skin disease. Crisaborole ointment, 2%, is a nonsteroidal phosphodiesterase 4 inhibitor approved for the treatment of mild to moderate AD. This post hoc analysis assesses the efficacy and safety of crisaborole in Chinese patients aged ≥ 2 years with mild to moderate AD. Methods We evaluated the efficacy and safety of crisaborole in Chinese patients from the vehicle-controlled, phase 3 CrisADe CLEAR study. Patients were randomly assigned 2:1 to receive crisaborole or vehicle twice daily, respectively, for 28 days. The primary endpoint was percent change from baseline in Eczema Area and Severity Index (EASI) total score at day 29. Key secondary endpoints were improvement in Investigator’s Static Global Assessment (ISGA), ISGA success, and change from baseline in weekly average Peak Pruritus Numerical Rating Scale (PP-NRS) score. Adverse events were documented. Results Of 391 patients in the overall study, 237 were from China, 157 assigned to crisaborole and 80 assigned to vehicle. A greater reduction in percent change from baseline in EASI total score at day 29 was shown in the crisaborole vs. vehicle group (least squares mean [LSM]: −66.34 [95% (confidence interval) CI −71.55 to −61.12] vs. −50.18 [95% CI −58.02 to −42.34]). Response rates for achievement of ISGA improvement (43.2% [95% CI 35.4–51.1] vs. 33.4% [95% CI 22.5–44.2]) and ISGA success (31.7% [95% CI 24.3–39.0] vs. 21.5% [95% CI 12.1–30.9]) at day 29 were higher in the crisaborole vs. vehicle group. A greater reduction in change from baseline in weekly average PP-NRS score at week 4 was observed in the crisaborole vs. vehicle group (LSM: −1.98 [95% CI −2.34 to −1.62] vs. −1.08 [95% CI −1.63 to −0.53]). No new safety signals were observed. Conclusion Crisaborole was effective and well tolerated in Chinese patients aged ≥ 2 years with mild to moderate AD. Trial Registration ClinicalTrials.gov, NCT04360187.

Abstract Background Hypopharyngeal squamous cell carcinoma (HPSCC) has the worst prognosis among all head-and-neck cancers, and treatment options are limited. Tumor microenvironment (TME) analysis can help identify new therapeutic targets and combined treatment strategies. Methods Six primary HPSCC tissues and two adjacent normal mucosae from six treatment-naïve patients with HPSCC were analyzed using scRNA-seq. Cell types were curated in detail, ecosystemic landscapes were mapped, and cell–cell interactions were inferred. Key results were validated with The Cancer Genome Atlas and cell biology experiments. Results Malignant HPSCC epithelial cells showed significant intratumor heterogeneity. Different subtypes exhibited distinct histological features, biological behaviors, and spatial localization, all affecting treatment selection and prognosis. Extracellular matrix cancer-associated fibroblasts (mCAFs) expressing fibroblast activation protein were the dominant CAFs in HPSCC tumors. mCAFs, constituting an aggressive CAF subset, promoted tumor cell invasion, activated endothelial cells to trigger angiogenesis, and synergized with SPP1+ tumor associated macrophages to induce tumor progression, ultimately decreasing the overall survival of patients with HPSCC. Moreover, the LAMP3+ dendritic cell subset was identified in HPSCC and formed an immunosuppressive TME by recruiting Tregs and suppressing CD8+ T cell function. Conclusions mCAFs, acting as the communication center of the HPSCC TME, enhance the invasion ability of HPSCC cells, mobilizing surrounding cells to construct a tumor-favorable microenvironment. Inhibiting mCAF activation offers a new anti-HPSCC therapeutic strategy. Graphical Abstract Video Abstract

Objectives. Despite the efficacy of surgical treatments, the high rate of recurrence in juvenile nasopharyngeal angiofibroma (JNA) after surgery remains an unresolved problem. The present study comprehensively analyzed the risk factors and characteristics of JNA recurrence, providing clinical guidance for reducing recurrence. Methods. A total of 123 patients who underwent surgery for JNA between 1997 and 2019 at a single hospital were analyzed retrospectively. Univariate and multivariate analyses were used to assess the clinical risk factors for the recurrence of JNA. The relapse-free survival and annual cumulative recurrence rates were analyzed for subgroups defined according to clinical parameters. Results. After screening, 78 of the 123 patients were included in the present study. The main risk factors associated with JNA recurrence included the year of diagnosis, tumor size, sphenoid bone invasion, Radkowski stage, surgical approach, and intraoperative bleeding. Importantly, the surgical approach and sphenoid bone invasion were independent prognostic factors affecting recurrence. Patients who underwent endoscopic surgery without sphenoid bone invasion exhibited longer relapse-free survival. In the present study, the overall cumulative recurrence rate of JNA was 38.7%, and recurrence occurred mainly in the first year after the initial surgery. Conclusion. Endoscopic surgery achieved better relapse-free survival in JNA patients, and patients with sphenoid bone invasion should be carefully explored to avoid residual JNA. The recurrence rate of JNA differed among subgroups defined based on clinical parameters and was highest in the first year after surgery. Computed tomography or magnetic resonance imaging, along with close follow-up, should be performed strictly within 1 year after the primary operation.

Flotation using sea water has been considered as a promising alternative to concentrate molybdenite (MoS2) under alkaline conditions due to scarcity of fresh water and increasingly strict regulations on the quality of discharged water. However, the MoS2 recovery with sea water during flotation has not been satisfactory, owing to the depressing effects from the hydrophilic metallic species onto MoS2 surface. This study combines experimental and theoretical studies of MoS2 flotation to investigate how the physicochemical properties of MoS2 vary with the addition of a dispersant, sodium hexametaphosphate (SHMP), and in sea and fresh water. Our experimental results show that the addition of SHMP during flotation has increased the recovery of MoS2, via reducing the adsorption of the hydrophilic metallic precipitation onto MoS2 surface. The DLVO calculation confirms that the addition of SHMP increases the floatability of MoS2 by dispersing the formed hydrophilic metallic precipitation (Mg(OH)2 colloids) from the MoS2 surface, via reversing attraction force to repulsion force, thereby improving MoS2 flotation recovery. [ABSTRACT FROM AUTHOR]

Our study mainly investigated ubiquitin-specific protease 4 (USP4) expression in pathogenesis of esophageal cancer. The data showed significantly increased expression of USP4 in cancer tissues compared to that in para-carcinoma tissues (68.38% ± 25.60% vs 13.04% ± 9.95%, P = 0.000) and positive correlation between USP4 and pathology grade (r = 0.249, P = 0.014), although survival analysis revealed that USP4 expression was positively associated with the prognosis (32.4% vs 10.9%, P = 0.043). Grouped analysis revealed that the prognosis of patients with high USP4 expression were significantly better only in the small tumor subgroup (diameter ≤ 5 cm) (52.6% VS 8.6%, P = 0.001) and the early stage subgroup (stages 1 and 2) (60.0% VS 16.7%, P = 0.006). Moreover, in the subgroup of clinical stages 1 and 2 with tumor diameter ≤ 5 cm, high USP4 expression prolonged the survival time of esophageal cancer patients more significantly (75.5% VS 5.9%, P = 0.000). Based on these results, we speculated that it was possible to significantly improve the prognosis of patients with low USP4 expression by targeted therapy in early esophageal cancer. Taken together, our study uncovered a previously unknown function of USP4 in esophageal cancer and more investigations would be carried out to further study its regulation gene network and molecular biological mechanism in esophageal cancer. [ABSTRACT FROM AUTHOR]

Background: BCR-ABL1 fusion proteins contain constitutively active tyrosine kinases that are potential candidates for targeted therapy with tyrosine kinase inhibitors such as imatinib in chronic myeloid leukemia (CML). However, uncharacterized BCR-ABL1 fusion genes can be missed by quantitative RT-PCR (qRT-PCR)-based routine screening methods, causing adverse effect on drug selection and treatment outcome. Case presentation: In this study, we demonstrated that the next-generation sequencing (NGS) can be employed to overcome this obstacle. Through NGS, we identified a novel BCR-ABL1 fusion gene with breakpoints in the BCR intron 14 and the ABL1 intron 2, respectively, in a rare case of CML. Its mRNA with an e14a3 junction was then detected using customized RT-PCR followed by Sanger sequencing. Subsequently, the patient received targeted medicine imatinib initially at 400 mg/day, and later 300 mg/day due to intolerance reactions. With this personalized treatment, the patient's condition was significantly improved. Interestingly, this novel fusion gene encodes a fusion protein containing a compromised SH3 domain, which is usually intact in the majority of CML cases, suggesting that dysfunctional SH3 domain may be associated with altered drug response and unique clinicopathological manifestations observed in this patient. Conclusion: We identified a novel BCR-ABL1 fusion gene using NGS in a rare case of CML while routine laboratory procedures were challenged, demonstrating the power of NGS as a diagnostic tool for detecting novel genetic mutations. Moreover, our new finding regarding the novel fusion variant will provide useful insights to improve the spectrum of the genomic abnormalities recognizable by routine molecular screening. [ABSTRACT FROM AUTHOR]

Abstract Background Laryngeal squamous cell carcinoma (LSCC) is considered to be a common malignancy of the head and neck with poor prognosis for its late diagnosis, metastasis and recurrence. Growing evidence demonstrates that the dysregulation of miR-29c-3p (microRNA-29c-3p) plays an important role in various tumor processes. Our study investigates the expression of miR-29c-3p in LSCC and analyzes the correlation of its dysregulation with clinicopathologic parameters and prognosis. Methods The expression of hsa-miR-29c-3p in LSCC tissues and the adjacent normal laryngeal tissues was detected in 96 LSCC formalin-fixed paraffin-embedded tissues by quantitative real-time PCR (qRT-PCR). The SPSS statistical software package (17.0) was used to analyze the associations between miR-29c-3p expressions and various clinicopathological characteristics. The overall survival (OS) was analyzed by the Kaplan-Meier method and log-rank test, and we analyzed the independent factor of prognosis by Cox proportional hazard analysis. Results A downregulation of miR-29c-3p expression in LSCC was significantly correlated with smoking index, tumor size, tumor site, differentiation, T classification, TNM stage, and lymph node metastasis (P 0.05). In the multivariate survival analysis, low miR-29c-3p expression was associated with shorter overall survival (P

Memristive behaviors are demonstrated in the single-layer oxide-based devices. The conduction states can be continually modulated with different pulses or voltage sweeps. Here, the p-CuAlO2- and n-ZnO-based memristors show the opposite bias polarity dependence with the help of tip electrode. It is well known that the conductivity of p-type and n-type semiconductor materials has the opposite oxygen concentration dependence. Thus, the memristive behaviors may attribute to the oxygen ion migration in the dielectric layers for the single-layer oxide based memristors. Further, based on the redox, the model of compressing dielectric layer thickness has been proposed to explain the memristive behavior.

Malignant melanoma is an aggressive skin cancer with a high mortality rate. Nucleolar protein 14 (NOP14) has been implicated in cancer development. However, the role of NOP14 in malignant melanoma progression remains largely unclear. In this study, we observed that malignant melanoma tissue showed NOP14 down-regulation compared to melanocytic nevi tissues. Moreover, we observed that NOP14 expression was significantly associated with melanoma tumor thickness and lymph node metastasis. NOP14 overexpression in melanoma cells suppressed proliferation, caused G1 phase arrest, promoted apoptosis, and inhibited melanoma cell migration and invasion. Further investigations revealed that NOP14 overexpression reduced the expression levels of Wnt3a, β-catenin, and GSK-3β of the Wnt/β-catenin pathway. In summary, we demonstrated that NOP14 inhibited melanoma cell proliferation and metastasis by regulating the Wnt/β-catenin signaling pathway.

The Sachdev-Ye-Kitaev (SYK) model is a concrete solvable model to study non-Fermi liquid properties, holographic duality, and maximally chaotic behavior. In this work, we consider a generalization of the SYK model that contains two SYK models with a different number of Majorana modes coupled by quadratic terms. This model is also solvable, and the solution shows a zero-temperature quantum phase transition between two non-Fermi liquid chaotic phases. This phase transition is driven by tuning the ratio of two mode numbers, and a nonchaotic Fermi liquid sits at the critical point with an equal number of modes. At a finite temperature, the Fermi liquid phase expands to a finite regime. More intriguingly, a different non-Fermi liquid phase emerges at a finite temperature. We characterize the phase diagram in terms of the spectral function, the Lyapunov exponent, and the entropy. Our results illustrate a concrete example of the quantum phase transition and critical behavior between two non-Fermi liquid phases. [ABSTRACT FROM AUTHOR]

In this sequel (to [Phys. Rev. Res. 3, 023044(2021)], arXiv:2006.10072), we study randomly driven $(1+1)$ dimensional conformal field theories (CFTs), a family of quantum many-body systems with soluble non-equilibrium quantum dynamics. The sequence of driving Hamiltonians is drawn from an independent and identically distributed random ensemble. At each driving step, the deformed Hamiltonian only involves the energy-momentum density spatially modulated at a single wavelength and therefore induces a M\"obius transformation on the complex coordinates. The non-equilibrium dynamics is then determined by the corresponding sequence of M\"obius transformations, from which the Lyapunov exponent $\lambda_L$ is defined. We use Furstenberg's theorem to classify the dynamical phases and show that except for a few \emph{exceptional points} that do not satisfy Furstenberg's criteria, the random drivings always lead to a heating phase with the total energy growing exponentially in the number of driving steps $n$ and the subsystem entanglement entropy growing linearly in $n$ with a slope proportional to central charge $c$ and the Lyapunov exponent $\lambda_L$. On the contrary, the subsystem entanglement entropy at an exceptional point could grow as $\sqrt{n}$ while the total energy remains to grow exponentially. In addition, we show that the distributions of the operator evolution and the energy density peaks are also useful characterizations to distinguish the heating phase from the exceptional points: the heating phase has both distributions to be continuous, while the exceptional points could support finite convex combinations of Dirac measures depending on their specific type. In the end, we compare the field theory results with the lattice model calculations for both the entanglement and energy evolution and find remarkably good agreement.

Motivated by the recent studies of out-of-time-order correlation functions and the holographic duality, we propose the quantum critical point conjecture, which is stated as: For a many-body quantum system with a quantum phase transition, the Lyapunov exponent extracted from the out-of-time-order correlators will exhibit a maximum around the quantum critical region. We first demonstrate that the Lyapunov exponent is well defined in the one-dimensional Bose-Hubbard model with the help of the out-of-time-order correlation-Rényi-entropy theorem. We then support the conjecture by numerically computing the out-of-time-order correlators. We also compute the butterfly velocity, and propose an experiment protocol of measuring this correlator without inverting the Hamiltonian. [ABSTRACT FROM AUTHOR]