Explore the vast range of titles available.

Optical control of structural and electronic properties of Weyl semimetals allows development of switchable and dissipationless topological devices at the ultrafast scale. An unexpected orbital-selective photoexcitation in type-II Weyl material WTe 2 is reported under linearly polarized light (LPL), inducing striking transitions among several topologically-distinct phases mediated by effective electron-phonon couplings. The symmetry features of atomic orbitals comprising the Weyl bands result in asymmetric electronic transitions near the Weyl points, and in turn a switchable interlayer shear motion with respect to linear light polarization, when a near-infrared laser pulse is applied. Consequently, not only annihilation of Weyl quasiparticle pairs, but also increasing separation of Weyl points can be achieved, complementing existing experimental observations. In this work, we provide a new perspective on manipulating the Weyl node singularity and coherent control of electron and lattice quantum dynamics simultaneously. Photoexcitation in Weyl semimetals is recently reported to induce topological phase transitions useful for ultrafast switching devices. Here, the authors predict that the symmetry of the atomic orbitals comprising the Weyl bands in response to linear light polarization allows for not only annihilation but also separation of Weyl quasiparticles.

Strong electron correlation can induce Mott insulating behaviour and produce intriguing states of matter such as unconventional superconductivity and quantum spin liquids. Recent advances in van der Waals material synthesis enable the exploration of Mott systems in the two-dimensional limit. Here we report characterization of the local electronic properties of single- and few-layer 1T-TaSe 2 via spatial- and momentum-resolved spectroscopy involving scanning tunnelling microscopy and angle-resolved photoemission. Our results indicate that electron correlation induces a robust Mott insulator state in single-layer 1T-TaSe 2 that is accompanied by unusual orbital texture. Interlayer coupling weakens the insulating phase, as shown by reduction of the energy gap and quenching of the correlation-driven orbital texture in bilayer and trilayer 1T-TaSe 2 . This establishes single-layer 1T-TaSe 2 as a useful platform for investigating strong correlation physics in two dimensions. The electrons that contribute to the Mott insulator state in single-layer 1T-TaSe2 are shown to also have a rich variation in their orbital occupation. As more layers are added, both the insulating state and orbital texture weaken.

Circulating tumor DNA (ctDNA) has potential as a promising biomarker for molecular residual disease (MRD) detection in lung cancer. As the next‐generation sequencing standardized panel for ctDNA detection emerges, its clinical utility needs to be validated. We prospectively recruited 184 resectable lung cancer patients from four medical centers. Serial postoperative ctDNAs were analyzed by a standardized panel. A total of 427 postoperative plasma samples from 177 eligible patients were enrolled. ctDNA positivity after surgery was an independent predictor for disease recurrence and preceded radiological recurrence by a median of 6.6 months (range, 0.7–27.0 months). ctDNA‐positive or ‐negative patients with tumors of any stage had similar disease‐free survival (DFS). Patients who received targeted therapy had significantly improved DFS than those not receiving adjuvant therapy or receiving chemotherapy, regardless of baseline/preadjuvant ctDNA status. According to whether the ctDNA variants were detected in its matched tissue, they were classified into tissue derived and non‐tissue derived. Patients with detectable postoperative ctDNA with tissue‐derived mutations had comparable DFS with those with non‐tissue‐derived mutations. Collectively, we demonstrated that postoperative ctDNA has the potential to stratify prognosis and optimize tumor stage in resectable lung cancer. ctDNA variants not identified in tissue samples should be considered in MRD test. Here, we examined the clinical utility of a standardized panel‐based circulating tumor DNA (ctDNA) test approach in 177 patients with resectable lung cancer. Our data demonstrated a significant correlation between postoperative ctDNA positivity and disease recurrence. Postoperative ctDNA positivity can further separate patients at high risk of recurrence in same tumor stage group. Postoperative ctDNA has the potential to stratify prognosis and optimize tumor stage in resectable lung cancer.

Background The physiological effects of prone ventilation in ARDS patients have been discussed for a long time but have not been fully elucidated. Electrical impedance tomography (EIT) has emerged as a tool for bedside monitoring of pulmonary ventilation and perfusion, allowing the opportunity to obtain data. This study aimed to investigate the effect of prone positioning (PP) on ventilation–perfusion matching by contrast-enhanced EIT in patients with ARDS. Design Monocenter prospective physiologic study. Setting University medical ICU. Patients Ten mechanically ventilated ARDS patients who underwent PP. Interventions We performed EIT evaluation at the initiation of PP, 3 h after PP initiation and the end of PP during the first PP session. Measurements and main results The regional distribution of ventilation and perfusion was analyzed based on EIT images and compared to the clinical variables regarding respiratory and hemodynamic status. Prolonged prone ventilation improved oxygenation in the ARDS patients. Based on EIT measurements, the distribution of ventilation was homogenized and dorsal lung ventilation was significantly improved by PP administration, while the effect of PP on lung perfusion was relatively mild, with increased dorsal lung perfusion observed. The ventilation–perfusion matched region was found to increase and correlate with the increased PaO 2 /FiO 2 by PP, which was attributed mainly to reduced shunt in the lung. Conclusions Prolonged prone ventilation increased dorsal ventilation and perfusion, which resulted in improved ventilation–perfusion matching and oxygenation. Trial registration : ClinicalTrials.gov, NCT04725227. Registered on 25 January 2021.

The role of corticosteroids in acute lung injury (ALI) remains uncertain. This study aims to determine the underlying mechanisms of corticosteroid treatment for lipopolysaccharide (LPS)‐induced inflammation and ALI. We used corticosteroid treatment for LPS‐induced murine ALI model to investigate the effect of corticosteroid on ALI in vivo. Moreover, LPS‐stimulated macrophages were used to explore the specific anti‐inflammatory effects of corticosteroids on NLRP3‐inflammasome in vitro. We found corticosteroids attenuated LPS‐induced ALI, which manifested in reduction of the alveolar structure destruction, the infiltration of neutrophils and the inflammatory cytokines release of interleukin‐1β (IL‐1β) and interleukin‐18 (IL‐18) in Lung. In vitro, when NLRP3‐inflammasome was knocked out, inflammatory response of caspase‐1 activation and IL‐1β secretion was obviously declined. Further exploration, our results showed that when corticosteroid preprocessed macrophages before LPS primed, it obviously inhibited the activation of caspase‐1 and the maturation of IL‐1β, which depended on inhibiting the nuclear factor‐κB (NF‐κB) signal pathway activation. However, when corticosteroids intervened the LPS‐primed macrophages, it also negatively regulated NLRP3‐inflammasome activation through suppressing mitochondrial reactive oxygen species (mtROS) production. Our results revealed that corticosteroids played a protection role in LPS‐induced inflammation and ALI by suppressing both NF‐κB signal pathway and mtROS‐dependent NLRP3 inflammasome activation.

Aim Soil abiotic and biotic conditions are often spatially variable, challenging plants with a heterogeneous environment consisting of favorable and unfavorable patches of soil. Many stoloniferous clonal plants can escape from unfavorable patches by elongating stolon internodes, but aggregate in favorable ones through shortening stolon internodes. However, whether the connected mother and daughter ramets of these plants can use their stolons to respond to plant-soil feedbacks (PSFs) is largely unknown. Methods In the conditioning phase, we grew either Hydrocotyle vulgaris or Glechoma longituba clonal plants separately in mesocosms to condition bulk soil. In the feedback phase, we grew connected mother and daughter ramets of each species in soil inoculated with the unsterilized or sterilized soil conditioned by conspecifics. We grew the plants for 12 weeks and measured the growth of the mother and daughter ramets separately. Results The daughter ramets of H. vulgaris produced more biomass, greater number of ramets and longer stolon internodes when grown in soil with sterilized inocula than with unsterilized inocula. However, no difference was found for the daughter ramets of G. longituba . In general, for both species, soil inoculum treatment on the mother ramet did not influence the performance of daughter or mother ramets. Conclusions We conclude that biotic PSFs differed not only among different species, but also in physically-connected ramets of the same clone. Moreover, physiological integration or plasticity in stolon internode lengths cannot help H. vulgaris alleviate the negative effects of PSFs.

Great progress has been made in the field of tumor immunotherapy in the past decade. However, the therapeutic effects of immune checkpoint blockade (ICB) against ovarian cancer are still limited. Recently, an inhibitor of cyclin-dependent kinases 4 and 6 (CDK4/6i) has been reported to enhance antitumor immunity in preclinical models. The combined use of CDK4/6i and ICB may be beneficial, but the effects of CDK4/6is on the tumor immune microenvironment and whether they can synergize with ICB in treating ovarian cancer remain unknown. In this study, we first assessed the antitumor efficacy of abemaciclib, an FDA-approved CDK4/6i, in a syngeneic murine ovarian cancer model. Then, immunohistochemistry, immunofluorescence and flow cytometry were performed to evaluate the number, proportion, and activity of tumor-infiltrating lymphocytes. Cytokine and chemokine production was detected both and by PCR array analysis and cytokine antibody arrays. The treatment efficacy of combined abemaciclib and anti-PD-1 therapy was evaluated , and CD8+ and CD4+ T cell activities were analyzed using flow cytometry. Lastly, the requirement for both CD8+ T cells and B cells in combination treatment was evaluated and potential cellular mechanisms were further analyzed by flow cytometry. We observed that abemaciclib monotherapy could enhance immune infiltration, especially CD8+ T cell and B cell infiltration, in the ID8 murine ovarian cancer model. Immunophenotyping analysis showed that abemaciclib induced a proinflammatory immune response in the tumor microenvironment. PCR array analysis suggested the presence of a Th1-polarized cytokine profile in abemaciclib-treated ID8 tumors. studies showed that abemaciclib-treated ID8 cells secreted more CXCL10 and CXCL13, thus recruiting more lymphocytes than control groups. Combination treatment achieved better tumor control than monotherapy, and the activities of CD8+ and CD4+ T cells were further enhanced when compared with monotherapy. The synergistic antitumor effects of combined abemaciclib and anti-PD-1 therapy depended on both CD8+ T cells and B cells. These findings suggest that combined treatment with CDK4/6i and anti-PD-1 antibody could improve the efficacy of anti-PD-1 therapy and hold great promise for the treatment of poorly immune-infiltrated ovarian cancer.

Background The adaption of brain region is fundamental to the development and maintenance of nervous system disorders. The prelimbic cortex (PrL) participates in the affective components of the pain sensation. However, whether and how the adaptation of PrL contributes to the comorbidity of neuropathic pain and depression are unknown. Methods Using resting-state functional magnetic resonance imaging (rs-fMRI), genetic knockdown or overexpression, we systematically investigated the activity of PrL region in the pathogenesis of neuropathic pain/depression comorbid using the combined approaches of immunohistochemistry, electrophysiology, and behavior. Results The activity of PrL and the excitability of pyramidal neurons were decreased, and the osteoclastic tartrate-resistant acid phosphatase 5 (Acp5) expression in PrL neurons was upregulated following the acquisition of spared nerve injury (SNI)-induced comorbidity. Genetic knockdown of Acp5 in pyramidal neurons, but not parvalbumin (PV) neurons or somatostatin (SST) neurons, attenuated the decrease of spike number, depression-like behavior and mechanical allodynia in comorbidity rats. Overexpression of Acp5 in PrL pyramidal neurons decreased the spike number and induced the comorbid-like behavior in naïve rats. Moreover, the expression of interleukin-6 (IL-6), phosphorylated STAT3 (p-STAT3) and acetylated histone H3 (Ac-H3) were significantly increased following the acquisition of comorbidity in rats. Increased binding of STAT3 to the Acp5 gene promoter and the interaction between STAT3 and p300 enhanced acetylation of histone H3 and facilitated the transcription of Acp5 in PrL in the modeled rodents. Inhibition of IL-6/STAT3 pathway prevented the Acp5 upregulation and attenuated the comorbid-like behaviors in rats. Conclusions These data suggest that the adaptation of PrL mediated by IL-6/STAT3/Acp5 pathway contributed to the comorbidity of neuropathic pain/depression induced by SNI.

Controlling complex systems is a fundamental challenge of network science. Recent advances indicate that control over the system can be achieved through a minimum driver node set (MDS). The existence of multiple MDS's suggests that nodes do not participate in control equally, prompting us to quantify their participations. Here we introduce control capacity quantifying the likelihood that a node is a driver node. To efficiently measure this quantity, we develop a random sampling algorithm. This algorithm not only provides a statistical estimate of the control capacity, but also bridges the gap between multiple microscopic control configurations and macroscopic properties of the network under control. We demonstrate that the possibility of being a driver node decreases with a node's in-degree and is independent of its out-degree. Given the inherent multiplicity of MDS's, our findings offer tools to explore control in various complex systems.