Observation of the Anomalous Hall Effect in a Collinear Antiferromagnet

Time-reversal symmetry breaking is the basic physics concept underpinning many magnetic topological phenomena such as the anomalous Hall effect (AHE) and its quantized variant. The AHE has been primarily accompanied by a ferromagnetic dipole moment, which hinders the topological quantum states and limits data density in memory devices, or by a delicate noncollinear magnetic order with strong spin decoherence, both limiting their applicability. A potential breakthrough is the recent theoretical prediction of the AHE arising from collinear antiferromagnetism in an anisotropic crystal environment. This new mechanism does not require magnetic dipolar or noncollinear fields. However, it has not been experimentally observed to date. Here we demonstrate this unconventional mechanism by measuring the AHE in an epilayer of a rutile collinear antiferromagnet RuO$_2$. The observed anomalous Hall conductivity is large, exceeding 300 S/cm, and is in agreement with the Berry phase topological transport contribution. Our results open a new unexplored chapter of time-reversal symmetry breaking phenomena in the abundant class of collinear antiferromagnetic materials.Comment: 33 pages, 14 figures, 2 table

Publisher Correction: An anomalous Hall effect in altermagnetic ruthenium dioxide

In the version of this article initially published, square brackets and parentheses were incorrect in Fig. 1g and throughout Fig. 2 (excepting lower labels in Fig. 2d–f). Further, in the second paragraph of the “Consistency with theoretical prediction” subsection of the main article, in the text now reading “the reorientation-field scale, namely, HC = (H2 AE − H2 d) /Hd,” the term “H2 AE” wasn’t shown as squared. The changes have been made in the HTML and PDF versions of the article

The drug tolerant persisters of Riemerella anatipestifer can be eradicated by a combination of two or three antibiotics

Abstract Background Riemerella anatipestifer (RA), the causative agent of duck infectious serositis, leads to high mortality in duck flocks and great economic losses in duck industry. Previous studies on RA are largely focused on its detection, virulence factors, serology, epidemiology as well as antibiotic resistance. Neither drug tolerant persisters nor the persister level under the treatment of antibiotics has been revealed. The persisters are non-growing or dormant cells within an isogenic bacterial population; they play important roles in recurrent infection and formation of drug resistant mutants. The aim of this study is to detect the drug tolerant persisters from the exponentially grown population of RA reference strain (RA 11845) or RA clinical isolate (RA TQ3), and address whether a single antibiotic or a combination of two or three antimicrobials can eradicate the persisters at respective maximum serum/plasma concentration (Cmax). Result With the concentration of a test antibiotic increased, a small fraction of cells in the exponentially grown culture of RA reference strain (RA 11845) or RA clinical isolate (RA TQ3) always survived, irrespective of treatment time, indicating the presence of drug tolerant presisters. A single antibiotic cannot eradicate the persisters of both RA strains at respective Cmax, except that the Cmax of ceftiofur wiped out the population of the reference strain (RA 11845). Besides, the clinical isolate RA TQ3 presented a higher tolerance to ceftiofur in comparison to that of the reference strain (RA 11845). Combination of any two or three antimicrobials eliminated the drug tolerant persisters of RA TQ3 completely at respective Cmax. Conclusion A sub-community of drug tolerant persisters was present in RA population. Persisters of RA TQ3 are single drug tolerant and not multidrug tolerant persisters

A Genetic Toolkit for Dissecting Dopamine Circuit Function in Drosophila.

The neuromodulator dopamine (DA) plays a key role in motor control, motivated behaviors, and higher-order cognitive processes. Dissecting how these DA neural networks tune the activity of local neural circuits to regulate behavior requires tools for manipulating small groups of DA neurons. To address this need, we assembled a genetic toolkit that allows for an exquisite level of control over the DA neural network in Drosophila. To further refine targeting of specific DA neurons, we also created reagents that allow for the conversion of any existing GAL4 line into Split GAL4 or GAL80 lines. We demonstrated how this toolkit can be used with recently developed computational methods to rapidly generate additional reagents for manipulating small subsets or individual DA neurons. Finally, we used the toolkit to reveal a dynamic interaction between a small subset of DA neurons and rearing conditions in a social space behavioral assay

A Genetic Toolkit for Dissecting Dopamine Circuit Function in Drosophila

Summary: The neuromodulator dopamine (DA) plays a key role in motor control, motivated behaviors, and higher-order cognitive processes. Dissecting how these DA neural networks tune the activity of local neural circuits to regulate behavior requires tools for manipulating small groups of DA neurons. To address this need, we assembled a genetic toolkit that allows for an exquisite level of control over the DA neural network in Drosophila. To further refine targeting of specific DA neurons, we also created reagents that allow for the conversion of any existing GAL4 line into Split GAL4 or GAL80 lines. We demonstrated how this toolkit can be used with recently developed computational methods to rapidly generate additional reagents for manipulating small subsets or individual DA neurons. Finally, we used the toolkit to reveal a dynamic interaction between a small subset of DA neurons and rearing conditions in a social space behavioral assay. : The rapid analysis of how dopaminergic circuits regulate behavior is limited by the genetic tools available to target and manipulate small numbers of these neurons. Xie et al. present genetic tools in Drosophila that allow rational targeting of sparse dopaminergic neuronal subsets and selective knockdown of dopamine signaling. Keywords: dopamine, genetics, behavior, neural circuits, neuromodulation, Drosophil

SERPINE2 promotes liver cancer metastasis by inhibiting c‐Cbl‐mediated EGFR ubiquitination and degradation

Abstract Background Liver cancer is a malignancy with high morbidity and mortality rates. Serpin family E member 2 (SERPINE2) has been reported to play a key role in the metastasis of many tumors. In this study, we aimed to investigate the potential mechanism of SERPINE2 in liver cancer metastasis. Methods The Cancer Genome Atlas database (TCGA), including DNA methylation and transcriptome sequencing data, was utilized to identify the crucial oncogene associated with DNA methylation and cancer progression in liver cancer. Data from the TCGA and RNA sequencing for 94 pairs of liver cancer tissues were used to explore the correlation between SERPINE2 expression and clinical parameters of patients. DNA methylation sequencing was used to detect the DNA methylation levels in liver cancer tissues and cells. RNA sequencing, cytokine assays, immunoprecipitation (IP) and mass spectrometry (MS) assays, protein stability assays, and ubiquitination assays were performed to explore the regulatory mechanism of SERPINE2 in liver cancer metastasis. Patient‐derived xenografts and tumor organoid models were established to determine the role of SERPINE2 in the treatment of liver cancer using sorafenib. Results Based on the public database screening, SERPINE2 was identified as a tumor promoter regulated by DNA methylation. SERPINE2 expression was significantly higher in liver cancer tissues and was associated with the dismal prognosis in patients with liver cancer. SERPINE2 promoted liver cancer metastasis by enhancing cell pseudopodia formation, cell adhesion, cancer‐associated fibroblast activation, extracellular matrix remodeling, and angiogenesis. IP/MS assays confirmed that SERPINE2 activated epidermal growth factor receptor (EGFR) and its downstream signaling pathways by interacting with EGFR. Mechanistically, SERPINE2 inhibited EGFR ubiquitination and maintained its protein stability by competing with the E3 ubiquitin ligase, c‐Cbl. Additionally, EGFR was activated in liver cancer cells after sorafenib treatment, and SERPINE2 knockdown‐induced EGFR downregulation significantly enhanced the therapeutic efficacy of sorafenib against liver cancer. Furthermore, we found that SERPINE2 knockdown also had a sensitizing effect on lenvatinib treatment. Conclusions SERPINE2 promoted liver cancer metastasis by preventing EGFR degradation via c‐Cbl‐mediated ubiquitination, suggesting that inhibition of the SERPINE2‐EGFR axis may be a potential target for liver cancer treatment