Antiferromagnetic to Ferrimagnetic Phase Transition and Possible Phase Coexistence in Polar Magnets (Fe1−x_{1-x}Mnx_x)2_2Mo3_3O8_8

In the present work, magnetic properties of single crystal (Fe$_{1-x}$Mn$_x$)$_2$Mo$_3$O$_8$ ($0<x<1$) have been studied by performing extensive measurements. A detailed magnetic phase diagram is built up, in which antiferromagnetic state dominates for $x<0.25$ and ferrimagnetic phase arises for $x>0.3$. Meanwhile, sizeable electric polarization of spin origin is commonly observed in all samples, no matter what the magnetic state is. For the samples hosting a ferrimagnetic state, square-like magnetic hysteresis loops are revealed, while the remnant magnetization and coercive field can be tuned drastically by simply varying the Mn-content or temperature. Possible coexistence of the antiferromagnetic and ferrimagnetic phases is proposed to be responsible for the remarkable modulation of magnetic properties in the samples

On Enriching the Levin-Wen model with Symmetry

Symmetry protected and symmetry enriched topological phases of matter are of great interest in condensed matter physics due to new materials such as topological insulators. The Levin-Wen model for spin/boson systems is an important rigorously solvable model for studying $2D$ topological phases. The input data for the Levin-Wen model is a unitary fusion category, but the same model also works for unitary multi-fusion categories. In this paper, we provide the details for this extension of the Levin-Wen model, and show that the extended Levin-Wen model is a natural playground for the theoretical study of symmetry protected and symmetry enriched topological phases of matter.Comment: 21 pages, 6 figure

Colossal linear magnetoelectricity in polar magnet Fe2Mo3O8

Linear magnetoelectric effect is an attractive phenomenon in condensed matters and provides indispensable technological functionalities. Here a colossal linear magnetoelectric effect with diagonal component alfa_33 reaching up to ~480 ps/m is reported in a polar magnet Fe2Mo3O8, and this effect can persist in a broad range of magnetic field (~20 T) and is orders of magnitude larger than reported values in literature. Such an exceptional experimental observation can be well reproduced by a theoretical model affirmatively unveiling the vital contributions from the exchange striction, while the sign difference of magnetocrystalline anisotropy can also be reasonably figured out.Comment: 14 pages and 4 figure

Crystal structure of the N‐terminal region of human Ash2L shows a winged‐helix motif involved in DNA binding

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/102216/1/embr2011101-sup-0001.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/102216/2/embr2011101.reviewer_comments.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/102216/3/embr2011101.pd

A Novel Germline ARMC5 Mutation in a Patient with Bilateral Macronodular Adrenal Hyperplasia: A Case Report

BACKGROUND: Bilateral macronodular adrenal hyperplasia (BMAH) is a rare cause of Cushing\u27s syndrome (CS). BMAH is predominantly believed to be caused by two mutations, a germline and somatic one, respectively, as described in the two-hit hypothesis. In many familial cases of BMAH, mutations in armadillo repeat containing 5 (ARMC5), a putative tumor suppressor gene, are thought to induce the disorder. The objective of this study was to report a case in which the patient presented with BMAH induced by a novel heterozygous germline ARMC5 mutation (c. 517C \u3e T, p. Arg173*) alone rather than a two-hit mutation. CASE PRESENTATION: A 51-year-old woman was identified with masses in the bilateral adrenals. Serum cortisol levels were increased significantly both in the morning (08:00 AM) and late at night (24:00 AM), while plasma adrenocorticotropic hormone was normal. The patient underwent a left adrenalectomy and histopathology substantiated the BMAH diagnosis. WES of the germline DNA discovered a novel heterozygous germline ARMC5 mutation (c. 517C \u3e T, p. Arg173*) and in silico analysis predicted that the mutation significantly impaired protein function, resulting in inactivated ARMC5. Subsequently, WES of the tumor specimen identified 79 somatic single nucleotide polymorphisms (SNPs)/insertion-deletion (indel) mutations, including 32 missense/nonsense/splice/stop-loss mutations. None of these mutations were CS-related. CONCLUSIONS: A novel germline ARMC5 mutation (c. 517C \u3e T, p. Arg173*) was identified that induced BMAH alone without a second mutation. ARMC5 sequencing may improve the identification of clinical forms of BMAH and allow earlier diagnosis of this disease

Adaptive Synaptic Memory via Lithium Ion Modulation in RRAM Devices

Biologically plausible computing systems require fine- grain tuning of analog synaptic characteristics. In this study, lithium- doped silicate resistive random access memory with a titanium nitride (TiN) electrode mimicking biological synapses is demonstrated. Biological plausibility of this RRAM device is thought to occur due to the low ionization energy of lithium ions, which enables controllable forming and filamentary retraction spontaneously or under an applied voltage. The TiN electrode can effectively store lithium ions, a principle widely adopted from battery construction, and allows state- dependent decay to be reliably achieved. As a result, this device offers multi- bit functionality and synaptic plasticity for simulating various strengths in neuronal connections. Both short- term memory and long- term memory are emulated across dynamical timescales. Spike- timing- dependent plasticity and paired- pulse facilitation are also demonstrated. These mechanisms are capable of self- pruning to generate efficient neural networks. Time- dependent resistance decay is observed for different conductance values, which mimics both biological and artificial memory pruning and conforms to the trend of the biological brain that prunes weak synaptic connections. By faithfully emulating learning rules that exist in human’s higher cortical areas from STDP to synaptic pruning, the device has the capacity to drive forward the development of highly efficient neuromorphic computing systems.In this study, lithium- doped silicate resistive random access memory with a titanium nitride (TiN) electrode is shown to mimic biological synapses. The TiN electrode effectively stores lithium ions, a principle widely adopted from battery construction, and enables reliable state- dependent decay. This device offers multi- bit functionality and synaptic plasticity, short- term memory and long- term memory, spike- timing- dependent plasticity and paired- pulse facilitation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/163426/3/smll202003964-sup-0001-SuppMat.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/163426/2/smll202003964_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/163426/1/smll202003964.pd

An Exposome Atlas of Serum Reveals the Risk of Chronic Diseases in the Chinese Population

Although adverse environmental exposures are considered a major cause of chronic diseases, current studies provide limited information on real-world chemical exposures and related risks. For this study, we collected serum samples from 5696 healthy people and patients, including those with 12 chronic diseases, in China and completed serum biomonitoring including 267 chemicals via gas and liquid chromatography-tandem mass spectrometry. Seventy-four highly frequently detected exposures were used for exposure characterization and risk analysis. The results show that region is the most critical factor influencing human exposure levels, followed by age. Organochlorine pesticides and perfluoroalkyl substances are associated with multiple chronic diseases, and some of them exceed safe ranges. Multi-exposure models reveal significant risk effects of exposure on hyperlipidemia, metabolic syndrome and hyperuricemia. Overall, this study provides a comprehensive human serum exposome atlas and disease risk information, which can guide subsequent in-depth cause-and-effect studies between environmental exposures and human health

Improvement of Morphine-Mediated Analgesia by Inhibition of β-Arrestin 2 Expression in Mice Periaqueductal Gray Matter

Morphine is a well-known μ-opioid receptor (MOR) agonist and an efficient analgesic, but its long-term use inevitably leads to drug addiction and tolerance. Here, we show that specific inhibition of β-arrestin2 with its siRNA lentivirus microinjected in mice periaqueductal gray matter (PAG) significantly improved both acute and chronic morphine analgesia and delayed the tolerance in the hotplate test. The specific effect of β-arrestin2 was proven by overexpression or knockdown of its homology β-arrestin1 in PAG, which showed no significant effects on morphine analgesia. These findings suggest that specific siRNA targeting β-arrestin2 may constitute a new approach to morphine therapy and other MOR agonist-mediated analgesia and tolerance

Antibiotic-Induced Gut Microbiota Dysbiosis Modulates Host Transcriptome and m6A Epitranscriptome via Bile Acid Metabolism.

Gut microbiota can influence host gene expression and physiology through metabolites. Besides, the presence or absence of gut microbiome can reprogram host transcriptome and epitranscriptome as represented by N6-methyladenosine (m6A), the most abundant mammalian mRNA modification. However, which and how gut microbiota-derived metabolites reprogram host transcriptome and m6A epitranscriptome remain poorly understood. Here, investigation is conducted into how gut microbiota-derived metabolites impact host transcriptome and m6A epitranscriptome using multiple mouse models and multi-omics approaches. Various antibiotics-induced dysbiotic mice are established, followed by fecal microbiota transplantation (FMT) into germ-free mice, and the results show that bile acid metabolism is significantly altered along with the abundance change in bile acid-producing microbiota. Unbalanced gut microbiota and bile acids drastically change the host transcriptome and the m6A epitranscriptome in multiple tissues. Mechanistically, the expression of m6A writer proteins is regulated in animals treated with antibiotics and in cultured cells treated with bile acids, indicating a direct link between bile acid metabolism and m6A biology. Collectively, these results demonstrate that antibiotic-induced gut dysbiosis regulates the landscape of host transcriptome and m6A epitranscriptome via bile acid metabolism pathway. This work provides novel insights into the interplay between microbial metabolites and host gene expression