Characterizing random-singlet state in two-dimensional frustrated quantum magnets and implications for the double perovskite Sr2_2CuTe1−x_{1-x}Wx_{x}O6_6

Motivated by experimental observation of the non-magnetic phase in the compounds with frustration and disorder, we study the ground state of the spin-$1/2$ square-lattice Heisenberg model with randomly distributed nearest-neighbor $J_1$ and next-nearest-neighbor $J_2$ couplings. By using the density matrix renormalization group (DMRG) calculation on cylinder system with circumference up to $10$ lattice sites, we identify a disordered phase between the N\'eel and stripe magnetic phase with growing $J_2 / J_1$ in the presence of strong randomness. The vanished spin-freezing parameter indicates the absent spin glass order. The large-scale DMRG results unveil the size-scaling behaviors of the spin-freezing parameter, the power-law decay of average spin correlation, and the exponential decay of typical spin correlation, which all agree with the corresponding behavior in the one-dimensional random singlet (RS) state and characterize the RS nature of this non-magnetic state. The DMRG simulation also opens new insight and opportunities for characterizing a class of non-magnetic states in two-dimensional frustrated magnets with disorder. We also compare with existing experiments and suggest more measurements for understanding the spin-liquid-like behavior in the double perovskite Sr$_2$CuTe$_{1-x}$W$_{x}$O$_6$.Comment: 11 pages,10 figure

Lack of an association of miR-938 SNP in IDDM10 with human type 1 diabetes

MicroRNAs (miRNAs) are a newly discovered type of small non-protein coding RNA that function in the inhibition of effective mRNA translation, and may serve as susceptibility genes for various disease developments. The SNP rs12416605, located in human type 1 diabetes IDDM10 locus, changes the seeding sequence (UGU[G/A]CCC) of miRNA miR-938 and potentially alters miR-938 targets, including IL-16 and IL-17A. In an attempt to test whether miR-938 may be a susceptibility gene for IDDM10, we assessed the possible association of the miR-938 SNP with T1D in an American Caucasian cohort of 622 patients and 723 healthy controls by TaqMan assay. Our current data do not support the association between the SNP in miR-938 and type 1 diabetes

PPARG rs3856806 C>T Polymorphism Increased the Risk of Colorectal Cancer: A Case-Control Study in Eastern Chinese Han Population

Purpose: Functional variants in the peroxisome proliferator-activated receptor gamma (PPARG) and PPARG co-activator 1 (PPARGC1) family (e.g., PPARGC1A and PPARGC1B) genes were predicted to confer susceptibility to colorectal cancer (CRC). The aim of the present study was to explore the relationship between PPARG, PPARGC1A, PPARGC1B polymorphism and the risk of CRC.Patients and methods: We conducted a case-control study with 1,003 CRC cases and 1,303 controls. We selected the PPARG rs3856806 C>T, PPARGC1A rs2970847 C>T, rs8192678 C>T, rs3736265 G>A and PPARGC1B rs7732671 G>C and rs17572019 G>A SNPs to assess the relationship between PPARG, PPARGC1A, PPARGC1B their variants and risk of CRC.Results: We found that the PPARG rs3856806 C>T polymorphism increased the risk of CRC (TT vs. CC: adjusted OR, 1.59, 95% CI 1.08–2.35, P = 0.020; TT/CT vs. CC: adjusted OR, 1.26; 95% CI 1.06–1.49; P = 0.009 and TT vs. CC/CT: adjusted OR, 1.54; 95% CI 1.05–2.26; P = 0.028), even after a Bonferroni correction test. The stratified analysis revealed that the PPARG rs3856806 C>T polymorphism also increased the risk of CRC, especially in male, ≥61 years old, never smoking, never drinking, BMI ≥ 24 kg/m2, colon cancer and rectum cancer subgroups.Conclusion: Our findings highlight that the PPARG rs3856806 C>T polymorphism may increase the risk of CRC. In the future larger sample size case-control studies with a detailed functional assessment are needed to further determine the relationship of the PPARG rs3856806 C>T polymorphism with CRC risk

Quantitative Phosphoproteomics of Proteasome Inhibition in Multiple Myeloma Cells

BACKGROUND: The proteasome inhibitor bortezomib represents an important advance in the treatment of multiple myeloma (MM). Bortezomib inhibits the activity of the 26S proteasome and induces cell death in a variety of tumor cells; however, the mechanism of cytotoxicity is not well understood. METHODOLOGY/PRINCIPAL FINDINGS: We investigated the differential phosphoproteome upon proteasome inhibition by using stable isotope labeling by amino acids in cell culture (SILAC) in combination with phosphoprotein enrichment and LC-MS/MS analysis. In total 233 phosphoproteins were identified and 72 phosphoproteins showed a 1.5-fold or greater change upon bortezomib treatment. The phosphoproteins with expression alterations encompass all major protein classes, including a large number of nucleic acid binding proteins. Site-specific phosphopeptide quantitation revealed that Ser38 phosphorylation on stathmin increased upon bortezomib treatment, suggesting new mechanisms associated to bortezomib-induced apoptosis in MM cells. Further studies demonstrated that stathmin phosphorylation profile was modified in response to bortezomib treatment and the regulation of stathmin by phosphorylation at specific Ser/Thr residues participated in the cellular response induced by bortezomib. CONCLUSIONS/SIGNIFICANCE: Our systematic profiling of phosphorylation changes in response to bortezomib treatment not only advanced the global mechanistic understanding of the action of bortezomib on myeloma cells but also identified previously uncharacterized signaling proteins in myeloma cells

The role of glucocorticoids in increasing cardiovascular risk

IntroductionDifferent studies provide conflicting evidence regarding the potential for glucocorticoids (GCs) to increase the risk of cardiovascular diseases. This study performed a systematic review and meta-analysis to determine the correlation between GCs and cardiovascular risk, including major adverse cardiovascular events (MACE), death from any cause, coronary heart disease (CHD), heart failure (HF), and stroke.MethodsWe performed a comprehensive search in PubMed and Embase (from inception to June 1, 2022). Studies that reported relative risk (RR) estimates with 95% confidence intervals (CIs) for the associations of interest were included.ResultsA total of 43 studies with 15,572,512 subjects were included. Patients taking GCs had a higher risk of MACE (RR = 1.27, 95% CI: 1.15–1.40), CHD (RR = 1.25, 95% CI: 1.11–1.41), and HF (RR = 1.92, 95% CI: 1.51–2.45). The MACE risk increased by 10% (95% CI: 6%–15%) for each additional gram of GCs cumulative dose or by 63% (95% CI: 46%–83%) for an additional 10 μg daily dose. The subgroup analysis suggested that not inhaled GCs and current GCs use were associated with increasing MACE risk. Similarly, GCs were linked to an increase in absolute MACE risk of 13.94 (95% CI: 10.29–17.58) cases per 1,000 person-years.ConclusionsAdministration of GCs is possibly related with increased risk for MACE, CHD, and HF but not increased all-cause death or stroke. Furthermore, it seems that the risk of MACE increased with increasing cumulative or daily dose of GCs

In Situ Construction of an Ultrarobust and Lithiophilic Li-Enriched Li–N Nanoshield for High-Performance Ge-Based Anode Materials

Alloy-based materials are promising anodes for rechargeable batteries because of their higher theoretical capacities in comparison to graphite. Unfortunately, the huge volume changes during cycling cause serious structural degradation and undesired parasitic reactions with electrolytes, resulting in fragile solid-electrolyte interphase formation and serious capacity decay. This work proposes to mitigate the volume changes and suppress the interfacial reactivity of Ge anodes without sacrificing the interfacial Li+ transport, through in situ construction of an ultrarobust and lithiophilic Li-enriched Li–N nanoshield, which demonstrated improved chemical, electrochemical, mechanical, and environmental stability. Therefore, it can serve as a versatile interlayer to facilitate Li+ transport and effectively block the attack of electrolyte solvents, thus boosting the long-term cycle stability and fast charging capability of Ge anodes. This work offers an alternative methodology to tune the interfaces of other electrode materials as well by screening for more N-containing compounds that can react with Li+ during battery operation

Boosting Superior Lithium Storage Performance of Alloy‐Based Anode Materials via Ultraconformal Sb Coating–Derived Favorable Solid‐Electrolyte Interphase

Alloy materials such as Si and Ge are attractive as high‐capacity anodes for rechargeable batteries, but such anodes undergo severe capacity degradation during discharge–charge processes. Compared to the over‐emphasized efforts on the electrode structure design to mitigate the volume changes, understanding and engineering of the solid‐electrolyte interphase (SEI) are significantly lacking. This work demonstrates that modifying the surface of alloy‐based anode materials by building an ultraconformal layer of Sb can significantly enhance their structural and interfacial stability during cycling. Combined experimental and theoretical studies consistently reveal that the ultraconformal Sb layer is dynamically converted to Li3Sb during cycling, which can selectively adsorb and catalytically decompose electrolyte additives to form a robust, thin, and dense LiF‐dominated SEI, and simultaneously restrain the decomposition of electrolyte solvents. Hence, the Sb‐coated porous Ge electrode delivers much higher initial Coulombic efficiency of 85% and higher reversible capacity of 1046 mAh g−1 after 200 cycles at 500 mA g−1, compared to only 72% and 170 mAh g−1 for bare porous Ge. The present finding has indicated that tailoring surface structures of electrode materials is an appealing approach to construct a robust SEI and achieve long‐term cycling stability for alloy‐based anode materials