Haoxiang Huang

Nonequilibrium molecular dynamics (NEMD) simulations on conceptual binary Lennard-Jones systems show that the thermal conductivity ($\ensuremath{\kappa}$) of a superlattice (SL) can be significantly reduced by randomizing the thicknesses of its layers, by which a SL becomes a random multilayer (RML). Such reduction in $\ensuremath{\kappa}$ is a clear signature of coherent phonon that can be localized in RMLs. We build a two-phonon model that divides the overall heat conduction into coherent and incoherent phonon contributions. In SL both coherent and incoherent phonons contribute to heat conduction, while in RML coherent phonons are localized so only incoherent phonons contribute. This model can fit the length dependence of the thermal conductances predicted in our NEMD simulations very well. The ballistic-limit thermal conductance and the intrinsic mean free path (MFP) of both coherent and incoherent phonons, and the localization length of coherent phonons, are obtained by fitting our model to the NEMD simulation results. The significant increase in $\ensuremath{\kappa}$ of SL with total length is due to the long MFP of coherent phonons, and the lower $\ensuremath{\kappa}$ of RML than SL is caused by the localization of coherent phonons.

AIMS: Metabolic switching during heart development contributes to postnatal cardiomyocyte (CM) cell cycle exit and loss of regenerative capacity in the mammalian heart. Metabolic control has potential for developing effective CM proliferation strategies. We sought to determine whether lactate dehydrogenase A (LDHA) regulated CM proliferation by inducing metabolic reprogramming. METHODS AND RESULTS: LDHA expression was high in P1 hearts and significantly decreased during postnatal heart development. CM-specific LDHA knockout mice were generated using CRISPR/Cas9 technology. CM-specific LDHA knockout inhibited CM proliferation, leading to worse cardiac function and a lower survival rate in the neonatal apical resection model. In contrast, CM-specific overexpression of LDHA promoted CM proliferation and cardiac repair post-MI. The α-MHC-H2B-mCh/CAG-eGFP-anillin system was used to confirm the proliferative effect triggered by LDHA on P7 CMs and adult hearts. Metabolomics, proteomics and Co-IP experiments indicated that LDHA-mediated succinyl coenzyme A reduction inhibited succinylation-dependent ubiquitination of thioredoxin reductase 1 (Txnrd1), which alleviated ROS and thereby promoted CM proliferation. In addition, flow cytometry and western blotting showed that LDHA-driven lactate production created a beneficial cardiac regenerative microenvironment by inducing M2 macrophage polarization. CONCLUSIONS: LDHA-mediated metabolic reprogramming promoted CM proliferation by alleviating ROS and inducing M2 macrophage polarization, indicating that LDHA might be an effective target for promoting cardiac repair post-MI.

Heating of Os3(CO)12 with 6 equiv of 2-(3-(trifluoromethyl)-1H-1,2,4-triazol-5-yl) pyridine (fptzH) in refluxing diethylene glycol monomethyl ether, followed by sequential treatment with stoichiometric Me3NO and addition of PPhMe2, afforded two isomeric mixtures of red-emitting [Os(fptz)2(PPhMe2)2] (1T and 1C), for which the notations T and C stand for the trans and cis-oriented fptz chelates, respectively. Alternatively, preparation of Os(II) complex using a 1:1 mixture of 5,5'-di(trifluoromethyl)-3,3'-di-1,2,4-triazole (dttzH2) and 2,2'-bipyridine (bpy), instead of fptzH, gave isolation of a mononuclear Os(II) complex [Os(bpy)(dttz)(CO)2] (2) in moderate yield. Replacement of CO with PPhMe2 on 2 afforded near-infrared (NIR)-emitting Os(II) complex [Os(bpy)(dttz)(PPhMe2)2] (3). The single-crystal X-ray structural analyses were executed on 1C, 2, and 3 to reveal the structural influence imposed by the various chelates. The photophysical and electrochemical properties were measured and discussed using the results of density functional theory (DFT) and time-dependent DFT calculations. Complex 3 is selected as the dopant to probe its electroluminescent properties by fabrication of the NIR emitting organic light-emitting diodes.

BACKGROUND: Major depressive disorder (MDD) and interstitial cystitis (IC) are two highly debilitating conditions that often coexist with reciprocal effect, significantly exacerbating patients' suffering. However, the molecular underpinnings linking these disorders remain poorly understood. METHODS: Transcriptomic data from GEO datasets including those of MDD and IC patients was systematically analyzed to develop and validate our model. Following removal of batch effect, differentially expressed genes (DEGs) between respective disease and control groups were identified. Shared DEGs of the conditions then underwent functional enrichment analyses. Additionally, immune infiltration analysis was quantified through ssGSEA. A diagnostic model for MDD was constructed by exploring 113 combinations of 12 machine learning algorithms with 10-fold cross-validation on the training sets following by external validation on test sets. Finally, the "Enrichr" platform was utilized to identify potential drugs for MDD. RESULTS: Totally, 21 key genes closely associated with both MDD and IC were identified, predominantly involved in immune processes based on enrichment analyses. Immune infiltration analysis revealed distinct profiles of immune cell infiltration in MDD and IC compared to healthy controls. From these genes, a robust 11-gene (ABCD2, ATP8B4, TNNT1, AKR1C3, SLC26A8, S100A12, PTX3, FAM3B, ITGA2B, OLFM4, BCL7A) diagnostic signature was constructed, which exhibited superior performance over existing MDD diagnostic models both in training and testing cohorts. Additionally, epigallocatechin gallate and 10 other drugs emerged as potential targets for MDD. CONCLUSION: Our work developed a diagnostic model for MDD employing a combination of bioinformatic techniques and machine learning methods, focusing on shared genes between MDD and IC.

Treatment of 2,6-di(5-trifluoromethylpyrazol-3-yl)pyridine (pz2py)H2 with Os3(CO)12 affords a mononuclear Os(II) complex [Os(pz2py)(CO)2(H2O)] (1) in excellent yield. Ligand substitution reactions were next executed to identify products with good photoluminescence at both fluid and solid states at RT. Therefore, substitutions with phosphorus donors such as PPh2Me and 2,6-bis(diphenylphosphinomethyl) pyridine (P2N), and nitrogen donors such as pyridine, 2,2′-bipyridine (bpy) and 2,2′:6′,2′′-terpyridine (tpy), afforded products with formula [Os(pz2py)(PPh2Me)2(CO)] (2), [Os(pz2py)(P2N)] (3), [Os(pz2py)(CO)2(py)] (4), [Os(pz2py)(CO)(bpy)] (5) and [Os(pz2py)(CO)(tpy)] (6). The single crystal X-ray structural analyses were executed on 1, 2, 3 and 6 to reveal the bonding of pz2py chelate as well as the structural effect imposed by the phosphorus and/or nitrogen donor groups. The photophysical properties were studied and discussed using the results of DFT and TDDFT calculations. For application, fabrication and analysis of organic light emitting diodes (OLEDs) were also carried out. OLEDs using 2 as a dopant exhibited an intense yellow emission with a maximum efficiency of 18.3%, 61.0 cd A−1, and 53.8 lm W−1, which are higher than those of most reported devices with greenish yellow/yellow emitters. Moreover, dopant 2 was combined with a red emitting dopant Os(bpftz)2(PPhMe2)2 (7) and two different sky-blue phosphors FIrpic and Ir(bptz)2(bdp) (8) to fabricate white OLEDs (WOLEDs). Device W1 achieved the highest efficiency of 18.0%, 33.9 cd A−1, and 31.2 lm W−1 while the maximized efficiency of device W2 was 15.3%, 29.3 cd A−1, and 27.0 lm W−1. Both devices showed stable warm-white emissions with a wide luminance range. In addition, device W2 exhibited a higher CRI of 84.2 with a low CCT of 2675 K at 103 cd m−2, making it a potential candidate for domestic lighting.