Phonon engineering in Yb:La2CaB10O19 crystal for extended lasing beyond the fluorescence spectrum.

Since the first invention of the laser in 1960, direct lasing outside the fluorescence spectrum is deemed impossible owing to the "zero-gain" cross-section. However, when electron-phonon coupling meets laser oscillation, an energy modulation by the quantized phonon can tailor the electronic transitions, thus directly creating some unprecedented lasers with extended wavelengths by phonon engineering. Here, we demonstrate a broadband lasing (1000-1280 nm) in a Yb-doped La2CaB10O19 (Yb:LCB) crystal, far beyond its spontaneous fluorescence spectrum. Numerical calculations and in situ Raman verify that such a substantial laser emission is devoted to the multiphonon coupling to lattice vibrations of a dangling "quasi-free-oxygen" site, with the increasing phonon numbers step-by-step (n = 1-6). This new structural motif provides more alternative candidates with strong-coupling laser materials. Moreover, the quantitative relations between phonon density distribution and laser wavelength extension are discussed. These results give rise to the search for on-demand lasers in the darkness and pave a reliable guideline to study those intriguing electron-phonon-photon coupled systems for integrated photonic applications.

Midbrain dopamine oxidation links ubiquitination of glutathione peroxidase 4 to ferroptosis of dopaminergic neurons.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the gradual loss of midbrain dopaminergic neurons in association with aggregation of α-synuclein. Oxidative damage has been widely implicated in this disease, though the mechanisms involved remain elusive. Here, we demonstrated that preferential accumulation of peroxidized phospholipids and loss of the antioxidant enzyme glutathione peroxidase 4 (GPX4) were responsible for vulnerability of midbrain dopaminergic neurons and progressive motor dysfunctions in a mouse model of PD. We also established a mechanism wherein iron-induced dopamine oxidation modified GPX4, thereby rendering it amenable to degradation via the ubiquitin-proteasome pathway. In conclusion, this study unraveled what we believe to be a novel pathway for dopaminergic neuron degeneration during PD pathogenesis, driven by dopamine-induced loss of antioxidant GPX4 activity.

Enhanced Electron-Phonon Coupling Effect in Rare-Earth Borate Crystals Containing a "Quasi-Free-Oxygen" Motif.

Revealing the interaction between electrons and phonons, e.g., electron-phonon coupling or decoupling, is a great challenge for physics and functional material communities. For rare-earth single crystals, the electron-phonon coupling and fluorescence behaviors strongly depend on the crystal structure and constituent motifs. Here, we proposed a universal "quasi-free O" as an effective structural motif to enhance phonon-assisted electronic transitions and photoluminescence. Using Gd3+ ion as a probe, we studied Gd:La2CaB10O19 (Gd:LCB) and GdMgB5O10 (GdMB) crystals composed of double B-O layers and dangling "quasi-free O", respectively, which enable strengthened phonon-involved luminescence. Especially, a GdMB crystal features an infinite [O-Gd-O-Gd-O] chain (O represents quasi-free oxygen), thus greatly promoting the energy transfer and electron-phonon coupling effect. As a result, its Huang-Rhys S factor is two times larger than that of a Gd:LCB crystal under room temperature. These results put forward "quasi-free O" to improve the electron-phonon coupling intensity and allow LCB and GdMB crystals to serve as potential hosts for phonon-terminated vibronic lasers.

Diode-pumped continuous-wave laser of a self-frequency-doubling Yb:La2CaB10O19 crystal.

We report the first, to the best of our knowledge, laser operation of acentric Yb3+-doped La2CaB10O19 (Yb:LCB) crystal since its discovery in 1998. The polarized absorption and emission cross-section spectra of Yb:LCB were calculated at room temperature. Using a fiber-coupled 976 nm laser diode (LD) as the pump source, we realized effective dual-wavelength laser generation at around 1030 and 1040 nm. The highest slope efficiency of 50.1% was obtained in the Y-cut Yb:LCB crystal. In addition, via resonant cavity design on a phase-matching crystal, a compact self-frequency-doubling (SFD) green laser at 521 nm was also realized in a single Yb:LCB crystal with an output power of 152 mW. These results promote Yb:LCB as a competitive multifunctional laser crystal, especially for highly integrated microchip laser devices ranging from the visible to the near-infrared regime.

Growth, Structure, and Properties of a Multifunctional Crystal Pr2CaB10O19.

A new praseodymium-based borate crystal Pr2CaB10O19 (PCB) has been grown through the high temperature solution method. PCB crystallizes in monoclinic space group C2 with unit cell parameters of a = 10.9475(10) Å, b = 6.5343(7) Å, c = 9.0336(8) Å, ß = 91.652(3)°, and Z = 2, in which B5O12 groups and PrO10 and CaO8 polyhedra constitute the three-dimensional framework. PCB exhibits a similar second harmonic response intensity to that of La2CaB10O19 and an intense orange fluorescence emission with a long fluorescence lifetime at about 610 nm excited by a xenon lamp light of 466 nm. The band gap, partial density of states, and birefringence have been investigated via theoretical calculations.

Large Magnetocaloric Effect in Li3K9Gd3(BO3)7 Crystal Featuring Sandwich-Like Three-Dimensional Framework.

A new Gd-based borate crystal, Li3K9Gd3(BO3)7, has been successfully obtained via the high-temperature solution method using Li2O-K2O-B2O3 self-flux. It crystallizes in monoclinic space group P2/n (no. 10) with lattice parameters a = 11.3454(6) Å, b = 9.9881(4) Å, c = 11.4467(7) Å, α = γ = 90 o, ß = 114.782(7) o, and Z = 2. Li3K9Gd3(BO3)7 exhibits an intriguing sandwich-like three-dimensional (3D) framework constructed from [Gd-B-O]∞ layers, KOn (n = 6 and 8) polyhedra, and LiO4 tetrahedra, in which [Gd-B-O]∞ layers are built from two types of GdO8 polyhedra and triangular BO3 units. Magnetic measurements showed that Li3K9Gd3(BO3)7 exhibits a large magnetocaloric effect with -ΔSm = 39.3 J kg-1 K-1 at 2.0 K for ΔH = 7 T, which is slightly higher than that of the commercial gadolinium gallium garnet under the same conditions. The powder X-ray diffraction, infrared spectrum, and UV-vis-NIR diffuse reflectance spectrum were also performed to characterize Li3K9Gd3(BO3)7. The electronic band structures, partial density of states, and refractive indices of Li3K9Gd3(BO3)7 were investigated via the first-principle calculations.

Gadolinium-Rich Borate Gd17.33(BO3)4(B2O5)2O16 Exhibiting a Magnetocaloric Effect.

A gadolinium-rich borate Gd17.33(BO3)4(B2O5)2O16 was successfully grown by the high-temperature solution method using the Rb2O-B2O3 flux. The crystal crystallizes in centrosymmetric space group C2/m with lattice constants a = 18.4300(2) Å, b = 3.7400(4) Å, c = 14.2047(16) Å, and ß = 119.8550(12)°. Two different honeycomb-like [GdO] layers alternately arrange in the order ABAB forming the three-dimensional framework, in which the isolated [B2O5] and [BO3] units fill in channels of the 12-membered and 10-membered [GdO] polyhedral rings, respectively. The UV cutoff edge of Gd17.33(BO3)4(B2O5)2O16 is less than 240 nm. The maximum -ΔSm,max is 26.53 J kg-1 K-1 or 174.70 mJ cm-3 K-1 (T = 4.4 K and ΔH = 7 T) as investigated by the isothermal magnetization method.

A new non-centrosymmetric Gd-based borate crystal Rb7SrGd2(B5O10)3: growth, structure, and nonlinear optical and magnetic properties.

A new non-centrosymmetric borate crystal, Rb7SrGd2(B5O10)3, was successfully grown via the spontaneous nucleation technique from the Rb2O-B2O3-SrO self-flux system. It crystallizes in the trigonal system space group R32 with lattice parameters a = b = 13.4975(5) Å, c = 15.3223(8) Å, α = ß = 90°, γ = 120°, and Z = 3. Its three-dimensional framework is composed of isolated GdO6 and SrO6 octahedra, RbOn (n = 6 and 8) polyhedra, and [B5O10]5- clusters. Rb7SrGd2(B5O10)3 exhibits multifunctional properties, and has both moderate second harmonic generation (SHG) responses (0.5 × KDP) and paramagnetic characteristics with µeff = 8.18µB. Thermal stability, Fourier transform infrared spectroscopy, and UV-Vis-NIR diffuse reflectance spectroscopy were performed to characterize the title compound. Its electronic band structures and density of states were also investigated via first-principles calculations.

Hydrogen gas alleviates blood-brain barrier impairment and cognitive dysfunction of septic mice in an Nrf2-dependent pathway.

Sepsis-associated encephalopathy (SAE) is a cognitive impairment caused by sepsis and is related to increased morbidity and mortality. Damage to the blood-brain barrier (BBB) has been proved to be one of the important causes of SAE. Molecular hydrogen (H2) is a promising method for the treatment of SAE, yet the underlying mechanism is not clear. This study was designed to demonstrate whether H2 can alleviate SAE by protecting the BBB, and whether it is protected by Nuclear factor erythroid-2-related factor 2 (Nrf2) and its downstream signaling pathways. Either a sham or a cecal ligation and puncture (CLP) procedure was applied to female wild-type (WT) and Nrf2-knock-out (Nrf2-/-) C57BL/6J mice. H2 (2%) was given for 60 min starting at 1 h and 6 h after the sham or CLP procedure. In addition, bEnd.3 cells cultured with medium which contained LPS, Saline, DMSO or ML385 (a Nrf2 inhibitor) were also used in the research. The 7-day survival rates were recorded. The Morris water maze was used to determine cognitive function. Pro-inflammatory and anti-inflammatory cytokines [tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), HMGB1, and IL-10), antioxidant enzymes, and oxidation products [superoxide dismutase (SOD), chloramphenicol acetyltransferase (CAT), malondialdehyde (MDA), and (8-iso-PGF2α)] were determined by enzyme-linked immunosorbent assay (ELISA). Brain water content, Dextran tracer, and Evans blue extravasation were used to detect the damage of the BBB. Western blot analysis was used to detect ß-catenin, phosphorylated ß-catenin, adhesion-linked protein VE-cadherin, and associated tight junction protein ZO-1. We found that H2 can improve survival in septic mice, decrease escape latency and platform crossing times, decrease pro-inflammatory cytokines and oxidative product levels in the mouse cortex, and increase the expression of anti-inflammatory factors in WT, but not Nrf2-/-, mice. Moreover, H2 can also decrease brain water content, extravascular dextran, extravascular Evans blue dye, and ß-catenin level, and increase ZO-1 and VE-cadherin expressions in WT mice, but not in Nrf2-/- mice. Our result shows that H2 can protect the BBB by decreasing its permeability, thereby reducing SAE and improving cognitive function, which is mediated through Nrf2 and its downstream signaling pathways.

Hydrogen alleviates mitochondrial dysfunction and organ damage via autophagy­mediated NLRP3 inflammasome inactivation in sepsis.

Sepsis is a highly heterogeneous syndrome that is caused by a dysregulated host response to infection. The disproportionate inflammatory response to invasive infection is a triggering event inducing sepsis. The activation of inflammasomes in sepsis can amplify inflammatory responses. It has been reported that damaged mitochondria contribute to NACHT, LRR and PYD domains­containing protein 3 (NLRP3) inflammasome­related sepsis. Our previous study revealed that hydrogen (H2) exerts anti­inflammatory effects in sepsis but the detailed mechanism remains to be elucidated. In the present study, septic mice induced by cecal ligation and puncture (CLP) and macrophages induced by lipopolysaccharide (LPS) were used as models of sepsis in vivo and in vitro, respectively. An inducer and inhibitor of autophagy and the NLRP3 inflammasome were administered to investigate the detailed mechanism of action of H2 treatment in sepsis. The results demonstrated that LPS and ATP led to NLRP3 inflammasome pathway activation, excessive cytokine release, mitochondrial dysfunction and the activation of autophagy. CLP induced organ injury and NLRP3 pathway activation. H2 treatment ameliorated vital organ damage, the inflammatory response, mitochondrial dysfunction and NLRP3 pathway activation, and promoted autophagy in macrophages induced by LPS and in CLP mice. However, the inhibitor of autophagy and the inducer of NLRP3 reversed the protective effect of H2 against organ damage, the inflammatory response and mitochondrial dysfunction in vivo and in vitro. Collectively, the results demonstrated that H2 alleviated mitochondrial dysfunction and cytokine release via autophagy­mediated NLRP3 inflammasome inactivation.

Dexmedetomidine alleviates LPS-induced apoptosis and inflammation in macrophages by eliminating damaged mitochondria via PINK1 mediated mitophagy.

The macrophage is an innate immune response cell that plays an important role in the development of sepsis. Dexmedetomidine (DEX) is a sedation drug, which have anti-oxidative, anti-inflammatory and anti-apoptosis effects and can be used on sepsis patients in the ICU. However, its mechanisms of action remain poorly understood. PTEN-induced putative kinase 1 (PINK1) is a mitochondrial serine/threonine protein kinase that recognizes damaged mitochondria and leads to mitophagy. This study investigated the effects of DEX on Lipopolysaccharides(LPS)-induced macrophage injury and explained the underlying mechanisms. The results showed that LPS treatment caused mitochondrial damage, mitochondria-dependent apoptosis and PINK1-mediated mitophagy; at the same time, PINK1 has a protective effect on LPS-induced macrophage apoptosis and inflammation by mitophagy that eliminates dysfunctional mitochondria. DEX could promote the clearance of damaged mitochondria characterized by low Mitochondrial membrane potential (MMP) and high reactive oxygen species(ROS), thus exerting a protective effect in LPS treated macrophages, and PINK1 mediated mitophagy is required for this protective effect.

Hydrogen gas inhalation attenuates sepsis-induced liver injury in a FUNDC1-dependent manner.

Sepsis-induced hepatic dysfunction is considered as an independent risk factor of multiple organ dysfunction syndrome (MODS) and death. Mitophagy, a selective form of autophagy, plays a major role in sepsis-induced organ damage. We have demonstrated that hydrogen gas (H2), a selective antioxidant, exerts protective effects in septic mice. Here, we hypothesize that the therapeutic effects of H2 on septic animals with liver damages may be exerted through regulation of the Fun14 domain-containing protein 1 (FUDNC1)-induced mitophagy pathway. Male C57BL/6J mice were subjected to sham or cecal ligation and puncture (CLP) operation and treated with 2% H2 gas inhalation for 3 h starting at 1 h after sham or CLP surgery. To verify the role of FUNDC1, the cell-penetrating peptide P (NH2-GRKKRRQRRRPQDYESDDESYEVLDLTEY-COOH) (1 mg/kg) that functions as a FUNDC1 inhibitor was intraperitoneally injected into mice 24 h before the sham or CLP operation. To evaluate the severity of septic liver injury, the 7-day survival rate, liver histopathologic score, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, respiration control ratio (RCR), and FUDNC1, P-18-FUDNC1, P62, LC3B-II, Tim23, and caspase-1 levels were evaluated after the sham or CLP operation. The results demonstrated that 2% H2 gas inhalation resulted in an increase in the 7-day survival rate, ALT and AST levels, RCR, and P62 and LC3B-II expression but decreased the histological score and FUDNC1, P-18-FUDNC1, Tim23, and caspase-1 levels after sepsis. However, no significant differences were reported between the CLP + peptide P and CLP + H2 + peptide P groups. These observations indicate that 2% H2 gas inhalation for 3 h may serve as an effective therapeutic strategy for sepsis-induced liver injury through the regulation of FUNDC1-dependent mitophagy.

Genome-wide identification and expression profiling of the auxin response factor (ARF) gene family in physic nut.

Auxin response factors (ARF) are important transcription factors which mediate the transcription of auxin responsive genes by binding directly to auxin response elements (AuxREs) found in the promoter regions of these genes. To date, no information has been available about the genome-wide organization of the ARF transcription factor family in physic nut. In this study, 17 ARF genes (JcARFs) are identified in the physic nut genome. A detailed investigation into the physic nut ARF gene family is performed, including analysis of the exon-intron structure, conserved domains, conserved motifs, phylogeny, chromosomal locations, potential small RNA targets and expression profiles under various conditions. Phylogenetic analysis suggests that the 17 JcARF proteins are clustered into 6 groups, and most JcARF proteins from the physic nut reveal closer relationships with those from Arabidopsis than those from rice. Of the 17 JcARF genes, eight are predicted to be the potential targets of small RNAs; most of the genes show differential patterns of expression among four tissues (root, stem cortex, leaf, and seed); and qRT-PCR indicates that the expression of all JcARF genes is inhibited or induced in response to exogenous auxin. Expression profile analysis based on RNA-seq data shows that in leaves, 11 of the JcARF genes respond to at least one abiotic stressor (drought and/or salinity) at, as a minimum, at least one time point. Our results provide valuable information for further studies on the roles of JcARF genes in regulating physic nut's growth, development and responses to abiotic stress.