Dendrimer-Encapsulated Halide Perovskite Nanocrystals for Self-Powered White Light-Emitting Glass.

Perovskite nanocrystals (PNCs) have attracted substantial attention due to their inspiring intrinsic merits such as low cost, high performance, and solution processability, but when it comes to the usage of blends of different colored PNCs with the purpose of covering the broadband spectrum field, the high degree of instability remains a major bottleneck. Herein, we report a family of dendritic ammonium ligands that act as stiff shell-encapsulating PNCs for improving their stability and suppressing ion permeability in mixed colloidal PNC solutions. The as-synthesized ligand-encapsulated PNCs notably achieve near-unity photoluminescence quantum yields (PLQYs) and strongly resist the unwanted ion exchange reaction under aggressive anion source attack. To fabricate self-powered white-emitting glass, the stabilized mixed colored PNCs were embedded into the laminated glass, which simultaneously acted as absorbers-emitters for luminescent solar concentrators (LSCs) and emitters for white light-emitting glass.

Monolithically-grained perovskite solar cell with Mortise-Tenon structure for charge extraction balance.

Although the power conversion efficiency values of perovskite solar cells continue to be refreshed, it is still far from the theoretical Shockley-Queisser limit. Two major issues need to be addressed, including disorder crystallization of perovskite and unbalanced interface charge extraction, which limit further improvements in device efficiency. Herein, we develop a thermally polymerized additive as the polymer template in the perovskite film, which can form monolithic perovskite grain and a unique "Mortise-Tenon" structure after spin-coating hole-transport layer. Importantly, the suppressed non-radiative recombination and balanced interface charge extraction benefit from high-quality perovskite crystals and Mortise-Tenon structure, resulting in enhanced open-circuit voltage and fill-factor of the device. The PSCs achieve certified efficiency of 24.55% and maintain >95% initial efficiency over 1100 h in accordance with the ISOS-L-2 protocol, as well as excellent endurance according to the ISOS-D-3 accelerated aging test.

Regulating Type H Vessel Formation and Bone Metabolism via Bone-Targeting Oral Micro/Nano-Hydrogel Microspheres to Prevent Bone Loss.

Postmenopausal osteoporosis is one of the most prevalent skeletal disorders in women and is featured by the imbalance between intraosseous vascularization and bone metabolism. In this study, a pH-responsive shell-core structured micro/nano-hydrogel microspheres loaded with polyhedral oligomeric silsesquioxane (POSS) using gas microfluidics and ionic cross-linking technology are developed. This micro/nano-hydrogel microsphere system (PDAP@Alg/Cs) can achieve oral delivery, intragastric protection, intestinal slow/controlled release, active targeting to bone tissue, and thus negatively affecting intraosseous angiogenesis and osteoclastogenesis. According to biodistribution data, PDAP@Alg/Cs can successfully enhance drug intestinal absorption and bioavailability through intestine adhesion and bone targeting after oral administration. In vitro and in vivo experiments reveal that PDAP@Alg/Cs promoted type H vessel formation and inhibited bone resorption, effectively mitigating bone loss by activating HIF-1α/VEGF signaling pathway and promoting heme oxygenase-1 (HO-1) expression. In conclusion, this novel oral micro/nano-hydrogel microsphere system can simultaneously accelerate intraosseous vascularization and decrease bone resorption, offering a brand-new approach to prevent postmenopausal osteoporosis.

Heterostructural Nanosheets Consisting of Polycyclic Aromatic Hydrocarbon Shields and Layered Perovskite Cores for Optical Image Encryption.

Optical image encryption technology, in which the emission on/off can be controlled by using specially appointed wavelengths, is useful in information storage and protection. Herein, we report a family of sandwiched heterostructural nanosheets, consisting of three-layered (n = 3) perovskite (PSK) frameworks in center with two different polycyclic aromatic hydrocarbons [triphenylene (Tp) and pyrene (Py)] in periphery. Both heterostructural nanosheets (Tp-PSK and Py-PSK) exhibit blue emissions under UVA-I irradiation; however, different photoluminescent properties are observed under UVA-II. A bright emission of Tp-PSK is attributed to the fluorescence resonance energy transfer (FRET) from Tp-shield to PSK-core, whereas the observed photoquenching phenomenon in Py-PSK is due to the competitive absorption between Py-shield and PSK-core. We exploited the unique photophysical features (on/off emission) of the two nanosheets in a narrow UV window (320-340 nm) for optical image encrypting.

Orientated crystallization of FA-based perovskite via hydrogen-bonded polymer network for efficient and stable solar cells.

Incorporating mixed ion is a frequently used strategy to stabilize black-phase formamidinum lead iodide perovskite for high-efficiency solar cells. However, these devices commonly suffer from photoinduced phase segregation and humidity instability. Herein, we find that the underlying reason is that the mixed halide perovskites generally fail to grow into homogenous and high-crystalline film, due to the multiple pathways of crystal nucleation originating from various intermediate phases in the film-forming process. Therefore, we design a multifunctional fluorinated additive, which restrains the complicated intermediate phases and promotes orientated crystallization of α-phase of perovskite. Furthermore, the additives in-situ polymerize during the perovskite film formation and form a hydrogen-bonded network to stabilize α-phase. Remarkably, the polymerized additives endow a strongly hydrophobic effect to the bare perovskite film against liquid water for 5 min. The unencapsulated devices achieve 24.10% efficiency and maintain >95% of the initial efficiency for 1000 h under continuous sunlight soaking and for 2000 h at air ambient of ~50% humid, respectively.

Osteoporotic bone loss from excess iron accumulation is driven by NOX4-triggered ferroptosis in osteoblasts.

Excess iron accumulation is a risk factor for osteopenia and osteoporosis, and ferroptosis is becoming well understood as iron-dependent form of cell death resulting from lipid peroxide accumulation. However, any pathological impacts of ferroptosis on osteoporosis remain unknown. Here, we show that ferroptosis is involved in excess-iron-induced bone loss and demonstrate that osteoporotic mice and humans have elevated skeletal accumulation of the NADPH oxidase 4 (NOX4) enzyme. Mechanistically, we found that the NOX4 locus contains iron-response element-like (IRE-like) sequences that are normally bound (and repressed) by the iron regulatory protein 1 (IRP1) protein. Binding with iron induces dissociation of IRP1 from the IRE-like sequences and thereby activates NOX4 transcription. Elevated NOX4 increases lipid peroxide accumulation and causes obvious dysregulation of mitochondrial morphology and function in osteoblasts. Excitingly, the osteoporotic bone loss which we initially observed in an excessive-iron accumulating mouse line (Hepc1-/-) was blocked upon treatment with the ferroptosis-inhibitor ferrostatin-1 (Ferr-1) and with the iron chelator deferoxamine (DFO), suggesting a potential therapeutic strategy for preventing osteoporotic bone loss based on disruption of ferroptosis.

Facile Synthesis of Highly Emissive All-Inorganic Manganese Bromide Compounds with Perovskite-Related Structures for White LEDs.

Lead-free all-inorganic halide materials with different Mn2+-based crystal structures (Cs3MnBr5 and CsMnBr3) were obtained using a convenient synthetic method. Cs3MnBr5 had a bright green emission (522 nm), with a unique single-exponential lifetime (τavg = 236 µs) and a high photoluminescence quantum yield (82 ± 5%). A red emission was observed in the case of the CsMnBr3 structure with a two-exponential fluorescence decay curve, and the lifetime was 1.418 µs (93%) and 18.328 µs (7%), respectively. By a judicious tuning of the synthetic conditions, a mixed phase of Cs3MnBr5/CsMnBr3 was also produced that emitted white light, covering almost the entire visible spectrum. White-light-emitting diodes (WLEDs) with color coordinates (0.4269, 0.4955), a color temperature of (3773 K), and a color rendering index (68) were then fabricated using the as-prepared powder of mixed phases of Cs3MnBr5/CsMnBr3 with a commercial UV LED chip (365 nm).

Deciphering core proteins of osteoporosis with iron accumulation by proteomics in human bone.

Iron accumulation is an independent risk factor for postmenopausal osteoporosis, but mechanistic studies of this phenomenon are still focusing on molecular and genetic researches in model animal. Osteoporosis with iron accumulation is a distinct endocrine disease with complicated pathogenesis regulated by several proteins. However, the comprehensive proteome-wide analysis of human bone is lacking. Using multiplex quantitative tandem mass tag-based proteomics, we detected 2900 and quantified 1150 proteins from bone of 10 postmenopausal patients undergoing hip replacement. Comparing with non-osteoporosis patients, a total of 75 differentially expressed proteins were identified, comprising 53 downregulated proteins and 22 upregulated proteins. These proteins primarily affect oxidoreductase activity, GTPase activity, GTP binding, and neural nucleus development, were mainly enriched in neural, angiogenesis and energy-related pathways, and formed complex regulatory networks with strong interconnections. We ultimately identified 4 core proteins (GSTP1, LAMP2, COPB1, RAB5B) that were significantly differentially expressed in the bone of osteoporosis patients with iron accumulation, and validated the changed protein level in the serum of the medical examination population. Our systemic analysis uncovers molecular insights for revealing underlying mechanism and clinical therapeutics in osteoporosis with iron accumulation.

Iron overload induced osteocytes apoptosis and led to bone loss in Hepcidin-/- mice through increasing sclerostin and RANKL/OPG.

BACKGROUND: Numerous studies have demonstrated that iron overload is a risk factor of osteoporosis. However, there has been no systematic and in-depth studies on the effect of iron overload on osteocytes and its role in iron overload-induced bone loss. Therefore, to address this problem, we carried out in vitro and in vivo studies using MLO-Y4 osteocyte-like cells and Hepcidin-/- mice as iron overload models. METHODS: (1) MLO-Y4 cells were treated with ferric ammonium citrate (FAC). Intracellular reactive oxygen species (ROS) levels and apoptosis of MLO-Y4 cells were determined by flow cytometry. Western blotting was performed to evaluate the effect of FAC on the expression of sclerostin and RANKL/OPG. (2) The conditioned medium of MLO-Y4 cells after treatment with FAC was collected and used to treat pre-osteoblasts and monocytes. Alkaline phosphatase (ALP) staining and alizarin red (AR) staining were used to evaluate osteogenic differentiation capacity, and tartrate-resistant acid phosphatase (TRAP) staining was performed to demonstrate osteoclast differentiation capacity. (3) In vivo studies included a wild type mouse, Hepcidin-/- mice, Hepcidin-/- mice + deferoxamine (DFO), and Hepcidin-/- mice + N-actyl-l-cysteine (NAC) group. Micro-CT was performed to evaluate the bone mineral density (BMD), bone volume, and bone micro-architecture of the mice, and three bending tests were used to assess bone strength. Histological analysis was used to detect alterations in bone turnover. TUNEL staining and scanning electron microscopy (SEM) were performed to evaluate the apoptosis and morphology of osteocytes. Immunohistochemical staining and Western blotting were used to determine alterations in sclerostin and RANKL/OPG expression levels in mice. RESULTS: (1) FAC increased intracellular ROS and apoptosis in MLO-Y4 cells, while FAC enhanced the expression of sclerostin and RANKL/OPG in MLO-Y4 cells. (2) Conditioned medium of MLO-Y4 cells inhibited the osteogenic capacity of osteoblasts while stimulating osteoclast differentiation. (3) By increasing oxidative stress, iron overload promotes the apoptosis of osteocytes and undermines the morphology of osteocytes in Hepcidin-/- mice, further increasing the expression levels of sclerostin and RANKL/OPG in osteocytes, which is considered to be the causative factor for reduced bone formation and enhanced bone resorption. DFO administration reduced iron levels, and NAC treatment decreased oxidative stress in Hepcidin-/- mice. Therefore, DFO or NAC treatment rescued the decrease in BMD, bone volume, and bone strength and attenuated the deterioration of bone architecture in Hepcidin-/- mice by attenuating the effect of iron overload on osteocytes. CONCLUSION: Osteocyte apoptosis due to increased ROS and resultant sclerostin and RANKL/OPG expression alteration was the main reason for bone loss in Hepcidin-/- mice. Osteocytes are the main targets for the prevention and treatment of iron overload-induced osteoporosis.

Mechanism of Pilose Antler in Treatment of Osteoporosis Based on Network Pharmacology.

Background: The purpose of this study was to demonstrate the pharmacodynamic material basis and molecular mechanism of pilose antler (PA) in the prevention and treatment of osteoporosis (OP) by the method of network pharmacology. Methods: First, the active components of PA were screened by BATMAN-TCM database, and the component targets were obtained from the SwissTargetPrediction online tool. Moreover, the relevant target genes of OP were obtained by searching the DisGeNET database. Second, the Venn diagram was drawn to obtain the PA-OP common targets, and the protein-protein interaction (PPI) network and drug-component-target (D-C-T) network were constructed by Cytoscape software. Finally, the GO functional annotation and KEGG pathway enrichment analysis of common targets were performed using the Metascape online tool. Results: 82 common targets were identified by generating a Venn diagram. The PPI network of 82 common targets indicated that the top 5 nodal targets, including PIK3CA, MAPK1, ESR1, AKT1, and SRC, were strongly associated with other proteins. The D-C-T network suggested that the active components with high degree of connectivity include Prostaglandin E1, 17-Beta-Estradiol, Alpha-Estradiol, and Estrone. Furthermore, the GO enrichment analysis revealed that the biological process categories were dominated by response to peptide, cellular response to lipid, regulation of MAPK cascade, and so on. Additionally, the KEGG pathway analysis indicated the estrogen signaling pathway, osteoclast differentiation, and HIF-1 signaling pathway might have critical effects on the development of OP. Conclusion: The study shows that PA has the characteristics of multi-component, multi-target, and multi-pathway in treating osteoporosis.

Ferrocene-Induced Perpetual Recovery on All Elemental Defects in Perovskite Solar Cells.

Lead halide perovskites always emerge complex interactions among different elemental ions, which lead to multiple intrinsic imperfections. Elemental defects, such as amine, Pb, and I vacancies at A-, B-, and X-sites, are main issues to deteriorate perovskite solar cells (PSCs). Unfortunately, most previous passivators can only temporarily fix partial inactive vacancies as sacrificial agents. Herein, we propose a recovery agent, ferrocene (Fc), which can form a one-dimensional perovskite with adequate steric cavities and suitable dissociation energy to recover all elemental defects back to active light-harvesting perovskites, and regenerate Fc itself meanwhile. Based on this perpetual chain-reaction cycle, corresponding PSCs maintain >10 000-hour lifetime in inert condition and >1000-hour durabilities under various extreme environments, including continuous 85 °C heating, 50 % relative humidity wetting, and 1-sun light soaking.

Hepcidin-induced reduction in iron content and PGC-1ß expression negatively regulates osteoclast differentiation to play a protective role in postmenopausal osteoporosis.

As a necessary trace element, iron is involved in many physiological processes. Clinical and basic studies have found that disturbances in iron metabolism, especially iron overload, might lead to bone loss and even be involved in postmenopausal osteoporosis. Hepcidin is a key regulator of iron homeostasis. However, the exact role of hepcidin in bone metabolism and the underlying mechanism remain unknown. In this study, we found that in postmenopausal osteoporosis cohort, the concentration of hepcidin in the serum was significantly reduced and positively correlated with bone mineral density. Ovariectomized (OVX) mice were then used to construct an osteoporosis model. Hepcidin overexpression in these mice significantly improved bone mass and rescued the phenotype of bone loss. Additionally, overexpression of hepcidin in OVX mice greatly reduced the number and differentiation of osteoclasts in vivo and in vitro. This study found that overexpression of hepcidin significantly inhibited ROS production, mitochondrial biogenesis, and PGC-1ß expression. These data showed that hepcidin protected osteoporosis by reducing iron levels in bone tissue, and in conjunction with PGC-1ß, reduced ROS production and the number of mitochondria, thus inhibiting osteoclast differentiation and bone absorption. Hepcidin could provide new targets for the clinical treatment of postmenopausal osteoporosis.

Lead-free Mn-doped antimony halide perovskite quantum dots with bright deep-red emission.

We reported the first synthesis of Mn2+ doped Cs3Sb2Clx/Br9-x (0 ≤ x ≤ 9) perovskite quantum dots (PQDs) by regulating the coprecipitation of Mn2+ and Sb3+ with thiol ligands. These lead-free PQDs demonstrated bright photoluminescence emission centered at 660 nm and a high quantum yield of ∼49%, making them suitable for optical applications.

Synthesis of two-dimensional phenylethylamine tin-lead halide perovskites with bandgap bending behavior.

Recently, two-dimensional (2D) metal halide perovskite materials with wide application in perovskite-based solar cells have attracted significant attention. Among them, 2D mixed lead-tin perovskites have not been systematically explored. Herein, we synthesize a 2D phenethylammonium (PEA) tin-lead bromide perovskite, PEA2Sn x Pb1-x Br4, via a simple solution-phase approach without toxic reagents and high temperatures. By tuning the ratio of Sn and Pb, the UV-vis absorption spectra showed unique bandgap bending behaviors. DFT calculations indicate the key effects of spin-orbital coupling (SOC) without the interference of lattice distortion. Moreover, we provided the standard equation with a correction term to introduce the influence of SOC. These results not only provide a step forward towards the bandgap engineering of perovskites, but also help to expand the application of 2D perovskite materials.

Bone Microthrombus Promotes Bone Loss in Iron Accumulation Rats.

In the present study, we investigated the changes of the coagulation state, bone microthrombus, microvascular bed and bone density levels in iron accumulation rats. Meanwhile,the effect of anticoagulation therapy on bone mineral density was further investigated. We established two groups: a control (Ctrl) group and an iron intervention (FAC) group. Changes in coagulation function, peripheral blood cell counts, bone microthrombus, bone vessels and bone mineral density were compared between the two groups. We designed the non-treatment group and treatment group to study the changes of bone mineral density by preventing microthrombus formation with the anticoagulant fondaparinux. We found that the fibrinogen and D-dimer contents were significantly higher, whereas the thrombin time (TT) and prothrombin time (PT) were significantly shorter in the FAC group. After ink staining, the microvascular bed in the FAC group was significantly reduced compared with that in the Ctrl group. HE and Martius Scarlet Blue (MSB) staining showed microthrombus in the bone marrow of the iron accumulation rats. Following anticoagulation therapy, the bone microcirculation vascular bed areas in the treatment group rats were significantly increased. Furthermore, the bone mineral density was increased in the treatment group compared with that in the non-treatment group. Through experiments, we found that the blood in iron accumulation rat was relatively hypercoagulable; moreover, there was microthrombus in the bone marrow, and the bone vascular bed was reduced. Additionally, anticoagulation was helpful for improving bone microcirculation, reducing microthrombus and decreasing bone loss.

Hepcidin deficiency causes bone loss through interfering with the canonical Wnt/ß-catenin pathway via Forkhead box O3a.

OBJECTIVE: Hepcidin deficiency is known to cause body iron accumulation and bone microarchitecture defects, but the exact underlying mechanisms of hepcidin deficiency-induced bone loss remain unclear. Our objective was to understand the molecular mechanism of hepcidin deficiency-induced bone loss. METHODS: The bone phenotypes of wild type (WT) and hepcidin knockout (Hepcidin-KO) mice were measured by microcomputed tomography. The osteoclastic marker of the bone was measured by tartrate-resistant acid phosphatase staining. The osteoblastic marker of the bone was measured by immunostaining of osteocalcin. Primary osteoblastic and osteoclastic differentiation was performed using bone marrow cells. The mature osteoclast was determined by tartrate-resistant acid phosphatase staining, pit formation assay and relative gene expression. The mature osteoblast was determined by alkaline phosphatase activity, alkaline phosphatase staining, Alizarin Red staining and relative gene expression. The protein expression of ß-catenin, TCF4/TCF7L2 and Forkhead box O3a (FOXO3a) was measured by Western blot and their combination by co-immunoprecipitation. In vivo study was performed by tail vein administration of FOXO3a-RNAi using an adeno-associated virus in Hepcidin-KO mice. RESULTS: We found that Hepcidin-KO mice exhibited iron accumulation and bone loss compared with WT mice. The osteoclastic differentiation of bone marrow-derived macrophages from Hepcidin-KO mice was not significantly different from that of bone marrow-derived macrophages from WT mice. However, the osteoblastic differentiation of bone marrow-derived mesenchymal stem cells from Hepcidin-KO mice was obviously decreased compared with that of bone marrow-derived mesenchymal stem cells from WT mice. Furthermore, it was confirmed in this study that upon hepcidin deficiency, ß-catenin, TCF4/TCF7L2 and FOXO3a expression in bone tissues was not altered, but ß-catenin combination with TCF4/TCF7L2 was strongly inhibited by ß-catenin combination with FOXO3a, indicating that the canonical Wnt/ß-catenin pathway was affected. Tail vein administration of FOXO3a-RNAi using an adeno-associated virus in Hepcidin-KO mice resulted in bone mass recovery. CONCLUSION: These findings suggested that hepcidin deficiency might cause bone loss by interfering with the canonical Wnt/ß-catenin pathway via FOXO3a, and FOXO3a inhibition would be a possible approach to treat hepcidin deficiency-induced bone loss. THE TRANSLATIONAL POTENTIAL OF THIS ARTICLE: Hepcidin deficiency, as well as iron accumulation, has been considered as a risk factor for osteoporosis. For this kind of osteoporosis, inhibition of FOXO3a either by neutralized antibody or AAV-mediated RNAi, represents an effective and promising method.

Efficient and Stable Thin-Film Luminescent Solar Concentrators Enabled by Near-Infrared Emission Perovskite Nanocrystals.

A novel triphenylphosphine (TPP) treatment strategy was developed to prepare the near-infrared emission CsPbI3 nanocrystal (NC)-polymer composite thin-film luminescent solar concentrators (LSCs) featuring high absolute photoluminescence quantum yield (PLQY), low reabsorption, and high stability. The PL emission of the LSCs is centered at about 700 nm with 99.4±0.4 % PLQY and narrow full width at half maximum (FWHM) of 75 meV (30 nm). Compared with LSCs prepared with classic CsPbI3 NCs, the stability of the LSCs after TPP treatments has been greatly improved, even after long-term (30 days) immersion in water and strong mercury-lamp irradiation (50 mW cm-2 ). Owing to the presence of lone-pair electrons on the phosphorus atom, TPP is also used as a photoinitiator, with higher efficiency than other common photoinitiators. Large-area (ca. 75 cm2 ) infrared LSCs were achieved with a high optical conversion efficiency of 3.1 % at a geometric factor of 10.

Aqueous acid-based synthesis of lead-free tin halide perovskites with near-unity photoluminescence quantum efficiency.

Recently, lead halide perovskites with outstanding emission performance have become new candidate materials for light-emitting devices and displays; however, the toxicity of lead and instability of halide perovskites remain significant challenges. Herein, we report the aqueous acid-based synthesis of highly emissive two-dimensional (2D) tin halide perovskites, (octylammonium)2SnX4 (X = Br, I, or mixtures thereof), which displayed a high absolute photoluminescence (PL) quantum yield of near-unity in the solid-state, PL emission centered at 600 nm with a broad bandwidth (136 nm), a large Stokes shift (250 nm), long-lived luminescence (τ = 3.3 µs), and zero overlap between their absorption and emission spectra. Significantly, the stability study of 2D tin halide perovskites monitored by the PL quantum yield showed no changes after 240 days of storage at room temperature under ambient air and humidity conditions. The PL emission of the 2D tin halide perovskites was tuned from yellow to deep red by controlling halide composition. Furthermore, new yellow phosphors with superior optical properties are used to fabricate UV pumped white light emitting diodes (WLEDs). We expect these results to facilitate the development of new environmentally friendly and high-performance phosphors for future lighting and display technologies.

Rapamycin improves bone mass in high-turnover osteoporosis with iron accumulation through positive effects on osteogenesis and angiogenesis.

Iron accumulation is an independent risk factor for type I osteoporosis, but the molecular mechanisms of the phenomenon are not well defined, and effective therapy has not been reported. Here, we found that the level of mTOR was increased both in wild-type mouse models with iron accumulation and transgenic mouse models (Hepc-/-) of high-turnover osteoporosis with iron accumulation. We show that an increased level of mTOR can depress osteogenesis and angiogenesis by Cxcl9 both in bone and in vitro. Suppression of mTOR in mouse models by rapamycin and in vitro by siRNA transfection recovered both osteogenesis and angiogenesis. These findings revealed the role of mTOR in osteogenesis and angiogenesis in high-turnover osteoporosis with iron accumulation and showed that rapamycin targeting of mTOR ameliorates osteogenesis and angiogenesis to improve bone mass.