Ce³⁺-Activated SrLu₂Al₃ScSiO₁₂ Cyan-Green-Emitting Garnet-Structured Inorganic Phosphor Materials toward Application in Blue-Chip-Based Phosphor-Converted Solid-State White Lighting

Phosphor-converted white-light-emitting diodes (WLEDs) with superhigh color rendering index (CRI) are the ongoing pursuit of next-generation solid-state lighting. One of the most important challenges is the limited improvement in CRI on account of the absence of a cyan component in the typical commercial combination. Here, a bright broad-band cyan-green-emitting phosphor with cubic garnet structure, SrLu2Al3ScSiO12:Ce3+ (SLASSO:Ce3+), was successfully reported, which can compensate for the absence of cyan cavity in the 480–520 nm blue-green emission region. With 439 nm blue-light irradiation, the as-fabricated SLASSO:Ce3+ phosphor yields a broad-band cyan-green emission with the maximum emission peak positioned at 525 nm and an appropriate full width at half-maximum (fwhm) of 111 nm, capable of providing more cyan emission component without sacrificing green emission. Meanwhile, the optimal SLASSO:2�3+ phosphor features CIE color coordinates of (0.3254, 0.5470) with cyan-green hue, along with a high internal quantum efficiency of up to 93%. Additionally, thermal stability measurements at different temperatures reveal that the luminescence emission intensity of the proposed phosphor retains 44% of its original integral emission intensity at 423 K with respect to room temperature, while also demonstrating an excellent color stability (ΔE = 5.4 × 10–3). This work shows that the highly efficient SLASSO:Ce3+ garnet phosphor can be utilized as a potential cyan-green-emitting phosphor for filling the cyan gap, resulting in the construction of a high-quality warm WLED with high CRI for “human-centric” sunlight-like full-spectrum solid-state illumination

Amphiphilic-Polymer-Guided Plasmonic Assemblies and Their Biomedical Applications

Plasmonic nanostructures with unique physical and biological properties have attracted increased attention for potential biomedical applications. Polymers grafted on metal nanoparticle surface can be used as assembly regulating molecules to guide nanoparticles organize into ordered or hierarchical structures in solution, within condensed phases, or at interfaces. In this Topical Review, we will highlight recent efforts on self-assembly of gold nanoparticles coated with polymer brushes. How and what kind of polymer graft can be used to adjust nanoparticle interactions, to dictate interparticle orientation, and to determine assembled nanostructures will be discussed. Furthermore, the Topical Review will shed light on the physicochemical properties, including self-assembly behavior and kinetics, tunable localized surface plasmon resonance effect, enhanced surface enhanced Raman scattering, and other optical and thermal properties. The potential of self-assembled nanostructures for applications in different fields, especially in biomedicine, will also be elaborated

LRP attenuated edema induced by stroke.

<p><b>A</b>. Diagram of the dissected regions of the ischemic penumbra and core for BBB leakage measurement. The penumbra (I) is defined as the ischemic region spared by LRP, while the core (II) is the ischemic part that developed into the infarction. The same regions were also dissected for Western blotting. <b>B</b>. LRP inhibited BBB leakage. Evans blue was injected 2 h before the rat was euthanized. The ischemic penumbra and core, as well as the corresponding non-ischemic hemisphere were dissected for Evans blue detection. LRP reduced BBB leakage at 48 h after stroke in the penumbra but not in the core (n = 6/group). * vs. control ischemia, <i>P</i><0.05. <b>C.</b> LRP mitigated edema after stroke. The ischemic and non-ischemic hemispheres from each rat brain were separated, weighed for wet weight, baked at 90±2°C for 1 wk, and weighed again for dry weight. Water contained in the brain tissues was calculated and is presented in the bar graph (n = 6–7/group). *** vs. contralateral hemisphere, <i>P</i><0.001; ### vs. sham and control ischemia, <i>P</i><0.001.</p

LRP attenuated behavioral deficits for up to 2 months post-ischemia.

<p>Three standard tests were performed. <b>A.</b> Vibrissae-elicited forelimb placement test. All sham rats showed normal forelimb placing. Control ischemic rats exhibited unsuccessful placing of the contralateral forelimb (right) after stroke. The reflex was tested 10 times on each side per trial, and 2 trials occurred per test session. The percentage of vibrissa stimulations in which a paw placement occurred was calculated. LRP attenuated the overall deficit from 2 to 60 d after stroke. <b>B.</b> Postural reflex test. Scores were increased in control rats at 1, 2, 7, 10, and 21 d after stroke; LRP reduced scores at 10 and 14 d after stroke compared with control stroke. <b>C.</b> Home cage forelimb use test. The number of times the animal used its forelimbs to brace itself against the wall of the cage was counted, with separate counting for the ipsilateral, contralateral, or both forelimbs until 20 contacts were reached. The percentage of times out of 20 that the ipsilateral forelimb (left) was used was computed. The ratio of left-limb-use was increased at 1, 2 and 7 d compared to control ischemia; LRP blocked this increase at 2 d. *, ** vs. control ischemia, and #, ##, vs. sham, <i>P</i><0.05, 0.01 at the corresponding time points, respectively. N = 6–8/group.</p

LRP blocked iNOS expression and nitrotyrosine after stroke.

<p><b>A and C.</b> Representative protein bands of iNOS and quantitative results in the penumbra are shown for control ischemia. <b>B and D.</b> Representative protein bands of iNOS in the penumbra and quantitative results for the animals receiving control ischemia and LRP. iNOS was increased from 1 to 24 h after stroke in rats receiving control ischemia. LRP inhibited iNOS expression. *, **, *** vs. sham, <i>P</i><0.05, 0.01. 0.001, respectively. n = 6/group. <b>E.</b> LRP blocked nitrotyrosine expression. Nitrotyrosine is a product of iNOS activities. Immunostaining suggested that nitrotyrosine expression was increased 24 h after stroke in control ischemic rats, and this was attenuated by LRP. Scale bar, 50 µM.</p

LRP reduced brain injury after focal ischemia.

<p><b>A.</b> Diagram of the LRP protocol. In the LRP group, 3 cycles of 15 min occlusion/reperfusion of the left femoral artery was induced before stroke onset. In the control group, 90 min of isoflurane was applied before ischemia, as a vehicle control for LRP. <b>B.</b> Top: Representative brain sections of TTC staining from rats receiving focal ischemia with and without LRP. Bottom: Bar graph showing the quantitation of infarct sizes in the ischemic cortex measured at each level and normalized to the non-ischemic contralateral cortex, and expressed as percentage. <b>C.</b> Top: Representative staining of cresyl/violet from rat brains 60 d post-stroke. The lost and damaged tissues are traced with dashed lines. Bottom: Bar graph showing the average value from 4 levels of brain sections. Control, control ischemia. LRP, limb remote preconditioning. N = 6–7/group. **, ***, <i>P</i><0.01, 0.001, respectively, vs. control.</p

Tim-3 expression was increased after stroke and inhibited by LRP.

<p><b>A and B.</b> Western blots showing representative protein bands of Tim-3 and β-actin in the ischemic penumbra for rats receiving control ischemia alone and ischemia plus LRP, respectively. <b>C.</b> Bar graphs indicating that Tim-3 was slightly increased as early as 1 h and peaked at 24 h after stroke. <b>D.</b> This was inhibited by LRP. ***, vs. sham, <i>P</i><0.001. n = 6/group. <b>E</b>. The results were further confirmed using immunofluorescent confocal microscopy in control ischemia and LRP 24 h after stroke. An ischemic brain was collected from a surviving rat 24 h after stroke, fixed for 24 h with 4% PFA, stained, and examined with confocal microscopy. <b>F.</b> Double staining of MAP-2 and Tim-3 suggests that Tim-3 was expressed in neurons. Scale bar, 50 µM.</p

Blocking nerve pathways enlarged infarct size in rats receiving LRP. A. Systemic injection of capsaicin enlarged infarction in rats receiving LRP.

<p>Capsaicin was subcutaneously injected into rats for 4 consecutive days. LRP and focal ischemia were conducted 2 wks after capsaicin injection, and infarct sizes were measured 2 d after stroke. The bar graphs represent the mean values of infarct size in 4 groups: 1) ischemia, control ischemia; 2) LRP, animals receiving LRP plus ischemia; 3) capsaicin+LRP, animals receiving capsaicin injection, LRP and ischemia; 4) capsaicin+ischemia, animals receiving capsaicin and control ischemia. <b>B.</b> Local application of capsaicin onto the thigh nerve in the hind limb abolished the protective effects of LRP. The nerve was soaked with a capsaicin solution for 30 min. Four days later LRP and focal ischemia were conducted. The bar graphs show average infarct sizes. <b>C</b>. The ganglion blocker hexamethonium blocked the protective effects of LRP. Hexamethonium was intravenously injected into rats 30 min before LRP induction. Infarct sizes were measured at 2 days after stroke. The bar graphs show the average values of infarct size of 4 groups. 1) Ischemia, control ischemia without LRP; 2) LRP, animals receiving ischemia and LRP; 3) Hex+LRP, animals receiving hexamethonium, LRP and ischemia; 4) Hex+ischemia, animals receiving hexamethonium and ischemia without LRP. N = 7/group. *, *** vs. ischemia, <i>P</i><0.05, 0.001, respectively. #, ##, vs. LRP.</p

New Generation of Gold Nanoshell-Coated Esophageal Stent: Preparation and Biomedical Applications

Esophageal cancer is one of the six most common cancers in the world, constituting ∼7% of the gastrointestinal cancers. Esophageal stents can be inserted into the esophagus to open the pathway as a palliative treatment for advanced esophageal cancer. For the treatment of esophageal cancer, a series of anticancer drug-loaded stents such as paclitaxel or 5-fluorouracil/esophageal stent combinations have been prepared by covering a nitinol stent with a polymer or hydrogel shell. For the first time, we developed a gold nanoshell (AuNS)-coated stent with high photothermal efficiency and used in the repetitive photothermal therapy of esophageal cancer. The functionalized stent was prepared by using surface-coated polydopamine as the Au³⁺ anchor and template. The thickness of the AuNS can be easily adjusted by controlling the reaction time and amount of Au³⁺. The AuNS-coated stent efficiently increased the temperature of pork and porcine intestines irradiated with a near-infrared (NIR) laser. The deep penetration of the NIR laser and excellent stability of the stent provide opportunity for the clinical applications of the newly functionalized stent. In vitro toxicity experiments showed excellent biocompatibility and safety of this device. Compared with bare metal stent, AuNS-modified stent exhibits great potential to open the duct passageway and suppress tumor growth in future clinical applications

Bioconjugated Manganese Dioxide Nanoparticles Enhance Chemotherapy Response by Priming Tumor-Associated Macrophages toward M1-like Phenotype and Attenuating Tumor Hypoxia

Hypoxia promotes not only the invasiveness of tumor cells, but also chemoresistance in cancer. Tumor associated macrophages (TAMs) residing at the site of hypoxic region of tumors have been known to cooperate with tumor cells, and promote proliferation and chemoresistance. Therefore, there is an urgent need for new strategies to alleviate tumor hypoxia and enhance chemotherapy response in solid tumors. Herein, we have taken advantage of high accumulation of TAMs in hypoxic regions of tumor and high reactivity of manganese dioxide nanoparticles (MnO₂ NPs) toward hydrogen peroxide (H₂O₂) for the simultaneous production of O₂ and regulation of pH to effectively alleviate tumor hypoxia by targeted delivery of MnO₂ NPs to the hypoxic area. Furthermore, we also utilized the ability of hyaluronic acid (HA) modification in reprogramming anti-inflammatory, pro-tumoral M2 TAMs to pro-inflammatory, antitumor M1 macrophages to further enhance the ability of MnO₂ NPs to lessen tumor hypoxia and modulate chemoresistance. The HA-coated, mannan-conjugated MnO₂ particle (Man-HA-MnO₂) treatment significantly increased tumor oxygenation and down-regulated hypoxia-inducible factor-1 α (HIF-1α) and vascular endothelial growth factor (VEGF) in the tumor. Combination treatment of the tumors with Man-HA-MnO₂ NPs and doxorubicin significantly increased apparent diffusion coefficient (ADC) values of breast tumor, inhibited tumor growth and tumor cell proliferation as compared with chemotherapy alone. In addition, the reaction of Man-HA-MnO₂ NPs toward endogenous H₂O₂ highly enhanced <i>T</i>₁- and <i>T</i>₂-MRI performance for tumor imaging and detection