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Accompanied by internal defect evolution in the perovskite lattice, the naturally formed “hollow” defects and obviously blue-shifted emission of CsEuCl3 nanocrystals were observed.

Mn4+-activated phosphors have become a hotspot in the development of inorganic red phosphors due to the fascinating photoluminescent properties. Herein, the synergetic manipulation of the flux effect and charge compensation was employed to improve the performance of Mn4+-activated CaAl12O19 red phosphors. The crystallinity was improved by appropriate Zn2+-doping, while nonradiative transition between Mn4+ ions is reduced by charge compensation of the formation of Mn4+–Mg2+ pairs with Mg2+ dopants. Thus, the emission of Mn4+-activated CaAl12O19 red phosphors has been remarkably enhanced. The low probability of nonradiative transition between Mn4+ ions was demonstrated by the thermal stability analysis. To depict the luminescent process, the crystal-field strength (Dq), and Racah parameters (B and C) were calculated to determine the sequence of the energy levels. Meanwhile, the warm WLEDs with high CRI and low CCT were obtained using the prepared phosphors as red-emitting composition. Our results clearly suggested that the synergetic strategy by combining the flux effect and charge compensation is an effective method to enhance the luminescence of CaAl12O19:Mn4+, and CaAl12O19:Mn4+/Zn2+/Mg2+ red-emitting phosphors, which have potential application value in warm WLEDs.

To research and develop the potential red emission phosphors for warm white-light-emitting diodes (WLED), we systematically investigated double alkaline rare-earth molybdates KGd1−xEux(MoO4)2 (0.05 ≤ x ≤ 1) phosphors. The crystal structure, morphology, chemical composition, and photoluminescence properties of the phosphors with different Eu3+ doping concentrations were investigated in detail. The results indicate that Eu3+ doping concentration can affect the crystal structure and morphology of KGd1−xEux(MoO4)2 phosphors. The luminescence performance reveals that KGd1−xEux(MoO4)2 phosphor could emit intense red emission under multiplexed excitations at 362, 382, 394, 465, and 535 nm, which are matched well with the commercial UV, blue and green LED chips. An abnormal quenching behavior was observed in the KGd1−xEux(MoO4)2 phosphors. And the quenching behavior at the excitation of Eu3+–O2− Charge-Transfer band and Eu3+ ions 4f–4f transitions is quite different. Finally, we fabricated a WLED lamp by coating the InGaN blue chip with a mixture of YAG: Ce3+ yellow phosphors and KEu(MoO4)2 red phosphors. The obtained WLED lamps showed warm white light with a lower CCT value (~ 5142 K) than that fabricated without the red phosphors (CCT = 5892 K). These results proved that the KGd1−xEux(MoO4)2 could be a very promising red-emitting phosphor for WLED.

Aim: To find out risk factors for postoperative cognitive dysfunction (POCD) after coronary artery bypass grafting (CABG), and to provide basis for clinical prevention of POCD. A total of 88 patients who underwent CABG were surveyed with Telephone Questionnaire (TICS-M) for their cognitive impairment after 3, 7, 21, 90, 180 days post-surgery. The occurrence of POCD was diagnosed by Neuropsychological Battery which included Vocabular Learning Test (VLT), Wisconsin Card Sorting Test (WCST), Trail Making Test (TMT) and Symbol Digit Modalities Test (SDMT). The preoperative, intraoperative and postoperative risk factors were assessed by the χ2 or t test. Multivariate analysis was used to study the correlation between the risk factors and the occurrence of POCD. Age, aortic plaque, carotid artery stenosis, cerebrovascular disease, anesthesia time, the rate of decline in intraoperative hemoglobin concentration (ΔHb) and systemic inflammatory response syndrome (SIRS) score on postoperative day 2 had statistically significant (P 1, P

Correction for ‘Enhanced photoluminescence stability and internal defect evolution of the all-inorganic lead-free CsEuCl3 perovskite nanocrystals’ by Yalei Gao et al., Phys. Chem. Chem. Phys., 2022, 24, 18860–18867, https://doi.org/10.1039/D2CP01374F.

The dictionary-aided sparse regression (SR) approach has been developed in hyperspectral unmixing (HU) in remote sensing. By using an available spectral library as a dictionary, the SR approaches unmix the spectral image by selecting the endmember matrix from the library which best represent the image and its fractional abundance. In this paper, we proposed a simultaneous dictionary refining and enhanced sparse regression method for hyperspectral unmixing(DRESR). The proposed method not only enhances the sparsity of fractional abundance through double weighted sparse regularization, and also improves the spectral signature mismatches between an actual spectra and its corresponding endmember in the spectral library by using dictionary sparse refining. Experimental results on both synthetic and real hyperspectral data sets demonstrate better performance compared with several state-of-art algorithms.

Increasing evidence indicates that stress potentiates pro-inflammatory response to a subsequent peripheral immune challenge. The present study investigated if prior exposure to inescapable tailshock (IS) delayed the recovery of surgery-induced spatial learning and memory impairment and prolonged hippocampus interleukin (IL)-1β and IL-6 expression. Methods A total of 192 aged rats were trained with Morris water-maze (MWM) for 6 consecutive days. A single session of inescapable tailshock was performed on day 6 after training. Then, the rats subjected to partial hepatectomy. Hippocampal-dependent spatial learning and memory were assessed on postoperative days 1, 3 and 7. The cytokines IL-1β and IL-6 and ionized calcium binding adaptor protein (Iba)-1 were measured at each time point. Cluster of differentiation 200 (CD200) was also measured to explore potential mechanisms of glial cell activation. Results Exposure of IS alone failed to affect the latency to platform and increase hippocampal cytokine levels at each time point. However, IS alone significantly increased the expression levels of Iba-1. A prolonged latency and additional significant increase in hippocampal levels of IL-1β and IL-6 were observed when partial hepatectomy was performed in aged rats exposed to IS 24 h later. The combination of IS and surgical trauma dramatically upregulated the levels of Iba-1 and significantly decreased the expression of CD200. Conclusion IS alone failed to induce cognitive deficits and increase pro-inflammatory cytokines expression. However, IS delayed the recovery of surgery-induced spatial learning and memory impairment and prolonged pro-inflammatory response to the subsequent surgery challenge.

Accumulated evidence indicates that stress sensitizes neuroinflammatory responses to a subsequent peripheral immune challenge. The present study investigated whether chronic unpredictable stress (CUS) aggravated surgery-induced sickness behavior and neuroinflammatory processes via glucocorticoids secretion in the adult brain. Methods Sprague-Dawley adult male rats (12–14 weeks old) were exposed to 14-day CUS and then subjected to partial hepatectomy 24 h after the last stress session. The rats were pretreated with an antagonist of the glucocorticoids (GCs) receptor RU486 (30 mg/kg, i.p.) 1 h prior to stress exposure. The behavioral changes were evaluated with open field test and elevated plus-maze test. The hippocampal cytokines interleukin (IL)-1β and IL-6 were measured on postoperative days 1, 3 and 7. Ionized calcium binding adaptor protein (Iba)-1, microglial M2 phenotype marker Arg1, brain derived neurotrophic factor (BDNF) and CD200 were also examined at each time point. Results CUS exacerbated surgery-induced sickness behavior. Exposure to CUS alone failed to alter the levels of pro-inflammatory cytokines in the brain. However, CUS exaggerated surgery-induced pro-inflammatory cytokines expression (e.g. IL-1β and IL-6) and upregulated the levels of Iba-1 on postoperative days 1 and 3. An additional significant decreased BDNF, CD200 and a lower level of Arg1 were also observed in the stressed rats following surgical procedure. Pretreatment with RU486 blunted the potentiating effects of CUS on surgery-induced sickness behavior and neuroinflammatory responses. Conclusion Chronic unpredictable stress enhanced surgery-induced sickness behavior and neuroinflammatory responses. Stress-induced GCs played a pivotal role in enhancing surgery-induced neuroinflammatory processes by modulation of microglia functions.