Long-term Efficacy and Safety of High-frequency Spinal Stimulation for Chronic Pain: A Meta-analysis of Randomized Controlled Trial.

OBJECTIVE: The aim of our meta-analysis was to systematically assess the enduring effectiveness and safety of high-frequency spinal stimulation (HF-SCS) in the management of chronic pain. METHODS: We developed a comprehensive literature search strategy to identify clinical trials investigating the efficacy of high-frequency spinal stimulation for chronic pain. The search was conducted in multiple databases, including Web of Science, Cochrane, PubMed, and Embase, covering the period from 2004 to 2023. The inclusion and exclusion criteria established for this study were applied to screen the eligible literature by carefully reviewing abstracts and, when necessary, examining the full text of selected articles. To assess the quality of the included studies, we utilized the risk of bias assessment tool provided by the Cochrane Collaboration.The PRISMA method was followed for the selection of articles, and the quality of the articles was evaluated using the risk assessment table for bias provided by the Cochrane Collaboration.Meta-analysis of the selected studies was performed using Review Manager 5.4 and STATA 16.0. Effect sizes for continuous data were reported as mean differences (MD) or standardized mean differences (SMD), while categorical data were analyzed using relative risks (RR). RESULTS: According to our predefined literature screening criteria, a total of seven English-language randomized controlled trials (RCTs) were included in the meta-analysis. The findings from the meta-analysis demonstrated that high-frequency spinal cord stimulation (HF-SCS) exhibited superior efficacy in the long-term treatment of chronic pain when compared to the control group (RR = 2.44, 95% CI [1.20, 4.96], P = 0.01). Furthermore, HF-SCS demonstrated a statistically significant improvement in the Oswestry Disability Index score (mean difference MD = 3.77, 95% CI [1.17, 6.38], P = 0.005).However, for pain assessment (standardized mean difference SMD = -0.59, 95% CI [-1.28, 0.10], P = 0.09), Patient Global Impression of Improvement (PGI-I) score (MD = 0.11, 95% CI [-0.66, 0.88], P = 0.78 for 6 months; MD = 0.02, 95% CI [-0.42, 0.43], P = 0.97 for 12 months), Clinical Global Impression of Improvement (CGI-I) score (MD = -0.58, 95% CI [-1.62, 0.43], P = 0.27 for 6 months; MD = -0.23, 95% CI [-0.94, 0.48], P = 0.52 for 12 months), and occurrence of adverse effects (odds ratio OR = 0.77, 95% CI [0.23, 2.59], P = 0.67) from a statistical point of view, HF-SCS did not show sufficient effect compared with the control group. Not significant enough to consider it. CONCLUSIONS: The findings from our comprehensive review and meta-analysis, encompassing research from 2004 to 2023, offer encouraging data about the prolonged efficacy and safety of HF-SCS in chronic pain management. Nonetheless, recognizing the constraints of the existing evidence is crucial. Upcoming clinical trials, meticulously planned and stringent, are essential to bolster the current body of evidence and reach more conclusive findings.

Morpho-physiological, Genomic, and Transcriptional Diversities in Response to Potassium Deficiency in Rapeseed (Brassica napus L.) Genotypes.

Variations in the resistance to potassium (K) deficiency among rapeseed genotypes emphasize complicated regulatory mechanisms. In this study, a low-K-sensitivity accession (L49) responded to K deficiency with smaller biomasses, severe leaf chlorosis, weaker photosynthesis ability, and deformed stomata morphology compared to a low-K resistant accession (H280). H280 accumulated more K+ than L49 under low K. Whole-genome resequencing (WGS) revealed a total of 5,538,622 single nucleotide polymorphisms (SNPs) and 859,184 insertions/deletions (InDels) between H280 and L49. RNA-seq identified more differentially expressed K+ transporter genes with higher expression in H280 than in L49 under K deficiency. Based on the K+ profiles, differential expression profiling, weighted gene coexpression network analysis, and WGS data between H280 and L49, BnaC4.AKT1 was proposed to be mainly responsible for root K absorption-mediated low K resistance. BnaC4.AKT1 was expressed preferentially in the roots and localized on the plasma membrane. An SNP and an InDel found in the promoter region of BnaC4.AKT1 were proposed to be responsible for its differential expression between rapeseed genotypes. This study identified a gene resource for improving low-K resistance. It also facilitates an integrated knowledge of the differential physiological and transcriptional responses to K deficiency in rapeseed genotypes.

Analysis of gut microbiota of ladybug beetle (Harmonia axyridis) after feeding on different artificial diets.

BACKGROUND: Harmonia axyridis is an effective natural enemy insect to a variety of phloem-sucking pests and Lepidopteran larvae, such as aphids, scabies, and phylloxera, while its industrial production is limited due to unmature artificial diet. Insect intestinal microbiota affect host development and reproduction. The aim of this study is to understand intestinal microbiota composition of H. axyridis and screen effective probiotics on artificial diet. Considering the role of the components and composition of the diet on the structure and composition of the intestinal microbiome, four kinds of diets were set up: (1) aphid; (2) basic diet; (3) basic diet + glucose; (4) basic diet + trehalose. The gut microbiota of H. axyridis was detected after feeding on different diets. RESULTS: Results showed that the gut microbiota between artificial diet group and aphid groups were far apart, while the basic and glucose groups were clearly clustered. Besides, the glucose group and trehalose group had one unique phylum, Cryptophyta and Candidatus Saccharibacteria, respectively. The highest abundance of Proteobacteria was found in the aphid diet. The highest abundance of Firmicutes was found in the basic diet. However, the addition of glucose or trehalose alleviated the change. In addition, the relative abundance of Enterobacter, Klebsiella, Enterobacteriaceae_unclassified, Enterobacteriales_unclassified and Serratia in the aphid group was higher than other groups. Moreover, the function of gut genes in each group also showed clear differences. CONCLUSION: These results have offered a strong link between artificial diets and gut microbes, and also have provided a theoretical basis for the screening of synergistic probiotics in artificial diet.

Genome-wide identification of the cation/proton antiporter (CPA) gene family and functional characterization of the key member BnaA05.NHX2 in allotetraploid rapeseed.

Rapeseed (Brassica napus L.) is susceptible to nutrient stresses during growth and development; however, the CPA (cation proton antiporter) family genes have not been identified in B. napus and their biological functions remain unclear. This study was aimed to identify the molecular characteristics of rapeseed CPAs and their transcriptional responses to multiple nutrient stresses. Through bioinformatics analysis, 117 BnaCPAs, consisting of three subfamilies: Na+/H+ antiporter (NHX), K+ efflux antiporter (KEA), and cation/H+ antiporter (CHX), were identified in the rapeseed genome. Transcriptomic profiling showed that BnaCPAs, particularly BnaNHXs, were transcriptionally responsive to diverse nutrient stresses, including Cd toxicity, K starvation, salt stress, NH4+ toxicity, and low Pi. We found that the salt tolerance of the transgenic rapeseed lines overexpressing BnaA05.NHX2 was significantly higher than that of wild type. Subcellular localization showed that BnaA05.NHX2 was localized on the tonoplast, and TEM combined with X-ray energy spectrum analysis revealed that the vacuolar Na+ concentrations of the BnaA05.NHX2-overexpressing rapeseed plants were significantly higher than those of wild type. The findings of this study will provide insights into the complexity of the BnaCPA family and a valuable resource to explore the in-depth functions of CPAs in B. napus.

Roles of GFAT and PFK genes in energy metabolism of brown planthopper, Nilaparvata lugens.

Glutamine:fructose-6-phosphate aminotransferases (GFATs) and phosphofructokinase (PFKs) are the principal rate-limiting enzymes involved in hexosamine biosynthesis pathway (HBP) and glycolysis pathway, respectively. In this study, the NlGFAT and NlPFK were knocked down through RNA interference (RNAi) in Nilaparvata lugens, the notorious brown planthopper (BPH), and the changes in energy metabolism were determined. Knockdown of either NlGFAT or NlPFK substantially reduced gene expression related to trehalose, glucose, and glycogen metabolism pathways. Moreover, trehalose content rose significantly at 72 h after dsGFAT injection, and glycogen content increased significantly at 48 h after injection. Glucose content remained unchanged throughout the experiment. Conversely, dsPFK injection did not significantly alter trehalose, but caused an extreme increase in glucose and glycogen content at 72 h after injection. The Knockdown of NlGFAT or NlPFK significantly downregulated the genes in the glycolytic pathway, as well as caused a considerable and significant decrease in pyruvate kinase (PK) activity after 48 h and 72 h of inhibition. After dsGFAT injection, most of genes in TCA cycle pathway were upregulated, but after dsNlPFK injection, they were downregulated. Correspondingly, ATP content substantially increased at 48 h after NlGFAT knockdown but decreased to an extreme extent by 72 h. In contrast, ATP content decreased significantly after NlPFK was knocked down and returned. The results have suggested the knockdown of either NlGFAT or NlPFK resulted in metabolism disorders in BPHs, highlighting the difference in the impact of those two enzyme genes on energy metabolism. Given their influence on BPHs energy metabolism, developing enzyme inhibitors or activators may provide a biological control for BPHs.

Regulation of Vicia faba L. Response and Its Effect on Megoura crassicauda Reproduction under Zinc Stress.

The heavy metal zinc (Zn) is known to be transmitted in the food chain; however, the effect of Zn stress on beans and herbivorous insects is largely unclear. This study aimed to investigate the resistance of broad bean plants to Zn stress and the consequent changes in their physiological and biochemical metabolism by simulating heavy metal pollution in soil. Simultaneously, the effects of aphid progeny treated with different Zn concentrations on the expression of carbohydrate and related genes were analyzed. The results showed that Zn had no effect on the germination rate of broad beans, but other effects mainly manifested as follows. (1) Chlorophyll content decreased. (2) The total soluble sugar and Zn content in stems and leaves increased with increasing Zn content. (3) The proline content first increased and then decreased with increasing Zn content. (4) The height of the seedlings indicates that low concentrations promote growth and high concentrations inhibit growth. In addition, only the first-generation fecundity decreased significantly when aphids fed on heavy metal broad beans. Continuous high Zn levels increase the trehalose content of aphid F1 and F2, while F3 decreases. These results can not only provide a theoretical basis for exploring the impact of soil heavy metal pollution on ecosystems but also preliminarily evaluate the possibility of broad beans as a means of pollution remediation.

Corneal endothelial cells and acoustic cavitation in phacoemulsification.

Postoperative complications of phacoemulsification, such as corneal edema caused by human corneal endothelial cell (CEC) injury, are still a matter of concern. Although several factors are known to cause CEC damage, the influence of ultrasound on the formation of free radicals during surgery should be considered. Ultrasound in aqueous humor induces cavitation and promotes the formation of hydroxyl radicals or reactive oxygen species (ROS). ROS-induced apoptosis and autophagy in phacoemulsification have been suggested to significantly promote CEC injury. CEC cannot regenerate after injury, and measures must be taken to prevent the loss of CEC after phacoemulsification or other CEC injuries. Antioxidants can reduce the oxidative stress injury of CEC during phacoemulsification. Evidence from rabbit eye studies shows that ascorbic acid infusion during operation or local application of ascorbic acid during phacoemulsification has a protective effect by scavenging free radicals or reducing oxidative stress. Both in experiments and clinical practice, hydrogen dissolved in the irrigating solution can also prevent CEC damage during phacoemulsification surgery. Astaxanthin (AST) can inhibit oxidative damage, thereby protecting different cells from most pathological conditions, such as myocardial cells, luteinized granulosa cells of the ovary, umbilical vascular endothelial cells, and human retina pigment epithelium cell line (ARPE-19). However, existing research has not focused on the application of AST to prevent oxidative stress during phacoemulsification, and the related mechanisms need to be studied. The Rho related helical coil kinase inhibitor Y-27632 can inhibit CEC apoptosis after phacoemulsification. Rigorous experiments are required to confirm whether its effect is realized through improving the ROS clearance ability of CEC.

Immigration Pathways of White-Backed Planthopper in the Confluence Area of the Two Monsoon Systems.

The white-backed planthopper, WBPH, Sogatella furcifera (Horváth) is a plant pest that migrates long-distances. The migration pathway of WBPH in eastern China coincides with the north-south round trip of the East Asian monsoon. However, in Yunnan China, which is affected by two monsoon systems, the migration pathway is unclear. Light-trap data and analysis of female ovarian development showed that the peak period of immigration of WBPH into western Yunnan was earlier than in eastern Yunnan. Using meteorological reanalysis data and flight parameters of WBPH, trajectory modeling showed that there are two immigration pathways to Yunnan. One is from Myanmar to western Yunnan, and the other is from Vietnam and Laos to eastern Yunnan. The reason for the differences in source areas and immigration pathways between eastern and western Yunnan is that the west wind prevails in western Yunnan and is controlled by South Asian monsoon, while southwesterly winds prevail in eastern Yunnan due to the combined influence of South Asian monsoon and East Asian monsoon. The results indicate that WBPH invades Yunnan via two pathways under a two-monsoon system. These data will allow earlier prediction and population management of WBPH.

Benefits of multidisciplinary collaborative care team-based nursing services in treating pressure injury wounds in cerebral infarction patients.

BACKGROUND: Cerebral infarction patients need to be bedridden for long periods of time often resulting in pressure injuries, which may represent a serious threat to patients' life and health. An effective nursing program should be adopted for timely intervention in patients with pressure wounds. AIM: To explore the value of nursing services based on a multidisciplinary collaborative treatment team in patients with pressure injury wounds following cerebral infarction. METHODS: Patients with cerebral infarction pressure injury wounds in our hospital from December 2016 to January 2021 were selected and divided into one study group and one control group based on the simple random number table method. The control group was treated with conventional nursing care (CNC), and the study group was treated with care services based on multidisciplinary collaborative care (MDCC). The Pressure Ulcer Scale for Healing (PUSH), healing effect, Self-Perceived Burden Score (SPBS), and satisfaction with the intervention were calculated before and after 2 and 4 wk of intervention in both groups. RESULTS: Sixty-two patients were enrolled, and 31 patients were assigned to each group. The results of the interventions were as follows: (1) There was no significant difference between the PUSH scores of the MDCC group (11.19 ± 2.46) and CNC group (12.01 ± 2.79) before the intervention (P > 0.05), and the PUSH scores were lower after 2 and 4 wk of intervention in the MDCC group (6.63 ± 1.97 and 3.11 ± 1.04) than in the CNC group (8.78 ± 2.13 and 4.96 ± 1.35 points) (P < 0.05); (2) The rate of wound healing in the MDCC group (96.77%) was higher than that in the CNC group (80.65%) (P < 0.05); (3) There was no significant difference between the SPBS scores of emotional factors (21.15 ± 3.11), economic factors (9.88 ± 2.15), and physical factors (8.19 ± 2.23) in the two groups before the intervention. The scores of emotional factors (13.51 ± 1.88), economic factors (6.38 ± 1.44), and physical factors (5.37 ± 1.08) were lower in the MDCC group than in the CNC group (16.89 ± 2.05, 7.99 ± 1.68 and 7.06 ± 1.19) after 4 wk of intervention (P < 0.05); and (4) Satisfaction with the intervention was higher in the MDCC group (93.55%) than in the CNC group (74.19%) (P < 0.05). CONCLUSION: Interventions for patients with cerebral infarction pressure wounds based on an MDCC treatment team can effectively reduce patients' self-perceived burden, improve pressure wound conditions, facilitate wound healing, and increase patient satisfaction with the intervention.

Sevoflurane preconditioning protects experimental ischemic stroke by enhancing anti-inflammatory microglia/macrophages phenotype polarization through GSK-3ß/Nrf2 pathway.

AIMS: Sevoflurane preconditioning (SPC) results in cerebral ischemic tolerance; however, the mechanism remains unclear. Promoting microglia/macrophages polarization from pro-inflammatory state to anti-inflammatory phenotype has been indicated as a potential treatment target against ischemic stroke. In this study, we aimed to assess the effect of SPC on microglia polarization after stroke and which signaling pathway was involved in this transition. METHODS: Mouse primary microglia with SPC were challenged by oxygen-glucose deprivation (OGD) or lipopolysaccharide (LPS), and mice with SPC were subjected to middle cerebral artery occlusion (MCAO). Then, the mRNA and protein levels of pro-inflammatory/anti-inflammatory factors were analyzed. GSK-3ß phosphorylation and Nrf2 nuclear translocation were measured. The mRNA and protein expression of pro-inflammatory/anti-inflammatory factors, neurological scores, infarct volume, cellular apoptosis, the proportion of pro-inflammatory/anti-inflammatory microglia/macrophages, and the generation of super-oxidants were examined after SPC or GSK-3ß inhibitor TDZD treatment with or without Nrf2 deficiency. RESULTS: Sevoflurane preconditioning promoted anti-inflammatory and inhibited pro-inflammatory microglia/macrophages phenotype both in vitro and in vivo. GSK-3ß phosphorylation at Ser9 was increased after SPC. Both SPC and TDZD administration enhanced Nrf2 nuclear translocation, reduced pro-inflammatory microglia/macrophages markers expression, promoted anti-inflammatory markers level, and elicited a neuroprotective effect. Nrf2 deficiency abolished the promoted anti-inflammatory microglia/macrophages polarization and ischemic tolerance induced by TDZD treatment. The reduced percentage of pro-inflammatory positive cells and super-oxidants generation induced by SFC or TDZD was also reversed by Nrf2 knockdown. CONCLUSIONS: Our results indicated that SPC exerts brain ischemic tolerance and promotes anti-inflammatory microglia/macrophages polarization by GSK-3ß-dependent Nrf2 activation, which provides a novel mechanism for SPC-induced neuroprotection.

Activation of CB1R-Dependent PGC-1α Is Involved in the Improved Mitochondrial Biogenesis Induced by Electroacupuncture Pretreatment.

Electroacupuncture (EA) pretreatment induces cerebral ischemic tolerance; however, the mechanism remains poorly understood. This study aimed to determine the participation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α)-mediated mitochondrial biogenesis in the neuroprotection of EA and whether cannabinoid receptor 1 (CB1R) is involved in this mechanism. At 2 hours after EA pretreatment, adult male C57BL/6j mice were subjected to 60-minute right middle cerebral artery occlusion (MCAO). Mitochondrial function, the level of mitochondrial biogenesis-related proteins (nuclear transcription factor 1, NRF1; mitochondrial transcription factor A, TFAM), and mitochondrial DNA (mtDNA) were measured. A small interfering RNA (siRNA) targeting PGC-1α and the CB1R antagonists AM251 and SR141716A were given to the animals before EA pretreatment, and mitochondrial function and biogenesis were examined after MCAO. EA ameliorated the mitochondrial function, upregulated the NRF1 and TFAM expression, and increased the mtDNA levels and the volume and number of mitochondria. EA pretreatment increased the expression of PGC-1α, whereas the PGC-1α siRNA and CB1R antagonists reversed the improved neuroprotection and increased mitochondrial biogenesis induced by EA. Our results indicated that EA pretreatment protects the mitochondria and promotes mitochondrial biogenesis by activating CB1R-dependent PGC-1α, which provides a novel mechanism for EA pretreatment-induced ischemic tolerance.

Apigenin-7-O-ß-D-(-6"-p-coumaroyl)-glucopyranoside treatment elicits a neuroprotective effect through GSK-3ß phosphorylation-mediated Nrf2 activation.

The current study was designed to seek the role of the glycogen synthase kinase-3ß (GSK-ß)-regulated NF-E2-related factor 2 (Nrf2) pathway in the antioxidant effect induced by Apigenin-7-O-ß-D-(-6"-p-coumaroyl)-glucopyranoside (APG). Rat primary cultured cortical neurons were challenged by oxygen and glucose deprivation/reoxygenation (OGD/R) and then treated with APG. Cell viability, phosphorylation of GSK-ß at Ser9 and nuclear expression of Nrf2 were measured. Male Sprague Dawley rats challenged by 2-h middle cerebral artery occlusion were treated with 50 mg/kg APG, and the neurological score, infarct volume, phosphorylation of GSK-3ß and nuclear expression of Nrf2 were analyzed. The neuroprotective effect of APG and the expression levels of antioxidant enzymes and oxidative products were also examined in the presence and absence of Nrf2-siRNA and PI3K inhibitors. APG reduced the apoptotic proportion, attenuated LDH release and increased cell viability, and in vivo, APG improved neurological scores and reduced infarct volume. APG increased GSK-3ß phosphorylation and Nrf2 nuclear translocation, while these effects were prevented by PI3K inhibitors or Nrf2-siRNA treatment in both OGD/R cell cultures and ischemic/reperfusion rats. These findings reveal that GSK-3ß phosphorylation-mediated Nrf2 activation is involved in the neuroprotective effect of APG.

Repetitive Transcranial Magnetic Stimulation Elicits Antidepressant- and Anxiolytic-like Effect via Nuclear Factor-E2-related Factor 2-mediated Anti-inflammation Mechanism in Rats.

Repetitive transcranial magnetic stimulation (rTMS) treatment is widely accepted as an evidence-based treatment option for depression and anxiety. However, the underlying mechanism of this treatment maneuver has not been clearly understood. The chronic unpredictable mild stress (CUMS) procedure was used to establish depression and anxiety-like behavior in rats. The rTMS was performed with a commercially available stimulator for seven consecutive days, and then depression and anxiety-like behaviors were subsequently measured. The expression of nuclear factor-E2-related factor 2 (Nrf2) was measured by western-blot, and the level of tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6) was measured with Enzyme-linked immunesorbent assay (ELISA) analyzing kits. Furthermore, a small interfering RNA was employed to knockdown Nrf2, after which the neurobehavioral assessment, Nrf2 nuclear expression, and the amount of inflammation factors were evaluated. Application of rTMS exhibited a significant antidepressant and anxiolytic-like effect, which was associated with the increased Nrf2 nuclear translocation and reduced level of TNF-α, iNOS, IL-1ß, and IL-6 in the hippocampus. Following Nrf2 silencing, the antidepressant and anxiolytic-like effect produced by rTMS was abolished. Moreover, the elevated Nrf2 nuclear translocation, and the reduced production of TNF-α, iNOS, IL-1ß, and IL-6 in hippocampus mediated by rTMS, were reversed by Nrf2 knockdown. Together, these results reveal that the Nrf2-induced anti-inflammation effect is crucial in regulating antidepressant-related behaviors produced by rTMS.

TREK-2 Mediates the Neuroprotective Effect of Isoflurane Preconditioning Against Acute Cerebral Ischemia in the Rat.

It is known that preconditional treatment with volatile anesthetics can induce tolerance of the brain to stroke. A previous study demonstrated that the involvement of TREK-1, a two-pore domain K+ channel, in sevoflurane preconditioning induced neuroprotection against focal cerebral ischemia in rats. The present study testified whether TREK-2, another anesthetic-target K+ channel, is also associated with volatile anesthetic-induced neuroprotection, and further explored its potential mechanism. Rats preconditioned with isoflurane were subjected to 1.4vol% isoflurane plus 98% O2 (1.5 L/min) inhalation for 1 hour daily and continuing for 5 consecutive days. Then, these rats were subjected to middle cerebral artery occlusion (MCAO) as focal cerebral ischemia model. The expression of TWIK-related K+ channel 2 (TREK-2) was analyzed by western blotting and quantitative real-time RT-PCR, and its downstream signaling molecules, protein kinase C (PKC) alpha, extracellular signal-regulated kinase 1/2 (ERK1/2), and pERK1/2 were detected by western blotting also. Subsequently, the expression of TREK-2 was regulated by siRNA transfection in the brain to clarify its role in the neuroprotection of isoflurane preconditioning. Neurological scores, infarction volume, and TdT-mediated dUTP Nick-End Labeling (TUNEL) staining were examined to evaluate the outcomes. The impact of TREK-2 on the expression of its downstream signaling molecules was also examined for preliminary analysis of the possible mechanisms. Isoflurane preconditioning reduced the infarct volume, inhibited the cell apoptosis, and improved the neurological outcome in rats subjected to MCAO. These effects were parallel with the increase in TREK-2 protein and inhibition of the ERK1/2 phosphorylation. The downregulation of TREK-2 through siRNA could significantly attenuate the isoflurane preconditioning-induced neuroprotective effects. Isoflurane preconditioning-induced neuroprotective effects against ischemia-reperfusion injury are associated with the increase in TREK-2 channel activation. These effects depend on the attenuation of PKC alpha and inhibition of ERK1/2 phosphorylation. Results enrich our understanding on the mechanism of two-pore domain K+ channel in preconditioning-induced tolerance to focal cerebral ischemia.

Single-Phase White-Light-Emitting and Photoluminescent Color-Tuning Coordination Assemblies.

Metal-organic complexes assembled from coordinative interactions are known to be able to display a wide range of photoluminescent behaviors benefiting from an extensive number of metal ions, organic linkers, and inclusion guests, depending on the multifaceted nature of their chemical structures and photophysical properties. In the past two decades, the white-light-emitting (WLE) and photoluminescent color-tuning (PLCT) materials based on the single-phase metal-organic coordination assemblies have merited particular attention and gained substantial advances. In this review, we give an overview of recent progress in this field, placing emphasis on the WLE and PLCT properties realized in the single-phase materials, which covers the origin, generation, and manipulation of different types of photoluminescence (PL) derived from ligand-centered (LC), metal/cluster-centered (MC or CC), excimer/exciplex-based (EX), metal-to-ligand or ligand-to-metal charge-transfer-based (MLCT or LMCT), or guest-included emissions. The coordination assemblies in this topic can be generally classified into three categories [(1) mono/homometallic coordination assemblies based on main group (s,p-block), transition (d-block), or lanthanide (f-block) metal centers, (2) s/p-f-, d-f-, or f-f-type heterometallic coordination assemblies, and (3) guest-included coordination assemblies] for which WLE and PLCT properties can be achieved by virtue of either a wide-band/overlapped emission covering the whole visible spectrum from a single emitting center or a combination of complementary color emissions from multiple emitting centers/origins. Some state-of-the-art assembly methods and successful design models relevant to the above three categories are elaborated to demonstrate how to achieve efficient and controllable white-light emission in a single-phase material through a tunable PL approach. Potential applications in the fields of lighting and displaying, sensing and detecting, and barcoding and patterning are surveyed, and at the end, possible prospects and challenges for future development along this line are proposed.

Anomalous thermally-activated NIR emission of ESIPT modulated Nd-complexes for optical fiber sensing devices.

Highly sensitized NIR emission was modulated using an ESIPT ligand in a Nd-complex, to achieve a substantially elongated NIR lifetime in cyclohexane suspension with a value of 16.89 µs at RT, and anomalous themally-activated NIR emission with the temperature increasing from 77 to 300 K for the first time, which was further designed into a remote and in situ optical fiber sensing device.

ESIPT-Modulated Emission of Lanthanide Complexes: Different Energy-Transfer Pathways and Multiple Responses.

Two series of isostructural lanthanide coordination complexes, namely, LIFM-42(Ln) (Ln=Eu, Tb, Gd, in which LIFM stands for the Lehn Institute of Functional Materials) and LIFM-43(Ln) (Ln=Er, Yb), were synthesized through the self-assembly of an excited-state intramolecular proton transfer (ESIPT) ligand, 5-[2-(5-fluoro-2-hydroxyphenyl)-4,5-bis(4-fluorophenyl)-1H-imidazol-1-yl]isophthalic acid (H2 hpi2cf), with different lanthanide ions. In the coordination structures linked by the ligands and oxo-bridged LnIII 2 clusters (for LIFM-42(Ln) series) or isolated LnIII ions (for LIFM-43(Ln) series), the ESIPT ligand can serve as both the host and antenna for protecting and sensitizing the photoluminescence (PL) of LnIII ions. Meanwhile, the -OH⋅⋅⋅N active sites on the ligands are vacant, which provides availability to systematically explore the PL behavior of Ln complexes with ESIPT interference. Based on the accepting levels of different lanthanide ions, energy transfer can occur from the T1 (K*) or T1 (E*) (K*=excited keto form, E*=excited enol form) excited states of the ligand. Furthermore, the sensitized lanthanide luminescence in both visible and near-infrared regions, as well as the remaining K* emission of the ligand, can be modulated by the ESIPT responsiveness to different solvents, anions, and temperature.

Analysis of the Huge Immigration of Sogatella furcifera (Hemiptera: Delphacidae) to Southern China in the Spring of 2012.

Sogatella furcifera (Horváth) is a migratory rice pest that periodically erupts across Asia, and early immigration is an important cause of its outbreak. The early immigration of S. furcifera into southern China shows evident annual fluctuations. In the spring of 2012, the huge size of the immigrant population and the large number of immigration peaks were at levels rarely seen prior to that year. However, little research has been done on the entire process of round-trip migration to clarify the development of the population, the long-distance migration and the final eruption. In this study, the light-trap data for S. furcifera in southern China and Vietnam in 2011-2016 were collected, and the trajectory modeling showed that the early immigrants to southern China came from the northern and central Vietnam, Laos, and northeastern Thailand. Analysis of the development of the population, the migration process and meteorological factors revealed the reasons for the huge size of the early immigration: 1) the expansion of the source area could be seen as a precondition; 2) the large size of the returned population in the last autumn and the warm temperature of southern Vietnam and Laos in the last winter increased the initial populations; 3) the sustained strong southwest winds were conducive to the northward migration of the population during the major immigration period in early May. Therefore, the large-scale immigration of S. furcifera to southern China in the spring of 2012 resulted from the combined effects of several factors involved in the process of round-trip migration.

Triggering Receptor Expressed on Myeloid Cells 2, a Novel Regulator of Immunocyte Phenotypes, Confers Neuroprotection by Relieving Neuroinflammation.

BACKGROUND: Microglia can not only detrimentally augment secondary injury but also potentially promote recovery. However, the mechanism underlying the regulation of microglial phenotypes after stroke remains unclear. METHODS: Mice were subjected to middle cerebral artery occlusion for 60 min. At 3 days after reperfusion, the effects of activation and suppression of triggering receptor expressed on myeloid cells 2 on immunocyte phenotypes (n = 5), neurobehavioral scores (n = 7), infarct volumes (n = 8), and neuronal apoptosis (n = 7) were analyzed. In vitro, cultured microglia were exposed to oxygen-glucose deprivation for 4 h. Inflammatory cytokines, cellular viability (n = 8), neuronal apoptosis (n = 7), and triggering receptor expressed on myeloid cells 2 expression (n = 5) were evaluated in the presence or absence of triggering receptor expressed on myeloid cell-specific small interfering RNA or triggering receptor expressed on myeloid cells 2 overexpression lentivirus. RESULTS: Triggering receptor expressed on myeloid cells 2 expression in the ischemic penumbra peaked at 3 days after ischemia-reperfusion injury (4.4 ± 0.1-fold, P = 0.0004) and was enhanced in interleukin-4/interleukin-13-treated microglia in vitro (1.7 ± 0.2-fold, P = 0.0119). After oxygen-glucose deprivation, triggering receptor expressed on myeloid cells 2 conferred neuroprotection by regulating the phenotypic conversion of microglia and inflammatory cytokine release. Intraperitoneal administration of triggering receptor expressed on myeloid cells 2 agonist heat shock protein 60 or unilateral delivery of a recombinant triggering receptor expressed on myeloid cells 2 lentivirus into the cerebral ventricle induced a significant neuroprotective effect in mice (apoptotic neurons decreased to 31.3 ± 7.6%; infarct volume decreased to 44.9 ± 5.3%). All values are presented as the mean ± SD. CONCLUSIONS: Activation or up-regulation of triggering receptor expressed on myeloid cells 2 promoted the phenotypic conversion of microglia and decreased the number of apoptotic neurons. Our study suggests that triggering receptor expressed on myeloid cells 2 is a novel regulator of microglial phenotypes and may be a potential therapeutic target for stroke.

Tanshinone IIA Elicits Neuroprotective Effect Through Activating the Nuclear Factor Erythroid 2-Related Factor-Dependent Antioxidant Response.

Tanshinone IIA (TSA), a principal component derived from the Traditional Chinese Medicine Danshen has been suggested to exert neuroprotective effect against experimental cerebral ischemic/reperfusion injury. But the associated underlying mechanisms still have not been understood. The current study characterized the role of nuclear factor erythroid two-related factor-induced antioxidant response in the neuroprotective efficacy of TSA treatment. The focal cerebral ischemia/reperfusion model was established by 60-minute middle cerebral artery occlusion. At the onset during reperfusion, mice were treated with 10 mg/kg TSA intraperitoneally. The mRNA and nuclear factor erythroid 2 (Nrf2) protein expression, the antioxidant enzymes, and oxidative production levels were measured. To further verify the role of Nrf2 in the neuroprotective effect induced by TSA, the Nrf2 small silenced RNA and Nrf2 knockout mice were used, the neurological function, brain infarct volume, and cellular apoptosis examination were assessed. TSA treatment improved neurological scores, reduced infarct volume, and attenuated the cellular apoptosis. TSA treatment upregulated the expression of Nrf2 mRNA and the contents of Nrf2 protein in nuclear extract. Nrf2 activation by TSA treatment increased the contents of antioxidant enzymes, and reduced the generation of oxidative productions. Either Nrf2 knockdown or Nrf2 knockout abolished the antioxidative and neuroprotective effect of TSA treatment. These results demonstrate that the Nrf2 activation contributes to TSA-induced neuroprotection from experimental ischemic stroke through maintaining antioxidant effect.