Search

Maintaining focus of attention over prolonged periods can be challenging, especially when the target stimulus is absent from the temporal sequence. Prior research has shown that a temporal attentional cue filling in the temporal blank can improve sustained attention: in a sustained visual attention task requiring synchronizing finger tapping with a temporally regular sequence composed of brief flash disks interleaved with blank periods, task performance was improved when a continuous fixation point that served as a temporal attentional cue was presented superimposed on the disk stimulus. To test the hypothesis that binding the temporal attentional cue with the target temporal sequence by spatial overlapping is crucial for enhancing sustained attention, the present study conducted a series of three experiments that deconstructed the bound connection between the cue and the sequence stimulus. In Experiment 1, the cue was placed above or below a flash disk. In Experiment 2, the cue was between two vertically arranged flash disks. In Experiment 3, the cue was in a flash ring. No significant effect of sustained attention improvement was found in any of the three experiments. Experiment 4 further replicated these null results and the previously observed effect of sustained attention improvement when the temporal cue was superimposed on the sequence stimulus. Our finding demonstrates that binding by spatial overlapping during the temporal blank when the sequence stimulus is absent is critical for enhancing sustained attention, which should be beneficial for improving performance across a broader range of tasks that require prolonged maintenance of attention. [ABSTRACT FROM AUTHOR]

Patients with diabetes are vulnerable to myocardial ischemia reperfusion (IR) injury, which may also induce acute lung injury (ALI) due to overaccumulation of reactive oxygen species (ROS) and inflammation cytokine in circulation. Despite autophagy plays a significant role in diabetes and pulmonary IR injury, the role of autophagy in ALI secondary to myocardial IR in diabetes remains largely elusive. We aimed to investigate pulmonary autophagy status and its roles in oxidative stress and inflammation reaction in lung tissues from diabetic rats subjected to myocardial IR. Control or diabetic rats were either treated with or without autophagy inducer rapamycin (Rap) or autophagy inhibitor 3-methyladenine (3-MA) before myocardial IR, which was achieved by occluding the left anterior descending coronary artery for 30 min and followed by reperfusion for 120 min. Diabetic rats subjected to myocardial IR showed more serious ALI with higher lung injury score and WET/DRY ratio and lower PaO2 as compared with control rats, accompanied with impaired autophagy indicated by reduced LC-3II/LC-3I ratio and Beclin-1 expression, decreased superoxide dismutase (SOD) activity, and increased 15-F2t-Isoprostane formation in lung tissues, as well as increased levels of leukocyte count and proinflammatory cytokines in BAL fluid. Improving autophagy with Rap significantly attenuated all these changes, but the autophagy inhibitor 3-MA exhibited adverse or opposite effects as Rap. In conclusion, diabetic lungs are more vulnerable to myocardial IR, which are involved in impaired autophagy. Improving autophagy could attenuate ALI induced by myocardial IR in diabetic rats, possibly through inhibiting inflammatory reaction and oxidative stress. [ABSTRACT FROM AUTHOR]

Increasing study has suggested that microRNAs (miRNAs) are pivotal regulators in regulating hypoxia-induced injury. miR-142-5p has been suggested as a critical regulator for cellular survival. However, the role of miR-142-5p in regulating hypoxia-induced injury remains unknown. In this study, we aimed to investigate the mechanistic roles of miR-142-5p in regulating cell survival during hypoxia treatment using H9C2 cardiomyoblasts and primary cardiomyocytes. We showed that miR-142-5p expression level was significantly repressed by hypoxia treatment. Overexpression of miR-142-5p during hypoxia induced extensive cell injury and apoptosis whereas suppression of miR-142-5p significantly promoted cell viability and attenuated cell apoptosis with hypoxia treatment. Sirtuin7 (SIRT7) was identified as a direct target gene of miR-142-5p by bioinformatics analysis and dual-luciferase reporter assays. Overexpression of miR-142-5p significantly decreased SIRT7 expression, while suppression of miR-142-5p increased SIRT7 expression. Furthermore, overexpression of SIRT7 protected H9C2 cardiomyoblasts and primary cardiomyocytes against hypoxia-induced injury and apoptosis. The silencing of SIRT7 markedly abrogated the protective effect induced by miR-142-5p suppression. Taken together, these results suggest that downregulation of miR-142-5p alleviates hypoxia-induced injury through upregulation of SIRT7. Our study suggests miR-142-5p/SIRT7 as potential therapeutic targets for ischemic heart disease. [ABSTRACT FROM AUTHOR]

The NMDA receptor is the most widely studied ionotropic glutamate receptor, and it is central to many physiological and pathophysiological processes in the central nervous system. GluN2A is one of the two main types of GluN2 NMDA receptor subunits in the forebrain. The proper activity of GluN2A is important to brain function, as the abnormal regulation of GluN2A may induce some neuropsychiatric disorders. This review will examine the regulation of GluN2A by endogenous and exogenous regulators in the central nervous system. [ABSTRACT FROM AUTHOR]

Carbon quantum dots (CQDs) were simply blended with platinum salts (K 2 PtCl 4 and K 2 PtCl 6 ) and converted into a hydrogen-evolution co-catalyst in situ , wherein Pt salts were dispersed on the surface of CQDs under photoirradiation of an aqueous solution of NADH (an electron and proton source) and 2-phenyl-4-(1-naphthyl)quinolinium ion (QuPh + −NA) employed as an organic photocatalyst. The co-catalyst (CQDs/Pt) exhibits similar catalytic reactivity in H 2 evolution as that of pure Pt nanoparticles (PtNPs) although the Pt amount of CQDs/Pt was only 1/200 that of PtNPs previously reported. CQDs were able to capture the Pt salt acting as Pt supports. Meanwhile, CQDs act as electron reservoir, playing an important role to enhance electron transfer from QuPh + −NA to the Pt salt, which was confirmed by kinetic studies, XPS and HRTEM. [ABSTRACT FROM AUTHOR]

The broadband light-absorption ability of carbon dots (CDs) has inspired their application in photocatalysis, however this has been impeded by poor electron transfer inside the CDs. Herein, we report the preparation of Cu-N-doped CDs (Cu-CDs) and investigate both the doping-promoted electron transfer and the performance of the CDs in photooxidation reactions. The Cu-N doping was achieved through a one-step pyrolytic synthesis of CDs with Na2[Cu(EDTA)] as precursor. As confirmed by ESR, FTIR, and X-ray photoelectron spectroscopies, the Cu species chelates with the carbon matrix through Cu-N complexes. As a result of the Cu-N doping, the electron-accepting and -donating abilities were enhanced 2.5 and 1.5 times, and the electric conductivity was also increased to 171.8 μs cm−1. As a result of these enhanced properties, the photocatalytic efficiency of CDs in the photooxidation reaction of 1,4-dihydro-2,6-dimethylpyridine-3,5-dicarboxylate is improved 3.5-fold after CD doping. [ABSTRACT FROM AUTHOR]

The broadband light-absorption ability of carbon dots (CDs) has inspired their application in photocatalysis, however this has been impeded by poor electron transfer inside the CDs. Herein, we report the preparation of Cu-N-doped CDs (Cu-CDs) and investigate both the doping-promoted electron transfer and the performance of the CDs in photooxidation reactions. The Cu-N doping was achieved through a one-step pyrolytic synthesis of CDs with Na2[Cu(EDTA)] as precursor. As confirmed by ESR, FTIR, and X-ray photoelectron spectroscopies, the Cu species chelates with the carbon matrix through Cu-N complexes. As a result of the Cu-N doping, the electron-accepting and -donating abilities were enhanced 2.5 and 1.5 times, and the electric conductivity was also increased to 171.8 μs cm−1. As a result of these enhanced properties, the photocatalytic efficiency of CDs in the photooxidation reaction of 1,4-dihydro-2,6-dimethylpyridine-3,5-dicarboxylate is improved 3.5-fold after CD doping. [ABSTRACT FROM AUTHOR]

Relative to audition, vision is considered much less trustworthy in sensorimotor timing such as synchronizing finger movements with a temporally regular sequence. Visuomotor timing requires maintaining attention over time, whereas the sustained visual attention may not be well held in conventional visuomotor timing task settings where flashing visual stimuli consisted of a briefly presented flash and a long blank period. In the present study, the potential attentional lapses in time due to the disappearance of the flash were carefully controlled in Experiment 1 by changing the color of the flash instead of its disappearance, or in Experiment 2 by adding an additional continuously presented fixation point serving as an external attentional cue when the flash disappeared. Improvement of visuomotor timing performance was found in both experiments. The finding suggests a role of enhanced sustained visual attention in improving visuomotor timing, by which vision could also be a trustworthy modality for processing temporal information in sensorimotor interactions. [ABSTRACT FROM AUTHOR]

Sepsis-induced ALI is marked by physiological, pathological, and biochemical irregularities caused by infection. Growth differentiation factor 3 (GDF3) is closely associated with the inflammatory response. Accumulating evidence has demonstrated a close relationship between GDF3 expression and the severity and prognosis of sepsis. However, the precise mechanism by which GDF3 protects against ALI induced by sepsis is still unclear. Following the intravenous administration of GDF3 in this research, we noted a rise in the survival rate, a decrease in the severity of histopathological damage as evaluated through HE staining, a decline in the count of inflammatory cells in bronchoalveolar lavage fluid (BALF), a reduction in the ratio of lung wet/dry (W/D) weight, and a noteworthy decrease in the levels of pro-inflammatory cytokines in both serum and BALF when compared to septic mice who underwent cecal ligation and puncture (CLP). These collective findings unequivocally indicate the protective effects of GDF3 against sepsis-induced ALI. In addition, the GDF3 group showed a significant reduction in the mRNA expression of Caspase-1 and NLRP3 when compared to the CLP group. Following this, we performed in vitro tests to confirm these discoveries and obtained comparable outcomes, wherein the administration of GDF3 notably decreased the levels of Caspase-1 and NLRP3 mRNA and protein in macrophages in comparison to the LPS group. Furthermore, GDF3 exhibited the capacity to reduce the secretion of inflammatory molecules from macrophages. By illuminating the mechanism by which GDF 3 regulates macrophages, this offers a theoretical basis for preventing and treating sepsis-induced ALI. [ABSTRACT FROM AUTHOR]

Objective: Tumour necrosis factor-α-induced protein 8-like 2 (TIPE2) has strong anti-inflammatory properties. However, it is unknown whether increased TIPE2 is protective against lipopolysaccharide (LPS)-induced ALI. In the current study, we aimed to investigate whether increased TIPE2 can exert protective effects in a mouse model of ALI induced by LPS. Methods: We administered TIPE2 adeno-associated virus (AAV-TIPE2) intratracheally into the lungs of mice. Three weeks later, ALI was induced by intratracheal injection of LPS into BALB/c mice. Twenty-four hours later, lung bronchoalveolar lavage fluid (BALF) was acquired to analyse cells and protein, arterial blood was collected for arterial blood gas analysis and the determination of pro-inflammatory factor levels, and lung issues were collected for histologic examination, transmission electron microscopy (TEM), TUNEL staining, wet/dry (W/D) weight ratio analysis, myeloperoxidase (MPO) activity analysis and blot analysis of protein expression. Results: We found that TIPE2 overexpression markedly mitigated LPS-induced lung injury, which was evaluated by the deterioration of histopathology, histologic scores, the W/D weight ratio, and total protein expression in the BALF. Moreover, TIPE2 overexpression markedly attenuated lung inflammation, as evidenced by the downregulation of polymorphonuclear neutrophils (PMNs) in the BALF, lung MPO activity, and pro-inflammatory cytokine levels in the serum. Moreover, TIPE2 overexpression not only dramatically prevented LPS-induced pulmonary cell apoptosis in mice but also blocked LPS-activated JNK phosphorylation and NF-κB p65 nuclear translocation. Conclusions: Our study shows that the increased expression of AAV-mediated TIPE2 in the lungs of mice inhibits acute inflammation and apoptosis and suppresses the activation of NF-κB and JNK in a murine model of ALI. [ABSTRACT FROM AUTHOR]

The role of ferroptosis in ischemic stroke has been hotly debated recently, but the mechanism is not clearly clarified. It has been reported that the NLRP3 inflammasome is essential for the progression of ischemic stroke. Whether the ferroptosis after ischemic stroke mediated by the activation of NLRP3 inflammasome is still not reported. In this study, we investigated the effect of NLRP3 deficiency on ferroptosis following cerebral ischemia-reperfusion injury (CIRI) in vivo and in vitro. In vivo , we used C57BL/6J mice and NLRP3-/- mice to establish a model of middle cerebral artery occlusion (MCAO). After 3 days of reperfusion, we assessed neurological function and then performed TTC staining to measure the infarct volume. Besides, we measured the expression of NLRP3 inflammasome-related proteins and the ferroptosis-inhibiting protein glutathione peroxidase 4 (GPX4) by western blotting (WB) and immunofluorescence (IF). Moreover, we evaluated the levels of ferroptosis-related factors (Fe2+, MDA and GSH) in the infarct area by using appropriate kits. Furthermore, we used WB to measure the expression of Kelch-like epichlorohydrin-associated protein 1 (Keap1) and nuclear factor erythroid 2-related factor 2 (Nrf2), which participate in the progression of ischemic stroke. In vitro , we knocked down NLRP3 with small interfering RNAs (siRNAs) and established an oxygen glucose deprivation/Reperfusion (OGD/R) model in BV2 cells to simulate ischemic conditions. Next, we assessed the viability of BV2 cells by the Cell Counting Kit (CCK)-8 cytotoxicity assay. Moreover, we used WB to measure the expression of NLRP3, IL-1β, GPX4, Keap1 and Nrf2 proteins which are involved in CIRI. Three days after MCAO, the NLRP3-/- mice exhibited smaller cerebral infarct volumes and lower neurological deficit scores. The expression of NLRP3 inflammasome-associated proteins (IL-18 and IL-1β) and Keap1/Nrf2 signaling pathway moleculars (Keap1 and Nrf2) in mice brain tissue and BV2 cells were inhibited by NLRP3 knockout/knockdown, while the expression of GPX4, one of the ferroptosis-related factors was increased. Furthermore, the contents of Fe2+ and MDA in the brain tissues of NLRP3-/- mice were decreased, while the content of GSH were increased significantly. Inhibition of the NLRP3 inflammasome alleviates CIRI by inhibiting ferroptosis and inflammation, possibly through a mechanism of the Keap1-Nrf2 pathway. • NLRP3 deficiency ameliorates neurological deficits and reduces the infarct volume after MCAO. • NLRP3 deficiency reduces OS and inflammation in mice after MCAO. • NLRP3 deficiency inhibits ferroptosis in mice after MCAO and in BV2 cells after OGD/R. • NLRP3 deficiency inhibits ferroptosis and OS may through down-regulating Keap1-Nrf2 signal pathway. [ABSTRACT FROM AUTHOR]

Introduction. Sepsis-induced myocardial dysfunction (SIMD) is the most common complications of sepsis and septic shock with extremely high incidence and mortality. Lipocalin 10 (Lcn10) has recently been identified as a potential biomarker for heart failure, yet its relation to sepsis has not been investigated. The purpose of this study was to explore whether circulating Lcn10 could be used as a prognostic tool in patients with SIMD. Methods. In this single-center observational pilot study, seventy-five sepsis patients were enrolled after sepsis diagnosis or ICU admission (45.3% female, median age 60 years), and 35 patients (46.7%) developed myocardial dysfunction. Serum Lcn10 levels of septic patients were measured using the enzyme-linked immunosorbent assay (ELISA) at the time of admission. Other biomarkers of cardiac function and Lcn10 concentration were compared between SIMD and non-SIMD groups. Results. We observed that the median Lcn10 levels were 2.780 ng/mL in patients with SIMD and 2.075 ng/mL in patients without SIMD (P < 0.05). The area under the receiver operating characteristic (ROC) curve for the diagnosis of SIMD was 0.797 (P < 0.05). In addition, elevated serum Lcn10 levels at the time of admission were positively associated with 28-day mortality in septic patients. Conclusions. Our study indicates that circulating Lcn10 levels may serve as a novel biomarker for the diagnosis and prognosis of myocardial dysfunction induced by sepsis. An additional large multicenter study may be warranted to confirm the findings of this study. [ABSTRACT FROM AUTHOR]

• Anti-CD1d treatment suppress Th2 cell responses in asthma by suppresses immunogenic maturation of LDCs. • Anti-CD1d treatment lowers the abundance and activation of lung iNKT cells in asthma. • The influences of anti-CD1d treatment in LDCs of asthma were dependent on lung iNKT cells. • The influences of anti-CD1d treatment in LDCs of asthma were relevant to the downregulation of CD40L expression on lung iNKT cells. Our previous findings show that invariant natural killer T (iNKT) cells can promote immunogenic maturation of lung dendritic cells (LDCs) to enhance Th2 cell responses in asthma. It has been accepted that recognition of glycolipid antigens presented by CD1d molecules by the T cell receptors of iNKT cells leads to iNKT cell activation. Therefore, we examine the immunoregulatory influences of anti-CD1d treatment on Th2 cell response and immunogenic maturation of LDCs and subsequently explored whether these influences were dependent on lung iNKT cells in asthmatic mice. We discovered that in wild-type mice sensitized and challenged with house dust mite or ovalbumin (OVA), anti-CD1d treatment inhibited Th2 cell response and immunogenic maturation of LDCs. LDCs from asthmatic mice with anti-CD1d treatment had a markedly decreased influence on Th2 cell responses in vivo and in vitro. Furthermore, anti-CD1d treatment reduced the abundance and activation of lung iNKT cells in asthmatic mice. Moreover, in asthmatic iNKT cell-deficient Jα18-/- mice, anti-CD1d treatment did not influence Th2 cell responses and immunogenic maturation of LDCs. Meanwhile, the quantity of CD40L+ iNKT cells in asthmatic mice was significant decreased by anti-CD1d treatment. Finally, the inhibition of anti-CD1d treatment on LDC immunogenic maturation and Th2 cell responses in asthmatic mice was reversed by anti-CD40 treatment. Our data suggest that anti-CD1d treatment can suppress Th2 cell responses through inhibiting immunogenic maturation of LDCs dependent on lung iNKT cells, which could be partially related to the downregulation of CD40L expression on lung iNKT cells in asthmatic mice. [ABSTRACT FROM AUTHOR]

The severity of sepsis may be associated with excessive inflammation, thus leading to acute liver injury. MicroRNA-21 is highly expressed in the liver of a variety of inflammation-related diseases, and PPARα is also proved to participate in regulating inflammation. In the present study, the LPS-induced sepsis model was established. We found that microRNA-21 expression was upregulated in the liver of sepsis mice, and microRNA-21 inhibition significantly reduced the liver injury. The expression of liver injury markers, inflammation cytokines, and PPARα in the septic mice was higher than in antagomir-21 treated septic mice. In addition, we also found that PPARα is the target gene of microRNA-21; PPARα antagonist GW6471 could reverse the effect of antagomir-21. In conclusion, our study illustrated that microRNA-21 exacerbate acute liver injury in sepsis mice by inhibiting PPARα expression. [ABSTRACT FROM AUTHOR]

Acute lung injury (ALI) is a critical syndrome that is associated with high morbidity and mortality rates. The activation of the Fas/Fas ligand (FasL) signaling pathway may be an important pathophysiological mechanism during ALI development. Penehyclidine hydrochloride (PHC) has been revealed to exhibit anti-apoptotic properties and may attenuate the observed systemic inflammatory response. The present study was performed to elucidate the molecular mechanism of PHC in the regulation of the Fas/FasL signaling pathway in rats with ALI. An ALI rat model was constructed by inducing blunt chest trauma and hemorrhagic shock (T/HS), with PHC administration prior to or following T/HS. At 6 h following T/HS, blood samples and lung tissues were collected. Western blotting, arterial blood gas analysis, ELISA, hematoxylin and eosin staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining and biochemical indicator analysis were performed to determine the degree of lung injury and the key signaling pathways associated with lung damage. The results indicated that the administration of PHC following T/HS effectively attenuates lung injury by improving pulmonary oxygenation, decreasing histopathological damage, decreasing polymorphonuclear neutrophil count and decreasing Fas, FasL, caspase-8, caspase-3, tumor necrosis factor-α, interleukin (IL)-6 and IL-1β expression. The results indicated that PHC exhibits anti-apoptotic functions and exerts protective effects in ALI rats induced by T/HS, which may be attributed to the inhibition of the Fas/FasL signaling pathway. [ABSTRACT FROM AUTHOR]

Background. Patients with diabetes are more vulnerable to myocardial ischemia reperfusion injury (IRI), which is involved in PKCβ2 activation and mitochondrial dysfunction. Glycine has been documented as a cytoprotective agent to attenuate diabetes-related abnormalities and reduce myocardial IRI, but the underlying mechanisms are still unclear. We determined whether glycine could attenuate high glucose- (HG-) and hypoxia/reoxygenation- (H/R-) induced injury by inhibiting PKCβ2 activation and improving mitochondrial quality in cultured H9C2 cells. Methods. H9C2 cells were either exposed to low glucose (LG) or HG conditions with or without treatment of glycine or CGP53353 (a selective inhibitor of PKCβ2) for 48 h, then subjected to 4 h of hypoxia followed by 2 h of reoxygenation (H/R). Cell viability, lactate dehydrogenase (LDH) release, mitochondrial membrane potential (MMP), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) concentration were detected using corresponding commercial kits. Mitochondrial quality control-related proteins (LC-3II, Mfn-2, and Cyt-C) and PKCβ2 activation were detected by Western blot. Results. HG stimulation significantly decreased cell viability and SOD activity and increased LDH release, MDA production, and PKCβ2 activation as compared to LG group, all of which changes were further increased by H/R insult. Glycine or CGP53353 treatment significantly reduced the increase of LDH release, MDA production, PKCβ2 activation, and Cyt-C expression and the decrease of cell viability, SOD activity, MMP, Mfn-2 expression, and LC-3II/LC-3I ratio induced by HG and H/R stimulation. Conclusions. Supplementary glycine protects H9C2 cells from HG- and H/R-induced cellular injury by suppressing PKCβ2 activation and improving mitochondria quality. [ABSTRACT FROM AUTHOR]

Background. Histone deacetylases (HDACs) play a pivotal role in signaling modification and gene transcriptional regulation that are essential for cardiovascular pathophysiology. Diabetic hearts with higher HDACs activity were more vulnerable to myocardial ischemia/reperfusion (MI/R) injury compared with nondiabetic hearts. We are curious about whether suppression of excessive HDACs activity in diabetic heart protects against MI/R injury. Methods. Diabetic rats were subjected to 45 min of ischemia, followed by 3 h of reperfusion. H9C2 cardiomyocytes were exposed to high glucose for 24 h, followed by 4 h of hypoxia and 2 h of reoxygenation (H/R). Results. Both MI/R injury and diabetes mellitus elevated myocardium HDACs activity. MI/R induced apoptotic cell death was significantly decreased in diabetic rats treated with HDACs inhibitor trichostatin A (TSA). TSA administration markedly moderated dissipation of mitochondrial membrane potential, protected the integrity of mitochondrial permeability transition pore (mPTP), and decreased cell apoptosis. Notably, cotreatment with Akt inhibitor partly or absolutely inhibited the protective effect of TSA in vivo and in vitro. Furthermore, TSA administration activated Akt/Foxo3a pathway, leading to Foxo3a cytoplasm translocation and attenuation proapoptosis protein Bim expression. Conclusions. Both diabetes mellitus and MI/R injury increased cardiac HDACs activity. Suppression of HDACs activity triggered protective effects against MI/R and H/R injury under hyperglycemia conditions through Akt-modulated mitochondrial apoptotic pathways via Foxo3a/Bim. [ABSTRACT FROM AUTHOR]

Photoinduced electron transfer process is a crucial step in photooxidation to obtain synthetic chemicals. However, the driving forces of electron transfer as priority in all have been rarely studied in stepwise detail. Herein, we report a series of BODIPY derivatives with an emphasis on the intramolecular charge transfer, enhancing the key step of photoinduced electron transfer process and photooxidation performances. A series of novel BODIPY photosensitizers ( B-1- B-5) were prepared, wherein diethylamine amino of B-3 as charge injection group was conjugated to the 2,6-diiodo-styryl-BODIPY, and the electron transfer impetus was enhanced 1.6 times due to its more negative redox potentials. These results were also confirmed by the DFT/TDDFT calculation. Without pure oxygen, B-3 still can exhibit an exceptional performance in photoxidative aromatization of 1,4-DHP under mild condition. After irradiation for 28 min, the conversion rate came to 98.2%. [ABSTRACT FROM AUTHOR]

We discovered that metal center confined in the porphyrin structure can process lower valence state (LV) via reversible photoinduced electron transfer in both singlet and triplet states, which are confirmed by X-ray photoelectron spectroscopy (XPS), X-ray absorption fine structure (XAFS), electron spin resonance (ESR) and density functional theory (DFT) calculations. More importantly, this controlling strategy was hardly influenced by the electronegative properties of surrounding porphyrin structures, at the same time, it can be widely applied to various metal elements such as Zn, Cu, Ni, Co, Fe. This work provides a new vision to fabricate and deeply understand the metal center with lower valence state from single atom level. Image 1 [ABSTRACT FROM AUTHOR]