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Substituting Sr2+ for Ba2+ ions in Ba(2−x)SrxMgWO6:Er3+,Yb3+,K+ led to the formation of tetragonal phase with a fourfold increase in Sa value. The effect of the phase transition on the optical properties of the phosphors was investigated.

A series of red-emitting BaLaLiWO6:Mn4+ (BLLW:Mn4+) phosphors were successfully synthesized by a high-temperature solid-state reaction method. The SrLLW:Mn4+ phosphor is a better candidate for plants illumination LED.

Ferroptosis is an iron-dependent cell death pathway and participates in various diseases. Current evidence suggests that ferroptosis can obviously affect the function of blood cells. This paper aims to elaborate the role of ferroptosis in blood cells and related diseases. First, abnormal ferroptosis damages the developing red blood cells by breaking systemic iron homeostasis, leading to erythropoiesis suppression and anaemia. Ferroptosis mediates neutrophils recruitment and neutrophil extracellular trap formation (NETosis). In T-cells, ferroptosis induces a novel point of synergy between immunotherapy and radiotherapy. Additionally, ferroptosis may mediate B cells differentiation, antibody responses and lymphoma. Nevertheless, increased ferroptosis can ameliorate acute myeloid leukaemia and T-cell leukaemia/lymphoma by inducing iron-dependent cancer cells death. Besides, ferroptosis activates platelets by increasing P-selectin, thus causing thromboembolism. Ferroptosis mediates virus infection and parasite infection by driving T-cell death and preventing T-cell immunity. Interestingly, ferroptosis is also considered as a critical player in COVID-19 infections, while targetting ferroptosis may also improve thromboembolism and prognosis in patients with COVID-19 infection. Overall, the crucial role of ferroptosis in blood cells will show a new therapeutic potential in blood cell-related diseases.HighlightsFerroptosis shows a new therapeutic potential for blood cell-related diseases.Ferroptosis damages erythropoiesis and thus induces anaemia.Ferroptosis induces platelet activation and leads to thromboembolism.Ferroptosis regulates T-cell and B-cell immunity, which participant in infectious diseases.Inversely, ferroptosis ameliorates acute myeloid leukaemia and T-cell leukaemia.

Hepatocellular carcinoma (HCC) is a primary malignancy of the liver and the third leading cause of cancer death worldwide. The incidence of HCC accounts for more than 90% of primary HCC. Like most solid malignancies, the occurrence and development of HCC are closely related to the Warburg effect. The Warburg effect of HCC is mainly manifested as increased glucose uptake by HCC cells, increased glycolysis, restricted mitochondrial oxidative phosphorylation, increased pentose phosphate pathway in HCC cells, and increased glutamine decomposition. As the contribution of glycolysis to the total ATP of tumor cells generally does not exceed 50% to 60%, oxidative phosphorylation (OXPHOS) still makes a considerable contribution to the ATP of tumor cells. In some cases, there will be an anti-Warburg effect. HCC Warburg effect is closely related to HCC cell proliferation, apoptosis, immune escape, migration and invasion, chemotherapy resistance, and treatment failure. The mechanism of the Warburg effect in HCC is complex, involving the expression of stimulating the key glycolysis enzymes by hypoxia-inducible factor-1(HIF-1), the activation of oncogenes and the inactivation of tumor suppressor genes, the continuous activation of related signaling pathways, the participation of noncoding RNA, and the rate of metabolism gene mutation of enzyme. This article synthetically discusses the characteristics of glucose metabolism in HCC cells, the mechanism of Warburg effect, clinical significance, and corresponding treatment strategies and provides new perspectives for the prevention and treatment of HCC.

Monoclinic Lu2WO6 undergoes diphase-to-perovskite BiLuWO6 transition via selective occupancy of Bi in three Lu sites. The transformation mechanism, process, and structure stabilities are revealed by variable cell nudged elastic band method, video, and phonon spectrum. Lattice transition brings about photogenerated charge separation in BiLuWO6. This is verified by indirect band gap transition, high electron migration rate, weak exciton binding energy, large photocurrent response, and small impedance. The electron–hole life time is elongated to produce abundant superoxide and hydroxyl radicals for the degradation of rhodamine B and phenol molecules. Bi–O antibonding states serve as immediate energy levels to change the recombination path, inducing 340 nm excitation band and 510 nm green light emission of Lu2WO6. Furthermore, multicolor emission of 1 at% Bi3+ + RE3+ (RE = Sm/Eu/Dy)-codoped Lu2WO6 is acquired via synergistic modification of the Bi–O antibonding state and RE3+ 4f states. Thus, the photogenerated charge motion in Lu2WO6 is tuned to expand application fields.

Small ubiquitin-like modifiers (SUMO) are highly conserved post-translational modification proteins that are present in eukaryotic cells. They are extensively expressed in diverse tissues, including the heart, liver, kidney, and lungs. SUMOylation, a crucial post-translational modification, exhibits a strong effect on DNA repair, transcriptional regulation, protein stability and cell cycle progression. Increasing evidence has demonstrated that SUMOylation is closely related to the development of liver disease. Therefore, the effects of SUMOylation in liver diseases, such as Hepatocellular carcinoma (HCC), viral hepatitis, non-alcoholic fatty liver disease (NAFLD), cirrhosis and primary biliary cirrhosis (PBC) were reviewed in this study. Specifically, SUMO1 was found to promote the invasion and metastasis of HCC and may promote hypoxia-mediated P65 nuclear transport while accelerating the progression of HCC. In addition, SUMO1-modified centrosomal P4.1-associated protein (CAPA) was observed to be overexpressed in Hepatitis B virus (HBV)-related HCC in response to TNF-α stimulation. Furthermore, SUMOylated CAPA was found to induce HBX-triggered NF-κB activation. Considering the diversity and significance of SUMOylation, targeting of the SUMOylation pathway may serve as an effective approach in the treatment of liver diseases.

Cell division cycle 42 (CDC42) can inhibit inflammation by regulating the activity of macrophage and T cells, which contributes to the pathophysiology of acute pancreatitis (AP). Therefore, CDC42 may have application as a potential biomarker for AP. The present study aimed to explore this possibility. Peripheral blood mononuclear cells (PBMCs) were collected from 149 patients with AP and 50 healthy controls (HCs). Subsequently, CDC42 expression in the PBMCs was measured using RT-qPCR; C-reactive protein (CRP), TNF-α and IL-6 in the serum of patients with AP were measured using ELISA. Meanwhile, Mann-Whitney U test, Kruskal-Wallis test, and Spearman's rank correlation test were performed on the data. The CDC42 expression levels were lower in patients with AP compared with those in HCs (P0.001). CDC42 expression was declined in patients with moderate-severe AP (MSAP) vs. patients with mild AP (MAP) (P=0.029), and in patients with severe AP (SAP) vs. patients with MAP (P=0.004). CDC42 expression correlated negatively with the Ranson's score (P0.001), APACEH II score (P=0.011) and SOFA score (P0.001) in patients with AP. CDC42 expression also correlated negatively with CRP (P0.001) and TNF-α (P=0.004) levels but not with IL-6 levels (P=0.177). Furthermore, CDC42 expression was lower in deceased patients with AP vs. AP survivors (P0.001) and in deceased patients with SAP vs. SAP survivors (P=0.026). CDC42 had good potential in predicting mortality from AP, with AUC of 0.829 and a 95% CI of 0.731-0.927, and it also had certain potential in predicting mortality from SAP and MSAP, with AUC (95% CI) of 0.794 (0.616-0.973) and 0.757 (0.558-0.956), respectively. In conclusion, data from the present study suggest that lower CDC42 expression levels correlate with higher disease susceptibility, disease severity, inflammation, and mortality risk in patients with AP.

Monoclinic Lu2WO6 undergoes diphase-to-perovskite BiLuWO6 transition via selective occupancy of Bi in three Lu sites. The transformation mechanism, process, and structure stabilities are revealed by variable cell nudged elastic band method, video, and phonon spectrum. Lattice transition brings about photogenerated charge separation in BiLuWO6. This is verified by indirect band gap transition, high electron migration rate, weak exciton binding energy, large photocurrent response, and small impedance. The electron-hole life time is elongated to produce abundant superoxide and hydroxyl radicals for the degradation of rhodamine B and phenol molecules. Bi-O antibonding states serve as immediate energy levels to change the recombination path, inducing 340 nm excitation band and 510 nm green light emission of Lu2WO6. Furthermore, multicolor emission of 1 at% Bi3+ + RE3+ (RE = Sm/Eu/Dy)-codoped Lu2WO6 is acquired via synergistic modification of the Bi-O antibonding state and RE3+ 4f states. Thus, the photogenerated charge motion in Lu2WO6 is tuned to expand application fields.

Dysregulated glycolysis is one of the mechanisms employed by cancer cells to facilitate growth and metastasis. Here we aimed to characterize the PPFIA4 gene, as a glycolysis-related oncogene in promoting the proliferation and migration of colon cancer cells. Using bioinformatical tools including The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA), we found that PPFIA4 expression and methylation levels were higher in colon cancer tissues of different stages than in normal tissues. Higher PPFIA4 level was also positively correlated with poorer survival of patients. PPFIA4 upregulation also correlated with poor prognosis and higher clinical stages of colon cancer patients. Colon cancer cell viability, migration and migration were enhanced after PPFIA4 overexpression. EMT markers and glycolysis were upregulated after PPFIA4 overexpression. PPFIA4 expression was found to be positively correlated with PFKFB3 and ENO2 levels, while knockdown of PFKFB3 and ENO2 reduced cell proliferation, migration, invasion and glycolysis. PPFIA4 upregulation is a potential biomarker in colon cancer which promotes proliferation, migration, invasion and glycolysis. The upregulation of PFKFB3/ENO2 signaling by PPFIA4 is a potential mechanism underlying the oncogenic effects of PPFIA4.

Cyclooxygenase-2 (COX-2) is an important rate-limiting enzyme in the synthesis of prostaglandins (PGs), which can be upregulated by various stimuli. COX-2 has been shown to be involved in the occurrence and development of hepatic fibrosis by regulating the proliferation and apoptosis of hepatic stellate cells (HSCs) in previous studies. The aims of the study are to study the mechanism of how COX-2 regulates the proliferation and apoptosis of HSCs and to provide new targets for the prevention and treatment of hepatic fibrosis. A short hairpin RNA targeting COX-2 was constructed, and the changes in proliferation and apoptosis of liver tissue cells and HSCs were observed, respectively. COX-2-shRNA-1 significantly suppressed the proliferation of HSCs in vivo. Moreover, knockdown of COX-2 significantly suppressed cell proliferation and accelerated cell cycle arrest and apoptosis in vitro. Among those differential genes related to cell proliferation and apoptosis, CDC27 and Sh3kbp1 were upregulated, but Plcd4 was suppressed. Mechanistically, the influence of COX-2 on HSCs partly depends on upregulating CDC27. Our results demonstrated that COX-2 regulates the proliferation and apoptosis of activated hepatic stellate cells through the CDC27 pathway. This study contributes to our understanding of the effect of COX-2 for the treatment of hepatic fibrosis.

The nuclear receptor superfamily is a family of ligand-activated transcription factors that play a key role in cell metabolism and human diseases. They can be modified after translation, such as acetylation, ubiquitination, phosphorylation and SUMOylation. Crosstalk between SUMO and ubiquitin, phosphorylation and acetylation regulates a variety of metabolic and physiological activities. Nuclear receptors play an important role in lipid metabolism, inflammation, bile acid homeostasis and autophagy. SUMOylation nuclear receptors can regulate their function and affect cell metabolism. It also provides a potential therapeutic target for atherosclerosis, tumor and other metabolic and inflammation-related diseases. This review focuses on the function of SUMOylation nuclear receptors.

The occupy of Eu3+ ions in the crystal lattice of NZPO:Eu3+ ions are studied by theoretical calculation and experimental. The electric structure and density of states of NZPO and NZPO:Eu3+ were comparatively studied by the first-principles, which indicated that the band gap of NZPO decreased after doping Eu3+ ions. The XRD patterns and PL spectra of NZ1-xPO:xEu3+ or N1-yZPO:yEu3+ phosphorare measured in the sake of prove the occupy of Eu3+ ions. The optimal sintering temperature are confirmed by the PL spectra and XRD patterns of a series NZPO:0.04Eu3+ phosphors prepared at different temperature.The effect of the charge compensator and different matrix component on the emission intensity of the phosphors was investigated. Moderate Na+ ions substitute for Zn2+ ions will enhance the emission intensity.The thermal quenching measurement revealed that NZPO:Eu3+ phosphor had better thermal stability. The results indicated that this phosphor can be used as a red supply light material for UV or blue based white LED.

BACKGROUND In December 2019, an ongoing outbreak of coronavirus disease 2019 (COVID-19) was first identified in Wuhan, China. The characteristics of COVID-19 patients treated in local hospitals in Wuhan are not fully representative of patients outside Wuhan. Therefore, it is highly essential to analyze the epidemiological and clinical characteristics of COVID-19 in areas outside Wuhan or Hubei Province. To date, a limited number of studies have concentrated on the epidemiological and clinical characteristics of COVID-19 patients with different genders, clinical classification, and with or without basic diseases. AIM To study the epidemiological and clinical characteristics of COVID-19 patients in Hengyang (China) and provide a reliable reference for the prevention and control of COVID-19. METHODS From January 16 to March 2, 2020, a total of 48 confirmed cases of COVID-19 were reported in Hengyang, and those cases were included in this study. The diagnostic criteria, clinical classification, and discharge standard related to COVID-19 were in line with the Diagnosis and Treatment Protocol for Novel Coronavirus Pneumonia (Trial Version 7) released by National Health Commission and National Administration of Traditional Chinese Medicine. The presence of SARS-CoV-2 in pharyngeal swab specimens was detected by quantitative reverse transcription polymerase chain reaction. All the data were imported into the excel worksheet and statistically analyzed by using SPSS 25.0 software. RESULTS A total of 48 cases of COVID-19 were collected, of which 1 was mild, 38 were moderate, and 9 were severe. It was unveiled that there were 31 (64.6%) male patients and 17 (35.4%) female patients, with a female-to-male ratio of 1.82:1. The range of age of patients with COVID-19 was dominantly 30-49 years old [25 (52.1%) of 48], followed by those aged over 60 years old [11 (22.9%)]. Besides, 29.2% (14 of 48) of patients had basic diseases, and 57.2% (8 of 14) of patients with basic diseases were aged over 60 years old. The occupations of 48 COVID-19 patients were mainly farmers working in agricultural production [15 (31.5%) of 48], rural migrant workers from Hengyang to Wuhan [15 (31.5%)], and service workers operating in the service sector [8 (16.7%)]. The mean latent period was 6.86 ± 3.57 d, and the median was 7 [interquartile range (IQR): 4-9] d. The mean time from onset of symptoms to the first physician visit was 3.38 ± 2.98 (95%CI: 2.58-9.18) d, with a median of 2 (IQR: 1-5) d, and the mean time from hospital admission to confirmed diagnosis was 2.29 ± 2.11 (95%CI: 1.18-6.42) d, with a median of 2 (IQR: 1-3) d. The main symptoms were fever [43 (89.6%) of 48], cough and expectoration [41 (85.4%)], fatigue [22 (45.8%)], and chills [22 (45.8%)]. Other symptoms included poor appetite [13 (27.1%)], sore throat [9 (18.8%)], dyspnea [9 (18.8%)], diarrhea [7 (14.6%)], dizziness [5 (10.4%)], headache [5 (10.4%)], muscle pain [5 (10.4%)], nausea and vomiting [4 (8.3%)], hemoptysis [4 (8.3%)], and runny nose [1 (2.1%)]. The numbers of peripheral blood leukocytes, lymphocytes, and eosinophils were significantly reduced in the majority of the patients. The levels of C-reactive protein, fibrinogen, blood glucose, lactate dehydrogenase, D-dimer, alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (γ-GT), myoglobin (MB), and creatine kinase (CK) were increased in 64.6%, 44.7%, 43.2%, 37.0%, 29.5%, 22.9%,20.8%, 21.6%, 13.6%, and 12.8% of patients, respectively. The incidence of ALT elevation in male patients was remarkably higher than that in females (P < 0.01), while the incidences of AST, CK, and blood glucose elevations in severe patients were remarkably higher than those in moderate patients (P < 0.05, respectively). Except for the mild patients, chest computed tomography showed characteristic pulmonary lesions. All the patients received antiviral drugs, 38 (79.2%) accepted traditional Chinese medicine, and 2 (4.2%) received treatment of human umbilical-cord mesenchymal stem cells. On March 2, 2020, 48 patients with COVID-19 were all cured and discharged. CONCLUSION Based on our results, patients with COVID-19 often have multiple organ dysfunction or damage. The incidences of ALT elevation in males, and AST, CK, and blood glucose elevations in severe patients are remarkably higher.

Olfactory receptors (ORs) are mainly distributed in olfactory neurons and play a key role in detecting volatile odorants, eventually resulting in the production of smell perception. Recently, it is also reported that ORs are expressed in non-olfactory tissues including heart, lung, sperm, skin, and cancerous tissues. Interestingly, ectopic ORs are associated with the development of diseases in non-olfactory tissues. For instance, ectopic ORs initiate the hypoxic ventilatory responses and maintain the oxygen homeostasis of breathing in the carotid body when oxygen levels decline. Ectopic ORs induce glucose homeostasis in diabetes. Ectopic ORs regulate systemic blood pressure by increasing renin secretion and vasodilation. Ectopic ORs participate in the process of tumor cell proliferation, apoptosis, metastasis, and invasiveness. Ectopic ORs accelerate the occurrence of obesity, angiogenesis and wound-healing processes. Ectopic ORs affect fetal hemoglobin levels in sickle cell anemia and thalassemia. Finally, we also elaborate some ligands targeting for ORs. Obviously, the diversified function and related signal pathway of ectopic ORs may play a potential therapeutic target in non-olfactory tissues. Thus, this review focuses on the latest research results about the diversified function and therapeutic potential of ectopic ORs in non-olfactory tissues.

A series of Dy3+, Ce3+/Dy3+, Eu2+/Dy3+ and Ce3+/Eu2+/Dy3+ doping LiBaB9O15 (LBB) phosphors were synthesized via a high temperature solid-state method. LBB:Dy3+ cannot create light under ultraviolet radiation, however, LBB:Ce3+, Dy3+ can produce yellow emission under 295 nm excitation. The energy transfer occurs from Ce3+ to Dy3+ ions via electric dipole-dipole interaction and the critical distance is estimated to be 21.15 A based on concentration quenching model. Generally, Eu2+ ion is a sensitizer to Dy3+ ion, however, there is only the emission of Eu2+ in LBB:Eu2+, Dy3+, which means there is no energy transfer from Eu2+ to Dy3+ ions. Interestingly enough, when doping Eu2+ ion into LBB:Ce3+, Dy3+, white emission can be achieved by increase the blue (350–425 nm) emission intensity. The spectral property, quantum efficiency, CIE chromaticity coordinates and thermal quenching property of LBB:Ce3+, Eu2+, Dy3+ are investigated. The results indicate that LBB:Ce3+, Eu2+, Dy3+ may be a potential application to white light emitting diodes.

Wing in ground effect vehicle is a type of the latest high performance vehicles. Due to the strong nonlinear change of aerodynamics with flight altitude and wind direction always being parallel in wind tunnel, the important aerodynamic derivative to climb angle is hardly to be tested. In this paper, a theoretical method of acquiring partial dynamic derivative of the wing in ground effect vehicle is derived by using the forced vibration of WIG vehicle above a certain flying height. At the same time, the aerodynamic characteristics of WIGS of XTW series are analyzed by means of fluent code using the theoretical method developed. It is shown that the numerical simulation method is reasonable compared with the experimental value, and the theoretical method of acquiring partial dynamic derivative of the wing in ground effect vehicle is feasible.

Mitochondrial unfolded protein response (mitoUPR) is a mitochondria stress response to maintain mitochondrial proteostasis during stress. Increasing evidence suggests that mitoUPR participates in diverse physiological processes especially metabolism and immunity. Although mitoUPR regulates metabolism in many aspects, it is mainly reflected in the regulation of energy metabolism. During stress, mitoUPR alters energy metabolism via suppressing oxidative phosphorylation (OXPHOS) or increasing glycolysis. MitoUPR also alters energy metabolism and regulates diverse metabolic diseases such as diabetes, cancers, fatty liver and obesity. In addition, mitoUPR also participates in immune process during stress. MitoUPR can induce innate immune response during various infections and may regulate inflammatory response during diverse inflammations. Considering the pleiotropic actions of mitoUPR, mitoUPR may supply diverse therapeutic targets for metabolic diseases and immune diseases.

Improving foam stability is an important issue in foam fractionation of proteins from their aqueous solutions with low foam properties. In this work, enhancing protein self-association at the gas–liquid interface by sodium citrate (Na-citrate), instead of adding surfactants, was used to improve the stability of protein foams. Using bovine serum albumin (BSA) as a model protein, the role of Na-citrate in enhancing self-association of BSA at the gas–liquid interface was studied at the molecular level. Then, the role of the enhanced protein self-association in intensifying foam fractionation of BSA was studied. The results show that by weakening electrostatic repulsion between the BSA molecules and unfolding their structures, Na-citrate induced the formation of 12 and 18 BSA aggregates at the gas–liquid interface. The enhanced protein self-association effectively increased the interfacial adsorption of BSA and improved the foam stability. At BSA concentration 50 mg/L, the recovery percentage of BSA with 30 mmol/L Na-citrate increased by 4 folds while its enrichment ratio just decreased by 11.5%, compared to those without Na-citrate. The results give a clear understanding of the role of protein self-association in foam fractionation of proteins.

Reduced graphene oxide/meso-TiO 2 /AuNPs (RGO/meso-TiO 2 /AuNPs) ternary composites were prepared via the addition of graphene oxide to the dispersion of meso-TiO 2 /AuNPs under hydrothermal conditions. The structure and the morphology of the RGO/meso-TiO 2 /AuNPs materials were characterized using X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), transmission electron microscopy (TEM), and scanning electron microscopy (SEM). The photocatalytic activity of RGO/meso-TiO 2 /AuNPs was evaluated by degradation of methyl blue (MB) under visible-light illumination. The ternary composites present an extended light absorption range, efficient charge separation properties, high adsorption ability for MB and high photocatalytic degradation activity of MB compared to the meso-TiO 2 and meso-TiO 2 /AuNPs.

Core-shell structured polyacrylic nanoparticles (named CSPN) impact modifiers consisting of a rubbery poly(n-butyl acrylate) core and a rigid poly(methyl methacrylate) shell with a size of about 352 nm were synthesized by seed emulsion polymerization. The CSPN modifier with core-shell weight ratio 80/20 was used to toughen poly(butylene terephthalate) (PBT) by melt blending. With an increase in CSPN content, the impact strength and the elongation at break of PBT/CSPN blends increased significantly compared with those of PBT; however, the tensile strength decreased. It was found that the polymerization had a very high instantaneous conversion (>93%) and overall conversion (99%). The core-shell structure of CSPN was examined by means of transmission electron microscope. Scanning electron microscope was used to observe the morphology of CSPN particle and fractured surfaces of the blends. The dynamic mechanical analyses of PBT/CSPN blends showed two merged transition peaks of PBT matrix, with the presence of CSPN modifier, which was responsible for the improvement of PBT toughness. The results indicated that the notched impact strength of PBT/CSPN blend with a weight ratio of 80/20 was 8.61 times greater than that of pure PBT where the brittle-ductile transition point appeared. Keywords: Core-shell structured polyacrylic nanoparticles (CSPN), Poly(butylene terephthalate) (PBT), Toughness, Emulsion polymerization, Structure–property relations