The association between plasma IgG N-glycosylation and neonatal hypoxic-ischemic encephalopathy: a case-control study.

Introduction: Hypoxic-ischemic encephalopathy (HIE) is one of severe neonatal brain injuries, resulting from inflammation and the immune response after perinatal hypoxia and ischemia. IgG N-glycosylation plays a crucial role in various inflammatory diseases through mediating the balance between anti-inflammatory and pro-inflammatory responses. This study aimed to explore the effect of IgG N-glycosylation on the development of HIE. Methods: This case-control study included 53 HIE patients and 57 control neonates. An ultrahigh-performance liquid chromatography (UPLC) method was used to determine the features of the plasma IgG N-glycans, by which 24 initial glycan peaks (GPs) were quantified. Multivariate logistic regression was used to examine the association between initial glycans and HIE, by which the significant parameters were used to develop a diagnostic model. Though receiver operating characteristic (ROC) curves, area under the curve (AUC) and 95% confidence interval (CI) were calculated to assess the performance of the diagnostic model. Results: There were significant differences in 11 initial glycans between the patient and control groups. The levels of fucosylated and galactosylated glycans were significantly lower in HIE patients than in control individuals, while sialylated glycans were higher in HIE patients (p < 0.05). A prediction model was developed using three initial IgG N-glycans and fetal distress, low birth weight, and globulin. The ROC analysis showed that this model was able to discriminate between HIE patients and healthy individuals [AUC = 0.798, 95% CI: (0.716-0.880)]. Discussion: IgG N-glycosylation may play a role in the pathogenesis of HIE. Plasma IgG N-glycans are potential noninvasive biomarkers for screening individuals at high risk of HIE.

Distribution characteristics, risk assessment, and relevance with surrounding soil of heavy metals in coking solid wastes from coking plants in Shanxi, China.

Heavy metal concentrations represent important pollution evaluation indices, and it is necessary to assess the potential environmental and health risks from heavy metals associated with coking wastes from coking plants. In this study, coking sludge (CS), tar residue (TR), coke powder (CP), and sulfur paste (SP) from three coking plants (Plant A, Plant B, and Plant C) in central, western, and southern Shanxi Province and from soils surrounding Plant A were selected as the research objects, and the distributions of Cu, Ni, Pb, Zn, Mn, Cd, and Cr were determined. The results showed that Cd in the four solid wastes far exceeded the soil background value by a factor of 16~195, and the contents of Pb in TR (three plants) and CS (Plant C) exceeded the soil background values 19.70-, 23.57-, 14.46-, and 12.56-fold, respectively. Similarly, the concentrations of Cu, Ni, Pb, Zn, and Cd in soils were higher than the background values by factors of 31.18, 8.35, 34.79, 29.48, and 3.43, respectively. In addition, the Cu, Ni, Pb, and Cr in the four solid wastes and soils mainly existed in the residual state. As depth increased, the overall Ni, Pb, Mn, and Cd concentrations in soils increased. The high ecological risks associated with the four solid wastes were mainly due to the enrichment of Cd. Workers in coking plants face certain Cr health risks. This study provides theoretical support for the coking industry with respect to the treatment, disposal, and management of solid wastes.

Spatial variability and risk assessment of heavy metals in the soil surrounding solid waste from coking plants in Shanxi, China.

Heavy metal pollution in the soil surrounding solid wastes from coking plants poses potential threats to human health and has attracted widespread attention. This study is the first to assess the spatial variability and risks of heavy metals in the soil surrounding solid waste from coking plants. The results showed that the concentrations of Cu, Ni, Pb, and Cd in the soil were much higher than the background value of the soil. Solid waste had a clear influence on the contents of Ni, Cd, Mn, Pb, and Cr in the soil. The ecological risk assessment of heavy metal pollution demonstrated that the pollution degree of Cu, Pb, and Cd was more serious than others, and the ecological risk of heavy metals was mainly caused by Cd in the soil. The human health risk assessment showed that adults and children near coking plants might face carcinogenic risk from exposure to Cr. This study can provide a theoretical basis for the prevention and management of soil heavy metal pollution surrounding solid waste in coking plants.

Expression Profile of Immunoglobulin G Glycosylation in Children With Epilepsy in Han Nationality.

Background: Epilepsy is a chronic brain disease that recurs during childhood, and more than half of adult epilepsy originates from childhood. Studies suggested that immunoglobulin G (IgG) glycosylation are closely related to neurological diseases. Here we analyzed the characteristics of the immunoglobulin glycosylation profile of children with epilepsy. Methods: Patients were recruited in Taian, Shandong Province from December 2019 to March 2020. Serum IgG glycome composition was analyzed by hydrophilic interaction liquid chromatography with ultra-high-performance liquid chromatography approach. Results: The proportion of fucosylated glycans in total IgG glycans was 93.72% in the epilepsy patients, which was significantly lower than that in the control group (94.94%). A lower level of total monogalactosylated and digalactosylated glycans were observed in the epilepsy patients group (30.76 and 40.14%) than that in the controls (36.17 and 42.69%). There was no significant difference between the two groups in bisected GlcNAc glycans and sialylated glycans. Conclusion: The decrease of core fucosylation and galactosylation may promote the inflammatory reaction of the body and participate in the occurrence of epilepsy in children.

Association Between Immunoglobulin G N-glycosylation and Vascular Cognitive Impairment in a Sample With Atherosclerosis: A Case-Control Study.

BACKGROUND: Atherosclerosis is considered a crucial component in the pathogenesis of decreased cognitive function, as occurs in vascular cognitive impairment (VCI). Inflammation and the immune response play a significant role in the development of many chronic diseases. Immunoglobulin G (IgG) N-glycosylation has been implicated in the development of a variety of diseases by affecting the anti-inflammatory and proinflammatory responses of IgG. This study aimed to investigate the association between IgG N-glycosylation and VCI in a sample of patients with atherosclerosis through a case-control study. METHOD: We recruited a total of 330 patients with atherosclerosis to participate in this case-control study, including 165 VCI patients and 165 sex- and age-matched participants with normal cognitive function. The plasma IgG N-glycans of participants were separated by ultrahigh-performance liquid chromatography. An enzyme-linked immunosorbent assay (ELISA) kit was used to determine the corresponding serum inflammatory factors. Atherosclerosis was diagnosed by carotid ultrasound, and the diagnosis of VCI was based on the "Guidelines for the Diagnosis and Treatment of Vascular Cognitive Impairment in China (2019)". A multivariate logistic regression model was used to explore the association between IgG N-glycans and VCI. We also analyzed the relationship between IgG N-glycans and the inflammatory state of VCI through canonical correlation analysis (CCA). RESULTS: Through the multivariate logistic regression analysis, 8 glycans and 13 derived traits reflecting decreased sialylation and galactosylation and increased bisecting GlcNAc significantly differed between the case and control groups after adjusting for confounding factors (P < 0.05, q < 0.05). Similarly, the differences in TNF-α, IL-6, and IL-10 were statistically significant between the case and control groups after adjusting for the effects of confounding factors (P < 0.05, q < 0.05). The CCA results showed that VCI-related initial N-glycans were significantly correlated with VCI-related inflammatory factors (r = 0.272, P = 0.004). The combined AUC value (AUC combined = 0.885) of 7 initial glycans and inflammatory factors was higher than their respective values (AUC initial glycans = 0.818, AUC inflammatory factors = 0.773). CONCLUSION: The findings indicate that decreased sialylation and galactosylation and increased bisecting GlcNAc reflected by IgG N-glycans might affect the occurrence of VCI in patients with atherosclerosis though promoting the proinflammatory function of IgG. IgG N-glycans may serve as potential biomarkers to distinguish VCI in individuals with atherosclerosis.

Theoretical and experimental investigation of the antioxidative activity of monascin.

Monascin, a specific type of monascus pigments, exhibits many bioactivities. In this study, the antioxidative activity of monascin was investigated by theoretical and experimental methods. First, the antioxidant potential of six monascus pigments was predicted by density functional theory (DFT) and time-dependent density functional theory (TDDFT) at the B3LYP/6-31+G (d, p) level, and monascus yellow pigments were predicted to have strong antioxidant capacity, as they can transfer hydrogen to free radicals and accept electrons from radicals. Then, the free radical-scavenging capacity of monascin for 2,2-diphenyl-1-picrylhydrazyl (DPPH), superoxide, and hydroxyl radicals was experimentally validated by electron spin resonance (ESR) measurement. Monascin exhibited a quenching effect on DPPH, superoxide, and hydroxyl radicals in a dose-dependent manner. Specifically, the scavenging activity of monascin for DPPH, superoxide, and hydroxyl radicals was 97.5%, 59.5%, and 68.6%, respectively, when 0.1 mg mL-1 monascin was present. Our study provides theoretical evidence for the strong antioxidative activity of monascin and offers a simple and reliable strategy to determine the antioxidative activity.

Efficient elimination of sulfadiazine in an anaerobic denitrifying circumstance: Biodegradation characteristics, biotoxicity removal and microbial community analysis.

Sulfadiazine (SDZ) is widely used in clinical treatment, livestock husbandry and aquaculture as an antibacterial agent, resulting in environmental risks. In this work, batch experiments were conducted to investigate the characteristics of SDZ biodegradation and reaction mechanisms in a nitrate anaerobic denitrifying system for the first time. The results showed that 98.52% of the SDZ, which had an initial concentration of 50 mg L-1, was degraded after 70 h, indicating that the removal efficiency of SDZ in anaerobic denitrifying system was 55.27% higher than that in anaerobic system. Furthermore, LC-MS-MS analysis confirmed that SDZ could be degraded into 16 byproducts via 3 main degradation pathways that contained 6 different reactions. After analyzing the microbial communities of the reactor, the denitrifying bacteria and desulfurizing bacteria Desulforhabdus, Ignavibacterium, SBR1031_norank, Nocardioides, etc. were highly associated with the removal of SDZ in the system. The biological toxicity test of the effluent indicated that the remaining organic matter and inorganic matter of the effluent could provide nutrients for E. coli and promote its growth. In other words, anaerobic denitrifying systems are highly efficient, simple and environmentally friendly, and have an impressive prospect in the biodegradation of sulfonamide antibiotics.

Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway.

BACKGROUND AND OBJECTIVE: Endometrial carcinoma (EC) is one of the most frequently diagnosed malignancies in females. Dysregulation of lncRNA TDRG1 has been widely documented in several cancers, including EC. However, the mechanism of this lncRNA involving in EC progression remains to be further elucidated. MATERIALS AND METHODS: The enrichment levels of TDRG1 in EC tissues and cell lines were examined by RT-qPCR. Flow cytometry, cell counting kit-8 (CCK-8), transwell, and Western blot assays were conducted to assess whether TDRG1 knockdown could affect cell cycle arrest, proliferation, migration, invasion, and apoptosis of EC cells. The phosphorylation levels of mTOR, AKT and PI3K that associated with PI3K/Akt/mTOR pathway were determined by Western blot assay. RESULTS: TDRG1 expression was markedly upregulated in EC tissues and cell lines. Knockdown of TDRG1 significantly induced cell cycle arrest and apoptosis, inhibited cell proliferation, restrained the invasion and migration abilities in EC cells. Moreover, TDRG1 silencing decreased the protein levels of p-AKT, p-PI3K, and p-mTOR of EC cells. CONCLUSION: Our data underlined the implication of TDRG1 in EC progression, proposing that targeting TDRG1 might be a potential therapeutic avenue in EC.

MiR-486-5p inhibits IL-22-induced epithelial-mesenchymal transition of breast cancer cell by repressing Dock1.

Epithelial-mesenchymal transition (EMT) is one of important steps that lead to cancer metastasis. Interleukin-22 (IL-22) is a T helper 17 (Th17) cells-secreted cytokine, it can promote invasion and metastasis of many cancers. MiR-486-5p is a microRNA that known to function as a tumor suppressor, and bioinformatics analysis predicts that Dock-1 has a binding site of miR-486-5p. In current research, we examined the relative expression levels of miR-486-5p and Dock-1 in 80 pairs of breast cancer tissues and corresponding adjacent normal tissues, also the effects of modifying their levels in cultured cells. We illustrated that IL-22 and Dock1 promote the invasion, metastasis, and EMT of breast cancer using Transwell invasion assay, western blot and immunofluorescence. MiR-486-5p directly bound the Dock1 mRNA 3' untranslated region and inhibited IL-22-induced EMT of breast cancer cells via the Dock1/NF-κB/Snail signaling pathway. Dock1 overexpression reversed the effect caused by the overexpression of miR-486-5p. Overexpression of miR-486-5p or downregulation of Dock1 reduced pulmonary metastasis in mice. This study provided insight into a potential mechanism where miRNAs regulate breast cancer metastasis and provided a novel therapeutic target for breast cancer treatment.

Ferroxidase-like and antibacterial activity of PtCu alloy nanoparticles.

Many metal nanoparticles are reported to have intrinsic enzyme-like activities and offer great potential in chemical and biomedical applications. In this study, PtCu alloy nanoparticles (NPs), synthesized through hydrothermal treatment of Cu2+ and Pt2+ in an aqueous solution, were evaluated for ferroxidase-like and antibacterial activity. Electron spin resonance (ESR) spectroscopy and colorimetric methods were used to demonstrate that PtCu NPs exhibited strong ferroxidase-like activity in a weakly acidic environment and that this activity was not affected by the presence of most other ions, except silver. Based on the color reaction of salicylic acid in the presence of Fe3+, we tested the ferroxidase-like activity of PtCu NPs to specifically detect Fe2+ in a solution of an oral iron supplement and compared these results with data acquired from atomic absorption spectroscopy and the phenanthroline colorimetric method. The results showed that the newly developed PtCu NPs detection method was equivalent to or better than the other two methods used for Fe2+ detection. The antibacterial experiments showed that PtCu NPs have strong antibacterial activity against Staphylococcus aureus and Escherichia coli. Herein, we demonstrate that the peroxidase-like activity of PtCu NPs can catalyze H2O2 and generate hydroxyl radicals, which may elucidate the antibacterial activity of the PtCu NPs against S. aureus and E. coli. These results showed that PtCu NPs exhibited both ferroxidase- and peroxidase-like activity and that they may serve as convenient and efficient NPs for the detection of Fe2+ and for antibacterial applications.

Long non-coding RNA ZEB2-AS1 promotes the proliferation, metastasis and epithelial mesenchymal transition in triple-negative breast cancer by epigenetically activating ZEB2.

The triple-negative breast cancer is the most malignant type of breast cancer. Its pathogenesis and prognosis remain poor despite the significant advances in breast cancer diagnosis and therapy. Meanwhile, long noncoding RNAs (LncRNAs) play a pivotal role in the progression of malignant tumors. In this study, we found that LncRNA-ZEB2-AS1 was dramatically up-regulated in our breast cancer specimens and cells (MDA231), especially in metastatic tumor specimens and highly invasive cells, and high lncRNA-ZEB2-AS1 expression is associated with clinicopathologic features and short survival of breast cancer patients. LncRNA-ZEB2-AS1 promotes the proliferation and metastasis of MDA231 cells in SCID mice. Thus, it is regarded as an oncogene in triple-negative breast cancer. It is mainly endo-nuclear and situated near ZEB2, positively regulating ZEB2 expression and activating the epithelial mesenchymal transition via the PI3K/Akt/GSK3ß/Zeb2 signaling pathway. Meanwhile, EGF-induced F-actin polymerization in MDA231 cells can be suppressed by reducing lncRNA-ZEB2-AS1 expression. The migration and invasion of triple-negative breast cancer can be altered through cytoskeleton rearrangement. In summary, we demonstrated that lncRNA-ZEB2-AS1 is an important factor affecting the development of triple-negative breast cancer and thus a potential oncogene target.

Seed yeast cultivation for salad oil manufacturing wastewater treatment.

The mixture of five yeast strains obtained from soil could remove about 85% TOC of oil-rich wastewater in batch test. While the highest MLSS was obtained at an N:C of 1:5, the oil removal decreased with the increase of N:C during yeast sludge cultivation. Ammonium chloride was the best nitrogen source for yeast cultivation from the viewpoint of yeast growth and oil utilization. An ammonia concentration of over 1300 mg/L led to mass death of yeast at a pH of 5. The ammonia concentration should be controlled at a level of 1000 mg/L or lower.