Well-ordered Au@Ag NBPs/SiO2 nanoarray for sensitive detection of chloramphenicol via DNAzyme-assisted SERS sensing.

Misuse of chloramphenicol (CAP) can lead to severe food safety issues. Therefore, the accurate and sensitive detection of CAP residues is important for public health. Herein, a convenient and reliable interfacial self-assembly technique was used to form a uniform Au@Ag nanobipyramids (NBPs) film on an ordered SiO2 nanosphere array (SiO2 NS), which served as a Raman-enhanced substrate. In conjunction with a deoxyribonucleic acid enzyme-induced signal amplification strategy, we developed a novel surface-enhanced Raman scattering (SERS) biosensor for the selective and sensitive detection of CAP. The biosensor exhibited a detection limit of 6.42 × 10-13 mol·L-1 and a detection range of 1.0 × 10-12-1.0 × 10-6 mol·L-1. The biosensor could detect CAP in spiked milk samples with a high accuracy, and its recovery rates ranged from 97.88% to 107.86%. The as-developed biosensor with the advantages of high sensitivity and high selectivity offers a new strategy for the rapid, reliable and sensitive detection of CAP, rendering it applicable to food safety control.

Quinoa alleviates osteoporosis in ovariectomized rats by regulating gut microbiota imbalance.

BACKGROUND: Postmenopausal osteoporosis (PMO) is associated with dysregulation of bone metabolism and gut microbiota. Quinoa is a grain with high nutritional value, and its effects and potential mechanisms on PMO have not been reported yet. Therefore, the purpose of this study is to investigate the bone protective effect of quinoa on ovariectomy (OVX) rats by regulating bone metabolism and gut microbiota. RESULTS: Quinoa significantly improved osteoporosis-related biochemical parameters of OVX rats and ameliorated ovariectomy-induced bone density reduction and trabecular structure damage. Quinoa intervention may repair the intestinal barrier by upregulating the expression of tight junction proteins in the duodenum. In addition, quinoa increased the levels of Firmicutes, and decreased the levels of Bacteroidetes and Prevotella, reversing the dysregulation of the gut microbiota. This may be related to estrogen signaling pathway, secondary and primary bile acid biosynthesis, benzoate degradation, synthesis and degradation of ketone bodies, NOD-like receptor signaling pathway and biosynthesis of tropane, piperidine and pyridine alkaloids. Correlation analysis showed that there is a strong correlation between gut microbiota with significant changes in abundance and parameters related to osteoporosis. CONCLUSION: Quinoa could significantly reverse the high intestinal permeability and change the composition of gut microbiota in OVX rats, thereby improving bone microstructure deterioration and bone metabolism disorder, and ultimately protecting the bone loss of OVX rats. © 2024 Society of Chemical Industry.

Revealing the mechanism of quinoa on type 2 diabetes based on intestinal flora and taste pathways.

To investigate the antidiabetic effects and mechanisms of quinoa on type 2 diabetes mellitus (T2DM) mice model. In this context, we induced the T2DM mice model with a high-fat diet (HFD) combined with streptozotocin (STZ), followed by treatment with a quinoa diet. To explore the impact of quinoa on the intestinal flora, we predicted and validated its potential mechanism of hypoglycemic effect through network pharmacology, molecular docking, western blot, and immunohistochemistry (IHC). We found that quinoa could significantly improve abnormal glucolipid metabolism in T2DM mice. Further analysis showed that quinoa contributed to the improvement of gut microbiota composition positively. Moreover, it could downregulate the expression of TAS1R3 and TRPM5 in the colon. A total of 72 active components were identified by network pharmacology. Among them, TAS1R3 and TRPM5 were successfully docked with the core components of quinoa. These findings confirm that quinoa may exert hypoglycemic effects through gut microbiota and the TAS1R3/TRPM5 taste signaling pathway.

Nursing students' experiences of workplace violence based on the perspective of gender differences: a phenomenological study.

BACKGROUND: Workplace violence is a worldwide concern, and particularly affects nursing students. It has a seriously negative impact on nursing students' clinical learning experience and their physical and mental health. This study explored whether there are differences in psychological responses and coping styles among different gender nursing students after exposure to workplace violence, and investigated the causes for these differences. METHODS: We enrolled 22 nursing undergraduates from Guangzhou Medical University and Zunyi Medical University, China. Phenomenological qualitative research and online semi-structured interviews were conducted. The data were analyzed by the Colaizzi seven-step content analysis method. RESULTS: Two categories were collated: psychological experience and coping styles. Three themes of the former were extracted: negative emotional experience, low level of professional identity, and negative effect on self-efficacy. Two themes of the latter: responses to violence and adjustment after violence. In addition, fourteen subthemes were extracted. CONCLUSIONS: Different gender nursing students have different psychological experience and coping styles in the face of workplace violence. The causes of the differences are likely related to sociocultural factors and psychological gender status.

Single-Hole Janus Hollow Sphere.

Cross-linked epoxy resin (EP) single-hole Janus hollow spheres are prepared by cross-linking induced phase separation within an emulsion droplet and selective modification. The droplet is composed of an EP oligomer, toluene, and hexadecane. 2-Ethyl-4-methylimidazole is used as the cross-linker added to the aqueous phase. During the cross-linking, hexadecane forms an eccentric core in the cross-linked EP sphere. A single hole forms across the shell after dissolving the solvents, and a single-hole hollow sphere is achieved. The hole and cavity size are controlled by adjusting the solvent content and cross-linker concentration. Furthermore, frozen wax is used as the core material instead of hexadecane to effectively protect the sphere's interior surface. Selective modification of the exterior and interior surfaces is thus permitted. As an example, a responsive single-hole Janus hollow sphere is prepared by the favorable growth of a silica-polyoxyethylene composite layer onto the exterior surface and a selective grafting of poly(2-diethylaminoethyl methacrylate) (PDEAEMA) by atom-transfer radical polymerization (ATRP) onto the interior. The Janus sphere is water-dispersible and controllably captures and releases oil from the aqueous environment as triggered by the pH value.

Biodegradation and Detoxification of Azo Dyes by Halophilic/Halotolerant Microflora Isolated From the Salt Fields of Tibet Autonomous Region China.

This study aimed to decolorize azo dyes in high-salt industrial wastewater under high-salt and low oxygen conditions using extreme halophilic/halotolerant bacteria screened from the salt fields of Tibet, which consisted of Enterococcus, unclassified Enterobacteriaceae, Staphylococcus, Bacillus, and Kosakonia. Under the optimal conditions, 600 mg/l Congo red, Direct Black G (DBG), Amaranth, methyl red, and methyl orange could be completely decolorized in 24, 8, 8, 12, and 12 h, respectively. When the DBG concentration was 600 mg/l, NADH-DCIP, laccase, and azo reductase were confirmed to be the primary reductase and oxidase during the degradation process, and the degradation pathways were verified. The microflora could not only tolerate changes in salt concentrations of 0-80 g/l, but also displayed strong degradative ability. Under high-salt concentrations (≥ 60 g/l NaCl), NADH-DCIP reductase was primarily used to decolorize the azo dye. However, under low salt concentrations (≤ 40 g/l NaCl), azo reductase began to function, and manganese peroxidase and lignin peroxidase could cooperate to participate in DBG degradation. Additionally, the halophilic/halophilic microflora was shown to convert the toxic DBG dye to metabolites of low toxicity based on phytotoxicity analysis, and a new mechanism for the microflora to degrade DBG was proposed based on intermediates identified by liquid chromatography-mass spectrometry (LC-MS). This study revealed that the halophilic/halophilic microflora has effective ecological and industrial value for treating wastewater from the textile industry.

Quinoa Reduces High-Fat Diet-Induced Obesity in Mice via Potential Microbiota-Gut-Brain-Liver Interaction Mechanisms.

The gut microbiota is important in the occurrence and development of obesity. It can not only via its metabolites, but also through microbiota-gut-brain-liver interactions, directly or indirectly, influence obesity. Quinoa, known as one kind of pseudocereals and weight loss food supplements, has been high-profile for its high nutritional value and broad applications. In this context, we produced high-fat diet-induced (HFD) obese mouse models and assessed the efficacy of quinoa with saponin and quinoa without saponin on obesity. We explored the potential therapeutic mechanisms of quinoa using methods such as 16S rRNA, Western blotting, Immunohistochemical (IHC). Our results indicated that quinoa can improve the obese symptoms significantly on HFD mice, as well as aberrant glucose and lipid metabolism. Further analyses suggest that quinoa can regulate microbiota in the colon and have predominantly regulation on Bacteroidetes, Actinobacteria and Desulfovibrio, meanwhile can decrease the F/B ratio and the abundance of Blautia. Contemporaneously, quinoa can upregulate the expression of TGR5 in the colon and brain, as well as GLP-1 in the colon, liver and brain. while downregulate the expression of TLR4 in the colon and liver, as well as markers of ER stress and oxidative stress in livers and serums. Beyond this, tight junctional proteins in colons and brains are also increased in response to quinoa. Therefore, quinoa can effectively reduce obesity and may possibly exert through microbiota-gut-brain-liver interaction mechanisms. IMPORTANCE Gut microbiota has been investigated extensively, as a driver of obesity as well as a therapeutic target. Studies of its mechanisms are predominantly microbiota-gut-brain axis or microbiota-gut-liver axis. Recent studies have shown that there is an important correlation between the gut-brain-liver axis and the energy balance of the body. Our research focus on microbiota-gut-brain-liver axis, as well as influences of quinoa in intestinal microbiota. We extend this study to the interaction between microbiota and brains, and the result shows obvious differences in the composition of the microbiome between the HFD group and others. These observations infer that besides the neurotransmitter and related receptors, microbiota itself may be a mediator for regulating bidirectional communication, along the gut-brain-liver axis. Taken together, these results also provide strong evidence for widening the domain of applicability of quinoa.

The role of ambra1 in Pb-induced developmental neurotoxicity in zebrafish.

Lead is a highly toxic metal that displays developmental neurotoxicity. Ambra1 plays a crucial role in embryonic neural development. At present, the role of Ambra1 in lead-induced developmental neurotoxicity remains unknown. In this study, we investigated the mechanism of Ambra1 concerning its role in lead-induced neurotoxicity. Zebrafish (Danio rerio) embryos were exposed to 0.1, 1, or 10 µM Pb until 5 days post-fertilization, and their locomotor activity was significantly impaired by the 10 µM treatment. Meanwhile, Pb reduced the expression of ambra1a and ambra1b in the brain at 48 and 72 h post-fertilization. Overexpression of ambra1a or ambra1b reversed Pb-induced alterations in locomotor activity, and decreased the apoptotic cell numbers in the brains of Pb-treated zebrafish. Our data reveal a novel protective role of Ambra1 against Pb-induced neural damage in the developing zebrafish.

Supplementation of quinoa regulates glycolipid metabolism and endoplasmic reticulum stress in the high-fat diet-induced female obese mice.

OBJECTIVE: To explore the effects of the quinoa diet on glycolipid metabolism and endoplasmic reticulum (ER) stress in an obese mouse model. METHODS: Six-week-old C57BL/6J female mice have received a high-fat diet (HFD) to induce obesity and subsequently were treated with a quinoa diet for 12 weeks. During this period, fasting blood glucose, body fat and insulin resistance were measured regularly. At the end of the experiment, mouse serum and liver tissue were collected. The differences in glucose and lipid metabolism were analyzed, and liver tissue pathological morphology, liver endoplasmic reticulum stress-related mRNA and protein levels, and serum oxidative stress levels were measured. RESULTS: Quinoa diet could significantly reduce the level of blood glucose, triglyceride, cholesterol, low-density lipoprotein, improve glucose tolerance, as well as improve histological changes of liver tissues in obese mice (P < 0.05 or < 0.01). Besides, quinoa could improve oxidative stress indicators such as GSH, and MDA (P < 0.05 or < 0.01). Furthermore, quinoa can down-regulate mRNA expression of ER stress markers eIF2α, GRP78, and CHOP in the liver of obese mice (P < 0.05 or < 0.01). CONCLUSIONS: Quinoa supplementation can improve glycolipid metabolism, regulate ER stress, and alleviate obesity in HFD-induced mice.

Association between attitude towards death and spiritual care competence of Chinese oncology nurses: a cross-sectional study.

BACKGROUNDS: An understanding of the oncology nurse spiritual care competence would help nurse managers recognize weakness in spiritual practice and improve the quality of spiritual care. But the relationship between attitude towards death and spiritual care competence is unknown. METHODS: We recruited 326 nurses from hospitals in Guangzhou, China. The nurses completed the Chinese Spiritual Care Competence Scale and the Chinese Death Attitude Profile-Revised questionnaires. RESULTS: The total score of spiritual care competence was 61.62 ± 16.10. And the lowest score of attitude towards death was for escape acceptance, 2.64 ± 0.82. Factors associated with nurse spiritual care competence were work department, whether trained in spiritual care, approaching acceptance, and escaping acceptance of attitude towards death. CONCLUSION: Nurses need to perfect their spiritual care competence and establish positive attitudes towards death.

Curcumin improves adipocytes browning and mitochondrial function in 3T3-L1 cells and obese rodent model.

Accumulating evidence suggests that mitochondrial dysfunction and adipocyte differentiation promote lipid accumulation in the development of obesity and diabetes. Curcumin is an active ingredient extracted from Curcuma longa that has been shown to exhibit antioxidant and anti-inflammatory potency in metabolic disorders. However, the underlying mechanisms of curcumin in adipocytes remain largely unexplored. We studied the effects of curcumin on adipogenic differentiation and mitochondrial oxygen consumption and analysed the possible mechanisms. 3T3-L1 preadipocytes were used to assess the effect of curcumin on differentiation of adipocytes. The Mito Stress Test measured by Seahorse XF Analyzer was applied to investigate the effect of curcumin on mitochondrial oxygen consumption in 3T3-L1 adipocytes. The effect of curcumin on the morphology of both white and brown adipose tissue (WAT and BAT) was evaluated in a high-fat diet-induced obese mice model. We found that curcumin dose-dependently (10, 20 and 35 µM) induced adipogenic differentiation and the intracellular fat droplet accumulation. Additionally, 10 µM curcumin remarkably enhanced mature adipocyte mitochondrial respiratory function, specifically, accelerating basic mitochondrial respiration, ATP production and uncoupling capacity via the regulation of peroxisome proliferator-activated receptor γ (PPARγ) (p < 0.01). Curcumin administration also attenuated the morphological changes in adipose tissues in high-fat diet-induced obese mice. Moreover, curcumin markedly increased the mRNA and protein expressions of mitochondrial uncoupling protein 1 (UCP1), PPARγ, peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and PR domain protein 16 (PRDM16) in vivo and in vitro. Collectively, the results demonstrate that curcumin promotes the adipogenic differentiation of preadipocytes and mitochondrial oxygen consumption in 3T3-L1 mature adipocytes by regulating UCP1, PRDM16, PPARγ and PGC-1α expression.

The elevated transcription of ADAM19 by the oncohistone H2BE76K contributes to oncogenic properties in breast cancer.

The recent discovery of the cancer-associated E76K mutation in histone H2B (H2BE76-to-K) in several types of cancers revealed a new class of oncohistone. H2BE76K weakens the stability of histone octamers, alters gene expression, and promotes colony formation. However, the mechanism linking the H2BE76K mutation to cancer development remains largely unknown. In this study, we knock in the H2BE76K mutation in MDA-MB-231 breast cancer cells using CRISPR/Cas9 and show that the E76K mutant histone H2B preferentially localizes to genic regions. Interestingly, genes upregulated in the H2BE76K mutant cells are enriched for the E76K mutant H2B and are involved in cell adhesion and proliferation pathways. We focused on one H2BE76K target gene, ADAM19 (a disintegrin and metalloproteinase-domain-containing protein 19), a gene highly expressed in various human cancers including breast invasive carcinoma, and demonstrate that H2BE76K directly promotes ADAM19 transcription by facilitating efficient transcription along the gene body. ADAM19 depletion reduced the colony formation ability of the H2BE76K mutant cells, whereas wild-type MDA-MB-231 cells overexpressing ADAM19 mimics the colony formation phenotype of the H2BE76K mutant cells. Collectively, our data demonstrate the mechanism by which H2BE76K deregulates the expression of genes that control oncogenic properties through a combined effect of its specific genomic localization and nucleosome destabilization effect.

Publisher Correction: Comparison of Alterations in miRNA Expression in Matched Tissue and Blood Samples during Spinal Cord Glioma Progression.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

A protective role of autophagy in Pb-induced developmental neurotoxicity in zebrafish.

Lead (Pb) is one of the most toxic heavy metals and has aroused widespread concern as it can cause severe impairments in the developing nervous system. Autophagy has been proposed as an injury factor in Pb-induced neurotoxicity. In this study, we used zebrafish embryo as a model, measured the general toxic effects of Pb, and investigated the effect of Pb exposure on autophagy, and its role in Pb-induced developmental neurotoxicity. Zebrafish embryos were exposed to Pb at concentrations of 0, 0.1, 1 or 10 µM until 4 days post-fertilization. Our data showed that exposure to 10 µM Pb significantly reduced survival rates and impaired locomotor activity. Uptake of Pb was enhanced as the concentration and duration of exposure increased. Inhibition of lysosomal degradation with bafilomycin A1 treatment abolished the suppression of Lc3-II protein expression by Pb. Furthermore, autophagosome formation was inhibited by Pb in the brain. In addition, mRNA expression of beclin1, one of the critical genes in autophagy, were decreased in Pb exposure groups at 72 h post-fertilization. Whole-mount in situ hybridization assay showed that beclin1 gene expression in the brain was reduced by Pb. Rapamycin, an autophagy inducer, partly resolved developmental neurotoxicity induced by Pb exposure. Our results suggest that autophagy plays a protective role in the developmental neurotoxicity of Pb in zebrafish embryos and larvae.

Comparison of Alterations in miRNA Expression in Matched Tissue and Blood Samples during Spinal Cord Glioma Progression.

Abnormal expression of microRNAs (miRNAs) contributes to glioma initiation. However, the expression of miRNAs in tumour tissue or blood of spinal cord glioma (SCG) patients, particularly in high-grade spinal gliomas (Grade IV) known as glioblastoma (GBM), remains largely unknown. In this study we aimed to determine differentially expressed miRNAs (DEmiRNAs) in the tissue and blood between spinal cord glioblastoma (SC-GBM) patients and low grade SCG (L-SCG) patients. Additionally, we predicted key miRNA targets and pathways that may be critical in glioma development using pathway and gene ontology analysis. A total of 74 miRNAs were determined to be differentially expressed (25 upregulated and 49 downregulated) in blood, while 207 miRNAs (20 up-regulated and 187 down-regulated) were identified in tissue samples. Gene ontology analysis revealed multicellular organism development and positive regulation of macromolecule metabolic process to be primarily involved. Pathway analysis revealed "Glioma", "Signalling pathways regulating pluripotency of stem cells" to be the most relevant pathways. miRNA-mRNA analysis revealed that hsa-miRNA3196, hsa-miR-27a-3p, and hsa-miR-3664-3p and their target genes are involved in cancer progression. Our study provides a molecular basis for SCG pathological grading based on differential miRNA expression.

E4F1 silencing inhibits the cell growth through cell-cycle arrest in malignant transformed cells induced by hydroquinone.

Hydroquinone (HQ), one of the most significant metabolic activation products of benzene in an organism, can cause hematological toxicity, such as acute myeloid leukemia. It is a clear carcinogen that can cause changes in the disorder of cell cycle and cell growth. However, its molecular mechanisms remain unclear. E4 transcription factor 1 (E4F1), an important transcription factor, participating in the regulation of cell cycle may be related to the occurrence of tumor. Here, we examined the HQ-induced malignant transformed TK6 cells (TK6-HT) to illustrate the role of E4F1 in carcinogenesis. The present study showed that both the expressions of E4F1 messenger RNA and protein increased obviously in TK6-HT, preliminarily indicating that E4F1 is associated with HQ-induced carcinogenesis. To further explore the role of E4F1, we established E4F1 silencing TK6-HT (pLVX-shE4F1) and its control cells (pLVX-shNC) using lentiviral short hairpin RNA (shRNA) interference expression plasmid vector pLVX-shRNA. Flow cytometry and cell counting kit-8 assay were used to determine the effects of E4F1 silencing on cell cycle and cell growth, respectively. E4F1 silencing inhibited cell growth in TK6-HT. The results from flow cytometry indicated that the inhibitory effect on cell growth may be the results of the E4F1 silencing-induced accumulation in G2/M compared with TK6-HT-shNC. Meanwhile, levels of DNA damage (γ-H2AX), proteins of Rb and phosphorylated Rb, and reactive oxygen species were increased in TK6-HT-shRNA2 cells, which is the critical reason of cell-cycle arrest. In conclusion, E4F1 silencing inhibits the cell growth through cell-cycle arrest in malignant transformed cells induced by HQ.

Salvianolic Acid B Improves Mitochondrial Function in 3T3-L1 Adipocytes Through a Pathway Involving PPARγ Coactivator-1α (PGC-1α).

Purpose: Mitochondrial dysfunction in adipose tissue has emerged as key to the development of obesity and diabetes. Salvianolic acid B (SalB) is a water-soluble ingredient derived from Salvia miltiorrhiza that has been shown to possess potential anti-obese and anti-diabetic activities. However, the cellular mechanism of SalB on mitochondrial function with respect to these metabolic disorders has not been elucidated. Therefore, we aim to investigate the effects of SalB on mitochondrial function in 3T3-L1 adipocytes and analyze the underlying molecular mechanism. Methods: The effects of SalB on adipocyte differentiation, glucose uptake, and glycerol release were evaluated in 3T3-L1 adipocytes. Differentiated adipocytes were treated with SalB (50 µM) with or without PPARγ antagonist (GW9662, 20 µM) for 48 h, and mitochondrial oxygen consumption rate (OCR) as well as extracellular acidification rate (ECAR) were assessed using an XF Extracellular Flux Analyzer. The mitochondrial distribution of adipocytes was assessed using Mito Tracker Green (MTG) and observed under a fluorescent microscope. In addition, the mRNA expression levels of peroxisome proliferators-activated receptor γ/α (PPARγ/α), CCAAT/enhancer binding proteinα (C/EBPα), Nuclear respiratory factor 1/2 (NRF1/2), Uncoupling protein 2 (UCP2), and phosphofructokinase 2/fructose-2, 6-bisphosphatase 2 (PFKFB2) were detected by RT-PCR. Finally, changes in the protein levels of peroxisome proliferators-activated receptor γ coactivator-1α (PGC-1α) were determined by western blotting and immunofluorescence analysis. Results: Treatment with SalB increased glucose uptake and mitochondrial respiration, reduced glycerol release and promoted adipocyte differentiation by increasing mRNA expression of adipogenic transcription factors including PPARγ, C/EBPα, and PPARα. Furthermore, SalB enhanced adipocytes mitochondrial content, mitochondrial respiration and glycolysis capacity, which had been attenuated by GW9662 treatment through the increased expression of PGC-1α. Conclusion: Our results provide novel insights into the role of PGC-1α and mitochondria as probable mediators of SalB activity in the regulation of adipocyte differentiation in 3T3-L1 adipocytes.