Toxic Effects of Arsenic on Four Freshwater Aquatic Species and Its Transformation Metabolism in Crucian Carp (Carassius auratus).

Inorganic arsenic is a well-known carcinogen that is much more toxic than its organic counterpart. While much is known about the accumulation and transformation of arsenic in marine organisms, little is known regarding these processes in freshwater aquatic species. In this study, the acute toxicity and toxicological effects of inorganic arsenic on four freshwater organisms (Cyprinus carpio, Misgurnus anguillicaudatus, Pseudorasbora parva, Eriocheir sinensis) commonly found in rice-fish farming systems were investigated. The organisms exhibited different levels of sensitivity to inorganic arsenic, with crustaceans being more sensitive than fish. Fish were found to be more tolerant to As(V) than As(III). The study also investigated the accumulation, transformation, and release of inorganic arsenic in crucian carp, an omnivorous species with high environmental tolerance. The fish accumulated As(III) rapidly in various tissues, and were able to transport it to other tissues through gills, intestines, and skin. The accumulated As(III) was converted into less toxic forms, such as monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA), via methylation. The fish also converted As(III) into arsenate (AsV) via enzymatic and oxidative reactions. After the transferal to clean water, the forms of arsenic in the various tissues decreased rapidly, but the rates of excretion of the four forms of arsenic were not the same among the different tissues. Our results suggest that crucian carp can reduce the environmental toxicity of As(III) at certain concentrations by transforming it into less toxic forms within their bodies.

Hepatotoxic effects of chronic exposure to environmentally relevant concentrations of Di-(2-ethylhexyl) phthalate (DEHP) on crucian carp: Insights from multi-omics analyses.

Di-(2-ethylhexyl) phthalate (DEHP) is an extensively used phthalate esters (PAEs) that raise growing ecotoxicological concerns due to detrimental effects on living organisms and ecosystems. This study performed hepatotoxic investigations on crucian carp under chronic low-dosage (CLD) exposure to DEHP at environmentally relevant concentrations (20-500 µg/L). The results demonstrated that the CLD exposure induced irreversible damage to the liver tissue. Multi-omics (transcriptomics and metabolomics) analyses revealed the predominant toxicological mechanisms underlying DEHP-induced hepatotoxicity by inhibiting energy production pathways and the up-regulation of the purine metabolism. Disruption of metabolic pathways led to excessive reactive oxygen species (ROS) production and subsequent oxidative stress. The adverse metabolic effects were exacerbated by an interplay between oxidative stress and endoplasmic reticulum stress. This study not only provides new mechanistic insights into the ecotoxicological effects of DEHP under chronic low-dosage exposure, but also suggests a potential strategy for further ecological risk assessment of PAEs.

Investigating the Impact of Disrupting the Glutamine Metabolism Pathway on Ammonia Excretion in Crucian Carp (Carassius auratus) under Carbonate Alkaline Stress Using Metabolomics Techniques.

With the gradual decline in freshwater resources, the space available for freshwater aquaculture is diminishing and the need to maximize saline water for aquaculture is increasing. This study aimed to elucidate the impact mechanisms of the disruption of the glutamate pathway on serum metabolism and ammonia excretion in crucian carp (Carassius auratus) under carbonate alkaline stress. A freshwater control group (C group), a 20 mmol/L NaHCO3 stress group (L group), and a 40 mmol/L NaHCO3 stress group (H group) were established. After 30 days of exposure, methionine sulfoximine (MSO) was injected to block the glutamate pathway metabolism, and the groups post-blocking were labeled as MC, ML, and MH. Ultra-high-performance liquid chromatography coupled with the quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) metabolomics technique was employed to detect changes in the composition and content of crucian carp serum metabolites. Significant differential metabolites were identified, and related metabolic pathways were analyzed. The results revealed that, following the glutamate pathway blockade, a total of 228 differential metabolites (DMs) were identified in the three treatment groups. An enrichment analysis indicated significant involvement in glycerophospholipid metabolism, arachidonic acid metabolism, sphingolipid metabolism, purine metabolism, arginine and proline biosynthesis, pantothenate and CoA biosynthesis, glutathione metabolism, and fatty acid degradation, among other metabolic pathways. The results showed that ROS imbalances and L-arginine accumulation in crucian carp after the glutamate pathway blockade led to an increase in oxidative stress and inflammatory responses in vivo, which may cause damage to the structure and function of cell membranes. Crucian carp improves the body's antioxidant capacity and regulates cellular homeostasis by activating glutathione metabolism and increasing the concentration of phosphatidylcholine (PC) analogs. Additionally, challenges such as aggravated ammonia excretion obstruction and disrupted energy metabolism were observed in crucian carp, with the upregulation of purine metabolism alleviating ammonia toxicity and maintaining energy homeostasis through pantothenate and CoA biosynthesis as well as fatty acid degradation. This study elucidated the metabolic changes in crucian carp under carbonate alkaline stress after a glutamate pathway blockade at the cellular metabolism level and screened out the key metabolic pathways, which provide a scientific basis for further in-depth studies on the ammonia excretion of freshwater scleractinian fishes under saline and alkaline habitats at a later stage.

Assessment of a training project of English as a media of instruction(EMI) using Kirkpatrick model.

BACKGROUND: English as a Media of Instruction (EMI) teacher development project is based upon the framework for teacher Continuing Professional Development (CPD) and aims to effectively improve both the confidence and overall capacity of EMI lecturers. Kunming Medical University(KMU) conducted the EMI training project to improve teachers' competence for MBBS education. This study aimed to assess teachers' changes following the implementation of this training project, via the Kirkpatrick evaluation model. METHODS: A total of trainees (n = 84) were invited as the research objects. The effects of the EMI training project implemented in KMU were evaluated in terms of the reaction, learning, and behavior dimensions based on the Kirkpatrick model. The self-administered online anonymous questionnaires and observations of participants' EMI lectures were administered to all participants to collect the data. Furthermore, to understand participants' perceptions of the management and trainers of the training project, some open-ended questions were required to answer. RESULTS: Based on 1-3 level of the Kirkpatrick model, all participants were highly satisfied with the EMI training implementation on the reaction level, and expressed positive comments about the management of the training and trainers. On the learning level, participants' scores on awareness of EMI teaching techniques increased significantly(t = 7.122, P < 0.001)with the training process. Concerning the behavior level, the participant's confidence as an EMI instructor increased dramatically at end of the whole training(p < 0.001). Moreover, trainees had applied some EMI skills in class and would like to make some commitment to implement learner-centered learning, to do more practice on EMI techniques. CONCLUSION: The findings of this study confirm that EMI training has an effective impact on the competence and confidence of participants as EMI instructors at levels 1-3 of the Kirkpatrick evaluation model. This training may be a potentially beneficial effect on the teaching quality of MBBS education.

Stress response and tolerance mechanisms of NaHCO3 exposure based on biochemical assays and multi-omics approach in the liver of crucian carp (Carassius auratus).

The development and utilization of saline-alkaline water, an important backup resource, has received widespread attention. However, the underuse of saline-alkaline water, threatened by the single species of saline-alkaline aquaculture, seriously affects the development of the fishery economy. In this work, a 30-day NaHCO3 stress experimental study combined with analyses of untargeted metabolomics, transcriptome, and biochemical approaches was conducted on crucian carp to provide a better understanding of the saline-alkaline stress response mechanism in freshwater fish. This work revealed the relationships among the biochemical parameters, endogenous differentially expressed metabolites (DEMs), and differentially expressed genes (DEGs) in the crucian carp livers. The biochemical analysis showed that NaHCO3 exposure changed the levels of several physiological parameters associated with the liver, including antioxidant enzymes (SOD, CAT, GSH-Px), MDA, AKP, and CPS. According to the metabolomics study, 90 DEMs are involved in various metabolic pathways such as ketone synthesis and degradation metabolism, glycerophospholipid metabolism, arachidonic acid metabolism, and linoleic acid metabolism. In addition, transcriptomics data analysis showed that a total of 301 DEGs were screened between the control group and the high NaHCO3 concentration group, of which 129 up-regulated genes and 172 down-regulated genes. Overall, NaHCO3 exposure could cause lipid metabolism disorders and induce energy metabolism imbalance in the crucian carp liver. Simultaneously, crucian carp might regulate its saline-alkaline resistance mechanism by enhancing the synthesis of glycerophospholipid metabolism, ketone bodies, and degradation metabolism, at the same time increasing the vitality of antioxidant enzymes (SOD, CAT, GSH-Px) and nonspecific immune enzyme (AKP). Herein, all results will provide new insights into the molecular mechanisms underlying the stress responses and tolerance to saline-alkaline exposure in crucian carp.

Effects of Saline-Alkaline Stress on Metabolome, Biochemical Parameters, and Histopathology in the Kidney of Crucian Carp (Carassius auratus).

The salinization of the water environment caused by human activities and global warming has increased which has brought great survival challenges to aquatic animals. Crucian carp (Carassius auratus) is an essential freshwater economic fish with superior adaptability to saline-alkali water. However, the physiological regulation mechanism of crucian carp adapting to saline-alkali stress remains still unclear. In this study, crucian carp were exposed to freshwater or 20, 40, and 60 mmol/L NaHCO3 water environments for 30 days, the effects of saline-alkali stress on the kidney were evaluated by histopathology, biochemical assays and metabolomics analysis from renal function, antioxidant capacity and metabolites level. Our results showed different degrees of kidney damage at different exposure concentrations, which were characterized by glomerular atrophy and swelling, renal tubular degranulation, obstruction and degeneration, renal interstitial edema, renal cell proliferation and necrosis. Saline-alkali stress could change the levels of several physiological parameters with renal function and antioxidant capacity, including creatinine (CREA), urea nitrogen (BUN), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA). In addition, metabolomics analysis showed that differential metabolites (DMs) were involved in various metabolic pathways, including phenylalanine, tyrosine, and tryptophan biosynthesis, aminoacyl-tRNA biosynthesis, purine metabolism, glycerophospholipid metabolism, sphingolipid metabolism, glycolysis/gluconeogenesis and the TCA cycle. In general, our study revealed that saline-alkaline stress could cause significant changes in renal function and metabolic profiles, and induce severe damage in the crucian carp kidney through destroying the anti-oxidant system and energy homeostasis, inhibiting protein and amino acid catabolism, as well as disordering purine metabolism and lipid metabolism. This study could contribute to a deeper understanding the adverse effects of saline-alkali stress on crucian carp kidney and the regulatory mechanism in the crucian carp of saline-alkali adaptation at the metabolic level.

UPLC-QTOF/MS Metabolomics and Biochemical Assays Reveal Changes in Hepatic Nutrition and Energy Metabolism during Sexual Maturation in Female Rainbow Trout (Oncorhynchus mykiss).

Mobilization and repartition of nutrients and energy are prerequisites for the normal sexual maturity of broodstock. However, there are few studies on the mechanisms of hepatic nutrients and energy metabolism during sexual maturation in female rainbow trout (Oncorhynchus mykiss). This study investigated hepatic metabolite changes and explored the potential nutritional regulation mechanism between mature and immature female rainbow trout by combining UPLC-QTOF/MS metabolomics and biochemical assays. It was observed that hepatic biochemical assays differed considerably between the two groups, such as glucose, triglycerides, hexokinase, lipase, and aspartate aminotransferase. Liver metabolomics showed that various differential metabolites involved in amino acid and lipid metabolism markedly increased, suggesting the enhancement of lipid metabolism and amino acid anabolism in the liver provides the necessary material basis for ovarian development. Meanwhile, glycogen catabolism and glycolysis hold the key to maintaining organismal energy homeostasis with normal sexual maturation of female rainbow trout. Overall, the results from this study suggested that the liver undergoes drastic reprogramming of the metabolic profile in response to mobilization and repartition of nutrients and energy during the sexual maturation of female rainbow trout. This study further deepened the understanding of the reproductive biology of rainbow trout, and provided the theoretical basis and practical ramifications for nutritional requirements of breeding high-quality broodstock in the artificial propagation of rainbow trout.

Revealing the pharmacological effect and mechanism of darutoside on gouty arthritis by liquid chromatography/mass spectrometry and metabolomics.

Darutoside is a diterpenoids compound with significant anti-inflammatory activity, however the pharmacological action and mechanism are still unclear. Metabolomics strategy was used to uncovering the pharmacological action and effective mechanism of darutoside against acute gouty arthritis rats. Liquid chromatography coupled with mass spectrometry technique was performed to explore the serum metabolites and potential pathways. We found that darutoside can up-regulate the level of glutamate, alanine, chenodeoxycholic acid, 1-methyladenosine, aspartic acid, citric acid, and down-regulate the level of valine, isoleucine, glutamine, alanyl-threonine, pyruvic acid, gamma-aminobutyric acid, uric acid. Metabolic pathway analysis showed that the therapeutic effect of darutoside was involved in amino acid metabolism, sugar metabolism, fatty acid metabolism, energy metabolism, purine metabolism and butanoate metabolism. It indicated that darutoside protect against acute gouty arthritis by regulating the expression of the key protein targets. It revealed that the mechanism of darutoside on acute gouty arthritis, which may be leading to the changes of serum metabolites, metabolic pathways and key protein targets to improve immune system response, inhibit oxidative stress and inflammatory response. It provides a novel method for molecular mechanisms of natural product in the disease treatment.

Multi-omics profiling and biochemical assays reveal the acute toxicity of environmental related concentrations of Di-(2-ethylhexyl) phthalate (DEHP) on the gill of crucian carp (Carassius auratus).

Di-(2-ethylhexyl) phthalate (DEHP) is one of the most extensively utilized plasticizers in the plastic manufacturing process. It is widely used in various fields due to its low cost and excellent effect. Although there is evidence that DEHP is harmful to animal and human health, DEHP-induced gill toxicity in aquatic organisms is inconclusive, and its mechanism has not been fully elucidated. Here, we investigated the effects of DEHP acute exposure on crucian carp gills at environmentally relevant concentrations of 20, 100, and 500 µg/L. Multi-omics profiling and biochemical assays were employed to characterize the potential toxicological mechanisms. The results showed that acute exposure to 100 and 500 µg/L of DEHP leads to oxidative stress in gills, as evidenced by overproduction of reactive oxygen species (ROS), increased antioxidant enzyme activity, and the transformation of glutathione from reduced to oxidized form, resulting in lipid peroxidation. Integrative analysis of transcriptomics and metabolomics indicated that increased purine metabolism was the potential source of increased ROS. Moreover, lipid metabolism disorder, including arachidonic acid metabolism, induces inflammation. Further, DEHP causes the imbalance of the CYP enzyme system in the gill, and DEHP-induced gill toxicity in crucian carp was associated with interference with CYP450 homeostasis. Taken together, this study broadens the molecular understanding of the DEHP-induced gill toxicity in aquatic organisms and provides novel perspectives for assessing the effects of DEHP on target and non-target aquatic organisms in the environment.

Physiological responses to heat stress in the liver of rainbow trout (Oncorhynchus mykiss) revealed by UPLC-QTOF-MS metabolomics and biochemical assays.

Rainbow trout (Oncorhynchus mykiss) is one of the world's most widely farmed cold-water fish. However, the rise in water temperature caused by global warming has seriously restricted the development of rainbow trout aquaculture. In this study, we investigated the physiological responses in the liver of rainbow trout exposed to 20 â„ƒ and 24 â„ƒ and returning to the initial temperature (14 â„ƒ) by combining biochemical analyses and UPLC-QTOF-MS metabolomics. The results of the biochemical analysis showed that serum aminotransferase, lysozyme, total bilirubin, alkaline phosphatase and liver superoxide dismutase, glutathione peroxidase, and malondialdehyde in rainbow trout under heat stress changed significantly. Even after the temperature recovery, some of the above indicators were still affected. Compared to the control group, 115, 130, and 121 differentially expressed metabolites were identified in the 20 â„ƒ, 24 â„ƒ, and recovery groups, respectively. Further pathway enrichment of these metabolites revealed that heat stress mainly affected the linoleic acid metabolism, α-linolenic acid metabolism, glycerophospholipid metabolism, and sphingolipid metabolism in the liver of rainbow trout, and continuously affected these metabolic pathways during the recovery period. Notably, the enrichment of glutathione metabolic pathways was consistent with the changes in glutathione peroxidase in the biochemical results. The results above suggest that heat stress can induce immune responses and oxidative stress inside the rainbow trout. After temperature recovery, some of the hepatic functions of fish return to normal gradually. The biochemical analysis and UPLC-QTOF-MS metabolomics tools provide insight into the physiological regulation of rainbow trout in response to heat stress.

miR-301b-5p and its target gene nfatc2ip regulate inflammatory responses in the liver of rainbow trout (Oncorhynchus mykiss) under high temperature stress.

Rainbow trout (Oncorhynchus mykiss) is a typical cold-water aquaculture fish and a high-end aquatic product. When water temperature exceeds its optimal range of 12-18 °C, the immune system of rainbow trout becomes weakened and unbalanced. High temperature in summer and global warming severely impact rainbow trout industry. The focus of this study was to explore the mechanisms regulating the immune response of rainbow trout under high temperature stress and identify molecular elements that account for resistance to high temperature. In this study, individual fish were screened in a high temperature stress experiment and divided into resistant (R) and sensitive (S) groups. The hepatic transcriptome sequencing and analysis of mRNAs and microRNAs of the R, S, and control groups showed that the number of the differentially expressed genes (DEGs) in the S group (9259) was higher than that in the R group (5313). Furthermore, the 1233 genes differentially expressed between S and R groups were mainly enriched in immune-related pathways, including cytokine-cytokine receptor interaction, TNF signaling and IL-17 signaling. Among these DEGs were miR-301b-5p and its target gene that encodes nuclear factor of activated T cells two interacting protein (nfatc2ip). The dual-luciferase reporter system and immunofluorescence experiments verified the relationship between miR-301b-5p and nfatc2ip. We also showed that expression levels of miR-301b-5p and nfatc2ip significantly negatively correlated in the liver of rainbow trout under high temperature stress. By performing functional experiments, we showed that activation of miR-301b-5p expression or inhibition of nfatc2ip expression stimulated the phosphorylation of p65, p38, and JNK in the classical nuclear factor kappa-B and mitogen-activated protein kinase pathways under high temperature stress. These manipulations initially promoted the secretion of the pro-inflammatory factor IL-1ß and then increased the levels of IL-6, IL-12, and TNF-α. In addition, activation of miR-301b-5p expression or inhibition of nfatc2ip expression stimulated the repair of the hepatic ultrastructural damage caused by high temperature stress by activating the inflammatory response in rainbow trout liver.

Integrated application of multi-omics approach and biochemical assays provides insights into physiological responses to saline-alkaline stress in the gills of crucian carp (Carassius auratus).

Given the decline of freshwater resources in recent years, the accessible space for freshwater aquaculture is rapidly shrinking, and aquaculture in saline-alkaline water has become a critical approach to meet the rising demand. However, the molecular mechanism behind the adverse effects of saline-alkaline water on fish and the regulatory mechanism in fish tolerance remains unclear. Here, adult crucian carp (Carassius auratus) were exposed to 60 mmol/L NaHCO3 for 30 days. It was observed that long-term carbonate alkalinity (CA) exposure not only caused gill oxidative stress but also changed the levels of several physiological parameters associated with ammonia transport, including blood ammonia, urea nitrogen (BUN), glutamine (Gln), and glutamine synthetase (GS). According to the metabolomics study, differential metabolites (DMs) engaged in various metabolic pathways, such as glycerophospholipid metabolism, sphingolipid metabolism, and arachidonic acid metabolism. In addition, transcriptomics data showed that differentially expressed genes (DEGs) were closely related to ammonia transport, apoptosis, and immunological response. In general, comprehensive multi-omics and biochemical analysis revealed that crucian carp might adopt Rh glycoprotein as a carrier to mediate ammonia transport and increase glutamine and urea synthesis under long-term high saline-alkaline stress to mitigate the adverse effects of blocked ammonia excretion. Simultaneously, saline-alkaline stress caused the destruction of the antioxidant system and the disorder of lipid metabolism in the crucian carp gills, which induced apoptosis and immunological response. To our knowledge, this is the first study to investigate fish's molecular and metabolic mechanisms under saline-alkaline stress using integrated metabolomics, transcriptomics, and biochemical assays. Overall, the results of this study provided new insights into the molecular mechanism behind the adverse effects of saline-alkaline water on fish and the regulatory mechanism in fish tolerance.

High-throughput metabolomics method based on liquid chromatography-mass spectrometry: Insights into the underlying mechanisms of salinity-alkalinity exposure-induced metabolites changes in Barbus capito.

It is critical to investigate the adaptive development and the physiological mechanism of fish in external stimulation. In this study, the response of Barbus capito to salinity-alkalinity exposure was explored by high-throughput nontargeted and liquid chromatography-mass spectrometry-based metabolomics to investigate metabolic biomarker and pathway changes. Meanwhile, the biochemical indexes of Barbus capito were measured to discover the chronic impairment response to salinity-alkalinity exposures. A total of 29 tissue metabolites were determined to deciphering the endogenous metabolic changes of fishes during the different concentration salinity-alkalinity exposures environment, which were mainly involved in the key metabolism including the phenylalanine, tyrosine, and tryptophan biosynthesis, arachidonic acid metabolism, pyruvate metabolism, citrate cycle, and glycerophospholipid metabolism. Finally, we found the amino acid metabolism as key target was associated with the endogenous metabolites and metabolic pathways of Barbus capito to salinity-alkalinity exposures. In conclusion, metabolomics is a potentially powerful tool to reveal the mechanism information of fish in various exposure environments.

Exploring the metabolic biomarkers and pathway changes in crucian under carbonate alkalinity exposure using high-throughput metabolomics analysis based on UPLC-ESI-QTOF-MS.

The aims of this study is to explore the metabolomic biomarker and pathway changes in crucian under carbonate alkalinity exposures using high-throughput metabolomics analysis based on ultra-performance liquid chromatography-electrospray ionization-quadrupole time of flight-tandem mass spectrometry (UPLC-ESI-QTOF-MS) for carrying out adaptive evolution of fish in environmental exposures and understanding molecular physiological mechanisms of saline-alkali tolerance in fishes. Under 60 day exposure management, the UPLC-ESI-QTOF-MS technology, coupled with a pattern recognition approach and metabolic pathway analysis, was utilized to give insight into the metabolic biomarker and pathway changes. In addition, biochemical parameters in response to carbonate alkalinity in fish were detected for chronic impairment evaluation. A total of twenty-seven endogenous metabolites were identified to distinguish the biochemical changes in fish in clean water under exposure to different concentrations of carbonate alkalinity (CA); these mainly involved amino acid synthesis and metabolism, arachidonic acid metabolism, glyoxylate and dicarboxylate metabolism, pyruvate metabolism and the citrate cycle (TCA cycle). Compared with the control group, CA exposure increased the level of blood ammonia; TP; ALB; Gln in the liver and gills; GS; urea in blood, the liver and gills; CREA; CPS; Glu and LDH; and decreased the level of weight gain rate, oxygen consumption, discharge rate of ammonia, SOD, CAT, ALT, AST and Na+/K+-ATPase. At low concentrations, CA can change the normal metabolism of fish in terms of changing the osmotic pressure regulation capacity, antioxidant capacity, ammonia metabolism and liver and kidney function to adapt to the CA exposure environment. As the concentration of CA increases, various metabolic processes in crucian are inhibited, causing chronic damage to the body. The results show that the metabolomic strategy is a potentially powerful tool for identifying the mechanisms in response to different environmental exposomes and offers precious information about the chronic response of fish to CA.

Structures and photocatalytic properties of two new Zn(ii) coordination polymers based on semi-rigid V-shaped multicarboxylate ligands.

Two new metal-organic coordination polymers (CPs), aqua-2,2'-bipyridine-5-(4'-carboxylphenoxy)isophthalatezinc(ii) polymer [Zn(HL)(2,2'-bipy)(H2O)] n (1) and tris-4,4'-bipyridine-bis-5-(4'-carboxylphenoxy)isophthalatetrizinc(ii) polymer [Zn3(L)2(4,4'-bipy)3] n (2) (H3L = 5-(4'-carboxylphenoxy)isophthalic acid, 4,4'-bipy = 4,4'-bipyridine and 2,2'-bipy = 2,2'-bipyridine), were obtained under hydrothermal conditions and characterized by microanalysis, FTIR spectroscopy and single crystal X-ray diffraction. The single crystal X-ray diffraction indicated that in both the CPs the coordination networks exhibited varied topologies and coordination modes around the Zn(ii) centers. CP 1 exhibits a one-dimensional (1D) chain structure, which further forms a 3D supramolecular architecture via intermolecular π⋯π and hydrogen bonding interactions, while 2 possesses a 3D framework generated from a 2D layered motif comprising zinc and tripodal carboxylate subunits pillared by 4,4'-bpy ligands. Apart from the structural investigation, the photocatalytic performances of both the coordination polymers to photodecompose an aqueous solution of methyl violet (MV) were examined. The results indicated that both the CPs displayed the potential to photodecompose aromatic dyes and in particular 2 showed good photocatalytic activity for dye degradation under light irradiation. The photocatalytic mechanism through which these CPs executed degradation of dyes has been explained with the assistance of band gap calculations using density of states (DOS) and its decomposed partial DOS calculations.

Cadmium exposure triggers mitochondrial dysfunction and oxidative stress in chicken (Gallus gallus) kidney via mitochondrial UPR inhibition and Nrf2-mediated antioxidant defense activation.

Cadmium (Cd) is a widespread environmental pollutant that accumulates in living systems and represents a significant global health hazard. Cd poses a toxicity threat to both human and animal health, including that of birds. Further knowledge of Cd toxicology pathways will allow for a better understanding of Cd-induced nephrotoxicity. To evaluate Cd-induced nephrotoxicity through potential oxidative damage, male chickens were treated with 0 mg/kg, 35 mg/kg or 70 mg/kg CdCl2 in diet for 90 days. Markedly, histopathology indicated renal tubular epithelial cell swelling, renal function CREA content abnormalities, biochemical and morphologic indices indicative of Cd-induced kidney injury. Cd toxicity induced the up-regulation of Nrf2 and downstream target genes that relieve oxidative stress. Meanwhile, Cd disrupted the homeostasis of trace elements and promoted oxidative damage. Cd interfered with mitochondrial unfolded protein response (UPRmt)-related factors (SIRT1, SIRT3, PGC-1α, TFAM, Nrf1, and HTRA2) and disrupted the homeostasis of mitochondrial dynamics (OPA1, MFN1, MFN2, Fis1 and MFF), thereby exacerbating mitochondrial structural damage and mitochondrial dysfunction. In conclusion, our study demonstrated that the nephrotoxicity of Cd exposure results in oxidative stress and mitochondrial dysfunction by activating the Nrf2 signaling pathway and inhibiting UPRmt in the kidneys.

Mixed Titanium Oxide Strategy for Enhanced Photocatalytic Hydrogen Evolution.

Titanium dioxide is a promising photocatalyst material for water splitting, but is limited by its low utilization of solar energy and rapid recombination of electron-hole pairs. Herein, a mixed titanium oxide strategy, utilizing TiO2/Ti2O3 heterostructures consisting of in situ grown TiO2 nanotubes with mixed anatase and rutile phases on bulk Ti2O3 materials, is demonstrated for efficient and recyclable hydrogen evolution from photocatalytic water splitting. Taking advantage of the formed heterostructures and the created porous structures, the photogenerated electrons from the conduction band of anatase TiO2 can be first delivered to rutile TiO2 and then transferred to Ti2O3. Meanwhile, the presence of Ti2O3 in TiO2/Ti2O3 heterostructures can substantially promote the charge mobility and suppress the recombination of photogenerated electron-hole pairs. Hence, with a tuned band gap structure that enables rapid electron-hole separation, increased charge carrier density, and enhanced light absorption, the TiO2/Ti2O3 heterostructures provide an enhanced photocatalytic hydrogen evolution rate as high as 1440 µmol g-1 h-1 under full-sunlight irradiation and without any other cocatalyst. This mixed titanium oxide strategy may open up new avenues for designing and constructing highly efficient TiO2-based photocatalytic materials for various applications.

Second-generation motion correction algorithm improves diagnostic accuracy of single-beat coronary CT angiography in patients with increased heart rate.

OBJECTIVE: To assess the effect of a second-generation motion correction algorithm on the diagnostic accuracy of coronary computed tomography angiography (CCTA) using a 256-detector row CT in patients with increased heart rates. METHODS: Eighty-one consecutive symptomatic cardiac patients with increased heart rates (≥ 75 beats per min) were enrolled. All patients underwent CCTA and invasive coronary angiography (ICA). CCTA was performed with a 256-detector row CT using prospectively ECG-triggered single-beat protocol. Images were reconstructed using standard (STD) algorithm, first-generation intra-cycle motion correction (MC1) algorithm, and second-generation intra-cycle motion correction (MC2) algorithm. The image quality of coronary artery segments was assessed by two experienced radiologists using a 4-point scale (1: non-diagnostic and 4: excellent), according to the 18-segment model. Diagnostic performance for segments with significant lumen stenosis (≥ 50%) was compared between STD, MC1, and MC2 by using ICA as the reference standard. RESULTS: The mean effective dose of CCTA was 1.0 mSv. On per-segment level, the overall image quality score and interpretability were improved to 3.56 ± 0.63 and 99.2% due to the use of MC2, as compared to 2.81 ± 0.85 and 92.5% with STD and 3.21 ± 0.79 and 97.2% with MC1. On per-segment level, compared to STD and MC1, MC2 improved the sensitivity (92.2% vs. 79.2%, 80.7%), specificity (97.8% vs. 82.1%, 90.8%), positive predictive value (89.9% vs. 48.4%, 65.1%), negative predictive value (98.3% vs. 94.9%, 95.7%), and diagnostic accuracy (96.8% vs. 81.5%, 89.0%). CONCLUSION: A second-generation intra-cycle motion correction algorithm for single-beat CCTA significantly improves image quality and diagnostic accuracy in patients with increased heart rate. KEY POINTS: • A second-generation motion correction (MC2) algorithm can further improve the image quality of all coronary arteries than a first-generation motion correction (MC1). • MC2 algorithm can significantly reduce the number of false positive segments compared to standard and MC1 algorithm.

Neuroprotective effects of pinocembrin on ischemia/reperfusion-induced brain injury by inhibiting autophagy.

BACKGROUND: Cerebral ischemia/reperfusion (I/R) injury is a common pathological process after cardiac arrest, shock and acute cerebral infarction recanalization, which causes serious injury in brain function. Pinocembrin (Pino), a natural flavonoid at the highest concentration in propolis, exhibited a variety of biological effects, including antitumor, antimicrobial and anti-inflammatory activities. However, the effects of Pino on brain injured after I/R and the mechanisms of its neuroprotective effects remain elusive. METHODS: In the present study, we used I/R model rats underwent transient cerebral ischemia inducing by four-vessel occlusion and reperfusion. Pino alone or in combination with autophagy inducer rapamycin (RAPA) was administered to I/R rats. The behavior and cognitive function were evaluated by open field test and Morris water maze test. HE staining was used to determine the survival of hippocampus CA1 pyramidal cells. Three key proteins of autophagy, LC3, Beclin1 and p62, were detected by Western blot. RESULTS: Our results showed that Pino could significantly reduce the damage of hippocampus CA1 pyramidal neurons and alleviate the impairments of behavior and cognitive function in I/R rats. Pino also decreased the expression of LC3II and Beclin1 and increased the level of p62 in hippocampus CA1 of I/R rats. In addition, Pino also decreased RAPA-induced neuronal damage and excessive activation of autophagy in I/R rats. CONCLUSIONS: Taken together, these results suggested that Pino could protect the brain injury induced by I/R and the potential mechanisms might attribute to inhibition of autophagy activity.

Development and validation of the pulmonary tuberculosis scale of the system of Quality of Life Instruments for Chronic Diseases (QLICD-PT).

BACKGROUND: Generic assessments are less responsive to subtle changes due to specific diseases, making it challenging to fully understand the impact of pulmonary tuberculosis (TB) on patient's quality of life (QOL). METHODS: We applied programmed decision procedures and theories on instrument development to develop the scale. Two hundred patients with pulmonary TB participated in measuring QOL three times before and after treatments. We assessed the validity, reliability, and responsiveness of QLICD-PT using correlation analysis, factor analysis, multi-trait scaling analysis, randomized block analyses of variance with Least Significant Difference post-hoc tests. RESULTS: We composed QLICD-PT with 3 domains (28 items) for general QOL and 1 pulmonary TB specific domain (12 items). Correlation and factor analysis confirmed good structure validity and criterion-related validity when using Chinese version of the Medical Outcomes Short-Form Health Survey (SF-36) as a criterion. The internal consistency of α values were higher than 0.70. The score changes after treatment were of statistical significance for the overall scale, physical domain and specific domain with effect size ranging from 0.32 to 0.72. No floor effects but small ceiling effects were observed at domain level. CONCLUSIONS: As the first pulmonary TB-specific QOL scale developed by a module approach in Chinese, QLICD-PT has an acceptable degree of validity, reliability and responsiveness, and can be used to measure the life quality of PT patients specifically and sufficiently.