High-Performance Contact-Doped WSe2 Transistors Using TaSe2 Electrodes.

Two-dimensional (2D) transitional metal dichalcogenides (TMDs) have garnered significant attention due to their potential for next-generation electronics, which require device scaling. However, the performance of TMD-based field-effect transistors (FETs) is greatly limited by the contact resistance. This study develops an effective strategy to optimize the contact resistance of WSe2 FETs by combining contact doping and 2D metallic electrode materials. The contact regions were doped using a laser, and the metallic TaSe2 flakes were stacked on doped WSe2 as electrodes. Doping the contact areas decreases the depletion width, while introducing the TaSe2 contact results in a lower Schottky barrier. This method significantly improves the electrical performance of the WSe2 FETs. The doped WSe2/TaSe2 contact exhibits an ultralow Schottky barrier height of 65 meV and a contact resistance of 11 kΩ·µm, which is a 50-fold reduction compared to the conventional Cr/Au contact. Our method offers a way on fabricating high-performance 2D FETs.

Foundation metrics for evaluating effectiveness of healthcare conversations powered by generative AI.

Generative Artificial Intelligence is set to revolutionize healthcare delivery by transforming traditional patient care into a more personalized, efficient, and proactive process. Chatbots, serving as interactive conversational models, will probably drive this patient-centered transformation in healthcare. Through the provision of various services, including diagnosis, personalized lifestyle recommendations, dynamic scheduling of follow-ups, and mental health support, the objective is to substantially augment patient health outcomes, all the while mitigating the workload burden on healthcare providers. The life-critical nature of healthcare applications necessitates establishing a unified and comprehensive set of evaluation metrics for conversational models. Existing evaluation metrics proposed for various generic large language models (LLMs) demonstrate a lack of comprehension regarding medical and health concepts and their significance in promoting patients' well-being. Moreover, these metrics neglect pivotal user-centered aspects, including trust-building, ethics, personalization, empathy, user comprehension, and emotional support. The purpose of this paper is to explore state-of-the-art LLM-based evaluation metrics that are specifically applicable to the assessment of interactive conversational models in healthcare. Subsequently, we present a comprehensive set of evaluation metrics designed to thoroughly assess the performance of healthcare chatbots from an end-user perspective. These metrics encompass an evaluation of language processing abilities, impact on real-world clinical tasks, and effectiveness in user-interactive conversations. Finally, we engage in a discussion concerning the challenges associated with defining and implementing these metrics, with particular emphasis on confounding factors such as the target audience, evaluation methods, and prompt techniques involved in the evaluation process.

The effects of Fc fusion protein glucagon-like peptide-1 and glucagon dual receptor agonist with different receptor selectivity in vivo studies.

BACKGROUND: Glucagon-like peptide-1 (GLP-1)/glucagon (GCG) dual receptor agonists with different receptor selectivity are under investigation and have shown significant improvement in both weight loss and glycemic control, but the optimal potency ratio between the two receptors to balance efficacy and safety remains unclear. EXPERIMENTAL APPROACH: We designed and constructed several dual receptor agonists with different receptor potency ratios using Fc fusion protein technology. The long-term effects of the candidates on body weight and metabolic dysfunction-associated steatotic liver disease (MASLD) were evaluated in diet-induced obese (DIO) model mice, high-fat diet (HFD)-ob/ob mice and AMLN diet-induced MASLD mice. Repeat dose toxicity assays were performed to investigate the safety profile of the candidate (HEC-C070) in Sprague Dawley (SD) rats. KEY RESULTS: The high GCG receptor (GCGR) selectivity of HEC-C046 makes it more prominent than other compounds for weight loss and most MASLD parameters but may lead to safety concerns. The weight change of HEC-C052 with the lowest GCG agonism was inferior to that of selective GLP-1 receptor agonist (GLP-1RA) semaglutide in DIO model mice. The GLP-1R selectivity of HEC-C070 with moderate GCG agonism has a significant effect on weight loss and liver function in obese mice, and its lowest observed adverse effect level (LOAEL) was 30 nmol/kg in the repeat dose toxicity study. CONCLUSION: We compared the potential of the Fc fusion protein GLP-1/GCG dual receptor agonists with different receptor selectivity to provide the setting for future GLP-1/GCG dual receptor agonists to treat obesity and MASLD.

Lineage regulators TFAP2C and NR5A2 function as bipotency activators in totipotent embryos.

During the first lineage segregation, a mammalian totipotent embryo differentiates into the inner cell mass (ICM) and trophectoderm (TE). However, how transcription factors (TFs) regulate this earliest cell-fate decision in vivo remains elusive, with their regulomes primarily inferred from cultured cells. Here, we investigated the TF regulomes during the first lineage specification in early mouse embryos, spanning the pre-initiation, initiation, commitment, and maintenance phases. Unexpectedly, we found that TFAP2C, a trophoblast regulator, bound and activated both early TE and inner cell mass (ICM) genes at the totipotent (two- to eight-cell) stages ('bipotency activation'). Tfap2c deficiency caused downregulation of early ICM genes, including Nanog, Nr5a2, and Tdgf1, and early TE genes, including Tfeb and Itgb5, in eight-cell embryos. Transcription defects in both ICM and TE lineages were also found in blastocysts, accompanied by increased apoptosis and reduced cell numbers in ICMs. Upon trophoblast commitment, TFAP2C left early ICM genes but acquired binding to late TE genes in blastocysts, where it co-bound with CDX2, and later to extra-embryonic ectoderm (ExE) genes, where it cooperatively co-occupied with the former ICM regulator SOX2. Finally, 'bipotency activation' in totipotent embryos also applied to a pluripotency regulator NR5A2, which similarly bound and activated both ICM and TE lineage genes at the eight-cell stage. These data reveal a unique transcription circuity of totipotency underpinned by highly adaptable lineage regulators.

Unveiling the mechanism of broad-spectrum blast resistance in rice: The collaborative role of transcription factor OsGRAS30 and histone deacetylase OsHDAC1.

Rice blast, caused by Magnaporthe oryzae, significantly impacts grain yield, necessitating the identification of broad-spectrum resistance genes and their functional mechanisms for disease-resistant crop breeding. Here, we report that rice with knockdown OsHDAC1 gene expression displays enhanced broad-spectrum blast resistance without effects on plant height and tiller numbers compared to wild-type rice, while rice overexpressing OsHDAC1 is more susceptible to M. oryzae. We identify a novel blast resistance transcription factor, OsGRAS30, which genetically acts upstream of OsHDAC1 and interacts with OsHDAC1 to suppress its enzymatic activity. This inhibition increases the histone H3K27ac level, thereby boosting broad-spectrum blast resistance. Integrating genome-wide mapping of OsHDAC1 and H3K27ac targets with RNA sequencing analysis unveils how OsHDAC1 mediates the expression of OsSSI2, OsF3H, OsRLR1 and OsRGA5 to regulate blast resistance. Our findings reveal that the OsGRAS30-OsHDAC1 module is critical to rice blast control. Therefore, targeting either OsHDAC1 or OsGRAS30 offers a promising approach for enhancing crop blast resistance.

Multifaceted SOX2-chromatin interaction underpins pluripotency progression in early embryos.

Pioneer transcription factors (TFs), such as OCT4 and SOX2, play crucial roles in pluripotency regulation. However, the master TF-governed pluripotency regulatory circuitry was largely inferred from cultured cells. In this work, we investigated SOX2 binding from embryonic day 3.5 (E3.5) to E7.5 in the mouse. In E3.5 inner cell mass (ICM), SOX2 regulates the ICM-trophectoderm program but is dispensable for opening global enhancers. Instead, SOX2 occupies preaccessible enhancers in part opened by early-stage expressing TFs TFAP2C and NR5A2. SOX2 then widely redistributes when cells adopt naive and formative pluripotency by opening enhancers or poising them for rapid future activation. Hence, multifaceted pioneer TF-enhancer interaction underpins pluripotency progression in embryos, including a distinctive state in E3.5 ICM that bridges totipotency and pluripotency.

DNA methylation and lipid metabolism are involved in GA-induced maize aleurone layers PCD as revealed by transcriptome analysis.

BACKGROUND: The aleurone layer is a part of many plant seeds, and during seed germination, aleurone cells undergo PCD, which is promoted by GA from the embryo. However, the numerous components of the GA signaling pathway that mediate PCD of the aleurone layers remain to be identified. Few genes and transcriptomes have been studied thus far in aleurone layers to improve our understanding of how PCD occurs and how the regulatory mechanism functions during PCD. Our previous studies have shown that histone deacetylases (HDACs) are required in GA-induced PCD of aleurone layer. To further explore the molecular mechanisms by which epigenetic modifications regulate aleurone PCD, we performed a global comparative transcriptome analysis of embryoless aleurones treated with GA or histone acetylase (HAT) inhibitors. RESULTS: In this study, a total of 7,919 differentially expressed genes (DEGs) were analyzed, 2,554 DEGs of which were found to be common under two treatments. These identified DEGs were involved in various biological processes, including DNA methylation, lipid metabolism and ROS signaling. Further investigations revealed that inhibition of DNA methyltransferases prevented aleurone PCD, suggesting that active DNA methylation plays a role in regulating aleurone PCD. GA or HAT inhibitor induced lipoxygenase gene expression, leading to lipid degradation, but this process was not affected by DNA methylation. However, DNA methylation inhibitor could regulate ROS-related gene expression and inhibit GA-induced production of hydrogen peroxide (H2O2). CONCLUSION: Overall, linking of lipoxygenase, DNA methylation, and H2O2 may indicate that GA-induced higher HDAC activity in aleurones causes breakdown of lipids via regulating lipoxygenase gene expression, and increased DNA methylation positively mediates H2O2 production; thus, DNA methylation and lipid metabolism pathways may represent an important and complex signaling network in maize aleurone PCD.

NR5A2 connects zygotic genome activation to the first lineage segregation in totipotent embryos.

Zygotic genome activation (ZGA) marks the beginning of the embryonic program for a totipotent embryo, which gives rise to the inner cell mass (ICM) where pluripotent epiblast arises, and extraembryonic trophectoderm. However, how ZGA is connected to the first lineage segregation in mammalian embryos remains elusive. Here, we investigated the role of nuclear receptor (NR) transcription factors (TFs), whose motifs are highly enriched and accessible from the 2-cell (2C) to 8-cell (8C) stages in mouse embryos. We found that NR5A2, an NR TF strongly induced upon ZGA, was required for this connection. Upon Nr5a2 knockdown or knockout, embryos developed beyond 2C normally with the zygotic genome largely activated. However, 4-8C-specific gene activation was substantially impaired and Nr5a2-deficient embryos subsequently arrested at the morula stage. Genome-wide chromatin binding analysis showed that NR5A2-bound cis-regulatory elements in both 2C and 8C embryos are strongly enriched for B1 elements where its binding motif is embedded. NR5A2 was not required for the global opening of its binding sites in 2C embryos but was essential to the opening of its 8C-specific binding sites. These 8C-specific, but not 2C-specific, binding sites are enriched near genes involved in blastocyst and stem cell regulation, and are often bound by master pluripotency TFs in blastocysts and embryonic stem cells (ESCs). Importantly, NR5A2 regulated key pluripotency genes Nanog and Pou5f1/Oct4, and primitive endoderm regulatory genes including Gata6 among many early ICM genes, as well as key trophectoderm regulatory genes including Tead4 and Gata3 at the 8C stage. By contrast, master pluripotency TFs NANOG, SOX2, and OCT4 targeted both early and late ICM genes in mouse ESCs. Taken together, these data identify NR5A2 as a key regulator in totipotent embryos that bridges ZGA to the first lineage segregation during mouse early development.

Non-inferiority of deep learning ischemic stroke segmentation on non-contrast CT within 16-hours compared to expert neuroradiologists.

We determined if a convolutional neural network (CNN) deep learning model can accurately segment acute ischemic changes on non-contrast CT compared to neuroradiologists. Non-contrast CT (NCCT) examinations from 232 acute ischemic stroke patients who were enrolled in the DEFUSE 3 trial were included in this study. Three experienced neuroradiologists independently segmented hypodensity that reflected the ischemic core on each scan. The neuroradiologist with the most experience (expert A) served as the ground truth for deep learning model training. Two additional neuroradiologists' (experts B and C) segmentations were used for data testing. The 232 studies were randomly split into training and test sets. The training set was further randomly divided into 5 folds with training and validation sets. A 3-dimensional CNN architecture was trained and optimized to predict the segmentations of expert A from NCCT. The performance of the model was assessed using a set of volume, overlap, and distance metrics using non-inferiority thresholds of 20%, 3 ml, and 3 mm, respectively. The optimized model trained on expert A was compared to test experts B and C. We used a one-sided Wilcoxon signed-rank test to test for the non-inferiority of the model-expert compared to the inter-expert agreement. The final model performance for the ischemic core segmentation task reached a performance of 0.46 ± 0.09 Surface Dice at Tolerance 5mm and 0.47 ± 0.13 Dice when trained on expert A. Compared to the two test neuroradiologists the model-expert agreement was non-inferior to the inter-expert agreement, [Formula: see text]. The before, CNN accurately delineates the hypodense ischemic core on NCCT in acute ischemic stroke patients with an accuracy comparable to neuroradiologists.

USE-Evaluator: Performance metrics for medical image segmentation models supervised by uncertain, small or empty reference annotations in neuroimaging.

Performance metrics for medical image segmentation models are used to measure the agreement between the reference annotation and the predicted segmentation. Usually, overlap metrics, such as the Dice, are used as a metric to evaluate the performance of these models in order for results to be comparable. However, there is a mismatch between the distributions of cases and the difficulty level of segmentation tasks in public data sets compared to clinical practice. Common metrics used to assess performance fail to capture the impact of this mismatch, particularly when dealing with datasets in clinical settings that involve challenging segmentation tasks, pathologies with low signal, and reference annotations that are uncertain, small, or empty. Limitations of common metrics may result in ineffective machine learning research in designing and optimizing models. To effectively evaluate the clinical value of such models, it is essential to consider factors such as the uncertainty associated with reference annotations, the ability to accurately measure performance regardless of the size of the reference annotation volume, and the classification of cases where reference annotations are empty. We study how uncertain, small, and empty reference annotations influence the value of metrics on a stroke in-house data set regardless of the model. We examine metrics behavior on the predictions of a standard deep learning framework in order to identify suitable metrics in such a setting. We compare our results to the BRATS 2019 and Spinal Cord public data sets. We show how uncertain, small, or empty reference annotations require a rethinking of the evaluation. The evaluation code was released to encourage further analysis of this topic https://github.com/SophieOstmeier/UncertainSmallEmpty.git.

RART-LAMP: One-Step Extraction-Free Method for Genotyping within 40 min.

Loop-mediated isothermal amplification (LAMP) is a commonly used alternative to PCR for point-of-care detection of nucleic acids due to its rapidity, sensitivity, specificity, and simpler instrumentation. While dual-labeled TaqMan probes are widely used in PCR for single-nucleotide polymorphism (SNP) genotyping, real-time LAMP primarily relies on turbidimetry or intercalator fluorescence measurements, which can be non-specific and generate false-positive results. In this study, we propose a closed-tube, dual-labeled RNA-modified probes and RNase H II-assisted real-time LAMP (RART-LAMP) method for SNP genotyping. Our findings indicate that (1) fluorescence signals were predominantly derived from probe hydrolysis rather than hybridization, (2) temperature-controlled hybridization between the probe and template ensured the specificity of SNP analysis, and (3) RNase H II hydrolysis between the target containing SNP sites and probes did not exhibit sequence specificity. Our RART-LAMP approach demonstrated excellent performance in genotyping C677T clinical samples, including gDNA extracted from blood, saliva, and swabs. More importantly, saliva and swab samples could be directly analyzed without any pretreatment, indicating promising prospects for nucleic acid analysis at the point of care in resource-limited settings.

Development of a novel Fc fusion protein dual glucagon-like peptide-1 and gastric inhibitory polypeptide receptor agonists.

AIM: To develop and investigate an imbalanced dual gastric inhibitory polypeptide receptor (GIPR)/glucagon-like peptide-1 receptor (GLP-1 R) agonist with Fc fusion protein structure. METHODS: We designed and constructed an Fc fusion protein that is a dual agonist (HEC-CG115) with an empirically optimized potency ratio for GLP-1R and GIPR. The long-term effects of HEC-CG115 on body weight and glycaemic control were evaluated in diet-induced obese mice and diabetic db/db mice. Repeat dose toxicity assays were performed to investigate the safety profile of HEC-CG115 in Sprague-Dawley rats. RESULTS: HEC-CG115 displayed high potency for GIPR and relatively low potency for GLP-1R, and we labelled it 'imbalanced'. In animal models, HEC-CG115 (3 nmol/kg) led to more weight loss than semaglutide at a higher dose (10 nmol/kg) in diet-induced obese model mice. HEC-CG115 (one dose every 3 days) reduced fasting blood glucose and glycated haemoglobin levels similar to those after semaglutide (once daily) at the same dose. In a 4-week subcutaneous toxicity study conducted to assess the biosafety of HEC-CG115, the no observed adverse effect level was determined to be 3 mg/kg. CONCLUSION: HEC-CG115 is a novel Fc fusion protein with imbalanced dual agonism that shows superior weight loss, glycaemic control and metabolic improvement in animal models, and has an optimal safety profile according to a repeat-dose toxicity study. Therefore, the use of HEC-CG115 appears to be safe and effective for the treatment of obesity and type 2 diabetes.

[Genetic analysis of a child with D bifunctional protein deficiency born to a consanguineous pedigree].

OBJECTIVE: To explore the genetic etiology of a child with D bifunctional protein deficiency (DBPD) born to a consanguineous pedigree. METHODS: A child with DBPD who was admitted to the First Affiliated Hospital of Hainan Medical College on January 6, 2022 due to hypotonia and global developmental delay was selected as the study subject. Clinical data of her pedigree members were collected. Peripheral blood samples of the child, her parents and elder sisters were collected and subjected to whole exome sequencing. Candidate variant was validated by Sanger sequencing and bioinformatic analysis. RESULTS: The child, a 2-year-and-9-month-old female, had featured hypotonia, growth retardation, unstable head lift, and sensorineural deafness. Serum long-chain fatty acids were elevated, and auditory brainstem evoked potentials had failed to elicit V waves in both ears with 90 dBnHL stimulation. Brain MRI revealed thinning of corpus callosum and white matter hypoplasia. The child's parents were secondary cousins. Their elder daughter had a normal phenotype and no clinical symptoms related to DBPD. Elder son had frequent convulsions, hypotonia and feeding difficulties after birth, and had died one and a half month later. Genetic testing revealed that the child had harbored homozygous c.483G>T (p.Gln161His) variants of the HSD17B4 gene, for which both of her parents and elder sisters were carriers. Based on the guidelines from the American College of Medical Genetics and Genomics, the c.483G>T (p.Gln161His) was rated as a pathogenic variant (PM1+PM2_Supporting+PP1+PP3+PP4). CONCLUSION: The homozygous c.483G>T (p.Gln161His) variants of the HSD17B4 gene caused by the consanguineous marriage probably underlay the DBPD in this child.

The CHCHD2/Sirt1 corepressors involve in G9a-mediated regulation of RNase H1 expression to control R-loop.

R-loops are regulators of many cellular processes and are threats to genome integrity. Therefore, understanding the mechanisms underlying the regulation of R-loops is important. Inspired by the findings on RNase H1-mediated R-loop degradation or accumulation, we focused our interest on the regulation of RNase H1 expression. In the present study, we report that G9a positively regulates RNase H1 expression to boost R-loop degradation. CHCHD2 acts as a repressive transcription factor that inhibits the expression of RNase H1 to promote R-loop accumulation. Sirt1 interacts with CHCHD2 and deacetylates it, which functions as a corepressor that suppresses the expression of downstream target gene RNase H1. We also found that G9a methylated the promoter of RNase H1, inhibiting the binding of CHCHD2 and Sirt1. In contrast, when G9a was knocked down, recruitment of CHCHD2 and Sirt1 to the RNase H1 promoter increased, which co-inhibited RNase H1 transcription. Furthermore, knockdown of Sirt1 led to binding of G9a to the RNase H1 promoter. In summary, we demonstrated that G9a regulates RNase H1 expression to maintain the steady-state balance of R-loops by suppressing the recruitment of CHCHD2/Sirt1 corepressors to the target gene promoter.

Investigation of soybean lipophilic proteins as carriers for vitamin B12: Focus on interaction mechanism, physicochemical functionality, and digestion characteristics.

This study aimed to explore the interaction mechanism between soybean lipophilic protein (LP) and vitamin B12 and the potential of LP as a vitamin B12 carrier. The results of spectroscopy indicated that the interaction between vitamin B12 and LP changed the conformation of LP and exposed hydrophobic groups largely. The results of molecular docking revealed that vitamin B12 interacted with LP through a hydrophobic pocket embedded on the surface of LP. With the enhancement of the interaction between LP and vitamin B12, the particle size of the LP-vitamin B12 complex gradually decreased to 588.31 nm and the absolute value of zeta potential gradually increased to 26.82 mV. Meanwhile, the LP-vitamin B12 complex showed excellent physicochemical properties and digestive characteristics. The present work enriched the means of vitamin B12 protection and provided a theoretical basis for applying the LP-vitamin B12 complex in food systems.

Encapsulating vitamins C and E using food-grade soy protein isolate and pectin particles as carrier: Insights on the vitamin additive antioxidant effects.

Functional factors show additive effects in the same nutraceutical food. In this study, a core-shell structure based on soy protein isolate (SPI) and pectin was constructed as a delivery system for vitamins C and E under neutral (pH 7.0) and acidic environment (pH 4.0). The SPI-vitamin-pectin complex formed at pH 4.0 showed larger particle size, higher turbidity, lower fluorescence intensity, and higher vitamin E encapsulation efficiency than those formed at pH 7.0. Also, the addition of vitamin C significantly enhanced the vitamin E encapsulation efficiency in the particles. Furthermore, the antioxidant properties of DPPH, ABTS, and hydroxyl radicals were increased by the addition of vitamin C, maximum values of 77%, 82%, and 65%, suggesting that vitamins C and E have additive antioxidant effects. These findings proposed a simple, structured protein-polysaccharide-based food-grade delivery system, which could serve as the basis for the design of products having multiple functional factors.

Determination of metabolisable and net energy contents of corn fed to Arbor Acres broilers and Beijing You chickens.

This study was done to compare the energy and nutrient utilisation of corn in Arbor Acres (AA) broilers and Beijing You (BJY) chickens. BJY chickens with the same age as AA broilers were named BJY1 chickens, and with the same body weight as AA broilers were named BJY2 chickens. Three groups of broilers (36 male AA broilers, 72 male BJY1 chickens, and 36 male BJY2 chickens), 2 treatments per group, 6 replicates per treatment, 3 chickens or 6 chickens per replicate. During each period, birds were fed in chambers for 11 days, including 5 days for adaptation to the feed, 3 days for excreta and gas data collection and another 3 days for fasting were recorded. Results showed that the fasting heat production (FHP) of AA, BJY1 and BJY2 chickens gradually stabilised after fasting for 72 h, the FHP of AA, BJY1 and BJY2 chickens were 486.54, 536.22 and 548.90 KJ/kg BW0.70 /day respectively. AA broilers had significantly lower (p < 0.01) apparent total tract digestibility (ATTD) of starch in corn than that of BJY1 and BJY2 chickens, whereas there were no significant differences (p > 0.05) observed in ATTD of dry matter, crude protein, ether extract and crude fibre. The apparent metabolisable energy (AME) values of corn in AA, BJY1 and BJY2 chickens were 16.18, 16.81, and 16.39 MJ/kg dry matter (DM) and the corresponding nitrogen-corrected AME (AMEn) values were 15.71, 16.38 and 15.99 MJ/kg DM respectively. The net energy (NE) values of corn in AA, BJY1 and BJY2 chickens were 12.03, 12.28 and 11.97 MJ/kg DM respectively. In conclusion, BJY chickens had a higher maintenance energy requirement than that of AA broilers, and AA broilers of the same age and weight as BJY chickens showed no significant differences in AME, AMEn and NE values of corn.

Genome-wide analysis of the CSN genes in land plants and their expression under various abiotic stress and phytohormone conditions in rice.

The CONSTITUTIVE PHOTOMORPHOGENIC9 (COP9) signalosome (CSN) is a multi-functional protein complex, which is involved in plant growth and abiotic stress response. However, the evolution and function of the CSN genes in land plants are still largely unclear. Here, we have identified 124 CSN genes and constructed phylogenetic trees of these CSN proteins to elucidate their feature and evolution in twelve land plants. Analysis of gene structure, protein property and protein motif composition shows the evolutional conservation and variation of the CSN proteins in land plants. These CSN genes might evolve through whole genome duplication (WGD)/segmental duplication (SD) and tandem duplication (TD). Analysis of promoter cis-elements shows that the CSN genes are implicated in diverse biological processes and different signaling pathways. RT-qPCR indicates that the transcript abundance of the OsCSN genes is up-regulated or down-regulated in response to abiotic stress and treatment with various hormones in rice. These results provide new insights into the CSN gene evolution and its possible function in land plants.

Comparison of soy protein isolate-(-)-epigallocatechin gallate complexes prepared by mixing, chemical polymerization, and ultrasound treatment.

The effects of the preparation method (mixing, chemical polymerization, or ultrasound treatment) on the structure and functional properties of soy protein isolate-(-)-epigallocatechin-3-gallate (SPI-EGCG) complexes were examined. The mixing treated SPI-EGCG samples (M-SE) were non-covalently linked, while the chemical polymerization and ultrasound treated SPI-EGCG samples (C-SE and U-SE, respectively) were bound covalently. The covalent binding of EGCG with protein improved the molecular weight and changed the structures of the SPI by decreasing the α-helix content. Moreover, U-SE samples had the lowest particle size (188.70 ± 33.40 nm), the highest zeta potential (-27.82 ± 0.53 mV), and the highest polyphenol binding rate (59.84 ± 2.34 %) compared with mixing and chemical polymerization-treated samples. Furthermore, adding EGCG enhanced the antioxidant activity of SPI and U-SE revealed the highest DPPH (84.84 ± 1.34 %) and ABTS (88.89 ± 1.23 %) values. In conclusion, the SPI-EGCG complexes prepared by ultrasound formed a more stable composite system with stronger antioxidant capacity, indicating that ultrasound technology may have potential applications in the preparation of protein-polyphenol complexes.

Effect of Dihydroquercetin on Energy Metabolism in LPS-Induced Inflammatory Mice.

This study investigated the effects and alterations of dihydroquercetin on the growth performance, nutriment metabolism, antioxidant and immune function, and energy substrate utilization in lipopolysaccharide-challenged mice. A total of 0, 50, and 200 mg/kg of dihydroquercetin were intragastrically administered once a day for 21 days. After the pretreatment with dihydroquercetin, each group was subjected to a lipopolysaccharide challenge (except for the control group). After lipopolysaccharide injection, food intake, body weight, metabolic indexes of blood and liver nutrients, blood inflammatory factors, and liver oxidative stress indexes were measured at 6, 12, 24, and 48 h, respectively. Indirect calorimetry analysis was performed by respiratory gas analysis for 48 h to calculate the energy substrate metabolism of carbohydrate, fat, and protein. Urinary nitrogen excretion was measured to evaluate the urinary protein metabolism to calculate the substrate utilization. The results showed that dihydroquercetin pretreatment can significantly increase the weight gain and average food intake and decrease the mortality rate in lipopolysaccharide-induced inflammation mice. Furthermore, dihydroquercetin pretreatment can alleviate the negative effects of lipopolysaccharides by increasing levels of superoxide dismutase and glutathione peroxidase and by decreasing the malondialdehyde and serum inflammatory cytokines (interleukin-1ß, nuclear factor κB, and interleukin-6). Dihydroquercetin pretreatment also can relieve nutrient metabolic disorder by increasing blood glucose, serum total protein, and liver glycogen levels and reducing serum and liver triglycerides, serum cholesterol, serum lactate dehydrogenase, and serum urea nitrogen levels. Meanwhile, it increases the relative utilization of carbohydrate, reducing relative utilization of protein and lipid, alleviating the change in energy metabolism pattern from glucose-predominant to lipid-predominant caused by lipopolysaccharide stimulation. In addition, the degree of metabolic pattern transformation depends on the dose of dihydroquercetin supplement. Finally, according to principal component analysis, we found that the inflammation was strongest in the mice at 24 h and was subsequently relieved in the LPS-stimulated group, whereas in the dihydroquercetin-pretreated group, the inflammation was initially relieved. To summarize, dihydroquercetin pretreatment can improve energy metabolism disorder and attenuate the negative effects of lipopolysaccharide challenge in mice from the initial stage of inflammation.