Effect of modified okara insoluble dietary fibre on the quality of yoghurt.

The aim of this study was to investigate the potential of adding soya bean dregs insoluble dietary fibre (IDF) modified by jet cavitation combined with cellulase to yoghurt to improve its functional properties (Yoghurt was prepared by adding 10 µL of yoghurt fermenter to 100 mL of milk, fermented to pH 4.5 in a constant temperature incubator at 42 °C, and then stored in a refrigerator at 4 °C after adding IDF separately). The results showed that the modified IDF had a rough structure with high water-holding capacity and sodium cholate adsorption capacity. The addition of modified IDF improved the pH, hardness, and elasticity of the yoghurt. During the entire storage period, the titratable acidity and whey precipitation rate of the modified IDF yoghurt gradually increased, and antioxidant activity gradually decreased, and its titratable acidity, whey precipitation rate, and antioxidant activity had a significant advantage compared with those of the blank group yoghurt. In conclusion, the modified soya bean dregs IDF-added yoghurt prepared by jet cavitation combined with the cellulase method has the potential for sodium cholate adsorption capacity and antioxidant activity, which can confer unique functional properties and improve the pH, texture, and reduce whey precipitation of yoghurt. This study provides a scientific basis for the application of soya bean dregs IDF as a fibre fortifier in yoghurt production and suggests innovative ideas for the design of functional dairy products.

Alpha-lipoic Acid Prevents Bone Loss in Type 2 Diabetes and Postmenopausal Osteoporosis Coexisting Conditions by Modulating the YAP/Glut4 Pathway.

This study aims to characterize the bone-protecting effects of Alpha-lipoic acid (ALA), a potent antioxidant, against the detrimental effects of the coexistence of type 2 diabetes mellitus (T2DM) and postmenopausal osteoporosis (POP) and identify the possible mechanisms with particular reference to its modulation of YAP/Glut4 pathway. The T2DM and POP coexisting model was induced in mice by high fat diet (HFD) + Streptozocin (STZ) + ovariectomy (OVX). The mice in the treatment groups were given ALA for 10 weeks. In the in vitro study, MC3T3-E1 cells were induced with 500 µM methylglyoxal for 24 h with or without pretreatment with ALA for 24 h. The oxidative and antioxidative biomarkers, bone microarchitecture, histo-morphology, and related protein expression of apoptosis, osteogenic differentiation and the YAP/Glut4 pathway were detected. The results showed ALA could improve glucose tolerance, inhibit oxidative stress and apoptosis and alleviate bone loss. Further study by siRNA technology revealed that the YAP/Glut4 pathway was implicated in the pathogenesis of bone loss due to the coexistence of T2DM and POP. Taken together, the present study has demonstrated for the first time that ALA exerts potent protective effects against bone loss in T2DM and POP coexisting conditions by modulating the YAP/Glut4 pathway.

FXR overexpression prevents hepatic steatosis through inhibiting AIM2 inflammasome activation in alcoholic liver disease.

BACKGROUND AND PURPOSE: Alcoholic liver disease (ALD), a metabolic liver disease caused by excessive alcohol consumption, has attracted increasing attention due to its high prevalence and mortality. Up to date, there is no effective and feasible treatment method for ALD. This study was to investigate whether Farnesoid X receptor (FXR, NR1H4) can alleviate ALD and whether this effect is mediated by inhibiting absent in melanoma 2 (AIM2) inflammasome activation. METHODS: The difference in FXR expression between normal subjects and ALD patients was analyzed using the Gene Expression Omnibus (GEO) database. Lieber-DeCarli liquid diet with 5% ethanol (v/v) (EtOH) was adopted to establish the mouse ALD model. Liver histopathological changes and the accumulation of lipid droplets were assessed by H&E and Oil Red O staining. Quantitative real-time PCR, Western blotting analysis and immunofluorescence staining were utilized to evaluate the expression levels of related genes and proteins. DCFH-DA staining was adopted to visualize reactive oxidative species (ROS). RESULTS: FXR was distinctly downregulated in liver tissues of patients with steatosis compared to normal livers using the GEO database, and in ethanol-induced AML-12 cellular steatosis model. FXR overexpression ameliorated hepatic lipid metabolism disorder and steatosis induced by ethanol by inhibiting the expression of genes involved in lipid synthesis and inducing the expression of genes responsible for lipid metabolism. Besides, FXR overexpression inhibited ethanol-induced AIM2 inflammasome activation and alleviated oxidative stress and ROS production during ethanol-induced hepatic steatosis. However, when FXR was knocked down, the results were completely opposite. CONCLUSIONS: FXR attenuated lipid metabolism disorders and lipid degeneration in alcohol-caused liver injury and alleviated oxidative stress and inflammation by inhibiting AIM2 inflammasome activation.

Coenzyme Q10 Protects Against Hyperlipidemia-Induced Osteoporosis by Improving Mitochondrial Function via Modulating miR-130b-3p/PGC-1α Pathway.

In hyperlipidemia-induced osteoporosis, bone marrow mesenchymal stem cells (BMSCs) differentiate into more adipocytes than osteoblasts, leading to decreased bone formation. It is vital to elucidate the effects of hyperlipidemia on bone metabolism and seek new agents that regulate adipocyte-osteoblast lineage allocation. CoQ10, a rate-limiting coenzyme of the mitochondrial respiratory chain, has been reported to decrease oxidative stress and lipid peroxidation by functioning as a mitochondrial antioxidant. However, its effect on hyperlipidemia-induced osteoporosis remains unknown. Here, we analyzed the therapeutic mechanisms of CoQ10 on hyperlipidemia-induced osteoporosis by using high-fat diet (HFD)-treated ApoE-/- mice or oxidized low-density lipoprotein (ox-LDL)-treated BMSCs. The serum lipid levels were elevated and bone formation-related markers were decreased in HFD-treated ApoE-/- mice and ox-LDL-treated BMSCs, which could be reversed by CoQ10. Additionally, PGC-1α protein expression was decreased in HFD-treated ApoE-/- mice and ox-LDL-treated BMSCs, accompanied by mitochondrial dysfunction, decreased ATP content and overgeneration of reactive oxygen species (ROS), which could also be antagonized by CoQ10. Furthermore, PGC-1α knockdown in vitro promoted ROS generation, BMSC apoptosis, and adipogenic differentiation while attenuating osteogenic differentiation in BMSCs. Mechanistically, it suggested that the expression of PGC1-α protein was increased with miR-130b-3p inhibitor treatment in osteoporosis under hyperlipidemia conditions to improve mitochondrial function. Collectively, CoQ10 alleviates hyperlipidemia-induced osteoporosis in ApoE-/- mice and regulates adipocyte-osteoblast lineage allocation. The possible underlying mechanism may involve the improvement of mitochondrial function by modulating the miR-130b-3p/PGC-1α pathway.

Farnesoid X receptor overexpression prevents hepatic steatosis through inhibiting AIM2 inflammasome activation in nonalcoholic fatty liver disease.

Oxidative stress-mediated activation of inflammasome has a significant effect on the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Farnesoid X receptor (NR1H4, FXR) has been implicated in biological function and many diseases, including NAFLD. The regulatory effect of FXR on oxidative stress and whether this process is related with the activation of absent melanoma 2 (AIM2) inflammasome in NAFLD remain unclear. In the present research, we confirmed that FXR in the livers of steatosis patients is significantly reduced compared with normal liver tissue by using the Gene Expression Omnibus (GEO) database and a palmitic acid (PA) - mediated steatosis model in AML-12 cells. Under the premise of ensuring the same food intake as the control group, overexpression of FXR in mice attenuated HFD-mediated weight gain and liver steatosis, facilitated lipid metabolism, improved fatty acid ß-oxidation, lipolysis, and reduced fatty acid synthesis and intake, which also inhibited the activation of AIM2 inflammasome. Overexpression of FXR alleviated PA-induced triglyceride (TG) accumulation, imbalance of lipid homeostasis, and the activation of AIM2 inflammasome in hepatic steatosis cells, while FXR knockdown appeared the opposite effects. FXR overexpression suppressed PA- and HFD-induced oxidative stress, but FXR siRNA demonstrated the opposite influence. The decreased ROS generation may be the reason why FXR weakens AIM2 activation when a fatty acid overload occurs. In conclusion, our results confirm that other than regulating lipid homeostasis and blocking NLRP3 inflammasome activation, FXR improves hepatic steatosis by a novel mechanism that inhibits oxidative stress and AIM2 inflammasome activation.

Logistic analysis of the recurrence of laparoscopic percutaneous extraperitoneal repair of pediatric inguinal hernia: A report of 486 cases.

BACKGROUND: Although the laparoscopic treatment of pediatric inguinal hernia (PIH) has more benefits than traditional surgery, it is difficult to completely avoid the problem of recurrence. The aim of this study was to use a logistic regression model to investigate the causes of recurrence after laparoscopic percutaneous extraperitoneal repair (LPER) of PIH. PATIENTS AND METHODS: From June 2017 to December 2021, 486 cases of PIH were performed using LPER in our department. We utilized a two-port approach to implement LPER for PIH. All cases were followed up and the recurrent cases were recorded in detail. We used a logistic regression model to analyze the clinical data in order to find the reasons for recurrence. RESULTS: We completed 486 cases with an internal inguinal ostium high ligation using laparoscopic surgery without conversion. Patients were followed for 10-29 months with an average of 18.2 months and 8 cases had recurrent ipsilateral hernia, including 4 recurrent cases in 89 cases (4.49%) using absorbable suture, 1 in 7 cases (14.29%) with internal inguinal ostium larger than 25 mm, 2 in 26 cases (7.69%) with BMI greater than 21, 2 in 41 cases (4.88%) with postoperative chronic constipation. The total recurrence rate was 1.65%. A foreign body reaction occurred in 2 cases, there were no complications such as scrotal hematoma, trocar umbilical hernia and testicular atrophy, and no deaths in this study. Univariate logistic regression analysis showed that patient BMI, ligation suture, diameter of the internal inguinal ostium and postoperative chronic constipation were significant variables (P values 0.093, 0.027, 0.060 and 0.081). The multivariate logistic regression analysis showed that the ligation suture and the diameter of the internal inguinal ostium were the main risk factors for postoperative recurrence, the odds ratio (OR) value were 5.374 and 2.801, the P values 0.018 and 0.046, and the 95% CI were 2.513-11.642 and 1.134-9.125. The area under ROC curve (AUC) for the logistic regression model was 0.735 (the 95% CI 0.677-0.801, P < 0.01). CONCLUSION: An LPER for PIH is a safe and effective operation, but there still remains a small probability of recurrence. In order to reduce the recurrence rate of LPER, we should improve surgical skills, choose an appropriate ligature and avoid using LPER for a huge internal inguinal ostium (especially over 25 mm). It is appropriate to be converted to open surgery for the patients with a very wide internal inguinal ostium.

Epigenetic modification of TWIST1 in macrophages promotes hypertension-induced atherosclerotic plaque instability.

It is accepted that hypertension is a major, independent risk factor for atherosclerotic cardiovascular ischemic events, which are mainly attributed to the formation of unstable, vulnerable atherosclerotic lesions. But the mechanisms by which hypertension aggravates atherosclerosis (AS) through increased macrophage recruitment are unknown. It has been reported that TWIST1 can regulate the shear stress of blood flow in endothelial cells to promote the development of atherosclerosis, but the function of TWIST1 in macrophage recruitment during hypertension remains undefined. Here, the roles of TWIST1 in macrophage activation during N w -nitro-l-arginine-methyl ester (L-NAME; NO-synthase (NOS) inhibitor)-induced hypertension were investigated in ApoE-/- mice fed a high-fat diet (HFD) and RAW264.7 cells treated with oxidized low-density lipoprotein(ox-LDL). Oil Red O staining and hematoxylin and eosin staining were adopted to analyze atherosclerotic lesions and plaque instability. Chromatin immunoprecipitation (ChIP)-PCR was used to explore whether Lysine-specific histone demethylase 1A (LSD1/KDM1A) and Variegated suppressor 3-9 homolog 1 (SUV39H1) could regulate histone modification of the TWIST1 promoter. We reported that L-NAME increased the expression of TWIST1 in the aortic tissues of ApoE-/- mice fed a high-fat diet (HFD) and RAW264.7 cells treated with ox-LDL. TWIST1 accelerated the development of an unstable atherosclerotic phenotype by promoting macrophage activation, inflammatory factor secretion, macrophage polarization, and lipid phagocytosis. Moreover, we found that H3K9me2 and H3K9me3 in the TWIST1 promoter could be coregulated by LSD1 and SUV39H1, and this process was modulated by CK2α. Taken together, these results revealed that TWIST1 in macrophages is a critical factor that mediates foam cell formation and enhances atherosclerotic plaque vulnerability during hypertension, and targeting TWIST1 may be a promising new therapeutic approach for delaying the progression of AS in hypertension.

Restoration and preservation effects of mung bean antioxidant peptides on H2O2-induced WRL-68 cells via Keap1-Nrf2 pathway.

Mung bean antioxidant peptides (MBAPs) were prepared from mung bean protein hydrolysate, and four peptide sequences including Ser-Asp-Arg-Thr-Gln-Ala-Pro-His (~953 Da), Ser-His-Pro-Gly-Asp-Phe-Thr-Pro-Val (~956 Da), Ser-Asp-Arg-Trp-Phe (~710 Da), and Leu-Asp-Arg-Gln-Leu (~644 Da) were identified. The effects of MBAPs on the oxidation-induced normal human liver cell line WRL-68 were analyzed to determine the mechanism protecting the oxidation-induced injury. The results showed that the cells were subjected to certain oxidative damage by H2O2 induction, as evidenced by decreased cell number and viability, overproduction of intracellular ROS, and decreased mitochondrial membrane potential. Compared with the H2O2-induced group, the MBAP-treated oxidation-induced group exhibited significantly higher cell number and viability, and the intracellular ROS was similar to that of the control group, suggesting that MBAP scavenges excessive intracellular free radicals after acting on the oxidation-induced cells. Combined with Western blotting results, it was concluded that the MBAP-treated oxidation-induced group also significantly promoted the expression of proteins related to the kelch-like ech-related protein 1 (Keap1)/ nuclear factor e2-related factor 2 (Nrf2) signaling pathway, which resulted in an approximately 2-fold increase in antioxidant enzymes, and a decrease in malondialdehyde content of approximately 55% compared to oxidatively-induced cells, leading to the recovery of both cell morphology and viability. These results suggest that MBAPs scavenge intracellular free radicals and improve oxidative stress in hepatocytes through the expression of Keap1/Nrf2 pathway-related protein, thereby reducing oxidative attack on the liver. Therefore, MBAP is applied as a nutritional ingredient in the functional food field, and this study provides a theoretical basis for the high utilization of mung bean proteins.

Catalpol ameliorates dexamethasone-induced osteoporosis by promoting osteogenic differentiation of bone marrow mesenchymal stem cells via the activation of PKD1 promoter.

OBJECTIVE: To investigate the effects of CA on glucocorticoid-induced osteoporosis (GIOP) and lucubrate the underlying mechanism of CA via the activation of polycystic kidney disease-1(PKD1) in bone marrow mesenchymal stem cells (BMSCs). METHODS: In vivo, a GIOP model in mice treated with dexamethasone (Dex) was established. Biomechanical, micro-CT, immunofluorescence staining of OCN, ALP and PKD1 and others were severally determined. qRT-PCR and Western blot methods were adopted to elucidate the particular mechanisms of CA on GIOP. In addition, BMSCs cultured in vitro were also induced by Dex to verify the effects of CA. Finally, siRNA and luciferase activity assays were performed to confirm the mechanisms. RESULTS: We found that CA could restore the destroyed bone microarchitecture and increase the bone mass in GIOP mice. CA could also upregulate PKD1 protein expression, reduce oxidative stress, and promote mRNA expression of bone formation-associated markers in GIOP mice. Furthermore, it was also observed that CA reduced oxidative stress and promoted osteogenic differentiation in Dex-induced BMSCs. Mechanically, CA could promote protein expression via increasing the activity of PKD1 promoter. CONCLUSION: This study provides important evidences for CA in the further clinical treatment of GIOP, reveals the activation of PKD1 promoter as the underlying mechanism.

Vitexin Regulates Heat Shock Protein Expression by Modulating ROS Levels Thereby Protecting against Heat-Stress-Induced Apoptosis.

Heat stress due to high temperatures can cause heat stroke, pyrexia, heat cramps, heart disease, and respiratory diseases, which seriously affect human health. Vitexin has been shown to alleviate heat stress; however, its mechanism of action remains unclear. Therefore, in this study, we used Caco-2 cells to establish a heat stress model and vitamin C as a positive control to investigate the regulatory effects of vitexin on heat-stress-induced apoptosis and the related mechanisms using Cell Counting Kit-8, flow cytometry, real-time quantitative polymerase chain reaction, and Western blot. The results showed that the mRNA expressions of Hsp27, Hsp70, and Hsp90 induced by heat stress could be effectively inhibited at vitexin concentrations as low as 30 µM. After heat stress prevention and heat stress amelioration in model cells based on this concentration, intracellular reactive oxygen species (ROS) levels and the mRNA level and the protein expression of heat shock proteins (Hsp70 and Hsp90) and apoptotic proteins were reduced. In addition, compared with the heat stress amelioration group, the expression of BCL2 mRNA and its protein (anti-apoptotic protein Bcl-2) increased in the heat stress prevention group, while the expression of BAX, CYCS, CASP3, and PARP1 mRNAs and their proteins (apoptotic proteins Bax, Cytochrome C, cle-Caspase-3, and cle-PARP1) were decreased. In summary, the heat-stress-preventive effect of vitexin was slightly better than its heat-stress-ameliorating effect, and its mechanism may be through the inhibition of intracellular ROS levels and thus the modulation of the expressions of Hsp70 and Hsp90, which in turn protects against heat-stress-induced apoptosis. This study provides a theoretical basis for the prevention and amelioration of heat stress using vitexin.

Improving cardiac function of angiotensin receptor/neprilysin inhibitor in patients with acute myocardial infarction: a systematic review and meta-analysis.

AIM: As the impact of angiotensin receptor/neprilysin inhibitor (ARNI) on cardiac function in acute myocardial infarction (AMI) patients is unclear in clinical therapy, we conducted this research to investigate the actual effects of improving cardiac function with ARNI in AMI patients. METHODS: Publications were checked up to June 2022. Standardised mean differences (SMD) and 95% confidence intervals (CI) were utilised for assessing the size of the effect of continuous variables. To assess the magnitude of the effect of dichotomous variables, a relative risk (RR) with 95% CI was used. RESULTS: ARNI could improve left ventricular ejection fraction (SMD = 0.40; 95% CI: 0.23 - 0.58), while lowering left ventricular end-diastolic volume (SMD = -0.43, 95% CI: -0.78 to -0.08), left ventricular end-systolic volume (SMD = -0.39, 95% CI: -0.66 to -0.11) and left ventricular enddiastolic diameter (SMD = -0.49; 95% CI: -0.65 to -0.33). Besides, it could decrease the rates of major adverse cardiac events (RR = 0.55; 95% CI: 0.43 - 0.69) and heart failure (RR = 0.42; 95% CI: 0.31 - 0.58). CONCLUSION: ARNI could greatly improve cardiac function in AMI patients.

The efficacy and safety assessment of oncolytic virotherapies in the treatment of advanced melanoma: a systematic review and meta-analysis.

BACKGROUND: The efficacy and safety of oncolytic virotherapies in the treatment of advanced melanoma still remains controversal. It is necessary to conduct quantitative evaluation on the basis of preclinical trial reports. METHODS: Publicly available databases (PubMed, Embase, Medline, Web of Science and Cochrane Library.) and register (Clinicaltrials.gov) were searched to collect treatment outcomes of oncolytic virotherapies (including herpes simplex virus type 1 (HSV), coxsackievirus A21 (CVA21), adenovirus, poxvirus and reovirus) for advanced/unresectable melanoma. Comparisons of treatment response, adverse events (AEs) and survival analyses for different virotherapies were performed by R software based on the extracted data from eligible studies. RESULTS: Finally, thirty-four eligible studies were analysed and HSV virotherapy had the highest average complete response (CR, 24.8%) and HSV had a slightly higher average overall response rate (ORR) than CVA21 (43.8% vs 42.6%). In the pooled results of comparing talimogene laherparepve (T-VEC) with or without GM-CSF/ICIs (immune checkpoint inhibitors) to GM-CSF/ICIs monotherapy suggested virotherapy was more efficient in subgroups CR (RR = 1.80, 95% CI [1.30; 2.51], P < 0.01), ORR (RR = 1.17, 95% CI [1.02; 1.34], P < 0.05), and DCR (RR = 1.27, 95% CI [1.15; 1.40], P < 0.01). In patients treated with T-VEC+ICIs, 2-year overall survival (12.1 ± 6.9 months) and progression-free survival (9.9 ± 6.9) were significantly longer than those treated with T-VEC alone. Furthermore, we found that AEs occurred frequently in virotherapy but decreased in a large cohort of enrolled patients, some of which, such as abdominal distension/pain, injection site pain and pruritus, were found to be positively associated with disease progression in patients treated with T-VEC monotherapy. CONCLUSION: Given the relative safety and tolerability of oncolytic viruses, and the lack of reports of dose-limiting-dependent toxicities, more patients treated with T-VEC with or without ICIs should be added to future assessment analyses. There is still a long way to go before it can be used as a first-line therapy for patients with advanced or unresectable melanoma.

An integrated neural network model for eye-tracking during human-computer interaction.

Improving the efficiency of human-computer interaction is one of the critical goals of intelligent aircraft cockpit research. The gaze interaction control method can vastly reduce the manual operation of operators and improve the intellectual level of human-computer interaction. Eye-tracking is the basis of sight interaction, so the performance of eye-tracking will directly affect the outcome of gaze interaction. This paper presents an eye-tracking method suitable for human-computer interaction in an aircraft cockpit, which can now estimate the gaze position of operators on multiple screens based on face images. We use a multi-camera system to capture facial images, so that operators are not limited by the angle of head rotation. To improve the accuracy of gaze estimation, we have constructed a hybrid network. One branch uses the transformer framework to extract the global features of the face images; the other branch uses a convolutional neural network structure to extract the local features of the face images. Finally, the extracted features of the two branches are fused for eye-tracking. The experimental results show that the proposed method not only solves the problem of limited head movement for operators but also improves the accuracy of gaze estimation. In addition, our method has a capture rate of more than 80% for targets of different sizes, which is better than the other compared models.

Circ_0114581 promotes osteogenic differentiation of BMSCs via the MiR-155-5p/HNRNPA3 axis.

Osteoporosis (OP) is a common metabolic bone disease characterized by deterioration of bone tissue structure, reduction of bone mass, and susceptibility to fracture. More and new suitable therapeutic targets need to be discovered. The purpose of this study was to explore the ceRNA mechanisms of circRNAs involved in osteoporosis. In this study, a competing endogenous RNA (ceRNA) regulatory network was obtained through the application of OP-related high throughput data sets. Our results provided evidence that HNRNPA3 was involved in the regulation of osteogenic differentiation in BMSCs. Testing of human bone tissues and ovariectomized mice bones proved that its expression level was negatively correlated with OP. The utilization of miRNA mimic or inhibitor proved that miR-155-5p could negatively regulate the expression of HNRNPA3, while overexpression of hsa_circ_0114581 with a circRNA overexpression vector proved that hsa_circ_0114581 could indirectly promoted HNRNPA3 expression and osteogenic differentiation by sponging hsa-miR-155-5p. A serious of luciferase reporter assay experiments further verified the binding site between miR-155-5p and HNRNPA3 and the binding site between miR-155-5p and hsa_circ_0114581. This study proved that the hsa_circ_0114581/hsa-miR-155-5p/HNRNPA3 axis was related with OP. The results reveal valuable insights into the pathogenesis of OP and noncoding RNA markers that may have a treatment role and will help to provide hypotheses for future studies.

DPP-IV Inhibitory Peptides from Coix Seed Prolamins: Release, Identification, and Analysis of the Interaction between Key Residues and Enzyme Domains.

Dipeptidyl peptidase IV (DPP-IV) inhibitory peptides can regulate type 2 diabetes by inhibiting the cleavage of glucagon-like peptide-1 and prolonging its half-life. The development of DPP-IV inhibitory peptides is still a hot topic. The primary structure of coix seed prolamins contains peptide sequence fragments that potentially inhibit DPP-IV; however, limited information is available regarding the extraction of peptides from coix seeds and the analysis of their conformational relationships. In this study, novel coix seed prolamin-derived peptides were obtained through single hydrolysis and double-enzyme stepwise hydrolysis. The inhibitory activity of these peptides against DPP-IV was evaluated to explore new functional properties of coix seeds. The results evidenced that the step-by-step enzymolysis (papain and alcalase) compared to single enzymolysis promoted the secondary structure disruption of the hydrolysates, enhanced the ß-turn structure, significantly increased the content of peptides below 1 kDa, and exhibited a substantial increase in DPP-IV inhibitory activity (97% inhibition). Three nontoxic DPP-IV inhibitory peptides, namely, LPFYPN, TFFPQ, and ATFFPQ (IC50 = 70.24, 176.87, 268.31 µM), were isolated and identified. All three peptides exhibited strong interactions with DPP-IV (all KA values >103). LPFYPN exhibited competitive inhibition, while TFFPQ and ATFFPQ demonstrated mixed competitive-noncompetitive inhibition. Hydrogen bonding and hydrophobic interactions were the main contributors to the coix seed prolamin peptides binding to DPP-IV. The central residue was a key amino acid in the parent peptide sequence, forming a more stable π-π stacking with residues in the active pocket, which may facilitate peptide activity. This study provides theoretical support for the development of coix seed-derived hypoglycemic peptides.

Ultrahigh Energy-Storage Density of BaTiO3-Based Ceramics via the Interfacial Polarization Strategy.

Lead-free dielectric capacitors are excellent candidates for pulsed power devices. However, their low breakdown strength (Eb) strongly limits their energy-storage performance. In this study, Sr0.7Bi0.2TiO3 (SBT) and Bi(Mg0.5Hf0.5)O3 (BMH) were introduced into BaTiO3 (BT) ceramics to suppress interfacial polarization and modulate the microstructure. The results show that the introduction of SBT and BMH increases the band gap width, reduces the domain size, and, most importantly, successfully attenuates the interfacial polarization. Significantly enhanced Eb values were obtained in (1 - x)(0.65BaTiO3-0.35Sr0.7Bi0.2TiO3)-xBi(Mg0.5Hf0.5)O3 (BSBT-xBMH) ceramics. Meanwhile, the interfacial polarization was reduced to near zero in the sample with x = 0.10, achieving an ultrahigh Eb (64 kV/mm) and a very large recoverable energy-storage density (Wrec ≈ 9.13 J/cm3). In addition, the sample has excellent thermal stability (in line with EIA-X7R standards) and frequency stability. These properties indicate that the BSBT-0.10BMH ceramic holds promising potential for the application of pulsed power devices.

Ganoderma lucidum polysaccharide peptide (GLPP) attenuates rheumatic arthritis in rats through inactivating NF-κB and MAPK signaling pathways.

BACKGROUND: Not many drugs with fewer side effects are available for the treatment of rheumatoid arthritis (RA). Ganoderma lucidum polysaccharide peptide (GLPP) has good immunomodulatory effects, but whether it is effective in managing RA is not clear. PURPOSE: This study was conducted to examine the anti-RA activity and possible mechanisms of GLPP in collagen-induced arthritis (CIA) rats. METHODS: Male Wistar rats were intradermally injected with bovine type II collagen in the tail base to establish the CIA model and were orally administered 100 or 200 mg/kg GLPP for 35 days. Paw thickness, clinical arthritis scores, gait analysis, organ index determination, blood cell counts, micro-CT imaging and pathological staining were performed on the rats. Liver and kidney function were measured by commercial kits, and antibody levels were measured by ELISA kits. RA-related protein levels were detected by Western blotting. RESULTS: GLPP effectively alleviated CIA symptoms and reduced immune organ indexes, antibody levels and systemic organ injury. GLPP decreased the protein expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, matrix metalloproteinase (MMP)2, MMP9, MMP13, BCL-2, OPN, ß-Catenin, and hypoxia inducible factor (HIF)-1α and increased the protein expression of BAX in the joint tissues of CIA rats. Moreover, GLPP decreased the phosphorylation levels of p65, IκB-α and ERK1/2. CONCLUSION: GLPP effectively alleviated RA symptoms in CIA rats by inhibiting the NF-κB and MAPK pathways. This study suggests a promising therapeutic effect of mushroom-derived polysaccharide peptides on RA.

Outstanding Energy Storage Performance of NBT-Based Ceramics under Moderate Electric Field Achieved via Antiferroelectric Engineering.

Ultrahigh energy-storage performance of dielectric ceramic capacitors is generally achieved under high electric fields (HEFs). However, the HEFs strongly limit the miniaturization, integration, and lifetime of the dielectric energy-storage capacitors. Thus, it is necessary to develop new energy-storage materials with excellent energy-storage densities under moderate electric fields (MEFs). Herein, the antiferroelectric material Ag0.9Ca0.05NbO3 (ACN) was used to modify the relaxor ferroelectric material 0.6Na0.5Bi0.5TiO3-0.4Sr0.7Bi0.2TiO3 (NBT-SBT). The introduction of ACN results in high polarization strength, regulated composition of rhombohedral (R3c) and tetragonal (P4bm), nanodomains, and refined grain size. An outstanding recoverable energy density (Wrec = 4.6 J/cm3) and high efficiency (η = 82%) were realized under an MEF of 260 kV/cm in 4 mol % ACN-modified NBT-SBT ceramic. The first-principles calculation reveals that the interaction between Bi and O is the intrinsic mechanism of the increased polarization. A new parameter ΔP/Eb was proposed to be used as the figure of merit to measure the energy-storage performance under MEFs (∼200-300 kV/cm). This work paves a new way to explore energy-storage materials with excellent-performance MEFs.

Recent advances in exploring and exploiting soybean functional peptides-a review.

Soybeans are rich in proteins and phytochemicals such as isoflavones and phenolic compounds. It is an excellent source of peptides with numerous biological functions, including anti-inflammatory, anticancer, and antidiabetic activities. Soy bioactive peptides are small building blocks of proteins that are released after fermentation or gastrointestinal digestion as well as by food processing through enzymatic hydrolysis, often in combination with novel food processing techniques (i.e., microwave, ultrasound, and high-pressure homogenization), which are associated with numerous health benefits. Various studies have reported the potential health benefits of soybean-derived functional peptides, which have made them a great substitute for many chemical-based functional elements in foods and pharmaceutical products for a healthy lifestyle. This review provides unprecedented and up-to-date insights into the role of soybean peptides in various diseases and metabolic disorders, ranging from diabetes and hypertension to neurodegenerative disorders and viral infections with mechanisms were discussed. In addition, we discuss all the known techniques, including conventional and emerging approaches, for the prediction of active soybean peptides. Finally, real-life applications of soybean peptides as functional entities in food and pharmaceutical products are discussed.