Arabidopsis protein S-acyl transferases positively mediate BR signaling through S-acylation of BSK1.

Protein S-acyl transferases (PATs) catalyze S-acylation, a reversible post-translational modification critical for membrane association, trafficking, and stability of substrate proteins. Many plant proteins are potentially S-acylated but few have corresponding PATs identified. By using genomic editing, confocal imaging, pharmacological, genetic, and biochemical assays, we demonstrate that three Arabidopsis class C PATs positively regulate BR signaling through S-acylation of BRASSINOSTEROID-SIGNALING KINASE1 (BSK1). PAT19, PAT20, and PAT22 associate with the plasma membrane (PM) and the trans-Golgi network/early endosome (TGN/EE). Functional loss of all three genes results in a plethora of defects, indicative of reduced BR signaling and rescued by enhanced BR signaling. PAT19, PAT20, and PAT22 interact with BSK1 and are critical for the S-acylation of BSK1, and for BR signaling. The PM abundance of BSK1 was reduced by functional loss of PAT19, PAT20, and PAT22 whereas abolished by its S-acylation-deficient point mutations, suggesting a key role of S-acylation in its PM targeting. Finally, an active BR analog induces vacuolar trafficking and degradation of PAT19, PAT20, or PAT22, suggesting that the S-acylation of BSK1 by the three PATs serves as a negative feedback module in BR signaling.

Antitumor efficacy and safety of unedited autologous CD5.CAR T cells in relapsed/refractory mature T-cell lymphomas.

ABSTRACT: Despite newer targeted therapies, patients with primary refractory or relapsed (r/r) T-cell lymphoma have a poor prognosis. The development of chimeric antigen receptor (CAR) T-cell platforms to treat T-cell malignancies often requires additional gene modifications to overcome fratricide because of shared T-cell antigens on normal and malignant T cells. We developed a CD5-directed CAR that produces minimal fratricide by downmodulating CD5 protein levels in transduced T cells while retaining strong cytotoxicity against CD5+ malignant cells. In our first-in-human phase 1 study (NCT0308190), second-generation autologous CD5.CAR T cells were manufactured from patients with r/r T-cell malignancies. Here, we report safety and efficacy data from a cohort of patients with mature T-cell lymphoma (TCL). Among the 17 patients with TCL enrolled, CD5 CAR T cells were successfully manufactured for 13 out of 14 attempted lines (93%) and administered to 9 (69%) patients. The overall response rate (complete remission or partial response) was 44%, with complete responses observed in 2 patients. The most common grade 3 or higher adverse events were cytopenias. No grade 3 or higher cytokine release syndrome or neurologic events occurred. Two patients died during the immediate toxicity evaluation period due to rapidly progressive disease. These results demonstrated that CD5.CAR T cells are safe and can induce clinical responses in patients with r/r CD5-expressing TCLs without eliminating endogenous T cells or increasing infectious complications. More patients and longer follow-up are needed for validation. This trial was registered at www.clinicaltrials.gov as #NCT0308190.

Myosin-binding protein 13 mediates primary seed dormancy via abscisic acid biosynthesis and signaling in Arabidopsis.

Dormancy is an essential characteristic that enables seeds to survive in unfavorable conditions while germinating when conditions are favorable. Myosin-binding proteins (MyoBs) assist in the movement of organelles along actin microfilaments by attaching to both organelles and myosins. In contrast to studies on yeast and metazoans, research on plant MyoBs is still in its early stages and primarily focuses on tip-growing cells. In this study, we found that Arabidopsis MyoB13 is highly expressed in dry mature seeds. The myob13 mutant, created using CRISPR/Cas9, exhibits a preharvest sprouting phenotype, which can be mitigated by after-ripening treatment, indicating that MyoB13 plays a positive role in primary seed dormancy. Furthermore, we show that MyoB13 negatively regulates ABA biosynthesis and signaling pathways. Notably, the expression of MyoB13 orthologs from maize and soybean can completely restore the phenotype of the Arabidopsis myob13 mutant, suggesting that the function of MyoB13 in ABA-induced seed dormancy is evolutionarily conserved. Therefore, the functional characterization of MyoB13 offers an additional genetic resource to help prevent vivipary in crop species.

Anomalous Raman Response in 2D Magnetic FeTe Under Uniaxial Strain: Tetragonal and Hexagonal Polymorphs.

2D Fe-chalcogenides emerge with rich structures, magnetisms, and superconductivities, which spark the growing research interests in the torturous transition mechanism and tunable properties for their potential applications in nanoelectronics. Uniaxial strain can produce a lattice distortion to study symmetry breaking induced exotic properties in 2D magnets. Herein, the anomalous Raman spectrum of 2D tetragonal (t-) and hexagonal (h-) FeTe is systematically investigated via uniaxial strain engineering strategy. It is found that both t- and h-FeTe keep the structural stability under different uniaxial tensile or compressive strain up to ± 0.4%. Intriguingly, the lattice vibrations along both in-plane and out-of-plane directions exceptionally harden (softened) under tensile (compressive) strain, distinguished from the behaviors of many conventional 2D systems. Further, the difference in thickness-dependent strain effect can be well explained by their structural discrepancy between two polymorphs of FeTe. These results can supply a unique platform to explore the vibrational properties of many novel 2D materials.

A novel pathogenic mitochondrial DNA variant m.4344T>C in tRNAGln causes developmental delay.

Mitochondrial diseases are a group of genetic diseases caused by mutations in mitochondrial DNA and nuclear DNA. However, the genetic spectrum of this disease is not yet complete. In this study, we identified a novel variant m.4344T>C in mitochondrial tRNAGln from a patient with developmental delay. The mutant loads of m.4344T>C were 95% and 89% in the patient's blood and oral epithelial cells, respectively. Multialignment analysis showed high evolutionary conservation of this nucleotide. TrRosettaRNA predicted that m.4344T>C variant would introduce an additional hydrogen bond and alter the conformation of the T-loop. The transmitochondrial cybrid-based study demonstrated that m.4344T>C variant impaired the steady-state level of mitochondrial tRNAGln and decreased the contents of mitochondrial OXPHOS complexes I, III, and IV, resulting in defective mitochondrial respiration, elevated mitochondrial ROS production, reduced mitochondrial membrane potential and decreased mitochondrial ATP levels. Altogether, this is the first report in patient carrying the m.4344T>C variant. Our data uncover the pathogenesis of the m.4344T>C variant and expand the genetic mutation spectrum of mitochondrial diseases, thus contributing to the clinical diagnosis of mitochondrial tRNAGln gene variants-associated mitochondrial diseases.

RGS20 promotes non-small cell lung carcinoma proliferation via autophagy activation and inhibition of the PKA-Hippo signaling pathway.

BACKGROUND: Novel therapeutic targets are urgently needed for treating drug-resistant non-small cell lung cancer (NSCLC) and overcoming drug resistance to molecular-targeted therapies. Regulator of G protein signaling 20 (RGS20) is identified as an upregulated factor in many cancers, yet its specific role and the mechanism through which RGS20 functions in NSCLC remain unclear. Our study aimed to identify the role of RGS20 in NSCLC prognosis and delineate associated cellular and molecular pathways. METHODS: Immunohistochemistry and lung cancer tissue microarray were used to verify the expression of RGS20 between NSCLC patients. CCK8 and cell cloning were conducted to determine the proliferation ability of H1299 and Anip973 cells in vitro. Furthermore, Transcriptome sequencing was performed to show enrichment genes and pathways. Immunofluorescence was used to detect the translocation changes of YAP to nucleus. Western blotting demonstrated different expressions of autophagy and the Hippo-PKA signal pathway. In vitro and in vivo experiments verified whether overexpression of RGS20 affect the proliferation and autophagy of NSCLC through regulating the Hippo pathway. RESULTS: The higher RGS20 expression was found to be significantly correlated with a poorer five-year survival rate. Further, RGS20 accelerated cell proliferation by increasing autophagy. Transcriptomic sequencing suggested the involvement of the Hippo signaling pathway in the action of RGS20 in NSCLC. RGS20 activation reduced YAP phosphorylation and facilitated its nuclear translocation. Remarkably, inhibiting Hippo signaling with GA-017 promoted cell proliferation and activated autophagy in RGS20 knock-down cells. However, forskolin, a GPCR activator, increased YAP phosphorylation and reversed the promoting effect of RGS20 in RGS20-overexpressing cells. Lastly, in vivo experiments further confirmed role of RGS20 in aggravating tumorigenicity, as its overexpression increased NSCLC cell proliferation. CONCLUSION: Our findings indicate that RGS20 drives NSCLC cell proliferation by triggering autophagy via the inhibition of PKA-Hippo signaling. These insights support the role of RGS20 as a promising novel molecular marker and a target for future targeted therapies in lung cancer treatment.

Targeting ferroptosis as a potential prevention and treatment strategy for aging-related diseases.

Ferroptosis, an emerging paradigm of programmed cellular necrosis posited in recent years, manifests across a spectrum of maladies with profound implications for human well-being. Numerous investigations substantiate that modulating ferroptosis, whether through inhibition or augmentation, plays a pivotal role in the etiology and control of numerous age-related afflictions, encompassing neurological, circulatory, respiratory, and other disorders. This paper not only summarizes the regulatory mechanisms of ferroptosis, but also discusses the impact of ferroptosis on the biological processes of aging and its role in age-related diseases. Furthermore, it scrutinizes recent therapeutic strides in addressing aging-related conditions through the modulation of ferroptosis. The paper consolidates the existing knowledge on potential applications of ferroptosis-related pharmacotherapies and envisages the translational prospects of ferroptosis-targeted interventions in clinical paradigms.

The effects of BMP2 and the mechanisms involved in the invasion and angiogenesis of IDH1 mutant glioma cells.

PURPOSE: This study investigated the effect of an isocitrate dehydrogenase 1 (IDH1) mutation (mutIDH1) on the invasion and angiogenesis of human glioma cells. METHODS: Doxycycline was used to induce the expression of mutIDH1 in glioma cells. Transwell and wound healing assays were conducted to assess glioma cell migration and invasion. Western blotting and cell immunofluorescence were used to measure the expression levels of various proteins. The influence of bone morphogenetic protein 2 (BMP2) on invasion, angiogenesis-related factors, BMP2-related receptor expression, and changes in Smad signaling pathway-related proteins were evaluated after treatment with BMP2. Differential gene expression and reference transcription analysis were performed. RESULTS: Successful infection with recombinant lentivirus expressing mutIDH1 was demonstrated. The IDH1 mutation promoted glioma cell migration and invasion while positively regulating the expression of vascularization-related factors and BMP2-related receptors. BMP2 exhibited a positive regulatory effect on the migration, invasion, and angiogenesis of mutIDH1-glioma cells, possibly mediated by BMP2-induced alterations in Smad signaling pathway-related factors.After BMP2 treatment, the differential genes of MutIDH1-glioma cells are closely related to the regulation of cell migration and cell adhesion, especially the regulation of Smad-related proteins. KEGG analysis confirmed that it was related to BMP signaling pathway and TGF-ß signaling pathway and cell adhesion. Enrichment analysis of gene ontology and genome encyclopedia further confirmed the correlation of these pathways. CONCLUSION: Mutation of isocitrate dehydrogenase 1 promotes the migration, invasion, and angiogenesis of glioma cells, through its effects on the BMP2-driven Smad signaling pathway. In addition, BMP2 altered the transcriptional patterns of mutIDH1 glioma cells, enriching different gene loci in pathways associated with invasion, migration, and angiogenesis.

Exposure to Short- and Medium-Chain Chlorinated Paraffins and the Risk of Gestational Diabetes Mellitus: A Nested Case-Control Study in Eastern China.

Toxicological studies have indicated that exposure to chlorinated paraffins (CPs) may disrupt intracellular glucose and energy metabolism. However, limited information exists regarding the impact of human CP exposure on glucose homeostasis and its potential association with an increased risk of developing gestational diabetes mellitus (GDM). Here, we conducted a prospective study with a nested case-control design to evaluate the link between short- and medium-chain CP (SCCPs and MCCPs) exposures during pregnancy and the risk of GDM. Serum samples from 102 GDM-diagnosed pregnant women and 204 healthy controls were collected in Hangzhou, Eastern China. The median (interquartile range, IQR) concentration of SCCPs was 161 (127, 236) ng/mL in the GDM group compared to 127 (96.9, 176) ng/mL in the non-GDM group (p < 0.01). For MCCPs, the GDM group had a median concentration of 144 (117, 174) ng/mL, while the control group was 114 (78.1, 162) ng/mL (p < 0.01). Compared to the lowest quartile as the reference, the adjusted odds ratios (ORs) of GDM were 7.07 (95% CI: 2.87, 17.40) and 3.34 (95% CI: 1.48, 7.53) in the highest quartile of ∑SCCP and ∑MCCP levels, respectively, with MCCPs demonstrating an inverted U-shaped association with GDM. Weighted quantile sum regression evaluated the joint effects of all CPs on GDM and glucose homeostasis. Among all CP congeners, C13H23Cl5 and C10H16Cl6 were the crucial variables driving the positive association with the GDM risk. Our results demonstrated a significant positive association between CP concentration in maternal serum and GDM risk, and exposure to SCCPs and MCCPs may disturb maternal glucose homeostasis. These findings contribute to a better understanding of the health risks of CP exposure and the role of environmental contaminants in the pathogenesis of GDM.

Melatonin alleviates LPS-induced depression-like behavior in mice by inhibiting ferroptosis by regulating RNA methylation-mediated SIRT6/Nrf2/HO-1 pathway.

PURPOSE: The objective of this study is to investigate the impact of ferroptosis on depression and elucidate the molecular mechanism underlying melatonin's inhibitory effect on ferroptosis in the treatment of depression. METHODS: In this study, a depression-like behavior model was induced in mice using LPS, and the effect of melatonin on depression-like behavior was evaluated through behavioral experiments (such as forced swimming test (FST) and sucrose preference test (SPT)). Additionally, molecular biological techniques (including real-time fluorescence quantitative PCR, Western blotting, immunoprecipitation) were employed to detect the expression levels and interactions of METTL3, SIRT6 and ferroptosis-related genes in mouse brain tissue. Furthermore, both in vitro and in vivo experiments were conducted to verify the regulatory effect of melatonin on Nrf2/HO-1 pathway and explore its potential molecular mechanism for regulating ferroptosis. RESULTS: Melatonin was found to significantly ameliorate depression-like behavior in mice, as evidenced by reduced immobility time in the forced swimming test and increased sucrose intake in the sucrose preference test. Subsequent investigations revealed that melatonin modulated SIRT6 stability through METTL3-mediated ubiquitination of SIRT6, leading to its degradation. As a deacetylase, SIRT6 plays a pivotal role in cellular metabolism regulation and antioxidative stress response. This study elucidated potential signaling pathways involving Nrf2/HO-1 through which SIRT6 may exert its effects. CONCLUSION: The findings suggest that melatonin can improve depressive behavior by suppressing ferroptosis and protecting neurons through its antioxidant properties. Additionally, targeting the Nrf2/HO-1 pathway via METTL3 and NEDD4 regulation may be a potential therapeutic approach for depression.

Uric acid promotes interleukin-17 expression to cause kidney injury.

Uric acid, an oxidation end-product of purine metabolism, is reportedly to be a risk factor for kidney injury. However, its underlying mechanism is still a mystery. This study aimed to reveal the detailed roles of uric acid in inducing kidney injury and the possible mechanisms. Injection of rats with uric acid significantly increased tubular injury score, and levels of blood urea nitrogen, serum creatinine, and urine kidney injury molecule-1. Uric acid increased the expression of collagen I, alpha-smooth muscle actin, tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6. Kyoto Encyclopedia of Genes and Genomes analysis result showed the IL-17 signaling pathway as the most significantly enriched pathway involved in hyperuricemia-related kidney injury. Long-term injection of uric acid induced significant production of IL-17 and recruitment of Th17 cells. Treating rats with the anti-IL-17 mAb attenuated uric acid-induced kidney injury, accompanied by the inactivation of nuclear factor-κB (NF-κB). In conclusion, uric acid was confirmed to be a risk factor for kidney injury via inducing IL-17 expression. Neutralization of IL-17 using the specific mAb relieved uric acid-induced kidney injury via inhibition of NF-κB signaling.

Fisetin ameliorates fibrotic kidney disease in mice via inhibiting ACSL4-mediated tubular ferroptosis.

Kidney fibrosis is the hallmark of chronic kidney disease (CKD) progression, whereas no effective anti-fibrotic therapies exist. Recent evidence has shown that tubular ferroptosis contributes to the pathogenesis of CKD with persistent proinflammatory and profibrotic responses. We previously reported that natural flavonol fisetin alleviated septic acute kidney injury and protected against hyperuricemic nephropathy in mice. In this study, we investigated the therapeutic effects of fisetin against fibrotic kidney disease and the underlying mechanisms. We established adenine diet-induced and unilateral ureteral obstruction (UUO)-induced CKD models in adult male mice. The two types of mice were administered fisetin (50 or 100 mg·kg-1·d-1, i.g.) for 3 weeks or 7 days, respectively. At the end of the experiments, the mice were euthanized, and blood and kidneys were gathered for analyzes. We showed that fisetin administration significantly ameliorated tubular injury, inflammation, and tubulointerstitial fibrosis in the two types of CKD mice. In mouse renal tubular epithelial (TCMK-1) cells, treatment with fisetin (20 µM) significantly suppressed adenine- or TGF-ß1-induced inflammatory responses and fibrogenesis, and improved cell viability. By quantitative real-time PCR analysis of ferroptosis-related genes, we demonstrated that fisetin treatment inhibited ferroptosis in the kidneys of CKD mice as well as in injured TCMK-1 cells, as evidenced by decreased ACSL4, COX2, and HMGB1, and increased GPX4. Fisetin treatment effectively restored ultrastructural abnormalities of mitochondrial morphology and restored the elevated iron, the reduced GSH and GSH/GSSG as well as the increased lipid peroxide MDA in the kidneys of CKD mice. Notably, abnormally high expression of the ferroptosis key marker ACSL4 was verified in the renal tubules of CKD patients (IgAN, MN, FSGS, LN, and DN) as well as adenine- or UUO-induced CKD mice, and in injured TCMK-1 cells. In adenine- and TGF-ß1-treated TCMK-1 cells, ACSL4 knockdown inhibited tubular ferroptosis, while ACSL4 overexpression blocked the anti-ferroptotic effect of fisetin and reversed the cytoprotective, anti-inflammatory, and anti-fibrotic effects of fisetin. In summary, we reveal a novel aspect of the nephroprotective effect of fisetin, i.e. inhibiting ACSL4-mediated tubular ferroptosis against fibrotic kidney diseases.

Internal and external microplastic exposure in young adults: A pilot study involving 26 college students in Changsha, China.

OBJECTIVE: This study aimed to systematically assess the total environmental exposure to microplastics and determine the internal exposure levels in the human body. METHODS: A total of 26 young college students were recruited. Exposure scenario estimation methods were used to establish evaluation models. The dietary and water intake behaviors of the participants were documented with questionnaires. The food and water consumed by the participants were sampled using weight and duplicate meal methods. Furthermore, air samples from the activity regions of the participants were collected. Fasting serum, 24-h urine, and fecal samples were also collected. Pyrolysis gas chromatography/mass spectrometry (Py-GCMS) helped identify the types and determine mass concentrations of microplastics across all samples, and the internal and external exposure levels of microplastics among the population were further evaluated. RESULTS: Microplastics were frequently observed in food samples, with mass concentrations ranging from 2.50 to 91.30 µg/g. Water samples also contained microplastics, with concentrations ranging from 0.02 to 18.41 µg/g. Indoor and outdoor air contained PS, PE, PP, PVC, and PET. The exposure levels of young college students in Changsha to microplastics through dietary intake, water intake, and inhalation were quantified at 346.65 µg/kg bw/d, 41.17 µg/kg bw/d, and 59.57 µg/kg bw/d, respectively. Cumulatively, the total exposure to microplastics from these three sources was 460.20 µg/kg bw/d. Median microplastic levels in serum and feces samples were 20.81 µg/g and 97.36 µg/g, respectively. Additionally, urine samples indicated the presence of seven types of microplastics (PS, PE, PP, PVC, PET, PA66, and PMMA), with a median exposure level of 5.06 µg/g. CONCLUSION: Among young college students in Changsha, the primary microplastic exposure source was dietary intake, followed by air and drinking water. The internal exposure level in serum was higher than that in urine.

Whole-genome resequencing reveals candidate genes associated with milk production trait in Guanzhong dairy goats.

Milk production is one of the most important economic utility of goats. Guanzhong dairy goat is a local dairy goat in Shaanxi Province of China and has high milk yield and quality. However, there are relatively few studies on molecular markers of milk production traits in Guanzhong dairy goats. In this study, we sequenced the whole genomes of 20 Guanzhong dairy goats, 10 of which had high milk yield (HM) and 10 of which had low milk yield (LM). We detected candidate signatures of selection in HM goats using Fst and π-ratio statistics and identified several candidate genes including ANPEP, ADRA1A and PRKG1 associated with milk production. Our results provide the basis for molecular breeding of milk production traits in Guanzhong dairy goats.

UBA3 promotes the occurrence and metastasis of intrahepatic cholangiocarcinoma through MAPK signaling pathway.

Intrahepatic cholangiocarcinoma (ICC) accounts for approximately 15% of primary liver cancers, and the incidence rate has been increasing in recent years. Surgical resection is the best treatment for ICC, but the 5-year survival rate is less than 30%. ICC signature genes are crucial for the early diagnosis of ICC, so it is especially important to identify signature genes. The aim of this study is to screen the signature genes of ICC and find the potential target for the treatment of ICC. We find that UBA3 is highly expressed in ICC, and knockdown of UBA3 inhibits ICC proliferation, invasion and migration. Mechanistic experiments show that UBA3 promotes ICC proliferation, invasion and migration by affecting ANXA2 through the MAPK signaling pathway. UBA3 is a target of bufalin, and bufalin targeting UBA3 inhibits ICC development and progression through the MAPK signaling pathway. In conclusion, our study shows that bufalin inhibits ICC by targeting UBA3, which has emerged as a new biomarker and potential therapeutic target for ICC.

Sex Differences in Antennal Transcriptome of Hyphantria cunea and Analysis of Odorant Receptor Expression Profiles.

Insects rely on olfaction for mating, finding oviposition sites, and locating hosts. Hyphantria cunea is a serious pest that severely damages forests. Differential expression analysis of olfactory-related genes between males and females is the basis for elucidating the functions of olfactory-related proteins in H. cunea. In this study, Illumina HiSeqTM 4000 high-throughput sequencing technology was used to perform transcriptome sequencing of the antennal tissues of adult male and female H. cunea. Functional annotation was conducted using the NR, Swiss-Prot, KOG, KEGG, and GO databases, and the results showed that the antennal transcriptome of adult H. cunea contained 50,158 unigenes. Differential expression analysis identified 3923 genes that were significantly differentially expressed between male and female antennae. A total of 221 olfactory-related genes were annotated, and 96 sex-biased genes were identified, including 13 odorant receptors (ORs), 48 odorant binding proteins (OBPs), 7 chemosensory proteins (CSPs), 10 ionotropic receptors (IRs), 10 sensory neuron membrane proteins (SNMPs), 2 gustatory receptors (GRs), and 6 odorant-degrading enzymes (ODEs), indicating that there were differences in olfaction between male and female H. cunea. Quantitative real-time PCR was used to verify the expression levels of 21 putative general odorant receptor genes in male and female antennae. HcunOR4 and HcunOR5 showed female-biased expression; HcunOR48, HcunOR49 and HcunOR50 showed male-biased expression. The results were consistent with the transcriptome differential analysis. The screening of male-biased odorant receptor genes might provide a theoretical basis for the functional characterization of odorant receptors for recognizing sex pheromones in H. cunea.

Genome-Wide Characterization of Fructose 1,6-Bisphosphate Aldolase Genes and Expression Profile Reveals Their Regulatory Role in Abiotic Stress in Cucumber.

The fructose-1,6-bisphosphate aldolase (FBA) gene family exists in higher plants, with the genes of this family playing significant roles in plant growth and development, as well as response to abiotic stresses. However, systematic reports on the FBA gene family and its functions in cucumber are lacking. In this study, we identified five cucumber FBA genes, named CsFBA1-5, that are distributed randomly across chromosomes. Phylogenetic analyses involving these cucumber FBAs, alongside eight Arabidopsis FBA proteins and eight tomato FBA proteins, were conducted to assess their homology. The CsFBAs were grouped into two clades. We also analyzed the physicochemical properties, motif composition, and gene structure of the cucumber FBAs. This analysis highlighted differences in the physicochemical properties and revealed highly conserved domains within the CsFBA family. Additionally, to explore the evolutionary relationships of the CsFBA family further, we constructed comparative syntenic maps with Arabidopsis and tomato, which showed high homology but only one segmental duplication event within the cucumber genome. Expression profiles indicated that the CsFBA gene family is responsive to various abiotic stresses, including low temperature, heat, and salt. Taken together, the results of this study provide a theoretical foundation for understanding the evolution of and future research into the functional characterization of cucumber FBA genes during plant growth and development.

New Insights into Mitochondria in Health and Diseases.

Mitochondria are a unique type of semi-autonomous organelle within the cell that carry out essential functions crucial for the cell's survival and well-being. They are the location where eukaryotic cells carry out energy metabolism. Aside from producing the majority of ATP through oxidative phosphorylation, which provides essential energy for cellular functions, mitochondria also participate in other metabolic processes within the cell, such as the electron transport chain, citric acid cycle, and ß-oxidation of fatty acids. Furthermore, mitochondria regulate the production and elimination of ROS, the synthesis of nucleotides and amino acids, the balance of calcium ions, and the process of cell death. Therefore, it is widely accepted that mitochondrial dysfunction is a factor that causes or contributes to the development and advancement of various diseases. These include common systemic diseases, such as aging, diabetes, Parkinson's disease, and cancer, as well as rare metabolic disorders, like Kearns-Sayre syndrome, Leigh disease, and mitochondrial myopathy. This overview outlines the various mechanisms by which mitochondria are involved in numerous illnesses and cellular physiological activities. Additionally, it provides new discoveries regarding the involvement of mitochondria in both disorders and the maintenance of good health.

Microfluidization improved hempseed yogurt's physicochemical and storage properties.

BACKGROUND: Plant-based yogurts are suffering from the common problems, such as an unattractive color, stratified texture state and rough taste. Therefore, it is urgent to develop a novel processing method to improve the quality and extend the storage life of hempseed yogurt. In the present study, hempseed yogurt was microfluidized prior to fermentation. The effects of microfluidization on microstructure, particle size, mechanical properties, sensory acceptability, variations in pH and titratable acidity, lactic acid bacteria (LAB) counts, and stability of hempseed yogurt during 20 days of storage were investigated. RESULTS: Microfluidization contributed to the production of hempseed yogurt as a result of the better physicochemical properties compared to normal homogenization. Specifically, microfluidization reduced the particle size of hempseed yogurt with a uniform particle distribution, increased water holding capacity, and improved texture and rheological properties. These advancements resulted in higher sensory scores for the yogurt. Furthermore, during storage, microfluidization effectively inhibited the post-acidification process of hempseed yogurt, and increased LAB counts and storage stability. CONCLUSION: Microfluidization improved the physicochemical properties and storage stability of hempseed yogurt. Our findings support the application of microfluidization in hempseed yogurt and provide a new approach for enhancing the quality of plant-based alternatives that meet consumers' demands for high-quality food products. © 2023 Society of Chemical Industry.

Metal cation-induced conformational changes of soybean protein isolate/soybean soluble polysaccharide and their effects on high-internal-phase emulsion properties.

BACKGROUND: Metal ions commonly inevitably appear in food products and have adverse effects on high-internal-phase emulsions (HIPEs) foods, but conformational conversion of soybean protein isolate (SPI)/soybean soluble polysaccharide (SSPS) on the interface layer of HIPEs influenced by different metal ions has rarely been reported. RESULTS: Here, the conformational conversion of SPI/SSPS induced by Na+ , K+ , Ca2+ , Mg2+ and Fe3+ ions and its effects on HIPEs were investigated. After adding the ions to SPI and SPI/SSPS dispersions, the particle size and zeta potential results showed different degrees of flocculation; the zeta potential and Fourier transform infrared spectra indicated that SPI and SPI/SSPS changes in structure involve electrostatic interactions and hydrogen bonding. Moreover, Raman spectra showed that the content of ß-sheet of SPI/SSPS HIPEs increased with the addition of Ca2+ , Mg2+ and Fe3+ , suggesting that SPI molecules at the interface formed a more orderly structure. The ultraviolet and fluorescence results showed that the hydrophobic environment of tryptophan and tyrosine residues inside protein molecules played a vital role in the emulsifying stability of SPI. CONCLUSION: These findings suggested that the SPI/SSPS complexes for food applications were not susceptible to ions, thus ensuring complex stability, showing potential for commercial application in the production of emulsions. © 2023 Society of Chemical Industry.