Chromosome-level genome assembly and characterization of the Calophaca sinica genome.

Calophaca sinica is a rare plant endemic to northern China which belongs to the Fabaceae family and possesses rich nutritional value. To support the preservation of the genetic resources of this plant, we have successfully generated a high-quality genome of C. sinica (1.06 Gb). Notably, transposable elements (TEs) constituted ~73% of the genome, with long terminal repeat retrotransposons (LTR-RTs) dominating this group of elements (~54% of the genome). The average intron length of the C. sinica genome was noticeably longer than what has been observed for closely-related species. The expansion of LTR-RTs and elongated introns emerged had the largest influence on the enlarged genome size of C. sinica in comparison to other Fabaceae species. The proliferation of TEs could be explained by certain modes of gene duplication, namely, whole genome duplication (WGD) and dispersed duplication (DSD). Gene family expansion, which was found to enhance genes associated with metabolism, genetic maintenance, and environmental stress resistance, was a result of transposed duplicated genes (TRD) and WGD. The presented genomic analysis sheds light on the genetic architecture of C. sinica, as well as provides a starting point for future evolutionary biology, ecology, and functional genomics studies centered around C. sinica and closely-related species.

The effect of intrahepatic cholestasis in pregnancy combined with different stages of hepatitis B virus infection on pregnancy outcomes: a retrospective study.

BACKGROUND AND AIMS: To investigate the impact of intrahepatic cholestasis of pregnancy (ICP) with hepatitis B virus (HBV) infection on pregnancy outcomes. METHODS: We selected 512 pregnant women, collected the data including maternal demographics, main adverse pregnancy outcomes and maternal HBV infected markers HBeAg and HBV-DNA loads status, then have a comparative analysis. RESULTS: There were 319 solitary ICP patients without HBV infection (Group I) and 193 ICP patients with HBV infection. Of the latter, there were 118 cases with abnormal liver function(Group II) and 80 cases with normal liver function(Group III). All HBV-infected pregnant women with ICP were divided into hepatitis Be antigen (HBeAg)-positive group (102 cases) and HBeAg-negative group (91 cases), according to the level of the serum HBeAg status; and into high viral load group (92 cases), moderate viral load group (46 cases) and low viral load group (55 cases) according to the maternal HBV-DNA level. Group II had a higher level of serum total bile acids, transaminase, bilirubin as well as a higher percentage of premature delivery, neonatal intensive care unit (NICU) admission and meconium-stained amniotic fluid (MSAF) compared with the other two groups(P < 0.05), but there were no significant differences in the above indicators between the Group I and Group III. Among the HBV-infected patients with ICP, HBeAg-positive group had a higher level of serum transaminase, bilirubin and bile acid as well as earlier gestational weeks of delivery, lower birth weight of new-borns and a higher rate of NICU admission than HBeAg-negative group (P < 0.05). Those with a high viral load (HBV-DNA > 106 IU/ml) had a higher level of transaminase, bilirubin, and bile acid as well as shorter gestational weeks of delivery, lower birth weight of new-borns and a higher rate of NICU admission compared with those with a low or moderate viral load (P < 0.05). CONCLUSION: HBV-infected pregnant women with ICP combined with abnormal liver function have more severe liver damage, a higher percentage of preterm birth and NICU admission. HBeAg-positive status and a high HBV-DNA load will increase the severity of conditions in HBV-infected pregnant women with ICP. HBV-infected patients with ICP who have abnormal liver function, HBeAg-positive or a high viral load should be treated more actively.

JNK signaling mediates acute rejection via activating autophagy of CD8+ T cells after liver transplantation in rats.

Background: Acute rejection (AR) after liver transplantation (LT) remains an important factor affecting the prognosis of patients. CD8+ T cells are considered to be important regulatory T lymphocytes involved in AR after LT. Our previous study confirmed that autophagy mediated AR by promoting activation and proliferation of CD8+ T cells. However, the underlying mechanisms regulating autophagy in CD8+ T cells during AR remain unclear. Methods: Human liver biopsy specimens of AR after orthotopic LT were collected to assess the relationship between JNK and CD8+ T cells autophagy. The effect of JNK inhibition on CD8+ T cells autophagy and its role in AR were further examined in rats. Besides, the underlying mechanisms how JNK regulated the autophagy of CD8+ T cells were further explored. Results: The expression of JNK is positive correlated with the autophagy level of CD8+ T cells in AR patients. And similar findings were obtained in rats after LT. Further, JNK inhibitor remarkably inhibited the autophagy of CD8+ T cells in rat LT recipients. In addition, administration of JNK inhibitor significantly attenuated AR injury by promoting the apoptosis and downregulating the function of CD8+ T cells. Mechanistically, JNK may activate the autophagy of CD8+ T cells through upregulating BECN1 by inhibiting the formation of Bcl-2/BECN1 complex. Conclusion: JNK signaling promoted CD8+ T cells autophagy to mediate AR after LT, providing a theoretical basis for finding new drug targets for the prevention and treatment of AR after LT.

Compositional transferability of deep potential in molten LiF-BeF2 and LaF3 mixtures: prediction of density, viscosity, and local structure.

The accumulation of lanthanide fission products carries the risk of altering the structure and properties of the nuclear fuel carrier salt LiF-BeF2 (Flibe), thereby downgrading the operating efficiency and safety of the molten salt reactor. However, the condition-limited experimental measurements, spatiotemporal-limited first-principles calculations, and accuracy-limited classical dynamic simulations are unable to capture the precise local structure and reliable thermophysical properties of heterogeneous molten salts. Therefore, the deep potential (DP) of LaF3 and Flibe molten mixtures is developed here, and DP molecular dynamics simulations are performed to systemically study the densities, diffusion coefficients, viscosities, radial distribution functions and coordination numbers of multiple molten Flibe + xLaF3, the quantitative relationships between these properties and LaF3 concentration are investigated, and the potential structure-property relationships are analyzed. Eventually, the transferability of DP on molten Flibe + LaF3 with different formulations as well as the predictability of structures and properties are achieved at the nanometer spatial scale and the nanosecond timescale.

The "depict" strategy for discovering new compounds in complex matrices: Lycibarbarspermidines as a case.

The comprehensive detection and identification of active ingredients in complex matrices is a crucial challenge. Liquid chromatography coupled with high-resolution mass spectrometry (LC-HRMS) is the most prominent analytical platform for the exploration of novel active compounds from complex matrices. However, the LC-HRMS-based analysis workflow suffers from several bottleneck issues, such as trace content of target compounds, limited acquisition for fragment information, and uncertainty in interpreting relevant MS2 spectra. Lycibarbarspermidines are vital antioxidant active ingredients in Lycii Fructus, while the reported structures are merely focused on dicaffeoylspermidines due to their low content. To comprehensively detect the new structures of lycibarbarspermidine derivatives, a "depict" strategy was developed in this study. First, potential new lycibarbarspermidine derivatives were designed according to the biosynthetic pathway, and a comprehensive database was established, which enlarged the coverage of lycibarbarspermidine derivatives. Second, the polarity-oriented sample preparation of potential new compounds increased the concentration of the target compounds. Third, the construction of the molecular network based on the fragmentation pathway of lycibarbarspermidine derivatives broadened the comprehensiveness of identification. Finally, the weak response signals were captured by data-dependent scanning (DDA) followed by parallel reaction monitoring (PRM), and the efficiency of acquiring MS2 fragment ions of target compounds was significantly improved. Based on the integrated strategy above, 210 lycibarbarspermidine derivatives were detected and identified from Lycii Fructus, and in particular, 170 potential new compounds were structurally characterized. The integrated strategy improved the sensitivity of detection and the coverage of low-response components, and it is expected to be a promising pipeline for discovering new compounds.

Sequence characteristics, genetic diversity and phylogenetic analysis of the Cucurbita ficifolia (Cucurbitaceae) chloroplasts genome.

BACKGROUND: Curcubita ficifolia Bouché (Cucurbitaceae) has high value as a food crop and medicinal plant, and also has horticultural value as rootstock for other melon species. China is home to many different cultivars, but the genetic diversity of these resources and the evolutionary relationships among them, as well as the differences between C. ficifolia and other Cucurbita species, remain unclear. RESULTS: We investigated the chloroplast (cp) genomes of 160 C. ficifolia individuals from 31 populations in Yunnan, a major C. ficifolia production area in China. We found that the cp genome of C. ficifolia is ~151 kb and contains 128 genes, of which 86 are protein coding genes, 34 encode tRNA, and eight encode rRNAs. We also identified 64 SSRs, mainly AT repeats. The cp genome was found to contain a total of 204 SNP and 57 indels, and a total of 21 haplotypes were found in the 160 study individuals. The reverse repeat (IR) region of C. ficifolia contained a few differences compared with this region in the six other Cucurbita species. Sequence difference analysis demonstrated that most of the variable regions were concentrated in the single copy (SC) region. Moreover, the sequences of the coding regions were found to be more similar among species than those of the non-coding regions. The phylogenies reconstructed from the cp genomes of 61 representative species of Cucurbitaceae reflected the currently accepted classification, in which C. ficifolia is sister to the other Cucurbita species, however, different interspecific relationships were found between Cucurbita species. CONCLUSIONS: These results will be valuable in the classification of C. ficifolia genetic resources and will contribute to our understanding of evolutionary relationships within the genus Cucurbita.

Stratifin promotes the malignant progression of HCC via binding and hyperactivating AKT signaling.

Hepatocellular carcinoma (HCC) is a highly aggressive malignant tumor with limited treatment options and poor prognosis. In this study, we reveal the pivotal role of Stratifin (SFN), also recognized as 14-3-3σ, in driving HCC progression. Our investigation underscores a substantial upregulation of SFN within HCC tissues, manifesting a significant association with worse prognostic outcomes among HCC patients. In vitro and in vivo experiments reveal that SFN overexpression significantly amplifies proliferation, mitigates sorafenib-induced effects on HCC cells, and enhances tumorigenesis. While SFN silencing exerts converse effects on HCC progression. Additionally, we unveil a critical interaction between SFN and AKT, where SFN boosts AKT kinase activity by disrupting the binding of PHLPP2 and AKT, thereby intensifying the malignant progression of HCC cells. In conclusion, this study identifies the oncogenic role of SFN and elucidates the regulatory mechanism of the SFN/AKT axis in HCC, which may provide valuable insights into the mechanisms of HCC progression and potential targets for therapeutic intervention.

IL-1ß induced down-regulation of miR-146a-5p promoted pyroptosis and apoptosis of corneal epithelial cell in dry eye disease through targeting STAT3.

AIM: To elaborate the underlying mechanisms by which IL-1ß promote progression of Dry eye disease(DED) through effect on pyroptosis and apoptosis of corneal epithelial cells(CECs). METHODS: 400 mOsM solutions were used to establish the DED model (hCECs- DED). RT-qPCR was performed to measure IL-1ß mRNA and miR-146a-5p in CECs. Western blotting was performed to measure STAT3, GSDMD, NLRP3, and Caspase-1 levels. Cell counting kit-8 assay was adopted to check cell viability. Apoptosis was detected by flow cytometry. ELISAs were performed to determine IL-18, IL-33 and LDH. The luciferase test detects targeting relationships. RESULTS: After treatment with 400 mOsM solution, cell viability decreased and apoptosis increased. Compared with hCECs, IL-1ß was increased and miR-146a-5p was decreased in hCECs-DED. At the same time, GSDMD, NLRP3, Caspase-1, IL-18, IL-33 and LDH were significantly higher in hCECs-DED than in hCECs, while IL-1ß silencing reversed this effect. In addition, IL-1ß negatively regulated miR-146a-5p. MiR-146a-5p mimics eliminated the inhibition of hCECs-DED pyroptosis and apoptosis caused by IL-1ß silencing. At the same time, miR-146a-5p reduced STAT3 levels in hCECs. CONCLUSION: Highly expressed IL-1ß promoted pyroptosis and apoptosis of hCECs- DED through downregulated miR-146a-5p and inhibited STAT3.

Comprehensive Assessment of Ischemic Stroke in Nonhuman Primates: Neuroimaging, Behavioral, and Serum Proteomic Analysis.

Ischemic strokes, prevalence and impactful, underscore the necessity of advanced research models closely resembling human physiology. Our study utilizes nonhuman primates (NHPs) to provide a detailed exploration of ischemic stroke, integrating neuroimaging data, behavioral outcomes, and serum proteomics to elucidate the complex interplay of factors involved in stroke pathophysiology. We observed a consistent pattern in infarct volume, peaking at 1-month postmiddle cerebral artery occlusion (MCAO) and then stabilized. This pattern was strongly correlated to notable changes in motor function and working memory performance. Using diffusion tensor imaging (DTI), we detected significant alterations in fractional anisotropy (FA) and mean diffusivity (MD) values, signaling microstructural changes in the brain. These alterations closely correlated with the neurological and cognitive deficits that we observed, highlighting the sensitivity of DTI metrics in stroke assessment. Behaviorally, the monkeys exhibited a reliance on their unaffected limb for compensatory movements, a common response to stroke impairment. This adaptation, along with consistent DTI findings, suggests a significant impact of stroke on motor function and spatial perception. Proteomic analysis through MS/MS functional enrichment identified two distinct groups of proteins with significant changes post-MCAO. Notably, MMP9, THBS1, MB, PFN1, and YWHAZ were identified as potential biomarkers and therapeutic targets for ischemic stroke. Our results underscore the complex nature of stroke and advocate for an integrated approach, combining neuroimaging, behavioral studies, and proteomics, for advancing our understanding and treatment of this condition.

Integrated metabolome and transcriptome analyses reveal the molecular mechanism underlying dynamic metabolic processes during taproot development of Panax notoginseng.

BACKGROUND: Panax notoginseng (Burk) F. H. Chen is one of the most famous Chinese traditional medicinal plants. The taproot is the main organ producing triterpenoid saponins, and its development is directly linked to the quality and yield of the harvested P. notoginseng. However, the mechanisms underlying the dynamic metabolic changes occurring during taproot development of P. notoginseng are unknown. RESULTS: We carried out metabolomic and transcriptomic analyses to investigate metabolites and gene expression during the development of P. notoginseng taproots. The differentially accumulated metabolites included amino acids and derivatives, nucleotides and derivatives, and lipids in 1-year-old taproots, flavonoids and terpenoids in 2- and 3-year-old taproots, and phenolic acids in 3-year-old taproots. The differentially expressed genes (DEGs) are related to phenylpropanoid biosynthesis, metabolic pathway and biosynthesis of secondary metabolites at all three developmental stages. Integrative analysis revealed that the phenylpropanoid biosynthesis pathway was involved in not only the development of but also metabolic changes in P. notoginseng taproots. Moreover, significant accumulation of triterpenoid saponins in 2- and 3-year-old taproots was highly correlated with the up-regulated expression of cytochrome P450s and uridine diphosphate-dependent glycosyltransferases genes. Additionally, a gene encoding RNase-like major storage protein was identified to play a dual role in the development of P. notoginseng taproots and their triterpenoid saponins synthesis. CONCLUSIONS: These results elucidate the molecular mechanism underlying the accumulation of and change relationship between primary and secondary metabolites in P. notoginseng taproots, and provide a basis for the quality control and genetic improvement of P. notoginseng.

Connective tissue disease as a challenge in heart failure: Three case reports.

RATIONALE: Connective tissue disease (CTD) is a heterogeneous group of chronic inflammatory autoimmune disorders derived from a systemically auto-immunological deregulation. CTD may affect cardiac structures through multiple pathophysiological mechanisms, and subclinical cardiac injury is common. Heart failure (HF) is one of the common complications in these patients. PATIENT CONCERNS: Patients with CTD suffer an increased risk of cardiovascular disease and may have chest pain and shortness of breath. DIAGNOSIS: HF is characterized by dyspnea or exertional limitation due to impaired ventricular filling and/or blood ejection. HF can be caused by other systemic diseases, not only by cardiovascular disorders but CTD. CTD may cause HF due to diffuse myocardial damage, heart valve damage, coronary ischemia, and so on. INTERVENTIONS: The patient with catastrophic antiphospholipid syndrome take prednisone and warfarin. The patient with anti-synthetase syndrome was treated with immunoglobulin, followed by long-term oral medicines of prednisone, methotrexate, and folic acid. OUTCOMES: The symptoms of chest pain and shortness of breath for patients with CTD improved. LESSONS: HF is one of the common complications in these patients with CTD, which has poor prognosis and severe aggravation. Once such patients experience chest pain, chest tightness, shortness of breath, etc, we should consider the possibility of HF. Early identification and correct treatment can delay the progression of HF, improve the prognosis, and enhance the quality of life for patients. Therefore, we should pay more attention to patients with CTD combined with HF.

Phosphorylation of AQP4 by LRRK2 R1441G impairs glymphatic clearance of IFNγ and aggravates dopaminergic neurodegeneration.

Aquaporin-4 (AQP4) is essential for normal functioning of the brain's glymphatic system. Impaired glymphatic function is associated with neuroinflammation. Recent clinical evidence suggests the involvement of glymphatic dysfunction in LRRK2-associated Parkinson's disease (PD); however, the precise mechanism remains unclear. The pro-inflammatory cytokine interferon (IFN) γ interacts with LRRK2 to induce neuroinflammation. Therefore, we examined the AQP4-dependent glymphatic system's role in IFNγ-mediated neuroinflammation in LRRK2-associated PD. We found that LRRK2 interacts with and phosphorylates AQP4 in vitro and in vivo. AQP4 phosphorylation by LRRK2 R1441G induced AQP4 depolarization and disrupted glymphatic IFNγ clearance. Exogeneous IFNγ significantly increased astrocyte expression of IFNγ receptor, amplified AQP4 depolarization, and exacerbated neuroinflammation in R1441G transgenic mice. Conversely, inhibiting LRRK2 restored AQP4 polarity, improved glymphatic function, and reduced IFNγ-mediated neuroinflammation and dopaminergic neurodegeneration. Our findings establish a link between LRRK2-mediated AQP4 phosphorylation and IFNγ-mediated neuroinflammation in LRRK2-associated PD, guiding the development of LRRK2 targeting therapy.

Functional characterization of genes related to triterpene and flavonoid biosynthesis in Cyclocarya paliurus.

MAIN CONCLUSION: The oxidosqualene cyclases (OSCs) generating triterpenoid skeletons in Cyclocarya paliurus were identified for the first time, and two uridine diphosphate (UDP)-glycosyltransferases (UGTs) catalyzing the glycosylation of flavonoids were characterized. Cyclocarya paliurus, a native rare dicotyledonous plant in China, contains an abundance of triterpenoid saponins and flavonoid glycosides that exhibit valuable pharmaceutical effects in preventing hypertension, hyperlipidemia, and diabetes. However, the molecular mechanism explaining the biosynthesis of triterpenoid saponin and flavonoid glycoside in C. paliurus remains unclear. In this study, the triterpene content in different tissues and the expression pattern of genes encoding the key enzymes associated with triterpenoid saponin and flavonoid glycoside biosynthesis were studied using transcriptome and metabolome analysis. The eight upstream oxidosqualene cyclases (OSCs) involved in triterpenoid saponin biosynthesis were functionally characterized, among them CpalOSC6 catalyzed 2,3;22,23-dioxidosqualene to form 3-epicabraleadiol; CpalOSC8 cyclized 2,3-oxidosqualene to generate dammarenediol-II; CpalOSC2 and CpalOSC3 produced ß-amyrin and CpalOSC4 produced cycloartenol, while CpalOSC2-CpalOSC5, CpalOSC7, and CpalOSC8 all produced lanosterol. However, no catalytic product was detected for CpalOSC1. Moreover, two downstream flavonoid uridine diphosphate (UDP)-glycosyltransferases (UGTs) (CpalUGT015 and CpalUGT100) that catalyze the last step of flavonoid glycoside biosynthesis were functionally elucidated. These results uncovered the key genes involved in the biosynthesis of triterpenoid saponins and flavonoid glycosides in C. paliurus that could be applied to produce flavonoid glycosides and key triterpenoid saponins in the future via a synthetic strategy.

Cytotoxic pyrone derivatives from the deep-sea-derived fungus Cladosporium halotolerans FS702.

Two new compounds (R)-6-((8S)-hydroxypropyl)-2-methyl-5,6-dihydro-4H-pyran-4-one (1) and (R)-6-((8R)-hydroxypropyl)-2-methyl-5,6-dihydro-4H-pyran-4-one (2), together with four known compounds were isolated from the marine-derived fungus Cladosporium halotolerans FS702. The structures of these compounds were determined on the basis of extensive spectroscopic analysis including 1D/2D NMR, IR, UV, HRESIMS, ECD calculations as well as the modified Mosher's method. Cytotoxic assay results showed that compound 2 had significant cytotoxic activity against SF-268, MCF-7, HepG-2, and A549 cells lines with IC50 values of 0.16, 0.47, 0.33 and 0.23 µM, respectively.

3-Carboxy-indole derivatives from the deep-sea-derived fungus Phomopsis tersa FS441.

Three new compounds phomtersines A-C (1-3) together with nine known compounds were isolated from the marine-derived fungus Phomopsis tersa FS441. Their structures were sufficiently established by spectroscopic methods, including extensive 1D and 2D NMR techniques and modified Snatzke's method. Moreover, compounds 1-12 were evaluated for cytotoxic and anti-inflammatory activities. As a result, phomtersine B (2) and the known compound 10 showed moderate cytotoxic activity against the four tested cell lines with IC50 values ranging from 20.21 to 36.53 µM, and phomtersine A (1) exhibited moderate inhibitory activity against LPS-induced NO production.

Carrier confinement activated explicit solvent dynamic of CdS/BiVO4/H2O and optimized photocatalytic hydrogen evolution performances.

Herein, using an electrophoretic deposition strategy, a S-scheme CdS (cubic)/BiVO4 (monoclinic) heterostructured photocatalyst is fabricated. The as-synthesized photocatalysts exhibit high carrier separation efficiency, prominent hydrogen evolution ability and high stability. The results of the detailed density functional theory (DFT) prove that the photogenerated electrons and holes are located in BiVO4 and CdS components, respectively. Besides, an explicit solvent model based on the electron-enriched region in CdS/BiVO4 heterojunction is designed deliberately to investigate the solid/liquid interface issues. Intriguing findings demonstrate that the surface hydrogen diffusing rate in CdS/BiVO4/H2O is faster than that of BiVO4/H2O and is highly associated with the electron-enrich effect, which has a greater capacity to promote water decomposition, the possibility of proton collision and photocatalytic hydrogen evolution. Notably, the H p orbital can participate in the electron-enrich effect during solvation, thus reforming the orbital energy level and activating the HER of the BiVO4 component in the CdS/BiVO4 system.

Systemic analysis of the prognostic significance and interaction network of miR-26b-3p in cholangiocarcinoma.

MicroRNAs (miRNAs) reportedly play significant roles in the progression of various cancers and hold huge potential as both diagnostic tools and therapeutic targets. Given the ongoing uncertainty surrounding the precise functions of several miRNAs in cholangiocarcinoma (CCA), this research undertakes a comprehensive analysis of CCA data sourced from Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. The present study identified a novel miRNA, specifically miR-26b-3p, which exhibited prognostic value for individuals with CCA. Notably, miR-26b-3p was upregulated within CCA samples, with an inverse correlation established with patient prognosis (Hazard Ratio = 8.19, p = 0.018). Through a combination of functional enrichment analysis, analysis of the LncRNA-miR-26b-3p-mRNA interaction network, and validation by qRT PCR and western blotting, this study uncovered the potential of miR-26b-3p in potentiating the malignant progression of CCA via regulation of essential genes (including PSMD14, XAB2, SLC4A4) implicated in processes such as endoplasmic reticulum (ER) stress and responses to misfolded proteins. Our findings introduce novel and valuable insights that position miR-26b-3p-associated genes as promising biomarkers for the diagnosis and treatment of CCA.

Population structure of wild soybean (Glycine soja) based on SLAF-seq have implications for its conservation.

Background: Glycine soja Sieb. & Zucc. is the wild ancestor from which the important crop plant soybean was bred. G. soja provides important germplasm resources for the breeding and improvement of cultivated soybean crops, however the species is threatened by habitat loss and fragmentation, and is experiencing population declines across its natural range. Understanding the patterns of genetic diversity in G. soja populations can help to inform conservation practices. Methods: In this study, we analyzed the genetic diversity and differentiation of G. soja at different sites and investigated the gene flow within the species. We obtained 147 G. soja accessions collected from 16 locations across the natural range of the species from China, Korea and Japan. Samples were analyzed using SLAF-seq (Specific-Locus Amplified Fragment Sequencing). Results: We obtained a total of 56,489 highly consistent SNPs. Our results suggested that G. soja harbors relatively high diversity and that populations of this species are highly differentiated. The populations harboring high genetic diversity, especially KR, should be considered first when devising conservation plans for the protection of G. soja, and in situ protection should be adopted in KR. G. soja populations from the Yangtze River, the Korean peninsula and northeastern China have a close relationship, although these areas are geographically disconnected. Other populations from north China clustered together. Analysis of gene flow suggested that historical migrations of G. soja may have occurred from the south northwards across the East-Asia land-bridge, but not across north China. All G. soja populations could be divided into one of two lineages, and these two lineages should be treated separately when formulating protection policies.

Effect of Starch on the Solubility of Quinoa Protein Isolates during Heat Treatment.

There is increasing interest in developing quinoa products due to their unique nutritional value. Starch and protein are the primary components in quinoa, and the interaction between them affects the quality of quinoa products. This study extracted the starch and protein from quinoa and simulated the thermal processing of quinoa to investigate the effects of starch on the solubility and structure of quinoa protein isolates during heat treatment. The structure of quinoa protein isolates was characterized by fluorescence spectroscopy, Fourier transform infrared spectroscopy, laser particle size analysis, and scanning electron microscopy. The results showed that starch decreased protein solubility, and the maximum solubility was obtained after heating for 5 min. After starch addition during heat treatment, the surface charge distribution of protein changed, the degree of protein aggregation increased, the particle size of proteins increased, the thermal stability increased, and the ß-sheet ratio of the proteins increased, suggesting that the protein structure is more ordered, which is the structural foundation of protein solubility decreasing. The research about the interaction between starch and protein and the effects on the solubility of protein could provide a reference for quinoa products processing.

Synergistic antitumor efficacy of aspirin plus lenvatinib in hepatocellular carcinoma via regulating of diverse signaling pathways.

It has been established that monotherapy yields limited efficacy in treating hepatocellular carcinoma (HCC), especially advanced HCC. Increasing evidence from preclinical studies and clinical trials indicates that combining multiple drugs can potentially refine treatment efficacy. Accordingly, it is crucial to explore more effective clinically feasible combination therapies to enhance the treatment outcomes of HCC patients. This study evaluated the antitumor efficacy and safety of combination therapy involving aspirin and lenvatinib in HCC. Through in vitro and in vivo assays, we demonstrated that this combination yielded stronger antitumor effects compared to lenvatinib or aspirin monotherapy. Furthermore, no significant adverse events were observed in an HCC mouse model during treatment. Mechanistic studies revealed that aspirin plus lenvatinib could target multiple oncogenes and tumor suppressors, affecting diverse signaling pathways in various biological processes conducive to antitumor effects. Overall, our findings suggest that aspirin plus lenvatinib could serve as a promising combination regimen to improve the therapeutic outcomes of HCC.