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Abstract Abscisic acid (ABA) plays a crucial role in promoting plant stress resistance and seed dormancy. However, how ABA regulates rice quality remains unclear. This study identifies a key transcription factor SLR1-like2 (SLRL2), which mediates the ABA-regulated amylose content (AC) of rice. Mechanistically, SLRL2 interacts with NF-YB1 to co-regulate Wx, a determinant of AC and rice quality. In contrast to SLR1, SLRL2 is ABA inducible but insensitive to GA. In addition, SLRL2 exhibits DNA-binding activity and directly regulates the expression of Wx, bHLH144 and MFT2. SLRL2 competes with NF-YC12 for interaction with NF-YB1. NF-YB1 also directly represses SLRL2 transcription. Genetic validation supports that SLRL2 functions downstream of NF-YB1 and bHLH144 in regulating rice AC. Thus, an NF-YB1-SLRL2-bHLH144 regulatory module is successfully revealed. Furthermore, SLRL2 regulates rice dormancy by modulating the expression of MFT2. In conclusion, this study revealed an ABA-responsive regulatory cascade that functions in both rice quality and seed dormancy.

Abstract The human gastrointestinal tract is populated with a diverse microbial community. The vast genetic and metabolic potential of the gut microbiome underpins its ubiquity in nearly every aspect of human biology, including health maintenance, development, aging, and disease. The advent of new sequencing technologies and culture-independent methods has allowed researchers to move beyond correlative studies toward mechanistic explorations to shed light on microbiome–host interactions. Evidence has unveiled the bidirectional communication between the gut microbiome and the central nervous system, referred to as the “microbiota–gut–brain axis”. The microbiota–gut–brain axis represents an important regulator of glial functions, making it an actionable target to ameliorate the development and progression of neurodegenerative diseases. In this review, we discuss the mechanisms of the microbiota–gut–brain axis in neurodegenerative diseases. As the gut microbiome provides essential cues to microglia, astrocytes, and oligodendrocytes, we examine the communications between gut microbiota and these glial cells during healthy states and neurodegenerative diseases. Subsequently, we discuss the mechanisms of the microbiota–gut–brain axis in neurodegenerative diseases using a metabolite-centric approach, while also examining the role of gut microbiota-related neurotransmitters and gut hormones. Next, we examine the potential of targeting the intestinal barrier, blood–brain barrier, meninges, and peripheral immune system to counteract glial dysfunction in neurodegeneration. Finally, we conclude by assessing the pre-clinical and clinical evidence of probiotics, prebiotics, and fecal microbiota transplantation in neurodegenerative diseases. A thorough comprehension of the microbiota–gut–brain axis will foster the development of effective therapeutic interventions for the management of neurodegenerative diseases.

Abstract Objective The conventional breast Diffusion-weighted imaging (DWI) was subtly influenced by microcirculation owing to the insufficient selection of the b values. However, the multiparameter derived from multiple b-value exhibits more reliable image quality and maximize the diagnostic accuracy. We aim to evaluate the diagnostic performance of stand-alone parameter or in combination with multiparameter derived from multiple b-value DWI in differentiating malignant from benign breast lesions. Methods A total of forty-one patients diagnosed with benign breast tumor and thirty-eight patients with malignant breast tumor underwent DWI using thirteen b values and other MRI functional sequence at 3.0 T magnetic resonance. Data were accepted mono-exponential, bi-exponential, stretched-exponential, aquaporins (AQP) model analysis. A receiver operating characteristic curve (ROC) was used to evaluate the diagnostic performance of quantitative parameter or multiparametric combination. The Youden index, sensitivity and specificity were used to assess the optimal diagnostic model. T-test, logistic regression analysis, and Z-test were used. P value

Objectives. Sepsis, caused by the body's response to infection, poses a life‐threatening condition and represents a significant global health challenge. Characterized by dysregulated immune response to infection, sepsis may lead to organ dysfunction and failure, ultimately resulting in high mortality rates. The liver plays a crucial role in sepsis, yet the role of differentially expressed genes in septic patients remains unclear in hepatocellular carcinoma (HCC). In this study, we aim to investigate the significance of differentially expressed genes related to sepsis in the occurrence and prognosis of tumors in HCC. Methods. We conducted analyses by obtaining gene transcriptome data and clinical data of HCC cases from The Cancer Genome Atlas (TCGA). Furthermore, we obtained transcriptomic sequencing results of septic patients from the Gene Expression Omnibus (GEO) database, identified intersecting differentially expressed genes between the two, and performed survival analysis on the samples using LASSO and Cox regression analysis. Combining analyses of tumor mutation burden (TMB) and immune function, we further elucidated the mechanisms of sepsis‐related genes in the prognosis and treatment of HCC. Results. We established a prognostic model consisting of four sepsis‐related genes: KRT20, PAEP, CCR3, and ANLN. Both the training and validation sets showed excellent outcomes in the prognosis of tumor patients, with significantly longer survival times observed in the low‐risk group based on this model compared to the high‐risk group. Furthermore, analyses, such as differential analysis of tumor mutation burden, immune function analysis, GO/KEGG pathway enrichment analysis, and drug sensitivity analysis, also demonstrated the potential mechanisms of action of sepsis‐related genes. Conclusions. Models constructed based on sepsis‐related genes have shown excellent predictive ability in prognosis and differential analysis of drug sensitivity among tumor patients. These predictive models can enhance patient prognosis and inform the creation of early treatment protocols for sepsis, consequently aiding in the prevention of sepsis‐induced HCC development through the modulation of the overall immune status. This may play a crucial role in patient management and immunotherapy, providing valuable reference for subsequent research. [ABSTRACT FROM AUTHOR]

AbstractMicro-145 down-regulation is frequently found in breast cancers, indicating its potential as a therapeutic target. The introduction of exogenous miR-145 directly to the tumor sites has been a hurdle due to limited delivery, low bioavailability, and hence lower therapeutic efficacy. Thus, this study aims to synthesize and characterize PEGylated liposome co-loaded with Dox-HCl and miR-145 mimics to investigate its in-vitro anti-proliferative activity against MDA-MB-231 cells. The formulations were developed using a composite central design to optimize nanoparticle size and encapsulation efficiency (EE%) of Dox-HCl and miR-145 mimics. The optimized formulation exhibited the highest desirability function (D = 0.814) and displayed excellent stability over 60 days at 4 °C, maintaining a stable nanoparticle size and zeta potential, with relative EE% of Dox-HCl and miR-145 mimics on the final incubation day 94.97 ± 0.53% and 51.96 ± 2.67%, respectively. The system displayed a higher rate of drug release within 4 h of incubation at an acidic condition. Additionally, the optimized formulation demonstrated a higher toxicity (IC50 = 0.58 μM) against MDA-MB-231 cells than the free Dox- HCl and miR-145 regimen (IC50 = 1.00 μM). Our findings suggest that PEGylated liposome is tunable for effective concurrent delivery of anticancer drugs and therapeutic miRNAs into tumor cells, necessitating further investigation. [ABSTRACT FROM AUTHOR]