Association between the hemoglobin A1c/High-density lipoprotein cholesterol ratio and stroke incidence: a prospective nationwide cohort study in China.

Background: Stroke has emerged as an escalating public health challenge among middle-aged and older individuals in China, closely linked to glycolipid metabolic abnormalities. The Hemoglobin A1c/High-Density Lipoprotein Cholesterol (HbA1c/HDL-C) ratio, an integrated marker of glycolipid homeostasis, may serve as a novel predictor of stroke risk.

Methods: Our investigation utilized data from the China Health and Retirement Longitudinal Study cohort (2011-2018).

AtFH5 recruits and transports the arabinogalactan protein AGP23 to maintain the tip growth of pollen tube.

Actin cytoskeleton drives the targeted transport of cell wall components to sustain the tip growth of pollen tubes for double fertilization; however, the underlying mechanism remains largely unknown. formin 5 (AtFH5), an actin-nucleating protein, localizes at secretory vesicles and mediates actin polymerization-based vesicle trafficking in pollen. Here, we demonstrate that AtFH5 determines the recruitment and transport of cell wall components in AtFH5-labeled vesicles during the tip growth of pollen tubes.

Moment-Consistent Contrastive CycleGAN for Cross-Domain Pancreatic Image Segmentation.

CT and MR are currently the most common imaging techniques for pancreatic cancer diagnosis. Accurate segmentation of the pancreas in CT and MR images can provide significant help in the diagnosis and treatment of pancreatic cancer. Traditional supervised segmentation methods require a large number of labeled CT and MR training data, which is usually time-consuming and laborious.

UCHL3 induces radiation resistance and acquisition of mesenchymal phenotypes by deubiquitinating POLD4 in glioma stem cells.

Background: The high degree of intratumoral genomic heterogeneity is a major obstacle for glioblastoma (GBM) tumors, one of the most lethal human malignancies, and is thought to influence conventional therapeutic outcomes negatively. The proneural-to-mesenchymal transition (PMT) of glioma stem cells (GSCs) confers resistance to radiation therapy in glioblastoma patients. POLD4 is associated with cancer progression, while the mechanisms underlying PMT and tumor radiation resistance have remained elusive.

E2F1-regulated USP5 contributes to the tumorigenic capacity of glioma stem cells through the maintenance of OCT4 stability.

Mesenchymal glioma stem cells (MES GSCs) are a subpopulation of cells in glioblastoma (GBM) that contribute to a worse prognosis owing to their highly aggressive nature and resistance to radiation therapy. Here, OCT4 is characterized as a critical factor in sustaining the stemness phenotype of MES GSC. We find that OCT4 is expressed intensively in MES GSC and is intimately associated with poor prognosis, moreover, OCT4 depletion leads to diminished invasive capacity and impairment of the stem phenotype in MES GSC.

Tumor neoantigens derived from RNA editing events show significant clinical relevance in melanoma patients treated with immunotherapy.

This study aimed to investigate the clinical significance of RNA editing (RE) and RNA editing derived (RED-) neoantigens in melanoma patients treated with immunotherapy. Vardict and VEP were used to identify the somatic mutations. RE events were identified by Reditools2 and filtered by the custom pipeline.

Experimental evidence for the functional importance and adaptive advantage of A-to-I RNA editing in fungi.

Adenosine-to-inosine (A-to-I) editing is the most prevalent type of RNA editing in animals, and it occurs in fungi specifically during sexual reproduction. However, it is debatable whether A-to-I RNA editing is adaptive. Deciphering the functional importance of individual editing sites is essential for the mechanistic understanding of the adaptive advantages of RNA editing.

An atlas of the binding specificities of transcription factors in directs prediction of novel regulators in virulence.

A high-throughput systematic evolution of ligands by exponential enrichment assay was applied to 371 putative TFs in , which resulted in the robust enrichment of 199 unique sequence motifs describing the binding specificities of 182 TFs. By scanning the genome, we predicted in total 33,709 significant interactions between TFs and their target loci, which were more than 11-fold enriched in the intergenic regions but depleted in the gene body regions. To further explore and delineate the physiological and pathogenic roles of TFs in , we constructed regulatory networks for nine major virulence-associated pathways and found that 51 TFs were potentially significantly associated with these virulence pathways, 32 of which had not been characterized before, and some were even involved in multiple pathways.

Directed Evolution of an Enhanced POU Reprogramming Factor for Cell Fate Engineering.

Transcription factor-driven cell fate engineering in pluripotency induction, transdifferentiation, and forward reprogramming requires efficiency, speed, and maturity for widespread adoption and clinical translation. Here, we used Oct4, Sox2, Klf4, and c-Myc driven pluripotency reprogramming to evaluate methods for enhancing and tailoring cell fate transitions, through directed evolution with iterative screening of pooled mutant libraries and phenotypic selection. We identified an artificially evolved and enhanced POU factor (ePOU) that substantially outperforms wild-type Oct4 in terms of reprogramming speed and efficiency.

Arabidopsis NHX5 and NHX6 regulate PIN6-mediated auxin homeostasis and growth.

NHX5 and NHX6, endosomal Na,K/H antiporters in Arabidopsis thaliana, play a vital role in growth and development. Our previous study has shown that NHX5 and NHX6 function as H leak to regulate auxin-mediated growth in Arabidopsis. In this report, we investigated the function of NHX5 and NHX6 in controlling PIN6-mediated auxin homeostasis and growth in Arabidopsis.

A compendium of DNA-binding specificities of transcription factors in Pseudomonas syringae.

Pseudomonas syringae is a Gram-negative and model pathogenic bacterium that causes plant diseases worldwide. Here, we set out to identify binding motifs for all 301 annotated transcription factors (TFs) of P. syringae using HT-SELEX.

CRISPR-assisted detection of RNA-protein interactions in living cells.

We have developed CRISPR-assisted RNA-protein interaction detection method (CARPID), which leverages CRISPR-CasRx-based RNA targeting and proximity labeling to identify binding proteins of specific long non-coding RNAs (lncRNAs) in the native cellular context. We applied CARPID to the nuclear lncRNA XIST, and it captured a list of known interacting proteins and multiple previously uncharacterized binding proteins. We generalized CARPID to explore binders of the lncRNAs DANCR and MALAT1, revealing the method's wide applicability in identifying RNA-binding proteins.

Identification of 3 subpopulations of tumor-infiltrating immune cells for malignant transformation of low-grade glioma.

Background: Tumor-infiltrating immune cells (TIICs) are highly relevant to clinical outcome of glioma. However, previous studies cannot account for the diverse functions that make up the immune response in malignant transformation (MT) from low-grade glioma (LGG) to high-grade glioma (HGG).

Methods: Transcriptome level, genomic profiles and its relationship with clinical practice were obtained from TCGA and CGGA database.

Ubiquitin-Specific Protease 3 Promotes Glioblastoma Cell Invasion and Epithelial-Mesenchymal Transition via Stabilizing Snail.

Epithelial-mesenchymal transition (EMT) represents one of the most important events in the invasion of glioblastomas (GBM); therefore, better understanding of mechanisms that govern EMT is crucial for the treatment of GBMs. In this study, we report that the deubiquitinase ubiquitin-specific protease 3 (USP3) is significantly upregulated in GBMs and correlates with a shorter median overall and relapse-free survival. Silencing of USP3 attenuates the migration and invasion abilities of GBM cells and tumor growth in an orthotopic xenograft mouse model.

USP9X deubiquitinates ALDH1A3 and maintains mesenchymal identity in glioblastoma stem cells.

The mesenchymal (MES) subtype of glioblastoma (GBM) stem cells (GSCs) represents a subpopulation of cancer cells that are notorious for their highly aggressive nature and resistance to conventional therapy. Aldehyde dehydrogenase 1A3 (ALDH1A3) has been recently suggested as a key determinant for the maintenance of MES features of GSCs. However, the mechanisms underpinning aberrant ALDH1A3 expression remain elusive.

K Efflux Antiporters 4, 5, and 6 Mediate pH and K Homeostasis in Endomembrane Compartments.

KEA4, KEA5, and KEA6 are members of the Arabidopsis () K efflux antiporter (KEA) family that share high sequence similarity but whose function remains unknown. Here, we show their gene expression pattern, subcellular localization, and physiological function in Arabidopsis. , , and had similar tissue expression patterns, and the three KEA proteins localized to the Golgi, the trans-Golgi network, and the prevacuolar compartment/multivesicular bodies, suggesting overlapping roles of these proteins in the endomembrane system.

Transcriptomic view of survival during early seedling growth of the extremophyte Haloxylon ammodendron.

Seedling establishment in an extreme environment requires an integrated genomic and physiological response to survive multiple abiotic stresses. The extremophyte, Haloxylon ammodendron is a pioneer species capable of colonizing temperate desert sand dunes. We investigated the induced and basal transcriptomes in H.

Na ,K /H antiporters regulate the pH of endoplasmic reticulum and auxin-mediated development.

AtNHX5 and AtNHX6 are endosomal Na ,K /H antiporters that are critical for growth and development in Arabidopsis, but the mechanism behind their action remains unknown. Here, we report that AtNHX5 and AtNHX6, functioning as H leak, control auxin homeostasis and auxin-mediated development. We found that nhx5 nhx6 exhibited growth variations of auxin-related defects.

MicroRNA-7 regulates glioblastoma cell invasion via targeting focal adhesion kinase expression.

Background: Invasion growth is the most characteristic biological phenotype of glioblastoma, but the molecular mechanism in glioma cell invasion is poorly understood. Recent data have showed that microRNA plays an essential role in tumor invasion. Our study aimed to explore the mechanism of miR-7 involved in the control of glioblastoma cell invasion.