In-depth profile of biosignatures for T2DM cohort utilizing an integrated targeted LC-MS platform.

The profiling of metabolites provides an immediate snapshot that depicts crucial physiological information, holding immense potential for the early diagnosis and prognosis of diseases, including diabetes. Herein, we proposed an optimized and in-depth target-based metabolome platform through an integration of six distinct conditions, including a normal phase, a pre-column chemical derivatization and four reversed phase separation methods for the quantification of a total of 1609 small molecules (32 sub-classes) in serum after normalization using isotope-labeled internal standards. After undergoing rigorous methodological validation and comprehensive comparison with untargeted strategies, we present a new dataset of metabolomic profile encompassing a cohort of 200 healthy individuals and 100 newly diagnosed Type 2 diabetes mellitus (T2DM) patients from the northern region of China.

Online monitoring of water quality in industrial wastewater treatment process based on near-infrared spectroscopy.

Water quality monitoring is one of the critical aspects of industrial wastewater treatment, which is important for checking the treatment effect, optimizing the treatment technology and ensuring that the water quality meets the standard. Chemical oxygen demand (COD) is a key indicator for monitoring water quality, which reflects the degree of organic matter pollution in water bodies. However, the current methods for determining COD values have drawbacks such as slow speed and complicated operation, which hardly meet the demand of online monitoring.

Causal association between COVID-19 vaccination and thrombosis-related biomarkers/thrombosis/ischemic stroke: Mendelian randomization study.

Background: Observational studies about the association between coronavirus disease 2019 (COVID-19) vaccination and thrombosis/ischemic stroke are inconsistent. The aim of this study is to assess the causality between COVID-19 vaccination and thrombosis-related biomarkers/thrombosis/ischemic stroke using mendelian randomization (MR) analysis.

Methods: A two-sample MR analysis using publicly available genome-wide association study (GWAS) data was conducted.

Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseases.

Ageing is a complex biological process in which a gradual decline in physiological fitness increases susceptibility to diseases such as neurodegenerative disorders and cancer. Cellular senescence, a state of irreversible cell-growth arrest accompanied by functional deterioration, has emerged as a pivotal driver of ageing. In this Review, we discuss how heterochromatin loss, telomere attrition and DNA damage contribute to cellular senescence, ageing and age-related diseases by eliciting genome instability, innate immunity and inflammation.

CRISPR screening uncovers nucleolar RPL22 as a heterochromatin destabilizer and senescence driver.

Dysfunction of the ribosome manifests during cellular senescence and contributes to tissue aging, functional decline, and development of aging-related disorders in ways that have remained enigmatic. Here, we conducted a comprehensive CRISPR-based loss-of-function (LOF) screen of ribosome-associated genes (RAGs) in human mesenchymal progenitor cells (hMPCs). Through this approach, we identified ribosomal protein L22 (RPL22) as the foremost RAG whose deficiency mitigates the effects of cellular senescence.

LINC02605 involved in paediatric Mycoplasma pneumoniae pneumonia complicated with diarrhoea via miR-539-5p/CXCL1 axis.

Background: To investigate the involvement of LINC02605 in the progression of paediatric Mycoplasma pneumoniae pneumonia (MPP).

Methods: One hundred and thirty-two children with MPP (90 simple MPP and 42 MPP + diarrhoea) were enrolled, and their plasma was collected for detection of LINC026505 expression. CCK-8 kit and commercial apoptosis kit were introduced to determine cell growth and apoptosis.

The sirtuin-associated human senescence program converges on the activation of placenta-specific gene PAPPA.

Sirtuins are pro-longevity genes with chromatin modulation potential, but how these properties are connected is not well understood. Here, we generated a panel of isogeneic human stem cell lines with SIRT1-SIRT7 knockouts and found that any sirtuin deficiency leads to accelerated cellular senescence. Through large-scale epigenomic analyses, we show how sirtuin deficiency alters genome organization and that genomic regions sensitive to sirtuin deficiency are preferentially enriched in active enhancers, thereby promoting interactions within topologically associated domains and the formation of de novo enhancer-promoter loops.

Emerging epigenetic insights into aging mechanisms and interventions.

Epigenetic dysregulation emerges as a critical hallmark and driving force of aging. Although still an evolving field with much to explore, it has rapidly gained significance by providing valuable insights into the mechanisms of aging and potential therapeutic opportunities for age-related diseases. Recent years have witnessed remarkable strides in our understanding of the epigenetic landscape of aging, encompassing pivotal elements, such as DNA methylation, histone modifications, RNA modifications, and noncoding (nc) RNAs.

A Nucleotide Metabolism-Related Gene Signature for Risk Stratification and Prognosis Prediction in Hepatocellular Carcinoma Based on an Integrated Transcriptomics and Metabolomics Approach.

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide. The in-depth study of genes and metabolites related to nucleotide metabolism will provide new ideas for predicting the prognosis of HCC patients. This study integrated the transcriptome data of different cancer types to explore the characteristics and significance of nucleotide metabolism-related genes (NMGRs) in different cancer types.

Stress, epigenetics, and aging: Unraveling the intricate crosstalk.

Aging, as a complex process involving multiple cellular and molecular pathways, is known to be exacerbated by various stresses. Because responses to these stresses, such as oxidative stress and genotoxic stress, are known to interplay with the epigenome and thereby contribute to the development of age-related diseases, investigations into how such epigenetic mechanisms alter gene expression and maintenance of cellular homeostasis is an active research area. In this review, we highlight recent studies investigating the intricate relationship between stress and aging, including its underlying epigenetic basis; describe different types of stresses that originate from both internal and external stimuli; and discuss potential interventions aimed at alleviating stress and restoring epigenetic patterns to combat aging or age-related diseases.

An experimental workflow for identifying RNA mA alterations in cellular senescence by methylated RNA immunoprecipitation sequencing.

N-methyladenosine (mA), the most prevalent mRNA modification in eukaryotic cells, is known to play regulatory roles in a wide array of biological processes, including aging and cellular senescence. To investigate such roles, the mA modification can be identified across the entire transcriptome by immunoprecipitation of methylated RNA with an anti-mA antibody, followed by high-throughput sequencing (meRIP-seq or mA-seq). Presented here is a protocol for employing meRIP-seq to profile the RNA mA landscape in senescent human cells.

CHIT1-positive microglia drive motor neuron ageing in the primate spinal cord.

Ageing is a critical factor in spinal-cord-associated disorders, yet the ageing-specific mechanisms underlying this relationship remain poorly understood. Here, to address this knowledge gap, we combined single-nucleus RNA-sequencing analysis with behavioural and neurophysiological analysis in non-human primates (NHPs). We identified motor neuron senescence and neuroinflammation with microglial hyperactivation as intertwined hallmarks of spinal cord ageing.

Deciphering RNA m A regulation in aging: Perspectives on current advances and future directions.

N -methyladenosine (m A) is a dynamic and reversible RNA modification that has emerged as a crucial player in the life cycle of RNA, thus playing a pivotal role in various biological processes. In recent years, the potential involvement of RNA m A modification in aging and age-related diseases has gained increasing attention, making it a promising target for understanding the molecular mechanisms underlying aging and developing new therapeutic strategies. This Perspective article will summarize the current advances in aging-related m A regulation, highlighting the most significant findings and their implications for our understanding of cellular senescence and aging, and the potential for targeting RNA m A regulation as a therapeutic strategy.

Distribution of drug-resistant genes in alveolar lavage fluid from patients with psittacosis and traceability analysis of causative organisms.

Background: is a small bacterium often found in birds, including poultry, and domesticated mammals, which causes psittacosis (or parrot fever) in humans. Different strains of respond variably to antibiotics, suggesting a possible risk of antibiotic resistance. In general, different genotypes of have relatively stable hosts and different pathogenicity.

Nuclear lamina erosion-induced resurrection of endogenous retroviruses underlies neuronal aging.

The primate frontal lobe (FL) is sensitive to aging-related neurocognitive decline. However, the aging-associated molecular mechanisms remain unclear. Here, using physiologically aged non-human primates (NHPs), we depicted a comprehensive landscape of FL aging with multidimensional profiling encompassing bulk and single-nucleus transcriptomes, quantitative proteome, and DNA methylome.

mA epitranscriptomic regulation of tissue homeostasis during primate aging.

How N-methyladenosine (mA), the most abundant mRNA modification, contributes to primate tissue homeostasis and physiological aging remains elusive. Here, we characterize the mA epitranscriptome across the liver, heart and skeletal muscle in young and old nonhuman primates. Our data reveal a positive correlation between mA modifications and gene expression homeostasis across tissues as well as tissue-type-specific aging-associated mA dynamics.

Destabilizing heterochromatin by APOE mediates senescence.

Apolipoprotein E (APOE) is a component of lipoprotein particles that function in the homeostasis of cholesterol and other lipids. Although APOE is genetically associated with human longevity and Alzheimer's disease, its mechanistic role in aging is largely unknown. Here, we used human genetic, stress-induced and physiological cellular aging models to explore APOE-driven processes in stem cell homeostasis and aging.

Morphological transformations of vesicles with confined flexible filaments.

A fundamental understanding of cell shaping with confined flexible filaments, including microtubules, actin filaments, and engineered nanotubes, has been limited by the complex interplay between the cell membrane and encapsulated filaments. Here, combining theoretical modeling and molecular dynamics simulations, we investigate the packing of an open or closed filament inside a vesicle. Depending on the relative stiffness and size of the filament to the vesicle as well as the osmotic pressure, the vesicle could evolve from an axisymmetric configuration to a general configuration with a maximum of three reflection planes, and the filament could bend in or out of plane or even coil up.

[Levels of neutrophil extracellular traps in neonates with acute respiratory distress syndrome].

Objectives: To study the changes in cell free-DNA (cf-DNA), a marker of neutrophil extracellular traps (NETs), in neonates with acute respiratory distress syndrome (ARDS), and to evaluate its relationship with the severity and early diagnosis of ARDS.

Methods: The neonates diagnosed with ARDS in the Affiliated Hospital of Jiangsu University from January 2021 to June 2022 were enrolled in the prospective study. The neonates were divided into mild, moderate, and severe ARDS groups based on the oxygen index (OI) (4≤OI<8, 8≤OI<16, and OI≥16, respectively).