Huashi Baidu granules alleviates LPS-induced acute lung injury by targeting TACE-mediated inflammatory signaling and stress granules disassembly.

Theoretical calculation of the amounts of nucleotide deletion impurities in oligonucleotides.

Collagen scaffold anisotropy and static tension maintain human tendon cell phenotype in culture.

Micro- and nanoplastics: Emerging environmental threats to the Developmental Origins of Health and Disease.

Barth syndrome is a mitochondrial disorder caused by Tafazzin (TAZ) mutations, which impair cardiolipin remodelling and contribute to systemic metabolic alterations. While islet dysfunction has been implicated in Barth syndrome, its underlying mechanisms remain unknown. We aimed to determine how Tafazzin (Taz) deficiency affects mouse pancreatic islet metabolism and hormone secretion, and whether systemic signals, such as circulating factors, modulate these effects in vivo. In vivo and in vitro models were used to separate direct islet effects from systemic influences of Taz deficiency. We used a mouse model of global Taz knockdown (Taz-KD) and combined in vivo and in vitro approaches to assess pancreatic islet metabolism, morphology and hormone secretion. Islet function was evaluated under basal and glucotoxic conditions. Transcriptomic profiling was performed to identify gene expression changes in isolated islets from Taz-KD mice and following in vitro Taz-KD. Additionally, we examined the role of the circulating factor fibroblast growth factor 21 (FGF-21) in modulating islet function. Despite impaired cardiolipin remodelling, pancreatic islets from Taz-KD mice maintained insulin secretion, supported by compensatory mechanisms such as increased glucose uptake, expanded mitochondrial volume and increased metabolic parameters. In addition, alpha cell mass and glucagon secretion were significantly increased in Taz-KD islets. These islet-specific adaptations occurred alongside improved whole-body glucose tolerance, elevated circulating FGF-21 levels and enhanced glucose uptake in brown adipose tissue. In contrast, in vitro Taz-KD led to impaired islet function and reduced insulin secretion. Transcriptomic analysis revealed distinct gene expression patterns between in vivo and in vitro Taz-KD models. While in vivo upregulation of genes related to N-acetylglucosamine biosynthesis and O-GlcNAcylation were related to compensatory mechanisms, in vitro Taz-KD affected, among others, the MAPK pathway, contributing to islet dysfunction. Notably, islet incubation with FGF-21 was able to restore insulin secretion after in vitro Taz-KD. Our findings demonstrate that while Taz and cardiolipin remodelling are essential for beta cell physiology, systemic and islet-specific compensatory mechanisms preserve insulin secretion in vivo in Taz-KD mice, alongside increased glucagon secretion. These adaptations probably contribute to the altered metabolic phenotype observed in Barth syndrome and highlight a potential role for hormones and circulating factors such as FGF-21 in maintaining islet function and glucose homeostasis.

Direct current electric field suppresses NPFFR2 expression in macrophages and alters its predicted conformational dynamics.

Amitriptyline and nortriptyline induce ocular toxicity in early life stage zebrafish (Danio rerio).

Transcriptomics-based approaches, particularly in human-derived cell systems, are emerging as key New Approach Methods (NAMs). These methods offer high-throughput, high-content, and human-relevant analyses of DNA damage. Transcriptomic profiling, which tracks gene expression changes resulting from chemical exposure, provides insights into both adverse and adaptive biological responses. This chapter gives an insight into the methodology (Wet Lab and Dry Lab) to be followed for the RNA sequencing and RNA data analysis, which can be used for identifying the biomarkers/signatures for the genotoxicity-based studies. RNA sequencing is a useful next-generation sequencing (NGS) technique, which has wide variety of applications which include studying altered gene expression, alternative spliced transcripts, gene fusion, post-transcriptional modifications, and mutations/single nucleotide polymorphisms (SNPs). Not only mRNA, RNA-Seq is used to study small RNAs as well as long non-coding RNA profiles in a cell or tissues. The basic steps for RNA-Seq include RNA isolation, cDNA synthesis, attachment of adapters, cDNA library preparation, followed by sequencing and bioinformatic data analysis workflow. The depth to which the library is sequenced depends on the usage of the output data. The sequencing usually follows either single-read or paired-end sequencing methods. Once the data is generated, it can be processed using R-programming, which is briefly discussed here as well.

Molecular responses to pollution stress in glass eels (Anguilla anguilla): Gene expression changes associated with varying contamination levels and temperature across estuaries.

Toxicity assessment of atmospheric particulate-bound polycyclic aromatic hydrocarbons on marine phytoplankton.

Temporal effects of perfluorononanoic acid (PFNA) exposure on metabolic disorders and gut-liver axis injury in large yellow croaker (Larimichthys crocea).

Genomechanical modeling of delayed fracture healing integrating transcriptomics and tissue mechanics.

SRSF1 is essential for pancreatic β-cell proliferation and the maintenance of glucose homeostasis in mice.

Organoid cultures mimic the composition, structure, and function of the organ they derive from to a certain extent, providing more physiologically and biologically relevant results to humans than the currently used monolayer cell cultures and animal models. Organoids have been derived for several organs, from both pluripotent and adult stem cells, and are becoming more commonly used in different areas of research, including development, disease, and pharmacological studies. Their potential in genotoxicity assessment has been reported, although it is still at an early stage. Methods to assess gene expression changes, DNA damage, and metabolite formation have been used and are outlined here.

Morphology and bioproduction potential of DCB-induced cell wall-deficient tobacco BY-2 cells and transcriptomic analysis.

Interplay between lung and intestine in responses to diesel exhaust particles: Contrasting intestinal effects of cleared and swallowed particles with lung-mediated effects using an in vitro approach.

Cortical reactive microglia activate astrocytes, increasing neurodegeneration in human alcohol use disorder.

Diabetic nephropathy is a serious and common complication among patients with both type 1 and type 2 diabetes, and it significantly reduces the patient’s quality of life. This study aimed to assess the reno preventive effects of valproate sodium (VPS) and metformin (MET) on alloxan-induced diabetic nephropathy and to elucidate their mechanisms of action, ‘type 1 diabetic mice’ (25–30 g) were established using a single dose of alloxan (‘120 mgkg-1’). and the diabetic mice were treated with three doses of VPS (10, 20, and 40 mg/kg) and MET (200 mg/kg) for a period of 28 days. Specific tests were performed to evaluate inflammatory gene expression (TNF-α, IL-6, and NF-κB) and histopathological changes and apoptotic factors (Bax/Bcl2, Caspase3). Our results have shown, VPS and MET led to significant decreases in blood glucose levels, thereby reflecting the improvement of impaired kidney function and decreasing elevated renal mRNA levels of inflammatory genes (TNF-α, IL-6, and NF-κB) in diabetic mice. A significant increase in the expression of be ‘Sirt1 and Bcl-2’ and decrease in (TNF-α, IL-6, and NF-κB) was observed in the kidneys of diabetic mice receiving MET/VPS Moreover, MET/VPS successfully prevented diabetes induced ‘histopathological deleterious changes’ in the kidneys of mice so it can concluded that MET and VPS alone or in combination can prevent alloxan-induced diabetic nephropathy through attenuating inflammatory markers and probably with suppression of apoptosis.

The differentiation potency of cells is governed by dynamic changes in gene expression, which can be inferred from single-cell RNA sequencing (scRNA-seq) data. While velocity-based approaches have been used to analyze cell state changes as vector fields, extracting acceleration (change of change) information remains challenging because of the sparsity and high-dimensionality of the data. Here, we develop ddHodge, a framework based on Hodge decomposition for precise vector-field reconstruction. ddHodge accurately recovers all basic components of the vector field, namely, the gradient, curl, and divergence, including the acceleration of the cell state, as second-order derivatives, even from biased and sparse samples. Furthermore, we extend the method to approximate high-dimensional gene expression dynamics on lower-dimensional data manifolds. By applying ddHodge to scRNA-seq data from mouse embryogenesis, we reveal that the gene expression dynamics during development follow a gradient system shaped by potential landscapes, which has not previously been validated with real data. Furthermore, we quantify differentiation potency as cell state stability on the basis of the divergence and identify key genes that drive potency. Our general computational framework for analyzing complex biological systems can elucidate cell fate decisions in developmental processes.

Flower blight is a fungal disease that significantly compromises the ornamental value of Rhododendron petals. However, the molecular mechanisms underlying the interaction between Rhododendron petals and pathogens remain poorly understood. To investigate the defense responses of Rhododendron hybridum petals to pathogenic infection, this study employed transcriptomic and widely targeted metabolomic approaches to analyze constitutive metabolites differences between the resistant cultivar Rhododendron hybridum 'Yangmeihong' (YMH) and the susceptible cultivar 'Xiaotaohong' (XTH), as well as changes in gene expression and metabolite accumulation following infection with Neopestalotiopsis clavispora. A total of 144 constitutive metabolites were identified in YMH petals, whereas 131 were upregulated in XTH petals, suggesting these metabolites may serve as part of the first line of defense during early pathogen infection. At 2 days post-inoculation (dpi), differentially expressed genes (DEGs) in YMH were predominantly enriched in pathways related to amino acid metabolism, central carbon and energy metabolism, nucleotide and sugar metabolism, defense metabolism, and photosynthetic metabolism. In contrast, DEGs in XTH were enriched in pathways secondary metabolite biosynthesis, antioxidant and redox metabolism, and cell structure and motility pathways. Overall, 612 metabolites were identified across both cultivars. Among them, 38 differentially accumulated metabolites (DAMs) were specifically induced in XTH, while 28 were specifically induced in YMH. Integrated transcriptomic and metabolomic analysis revealed that the plant hormone signal transduction pathway likely plays distinct roles in mediating the immune responses of the two cultivars to pathogen infection. These findings enhance our understanding of the moleculer mechanisms governing the interaction between Rhododendron petals and pathogens and provide new insights into the genetic and metabolic basis of disease resistance in Rhododendron.