Yam polysaccharide extraction, purification, structural features, and biological properties: A review.

Oxaliplatin resistance remains a critical barrier to effective colorectal cancer treatment. The molecular mechanisms underlying this resistance are not fully understood, highlighting the need to define the transcriptional alterations that contribute to therapeutic failure. Accordingly, a comparative transcriptome analysis was performed on oxaliplatin-resistant colorectal cancer cells (HCT-116-ROx) and their parental counterparts (HCT-116) using RNA sequencing in this study. Differentially expressed gene (DEG) analysis was conducted using a quasi-likelihood negative binomial model. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were carried out using the topGO and clusterProfiler packages, respectively. To confirm the robustness of the transcriptomic data, the genes with the most significant expression changes, based on false discovery rate-adjusted P value less than 0.05 and a |logFC| > 2 thresholds, were selected for validation by quantitative real-time PCR (qRT-PCR). A total of 313 DEGs were identified, including ALDH3A1 and TACSTD2 (upregulated) and IFITM1 (downregulated); these three genes were chosen for validation by qRT-PCR. Gene Ontology enrichment revealed significant changes in cell motility, redox regulation, and extracellular matrix remodeling. KEGG analysis indicated upregulation of ferroptosis, glutathione metabolism, and lysosome-related pathways, and downregulation of p53 signaling, oxidative phosphorylation, and cancer-specific pathways. Oxaliplatin-resistant colorectal cancer cells undergo multifaceted transcriptional reprogramming that promotes redox homeostasis, metabolic adaptation, and structural plasticity while suppressing apoptotic and mitochondrial functions. These changes support chemoresistance and may represent potential therapeutic targets to restore drug sensitivity.

Photocrosslinkable carbohydrate-based hydrogels for cartilage regeneration: Current insights and future perspectives.

The naked mole-rat (Heterocephalus glaber) is a fascinating model organism which challenges conventional paradigms in evolutionary developmental biology. As one of the two known eusocial mammals with a reproductive hierarchy akin to social insects, the naked mole-rat presents an exceptional system for studying the interplay between social structure, environmental adaptation, and developmental plasticity. This chapter explores how the species' unique reproductive strategies-including lifelong fertility, postnatal oogenesis, and social suppression of reproduction-reshape our understanding of mammalian reproductive aging. The queen, the sole breeding female within a colony, maintains an exceptionally large ovarian reserve throughout life, defying the prevailing dogma of a fixed oocyte pool and progressive depletion. Unlike other mammals, germ cells in the naked mole-rat continue to proliferate postnatally, offering unprecedented insights into the regulation of ovarian function and reproductive longevity. Additionally, the integration of genomic, epigenetic, and neuroendocrine mechanisms underlying eusociality provides a rare perspective on how developmental processes can be shaped by cooperative behaviors and environmental constraints. By situating these traits within an evo-devo framework, this chapter underscores the naked mole-rat's potential to advance research in several fields such as aging, reproductive biology, and the evolution of complex social systems.

Selective eIF4E-eIF4G Pairing and Cap-4 Recognition Mechanisms in Trypanosomatids: Insights From EIF4E5-EIF4G1 and EIF4E6-EIF4G5 Complexes.

A hyperexcited basolateral amygdala complex state determines the hippocampal structural plasticity associated with the reconsolidation of a fear memory.

Decoding chromatin nanoscale plasticity in situ: Insights from native AFM imaging.

Background Subjective tinnitus is an auditory perception occurring without an external sound source. The medial geniculate body (MGB) plays a critical role in tinnitus pathology. The order of this study is to investigate whether mid-infrared (MIR) modulation of the MGB can mitigate tinnitus-like behavior in mice. Methods RNA sequencing was employed to analyze and compare gene expression levels in the MGB of mice with tinnitus to those of control mice. Golgi staining and transmission electron microscopy were used to confirm alterations in the structural plasticity of neurons. The whole-cell patch-clamp technique was applied to assess changes in neuronal functional plasticity. MIR optical fibers were employed to modulate MGB neuronal activity. Molecular dynamics simulations were performed to investigate the regulatory effect of MIR on hyperpolarization-activated cyclic nucleotide-gated (HCN) ion channel function. Results The results of this study illustrates that MIR modulation reversed the abnormal electrophysiological properties of neurons associated with tinnitus-like behavior. Furthermore, molecular dynamics simulations revealed that MIR regulates HCN channel function, reducing the increased firing frequency of MGB neurons in tinnitus mice. Conclusions MIR intervention may alleviate the abnormal increase in neuronal firing frequency in the MGB of tinnitus mice by modulating HCN channel function. This regulatory mechanism involves influencing the secondary structure of HCN channels, enhancing hyperpolarization-activated current amplitude, and restoring reduced amplitudes observed in tinnitus mice.

This review examines convergent neurobiological mechanisms linking stress and drugs that drive stress-induced drug-related behaviors. It first outlines the main theoretical frameworks explaining substance use disorders (SUDs), emphasizing vulnerability factors-particularly stressful life events-that increase addiction risk. The analysis integrates preclinical evidence demonstrating that chronic stress facilitates cross-sensitization to psychostimulants and accelerates drug self-administration, underscoring how stress and drugs converge on glutamatergic and dopaminergic transmission within the Nucleus Accumbens (NAc). Special attention is given to the glial cells, particularly microglia and astrocytes, in mediating stress-induced neuroimmune activation and glutamate dysregulation in the NAc. Three major themes related to microglia-astrocyte crosstalk are addressed: (i) the contribution of these glial cells to neuroimmune and glutamatergic alterations induced by stress; (ii) their role in synaptic and structural plasticity changes within the NAc; and (iii) the mechanisms by which stress and drug exposure reshape glial-neuronal communication, driving the comorbidity between stress and SUDs. A dedicated section focuses on key neuroimmune signaling pathways-particularly the TNF-α/NF-κB axis-and their involvement in stress-induced vulnerability to cocaine addiction. Finally, the review discusses preclinical evidence supporting the therapeutic potential of repurposed glutamate-modulating agents as promising pharmacological candidates for treating comorbid stress and cocaine-use disorder.

NDM-type metallo-β-lactamases (MBLs) are among the most widespread acquired carbapenemases in carbapenem-resistant Enterobacterales. As with other β-lactamases, allelic variability occurs among NDM-type MBLs, with almost 100 variants so far reported, differing by single or multiple amino acid substitutions or insertions, which may have implications for enzymatic activity. In this study, we report on a novel NDM variant, NDM-63, identified in a carbapenem-resistant ST147 Klebsiella pneumoniae from a surveillance rectal swab. Compared to NDM-1, NDM-63 features an original array of changes in the L3 loop, including deletion of phenylalanine at position 70 and two amino acid substitutions (G69S and A72H), due to a four-nucleotide deletion plus a nucleotide insertion in the gene region encoding the L3 loop. When expressed in Escherichia coli under isogenic conditions, NDM-63 conferred a resistance profile overall similar to NDM-1, but exhibiting a lower level of resistance to carbapenems and cefepime, while remaining susceptible to inhibition by taniborbactam. Present findings expand current knowledge on the structural plasticity of NDM-type MBLs and highlight that variability in the L3 loop, which contributes to delimitation of the active site, could also tolerate amino acid deletions without loss of enzymatic activity. A virtually identical K. pneumoniae carrying a non-functional blaNDM allele entailing only the nucleotide insertion observed in blaNDM-63 (which might have played a role in the evolution of blaNDM) was also isolated from a bloodstream infection that occurred in the same patient, yielding a misleading result of molecular diagnostic testing due to the lack of enzyme activity despite the presence of the target gene.

Introduction. Sleep disorders are a group of conditions that disrupt normal sleep patterns. They are one of the most common clinical problems. Insufficient or non-restorative sleep can interfere with normal physical, mental, social, and emotional functioning. Sleep disorders can affect overall health, safety, and quality of life. Sleep disorders have a broad differential diagnosis; therefore, standardized definitions and classifications are important. Aim. To identify the main trends in modern scientific understanding of the pathophysiology of sleep disorders. Materials and methods. Theoretical review of modern scientific works on the topic of the study, which are freely available in scientific information search systems, international databases of scientific information. Results. Based on the literature review, current understanding of the pathophysiology of sleep disorders and their role in the development of somatic and mental diseases was systematized. Cellular changes induced by sleep dysfunction underlie functional and structural alterations in brain regions and circuits. Alterations in neuronal plasticity and glial activation in brain structures contribute to sleep disorders. These alterations in neurotransmitter system function are of key importance. Modern approaches to the classification of sleep disorders, based on clinical manifestations and pathophysiological mechanisms, have received special attention. Conclusions. Analysis of modern data shows that sleep disorders are based on an imbalance of neurotransmitter systems, changes in the regulation of circadian rhythms, dysfunction of the hypothalamic-pituitary-adrenal axis, as well as structural and functional disorders of the central nervous system. Of particular importance are neurohumoral mechanisms that mediate the relationship between sleep, the emotional sphere and somatic health.

The axon initial segment (AIS) is the site of action potential generation and exhibits structural and functional plasticity upon adaptation of neuronal excitability and disease. Performing in vivo longitudinal two-photon imaging of AIS in the medial prefrontal cortex of male mice, we reveal dynamic AIS remodeling during associative fear learning and extinction. These results demonstrate that AIS plasticity is not only crucial for homeostatic adaptation but also a hallmark of memory formation.

Muscle structure is dynamically shaped by mechanical use, yet how distinct locomotor behaviors influence sarcomere organization remains poorly understood. In Caenorhabditis elegans, crawling and swimming constitute discrete gaits that differ in curvature, frequency, and mechanical load, providing a tractable model for studying activity-dependent remodeling. Using confocal imaging of phalloidin-stained body-wall myocytes, we quantified myocyte geometry, sarcomere length, and sarcomere number across anterior, mid-body, and posterior regions in animals reared exclusively under crawling or swimming conditions. Quantification and hypothesis testing used linear mixed models that accounted for repeated myocyte measurements within animals, with interaction terms testing region-specific effects of locomotor condition after IQR-based outlier removal. Swimming produced characteristic remodeling of body-wall muscles. Myocytes elongated globally, while selectively thinning in the mid-body, reducing cell area by ∼13 % relative to crawlers. Shape metrics confirmed this shift: circularity declined at mid- and tail-regions and anisotropy increased by ∼2-3 units. Sarcomere architecture exhibited parallel remodeling. Average sarcomere length shortened across the body (-0.19 µm in head, -0.35 µm in mid-body, -0.20 µm in tail), while sarcomere number increased in anterior and mid-body regions (+0.77 and +0.65 sarcomeres per myocyte). The mid-body region also showed a significant rise in sarcomere density, indicating tighter serial packing. These adaptations mirror functional compartmentalization predicted from gait kinematics and parallel fast-fiber remodeling observed in vertebrate muscles. The results indicate that C. elegans muscles adapt their contractile lattice to sustained mechanical demand, linking neural gait selection and mechanosensitive signaling to long-term structural plasticity. This work establishes C. elegans as a model for dissecting the conserved pathways that couple muscle use to cellular architecture and provides a foundation for future comparisons of healthy and diseased muscle remodeling.

The evolutionary history of the Hypericaceae Juss. family remains poorly understood despite previous phylogenomic efforts. A prior study on Hypericum ascyron revealed exceptional plastome rearrangements and gene loss events, prompting questions about whether such genomic patterns are unique to Hypericum or reflect broader evolutionary trends within the family. To explore plastome evolution across Hypericaceae, we sequenced 12 complete chloroplast genomes representing seven genera from the three major tribes, Hypericeae, Vismieae, and Cratoxyleae, and two outgroup plastomes from Clusiaceae. Comparative analysis of 281 Malpighiales plastomes showed that Hypericaceae differ significantly in total plastome size and SSC region length, while LSC and IR regions showed no significant differences.. Plastome sizes in Hypericaceae ranged from 138 to 176kb, reflecting extensive structural variation, multiple inversions, IR expansions, and lineage-specific rearrangements. Cratoxyleae exhibited a relatively conserved plastome structure with one major inversion and minimal gene loss, representing the most stable lineage within the family. Species within Vismieae showed markedly expanded IR regions, while Hypericeae exhibited frequent gene and intron losses associated with structural instability. In Hypericum, genes such as matK and accD were relocated into or near the IR regions, accompanied by lineage-specific ORFs likely formed through repeat-mediated recombination. Several genes (rpl23, rpl32, rps7, rps16, infA, ycf1, ycf2) showed independent losses across the family. Across the Hypericaceae, the protein-coding genes matK, accD and clpP also showed domain-disrupting expansions, potentially impacting their functional roles. Our results demonstrate that plastome evolution in Hypericaceae is highly dynamic, characterized by substantial structural plasticity, gene loss, and lineage-specific innovation. These findings provide new insights into plastome diversification across the family and lay the groundwork for further phylogenomic and evolutionary studies within Malpighiales.

We present a multiscale model of taste that is both biophysically faithful and computationally efficient, enabling end-to-end simulation from receptor transduction to network-level coding. The novelty lies in coupling Hodgkin–Huxley taste receptor cells with Goldman–Hodgkin–Katz ion currents and modality-specific receptors (T1R/T2R, ENaC), to an Izhikevich spiking network equipped with realistic glutamatergic synapses and spike-timing-dependent plasticity. Training combines spike synchrony and a genetic approach in order to reach both globally optimized network structure and biomorphic synaptic plasticity. This hybrid design yields distinct, sparse spiking “fingerprints” for taste qualities and mixtures, and provides a practical foundation for neuromorphic gustatory sensors that require real-time, energy-efficient operation.

In the current study, the surface characteristics and deformation behavior of raw and washed denim fabrics were investigated using Tactile Sensation Analyzer (TSA) which measures surface variations through sound analysis and determines out-of-plane deformation behavior during the deformation test phase. A total of 30 denim fabrics with various raw materials and production parameters were examined. Two different denim washing processes were applied to the raw denim fabrics, one involving cellulase enzyme and the other combined with pumice stones. The effects of washing on structural properties, surface characteristics, deformation, elasticity, hysteresis, plasticity, and tactile comfort were analyzed. The results indicated that denim washing significantly increased the thickness and decreased the magnitude of micro-surface variations across all tested samples, and most fabrics exhibited a less rigid structure after washing. It was detected that enzyme washing has a moderate effect on fabric properties. Meanwhile, the combination of cellulase enzyme and pumice stones resulted in significant improvements in surface smoothness, fullness, unit mass, deformability, elasticity and total hand scores.

Multiphoton imaging allows for the visualization of structural and functional plasticity within the central nervous system. However, gaining optical access to deep brain structures, such as the hippocampal dentate gyrus (DG), requires invasive approaches, causing brain damage. Here we optimize three-photon (3P) microscopy to perform longitudinal imaging of the DG in the intact brain at unprecedented depth of up to 1800 µm. We apply this approach to follow the dynamics of neural stem cells (NSCs) in the adult and developing DG, allowing for novel insights into structural plasticity deep within the intact mouse brain.

​ Background : Podocytes are specialized epithelial cells that constitute the glomerular filtration barrier. Because adult kidneys lack podocyte stem cells, the cells produced during development must persist throughout life. However, podocyte numbers decline with aging and disease, suggesting that surviving podocytes may undergo structural adaptations to maintain the glomerular epithelium. The nature of these changes, however, remains poorly understood. Methods: We used volume electron microscopy to analyze and compare the three-dimensional ultrastructure of podocytes in young adult (1.5-month-old), adult (6-month-old), and aged (24-month-old) male Wistar rats. Results: Aged podocytes exhibited eight characteristic structural alterations: hypertrophy, pseudocystic changes, irregularity of foot processes, fragmentation, pruning of foot processes, autocellular interdigitation, release of lysoendosomal and multivesicular body contents, and an increase in lysosomal volume. Among these, hypertrophy was particularly notable—it resulted in an approximately 4.6-fold increase in podocyte volume and a 3.0-fold increase in total surface area, enabling adequate coverage of the enlarged glomerular surface. Furthermore, in areas where portions of podocytes appeared to be lost due to fragmentation, adjacent podocytes formed de novo autocellular junctions/interdigitation, thereby preventing exposure of the basement membrane. Additionally, aged podocytes showed clustering of lysoendosomes and multivesicular bodies, with evidence of their exocytotic release into the urinary space. This process may compensate for the reduced intracellular degradation capacity associated with aging. Conclusions: Our study demonstrated the remarkable plasticity of podocytes during aging.

Reversal of auditory cortical hyperexcitability and restoration of synaptic plasticity balance by GluN1-mediated photobiomodulation in noise-induced tinnitus.

Sex differences are found in brain structure and function across species, and across brain disorders in humans. A major source of brain sex differences is differential secretion of steroid hormones from the gonads across the lifespan. Specifically, ovarian hormones oestrogens and progesterone are known to dynamically change structure and function of the adult female brain, having a major impact on psychiatric risk. However, due to limited molecular studies in female rodents, very little is still known about molecular drivers of female-specific brain and behavioural plasticity. Here we show that ventral hippocampal (vHIP) overexpression of Egr1, an oestrous cycle-dependent transcription factor, induces sex-dependent changes in vHIP neuronal chromatin, gene expression, and structural plasticity, along with female-specific effects on vHIP-dependent behaviours. Importantly, Egr1 overexpression and knockdown partially mimic the vHIP chromatin state associated with the high and low-oestrogenic phase of the oestrous cycle, respectively. We demonstrate that Egr1 directs neuronal chromatin opening across the sexes, although with limited genomic overlap. Our study not only reveals a sex-dependent chromatin regulator in the brain, but also provides functional evidence that this sex-dependent gene regulation drives structural and behavioural plasticity, informing sex-based treatments for brain disorders.