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Root colonization ability results from the long-term evolutionary adaptation of certain bacteria to the plant rhizosphere, involving extensive bacterial genetic resources. Understanding colonization mechanisms is crucial for fully exploiting the potential of PGPRs. Pseudomonas spp. are important biocontrol agents for plant diseases, with strong affinity for plant roots and large populations in the rhizosphere, making them key models for studying PGPR colonization mechanisms. Most studies on Pseudomonas colonization rely on molecular genetics and omics approaches, which reveal many bacterial traits and mechanisms involved in rhizosphere colonization but are limited in detecting continuous genomic changes and subtle nucleotide variations. In this study, we established an experimental evolution system using Pseudomonas bijieensis 2P24 in the wheat rhizosphere to simulate bacterial evolution in the plant rhizosphere. We observed that bacteria enhance colonization ability by fine-tuning the flagellar number, revealing a novel adaptive mutation in plant rhizobacteria.

While stroke survivors with moderate or mild impairment are typically able to open their hand at will, those with severe impairment cannot. Abnormal synergies govern the arm and hand in stoke survivors with severe impairment, so hand opening, which is required to overcome the working synergy, is an extremely difficult task for them to achieve. It is universally accepted that alternative tracts including the cortico-reticulospinal tract (CRST), employed in the case that the corticospinal tract (CST) is damaged by stroke, brings about such abnormal synergies. Here we note that hand closing is enabled by alternative tracts as well as the CST, and a research question arises: Does motor characteristics while closing the hand depend on the integrity of the CST? In this study, we evaluate the abilities of 17 stroke survivors to flex and relax the metacarpophalangeal (MCP) joints and investigate whether motor characteristics can be distinguished based on CST integrity which is estimated using upper-extremity Fugl-Meyer (UEFM) scores. UEFM scores have been perceived as an indirect indicator of CST integrity. We found that participants with the UEFM score above a certain value, who are assumed to use the CST, moves the MCP joints more smoothly ( P  < 0.05) and activates the flexors to flex the joints faster ( P  < 0.05), in comparison to participants with low UEFM scores, who are assumed to preferentially use alternative tracts. The results imply that use of alternative tracts (i.e. the CRST) results in a degradation in movement smoothness and slow activation of MCP flexors. We present evidence that responses of flexors of the MCP joints following stroke depend on the degree of impairment which is hypothesized to originate from preferentially use of different neural motor pathways.

Understanding abnormal synergy of the upper extremity (UE) in stroke survivors is critical for better identification of motor impairment. Here, we investigated to what extent stroke survivors retain the ability to coordinate multiple joints of the arm during a reaching task. Using an exoskeleton robot, 37 stroke survivors’ arm joint angles (θ) and torques (τ) during hand reaching in the horizontal plane was compared to that of 13 healthy controls. Kinematic and kinetic coordination patterns were quantified as variances of the multiple-joint angles and multiple-joint torques across trials, respectively, that were partitioned into task-irrelevant variance ( TIV θ and TIV τ ) and task-relevant variance ( TRV θ and TRV τ ). TIV θ and TRV θ (or TIV τ and TRV τ ) led to consistent and inconsistent hand position (or force), respectively. The index of synergy ( IS θ and IS τ ) was determined as IS θ = ( TIV θ - TRV θ ) / ( TIV θ + TRV θ ) and IS τ = ( TIV τ - TRV τ ) / ( TIV τ + TRV τ ) for kinematic and kinetic coordination patterns, respectively. Both kinematic IS θ and kinetic IS τ in the stroke group were significantly lower than that of the control group, indicating stroke survivors had impaired reaching abilities in utilizing the multiple joints of the UE for successful completion of a reaching task. The reduction of kinematic IS θ in the stroke group was mainly attributed to the lower TIV θ as compared to the control group, while the reduction of kinetic IS τ was mainly due to the higher TRV τ as well as lower TIV τ . Our results also indicated that stroke may lead to motor deficits in formation of abnormal kinetic synergistic movement of UE, especially during outward movement. The findings in abnormal synergy patterns provides a better understanding of motor impairment, suggesting that impairment-specific treatment could be identified to help improve UE synergies, focusing on outward movements.

Myocardial ischemia, while causing cardiomyocyte injury, can activate innate protective processes, enhancing myocardial tolerance to ischemia. Such processes are present in not only the heart, but also remote organs. In this investigation, we demonstrated a cardioprotective process involving FGF21 from the liver and adipose tissue. In response to myocardial ischemia/reperfusion injury in the mouse, FGF21 was upregulated and released from the hepatic cells and adipocytes into the circulation and interacted with FGFR1 in cardiomyocytes under the mediation of the cell membrane protein β-Klotho, inducing FGFR1 phosphorylation. This action caused phosphorylation of the signaling molecules PI3K p85, Akt1 and BAD, thereby reducing caspase 3 activity, cell death and myocardial infarction in association with improvement of myocardial function. These observations suggest that FGF21 is upregulated and released from the liver and adipose tissue in myocardial injury, contributing to myocardial protection by the mediation of the FGFR1/β-Klotho–PI3K–Akt1–BAD signaling network.

NUDIX hydrolase type 5 (NUDT5) is a kind of ADP-ribose pyrophosphatase and nucleotide metabolizing enzyme in cell metabolism. Previous studies have shown NUDT5 expression affected chromosome remodeling, involved in cell adhesion, cancer stem cell maintenance and epithelial to mesenchyme transition in breast cancer cells. Nevertheless, the role of NUDT5 in breast cancer progression and prognosis has not yet been systematically studied. This study explored the association of NUDT5 with the tumor development and poor prognosis in patients with breast cancer. Our results show that the levels of NUDT5 were upregulated in breast cancer cell lines and breast tumor tissues, and the expression of NUDT5 in breast tumor tissues increased significantly when compared with adjacent non-tumorous tissues by immunohistochemical staining of tissue microarrays. Breast cancer patients with high NUDT5 expression had a worse prognosis than those with low expression of NUDT5. In addition, the knockdown of NUDT5 suppressed breast cancer cell lines proliferation, migration and invasion, and dramatically inhibited the AKT phosphorylation at Thr308 and expression of Cyclin D1. The opposite effects were observed in vitro following NUDT5 rescue. Our findings indicated that the high expression of NUDT5 is probably involved in the poor prognosis of breast cancer via the activation of the AKT / Cyclin D pathways, which could be a prognostic factor and potential target in the diagnosis and treatment of breast cancer.

Reactive oxygen species formed within the mammalian cell can produce 8-oxo-7,8-dihydroguanine (8-oxoG) in mRNA, which can cause base mispairing during gene expression. Here we found that administration of 8-oxoGTP in MTH1-knockdown cells results in increased 8-oxoG content in mRNA. Under this condition, an amber mutation of the reporter luciferase is suppressed. Using secondgeneration sequencing techniques, we found that U-to-G changes at preassigned sites of the luciferase transcript increased when 8-oxoGTP was supplied. In addition, an increased level of 8-oxoG content in RNA induced the accumulation of aggregable amyloid β peptides in cells expressing amyloid precursor protein. Our findings indicate that 8-oxoG accumulation in mRNA can alter protein synthesis in mammalian cells. Further work is required to assess the significance of these findings under normal physiological conditions.

The coordination of public and private goods production is essential for bacterial adaptation to environmental changes. Quorum sensing (QS) regulates this balance by mediating the trade‐off between the communal benefits of “public goods,” such as siderophores and antibiotics, and the individual metabolic needs fulfilled by “private goods,” such as intracellular metabolites utilized for growth and survival. Pseudomonas fluorescens 2P24 harbors a LasI/LasR‐type QS system, MupI/MupR, which regulates mupirocin production through signaling molecules. This study explores how QS coordinates carbon and nitrogen metabolism to optimize the production of key secondary metabolites, including 2,4‐diacetylphloroglucinol (2,4‐DAPG), mupirocin, and siderophores, which serve as public goods. Loss of QS disrupts this balance by enhancing the Krebs cycle, denitrification, pyruvate anaplerosis, and ammonium assimilation, lead to halted 2,4‐DAPG and mupirocin synthesis and increased siderophore production. In the absence of QS, elevated siderophore production compensates for iron acquisition, ensuring rapid cellular growth. Under nutrient‐limited or high cell density conditions, MupR regulates carbon and nitrogen fluxes to sustain public goods production. These findings highlight QS as a key environmental sensor that fine‐tunes resource allocation, bacterial fitness, and adaptation to ecological and nutritional conditions, suggesting the potential for QS‐targeted approaches to enhance antibiotic production and agricultural sustainability. Pseudomonas fluorescens 2P24 utilizes a LasI/LasR‐type quorum sensing (QS) system, MupI/MupR, to regulate carbon and nitrogen metabolism for optimal production of secondary metabolites as public goods, including 2,4‐diacetylphloroglucinol, mupirocin, and siderophores. QS acts as a sensor, regulating metabolic fluxes to maintain energy and nutrient homeostasis, enabling facultative cooperation, and supporting long‐term adaptation to environmental changes.

The primary aim of this study was to investigate how measurements from different regions along the rectus femoris (RF) and vastus lateralis (VL) influence muscle morphology, including muscle thickness (MT), muscle stiffness, and muscle quality. An exploratory aim was to examine whether an association exists between voluntary and involuntary force and muscle morphology across the same regions. In one session, participants ( n  = 13) underwent ultrasound imaging (US), followed by knee extension maximal isometric voluntary contractions and evoked contractions. US recordings (at rest) and testing were conducted while participants were seated at 90º knee flexion (dominant leg) on an isokinetic dynamometer. Muscle morphology was recorded at proximal, medial, and distal regions of RF and VL. During maximum contractions, participants were instructed to exert maximal effort as fast and as forcefully as possible for 5 s, while evoked contractions were performed via femoral nerve stimulation. A one-way repeated measures ANOVA was used for the main aim, while Spearman bivariate correlations were used for the exploratory aim. The primary findings showed that the RF and VL muscles were significantly larger in the medial region ( P  ≤ 0.023), with no significant differences in muscle quality or stiffness within the same muscle. Additionally, a significant overall relationship was observed between muscle quality and the rate of force development in both muscles ( P  ≤ 0.037). In conclusion, muscle size varies across the length of the VL and RF muscles, with no changes in muscle quality or stiffness. Furthermore, muscle quality demonstrates a significant association with rate of force development.

Among the potential biological signals for human-machine interactions (brain, nerve, and muscle signals), electromyography (EMG) widely used in clinical setting can be obtained non-invasively as motor commands to control movements. The aim of this study was to develop a model for continuous and simultaneous decoding of multi-joint dynamic arm movements based on multi-channel surface EMG signals crossing the joints, leading to application of myoelectrically controlled exoskeleton robots for upper-limb rehabilitation. Twenty subjects were recruited for this study including 10 stroke subjects and 10 able-bodied subjects. The subjects performed free arm reaching movements in the horizontal plane with an exoskeleton robot. The shoulder, elbow and wrist movements and surface EMG signals from six muscles crossing the three joints were recorded. A non-linear autoregressive exogenous (NARX) model was developed to continuously decode the shoulder, elbow and wrist movements based solely on the EMG signals. The shoulder, elbow and wrist movements were decoded accurately based only on the EMG inputs in all the subjects, with the variance accounted for (VAF) > 98% for all three joints. The proposed approach is capable of simultaneously and continuously decoding multi-joint movements of the human arm by taking into account the non-linear mappings between the muscle EMGs and joint movements, which may provide less effortful control of robotic exoskeletons for rehabilitation training of individuals with neurological disorders and arm impairment.

Background Pseudomonas fluorescens 2P24 is a rhizosphere bacterium that produces 2,4-diacetyphloroglucinol (2,4-DAPG) as the decisive secondary metabolite to suppress soilborne plant diseases. The biosynthesis of 2,4-DAPG is strictly regulated by the RsmA family proteins RsmA and RsmE. However, mutation of both of rsmA and rsmE genes results in reduced bacterial growth. Results In this study, we showed that overproduction of 2,4-DAPG in the rsmA rsmE double mutant influenced the growth of strain 2P24. This delay of growth could be partially reversal when the phlD gene was deleted or overexpression of the phlG gene encoding the 2,4-DAPG hydrolase in the rsmA rsmE double mutant. RNA-seq analysis of the rsmA rsmE double mutant revealed that a substantial portion of the P. fluorescens genome was regulated by RsmA family proteins. These genes are involved in the regulation of 2,4-DAPG production, cell motility, carbon metabolism, and type six secretion system. Conclusions These results suggest that RsmA and RsmE are the important regulators of genes involved in the plant-associated strain 2P24 ecologic fitness and operate a sophisticated mechanism for fine-tuning the concentration of 2,4-DAPG in the cells.