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This study focused on the preparation of microcapsules that simulate adipose tissue cells via complex coacervation, followed by the formation of block-like fat analogue products through gelation. The results indicated that microcapsules obtained by encapsulating coconut oil with soy protein isolate (SPI) and sodium alginate (SA) through a complex coacervation process could serve as effective fat substitutes in meat products. When the mass ratio of SPI to SA was 3:1, the core-to-wall mass ratio was 1:1, and the total wall material concentration was 3% (w/v), the oil loading rate of the microcapsules reached 39.17%. The particle size of the oil-loaded microcapsules was mainly distributed between 40–180 μm, which was comparable to the size of fat cells in animal adipose tissue. Microcapsules (50%, w/w) were mixed with a 5% (w/v) curdlan dispersion and heated at 95 °C for 60 min to form fat analogues. The fat analogues demonstrated significantly reduced cooking loss, enhanced textural rigidity, and superior chew resistance, achieving performance metrics comparable to those of natural adipose tissue. This dual-phase strategy—combining interfacial engineering of lipid microcapsules with polysaccharide-mediated gelation—provides a promising approach for developing sustainable, plant-based fat alternatives in meat product reformulation. The methodology not only addresses texture and flavour challenges in fat replacement but also enables precise control over lipid content, supporting applications in healthier food systems.

Rotating machines are widely used as components of various industries around the world, and its normal operation of rotating machines is important. Thus, condition monitoring and fault diagnosis of rotating machines have considerable attention in recent years. Industrial statistics illustrate that 40% of total large machine breakdowns happened due to broken bearings, while for small machines, the analogous number reaches up to 90%. This study aimed at researching fault diagnosis of journal bearings using the support vector machine (SVM) method. The experimental systems of vertical and horizontal rotating shafts were developed. There was no adding any initial artificial failure in the bearing, and a little muddy water was used, and long-term vibration data in both systems were obtained in the normal operation of the machines until bearing damages occurred in the journal bearing (3-hour tests were conducted repeatedly and total 128 datasets for vertical shaft and 24 datasets for horizontal shaft were obtained). A feature selection method is focused, and a hybrid feature selection method by combining Fisher score (FS) and a sequential forward selection (SFS) method was proposed. Its accuracy and efficiency was proved experimentally with 97.14% and 100% for vertical shaft and 100% for horizontal shaft. Furthermore, as a result of the SVM model and hybrid feature selection method, the most important feature for journal bearing of horizontal rotor system was clarified as mean value of RMS, and only this feature can give good diagnosis result. It is useful suggestion in selecting the features for the fault diagnosis of horizontal rotating machines.

Fibroblast growth factor (FGF) 23 is a member of the FGF family involved in bone development by interacting with FGFRs. In a previous study, we discovered a mutant human FGF (hFGF) 23 (A12D) in the mandibular prognathism (MP) pedigree. However, the exact role of hFGF23(A12D) during bone formation remains unclear. The aim of this study was to identify the function of hFGF23(A12D) in bone formation. We infected isolated rat calvaria (RC) cells with the recombinant lentivirus containing mutant hFGF23(A12D) and WT hFGF23 respectively. Real‐time PCR, western blot and enzyme‐linked immunosorbent assay confirmed that hFGF23(A12D) failed to be secreted. We measured cell growth via the CCK‐8 assay based on Zsgreen expression, detected cell differentiation ability via alkaline phosphatase staining, performed RT‐PCR and found that hFGF23(A12D) inhibited proliferation of RC cells and stimulated the differentiation of RC cells to osteoblasts. Through RNA sequencing, RT‐PCR and western blot, we found increased expression of FGFR3. Through co‐immunoprecipitation assays and immunofluorescence staining, we revealed that hFGF23(A12D) activated the mitogen‐activated protein kinase signalling pathway through interactions with the intracellular domain of FGFR3. In summary, we determined the mechanisms of hFGF23(A12D) involved in osteoblast generation and formation which is specifically due to its interaction with FGFR3.

Even though metagenomics have revolutionized the characterization of the human microbiome, detailed mechanistic studies are impracticable, as there is a dearth of robust culture collections. We now describe the development and use of a laser-assisted culturomics platform, incorporating the elements of a bioprinter, the culture conditions, the methods to characterize the microorganisms and a biobank. With laser-assisted bioprinting, the microorganisms can be rapidly and precisely transferred from clinical biofilms to highly organized arrays of microbial colonies, which are suitable for co-culturing and molecular analyses. The presented technique has propagated 99 of 100 microbial species and recovered 79% of abundant species from dental plaque in accordance with full 16S rRNA gene profiling of 691,199 sequences. Microscopy, spectroscopy and enzyme assays have been used to guide isolations. Processing of oral biofilms from four individuals has yielded 249 representative isolates, from 14 classes and 124 species in total. Functional profiling with bioprinting has indicated commensals which could potentially contribute to disease development. Isolates from peri-implantitis cover 85.4% of the transcriptionally active clinical biofilms at genus level. Taken together, this work provides the basis for generating on-demand culture collections and biofilms for research and clinical use. Representative microbial isolates and patient-specific biobanks are crucial for microbiome investigation and management. Here, authors develop laser-assisted microbial culturomics, combining high-throughput, precise bioprinting on diverse media with rapid, non-invasive analyses.

This article aims to evaluate the effects of mesh size change on the mechanical properties of GFRP laminates, via low-velocity impact and compression-after-impact (CAI) test, and the failure mechanism was analyzed. Through vacuum-assisted resin infusion, wire meshes with different mesh numbers and wire diameters were incorporated into GFRP. Based on response history and failure morphology, the results show that the addition of wire mesh can disperse the incident energy from the impact center to the outer region, thereby improving the impact resistance of GFRP. It is worth noting that increasing the number of mesh could improve the stiffness of the panels and enhance their ability in CAI events compared with increasing the diameter of wires, their failure evolution was presented from the perspective of digital image correlation (DIC). For example, the maximum displacement of 0.50–40 J decreased by 10.6% from 2.5 to 2.26 mm compared with 20–60 J.

To study the impact response and compression-after-impact (CAI) behavior of perforated sandwich panels comprised of foam core and glass fiber-reinforced epoxy hybrid facesheets, the hole diameter of specimens is changed in the fabrication via vacuum-assisted resin infusion. Furthermore, low-velocity-impact tests with various impact distances between the impact point and hole are carried out. With the help of the digital image correlation technique, CAI testing is conducted, and the strain evolution of specimens is monitored carefully. The mechanical response history, damage morphology, and compressive process are discussed in detail. The results show that the impact and CAI performance of specimens are weakened because of open holes. Compared with the non-perforated specimen, the maximum force of the specimen with a 6-mm hole and the 5-mm impact distance decreases by 41.21%, and its maximum displacement increases by 38.60%. During the CAI process, in comparison with the impact damage, more significant stress concentration and buckling around the hole are found.

The problem of input-to-state stability (ISS) was studied in this paper for a class of nonlinear time-delay systems with delayed impulses under event-triggered impulsive control (ETIC), where delays were flexible and external inputs in continuous and impulse dynamics were different. To avoid Zeno behavior, an event-triggered mechanism (ETM) that used the information of the system state and external disturbances was proposed, and the feasibility was enhanced by introducing a forced impulse sequence. Furthermore, some sufficient conditions were formulated to enable ISS for the considered system by using Lyapunov-Razumikhin-like methods. For a class of nonlinear impulse control systems, an application was introduced that utilizes linear matrix inequalities (LMIs) to design an ETM and control gain. Finally, two numerical examples were given to validate the theoretical results.

Acute pancreatitis (AP) is a disease characterized by local and systemic inflammation with an increasing incidence worldwide. Receptor-interacting serine/threonine protein kinase 3 (RIPK3), mixed-lineage kinase domain-like protein (MLKL), and innate immune cell macrophages have been reported to be involved in the pathogenesis of AP. However, the mechanisms by which RIPK3 and MLKL regulate pancreatic injury, as well as the interactions between injured pancreatic acinar cells and infiltrating macrophages in AP, remain poorly defined. In the present study, experimental pancreatitis was induced in C57BL/6J, Ripk3 -/- and Mlkl -/- mice by cerulein plus lipopolysaccharide in vivo, and primary pancreatic acinar cells were also isolated to uncover cellular mechanisms during cerulein stimulation in vitro. The results showed that MLKL and its phosphorylated protein p-MLKL were upregulated in the pancreas of the mouse AP model and cerulein-treated pancreatic acinar cells, independent of its canonical upstream molecule Ripk3 , and appeared to function in a cell death-independent manner. Knockout of Mlkl attenuated AP in mice by reducing the polarization of pancreatic macrophages toward the M1 phenotype, and this protective effect was partly achieved by reducing the secretion of CXCL10 from pancreatic acinar cells, whereas knockout of Ripk3 did not. In vitro neutralization of CXCL10 impaired the pro-M1 ability of the conditioned medium of cerulein-treated pancreatic acinar cells, whereas in vivo neutralization of CXCL10 reduced the polarization of pancreatic macrophages toward M1 and the severity of AP in mice. These findings suggested that targeting the MLKL-CXCL10-macrophage axis might be a promising strategy for the treatment of AP.

Despite long-standing recognition in the significance of mucus overproduction in asthma, its etiology remains poorly understood. Muc5ac is a secretory mucin that has been associated with reduced pulmonary function and asthma exacerbations. We sought to investigate the immunological pathway that controls Muc5ac expression and allergic airway inflammation in asthma. Cockroach allergen-induced Muc5ac expression and aryl hydrocarbon receptor (AhR) signaling activation was examined in the human bronchial epithelial cells (HBECs) and mouse model of asthma. AhR regulation of Muc5ac expression, mitochondrial ROS (Mito-ROS) generation, and NLRP3 inflammasome was determined by AhR knockdown, the antagonist CH223191, and AhR mice. The role of NLRP3 inflammasome in Muc5ac expression and airway inflammation was also investigated. Cockroach allergen induced Muc5ac overexpression in HBECs and airways of asthma mouse model. Increased expression of AhR and its downstream genes CYP1A1 and CYP1B1 was also observed. Mice with AhR deletion showed increased allergic airway inflammation and MUC5AC expression. Moreover, cockroach allergen induced epithelial NLRP3 inflammasome activation (e.g., NLRP3, Caspase-1, and IL-1β), which was enhanced by AhR knockdown or the antagonist CH223191. Furthermore, AhR deletion in HBECs led to enhanced ROS generation, particularly Mito-ROS, and inhibition of ROS or Mito-ROS subsequently suppressed the inflammasome activation. Importantly, inhibition of the inflammasome with MCC950, a NLRP3-specifc inhibitor, attenuated allergic airway inflammation and Muc5ac expression. IL-1β generated by the activated inflammasomes mediated cockroach allergen-induced Muc5ac expression in HBECs. These results reveal a previously unidentified functional axis of AhR-ROS-NLRP3 inflammasome in regulating Muc5ac expression and airway inflammation.