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The spectrum scanned by a Fourier transform spectrometer (FTIR) often has a baseline drift. However, baseline distortion rarely occurs in a laboratory owing to the insignificant effects of environmental vibrations and electromagnetic factors. Even if it occurs, the distorted spectrum can be manually eliminated. However, in a complex environment, especially after the long-term operation of a spectrometer, the scanned spectrum may be distorted to different degrees. Herein, the origins of spectral baseline drifts and distortions are analyzed and simulated using MATLAB; furthermore, a baseline correction method based on the baseline-type model is proposed. The results of experiments performed on the methane spectrum confirm that the proposed method outperformed the improved modified multi-polynomial fitting and iterative averaging methods.

Allogeneic mesenchymal stem cells (MSCs) exhibit immunoregulatory function in human autoimmune diseases such as systemic lupus erythematosus (SLE), but the underlying mechanisms remain incompletely understood. Here we show that the number of peripheral tolerogenic CD1c + dendritic cells (DCs) and the levels of serum FLT3L are significantly decreased in SLE patients especially with lupus nephritis, compared to healthy controls. Transplantation of allogeneic umbilical cord-derived MSCs (UC-MSCs) significantly up-regulates peripheral blood CD1c + DCs and serum FLT3L. Mechanistically, UC-MSCs express FLT3L that binds to FLT3 on CD1c + DCs to promote the proliferation and inhibit the apoptosis of tolerogenic CD1c + DCs. Conversely, reduction of FLT3L with small interfering RNA in MSCs abolishes the up-regulation of tolerogenic CD1c + DCs in lupus patients treated with MSCs. Interferon-γ induces FLT3L expression in UC-MSCs through JAK/STAT signaling pathway. Thus, allogeneic MSCs might suppress inflammation in lupus through up-regulating tolerogenic DCs. Promising pilot clinical trials of mesenchymal stem cells (MSCs) therapy of lupus await validation in larger, controlled trials. Here the authors show that MSCs expand CD1c + dendritic cells in cell culture by producing FLT3L, and that in lupus patients, circulating CD1c + dendritic cells and FLT3L are increased following MSCs therapy.

Baseline drift spectra are used for quantitative and qualitative analysis, which can easily lead to inaccurate or even wrong results. Although there are several baseline correction methods based on penalized least squares, they all have one or more parameters that must be optimized by users. For this purpose, an automatic baseline correction method based on penalized least squares is proposed in this paper. The algorithm first linearly expands the ends of the spectrum signal, and a Gaussian peak is added to the expanded range. Then, the whole spectrum is corrected by the adaptive smoothness parameter penalized least squares (asPLS) method, that is, by turning the smoothing parameter λ of asPLS to obtain a different root-mean-square error (RMSE) in the extended range, the optimal λ is selected with minimal RMSE. Finally, the baseline of the original signal is well estimated by asPLS with the optimal λ. The paper concludes with the experimental results on the simulated spectra and measured infrared spectra, demonstrating that the proposed method can automatically deal with different types of baseline drift.

An automated camera exposure control method, which allows a two-camera stereo-digital image correlation (stereo-DIC) system to capture high-quality speckle image pairs, is presented for accuracy-enhanced stereo-DIC measurement. By using this method, the two synchronized cameras can automatically determine the optimal camera exposure and ideal average grayscale for capturing the optimal reference image pair in the reference state. Furthermore, high-quality deformed image pairs can be recorded during the test by adaptively adjusting the camera exposure in case of serious ambient light variations. Validation tests, including varying illumination tests and translation tests, were performed to verify the effectiveness and robustness of this method. Experimental results indicate that the proposed method overperforms the existing stereo-DIC technique with empirically determined fixed camera exposure time. The practicality of the proposed automated camera exposure control method was verified using real high-temperature experiments.

At present, the understanding of structural failure and energy analysis of sandstone under hydrofracture is still insufficient. This time, we selected the sandstone in Chongqing Three Gorges Reservoir Area as the main analysis object to discuss and compare the characteristics of conventional uniaxial (triaxial) compression strength test and uniaxial (triaxial) compression hydraulic fracturing strength test and conduct instability analysis from the perspective of energy. Based on the mechanical characteristics and parameters about the uniaxial (triaxial) compressive strength test and uniaxial (triaxial) compressive hydrofracture strength test, we focus on the analysis of the evolution rules of the hydraulic pressure-strain curve, analyzing the criteria of crack expanding and instability by using energy principle. According to the viewpoint of fracture mechanics, the fracture morphology and failure type of sandstone under hydrofracture were discussed. The test results show that the deformation evolution rules of rock hydrofracture can be divided into four stages, including the characteristics of pore fissure water injection stage (OA), the elastic deformation stage (AB), the volume expansion stage (BC), and global rupture stage (CD). Using the P/C modulus (the ratio of hydraulic pressure and cohesive force, abbreviated as P/C), the ability of hydraulic pressure overcoming cohesive force can be evaluated during hydrofracture. Using energy variables (expressed by Ek) about crack expanding from beginning to end, the unexpanded state, critical state, unstable state, and unstable failure of crack can be estimated. There is an interaction between tensile deformation and shear deformation from the crack initial stage to crack expanding stage.

Sagittal craniosynostosis, a congenital cranial suture disorder, is treated with spring-assisted cranioplasty (SAC), but optimal surgical parameters remain unclear. This study explores computational models to predict surgical outcomes of SAC by linking biomechanics with bone regeneration and cranial remodeling. Fifteen 3-week-old Sprague–Dawley (SD) rats underwent SAC with nickel-titanium springs (0–100 g forces). Bone regeneration was tracked via fluorescence labeling, while micro-CT scans measured cephalic index (CI), bone mineral density (BMD), and bone volume fraction (BV/TV). Finite element analysis (FEA) simulated stress and strain distributions. Regression models were established to predict the relationship between mechanical indicators and surgical outcomes. The 50 g group achieved optimal bone regeneration and cranial correction, while > 80 g forces risked bone damage. FEA indicates stress and strain over the bone are influenced by spring force, rat geometry, and bone density. Regression analysis revealed linear strain-CI relationships and quadratic strain-BV/TV and strain-BMD relationship. Moderate spring force (50 g) or strain (1.0%) enhances osteogenesis without structural compromise. Computational models provide a biomechanically grounded framework for SAC optimization, advancing precision treatment for sagittal craniosynostosis. Future studies should validate findings in disease-specific models and assess long-term outcomes.

Resolvin D1 (RvD1) prompts inflammation resolution and regulates immune responses. We explored the effect of RvD1 on systemic lupus erythematosus (SLE) and investigated the correlation between RvD1 and Treg/Th17 imbalance, which is one of the major factors contributing to the pathogenesis of disease. SLE patients and healthy controls were recruited to determine plasma RvD1 levels. MRL/ lpr lupus model was used to verify rescue of the disease phenotype along with Treg/Th17 ratio. Purified naive CD4+ T cells were used to study the effect of RvD1 on Treg/Th17 differentiation in vitro . Furthermore, small RNA Sequencing and transfection were performed successively to investigate downstream microRNAs. The result showed that the RvD1 level was significantly lower in active SLE patients compared with inactive status and controls. Moreover, The SLE disease activity index (SLEDAI) score had a significant negative correlation with RvD1 level. As expected, RvD1 treatment ameliorated disease phenotype and inflammatory response, improved the imbalanced Treg/Th17 in MRL/ lpr mice. In addition, RvD1 increased Treg while reduced Th17 differentiation in vitro . Furthermore, miR-30e-5p was verified to modulate the Treg/Th17 differentiation from naïve CD4+ T cells as RvD1 downstream microRNA. In conclusion, RvD1 effectively ameliorates SLE progression through up-regulating Treg and down-regulating Th17 cells via miR-30e-5p.

Objectives Research indicates that low doses of interleukin-2 (IL-2) can effectively mitigate Rheumatoid arthritis (RA) symptoms by promoting Treg cells, while high doses may enhance immune responses and exacerbate the disease. Consequently, this study employed mutated IL-2 to minimize its impact on CD8 + T and NK cell activation while preserving its influence on Treg cells. Methods We used a previously published mutation sites to construct the murine IL-2 mutants by overlap PCR. Then we assessed its impact on the proliferation and functionality of Treg cells by flow cytometry and PCR. The synergistic effects of mutated IL-2 and MSC on collagen-induced arthritis (CIA) in mice were evaluated through the infusion of lentiviral-transduced umbilical cord-derived mesenchymal stromal cell (UC-MSC) for CIA treatment and through pathological section staining to assess inflammatory joint injury, cartilage destruction, and osteoclast infiltration. Results Mutant IL-2 demonstrated targeted enhancement of both the proportion and proliferative activity of Treg cells with a diminished capacity to stimulate the proliferation of CD8 + T cells and NK cells relative to wild-type IL-2. Moreover, MSC-mutant IL-2 significantly augmented the proportion of Treg cells compared to either MSC or mutant IL-2 in isolation. Treatment with MSC-mutant IL-2 infusion in CIA mice ameliorated arthritis symptoms and reduced inflammatory infiltration and cartilage damage in their joints. Conclusion Mutant IL-2 enhances Treg function and proliferation while exerting reduced effects on CD8 + T and NK cell activation. MSC expressing mutant IL-2 demonstrates therapeutic benefits in CIA by increasing the proportion of Treg cells and reducing the proportion of CD8 + T cells.

Background Metastasis of cancer causes more than 90% of cancer deaths and is severely damaging to human health. In recent years, several studies have linked sarcopenia to shorter survival in patients with metastatic cancer. Several predictive models exist to predict mortality in patients with metastatic cancer, but have reported limited accuracy. Methods We systematically searched Medline, EMBASE, and the Cochrane Library for articles published on or before October 14, 2022. Pooled Hazard Ratio (HR) estimates with 95% confidence intervals (CIs) were calculated using a random effects model. The primary outcome was an increased risk of death or tumor progression in patients with metastatic cancer, which is expressed as progression-free survival (PFS). In addition, we performed subgroup analyses and leave-one-out sensitivity analyses to explore the main sources of heterogeneity and the stability of the results. Results Sixteen retrospective cohort studies with 1,675 patients were included in the 888 papers screened. The results showed that sarcopenia was associated with lower progression-free survival (HR = 1.56, 95% CI = 1.19–2.03, I2 = 76.3%, P  < 0.001). This result was further confirmed by trim-and-fill procedures and leave-one-out sensitivity analysis. Conclusions This study suggests that sarcopenia may be a risk factor for reduced progression-free survival in patients with metastatic cancer. Further studies are still needed to explain the reason for this high heterogeneity in outcome. Trial registration CRD42022325910.

To explore the molecular network mechanism of Celastrol in the treatment of rheumatoid arthritis (RA) based on a novel strategy (integrated systems pharmacology, proteomics, transcriptomics and single-cell transcriptomics). Firstly, the potential targets of Celastrol and RA genes were predicted through the database, and the Celastrol-RA targets were obtained by taking the intersection. Then, transcriptomic data and proteomic data of Celastrol treatment of RA were collected. Subsequently, Celastrol-RA targets, differentially expressed genes, and differentially expressed proteins were imported into Metascape for enrichment analysis, and related networks were constructed. Finally, the core targets of Celastrol-RA targets, differentially expressed genes, and differentially expressed proteins were mapped to synoviocytes of RA mice to find potential cell populations for Celastrol therapy. A total of 195 Celastrol-RA targets, 2068 differential genes, 294 differential proteins were obtained. The results of enrichment analysis showed that these targets, genes and proteins were mainly related to extracellular matrix organization, TGF-β signaling pathway, etc. The results of single cell sequencing showed that the main clusters of these targets, genes, and proteins could be mapped to RA synovial cells. For example, Mmp9 was mainly distributed in Hematopoietic cells, especially in Ptprn+fibroblast. The results of molecular docking also suggested that Celastrol could stably combine with molecules predicted by network pharmacology. In conclusion, this study used systems pharmacology, transcriptomics, proteomics, single-cell transcriptomics to reveal that Celastrol may regulate the PI3K/AKT signaling pathway by regulating key targets such as TNF and IL6, and then play an immune regulatory role.