Nanofiltration (NF) is an effective method for removing various emerging pollutants in drinking water. However, its conventional application, primarily adapted from desalination practices, faces challenges such as stringent pretreatment requirements, high energy consumption, and severe membrane fouling. To address these issues, we modified the NF process by transitioning from the traditional spiral-wound configuration to a submerged flat-sheet configuration and incorporating riverbank filtration (RBF) as a pretreatment. Experimental results demonstrated that the RBF-NF system could selectively remove natural organic matter (60.6 %) and various trace organic compounds (30.7 %–68.0 %), without the losses of beneficial ions. Additionally, the RBF-NF system reduced the risk of microbial regrowth in treated water by effectively lowering assimilable organic carbon and phosphorus levels, with removal of 52.1 % and 35.0 %, respectively. More importantly, a membrane biofilm naturally developed on the NF membrane surface over a 6-month filtration period, which facilitated the self-cleaning of the NF by biodegrading foulants and loosening the fouling cake structure. This resulted in stabilized filtration without an increase in transmembrane pressure, highlighting the potential for cleaning-free and low-maintenance operation. Additionally, the RBF-NF process reduced energy consumption by 94.6 % and carbon emissions by 87.4 % compared to traditional NF processes, primarily through the reduction of driving pressure and the elimination of crossflow. These findings demonstrate that RBF-NF is an efficient, chemical-free, and nature-based water treatment technology with significant operational and environmental benefits.

Rationale: Chronic inflammation plays an important role in alveolar tissue damage in emphysema, but the underlying immune alterations and cellular interactions are incompletely understood. Objectives: To explore disease-specific pulmonary immune cell alterations and cellular interactions in emphysema. Methods: We used single-cell mass cytometry (CyTOF) to compare the immune compartment in alveolar tissue from 15 patients with severe emphysema and 5 control subjects. Imaging mass cytometry (IMC) was applied to identify altered cell-cell interactions in alveolar tissue from patients with emphysema (n = 12) compared with control subjects (n = 8). Measurements and Main Results: We observed higher percentages of central memory CD4 T cells in combination with lower proportions of effector memory CD4 T cells in emphysema. In addition, proportions of cytotoxic central memory CD8 T cells and CD127+CD27+CD69- T cells were higher in emphysema, the latter potentially reflecting an influx of circulating lymphocytes into the lungs. Central memory CD8 T cells, isolated from alveolar tissue from patients with emphysema, exhibited an IFN-γ response upon anti-CD3 and anti-CD28 activation. Proportions of CD1c+ dendritic cells, expressing migratory and costimulatory markers, were higher in emphysema. Importantly, IMC enabled us to visualize increased spatial colocalization of CD1c+ dendritic cells and CD8 T cells in emphysema in situ. Conclusions: Using CyTOF, we characterized the alterations of the immune cell signature in alveolar tissue from patients with chronic obstructive pulmonary disease stage III or IV emphysema versus control lung tissue. These data contribute to a better understanding of the pathogenesis of emphysema and highlight the feasibility of interrogating the immune cell signature using CyTOF and IMC in human lung tissue. Clinical trial registered with www.clinicaltrials.gov (NCT04918706).

In this article, we’ll show how to solve the time-fractional seventh-order Lax’s Korteweg–de Vries and Kaup–Kupershmidt equations analytically using the homotopy perturbation approach, the Adomian decomposition method, and the Elzaki transformation. The KdV equation is a general integrable equation with an inverse scattering transform-based solution that arises in a variety of physical applications, including surface water waves, internal waves in a density stratified fluid, plasma waves, Rossby waves, and magma flow. Fractional derivative is described in the Caputo sense. The solutions to fractional partial differential equation is computed using convergent series. The numerical computations and graphical representations of the analytical results obtained using the homotopy perturbation and decomposition techniques. Moreover, plots that are simple to grasp are used to compare the integer order and fractional-order solutions. After only a few iterations, we may easily obtain numerical results that provide us better approximations. The exact solutions and the derived solutions were observed to be very similar. The suggested methods have also acquired the highest level of accuracy. The most prevalent and convergent techniques for resolving nonlinear fractional-order partial differential issues are the applied techniques.

Due to the increase in bacterial resistance, improving the anti-infectious immunity of the host is rapidly becoming a new strategy for the prevention and treatment of bacterial pneumonia. However, the specific lung immune responses and key immune cell subsets involved in bacterial infection are obscure. Actinobacillus pleuropneumoniae (APP) can cause porcine pleuropneumonia, a highly contagious respiratory disease that has caused severe economic losses in the swine industry. Here, using high-dimensional mass cytometry, the major immune cell repertoire in the lungs of mice with APP infection was profiled. Various phenotypically distinct neutrophil subsets and Ly-6C+ inflammatory monocytes/macrophages accumulated post-infection. Moreover, a linear differentiation trajectory from inactivated to activated to apoptotic neutrophils corresponded with the stages of uninfected, onset, and recovery of APP infection. CD14+ neutrophils, which mainly increased in number during the recovery stage of infection, were revealed to have a stronger ability to produce cytokines, especially IL-10 and IL-21, than their CD14- counterparts. Importantly, MHC-II+ neutrophils with antigen-presenting cell features were identified, and their numbers increased in the lung after APP infection. Similar results were further confirmed in the lungs of piglets infected with APP and Klebsiella pneumoniae infection by using a single-cell RNA-seq technique. Additionally, a correlation analysis between cluster composition and the infection process yielded a dynamic and temporally associated immune landscape where key immune clusters, including previously unrecognized ones, marked various stages of infection. Thus, these results reveal the characteristics of key neutrophil clusters and provide a detailed understanding of the immune response to bacterial pneumonia.

Chronic intestinal inflammation underlies inflammatory bowel disease (IBD). Previous studies indicated alterations in the cellular immune system; however, it has been challenging to interrogate the role of all immune cell subsets simultaneously. Therefore, we aimed to identify immune cell types associated with inflammation in IBD using high-dimensional mass cytometry. We analyzed 188 intestinal biopsies and paired blood samples of newly-diagnosed, treatment-naive patients (n=42) and controls (n=26) in two independent cohorts. We applied mass cytometry (36-antibody panel) to resolve single cells and analyzed the data with unbiased Hierarchical-SNE. In addition, imaging-mass cytometry (IMC) was performed to reveal the spatial distribution of the immune subsets in the tissue. We identified 44 distinct immune subsets. Correlation network analysis identified a network of inflammation-associated subsets, including HLA-DR⁺CD38⁺ EM CD4⁺ T cells, T regulatory-like cells, PD1⁺ EM CD8⁺ T cells, neutrophils, CD27⁺ TCRγδ cells and NK cells. All disease-associated subsets were validated in a second cohort. This network was abundant in a subset of patients, independent of IBD subtype, severity or intestinal location. Putative disease-associated CD4⁺ T cells were detectable in blood. Finally, imaging-mass cytometry revealed the spatial colocalization of neutrophils, memory CD4⁺ T cells and myeloid cells in the inflamed intestine. Our study indicates that a cellular network of both innate and adaptive immune cells colocalizes in inflamed biopsies from a subset of patients. These results contribute to dissecting disease heterogeneity and may guide the development of targeted therapeutics in IBD.