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The lung is an organ that is directly exposed to the external environment. Given the large surface area and extensive ventilation of the lung, it is prone to exposure to airborne substances, such as pathogens, allergens, chemicals, and particulate matter. Highly elaborate and effective mechanisms have evolved to protect and maintain homeostasis in the lung. Despite these sophisticated defense mechanisms, the respiratory system remains highly susceptible to environmental challenges. Because of the impact of respiratory exposure on human health and disease, there has been considerable interest in developing reliable and predictive in vitro model systems for respiratory toxicology and basic research. Human air-liquid-interface (ALI) organotypic airway tissue models derived from primary tracheobronchial epithelial cells have in vivo-like structure and functions when they are fully differentiated. The presence of the air-facing surface allows conducting in vitro exposures that mimic human respiratory exposures. Exposures can be conducted using particulates, aerosols, gases, vapors generated from volatile and semi-volatile substances, and respiratory pathogens. Toxicity data have been generated using nanomaterials, cigarette smoke, e-cigarette vapors, environmental airborne chemicals, drugs given by inhalation, and respiratory viruses and bacteria. Although toxicity evaluations using human airway ALI models require further standardization and validation, this approach shows promise in supplementing or replacing in vivo animal models for conducting research on respiratory toxicants and pathogens.

The traditional liquid electrolytes pose safety hazards primarily attributed to the flammability of organic solvent, whereas solid-state electrolytes can significantly enhance the safety of lithium-ion batteries. Polymer solid electrolytes are being considered as an effective solution due to their excellent flexibility and low cost, but they suffer low ionic conductivity or high interface impedance. Here, the ketone-containing allyl acetoacetate monomers were polymerized within the cellulose membrane via UV photopolymerization to prepare a cellulose-supported poly-allyl acetoacetate polymer electrolyte. The PAAA electrolyte shows the ion conductivity of 1.14 × 10−4 S cm−1 and the electrochemical stability window of 4.5 V. The Li symmetric battery can stably cycle for 1500 h at 0.1 mA cm−2. The LiFeO4‖Li cell achieves a discharge specific capacity of 160 mAh g−1 and demonstrates excellent cycling stability. Matching with Ni-rich cathodes also delivers decent performance. The designed polymer electrolyte with high ionic conductivity offers new ideas and directions for the development of future energy storage technology.

This study investigated the comparative effectiveness of unilateral biportal endoscopic discectomy (UBED) and percutaneous endoscopic lumbar discectomy (PELD) in managing lumbar disc herniation (LDH). Clinical data from 146 LDH patients treated surgically at the First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine (January 2020–January 2023) were retrospectively analyzed. Patients were categorized into UBED ( n  = 84) and PELD ( n  = 62) groups. Key metrics such as surgical time, incision length, fluoroscopy frequency, blood loss, hospital stay, complications, visual analog scale (VAS) scores, and the Oswestry Disability Index (ODI) were compared. The average age of patients in the UBED group was 53.46 ± 15.60 years, whereas the average age of patients in the PELD group was 55.61 ± 15.52 years ( P =  0.411). Their BMI was 24.17 ± 2.94 and 23.90 ± 2.61, respectively ( P =  0.558). The duration of symptoms was 10.52 ± 5.23 months in the UBED group and 11.66 ± 6.02 months in the PELD group ( P =  0.225). The surgical time was 66.67 ± 15.83 min in the UBED group and 69.11 ± 25.84 min in the PELD group ( P =  0.481). Intraoperative blood loss was 76.81 ± 26.74 ml in the UBED group and 69.44 ± 25.74 ml in the PELD group ( P =  0.096). The hospital stay was 5.39 ± 1.83 days in the UBED group and 5.11 ± 3.42 days in the PELD group ( P =  0.525). The average follow-up time was 16.46 ± 4.52 months in the UBED group and 15.71 ± 3.83 months in the PELD group ( P =  0.289). Compared with those before the operation, the VAS score, JOA score, and ODI of both groups significantly improved on the first day postoperatively, at 3 months, and at 6 months. No significant intergroup differences were noted in terms of intraoperative blood loss, hospital stay, or postoperative functional scores. Both groups showed marked postoperative improvements in functional outcomes. The postoperative satisfaction rates of patients in the UBED group and PELD group were 91.7% and 87.1%, respectively. Notably, the UBED group demonstrated a reduced fluoroscopy frequency and significantly lower rates of complications and recurrence. In terms of imaging, the disc Height of the two groups of patients showed a slight decrease after surgery, whereas the spinal canal area increased compared to before surgery, and there was no difference between the groups. UBED and PELD effectively alleviate LDH symptoms, but UBED has advantages in reducing fluoroscopy dependence, complications, and recurrence.

Photoluminescent flexible nanopaper-based Fe3+ sensors were fabricated by carbon quantum dot (CQD) grafted oxidized cellulose nanofibrils (OCNF). Transparent and tunable luminescent CQD–OCNF nanopapers were facilely synthesized from citric acid, ethanediamine and an OCNF suspension using a one-pot hydrothermal method without catalysts. The morphology and chemical structures of the CQD–OCNF nanopapers were investigated by TEM, SEM, XRD, FT-IR spectroscopy, XPS and CP/MAS 13C NMR spectroscopy. The carboxyl groups of OCNF were covalently bonded to the amino groups of the newly-formed CQDs. The resultant CQD–OCNF nanopapers presented high transparency in bright field imaging and strong blue emission under ultraviolet excitation. The CQD–OCNF nanopaper was used as a highly sensitive and selective fluorescent sensor for Fe3+ ions. This study provides a facile and effective method for fabricating luminescent CQD–OCNF nanopapers with high selectivity for the detection of Fe3+.Graphic abstract

Glutaraldehyde (GA) has been cleared by the Center for Devices and Radiological Health (CDRH) of the Food and Drug Administration (FDA) as a high-level disinfectant for disinfecting heat-sensitive medical equipment in hospitals and healthcare facilities. Inhalation exposure to GA is known to cause respiratory irritation and sensitization in animals and humans. To reproduce some of the known in vivo effects elicited by GA, we used a liquid aerosol exposure system and evaluated the tissue responses in a human in vitro airway epithelial tissue model. The cultures were treated at the air interface with various concentrations of GA aerosols on five consecutive days and changes in tissue function and structure were evaluated at select timepoints during the treatment phase and after a 7-day recovery period. Exposure to GA aerosols caused oxidative stress, inhibition of ciliary beating frequency, aberrant mucin production, and disturbance of cytokine and matrix metalloproteinase secretion, as well as morphological transformation. Some effects, such as those on goblet cells and ciliated cells, persisted following the 7-day recovery period. Of note, the functional and structural disturbances observed in GA-treated cultures resemble those found in ortho-phthaldehyde (OPA)-treated cultures. Furthermore, our in vitro findings on GA toxicity partially and qualitatively mimicked those reported in the animal and human survey studies. Taken together, observations from this study demonstrate that the human air-liquid-interface (ALI) airway tissue model, integrated with an in vitro exposure system that simulates human inhalation exposure, could be used for in vitro-based human hazard identification and the risk characterization of aerosolized chemicals.

Exposure to cigarette smoke (CS) is a known risk factor in the pathogenesis of smoking-caused diseases, such as chronic obstructive pulmonary diseases (COPD) and lung cancer. To assess the effects of CS on the function and phenotype of airway epithelial cells, we developed a novel repeated treatment protocol and comprehensively evaluated the progression of key molecular, functional, and structural abnormalities induced by CS in a human in vitro air–liquid-interface (ALI) airway tissue model. Cultures were exposed to CS (diluted with 0.5 L/min, 1.0 L/min, and 4.0 L/min clean air) generated from smoking five 3R4F University of Kentucky reference cigarettes under the International Organization for Standardization (ISO) machine smoking regimen, every other day for 4 weeks (3 days per week, 40 min/day). By integrating the transcriptomics-based approach with the in vitro pathophysiological measurements, we demonstrated CS-mediated effects on oxidative stress, pro-inflammatory cytokines and matrix metalloproteinases (MMPs), ciliary function, expression and secretion of mucins, and squamous cell differentiation that are highly consistent with abnormalities observed in airways of smokers. Enrichment analysis on the transcriptomic profiles of the ALI cultures revealed key molecular pathways, such as xenobiotic metabolism, oxidative stress, and inflammatory responses that were perturbed in response to CS exposure. These responses, in turn, may trigger aberrant tissue remodeling, eventually leading to the onset of respiratory diseases. Furthermore, changes of a panel of genes known to be disturbed in smokers with COPD were successfully reproduced in the ALI cultures exposed to CS. In summary, findings from this study suggest that such an integrative approach may be a useful tool for identifying genes and adverse cellular events caused by inhaled toxicants, like CS.

Functional MRI (fMRI) is a popular approach to investigate brain connections and activations when human subjects perform tasks. Because fMRI measures the indirect and convoluted signals of brain activities at a lower temporal resolution, complex differential equation modeling methods (e.g., Dynamic Causal Modeling) are usually employed to infer the neuronal processes and to fit the resulting fMRI signals. However, this modeling strategy is computationally expensive and remains to be mostly a confirmatory or hypothesis-driven approach. One major statistical challenge here is to infer, in a data-driven fashion, the underlying differential equation models from fMRI data. In this paper, we propose a causal dynamic network (CDN) method to estimate brain activations and connections simultaneously. Our method links the observed fMRI data with the latent neuronal states modeled by an ordinary differential equation (ODE) model. Using the basis function expansion approach in functional data analysis, we develop an optimization-based criterion that combines data-fitting errors and ODE fitting errors. We also develop and implement a block coordinate-descent algorithm to compute the ODE parameters efficiently. We illustrate the numerical advantages of our approach using data from realistic simulations and two task-related fMRI experiments. Compared with various effective connectivity methods, our method achieves higher estimation accuracy while improving the computational speed by from tens to thousands of times. Though our method is developed for task-related fMRI, we also demonstrate the potential applicability of our method (with a simple modification) to resting-state fMRI, by analyzing both simulated and real data from medium-sized networks.

In the field of remote sensing image interpretation, automatically extracting water body information from high-resolution images is a key task. However, facing the complex multi-scale features in high-resolution remote sensing images, traditional methods and basic deep convolutional neural networks are difficult to effectively capture the global spatial relationship of the target objects, resulting in incomplete, rough shape and blurred edges of the extracted water body information. Meanwhile, massive image data processing usually leads to computational resource overload and inefficiency. Fortunately, the local data processing capability of edge computing combined with the powerful computational resources of cloud centres can provide timely and efficient computation and storage for high-resolution remote sensing image segmentation. In this regard, this paper proposes PMNet, a lightweight deep learning network for edge-cloud collaboration, which utilises a pipelined multi-step aggregation method to capture image information at different scales and understand the relationships between remote pixels through horizontal and vertical spatial dimensions. Also, it adopts a combination of multiple decoding branches in the decoding stage instead of the traditional single decoding branch. The accuracy of the results is improved while reducing the consumption of system resources. The model obtained F1-score of 90.22 and 88.57 on Landsat-8 and GID remote sensing image datasets with low model complexity, which is better than other semantic segmentation models, highlighting the potential of mobile edge computing in processing massive high-resolution remote sensing image data.

Background The cadmium (Cd) present in air pollutants and cigarette smoke has the potential of causing multiple adverse health outcomes involving damage to pulmonary and cardiovascular tissue. Injury to pulmonary epithelium may include alterations in tight junction (TJ) integrity, resulting in impaired epithelial barrier function and enhanced penetration of chemicals and biomolecules. Herein, we investigated mechanisms involved in the disruption of TJ integrity by Cd exposure using an in vitro human air-liquid-interface (ALI) airway tissue model derived from normal primary human bronchial epithelial cells. Methods ALI cultures were exposed to noncytotoxic doses of CdCl 2 basolaterally and TJ integrity was measured by Trans-Epithelial Electrical Resistance (TEER) and immunofluorescence staining with TJ markers. PCR array analysis was used to identify genes involved with TJ collapse. To explore the involvement of kinase signaling pathways, cultures were treated with CdCl 2 in the presence of kinase inhibitors specific for cellular Src or Protein Kinase C (PKC). Results Noncytotoxic doses of CdCl 2 resulted in the collapse of barrier function, as demonstrated by TEER measurements and Zonula occludens-1 (ZO-1) and occludin staining. CdCl 2 exposure altered the expression of several groups of genes encoding proteins involved in TJ homeostasis. In particular, down-regulation of select junction-interacting proteins suggested that a possible mechanism for Cd toxicity involves disruption of the peripheral junctional complexes implicated in connecting membrane-bound TJ components to the actin cytoskeleton. Inhibition of kinase signaling using inhibitors specific for cellular Src or PKC preserved the integrity of TJs, possibly by preventing occludin tyrosine hyperphosphorylation, rather than reversing the down-regulation of the junction-interacting proteins. Conclusions Our findings indicate that acute doses of Cd likely disrupt TJ integrity in human ALI airway cultures both through occludin hyperphosphorylation via kinase activation and by direct disruption of the junction-interacting complex.

Exposure to cigarette smoke (CS) is strongly associated with impaired mucociliary clearance (MCC), which has been implicated in the pathogenesis of CS-induced respiratory diseases, such as chronic obstructive pulmonary diseases (COPD). In this study, we aimed to identify microRNAs (miRNAs) that are associated with impaired MCC caused by CS in an in vitro human air–liquid-interface (ALI) airway tissue model. ALI cultures were exposed to CS (diluted with 0.5 L/min, 1.0 L/min, and 4.0 L/min of clean air) from smoking five 3R4F University of Kentucky reference cigarettes under the International Organization for Standardization (ISO) machine smoking regimen, every other day for 1 week (a total of 3 days, 40 min/day). Transcriptome analyses of ALI cultures exposed to the high concentration of CS identified 5090 differentially expressed genes and 551 differentially expressed miRNAs after the third exposure. Genes involved in ciliary function and ciliogenesis were significantly perturbed by repeated CS exposures, leading to changes in cilia beating frequency and ciliary protein expression. In particular, a time-dependent decrease in the expression of miR-449a, a conserved miRNA highly enriched in ciliated airway epithelia and implicated in motile ciliogenesis, was observed in CS-exposed cultures. Similar alterations in miR-449a have been reported in smokers with COPD. Network analysis further indicates that downregulation of miR-449a by CS may derepress cell-cycle proteins, which, in turn, interferes with ciliogenesis. Investigating the effects of CS on transcriptome profile in human ALI cultures may provide not only mechanistic insights, but potential early biomarkers for CS exposure and harm.