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Amidst the rapid advancements in materials science, the exploration of aerogel-based biomaterials has garnered extensive attention across diverse sectors, including biomedicine, energy, architecture, and sensing. Comprehensive studies have unveiled the utilization of organic, inorganic, and hybridized materials for aerogel preparation, catapulting aerogel-based biomaterials to global prominence. Endowed with distinctive properties, including low density, a hierarchical porous network, high porosity, and nanoscale micropores, aerogels have exhibited a broad spectrum of applications, particularly in the realm of tissue engineering. The deployment of aerogel-based biomaterials in tissue engineering is in a dynamic phase of development, with available reports indicating varying degrees of exploration in fields such as blood vessels, soft tissues, nerves, skin, muscles, heart, bronchial tubes, bone, and cartilage—an evolutionary process. This paper offers a comprehensive review of the evolution of aerogel properties and preparation processes, encapsulating strategic insights for the application of aerogel-based biomaterials in tissue engineering. It succinctly summarizes recent developments in tissue engineering research, emphasizing their significance. Additionally, the review outlines future prospects for the application of aerogels in tissue engineering and envisions challenges arising from current studies. Through this thorough exploration of aerogel-based biomaterials in tissue engineering, the paper aspires to make a profound impact on regenerative medicine, offering innovative and effective application strategies for biomedicine.

Abstract Analyzing the influence of tourism on carbon emission has significant implications for promoting the sustainable development of tourism. Based on the panel data of 31 tourist cities in China from 2005 to 2022, this study utilizes a structural equation model to explore the carbon reduction effect of tourism development and its influencing mechanism. The results show that: (1) The overall carbon emission efficiency of tourism cities first decreased and then increased, rised to a peak of 0.923 in 2022. (2) Tourism development has a significant positive impact on carbon emission efficiency, and there are three influence paths: tourism → environmental regulation → carbon emission efficiency, tourism → environmental regulation → industrial structure → carbon emission efficiency, and tourism → industrial structure → carbon emission efficiency. (3) The influence of tourism development on carbon emission efficiency mainly depends on the direct effect, and the development of tourism also indirectly affect the industrial structure. Environmental regulation also mainly depends on the direct effect on carbon emission efficiency. (4) Foreign direct investment lead to the reduction of carbon emission efficiency in both direct and indirect aspects.

Abstract Background Characterizing cancer molecular subtypes is crucial for improving prognosis and individualized treatment. Integrative analysis of multi-omics data has become an important approach for disease subtyping, yielding better understanding of the complex biology. Current multi-omics integration tools and methods for cancer subtyping often suffer challenges of high computational efficiency as well as the problem of weight assignment on data types. Results Here, we present an efficient multi-omics integration via weighted affinity and self-diffusion (MOSD) to dissect cancer heterogeneity. MOSD first construct local scaling affinity on each data type and then integrate all affinities by weighted linear combination, followed by the self-diffusion to further improve the patients’ similarities for the downstream clustering analysis. To demonstrate the effectiveness and usefulness for cancer subtyping, we apply MOSD across ten cancer types with three measurements (Gene expression, DNA methylation, miRNA). Conclusions Our approach exhibits more significant differences in patient survival and computationally efficient benchmarking against several state-of-art integration methods and the identified molecular subtypes reveal strongly biological interpretability. The code as well as its implementation are available in GitHub: https://github.com/DXCODEE/MOSD .

BackgroundIn elderly individuals suffering from hip fractures, a prolonged hospital length of stay (PLOS) not only heightens the probability of patient complications but also amplifies mortality risks. Yet, most elderly hip fracture patients present compromised baseline health conditions. Additionally, PLOS leads to increased expenses for patient treatment and care, while also diminishing hospital turnover rates. This, in turn, jeopardizes the prompt allocation of beds for urgent cases.MethodsA retrospective study was carried out from October 2021 to November 2023 on 360 elderly hip fracture patients who underwent surgical treatment at West China Hospital. The 75th percentile of the total patient cohort’s hospital stay duration, which was 12 days, was used to define prolonged hospital length of stay (PLOS). The cohort was divided into training and testing datasets with a 70:30 split. A predictive model was developed using the random forest algorithm, and its performance was validated and compared with the Lasso regression model.ResultsOut of 360 patients, 103 (28.61%) experienced PLOS. A Random Forest classification model was developed using the training dataset, identifying 10 essential variables. The Random Forest model achieved perfect performance in the training set, with an area under the curve (AUC), balanced accuracy, Kappa value, and F1 score of 1.000. In the testing set, the model’s performance was assessed with an AUC of 0.846, balanced accuracy of 0.7294, Kappa value of 0.4325, and F1 score of 0.6061.ConclusionThis study aims to develop a prognostic model for predicting delayed discharge in elderly patients with hip fractures, thereby improving the accuracy of predicting PLOS in this population. By utilizing machine learning models, clinicians can optimize the allocation of medical resources and devise effective rehabilitation strategies for geriatric hip fracture patients. Additionally, this method can potentially improve hospital bed turnover rates, providing latent benefits for the healthcare system.

NAD(P)HX dehydratase (NAXD) gene is one of the key enzymes encoding the nicotinamide nucleotide repair system, reportedly associated with Encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy, 2 (PEBEL2). Here, we generated an induced pluripotent stem cell (iPSC) line from the dermal fibroblasts (HDFs) of a PEBEL2 patient who carried biallelic mutations, c.101_102delTA(p.Thr35Phefs*63) and c.318C > G (p.Ile160Met) in NAXD. These iPSCs showed stable amplification in vitro, expressed pluripotent markers, and differentiated spontaneously into three germ layers, as well as NAXD mutations with normal karyotype.

Drosophila spermatogenesis involves the renewal of germline stem cells, meiosis of spermatocytes, and morphological transformation of spermatids into mature sperm. We previously demonstrated that Ocnus (ocn) plays an essential role in spermatogenesis. The ValRS-m (Valyl-tRNA synthetase, mitochondrial) gene was down-regulated in ocn RNAi testes. Here, we found that ValRS-m-knockdown induced complete sterility in male flies. The depletion of ValRS-m blocked mitochondrial behavior and ATP synthesis, thus inhibiting the transition from spermatogonia to spermatocytes, and eventually, inducing the accumulation of spermatogonia during spermatogenesis. To understand the intrinsic reason for this, we further conducted transcriptome-sequencing analysis for control and ValRS-m-knockdown testes. The differentially expressed genes (DEGs) between these two groups were selected with a fold change of ≥2 or ≤1/2. Compared with the control group, 4725 genes were down-regulated (dDEGs) and 2985 genes were up-regulated (uDEGs) in the ValRS-m RNAi group. The dDEGs were mainly concentrated in the glycolytic pathway and pyruvate metabolic pathway, and the uDEGs were primarily related to ribosomal biogenesis. A total of 28 DEGs associated with mitochondria and 6 meiosis-related genes were verified to be suppressed when ValRS-m was deficient. Overall, these results suggest that ValRS-m plays a wide and vital role in mitochondrial behavior and spermatogonia differentiation in Drosophila.

Calcium silicate-based cement is a promising material for filling root canals. However, it has several drawbacks to its clinical application, including difficult operation and low curing strength. In this study, we successfully prepared an ultrafine tricalcium silicate powder and investigated the effects of this ultrafine powder on the performance of the premixed tricalcium silicate cement, including the curing process, setting time, hydration products, microstructure, injectivity, fluidity, and compressive strength. The results demonstrate that the addition of ultrafine tricalcium silicate powder alters the hydration product content and product morphology of the premixed cement. By increasing the content of the ultrafine powder, the injectable property of the cement can be increased to more than 95%, the fluidity can be increased from 18 mm to 35 mm, and the curing time can be shortened from 13 h to 11 h. Notably, the addition of the ultrafine powder greatly enhances the compressive strength of the hardened cement, which increases from 20.6 MPa to 51.0 MPa. These results indicate that altering the particle size distribution of the powder is an effective method for enhancing the physicochemical and mechanical properties of tricalcium silicate cement as a root canal filling material.

Maintaining precise synaptic contacts between neuronal partners is critical to ensure the proper functioning of the mammalian central nervous system (CNS). Diverse cell recognition molecules, such as classic cadherins (Cdhs), are part of the molecular machinery mediating synaptic choices during development and synaptic maintenance. Yet, the principles governing neuron-neuron wiring across diverse CNS neuron types remain largely unknown. The retinotectal synapses, connections from the retinal ganglion cells (RGCs) to the superior collicular (SC) neurons, offer an ideal experimental system to reveal molecular logic underlying synaptic choices and formation. This is due to the retina's unidirectional and laminar-restricted projections to the SC and the large databases of presynaptic RGC subtypes and postsynaptic SC neuronal types. Here, we focused on determining the role of Type II Cdhs in wiring the retinotectal synapses. We surveyed Cdhs expression patterns at neuronal resolution and revealed that Cdh13 is enriched in the wide-field neurons in the superficial SC (sSC). In either the Cdh13 null mutant or selective adult deletion within the wide-field neurons, there is a significant reduction of spine densities in the distal dendrites of these neurons in both sexes. Additionally, Cdh13 removal from presynaptic RGCs reduced dendritic spines in the postsynaptic wide-field neurons. Cdh13-expressing RGCs use differential mechanisms than aRGCs and On-Off Direction-Selective Ganglion Cells (ooDSGCs) to form specific retinotectal synapses. The results revealed a selective transneuronal interaction mediated by Cdh13 to maintain proper retinotectal synapses in vivo. [ABSTRACT FROM AUTHOR]

Based on panel data from 277 cities in China from 2003 to 2019, this paper uses a multi-period difference-in-differences (DID) model to analyze the effect of civilized city construction on urban carbon emission intensity. The findings of the research are as follows: Firstly, the construction of civilized cities is conducive to curbing the carbon emission intensity of cities, and the construction of civilized cities has reduced urban carbon emission intensity by 14.5%. Secondly, this inhibitory effect can be achieved by optimizing the industrial structure, reducing urban energy consumption, and improving technological innovation. Thirdly, the impact of civilized city construction on urban carbon emissions varies significantly depending on urban location, urban administrative level, urban resource endowment, and urban cultural tourism resources. In addition, the construction of civilized cities in China has resulted in a reduction of carbon emission intensity by 13.2% in non-resource-based cities, and tourist cities have witnessed a 16.8% decrease in carbon emission intensity due to the construction of civilized cities. Finally, based on the analysis results, some suggestions are put forward for promoting the construction of civilized cities in China to reduce carbon emission intensity. [ABSTRACT FROM AUTHOR]

Abstract Background Liquid biopsies, for example, exosomal circular RNA (circRNA) can be used to assess potential predictive markers for hepatocellular carcinoma (HCC) in patients after curative resection. This study aimed to search for effective prognostic biomarkers for HCC in patients after surgical resection based on exosomal circRNA expression profiles. We developed two nomograms incorporating circRNAs to predict the postoperative recurrence-free survival (RFS) and overall survival (OS) of HCC patients. Method Plasma exosomes isolated from HCC patients and healthy individuals were used for circRNA microarray analysis to explore differentially expressed circRNAs. Pearson correlation analysis was used to evaluate the correlation between circRNAs and clinicopathological features. Cox regression analysis was used to explore the correlation between circRNA and postoperative survival time as well as recurrence time. A nomogram based on circRNA and clinicopathological characteristics was established and further evaluated to predict prognosis and recurrence. Result Among 60 significantly upregulated circRNAs and 25 downregulated circRNAs, hsa_circ_0029325 was selected to verify its power for predicting HCC outcomes. The high expression level of exosomal hsa_circ_0029325 was significantly correlated with OS (P = 0.001, HR = 2.04, 95% CI 1.41–3.32) and RFS (P = 0.009, HR = 1.62, 95% CI 1.14–2.30). Among 273 HCC patients, multivariate regression analysis showed that hsa_circ_0029325 (HR = 1.96, 95% CI 1.21–3.18), tumor size (HR = 2.11, 95% CI 1.33–3.32), clinical staging (HR = 2.31, 95% CI 1.54–3.48), and tumor thrombus (HR = 1.74, 95% CI 1.12–2.7) were independent risk factors for poor prognosis in HCC patients after radical resection. These independent predictors of prognosis were incorporated into the two nomograms. The AUCs under the 1-year, 3-year, and 5-year survival and recurrence curves of the OS and RFS nomograms were 0.755, 0.749, and 0.742 and 0.702, 0.685, and 0.642, respectively. The C-index, calibration curves, and clinical decision curves showed that the two prediction models had good predictive performance. These results were verified in the validation cohort with 90 HCC patients. Conclusion Our study established two reliable nomograms for predicting recurrence and prognosis in HCC patients. We also show that it is feasible to screen potential predictive markers for HCC after curative resection through exosomal circRNA expression profile analysis.

Abstract Osteoarthritis is a highly prevalent progressive joint disease that still requires an optimal therapeutic approach. Intermittent fasting is an attractive dieting strategy for improving health. Here this study shows that intermittent fasting potently relieves medial meniscus (DMM)‐ or natural aging‐induced osteoarthritic phenotypes. Osteocytes, the most abundant bone cells, secrete excess neuropeptide Y (NPY) during osteoarthritis, and this alteration can be altered by intermittent fasting. Both NPY and the NPY‐abundant culture medium of osteocytes (OCY‐CM) from osteoarthritic mice possess pro‐inflammatory, pro‐osteoclastic, and pro‐neurite outgrowth effects, while OCY‐CM from the intermittent fasting‐treated osteoarthritic mice fails to induce significant stimulatory effects on inflammation, osteoclast formation, and neurite outgrowth. Depletion of osteocyte NPY significantly attenuates DMM‐induced osteoarthritis and abolishes the benefits of intermittent fasting on osteoarthritis. This study suggests that osteocyte NPY is a key contributing factor in the pathogenesis of osteoarthritis and intermittent fasting represents a promising nonpharmacological antiosteoarthritis method by targeting osteocyte NPY.

Abstract Background Major depressive disorder (MDD) is a common but severe psychiatric illness characterized by depressive mood and diminished interest. Both nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 1 (NLRP1) inflammasome and autophagy have been reported to implicate in the pathological processes of depression. However, the mechanistic interplay between NLRP1 inflammasome, autophagy, and depression is still poorly known. Methods Animal model of depression was established by chronic social defeat stress (CSDS). Depressive-like behaviors were determined by social interaction test (SIT), sucrose preference test (SPT), open field test (OFT), forced swim test (FST), and tail-suspension test (TST). The protein expression levels of NLRP1 inflammasome complexes, pro-inflammatory cytokines, phosphorylated-phosphatidylinositol 3-kinase (p-PI3K)/PI3K, phosphorylated-AKT (p-AKT)/AKT, phosphorylated-mechanistic target of rapamycin (p-mTOR)/mTOR, brain-derived neurotrophic factor (BDNF), phosphorylated-tyrosine kinase receptor B (p-TrkB)/TrkB, Bcl-2-associated X protein (Bax)/B-cell lymphoma-2 (Bcl2) and cleaved cysteinyl aspartate-specific proteinase-3 (caspase-3) were examined by western blotting. The mRNA expression levels of pro-inflammatory cytokines were tested by quantitative real-time PCR. The interaction between proteins was detected by immunofluorescence and coimmunoprecipitation. Neuronal injury was assessed by Nissl staining. The autophagosomes were visualized by transmission electron microscopy. Nlrp1a knockdown was performed using an adeno-associated virus (AAV) vector containing Nlrp1a–shRNA–eGFP infusion. Results CSDS exposure caused a bidirectional change in hippocampal autophagy function, which was activated in the initial period but impaired at the later stage. In addition, CSDS exposure increased the expression levels of hippocampal NLRP1 inflammasome complexes, pro-inflammatory cytokines, p-PI3K, p-AKT and p-mTOR in a time-dependent manner. Interestingly, NLRP1 is immunoprecipitated with mTOR but not PI3K/AKT and CSDS exposure facilitated the immunoprecipitation between them. Hippocampal Nlrp1a knockdown inhibited the activity of PI3K/AKT/mTOR signaling, rescued the impaired autophagy and ameliorated depressive-like behavior induced by CSDS. In addition, rapamycin, an autophagy inducer, abolished NLRP1 inflammasome-driven inflammatory reactions, alleviated depressive-like behavior and exerted a neuroprotective effect. Conclusions Autophagy dysfunction contributes to NLRP1 inflammasome-linked depressive-like behavior in mice and the regulation of autophagy could be a valuable therapeutic strategy for the management of depression.

Obesity is a multifactorial chronic inflammatory metabolic disorder, with pathogenesis influenced by genetic and non-genetic factors such as environment and diet. Intestinal microbes and their metabolites play significant roles in the occurrence and development of obesity by regulating energy metabolism, inducing chronic inflammation, and impacting intestinal hormone secretion. Epigenetics, which involves the regulation of host gene expression without changing the nucleotide sequence, provides an exact direction for us to understand how the environment, lifestyle factors, and other risk factors contribute to obesity. DNA methylation, as the most common epigenetic modification, is involved in the pathogenesis of various metabolic diseases. The epigenetic modification of the host is induced or regulated by the intestinal microbiota and their metabolites, linking the dynamic interaction between the microbiota and the host genome. In this review, we examined recent advancements in research, focusing on the involvement of intestinal microbiota and DNA methylation in the etiology and progression of obesity, as well as potential interactions between the two factors, providing novel perspectives and avenues for further elucidating the pathogenesis, prevention, and treatment of obesity.