Ulcerative colitis (UC) is a systemic disease that can involve multiple organs, and hepatobiliary diseases in UC patients are frequently observed. However, the pathogenesis of UC and its associated hepatobiliary complications remains elusive, and limited therapeutic options are available. This study revealed that disrupted hepatic lipid metabolism plays a pivotal role in driving the progression of UC and its extraintestinal hepatobiliary manifestations. Mechanistically, colitis-elevated circulating endogenous corticosterone (CORT) mediates the downregulation of hepatic LXRα-SCD1 signaling, resulting in diminished monounsaturated fatty acid (MUFA), reduced unsaturated lysophospholipids, and the accumulation of alkyl lysophospholipids, ceramide and hexosylceramide. These alterations contribute to liver lipotoxicity and, in turn, exacerbate colitis. A similar lipid profile is observed in UC patients. Importantly, pristimerin, a natural compound structurally similar to the star molecule celastrol, has been demonstrated to alleviate UC and concomitant liver injury by remodeling hepatic lipid metabolism in a microbiota-dependent manner. The gut commensal Lactobacillus johnsonii mediates the effects of PSM by activating hepatic LXRα-SCD1 signaling and increasing the potential anti-inflammation lipid species LPC20:2 and LPC20:3. This investigation suggests a novel therapeutic strategy for UC and associated liver injury based on the L. johnsonii-hepatic LXRα-SCD1 axis. This study also opens new avenues for mechanistic exploration of systemic diseases and therapeutic strategies of multi-organ comorbidity.

Background: Tripartite motif containing 59 (TRIM59) functions as an E3 ubiquitin ligase contributing to host immune responses including innate and adaptive immunity. This study investigated the influence of myeloid cell TRIM59 deletion on experimental abdominal aortic aneurysms (AAAs). Methods: Nine- to ten-week-old male, myeloid cell-specific TRIM59 deficient (Lysozyme 2 Cre + /TRIM59 flox +/+ , CKO) and TRIM59 flox +/+ (wild type, WT) mice were used in all experiments. Experimental AAAs were induced in all mice by transient intra-infrarenal aortic infusion of porcine pancreatic elastase. Experimental AAA progression was assessed via serial in vivo infrarenal ultrasonographic aortic diameter measurements and histopathologic analysis at sacrifice. Results: Major findings are summarized in the Figure. On days 7 and 14 following elastase infusion, aortic diameters were significantly larger in CKO than those in WT mice. On histological analysis, elastin degradation was enhanced in CKO mice with a trend toward aortic macrophage accumulation. Aortic accumulation of CD4 + and CD8 + T cells and B220 + B cells, as well as mural neoangiogenesis (identified by CD31 + antibody staining) were all more prominent in CKO mice. No difference in α actin-positive aortic medial smooth muscle cell depletion was noted between strains. Conclusions: Deficiency of myeloid cell TRIM59 augments progression of experimental AAAs.

Ischemic stroke is a cerebrovascular disease that activates the complement system, leading to inflammation and neuronal injury. TRIM59, an E3 ubiquitin ligase, has been extensively studied in cancer, sepsis, and myocardial infarction, and is upregulated in macrophages after ischemic stroke. This study used myeloid cell Trim59 conditional knockout and macrophage-specific Trim59 overexpression mice to investigate the role of macrophage TRIM59 in regulating complement C3 release and neuronal phagocytosis following cerebral ischemia. Myeloid cell Trim59 conditional knockout (Trim59-cKO) mice were generated and bred using the Cre-loxP system, and macrophage-specific Trim59 overexpressing (AAV-Trim59) mice were constructed via intra-bone marrow injection. Middle cerebral artery occlusion/reperfusion (MCAO/R) and photothrombotic (PT) surgery were used to mimic the cerebral ischemia in mice. RT-qPCR, ELISA and immunofluorescence staining were performed to detect the expression of complement molecules and synaptic engulfment. Neurobehavioral tests were performed during recovery phase. Western blot and co-immunoprecipitation (Co-IP) assay were utilized to analyze the effect of TRIM59 on C3 expression and its transcription factor CCAAT/enhancer binding protein β (c/EBPβ). Compared to Trim59flox/flox mice, Trim59-cKO promoted excessive expression and release of complement components C3 and C9 in macrophages after cerebral ischemia, resulting in aggravated pathological injury and reduced neuronal survival. In contrast, macrophage-specific TRIM59 overexpression reversed the above results and alleviated acute-phase injury. Furthermore, deficiency of Trim59 led to excessive macrophage-derived C3 deposition around neurons, enhanced phagocytic activity, and aggravated synaptic loss during the acute phase after MCAO/R injury, ultimately causing delayed recovery of cerebral blood flow, impaired learning and memory function, and lower survival rates during the chronic phase after PT induced ischemic stroke. The transcription factor c/EBPβ was identified as a key mediator of macrophage TRIM59-dependent regulation of C3 expression, verified by silencing of c/EBPβ in Trim59 knockout macrophages could attenuate the neuronal C3 deposition and synaptic damage. Further research shows that TRIM59 promotes K48-linked ubiquitination and proteasomal degradation of c/EBPβ through its RING domain. Macrophage TRIM59 is critical for controlling excessive complement C3 activation, release, and phagocytosis after ischemic stroke by promoting ubiquitin-mediated degradation of its transcription factor c/EBPβ, providing a potential therapeutic target for cerebral ischemia.

Ischemic stroke (IS) accounts for ~85% of all stroke cases and stands as one of the leading global causes of disability and mortality. Its pathological progression is closely intertwined with intricate inflammatory responses, among which post-stroke activated macrophages are widely recognized as the core drivers and regulators of IS pathogenesis. This review systematically elucidates the dual role of macrophages in stroke: they act as the primary drivers of the acute neuroinflammatory storm, while also serving as key regulators of neurorepair during the subacute and chronic phases. By focusing on the spatiotemporal dynamic changes, polarization regulatory mechanisms, and phenotypic/functional transition patterns of macrophages. This review provides a theoretical foundation for the development of precise therapeutic strategies that target the spatiotemporal dynamics and functional transitions of macrophages.

Allergic asthma, known for its airway hyperresponsiveness and remodeling, is a prevalent chronic respiratory disease. Recent investigations have emphasized the crucial role of ubiquitination, a post-translational modification, in the pathogenesis of allergic asthma. Ubiquitination involves the addition of ubiquitin molecules to substrates, caused their degradation or alteration in activity. Ubiquitination affects various aspects of immune cell function, such as activation of Th2 cells, B cells, and antigen-presenting cells, which are vital to allergic asthma.In this review, we explore the role of ubiquitination in modulating immune responses during allergic asthma. We discuss the interplay between ubiquitin ligases, their substrates, and the impact on immune cell function, including Th2 differentiation and Th2 cytokines production. Our study also considers the potential therapeutic outcomes of targeting ubiquitination in asthma management. By understanding the complex interplay between ubiquitination, immune cells and immune responses, we can identify new molecules for treating allergic asthma, potentially leading to more effective therapies that modulate immune responses and ameliorate disease symptoms.

Introduction: Lactobacilli are a group of Gram-positive bacteria belonging to the family Lactobacillaceae within the phylum Firmicutes. They colonize the intestinal tract and play a significant role in human health and disease treatment, serving irreplaceable functions in numerous disease domains. These include intestinal diseases (such as inflammatory bowel disease, diarrhea, colorectal cancer, etc.), viral respiratory infections, type 2 diabetes-related periodontitis, and urinary system diseases (prevention of vaginal diseases and urinary tract infections). Aim of the Review: This review focuses on the mechanisms of action of lactobacilli in diseases, the regulatory effects of diet and Chinese herbal medicine, and summarizes the impacts of Chinese herbal medicine on lactobacilli. It aims to explain the relationships among diseases, lactobacilli, and Chinese herbal medicine, providing theoretical support for promoting the research and development of related products. Methods: Literature related to lactobacilli was collected by searching the academic databases PubMed and CNKI using keywords such as characteristics of lactobacilli, biological functions, metabolic pathways, roles in diseases, mechanisms of action, and regulation by Chinese herbal medicine. Results: Based on the collected literature, this review summarizes the characteristics, biological functions, metabolic pathways, roles in diseases, and mechanisms of action of lactobacilli, as well as the regulatory effects of diet, single Chinese herbal medicines, and Chinese herbal compound formulas on the abundance of lactobacilli. Discussion: Dietary and Chinese herbal medicine interventions significantly influence the growth and reproduction of intestinal lactobacilli. A high-protein diet and specific carbohydrates can regulate lactobacilli levels, but their specific mechanisms of action remain unclear. The molecular-level interactions with host cells and the signaling pathways under different disease states are not yet fully understood. Future research could deeply analyze the molecular-level interactions between lactobacilli and host cells, clarify the key signaling pathways activated or inhibited under different disease conditions, and provide a theoretical basis for precision treatment.

Demethylzeylasteral (DMLL) is a natural compound isolated from the root of the herbal plant Tripterygium wilfordii Hook. F. It exhibits various pharmacological activities, yet the therapeutic effects against ulcerative colitis (UC) remain poorly understood. In this study, multiomics analysis revealed that DMLL alleviated DSS-induced experimental colitis by reconstructing gut microbiota and improving metabolic dysbiosis. The Bacteroidota phylum and genera of norank_f_Muribaculaceae and Ruminococcus with beneficial potential for UC were the major gut flora influenced by DMLL treatment. In terms of microbiota-derived metabolites, DMLL primarily enriched tryptophan metabolites, secondary bile acids, and nicotinamide. These compounds possess anti-inflammatory activity and protective effects for intestinal epithelial barrier, subsequently altered metabolic pathways, and improved impaired host gut homeostasis. In addition, we found significantly elevated levels of indolelactic acid (ILA) in the cecum of colitis mice and showed a strong positive correlation with UC symptoms, whereas serum levels of ILA were remarkably reduced and exhibited a negative association with UC, suggesting its dual role in colitis. Importantly, DMLL treatment effectively restored ILA levels in both the cecum and the systemic circulation. These findings provide novel mechanistic insights into the anticolitis effect of DMLL in mice, highlighting the crucial role of gut microbiota in its therapeutic action.

Bacillus Calmette-Gu & eacute;rin (BCG) immunotherapy is limited by resistance in similar to 50% of patients, linked to tumor microenvironment (TME) angiogenesis. The work explored if BCG-activated tumor-associated macrophages (TAMs) drive angiogenesis via hypoxia-inducible factor-1 alpha (HIF-1 alpha) to impair BCG efficacy. Results demonstrated that macrophages stimulated with BCG significantly enhanced the proliferation, migration, and tube formation of endothelial cells. Further mechanistic studies revealed that this pro-angiogenic effect was mediated through the activation of the NF-kappa B, PI3K/AKT and p38/MAPK signaling pathways. Activation of these pathways subsequently led to the upregulated expression of HIF-1 alpha and vascular endothelial growth factor A (VEGFA). Critically, HIF-1 alpha deficiency in macrophages effectively inhibited BCG-induced angiogenesis without exerting a significant impact on the infiltration of CD8+ T cells or B cells. Additionally, BCG stimulation enhanced the secretion of VEGF encapsulated in exosomes in an HIF-1 alpha-dependent manner, and these VEGF-enriched exosomes further facilitated the activation of endothelial cell functions. In conclusion, the present study confirms that BCG can promote tumor angiogenesis by activating macrophages to induce the release of exosome-derived VEGF through an HIF-1 alpha-dependent pathway. Targeting the HIF-1 alpha-exosome-derived VEGF (HIF-1 alpha-exoVEGF) axis holds promise as a potential strategy to overcome BCG resistance and improve its therapeutic efficacy.

Molnupiravir (MO) is a pyrimidine nucleoside anti-SARS-CoV-2 drug. MO treatment could cause mild liver injury. However, the underlying mechanism of MO-induced liver injury and the metabolic pathway of MO in vivo are unclear. In this study, metabolomics analysis and molecular biology methods were used to explore these issues. Through metabolomics analysis, it was found that the homeostasis of pyrimidine, purine, lysophosphatidylcholine (LPC), and amino acids in mice was destroyed after MO treatment. A total of 80 changed metabolites were detected. Among these changed metabolites, 4-ethylphenyl sulfate, dihydrouracil, and LPC 20:0 was related to the elevation of alkaline phosphatase (ALP), interleukin-6 (IL6), and nuclear factor kappa-B (NF-κB). The levels of 4-ethylphenyl sulfate, dihydrouracil, and LPC 20:0 in plasma were positively correlated with their levels in the liver, suggesting that these metabolites were associated with MO-induced liver injury. MO treatment could increase NHC and cytidine levels, activate cytidine deaminase (CDA), and increase LPC levels. CDA and LPC could increase the mRNA expression level of toll-like receptor (TLR). The current study indicated that the elevation of hepatic TLR may be an important reason for MO leading to the liver injury.

Bladder cancer (BLCA) is a common type of urogenital malignancy worldwide. The recurrence and metastasis of bladder cancer are closely related to angiogenesis, but the underlying mechanisms are unclear. In this study, we developed a method to predict survival outcomes among BLCA patients, which could be used to guide immunotherapy and chemotherapy. We obtained patient data from The Cancer Genome Atlas (TCGA) and identified angiogenesis-related genes from the GeneCards database. First, we used differential expression analysis and univariate Cox analysis to identify angiogenesis-related genes and used correlation analysis to generate molecular subtypes based on M2 macrophages. Next, we constructed a prognostic signature consisting of four genes (ECM1, EFEMP1, SLIT2, and PDGFRΑ), which was found to be an independent prognostic factor. Higher risk scores were associated with worse overall survival and higher expression of immune checkpoints. We also evaluated immune cell infiltration using the CIBERSORT and ssGSEA algorithms. Additionally, we performed stratification analyses, constructed a nomogram, and predicted chemotherapeutic responses based on the risk signature. Finally, we validated our findings by using qRT-PCR as well as IHC data to detect the expression levels of the four genes at mRNA and protein levels in BLCA patients and obtained results that were consistent with our predictions. Our study demonstrates the utility of a four-gene prognostic signature for prognostication in bladder cancer patients and designing personalized treatments, which could provide new avenues for personalized management of these patients.

PLAIN LANGUAGE SUMMARY The immune system plays an important role in maintaining physiology. When immune system is in disorder, there are a series of diseases such as allergy, immune deficiency diseases and persistent infections. Immune system is composed of a large number of immune cells, which plays a major role in fighting bacteria, viruses, parasites fungi, or cancer cells. There are many molecules involved in the regulation of immune balance, including TRIM59. Like other TRIM proteins, TRIM59 is important in tumor invasion and metastasis, immune response and thus pathogenesis of various immune diseases. In this study, we summarized the structure and expression regulation of TRIM59, expounded its effect and mechanism on immunity and immune-related diseases, and discussed the possibility of TRIM59 as a therapeutic target. TRIM59 is a member of the tripartite motif containing (TRIM) protein family. It functions as an E3 ubiquitin ligase through its RING domain and is expressed by multiple types of cells. Physiogically, TRIM59 is involved in development, immune response, and the invasion and metastasis of tumors. In this review, we first describe the structure, expression, and subcellular location of TRIM59. Then, we summarize emerging evidence for TRIM59 in immunological diseases including infection, vascular diseases, autoimmunity, and tumor immunity. Additionally, we discuss important molecular signaling pathways that mediate TRIM59 activity. Altogether, the accumulating evidence suggests that manipulating TRIM59 levels and activity may open an avenue for innovative therapies for immune diseases and tumors.

Chiral nanophotonic materials have emerged as ideal candidates for biosensing applications due to their exceptional sensitivity. However, the inability to directly visualize chiral signals limits their broader application, particularly in disease diagnosis and treatment. In this study, we introduce a chiral nanocomposite based on upconversion nanoparticles (UCNPs), denoted UCNPs@L-POM, that exhibits both upconversion luminescence (UCL) and circular dichroism (CD) signals. This dual-signal system enables ultrasensitive detection and in vivo imaging of ·OH. The detection limits for UCL and CD signals in aqueous solution are 6.258 and 0.912 μM, respectively. This dual-mode sensing approach is also effective at the cellular level. As a demonstration, UCNPs@L-POM enables in situ imaging diagnosis of rheumatoid arthritis (RA), characterized by elevated levels of ·OH expression. Additionally, through the oxidation reaction induced by ·OH, UCNPs@L-POM effectively alleviates paw inflammation and promotes the healing of RA. This work offers new prospects for biological applications of chiral nanocomposites.

Abstract Background Cancer‐associated cachexia (CAC) is a debilitating syndrome associated with poor quality of life and reduced life expectancy of cancer patients. CAC is characterized by unintended body weight reduction due to muscle and adipose tissue loss. A major hallmark of CAC is systemic inflammation. Several non‐steroidal anti‐inflammatory drugs (NSAIDs) have been suggested for CAC treatment, yet no single medication has proven reliable. R‐ketorolac (RK) is the R‐enantiomer of a commonly used NSAID. The effect of RK on CAC has not yet been evaluated. Methods Ten‐ to 11‐week‐old mice were inoculated with C26 or CHX207 cancer cells or vehicle control (phosphate‐buffered saline [PBS]). After cachexia onset, 2 mg/kg RK or PBS was administered daily by oral gavage. Body weight, food intake and tumour size were continuously measured. At study endpoints, blood was drawn, mice were sacrificed and tissues were excised. Immune cell abundance was analysed using a Cytek® Aurora spectral flow cytometer. Cyclooxygenase (COX) activity was determined in lung homogenates using a fluorometric kit. Muscle tissues were analysed for mRNA and protein expression by quantitative real‐time PCR and western blotting analysis, respectively. Muscle fibre size was determined on histological slides after haematoxylin/eosin staining. Results Ten‐day survival rate of C26‐bearing animals was 10% while RK treatment resulted in a 100% survival rate (P = 0.0009). Chemotherapy resulted in a 10% survival rate 14 days after treatment initiation, but all mice survived upon co‐medication with RK and cyclophosphamide (P = 0.0001). Increased survival was associated with a protection from body weight loss in C26 (−0.61 ± 1.82 vs. −4.48 ± 2.0 g, P = 0.0004) and CHX207 (−0.49 ± 0.33 vs. −2.49 ± 0.93 g, P = 0.0003) tumour‐bearing mice treated with RK, compared with untreated mice. RK ameliorated musculus quadriceps (−1.7 ± 7.1% vs. −27.8 ± 8.3%, P = 0.0007) and gonadal white adipose tissue (−18.8 ± 49% vs. −69 ± 15.6%, P = 0.094) loss in tumour‐bearing mice, compared with untreated mice. Mechanistically, RK reduced circulating interleukin‐6 (IL‐6) concentrations from 334 ± 151 to 164 ± 123 pg/mL (P = 0.047) in C26 and from 93 ± 39 to 35 ± 6 pg/mL (P = 0.0053) in CHX207 tumour‐bearing mice. Moreover, RK protected mice from cancer‐induced T‐lymphopenia (+1.8 ± 42% vs. −49.2 ± 12.1% in treated vs. untreated mice, respectively). RK was ineffective in ameliorating CAC in thymus‐deficient nude mice, indicating that the beneficial effect of RK depends on T‐cells. Conclusions RK improved T‐lymphopenia and decreased systemic IL‐6 concentrations, resulting in alleviation of cachexia and increased survival of cachexigenic tumour‐bearing mice, even under chemotherapy and independent of COX inhibition. Considering its potential, we propose that the use of RK should be investigated in patients suffering from CAC.

Background In tropical and subtropical region, Cassia (Fabaceae) is widely distributed, and many species of this genus are used for medicinal purposes such as hypertension, hyperlipidemia, obesity, diabetes in China and India. However, there are limited reviews describing the biological activity on metabolic syndrome associated with Cassia species. Methods Online databases including SciFinder, Web of Science, PubMed, Science Direct, ACS Journals, Springer, Tailor & Francis, Wiley, The Plant List Database, Google Scholar, and China National Knowledge Infrastructure (CNKI), were consulted by using “Cassia”, “决明属(Cassia)”, “Senna”, “ethnobotany”, “traditional use”, “ethnomedicine”, “phytochemistry”, “Lipid Metabolism”, “metabolic syndrome”, “anti-obesity”, “anti-diabetes” and “anti- hyperlipidemia” as keywords. Results Extracts, a total of 23 non-volatile natural products and one peptide from 18 Cassia species have demonstrated efficacy in treating metabolic syndrome and related complications. Sixty-five commercial Chinese polyherbal preparation with ingredients of Cassia seeds or Senna leaves showed effects on MetS. Conclusions This review presents an in-depth analysis of the chemical constituents and medicinal properties of the ethnomedicinally important Cassia species on metabolic syndrome and related complications such as hyperlipidemia, obesity and diabetes etc. Overall, most publications focused on species of C. angustifolia, C. auriculate, C. fistula, C. glauca, and C. obtusifolia. It is not fully understood how chemical compounds interact with the corresponding target proteins. In spite of this, preliminary data from other Cassia species indicate the potential of this genus for research on metabolic syndrome, both phytochemically, pharmacologically and clinical uses of C. species.

Chiral assemblies have become one of the most active research areas due to their versatility, playing an increasingly important role in bio-detection, imaging and therapy. In this work, chiral UCNPs/CuxOS@ZIF nanoprobes are prepared by encapsulating upconversion nanoparticles (UCNPs) and CuxOS nanoparticles (NPs) into zeolitic imidazolate framework-8 (ZIF-8). The novel excited-state energy distribution-modulated upconversion nanostructure (NaYbF4@NaYF4: Yb, Er) is selected as the fluorescence source and energy donor for highly efficient fluorescence resonance energy transfer (FRET). CuxOS NP is employed as chiral source and energy acceptor to quench upconversion luminescence (UCL) and provide circular dichroism (CD) signal. Utilizing the natural adsorption and sorting advantages of ZIF-8, the designed nanoprobe can isolate the influence of other common disruptors, thus achieve ultra-sensitive and highly selective UCL/CD dual-mode quantification of H2S in aqueous solution and in living cells. Notably, the nanoprobe is also capable of in vivo intra-tumoral H2S tracking. Our work highlights the multifunctional properties of chiral nanocomposites in sensing and opens a new vision and idea for the preparation and application of chiral nanomaterials in biomedical and biological analysis. The schematic of the preparation process of chiral UCNPs/CuxOS@ZIF nanoprobe, in vitro highly selective UCL/CD dual-mode sensing for hydrogen sulfide, and in vivo bioimaging.

Background:Tripartite motif containing 59 (TRIM59) is a ubiquitin ligase and is involved in the pathogenesis of various diseases, including cancers, sepsis, and other immune-related diseases. However, it has not been defined whether TRIM59 plays a role in ischemic stroke in mice. Methods:This study determined the influence of Trim59 deficiency on experimental stroke outcomes and the cerebral proteomic profile using myeloid cell Trim59 conditional knockout (Trim59-cKO) mice and a label-free quantitative proteomic profiling technique. The possible mechanisms by which TRIM59 affected stroke onset were elucidated by in vivo and in vitro experiments. Results:Immunofluorescence staining results showed that TRIM59 expression was up-regulated after cerebral ischemia and co-localized with macrophages. Myeloid cell Trim59 deficiency exacerbated ischemic injury on day 3 after experimental stroke. In proteomic analysis, 23 differentially expressed proteins were identified in ischemic brain of Trim59-cKO mice as compared to Trim59flox/flox mice. Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed that the differentially expressed proteins were enriched in complement and coagulation cascades. Protein-protein interaction analysis suggested the central role of clusterin in the interaction network. ELISA and Western blot assays confirmed the reduced levels of clusterin protein in the ischemic brains of Trim59-cKO mice. Further experimental results showed that clusterin was expressed in neurons. Conditional co-culture experiments of primary neurons and bone marrow-derived macrophages demonstrated that LPS stimulated macrophages to secrete complement C3. In addition, TRIM59 may affect the changes in clusterin expression in an indirect manner by influencing the secretion of complement C3 in macrophages. In vivo experiments also proved a significant increase in C3 levels in the brains of Trim59-cKO mice after ischemia. Conclusion:Myeloid cell Trim59 deficiency aggravated ischemic stroke outcomes in conjunction with a distinct cerebral proteomic profile, and the underlying mechanism may be related to the regulation of macrophage C3 expression by TRIM59.

It is crucial to detect and classify industrial heat sources for sustainable industrial development. Sustainable Development Science Satellite 1 (SDGSAT-1) thermal infrared spectrometer (TIS) data were first introduced for detecting industrial heat source production areas to address the difficulty in identifying factories with low combustion temperatures and small scales. In this study, a new industrial heat source identification and classification model using SDGSAT-1 TIS and Landsat 8/9 Operational Land Imager (OLI) data was proposed to improve the accuracy and granularity of industrial heat source recognition. First, multiple features (thermal and optical features) were extracted using SDGSAT-1 TIS and Landsat 8/9 OLI data. Second, an industrial heat source identification model based on a support vector machine (SVM) and multiple features was constructed. Then, industrial heat sources were generated and verified based on the topological correlation between the identification results of the production areas and Google Earth images. Finally, the industrial heat sources were classified into six categories based on point-of-interest (POI) data. The new model was applied to the Beijing–Tianjin–Hebei (BTH) region of China. The results showed the following: (1) Multiple features enhance the differentiation and identification accuracy between industrial heat source production areas and the background. (2) Compared to active-fire-point (ACF) data (375 m) and Landsat 8/9 thermal infrared sensor (TIRS) data (100 m), nighttime SDGSAT-1 TIS data (30 m) facilitate the more accurate detection of industrial heat source production areas. (3) Greater than 2~6 times more industrial heat sources were detected in the BTH region using our model than were reported by Ma and Liu. Some industrial heat sources with low heat emissions and small areas (53 thermal power plants) were detected for the first time using TIS data. (4) The production areas of cement plants exhibited the highest brightness temperatures, reaching 301.78 K, while thermal power plants exhibited the lowest brightness temperatures, averaging 277.31 K. The production areas and operational statuses of factories could be more accurately identified and monitored with the proposed approach than with previous methods. A new way to estimate the thermal and air pollution emissions of industrial enterprises is presented.

Photothermal therapy (PTT) has attracted much attention due to its less invasive, controllable and highly effective nature. However, PTT also suffers from intrinsic cancer resistance mediated by cell survival pathways. These survival pathways are regulated by a variety of proteins, among which heat shock protein (HSP) triggers thermotolerance and protects tumor cells from hyperthermia-induced apoptosis. Confronted by this challenge, we propose and validate here a novel MXene-based HSP-inhibited mild photothermal platform, which significantly enhances the sensitivity of tumor cells to heat-induced stress and thus improves the PPT efficacy. The Ti3C2@Qu nanocomposites are constructed by utilizing the high photothermal conversion ability of Ti3C2 nanosheets in combination with quercetin (Qu) as an inhibitor of HSP70. Qu molecules are loaded onto the nanoplatform in a pH-sensitive controlled release manner. The acidic environment of the tumor causes the burst-release of Qu molecules, which deplete the level of heat shock protein 70 (HSP70) in tumor cells and leave the tumor cells out from the protection of the heat-resistant survival pathway in advance, thus sensitizing the hyperthermia efficacy. The nanostructure, photothermal properties, pH-responsive controlled release, synergistic photothermal ablation of tumor cells in vitro and in vivo, and hyperthermia effect on subcellular structures of the Ti3C2@Qu nanocomposites were systematically investigated.

医学免疫学作为一门联系基础医学与临床医学的重要学科,依照"两性一度"标准,如何推进医学免疫学课程建设的改革,是影响医学生培养质量的重要环节之一.传统教学方式的学生往往处于被动接受知识状态,因此不能充分发挥其主动性,学生学习热情不高,严重影响教学效果,很难保证现代大学教育"两性一度"的建设标准.因此需改变教学方式,调动学生学习积极性.本研究尝试将对分课堂与情境教学法相结合,通过创设免疫学相关的情境问题,利用对分课堂充分讨论与自主学习,推动具有"两性一度"的高质量医学免疫学课程建设.