A review on the evaluation models and impact factors of greenhouse gas emissions from municipal solid waste management processes.

The total amount of global municipal solid waste (MSW) will reach 3.5 billion tons by 2050, thereby bringing tremendous environmental pressure, especially global warming. Large amounts of greenhouse gases (GHGs) have been released during MSW management (MSWM). Accounting for GHG emissions is a prerequisite for providing recommendations on appropriate treatment options to mitigate emissions from MSWM systems. There are many methods involved in estimating emissions. This paper summarizes the computing models commonly used in each process of the integrated MSWM system and emphasizes the influence of parameters and other factors. Compared with other disposal methods, landfilling has the highest emissions, commonly estimated using first-order decay (FOD) methods. Emission reduction can be realized through waste to energy (WtE) and resource recovery measures. IPCC is commonly used for calculating direct emissions, while LCA-based models can calculate emissions including upstream and downstream processes, whose results depend on assumptions and system boundaries. The estimation results of models vary greatly and are difficult to compare with each other. Besides, large gaps exist between the default emission factors (EFs) provided by models and those F measured in specific facilities. These findings provide a systematic view for a bettering understanding of MSW emissions as well as the estimating methods and also reveal the key points that need be developed in the future.

Two undescribed coumarins from Hansenia weberbaueriana.

Two previously undescribed coumarins (1 and 2) were isolated from the root of Hansenia weberbaueriana which have been used to cure inflammatory diseases over thousands of years by Chinese. The structures of new findings were confirmed by comprehensive analyses of spectral evidences in HRESIMS, 1D and 2D NMR combined with chemical calculations. Compounds 1 and 2 exhibited potential anti-inflammatory properties by reducing the mRNA expression levels of TNF-α, IL-6 and IL-1ß in lipopolysaccharide (LPS)-induced RAW264.7 macrophages at a concentration of 15 µM.

RUNX1 C-terminal Mutations Impair Blood Cell Differentiation by Perturbing Specific Enhancer-Promoter Networks.

The transcription factor RUNX1 is a master regulator of hematopoiesis and is frequently mutated in myeloid malignancies. Mutations in its runt homology domain (RHD) frequently disrupt DNA binding and result in loss of RUNX1 function. However, it is not clearly understood how other RUNX1 mutations contribute to disease development. Here, we characterize RUNX1 mutations outside of the RHD. Our analysis of patient datasets revealed that mutations within the C-terminus frequently occur in hematopoietic disorders. Remarkably, most of these mutations were nonsense or frameshift and predicted to be exempt from nonsense mediated mRNA decay. Therefore, this class of mutation is projected to produce DNA-binding proteins that contribute to pathogenesis in a distinct manner. To model this, we introduced the RUNX1R320* mutation into the endogenous gene locus and demonstrated the production of RUNX1R320* protein. Expression of RUNX1R320* resulted in the disruption of RUNX1 regulated processes such as megakaryocytic differentiation through a transcriptional signature different from RUNX1 depletion. To understand the underlying mechanisms, we utilized Global RNA Interactions with DNA by deep sequencing (GRID-seq) to examine enhancer-promoter connections. We identified wide-spread alteration of enhancer-promoter networks within RUNX1 mutant cells. Additionally, we uncovered enrichment of RUNX1R320* and FOXK2 binding at the MYC super enhancer locus, significantly upregulating MYC transcription and signaling pathways. Together, our study demonstrates that most RUNX1 mutations outside the DNA binding domain are not subject to nonsense mediated decay, producing protein products that act in concert with additional cofactors to dysregulate hematopoiesis through mechanisms distinct from that induced by RUNX1 depletion.

Summary of the best evidence for the management of dysphagia in elderly patients.

OBJECTIVE: To search for and summarize the best evidence for themanagement of elderly patients with dysphagia. METHODS: Clinical decisions, recommended practices, evidence summaries, clinical practice guidelines, expert consensus, and systematic reviews on the management of dysphagia among elderly patients were systematically reviewed from domestic and foreign guideline websites, association websites, and Chinese and English databases according to the 6S model of evidence-based resources. The search period was between January 1, 2010 and November 1, 2023. Two researchers evaluated the quality of the included literature respectively and extracted evidence. RESULTS: A total of 14 literatures were identified, including 2 guidelines, 2 clinical decisions, 5 evidence summaries, 3 expert consensus statements, and 2 systematic reviews. Twenty-four pieces of evidence from 7 aspects were summarized, including assessment, treatment and rehabilitation, medication care, nutrition management, oral care, complication management, and psychological care. CONCLUSION: The best evidence-based recommendations for the management of dysphagia in elderly patients is summarized, it is suggested that the best evidence should be selected according to the actual situation of patients, and a personalized management plan should be formulated to improve the quality of life of patients and achieve high-quality nursing.

Secondary metabolites isolated from Trichoderma hamatum b-3 and their fungicidal activity.

An undescribed trichodenone derivative (1), two new diketopiperazines (3 and 4) along with a bisabolane analog (2) were isolated from Trichoderma hamatum b-3. The structures of the new findings were established through comprehensive analyses of spectral evidences in HRESIMS, 1D and 2D NMR, Marfey's analysis as well as comparisons of ECD. The absolute configuration of 2 was unambiguously confirmed by NMR, ECD calculation and Mo2(AcO)4 induced circular dichroism. Compounds 1-4 were tested for their fungicidal effects against eight crop pathogenic fungi, among which 1 showed 51% inhibition against Sclerotinia sclerotiorum at a concentration of 50 µg/mL.

Application of IMB model in preventing venous thromboembolism in elderly lung cancer patients.

Objective: This study aims to explore the effects of the Information-Motivation-Behavioral (IMB) Skills Model on the prevention of Venous Thromboembolism (VTE) in elderly lung cancer patients. Methods: A convenience sampling method was used to select study participants who were hospitalized for treatment between November 2022 and August 2023 at a tertiary hospital in Neijiang and met the inclusion and exclusion criteria. The control group (n = 41) received conventional health education, while the intervention group (n = 40) received health education based on the IMB Skills Model over three months. The scores of the Venous Thrombosis Knowledge, Participation in Thrombosis Prevention Willingness and Behavior Questionnaire, and Quality of Life Measurement Scale (QLQ-C30) were compared before the intervention and after three months. After three months of intervention, the hospital satisfaction and VTE incidence rates in both groups were investigated and compared. Results: After three months of intervention, the scores for the Venous Thrombosis Knowledge, (Participation in Thrombosis Prevention Willingness and Behavior Questionnaire in the intervention group were higher than those in the control group (P < 0.05). The QLQ-C30 scores in the intervention group for physical function, role function, emotional function, insomnia, appetite loss, and overall health status were higher than those in the control group (P < 0.05). The intervention group rated higher in doctor's professional skills, information provision, accessibility; nurse's professional skills, humanistic care, information provision, accessibility; team communication, services of other personnel, overall satisfaction compared to the control group (P < 0.05). The rate of VTE in the intervention group was 2.5%(1/40), and that in the control group was 19.5%(8/41). There was a significant difference (χ2 = 4.336, P = 0.037). Conclusion: Nursing interventions based on the IMB Skills Model for elderly lung cancer patients can enhance patients' understanding of venous thrombosis, increase willingness and active participation in thrombosis prevention, improve quality of life, increase hospital satisfaction, and reduce the incidence of VTE.

Eosinophils preserve bone homeostasis by inhibiting excessive osteoclast formation and activity via eosinophil peroxidase.

Eosinophils are involved in tissue homeostasis. Herein, we unveiled eosinophils as important regulators of bone homeostasis. Eosinophils are localized in proximity to bone-resorbing osteoclasts in the bone marrow. The absence of eosinophils in ΔdblGATA mice results in lower bone mass under steady-state conditions and amplified bone loss upon sex hormone deprivation and inflammatory arthritis. Conversely, increased numbers of eosinophils in IL-5 transgenic mice enhance bone mass under steady-state conditions and protect from hormone- and inflammation- mediated bone loss. Eosinophils strongly inhibit the differentiation and demineralization activity of osteoclasts and lead to profound changes in the transcriptional profile of osteoclasts. This osteoclast-suppressive effect of eosinophils is based on the release of eosinophil peroxidase causing impaired reactive oxygen species and mitogen-activated protein kinase induction in osteoclast precursors. In humans, the number and the activity of eosinophils correlates with bone mass in healthy participants and rheumatoid arthritis patients. Taken together, experimental and human data indicate a regulatory function of eosinophils on bone.

Age-related genes USP2 and ARG2 are involved in the reduction of immune cell infiltration in elderly patients with rheumatoid arthritis.

BACKGROUND: There are large differences in clinical manifestations and biological markers between elderly patients with rheumatoid arthritis (EPRA, age >60) and younger patients with RA (YPRA, age ≤60), partly owing to variations in the immune system of different age groups. Here, we focused on the changes of immune cell infiltration in YPRA and EPRA. METHODS: The R packages "ssGSEA" and "GSEA" were used to identify the changes in immune cell infiltration and immune-related pathways between the two groups. The R packages "WGCNA" and "DEseq2" were used to screen and verify age-related differentially expressed genes (DEGs). Hub genes were identified using Cytoscape and cytoHubba. Spearman correlation coefficient was conducted to evaluate correlations between hub age-related genes and immune cells. RESULTS: Compared with 54 established YPRA, several immune cells and immune-related pathways were markedly decreased in 29 EPRA synovial tissues. Moreover, 78 age-related DEGs related to amino acid and glycosphingolipid synthesis and metabolism were identified. USP2 and ARG2 were verified to be upregulated in EPRA, signifying that these two genes could effectively distinguish YPRA and EPRA and have potential as biomarkers. In addition, we found that USP2 was significantly negatively correlated with B cells and monocytes, while there was a significant negative association between ARG2 and T cells. CONCLUSIONS: In conclusion, this study is the first to systematically analyze changes in immune cell infiltration between YPRA and EPRA patients and obtain hub age-related genes, which may provide the basis for illuminating the pathogenesis of EPRA and informing treatment strategies.

Single-cell RNA sequencing of a new transgenic t(8;21) preleukemia mouse model reveals regulatory networks promoting leukemic transformation.

T(8;21)(q22;q22), which generates the AML1-ETO fusion oncoprotein, is a common chromosomal abnormality in acute myeloid leukemia (AML) patients. Despite having favorable prognosis, 40% of patients will relapse, highlighting the need for innovative models and application of the newest technologies to study t(8;21) leukemogenesis. Currently, available AML1-ETO mouse models have limited utility for studying the pre-leukemic stage because AML1-ETO produces mild hematopoietic phenotypes and no leukemic transformation. Conversely, overexpression of a truncated variant, AML1-ETO9a (AE9a), promotes fully penetrant leukemia and is too potent for studying pre-leukemic changes. To overcome these limitations, we devised a germline-transmitted Rosa26 locus AE9a knock-in mouse model that moderately overexpressed AE9a and developed leukemia with long latency and low penetrance. We observed pre-leukemic alterations in AE9a mice, including skewing of progenitors towards granulocyte/monocyte lineages and replating of stem and progenitor cells. Next, we performed single-cell RNA sequencing to identify specific cell populations that contribute to these pre-leukemic phenotypes. We discovered a subset of common myeloid progenitors that have heightened granulocyte/monocyte bias in AE9a mice. We also observed dysregulation of key hematopoietic transcription factor target gene networks, blocking cellular differentiation. Finally, we identified Sox4 activation as a potential contributor to stem cell self-renewal during the pre-leukemic stage.

Mediating effects of depression on sleep disturbance and frailty in older adult type 2 diabetes patients in the community.

Introduction: With the progressive aging of the population, frailty is now a significant challenge in geriatrics research. A growing amount of evidence suggests that sleep disturbance and depression have independent effects on frailty, although the underlying mechanisms are not yet clear. This study aimed to investigate the mediating role of depression in the relationship between sleep disturbance and frailty in older adult patients with type 2 diabetes (T2DM) in the community. Method: Purposive sampling was used to collect face-to-face data from 342 community-dwelling T2DM patients in Chengdu, Sichuan Province, China, between February and May 2023. The Pittsburgh Sleep Quality Index (PSQI) scale was used to evaluate sleep quality, the Simple Geriatric Depression Scale (GDS-15) was used to evaluate depressive symptoms, and the FRAIL Scale (FRAIL) was used to evaluate frailty. Linear regression equation and bootstrap self-sampling were used to verify the mediating role of depressive symptoms in sleep disturbance and frailty. Result: The study found that sleep disturbance had a direct positive effect with frailty [ß = 0.040, 95% CI: (0.013, 0.069)]. Additionally, depression had a direct positive effect on frailty [ß = 0.130, 95% CI: (0.087, 0.173)], and depression was found to partially mediate the relationship between sleep disturbance and frailty. Conclusion: Poor sleep quality and frailty are common in patients with T2DM. To reduce the frailty of older adult T2DM patients, all levels of society (government, medical institutions, and communities) must pay more attention to mental health. A variety of interventions should be considered to improve sleep quality and depression, which in turn may prevent or control frailty.

Reprogramming of tumor-associated macrophages via NEDD4-mediated CSF1R degradation by targeting USP18.

Tumor-associated myeloid cells modulate the tumor microenvironment and affect tumor progression. Type I interferon (IFN-I) has multiple effects on tumors and immune response, and ubiquitin-specific peptidase 18 (USP18) functions as a negative regulator of IFN-I signal transduction. This study aims to examine the function of IFN-I in myeloid cells during tumor progression. Here, we show that deletion of USP18 in myeloid cells suppresses tumor progression. Enhanced IFN-I signaling and blocked USP18 expression prompt downregulation of colony stimulating factor 1 receptor (CSF1R) and polarization of tumor-associated macrophages toward pro-inflammatory phenotypes. Further in vitro experiments reveal that downregulation of CSF1R is mediated by ubiquitin-proteasome degradation via E3 ligase neural precursor cell-expressed, developmentaly downregulated 4 (NEDD4) and the IFN-induced increase in ubiquitin E2 ubiquitin-conjugating enzyme H5. USP18 impairs ubiquitination and subsequent degradation of CSF1R by interrupting NEDD4 binding to CSF1R. These results reveal a previously unappreciated role of IFN-I in macrophage polarization by regulating CSF1R via USP18 and suggest targeting USP18 in myeloid-lineage cells as an effective strategy for IFN-based therapies.

Expansion of interferon inducible gene pool via USP18 inhibition promotes cancer cell pyroptosis.

While immunotherapy has emerged as a breakthrough cancer therapy, it is only effective in some patients, indicating the need of alternative therapeutic strategies. Induction of cancer immunogenic cell death (ICD) is one promising way to elicit potent adaptive immune responses against tumor-associated antigens. Type I interferon (IFN) is well known to play important roles in different aspects of immune responses, including modulating ICD in anti-tumor action. However, how to expand IFN effect in promoting ICD responses has not been addressed. Here we show that depletion of ubiquitin specific protease 18 (USP18), a negative regulator of IFN signaling, selectively induces cancer cell ICD. Lower USP18 expression correlates with better survival across human selected cancer types and delays cancer progression in mouse models. Mechanistically, nuclear USP18 controls the enhancer landscape of cancer cells and diminishes STAT2-mediated transcription complex binding to IFN-responsive elements. Consequently, USP18 suppression not only enhances expression of canonical IFN-stimulated genes (ISGs), but also activates the expression of a set of atypical ISGs and NF-κB target genes, including genes such as Polo like kinase 2 (PLK2), that induce cancer pyroptosis. These findings may support the use of targeting USP18 as a potential cancer immunotherapy.

On-Treatment Platelet Reactivity and Ischemic Outcomes in Patients With Diabetes Mellitus: Two-Year Results From ADAPT-DES.

Background Diabetes mellitus and high platelet reactivity (HPR) on clopidogrel are both associated with increased risk of ischemic events after percutaneous coronary intervention, but whether the HPR-associated risk of adverse ischemic events differs by diabetes mellitus status is unknown. Methods and Results ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents) was a prospective, multicenter registry of patients treated with coronary drug-eluting stents. HPR was defined as P2Y12 reaction units >208 by the VerifyNow point-of-care assay. Cox multivariable analysis was used to assess whether HPR-associated risk of major adverse cardiac events (MACE; cardiac death, myocardial infarction, or stent thrombosis) varied for patients with insulin-treated diabetes mellitus (ITDM), non-ITDM, and no diabetes mellitus. Diabetes mellitus and HPR were included in an interaction analysis. Of 8582 patients enrolled, 2429 (28.3%) had diabetes mellitus, of whom 998 (41.1%) had ITDM. Mean P2Y12 reaction units were higher in patients with diabetes mellitus versus without diabetes mellitus, and HPR was more frequent in patients with diabetes mellitus. HPR was associated with consistently increased 2-year rates of MACE in patients with and without diabetes mellitus (Pinteraction=0.36). A significant interaction was present between HPR and non-insulin-treated diabetes mellitus versus ITDM for 2-year MACE (adjusted hazard ratio [HR] for non-ITDM, 2.28 [95% CI, 1.39-3.73] versus adjusted HR for ITDM, 1.02 [95% CI, 0.70-1.50]; Pinteraction=0.01). Conclusions HPR was more common in patients with diabetes mellitus and was associated with an increased risk of MACE in both patients with and without diabetes mellitus. In patients with diabetes mellitus, a more pronounced effect of HPR on MACE was present in lower-risk non-ITDM patients than in higher-risk patients with ITDM. Registration URL: https://clinicaltrials.gov/ct2/show/NCT00638794; Unique identifier: NCT00638794. ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents).

Dietary Inflammatory Potential, Inflammation-Related Lifestyle Factors, and Incident Anxiety Disorders: A Prospective Cohort Study.

It is unclear whether diet-associated inflammation is related to the development of anxiety disorders. We aimed to investigate the association between energy-adjusted dietary inflammatory index (E-DII) scores and the incidence of anxiety disorders, and explore the joint effects of E-DII scores with other inflammatory lifestyles in enhancing anxiety risk. In the UK Biobank Study of 96,679 participants, baseline E-DII scores were calculated from the average intake of at least two 24 h dietary recalls. Multivariable-adjusted Cox models were used to evaluate the associations between E-DII scores and the incidence of total anxiety disorders, and primary types and subtypes; additive and multiplicative interactions of a pro-inflammatory diet and seven inflammatory lifestyles were examined. After a median follow-up of 9.4 years, 2785 incident cases of anxiety disorders occurred. Consuming a pro-inflammatory diet was significantly associated with a higher risk of total anxiety disorders (HRQ4vsQ1 = 1.12, 95% CI = 1.00-1.25), and positive associations were consistently identified for primary types and subtypes of anxiety disorders, with HRs ranging from 1.08 to 1.52, and were present in women only. Both additive and multiplicative interactions of current smoking and a proinflammatory diet on total anxiety risk were identified. A proinflammatory diet was associated with a higher incidence of anxiety disorders, and current smoking may synergize with a proinflammatory diet to promote anxiety risk, particularly among women.

Impact of Intravascular Ultrasound-Derived Lesion-Specific Virtual Fractional Flow Reserve Predicts 3-Year Outcomes of Untreated Nonculprit Lesions: The PROSPECT Study.

BACKGROUND: Hemodynamic assessment of untreated nonculprit lesions was not studied in the PROSPECT study (Providing Regional Observations to Study Predictors of Events in the Coronary Tree). We developed a virtual intravascular ultrasound-derived lesion-specific fractional flow reserve (lesion-specific IVUS-FFR) algorithm to assess individual lesion-level FFR. We sought to investigate the relation between lesion-specific IVUS-FFR and major adverse cardiovascular events (MACE) arising from untreated nonculprit lesions in the PROSPECT study. METHODS: In PROSPECT, 697 patients with acute coronary syndromes underwent 3-vessel grayscale and virtual histology-IVUS to correlate untreated nonculprit plaque morphology with 3-year nonculprit related MACE (composite of cardiac death, cardiac arrest, myocardial infarction, or rehospitalization due to unstable or progressive angina). Lesion-specific IVUS-FFR was calculated from volumetric IVUS lumen area measurements at 0.4 mm intervals by applying a mathematical circulation model using basic fluid dynamics equations. RESULTS: Lesion-specific IVUS-FFR was analyzable in 3227 nonculprit lesions in 660 patients among whom 54 nonculprit MACE events (3 myocardial infarctions) occurred at median 3.4-year follow-up. By receiver-operating characteristic analysis, the best cutoff value of lesion-specific IVUS-FFR to predict nonculprit MACE was ≤0.95. After adjusting for patient and lesion characteristics, lesion-specific IVUS-FFR (hazard ratio, 4.83 [95% CI, 2.20-10.61]; P<0.001) was an independent predictor of 3-year nonculprit MACE, in addition to minimum lumen area≤4.0 mm2, plaque burden ≥70%, and virtual histology thin-cap fibroatheroma. CONCLUSIONS: Minor reductions in lesion-specific IVUS-FFR were independently associated with future nonculprit MACE arising from untreated angiographically mild stenoses along with previously established high-risk lesion morphological characteristics. REGISTRATION: URL: https://www. CLINICALTRIALS: gov; Unique identifier: NCT00180466.

Research advances in the structures and biological activities of secondary metabolites from Talaromyces.

The genus Talaromyces belongs to the phylum Ascomycota of the kingdom Fungi. Studies have shown that Talaromyces species yield many kinds of secondary metabolites, including esters, terpenes, steroids, alkaloids, polyketides, and anthraquinones, some of which have biological activities such as anti-inflammatory, bacteriostatic, and antitumor activities. The chemical constituents of fungi belonging to the genus Talaromyces that have been studied by researchers over the past several years, as well as their biological activities, are reviewed here to provide a reference for the development of high-value natural products and innovative uses of these resources.

Trichodimerol inhibits inflammation through suppression of the nuclear transcription factor-kappaB/NOD-like receptor thermal protein domain associated protein 3 signaling pathway.

Excessive inflammation causes chronic diseases and tissue damage. Although there has been drug treatment, its side effects are relatively large. Searching for effective anti-inflammatory drugs from natural products has become the focus of attention. First isolated from Trichoderma longibraciatum, trichodimerol is a natural product with TNF inhibition. In this study, lipopolysaccharide (LPS)-induced RAW264.7 macrophages were used as a model to investigate the anti-inflammatory activity of trichodimerol. The results of nitric oxide (NO) detection, enzyme-linked immunosorbent assay (ELISA), and reactive oxygen species (ROS) showed that trichodimerol could reduce the production of NO, ROS, and the proinflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α. Western blotting results showed that trichodimerol could inhibit the production of inflammatory mediators such as cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) and the protein expression of nuclear transcription factor-kappaB (NF-κB), p-IKK, p-IκB, Toll-like receptor 4 (TLR4), NOD-like receptor thermal protein domain associated protein 3 (NLRP3), cysteinyl aspartate specific proteinase (Caspase)-1, and ASC, which indicated that trichodimerol may inhibit inflammation through the NF-κB and NLRP3 pathways. At the same time, molecular docking showed that trichodimerol can directly combine with the TLR4-MD2 complex. Hence, trichodimerol inhibits inflammation by obstructing the interaction between LPS and the TLR4-MD2 heterodimer and suppressing the downstream NF-κB and NLRP3 pathways.

Recycling municipal solid waste incineration fly ash in super-lightweight aggregates by sintering with clay and using SiC as bloating agent.

Municipal solid waste incineration (MSWI) fly ash is classified as hazardous waste and requires proper treatments. Sintering of MSWI fly ash for the production of lightweight aggregate (LWA) is a promising treatment technology, while the dependence on natural bloating clay to produce high quality LWA has limited its wide application. In this study, by using SiC as a bloating agent, normal clay could be used to produce super-lightweight aggregate (bulk density <500 kg/m3) with MSWI fly ash. Effects of SiC addition amount, sintering temperature and duration on LWA performance were studied. The results showed that LWA with SiC addition of 0.1-0.5 wt% had significant expansion at sintering temperature of 1120 °C-1160 °C. The optimal conditions were 0.3 wt% SiC addition and sintering at 1120 °C for 30 min, and the bulk density could reach 212 kg/m3 with other properties meeting the LWA standard (GB/T 17431.1-2010). Further, the heavy metal leaching toxicity was significantly decreased after sintering and met the MSWI fly ash utilization standard (HJ 1134-2020). The X-ray diffraction results revealed the formation of a complex diopside-based phase after sintering. This study provides a new approach for recycling MSWI fly ash in LWA without dependence on specific clay resources, and makes this technology wider applicability.

Recent Insights Into the Role of Macrophages in Acute Gout.

Gout is a common type of inflammatory arthritis characterized by the presence of monosodium urate crystals (MSU) in the joints. Macrophages are believed to be involved in gout flares. It has long been recognized that resident macrophage and monocyte derived macrophages are distinct subsets and there have been attempts to investigate their roles in acute gout, respectively. Previous studies revealed that resident macrophages initiate and drive the inflammation, while monocyte derived macrophages differentiated into M1-like macrophages in response to MSU crystals. With the advancement of technologies, subpopulations of synovial resident macrophages have been defined with the characteristics more accurately described. Resident macrophages in the synovial lining layer showed an anti-inflammatory effect in rheumatoid arthritis, but specific Trpv4 depletion of them reduced MSU crystals induced murine arthritis. CD14+ monocytes in the synovial fluid from patients with gout exhibit phenotypes of anti-inflammatory as well as pro-inflammatory characteristics. Here, we review the main aspects of macrophages in the initiation and resolution of acute gout and try to clarify the specific role of each subpopulation. Building a reliable diagram of the effect of monocytes and macrophages during MSU crystals induced arthritis will bring us closer to targeting macrophages for improving the management of gout.