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Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer-related death worldwide. Countless CRC patients undergo disease progression. As a hallmark of cancer, Warburg effect promotes cancer metastasis and remodels the tumor microenvironment, including promoting angiogenesis, immune suppression, cancer-associated fibroblasts formation and drug resistance. Targeting Warburg metabolism would be a promising method for the treatment of CRC. In this review, we summarize information about the roles of Warburg effect in tumor microenvironment to elucidate the mechanisms governing Warburg effect in CRC and to identify novel targets for therapy.

Background Mounting evidence has demonstrated the vital importance of tumor-associated macrophages (TAMs) and exosomes in the formation of the premetastatic niche. However, the molecular mechanisms by which tumor-derived exosomal miRNAs interact with TAMs underlying premetastatic niche formation and colorectal cancer liver metastasis (CRLM) remain largely unknown. Methods Transmission electron microscopy and differential ultracentrifugation were used to verify the existence of exosomes. In vivo and in vitro assays were used to identify roles of exosomal miR-934. RNA pull-down assay, dual-luciferase reporter assay, etc. were applied to clarify the mechanism of exosomal miR-934 regulated the crosstalk between CRC cells and M2 macrophages. Results In the present study, we first demonstrated the aberrant overexpression of miR-934 in colorectal cancer (CRC), especially in CRLM, and its correlation with the poor prognosis of CRC patients. Then, we verified that CRC cell-derived exosomal miR-934 induced M2 macrophage polarization by downregulating PTEN expression and activating the PI3K/AKT signaling pathway. Moreover, we revealed that hnRNPA2B1 mediated miR-934 packaging into exosomes of CRC cells and then transferred exosomal miR-934 into macrophages. Interestingly, polarized M2 macrophages could induce premetastatic niche formation and promote CRLM by secreting CXCL13, which activated a CXCL13/CXCR5/NFκB/p65/miR-934 positive feedback loop in CRC cells. Conclusions These findings indicate that tumor-derived exosomal miR-934 can promote CRLM by regulating the crosstalk between CRC cells and TAMs. These findings reveal a tumor and TAM interaction in the metastatic microenvironment mediated by tumor-derived exosomes that affects CRLM. The present study also provides a theoretical basis for secondary liver cancer.

Colorectal cancer liver metastasis (CRLM) is one of the leading causes of death among patients with colorectal cancer (CRC). Although immunotherapy has demonstrated encouraging outcomes in CRC, its benefits are minimal in CRLM. The complex immune landscape of the hepatic tumour microenvironment is essential for the development of a premetastatic niche and for the colonisation and metastasis of CRC cells; thus, an in-depth understanding of these mechanisms can provide effective immunotherapeutic targets for CRLM. This review summarises recent studies on the immune landscape of the tumour microenvironment of CRLM and highlights therapeutic prospects for targeting the suppressive immune microenvironment of CRLM.

Ternary lithium-ion batteries (LIBs), widely used in new energy vehicles and electronic products, are known for their high energy density, wide operating temperature range, and excellent cycling performance. With the rapid development of the battery industry, the recycling of spent ternary LIBs has become a hot topic because of their economic value and environmental concerns. To date, a considerable amount of literature has reported on the recycling of spent ternary LIBs designed to provide an efficient, economical, and environmentally friendly method for battery recycling. This article examines the latest developments in various technologies for recycling spent ternary LIBs in both research and practical production, including pretreatment, pyrometallurgy, hydrometallurgy, pyro-hydrometallurgy, and direct regeneration. Suggestions for addressing challenges based on the benefits and disadvantages of each method are made. Finally, through a comparison of the feasibility and economic benefits of various technologies, the challenges faced during battery recycling are summarized, and future development directions are proposed.

The self‐thinning rule in forest stands is fundamental to the development of density management strategies, as it determines the maximum stand density achievable for a given tree size. Accurate modeling of the maximum density line is crucial, but selecting representative data points for this purpose remains a challenge. Using 18 years of data from five Cunninghamia lanceolata plantations with varying initial planting densities, this study investigated whether relationships between mean tree basal area (g) and height (H) can reveal forest developmental stages and identify when stands begin self‐thinning and reach maximum density. Our results showed a significant linear relationship (p < 0.05) between g and H after self‐thinning was established, supporting the presence of self‐regulatory growth mechanisms. These findings enabled the development of a novel sample selection method for constructing more accurate maximum density line models, outperforming traditional methods that rely on arbitrary thresholds. Additionally, we derived formulas to describe total stand basal area (G1.0) during different growth stages, revealing positive correlations with mean height during early growth and negative correlations with mean diameter during self‐thinning. This research advances the understanding of self‐thinning dynamics and provides practical tools for improving density management in plantation forestry. The mean basal area and height showed a significant linear relationship during two growth stages (from canopy closure to prethinning, anaphase self‐thinning). The forest may have a self‐regulatory mechanism that ensures a relative balance of mean basal area and height.

Background Skin cutaneous melanoma (SKCM) is the most aggressive skin cancer, accounting for more than 75% mortality rate of skin-related cancers. As a newly identified programmed cell death, pyroptosis has been found to be closely associated with tumor progression. Nevertheless, the prognostic significance of pyroptosis in SKCM remains elusive. Methods A total of 469 SKCM samples and 812 normal samples were obtained from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases. Firstly, differentially expressed pyroptosis-related genes (PRGs) between normal samples and SKCM samples were identified. Secondly, we established a prognostic model based on univariate Cox and LASSO Cox regression analyses, which was validated in the test cohort from GSE65904. Thirdly, a nomogram was used to predict the survival probability of SKCM patients. The R package “pRRophetic” was utilized to identify the drug sensitivity between the low- and high-risk groups. Tumor immune infiltration was evaluated using “immuneeconv” R package. Finally, the function of GSDMD and SB525334 was explored in A375 and A2058 cells. Results Based on univariate Cox and LASSO regression analyses, we established a prognostic model with identified eight PRGs (AIM2, CASP3, GSDMA, GSDMC, GSDMD, IL18, NLRP3, and NOD2), which was validated in the test cohort. SKCM patients were divided into low- and high-risk groups based on the median of risk score. Kaplan–Meier survival analysis showed that high-risk patients had shorter overall survival than low-risk patients. Additionally, time-dependent ROC curves validated the accuracy of the risk model in predicting the prognosis of SKCM. More importantly, 4 small molecular compounds (SB525334, SR8278, Gemcitabine, AT13387) were identified, which might be potential drugs for patients in different risk groups. Finally, overexpression of GSDMD and SB525334 treatment inhibit the proliferation, migration, and invasion of SKCM cells. Conclusion In this study, we constructed a prognostic model based on PRGs and identified GSDMD as a potential therapeutic target, which provide new insights into SKCM treatment.

The wind-induced vibration energy harvester is a type of ideal power source for wireless sensor nodes. To adapt to the uncertainty of wind direction in natural environments, this paper proposes a three-dimensional multi-directional piezoelectric wind energy harvester (WEH), whose bluff body is an external shell with the shape like a lampshade, supported by three internal piezoelectric composite beams. A harvester prototype was made using 3D printing technology, and its multi-directional energy harvesting characteristics were systematically tested in a wind tunnel. Experiments show that it can harvest wind energy from any direction in three-dimensional space. When the wind speed is about 15 m/s and the wind direction changes in the horizontal plane, the minimum to maximum total average output power ratio is about 0.84. This work provides an experimental basis for the future development of three-dimensional multi-directional WEHs to some extent.

The urgent demand of wireless sensor nodes for long-life and maintenance-free miniature electrical sources with output power ranging from microwatts to milliwatts has accelerated the development of energy harvesting technologies. For the abundant and renewable nature of wind in environments, flow-induced vibration (FIV)-based wind energy harvesting has emerged as a promising approach. Electromagnetic FIV wind energy harvesters (WEHs) show great potential for realistic applications due to their excellent durability and stability. However, electromagnetic WEHs remain less studied than piezoelectric WEHs, with few dedicated review articles available. This review analyzes the working principle, device structure, and performance characteristics of electromagnetic WEHs based on vortex-induced vibration, galloping, flutter, wake galloping vibration, and Helmholtz resonator. The methods to improve the output power, broaden the operational wind speed range, broaden the operational wind direction range, and enhance the durability are then discussed, providing some suggestions for the development of high-performance electromagnetic FIV WEHs.

lncRNA can regulate tumorigenesis development and distant metastasis of colorectal cancer (CRC). However, the detailed molecular mechanisms are still largely unknown. Using RNA-sequencing data, RT-qPCR, and FISH assay, we found that HIF1A-AS2 was upregulated in CRC tissues and associated with poor prognosis. Functional experiments were performed to determine the roles of HIF1A-AS2 in tumor progression and we found that HIF1A-AS2 can promote the proliferation, metastasis, and aerobic glycolysis of CRC cells. Mechanistically, HIF1A-AS2 can promote FOXC1 expression by sponging miR-141-3p. SP1 can transcriptionally activate HIF1A-AS2. Further, HIF1A-AS2 can be packaged into exosomes and promote the malignant phenotype of recipient tumor cells. Taken together, we discovered that SP1-induced HIF1A-AS2 can promote the metabolic reprogramming and progression of CRC via miR-141-3p/FOXC1 axis. HIF1A-AS2 is a promising diagnostic marker and treatment target in CRC.

Hemophagocytic lymphohistiocytosis (HLH) is a severe disorder characterized by excessive secretion of cytokines. Even with the recommended HLH-94/2004 regimen, over 30% of patients remain refractory to frontline therapy or relapse after an initial response, leading to poor clinical outcomes. Ruxolitinib, a JAK1/2 inhibitor targets key cytokines in HLH, has shown promising therapeutic effects. However, there has been little attention given to patients who do not respond to ruxolitinib and whether an escalating dose can provide a resolution. This study analyzed eight HLH patients who received dose-escalating ruxolitinib who had previously failed to respond to the general dose. The efficacy and safety were mainly analyzed. Overall, four out of eight (50%) patients achieved better remission after dose escalation. Two patients who only showed improvement with the general dose achieved complete remission (CR) after dose escalation, and the other two patients also achieved CR after dose escalation when they did not respond to the general dose. The median time to achieve the best overall response was 18.5 days (IQR 13.25-23.75 days). There was no correlation of treatment outcome with blood count, liver function, LDH, cytokines, ferritin levels, NK cell activity, or the time to initiation of ruxolitinib and maximum dosage. The etiology of HLH (p=0.029) and level of sCD25 (p=0.021) correlated with treatment response to dose-escalating ruxolitinib. The area of sCD25 under the ROC curve was 0.8125 (95% CI 0.5921 to 1.033, p=0.035) when using 10,000 pg/ml as the cut-off value for predicting therapeutic effects. After a median follow-up of 159 days, two patients died, and the estimated 2-month overall survival rate was 75%. Adverse effects possibly related to the dose-escalating of ruxolitinib included two cases of extremity pain and one of aminotransferase increased. No grade 3 or higher adverse events were reported. This is the first comprehensive study on the use of dose-escalating ruxolitinib in HLH. Ruxolitinib at an escalated dose represent a viable and relatively safe solution for managing refractory HLH. The levels of sCD25 (with a cut-off of 10000pg/ml) can serve as an indicator for early consideration of chemotherapy during treatment.