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Cancer metabolism mainly includes carbohydrate, amino acid and lipid metabolism, each of which can be reprogrammed. These processes interact with each other to adapt to the complicated microenvironment. Ferroptosis is a regulated cell death induced by iron-dependent lipid peroxidation, which is morphologically different from apoptosis, necrosis, necroptosis, pyroptosis, autophagy-dependent cell death and cuprotosis. Cancer metabolism plays opposite roles in ferroptosis. On the one hand, carbohydrate metabolism can produce NADPH to maintain GPX4 and FSP1 function, and amino acid metabolism can provide substrates for synthesizing GPX4; on the other hand, lipid metabolism might synthesize PUFAs to trigger ferroptosis. The mechanisms through which cancer metabolism affects ferroptosis have been investigated extensively for a long time; however, some mechanisms have not yet been elucidated. In this review, we summarize the interaction between cancer metabolism and ferroptosis. Importantly, we were most concerned with how these targets can be utilized in cancer therapy.

In this study, a piezoelectric active sensing-based time reversal method was investigated for monitoring pipeline internal corrosion. An effective method that combines wavelet packet energy with a Convolutional Neural Network (CNN) was proposed to identify the internal corrosion status of pipelines. Two lead zirconate titanate (PZT) patches were pasted on the outer surface of the pipeline as actuators and sensors to generate and receive ultrasonic signals propagating through the inner wall of the pipeline. Then, the time reversal technique was employed to reverse the received response signal in the time domain, and then to retransmit it as an excitation signal to obtain the focused signal. Afterward, the wavelet packet transform was used to decompose the focused signal, and the wavelet packet energy (WPE) with large components was extracted as the input of the CNN model to rapidly identify the corrosion degree inside the pipeline. The corrosion experiments were conducted to verify the correctness of the proposed method. The occurrence and development of corrosion in pipelines were generated by electrochemical corrosion, and nine different depths of corrosion were imposed on the sample pipeline. The experimental results indicated that the classification accuracy exceeded 99.01%. Therefore, this method can quantitatively monitor the corrosion status of pipelines and can pinpoint the internal corrosion degree of pipelines promptly and accurately. The WPE-CNN model in combination with the proposed time reversal method has high application potential for monitoring pipeline internal corrosion.

Metastatic colorectal cancer (mCRC) patients have poor overall survival despite using irinotecan- or oxaliplatin-based chemotherapy combined with anti-EGFR (epidermal growth factor receptor) drugs, especially those with the oncogene mutation of KRAS. Metformin has been reported as a potentially novel antitumor agent in many experiments, but its therapeutic activity is discrepant and controversial so far. Inspiringly, the median survival time for KRAS-mutation mCRC patients with diabetes on metformin is 37.8 mo longer than those treated with other hypoglycemic drugs in combination with standard systemic therapy. In contrast, metformin could not improve the survival of mCRC patients with wild-type KRAS. Interestingly, metformin is preferentially accumulated in KRAS-mutation mCRC cells, but not wild-type ones, in both primary cell cultures and patient-derived xenografts, which is in agreement with its tremendous effect in KRAS-mutation mCRC. Mechanistically, the mutated KRAS oncoprotein hypermethylates and silences the expression of multidrug and toxic compound extrusion 1 (MATE1), a specific pump that expels metformin from the tumor cells by upregulating DNA methyltransferase 1 (DNMT1). Our findings provide evidence that KRAS-mutation mCRC patients benefit from metformin treatment and targeting MATE1 may provide a strategy to improve the anticancer response of metformin.

The lower surface hardness limits the further application of 316 L stainless steel. In this study, selective laser melting (SLM)/laser metal deposition (LMD) composite additive manufacturing technology was used to prepare five kinds of 316L-nano-TiC cermet strengthening layers on the surface of 316L stainless steel, and to study the effect of nano-TiC particle content on the microstructure and the influence of microhardness. Use Laser microscope, scanning electron microscope (SEM), X-ray diffractometer (XRD) to analyze the structure, element distribution and phase composition of the strengthening layer. The hardness of the strengthened layer was analyzed using a Vickers micro-hardness tester. The study found that the composite SLM/LMD formed samples changed continuously from LMD forming to SLM forming, showing good metallurgical bonding. Diffusion of TiC particles was observed in the SLM strengthening layer, and TiC phase was detected in the strengthening layer. Compared with the 316L matrix, the microhardness of the strengthened layer is significantly improved. When 50 wt% TiC is added, the average hardness of the strengthened layer is 1.9 times that of the 316L matrix, and the highest is 408.9 HV. The results of this study show that the strengthening layer manufactured by composite additive materials can effectively improve the hardness of the 316L stainless steel matrix. As the content of nano-TiC in the preset powder increases, the microhardness of the strengthening layer first increases and then decreases, and the hardness of the 50wt% TiC strengthening layer is the highest. There are distributed nano-TiC particles in the structure of the strengthening layer, and the distribution of nano-TiC particles in the 50wt% TiC strengthening layer is more uniform than other samples. This research provides a new reference for the strengthening of 316L stainless steel through SLM/LMD composite additive manufacturing technology and the addition of nano-TiC particles.

Two new sulfur glycosides, bursapastoris A–B (3–4), were extracted and isolated from shepherd’s purse seed, along with two new natural products, 11-(methylsulfinyl)undecanoic acid (2) and 10-(methylsulfinyl)decanoic acid (1). Their structures were determined though infrared spectroscopy, one-dimensional nuclear magnetic resonance (1H and 13C), and electrospray ionization mass spectrometry. Additionally, the structures of 3–4 were further identified by two-dimensional nuclear magnetic resonance (HMBC, HSQC, 1H-1H COSY, and NOESY). Compounds 1–4 showed relatively favorable docking to NF-κB. Unfortunately, we only discovered that compound 1–4 had weak anti-radiation activity at present. Therefore, further research regarding the biological activity of these organosulfur compounds is required at a later stage.

Beige fat dissipates energy and functions as a defense against cold and obesity, but the mechanism for its development is unclear. We found that interleukin (IL)-25 signaling through its cognate receptor, IL-17 receptor B (IL-17RB), increased in adipose tissue after cold exposure and β3-adrenoceptor agonist stimulation. IL-25 induced beige fat formation in white adipose tissue (WAT) by releasing IL-4 and IL-13 and promoting alternative activation of macrophages that regulate innervation and up-regulate tyrosine hydroxylase (TH) up-regulation to produce more catecholamine including norepinephrine (NE). Blockade of IL-4Rα or depletion of macrophages with clodronate-loaded liposomes in vivo significantly impaired the beige fat formation in WAT. Mice fed with a high-fat diet (HFD) were protected from obesity and related metabolic disorders when given IL-25 through a process that involved the uncoupling protein 1 (UCP1)-mediated thermogenesis. In conclusion, the activation of IL-25 signaling in WAT may have therapeutic potential for controlling obesity and its associated metabolic disorders.

Gastric cancer and breast cancer have a clear tendency toward metastasis and invasion to the microenvironment predominantly composed of adipocytes. Oleic acid is an abundant monounsaturated fatty acid that releases from adipocytes and impinges on different energy metabolism responses. The effect and underlying mechanisms of oleic acid on highly metastatic cancer cells are not completely understood. We reported that AMP-activated protein kinase (AMPK) was obviously activated in highly aggressive carcinoma cell lines treated by oleic acid, including gastric carcinoma HGC-27 and breast carcinoma MDA-MB-231 cell lines. AMPK enhanced the rates of fatty acid oxidation and ATP production and thus significantly promoted cancer growth and migration under serum deprivation. Inactivation of AMPK attenuated these activities of oleic acid. Oleic acid inhibited cancer cell growth and survival in low metastatic carcinoma cells, such as gastric carcinoma SGC7901 and breast carcinoma MCF-7 cell lines. Pharmacological activation of AMPK rescued the cell viability by maintained ATP levels by increasing fatty acid β-oxidation. These results indicate that highly metastatic carcinoma cells could consume oleic acid to maintain malignancy in an AMPK-dependent manner. Our findings demonstrate the important contribution of fatty acid oxidation to cancer cell function.

Distant metastasis is, unfortunately, the leading cause of death in colorectal cancer (CRC). Approximately 50% of CRC patients develop liver metastases, while 10–30% of patients develop pulmonary metastases. The occurrence of metastasis is considered to be almost exclusively driven by cancer stem cells (CSCs) formation. However, the key molecules that confer the transformation to stem cells in CRC, and subsequent metastasis, remain unclear. Far upstream element‐binding protein 1 (FUBP1), a transcriptional regulator of c‐Myc, was screened in CSCs of CRC by mass spectrometry and was examined by immunohistochemistry in a cohort of CRC tissues. FUBP1 was upregulated in 85% of KRAS‐mutant and 25% of wild‐type CRC patients. Further, whether in KRAS‐mutant or wild‐type patients, elevated FUBP1 was positively correlated with CRC lymph node metastasis and clinical stage, and negatively associated with overall survival. Overexpression of FUBP1 significantly enhanced CRC cell migration, invasion, tumor sphere formation, and CD133 and ALDH1 expression in vitro, and tumorigenicity in vivo. Mechanistically, FUBP1 promoted the initiation of CSCs by activating Wnt/β‐catenin signaling via directly binding to the promoter of DVL1, a potent activator of β‐catenin. Knockdown of DVL1 significantly inhibited the transformation to stem cells in, as well as the tumorigenicity of, CRC. Activation of Wnt/β‐catenin signaling by DVL1 increased pluripotent transcription factors, including c‐Myc, NANOG, and SOX2. Moreover, FUBP1 was upregulated at the post‐transcriptional level. Elevated FUBP1 levels in KRAS wild‐type CRC patients is due to the decrease in Smurf2, which promotes ubiquitin‐mediated degradation of FUBP1. In contrast, FUBP1 was upregulated in KRAS‐mutant patients through both inhibition of caspase 3‐dependent cleavage and decreased Smurf2. Our results demonstrate, for the first time, that FUBP1 is an oncogene, initiating the development of CSCs, as well as a new powerful endogenous Wnt‐signaling agonist that could provide an important prognostic factor and therapeutic target for metastasis in both KRAS‐mutant and wild‐type CRC. Distant metastasis represents the leading cause of death in colorectal cancer (CRC). Cancer stem cells (CSCs) formation is considered to drive metastasis in patients with CRC; however, the key molecules guiding CSC formation remain elusive. Here, we investigated the role of the FUBP1 oncogene and DVL1, a novel agonist of endogenous Wnt signaling in CSCs development. Our data indicate that FUBP1 acts in initiating the development of CSC and could serve as a prognostic factor, as well as a potential therapeutic target in both KRAS‐mutant and wild‐type patients with CRC metastasis.

Combined with NMR, core experiment, slim-tube tests, nano-CT and oil composition analysis, the mechanism of CO2 enhanced oil recovery had been studied. CO2 flooding under supercritical state could achieve higher oil recovery. In the process of crude oil displaced by supercritical CO2, the average oil recovery was 46.98% at low displacement pressures and 73.35% at high displacement pressures. The permeability of cores after CO2 flooding was only 28%–64% of those before flooding. As to the expelled oil, the contents of asphaltenes and non-hydrocarbons decreased, and saturated hydrocarbons of above C25 were absent in some samples, indicating that they had been retained in cores as demonstrated by CT and NMR experiments. In slim-tube tests, the heavy components of oil were expelled when the pressure increased to 30 MPa. There was a reasonable bottom hole pressure (BHP) below which the heavy components driven out from the far-well zone would deposit in the near-well zone, and when the pressure was too high, the nonhydrocarbon detention may cause block. The smaller throat and worse physical properties the porous media had, the higher displacement pressure would be required to achieve a good oil displacement efficiency. The increase in displacement pressure or time of interaction between oil and CO2 could effectively enhance oil recovery.

This study explores the mechanisms underlying the enhanced anti-wear and thermal fatigue performance of laser-treated bionic brake drums, aiming to extend their service life and improve design quality. Bionic brake drums treated with laser patterns—point, stripe, and grid—were tested with semi-metallic, non-asbestos organic (NAO), and ceramic brake pads. A mechanical model was developed to analyze wear performance, and bench tests were conducted to assess wear patterns. Thermal fatigue tests examined the impact of thermal cycling on the treated drums’ wear behavior. The results reveal that laser-treated bionic brake drums significantly outperformed untreated ones in both wear resistance and thermal fatigue. Among the treatments, the grid pattern showed the best wear performance, and thermal fatigue life was improved by 27% for the striped pattern and 38% for the grid pattern. The study concludes that laser treatment effectively enhances both wear resistance and thermal fatigue performance in bionic brake drums, especially for the grid pattern, offering valuable insights for future brake drum design.