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Lipid metabolic reprogramming is an emerging hallmark of cancer. In order to sustain uncontrolled proliferation and survive in unfavorable environments that lack oxygen and nutrients, tumor cells undergo metabolic transformations to exploit various ways of acquiring lipid and increasing lipid oxidation. In addition, stromal cells and immune cells in the tumor microenvironment also undergo lipid metabolic reprogramming, which further affects tumor functional phenotypes and immune responses. Given that lipid metabolism plays a critical role in supporting cancer progression and remodeling the tumor microenvironment, targeting the lipid metabolism pathway could provide a novel approach to cancer treatment. This review seeks to: (1) clarify the overall landscape and mechanisms of lipid metabolic reprogramming in cancer, (2) summarize the lipid metabolic landscapes within stromal cells and immune cells in the tumor microenvironment, and clarify their roles in tumor progression, and (3) summarize potential therapeutic targets for lipid metabolism, and highlight the potential for combining such approaches with other anti-tumor therapies to provide new therapeutic opportunities for cancer patients.

The demand for fluency in human–computer interaction is on an increase globally; thus, the active localization of the speaker by the machine has become a problem worth exploring. Considering that the stability and accuracy of the single-mode localization method are low, while the multi-mode localization method can utilize the redundancy of information to improve accuracy and anti-interference, a speaker localization method based on voice and image multimodal fusion is proposed. First, the voice localization method based on time differences of arrival (TDOA) in a microphone array and the face detection method based on the AdaBoost algorithm are presented herein. Second, a multimodal fusion method based on spatiotemporal fusion of speech and image is proposed, and it uses a coordinate system converter and frame rate tracker. The proposed method was tested by positioning the speaker stand at 15 different points, and each point was tested 50 times. The experimental results demonstrate that there is a high accuracy when the speaker stands in front of the positioning system within a certain range.

Background Right upper lobectomy (RUL) for lung cancer with different dissecting orders involves the most variable anatomical structures, but no studies have analyzed its effects on postoperative recovery. This study compared the conventional surgical approach, VAB (dissecting pulmonary vessels first, followed by the bronchus), and the alternative surgical approach, aBVA (dissecting the posterior ascending arterial branch first, followed by the bronchus and vessels) on improving surgical feasibility and postoperative recovery for lung cancer patients. Methods According to the surgical approach, consecutive lung cancer patients undergoing RUL were grouped into aBVA and VAB cohorts. Their clinical, pathologic, and perioperative characteristics were collected to compare perioperative outcomes. Results Three hundred one patients were selected (109 in the aBVA cohort and 192 in the VAB cohort). The mean operation time was shorter in the aBVA cohort than in the VAB cohort (164 vs. 221 min, P < 0.001), and less blood loss occurred in the aBVA cohort (92 vs. 141 mL, P < 0.001). The rate of conversion to thoracotomy was lower in the aBVA cohort than in the VAB cohort (0% vs. 11.5%, P < 0.001). The mean duration of postoperative chest drainage was shorter in the aBVA cohort than in the VAB cohort (3.6 vs. 4.5 days, P = 0.001). The rates of postoperative complications were comparable (P = 0.629). The median overall survival was not arrived in both cohorts (P > 0.05). The median disease‐free survival was comparable for all patients in the two cohorts (not arrived vs. 41.97 months) and for patients with disease recurrences (13.25 vs. 9.44 months) (both P > 0.05). The recurrence models in two cohorts were also comparable for patients with local recurrences (6.4% vs. 7.8%), distant metastases (10.1% vs. 8.3%), and both (1.8% vs. 1.6%) (all P > 0.05). Conclusions Dissecting the right upper bronchus before turning over the lobe repeatedly and dissecting veins via the aBVA approach during RUL would promote surgical feasibility and achieve comparable postoperative recovery for lung cancer patients.

Compatibility between host cells and heterologous pathways is a challenge for constructing organisms with high productivity or gain of function. Designer yeast cells incorporating the Synthetic Chromosome Rearrangement and Modification by LoxP-mediated Evolution (SCRaMbLE) system provide a platform for generating genotype diversity. Here we construct a genetic AND gate to enable precise control of the SCRaMbLE method to generate synthetic haploid and diploid yeast with desired phenotypes. The yield of carotenoids is increased to 1.5-fold by SCRaMbLEing haploid strains and we determine that the deletion of YEL013W is responsible for the increase. Based on the SCRaMbLEing in diploid strains, we develop a strategy called Multiplex SCRaMbLE Iterative Cycling (MuSIC) to increase the production of carotenoids up to 38.8-fold through 5 iterative cycles of SCRaMbLE. This strategy is potentially a powerful tool for increasing the production of bio-based chemicals and for mining deep knowledge. The SCRaMbLE system integrated into Sc2.0’s synthetic yeast chromosome project allows rapid strain evolution. Here the authors use a genetic logic gate to control induction of recombination in a haploid and diploid yeast carrying synthetic chromosomes.

The purpose of the present study was to investigate whether catalpol exhibited neuroprotective effects in chronic unpredictable mild stress (CUMS) mice through oxidative stress-mediated nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin-domain-containing 3 (NLRP3) inflammasome and neuroinflammation. Deficits in behavioral tests, including open field test (OFT), forced swim test (FST), and elevated plus-maze test (EPM), were ameliorated following catalpol administration. To study the potential mechanism, western blots, quantitative real-time PCR (qRT-PCR) analysis and immunofluorescence imaging were performed on the hippocampus samples. We found that the defects of behavioral tests induced by CUMS could be reversed by the absence of NLRP3 and NLRP3 inflammasome might be involved in the antidepressant effects of catalpol on CUMS mice. Similar to the NLRP3 inflammasome, the expression of interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and inducible nitride oxide synthase (iNOS) were increased after CUMS. The current study demonstrated that catalpol possessed anti-inflammatory effect on CUMS mice and inhibited microglial polarization to the M1 phenotype. In addition, the activity of mitochondrial oxidative stress might be involved in the NLRP3 activation, which was proved by the downregulation of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and cleaved IL-1β, after the administration of mitochondrion-targeted antioxidant peptide SS31. Taken together, we provided evidence that catalpol exhibited antidepressive effects on CUMS mice possibly via the oxidative stress-mediated regulation of NLRP3 and neuroinflammation.

Inflammatory cell infiltration contributes to the pathogenesis of acute respiratory distress syndrome (ARDS). Protectin DX (PDX), an endogenous lipid mediator, shows anti‐inflammatory and proresolution bioactions. In vivo, the mice were intraperitoneally injected with PDX (0.1 µg/mouse) after intratracheal (1 mg/kg) or intraperitoneal (10 mg/kg) LPS administration. Flow cytometry was used to measure inflammatory cell numbers. Clodronate liposomes were used to deplete resident macrophages. RT‐PCR, and ELISA was used to measure MIP‐2, MCP‐1, TNF‐α and MMP9 levels. In vitro, sorted neutrophils, resident and recruited macrophages (1 × 106) were cultured with 1 μg/mL LPS and/or 100 nmol/L PDX to assess the chemokine receptor expression. PDX attenuated LPS‐induced lung injury via inhibiting recruited macrophage and neutrophil recruitment through repressing resident macrophage MCP‐1, MIP‐2 expression and release, respectively. Finally, PDX inhibition of neutrophil infiltration and transmembrane was associated with TNF‐α/MIP‐2/MMP9 signalling pathway. These data suggest that PDX attenuates LPS‐stimulated lung injury via reduction of the inflammatory cell recruitment mediated via resident macrophages.

Acute respiratory distress syndrome (ARDS) is a fatal disease characterized by excessive infiltration of inflammatory cells. MCTR1 is an endogenously pro‐resolution lipid mediator. We tested the hypothesis that MCTR1 accelerates inflammation resolution through resident M2 alveolar macrophage polarization. The mice received MCTR1 via intraperitoneal administration 3 days after LPS stimulation, and then, the bronchoalveolar lavage (BAL) fluid was collected 24 hours later to measure the neutrophil numbers. Flow cytometry was used to sort the resident and recruited macrophages. Post‐treatment with MCTR1 offered dramatic benefits in the resolution phase of LPS‐induced lung injury, including decreased neutrophil numbers, reduced BAL fluid protein and albumin concentrations and reduced histological injury. In addition, the expression of the M2 markers Arg1, FIZZ1, Remlα, CD206 and Dectin‐1 was increased on resident macrophages in the LPS + MCTR1 group. Resident macrophage depletion abrogated the therapeutic effects of MCTR1, and reinjection of the sorted resident macrophages into the lung decreased neutrophil numbers. Finally, treatment with MCTR1 increased STAT6 phosphorylation. The STAT6 inhibitor AS1517499 abolished the beneficial effects of MCTR1. In conclusion, MCTR1 promotes resident M2 alveolar macrophage polarization via the STAT6 pathway to accelerate resolution of LPS‐induced lung injury.

Background Hidden blood loss (HBL) is often ignored unilateral biportal endoscopic interbody fusion surgery (ULIF). We investigated the amount and influencing factors of HBL in ULIF surgery in this study. Methods From October 2020 to November 2023, 100 patients’ clinical and radiological data were retrospectively analyzed. Pearson or Spearman correlation and multivariate linear regression were used to identify factors linked to HBL. Results The mean hidden blood loss (HBL) was 255.84 ± 290.89 ml, making up 62.48% of total blood loss. Correlation analysis showed HBL positively related to ASA classification ( P  = 0.009), operation time ( P  = 0.004), number of operation levels ( P  = 0.046), and paraspinal muscle thickness ( P  = 0.043), but negatively related to tranexamic acid use ( P  = 0.001). A multivariate linear regression analysis showed that HBL was positively associated with ASA classification ( P  = 0.038) and operation time ( P  = 0.046), but negatively associated with tranexamic acid use ( P  = 0.001). Conclusion Patients undergoing ULIF surgery incurred a great deal of HBL. More importantly, ASA classification, operation time and tranexamic acid use were independent risk factors for HBL.

Perchlorate is a toxic, explosive, and water-soluble pollutant but while efficient and low-cost removal of ClO 4 − from water is an important challenge, suitable methods for precipitation of ClO 4 − from water are underdeveloped. Here, we demonstrate a hydrogen-bonded supramolecular polymer network crystal ( HBPC ) for efficient complexation of ClO 4 − . The HBPC network is constructed by an A,A’-bis-pyridyl-hydrazone-phenyl conjugate-functionalized pillar[5]arene ( PYP5 ), which self-assembles via the formation of clustered hydrogen-bonds. Two-pyridyl-hydrazone moieties provide coordination sites while the eight ethoxyl moieties on the pillar[5]arene enable multiple hydrogen bonding motifs to tightly bind to the ClO 4 − . The HBPC network therefore adsorbs ClO 4 − ions and facilitates the separation of these ions from water. Perchlorate is a toxic, explosive pollutant, and is difficult to precipitate due to its water solubility. Here, the authors report a pillar[5]arene-based supramolecular polymer network that can bind with perchlorate by clustered hydrogen-bonds for removal from water.

Background Bone tissue engineering for alveolar clefts is in the early stages of development, and more research is needed to determine the optimal cell types, growth factors and delivery methods for the therapy. Methods We co-cultured Carbonic anhydrase 1 (CA1) induced dental follicle stem cells (DFSCs) with dental pulp stem cells (DPSCs). In vitro, the Lentivirus vector overexpressing CA1 (LV-CA1) gene was constructed, transfected into DFSCs, and co-cultured with DPSCs indirectly. Osteoblast biomarkers in differentiated DFSCs were detected using quantitative real-time polymerase chain reaction and Western blotting. In vivo, establish a rat alveolar cleft model, transplanted stem cell Polycaprolactone/β-tricalcium phosphate (PCL/β-TCP) three-dimensional printed composite scaffold and samples were collected at 4 and 8 weeks postoperatively. The osteogenic effect was evaluated through micro computed tomography and histomorphometric analysis. Results In vitro, the activity of DFSCs in the LV-CA1+Co-culture group was increased, and the mRNA and protein expressions of CA1, Alkaline phosphatase (ALP), Bone morphogenetic proteins 2 (BMP2), and Runt-related transcription factor 2 (RUNX2) were amplified to varying degrees (P  < 0.05 ) . In vivo, micro-CT displayed at 4 and 8 weeks postoperatively, the LV-CA1+Co-culture group had a considerably higher percentage of new bone development (39.1% and 56.9%) ( P  < 0.05) than the other two groups. Histomorphometric analysis displayed the LV-CA1+Co-culture group had more newly formed bone trabeculae and immature collagen. Conclusion A strategy based on a novel osteogenic gene CA1 and dental-derived mesenchymal stem cells co-culture is applied to the alveolar cleft, providing a novel idea for the application of bone tissue engineering in alveolar cleft bone grafting. Graphical Abstract