Search

Abstract Talin-1 (TLN1), encoded by the TLN1 gene, is a focal adhesion-related protein capable of binding various proteins in the cytoskeleton. It is also expressed at high levels in many cancers wherein it influences cellular adhesion and the activation of integrins. TLN1 is also capable of promoting tumor cell invasivity, proliferation, and metastatic progression, in addition to being a relevant biomarker and therapeutic target in certain cancers. The present review offers a comprehensive overview of current knowledge regarding TLN1 with respect to its structural properties, functions, and role in tumor development.

Abstract Background Abnormal sensory perception, particularly pain insensitivity (PAI), is a typical symptom of autism spectrum disorder (ASD). Despite the role of myelin metabolism in the regulation of pain perception, the mechanisms underlying ASD-related PAI remain unclear. Methods The pain-associated gene sphingosine-1-phosphate receptor 1 (S1PR1) was identified in ASD samples through bioinformatics analysis. Its expression in the dorsal root ganglion (DRG) tissues of BTBR ASD model mice was validated using RNA-seq, western blot, RT-qPCR, and immunofluorescence. Pain thresholds were assessed using the von Frey and Hargreaves tests. Patch-clamp techniques measured KCNQ/M channel activity and neuronal action potentials. The expression of S1PR1, KCNQ/M, mitogen-activated protein kinase (MAPK), and cyclic AMP/protein kinase A (cAMP/PKA) signaling proteins was analyzed before and after inhibiting the S1P-S1PR1-KCNQ/M pathway via western blot and RT-qPCR. Results Through integrated transcriptomic analysis of ASD samples, we identified the upregulated gene S1PR1, which is associated with sphingolipid metabolism and linked to pain perception, and confirmed its role in the BTBR mouse model of ASD. This mechanism involves the regulation of KCNQ/M channels in DRG neurons. The enhanced activity of KCNQ/M channels and the decreased action potentials in small and medium DRG neurons were correlated with PAI in a BTBR mouse model of ASD. Inhibition of the S1P/S1PR1 pathway rescued baseline insensitivity to pain by suppressing KCNQ/M channels in DRG neurons, mediated through the MAPK and cAMP/PKA pathways. Investigating the modulation and underlying mechanisms of the non-opioid pathway involving S1PR1 will provide new insights into clinical targeted interventions for PAI in ASD. Conclusions S1PR1 may contribute to PAI in the PNS in ASD. The mechanism involves KCNQ/M channels and the MAPK and cAMP/PKA signaling pathways. Targeting S1PR1 in the PNS could offer novel therapeutic strategies for the intervention of pain dysesthesias in individuals with ASD.

Abstract Substituting thermodynamically favorable ethanol oxidation reaction (EOR) for oxygen evolution reaction (OER) engenders high‐efficiency hydrogen production and generates high value‐added products as well. However, the main obstacles have been the low activity and the absence of an explicit catalytic mechanism. Herein, a heterostructure composed of amorphous vanadium oxide and crystalline nickel nitride (VOx−Ni3N) is developed. The heterostructure immensely boosts the EOR process, achieving the current density of 50 mA cm−2 at the low potential of 1.38 V versus reversible hydrogen electrode (RHE), far surpassing the sluggish OER (1.65 V vs RHE). Electrochemical impedance spectroscopy indicates that the as‐fabricated heterostructure can promote the adsorption of OH− and the generation of the reactive species (O*). Theoretical calculations further outline the dual polarization of the Ni site at the interface, specifically the asymmetric charge redistribution (interfacial polarization) and in‐plane polarization. Consequently, the dual polarization modulates the d‐band center, which in turn regulates the adsorption/desorption strength of key reaction intermediates, thereby facilitating the entire EOR process. Moreover, a VOx−Ni3N‐based electrolyzer, coupling hydrogen evolution reaction (HER) and EOR, attains 50 mA cm−2 at a low cell voltage of ≈1.5 V. This work thus paves the way for creating dual polarization through interface engineering toward broad catalysis.

Abstract Matrix metalloproteinases (MMPs) had a variety of subtypes, which may be related to tumor invasion and angiogenesis, and the polymorphisms from MMPs have been also associated with the susceptibility to a variety of tumors, including prostate cancer (PCa). However, previous studies have not systematically analyzed the association between MMP and prostate cancer, so we conducted systematic data collection and analyzed to evaluate the relationship among polymorphisms in MMPs and PCa susceptibility. We searched PubMed, Web of Science, Embase and Google Scholar for all papers published up to Apr 3rd, 2023, and systematically analyzed the relationship among MMP1-1607 2G/1G, MMP2-1306 T/C, MMP2-735 T/C, MMP7-181 G/A, MMP9-1562 T/C and PCa susceptibility using multiple comparative models and subgroup analyses. We found that MMP2-1306 T/C polymorphism showed associations with PCa susceptibility, with the Ethnicity subgroup (Asian) being more pronounced. Similarly, MMP9-1562 T/C has also had associations with PCa susceptibility. Our current study found that the polymorphisms of, MMP2-1306 T/C, and MMP9-1562 T/C had strong associations with PCa risk.

Tropomyosin (TPM) is an important regulatory protein that binds to actin in fine myofilaments, playing a crucial role in the regulation of muscle contraction. TPM3, as one of four tropomyosin genes, is notably prevalent in eukaryotic cells. Traditionally, abnormal gene expression of TPM3 has been exclusively associated with myopathy. However, recent years have witnessed a surge in studies highlighting the close correlation between abnormal expression of TPM3 and the onset, progression, metastasis, and prognosis of various malignant tumors. In light of this, investigating the mechanisms underlying the pathogenetic role of TPM3 holds significant promise for early diagnosis and more effective treatment strategies. This article aims to provide an insightful review of the structural characteristics of TPM3 and its intricate role in the occurrence and development of malignant tumors.

The rapid development of cities has led to severe fragmentation of wetland landscapes, destroying their ecological function in climate regulation. However, most studies on the climate regulation services of wetlands focused on isolated wetland units, ignoring the overall function of wetland networks. The climate regulation function of wetlands can be improved by integrating fragmented wetland resources and building a stable wetland network. A case study was carried out in Changchun City, China, to improve the method of identifying ecological networks by considering the network energy flows. First, morphological spatial pattern analysis and landscape connectivity index combined with the wetland cooling index were used to identify ecological sources with high cooling capacity, and an ecological resistance surface was constructed with surface temperature as the main factor. The minimum cumulative resistance model was then used to identify the ecological network, which was then optimized by integrating patches as stepping stones to form the optimized ecological network. Finally, the importance of ecological corridors was evaluated by identifying ventilation corridors and integrated with the complex network theory to determine the ecological network robustness. We found that the degree of fragmentation in the studied wetlands was relatively high, and that construction of an ecological network with patches as stepping stones can improve its robustness. Each component in the ecological network had a high potential to mitigate the urban heat island effect, which can be further promoted by ecological corridors with high ventilation potential. Mutations in ecological nodes that cause network robustness played a key role in maintaining ecological network stability. This improved methodology effectively improves the scientific and practical application of wetland networks to mitigate the urban heat island effect and provides regions facing the contradiction of rapid development and wetland protection with strategies to reduce the threat of this effect.