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Age-related osteoporosis is characterized by the deterioration in bone volume and strength, partly due to the dysfunction of bone marrow mesenchymal stromal/stem cells (MSCs) during aging. Alpha-ketoglutarate (αKG) is an essential intermediate in the tricarboxylic acid (TCA) cycle. Studies have revealed that αKG extends the lifespan of worms and maintains the pluripotency of embryonic stem cells (ESCs). Here, we show that the administration of αKG increases the bone mass of aged mice, attenuates age-related bone loss, and accelerates bone regeneration of aged rodents. αKG ameliorates the senescence-associated (SA) phenotypes of bone marrow MSCs derived from aged mice, as well as promoting their proliferation, colony formation, migration, and osteogenic potential. Mechanistically, αKG decreases the accumulations of H3K9me3 and H3K27me3, and subsequently upregulates BMP signaling and Nanog expression. Collectively, our findings illuminate the role of αKG in rejuvenating MSCs and ameliorating age-related osteoporosis, with a promising therapeutic potential in age-related diseases. α-ketoglutarate is an intermediate of the Krebs Cycle that was recently reported to extend lifespan in C.Elegans. Here, the authors show that administration of α-ketoglutarate to mice reduces age-related bone loss, by ameliorating senescence of bone-marrow derived mesenchymal stem cells.

In this work, laminated ammonium perchlorate-based composite (LAPC) with high thermal decomposition performance was prepared by ice-template freezing-induced assembly strategy. Cobalt-Konjac glucomannan (Co 2+ -KGM) hydrosol with rich AP embedded was designed and used as a frozen precursor. LAPC was obtained from the ice-template freezing of the hydrosol precursor and crystallization of AP molecules. The structure and morphology of as-obtained composite were characterized, and the thermal decomposition performances were investigated. The results showed that LAPC materials have micro-/nano-lamellar structures with the thickness size of 20 μm, which are composed of AP micro-/nanoparticles formed in the freezing crystalline progress and uniformly dispersed Co 2+ -KGM coated on the surface and inside of the micro-/nanoparticles. Thermal analysis results show that LAPC-2 has a lower decomposition temperature than raw AP, which have decreased by 114.3 °C. The activation energy of LAPC-2 thermal decomposition was reduced by 87 kJ/mol from 200 kJ/mol of AP to 113 kJ/mol of LAPC-2. A possible catalytic mechanism of thermal decomposition of LAPC is proposed. Under heating condition, the Co 2+ -KGM molecules firstly decomposed, and Co-based oxides can be in situ generated on the surface and inside of AP particles, resulting in enhancing the catalytic contact areas. Abundant distributed nanoscale Co-based oxides boosted the thermal decomposition of AP and exhibited excellent catalytic performances. Graphic abstract

This study elucidates the mechanism by which GLIS Family Zinc Finger 2 (GLIS2) promotes epithelial‐mesenchymal transition (EMT) in gastric cancer through biglycan (BGN) activation and Wnt/β‐catenin stimulation. By analyzing 18 pairs of GC tissues and establishing in vitro models (combining GLIS2 knockdown/BGN overexpression with Wnt pathway modulators), we demonstrated that GLIS2 directly binds to the BGN promoter to enhance its transcription, thereby activating Wnt/β‐catenin signaling and significantly promoting GC cell migration, invasion, and EMT. Functional rescue experiments confirmed that BGN overexpression reverses the inhibitory effects of GLIS2 knockdown, while the Wnt/β‐catenin inhibitor XAV‐939 effectively blocks BGN's tumor‐promoting effects. These findings establish the crucial role of the GLIS2‐BGN‐Wnt/β‐catenin axis in regulating GC EMT and identify novel potential therapeutic targets for GC treatment.

Observations of topological surface states provide strong evidence that MoTe 2 is a type-II Weyl semimetal, hosting Weyl fermions that have no counterpart in high-energy physics. Weyl semimetal is a new quantum state of matter 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 hosting the condensed matter physics counterpart of the relativistic Weyl fermions 13 originally introduced in high-energy physics. The Weyl semimetal phase realized in the TaAs class of materials features multiple Fermi arcs arising from topological surface states 10 , 11 , 14 , 15 , 16 and exhibits novel quantum phenomena, such as a chiral anomaly-induced negative magnetoresistance 17 , 18 , 19 and possibly emergent supersymmetry 20 . Recently it was proposed theoretically that a new type (type-II) of Weyl fermion 21 , 22 that arises due to the breaking of Lorentz invariance, which does not have a counterpart in high-energy physics, can emerge as topologically protected touching between electron and hole pockets. Here, we report direct experimental evidence of topological Fermi arcs in the predicted type-II Weyl semimetal MoTe 2 (refs  23 , 24 , 25 ). The topological surface states are confirmed by directly observing the surface states using bulk- and surface-sensitive angle-resolved photoemission spectroscopy, and the quasi-particle interference pattern between the putative topological Fermi arcs in scanning tunnelling microscopy. By establishing MoTe 2 as an experimental realization of a type-II Weyl semimetal, our work opens up opportunities for probing the physical properties of this exciting new state.

This study aimed to determine long non‐coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) expression in pancreatic cancer and to explore the potential molecular actions of SNHG14 in mediating pancreatic cancer progression. Gene expression was detected by quantitative real‐time PCR. Cell proliferation, growth and invasion were detected by respective CCK‐8, colony formation, and transwell invasion assays. Protein levels were measured by Western blotting. Cell apoptosis and caspase‐3 activity were detected by flow cytometry and caspase‐3 activity assay. The link between miR‐613 and its targets was evaluated by luciferase reporter assay. In vivo tumour growth was evaluated using a xenograft model of nude mice. SNHG14 expression was up‐regulated in cancerous tissues from pancreatic cancer patients. High expression of SNHG14 was associated with poor tumour differentiation, advanced TNM stage and nodal metastasis. SNHG14 overexpression enhanced cell proliferative, growth and invasive abilities, and suppressed apoptotic rates and caspase‐3 activity in pancreatic cancer cells, while SNHG14 knockdown exerted opposite effects. Mechanistic studies revealed that miR‐613 was targeted by SNHG14, and Annexin A2 (ANXA2) was targeted and inversely regulated by miR‐613 in pancreatic cancer cells. In vivo studies showed that SNHG14 knockdown attenuated tumour growth. MiR‐613 was down‐regulated and ANXA2 was up‐regulated in the pancreatic cancer tissues, and SNHG14 expression levels were inversely correlated with miR‐613 expression levels and positively correlated with the ANXA2 mRNA expression levels. Collectively, our results suggest that SNHG14 potentiates pancreatic cancer progression through modulation of annexin A2 expression via acting as a competing endogenous RNA for miR‐613.

NaClO4-based molecular perovskite (H2dabco)[Na(ClO4)3] combined with the inorganic oxidizer and organic fuel was prepared by molecular assembly strategy. The high-yield samples were obtained by the one-pot reaction of NaClO4, HClO4, and triethylenediamine (dabco). The thermal analysis results showed molecular perovskite (H2dabco)[Na(ClO4)3] with ABX3-type closely ternary molecular stacking structure had a lower decomposition temperature (381.7 °C) and a higher heat release (2770 J/g) than NaClO4 (569.2 °C and 353 J/g). The apparent activation energy of thermal decomposition process was reduced by 25 kJ/mol from 184.8 kJ/mol of NaClO4 to 159.8 kJ/mol of (H2dabco)[Na(ClO4)3]. A synergistic catalysis thermal decomposition mechanism was proposed. The H2dabco2+ from the unique ternary molecular perovskite structure can be favorable for proton excitation under thermal stimuli, and promote the formation of HClO4 and superoxide radical anions ·O2− further, resulted in the redox thermal decomposition reaction between oxidizer ClO4− and fuel dabco more completely.

Sensorimotor impairments-such as reduced gait speed, diminished balance, and lower muscle strength-are common in older adults and have been suggested as early markers of cognitive decline. However, evidence from real-world hospital settings remains limited. This study investigated the associations between multiple sensorimotor functions and cognitive performance in hospitalized older adults. A retrospective cross-sectional study was conducted among 548 inpatients aged ≥ 60 years. Sensorimotor measures included gait speed, Timed Up and Go (TUG), handgrip strength, balance score, and activities of daily living (ADL). Cognitive performance was assessed using the Mini-Mental State Examination (MMSE). Correlations were analyzed using Pearson coefficients, followed by multivariable linear and logistic regression models adjusting for demographic, clinical, and laboratory covariates. Only handgrip strength showed a significant positive correlation with MMSE score ( = 0.085, = 0.046), whereas gait speed, TUG, balance score, and ADL were not significantly associated with cognitive performance. In multivariable linear regression, none of the sensorimotor measures independently predicted MMSE score after covariate adjustment. Education level was the strongest independent predictor of cognitive performance (β = 0.41, < 0.001). In the fully adjusted logistic regression model, gait speed was significantly associated with cognitive impairment, whereas other sensorimotor indicators were not independently associated. In this real-world hospital cohort, sensorimotor measures were not independently associated with continuous MMSE performance after adjustment. However, gait speed was associated with cognitive impairment status in the fully adjusted logistic regression model, suggesting limited utility of routine sensorimotor assessments for cognitive screening during acute hospitalization. These findings should be interpreted cautiously given the retrospective, single-center design and potential measurement variability during hospitalization.

In the context of peptide drug development, glycosylation plays a pivotal role. Accordingly, L-type peptides were synthesized predicated upon the PD-1/PD-L1 blocker DPPA-1. Subsequent glycosylation resulted in the production of two distinct glycopeptides, D-glu-LPPA-1 and D-gal-LPPA-1, by using D-glucose (D-glu) and D-galactose (D-gal), respectively, during glycosylation. Both glycopeptides significantly inhibited the interaction between PD-1 and PD-L1, and the measured half maximal inhibitory concentrations (IC50s) were 75.5 μM and 101.9 μM for D-glu-LPPA-1 and D-gal-LPPA-1, respectively. Furthermore, D-gal-LPPA-1 displayed a pronounced ability to restore T-cell functionality. In an MC38 tumor-bearing mouse model, D-gal-LPPA-1 demonstrated a significant inhibitory effect. Notably, D-gal-LPPA-1 substantially augmented the abundance and functionality of CD8+ T cells in the tumor microenvironment. Additionally, in the lymph nodes and spleens, D-gal-LPPA-1 significantly increased the proportion of CD8+ T cells secreting interferon-gamma (IFN-γ). These strong findings position D-gal-LPPA-1 as a potent enhancer of the antitumor immune response in MC38 tumor-bearing mice, underscoring its potential as a formidable PD-1/PD-L1 blocking agent.

Background Reprogrammed glucose metabolism of enhanced Warburg effect (or aerobic glycolysis) is considered as a hallmark of cancer. Long non-coding RNAs (lncRNAs) have been certified to play a crucial role in tumor progression. The current study aims to inquire into the potential regulatory mechanism of long intergenic non-protein coding RNA 242 (LINC00242) on aerobic glycolysis in gastric cancer. Method LINC00242, miR-1-3p and G6PD expression levels in gastric cancer tissues and cells were determined by qRT-PCR. Cell apoptosis or viability were examined by Flow cytometry or MTT assay. Western blot was utilized to investigate G6PD protein expression levels. Immunohistochemical (IHC) and hematoxylin and eosin (H&E) staining were used for histopathological detection. The targeted relationship between LINC00242 or G6PD and miR-1-3p was verified by luciferase reporter gene assay. Nude mouse xenograft was utilized to detect tumor formation in vivo. Result LINC00242 and G6PD was high-expressed in gastric cancer tissues and cells, and LINC00242 is positively correlated with G6PD . Silencing of LINC00242 or G6PD within gastric cancer cells prominently inhibited cell proliferation and aerobic glycolysis in vitro and relieved the tumorigenesis of gastric cancer in vivo. miR-1-3p was predicted to directly target both LINC00242 and G6PD . Overexpression of miR-1-3p suppressed gastric cancer cells proliferation and aerobic glycolysis. LINC00242 competitively combined miR-1-3p, therefore relieving miR-1-3p-mediated suppression on G6PD . Conclusion LINC00242 plays a stimulative role in gastric cancer aerobic glycolysis via regulation of miR-1-3p/ G6PD axis, therefore affecting gastric cancer cell proliferation.

Marine innovation, as a fundamental driving force behind the development of the marine economy, is crucial for the realization of the maritime power strategy. The reports from the 19th and 20th National Congresses of the Communist Party of China explicitly advocate for the acceleration of maritime power construction and emphasize the innovation-driven development strategy. Marine innovation and the resilience of the marine economy dynamically interact and mutually reinforce one another. Investigating the coordination between marine innovation and the resilience of the marine economy can provide theoretical support for regional marine technological innovation and sustainable economic development, thereby facilitating the achievement of innovation-driven development goals. This article establishes an evaluation index system for regional marine innovation capacity, considering two perspectives: marine innovation input and output. Additionally, it constructs an evaluation index system for marine economic resilience, which is based on three dimensions: resistance, robustness, and recovery. The entropy weight TOPSIS method is employed to calculate the sub-indices for China’s regional marine technological innovation capacity and marine economic resilience. Furthermore, a coordination degree and coordinated development degree model is developed to assess the coordination and development of marine innovation capacity and economic resilience across 11 coastal provinces (municipalities and autonomous regions) in China from 2013 to 2022. The research results indicate that from 2013 to 2022, the coordination degree of marine innovation capacity and economic resilience in the 11 coastal provinces (municipalities and autonomous regions) of China has exhibited a positive development trend. The southern and eastern economic circles display synchronized development patterns, with the southern economic circle experiencing the fastest improvements, while the northern economic circle shows slight regression. The marginal contribution of this study lies in the integration of marine innovation capacity and economic resilience for the first time, further exploring the degree of coordinated development based on coordination degree and providing a systematic analysis of the coordinated development of regional marine innovation and economic resilience from the perspectives of individual provinces and economic circles.