Yingyu Zhou

Early‐onset colorectal cancer (EOCRC), defined as colorectal cancer diagnosed before 50 years of age, has increased markedly over the past decades, especially in high‐income settings. In parallel, obesity and related metabolic disturbances have become more common in both adults and younger populations, raising the possibility that excess adiposity contributes to the changing EOCRC burden. Epidemiological studies increasingly support this association, particularly for early‐life adiposity and persistent metabolic dysfunction. Most EOCRC cases are sporadic, indicating that environmental and lifestyle‐related exposures likely play a major role. Among these, obesity may be especially important because it links systemic metabolic stress with intestinal inflammation, microbial imbalance, and epigenetic change. However, the mechanisms through which obesity promotes early colorectal carcinogenesis are still not fully defined. In this review, we examine how obesity may shape EOCRC development across four interacting domains: chronic inflammation, metabolic reprogramming, gut microbiota dysbiosis, and epigenetic remodeling. We also discuss how these pathways may converge during early‐life windows of susceptibility and consider their implications for risk identification, prevention, and early intervention in younger populations.

Complicated relationships exist among lifestyles, gut microbiome (GM), and human health. Lifestyles can modulate the composition and function of GM, hence influencing the development of non-communicable diseases (NCDs). Recently, the socio-economic growth in China has led to the emergence of urbanized lifestyles, including unbalanced eating patterns and a sedentary lifestyle, causing an increased incidence of lifestyle-related NCDs among the Chinese population. In this review, we discussed the impact of lifestyle specific to the Chinese population on the GM and highlighted the mechanistic evidence that the commensals and their metabolites prevent or promote the pathogenesis of common lifestyle-related NCDs in China. Additionally, we described several microbiome-targeted therapies derived from traditional Chinese health practices, including traditional Chinese medicine treatments, the intake of fermented foods and tea, and Tai Chi intervention. In conclusion, we emphasized the significance of lifestyle-induced dysbiosis in the etiology of prevalent NCDs in China and provided relevant solutions, which should offer new insight into the treatment of these diseases to improve the overall health status of Chinese citizens.

Foodomics aids colorectal cancer management via diet and biomarkers, showing promise despite challenges.

Electrets can be used to develop self‐powered vibration sensors that rely on charged dielectrics to measure vibration parameters. A critical challenge in the sensor design is to simultaneously enlarge vibration amplitude and maintain a high surface voltage of the electret. In this study, an electret‐based flexible vibration sensor (E‐FVS) featuring a multifunctional PDMS seismic mass (MPSM) is proposed. Fabricated via molding, the MPSM comprises three parts: 1) a protruded additional mass for increasing the resonance vibration amplitude to enhance peak sensitivity, 2) a perforated film that reduces air damping to improve the overall sensitivity, and 3) a micro‐protrusion stopper that improves the durability by suppressing contact discharge in case of exposure to unexpectedly large accelerations. The E‐FVS operates effectively with excellent sensitivity (up to 1.154 V·g ⁻¹ ) in a frequency range of 15–600 Hz and good linearity ( R ² > 0.99) within an acceleration range of 0–5 g . Remarkably, the output voltage of the sensor has only attenuated by 0.75% after one million vibration tests. Combined with deep learning, the E‐FVS achieves a 99.17% accuracy in state identification of a self‐made fan. Monitoring of other vibrating machinery and human motion is also demonstrated, showing the sensor's broad application scenario.

Space flight has many adverse effects on the physiological functions of astronauts. Certain similarities have been observed in some physiological processes of rodents and astronauts in space, although there are also differences. These similarities make rodents helpful models for initial investigations into space-induced physiological changes. This study uses a 3D-Clinostat to simulate microgravity and explores the role of microgravity in space flight-induced liver and brain abnormalities by comparing changes in the gut microbiota, serum metabolites, and the function and physiological biochemistry of liver and brain tissues between the simulated microgravity (SMG) group mice and the wild type (WT) group mice. The study, based on hematoxylin-eosin (HE) staining, 16S sequencing technology, and non-targeted metabolomics analysis, shows that the gut tissue morphology of the SMG group mice is abnormal, and the structure of the gut microbiota and the serum metabolite profile are imbalanced. Furthermore, using PICRUST 2 technology, we have predicted the functions of the gut microbiota and serum metabolites, and the results indicate that the liver metabolism and functions (including lipid metabolism, amino acid metabolism, and sugar metabolism, etc.) of the SMG group mice are disrupted, and the brain tissue metabolism and functions (including neurotransmitters and hormone secretion, etc.) are abnormal, suggesting a close relationship between microgravity and liver metabolic dysfunction and brain dysfunction. Additionally, the high similarity in the structure of the gut microbiota and serum metabolite profile between the fecal microbiota transplant (FMT) group mice and the SMG group mice, and the physiological and biochemical differences in liver and brain tissues compared to the WT group mice, suggest that microgravity induces imbalances in the gut microbiota, which in turn triggers abnormalities in liver and brain metabolism and function. Finally, through MetaMapp analysis and Pearson correlation analysis, we found that valeric acid, a metabolite of gut microbiota, is more likely to be the key metabolite that relates to microgravity-induced gut microbiota abnormalities, disorders of amino acid and lipid metabolism, and further induced metabolic or functional disorders in the liver and brain. This study has significant practical application value for deepening the understanding of the adaptability of living organisms in the space environment.

Early detection of cancer significantly improves patient outcomes, with biomarkers offering a promising avenue for earlier and more precise diagnoses. Microfluidic biosensors have emerged as a powerful tool for detecting these biomarkers in body fluids, providing enhanced sensitivity, specificity, and rapid analysis. This review focuses on recent advances in microfluidic biosensors from 2018 to 2024, detailing their operational principles, fabrication techniques, and integration with nanotechnology for cancer biomarker detection. Additionally, we have reviewed recent innovations in several aspects of microfluidic biosensors, such as novel detection technologies, nanomaterials and novel microfluidic chip structures, which significantly enhance detection capabilities. We highlight key biomarkers pertinent to early cancer detection and explore how these innovations in biosensor technology contribute to the evolving landscape of personalized medicine. We further explore how these technologies could be incorporated into clinical cancer diagnostic workflows to improve early detection and treatment outcomes. These innovations could help enable more precise and personalized cancer diagnostics. In addition, this review addresses several important issues such as enhancing the scalability and sensitivity of these biosensors in clinical settings and points out future possibilities of combining artificial intelligence diagnostics with microfluidic biosensors to optimize their practical applications. This overview aims to guide future research and clinical applications by addressing current challenges and identifying opportunities for further development in the field of biomarker research.

As a kind of metabolically triggered inflammation, obesity influences the interplay between the central nervous system and the enteral environment. The present study showed that β-elemene, which is contained in various plant substances, had effects on recovering the changes in metabolites occurring in high-fat diet (HFD)-induced obese C57BL/6 male mice brains, especially in the prefrontal cortex (PFC) and hippocampus (HIP). β-elemene also partially reversed HFD-induced changes in the composition and contents of mouse gut bacteria. Furthermore, we evaluated the interaction between cerebral metabolites and intestinal microbiota via Pearson correlations. The prediction results suggested that Firmicutes were possibly controlled by neuron integrity, cerebral inflammation, and neurotransmitters, and Bacteroidetes in mouse intestines might be related to cerebral aerobic respiration and the glucose cycle. Such results also implied that Actinobacteria probably affected cerebral energy metabolism. These findings suggested that β-elemene has regulatory effects on the imbalanced microbiota-gut-brain axis caused by obesity and, therefore, would contribute to the future study in on the interplay between cerebral metabolites from different brain regions and the intestinal microbiota of mice.

The active compounds in Acanthopanax senticosus (AS) have different pharmacokinetic characteristics in mouse models. C_max and AUC of Acanthopanax senticosus polysaccharides (ASPS) were significantly reduced in radiation-injured mice, suggesting that the blood flow of mouse was blocked or slowed, due to the pathological state of ischemia and hypoxia, which are caused by radiation. In contrast, the ability of various metabolizing enzymes to inactivate, capacity of biofilm transport decrease, and lessening of renal blood flow accounts for radiation, resulting in the accumulation of syringin and eleutheroside E in the irradiated mouse. Therefore, there were higher pharmacokinetic parameters—AUC, MRT, and t_1/2 of the two compounds in radiation-injured mouse, when compared with normal mouse. In order to investigate the intrinsic mechanism of AS on radiation injury, AS extract’s protective effects on brain, the main part of mouse that suffered from radiation, were explored. The function of AS extract in repressing expression changes of radiation response proteins in prefrontal cortex (PFC) of mouse brain included tubulin protein family (α-, β-tubulin subunits), dihydropyrimidinase-related protein 2 (CRMP2), γ-actin, 14-3-3 protein family (14-3-3ζ, ε), heat shock protein 90β (HSP90β), and enolase 2. The results demonstrated the AS extract had positive effects on nerve cells’ structure, adhesion, locomotion, fission, and phagocytosis, through regulating various action pathways, such as Hippo, phagosome, PI3K/Akt (phosphatidylinositol 3 kinase/protein kinase B), Neurotrophin, Rap1 (Ras-related protein RAP-1A), gap junction glycolysis/gluconeogenesis, and HIF-1 (Hypoxia-inducible factor 1) signaling pathways to maintain normal mouse neurological activity. All of the results indicated that AS may be a promising alternative medicine for the treatment of radiation injury in mouse brain. It would be tested that whether the bioactive ingredients of AS could be effective through the blood–brain barrier in the future.