（Phenomics期刊2024年第四期封面图）
01
Living Conditions Alter Ketogenic Diet-induced Metabolic Consequences in Mice through Modulating Gut Microbiota
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引用格式：
Yang, J., Li, X., Dai, C. et al. Living Conditions Alter Ketogenic Diet-induced Metabolic Consequences in Mice through Modulating Gut Microbiota. Phenomics 4, 313–326 (2024). https://doi.org/10.1007/s43657-024-00161-1
Abstract
Many laboratories have demonstrated that the ketogenic diet (KD) can lead to weight loss and reduced fasting glucose levels, while also increasing total serum cholesterol levels. However, it's worth noting that the specific outcomes induced by KD can vary across different research settings. Certain studies have indicated that environmental factors, such as housing conditions and the acidity of drinking water, can influence physiological parameters and gut microbes in mice. Thus, our current study aimed to investigate whether differences in housing conditions and pH levels of drinking water contribute to variations in KD-induced phenotypes and gut microbes. Our findings revealed that mice housed in conventional (CV) conditions experienced more significant weight loss, lower fasting blood glucose levels, and a greater elevation of blood cholesterol levels compared to those in the specific pathogen-free (SPF) condition. Additionally, similar differences were observed when comparing mice fed with non-acidified water versus acidified water. Furthermore, we analyzed cecum content samples using 16S rRNA sequencing to assess gut microbial composition and found that the tested environmental variables also had an impact on the gut microbial composition of KD-fed mice, which was correlated with their phenotypic alterations. In summary, both housing conditions and the pH of drinking water were identified as crucial environmental factors that influenced KD-induced changes in metabolic phenotypes and gut microbes. Our study emphasizes the importance of considering these factors in animal studies related to KD and gut microbes, as well as in other types of animal research.
Housing conditions influence KD-induced decreasing of body weight and fasting blood glucose and increasing of serum TC
02
Risk of Cardiovascular Disease Hospitalization After Common Psychiatric Disorders: Analyses of Disease Susceptibility and Progression Trajectory in the UK Biobank
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引文格式：
Han, X., Zeng, Y., Shang, Y. et al. Risk of Cardiovascular Disease Hospitalization After Common Psychiatric Disorders: Analyses of Disease Susceptibility and Progression Trajectory in the UK Biobank. Phenomics 4, 327–338 (2024). https://doi.org/10.1007/s43657-023-00134-w
Abstract
Whether associations between psychiatric disorders and hospitalization for cardiovascular diseases (CVDs) can be modified by disease susceptibility and the temporal pattern of these associated CVDs remain unknown. In our study, we conducted a matched cohort study of the UK Biobank including 44,430 patients with common psychiatric disorders (anxiety, depression, and stress-related disorders) between 1997 and 2019, together with 222,150 sex-, Townsend deprivation index-, and birth year- individually matched unexposed individuals. The hazard ratios (HRs) for CVD hospitalization associated with a prior psychiatric disorder were derived from Cox models, adjusted for multiple confounders. We then stratified the analyses by self-reported family history of CVD and CVD polygenic risk score (PRS) calculated based on summary statistics of independent genome-wide association studies. We further conducted disease trajectory analysis and visualized the temporal pattern of CVDs after common psychiatric disorders. During a mean follow-up of 12.28 years, we observed an elevated risk of CVD hospitalization among patients with psychiatric disorders, compared with matched unexposed individuals (hazard ratios [HRs] = 1.20, 95% confidence interval [CI]: 1.18–1.23), especially during the first six months of follow-up (1.72 [1.55–1.91]). The stratification analyses by family history of CVD and by CVD PRS obtained similar estimates between subgroups with different susceptibilities to CVD. We conducted trajectory analysis to visualize the temporal pattern of CVDs after common psychiatric disorders, identifying primary hypertension, acute myocardial infarction, and stroke as three main intermediate steps leading to further increased risk of other CVDs. In conclusion, the association between common psychiatric disorders and subsequent CVD hospitalization is not modified by predisposition to CVD. Hypertension, acute myocardial infarction, and stroke are three initial CVDs linking psychiatric disorders to other CVD sequelae, highlighting a need of timely intervention on these targets to prevent further CVD sequelae among all individuals with common psychiatric disorders.
Flowchart of the participants' selection
03
Cell-Free DNA in Plasma Reveals Genomic Similarity Between Biliary Tract Inflammatory Lesion and Biliary Tract Cancer
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引文格式：
Liu, R., Song, Y., Hua, R. et al. Cell-Free DNA in Plasma Reveals Genomic Similarity Between Biliary Tract Inflammatory Lesion and Biliary Tract Cancer. Phenomics 4, 339–351 (2024). https://doi.org/10.1007/s43657-024-00160-2
Abstract
Similar clinical manifestations and imaging features between biliary tract inflammatory lesion (BTI) and biliary tract cancer (BTC) pose significant challenges for the management of BTC. To date, the molecular characteristics of the relationship between biliary tract inflammatory lesion and biliary tract cancer remain poorly elucidated. Here, we performed target deep sequencing on 45 BTC patients and 31 BTI patients based on cell-free DNA (cfDNA) in plasma. We characterized the mutational features of 93 cancer-related genes for BTI and BTC. A total of 41% of genes showed concordance between BTI and BTC patients. Mutation burden in cfDNA exhibits a correlation with the levels of cancer antigen 19-9 (CA19-9) (r = 0.420) and carcinoembryonic antigen (CEA) (r = 0.580). Tumor protein p53 (TP53) and low-density lipoprotein receptor-related protein 1B (LRP1B) exhibit the most significant disparity in mutation frequencies between BTC and BTI. Additionally, based on cfDNA, we developed an algorithm, allele fraction variance (AFV), as a supplemental tool for BTC prognosis. Preoperative AFV performed better in predicting prognosis than postoperative one. These findings indicate that genetic mutations in cfDNA accumulate during the progression from BTI to BTC. cfDNA in plasma implies a prognostic value for the BTC.
Overview of the study
04
Associations of Plasma Lipidomic Profiles with Uric Acid and Hyperuricemia Risk in Middle-Aged and Elderly Chinese
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引文格式：
Kang, W., Xu, X., Yang, X. et al. Associations of Plasma Lipidomic Profiles with Uric Acid and Hyperuricemia Risk in Middle-Aged and Elderly Chinese. Phenomics 4, 352–364 (2024). https://doi.org/10.1007/s43657-024-00157-x
Abstract
Little is known about the links of disturbed lipid metabolism with hyperuricemia (HUA). We aimed to investigate the associations of lipidomic profiles with uric acid (UA)/HUA and their modifying factors in middle-aged and elderly Chinese. A total of 350 lipids were quantified in 2247 community-based Chinese aged 50–70 years by high-coverage targeted lipidomics. HUA was defined by plasma UA > 420 μmol/L in men or > 360 μmol/L in women. The prevalence of HUA in this population was 10.4%. After multivariable adjustment including BMI and lifestyle, 123 lipids were significantly associated with UA, predominantly glycerolipids (GLs) and glycerophospholipids (GPs). Specifically, diacylglycerol [DAG (16:0/22:5), DAG (16:0/22:6), DAG (18:1/20:5), DAG (18:1/22:6)], phosphatidylcholine [PC (16:0/20:5)), and triacylglycerol (TAG (53:0)] were the most significant lipid signatures positively associated with HUA risk, while lysophosphatidylcholine (LPC (20:2)) was inversely associated with HUA risk (p < 0.05). Network analysis also showed a positive association between TAGs/PCs/DAGs contained module and HUA risk (p < 0.01). Notably, HUA-related lipids were associated with de novo lipogenesis fatty acids, especially 16:1n-7 (Spearman correlation coefficients = 0.32–0.41, p < 0.001). Reduced rank regression showed that increased aquatic products intake was correlated to elevated HUA risk and HUA-associated lipids; while high dairy consumption was correlated with low level of HUA-associated lipids (|factor loadings| ≥ 0.2). Moreover, mediation analyses suggested that the lipid-HUA associations were partially mediated by retinol-binding protein 4 (RBP4, mediation proportion 5–14%), an adipokine linked with dyslipidemia and insulin resistance. In conclusion, disturbed specific metabolisms of GLs and GPs were associated with high prevalent HUA, partially mediated by RBP4 and/or influenced by certain dietary factors.
Manhattan plot for the associations of 350 lipids with uric acid within each subclass
05
Dissecting the Implications of Calumenin in Malignancy and Heterogeneity of the Microenvironment of Clear Cell Renal Cell Carcinoma Using Multi-Omics Data
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引文格式：
Wu, XQ., Shang, Z., Xiong, C. et al. Dissecting the Implications of Calumenin in Malignancy and Heterogeneity of the Microenvironment of Clear Cell Renal Cell Carcinoma Using Multi-Omics Data. Phenomics 4, 365–378 (2024). https://doi.org/10.1007/s43657-024-00169-7
Abstract
Increasing evidence indicates that Calumenin (CALU), which is localized in the endoplasmic reticulum, is significantly associated with tumor progression. However, the effect of CALU on patients with clear cell renal cell carcinoma (ccRCC) is unknown. By integrating multi-omics data and molecular biology experiments, we found that CALU expression was significantly increased in tumors compared with normal tissues, and the pathological grade and prognosis of patients were correlated with CALU expression. Next, knockdown or ectopic expression of CALU could affect the proliferative and invasive abilities of ccRCC cells. Moreover, immune landscape characterization revealed that CALU expression was positively associated with neutrophils and macrophages, whereas it was negatively associated with natural killer T cells and CD8+ T cells. Single-cell sequencing showed that the localization and binding targets of CALU mainly involved monocytes/macrophages and CD4+ and CD8+ T-cells. Sensitivity analysis of common chemotherapeutic drugs showed that high expression of CALU could sensitize chemotherapeutic drugs such as 5Z-7-Oxozeaenol, AMG-706 and Cytarabine, but could lead to drug resistance to chemotherapeutic drugs such as Embelin, Salubrinal and Tipifarnib. We demonstrated a significant correlation between high CALU expression and poor patient survival. Further, we demonstrated a correlation between CALU expression, tumor microenvironment, and the sensitivity of patients to common chemo- and immuno-therapy drugs. Thus, our results indicate that CALU could be a biomarker and designing personalized treatment approaches for ccRCC patients.
High CALU expression in patients with ccRCC indicates a poor prognosis
06
Senescence-Related LncRNAs: Pioneering Indicators for Ovarian Cancer Outcomes
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引文格式：
Fan, SB., Xie, XF., Wei, W. et al. Senescence-Related LncRNAs: Pioneering Indicators for Ovarian Cancer Outcomes. Phenomics 4, 379–393 (2024). https://doi.org/10.1007/s43657-024-00163-z
Abstract
In gynecological oncology, ovarian cancer (OC) remains the most lethal, highlighting its significance in public health. Our research focused on the role of long non-coding RNA (lncRNA) in OC, particularly senescence-related lncRNAs (SnRlncRNAs), crucial for OC prognosis. Utilizing data from the genotype-tissue expression (GTEx) and cancer genome Atlas (TCGA), SnRlncRNAs were discerned and subsequently, a risk signature was sculpted using co-expression and differential expression analyses, Cox regression, and least absolute shrinkage and selection operator (LASSO). This signature's robustness was validated through time-dependent receiver operating characteristics (ROC), and multivariate Cox regression, with further validation in the international cancer genome consortium (ICGC). Gene set enrichment analyses (GSEA) unveiled pathways intertwined with risk groups. The ROC, alongside the nomogram and calibration outcomes, attested to the model's robust predictive accuracy. Of particular significance, our model has demonstrated superiority over several commonly utilized clinical indicators, such as stage and grade. Patients in the low-risk group demonstrated greater immune infiltration and varied drug sensitivities compared to other groups. Moreover, consensus clustering classified OC patients into four distinct groups based on the expression of 17 SnRlncRNAs, showing diverse survival rates. In conclusion, these findings underscored the robustness and reliability of our model and highlighted its potential for facilitating improved decision-making in the context of risk assessment, and demonstrated that these markers potentially served as robust, efficacious biomarkers and prognostic tools, offering insights into predicting OC response to anticancer therapeutics.
Flowchart for the study
07
Site-Specific Quantitative N-Glycoproteomics: The Great Clinical Application Potential of GlycoQuant
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引文格式：
Yang, H., Yang, G., Lv, J. et al. Site-Specific Quantitative N-Glycoproteomics: The Great Clinical Application Potential of GlycoQuant. Phenomics 4, 394–396 (2024). https://doi.org/10.1007/s43657-024-00185-7
Conclusion
In all, Zhao et al. (2024) have made a significant contribution to the field of glycoproteomics with their novel and comprehensive approach to quantifying N-glycosylation. The GlycoQuant pipeline has the potential to discover new biomarkers for CKDs and enhance diagnostic accuracy. We anticipate that this pipeline will be widely applied to improve glycoproteoomics in clinical diagnosis, including O-glycoproteomics and other diseases. However, before clinical application, it is crucial to conduct external quality assessment (EQA) as mandated by regulatory agencies.
08
Dissecting the Implications of Calumenin in Malignancy and Heterogeneity of the Microenvironment of Clear Cell Renal Cell Carcinoma Using Multi-Omics Data
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引文格式：
Cheng, H., Li, B. True Ageing: An Up-to-date Model for Evaluating the Immune Age of the Chinese Population. Phenomics 4, 397–400 (2024). https://doi.org/10.1007/s43657-024-00166-w
Abstract
The pursuit of immortality has always been a long-standing aspiration of humanity. However, with increasing age comes the unexpected onset of aging. Although time is impartial, the process of ageing lacks uniformity. The human immune system changes with age and immune ageing significantly weakens an individual's resistance against various pathogens and cancer cells while simultaneously elevating the risk of immune disorders and chronic inflammation. Consequently, individuals who share the same chronological age may exhibit varying disease-fighting abilities. The substantial inter-individual variability underscores the imperative of precise monitoring to investigate the progressive alterations experienced by the immune system during ageing. Actually, numerous studies have focused on the changes in different lymphocyte subsets in diseases and immuno-senescence. However, quantitatively assessing host immunity remains a challenge, a comprehensive analysis of the alterations in both lymphocyte number and phenotype alterations induced by ageing remains lacking in China. Previous studies have primarily focused on the phenotypic changes in immune subsets during ageing, often utilizing a limited control cohort or lacking appropriate age-matched controls. Therefore, the standard immune markers and immune age evaluation model tailored to the Chinese population were currently needed. In a recent study, Jia et al. conducted a comprehensive investigation on a large-scale healthy Chinese cohort and successfully developed the first and largest immune age prediction model specifically tailored for the Chinese population. Here, we discussed this immune age evaluation model for the Chinese population and gave some suggestions for further improvement.
Schematic of the immune age prediction model for the Chinese population
09
Modulating and Imaging Macrophage Reprogramming for Cancer Immunotherapy
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引文格式：
Wang, J., Lu, Y., Zhang, R. et al. Modulating and Imaging Macrophage Reprogramming for Cancer Immunotherapy. Phenomics 4, 401–414 (2024). https://doi.org/10.1007/s43657-023-00154-6
Abstract
Cancer immunotherapy has made great progress in effectively attacking or eliminating cancer. However, the challenges posed by the low reactivity of some solid tumors still remain. Macrophages, as a key component of the tumor microenvironment (TME), play an important role in determining the progression of solid tumors due to their plasticity and heterogeneity. Targeting and reprogramming macrophages in TME to desired phenotypes offers an innovative and promising approach for cancer immunotherapy. Meanwhile, the rapid development of in vivo molecular imaging techniques provides us with powerful tools to study macrophages. In this review, we summarize the current progress in macrophage reprogramming from conceptual roadmaps to therapeutic approaches, including monoclonal antibody drugs, small molecule drugs, gene therapy, and chimeric antigen receptor-engineered macrophages (CAR-M). More importantly, we highlight the significance of molecular imaging in observing and understanding the process of macrophage reprogramming during cancer immunotherapy. Finally, we introduce the therapeutic applications of imaging and reprogramming macrophages in three solid tumors. In the future, the integration of molecular imaging into the development of novel macrophage reprogramming strategies holds great promise for precise clinical cancer immunotherapy.
The typical markers and morphology of polarized macrophages
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