Hypoxia plays a critical role in both physiological and pathological processes. Cells adapt to hypoxia through the extensive reprogramming of gene expression. While the transcriptional regulations of hypoxia-inducible factors (HIFs) are well-studied, recent advances have emphasized the importance of post-transcriptional regulation, including mRNA translation, modification, stability, and degradation. Summarizing the regulation of mRNA homeostasis under hypoxia will improve our understanding of how hypoxia contributes to diseases such as cancer and ischemic injury. This review systematically summarizes the regulation of mRNA metabolism by hypoxia across multiple levels. First, hypoxia remodels mRNA transcription initiation and elongation. HIF-1 plays a critical role in this process by recruiting RNA polymerase II and releasing promoter-proximal pausing. Second, hypoxia suppresses global protein synthesis by phosphorylating eIF2α and inhibiting mTOR, while selectively upregulating key mRNAs (e.g., VEGFA) via internal ribosome entry sites (IRES). Third, hypoxia influences mRNA modifications, including m6A, m5C, and ac4C, thereby modulating mRNA stability and translation. Lastly, hypoxia influences mRNA stability and degradation through poly(A) tail dynamics and AU-rich elements. Hypoxia orchestrates mRNA metabolism through interconnected transcriptional and post-transcriptional mechanisms, enabling cells to adapt to oxygen deprivation. RNA-binding proteins play a role throughout the entire lifespan of mRNA and could serve as potential therapeutic targets for the treatment of hypoxia-related diseases. Oxygen is essential for normal life activities in a wide range of organisms, especially mammals. An adequate supply of oxygen is necessary for cellular and tissue metabolism. Certain physiological or pathological conditions, such as high altitudes, cancer, or ischemic disease, result in low oxygen levels and pressure within cells. This phenomenon is called hypoxia. The central aim of the hypoxia response is to restore oxygen homeostasis. Previous studies have shown that cells primarily adapt to hypoxia through hypoxia-inducible factor-mediated transcriptional regulation. Recent studies indicate that hypoxia regulates the mRNA life cycle through processes such as synthesis, processing, translation, and degradation. This review illustrates how mRNA homeostasis is regulated under hypoxic conditions and provides potential therapeutic targets for hypoxia-related diseases.

Introduction Sishen Wan (SSW), a classical traditional Chinese medicine decoction, is described to treat ulcerative colitis (UC) patients, but the molecular mechanisms of the main active ingredients of SSW on the interaction between mitochondria and T cells are still unclear. This study aimed to determine the main active ingredients of SSW, predict and explore the possible regulatory mechanism of main active ingredients of SSW in modulating mitochondrial function and ameliorating mitochondrial damage, followed by regulating T cell balance during UC development. Methods Colorimetric test and quantitative real-time polymerase chain reaction (qRT-PCR) were performed to evaluate the efficacy of SSW on inflammatory injuries of UC and preliminarily explore the mechanisms of SSW against oxidative stress. The main active components and their possible ligands were predicted by network pharmacology, molecular docking, dynamic simulation and three-dimensional-quantitative structure activity relationship (3D-QSAR). RNA-seq analysis and western blot (WB) was conduct to discover the impact of SSW on genetic profile changes, and discover and predict the potentials of anti-mitochondrial damage and proinflammatory T-cells of the selected bioactive compounds. Results SSW effectively ameliorated the colonic injuries and alleviated the oxidative stress in the dextran sulphate sodium (DSS)-induced UC. Angelicin, corylifolinin, psoralen and rutaecarpine, derived from SSW, were identified as the main components of SSW, and might interact with CYP2C9 and CYP1A1 due to the lowest binding energy. SSW alleviated UC via regulating genes related to mitochondrial function and T cell responses based on RNA-seq data. Cytc-related targets and T cell-associated proinflammatory cytokines were downregulated, while mtDNA repairing-related targets were upregulated with SSW intervention. Moreover, the caspase, inflammasome and Th1 and Th17 polarizing-related genes are positively correlated with cytochrome C oxidase (COX), caspase and inflammasome-associated genes, respectively. Conclusion Taken together, this study not only identifies the main bioactive ingredients of SSW and their possible ligands, but also provides angelicin, corylifolinin, psoralen and rutaecarpine may alleviate oxidative stress and mitochondrial damage, followed by modulating Th1 and Th17-related proinflammatory cytokines.

Alzheimer's disease (AD) incidence is rising with no effective treatments. Eleutheroside B (EB) has neuroprotective potential, but its therapeutic effects and mechanisms in AD are unclear. This study investigated EB's effects on AD pathologies and elucidated its underlying mechanisms using a transgenic Caenorhabditis elegans (C. elegans) model. We found that EB could ameliorate cognitive impairment, locomotor dysfunction, and shortened lifespan induced by amyloid-β(Aβ) and Tau aggregation in C. elegans, and reduce the relative expression levels of Aβ, Tau, and phosphorylated Tau (p-Tau) proteins. EB improved the health status and anti-aging capacity of the worms, as evidenced by prolonged healthspan, elevated pharyngeal pumping rate and body bend frequency, and increased body length and width. Notably, EB exhibited no observable toxicity even at high-dose administration. Furthermore, EB activated key stress-responsive transcription factors skn-1, daf-16, and hsf-1; it also increased the expression levels of antioxidant enzymes superoxide dismutase-3(SOD-3) and glutathione S-transferase 4(GST-4), decreased reactive oxygen species (ROS) levels, and elevated the expression of heat shock proteins Hsp-4 and Hsp-6. EB also reduced the accumulation of p62/SQST-1 protein, promoted the colocalization of lgg-1:GFP with lysosomes, and increased the relative mRNA expression of autophagy-related genes aak-2, unc-51, bec-1, vps-34, and lgg-1. After targeted knockdown of these genes, the protective effects of EB against AD-related pathologies were abolished. Our findings demonstrate that EB exhibits anti-aging properties and potential for ameliorating AD, which is likely mediated via antioxidative activities and autophagy induction.

Ulcerative colitis (UC) is a nonspecific inflammatory disease. Baicalein has potential value in treating UC, but its mechanism is unclear. This study aims to evaluate the protective effects of baicalein on dextran sodium sulfate (DSS)-induced UC mice. The UC model was established by 4% DSS solution for 7 days. Treatments included baicalein (10 mg/kg, 20 mg/kg) and sulfasalazine (200 mg/kg) via oral gavage. Colonic damage was assessed through body weight, disease activity index (DAI), histopathology (H&E staining) and colon length. Inflammatory cytokines were measured by ELISA, while oxidative stress markers and iron content were analyzed by colorimetric assays. Protein expression was evaluated by Western blot, and gene levels by RT-qPCR. Intestinal microbiota changes were characterized using 16S rRNA gene sequencing. Results demonstrated that Baicalein ameliorated UC mice, particularly in high-dose of baicalein group. After baicalein treatment, the proinflammatory cytokines (TNF-α, IL-1β), and anti-inflammatory cytokine (IL-10) has decreased. Additionally, high-dose of baicalein strongly reversed oxidative stress alterations caused by DSS, as evidenced by Fe2+, MDA, ROS significantly depleted, and MPO, SOD, GSH significantly increased. Protein and mRNA expression analyses revealed that high-dose baicalein upregulated the expression of FTH1, GPX4, SLC7A11, SLC3A2 and Nrf2, while downregulating ACSL4 significantly. Microbiological analysis showed that baicalein ameliorated intestinal dysbiosis, increased Ligilactobacillus and NK4A136, while reduced Clostridium_sensu_stricto_1 and Escherichia-Shigella. These findings suggest that baicalein mitigates DSS-induced UC mice by reducing oxidative stress and inflammation, suppressing ferroptosis and modulating gut microbiota composition, Proposing a potentially effective therapeutic approach for UC.

Fluoride, a naturally occurring element found in water, soil, food, and atmospheric precipitation, can lead to fluorosis and various health issues when consumed excessively. However, the mechanism of fluorosis is still under investigation. This study utilizes Caenorhabditis elegans as a model organism to investigate the effects of fluoride exposure on biological systems and to explore the mechanisms by which curcumin mitigates fluoride-induced toxicity. Three groups were established: a blank control, a sodium fluoride (NaF) exposure group (concentration 5 mmol/L), and a curcumin intervention group (concentration 25 μmol/L). Physiological parameters, lipofuscin levels, intracellular reactive oxygen species (ROS) levels, mitochondrial membrane potential, and mitochondrial copy numbers were measured to assess the effects of fluoride toxicity and curcumin protection. RNA-seq and qRT-PCR were utilized to investigate the molecular mechanisms underlying fluoride-induced damage and curcumin's mitigating effects. Results indicated that fluoride-exposed nematodes displayed physiological abnormalities, increased ROS production, higher lipofuscin levels, altered mitochondrial membrane potential and mitochondrial copy number, and activated MAPK signaling pathway genes. Curcumin exhibited protective effects on these parameters, suggesting its potential in preventing fluoride-induced harm by modulating oxidative stress and preserving mitochondrial function. This research enhances our understanding of the mechanisms of fluoride toxicity and highlights the potential benefits of curcumin.

Alternative splicing (AS) is a universal phenomenon in eukaryotes, and it is still challenging to identify AS events. Several methods have been developed to identify AS events, such as expressed sequence tags (EST), microarrays and RNA-seq. However, EST has limitations in identifying low-abundance genes, while microarray and RNA-seq are high-throughput technologies, and PCR-based technology is needed for validation. To overcome the limitations of EST and shortcomings of high-throughput technologies, we established a method to identify AS events, especially for low-abundance genes, by reverse transcription (RT) PCR with gene-specific primers (GSPs) followed by nested PCR. This process includes two major steps: 1) the use of GSPs to amplify as long as the specific gene segment and 2) multiple rounds of nested PCR to screen the AS and confirm the unknown splicing variants. With this method, we successfully identified three new splicing variants, namely, GenBank Accession No. HM623886 for the bdnf gene (GenBank GeneID: 12064), GenBank Accession No. JF417977 for the trkc gene (GenBank GeneID: 18213) and GenBank Accession No. HM623888 for the glb-18 gene (GenBank GeneID: 172485). In addition to its reliability and simplicity, the method is also cost-effective and labor-intensive. In conclusion, we developed an RT-nested PCR method using gene-specific primers to efficiently identify known and novel AS variants. This approach overcomes the limitations of existing methods for detecting rare transcripts. By enabling the discovery of new isoforms, especially for low-abundance genes, this technique can aid research into aberrant splicing in disease. Future studies can apply this method to uncover AS variants involved in cancer, neurodegeneration, and other splicing-related disorders.

Non-coding genomic variants constitute the majority of trait-associated genome variations; however, the identification of functional non-coding variants is still a challenge in human genetics, and a method for systematically assessing the impact of regulatory variants on gene expression and linking these regulatory variants to potential target genes is still lacking. Here, we introduce a deep neural network (DNN)-based computational framework, RegVar, which can accurately predict the tissue-specific impact of non-coding regulatory variants on target genes. We show that by robustly learning the genomic characteristics of massive variant-gene expression associations in a variety of human tissues, RegVar vastly surpasses all current non-coding variant prioritization methods in predicting regulatory variants under different circumstances. The unique features of RegVar make it an excellent framework for assessing the regulatory impact of any variant on its putative target genes in a variety of tissues. RegVar is available as a web server at https://regvar.omic.tech/.

目的 探讨黄连素对高盐高糖诱发的秀丽隐杆线虫形态和寿命改变的干预作用.方法 取秀丽线虫进行培养,随机分为正常对照组、高盐组、高糖组、高盐高糖组.正常对照组加入线虫NGM培养基;高盐组、高糖组、高盐高糖组下设模型对照组、10 mg/L黄连素干预组、20 mg/L黄连素干预组,先分别加入高盐培养基(含0.7%氯化钠的线虫NGM培养基)、高糖培养基(含1%葡萄糖的线虫NGM培养基)、高盐高糖培养基(含0.7%氯化钠和1%葡萄糖的线虫NGM培养基),然后向黄连素干预组中加入相应浓度的黄连素溶液,培养6 d.于第1、3、6天测定各组线虫体长、体宽及寿命,培养第6天采用RT-qPCR法检测线虫类似人胰岛素代谢相关基因daf-2、daf-16 mRNA.结果 与正常对照组相比,高盐、高糖以及高盐高糖组线虫体宽增加、寿命缩短(P均<0.05),体长无明显变化(P均>0.05),daf-2 mRNA表达升高、daf-16 mRNA表达降低(P均<0.05);与高盐、高糖以及高盐高糖组相比,添加黄连素组线虫的体宽降低、寿命延长(P均<0.05),体长无明显变化(P均>0.05),daf-2 mRNA表达降低、daf-16 mRNA表达升高(P均<0.05).结论 黄连素可抑制高盐高糖诱发的秀丽线虫形态改变以及寿命缩短,其机制可能是通过下调daf-2 mRNA表达、上调daf-16 mRNA表达来发挥作用.

目的 肥胖比例逐年增高,严重影响生命健康和生活质量.前期研究将柔性辟谷技术用于肥胖等慢病获得良好结果,但体验感有待进一步提高,此次研究将该方法与中药茶饮相结合,旨在有效减肥的基础上提升体验感,优化干预效果.方法 应用茯苓陈皮茶饮联合柔性辟谷技术对单纯性肥胖志愿者进行为期2周的限食干预,通过益生元调控肠道菌群来减除饥饿感,促进自身脂肪分解供能而减肥.结果 与干预前相比,辟谷第7天及复食第7天,志愿者体质量、体质量指数(BMI)均显著降低(P<0.01),脂肪率、腰臀比均下降(P<0.05),内脏脂肪面积在复食第7天较干预前明显减少(P<0.01);血压、心率在正常范围内有所降低(P<0.05);骨内矿物质、无机盐、蛋白质、全身肌肉量、骨骼肌、基础代谢量(BMR),在辟谷第7天较干预前有所下降(P<0.01),恢复饮食后与干预前相比无明显差异(P>0.05);辟谷第7天及复食第7天睡眠状况评分较干预前均有明显改善(P<0.01).饮食欲望、饥饿感、疲劳感在恢复饮食后低于干预前水平(P<0.05),精力及自律性较干预前明显提高(P<0.01).与干预前比较,恢复饮食后平和与基本平和体质增加,平和质与偏颇质构成比差异无统计学意义(P>0.05).结论 中药茶饮联合柔性辟谷可有效控制体质量,调节生理及心理状态,且安全性良好.

Curcumin is well known as a potent antioxidant and free radical scavenger and has great potential for anti-aging applications. In this study, we investigate the molecular mechanism of curcumin in prolonging the lifespan of C. elegans. Four concentrations of curcumin (10, 25, 50, and 100 µM) were administered, and the optimal treatment concentration was determined by analyzing the nematode lifespan, physiology, and biochemistry. Additionally, RNA-seq and qRT-PCR were performed to explore the antioxidant effect of curcumin and its underlying mechanism. Results revealed that curcumin could significantly improve the survival capacity of C. elegans without influencing its growth. Curcumin was observed to significantly decrease the levels of reactive oxygen species (ROS) under extreme conditions such as heat stress and paraquat stress. In addition, curcumin increased the amount of nematode mitochondrial DNA (mtDNA) replication. RNA-seq results revealed that the underlying mechanism of curcumin in C. elegans is related to the mitogen-activated protein kinase (MAPK) pathway. qRT-PCR results confirmed that the expression of oxidative stress-related genes (sod-1, sod-2, sod-3, gst-4) was increased, and the expression of MAPK signaling pathway-related genes (sek-1, pmk-1, nsy-1) was significantly downregulated. Furthermore, the administration of curcumin extended the lifespan of nematodes, potentially through the enhancement of oxidative stress resistance and the downregulation of the MAPK signaling pathway. These findings improve our understanding of both lifespan extension and the potential mechanism of curcumin in C. elegans.

随着生命科学与生物技术研究和应用的快速发展,生物经济也迎来了迅猛的发展时期,为21世纪是生命科学的世纪提供了有力的注解.然而,在看到生物经济发展的同时,也需要关注生物安全的问题.生物经济的良性发展和健康发展,既需要确保环境生物安全即体外生物安全,同时也要确保体内生物安全即人体共生微生物系统的健康安全.因此,亟需以科技向善、为人类谋福祉的负责任创新发展理念为先导,在确保体外生物安全和体内生物安全的前提下,促进生物经济又好又快发展.

Alzheimer's disease (AD) is the most common form of dementia without effective clinical treatment. Here, we show that intermittent fasting (IF) improves cognitive functions and AD-like pathology in a transgenic AD mouse model (5XFAD). IF alters gut microbial composition with a significant enrichment in probiotics such as Lactobacillus. The changes in the composition of the gut microbiota affect metabolic activities and metabolite production. Metabolomic profiling analysis of cecal contents revealed IF leads to a decreased carbohydrate metabolism (for example, glucose) and an increased abundance in amino acids (for example, sarcosine and dimethylglycine). Interestingly, we found that the administration of IF-elevated sarcosine or dimethylglycine mimics the protective effects of IF in 5XFAD mice, including the amelioration of cognitive decline, amyloid-β (Aβ) burden and glial overactivation. Our findings thus demonstrate an IF regimen is a potential approach to prevent AD progression, at least through the gut-microbiota-metabolites-brain axis, and constitutes an innovative AD therapeutic avenue.

Purpose Propofol is commonly used as an intravenous anesthetic in surgical patients. However, its usage is associated with adverse effects. Auxiliary medication can reduce the dose of intravenous anesthetics. Hence, we investigated whether vitamin C could lower propofol dosage in elderly patients undergoing total knee replacement surgery. Patients and Methods The trial was carried out in PLA General Hospital in Beijing, China. We enrolled patients aged ≥50 years who were undergoing unilateral total knee arthroplasty with total intravenous anesthesia combined with lumbar sciatic nerve block. The patients were randomly assigned to either the vitamin C (Vc) group (0.067 g/kg) or the control group (an equivalent dose of normal saline). Nerve block was done for all the patients before the general anesthesia. The same depth of anesthesia was maintained during the operation. We compared the propofol dosage and adverse events (eg hypotension) during anesthesia between the two groups. This study was registered with the Chinese Clinical Trial Registry, www.chictr.org.cn, number ChiCTR-TRC-16010112. Results There were significant differences in the total infusion dose (Vc group: 704.3 ± 188.6 mg; control group: 888.6 ± 232.7 mg; p = 0.016) and the average maintenance dose of propofol (Vc group: 5.8 ± 1.0 mg/kg/h; control group: 6.9 ± 1.6 mg/kg/h; p = 0.013). But there were no significant differences in the induction dose of propofol (control group: 90 mg, range 80–115 mg; Vc group: 100 mg, range 90–110 mg, p = 0.379) between the Vc and control groups. Furthermore, there were no significant differences in the hemodynamics and the incidence of intraoperative hypotension. Conclusion Vitamin C can reduce the dosage of propofol in patients undergoing total knee replacement.

ALT The Intake of Extremely Low Minerals and Bacteria Consumable Saccharides Secured Safety and Persistent of 7-14 Days Prolonged Total Dietary Deprivation Regimen. In: Abstract Objectives: The aim of this study was to evaluate a total fasting regimen assisted by a novel prebiotic, Flexible Abrosia (FA), in more than 7 days of continual dietary deprivation (7D-CDD). Our analysis included basic physical examinations, bioelectrical impedance analysis, and clinical lab and ELISA analysis in normal volunteers. Methods : Eight healthy subjects with normal body weight participated in 7D-CDD with the assistance of a specially designed probiotic. Individuals were assigned to take FA (113.4 KJ/10g/dose) at each mealtime to avoid possible injuries to intestinal flora and smooth the hunger sensation. During 7D-CDD, the subjects were advised to avoid any food intake, especially carbohydrates, except for drinking plentiful amounts of water. The examination samples were collected before CDD as self-control, at 7-d fasting, and after 7~14 d of refeeding. Four subjects were also tested after 6-m refeeding. Results: The FA-CDD regimen significantly decreased suffering from starvation, with tolerable hunger sensations during the treatment. With the addition of daily mineral electrolytes, the subjects not only passed through the entire 7D-CDD regimen but also succeed in up to 14D total fasting in three subjects. There was a significant reduction in blood glucose, insulin, and high-density lipoprotein levels during fasting, and the blood concentrations of uric acid (UA), alanine aminotransferase (ALT), and creatine kinase (CK) were increased. However, after more than 2 months of refeeding, the disease markers ALT, GOT, and CK either remained stable or were slightly downregulated compared to their initial 0 D control level. Conclusion: Our experiment has supplied the first positive evidence that, with the assistance of a daily nutritional supply around 100 kcal total calories to their intestinal flora, human subjects were able to tolerate hunger sensations. We have found that, although 7D-CDD induced increases in UA, CK, and transferases during fasting, refeeding led the markers to become either down-regulated or unchanged compared to their initial levels. This phenomenon was further confirmed in longer-term (6 m) recovery. Our results failed to support the hypothesis that fasting induced liver damage, since ALT, GOT, and CK remained low after longer-term refeeding. Our findings indicate that our 7D-CDD regimen which target of Intestinal flora saturation might be practical and that it might be valuable to design larger clinical fasting trials for improvement of health strategy-targeting in metabolic disorders.

本文在上一篇论文提出人体结构与功能的四元数矢量模型(→z)=a+b→i+c→j+d→k的基础上,从结构角度确定对应关系为(→z)(人的矢量)=a(人体标量)+b→i(菌群矢量)+c→j(线粒体矢量)+d→k(人脑矢量),从功能角度确定对应关系为(→z)(整体的人)=a(人体主动)+b→i(菌脑主吃)+c→j(粒脑主吸)+d→k(人脑主思),由此获得对人体结构与功能的新认识,即将"人"视为由1个标量和3个矢量组成的联合体,从而体现出自然界在"人类起源"过程中"先造菌、再造线粒体、后造人"的逻辑.据此可以合理解释"慢病源于肠道""饥饿源于菌群""吃五谷、得百病"等观点与问题,并可将慢病起源从以往关注的"人类基因致病论"推进发展为"肠道菌群基因致病在先、人类基因致病在后"的新认识,从而为慢病防控与健康管理提供新思路.该模型也支持了人与共生微生物之间具有"和合"思想而非"对抗"理念的传统认识,为正确理解"人与自然"以及"身心健康"提供了参考依据.

总是胃胀要注意 胃肠道是人体消化系统的重要组成部分.在日常生活中,由于生活方式和饮食习惯的变化,身体往往会出现不适,如胃部胀气(胃胀)、反酸呃逆等情况.这些虽然不是什么大事,但如果经常出现这样的情况,就说明身体健康已经发出危险信号,需要引起关注,以免发展为疾病状态.毕竟人体十分精密,无时不刻不在确保自身的健康运行,通常不会无缘无故地拉响警报,除非已经到了疾病边缘.

生命起源与进化是地球历史发展过程中的一个自然现象.即便是能够通过考古学和历史学研究等知晓人类是从动物进化而来的,然而通常也很难理解自然界进化出复杂生命现象的目的、动机和意义.虽然有"存在即合理"的说法,但如果进化是随机的,那么,自然界又怎么会进化出号称"万物之灵"的人类这一特殊的高级物种呢?从原始社会发展到现代社会,人类经历了数不胜数的自然灾害、疾病和战争等痛苦与磨难,其成长和发展过程实属不易.当前虽已进入21世纪,人类在物质文明与精神文明获得大发展的同时,却依然面临病毒疫情、慢病顽疾、焦虑抑郁、恐怖袭击、难民危机、战争阴云等压力,这就不得不令人深思,人类的出现与发展是否必须面对这些痛苦.在此前提出"菌心进化论"的基础上,进一步从"动机进化论"的角度进行学术探讨,旨在为人类存在与发展的意义和价值提供一种新解释,有利于对人类社会未来健康美好的生活图景进行科学展望.

肠道菌群作为隐形的"内分泌器官",广泛参与机体神经、内分泌、循环及消化等系统的调节,与宿主健康和多种慢性疾病的发生与发展息息相关.综述运动与肠道菌群相关文献发现:肠道菌群可通过调节运动系统的骨骼和骨骼肌的代谢,进而从免疫功能、能量代谢、代谢产物、抗氧化能力等方面影响机体的运动机能,并在延缓运动性疲劳的产生和消除等方面具有潜在的应用价值.因此本文以肠道菌群对骨骼与骨骼肌的影响为切入点,总结肠道菌群与运动系统、运动机能的研究现状,深入分析其潜在的相关作用机制,为肠道菌群在运动科学领域的后续研究和应用提供借鉴与参考.

当前我国仍处在慢性病高发阶段,而老龄化社会的到来,更是给当前的慢病防控工作带来了压力.医学领域和药物研发机构持续发力,希望能够找到有效防控慢性病的新策略和新方法.令人意外的是,越来越多的信息指向了慢性病与肠道菌群之间的相关性. 很难想象,作为与人体相生相伴、终生共存的熟悉的"陌生人",肠道菌群在慢性病中的作用正逐渐从相关性向因果性发展.在此简要梳理一下肠道菌群目前看来前沿的、有意思的科研进展,帮助大家熟悉与理解肠道菌群的作用.