Longitudinal assessment of peripheral organ metabolism and the gut microbiota in an APP/PS1 transgenic mouse model of Alzheimer’s disease

Alzheimer’s disease not only affects the brain,but also induces metabolic dysfunction in peripheral organs and alters the gut microbiota.The aim of this study was to investigate systemic changes that occur in Alzheimer’s disease,in particular the association between changes in peripheral organ metabolism,changes in gut microbial composition,and Alzheimer’s disease development.To do this,we analyzed peripheral organ metabolism and the gut microbiota in amyloid precursor protein-presenilin 1(APP/PS1)transgenic and control mice at 3,6,9,and 12 months of age.Twelve-month-old APP/PS1 mice exhibited cognitive impairment,Alzheimer’s disease-related brain changes,distinctive metabolic disturbances in peripheral organs and fecal samples(as detected by untargeted metabolomics sequencing),and substantial changes in gut microbial composition compared with younger APP/PS1 mice.Notably,a strong correlation emerged between the gut microbiota and kidney metabolism in APP/PS1 mice.These findings suggest that alterations in peripheral organ metabolism and the gut microbiota are closely related to Alzheimer’s disease development,indicating potential new directions for therapeutic strategies.

基于ARIMA模型与GM(1,1)模型比较的宁夏卫生总费用及其构成预测研究

目的比较ARIMA模型和GM(1,1)模型对宁夏卫生费用的拟合效果,并预测宁夏卫生总费用及其构成的未来发展趋势,为相关部门制定和调整医疗卫生政策提供参考。方法利用2016年—2022年宁夏卫生总费用及其构成的相关数据,分别构建ARIMA模型和GM(1,1)模型,进行卫生总费用构成的拟合,采用平均绝对误差(Mean Absolute Error,MAE)和均方根误差(Root Mean Square Error,RMSE)比较拟合效果,基于优势模型对宁夏2023年—2028年卫生总费用及其构成进行预测。结果GM(1,1)模型拟合效果较好,为优势模型。预测结果显示,2023年—2028年,宁夏卫生总费用平稳增长,从465.38亿元增长至671.50亿元,政府和个人卫生支出占卫生总费用的比重分别从32.35%和25.39%下降至31.63%和22.53%,社会卫生支出占卫生总费用的比重从42.25%上升至45.84%。结论经预测,2023年—2028年宁夏卫生总费用呈逐年增长趋势,卫生费用筹资结构趋于合理化,相关部门应继续保持目前发展态势,采取有效措施以促进医疗卫生事业的可持续发展。

EEMD-LASSO-优化GM(1,N)管道腐蚀速率预测模型

【目的】为了评价管道的剩余强度与剩余寿命,并针对性地制定防腐措施,亟需提高管道腐蚀速率的预测精度。【方法】建立了一种基于集成经验模态分解(Ensemble Empirical Mode Decomposition,EEMD)-套索回归(Least Absolute Shrinkage and Selection Operator,LASSO)-优化一阶多维灰色模型〔First Order Multidimensional Grey Model,GM(1,N)〕的腐蚀速率预测模型。首先,采用EEMD算法增加原始自变量的多样性,降低序列波动对预测结果的影响,将隐藏在数据中的信息按照频域尺度逐层分解;之后,采用LASSO算法进行自变量筛选,降低序列间的相关性、冗余性;最后,引入线性修正量和灰色作用量对GM(1,N)模型进行优化,将微分方程变为差分方程,形成优化GM(1,N)模型,并将输入变量代入优化GM(1,N)模型完成训练和预测。【结果】与CO_(2)分压、SRB(Sulfate Reducing Bacteria)个数相关的影响权重较大,腐蚀过程由CO_(2)控制,共筛选出包括分解变量和残余变量在内的8个自变量;与灰色关联法筛选得到的影响因素相比,LASSO算法具有一定的客观性和科学性;EEMD-LASSO-GM(1,N)模型的平均相对误差为1.25%、标准差为0.72,模型精度超过常规GM(1,N)、EEMD-常规GM(1,N)、EEMD-优化GM(1,N)、EEMD-主成分分析-优化GM(1,N)等模型;通过与文献数据相对比,EEMD-LASSO-GM(1,N)模型的预测精度更高,其在泛化能力和鲁棒性上具有优越性,并在腐蚀影响因素和数据条数不同时,仍具有良好的适应性。【结论】研究结果可为多因素耦合的管道腐蚀行为预测和腐蚀速率发展趋势的预测提供理论依据及实际参考。

Liver as a new target organ in Alzheimer's disease:insight from cholesterol metabolism and its role in amyloid-beta clearance

Alzheimer's disease,the primary cause of dementia,is characterized by neuropathologies,such as amyloid plaques,synaptic and neuronal degeneration,and neurofibrillary tangles.Although amyloid plaques are the primary characteristic of Alzheimer's disease in the central nervous system and peripheral organs,targeting amyloid-beta clearance in the central nervous system has shown limited clinical efficacy in Alzheimer's disease treatment.Metabolic abnormalities are commonly observed in patients with Alzheimer's disease.The liver is the primary peripheral organ involved in amyloid-beta metabolism,playing a crucial role in the pathophysiology of Alzheimer's disease.Notably,impaired cholesterol metabolism in the liver may exacerbate the development of Alzheimer's disease.In this review,we explore the underlying causes of Alzheimer's disease and elucidate the role of the liver in amyloid-beta clearance and cholesterol metabolism.Furthermore,we propose that restoring normal cholesterol metabolism in the liver could represent a promising therapeutic strategy for addressing Alzheimer's disease.

Astrocytic endothelin-1 overexpression impairs learning and memory ability in ischemic stroke via altered hippocampal neurogenesis and lipid metabolism

Vascular etiology is the second most prevalent cause of cognitive impairment globally.Endothelin-1,which is produced and secreted by endothelial cells and astrocytes,is implicated in the pathogenesis of stroke.However,the way in which changes in astrocytic endothelin-1 lead to poststroke cognitive deficits following transient middle cerebral artery occlusion is not well understood.Here,using mice in which astrocytic endothelin-1 was overexpressed,we found that the selective overexpression of endothelin-1 by astrocytic cells led to ischemic stroke-related dementia(1 hour of ischemia;7 days,28 days,or 3 months of reperfusion).We also revealed that astrocytic endothelin-1 overexpression contributed to the role of neural stem cell proliferation but impaired neurogenesis in the dentate gyrus of the hippocampus after middle cerebral artery occlusion.Comprehensive proteome profiles and western blot analysis confirmed that levels of glial fibrillary acidic protein and peroxiredoxin 6,which were differentially expressed in the brain,were significantly increased in mice with astrocytic endothelin-1 overexpression in comparison with wild-type mice 28 days after ischemic stroke.Moreover,the levels of the enriched differentially expressed proteins were closely related to lipid metabolism,as indicated by Kyoto Encyclopedia of Genes and Genomes pathway analysis.Liquid chromatography-mass spectrometry nontargeted metabolite profiling of brain tissues showed that astrocytic endothelin-1 overexpression altered lipid metabolism products such as glycerol phosphatidylcholine,sphingomyelin,and phosphatidic acid.Overall,this study demonstrates that astrocytic endothelin-1 overexpression can impair hippocampal neurogenesis and that it is correlated with lipid metabolism in poststroke cognitive dysfunction.

Exploring the therapeutic potential of glucagon-like peptide 1agonists in metabolic disorders

This article comments on the work by Soresi and Giannitrapani.The authors have stated that one of the most novel and promising treatments for metabolic dysfunction-associated steatotic liver disease(MASLD)is the use of glucagon-like peptide 1 receptor agonists,especially when used in combination therapy.However,despite their notable efficacy,these drugs were not initially designed to target MASLD directly.In a groundbreaking development,the Food and Drug Administration has recently approved resmetirom,the first treatment specifically aimed at reducing liver fibrosis in metabolic-associated steatohepatitis.Resmetirom,an orally administered,liver-directed thyroid hormone beta-selective agonist,acts directly on intrahepatic pathways,enhancing its therapeutic potential and marking the beginning of a new era in the treatment of MASLD.Furthermore,the integration of lifestyle modifications into liver disease management is an essential component that should be considered and reinforced.By incorporating dietary changes and regular physical exercise into treatment,patients may achieve improved outcomes,reducing the need for pharmacological interventions and/or improving treatment efficacy.As a complement to medical therapies,lifestyle factors should not be overlooked in the broader strategy for managing MASLD.

基于GM(1,1)模型的河北省生鲜农产品冷链物流需求预测及其影响因素研究

为了掌握河北省生鲜农产品冷链物流的发展趋势,为政府制定发展冷链物流产业政策提供参考,文章以2012—2021年河北省生鲜农产品的产量作为原始数据,通过灰色预测模型进行预测,针对2024—2031年共八年河北省生鲜农产品冷链物流需求量进行预测;另一方面从区域经济发展水平、物流运输技术能力、冷链物流市场规模、冷链支撑条件水平、人文因素五个方面,构建一个能够反映影响河北省生鲜农产品冷链物流需求的各种因素的指标体系,在构建指标的过程中,采用灰色关联分析方法。在建立影响河北省生鲜农产品冷链物流需求的指标体系过程中,进行指标选取时,应用灰色关联分析的方法。经测算,本次生鲜农产品冷链物流需求量预测的精确度为95.7%,能够进行较为精确的预测,可以得出河北省生鲜农产品冷链物流的需求量逐年增长的结果。同时灰色关联分析表明,物流交通运输能力和人文因素对生鲜农产品冷链物流需求影响最为显著,其次是冷链物流市场规模,而区域经济发展水平和冷链支撑条件水平对河北省生鲜品冷链物流需求量的影响程度相对较弱。

Bletilla striata polysaccharides alleviate metabolic dysfunctionassociatedsteatotic liver disease through enhancing hepatocyteRelA/HNF1αsignal

BACKGROUND Bletilla striata polysaccharides(BSP)have antioxidant,immune regulation,and anti-fibrotic activities.However,the therapeutic effect and mechanisms underlying the action of BSP in metabolic dysfunction-associated steatotic liver disease(MASLD)have not been fully understood.AIMTo investigate the therapeutic effects and mechanisms of BSP on MASLD by centering on the hepatocyte nuclearfactor kappa B p65(RelA)/hepatocyte nuclear factor-1 alpha(HNF1α)signaling.METHODSA mouse model of MASLD was induced by feeding with a high-fat-diet(HFD)and a hepatocyte model of steatosiswas induced by treatment with sodium oleate(SO)and sodium palmitate(SP).The therapeutic effects of BSP onMASLD were examined in vivo and in vitro.The mechanisms underlying the action of BSP were analyzed for theireffect on lipid metabolism disorder,endoplasmic reticulum(ER)stress,and the RelA/HNF1αsignaling.RESULTSHFD feeding reduced hepatocyte RelA and HNF1αexpression,induced ER stress,lipid metabolism disorder,andnecroptosis in mice,which were significantly mitigated by treatment with BSP.Furthermore,treatment with BSP orBSP-containing conditional rat serum significantly attenuated the sodium oleate/sodium palmitate(SO/SP)-induced hepatocyte steatosis by decreasing lipid accumulation,and lipid peroxidation,and enhancing theexpression of RelA,and HNF1α.The therapeutic effects of BSP on MASLD were partially abrogated by RELAsilencing in mice and RELA knockout in hepatocytes.RELA silencing or knockout significantly down-regulatedHNF1αexpression,and remodeled ER stress and oxidative stress responses during hepatic steatosis.CONCLUSIONTreatment with BSP ameliorates MASLD,associated with enhancing the RelA/HNF1αsignaling,remodeling ERstress and oxidative stress responses in hepatocytes.

Mepiquat chloride increases the Cry1Ac protein content of Bt cotton under high temperature and drought stress by regulating carbon and amino acid metabolism

The effects of mepiquat chloride(DPC)on the Cry1Ac protein content in Bacillus thuringiensis(Bt)cotton boll shells under high temperature and drought stress were investigated to provide a theoretical reference for Bt cotton breeding and high-yield and-efficiency cotton cultivation.This study was conducted using Bt cotton cultivar‘Sikang 3'during the 2020 and 2021 growing seasons at Yangzhou University Farm,Yangzhou,Jiangsu Province,China.Potted cotton plants were exposed to high temperature and drought stress,and sprayed with either 20 mg L^(-1)DPC or water(CK).Seven days after treatment,the Cry1Ac protein content,α-ketoglutarate content,pyruvic acid content,glutamate synthase activity,glutamic oxaloacetic transaminase activity,soluble protein content,and amino acid content were measured,and transcriptome sequencing was performed.DESeq was used for differential gene analysis.Under the DPC treatment,the Cry1Ac protein content increased by 4.7-11.9% compared to CK.Theα-ketoglutarate content,pyruvic acid content,glutamate synthase activity,glutamic oxaloacetic transaminase activity,soluble protein content,and amino acid content all increased.Transcriptome analysis revealed 7,542 upregulated genes and 10,449 downregulated genes for DPC vs.CK.Gene ontology(GO)and Kyoto Encyclopedia of Gene and Genomes(KEGG)analyses showed that the differentially expressed genes were mainly involved in biological processes,such as carbon and amino acid metabolism.For example,genes encoding 6-phosphofructokinase,pyruvate kinase,glutamic pyruvate transaminase,pyruvate dehydrogenase,citrate synthase,isocitrate dehydrogenase,2-oxoglutarate dehydrogenase,glutamate synthase,1-pyrroline-5-carboxylate dehydrogenase,glutamic oxaloacetic transaminase,amino-acid N-acetyltransferase,and acetylornithine deacetylase were all significantly upregulated.The DPC treatment increased pyruvate,α-ketoglutarate,and oxaloacetate by increasing the operational rate of the glycolytic pathway of the citric acid cycle.It also significantly upregulated the genes encoding glutamate synthase,pyrrolidine-5-carboxylic acid dehydrogenase,glutamate oxaloacetate transaminase,and N-acetylglutamate synthetase,while it downregulated the genes encoding glutamine synthetase.Therefore,the synthesis of aspartic acid,glutamic acid,pyruvate,and arginine increased after treatment with DPC,and the Cry1Ac protein content was increased by regulating carbon and amino acid metabolism.

GLP-1 receptor agonists and myocardial metabolism in atrial fibrillation

Atrial fibrillation(AF)is the most common cardiac arrhythmia.Many medical conditions,including hypertension,diabetes,obesity,sleep apnea,and heart failure(HF),increase the risk for AF.Cardiomyocytes have unique metabolic characteristics to maintain adenosine triphosphate production.Significant changes occur in myocardial metabolism in AF.Glucagon-like peptide-1 receptor agonists(GLP-1RAs)have been used to control blood glucose fluctuations and weight in the treatment of type 2 diabetes mellitus(T2DM)and obesity.GLP-1RAs have also been shown to reduce oxidative stress,inflammation,autonomic nervous system modulation,and mitochondrial function.This article reviews the changes in metabolic characteristics in cardiomyocytes in AF.Although the clinical trial outcomes are unsatisfactory,the findings demonstrate that GLP-1 RAs can improve myocardial metabolism in the presence of various risk factors,lowering the incidence of AF.

Hepatic protein phosphatase 1 regulatory subunit 3G alleviates obesity and liver steatosis by regulating the gut microbiota and bile acid metabolism

Intestinal dysbiosis and disrupted bile acid(BA)homeostasis are associated with obesity,but the precise mechanisms remain insufficiently explored.Hepatic protein phosphatase 1 regulatory subunit 3G(PPP1R3G)plays a pivotal role in regulating glycolipid metabolism;nevertheless,its obesity-combatting potency remains unclear.In this study,a substantial reduction was observed in serum PPP1R3G levels in high-body mass index(BMI)and high-fat diet(HFD)-exposed mice,establishing a positive correlation between PPP1R3G and non-12a-hydroxylated(non-12-OH)BA content.Additionally,hepatocyte-specific overexpression of Ppp1r3g(PPP1R3G HOE)mitigated HFD-induced obesity as evidenced by reduced weight,fat mass,and an improved serum lipid profile;hepatic steatosis alleviation was confirmed by normalized liver enzymes and histology.PPP1R3G HOE considerably impacted systemic BA homeostasis,which notably increased the non-12-OH BAs ratio,particularly lithocholic acid(LCA).16S ribosomal DNA(16S rDNA)sequencing assay indicated that PPP1R3G HOE reversed HFD-induced gut dysbiosis by reducing the Firmicutes/Bacteroidetes ratio and Lactobacillus population,and elevating the relative abundance of Blautia,which exhibited a positive correlation with serum LCA levels.A fecal microbiome transplantation test confirmed that the anti-obesity effect of hepatic PPP1R3G was gut microbiotadependent.Mechanistically,PPP1R3G HOE markedly suppressed hepatic cholesterol 7a-hydroxylase(CYP7A1)and sterol-12a-hydroxylase(CYP8B1),and concurrently upregulated oxysterol 7-a hydroxylase and Takeda G protein-coupled BA receptor 5(TGR5)expression under HFD conditions.Furthermore,LCA administration significantly mitigated the HFD-induced obesity phenotype and elevated non-12-OH BA levels.These findings emphasize the significance of hepatic PPP1R3G in ameliorating diet-induced adiposity and hepatic steatosis through the gut microbiota-BA axis,which may serve as potential therapeutic targets for obesity-related disorders.

Effects of altering the ratio of C16:0 and cis-9 C18:1 in rumen bypass fat on growth performance, lipid metabolism, intestinal barrier, cecal microbiota, and inflammation in fattening bulls

Background C16:0 and cis-9 C18:1 may have different effects on animal growth and health due to unique metabolism in vivo.This study was investigated to explore the different effects of altering the ratio of C16:0 and cis-9 C18:1 in fat supplements on growth performance,lipid metabolism,intestinal barrier,cecal microbiota,and inflammation in fattening bulls.Thirty finishing Angus bulls(626±69 kg,21±0.5 months)were divided into 3 treatments according to the randomized block design:(1)control diet without additional fat(CON),(2)CON+2.5%palmitic acid calcium salt(PA,90%C16:0),and(3)CON+2.5%mixed fatty acid calcium salt(MA,60%C16:0+30%cis-9 C18:1).The experiment lasted for 104 d,after which all the bulls were slaughtered and sampled for analysis.Results MA tended to reduce 0–52 d dry matter intake compared to PA(DMI,P=0.052).Compared with CON and MA,PA significantly increased 0–52 d average daily gain(ADG,P=0.027).PA tended to improve the 0–52 d feed conversion rate compared with CON(FCR,P=0.088).Both PA and MA had no significant effect on 52–104 days of DMI,ADG and FCR(P>0.05).PA tended to improve plasma triglycerides compared with MA(P=0.077),significantly increased plasma cholesterol(P=0.002)and tended to improve subcutaneous adipose weight(P=0.066)when compared with CON and MA.Both PA and MA increased visceral adipose weight compared with CON(P=0.021).Only PA increased the colonization of Rikenellaceae,Ruminococcus and Proteobacteria in the cecum,and MA increased Akkermansia abundance(P<0.05).Compared with CON,both PA and MA down-regulated the m RNA expression of Claudin-1 in the jejunum(P<0.001),increased plasma diamine oxidase(DAO,P<0.001)and lipopolysaccharide(LPS,P=0.045).Compared with CON and MA,PA down-regulated the ZO-1 in the jejunum(P<0.001)and increased plasma LPS-binding protein(LBP,P<0.001).Compared with CON,only PA down-regulated the Occludin in the jejunum(P=0.013).Compared with CON,PA and MA significantly up-regulated the expression of TLR-4 and NF-κB in the visceral adipose(P<0.001)and increased plasma IL-6(P<0.001).Compared with CON,only PA up-regulated the TNF-αin the visceral adipose(P=0.01).Compared with CON and MA,PA up-regulated IL-6 in the visceral adipose(P<0.001),increased plasma TNF-α(P<0.001),and reduced the Ig G content in plasma(P=0.035).Compared with CON,PA and MA increased C16:0 in subcutaneous fat and longissimus dorsi muscle(P<0.05),while more C16:0 was also deposited by extension and desaturation into C18:0 and cis-9 C18:1.However,neither PA nor MA affected the content of cis-9 C18:1 in longissimus dorsi muscle compared with CON(P>0.05).Conclusions MA containing 30%cis-9 C18:1 reduced the risk of high C16:0 dietary fat induced subcutaneous fat obesity,adipose tissue and systemic low-grade inflammation by accelerating fatty acid oxidative utilization,improving colonization of Akkermansia,reducing intestinal barrier damage,and down-regulating NF-κB activation.

Regulation role of miR-204 on SIRT1/VEGF in metabolic memory induced by high glucose in human retinal pigment epithelial cells

AIM:To examine the regulatory role of microRNA-204(miR-204)on silent information regulator 1(SIRT1)and vascular endothelial growth factor(VEGF)under highglucose-induced metabolic memory in human retinal pigment epithelial(hRPE)cells.METHODS:Cells were cultured with either normal(5 mmol/L)or high D-glucose(25 mmol/L)concentrations for 8d to establish control and high-glucose groups,respectively.To induce metabolic memory,cells were cultured with 25 mmol/L D-glucose for 4d followed by culture with 5 mmol/L D-glucose for 4d.In addition,exposed in 25 mmol/L D-glucose for 4d and then transfected with 100 nmol/L miR-204 control,miR-204 inhibitor or miR-204 mimic in 5 mmol/L D-glucose for 4d.Quantitative reverse transcription-polymerase chain reaction(RT-qPCR)was used to detect miR-204 mRNA levels.SIRT1 and VEGF protein levels were assessed by immunohistochemical and Western blot.Flow cytometry was used to investigate apoptosis rate.RESULTS:It was found that high glucose promoted miR-204 and VEGF expression,and inhibited SIRT1 activity,even after the return to normal glucose culture conditions.Upregulation of miR-204 promoted apoptosis inhibiting SIRT1 and increasing VEGF expression.However,downregulation of miR-204 produced the opposite effects.CONCLUSION:The study identifies that miR-204 is the upstream target of SIRT1and VEGF,and that miR-204 can protect hRPE cells from the damage caused by metabolic memory through increasing SIRT1 and inhibiting VEGF expression.

基于灰色GM(1,1)模型的我国医院感染患病率变化趋势及预测

目的了解我国医院感染患病率变化趋势,并采用灰色GM(1,1)模型对我国不同规模医院的医院感染患病率进行预测,为医院感染防控提供数据支持和新思路。方法采用描述性流行病学方法分析我国医院感染患病率变化趋势,2008—2016年我国医院感染患病率数据进行灰色GM(1,1)模型构建,2018—2020年数据进行模型验证。采用构建的灰色GM(1,1)模型对2022—2024年我国医院感染患病率进行预测。结果我国医院感染患病率呈下降趋势,随着医院规模的增加医院感染患病率升高。医院感染患病率灰色GM(1,1)模型的精度良好、拟合效果较高。2024年全国、<300张床位医院、300~599张床位医院、600~899张床位医院和≥900张床位医院的医院感染患病率可降为1.00%、0.49%、0.90%、1.13%和2.05%。结论我国医院感染防控效果明显,灰色GM(1,1)模型对我国医院感染患病率有较好的预测效果。

基于灰色GM(1,1)模型的2023—2027年闵行区脑卒中死亡趋势预测

目的分析2012—2022年上海市闵行区脑卒中死亡变化趋势,预测2023—2027年脑卒中死亡情况。方法测算2012—2022年上海市闵行区脑卒中死亡的年度变化百分比(annual percentage change,APC),运用Joinpoint线性回归模型进行时间趋势分析。以2012—2022年上海市闵行区脑卒中死亡率构建灰色GM(1,1)模型,运用相对误差和级比偏差评估模型拟合效果,对2023—2027年上海市闵行区脑卒中死亡率进行预测分析。结果2012—2022年上海市闵行区脑卒中全人群、男性和女性粗死亡率均呈上升趋势(全人群:APC=2.50%,P<0.001;男性:APC=3.41%,P<0.001;女性:APC=1.46%,P=0.008)。灰色GM(1,1)模型预测2023—2027年上海市闵行区脑卒中死亡率呈上升趋势,2027年全人群脑卒中粗死亡率为97.55/10万,男性为112.31/10万,女性为83.33/10万,检验评估模型拟合效果达到较高要求。结论近十年来上海市闵行区脑卒中死亡率呈明显上升趋势,5年预测结果显示死亡率呈逐年上升趋势。

基于新陈代谢GM(1,1)++的疫情应急物资需求量预测研究

当大规模疫情发生时,应急物资的供给至关重要.在新陈代谢GM(1,1)模型的基础上提出了一种新陈代谢GM(1,1)++模型,即再加入新信息,移除原始数据中的旧信息的同时,将原始数据中与拟合值相对残差最大的数据项用拟合值替代.提出的方法既能够及时去掉意义逐渐降低的老信息,加入更能够反应系统目前特征的新信息,又能够降低其他因素对原始数据的扰动性,使原始数据更具规律性.为了检验新陈代谢GM(1,1)++模型的有效性,将其预测结果分别与传统GM(1,1)、新信息GM(1,1)、新陈代谢GM(1,1)的预测结果进行比较研究.试验结果显示,新陈代谢GM(1,1)++模型的误差平方和最小,预测准确性远优于另外3种预测模型.

臭氧结合1-MCP处理对油桃贮藏色泽和品质的影响

为探究臭氧调控方式对经1-甲基环丙烯(1-MCP)处理后的油桃在冷藏过程中的色泽和品质变化的影响,以油桃为试材,采后用1μL/L 1-MCP熏蒸24 h以及1-MCP熏蒸分别结合臭氧水雾化和臭氧气体熏蒸30 min后包装,然后于0±0.5℃条件下贮藏,定期测定相关理化指标。结果表明,1-MCP联合臭氧处理能有效抑制呼吸速率和乙烯产量。单独1-MCP处理抑制果肉中花青素的积累,阻碍了果肉的红色着色,而1-MCP联合臭氧处理在贮藏后期促进了果肉的红色着色。与单独1-MCP组相比,1-MCP联合臭氧处理组在贮藏后期花青素含量、矢车菊素-3-O-葡萄糖苷、矢车菊素-3-O-芸香糖苷含量和花青素代谢相关酶活性较高,同时,臭氧气体熏蒸的方式更有利于贮藏后期花青素的积累,果肉红色度更高。该研究为改善果实采后色泽调控以及优化1-MCP在采后保鲜中的应用提供了新的思路。

吉兰⁃巴雷综合征患者抗GM1抗体与抗甲状腺抗体的相关性研究

目的:探讨吉兰⁃巴雷综合征(Guillain⁃Barrésyndrome,GBS)患者抗甲状腺抗体与抗神经节苷脂GM1抗体的相关性。方法:收集2018年7月—2023年2月南京大学医学院附属鼓楼医院神经内科收治的同时检测抗甲状腺抗体和抗神经节苷脂抗体(antiganglioside antibody,AGA)水平的60例GBS患者,根据抗甲状腺抗体结果将患者分为正常组和异常组,比较两组患者的临床特征、甲状腺功能以及AGA比例。结果:与正常组相比,甲状腺功能异常组中GBS患者抗神经节苷酯GM1抗体和GM2抗体水平人明显升高,并伴有更严重的临床症状(P<0.05)。多因素Logistic回归分析显示,GBS患者抗甲状腺抗体异常(OR=5.184,95%CI:1.377~19.518,P=0.015)以及游离甲状腺素(free thyroxine,FT4)水平升高(OR=1.266,95%CI:1.009~1.588,P=0.030),是导致抗GM1抗体阳性率增加的独立危险因素。受试者工作特征(receiver operation characteristic,ROC)曲线显示甲状腺过氧化物酶抗体(thyroperoxidase antibody,TPO⁃Ab)预测GM1阳性的最佳阈值为47.9 U/mL,灵敏度为66.7%,特异度为77.8%。甲状腺球蛋白抗体(thyroglobulin antibody,Tg⁃Ab)预测GM1阳性的最佳阈值为20.0 U/mL,灵敏度为73.3%,特异度为73.3%。结论:合并抗甲状腺抗体异常的GBS患者更易出现抗GM1抗体阳性,这可能是合并甲状腺功能异常的GBS患者预后更差的可能机制。

Role of gut-liver axis and glucagon-like peptide-1 receptor agonists in the treatment of metabolic dysfunction-associated fatty liver disease

Metabolic dysfunction-associated fatty liver disease(MAFLD)is a hepatic manifestation of the metabolic syndrome.It is one of the most common liver diseases worldwide and shows increasing prevalence rates in most countries.MAFLD is a progressive disease with the most severe cases presenting as advanced fibrosis or cirrhosis with an increased risk of hepatocellular carcinoma.Gut microbiota play a significant role in the pathogenesis and progression of MAFLD by disrupting the gut-liver axis.The mechanisms involved in maintaining gut-liver axis homeostasis are complex.One critical aspect involves preserving an appropriate intestinal barrier permeability and levels of intestinal lumen metabolites to ensure gutliver axis functionality.An increase in intestinal barrier permeability induces metabolic endotoxemia that leads to steatohepatitis.Moreover,alterations in the absorption of various metabolites can affect liver metabolism and induce liver steatosis and fibrosis.Glucagon-like peptide-1 receptor agonists(GLP-1 RAs)are a class of drugs developed for the treatment of type 2 diabetes mellitus.They are also commonly used to combat obesity and have been proven to be effective in reversing hepatic steatosis.The mechanisms reported to be involved in this effect include an improved regulation of glycemia,reduced lipid synthesis,β-oxidation of free fatty acids,and induction of autophagy in hepatic cells.Recently,multiple peptide receptor agonists have been introduced and are expected to increase the effectiveness of the treatment.A modulation of gut microbiota has also been observed with the use of these drugs that may contribute to the amelioration of MAFLD.This review presents the current understanding of the role of the gutliver axis in the development of MAFLD and use of members of the GLP-1 RA family as pleiotropic agents in the treatment of MAFLD.

RARRES2's impact on lipid metabolism in triplenegative breast cancer:a pathway to brain metastasis

Breast cancer brain metastasis(BCBrM)is a crucial and hard area of research which guarantees an urgent need to understand the underlying molecular mechanisms.A recent study by Li et al.[1]published in Military Medical Research investigated the role of retinoic acid receptor responder 2(RARRES2)in regulating lipid metabolism in BCBrM,highlighting the clinical relevance of alterations in lipid metabolites,such as phosphatidylcholine(PC)and triacylglycerols(TAGs),by RARRES2 through the modulation of phosphatase and tensin homologue(PTEN)-mammalian target of rapamycin(mTOR)-sterol regulatory element-binding protein 1(SREBP1)signaling pathway.This commentary aims to elaborate on the key findings and their relevance to the field.