Nutritional disorders and muscle wasting associated with liver disease are key determinants of poor prognosis in patients with chronic liver disease. The formation of these conditions involves multiple factors, including impaired energy metabolism, enhanced protein degradation, and gut microbiota imbalance. In recent years, with the deepening of microbiome research, the concept of the “gut-liver-muscle axis” has gradually emerged to explain the more systematic interaction between gut microbiota, liver metabolism, and skeletal muscle homeostasis. Gut dysbiosis can promote liver inflammation and metabolic disorders through various pathways, further weakening muscle energy utilization and protein synthesis, ultimately leading to malnutrition and sarcopenia. This review systematically explores the crucial role of gut microbiota in liver disease-related malnutrition and muscle wasting, elucidates its potential mechanisms in influencing host metabolism and nutritional status through the “gut-liver-muscle axis,” and discusses the prospects of microbiome interventions in improving nutritional outcomes in liver disease.

TRIM56 plays a role in tumor development through the ubiquitination of several key substrate molecules. However, its relationship with tumor prognosis and immune infiltration remains unclear. The expression and localization of TRIM56 were analyzed from TCGA_GTEx, TCGA and HPA database. The effects of TRIM56 on the proliferation and migration of lung cancer cells A549 were evaluated by CCK-8 and wound healing assays. Correlations between TRIM56 expression and survival in patients were analyzed using the Kaplan-Meier Plotter and a nomogram model. Additionally, the relationship between TRIM56 and immune cell infiltration in tumors was explored via TIMER 2.0. Functional interactions and associated proteins of TRIM56 were examined using GEPIA 2.0 and the STING database. The signaling pathways influenced by TRIM56 were identified through GO and KEGG analyses. TRIM56 expression showed significant variation across 11 different tumor types when compared to normal tissues, with some tumors displaying high expression and others showing the opposite. TRIM56 inhibited the proliferation and migration of A549 cells. High TRIM56 expression was associated with shorter overall survival (OS) in patients with COAD, GBM, and LGG, but with longer OS in BLCA, KIRC, MESO, and SKCM. In BLCA and KIRC, high TRIM56 expression was closely linked to B cells, macrophages, and CD4(+) and CD8(+) T cell infiltration, contributing to a favorable prognosis. TRIM56 appears to affect tumor development through transcriptional regulatory complexes, transcriptional co-regulatory factor activity, and immune-related pathways.TRIM56 may play a critical role in tumor immunity and influence tumor prognosis. It holds potential as both a target for immunotherapy and a prognostic marker.

Colorectal cancer (CRC) is one of the most prevalent and life-threatening cancers. Rapid cell proliferation is the leading cause of cancer-related death in CRC. MicroRNAs (miRNAs) have been identified to play essential roles in the proliferation of CRC. Differential expression of let-7c-5p in CRC was assessed using a GEO dataset, and confirmed through RT-qPCR using CRC subject tissues. Let-7c-5p-overexpressing HCT8 cell line was constructed by transfecting let-7c-5p. Bioinformatics analysis identified that DUSP7 is the target gene of let-7c-5p. Further experimental assays, including Cell Counting Kit-8 (CCK8), EdU staining, cell colony, and Western Blot assays, confirmed the target genes and pathway of let-7c-5p. Receiver operator characteristic curve (ROC) analysis was performed to evaluate the diagnostic value of let-7c-5p for CRC. Finally, survival analysis was performed to determine the effect of DUSP7 and let-7c-5p on the prognosis of CRC patients. RT-qPCR analysis showed that the expression level of let-7c-5p was significantly increased in CRC subject tissues compared to the adjacent tissue. Overexpression of let-7c-5p promoted cell proliferation in HCT8 cell line. Furthermore, the MAPK-ERK pathway’s protein expression of p-ERK1/2 was downregulated, while the ratio of Bcl-2/Bax was increased by let-7c-5p transfection in HCT 8. ROC analysis demonstrated that the expressive level of let-7c-5p had higher diagnostic value for CRC. Survival curve analysis indicated that high expression of DUSP7 and low expression of let-7c-5p were associated with poor prognosis in CRC patients. The findings suggest that let-7c-5p exerts an antitumor function by inhibiting the DUSP7-mediated MAPK-ERK pathway. Both DUSP7 and let-7c-5p have the potential to serve as prognostic biomarkers in CRC patients.

结直肠癌(CRC)患者约占全球所有新发肿瘤患者的10%,健康人群患CRC的风险为4%～5%,是肿瘤相关死亡的常见原因之一.目前筛查CRC的方法很多,如结肠镜、肿瘤标志物、影像学、微环境、病理学等,但是都有其不足之处.近年来随着深度学习、机器学习算法(ML)、硬件水平和数据库的提升,人工智能(AI)技术迎来第三次发展热潮,将ML与CRC的筛查方法相结合,能有效提高其敏感度及特异度,减少人工检测所带来的失误.目前研究显示,基于结肠镜检查、肿瘤标志物、影像学检查、肠道微环境、病理学检查的ML预测模型可以提高CRC筛查的准确性,减少不必要的人为错误,在提高效率的同时也减少了不必要的劳动浪费.ML有很多种预测模型,每个模型都有其自身的优势,我们要根据目标的不同特点进行合理选择,以提高CRC的筛查效果.

1 概述 结直肠癌(colorectal cancer,CRC)是目前常见的消化道恶性肿瘤之一,根据国家癌症中心数据显示,2015年,我国结直肠癌发病率位居全部恶性肿瘤第3位,新增死亡病例数为18.7万例[1].近些年,随着我国经济水平的发展,生活方式、饮食结构的改变,结直肠癌的发病率和死亡率呈上升趋势[1].

目的 观察结直肠癌组织中血浆激肽释放酶B1(KLKB1)蛋白的表达变化,并探讨其临床意义.方法 结直肠癌患者86例,均接受根治性手术治疗,术中留取癌组织及癌旁组织,采用免疫组织化学法检测结直肠癌组织及癌旁正常组织中KLKB1蛋白,分析KLKB1蛋白阳性表达与结直肠癌患者临床病理参数的关系及相关性.结果 结直肠癌组织及癌旁正常组织中KLKB1蛋白阳性表达率分别为45.3％、72.1％,两者相比,P<0.05.KLKB1蛋白阳性表达与结直肠癌患者肿瘤直径、淋巴结转移、临床分期有关,且呈负相关关系(r分别为-0.260、-0.231、-0.231,P均<0.05).结论 结直肠癌组织中KLKB1蛋白呈低表达,可能参与了结直肠癌的发生发展.

目的 检测结直肠癌(CRC)患者血浆激肽释放酶B1(KLKB1)水平,评估其对CRC的诊断价值.方法 采集65例CRC患者(CRC组)和20例同期门诊健康体检者(对照组)的空腹静脉血,采用ELISA法检测血浆KLKB1水平,免疫荧光法检测血清CEA水平.分析比较不同临床特征患者的血浆KLKB1水平;通过受试者工作特征(ROC)曲线评估KLKB1和CEA对CRC的诊断价值.结果 CRC组血浆KLKB1水平高于对照组(P<0.05).有淋巴结转移、远处转移、临床分期Ⅲ～Ⅳ期CRC患者的血浆KLKB1分别高于无淋巴结转移、未发生远处转移、临床分期Ⅰ～Ⅱ期患者(P均<0.01).KLKB1诊断CRC的敏感度为78.5％、特异度为95.0％,CEA诊断CRC的敏感度为75.4％、特异度为85％;KLKB1的ROC曲线下面积(0.885)高于CEA(0.830).结论 CRC患者血浆KLKB1水平升高,尤其是发生转移及临床分期高者,可作为诊断CRC的生物标志物.

To explore how insulin resistance promotes colorectal adenomas by disrupting the balance of glucose and lipid metabolism.

目的 观察酒精性肝病不同阶段患者的血清白细胞介素17(IL-17)水平,以及IL-17197A/G位点单核苷酸多态性(SNP)特点.方法 选择124例酒精性肝病患者,其中脂肪肝32例(脂肪肝组)、肝硬化68例(肝硬化组)、肝癌24例(肝癌组);另选择58例健康体检者作为对照组.采用ELISA法检测各组血清IL-17水平;贝克曼SNP分析仪检测IL-17197A/G位点基因型及等位基因分布频率,比较四组基因型和等位基因分布频率.结果 肝癌组血清IL-17水平高于其他三组,肝硬化组高于脂肪肝组和对照组(P均<0.05),脂肪肝组与对照组比较差异无统计学意义(P>0.05).四组IL-17197A/G位点AA、AG、GG基因型分布频率比较差异有统计学意义,脂肪肝组和对照组的GG基因型分布频率高于肝硬化组和肝癌组,肝癌组的AA基因型分布频率高于其他三组(P均<0.05).等位基因A在肝癌组的分布频率高于脂肪肝组和对照组,等位基因G在脂肪肝组和对照组的分布频率高于肝硬化组和肝癌组(P均<0.05).结论 酒精性肝病患者发展至肝硬化、肝癌阶段后血清IL-17水平升高;IL-17197A/G位点AA基因型和A等位基因是酒精性肝病患者发展至肝硬化、肝癌阶段的易感基因,可能增加酒精性脂肪肝进展为肝硬化的发生风险.

目的 探讨思维导图在局部血液循环障碍一章教学中的应用效果.方法 将承德医学院2015级麻醉医学专业学生分为观察组和对照组,在局部血液循环障碍教学中应用思维导图和传统教学两种方法,并在教学结束后对两组学生进行教学内容检测,对观察组学生发放教学满意度调查问卷.结果 观察组学生课后病例分析题测试[(82.26±6.28)分]明显高于对照组[(73.73±9.81)分],差异有统计学意义(P<0.05),但选择题[(85.77±5.42)分]与对照组[(83.33±7.86)分]差异无统计学意义(P>0.05).调查问卷显示观察组学生认为思维导图模式教学可提高学习效率、培养临床思维、激发学习兴趣、促进学习主动性、增强自主学习能力、利于知识巩固及宏观把握、提高综合素质及提高课堂气氛活跃度满意度分别为97.44%、92.31%、92.31%、92.31%、100.00%、100.00%、94.87%、84.62%.结论 思维导图可以有效提高学生综合分析能力和学习兴趣,为医学教育提供了科学有效的教学模式.

The objectives of the present study were to identify the aberrant expression of microRNA (miRNA) in colorectal carcinoma (CRC) tissues from published miRNA profiling studies and to investigate the effects of the identified miRNA inhibitor and mimic miR-96-5p on CRC cell migration and invasion. The altered expression of the regulators of cytoskeleton mRNA in miR-96-5p inhibitor-transfected cells was determined. The miR-96-5p expression level in five CRC cell lines, HCT11, CaCo2, HT29, SW480 and SW620, and 26 archived paraffin-embedded CRC tissues were also investigated by reverse-transcriptase quantitative polymerase chain reaction (RT-qPCR). Cell viability in response to the miR-96-5p inhibitor and mimic transfections was determined by an MTT assay. A Matrigel invasion assay was conducted to select the invasive subpopulation designated SW480-7, by using the parental cell line SW480. The effects of miR-96-5p mimic- or inhibitor-transfected SW480-7 cells on cell migration and invasion were evaluated using the Transwell and Matrigel assays, and the change in expression of the regulators of cytoskeleton mRNAs was identified by Cytoskeleton Regulators RT2-Profiler PCR array followed by validation with RT-qPCR. CRC tissues exhibited a significant increase in miR-96-5p expression, compared with their matched normal adjacent tissues, indicating an oncogenic role for miR-96-5p. The results demonstrated that the miR-96-5p inhibitor decreased the migration of SW480-7 cells, but had no effect on invasion. This may be due to the promotion of cell invasion by Matrigel, which counteracts the blockade of cell invasion by the miR-96-5p inhibitor. The miR-96-5p mimic enhanced SW480-7 cell migration and invasion, as expected. It was determined that there was a >2.5 fold increase in the expression of genes involved in cytoskeleton regulation, myosin light chain kinase 2, pleckstrin homology like domain family B member 2, cyclin A1, IQ motif containing GTPase activating protein 2, Brain-specific angiogenesisinhibitor 1-associated protein 2 and microtubule-actin crosslinking factor 1, in miR-96-5p inhibitor-transfected cells, indicating that they are negative regulators of cell migration. In conclusion, the miR-96-5p inhibitor blocked cell migration but not invasion, and the latter may be due to the counteraction of Matrigel, which has been demonstrated to stimulate cell invasion.

酒精性肝病(ALD)的发病率呈逐年增高趋势,每年因过量饮酒引起的个体健康危害、公共安全危害和公共卫生负担已经成为我国亟待解决的健康问题.本研究以酒精性脂肪肝患者为研究对象,观察肥胖和糖耐量异常对其氧化应激状态与凋亡通路的影响,探讨肥胖和糖耐量异常协同促进酒精性脂肪肝发展的机制.结果表明肥胖与乙醇协同作用,通过胰岛素抵抗激活氧化应激通路调控Caspase 3促进细胞凋亡,从而加重酒精性肝损伤.

目的 探讨miR-9-5p通过靶向叉头框转录因子O1(FOXO1)对食管癌Eca-109细胞体外增殖、侵袭和迁移能力的调控作用.方法 在食管癌Eca-109细胞中分别转染miR-9-5p inhibitor和NC-inhibitor,分别设置为anti-miR-9-5p组和NC组,并设置未转染的细胞为Blank组.采用实时荧光定量PCR(qRT-PCR)技术检测各组细胞中miR-9-5p的表达水平,噻唑蓝(MTT)法、Transwell实验分别检测细胞增殖、侵袭和迁移能力.通过生物信息学在线软件预测miR-9-5p与FOXO1互补结合位点,双荧光素酶报告基因实验验证二者靶向关系.采用qRT-PCR和蛋白免疫印迹法(Western blotting)分析miR-9-5p对FOXO1的调控作用.结果 anti-miR-9-5p组Eca-109细胞中miR-9-5p的表达水平、OD值、侵袭和迁移细胞数均显著低于NC组和Blank组(P＜0.05).miR-9-5p与FOXO1存在互补结合位点,双荧光素酶报告基因实验分析结果显示,miR-9-5p和FOXO1能够靶向结合.anti-miR-9-5p组Eca-109细胞中FOXO1 mRNA和蛋白表达水平明显高于NC组和Blank组(P＜0.05).NC组和Blank组细胞中以上指标均无明显改变(P＞0.05).结论 干扰miR-9-5p的表达可通过靶向FOXO1基因抑制食管癌Eca-109细胞的体外增殖、侵袭和迁移能力.

Objective To investigate the mechanistic basis for the attenuation of bone degeneration by edible bird’s nest (EBN) in ovariectomized rats. Methods Forty-two female Sprage-Dawley rats were randomized into 7 groups (6 in each group). The ovariectomized (OVX) and OVX + 6%, 3%, and 1.5% EBN and OVX +estrogen groups were given standard rat chow alone, standard rat chow +6%, 3%, and 1.5% EBN, or standard rat chow +estrogen therapy (0.2mg/kg per day), respectively. The sham-operation group was surgically opened without removing the ovaries. The control group did not have any surgical intervention. After 12 weeks of intervention, blood samples were taken for serum estrogen, osteocalcin, and osteoprotegerin, as well as the measurement of magnesium, calcium abd zinc concentrations. While femurs were removed from the surrounding muscles to measure bone mass density using the X-ray edge detection technique, then collected for histology and estrogen receptor (ER) immunohistochemistry. Results Ovariectomy altered serum estrogen levels resulting in increased food intake and weight gain, while estrogen and EBN supplementation attenuated these changes. Ovariectomy also reduced bone ER expression and density, and the production of osteopcalcin and osteorotegerin, which are important pro-osteoplastic hormones that promote bone mineraliztion and density. Conversely, estrogen and EBN increased serum estrogen levels leading to increased bone ER expression, pro-osteoplastic hormone production and bone density (all P <0.05). Conclusion EBN could be used as a safe alternative to hormone replacement therapys for managing menopausal complications like bone degeneration.

目的 探讨Hsa-miR-182-5p在结直肠癌癌组织及癌旁正常组织中表达水平的差异对结肠癌的病理特征及临床意义的影响.方法 收集2017年1月至2017年11月期间在承德医学院附属医院手术的42例结直肠癌患者癌组织样本及距肿瘤边缘5厘米处癌旁粘膜组织标本,利用实时荧光定量 PCR(qRT-PCR)检测结直肠癌组织和癌旁正常组织中Hsa-miR-182-5p的表达水平,并分析其表达的差异与结直肠癌临床病理特征的相关性.结果 结直肠癌组织中Hsa-miR-182-5p表达水平显著高于癌旁正常组织,差异有统计学意义(P＜0.05).Hsa-miR-182-5p表达量变化与患者年龄、性别、肿瘤大小、肿瘤部位均无关,P值均＞0.05;但在肿瘤分化程度、浸润深度、远处转移及淋巴结转移组Hsa-miR-182-5p表达量明显升高,差异具有统计学意义;miR-182-5p在临床Ⅲ/Ⅳ期结肠癌患者中表达量显著高于Ⅱ期患者.结论 Hsa-miR-182-5p在结直肠癌患者直肠粘膜组织中存在异常表达,其表达量增高与结直肠癌疾病进展及不良预后呈正相关,说明直肠粘膜中异常表达的Hsa-miR-182-5p可能成为判断结直肠癌预后的潜在靶点.

目的 探讨双歧杆菌四联活菌片治疗非酒精性脂肪肝疗效分析. 方法 选择2012年1月至201 5年1月在该院门诊就诊的非酒精性脂肪肝(non-alcoholic fatty liver disease,NAFLD)患者60例随机分为2组,A组采用常规方法治疗非酒精性脂肪肝48周,B组在常规方法治疗非酒精性脂肪肝基础上加用双歧杆菌四联活菌片3粒/次日3次口服48周,观察2组治疗前后肝功能指标、体质量指数(body mass index,BMI)、腰围、胆固醇及甘油三酯指标及CT下肝脏形态学变化情况. 结果 B组在治疗后的上述各项指标均明显低于A组,差异具有统计学意义.结论 双歧杆菌四联活菌片治疗非酒精性脂肪肝作用明显,具有重要的临床实践意义.

目的：观察河北汉族慢性乙型肝炎病毒（HBV）感染者血清 IL-10水平变化及 IL-10基因启动子区-592 A ／C 和-819 C ／T 位点的多态性。方法慢性 HBV 感染者122例，其中无症状慢性 HBV 携带者56例（病例组1）、慢性乙型肝炎（乙肝）患者24例（病例组2）、慢性乙肝肝硬化患者42例（病例组3）。将88例自限性 HBV 清除者纳入对照组。采用 ELISA 法检测各组血清 IL-10；采用 PCR 法及贝克曼 SNP 分析仪检测 IL-10基因启动子区-592 A ／C、-819 C ／T 位点多态性，计算基因型及等位基因分布频率。结果病例组1、病例组2、病例组3及对照组血清IL-10水平分别为（8．76±1．54）、（23．65±10．32）、（11．54±5．78）、（4．57±0．22）pg／mL，两两组间比较，P 均＜0．01。病例组2 IL-10基因-819 C 等位基因频率高于对照组，T 等位基因频率低于对照组（P 均＜0．05）。各病例组IL-10基因-819 TT 基因型频率低于对照组（P 均＜0．05）。病例组2 IL-10基因-592 CC 基因型频率高于其余三组，病例组1、病例组3 CC 基因型频率低于对照组（P 均＜0．05）。结论河北汉族慢性乙肝患者血清 IL-10水平高于HBV 携带者、慢性乙肝肝硬化患者及自限性 HBV 清除者；HBV 感染者 IL-10基因启动子区-592 A ／C 和-819 C ／T 位点存在多态性，其中 HBV 携带者、慢性乙肝患者及慢性乙肝肝硬化患者-819 C ／T 位点 TT 基因型频率升高，慢性乙肝患者-592 A ／C 位点 CC 基因型频率升高；IL-10基因多态性可能与 IL-10分泌水平有关，进而影响 HBV 感染的结局及转归。

Menopause causes cognitive and memory dysfunction due to impaired neuronal plasticity in the hippocampus. Sirtuin-1 (SIRT1) downregulation in the hippocampus is implicated in the underlying molecular mechanism. Edible bird's nest (EBN) is traditionally used to improve general wellbeing, and in this study, we evaluated its effects on SIRT1 expression in the hippocampus and implications on ovariectomy-induced memory and cognitive decline in rats. Ovariectomized female Sprague-Dawley rats were fed with normal pellet alone or normal pellet + EBN (6, 3, or 1.5%), compared with estrogen therapy (0.2 mg/kg/day). After 12 weeks of intervention, Morris water maze (four-day trial and one probe trial) was conducted, and serum estrogen levels, toxicity markers (alanine transaminase, alkaline phosphatase, urea, and creatinine), and hippocampal SIRT1 immunohistochemistry were estimated after sacrifice. The results indicated that EBN and estrogen enhanced spatial learning and memory and increased serum estrogen and hippocampal SIRT1 expression. In addition, the EBN groups did not show as much toxicity to the liver as the estrogen group. The data suggested that EBN treatment for 12 weeks could improve cognition and memory in ovariectomized female rats and may be an effective alternative to estrogen therapy for menopause-induced aging-related memory loss.

The aim of this study was to investigate the hepatoprotective effects of resveratrol in alcoholic liver disease (ALD). Alcohol was administered to healthy female rats starting from 6% (v/v) and gradually increased to 20% (v/v) by the fifth week. After 16 weeks of intervention, liver enzymes (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) were analyzed using a chemistry analyzer, while hepatic antioxidant enzymes, oxidative stress markers, and caspase 3 activity were assessed using ELISA kits. Furthermore, hepatic CYP2E1 protein levels and mRNA levels of antioxidant and inflammation-related genes were determined using western blotting and RT-PCR, respectively. The results showed that resveratrol significantly attenuated alcohol-induced elevation of liver enzymes and improved hepatic antioxidant enzymes. Resveratrol also attenuated alcohol-induced CYP2E1 increase, oxidative stress, and apoptosis (caspase 3 activity). Moreover, genes associated with oxidative stress and inflammation were regulated by resveratrol supplementation. Taken together, the results suggested that resveratrol alleviated ALD through regulation of oxidative stress, apoptosis, and inflammation, which was mediated at the transcriptional level. The data suggests that resveratrol is a promising natural therapeutic agent against chronic ALD.