目的探究2型糖尿病并发骨质疏松患者血清白脂素(Asprosin)、巨噬细胞炎症蛋白-1β(macrophageinflammato-ry protein-1β,MIP-1β)水平与骨密度及骨代谢指标的相关性。方法选取2022年4月~2023年4月在承德市中心医院就诊的172例2型糖尿...目的探究2型糖尿病并发骨质疏松患者血清白脂素(Asprosin)、巨噬细胞炎症蛋白-1β(macrophageinflammato-ry protein-1β,MIP-1β)水平与骨密度及骨代谢指标的相关性。方法选取2022年4月~2023年4月在承德市中心医院就诊的172例2型糖尿病患者为研究对象,并根据骨密度值结果分为2型糖尿病组(n=103)和2型糖尿病并发骨质疏松组(n=69);采用ELISA法测定血清Asprosin,MIP-1β水平;Pearson法分析血清Asprosin,MIP-1β表达水平与骨密度的相关性;Logistic回归分析2型糖尿病并发骨质疏松的影响因素;受试者工作特征(ROC)曲线分析血清Asprosin,MIP-1β水平对2型糖尿病并发骨质疏松的预测价值。结果与2型糖尿病组比,2型糖尿病并发骨质疏松组患者血清β-CTX(0.48±0.08ng/ml vs 0.42±0.04ng/ml),Asprosin(2.26±0.56ng/ml vs 1.65±0.36ng/ml),MIP-1β(26.01±6.43pg/ml vs 19.46±4.27pg/ml)水平均显著升高,骨密度(0.67±0.13g/cm2 vs 0.84±0.17g/cm2),BGP(8.33±1.23ng/ml vs 9.54±1.42ng/ml),T-P1NP(30.38±3.27ng/ml vs 32.49±3.29ng/ml)水平降低,差异具有统计学意义(t=6.501,8.699,8.032,7.039,5.773,4.133,均P<0.05);Pearson法分析显示,2型糖尿病并发骨质疏松组患者血清Asprosin,MIP-1β水平均与骨密度呈负相关(r=-0.484,-0.498,均P<0.05);Logistic回归分析显示血清Asprosin,MIP-1β水平均为影响2型糖尿病并发骨质疏松发生的独立危险因素(均P<0.05);ROC曲线分析显示,血清Asprosin,MIP-1β水平预测2型糖尿病患者并发骨质疏松的AUC分别为0.768,0.704,联合预测的AUC为0.859,优于二者单独预测(Z=1.812,2.895,均P<0.05)。。结论2型糖尿病患者并发骨质疏松患者血清Asprosin,MIP-1β水平显著升高,二者水平与骨密度密切相关,血清Asprosin,MIP-1β是2型糖尿病发生骨质疏松的独立危险因素,二者联合检测对疾病发展有较高的预测价值。展开更多
BACKGROUND MicroRNAs(miRNAs)regulate gene expression and play a critical role in cancer physiology.However,there is still a limited understanding of the function and regulatory mechanism of miRNAs in gastric cancer(GC...BACKGROUND MicroRNAs(miRNAs)regulate gene expression and play a critical role in cancer physiology.However,there is still a limited understanding of the function and regulatory mechanism of miRNAs in gastric cancer(GC).AIM To investigate the role and molecular mechanism of miRNA-145-5p(miR145-5p)in the progression of GC.METHODS Real-time polymerase chain reaction(RT-PCR)was used to detect miRNA expression in human GC tissues and cells.The ability of cancer cells to migrate and invade was assessed using wound-healing and transwell assays,respectively.Cell proliferation was measured using cell counting kit-8 and colony formation assays,and apoptosis was evaluated using flow cytometry.Expression of the epithelial-mesenchymal transition(EMT)-associated protein was determined by Western blot.Targets of miR-145-5p were predicated using bioinformatics analysis and verified using a dual-luciferase reporter system.Serpin family E member 1(SERPINE1)expression in GC tissues and cells was evaluated using RT-PCR and immunohistochemical staining.The correlation between SERPINE1 expression and overall patient survival was determined using Kaplan-Meier plot analysis.The association between SERPINE1 and GC progression was also tested.A rescue experiment of SERPINE1 overexpression was conducted to verify the relationship between this protein and miR-145-5p.The mechanism by which miR-145-5p influences GC progression was further explored by assessing tumor formation in nude mice.RESULTS GC tissues and cells had reduced miR-145-5p expression and SERPINE1 was identified as a direct target of this miRNA.Overexpression of miR-145-5p was associated with decreased GC cell proliferation,invasion,migration,and EMT,and these effects were reversed by forcing SERPINE1 expression.Kaplan-Meier plot analysis revealed that patients with higher SERPINE1 expression had a shorter survival rate than those with lower SERPINE1 expression.Nude mouse tumorigenesis experiments confirmed that miR-145-5p targets SERPINE1 to regulate extracellular signal-regulated kinase-1/2(ERK1/2).CONCLUSION This study found that miR-145-5p inhibits tumor progression and is expressed in lower amounts in patients with GC.MiR-145-5p was found to affect GC cell proliferation,migration,and invasion by negatively regulating SERPINE1 levels and controlling the ERK1/2 pathway.展开更多
目的:探究床旁超声联合可溶性髓系细胞触发受体-1 (sTREM-1)、可溶性白细胞介素-2受体(sIL-2R)在新生儿肺炎早期诊断中的应用价值。方法:选取2019年1月~2021年6月本院接收的新生儿肺炎的患儿120例,依据X线诊断结果分为轻症肺炎组(n = 75...目的:探究床旁超声联合可溶性髓系细胞触发受体-1 (sTREM-1)、可溶性白细胞介素-2受体(sIL-2R)在新生儿肺炎早期诊断中的应用价值。方法:选取2019年1月~2021年6月本院接收的新生儿肺炎的患儿120例,依据X线诊断结果分为轻症肺炎组(n = 75)和重症肺炎组(n = 45),选取同期在本院分娩的健康新生儿50例为对照组,以X线诊断为金标准,三组均行床旁肺部超声检查及病原学检测,分析超声诊断结果,根据病原学检测结果分为细菌性肺炎组(n = 65)和非细菌性肺炎组(n = 55)。应用双抗体夹心酶联免疫吸附法(DAS-ELISA)检测三组sTREM-1、sIL-2R水平,应用受试者工作特征(ROC)曲线分析血清sTREM-1、sIL-2R在新生儿肺炎早期诊断中的应用价值。结果:床旁肺部超声检出新生儿肺炎115例,诊断准确率为95.83%;细菌性肺炎组与非细菌性肺炎组sTREM-1、sIL-2R水平明显高于对照组(P P P P P < 0.05)。结论:床旁肺部超声检查具较高诊断准确率,具明显超声图像特点,sTREM-1、sIL-2R可有效诊断新生儿肺炎,其中sTREM-1可为细菌性新生儿肺炎重要诊断指标。展开更多
BACKGROUND Increasing data indicated that long noncoding RNAs(lncRNAs)were directly or indirectly involved in the occurrence and development of tumors,including hepatocellular carcinoma(HCC).Recent studies had found t...BACKGROUND Increasing data indicated that long noncoding RNAs(lncRNAs)were directly or indirectly involved in the occurrence and development of tumors,including hepatocellular carcinoma(HCC).Recent studies had found that the expression of lncRNA HAND2-AS1 was downregulated in HCC tissues,but its role in HCC progression is unclear.Ultrasound targeted microbubble destruction mediated gene transfection is a new method to overexpress genes.AIM To study the role of ultrasound microbubbles(UTMBs)mediated HAND2-AS1 in the progression of HCC,in order to provide a new reference for the treatment of HCC.METHODS In vitro,we transfected HAND2-AS1 siRNA into HepG2 cells by UTMBs,and detected cell proliferation,apoptosis,invasion and epithelial-mesenchymal transition(EMT)by cell counting kit-8 assay,flow cytometry,Transwell invasion assay and Western blotting,respectively.In addition,we transfected miR-837-5p mimic into UTMBs treated cells and observed the changes of cell behavior.Next,the UTMBs treated HepG2 cells were transfected together with miR-837-5p mimic and tissue inhibitor of matrix metalloproteinase-2(TIMP2)overexpression vector,and we detected cell proliferation,apoptosis,invasion and EMT.In vivo,we established a mouse model of subcutaneous transplantation of HepG2 cells and observed the effect of HAND2-AS1 silencing on tumor formation ability.RESULTS We found that UTMBs carrying HAND2-AS1 restricted cell proliferation,invasion,and EMT,encouraged apoptosis,and HAND2-AS1 silencing eliminated the effect of UTMBs.Additionally,miR-873-5p targets the gene HAND2-AS1,which also targets the 3’UTR of TIMP2.And miR-873-5p mimic counteracted the impact of HAND2-AS1.Further,miR-873-5p mimic solely or in combination with pcDNA-TIMP2 had been transformed into HepG2 cells exposed to UTMBs.We discovered that TIMP2 reversed the effect of miR-873-5p mimic caused by the blocked signalling cascade for matrix metalloproteinase(MMP)2/MMP9.In vivo results showed that HAND2-AS1 silencing significantly inhibited tumor formation in mice.CONCLUSION LncRNA HAND2-AS1 promotes TIMP2 expression by targeting miR-873-5p to inhibit HepG2 cell growth and delay HCC progression.展开更多
文摘目的探究2型糖尿病并发骨质疏松患者血清白脂素(Asprosin)、巨噬细胞炎症蛋白-1β(macrophageinflammato-ry protein-1β,MIP-1β)水平与骨密度及骨代谢指标的相关性。方法选取2022年4月~2023年4月在承德市中心医院就诊的172例2型糖尿病患者为研究对象,并根据骨密度值结果分为2型糖尿病组(n=103)和2型糖尿病并发骨质疏松组(n=69);采用ELISA法测定血清Asprosin,MIP-1β水平;Pearson法分析血清Asprosin,MIP-1β表达水平与骨密度的相关性;Logistic回归分析2型糖尿病并发骨质疏松的影响因素;受试者工作特征(ROC)曲线分析血清Asprosin,MIP-1β水平对2型糖尿病并发骨质疏松的预测价值。结果与2型糖尿病组比,2型糖尿病并发骨质疏松组患者血清β-CTX(0.48±0.08ng/ml vs 0.42±0.04ng/ml),Asprosin(2.26±0.56ng/ml vs 1.65±0.36ng/ml),MIP-1β(26.01±6.43pg/ml vs 19.46±4.27pg/ml)水平均显著升高,骨密度(0.67±0.13g/cm2 vs 0.84±0.17g/cm2),BGP(8.33±1.23ng/ml vs 9.54±1.42ng/ml),T-P1NP(30.38±3.27ng/ml vs 32.49±3.29ng/ml)水平降低,差异具有统计学意义(t=6.501,8.699,8.032,7.039,5.773,4.133,均P<0.05);Pearson法分析显示,2型糖尿病并发骨质疏松组患者血清Asprosin,MIP-1β水平均与骨密度呈负相关(r=-0.484,-0.498,均P<0.05);Logistic回归分析显示血清Asprosin,MIP-1β水平均为影响2型糖尿病并发骨质疏松发生的独立危险因素(均P<0.05);ROC曲线分析显示,血清Asprosin,MIP-1β水平预测2型糖尿病患者并发骨质疏松的AUC分别为0.768,0.704,联合预测的AUC为0.859,优于二者单独预测(Z=1.812,2.895,均P<0.05)。。结论2型糖尿病患者并发骨质疏松患者血清Asprosin,MIP-1β水平显著升高,二者水平与骨密度密切相关,血清Asprosin,MIP-1β是2型糖尿病发生骨质疏松的独立危险因素,二者联合检测对疾病发展有较高的预测价值。
文摘BACKGROUND MicroRNAs(miRNAs)regulate gene expression and play a critical role in cancer physiology.However,there is still a limited understanding of the function and regulatory mechanism of miRNAs in gastric cancer(GC).AIM To investigate the role and molecular mechanism of miRNA-145-5p(miR145-5p)in the progression of GC.METHODS Real-time polymerase chain reaction(RT-PCR)was used to detect miRNA expression in human GC tissues and cells.The ability of cancer cells to migrate and invade was assessed using wound-healing and transwell assays,respectively.Cell proliferation was measured using cell counting kit-8 and colony formation assays,and apoptosis was evaluated using flow cytometry.Expression of the epithelial-mesenchymal transition(EMT)-associated protein was determined by Western blot.Targets of miR-145-5p were predicated using bioinformatics analysis and verified using a dual-luciferase reporter system.Serpin family E member 1(SERPINE1)expression in GC tissues and cells was evaluated using RT-PCR and immunohistochemical staining.The correlation between SERPINE1 expression and overall patient survival was determined using Kaplan-Meier plot analysis.The association between SERPINE1 and GC progression was also tested.A rescue experiment of SERPINE1 overexpression was conducted to verify the relationship between this protein and miR-145-5p.The mechanism by which miR-145-5p influences GC progression was further explored by assessing tumor formation in nude mice.RESULTS GC tissues and cells had reduced miR-145-5p expression and SERPINE1 was identified as a direct target of this miRNA.Overexpression of miR-145-5p was associated with decreased GC cell proliferation,invasion,migration,and EMT,and these effects were reversed by forcing SERPINE1 expression.Kaplan-Meier plot analysis revealed that patients with higher SERPINE1 expression had a shorter survival rate than those with lower SERPINE1 expression.Nude mouse tumorigenesis experiments confirmed that miR-145-5p targets SERPINE1 to regulate extracellular signal-regulated kinase-1/2(ERK1/2).CONCLUSION This study found that miR-145-5p inhibits tumor progression and is expressed in lower amounts in patients with GC.MiR-145-5p was found to affect GC cell proliferation,migration,and invasion by negatively regulating SERPINE1 levels and controlling the ERK1/2 pathway.
文摘目的:探究床旁超声联合可溶性髓系细胞触发受体-1 (sTREM-1)、可溶性白细胞介素-2受体(sIL-2R)在新生儿肺炎早期诊断中的应用价值。方法:选取2019年1月~2021年6月本院接收的新生儿肺炎的患儿120例,依据X线诊断结果分为轻症肺炎组(n = 75)和重症肺炎组(n = 45),选取同期在本院分娩的健康新生儿50例为对照组,以X线诊断为金标准,三组均行床旁肺部超声检查及病原学检测,分析超声诊断结果,根据病原学检测结果分为细菌性肺炎组(n = 65)和非细菌性肺炎组(n = 55)。应用双抗体夹心酶联免疫吸附法(DAS-ELISA)检测三组sTREM-1、sIL-2R水平,应用受试者工作特征(ROC)曲线分析血清sTREM-1、sIL-2R在新生儿肺炎早期诊断中的应用价值。结果:床旁肺部超声检出新生儿肺炎115例,诊断准确率为95.83%;细菌性肺炎组与非细菌性肺炎组sTREM-1、sIL-2R水平明显高于对照组(P P P P P < 0.05)。结论:床旁肺部超声检查具较高诊断准确率,具明显超声图像特点,sTREM-1、sIL-2R可有效诊断新生儿肺炎,其中sTREM-1可为细菌性新生儿肺炎重要诊断指标。
文摘BACKGROUND Increasing data indicated that long noncoding RNAs(lncRNAs)were directly or indirectly involved in the occurrence and development of tumors,including hepatocellular carcinoma(HCC).Recent studies had found that the expression of lncRNA HAND2-AS1 was downregulated in HCC tissues,but its role in HCC progression is unclear.Ultrasound targeted microbubble destruction mediated gene transfection is a new method to overexpress genes.AIM To study the role of ultrasound microbubbles(UTMBs)mediated HAND2-AS1 in the progression of HCC,in order to provide a new reference for the treatment of HCC.METHODS In vitro,we transfected HAND2-AS1 siRNA into HepG2 cells by UTMBs,and detected cell proliferation,apoptosis,invasion and epithelial-mesenchymal transition(EMT)by cell counting kit-8 assay,flow cytometry,Transwell invasion assay and Western blotting,respectively.In addition,we transfected miR-837-5p mimic into UTMBs treated cells and observed the changes of cell behavior.Next,the UTMBs treated HepG2 cells were transfected together with miR-837-5p mimic and tissue inhibitor of matrix metalloproteinase-2(TIMP2)overexpression vector,and we detected cell proliferation,apoptosis,invasion and EMT.In vivo,we established a mouse model of subcutaneous transplantation of HepG2 cells and observed the effect of HAND2-AS1 silencing on tumor formation ability.RESULTS We found that UTMBs carrying HAND2-AS1 restricted cell proliferation,invasion,and EMT,encouraged apoptosis,and HAND2-AS1 silencing eliminated the effect of UTMBs.Additionally,miR-873-5p targets the gene HAND2-AS1,which also targets the 3’UTR of TIMP2.And miR-873-5p mimic counteracted the impact of HAND2-AS1.Further,miR-873-5p mimic solely or in combination with pcDNA-TIMP2 had been transformed into HepG2 cells exposed to UTMBs.We discovered that TIMP2 reversed the effect of miR-873-5p mimic caused by the blocked signalling cascade for matrix metalloproteinase(MMP)2/MMP9.In vivo results showed that HAND2-AS1 silencing significantly inhibited tumor formation in mice.CONCLUSION LncRNA HAND2-AS1 promotes TIMP2 expression by targeting miR-873-5p to inhibit HepG2 cell growth and delay HCC progression.
