目的优化点分辨波谱(PRESS)的回波时间(TE),以检测胶质瘤中的胱硫醚,并评估PRESS波谱在识别1p/19q共缺失分子分型方面的诊断准确性。方法通过计算机模拟激发和模体实验优化PRESS的TE,以更好地区分胱硫醚和重叠的天冬氨酸多重峰。随后,...目的优化点分辨波谱(PRESS)的回波时间(TE),以检测胶质瘤中的胱硫醚,并评估PRESS波谱在识别1p/19q共缺失分子分型方面的诊断准确性。方法通过计算机模拟激发和模体实验优化PRESS的TE,以更好地区分胱硫醚和重叠的天冬氨酸多重峰。随后,将优化后的PRESS序列和97 ms TE PRESS序列应用于前瞻性纳入的84例疑似胶质瘤或胶质瘤复发的患者。通过拟合包含和不包含天冬氨酸的基组集来研究天冬氨酸对胱硫醚量化的影响,并评估PRESS对1p/19q共缺失胶质瘤的诊断表现。结果PRESS的TE优化为TE=45 ms,胱硫醚和天冬氨酸的谱峰模式在模拟激发和模体实验中一致。在临床实验中,97 ms TE PRESS中不包含天冬氨酸拟合得到的胱硫醚平均浓度显著高于使用完整基组集拟合的浓度[(1.97±2.01)mM vs.(1.55±1.95)mM,P<0.01],而45 ms TE PRESS方法则无显著差异[(0.801±1.217)mM vs.(0.796±1.217)mM,P=0.494]。45 ms方法的胱硫醚浓度与编辑MRS的相关性优于97 ms方法(r=0.68 vs.0.49,P<0.01)。在鉴别1p/19q共缺失胶质瘤方面,45 ms TE PRESS的敏感度和特异度分别为66.7%和73.7%,97 ms TE PRESS的敏感度和特异度分别为44.4%和52.5%。结论45 ms TE PRESS较97 ms方法提供了更精确的胱硫醚检测,将有助于1p/19q共缺失胶质瘤的无创诊断和患者的治疗反应监测。PRESS在1p/19q共缺失胶质瘤中表现出中等诊断性能,表明需要进一步研究。展开更多
Myocardial fibrosis is a major pathogenic factor contributing to cardiac remodeling and heart failure. Recent research has indicated that micro RNAs play a crucial role in the progression of cardiac fibrosis. Bone mor...Myocardial fibrosis is a major pathogenic factor contributing to cardiac remodeling and heart failure. Recent research has indicated that micro RNAs play a crucial role in the progression of cardiac fibrosis. Bone morphogenetic protein and activin membrane-bound inhibitor(BAMBI) have been shown to alleviate myocardial fibrosis by inhibiting the transforming growth factor β1(TGF-β1) signaling pathway. Therefore, the current study aimed to elucidate the post-transcriptional regulation of BAMBI by miR-19a-3p and its role in TGF-β1-induced cardiac fibroblast activation. We found that transverse aortic constriction induced both myocardial interstitial and perivascular collagen deposition. Quantitative reverse transcription-PCR(q RT-PCR) analysis showed that the expression level of miR-19a-3p was increased in the myocardial tissues of cardiac fibrosis, and TGF-β1 induced an upregulation in miR-19a-3p expression in cardiac fibroblasts. The dual-luciferase reporter assay and q RT-PCR verified that miR-19a-3p directly bound to the 3 ′ untranslated regions of BAMBI m RNA, thereby reducing BAMBI expression and diminishing its ability to inhibit the TGF-β1 signaling pathway. Furthermore,overexpression of miR-19a-3p mimic increased the activation of TGF-β1/SMAD2/3 pathway signaling,promoting cardiac fibroblast activation. However, this activation was blocked by BAMBI overexpression. These findings imply that miR-19a-3p enhances the activation of TGF-β1/SMAD2/3 by inhibiting BAMBI, further boosting the activation of cardiac fibroblasts and contributing to myocardial fibrosis.展开更多
文摘目的优化点分辨波谱(PRESS)的回波时间(TE),以检测胶质瘤中的胱硫醚,并评估PRESS波谱在识别1p/19q共缺失分子分型方面的诊断准确性。方法通过计算机模拟激发和模体实验优化PRESS的TE,以更好地区分胱硫醚和重叠的天冬氨酸多重峰。随后,将优化后的PRESS序列和97 ms TE PRESS序列应用于前瞻性纳入的84例疑似胶质瘤或胶质瘤复发的患者。通过拟合包含和不包含天冬氨酸的基组集来研究天冬氨酸对胱硫醚量化的影响,并评估PRESS对1p/19q共缺失胶质瘤的诊断表现。结果PRESS的TE优化为TE=45 ms,胱硫醚和天冬氨酸的谱峰模式在模拟激发和模体实验中一致。在临床实验中,97 ms TE PRESS中不包含天冬氨酸拟合得到的胱硫醚平均浓度显著高于使用完整基组集拟合的浓度[(1.97±2.01)mM vs.(1.55±1.95)mM,P<0.01],而45 ms TE PRESS方法则无显著差异[(0.801±1.217)mM vs.(0.796±1.217)mM,P=0.494]。45 ms方法的胱硫醚浓度与编辑MRS的相关性优于97 ms方法(r=0.68 vs.0.49,P<0.01)。在鉴别1p/19q共缺失胶质瘤方面,45 ms TE PRESS的敏感度和特异度分别为66.7%和73.7%,97 ms TE PRESS的敏感度和特异度分别为44.4%和52.5%。结论45 ms TE PRESS较97 ms方法提供了更精确的胱硫醚检测,将有助于1p/19q共缺失胶质瘤的无创诊断和患者的治疗反应监测。PRESS在1p/19q共缺失胶质瘤中表现出中等诊断性能,表明需要进一步研究。
基金National Natural Science Foundation of China (Grant Nos. 82070234 and 82100254)。
文摘Myocardial fibrosis is a major pathogenic factor contributing to cardiac remodeling and heart failure. Recent research has indicated that micro RNAs play a crucial role in the progression of cardiac fibrosis. Bone morphogenetic protein and activin membrane-bound inhibitor(BAMBI) have been shown to alleviate myocardial fibrosis by inhibiting the transforming growth factor β1(TGF-β1) signaling pathway. Therefore, the current study aimed to elucidate the post-transcriptional regulation of BAMBI by miR-19a-3p and its role in TGF-β1-induced cardiac fibroblast activation. We found that transverse aortic constriction induced both myocardial interstitial and perivascular collagen deposition. Quantitative reverse transcription-PCR(q RT-PCR) analysis showed that the expression level of miR-19a-3p was increased in the myocardial tissues of cardiac fibrosis, and TGF-β1 induced an upregulation in miR-19a-3p expression in cardiac fibroblasts. The dual-luciferase reporter assay and q RT-PCR verified that miR-19a-3p directly bound to the 3 ′ untranslated regions of BAMBI m RNA, thereby reducing BAMBI expression and diminishing its ability to inhibit the TGF-β1 signaling pathway. Furthermore,overexpression of miR-19a-3p mimic increased the activation of TGF-β1/SMAD2/3 pathway signaling,promoting cardiac fibroblast activation. However, this activation was blocked by BAMBI overexpression. These findings imply that miR-19a-3p enhances the activation of TGF-β1/SMAD2/3 by inhibiting BAMBI, further boosting the activation of cardiac fibroblasts and contributing to myocardial fibrosis.
