目的 总结彩色多普勒超声（彩超）结合钼靶X线摄片标记定位对无临床体征乳腺肿块的定位诊断价值。 方法 2010年3月－2011年10月对48例彩超和钼靶X线检查发现可疑病灶而无任何临床体征的患者，在彩超引导下穿刺病灶金属导丝标记定位，并结合钼靶X线检查切除病灶，同时快速冰冻活检明确诊断。 结果 48倒中有11例确诊为乳腺癌（浸润性导管癌7例，导管内癌4例），37例为良性病变（纤维瘤5例，导管内乳头状瘤4例，乳腺腺病28例）。冰冻切片病理检查与术后石蜡病检结果一致。 结论 彩超引导下穿刺钢丝标记定位活检结合钼靶X线摄片，有效地解决了乳腺细小钙化和微小病灶活检术中精确定位和完整切除的难题，对无临床体征的微小乳腺肿块的诊断准确、可靠、实用。
The aim of this study was to observe whether necroptosis is involved in the process of cardiac hypertrophy induced by pressure overload. SD rats underwent transverse abdominal aortic constriction (TAC) operation for establishing cardiac hypertrophy model. The structure and function of the left ventricle of rats were evaluated via echocardiography, left ventricular mass index, the expression of markers of cardiac hypertrophy and histological detection. Real-time PCR and Western blot were used to measure the gene and protein expression of receptor interacting protein kinase 1 and 3 (RIPK1 and RIPK3, the necroptosis markers) respectively. Four weeks after TAC operation, rat model for cardiac hypertrophy was established. The experimental data showed that the gene and protein expressions of RIPK1 and RIPK3 in the rat heart hypertrophic tissues after TAC for 4 weeks were increased significantly compared with those in the sham group. HE staining showed cardiomyocytes injury and hypertrophy in the hearts of TAC rat models. By transmission electron microscope, we observed that mitochondria of cardiomyocytes were damaged seriously in the TAC models. Treatment with losartan used, the selective antagonist of angiotensinⅡtypeⅠreceptor could improve the cardiac function of TAC rats. Moreover, losartan treatment decreased the expression of RIPK1 and RIPK3 in heart tissues of TAC rats. The results suggest that necroptosis occurrs in the process of cardiac hypertrophy with pressure overload, and losartan could alleviate the cardiac hypertrophy and inhibit necroptosis.
This study aims to investigate the role of calreticulin in (CRT) pressure overload induced cardiac hypertrophy. In our study, cardiac hypertrophy was induced by left ventricular pressure overload in male SD rats subjected to transverse aortic constriction (TAC) operation. Expression of gene and protein of calreticulin, markers of cardiac hypertrophy and endoplasmic reticulum stress (ERS) were measured with real-time qPCR and Western blot respectively. Meanwhile, atorvastatin (a known ERS inhibitor) and calreticulin-specific small interference ribonucleic acid (siRNA) were used to inhibit the expression of ERS and calreticulin respectively. The experimental data demonstrated that the gene and protein levels of calreticulin, hypertrophic and ERS markers were increased significantly in the heart tissues of TAC rat models after 4 weeks. Moreover, atorvastatin administration improved the cardiac function and reduced the expression of calreticulin and ERS markers in TAC rats. In addition, cultured primary neonatal rat cardiomyocytes (NCMs) were treated with norepinephrine (NE), angiotensionⅡ (AngⅡ) or isoprenaline (ISO) to induce hypertrophic phenotype and ERS. The expression of hypertrophic markers was reduced in NCMs transfected with calreticulin-siRNA. The results suggested that calreticulin might be a promising target for the treatment of cardiac hypertrophy.