Objective To explore the role of estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) in estrogen-induced proliferation of endometrial cancer, and explore whether metformin inhibits the proliferation of endometrial cancer cells through ERα and ERβ. Methods Stable transfected Ishikawa cells were constructed by lentivirus. The effects of down-regulated ERα and ERβ on estrogen-induced Ishikawa cell proliferation were detected by methyl thiazolyl tetrazolium assay. The effects of down-regulated ERα and ERβ on estrogen-induced Ishikawa cell cycle were detected by flow cytometry. In addition, quantitative real-time polymerase chain reaction and Western blotting assays were used to detect changes in the expression of cyclinD1 and P21 involved in cell cycle regulation. The effects of down-regulated ERα and ERβ on estrogen-induced Ishikawa cell proliferation were observed by adding metformin to estrogen treatment. Results Down-regulation of ERα inhibited the proliferation and cell cycle of Ishikawa cells (P<0.05). Down-regulation of ERα also inhibited the expression of cyclinD1 and promoted the expression of P21 (P<0.05). Down-regulation of ERα counteracted the effect of estrogen-induced cell proliferation, cell cycle, and the expression changes of cyclinD1 and P21 (P<0.05). Down-regulation of ERβ promoted the proliferation and cell cycle of Ishikawa cells (P<0.05). Down-regulation of ERβ also promoted the expression of cyclinD1 and inhibited the expression of P21 (P<0.05). Down-regulation of ERβ enhanced the effect of estrogen-induced cell proliferation, cell cycle, and the expression changes of cyclinD1 and P21 (P<0.05). Metformin inhibited the proliferation of estrogen-induced Ishikawa cells (P<0.05), while in the down-regulated ERα Ishikawa cells or down-regulated ERβ Ishikawa cells, the inhibition of metformin on Ishikawa cells disappeared (P<0.05). Conclusions ERα may promote estrogen-induced proliferation of endometrial cancer cells, while ERβ may inhibit estrogen-induced proliferation of endometrial cancer cells. In addition, ERα and ERβ may also mediate the inhibitory effect of metformin on endometrial cancer cells.
Conventional transcatheter aortic valve replacement is normally recommended with transthoracic echocardiography, and contrast agent mediated fluoroscopy under anesthesia to guide a better implantation of the transcatheter valve. However, iodine-containing contrast agent possibly damages the patient’s kidney, and even induces the acute kidney injury. We reported a 75-year-old patient diagnosed with severe aortic valve stenosis, moderate regurgitation, and chronic renal failure. We performed the aortic valve replacement under the guidance of fluoroscopy and transesophageal ultrasound without contrast agent. Seven days after surgery, the patient recovered well and discharged with alleviated aortic stenosis and fixed transcatheter aortic valve.
Artificial chords is a mature mitral valve repair technique, especially in adult mitral valve repair. It is still challenging to repair mitral valve in children with artificial chords because the quality of mitral valve is soft and immature. There are some differences in the methods of suture, the choice of suture size and the number of artificial chords. Although the artificial chords could not grow naturally, we found through the long-term research that most children did not have mitral valve restriction or even chords rupture due to itself can compensate through the growth of the flap and papillary muscle. This article summarizes the recent research progress on the treatment of mitral valve insufficiency in children with artificial chordae and provides advise for clinical treatment.
Objective To summarize the characteristics of children diagnosed with secondary subaortic stenosis after the surgical closure for ventricular septal defect and explore its potential mechanism. Methods We retrospectively collected patients aged from 0 to 18 years, who underwent ventricular septal defect closure and developed secondary subaortic stenosis, and subsequently received surgical repair from 2008 to 2019 in Fuwai Hospital. Their surgical details, morphological features of the subaortic stenosis, and the follow-up information were analyzed. Results Six patients, including 2 females and 4 males, underwent the primary ventricular septal defect closure at the median age of 9 months (ranging from 1 month to 3 years). After the first surgery, patients were diagnosed with secondary subaortic stenosis after 2.9 years (ranging from 1 to 137 months). Among them, 2 patients underwent the second surgery immediately after diagnosis, and the other 4 patients waited 1.2 years (ranging from 6 to 45 months) for the second surgery. The most common type of the secondary subaortic stenosis after ventricular septal defect closure was discrete membrane, which located underneath the aortic valve and circles as a ring. In some patients, subaortic membrane grew along with the ventricular septal defect closure patch. During the median follow-up of 8.1 years (ranging from 7.3 to 8.9 years) after the sencond surgery, all patients recovered well without any recurrence of left ventricular outflow tract obstruction. Conclusion Regular and persistent follow-up after ventricular septal defect closure combining with or without other cardiac malformation is the best way to diagnose left ventricular outflow tract obstruction in an early stage and stop the progression of aortic valve regurgitation.