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.
Objective To explore the relationship between imbalance in sagittal plane as well as structural factors and lumbar degenerative disease. Methods Patients diagnosed between July 2012 and May 2015 were divided into 4 groups according to corresponding diagnostic criteria: lumbar disc herniation group (LDH), lumbar disc protrusion group (LDP), degenerative lumbar spondylisthesis group (DLS) and nonspecific low back pain group (NLBP); 40 patients were included in each group according to their visiting time. All patients underwent X-ray, CT, and MRI. Sagittal parameters and evaluate degeneration level of structural factors were measured, and the difference among the groups were analyzed. Results There was statistical significance in differences of pelvic incidence (PI) and lumbar lordosis (LL) among 4 groups (P<0.05). Average PI was followed in descending order: DLS, LDP, NLBP, and LDH; average LL was followed in descending order: DLS, NLBP, LDP, and LDH. There was no statistical differences in sacral slope and pelvic tilting among 4 groups (P>0.05). The difference in the level of lumbar disc degeneration between NLBP group (which had slightest lumbar disc degeneration) and the other groups was significant (P<0.001) while no statistical differences in level and rate of lumbar disc degeneration among the other three groups was found (P>0.05). As to the level of lumbar zygapophyseal joint degeneration, there was statistical differences between NLBP group (which had the lowest level of lumbar zygapophyseal joint degeneration) and the other groups (P<0.001) while no statistical differences in the grade of lumbar zygapophyseal joint degeneration among the other three groups (P>0.05). There was statistical differences in the rate of lumbar zygapophyseal joint degeneration between LDH and DLS group (χ2=11.429,P=0.001). Conclusions Vertical lunbar spine is combined with LDH of which the level of lumbar zygapophyseal joint degeneration is minimized, while crooked lunbar spine is combined with DLS of which the level of lumbar zygapophyseal joint degeneration is maximization. NLBP has the lowest level of degeneration of lumbar disc and lumbar zygapophyseal joint degeneration.
Chronic obstructive pulmonary disease (COPD) is one of the major chronic diseases that seriously endanger the health of residents in our country. Exercise is one of the effective interventions to improve the cardiopulmonary function and quality of life of COPD patients. An exercise prescription specifies the frequency, intensity, duration, mode, total exercise volume, and progression of exercise, forming a clear - purpose and systematic exercise guidance plan. Clinical pathways standardize and proceduralize the patient's diagnosis and treatment process. Developing an exercise prescription for the entire process of issuing and implementing exercise prescriptions for COPD patients helps to promote the application of exercise prescriptions and assist in the implementation of related work in primary - level medical institutions. Therefore, we invited a number of COPD experts and sports medicine experts to develop this clinical pathway in combination with domestic and international guidelines, consensuses, and personal experience. Its aims are to simplify the exercise prescription development process, reduce the required level of expertise, enhance the capacity of primary healthcare institutions, and facilitate the application of exercise prescriptions within these settings.