ABSTRACT
Chronic disease management is a challenging issue in China. To address the needs of talents and mature innovation ecosystem related to chronic disease management, The First Affiliated Hospital of Sun Yat-sen University(FAH-SYSU) actively responds to the national strategy to promote the high-quality development of the hospital through strengthening strategic planning, top-level design, and systematic consideration. Precise management of chronic diseases was taken as key measure for the construction of a national medical center. With continuous exploration in establishing talent pool, innovation center and application platform, and chronic disease management system that focuses on core elements of talent and innovation, the FAH-SYSU Model for the precise management of chronic diseases has been initially formed.
ABSTRACT
Objective To investigate the reasons of HOXA5 overexpression in GBM and the molecular mechanism of miR-128-3p regulating the proliferation, invasion and apoptosis of glioblastoma multiforme. Methods After increasing and decreasing miR-128-3p expression in U87 cell lines by lentivirus transfection, the changes of HOXA5 expression were detected by Western blot, to explore the correlation between miR-128-3p and HOXA5 in GBM. The dual-luciferase reporter tests were performed to detect the target interaction of miR-128-3p with HOXA5. Through CCK-8 test, Transwell test, flow cytometric assay and tumor cell xenograft in nude mice, we verified molecular mechanism of miR-128-3p regulating the proliferation, invasion and apoptosis of GBM in vitro and in vivo. Results The expression level of HOXA5 was decreased in U87 cell line after miR-128-3p upregulation. In addition, the expression level of HOXA5 was increased in U87 cell line after miR-128-3p downregulation (P < 0.05). The expression level of HOXA5 was correlated negatively with the expression of miR-128-3p in U87 cell lines. MiR-128-3p targetedly interacted with 3'UTR of HOXA5 and inhibited the expression of HOXA5. The proliferation, invasion and anti-apoptosis of U87 cells were significantly decreased in the miR-128-3p+control group. Conclusion MiR-128-3p regulates negatively the proliferation, invasion and anti-apoptosis of GBM cells by targeting HOXA5. The overexpression of HOXA5 is induced by downregulation of miR-128-3p in GBM.
ABSTRACT
Objective To analyze the clinical features of systemic lupus erythematosus (SLE) com-plicated by noncirrhotic portal hypertention (NCPH),and improve the recognition of NCPH.Methods Clinical data from SLE complicated by NCPH in our hospital were retrospectively analyzed and summarized,while the related literatures were reviewed.Results Four patients diagnosed as SLE complicated by NCPH were all women.NCPH presented with the clinical features of portal hypertension with normal or slightly elevated transaminase.Anticardiolipin (ACL) antibodies were positive in 2 patients.Two patients underwent liver needle biopsy,showing nodular regenerative hyperplasia,of which,one with liver portal fibrosis.The treatment strategy was managing the primary disorder and controling of portal hypertention in four patients.Twenty-two cases of SLE complicated by NCPH were reviewed and analyzed,including 18 cases from related literatures and our 4 cases.Among the 22 cases,the mean time between the diagnosis of SLE and NCPH was eight years,of which one patient with NCPH before SLE,one diagnosed at the same time and the rest with NCPH after SLE.19％ (4/21) of patients presented with Raynaud's phenomenon and 18％ (4/22) complicated by pulmonary hypertension.In serological tests,patients presented with positive ACL anti-bodies [33％(7/21)] and anti-dsDNA [48％(10/21)],as well as increased IgG and γ-Globulin [38％(8/21)].Liver needle biopsy showed nodular regenerative hyperplasia or liver portal fibrosis with the prevalence of 80％ (16/20) and 25％ (5/20),respectively.Conclusion SLE complicated by NCPH is very rare clinically and is easily being misdiagnosed without obvious symptoms and signs in the early stage.Positive ACL antibodies and Raynaud's phenomenon maybe be closely related to SLE complicated by NCPH.