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OBJECTIVE: To investigate the correlation between clinicopathological features and BRAF~(V600E) gene mutation in papillary thyroid carcinoma(PTC). METHODS: The data of 290 cases of PTC admitted from August 2016 to May 2018 in Beijing Tongren Hospital,Capital Medical University were analyzed retrospectively. All the cases of PTC were examined by BRAF~(V600E) immunohistochemistry after operation. Mutation positive group included 192 cases. Mutation negative group included 59 cases and partial mutation group included 39 cases. The cases of partial mutantion were excluded. The clinicopathological differences between the two groups were compared. RESULTS: By statistical analysis,there was a statistical difference between two groups in the invasion of the capsule(P<0.05). In the two groups(microcarcinoma and non-microcarcinoma),there was the same result.There was no statistical difference in other indexes. CONCLUSION: In patients with PTC,BRAF~(V600E) gene mutation is not associated with the clinicopathological features of the PTC. Patients with non-BRAF~(V600E) gene mutations are more likely to invade the membranes of microcarcinomas and non-microcarcinomas.
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Objective To examine the expression of autoantibodies against angiotensin Ⅱ type 1 receptor (AT1-AAs),monocyte chemoattractant protein-1 (MCP-1) and high-sensitivity C-reactive protein (hs-CRP) in patients of acute coronary syndrome (ACS),and study the role of AT1-AAs in plaque stability and pathogenesis of ACS.Methods Sixty patients with ACS were selected as ACS group,60 patients with stable angina pectoris (SAP) were selected as SAP group,and 60 healthy people were selected as control groups.The epitopes of the second extracellular loop of angiotensin Ⅱ type 1 receptor (165-191) were synthesized and used as antigen to screen the serum autoantibodies by enzyme-linked immunosorbent assay (ELISA).The peripheral blood levels of MCP-1 and hs-CRP were also evaluated.Results The positive rates of AT1-AAs in ACS group,SAP group and control group were 45.0%(27/60),21.7%(13/60) and 5.0%(3/60),respectively.The positive rates of AT1-AAs in ACS group and SAP group were significantly higher than those in control group,the positive rate of AT1-AAs in ACS group was significantly higher than that in SAP group,and there were statistical differences (P < 0.01).The MCP-1 and hs-CRP levels in ACS group and SAP group were significantly higher than those in control group,the MCP-1 and hs-CRP levels in ACS group were significantly higher than those in SAP group,and there were statistical differences (P < 0.01).The MCP-1 and hs-CRP levels in AT1-AAs positive patients in ACS group and SAP group were significantly higher than those in AT1-AAs negative patients,and there were statistical differences (P <0.01).Conclusions AT1-AAs may play an important role in the pathogenesis of ACS.Inducing the expression of inflammatory factor through AT1-AAs maybe an important mechanism for plaque instability.
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<p><b>OBJECTIVE</b>To explore the underlying mechanism of mesenchymal stem cells (MSCs) transfer induced cardiac function improvement in failing hearts.</p><p><b>METHODS</b>Congestive heart failure (CHF) was induced in rats by cauterization of the heart wall. MSCs were cultured from autologous bone marrow and injected into the border zone and the remote myocardium 5 days after cauterization.</p><p><b>RESULTS</b>Ten weeks later, cardiomyocyte nucleus mitotic index, capillary density and expression of insulin-like growth factor 1 (IGF-1), hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) were significantly increased in the border zone and significantly reduced in the remote myocardium in CHF rats (all P<0.05 vs. sham). Besides cardiac function improvement and left ventricular remodeling attenuation evidenced by hemodynamic and echocardiographic examinations, expressions of IGF-1, HGF and VEGF in the remote myocardium and in the border zone were also significantly upregulated (P<0.05 or P<0.01 vs. CHF), and cardiomyocyte nucleus mitotic index as well as capillary density were significantly increased in CHF rats with MSCs (P<0.05 or P<0.01 vs. CHF). Moreover, collagen area was significantly reduced and myocardial area was significantly increased in the border zone in these rats too.</p><p><b>CONCLUSION</b>Autologous MSC implantation upregulated expressions of growth factors enhanced cardioangiogenesis which might be the underlying mechanisms for improved cardiac function and attenuated left ventricular remodeling induced by MSCs transplantation in failing rat myocardium.</p>
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Animais , Masculino , Ratos , Modelos Animais de Doenças , Insuficiência Cardíaca , Metabolismo , Terapêutica , Fator de Crescimento de Hepatócito , Metabolismo , Fator de Crescimento Insulin-Like I , Metabolismo , Transplante de Células-Tronco Mesenquimais , Miocárdio , Metabolismo , Ratos Sprague-Dawley , Transplante Autólogo , Fator A de Crescimento do Endotélio Vascular , Metabolismo , Remodelação VentricularRESUMO
<p><b>OBJECTIVE</b>To gain insight into the role of dendritic cells in graft rejection following penetrating keratoplasty by investigating their distribution in rat cornea.</p><p><b>METHODS</b>Orthotopical corneal transplantation was performed and immunohistochemical staining of the whole-mount cornea and the spleen tissue specimen employed to determine the distribution of the dendritic cells in the cornea.</p><p><b>RESULTS</b>Graft rejection occurred in all rats following the transplantation. No OX-62(+) dendritic cells were found in normal cornea but they were present in the epithelium of the cornea graft with allograft rejection.</p><p><b>CONCLUSION</b>OX-62(+) dendritic cells presenting in the rejected cornea may be related to acute graft rejection after penetrating keratoplasty.</p>