Central nervous system infection and AEDs withdrawal in epilepsy patients were the most important causes of CSE. There is a large gap between antiepileptic therapy in China and European Status Epilepticus guidelines.
Cardiac hypertrophy is a crucial predictor of heart failure and is regulated by microRNAs. MicroRNA-124 (miR-124) is regarded as a prognostic indicator for outcomes after cardiac arrest. However, whether miR-124 participates in cardiac hypertrophy remains unclear. Therefore, our study aimed to determine the role of miR-124 in angiotensin II(AngII)-induced myocardial hypertrophy and the possible mechanism. Primary cultured rat neonatal cardiomyocytes(NCMs) were transfected with miR-124 mimics or inhibitor, followed by AngII stimulation. Quantitative RT-PCR, western blot analysis and determination of cell surface area of NCMs were used to detect the hypertrophic phenotypes. We observed that miR-124 was elevated in AngII-induced hypertrophic cardiomyocytes. Cell surface area of NCMs and mRNA expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC), indicators of myocardial hypertrophy, were higher in NCMs transfected with miR-124 mimics in the presence of AngII. On the contrary, knockdown of miR-124 by its specific inhibitor could restore these courses. Furthermore, downregulation of miR-124 alleviated the increased protein level of endoplasmic reticulum (ER) stress markers 78-kDa glucose-regulated protein (Grp78) and calreticulin(CRT) in AngII-induced NCMs. In conclusion, our study shows that inhibition of miR-124 effectively suppresses AngII-induced myocardial hypertrophy, which is associated with attenuation of ER stress.
The number of pulmonary nodules identified incidentally or through lung cancer screening programs has dramatically increased. The role of radiation therapy (RT) in this patient population is not defined. Our institution established a multidisciplinary Pulmonary Nodule and Lung Cancer Screening Clinic (PNLCSC) to optimize the management of these patients. In this study, we describe the role of radiation oncologists in the multidisciplinary evaluation and management of incidental and screening-identified pulmonary nodules. Materials/Methods: This study included patients referred to the PNLCSC between 10/2012 and 9/2019. Indications for referral included a Lung-RADS 4 finding on screening CT or an incidental pulmonary nodule measuring 6 mm. At each clinic session, a multidisciplinary team including diagnostic/interventional radiologists, pulmonologists, medical oncologists, thoracic surgeons, and radiation oncologists made recommendations regarding the work-up, management, and follow-up of each patient. Demographic and clinical characteristics as well as data on followup and treatments were prospectively recorded. Collection and analysis of the data was approved by institutional IRB. Results: Of 1,150 patients evaluated by the PNLCSC, 234 (20.3%) were screening patients, and 916 (79.7%) had incidental nodules. Among screening patients, 41 (17.5%) underwent therapeutic intervention, 31 (13.2%) with surgical resection and 10 (4.3%) with RT. RT represented 24.4% of all treatments received by screening patients. Among patients with incidental pulmonary nodules, 227 underwent therapeutic intervention, with 167 (18.2%) and 60 (6.6%) receiving surgery and RT, respectively. The overall rate of patients undergoing RT was stable over time, ranging from 6.
BackgroundOur previous research has demonstrated decreased expression of CD4+CD25+Foxp3+ regulatory T cells (Tregs) enrolled in the pathogenesis of rheumatoid arthritis (RA). Anti-TNF-α mAb therapy could improve Tregs expansion in RA and associate with clinical amelioration of RA patients. STAT5 is reported to have effects on many aspects of immune function, particularly in regulatory T cell development.ObjectivesIn this study, we aim to monitor phosphoSTAT5 expression in Tregs and investigate its role in RA disease.MethodsFlowcytometry was employed to detect the phosphorylation level of STAT5 in CD3+CD4+ T cells, CD4+CD25high regulatory T cells and the expression of CD4+CD25+Foxp3+Tregs in peripheral blood of 20 patients with RA disease and 20 age and gender-matched normal controls. STAT5 mRNA expression in peripheral blood mononuclear cells (PBMC) were also monitored of these RA patients and normal controls.ResultsPhosphorylation level of STAT5 deceased in RA patients both in CD3+CD4+ T cells and in CD4+CD25high regulatory T cells, along with reduction of expression of CD4+CD25+Foxp3+ Tregs. Detection of mRNA also confirmed STAT5 down regulation in Tregs in RA patients.ConclusionsCompared with normal controls, the expression of CD4+CD25+Foxp3+Tregs decreased in RA patients. PhosphoSTAT5 reduction in CD3+CD4+ T cells, mainly in CD4+CD25high regulatory T cells contributed to impairment of CD4+CD25+Foxp3+ regulatory T cells in RA.ReferencesNiu Q, Cai B, Huang ZC, Shi YY, Wang LL. Disturbed Th17/Treg balance in patients with rheumatoid arthritis. Rheumatol Int. 2012 Sep;32(9):2731–6.Huang Z, Yang B, Shi Y, Cai B, Li Y, Feng W, Fu Y, Luo L, Wang L. Anti-TNF-α therapy improves Treg and suppresses Teff in patients with rheumatoid arthritis. Cell Immunol. 2012 Sep;279(1):25–9.Disclosure of InterestNone declared
The aim of this study was to retrospectively review our experience of performing simultaneous operations on concomitant diseases in the esophagus and lungs. From January 1998 to July 2009, simultaneous operations were performed on 13 patients with concomitant esophageal and pulmonary diseases, using coordinated surgical approaches. Among the 13 patients, six had primary cancers in the esophagus and lungs, five had primary esophageal cancer accompanied by a benign pulmonary disease, one had benign diseases in both esophagus and lung, and one had primary esophageal cancer with metastasis to the left lower lung. All patients survived the operations. Two major complications occurred postoperatively. One complication was bronchopleural fistula and the other was intrathoracic gastric laceration. Both patients recovered after additional treatments. Simultaneous operation of concomitant diseases in the esophagus and lungs is feasible and safe in selected patients who have received careful preoperative assessment, well-designed surgical approach, and proper perioperative management.
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