L-carnosine, a dipeptide of the amino acids β-alanine and histidine, is found in various tissues, such as the central nervous system and skeletal muscles. Recently, L-carnosine has been reported to possess anti-tumor activity; however, the molecular mechanism underlying its activity in colorectal cancer is still unknown. Therefore, we investigated the effect of L-carnosine using a human colorectal cancer cell line, HCT116. Treatment with L-carnosine (0, 100, or 200 mM) for 24 h gradually reduced cellular proliferation according to immunochemistry and 7-aminoactinomycin D (7-AAD) analyses and induced G0/G1 phase arrest. In the RT-PCR analysis, L-carnosine decreased the mRNA levels of cell cycle-related genes in HCT116 cells. In the Western blot analysis, levels of the cyclin D1, BAX/Bcl-2, cleaved caspase-3, p21, and p53 proteins were significantly increased in cells treated with L-carnosine. We next determined whether STAT1/NF-κB pathway is involved in regulation of cell cycle arrest- and cell death-associated gene in HCT116. The L-carnosine treatment significantly inhibited the phosphorylation of STAT1 on Tyr701 and NF-κB p65 on Ser276 and Ser536, and then, we exogenously blocked the NF-κB phosphorylation using Bay 11-7082. Based on our findings, L-carnosine induces cell cycle arrest and apoptosis in human colorectal cancer cells by suppressing of NF-κB/STAT1 signaling.
Background. In most reports on ECMO treatment, advanced age is classified as a contraindication to VA ECMO. We attempted to investigate whether advanced age would be a main risk factor deciding VA ECMO application and performing VA ECMO support. We determined whether advanced age should be regarded as an absolute or relative contraindication to VA ECMO and could affect weaning and survival rates of VA ECMO patients. Methods. VA ECMO was performed on 135 adult patients with primary cardiogenic shock between January 2010 and December 2014. Successful weaning was defined as weaning from ECMO followed by survival for more than 48 hours. Results. Among the 135 patients, 35 survived and were discharged uneventfully, and the remaining 100 did not survive. There were significant differences in survival between age groups, and older age showed a lower survival rate with statistical significance (P = .01). By multivariate logistic regression analysis, age was not significantly associated with in-hospital mortality (P = .83) and was not significantly associated with VA ECMO weaning (P = .11). Conclusions. Advanced age is an undeniable risk factor for VA ECMO; however, patients of advanced age should not be excluded from the chance of recovery after VA ECMO treatment.
Cigarette smoking (CS) is considered one of the major risk factors to cause neurodegenerative disorders. Nicotine is the main chemical in CS which is responsible for dysfunction of the brain as a neuroteratogen. Also, nicotine dependency is a real mental illness and disease. Recently, chronic nicotine exposure has been shown to cause oxidative/nitrosative stress leading to a deleterious condition to cellular death in different brain regions. However, little is known about the effects of nicotine on mouse neural stem cells (mNSCs). The aim of this study is to investigate the effects of nicotine on mNSCs and elucidate underlying mechanisms involved in expression of a diversity of genes regulated by nicotine. When mNSCs were isolated from the whole brain of embryonic day 16 mice treated with nicotine at vehicle, 100, 400, and 800 μM for 5 d, nicotine significantly decreased the number and size of neurospheres. In immunocytochemistry, nicotine-exposed mNSCs expressing nestin showed the shortened filaments and condensed nuclei. In RT-PCR, messenger RNA (mRNA) levels of proliferating cell nuclear antigen (PCNA) and sirtuin1 (SIRT1) were significantly decreased, while the production of nitric oxide and mRNA levels of cyclooxygenase2 (COX-2), tumor necrosis factor-alpha TNF-α, and histone deacetylase 1 (HDAC1) were increased in a dose-dependent manner. In addition, sodium butyrate and valproic acid, HDAC inhibitors, partially rescue proliferation of mNSCs via inhibition of HDAC1 expression and NO production. Taken together, these data demonstrate that prolonged exposure of nicotine decreased proliferation of mNSCs by increased NO and inflammatory cytokine through increased HDAC1. Furthermore, this study could help in the development of a therapy for nicotine-induced neurodegenerative disorder and drug abuse.
A 66-year-old male patient arrived at the emergency room with a crush injury to his chest. Multiple rib fractures, hemothorax on both sides, left scapular fracture, liver laceration, and retroperitoneal hematoma were found upon the radiologic examination. After closed thoracostomy, the patient had been initially admitted to the intensive care unit, but he was transferred to the general ward on the next day. On the 4th post-trauma day, the patient complained of severe pain and there was bloody drainage through the chest tube. This case is an exploration with the consideration of the possibility of major bleeding and the subsequent repair of the descending thoracic aorta. This case is regarded as a case in which the aorta wall was damaged as the sharp margin of the fractured ribs caused continuous irritation.
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