REFERENCES 1. Go AS, Mozaffarian D, Roger VL, et al. Heart Disease and Stroke Statistics—2014 Update. Circulation. 2014;129:e28-e292. https://doi.org/10.1161/01.cir.0000441139.02102.80 2. Berdowski J, Berg RA, Tijssen JG, Koster RW. Global incidences of out-of-hospital cardiac arrest and survival rates: Systematic review of 67 prospective studies. Resuscitation. 2010;81:1479-1487. doi: 10.1016/j.resuscitation.2010.08.006. 3. Fukuda T, Ohashi-Fukuda N, Kondo Y, Sera T, Doi K, Yahagi N. Epidemiology, Risk Factors, and Outcomes of Out
Monica Marton-Popovici and Dietmar Glogar
Sebastian Adeberg, Denise Bernhardt, Semi B. Harrabi, Nils H. Nicolay, Juliane Hörner-Rieber, Laila König, Michael Repka, Angela Mohr, Amir Abdollahi, Klaus-Josef Weber, Juergen Debus and Stefan Rieken
ATP production, induction of cell cycle arrest, autophagy, and apoptotic processes through activation of adenosine-5’-monophosphate-activated protein kinase (AMPK) 5 and inhibition of the mTOR (mammalian target of rapamycin) pathway in glioblastoma cells. 6 , 7 AMPK is a serine/threonine kinase that functions as a cellular energy sensor. AMPK is an obligate heterotrimer, consisting of one catalytic subunit (α) and two regulatory subunits (β and γ). 8 Under cellular stress conditions, AMPK is activated by increased AMP-to-ATP ratios to promote catabolism and
Cardiology. 2010;26:8C-13C. 4. Kozinski M, Pstragowski K, Kubica JM, et al. ACS networkbased implementation of therapeutic hypothermia for the treatment of comatose out-of-hospital cardiac arrest survivors improves clinical outcomes: the first European experience. Scand J Trauma Resusc Emerg Med. 2013;21:22. doi: 10.1186/1757-7241-21-22. 5. Tubaro M, Danchin N, Goldstein P, et al. Pre-hospital treatment of STEMI patients. A scientific statement of the Working Group Acute Cardiac Care of the European Society of Cardiology. Acute Card Care
Jakob Liermann, Patrick Naumann, Franco Fortunato, Thomas E. Schmid, Klaus-Josef Weber, Jürgen Debus and Stephanie E. Combs
ponicidin have been published. 6 , 7 , 8 In pancreatic cancer oridonin induces apoptosis and leads to an arrest in the G2/M-phase of the cell cycle. 9 , 10 , 11 , 12 Further, oridonin inhibits nuclear factor-kB. 13 Ponicidin is also known to induce apoptosis 14 , 15 , 16 , 17 but to our knowledge, there is no data for ponicidin in pancreatic cancer. Potential radiosensitization could be observed in chinese-hamster-V79 cells by oridonin. 18 Apart from this study we found no publication concerning oridonin or ponicidin induced radiomodulation. As natural occurring
Andreea Barcan, Istvan Kovacs, Ciprian Blendea, Marius Orzan and Monica Chitu
References 1. Windecker S, Kolh P, Fernando A et al. 2014 ESC/EACTS Guidelines on myocardial revascularization. European, The Task Force on Myocardial Revascularization of the Society of Cardiology (ESC) and the European Association for Cardio- Thoracic Surgery (EACTS). Eur Heart J. 2014;35:2541-2619. 2. Garot P, Lefevre T, Eltchaninoff H, et al. Six-Month Outcome of Emergency Percutaneous Coronary Intervention in Resuscitated Patients After Cardiac Arrest Complicating STElevation Myocardial Infarction. Circulation. 2007
Xinyu Wu, Daixing Zhong, Bin Lin, Wenliang Zhai, Zhenqi Ding and Jin Wu
correlation with BRAF V600E and different KRAS mutations in metastatic colorectal cancer - a single institution retrospective analysis. Radiol Oncol 2011; 45: 285-91. 25. Bulavin DV, Kovalsky O, Hollander MC, Fornace AJ Jr. Loss of oncogenic H-ras-induced cell cycle arrest and p38 mitogen-activated protein kinase activation by disruption of Gadd45a. Mol Cell Biol 2003; 23: 3859-71. 26. Cardaci S, Filomeni G, Rotilio G, Ciriolo MR. p38(MAPK)/p53 signalling axis mediates neuronal apoptosis in response to tetrahydrobiopterin
Valerija Zager, Maja Cemazar, Irena Hreljac, Tamara Lah, Gregor Sersa and Metka Filipic
genotoxins. Mutat Res-Gen Tox En 2008; 653 : 63-9. Zhou B-BS, Elledge SJ. The DNA damage response: putting checkpoints in perspective. Nature 2000; 408 : 433-9. Sionov RV, Haupt Y. The cellular response to p53: the decision between life and death. Oncogene 1999; 18 : 6145-57. Waldman T, Kinzler KW, Vogelstein B. P21 is necessary for the P53-mediated G1 arrest in human cancer cells. Cancer Res 1995; 55 : 5187-90. Vogelstein B, Lane D, Levine AJ. Surfing the p
Ivana Steiner, Nikolina Stojanovic, Aljosa Bolje, Anamaria Brozovic, Denis Polancec, Andreja Ambriovic-Ristov, Marijana Radic Stojkovic, Ivo Piantanida, Domagoj Eljuga, Janez Kosmrlj and Maja Osmak
flow cytometric analysis is presented in Figure 2 , and Table 3 . They show that compound 2b arrested the cells in the G1 phase of the cell cycle in dose-dependent manner, even after 24 hours of treatment. At later time points a dose- and time-dependent increase was detected in a fraction of cells with reduced DNA content (subG1), which represents the apoptotic cells subG1 fraction. These results suggest that 2b induces apoptosis in treated cells. Table 3 Effect of compound 2b on the cell cycle of H460 cells Conc. (μM) 24 h 48 h 72 h G1 S
Ioan Țilea, Codruța Gal, Andreea Varga and Roxana Rudzik
Left ventricular non-compaction (LVNC) is a cardiomyopathy that can either result from arrested or abnormal myocardial morphogenesis during heart development, or can be acquired later in life. Current practice guidelines recommend different strategies for the management of patients with LVNC. Common clinical features of this disease include cardiac failure, thromboembolism, life-threatening arrhythmia or sudden cardiac death, which could indicate a worse prognosis. The disease may occur alone or in association with other congenital cardiac, neuromuscular, mitochondrial or metabolic disorders. The association of left ventricular non-compaction with other structural cardiac congenital diseases (such as atrial or ventricular septal defect, patent ductus arteriosus, obstruction of ventricular outflow tract) is rare. As clinical manifestations of LVNC are non-specific, particular imaging modalities (echocardiography, cardiovascular magnetic resonance imaging or ECG gated computed tomography) should be used in order to establish the diagnosis of LVNC. Antiarrhythmic drugs and implantable cardioverter defibrillators may be considered for the management of ventricular arrhythmias in patients with ventricular non-compaction. We report the presentation, diagnosis and management of a 46 year-old female with refractory severe cardiac failure, repeated syncope due to LVNC and atrial septal defect, requiring medical therapy and an implantable cardioverter defibrillator as a "life bridge" to heart transplantation.
Shu-Hua Zhao, Fan Zhao, Jing-Ying Zheng, Li-Fang Gao, Xue-Jian Zhao and Man-Hua Cui
Knockdown of stat3 expression by RNAi inhibits in vitro growth of human ovarian cancer
Background. The aim of the study was to investigate the suppressive effects of pSilencer2.1-U6-siRNA-stat3 recombinant plasmids on the growth of ovarian cancer in vitro.
Material and methods. Three pairs of DNA template (stat3-1, stat3-2, stat3-3) specific for different target sites on stat3 mRNA were synthesized to reconstruct pSilencer2.1-U6-siRNA-stat3s, which were transfected into SKOV3 cells. The expressions of STAT3, BcL-2, cyclin D1 and C-myc in these cells were detected by Western blot and Northern blot. The cell cycle and the growth were determined by flow cytometry (FCM) and MTT assay, respectively. Cell apoptosis was determined by TUNEL staining.
Results. Of the three siRNAs, only siRNA targeting stat3-3 markedly suppressed the protein expression of stat3 in SKOV3 cells; MTT assay and FCM showed that transfection of stat3-3 siRNA could significantly suppress the growth of SKOV3 cells and arrest the cell cycle in vitro. TUNEL staining also showed massive apoptosis in SKOV3 cells transfected with stat3-3 siRNA.
Conclusions. pSilencer2.1-U6-siRNA-stat3-3 can significantly inhibit the STAT3 expression in human ovarian cancer cells resulting in the inhibition of the cancer growth and the increase of apoptosis of cancer cells.