Experimental Research Center

Pikérmi, Greece

Experimental Research Center

Pikérmi, Greece
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Triantafillidis J.K.,Saint Panteleimon General Hospital | Merikas E.,Saint Panteleimon General Hospital | Nikolakis D.,Saint Panteleimon General Hospital | Papalois A.E.,Experimental Research Center
World Journal of Gastroenterology | Year: 2013

Diagnostic and therapeutic endoscopy can successfully be performed by applying moderate (conscious) sedation. Moderate sedation, using midazolam and an opioid, is the standard method of sedation, although propofol is increasingly being used in many countries because the satisfaction of endoscopists with propofol sedation is greater compared with their satisfaction with conventional sedation. Moreover, the use of propofol is currently preferred for the endoscopic sedation of patients with advanced liver disease due to its short biologic half-life and, consequently, its low risk of inducing hepatic encephalopathy. In the future, propofol could become the preferred sedation agent, especially for routine colonoscopy. Midazolam is the benzodiazepine of choice because of its shorter duration of action and better pharmacokinetic profile compared with diazepam. Among opioids, pethidine and fentanyl are the most popular. A number of other substances have been tested in several clinical trials with promising results. Among them, newer opioids, such as remifentanil, enable a faster recovery. The controversy regarding the administration of sedation by an endoscopist or an experienced nurse, as well as the optimal staffing of endoscopy units, continues to be a matter of discussion. Safe sedation in special clinical circumstances, such as in the cases of obese, pregnant, and elderly individuals, as well as patients with chronic lung, renal or liver disease, requires modification of the dose of the drugs used for sedation. In the great majority of patients, sedation under the supervision of a properly trained endoscopist remains the standard practice worldwide. In this review, an overview of the current knowledge concerning sedation during digestive endoscopy will be provided based on the data in the current literature. © 2013 Baishideng. All rights reserved.

Karlis G.,Sismanoglio General Hospital | Iacovidou N.,National and Kapodistrian University of Athens | Lelovas P.,National and Kapodistrian University of Athens | Niforopoulou P.,National and Kapodistrian University of Athens | And 5 more authors.
Acta Anaesthesiologica Scandinavica | Year: 2014

Background Aim of this experimental study was to compare haemodynamic effects and outcome with early administration of amiodarone and adrenaline vs. adrenaline alone in pigs with prolonged ventricular fibrillation (VF). Methods After 8 min of untreated VF arrest, bolus doses were administered of adrenaline (0.02 mg/kg) and either amiodarone (5 mg/kg) or saline (n = 8 per group) after randomisation. Cardiopulmonary resuscitation (CPR) was commenced immediately after drug administration, and defibrillation was attempted 2 min later. CPR was resumed for another 2 min after each defibrillation attempt, and the same dose of adrenaline was given every 4th minute during CPR. Haemodynamic monitoring and mechanical ventilation continued for 6 h after return of spontaneous circulation (ROSC), and the pigs were euthanised at 48 h. Researchers were blinded for drug groups throughout the study. Results There was no difference in rates of ROSC and 48-h survival with amiodarone vs. saline (5/8 vs. 7/8 and 0/8 vs. 3/8, respectively). Diastolic aortic pressure and coronary perfusion pressure were significantly lower with amiodarone during CPR and 1 min after ROSC (P < 0.05). The number of electric shocks required for terminating VF, time to ROSC and adrenaline dose were significantly higher with amiodarone (P < 0.01). The incidence of post-resuscitation tachyarrhythmias tended to be higher in the saline group (P = 0.081). Conclusion Early administration of amiodarone did not improve ROSC or 48-h survival rates, and was associated with worse haemodynamics in this swine model of cardiac arrest. © 2013 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.

Karagianni V.T.,Saint Panteleimon General Hospital | Papalois A.E.,Experimental Research Center | Triantafillidis J.K.,Saint Panteleimon General Hospital
Indian Journal of Surgical Oncology | Year: 2012

Cachexia, malnutrition, significant weight loss, and reduction in food intake due to anorexia represent the most important pathophysiological consequences of pancreatic cancer. Pathophysiological consequences result also from pancreatectomy, the type and severity of which differ significantly and depend on the type of the operation performed. Nutritional intervention, either parenteral or enteral, needs to be seen as a method of support in pancreatic cancer patients aiming at the maintenance of the nutritional and functional status and the prevention or attenuation of cachexia. Oral nutrition could reduce complications while restoring quality of life. Enteral nutrition in the post-operative period could also reduce infective complications. The evidence for immune-enhanced feed in patients undergoing pancreaticoduodenectomy for pancreatic cancer is supported by the available clinical data. Nutritional support during the post-operative period on a cyclical basis is preferred because it is associated with low incidence of gastric stasis. Postoperative total parenteral nutrition is indicated only to those patients who are unable to be fed orally or enterally. Thus nutritional deficiency is a relatively widesoread and constant finding suggesting that we must optimise the nutritional status both before and after surgery. © 2012 Indian Association of Surgical Oncology.

Kandarakis S.A.,National and Kapodistrian University of Athens | Piperi C.,National and Kapodistrian University of Athens | Moschonas D.P.,National and Kapodistrian University of Athens | Korkolopoulou P.,National and Kapodistrian University of Athens | And 2 more authors.
Experimental Eye Research | Year: 2015

Exogenous intake of glycotoxins present in western diet accelerates the accumulation of advanced glycation end products (AGEs) in multiple organs leading to potential tissue damage. Advanced ageing and diabetic conditions have been associated with AGEs deposition in multiple eye compartments including Bruch's membrane, optic nerve, lens and cornea. However, the impact of dietary AGEs in ocular physiology has not been extensively studied. The present study investigates the direct effects of a high AGE content diet in the ocular tissues of normal rats of different age. Two groups of baby (4 weeks of age) and adult (12 weeks of age) female Wistar rats (n=73) were allocated to high- or low-AGE diet for 3 months. Upon completion of experimental protocol, somatometric, hormonal and biochemical parameters were evaluated in all groups. Circulating and tissue AGE levels were estimated along with their signaling receptor (receptor for AGEs, RAGE) and vascular endothelial growth factor A (VEGF-A) expression in ocular tissues of the different subgroups. High AGE intake was associated with elevated serum AGEs (. p=0.0001), fructosamine (. p=0.0004) and CRP levels (. p=0.0001) compared to low AGE. High peripheral AGE levels were positively correlated with significant increased tissue immunoreactivity of AGEs and RAGE in retinal and uveal tissues as well as retinal VEGF-A expression. Up-regulation of RAGE and VEGF-A expression was observed in the ocular tissue of both baby and adult animals fed with high-AGE diet. Co-localization of AGEs and RAGE staining was observed mainly in the inner retinal layers and the retinal pigment epithelium (RPE) of all groups. VEGF-A expression was elevated in the RPE, the inner nuclear layer and the retinal ganglion cell layer of the animals exposed to high-AGE diet. In conclusion, dietary AGEs intake affects the physiology of ocular tissues by up-regulating RAGE and VEGF-A expression contributing to enhanced inflammatory responses and pathologic neovascularization in normal organisms independent of ageing. © 2015 Elsevier Ltd.

Bimpis A.,National and Kapodistrian University of Athens | Papalois A.,Experimental Research Center | Voumvourakis K.,National and Kapodistrian University of Athens | Olah O.,University of Szeged | And 2 more authors.
Brain Research | Year: 2015

Tumour necrosis factor α (TNF-α) and interleukin 1β (IL-1β) are important mediators of intracerebral haemorrhage (ICH) inflammatory response. Lazaroids, established antioxidants and neuroprotectants, have been studied in several brain pathologies. The present study was designed to investigate: a) TNF-α and IL-1β changes, in neurons and b) U-74389G effects, 4 and 24. h after haematoma induction in a porcine model of intracerebral haemorrhage.In twenty male landrace pigs (swines) aged 135-150 days old, autologous whole blood was injected around the right basal ganglia territory; in ten of the pigs the lazaroid compound U-74389G was administered. Brain TNF-α and IL-1β immunopositive neurons were determined by immunoarray techniques at 4 and 24. h timepoints.After the haematoma induction the number of TNF-α immunopositive neurons ipsilateral to the haematoma was significantly higher compared to the contralateral site at 4. h (p<0.0005), while U-74389G significantly reduced the number of TNF-α immunopositive neurons, ipsilateral to the haematoma, at 4. h (p=0.002); at 24. h, TNF-α immunopositive neurons were found significantly lower in the control group ipsilateral to the haematoma in comparison to 4. h timepoint(p<0.0005).The number of IL-1β immunopositive neurons at 4. h after the hematoma induction was significantly higher ipsilateral to the haematoma site (p<0.0005). U-74389G had no statistical significant effect.TNF-α and IL-1β, increase in neurons, 4. h after the haematoma induction, ipsilateral to the haematoma site. The administration of the antioxidant compound U-74389G, results in early (at 4. h) decrease of TNF-α immunopositive neurons but shows no statistical significant effect to IL-1β immunopossitive neurons. © 2015.

Chatzigeorgiou A.,National and Kapodistrian University of Athens | Chatzigeorgiou A.,TU Dresden | Kandaraki E.,National and Kapodistrian University of Athens | Piperi C.,National and Kapodistrian University of Athens | And 5 more authors.
Journal of Endocrinology | Year: 2013

The levels of advanced glycation end products (AGEs) are increased under conditions of impaired glucose metabolism and/or oxidative stress, promoting insulin resistance and other endocrine abnormalities. AGEs play a major role in the pathogenesis of several diseases such as diabetes, atherosclerosis, polycystic ovary syndrome and Alzheimer's disease, contributing to progressive ageing. Receptor-based clearance of AGEs by the receptor for AGE (RAGE) and/or the macrophage scavenger receptor A (SR-A) is considered as a main factor for the regulation of the concentration of AGEs under these conditions. This study aimed to investigate the expression of RAGE (AGER) and SR-A (MSR1) under high/low-dietary AGE conditions in vivo and their potential contribution to the metabolic and sex hormonal profile of female rats. Female Wistar rats were fed a low-AGE or high-AGE diet for 3 months. Serum samples were collected at baseline and at the completion of the 3-month period for the measurements of metabolic and hormonal parameters. Peripheral blood mononuclear cells (PBMCs) were isolated for the determination of the expression of RAGE and SR-A. The high-AGE diet-fed rats exhibited increased glucose, insulin and testosterone levels as well as decreased oestradiol and progesterone levels compared with the low-AGE diet-fed ones, thus indicating a metabolic and hormonal dysregulation attributed to high-AGE dietary exposure. The expression of RAGE was significantly down-regulated in the PBMCs of the high-AGE diet-fed rats (PZ0.041), and it was correlated negatively with insulin and testosterone levels and positively with progesterone levels. The expression of SR-A was also decreased in the high-AGE diet-fed rats to marginal significance. Decreased monocytic expression of scavenger receptors such as RAGE and SR-A may result in a higher deposition of AGEs in peripheral endocrine tissues, thus promoting endocrine-related abnormalities and diseases. © 2013 Society for Endocrinology.

Triantafillidis J.K.,IASO General Hospital | Papalois A.E.,Experimental Research Center
Scandinavian Journal of Gastroenterology | Year: 2014

Total parenteral nutrition (TPN) represents a therapeutic modality that could save the life of a patient with inflammatory bowel disease (IBD) facing severe nutritional problems, by restoring the patient's impaired nutritional status. TPN does not compete with enteral nutrition (EN), the latter being the first choice for all patients having anatomically intact and functionally normal digestive tract. TPN allows bowel rest while supplying adequate calorific intake and essential nutrients, and removes antigenic mucosal stimuli. The value of TPN in malnourished patients with intestinal failure due to CD is beyond doubt. However, it is difficult to suggest TPN as a sole treatment for active CD. An increased rate of remission could not be expected by applying TPN. The utility of TPN is restricted to certain cases involving efforts to close enterocutaneous or other complicated fistulas in patients with fistulizing CD, the treatment of short bowel syndrome following extensive resections for CD, or when EN is impractical for other reasons. There are no advantages of TPN therapy over EN therapy regarding fistula healing. TPN has no influence on the surgical intervention rate and little benefit by bypassing the intestinal passage could be expected. Also TPN shows no advantage if the disease is chronically active. However, an optimal supply of nutrients improves bowel motility, intestinal permeability and nutritional status, and reduces inflammatory reactions. TPN might be associated with an increased risk of adverse events, although TPN undertaken by experienced teams does not cause more complications than does EN. © 2014 Informa Healthcare.

Lampropoulos P.,Democritus University of Thrace | Lambropoulou M.,Democritus University of Thrace | Papalois A.,Experimental Research Center | Basios N.,Democritus University of Thrace | And 3 more authors.
Journal of Surgical Research | Year: 2013

Aim: The aim of the present study is to evaluate pathologic changes in the pancreatic parenchyma in an experimental model of acute pancreatitis (AP) following bilio-pancreatic duct ligation. An effort was made to clarify the role of apigenin, a substance that is well-known for its antioxidant and anti-inflammatory role and its likely beneficial activity to the pancreatic parenchyma following AP in rats. Material and method: One hundred twenty-six male Wistar rats 3-4 mo old and weighing 220-350 g were used. At time 0, the following groups were randomly assigned: group sham: rats were subjected to virtual surgery; group control: rats were subjected to surgery for induction of AP, by ligation of the bilio-pancreatic duct; group apigenin: rats were subjected to surgery for induction of AP and enteral feeding with apigenin. Pathologic changes of the pancreatic parenchymal and myeloperoxidase activity were measured at predetermined time intervals 6, 12, 24, 48, and 72 h. Result: From the pathologic reports, by comparing the control group with the apigenin group, an improvement of pancreatic tissue architecture following apigenin administration was observed. Inflammatory infiltration, edema, ductal dilation, and necrosis were reduced following apigenin administration over time (P = 0.049, P = 0.228, P = 0.387, P = 0.046). Treatment with apigenin significantly reduced the bilio-pancreatic duct ligation and evoked an increase in pancreatic myeloperoxidase activity (P = 0.030). Conclusion: Oral apigenin administration in rats, following experimentally induced pancreatitis, seems to protect the pancreatic tissue. Thus, apigenin administration to humans could potentially ameliorate the damages to the pancreas. © 2013 Elsevier Inc. All rights reserved.

Natoudi M.,Hippokration Hospital | Theodorou D.,Hippokration Hospital | Papalois A.,Experimental Research Center | Drymousis P.,Hippokration Hospital | And 5 more authors.
Obesity Surgery | Year: 2014

Background: Staple line leak, although rare, is among the most common postoperative complications after sleeve gastrectomy (SG) and usually occurs in the gastroesophageal (GE) junction. Increased intragastric pressure, regional ischemia, and technical failure of stapling devices have been reported as the main risk factors of postoperative leak. The aim of this study was to evaluate the impact of ischemia and intraluminal pressure in leak appearance. Methods: Landrace swine (n = 12) were subjected to SG and total gastrectomy subsequently. Lactic acid, glycerol, and pyruvate were measured by microdialysis in GE junction and pylorus before and nine times after operation, and lactate/pyruvate (L/P) ratio was calculated as well. Moreover, ex vivo air was insufflated inside the tubularized stomach till a rupture of the staple line occurs. Maximum air pressure reached and location of rupture were recorded. Results: Increase of lactic acid and L/P ratio were demonstrated in GE junction measurements; however, when the measurements between GE junction and pylorus were compared, no statistically significant differences were found, with the exception of a slightly increased lactate concentration in pylorus in the midst of measurements. The maximum air pressure recorded varied from 3 to 75 mmHg (mean 24.5 mmHg) and the majority of ruptures (n = 8) occurred in GE junction. In one of them, clip displacement was noticed. Conclusions: No evidence of increased ischemia in GE junction compared to pylorus was recorded. Increased intraluminal pressure and stapling malfunction may play the most important role in leak appearance. © 2014 Springer Science+Business Media New York.

Kaptchuk T.J.,Harvard University | Chen K.-J.,Chinese Academy of Sciences | Song J.,Experimental Research Center | Song J.,Chinese Academy of Sciences
Chinese Journal of Integrative Medicine | Year: 2010

In the West, hundreds of randomized controlled trials (RCTs) have been performed testing acupuncture. They include two types: those that compare acupuncture to other therapies, usual care or no treatment (pragmatic trials), and those that have placebo controls (efficacy trials). Acupuncture has generally performed well against other therapies or no treatment, but until recently, the evidence from placebo controlled trials has been considered equivocal or contradictory. A recent series of large RCTs, mostly performed in Germany and also in the US have included both pragmatic and placebo comparisons. The evidence poises a conundrum for the profession of acupuncture. This essay first describes the two types of RCTs used to examine acupuncture and examine the results of two recent large RCTs for chronic low back pain as representative examples of recent large studies. The essay then presents the most common Euro-American acupuncture professions' interpretation of these results. Western responses have included: (1) methodological weaknesses; (2) inappropriateness of placebo controls; (3) questions as to whether acupuncture placebo controls are "inert"; (4) rejection of evidence-based medicine epistemology; (5) discrepancy between acupuncture performed in RCTs with real world acupuncture; (6) enhanced placebo effects of acupuncture; and (7) needs to re-evaluate acupuncture theory. The authors do not necessarily agree with all of these responses; they are presented in an attempt to foster critical discussion. The paper also looks at recent neuroimaging experiments on acupuncture that may point to some worthwhile new avenues of investigation. Finally, the Euro-American health care policy consequences of these recent RCTs are discussed. © The Chinese Journal of Integrated Traditional and Western Medicine Press and Springer-Verlag Berlin Heidelberg 2010.

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