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Conventional synthetic sorbents for oil spill removal are the most widely applied materials, although they are not the optimal choices from an economic and environmental point of view. The use of inexpensive, abundant, non-toxic, biodegradable, and reusable lignocellulosic materials might be an alternative to conventional sorbents, with obvious positive impact on sustainability and circular economy. The objective of this paper was to review reports on the use of natural-based adsorbing materials for the restoration of water bodies threatened by oil spills. The use of raw and modified natural sorbents as a restoration tool, their sorption capacity, along with the individual results in conditions that have been implemented, were examined in detail. Modification methods for improving the hydrophobicity of natural sorbents were also extensively highlighted. Furthermore, an attempt was made to assess the advantages and limitations of each natural sorbent since one material is unlikely to encompass all potential oil spill scenarios. Finally, an evaluation was conducted in order to outline an integrated approach based on the terms of material-environment-economy.

Helicobacter pylori infection (Hp-I) has been associated with a wide spectrum of gastrointestinal and extra-digestive manifestations, including neurodegenerative diseases. Contradictory data have been published on Hp-I and multiple sclerosis (MS) association, with studies mainly using serology for Hp-I detection that cannot distinguish between active and past infections. We herein hypothesize that humoral and cellular immune responses induced by active Hp-I, beyond damaging locally the gastric mucosa, they may shape the character of systemic autoimmune responses, contributing to MS pathogenesis. To investigate our hypothesis, active Hp-I has been diagnosed in two small MS Greek cohorts by using primarily gastric mucosa histology. A higher prevalence of active Hp-I was documented in MS patients vs. controls (86.4 vs. 50%, P = 0.002)accompanied by exclusive existence of duodenal ulcer and autoimmune diseases with endoscopic and histological findings of chronic active gastritis for the MS group. Our preliminary data suggested that active Hp-Iunlike other studies, may not protect, but contribute to MS and we proposed possibleHp-relating mechanisms involved in MS pathophysiology, that merit further evaluation., Competing Interests: Declaration of Competing Interest Dr. Doulberis has received a travel grant by Gilead Sciences Switzerland Sàrl. Rest of the authors declare that they have no competing interest., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Gastroesophageal reflux disease (GERD) and the increasing rate of its associated complications, including esophageal adenocarcinoma (EAC), has stimulated a plethora of studies attempting to evaluate provocative and protective factors. Helicobacter pylori (Hp) infection (Hp-I) was initially considered as a beneficial condition in GERD management based on rather limited data. Large-scale regional studies revealed an alternative approach, by suggesting a positive relationship between Hp-I and EAC development. Regarding pathophysiology, Hp-I induces gastric microbiota disturbances through hypochlorhydria and chronic inflammation, with a subsequent possible effect on the GERD-Barrett's esophagus (BE)-EAC cascade. Additionally, both direct effects on esophageal mucosa and indirect effects on known mechanisms of GERD, such as acid pocket and transient lower esophageal sphincter relaxation, remain to be elucidated. Hp contribution to carcinogenesis is related to oncogenic gastrin, cyclooxygenase-2, and prostaglandins; Ki-67 is also expressed and represents an index of BE-related malignancy. Moreover, Hp-I is vigorously suggested as a risk factor for metabolic syndrome, which may be the link between Hp-I and EAC. Although further studies are necessary to establish a pathophysiologic risk between Hp-I and the GERD-BE-EAC sequence, the theory of Hp protection against GERD seems outdated., (© 2019 New York Academy of Sciences.)

Acute liver failure is a rare hepatic emergent situation that affects primarily young people and has often a catastrophic or even fatal outcome. Definition of acute liver failure has not reached a universal consensus and the interval between the appearance of jaundice and hepatic encephalopathy for the establishment of the acute failure is a matter of debate. Among the wide variety of causes, acetaminophen intoxication in western societies and viral hepatitis in the developing countries rank at the top of the etiology list. Identification of the clinical appearance and initial management for the stabilization of the patient are of vital significance. Further advanced therapies, that require intensive care unit, should be offered. The hallmark of treatment for selected patients can be orthotopic liver transplantation. Apart from well-established treatments, novel therapies like hepatocyte or stem cell transplantation, additional new therapeutic strategies targeting acetaminophen intoxication and/or hepatic encephalopathy are mainly experimental, and some of them do not belong, yet, to clinical practice. For clinicians, it is substantial to have the alertness to timely identify the patient and transfer them to a specialized center, where more treatment opportunities are available.

Both Helicobacter pylori infection and metabolic syndrome present significant global public health burdens. Metabolic syndrome is closely related to insulin resistance, the major underlying mechanism responsible for metabolic abnormalities, and Helicobacter pylori infection has been proposed to be a contributing factor. There is growing evidence for a potential association between Helicobacter pylori infection and insulin resistance, metabolic syndrome and related morbidity, including abdominal obesity, type 2 diabetes mellitus, dyslipidemia, hypertension, all of which increase mortality related to cardio-cerebrovascular disease, neurodegenerative disorders, nonalcoholic fatty liver disease and malignancies. More specifically, insulin resistance, metabolic syndrome and hyperinsulinemia have been associated with upper and lower gastrointestinal tract oncogenesis. Apart from cardio-cerebrovascular, degenerative diseases and nonalcoholic fatty liver disease, a number of studies claim that Helicobacter pylori infection is implicated in metabolic syndrome-related Barrett's esophagus and esophageal adenocarcinoma development, gastric and duodenal ulcers and gastric oncogenesis as well as lower gastrointestinal tract oncogenesis. This review summarizes evidence on the potential impact of Helicobacter pylori-related metabolic syndrome on gastroesophageal reflux disease-Barrett's esophagus-esophageal adenocarcinoma, gastric atrophy-intestinal metaplasia-dysplasia-gastric cancer and colorectal adenoma-dysplasia-colorectal cancer sequences. Helicobacter pylori eradication might inhibit these oncogenic processes, and thus further studies are warranted., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Neurodegeneration represents a component of the central nervous system (CNS) diseases pathogenesis, either as a disability primary source in the frame of prototype neurodegenerative disorders, or as a secondary effect, following inflammation, hypoxia or neurotoxicity. Galectins are members of the lectin superfamily, a group of endogenous glycan-binding proteins, able to interact with glycosylated receptors expressed by several immune cell types. Glycan-lectin interactions play critical roles in the living systems by involving and mediating a variety of biologically important normal and pathological processes, including cell-cell signaling shaping cell communication, proliferation and migration, immune responses and fertilization, host-pathogen interactions and diseases such as neurodegenerative disorders and tumors. This review focuses in the role of Galectin-3 in shaping responses of the immune system against microbial agents, and concretely, Helicobacter pylori (Hp), thereby potentiating effect of the microbe in areas distant from the ordinary site of colonization, like the CNS. We hereby postulate that gastrointestinal Hp alterations in terms of immune cell functional phenotype, cytokine and chemokine secretion, may trigger systemic responses, thereby conferring implications for remote processes susceptible in immunity disequilibrium, namely, the CNS inflammation and/or neurodegeneration., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Background: With advancing age there is progressive pancreatic atrophy and fibrosis, leading to tissue destruction and chronic pancreatitis that has been found to be protective against post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP). However, there are no reports regarding the potential effect of the aging pancreatic changes on the incidence and severity of PEP. Therefore, the aim of the present study was to investigate the impact of senile changes in the pancreas on the incidence and severity of PEP., Methods: A total of 2688 patients who underwent the first therapeutic ERCP at a single center were included in the final analysis of the study. Patients were classified into two groups: 1644 patients aged ≤75 years (mean age 61.56+1.26 years), group A; and 1044 patients aged >75 years (mean age 81.97+4.29 years), group B. Patients' files were identified using a retrospective database linked to the endoscopy reporting system. Patients' characteristic, endoscopic findings, details of intervention and rate and severity of PEP were evaluated., Results: No significant differences between the two groups were observed with regard to ERCP indication, patient- and technique-related risk factors for PEP, presence of periampullary diverticulum, and type of therapeutic intervention. The incidence of PEP was 5.2% in group A and 4% in group B (P=NS) with comparable grades of severity. All episodes of pancreatitis had full recovery with conventional treatment. One death occurred from respiratory arrest in each group of patients., Conclusion: This study shows that the pancreatic changes associated with aging do not influence the incidence and severity of PEP., Competing Interests: Conflict of Interest: None

Helicobacter pylori (H. pylori) induces reactive oxygen species (ROS) production that contribute to pathogenesis of a variety of H. pylori-related gastric diseases, as shown in animal and human studies. Helicobacter pylori infection is also associated with variety of systemic extragastric diseases in which H. pylori-related ROS production might also be involved in the pathogenesis of these systemic conditions. We proposed that Hp-related ROS may play a crucial role in the pathophysiology of Hp-related systemic diseases including Alzheimer's disease, multiple sclerosis, glaucoma and other relative neurodegenerative diseases, thereby suggesting introduction of relative ROS scavengers as therapeutic strategies against these diseases which are among the leading causes of disability and are associated with a large public health global burden. Moreover, we postulated that H. pylori-related ROS might also be involved in the pathogenesis of extragastric common malignancies, thereby suggesting that H. pylori eradication might inhibit the development or delay the progression of aforementioned diseases. However, large-scale future studies are warranted to elucidate the proposed pathophysiological mechanisms, including H. pylori-related ROS, involved in H. pylori-associated systemic and malignant conditions.

Objective. To evaluate the prognostic significance of microscopically assessed DNA ploidy and other clinical and laboratory parameters in stage IV colorectal cancer (CRC). Methods. 541 patients with histologically proven stage IV CRC treated with palliative chemotherapy at our institution were included in this retrospective analysis, and 9 variables (gender, age, performance status, carcinoembryonic antigen, cancer antigen 19-9, C-Reactive Protein (CRP), anaemia, hypoalbuminaemia, and ploidy (DNA Index)) were assessed for their potential relationship to survival. Results. Mean survival time was 12.8 months (95% confidence interval (CI) 12.0-13.5). Multivariate analysis revealed that DNA indexes of 2.2-3.6 and >3.6 were associated with 2.94 and 4.98 times higher probability of death, respectively, compared to DNA index <2.2. CRP levels of >15 mg/dL and 5-15 mg/dL were associated with 2.52 and 1.72 times higher risk of death, respectively. Hazard ratios ranged from 1.29 in patients mild anaemia (Hb 12-13.5 g/dL) to 1.88 in patients with severe anaemia (Hb < 8.5 g/dL). Similarly, the presence of hypoalbuminaemia (albumin < 5 g/dL) was found to confer 1.41 times inferior survival capability. Conclusions. Our findings suggest that patients with stage IV CRC with low ploidy score and CRP levels, absent or mild anaemia, and normal albumin levels might derive greatest benefit from palliative chemotherapy.

Background: Recent data indicate that gastroenteropancreatic neuroendocrine tumours (GEP-NETs) have a hypomethylated long interspersed element (LINE1) promoter. To answer the question, of whether LINE1 may be of value in assessing the malignant potential of GEP-NETs, we analysed LINE1 methylation in different organs., Materials and Methods: A total of 58 GEP-NETs of gastric (n=14), pancreatic (n=15), small intestine (n=17), appendix (n=8), colorectal (n=4) and non-neoplastic tissues were analysed using DNA isolation, bisulphite-treatment and pyrosequencing., Results: LINE1 hypomethylation was detected in 50% of gastric, 100% pancreatic, 82% small intestine, 87.5% appendix and 100% colorectal NETs. G1 (p<0.001) and G2 (p<0.05) colorectal, and G1 (p<0.001) and G2 (p<0.001) pancreatic NETs exhibited significant LINE1 hypomethylation compared with non-neoplastic tissues. Higher rates of LINE1 hypomethylation in G2 pancreatic NETs than in G1 NETs (p<0.05) were observed. NETs exhibited a significantly lower frequency of hypomethylation in cases with lymph node metastases (p<0.05)., Conclusion: LINE1 hypomethylation may serve as a marker of tumour grade and lymph node metastasis.

Objectives: Many studies have linked irritable bowel syndrome (IBS) with small intestinal bacterial overgrowth (SIBO), although they have done so on a qualitative basis using breath tests even though quantitative cultures are the hallmark of diagnosis. The purpose of this study was to underscore the frequency of SIBO in a large number of Greeks necessitating upper gastrointestinal (GI) tract endoscopy by using quantitative microbiological assessment of the duodenal aspirate., Methods: Consecutive subjects presenting for upper GI endoscopy were eligible to participate. Quantitative culture of aspirates sampled from the third part of the duodenum during upper GI tract endoscopy was conducted under aerobic conditions. IBS was defined by Rome II criteria., Results: Among 320 subjects enrolled, SIBO was diagnosed in 62 (19.4%); 42 of 62 had IBS (67.7%). SIBO was found in 37.5% of IBS sufferers. SIBO was found in 60% of IBS patients with predominant diarrhea compared with 27.3% without diarrhea (P = 0.004). Escherichia coli, Enterococcus spp and Klebsiella pneumoniae were the most common isolates within patients with SIBO. A step-wise logistic regression analysis revealed that IBS, history of type 2 diabetes mellitus and intake of proton pump inhibitors were independently and positively linked with SIBO; gastritis was protective against SIBO., Conclusions: Using culture of the small bowel, SIBO by aerobe bacteria is independently linked with IBS. These results reinforce results of clinical trials evidencing a therapeutic role of non-absorbable antibiotics for the management of IBS symptoms.

Background: Members of the immunoglobulin superfamily of endothelial adhesion molecules, vascular cell adhesion molecule (VCAM-1) and intercellular cell adhesion molecule (ICAM-1), participate in leukocyte adhesion to the endothelium and play an important role in all stages of atherosclerosis. The aim of the study was to examine the expression of VCAM-1 and ICAM-1 in the aorta of rats at the early stages of atherosclerosis and the correlation with their plasma concentrations., Materials and Methods: Male rats (n=44), 10 weeks of age, were divided in 4 groups. Groups A and C (n=12) were fed with rich cholesterol diet for 12 and 16 weeks, respectively. Group B (regression group, n=12) was fed for the first 12 weeks with rich cholesterol diet and for another 4 weeks with normal diet. Group D (control group, n=8) was fed with normal diet for 12 weeks. We measured the serum lipid profile, the concentration of soluble ICAM-1 and the immunohistochemical expression of ICAM-1 and VCAM-1 in the endothelium, media and vasa vasorum of the aorta., Results: There were significant differences (p<0.05) in the expression of ICAM-1 between group C (maximum time of rich cholesterol diet) and all other groups in the 3 groups of the aorta studied. There was regression of the expression of ICAM-1 in group B and significant differences (p<0.05) between group B and all the other groups, except group D in the expression of ICAM-1. There were no significant differences in the expression of VCAM-1 between any groups. The serum concentration of soluble ICAM-1 positively correlated with the expression of the molecule in the vasa vasorum (r=0.35, p<0.05) and fibroblasts/smooth muscular cells (r=0.34, p<0.05) of the aorta., Conclusion: A cholesterol diet plays a role in the expression of ICAM-1 but not in that of VCAM-1 in the rat aorta. The expression of ICAM-1 in the aorta regresses after the withdrawal of a cholesterol-rich diet. Soluble ICAM-1 is a reliable measure of ICAM-1 expression in the aorta, vasa vasorum and fibroblasts/smooth muscle cells.

Background and Aim: The treatment-of-choice for the optimal management of the dyslipidemia of the metabolic syndrome (MetS) is not clearly defined. We compared the efficacy of 4 drug regimes for the management of this dyslipidemia in a mouse model., Materials and Methods: A total of 60 C57Bl6 mice comprised the study group. The first 10 received standard mouse food for the whole experiment (control group). The remaining 50 mice received atherogenic diet for 14 weeks until the development of the MetS. The mice were then divided into 5 groups: the 1st group continued receiving atherogenic diet, while the other 4 groups received atherogenic diet plus ezetimibe (10 mg/kg per day), fenofibrate (100 mg/kg per day), low-dose atorvastatin (10 mg/kg per day), or high-dose (40 mg/kg per day) atorvastatin, respectively, for another 8 weeks., Results: High-dose atorvastatin treatment achieved the best lipid profile compared with low-dose atorvastatin, ezetimibe, and fibrate therapy. The lipid profile of mice receiving atherogenic diet plus high-dose atorvastatin treatment was similar with mice on regular chow., Conclusions: High-dose atorvastatin treatment resulted in optimization of the lipid profile in the presence of a high-fat atherogenic diet in a mouse model. Our results suggest that high-dose atorvastatin treatment may be the optimal treatment option for the dyslipidemia associated with MetS. Nevertheless, verification of these results in humans is required before any definite conclusions can be drawn.

Background: Acute pancreatitis is a form of inflammation with clinical features ranging from pancreatic inflammation to fatal systemic manifestations. The aim of this study was to clarify changes in lymphocyte subsets and alterations in the functioning of natural killer (NK) cells., Patients and Methods: Forty-five patients were enrolled into the study; 35 with acute pancreatitis and systemic inflammatory response syndrome (SIRS) and 10 healthy subjects. Blood was sampled early from all patients. Blood immune cells were studied on days 1 and 4 by flow cytometry. Tumor necrosis factor-α (TNFα) and interleukin (IL)-6 were estimated from supernatants of NK cells before/after stimulation with lipopolysaccharide (LPS)., Results: Apoptosis in patients was significantly different on days 1 and 4 compared with controls. Apoptosis of CD4(+) lymphocytes was significantly correlated with the days to resolution of SIRS (r = +0.586, p = 0.022). Significant differences were observed in TNFα and IL-6 on day 1 with/without LPS stimulation between patients and healthy individuals. Significantly increased levels of TNFα and IL-6 were found after LPS stimulation compared with unstimulated supernatants in day 1., Conclusion: NK cells altered their secretory status when stimulated with LPS. This finding could be explained by the cellular reprogramming of NK cells in the field of acute pancreatitis and SIRS., (Copyright © 2011 S. Karger AG, Basel.)

Aim: To investigate the probable role of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) in the pathogenesis of inflammatory bowel disease (IBD)., Methods: Fifty-eight patients were enrolled; nineteen healthy volunteers served as controls; 8 patients were diagnosed with Crohn's disease, and 31 with ulcerative colitis. Clinical and endoscopic activity indexes of patients with Crohn's disease and ulcerative colitis respectively were estimated. Upon admission blood was sampled; sTREM-1 and TNFalpha were measured by an immunoassay and malondialdehyde (MDA) by the thiobarbitourate assay, after passage through an HPLC system., Results: Median +/- SE of TNFalpha of controls, patients with Crohn's disease and patients with ulcerative colitis were 6.02 +/- 3.94, 7.98 +/- 5.08 (P = NS vs controls), and 8.45 +/- 4.15 ng/L (P = 0.018 vs controls) respectively. Respective values of sTREM-1 were 53.31 +/- 32.93, 735.10 +/- 197.17 (P = 0.008 vs controls) and 435.82 +/- 279.71 ng/L (P = 0.049 vs controls). sTREM-1 was positively correlated with Crohn's disease activity index and clinical and endoscopic activity indexes of ulcerative colitis (P = 0.002, 0.001 and 0.009, respectively). sTREM-1 of patients with ulcerative colitis was positively correlated with TNFalpha (P = 0.001)., Conclusion: sTREM-1 seems to behave as a novel mediator in IBD in correlation with the degree of the inflammatory reaction of the intestinal mucosa.