Acute and chronic excessive intracellular increase of reactive oxygen species (ROS) is involved in the development and progression of cardiovascular diseases. ROS are by-products of various oxidative physiological and biochemical processes. Sources of ROS are mitochondrial respiration, NADH/NADPH oxidase, xanthine oxidoreductase or the uncoupling of nitric oxide synthase (NOS) in vascular cells. ROS mediate various signaling pathways that underlie cardiovascular pathophysiology. The delicate equilibrium between free-radical generation and antioxidant defense is altered in favor of the former, thus leading to redox imbalance, oxidative stress, and increased cellular injury. An understanding of the pathophysiological mechanisms mediated by oxidative stress is crucial to the prevention and treatment of cardiovascular diseases.

Reactive oxygen species (ROS) are subcellular messengers in gene regulatory and signal transduction pathways. In pathological situations, ROS accumulate due to excessive production or insufficient degradation, leading to oxidative stress (OS). OS causes oxidation of DNA, membranes, cellular lipids, and proteins, impairing their normal function and leading ultimately to cell death. OS in the heart is increased in response to ischemia/reperfusion, hypertrophy, and heart failure. The concentration of ROS is determined by their rates of production and clearance by antioxidants. Increases in OS in heart failure are primarily a result of the functional uncoupling of the respiratory chain due to inactivation of complex I. However, increased ROS in the failing myocardium may also be caused by impaired antioxidant capacity, such as decreased activity of Cu/Zn superoxide dismutase (SOD) and catalase (CAT) or stimulation of enzymatic sources, including, cyclooxygenase, xanthine oxidase (XO), nitric oxide synthase, and nonphagocytic NAD(P)H oxidases (Noxs). Mitochondria are the main source of ROS during heart failure and aging. Increased production of ROS in the failing heart leads to mitochondrial permeability transition, which results in matrix swelling, outer membrane rupture, a release of apoptotic signaling molecules, and irreversible injury to the mitochondria. Alterations of "redox homeostasis" leads to major cellular consequences, and cellular survival requires an optimal regulation of the redox balance.

Background/Aim: The occurrence of an incisional hernia after liver transplantation consists of a potential complication that may seriously affect the postoperative course and the quality of patient's life in general. The purpose of this study was to report the current epidemiological data, analyze the risk factors, evaluate the role of laparoscopic repair in this condition, and present the technical difficulties in the management of this special patient group. Materials and Methods: A literature search was performed through PubMed. Our criteria included all studies published from March 1982 to February 2019 in English, regarding incisional posttransplant hernias and open or laparoscopic repair. Finally, we collected 19 relevant studies. Results: Incisional hernia may occur independently of the type of abdominal incision. Risk factors are both patient-and technique-related. Conclusion: Well-organized randomized controlled studies are needed, in order to estimate the best treatment strategy for these patients. An incisional hernia may complicate any abdominal incision, regardless of the type of incision (Figure 1A and B). However, median abdominal incisions have been documented to be more prone to incisional hernia formation, compared with other abdominal incisions (1, 2). According to a systematic review, median incisions carry a significantly higher risk of herniation compared to transversal [relative risk (RR) 1.77, 95%CI=1.09-2.87], and paramedian incisions (RR=3.41, 95%CI=1.02-11.45), respectively (3). Risk factors predisposing to incisional hernia are both patient-and technique-related. Patient-related factors that increase such a risk include obesity, smoking, malnutrition, connective tissue disorders, preoperative chemo-radiation and immunosuppressive therapy (4, 5). As for techniquerelated factors, excess wound tension, suturing material failure, poor surgical technique, as well as the need for emergency surgery, are amongst the most important factors predisposing to the development of incisional hernia. The development of an incisional hernia following liver transplantation (LT) comprises a potential complication that may seriously affect the postoperative course and the quality of patient's life. The purpose of the present study was to investigate the current epidemiological data, analyse the risk 1059 This article is freely accessible online.

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Background/Aim: Adrenal glands are one of the most common sites of cancer metastasis. The treatment options include either surgery or chemotherapy and/or radiotherapy while certain diagnosis is made via percutaneous biopsy or fine needle aspiration (FNA), guided by CT scan. This review aimed to present the current practice regarding the diagnosis and treatment of adrenal cancer metastasis.

The repair of an abdominal aortic aneurysm (AAA) is a high-risk surgical procedure related to hormonal and metabolic stress-related response with an ensuing activation of the inflammatory cascade. In contrast to open repair (OR), endovascular aortic aneurysm repair (EVAR) seems to decrease the postoperative stress by offering less extensive incisions, dissection, and tissue manipulation. However, these beneficial effects may be offset by the release of cytokines and arachidonic acid metabolites during intra-luminal manipulation of the thrombus using catheters in endovascular repair, resulting in systemic inflammatory response (SIR), which is clinically called post-implantation syndrome. In this systematic review we compared OR with EVAR in terms of the post-interventional inflammatory response resulting from alterations in the circulating cytokine levels. We sought to summarize all the latest evidence regarding post-implantation syndrome after EVAR. We searched Medline (PubMed), ClinicalTrials.gov and the Cochrane library for clinical studies reporting on the release of cytokines as part of the inflammatory response after both open/conventional and endovascular repair of the AAA. We identified 17 studies examining the cytokine levels after OR versus EVAR. OR seemed to be associated with a greater SIR than EVAR, as evidenced by the increased cytokine levels, particularly IL-6 and IL-8, whereas IL-1β, IL-10 and TNF-α showed conflicting results or no difference between the two groups. Polyester endografts appear to be positively correlated with the incidence of post-implantation syndrome after EVAR. Future large prospective studies are warranted to delineate the underlying mechanisms of the cytokine interaction in the post-surgical inflammatory response setting.

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The aim of this article is to review the literature regarding the relationship between vitamin D deficiency and cardiovascular disease (CVD) and its modification in the presence of obesity. Despite the strong association between vitamin D status and cardiovascular outcomes, vitamin D supplementation trials in the general population have failed to decrease the incidence of cardiovascular events and mortality. A comprehensive study of the published literature and a comparison with experimental data lead to the conclusion that obesity, due to its high prevalence and strong association with both vitamin D deficiency and CVD, may act as a critical confounder, which is responsible for the different results on this association. Adoption of a vitamin D preventive supplementation strategy for CVD is unlikely to yield any benefit to the general population. However, it might be particularly useful in obese adults with increased risk for CVD.