There is, I think, something ethereal about i —the square root of minus one. I remember first hearing about it at school. It seemed an odd beast at that time—an intruder hovering on the edge of reality.

Usually familiarity dulls this sense of the bizarre, but in the case of i it was the reverse: over the years the sense of its surreal nature intensified. It seemed that it was impossible to write mathematics that described the real world in …

I and i

Retrospective study: The diagnostic accuracy of conventional forceps biopsy of gastric epithelial compared to endoscopic submucosal dissection (STROBE compliant).

Mini Mental State

Obesity and its associated comorbidities are among the most prevalent and challenging conditions confronting the medical profession in the 21st century. A major metabolic consequence of obesity is insulin resistance, which is strongly associated with the deposition of triglycerides in the liver. Hepatic steatosis can either be a benign, noninflammatory condition that appears to have no adverse sequelae or can be associated with steatohepatitis: a condition that can result in end-stage liver disease, accounting for up to 14% of liver transplants in the US. Here we highlight recent advances in our understanding of the molecular events contributing to hepatic steatosis and nonalcoholic steatohepatitis.

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Molecular mediators of hepatic steatosis and liver injury

Electrical stimulation of excitable tissue: design of efficacious and safe protocols.

The diatomic molecule of oxygen contains two uncoupled electrons and can therefore undergo reduction, yielding several different oxygen metabolites, which are collectively called Reactive Oxygen Species or ROS. They are invariably produced in aerobic environments through a variety of mechanisms, which include electron “leakage” during biologic oxidations, action of flavin dehydrogenases and specific membrane associated secretion, as well as by physical activation of oxygen by irradiation, e.g. UV sun-light. Organisms have developed efficient protective mechanisms against excessive accumulation of ROS, which include superoxide anion, hydrogen peroxide and hydroxyl radical, since all these metabolites are highly reactive and affect almost every kind of organism, either directly or through conversion into other derivatives, notably NO-derived radicals or RNS. Depending on their tissue concentration they can either exert beneficial physiologic effects (control of gene expression and mitogenesis) or damage cell structures, including lipids and membranes, proteins and nucleic acids, leading to cell death. In this brief overview we summarize the present state-of-theart, restricting the discussion to the role of ROS in physiology and pathology, not taking into account RNS. Discussion will focus on basic chemical and biochemical features of ROS, underlining how ROS can promote severe diseases, including neoplastic, cardiovascular and neurodegenerative diseases. This brief discussion should clarify the present huge interest in ROS, in the perspective to develop new and specific therapeutic approaches.

Oxygen, Reactive Oxygen Species and Tissue Damage

Living organisms are continuously exposed to environmental pollutants Because of its critical location, the skin is a major interface between the body and the environment and provides a biological barrier against an array of chemical and physical environmental pollutants The skin can be defined as our first defense against the environment because of its constant exposure to oxidants, including ultraviolet (UV) radiation and other environmental pollutants such as diesel fuel exhaust, cigarette smoke (CS), halogenated hydrocarbons, heavy metals, and ozone (O3) The exposure to environmental pro-oxidant agents leads to the formation of reactive oxygen species (ROS) and the generation of bioactive molecules that can damage skin cells This short review provides an overview of the effects and mechanisms of action of CS, O3, and UV on cutanous tissues

Cutaneous responses to environmental stressors.

Inflammation is a complex systemic response evolved to cope with cellular injury, either due to infectious agents or, in general, with sporadic events challenging tissue integrity and function. Researchers involved in different fields have the tendency to look at the inflammatory response with different angles, according to their specific interest. Established its complexity, one of the most evident features of the inflammatory response is the generation of a pro-oxidative environment due to the production of high fluxes of pro-oxidant species. This production starts locally, at the site of injury or infection, but eventually becomes a chronic challenge for the organism, if the inflammatory response is not properly controlled. In this review, we focus on this specific aspect of chronic, low-level sub-clinical inflammatory response. We propose the term “OxInflammation” as a novel operative term describing a permanent pro-oxidative feature that interact, in a positive feed-back manner, to a not yet clinically detectable inflammatory process, leading in a long run (chronically) to a systemic/local damage, as a consequence of the cross talk between inflammatory and oxidative stress mediators. Therefore, it could be useful to analyse inflammatory markers in pathologies where there is an alteration of the redox homeostasis although an inflammatory status is not clinically evident.

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OxInflammation: from subclinical condition to pathological biomarker

The underlying mechanism in postmenopausal osteoporosis (PO) is an imbalance between bone resorption and formation. This study was conducted to investigate whether oxidative stress (OxS) might have a role in this derangement of bone homeostasis. In a sample of 167 postmenopausal women, we found that increased serum levels of a lipid peroxidation marker, hydroperoxides, were negatively and independently associated with decreased bone mineral density (BMD) in total body (, ), lumbar spine (, ), and total hip (, ), as well as with increased bone resorption rate (, ), as assessed by the serum concentration of C-terminal telopeptide of type I collagen (CTX-1). On the contrary, the OxS marker failed to be correlated with the serum levels of bone-specific alkaline phosphatase (BAP), that is, elective marker of bone formation. Importantly, multiple regression analysis revealed that hydroperoxides is a determinant factor for the statistical association between lumbar spine BMD and CTX-1 levels. Taken together, our data suggest that OxS might mediate, by enhancing bone resorption, the uncoupling of bone turnover that underlies PO development.

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Oxidative stress and bone resorption interplay as a possible trigger for postmenopausal osteoporosis.

Background: Post-menopausal osteoporosis (PO) affecting a large fraction of elderly women, is triggered by the decline in 17 β -estradiol (E2) level. Experimental studies in animal models and cell cultures have suggested that the fall in E2 might contribute to developing oxidative stress (OS) which in turn is believed to play an important role in PO pathogenesis. The scarcity of human studies focusing on this issue prompted us to investigate the effects of the reproductive and postreproductive phase of women ’ s life on OS and bone health. Methods: Serum parameters of oxidative challenge (lipid hydroperoxides and protein advanced oxidation products) and antioxidant defence (total serum antioxidants levels) along with bone mineral density (BMD) at femoral neck and lumbar spine were assessed in a sample of 191 women (98 pre- and 93 post-menopausal, of whom 30 osteoporotic). Results: Pearson ’ s correlation analysis unveiled that spinal BMD was negatively correlated with lipid hydroperoxides in overall postmenopausal subsample (r = – 0.251, p = 0.012), while no signifi cant link between these two variables was detected in women in reproductive age (r = – 0.022, p = 0.833). Noteworthy, stepwise multiple regression analysis showed that the association found in post-menopausal women retained signifi cance after adjusting for potential confounding factors (p = 0.001). Conclusions: Our data showed that markers of oxidative challenge are associated with bone loss in women in postmenopausal status. We suggest that menopause-related estrogen withdrawal might contribute to make bone more vulnerable to oxidative injury thereby increasing the risk of PO development.

Carlo Cervellati

Papers

Oxygen, Reactive Oxygen Species and Tissue Damage

Cutaneous responses to environmental stressors.

OxInflammation: from subclinical condition to pathological biomarker

Oxidative stress and bone resorption interplay as a possible trigger for postmenopausal osteoporosis.

Bone mass density selectively correlates with serum markers of oxidative damage in post-menopausal women