Altered accumulation of hepatic mitochondrial antioxidant proteins with age and environmental heat stress.

Aging impairs overall physiological function, particularly the response to environmental stressors. Repeated heat stress elevates reactive oxygen species and macromolecular damage in the livers of aged animals, likely due to mitochondrial dysfunction. The goal of this investigation was to determine potential mechanisms for mitochondrial dysfunction after heat stress by evaluating key redox-sensitive and antioxidant proteins (Sirt-3, MnSOD, Trx-2, and Ref-1).

Hormonal contraceptive use and women's well-being: links with body image, eating behavior, and sleep.

The goal of the current study was to examine associations between hormonal contraceptive use and indicators of well-being including body image, eating behavior, sleep and energy level. Drawing on a health protection framework, we expected that individuals who use hormonal contraceptives would be more attuned to health and report more positive health attitudes and behaviors on these dimensions. Undergraduate college women ( = 270;  = 19.

The effects of sleep on body image: examining the roles of depression, perceived stress, and anxiety.

Although health and wellness behaviors are associated with positive body image, research is limited regarding the relationship between sleep and positive body image. We propose that negative affective states may link sleep and body image. Specifically, we examined whether better sleep may relate to positive body image through reductions in negative affective experiences.

Hepatic Macrophage Abundance and Phenotype in Aging and Liver Iron Accumulation.

Liver macrophages serve important roles in iron homeostasis through phagocytosis of effete erythrocytes and the export of iron into the circulation. Conversely, intracellular iron can alter macrophage phenotype. Aging increases hepatic macrophage number and nonparenchymal iron, yet it is unknown whether age-related iron accumulation alters macrophage number or phenotype.

Hepcidin and Iron Metabolism in Experimental Liver Injury.

The liver plays a pivotal role in the regulation of iron metabolism through its ability to sense and respond to iron stores by release of the hormone hepcidin. Under physiologic conditions, regulation of hepcidin expression in response to iron status maintains iron homeostasis. In response to tissue injury, hepcidin expression can be modulated by other factors, such as inflammation and oxidative stress.

Hepatic macrophage accumulation with aging: cause for concern?

Aging is associated with chronic, low-grade inflammation that adversely affects physiological function. The liver regulates systemic inflammation; it is a source of cytokine production and also scavenges bacteria from the portal circulation to prevent infection of other organs. The cells with primary roles in these functions, hepatic macrophages, become more numerous in the liver with "normal" aging (i.

Effects of long-term ethanol ingestion on hepatic iron metabolism in two mouse strains.

The mechanisms responsible for dysregulation of iron metabolism in response to ethanol ingestion are poorly understood. Relatively brief ethanol exposures in rodents are associated with reduced hepatic hepcidin expression without increases in hepatic iron content. This study evaluated the effects of long-term ethanol treatment on hepatic iron metabolism in two mouse strains.

Aging results in accumulation of M1 and M2 hepatic macrophages and a differential response to gadolinium chloride.

Macrophages have vital roles in innate immunity by modulating the inflammatory response via their ability to alter their phenotype from pro-inflammatory (M1) to anti-inflammatory (M2). Aging increases activation of the innate immune system, and macrophage numbers increase in the aged liver. Since macrophages also produce free radical molecules, they are a potential source of age-related oxidative injury in the liver.

Iron-Induced Liver Injury: A Critical Reappraisal.

Iron is implicated in the pathogenesis of a number of human liver diseases. Hereditary hemochromatosis is the classical example of a liver disease caused by iron, but iron is commonly believed to contribute to the progression of other forms of chronic liver disease such as hepatitis C infection and nonalcoholic fatty liver disease. In this review, we present data from cell culture experiments, animal models, and clinical studies that address the hepatotoxicity of iron.

Renal Iron Accumulation and Oxidative Injury With Aging: Effects of Treatment With an Iron Chelator.

Dysregulation of iron metabolism in the kidney may contribute to age-related increases in renal oxidative stress and dysfunction. This study assessed the effects of short-term iron chelation on markers of iron status, oxidative stress, inflammation, and autophagy in the kidneys of old rats. Old Fischer 344 rats (24 months) were treated with deferoxamine (DFO; 200 mg/kg, twice daily for 4.

Sexual dimorphism in the hepatic protein response to a moderate trans fat diet in senescence-accelerated mice.

Background: Aging is characterized by increases in inflammation and oxidative stress, conditions that are exacerbated by environmental factors such as diet. In this study, we investigated the effects of a trans-fatty acid (TFA) diet on the liver in adult (25 wk) and old (60 wk) senescence-accelerated mice (SAMP8 strain) of both sexes. Our goal was to assess the effects of the diet on protein markers of inflammation and oxidative stress in the liver.

Expertise and infrastructure capacity impacts acute coronary syndrome outcomes.

Objective Effective translation of evidence to practice may depend on systems of care characteristics within the health service. The present study evaluated associations between hospital expertise and infrastructure capacity and acute coronary syndrome (ACS) care as part of the SNAPSHOT ACS registry. Methods A survey collected hospital systems and process data and our analysis developed a score to assess hospital infrastructure and expertise capacity.

Strain- and time-dependent alterations in hepatic iron metabolism in a murine model of nonalcoholic steatohepatitis.

Unlabelled: Nonalcoholic steatohepatitis is a common liver disease that is often accompanied by dysregulated iron metabolism. The aim of the study was to test the hypothesis that aberrant iron metabolism in nonalcoholic steatohepatitis is modulated by genetic susceptibility to inflammation and oxidative stress. Hepatic histology and iron content were assessed in 3 inbred strains of mice (C57BL/6, BALB/c, and C3H/HeJ) fed an atherogenic diet (AD).

Strategies for engaging with future radiation protection professionals: a public outreach case study.

It is evident that there is a nuclear skills shortage within the UK, and logically it can be assumed that the shortfall extends to the radiation protection arena. Plans for nuclear new-build and the decommissioning of existing nuclear sites will require many more people with radiological knowledge and practical competencies. This converts to a nuclear industry requirement in the order of 1000 new recruits per year over at least the next ten years, mainly as new apprentices and graduates.

Aging impairs induction of redox factor-1 after heat stress: a potential mechanism for heat-induced liver injury.

Aging is associated with reduced tolerance to physiological stressors such as hyperthermia. In animal models, heat stress is associated with increased oxidative damage in the livers of old rats. In this study, we evaluated the expression of redox factor-1 (Ref-1), a DNA repair enzyme, and thioredoxin-1 (Trx-1), an antioxidant protein.

Tumour promotion versus tumour suppression in chronic hepatic iron overload.

Although iron-catalysed oxidative damage is presumed to be a major mechanism of injury leading to cirrhosis and hepatocellular carcinoma in hemochromatosis, these events have been difficult to recapitulate in an animal model. In this study, we evaluated regulators of hepatocarcinogenesis in a rodent model of chronic iron overload. Sprague-Dawley rats were iron loaded with iron dextran over 6 months.

A utility of peroral endoscopic myotomy (POEM) across the spectrum of esophageal motility disorders.

Background: Peroral endoscopic myotomy (POEM) has been performed as a novel endoscopic procedure to treat achalasia with favorable outcome. The objective of this study was to assess the outcome of POEM in our initial series and to assess the safety and efficacy of POEM in a variety of esophageal motility-related clinical problems.

Methods: This is a retrospective cross-sectional study involving all patients with esophageal motility disorders defined by the Chicago classification, who had undergone consideration for POEM at our institution.

Comparison of the management and in-hospital outcomes of acute coronary syndrome patients in Australia and New Zealand: results from the binational SNAPSHOT acute coronary syndrome 2012 audit.

Background/aims: We aimed to assess differences in patient management, and outcomes, of Australian and New Zealand patients admitted with a suspected or confirmed acute coronary syndrome (ACS).

Methods: We used comprehensive data from the binational Australia and New Zealand ACS 'SNAPSHOT' audit, acquired on individual patients admitted between 00.00 h on 14 May 2012 to 24.

Heat stress stimulates hepcidin mRNA expression and C/EBPα protein expression in aged rodent liver.

Elevations in hepatic iron content occur with aging and physiological stressors, which may promote oxidative injury to the liver. Since dysregulation of the iron regulatory hormone, hepcidin, can cause iron accumulation, our goal was to characterize the regulation of hepcidin in young (6 mo) and old (24 mo) Fischer 344 rats exposed to environmental heat stress. Liver and blood samples were taken in the control condition and after heating.

Acute coronary syndrome care across Australia and New Zealand: the SNAPSHOT ACS study.

Objectives: To characterise management of suspected acute coronary syndrome (ACS) in Australia and New Zealand, and to assess the application of recommended therapies according to published guidelines.

Design, Setting And Patients: All patients hospitalised with suspected or confirmed ACS between 14 and 27 May 2012 were enrolled from participating sites in Australia and New Zealand, which were identified through public records and health networks. Descriptive and logistic regression analysis was performed.

Altered expression of iron regulatory proteins with aging is associated with transient hepatic iron accumulation after environmental heat stress.

An increasing body of evidence suggests that dysregulation of iron metabolism contributes to age-related pathologies. We have previously observed increased hepatic iron with aging, and that environmental heat stress stimulates a further increase in iron and oxidative liver injury in old rats. The purpose of this study was to determine a mechanism for the increase in hepatic iron in old rats after heat stress.

Differential regulation of hepatic heme oxygenase-1 protein with aging and heat stress.

Increased expression of heme oxygenase-1 (HO-1) in response to physiological stress is considered to be a protective response, which may be altered with aging. In this study, HO-1 expression was assessed following heat stress by immunoblotting of liver homogenates and isolated hepatocytes from young (6 months) and old (24 months) Fischer 344 rats and by immunohistochemistry. Livers of old rats showed higher baseline levels of HO-1, which was predominately localized to Kupffer cells.