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Hammer K.,University of the Faroe Islands | Hall E.O.C.,University of Aarhus | Mogensen O.,Institute of Clinical Research
Cancer Nursing | Year: 2013

BACKGROUND:: In mysterious ways, hope makes life meaningful even in chaotic and uncontrolled situations. When a woman is newly diagnosed with gynecologic cancer, hope is ineffable and needs exploring. Drawings help express ineffable phenomena. OBJECTIVE:: The aim of the study was to explore how women newly diagnosed with gynecologic cancer express the meaning of hope in drawings. METHOD:: Participants were 15 women who on the same day had received the diagnosis of gynecologic cancer. They were between 24 and 87 years (median, 52 years) with a variety of gynecologic cancer diagnoses. Data from 15 drawings and postdrawing interviews with the women were analyzed using visual and hermeneutic phenomenology. RESULTS:: Three themes emerged: hope as a spirit to move on, hope as energy through nature, and hope as a communion with families. CONCLUSION:: Hope as pictured in drawings often appears through metaphors and incorporates internal, external, and relational aspects. With other words, inner willpower, experiences in open nature, and closeness to loved ones contribute to hope when newly diagnosed with gynecologic cancer. IMPLICATION FOR PRACTICE:: The use of drawings in clinical situations might give cancer nurses new perceptions of hope and other phenomena. Patients might feel threat and despair when diagnosed with cancer; they need gentle truth about reality, and they long for being together with loved ones. Nurses are in a unique position to enable hope in this situation through listening and active engagement. Drawing might be a tool in understanding the hope. Drawings picture where words come short. Copyright © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins. Source


Matsuda M.,Institute of Clinical Research | Shimomura I.,Osaka University
Obesity Research and Clinical Practice | Year: 2013

Obesity, especially of the abdominal type, is a health problem that constitutes metabolic syndrome and increases the incidence of various diseases, including diabetes, hypertension, dyslipidemia, atherosclerosis, and cancer. Various mechanisms linking obesity to these associated diseases have been postulated. One candidate is oxidative stress, which has been implicated in vascular complications of diabetes and in pancreatic β-cell failure in diabetes. Notably, obese people without diabetes also display elevated levels of systemic oxidative stress. In addition, levels of oxidative stress are increased in the adipose tissue in obese mice. Treating obese mice with antioxidant agents attenuates the development of diabetes. In 3T3-L1 adipocytes, increases in reactive oxygen species (ROS) occur with lipid accumulation; the addition of free fatty acids elevates ROS generation further. Thus, adipose tissue represents an important source of ROS; ROS may contribute to the development of obesity-associated insulin resistance and type 2 diabetes. Moreover, the levels of oxidative stress present in several other types of cells or tissues, including those in the brain, arterial walls, and tumors, have been implicated in the pathogenesis associated with hypertension, atherosclerosis, and cancer. The increased levels of systemic oxidative stress that occur in obesity may contribute to the obesity-associated development of these diseases. © 2013 Asian Oceanian Association for the Study of Obesity. Source


Matsuda M.,Institute of Clinical Research | Shimomura I.,Osaka University
Reviews in Endocrine and Metabolic Disorders | Year: 2014

The recent increase in populations with obesity is a worldwide social problem, and the enhanced susceptibility of obese people to metabolic and cardiovascular diseases has become a growing health threat. An understanding of the molecular basis for obesity-associated disease development is required to prevent these diseases. Many studies have revealed that the mechanism involves various bioactive molecules that are released from adipose tissues and designated as adipocytokines/adipokines. Adiponectin is an adipocytokine that exerts insulin-sensitizing effects in the liver and skeletal muscle via adenosine monophosphate-activated protein kinase and proliferator-activated receptor α activation. Additionally, adiponectin can suppress atherosclerosis development in vascular walls via various anti-inflammatory effects. In contrast, oxidative stress is a harmful factor that systemically increases during obesity and promotes the development of diabetes, atherosclerosis, and various other diseases. In obese mice, oxidative stress is enhanced in adipose tissue before diabetes development, but not in the liver, skeletal muscle, and aorta, suggesting that in obesity, adipose tissue may be a major source of reactive oxygen species (ROS). ROS suppress adiponectin production in adipocytes. Treatment of obese mice with anti-oxidative agents improves insulin resistance and restores adiponectin production. Recent studies have demonstrated that adiponectin protects against oxidative stress-induced damage in the vascular endothelium and myocardium. Thus, decreased circulating adiponectin levels and increased oxidative stress, which are closely linked to each other, should be deeply involved in obesity-associated metabolic and cardiovascular disease pathogenesis. © 2013 Springer Science+Business Media. Source


Shetty K.,Johns Hopkins University | Chen J.,University of Houston | Shin J.-H.,University of Houston | Jogunoori W.,Institute of Clinical Research | Mishra L.,University of Houston
Current Hepatitis Reports | Year: 2015

Non-alcoholic fatty liver disease (NAFLD) is being recognized as an increasingly important contributor to the burden of hepatocellular carcinoma (HCC) worldwide. It is  often accompanied by obesity and diabetes mellitus and isbelieved to be the hepatic representation of the metabolic syndrome. HCC development in NAFLD is multifactorial and complex. It is dependent on not only the well-describedmechanisms noted in chronic liver injury but also on the molecular derangements associated with obesity and dysmetabolism. These include adipocyte remodeling, adipokine secretion, lipotoxicity, and insulin resistance. Recent advances focus on the importance of the gut-liver axis in accelerating the process of oncogenesis in NAFLD. The Farnesoid X receptor (FXR) has been demonstrated to have important metabolic effects, and its pharmacological activation by obeticholic acid has been recently reported to produce histological improvement in non-alcoholic steatohepatitis (NASH). It is hoped that delineating the mechanisms o f hepatic fibrosis and oncogenesis in NASH will lead to enhanced strategies for cancer prevention, surveillance, and therapy in this population. © Springer Science+Business Media New York 2015. Source


Okuno Y.,Osaka University | Matsuda M.,Osaka University | Matsuda M.,Institute of Clinical Research | Miyata Y.,Osaka University | And 4 more authors.
Endocrine Journal | Year: 2010

Oxidative stress has been implicated as a causal role in atherosclerosis, microvascular complications of diabetes as well as in beta cell failure in type 2 diabetes. PPARγ agonists not only improve insulin sensitivity but also eliminate oxidative stress. In mouse, catalase, a major antioxidant enzyme, is directly regulated by PPARγ through two PPARγ binding elements in its promoter. This study examined the regulatory mechanisms of catalase expression in human. Expression of catalase was significantly upregulated in human primary adipocytes upon treatment with a PPARγ agonist. However, the mouse PPARγ response elements are not functionally conserved in human catalase promoter. In luciferase reporter assay containing human catalase promoter, PPARγ/RXRα, in combination of a PPARγ agonist significantly transactivated 19 kb of promoter and this was mediated via a novel PPARγ response element (PPRE) at -12 kb from transcription initiation site of human catalase gene. Electrophoretic mobility shift assay showed direct binding of PPARγ to this PPRE. Together, our results indicate that PPARγ regulates the expression of catalase gene in human through a PPRE distinct from that of mouse, and could explain, at least in part, the observed inhibitory effects of PPARγ on oxidative stress in human. Source

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