Lived Bodily Experience of Worsening Heart Failure from Acute Exacerbation to Recovery: A Phenomenological Study.

Patients with heart failure have difficulty recognizing and identifying changes in bodily sensations, despite the importance of symptom monitoring. The way patients with heart failure experience their bodies from exacerbation to recovery is poorly understood. We aimed to describe the lived bodily experience of heart failure from exacerbation to recovery. Participatory observations and interviews were conducted in seven patients admitted to the intensive care unit with worsening heart failure. Benner's interpretive phenomenology was used for analysis. Four major themes were identified: a non-functional body becomes the central concern and an object; being conscious of bodily changes before hospitalization when asked; the central concern shifted to daily life and the body becomes the background; and having a feeling of death in the body that no longer functions or a weakened body after recovery. This study found that patients with heart failure were conscious and concerned about their bodies changing as they underwent rapid changes during exacerbations and recovery. In addition, immediately after their bodies recovered and until they were discharged from the hospital, they looked toward their daily lives through their bodily experiences during heart failure exacerbation. The lived bodily experience of heart failure, which is less conscious in daily life, is made conscious through storytelling in the period immediately following recovery from an acute exacerbation and can be the basis for subsequent self-care exploration.

Differentiation-specific localization of catalase and hydrogen peroxide, and their alterations in rat skin exposed to ultraviolet B rays.

BACKGROUND: It is now well known that to counteract oxidative stress and maintain a redox balance within the cells, the skin is equipped with a network of antioxidant enzymes. Among these enzymes, SOD and CAT are the major antioxidant enzymes protecting the epidermis. OBJECTIVE: In the present study, we have attempted to demonstrate the distribution of endogenous H(2)O(2) and the expression of CAT in the epidermis of newborn rats, in relation to epidermal differentiation, and alterations after UVB irradiation. METHODS: We have localized the antioxidant enzyme catalase (CAT) using immunohistochemical analysis, and hydrogen peroxide (H(2)O(2)) using in situ H(2)O(2) assay. RESULTS: We demonstrated that keratinocytes in the stratum granulosum produced H(2)O(2), and CAT was mainly expressed in the cytoplasm of cells from the stratum granulosum to the lower corneum, and in the cell periphery in the stratum granulosum of newborn rat skin. The results suggested that generation of H(2)O(2) and expression of CAT were coordinated and were indicative of epidermal differentiation as well as of the role of CAT in repairing redox damage by discomposing H(2)O(2). When rat skin was exposed to 50 mJ/cm(2) of ultraviolet B (UVB) rays, the accumulation of H(2)O(2) in the upper epidermis increased twenty-four hours later, while CAT immunoreactivity decreased. CONCLUSION: The results suggested that generation of H(2)O(2) and expression of CAT were coordinated and were indicative of epidermal differentiation as well as of the role of CAT in repairing redox damage by discomposing H(2)O(2). In addition, UVB-induced oxidative stress in the present study seemed to alter the endogenous and differentiation-specific redox balance between H(2)O(2) and CAT.

Sulfhydryl oxidase (SOx) from mouse epidermis: molecular cloning, nucleotide sequence, and expression of recombinant protein in the cultured cells.

Skin sulfhydryl oxidase (SOx) is an enzyme that catalyzes disulfide (S-S) cross-linking through the oxidation of sulfhydryl compounds in the skin. In this study, using the enzyme purified from rat seminal vesicle, we obtained peptide sequences for SOx by mass spectrometry. We then searched for SOx nucleotides corresponding highly to the rat peptide sequences by assembling murine-expressed sequence tags (ESTs) from the GeneBank database. The assembled mouse SOx cDNA has an open reading frame of 1704-bp nucleotides, translating into a size of 568 amino acids. The calculated molecular mass of the mouse SOx protein is 65 kDa. This mouse sequence can be amplified from total RNAs of various mouse tissue samples by reverse transcription polymerase chain reaction, especially highly amplified from those of the seminal vesicles and epidermis. The cDNA fragment was subsequently cloned into the mammalian expression vector (pTARGET-MSSOx), allowing us to express mouse recombinant SOx protein in cultured cells. When pTARGET-MSSOx was transfected, Western blot analysis using anti-SOx antiserum could detect a 65 kDa-band of recombinant SOx in both samples from the whole cell extract and the medium after the harvest of the HEK cells. In immunohistochemical analysis, the Pt-K2 cells, following the introduction of pTARGET-MSSOx, seemed to generate a SOx protein reactive to anti-SOx antiserum in the cells. Moreover, the indirect staining of the S-S bonds using N-(7-dimethylamino-4-methyl coumarinyl) maleimide (DACM), following the addition of N-ethylmaleimide and dithiothreitol, showed that the formation of S-S bridges almost matched the localization of SOx expression in the Pt-K2 cells after the transfection. In essence, we cloned skin SOx cDNA and characterized it as one of the S-S cross-linking enzymes. The SOx clone from mouse epidermis seems to be useful for investigating the potential function of the enzyme in the epidermis, especially for understanding the physiological role of SOx in the differentiation of keratinocytes.