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Methotrexate (MTX) is a commonly used chemotherapy agent for a variety of cancers. However, therapeutic levels are associated with numerous untoward effects such as central nervous system damage in children with acute lymphoblastic leukemia. The purpose of this study was to determine if MTX caused injury to endothelial cells using cultured bovine pulmonary artery endothelial cells as a model. Light microscopy showed gaps between cells and reduced numbers of endothelial cells after exposure to MTX (10 M), a range consistent with therapeutic drug levels. Proliferation and viability of subconfluent and confluent MTX-treated endothelial cells were measured by colorimetric (MTS) assay. There was a significant decline in cell numbers in MTX-treated subconfluent (growing) cells cultured after 4 days of MTX exposure compared to controls, as expected. However, there was also an unexpected decline in cell numbers in MTX-treated postmitotic endothelial cells after 1, 3, and 4 days of drug exposure. This suggested that MTX induced endothelial cell death. Fluorescent ApoAlert™
The natriuretic peptides (NPs), atrial natriuretic peptide, and brain natriuretic peptide (BNP) have been shown to have important roles in fluid volume homeostasis and blood pressure regulation. In addition, plasma NP levels are elevated in a number of cardiac pathologies and have been used as biochemical markers of left-ventricular dysfunction (LVD) in small-and large-scale clinical studies. In this review, the authors describe NP physiology and summarize the findings of selected studies that have examined the reliability and feasibility of NP measurement in LVD. In particular, BNP is proposed to be a biochemical marker that may provide a useful and inexpensive screening test of LVD. In addition, the authors discuss possible roles of the NPs in the etiology and progression of LVD. The findings of these studies suggest that the NPs may directly contribute to cardiac pathophysiology and LVD progression.
This is the first of a 2-part article on understanding cytokines. Cytokines are intercellular signaling proteins released from virtually all nucleated cells that influence growth and cellular proliferation in a wide range of tissues. Cytokines have immune modulating effects and are understood to control most of the physical and psychological symptoms associated with infection and inflammation. Cytokines also influence reproduction and bone remodeling. Dysregulation of the cytokine cellular system has significant implications in the development of a variety of illnesses, including most autoimmune disorders, many diseases of the cardiovascular system, osteoporosis, asthma, and depression. For nurses to be adequately informed when caring for clients with chronic illnesses and to be sufficiently knowledgeable when evaluating client outcomes, an understanding of the physiology of cytokines, the occurrences of dysregulation, and the role of cytokines in health and illness is essential. In Part I of this review, cytokine physiology is presented, with an emphasis on characteristics, categories, and mechanism of action. Specific instances of cytokine function in health and disease and implications for nursing research and practice are presented in Part II.
Cytokines are small signaling proteins released from a variety of cells that influence virtually every aspect of growth and development and every host response to infection, injury, and inflammation. Because of their widespread and potent effects across the life span, cytokines without a doubt influence nursing research and practice. From physiological and adaptive effects of cytokines to cytokine-induced diseases, nurses and nursing care are involved. Part II of this review highlights a few of the many examples of cytokines functioning in response to infection and inflammation, during the processes of reproduction, and in a variety of pathophysiological states. Implications for nursing research and practice are emphasized.
Iron-overload cardiomyopathy is a restrictive cardiomyopathy that manifests itself as systolic or diastolic dysfunction secondary to increased deposition of iron in the heart and occurs with common genetic disorders such as primary hemochromatosis and betathalassemia major. Although the exact mechanism of iron-induced heart failure remains to be elucidated, the toxicity of iron in biological systems is believed to be attributed to its ability to catalyze the generation of oxygen-free radicals. In the current investigation, the dose-dependent effects of chronic iron-loading on heart tissue concentrations of iron, glutathione peroxidase (GPx) activity, free-radical production, and cardiac dysfunction were investigated in a murine model of iron-overload cardiomyopathy. It was shown that chronic iron-overload results in dose-dependent (a) increases in myocardial iron burden, (b) decreases in the protective antioxidant enzyme GPx activity, (c) increased free-radical production, and (d) increased mortality. These findings show that the mechanism of iron-induced heart dysfunction involves in part free radical–mediated processes.
Many preterm infants cared for in incubators do not experience Kangaroo Care (KC), skin-to-skin contact with their mothers, due to fear of body heat loss when being held outside the incubator. A randomized clinical trial of 16 KC and 13 control infants using a pretest-test-posttest design of three consecutive interfeeding intervals of 2.5 to 3.0 h duration each was conducted over 1 day. Infant abdominal and toe temperatures were measured in and out of the incubator; maternal breast temperature was measured during KC. Repeated measures ANOVA showed no change in abdominal temperature across all periods and between groups. Toe temperatures were significantly higher during KC than incubator periods, and maternal breast temperature met each infant’s neutral thermal zone requirements within 5 min of onset of KC. Preterm infants similar to those studied here will maintain body warmth with up to 3 h of KC.