Effects of a tailored inhaler use education program for chronic obstructive pulmonary disease patients.

OBJECTIVES: This study compared the effects of a tailored inhaler use education program with routine clinical practice in asthma and chronic obstructive pulmonary disease patients treated with inhalers. METHODS: The participants included 59 patients from a ≥900-bed university hospital in J city. Participants were divided into two groups and received either the tailored inhaler use education program (n = 29) or routine clinical care (n = 30). Disease knowledge and correct inhaler use were assessed using a questionnaire and observational checklists at admission and discharge. Chi-square and Mann-Whitney U tests were used for data analysis. RESULTS: Disease knowledge (asthmaz = -2.69, p = .007; chronic obstructive pulmonary disease z = -6.08, p < .001) and correct inhaler use (z = -5.51, p < .001) were significantly higher in the tailored inhaler use education program group compared to the control group. CONCLUSIONS: Nurses play a pivotal role in educating patients. Our results indicate that nurses are needed to identify diseases and inhaler types and to provide patients with individually tailored education that includes demonstration and feedback. PRACTICE IMPLICATIONS: One-on-one health literacy education tailored to inhaler type and patient age shows promise for chronic disease interventions provided by nurses, physicians, and pharmacists--all the parties involved in patient care.

Effect of retinoic acid on renal development in newborn mice treated with an angiogenesis inhibitor.

BACKGROUND: A mouse model of impaired renal development was developed and the effect of retinoic acid (RA) was investigated in this animal model. METHODS: An angiogenesis inhibitor (SU1498) was injected s.c. into day 3 C57BL/6 newborn mice to create a model of arrested renal development. RA (2 mg/kg) was injected i.p. for 10 days. Morphometry and immunohistochemistry were done. RESULTS: Mice injected with SU1498 demonstrated deranged renal development in tubular structure and glomerular tuft area. Cortical thickness and area of glomerular tuft were significantly decreased after vascular endothelial growth factor (VEGF) inhibitor, and were significantly restored by RA. The length of capillary loops/glomerulus, the number of podocytes/glomerulus, and density of peritubular capillaries on CD31 immunostaining were significantly decreased by VEGF blocking and recovered by RA. CONCLUSIONS: VEGF plays a major role in renal development, and RA reverses the inhibited development caused by an angiogenesis inhibitor.

Mesenchymal stem cells showed the highest potential for the regeneration of injured liver tissue compared with other subpopulations of the bone marrow.

We have previously reported that bone marrow cells (BMCs) participate in the regeneration after liver injury. However, it is not established that this is the result of differentiation of hematopoietic stem cells (HSCs), mesenchymal stem cells (MSCs) or the combination of both. We investigated the contribution of each cell fraction to the regenerative process. First, we confirmed that transplanted stem cells migrate directly to injured liver tissue without dispersing to other organs. Next, we divided green fluorescent protein (GFP)-expressing BMCs into three populations as mononuclear cells, MSCs and HSCs. We then compared the engraftment capacity after transplantation of each fraction of cells into liver-injured mice. Of these, the MSCs transplanted group showed the highest GFP fluorescence intensities in liver tissue by flow cytometry analysis and confocal microscopic observation. Furthermore, MSCs showed differentiation potential into hepatocytes when co-cultured with injured liver cells, which suggests that MSCs showed highest potential for the regeneration of injured liver tissue compared with those of the other two cell refractions.

Effect of hypoxic treatment on bone marrow cells that are able to migrate to the injured liver.

Restricted numbers and poor regenerative properties limit the use of adult stem cells. We tested the effect of hypoxic treatment as a method by which to increase cell migration. Bone marrow cells (BMCs) were cultured under oxygen saturations of 0.1, 3, and 20% for 24h. After hypoxic treatment, BMCs of apoptotic fraction were decreased. The expression of CXCR4 was noticeably increased in the hypoxia-treated BMCs and their migration in response to SDF-1alpha was enhanced compared with cells cultured under normoxic condition. Hypoxic BMCs had a higher degree of engraftment to the CCl(4)-injured liver than the normoxic cells. Hypoxic treatment of BMCs may have merits in decreasing apoptosis of those cells as well as in enhancing cellular migration to SDF-1alpha, the chemokine which binds to BMCs expressed CXCR4 and to the injured tissue, such as CCl(4) damaged liver.

Gene expression profile of mesenchymal stromal cells after co-culturing with injured liver tissue.

Mesenchymal stromal cells (MSCs) are a potential cell source for the development of therapeutic products. Recent studies have shown that the transplantation of MSCs to damaged organs, including the heart, liver and kidneys, results in the restoration of the damaged tissues. However, the mechanisms underlying this regeneration process have yet to be clearly characterized. Consequently, in this study, we focused on the therapeutic potential of MSCs in injured liver tissue by evaluating the gene expression profiles of MSCs in the presence of injured liver and normal liver cells using a microarray chip containing 44,000 genes. In order to mimic the state of liver cell regeneration in vitro, we respectively co-cultured MSCs with CCl4-injured liver cells and normal liver cells from C57BL/6 female mice. After 48 h of co-culturing, MSCs were collected and the RNA was extracted for microarray analysis. Under conditions of co-culture with normal liver cells, upregulated expression of CXCR6, CCR3, IL-2, IL-11, CD34, CD74, procollagen, FMS-like tyrosine kinase, neuregulin 4, Wnt2 and catenins was noted. Under conditions of co-culture with the CCl4-injured liver cells, expression of CXCL2, cytoglobin, erythropoietin, v-Erb, hypoxia-inducible factor 3 (α subunit), retinoic acid receptor ß and Vav2 was upregulated. Our research provides information regarding the differential molecular mechanisms that regulate the properties of MSCs in the regeneration of injured liver tissue.

Effect on cell cycle progression by N-Myc knockdown in SK-N-BE(2) neuroblastoma cell line and cytotoxicity with STI-571 compound.

PURPOSE: Neuroblastoma is a common tumor in childhood, and generally exhibits heterogeneity and a malignant progression. MYCN expression and amplification profiles frequently correlate with therapeutic prognosis. Although it has been reported that MYCN silencing causes differentiation and apoptosis in human neuroblastoma cells, MYCN expression influences the cytotoxic potential of chemotherapeutic drugs via the deregulation of the cell cycle. STI-571 may constitute a promising therapeutic agent against neuroblastoma, particularly in cases in which c-Kit is expressed preferentially in MYCN-amplified neuroblastoma. MATERIALS AND METHODS: To determine whether STI-571 exerts a synergistic effect on cytotoxicity with MYCN expression, we assessed apoptotic cell death and cell cycle distribution after 72 h of exposure to STI-571 with or with out treatment of SK-N-BE(2) neuroblastoma cells with MYCN siRNA. RESULTS: MYCN siRNA-treated SK-N-BE(2) cells did not affect apoptosis and cells were arrested in G0/G1 phase after STI-571 treatment. CONCLUSIONS: siRNA therapy targeted to MYCN may not be effective when administered in combination with STI-571 treatment in cases of neuroblastoma. Therefore, chemotherapeutic drugs that target S or G2-M phase may prove ineffective when applied to cells arrested in the G0/1 phase as the result of MYCN knockdown and STI-571 treatment.