ABSTRACT
BACKGROUND: Caring consciousness and care action are core nursing values. The concept of internal temporal flow offers the potential to provide patients a richer and more meaningful life and better care. The family care phenomenon of psychiatric patients merits re-exploration. PURPOSE: This study identifies and describes relationships and issues within and between caring consciousness, care actions, and internal temporal flow by describing and interpreting the family care phenomenon of psychiatric patients. This study targets the care-recipient as a primary subject and highlights the orientation of co-existing and co-presenting caring-temporal flow for family and professional care applications and references. METHODS: This study conducts secondary data analysis using hermeneutic phenomenology inquiry. Research work was completed using multi-perspectives and multi-methods of data collection, including participant observation, individual in-depth and focus group interviews with psychiatric patients and their family members regarding their feelings, and thoughts and experiences of psychiatric family care. RESULTS: Data analysis results are divided into two parts: (1) the intersection of caregiver's and care receiver's caring-temporal flow and (2) The trajectory and construction of psychiatric patients' self-care temporal flow. Multiple appearances of the caring-temporal flow were formed when caregivers and care receivers engaged in different time and diverse care patterns. CONCLUSION: Fluctuation and competition among psychiatric patients' and their family members' control and transfer in terms of their lived temporality were influenced by mutual maturity as well as the demand and offering of caring consciousness and care action. The psychiatric patient as a primary subject should return and take control over his or her own mainstream lived temporality, which is the core essence of care.
Subject(s)
Caregivers/psychology , Family/psychology , Mental Disorders/therapy , Adolescent , Adult , Female , Humans , Male , Middle AgedABSTRACT
Increased cell death of cardiomyocyte by oxidative stress is known to cause dysfunction of the heart. O. gratissimum is one of the more well-known medicinal plants among the Ocimum species and widely used in treatment of inflammatory diseases. In this study, we hypothesized that aqueous extract of O. gratissimum leaf (OGE) may protect myocardiac cell H9c2 from oxidative injury by hydrogen peroxide (H(2)O(2)). Our results revealed that OGE pretreatment dose-dependently protects H9c2 cells from cell death when exposed to H(2)O(2). Additionally, DNA condensation induced by H(2)O(2) was also reduced by OGE pretreatment, suggesting that Ocimum gratissimum extract may attenuate H(2)O(2)-induced chromosome damage. Further investigation showed that OGE pretreatment inhibited H(2)O(2)-induced activation of caspase-3 and caspase-9, as well as H(2)O(2)-induced upregulation of proapoptotic Apaf-1 and the release of cytosolic cytochrome c, but has little effect on the activation of caspase-8. Additionally, OGE pretreatment significantly upregulated Bcl-2 expression and Akt phosphorylation, and slightly affected the phosphorylation of mitogen-activated protein kinases including p38 MAPK and JNK. Taken together, our findings revealed that Ocimum gratissimum extract effectively inhibited the mitochondrial pathway and upregulated Bcl-2 expression, which may be important in protecting H9c2 cells from H(2)O(2)-induced cell death.
ABSTRACT
Collapsin response mediator protein-1 (CRMP-1) controls neural development and axonal growth but also acts as a cancer invasion suppressor. In this study, we investigated the transcriptional regulation of CRMP-1 expression. Using a serial deletion strategy, we identified a basal promoter region between nucleotides -100 and -180 in the 5' flanking region of CRMP-1 (nucleotides -1,920 to +50) that contains multiple putative Sp1 and C/EBPalpha sites. Site-directed mutagenesis and deletion analysis revealed that the two C/EBPalpha sites, from nucleotides -122 to -133 and from nucleotides -101 to -113, are the most important regulatory elements. Gel-shift and antibody supershift assays showed that Sp1 protein was also present at this C/EBPalpha site, which overlaps with a Sp1 site. Overexpression of Sp1 decreased CRMP-1 promoter activity and protein expression, whereas overexpression of C/EBPalpha produced the opposite effect. Chromatin immunoprecipitation assays confirmed that Sp1 and C/EBPalpha compete for binding at the overlapping C/EBPalpha and Sp1 sites and reciprocally regulate CRMP-1 expression. Overexpression of cyclooxygenase-2 (COX-2) decreased CRMP-1 mRNA and protein expression. Conversely, the COX-2 inhibitor, celecoxib, induced a dose-dependent increase in CRMP-1 expression. COX-2 inhibition also decreased Sp1-DNA complex formation and inhibited cell invasion. We conclude that transcription of the invasion suppressor, CRMP-1, is reciprocally regulated at the promoter region by C/EBPalpha and Sp1. COX-2 inhibitors increase CRMP-1 expression by inhibiting Sp1-DNA complex formation and enhancing DNA binding of C/EBPalpha at the promoter.