Negotiating The Maze: Confronting Dysphagia Together With My Stroke-Afflicted Family Member

Aim: To generate a descriptive theory grounded in the responses of family caregivers caring for their family stroke survivors with dysphagia during hospitalization. Design and Method: A qualitative study employing the grounded theory method was used. Fifteen family caregivers participated in comprehensive interviews. The interview data were analyzed using the constant comparative method. Findings: ‘Negotiating the maze: Confronting dysphagia with my stroke-afflicted family member’ was the core category guiding the care process for dysphagia family members among caregivers. After surviving stroke, the caregivers felt ‘more confusion less rejoicing’ as the antecedent condition. The following three interaction categories were identified: (1) ‘being overwhelmed by nasogastric (NG) tube issues’; (2) ‘searching for the right helper and information’; and (3) ‘food culture conflicts with the formula diet administered through the NG tube’. Additionally, ‘Maintaining positivity’ described the consequence of this process. Conclusions: This study highlights the critical perspective of family members who care for dysphagia stroke survivors in the hospital. Participants were under tremendous pressure during the disease treatment process. However, all attempted to maintain a positive attitude and treasured the chance to accompany their family members. Clinical Relevance: These findings can assist health professionals in charting the effects of dysphagia and in understanding the problems and needs according to the subjective perspectives of family caregivers. They can also provide a necessary foundation for comprehensive care interventions for family caregivers of stroke survivors with dysphagia

Identification of the initial molecular changes in response to circulating angiogenic cells-mediated therapy in critical limb ischemia

BackgroundCritical limb ischemia (CLI) constitutes the most aggressive form of peripheral arterial occlusive disease, characterized by the blockade of arteries supplying blood to the lower extremities, significantly diminishing oxygen and nutrient supply. CLI patients usually undergo amputation of fingers, feet, or extremities, with a high risk of mortality due to associated comorbidities.Circulating angiogenic cells (CACs), also known as early endothelial progenitor cells, constitute promising candidates for cell therapy in CLI due to their assigned vascular regenerative properties. Preclinical and clinical assays with CACs have shown promising results. A better understanding of how these cells participate in vascular regeneration would significantly help to potentiate their role in revascularization.Herein, we analyzed the initial molecular mechanisms triggered by human CACs after being administered to a murine model of CLI, in order to understand how these cells promote angiogenesis within the ischemic tissues.MethodsBalb-c nude mice (n:24) were distributed in four different groups: healthy controls (C, n:4), shams (SH, n:4), and ischemic mice (after femoral ligation) that received either 50 mu l physiological serum (SC, n:8) or 5x10(5) human CACs (SE, n:8). Ischemic mice were sacrificed on days 2 and 4 (n:4/group/day), and immunohistochemistry assays and qPCR amplification of Alu-human-specific sequences were carried out for cell detection and vascular density measurements. Additionally, a label-free MS-based quantitative approach was performed to identify protein changes related.ResultsAdministration of CACs induced in the ischemic tissues an increase in the number of blood vessels as well as the diameter size compared to ischemic, non-treated mice, although the number of CACs decreased within time. The initial protein changes taking place in response to ischemia and more importantly, right after administration of CACs to CLI mice, are shown.ConclusionsOur results indicate that CACs migrate to the injured area; moreover, they trigger protein changes correlated with cell migration, cell death, angiogenesis, and arteriogenesis in the host. These changes indicate that CACs promote from the beginning an increase in the number of vessels as well as the development of an appropriate vascular network.Institute of Health Carlos III, ISCIII; Junta de Andaluci

Val-9Ala and Ile + 58Thr polymorphism of MnSOD in Parkinson's disease

100學年度研究獎補助論文[[abstract]]Objectives: To investigate the polymorphism distribution of Val-9Ala and Ile + 58Thr of the Mn-superoxide dismutase (Mn-SOD) gene among subjects with Parkinson's disease (PD) by analyses of genders and clinical severity. Design and Methods: We examined the DNA genotypes of Val-9Ala and Ile + 58Thr from 295 PD subjects and 111 controls by nucleotide sequencing and BsaWI restriction. Results: Ala/Ala homozygosity was found in four PD subjects but not in the controls. All of the genotypes at codon + 58 among the examined samples were Ile/Ile homozygotes. Although higher carrier rate of Ala allele among PD subjects than the controls, there were no differences by analyses of the genders and clinical severity. Conclusion: The higher Ala-allele carrier rate among PD subjects may suggest a possible higher amount of mitochondrial Mn-SOD rendering higher intracellular stress in PD. In this study the polymorphisms at codons -9 and + 58 did not give informative association evidences with PD.[[incitationindex]]SCI[[booktype]]紙

Octarepeat changes of prion protein in Parkinson's disease

100學年度莊子超升等參考著作[[abstract]]Polymorphism in prion protein (PrP) is related to different phenotypes of spongiform encephalopathies and some mental illnesses. The octarepeat region of PrP, encompassing the codon 51 through 91, is related to cellular anti-oxidation function and may play a role in genetic contribution of PrP polymorphism to neurodegeneration, such as Parkinson's disease (PD). We analyzed the genomic patterns of PrP gene from 528 subjects and found a predominance of Met/Met variant at codon 129 of PD subjects without significant difference (97.3%, and 96.5% in controls). But among PD subjects there were one with heterozygosity of silent nucleotide substitution (NS) on octarepeats (R1–2–3g–3–4/R1–2–2–3–4) and three with heterozygosity of single copy deletion (CD) on octarepeats (R1–2–3–4/R1–2–2–3–4). Consistent genomic DNA and cDNA sequences were found in a PD subject without any octarepeat changes and the one with NS, but R1–2–3g–3–4/R1–2–2–3–4 of cDNA pattern occurred in the one with genomic CD. This is the first report of the polymorphic PrP octarepeat change among those with parkinsonism. We proposed a hypothesis about an initial secondary hairpin structure of the template strand followed by the transcript “shift backward” due to the high homology of the sequences between R2 and R3 motifs while synthesizing RNA. This phenomenon may be a key step of neurodegeneration resulting from PrP polymorphism and require further studies.[[notice]]補正完畢[[journaltype]]國外[[incitationindex]]SCI[[countrycodes]]GBR[[countrycodes]]紙

Nitric Oxide Induces Prion Protein via MEK and p38 MAPK signaling

[[journaltype]]國外[[incitationindex]]SC

Baicalein Induces G₂/M Cell Cycle Arrest Associated with ROS Generation and CHK2 Activation in Highly Invasive Human Ovarian Cancer Cells

Ovarian cancer is a lethal gynecological cancer because drug resistance often results in treatment failure. The CHK2, a tumor suppressor, is considered to be an important molecular target in ovarian cancer due to its role in DNA repair. Dysfunctional CHK2 impairs DNA damage-induced checkpoints, reduces apoptosis, and confers resistance to chemotherapeutic drugs and radiation therapy in ovarian cancer cells. This provides a basis for finding new effective agents targeting CHK2 upregulation or activation to treat or prevent the progression of advanced ovarian cancer. Here, the results show that baicalein (5,6,7-trihydroxyflavone) treatment inhibits the growth of highly invasive ovarian cancer cells, and that baicalein-induced growth inhibition is mediated by the cell cycle arrest in the G2/M phase. Baicalein-induced G2/M phase arrest is associated with an increased reactive oxygen species (ROS) production, DNA damage, and CHK2 upregulation and activation. Thus, baicalein modulates the expression of DNA damage response proteins and G2/M phase regulatory molecules. Blockade of CHK2 activation by CHK2 inhibitors protects cells from baicalein-mediated G2/M cell cycle arrest. All the results suggest that baicalein has another novel growth inhibitory effect on highly invasive ovarian cancer cells, which is partly related to G2/M cell cycle arrest through the ROS-mediated DNA breakage damage and CHK2 activation. Collectively, our findings provide a molecular basis for the potential of baicalein as an adjuvant therapeutic agent in the treatment of metastatic ovarian cancer

Effects of Repetitive Hyperbaric Oxygen Treatment in Patients with Acute Cerebral Infarction: A Pilot Study

The role of hyperbaric oxygen therapy (HBOT) in the treatment of acute ischemic stroke is controversial. This prospective study assessed the efficacy and safety of HBOT as adjuvant treatment on 46 acute ischemic stroke in patients who did not receive thrombolytic therapy. The HBOT group (n=16) received conventional medical treatment with 10 sessions of adjunctive HBOT within 3–5 days after stroke onset, while the control group (n=30) received the same treatment but without HBOT. Early (around two weeks after onset) and late (one month after onset) outcomes (National Institutes of Health Stroke Scale, NIHSS scores) and efficacy (changes of NIHSS scores) of HBOT were evaluated. The baseline clinical characteristics were similar in both groups. Both early and late outcomes of the HBOT group showed significant difference (P≤0.001). In the control group, there was only significant difference in early outcome (P=0.004). For early efficacy, there was no difference when comparing changes of NIHSS scores between the two groups (P=0.140) but there was statistically significant difference when comparing changes of NIHSS scores at one month (P≤0.001). The HBOT used in this study may be effective for patients with acute ischemic stroke and is a safe and harmless adjunctive treatment