• 한국융합학회논문지
• /
• 제11권10호
• /
• pp.401-407
• /
• 2020

본 연구는 생명윤리의식과 뇌사자의 장기기증에 대한 교육을 받은 학생과 받지 않은 학생의 생명의료 윤리의식과 뇌사자 장기기증 지식을 측정하고 비교하기 위한 비동등성 대조군 유사 실험연구이다. 연구대상자는 C시에 소재한 1개 대학 간호학과에 재학 중인 2학년 학생 76명을 대상으로 하였으며, 실험군 37명에게는 생명윤리의식과 뇌사자 장기기증에 대한 교육을 제공하였다. 수집된 자료는 SPSS 23.0프로그램을 이용하여 Fisher's exact test, t-test, ANCOVA로 분석하였다. 검증결과 뇌사자 장기기증에 관한 지식이 실험군과 대조군 두 집단간 유의한 차이(F=35.21, p=.000)가 있는 것으로 나타났다. 이에 간호대학생의 생명의료윤리에 대한 교육과 생명의료윤리 의식에 영향을 미치는 변수를 고려한 교육과정 개발이 이루어져야 할 것이다.

• The Korean Journal of Physiology and Pharmacology
• /
• 제12권2호
• /
• pp.65-71
• /
• 2008

The present study examined the inhibitory effect of licorice compounds glycyrrhizin and a metabolite $18{\beta}$-glycyrrhetinic acid on the neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse and on the 1-methyl-4-phenylpyridinium ($MPP^+$)-induced cell death in differentiated PC12 cells. MPTP treatment increased the activities of total superoxide dismutase, catalase and glutathione peroxidase and the levels of malondialdehyde and carbonyls in the brain compared to control mouse brain. Co-administration of glycyrrhizin (16.8 mg/kg) attenuated the MPTP effect on the enzyme activities and formation of tissue peroxidation products. In vitro assay, licorice compounds attenuated the $MPP^+$-induced cell death and caspase-3 activation in PC12 cells. Glycyrrhizin up to $100{\mu}M$ significantly attenuated the toxicity of $MPP^+$. Meanwhile, $18{\beta}$-glycyrrhetinic acid showed a maximum inhibitory effect at $10{\mu}M$; beyond this concentration the inhibitory effect declined. Glycyrrhizin and $18{\beta}$-glycyrrhetinic acid attenuated the hydrogen peroxide- or nitrogen species-induced cell death. Results from this study indicate that glycyrrhizin may attenuate brain tissue damage in mice treated with MPTP through inhibitory effect on oxidative tissue damage. Glycyrrhizin and $18{\beta}$-glycyrrhetinic acid may reduce the $MPP^+$ toxicity in PC12 cells by suppressing caspase-3 activation. The effect seems to be ascribed to the antioxidant effect.

• BMB Reports
• /
• 제46권8호
• /
• pp.383-390
• /
• 2013

Mammalian neural stem cells (NSCs) are of particular interest because of their role in brain development and function. Recent findings suggest the intimate involvement of programmed cell death (PCD) in the turnover of NSCs. However, the underlying mechanisms of PCD are largely unknown. Although apoptosis is the best-defined form of PCD, accumulating evidence has revealed a wide spectrum of PCD encompassing apoptosis, autophagic cell death (ACD) and necrosis. This mini-review aims to illustrate a unique regulation of PCD in NSCs. The results of our recent studies on autophagic death of adult hippocampal neural stem (HCN) cells are also discussed. HCN cell death following insulin withdrawal clearly provides a reliable model that can be used to analyze the molecular mechanisms of ACD in the larger context of PCD. More research efforts are needed to increase our understanding of the molecular basis of NSC turnover under degenerating conditions, such as aging, stress and neurological diseases. Efforts aimed at protecting and harnessing endogenous NSCs will offer novel opportunities for the development of new therapeutic strategies for neuropathologies.

• Anatomy and Cell Biology
• /
• 제57권2호
• /
• pp.155-162
• /
• 2024

Cerebral ischemia is the important cause of worldwide disability and mortality, that is one of the obstruction of blood vessels supplying to the brain. In early stage, glutamate excitotoxicity and high level of intracellular calcium (Ca²⁺) are the major processes which can promote many downstream signaling involving in neuronal death and brain tissue damaging. Moreover, autophagy, the reusing of damaged cell organelles, is affected in early ischemia. Under ischemic conditions, autophagy plays an important role to maintain energy of the brain and its function. In the other hand, over intracellular Ca²⁺ accumulation triggers excessive autophagic process and lysosomal degradation leading to autophagic process impairment which finally induce neuronal death. This article reviews the association between intracellular Ca²⁺ and autophagic process in acute stage of ischemic stroke.

• Animal cells and systems
• /
• 제12권4호
• /
• pp.211-217
• /
• 2008

Bax, a pro-apoptotic member of Bcl-2 family proteins, plays a central role in the mitochondria-dependent apoptosis. Apoptotic signals induce the translocation of Bax from cytosol into the mitochondria, which triggers the release of apoptogenic molecules such as cytochrome C and apoptosis-inducing factor, AIF. Bax-inhibiting peptide(BIP) is a cell permeable peptide comprised of five amino acids designed from the Bax-interaction domain of Ku70. Because BIP inhibits Bax translocation and Bax-mediated release of cytochrome C, BIP suppresses Bax-dependent apoptosis. In this study, we observed that BIP inhibited staurosporine-induced neuronal death in cultured cerebral cortex and cerebellar granule cells, but BIP failed to rescue granule cells from trophic signal deprivation-induced neuronal death, although both staurosporine-induced and trophic signal deprivation-induced neuronal death are dependent on Bax. These findings suggest that the mechanisms of the Bax activation may differ depending on the type of cell death induction, and thus BIP exhibits selective suppression of a subtype of Bax-dependent neuronal death.

• 대한핵의학회지
• /
• 제29권1호
• /
• pp.15-21
• /
• 1995

To evaluate availability of cerebral radionuclide imaging for diagnosis of brain death, we examined 25 patients with a suspected clinical diagnosis of brain death. 8 patients were studied by $^{99m}Tc$ DTPA and 15 patients were studied by $^{99m}Tc$ HMPAO (Hexamethyl propyleneamine oxime). Seven patients with $^{99m}Tc$ DTPA studies revealed absence of cerebral blood flow and sagittal sinus activity. All of 15 patients with $^{99m}Tc$ HMPAO studies revealed complete absence of cerebral perfusion. The results of the cerebral radionuclide studies of brain death correlated with other clinical conditions, such as intracranial pressure(ICP), EEG, transcranial doppler sonography(TCDS), and neurologic examination. The ICP of 8 patients, who are confirmed by brain death with $^{99m}Tc$ HMPAO study are elevated in all cases. In conclusion, cerebral radionuclide imaging for diagnosis of brain death is available. $^{99m}Tc$ HMPAO imaging is unequivocal, easily interpreted, well reflect the physiologic state of increased ICP, and provides adequate assessment of posterior fossa activity. In addition, the SPECT imaging with $^{99m}Tc$ HMPAO produces more accurate results due to it's superiority of image contrast and proper localization of radiopharmaceutical distribution than conventional planar imaging.

• 한국가족관계학회지
• /
• 제21권2호
• /
• pp.3-23
• /
• 2016

Objectives: The purpose of this study is to conduct a meta-analysis of results of death education program implemented with a wide range of learners from preschoolers to the elderly and use the findings to suggest effect sizes of the intervention program, variables, and measurement tools and activity elements of the variables. Method: Among preceding studies conducted domestically until 2015, 21 studies that meet the meta-analysis criteria were selected and analyzed using CMA(Comprehensive Meta-Analysis 3.0 version). Results: The findings are as follows. The overall average effect size was rather large at 0.997. Reviewing by research subject group, victims of domestic violence indicated the largest effect size(2.381). As for variables, death awareness showed the largest effect size(2.908). In terms of activity elements, the largest effect size for total number of sessions was 16 sessions (4.972), while that for per week sessions was 2 sessions/week (2.327). With effect size for activity hours largest at 30 minutes(5.365) followed by 108 minutes(2.381) and 360 minutes(1.607), it was found that there is no positive relationship between activity time and effect size. In terms of publication type, effect size of academic journal paper was 1.107 while that of thesis or dissertation was 0.894, indicating that academic journal papers are relatively highly effective. Conclusions: The present study is meaningful in that it provides baseline data applicable to program development and implementation by verifying the effectiveness of domestically implemented death education programs and variables relevant to such programs.

• Journal of Ginseng Research
• /
• 제44권4호
• /
• pp.593-602
• /
• 2020

Background: Heat stress orchestrates neurodegenerative disorders and results in the formation of reactive oxygen species that leads to cell death. Although the immunomodulatory effects of ginseng are well studied, the mechanism by which ginseng alleviates heat stress in the brain remains elusive. Methods: Rats were exposed to intermittent heat stress for 6 months, and brain samples were examined to elucidate survival and antiinflammatory effect after Korean Red Ginseng (KRG) treatment. Results: Intermittent long-term heat stress (ILTHS) upregulated the expression of cyclooxygenase 2 and inducible nitric oxide synthase, increasing infiltration of inflammatory cells (hematoxylin and eosin staining) and the level of proinflammatory cytokines [tumor necrosis factor α, interferon gamma (IFN-γ), interleukin (IL)-1β, IL-6], leading to cell death (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) and elevated markers of oxidative stress damage (myeloperoxidase and malondialdehyde), resulting in the downregulation of antiapoptotic markers (Bcl-2 and Bcl-x_L) and expression of estrogen receptor beta and brain-derived neurotrophic factor, key factors in regulating neuronal cell survival. In contrast, KRG mitigated ILTHS-induced release of proinflammatory mediators, upregulated the mRNA level of the antiinflammatory cytokine IL-10, and increased myeloperoxidase and malondialdehyde levels. In addition, KRG significantly decreased the expression of the proapoptotic marker (Bax), did not affect caspase-3 expression, but increased the expression of antiapoptotic markers (Bcl-2 and Bcl-x_L). Furthermore, KRG significantly activated the expression of both estrogen receptor beta and brain-derived neurotrophic factor. Conclusion: ILTHS induced oxidative stress responses and inflammatory molecules, which can lead to impaired neurogenesis and ultimately neuronal death, whereas, KRG, being the antioxidant, inhibited neuronal damage and increased cell viability.

• BMB Reports
• /
• 제35권1호
• /
• pp.94-105
• /
• 2002

Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to actively participate in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents that target this cell death process. This review will focus on molecular cell death pathways that are responsible for generating the apoptotic phenotype. It will also summarize what is currently known about the apoptotic signals that are activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.

• Journal of Chest Surgery
• /
• 제55권4호
• /
• pp.283-287
• /
• 2022

The shortage of donor lungs has become a serious obstacle to implementing lung transplantation (LTx). Donation after circulatory death (DCD) donors are among the several donor pools utilized to overcome the problem posed by the shortage of donation after brain death (DBD) donors. The active use of DCD donors is expected to significantly reduce mortality on the waiting list for LTx, as LTx from DCD donors has comparable outcomes to LTx from DBD donors. Further studies on efforts to shorten the warm ischemic time and use uncontrolled DCD are required.