• Title/Summary/Keyword: BRAIN DEATH

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Nurse's Attitudes on Organ Donation in Brain Dead Donors (뇌사자 장기기증에 대한 간호사의 태도)

  • Kim, Sang-Hee
    • Journal of Hospice and Palliative Care
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    • v.9 no.1
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    • pp.11-16
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    • 2006
  • Purpose: This study is aimed to confirm nurse's attitudes and to investigate the factor analysis on organ donation in brain dead donors. Methods: This survey were collected from 198 nurses in three university hospitals and four general hospitals in B city with questionnaires developed by the author. The consent for this research was obtained from nursing managers, head nurses, and staff nurses after explaining the purpose of this research. Results: In questionnaires, 45 items about attitudes were included and positive and negative attitude were analyzed. The contents of factors are 'legal permission of brain death', 'one's will of organ donation at the brain death', 'need for educational program about brain dead during college curriculum', 'organ donation is good presents for others', 'connection with professional institutes', 'necessity of brain death', 'convenient to control of brain death' and 'the goods for organ transplantation in brain dead donors' as positive attitudes. Meanwhile, 'contrast to certain religion and dignity to life', 'negative dangers on brain dead permission', 'unbelief to the medical teams', 'burdens to ask organ donation to brain deads/families' and 'economical compensation' are factors as negative attitudes about organ donation in brain dead. The total mean point score of positive attitudes about organ donation in brain dead donors was $3.753{\pm}3.398$. The total mean point score of negative attitudes about organ donation in brain dead donors was $2.915{\pm}0.472$. Conclusion: The results of this study may be of help for the nurses who concern organ sharing and make effective interventions and educations to facilitate the decision making process for organ donation in brain dead donors or families.

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Factors Affecting Nurse Clinicians' Knowledge and Attitude of Organs Procurement from Brain Dead Patients (임상간호사의 뇌사자 장기기증에 대한 지식과 태도에 영향을 미치는 요인)

  • Lee, Hyun Ah;Hur, Yujin;Lee, Young Gew;Song, Garam;Lee, Eunji;Shin, Sujin
    • Journal of Korean Critical Care Nursing
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    • v.10 no.3
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    • pp.19-30
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    • 2017
  • Purpose : This study investigated factors affecting the knowledge and attitude of organ procurement from brain dead patients in nurse clinicians. Methods : A survey was conducted with 160 clinical nurses from a university hospital in Seoul. Descriptive statistics, t-tests, an ANOVA, $Scheff{\acute{e}}^{\prime}s$ test, Pearson's correlation coefficient, and a multiple regression analysis were used. Results : The mean score for knowledge of organ procurement from brain dead patients was $12.41{\pm}2.16$ (mean correct answers = 62.1). Factors influencing the knowledge of organ procurement among nurse clinicians were working department (${\beta}=.454$, p < .001), a recent family death (${\beta}=.187$, p = .014), experience recognizing potential brain dead patients (${\beta}=.182$, p = .033), and experience referring to potential brain dead patients (${\beta}=-.192$, p = .048). Conclusion : To ensure effective organ procurement from brain dead patients, it is necessary to continually educate nurse clinicians to improve their attitude and knowledge concerning organ donation.

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Involvement of Caspases and Bcl-2 Family in Nitric Oxide-Induced Apoptosis of Rat PC12 Cells

  • Jeong, Yeon-Jin;Jung, Ji-Yeon;Lee, Jin-Ha;Cho, Jin-Hyoung;Lee, Guem-Sug;Kim, Sun-Hun;Kim, Won-Jae
    • The Korean Journal of Physiology and Pharmacology
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    • v.10 no.6
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    • pp.329-335
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    • 2006
  • This study was aimed to investigate the nitric oxide (NO)-induced cytotoxic mechanism in PC12 cells. Sodium nitroprusside (SNP), an NO donor, decreased the viability of PC12 cells in dose-and time-dependent manners. SNP enhanced the production of reactive oxygen species (ROS), and gave rise to apoptotic morphological changes including cell shrinkage, chromatin condensation, and DNA fragmentation. Expression of Bax was not affected, whereas Bcl-2 was downregulated in SNP-treated PC12 cells. SNP augmented the release of cytochrome c from mitochondria into cytosol and enhanced caspase -8, -9, and -3 activities. SNP upregulated both Fas and Fas-L, which are known to be components of death receptor assembly. These results suggest that NO induces apoptosis of PC12 cells through both mitochondria-and death receptor-mediated pathways mediated by ROS and Bcl-2 family.

Pediatric Severe Traumatic Brain Injury : Updated Management

  • Ha, Eun Jin
    • Journal of Korean Neurosurgical Society
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    • v.65 no.3
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    • pp.354-360
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    • 2022
  • Traumatic brain injury (TBI) is the leading cause of death and disability in children. Survivors of severe TBI are more susceptible to functional deficits, resulting in disability, poor quality of life, cognitive decline, and mental health problems. Despite this, little is known about the pathophysiology of TBI in children and how to manage it most effectively. Internationally, efforts are being made to expand knowledge of pathophysiology and develop practical clinical treatment recommendations to improve outcomes. Here we discuss recently updated evidence and management of severe pediatric TBI.

Tensile Characteristics and Behavior of Blood Vessels from Human Brain in Uniaxial Tensile Test

  • Suh, Chang-Min;Kim, Sung-Ho;Ken L. Monson;Werner Goldsmith
    • Journal of Mechanical Science and Technology
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    • v.17 no.7
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    • pp.1016-1025
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    • 2003
  • The rupture of blood vessels in the human brain results in serious pathological and medical problems. In particular, brain hemorrhage and hematomas resulting from impact to the head are a major cause of death. As such, investigating the tensile behavior and rupture of blood vessels in the brain is very important from a medical point of view. In the present study, the tensile characteristics of the blood vessels in the human brain were analyzed using a quasi-static uniaxial tensile test, and the properties of the arteries and veins compared. In addition, to compare the tensile behavior and demonstrate the validity of the experimental results, blood vessels from the legs of pigs were also tested and analyzed. The overall results were in accordance with the histological structures and previous medical reports.

Evaluation of Probability of Survival Using Trauma and Injury Severity Score Method in Severe Neurotrauma Patients

  • Moon, Jung-Ho;Seo, Bo-Ra;Jang, Jae-Won;Lee, Jung-Kil;Moon, Hyung-Sik
    • Journal of Korean Neurosurgical Society
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    • v.54 no.1
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    • pp.42-46
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    • 2013
  • Objective : Despite several limitations, the Trauma Injury Severity Score (TRISS) is normally used to evaluate trauma systems. The aim of this study was to evaluate the preventable trauma death rate using the TRISS method in severe trauma patients with traumatic brain injury using our emergency department data. Methods : The use of the TRISS formula has been suggested to consider definitively preventable death (DP); the deaths occurred with a probability of survival (Ps) higher than 0.50 and possible preventable death (PP); the deaths occurred with a Ps between 0.50 and 0.25. Deaths in patients with a calculated Ps of less than 0.25 is considered as non-preventable death (NP). A retrospective case review of deaths attributed to mechanical trauma occurring between January 1, 2011 and December 31, 2011 was conducted. Results : A total of 565 consecutive severe trauma patients with ISS>15 or Revised Trauma Score<7 were admitted in our institute. We excluded a total of 24 patients from our analysis : 22 patients younger than 15 years, and 2 patients with burned injury. Of these, 221 patients with head injury were analyzed in the final study. One hundred eighty-two patients were in DP, 13 in PP and 24 in NP. The calculated predicted mortality rates were 11.13%, 59.04%, and 90.09%. The actual mortality rates were 12.64%, 61.547%, and 91.67%, respectively. Conclusion : Although it needs to make some improvements, the present study showed that TRISS performed well in predicting survival of traumatic brain injured patients. Also, TRISS is relatively exact and acceptable compared with actual data, as a simple and time-saving method.

Risk Factors Predicting Unfavorable Neurological Outcome during the Early Period after Traumatic Brain Injury

  • Park, Jung-Eon;Kim, Sang-Hyun;Yoon, Soo-Han;Cho, Kyung-Gi;Kim, Se-Hyuk
    • Journal of Korean Neurosurgical Society
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    • v.45 no.2
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    • pp.90-95
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    • 2009
  • Objective : We aimed to identify clinico-radiological risk factors that may predict unfavorable neurological outcomes in traumatic brain injury (TBI), and to establish a guideline for patient selection in clinical trials that would improve neurological outcome during the early post TBI period. Methods : Initial clinico-radiological data of 115 TBI patients were collected prospectively. Regular neurological assessment after standard treatment divided the above patients into 2 groups after 6 months : the Favorable neurological outcome group (GOS : good & moderate disability, DRS : 0-6, LCFS : 8-10) and the Unfavorable group (GOS : severe disability-death, DRS : 7-29 and death, LCFS : 1-7 and death). Results : There was a higher incidence of age $\geq$35 years, low initial GCS score, at least unilateral pupil dilatation, and neurological deficit in the Unfavorable group. The presence of bilateral parenchymal lesions or lesions involving the midline structures in the initial brain CT was observed to be a radiological risk factor for unfavorable outcome. Multivariate analysis demonstrated that age and initial GCS score were independent risk factors. The majority of the Favorable group patients with at least one or more risk factors showed improvement of GCS scores within 2 months after TBI. Conclusion : Patients with the above mentioned clinico-radiological risk factors who received standard treatment, but did not demonstrate neurological improvement within 2 months after TBI were deemed at risk for unfavorable outcome. These patients may be eligible candidates for clinical trials that would improve functional outcome after TBI.

Activation of Autophagy Pathway Suppresses the Expression of iNOS, IL6 and Cell Death of LPS-Stimulated Microglia Cells

  • Han, Hye-Eun;Kim, Tae-Kyung;Son, Hyung-Jin;Park, Woo Jin;Han, Pyung-Lim
    • Biomolecules & Therapeutics
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    • v.21 no.1
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    • pp.21-28
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    • 2013
  • Microglia play a role in maintaining and resolving brain tissue homeostasis. In pathological conditions, microglia release pro-inflammatory cytokines and cytotoxic factors, which aggravate the progression of neurodegenerative diseases. Autophagy pathway might be involved in the production of pro-inflammatory cytokines and cytotoxic factors in microglia, though details of the mechanism remain largely unknown. In the present study, we examined the role of the autophagy pathway in activated BV2 microglia cells. In BV2 cells, rapamycin treatment activated the formation of anti-LC3-labeled autophagosomes, whereas the ATG5 depletion using siRNA-ATG5 prevented the formation of LC3-labeled autophagosomes, indicating that BV2 cells exhibit an active classical autophagy system. When treated with LPS, BV2 cells expressed an increase of anti-LC3-labeled dots. The levels of LC3-labeled dots were not suppressed, instead tended to be enhanced, by the inhibition of the autophagy pathway with siRNA-ATG5 or wortmannin, suggesting that LPS-induced LC3-labeled dots in nature were distinct from the typical autophagosomes. The levels of LPS-induced expression of iNOS and IL6 were suppressed by treatment with rapamycin, and conversely, their expressions were enhanced by siRNA-ATG5 treatment. Moreover, the activation of the autophagy pathway using rapamycin inhibited cell death of LPS-stimulated microglia. These results suggest that although microglia possess a typical autophagy pathway, the glial cells express a non-typical autophagy pathway in response to LPS, and the activation of the autophagy pathway suppresses the expression of iNOS and IL6, and the cell death of LPS-stimulated microglia.

Adult Neurogenesis in Insulted Brain

  • Kim, Byung-Woo;Son, Hyeon
    • Toxicological Research
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    • v.23 no.2
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    • pp.107-114
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    • 2007
  • Although there are some questions about the venues of adult neurogenesis, it is undoubtedly accepted that new neurons are born in adult brains. Adult neurogenesis is regulated by a wide array of factors. Insults harmful to brain, such as neurodegenerative diseases, seizure, ischemia and exposure to drugs of abuse, are intricately related to adult neurogenesis. Whereas neurodegenerative diseases are characterized by death or functional loss of specific neurons, recent studies report that they can be accompanied by neurogenesis. In addition, alcohol and drugs of abuse which have been reputed to cause irreversible damage to brain can also generate newly born cells in adult brain. As yet, however, we have little knowledge of the functional significance and roles of adult neurogenesis under pathological settings, not to mention under physiological settings. Accordingly, in this review we briefly summarize the results of studies which focus on adult neurogenesis in insulted brain, instead of trying to draw hurried conclusion regarding the relationship between adult neurogenesis and brain insults.

Insulin resistance and Alzheimer's disease

  • De La Monte, Suzanne M.
    • BMB Reports
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    • v.42 no.8
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    • pp.475-481
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    • 2009
  • Emerging data demonstrate pivotal roles for brain insulin resistance and insulin deficiency as mediators of cognitive impairment and neurodegeneration, particularly Alzheimer's disease (AD). Insulin and insulin-like growth factors (IGFs) regulate neuronal survival, energy metabolism, and plasticity, which are required for learning and memory. Hence, endogenous brain-specific impairments in insulin and IGF signaling account for the majority of AD-associated abnormalities. However, a second major mechanism of cognitive impairment has been linked to obesity and Type 2 diabetes (T2DM). Human and experimental animal studies revealed that neurodegeneration associated with peripheral insulin resistance is likely effectuated via a liver-brain axis whereby toxic lipids, including ceramides, cross the blood brain barrier and cause brain insulin resistance, oxidative stress, neuro-inflammation, and cell death. In essence, there are dual mechanisms of brain insulin resistance leading to AD-type neurodegeneration: one mediated by endogenous, CNS factors; and the other, peripheral insulin resistance with excess cytotoxic ceramide production.