• Title/Summary/Keyword: 돌연사

Search Result 64, Processing Time 0.02 seconds

Effects of Myostatin Prodomains on the Reproduction of Rotifer Brachionus rotundiformis (Myostatin prodomains이 rotifer 생활사에 미치는 영향)

  • Jo, Mi-Jin;Jin, Hyung-Joo
    • Journal of Life Science
    • /
    • v.22 no.4
    • /
    • pp.486-491
    • /
    • 2012
  • Myostatin (MSTN), a member of the transforming growth factor (TGF)-beta family, is a potent negative regulator of skeletal muscle growth and maintenance. The MSTN prodomain inhibits MSTN biological activity. The rotifer Brachionus rotundiformis is an excellent primary live feed for fish larvae in aquaculture; however, it is not known whether the rotifer expresses MSTN and the MSTN prodomain along with its activity. The objective of this study was to examine the effects of recombinant MSTN prodomains. Individual cultures of the rotifer B. rotundiformis were carried out to determine the effect of recombinant MSTN prodomains (pMALc2x-poMSTNpro and pMALc2x-sMSTNpro) on the pre-reproductive phase, reproductive phase, post-reproductive phase, offspring, lifespan, fecundity, and male ratio. In addition, a population culture of the rotifer was performed to confirm the effects of pMALc2x-poMSTNpro and pMALc2x-sMSTNpro on population growth. The results showed that the rotifer treated with pMALc2x-pMSTNpro had a reduced pre-reproductive phase at higher concentrations (1, 2, and 4 ${\mu}g/ml$) compared to the non-treated control group. Moreover, the pMALc2xsMSTNpro treated rotifer effectively decreased the pre-reproductive phase at a lower concentration (0.25 ${\mu}g/ml$) compared to the pMALc2x-pMSTNpro treated and control group. Interestingly, pMALc2x-poMSTNpro and pMALc2x-sMSTNpro significantly increased the population of $B.$ $rotundiformis$.

Development of an Infants' Sleep Health Program Using a Video for SIDS Prevention Education and Measurement of the Program's Effects (영아 수면건강 교육프로그램의 개발 및 효과)

  • Jang, Sook;Kim, Il-Ok
    • Child Health Nursing Research
    • /
    • v.21 no.1
    • /
    • pp.11-19
    • /
    • 2015
  • Purpose: The purposes of this study were to develop an infant sleep health education program using a video for SIDS prevention education and to measure the effects of the program. Methods: The infant sleep health education program consisted of presentations and motor images. The formation of educational material was directed by the systematic design of instruction. Participants in this study were 59 primiparous women from postpartum care centers. The instruments used in this study were criterion referenced test items for knowledge about infant sleep health and confidence inventory. Experimental group I was given the treatment of infant sleep health education program. Experimental group II was given the program using a video reinforcement after 2 weeks. On the other hand, control group was given no treatment. Results: There was a significant increase in knowledge and confidence in the performance of mother's roles of both experimental group I and experimental group II over the control group. No significant difference was founds for knowledge and confidence in the performance of mother's roles between experimental group I and II. Conclusion: The results indicate that this program is a very effective intervention for better sleep health in infants by helping the mothers increase confidence in their role performance.

Neuroprotective Effects of Parkin and Bcl-2 against Dieldrin-induced Endoplasmic Reticulum Stress (디엘드린 유도성 소포체 스트레스에서의 parkin과 Bcl-2의 신경보호 효과)

  • Seo, Jeong-Yeon;Kim, Jae-Sung;Kim, Do Kyung;Chun, Hong Sung
    • Journal of Life Science
    • /
    • v.32 no.10
    • /
    • pp.771-777
    • /
    • 2022
  • Dopaminergic (DA) cell death in Parkinson's disease (PD) has been attributed to multiple, distinct genetic and environmental factors. In rare familial PD loss of parkin function mutations play a key role in nigral DA neuron-specific pathogenesis primarily via endoplasmic reticulum (ER) stress. In more prevalent sporadic PD, environmental exposure to pesticides has a significant epidemiological role. However, it is largely unknown how environmental exposure to xenobiotics is etiologically linked with the known etiology in familial PD. In the present study biochemical evidence for a common pathogenic mechanism between sporadic and familial PD has been identified employing the recently characterized mesencephalic DA cell line, N27-A. Dieldrin, an organochlorine pesticide epidemiologically implicated in sporadic PD, induced the markers of ER stress response such as a chaperone BiP/Grp78, heme oxygenase-1 and especially, parkin. Accordingly, dieldrin activated the ER resident Caspase-12, a mediator of ER stress-specific apoptosis, during cell death of N27-A cells. Of great interest the dieldrin-induced DA neuronal cell death was synergistically rescued by the overexpression of ER resident neuroprotective proteins, parkin and Bcl-2. The present findings implicate that accumulation of ER stress could be one of common pathogenic mechanisms in idiopathic and familial PD, and some ER proteins, such as parkin and Bcl-2 may effectively attenuate ER stress-mediated N27-A DA cell death.

Generation of a transgenic mouse model to study cranial suture development; Apert syndrome (두개봉합 발육 연구를 위한 형질변환 쥐의 개발 : 어퍼트 신드롬)

  • Lee, Kee-Joon;Ratisoontorn, Chootima;Baik, Hyoung-Seon;Park, Young-Chel;Park, Kwang-Kyun;Nah, Hyun-Duck
    • The korean journal of orthodontics
    • /
    • v.33 no.6 s.101
    • /
    • pp.485-497
    • /
    • 2003
  • The form and function of the craniofacial structure critically depend on genetic information. With recent advances in the molecular technology, genes that are important for normal growth and morphogenesis of the craniofacial skeleton are being rapidly uncovered, shaping up modem craniofacial biology. One of them is fibroblast growth factor receptor 2 (FGFR2). Specific point mutations in the. FGFR2 gene have been linked to Apert syndrome, which is characterized by premature closure of cranial sutures and craniofacial anomalies as well as limb deformities. To study pathogenic mechanisms underlying craniosynostosis phenotype of Apert syndrome, we used a transgenic approach; an FGFR2 minigene construct containing an Apert mutation (a point mutation that substitute proline at the position 253 to arginine; P253R) was introduced into fertilized mouse germ cells by DNA microinjection. The injected cells were then allowed to develop into transgenic mice. We used a bone-specific promoter (a DNA fragment from the type I collagen gene) to confine the expression of mutant FGFR2 gene to the bone tissue, and asked whether expression of mutant FGFR2 in bone is sufficient to cause the craniosynostosis phenotype in mice. Initial characterization of these mice shows prematurely closed cranial sutures with facial deformities expected from Apert patients. We also demonstrate that the transgene produces mutant FGFR2 protein with increased functional activities. Having this useful mouse model, we now can ask questions regarding the role of FGFR2 in normal and abnormal development of cranial bones and sutures.