• Title/Summary/Keyword: Primate

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Comparative Anatomic Structures of Nonhuman Primate Lungs 2. Tracheobronchial Geometry and Lung Lobe Weight (영장동물폐(靈長動物肺)의 비교해부학적연구(比較解剖學的硏究) 2. 기관(氣管) 및 기관지(氣管枝)의 기하학적계측(幾何學的計測)과 폐중량(肺重量)에 관(關)한 연구(硏究))

  • Kim, Moo Gang;Kim, James C.S.
    • Korean Journal of Veterinary Research
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    • v.19 no.1
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    • pp.9-15
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    • 1979
  • Anatomical measurements were made at the necoropsy and sacrifice in a group of 41 adult female Rhesus monkey to determine the 34 characteristcs found in tracheas snd bronchus. Table 1, 2, 3, 4, and figure 1 were therefore prepared as a guide in the further use for illustrating monkey lung research. Summary of this report is as follows: 1. Accurate Knowledge of these measurements may have some value in pulmonary dissection and reconstructive procedures. 2. These studies may provide a more accurate determination of the monkey lungs. 3. The right and left bronchus length of the monkey is shorter than fornd in man. 4. The left bronchus length is more longer than the rrght bronchas. 5. There were large variation among the weight of adult female Rhesus monkey.

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Role of gangliosides in the differentiation of human mesenchymal-derived stem cells into osteoblasts and neuronal cells

  • Moussavou, Ghislain;Kwak, Dong Hoon;Lim, Malg-Um;Kim, Ji-Su;Kim, Sun-Uk;Chang, Kyu-Tae;Choo, Young-Kug
    • BMB Reports
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    • v.46 no.11
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    • pp.527-532
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    • 2013
  • Gangliosides are complex glycosphingolipids that are the major component of cytoplasmic cell membranes, and play a role in the control of biological processes. Human mesenchymal stem cells (hMSCs) have received considerable attention as alternative sources of adult stem cells because of their potential to differentiate into multiple cell lineages. In this study, we focus on various functional roles of gangliosides in the differentiation of hMSCs into osteoblasts or neuronal cells. A relationship between gangliosides and epidermal growth factor receptor (EGFR) activation during osteoblastic differentiation of hMSCs was observed, and the gangliosides may play a major role in the regulation of the differentiation. The roles of gangliosides in osteoblast differentiation are dependent on the origin of hMSCs. The reduction of ganglioside biosynthesis inhibited the neuronal differentiation of hMSCs during an early stage of the differentiation process, and the ganglioside expression can be used as a marker for the identification of neuronal differentiation from hMSCs.

Molecular Characterization of the HERV-W Env Gene in Humans and Primates: Expression, FISH, Phylogeny, and Evolution

  • Kim, Heui-Soo;Kim, Dae-Soo;Huh, Jae-Won;Ahn, Kung;Yi, Joo-Mi;Lee, Ja-Rang;Hirai, Hirohisa
    • Molecules and Cells
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    • v.26 no.1
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    • pp.53-60
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    • 2008
  • We characterized the human endogenous retrovirus (HERV-W) family in humans and primates. In silico expression data indicated that 22 complete HERV-W families from human chromosomes 1-3, 5-8, 10-12, 15, 19, and X are randomly expressed in various tissues. Quantitative real-time RT-PCR analysis of the HERV-W env gene derived from human chromosome 7q21.2 indicated predominant expression in the human placenta. Several copies of repeat sequences (SINE, LINE, LTR, simple repeat) were detected within the complete or processed pseudo HERV-W of the human, chimpanzee, and rhesus monkey. Compared to other regions (5'LTR, Gag, Gag-Pol, Env, 3'LTR), the repeat family has been mainly integrated into the region spanning the 5'LTRs of Gag (1398 bp) and Pol (3242 bp). FISH detected the HERV-W probe (fosWE1) derived from a gorilla fosmid library in the metaphase chromosomes of all primates (five hominoids, three Old World monkeys, two New World monkeys, and one prosimian), but not in Tupaia. This finding was supported by molecular clock and phylogeny data using the divergence values of the complete HERV-W LTR elements. The data suggested that the HERV-W family was integrated into the primate genome approximately 63 million years (Myr) ago, and evolved independently during the course of primate radiation.

Enhancer Function of MicroRNA-3681 Derived from Long Terminal Repeats Represses the Activity of Variable Number Tandem Repeats in the 3' UTR of SHISA7

  • Lee, Hee-Eun;Park, Sang-Je;Huh, Jae-Won;Imai, Hiroo;Kim, Heui-Soo
    • Molecules and Cells
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    • v.43 no.7
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    • pp.607-618
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    • 2020
  • microRNAs (miRNAs) are non-coding RNA molecules involved in the regulation of gene expression. miRNAs inhibit gene expression by binding to the 3' untranslated region (UTR) of their target gene. miRNAs can originate from transposable elements (TEs), which comprise approximately half of the eukaryotic genome and one type of TE, called the long terminal repeat (LTR) is found in class of retrotransposons. Amongst the miRNAs derived from LTR, hsa-miR-3681 was chosen and analyzed using bioinformatics tools and experimental analysis. Studies on hsa-miR-3681 have been scarce and this study provides the relative expression analysis of hsa-miR-3681-5p from humans, chimpanzees, crab-eating monkeys, and mice. Luciferase assay for hsa-miR-3681-5p and its target gene SHISA7 supports our hypothesis that the number of miRNA binding sites affects target gene expression. Especially, the variable number tandem repeat (VNTR) and hsa-miR-3681-5p share the binding sites in the 3' UTR of SHISA7, which leads the enhancer function of hsamiR-3681-5p to inhibit the activity of VNTR. In conclusion, hsa-miR-3681-5p acts as a super-enhancer and the enhancer function of hsa-miR-3681-5p acts as a repressor of VNTR activity in the 3' UTR of SHISA7.

Effects of Newly Synthesized Recombinant Human Amyloid-β Complexes and Poly-Amyloid-β Fibers on Cell Apoptosis and Cognitive Decline

  • Park, Soojin;Huh, Jae-Won;Eom, Taekil;Park, Naeun;Lee, Youngjeon;Kim, Ju-Sung;Kim, Sun-Uk;Shim, Insop;Lee, Sang-Rae;Kim, Ekyune
    • Journal of Microbiology and Biotechnology
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    • v.27 no.11
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    • pp.2044-2051
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    • 2017
  • The main pathological hallmark of Alzheimer's disease is the deposition of amyloid-beta ($A{\beta}$) peptides in the brain. $A{\beta}$ has been widely used to mimic several aspects of Alzheimer's disease. However, several characteristics of amyloid-induced Alzheimer's disease pathology are not well established, especially in mice. The present study aimed to develop a new Alzheimer's disease model by investigating how $A{\beta}$ can be effectively aggregated using prokaryotes and eukaryotes. To express the $A{\beta}42$ complex in HEK293 cells, we cloned the $A{\beta}42$ region in a tandem repeat and incorporated the resulting construct into a eukaryotic expression vector. Following transfection into HEK293 cells via lipofection, cell viability assay and western blotting analysis revealed that exogenous $A{\beta}42$ can induce cell death and apoptosis. In addition, recombinant His-tagged $A{\beta}42$ was successfully expressed in Escherichia coli BL21 (DE3) and not only readily formed $A{\beta}$ complexes, but also inhibited the proliferation of SH-SY5Y cells and E. coli. For in vivo testing, recombinant His-tagged $A{\beta}42$ solution ($3{\mu}g/{\mu}l$ in $1{\times}PBS$ containing $1mM\;Ni^{2+}$) was injected stereotaxically into the left and right lateral ventricles of the brains of C57BL/6J mice (n = 8). Control mice were injected with $1{\times}PBS$ containing $1mM\;Ni^{2+}$ following the same procedure. Ten days after the sample injection, the Morris water maze test confirmed that exogenous $A{\beta}$ caused an increase in memory loss. These findings demonstrated that $Ni^{2+}$ is capable of complexing the 50-kDa amyloid and that intracerebroventricular injection of $A{\beta}42$ can lead to cognitive impairment, thereby providing improved Alzheimer's disease models.