• The Korean Journal of Zoology
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• v.38 no.4
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• pp.542-549
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• 1995

The effect of extraceflular matrix (ECM) protein on the neuronai differentiation of SI(-N-SH and IMR-32 human neuroblastoma cell lines was examined. When ceils were cultured on the laminin/collagen coated plate for 7 days, the extensive neurite outgrowth was observed In IMR-32. To address the reason why IMR-32 cell llne did not respond to ECM proteins, the ECM mediated early signalling mechanisms were analysed in both SK-N-SH and IMR-32. When cells were plated on the laminin/collagen coated plates, tyrosine phosphorylated proteins were Increased within an hour In both of these cells. Moreover, the foaal adhesion IlInase (FAK) was tyrosine phosphorylated in both of these two cell lines. These results suggest that the ECM mediated early signalling mechanism was normal in IMR-32 cell line. The expression of both NSE and Bcl-2 was increased by ECM treatment in SK-N-SH. However, these components were not changed by ECM In IMR 32 cells to ECM component Is likely due to the abnomality of the transcriptional regulation mechanism which Is responsible for the neuronal differentiation.

• Biomedical Science Letters
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• v.3 no.1
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• pp.11-20
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• 1997

A regulation of differentiation in human neuroblastoma cells remains poorly understood, although it is of great importance in the clinical therapy of neuroblastoma. This study was aimed to elucidate effects of DNA synthesis inhibitors on the differentiation of neuroblastoma cells on the basis of morphological, biochemical and molecular respects. Three DNA synthesis inhibitors, sodium butyrate, hydroxyurea, cytosine arabinoside were used to explore their effects on the cellular morphology, the expression of c-myc and the elevation of choline acetyltransferase activity. They led to the extension or neurite-like processes reflecting differentiation or IMR-32 cells. In addition, the treatment of three DNA synthesis inhibitors resulted in the remarkable increases in the expression of c-myc as well as the stimulation of choline acetyltransferase activity which is involved in the synthesis of acetylcholine in the differentiated cholinergic neurons. Taken together, these results indicate that DNA synthesis inhibitors play an important role in the induction of cellular differentiation in IMR-32 cells. Furthermore these DNA synthesis inhibitors seem to be future useful to give an important clue (for the treatment of neuroblastoma).

• Biomolecules & Therapeutics
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• v.14 no.3
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• pp.137-142
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• 2006

Apigenin, a natural flavonoid found in a variety of vegetables and fruits, has been shown to possess many biological functions. In this study we investigated the role of apigenin in the production of reactive oxygen species (ROS) through the modulation of activity of $K^+-Cl^-$-cotransport (KCC) in IMR-32 human neuroblastoma cells. Apigenin induced $Cl^-$-dependent $K^+$ efflux, a hallmark of KCC activity, which was markedly prevented by different kinds of KCC inhibitors (calyculin-A, genistein and $BaCl_2$). These results indicate that KCC is functionally present, and activated by apigenin in the IMR-32 cells. Treatment with apigenin also induced a sustained increase in the level of intracellular ROS. The KCC inhibitors also significantly inhibited the apigenin-induced ROS generation. Taken together, these results suggest that apigenin can modulate ROS generation through the activation of a membrane ion transporter, KCC. These results further suggest that the alteration of KCC activity may play a role in the mechanism of degenerative diseases and/or carcinogenesis in neuronal tissues through the regulation of ROS production.

• Journal of Genetic Medicine
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• v.1 no.1
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• pp.45-50
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• 1997

Neuroblastoma, a pediatric malignant neoplasm of neural crest origin, has a wide range of clinical virulence. The mechanisms contributing to the development of neuroblastomas are largely unclear, but non-random chromosomal changes identified over the past years suggest the involvement of genetic alterations. Amplification of the human N-myc proto-oncogene is frequently seen either in extrachromosomal double minutes or in homogeneously staining regions (HSRs) of aggressively growing neuroblastomas. N-myc maps to chromosome 2 band 24, but HSR have never been observed at this band, suggesting transposition of N-myc during amplification. We have constructed and analyzed the region-specific painting probe for HSR in neuroblastoma IMR-32 to determine the derivative chromosomes. Microdissection was performed on HSR using an inverted microscope with the help of microglass needles and an micromanipulator. We pretreated the microdissected fragments with Topoisomerase I which catalyzes the relaxation of supercolled DNA, and performed two initial rounds of DNA synthesis with T7 DNA polymerase followed by conventional PCR to enable the reliable preparation of Fluorescent in situ hybridization probe from a single microdissected chromosome. With this method, it was possible to construct the region-specific painting probe for HSR. The probe hybridized specifically to the HSRs of IMR-32, and to 2p24, 2p13 of normal chromosome. Our results suggest there was coamplification of N-myc together with DNA of the chromosome 2p24 and 2p13. Moreover, the fluorescent signals for the amplified chromosomal regions in IMR-32 cells were also easily recognized at a Thus this painting probe can be applied to detect the similar amplification of N-myc in neuroblastoma tissue, and the probe pool for HSR may be used to identify the cancer-relevant genes.

• Progress in Medical Physics
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• v.32 no.4
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• pp.92-98
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• 2021

Purpose: This study automatically discriminates homogeneous and structure edge regions on computed tomography (CT) images, and it evaluates the noise level and edge preservation ratio (EPR) according to the different types of iterative reconstruction (IR). Methods: The dataset consisted of CT scans of 10 patients reconstructed with filtered back projection (FBP), statistical IR (iDose⁴), and iterative model-based reconstruction (IMR). Using the 10th and 85th percentiles of the structure coherence feature, homogeneous and structure edge regions were localized. The noise level was estimated using the averages of the standard deviations for five regions of interests (ROIs), and the EPR was calculated as the ratio of standard deviations between homogeneous and structural edge regions on subtraction CT between the FBP and IR. Results: The noise levels were 20.86±1.77 Hounsfield unit (HU), 13.50±1.14 HU, and 7.70±0.46 HU for FBP, iDose⁴, and IMR, respectively, which indicates that iDose⁴ and IMR could achieve noise reductions of approximately 35.17% and 62.97%, respectively. The EPR had values of 1.14±0.48 and 1.22±0.51 for iDose⁴ and IMR, respectively. Conclusions: The iDose⁴ and IMR algorithms can effectively reduce noise levels while maintaining the anatomical structure. This study suggested automated evaluation measurements of noise levels and EPRs, which are important aspects in CT image quality with patients' cases of FBP, iDose⁴, and IMR. We expect that the inclusion of other important image quality indices with a greater number of patients' cases will enable the establishment of integrated platforms for monitoring both CT image quality and radiation dose.

• Animal cells and systems
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• v.9 no.4
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• pp.191-198
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• 2005

The effects of 6-aminonicotinamide (6-AN) on viability of IMR32 neuroblastoma cells in the presence of ATP or $NAD^+$ have been investigated. 6-AN caused marked reduction in cell viability and similar observations were also made with cells treated with 6-AN+ATP. However, cells treated with $6-AN+NAD^+$ showed cell viability similar to untreated cells. Morphologically, 6-AN and 6-AN+ATP treated cells showed loss of neurites, polyhedric shapes, shrinkage of cell bodies and formation of lysed cells, while $6-AN+NAD^+$ cells did not show any such changes. The flow cytometry analysis demonstrated that 6-AN increased cell population in $G_0/G_1$ phase and decreased cell population in Sand $G_2/M$ phase following a 72 h exposure. Western blot analysis showed that 6-AN stimulated a substantial increase in the level of the cdk inhibitor $p27^{kip1}$, but lowered the levels of cdk2, cyclin E and p-Rb. However, cdc25A and p53R2 were not significantly affected. Immunofluorscence staining of $p27^{kip1}$, cdk2, cyclin E and p-Rb revealed close correlation between the signal observed in the Western blot analysis. 6AN+ATP treated cells showed similar results obtained with 6-AN treated cells in expression of cdk2, cyclin E, p-Rb proteins and $p27^{kip1}$, $6-AN+NAD^+$ cells showed greater expression of cdk2, cyclin E and p-Rb than those in 6-AN and 6-AN+ATP treated cells. The results suggest that 6-AN induced the $G_0/G_1$ phase arrest in IMR32 neuroblastoma cell lines through the increase of $p27^{kip1}$ and the decrease of cdk2, cyclin E and p-Rb.

• Neonatal Medicine
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• v.18 no.2
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• pp.182-188
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• 2011

Purpose: Recently in Korea, there have been significant improvements in neonatal mortality rate (NMR) and infant mortality rate (IMR). This study aimed to investigate the proportion of the NMR among IMR, with the goal of discerning the influence of improved NMR on the reduction of IMR in the last 5 years in Korea. Methods: All data were from Statistics Korea. Changes in the NMR percentage among IMR and the percentage of the death by the distribution of the birth weight and gestational were investigated. Results: The total birth rate decreased, but the total number of preterm and low birth weight infants increased. These was a large decrease in NMR and IMR. The proportion of NMR among INR exceeded 50%. Early NMR was higher than late NMR. Among the total infant death, the mortality of preterm and low birth weight infants was high. Conclusion: Between 2005 and 2009, the total birth has declined in Korea, but the frequency of low birth weight infants is trending upward. The improvements in NMR and IMR, and the downtrend of the NMR percentage in IMR, are encouraging. It seems that the continued decrease of mortality of preterm and LBWI is required for better improvements NMR and IMR in Korea. This result is expected to be used for the basic data to improve the management of the newborns in Korea.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.1
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• pp.19-27
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• 1999

Apoptosis has been implicated in the pathophysiological mechanisms of various neurodegenerative diseases. In a variety of cell types, oxidative stress has been demonstrated to play an important role in the apoptotic cell death. However, the exact mechanism of oxidative stress-induced apoptosis in neuronal cells is not known. In this study, we induced oxidative stress in IMR-32 human neuroblastoma cells with tert- butylhydroperoxide (TBHP), which was confirmed by significantly reduced glutathione content and glutathione reductase activity, and increased glutathione peroxidase activity. TBHP induced decrease in cell viability and increase in DNA fragmentation, a hallmark of apoptosis, in a dose-dependent manner. TBHP also induced a sustained increase in intracellular $Ca^{2+}$ concentration, which was completely prevented either by EGTA, an extracellular $Ca^{2+}$ chelator or by flufenamic acid (FA), a non-selective cation channel (NSCC) blocker. These results indicate that the TBHP-induced intracellular $Ca^{2+}$ increase may be due to $Ca^{2+}$ influx through the activation of NSCCs. In addition, treatment with either an intracellular $Ca^{2+}$ chelator (BAPTA/AM) or FA significantly suppressed the TBHP-induced apoptosis. Moreover, TBHP increased the expression of p53 gene but decreased c-myc gene expression. Taken together, these results suggest that the oxidative stress-induced apoptosis in neuronal cells may be mediated through the activation of intracellular $Ca^{2+}$ signals and altered expression of p53 and c-myc.

• Women's Health Nursing
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• v.27 no.4
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• pp.286-296
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• 2021

Purpose: This study compared infant mortality and its associated factors between Korean and immigrant women using vital statistics gathered by Statistics Korea. Methods: Birth and death statistics from the period between 2009 and 2019 were extracted from the census of population dynamics data of the Microdata Integrated Service, Korea. Statistical data were derived from a complete survey and infant mortality was analyzed from mortality statistics data. Descriptive statistics were used for comparison. Results: The average infant mortality rate (IMR) of Korean women was 2.7 in Korea, which did not change significantly between 2009 and 2019; however, the IMR of immigrant women increased significantly in 2018 to 4.2 and subsequently decreased to 2.6 in 2019. Moreover, the age of Korean and immigrant women at the time of infant death gradually increased from 31.1 years and 25.9 years in 2009 to 32.8 years and 30.9 years in 2019, respectively. The gestational age was lower for deceased infants born to immigrant women (mean, 31.04 weeks; standard deviation [SD], 6.42; median, 30.00) compared to infants born to Korean women (mean, 31.71 weeks; SD, 6.48; median, 32.00). Immigrant women (91.7%) received slightly fewer antenatal care visits compared to Korean women (93.1%). Conclusion: It is vital to devise a plan to lower the IMR of immigrant women in Korea. Moreover, it is necessary to explore the factors related to infant mortality among immigrant women within the context of Korean societal situation, culture, and home environment.

• Archives of Pharmacal Research
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• v.22 no.4
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• pp.404-409
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• 1999

The inhibitory effects of the constituents of Gastrodia elata Bl. (GE) on glutamate-induced apoptosis in human neuronal cells were investigated using IMR32 human neuroblastoma cells. Glutamate (GLU) induced DNA fragmentation, a hallmark of apoptosis, in a dose-dependent manner. GLU also induced a slow and sustained increase in intracellular $Ca^{2+}$ concentration. Treatment with EGTA, an extracellular $Ca^{2+}$ chelator, in a nominal $Ca^{2+}$ -free buffer solution abolished the GLU-induced intracellular $Ca^{2+}$ increase, indicating that GLU stimulated Ca2+ influx pathway in the IMR32 cells. BAPTA, an intracellualr $Ca^{2+}$ chelator, significantly inhibited the GLU-induced apoptosis assessed by the flow cytometry measuring hypodiploid DNA content indicative of apoptosis, implying that intracellular $Ca^{2+}$ rise may mediate the apoptotic action of GLU. Vanillin (VAN) and p-hydroxybenzaldehyde(p-HB), known constituents of GE, significantly inhibited both intracellular $Ca^{2+}$ rise and apoptosis induced by GLU. These results suggest that the apoptosis-inhibitory actions of the constituents of GE may account, at least in part, for the basis of their antiepileptic activities. These results further suggest that intracelluarl $Ca^{2+}$ signaling pathway may be a molecular target of the constituents of GE.