• Journal of Life Science
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• v.25 no.1
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• pp.101-112
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• 2015

A type of cell junction that is formed between different parts within the same cell is called autotypic cell junction. Autotypic junction proteins form tight junctions found between membrane lamellae of a cell, especially in myelinating glial cells. Some of them have postsynaptic density-95/disks large/zonula occludens-1 (PDZ) domains, which interact with the carboxyl (C)-terminal PDZ-binding motif of other proteins. PDZ domains are protein-protein interaction modules that play a role in protein complex assembly. The PDZ domain, which is widespread in bacteria, plants, yeast, metazoans, and Drosophila, allows the assembly of large multi-protein complexes. The multi-protein complexes act in intracellular signal transduction, protein targeting, and membrane polarization. The identified PDZ domain-containing proteins located at autotypic junctions include zonula occludens-1 (ZO-1), ZO-2, pals-1-associated tight junction protein (PATJ), multi-PDZ domain proteins (MUPPs), membrane-associated guanylate kinase inverted 2 (MAGI2), and protease-activated receptor (PAR)-3. PAR-3 interacts with atypical protein kinase C and PAR-6, forming a ternary complex, which plays an important role in the regulation of cell polarity. MAGI2 interacts with ${\alpha}$-amino-3-hydroxyl-5-methyl-4-isoxazole propionate (AMPA) receptor at excitatory synapses. PATJ is detected in paranodal loops associated with claudin-1. On the other hand, MUPP1 is found in mesaxons and Schmidt-Lanterman incisures with claudin-5. ZO-1, ZO-2, and PAR-3 are found at all three sites. Different distributions of PDZ domain-containing proteins affect the development of autotypic junctions. In this review, we will describe PDZ domain-containing proteins at autotypic tight junctions in myelinating Schwann cells and their roles.

• Korean Journal of Veterinary Research
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• v.28 no.1
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• pp.125-135
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• 1988

Attempts of these studies were made to investigate the nonspecific congenital focal accumulation of ectodermal glial cells in the brain of normal piglets. The brain samples were taken from 1-,10-,20-,35-,45- and 70-day-old piglets from a SPF-pig farm and three model pig farms. Occurrences of neuroglial cell foci (NCF) on the brain were observed with light microscope. Appearance degrees of the congenital NCF on 10 to 16 cross section slides per a piglets brain were tentatively designed on a scale from degree+ to ⧻by NCF number: +, less than 20 of NCF number; ⧺, 21-40 of NCF number: ⧻, more than 41 of NCF number. The results obtained were as follows: 1. NCF in the brain were observed mainly on the cerebrum. Regions of higher frequencies on the cerebrum were ordered as subependymal layers of the lateral ventricles, peripheral regions of lateral ventricles in the white matter and some neuron layers under the molecular layer of the gray matter. But NCF were not observed in the cerebellum, pons, medulla oblongata and spinal cords. 2. On the subependymal layers of the lateral ventricles, NCF were observed in 100% of 27 piglets, and appearance degree of ⧻ was observed in 10 piglets(37.0%), ⧺ in 10 piglets(37.0%) and + in 7 Piglets(26.0%) of 27 piglets, respectively. 3. On the white matter of the cerebrum, NCF were observed in 25 piglets(92.6%) of 27 piglets, and appearance degree of ⧻ was observed in 3 piglets(11.1%), ⧺ in 13 piglets(48.2%), + in 9 piglets(33.3%) and - in 2 piglets(7.4%) of 27 piglets, respectively. 4. On the gray matter of the cerebrum, NCF were observed in 21 piglets(77.8%) of 27 piglets, and appearance degree of ⧻ was not observed, appearance degree of ⧺ was observed in 6 piglets(22.2%), + in 15 Piglets(55.6%) and - in 6 piglets(22.2%) of 27 Piglets, respectively. 5. NCF tended to be converged appearance on some regions and tended to be decreased markedly from 35th day after birth, and the shapes of NCF were: global or oval forms crowded by analogous shaped and stained cells in the empty spaces of the brain substrate or on one side of the blood vessels.

• The Journal of Internal Korean Medicine
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• v.34 no.2
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• pp.178-191
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• 2013

Objectives : In this study, we made an effort to investigate the protective mechanism of Ukgan-san (UGS) extracts on hypoxia-induced C6 glial cell death. Methods : The cell viability was assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MMT) assay and cell morphological changes were analysed with microscope after staining with crystal violet (CV). Reactive oxygen species (ROS) formation was assessed by flow cytometer after staining with 2'7'-dichlorofluorescein diacetate (DCF-DA). We also analyzed expression of hypoxia-inducible factor-1 alpha (HIF-$1{\alpha}$) and p53, processing of procaspase-3 and procyclic acidic repetitive protein (PARP) by western blot method. Results : We estimated the elevated cell viability by UGS extract on $CoCl_2$-induced C6 glial cells. UGS attenuated $CoCl_2$-induced ROS formation in C6 glial cells and also showed a protective activity compared to antioxidants and exhibited abrogation of LDH-released by $CoCl_2$. UGS suppressed the typical apoptotic cell death markers, caspase-3 and PARP activation. UGS inhibited $CoCl_2$-induced HIF-1${\alpha}$ expression which is known as a major regulator for hypoxia-induced cell death, and suppressed p53 expression. Conclusions : These results suggest that UGS extract contains protective constituents for hypoxia-induced C6 glial cell death.

• The Korean Journal of Nuclear Medicine
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• v.34 no.5
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• pp.371-380
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• 2000

Purpose: Thallim-201 ($^{201}Tl$) brain SPECT, which can represent cellular activity of brain lesions, may provide more useful information in differentiating between benign and malignant brain lesions more so than CT of MRI, that merely represents anatomic changes or breakdown of blood brain barrier. We used $^{201}Tl$ brain SPECT prospectively to evaluate the utility of $^{201}Tl$-indices as an indicator of benign or malig nant lesions. Materials and Methods: We studied 28 patients. There were 13 cases of benign lesions (3: nonspecific benign lesion, 3: meningioma, 2: low grade glioma, 1: tuberculoma, central neurocytoma, hemangioblastoma, radiation necrosis, and choroid plexus papilloma) and 15 cases of malignant lesions (6: glioblastoma multiforme, 5: anaplastic glioma, 2: medulloblastoma, 1: metastasis and lymphoma). In all patients, CT and/or MRI were obtained and then $^{201}Tl$ brain SPECT was obtained with measuring mean $^{201}Tl$ index and peak $^{201}Tl$ index. An unpaired t-test was performed to compare the $^{201}Tl$-indices and pathologic diagnoses to evaluate the utility of $^{201}Tl$-indices as all indicator of benign or malignant lesions. Results: There were no statistically significant difference in $^{201}Tl$-indices between benign and malignant brain lesion (p>0.05). Conclusion: These results demonstrated that we could not use $^{201}Tl$ indices on brain SPECT alone as an indicator of benign or malignant brain lesions.

• Proceedings of the KOR-BRONCHOESO Conference
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• 1993.05a
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• pp.97-97
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• 1993

Primary tumor arises infrequently in the parotid gland and generally, only about 20 to 40 percent of which prove to be malignant. They are characterized by histopathologic diversity, slow tumor growth, significant proportion of patients who have received previous treatment elsewhere. We have reviewed retrospectively 101 cases of parotid gland tumors which were treated for the recent eight years (1985-1992), Non-neoplastic tumor-like lesions were all excluded.

• Journal of Korean Neurosurgical Society
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• v.30 no.6
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• pp.688-698
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• 2001

Objectives : Parkinson's disease is a well-known neurodegenerative disease characterized by dopaminergic cell death in the substantia nigra. The reactive gliosis by activated astrocytes and microglias is no more regarded as a simple sequel of neuronal cell death. Microglial activation takes place in a stereotypic pattern with graded morphologic and functional(resting, activated and phagocytic) changes. In Parkinson's disease animal model, the degree of microglial activation along the nigro-striatal dopaminergic tract has not been studied intensively. The purpose of this study was to elucidate the characteristics of microglial reaction and to grade its degree of activation at substantia nigra and corpus striatum using 6-hydroxydopamine induced rat model of Parkinson's disease. Methods : Using Sprague-Dawley rat, parkinsonian model was made by 6-hydroxydopamine(OHDA) induced destruction of medial and lateral substantia nigra(SN). The rat was sacrificed 3-, 5-, 7-, 14- and 21-day-after operation. For control group, we injected saline with same manner and sacrificed 3-day after operation. With immunohistochemistry, we examined dopaminergic neuronal cells and microglial expression using tyrosine hydroxylase (TH) and OX-42 antibodies, respectively. Also we performed in situ hybridization for osteopontin, a possible marker of subset in activated microglia. Results : 1) In lesioned side of substantia nigra and corpus striatum, the TH immunoreactivity was markedly decreased in whole experimental groups. 2) Using optical densitometry, microglia induced immunoreactivity of OX-42 was counted at SN and corpus striatum. At SN, it was increased significantly on the lesioned side in control and all time-dependent experimental groups. At striatum, it was increased significantly in post lesion 3-day group only(p <0.05). Compared to control group, immunoreactivity of OX-42 on lesioned side was increased in groups, except post lesion 21-day group, at SN. Only post lesion 3-day group showed significance at striatum(p <0.05). Compared to SN region, immunoreactivity of OX-42 was much weaker in striatum. 3) Microscopically, the microglias showed typically different activation pattern. At SN, numerous phagocytic microglias were found at pars compacta and reticularis of lesion side. At striatum, no phagocytic form was found and the intensity of staining was much weaker. 4) At SN, the immunoreactivity of osteopontin showed definite laterality and it was markedly increased at pars compacta of lesion side with relatively short duration time. At striatum, however, it was not detected by in situ hybridization technique. Conclusion : The nigral 6-OHDA induced rat model of Parkinson's disease revealed several characteristic patterns of microglial reaction. At SN, microglias was activated shortly after direct neuronal damage and maintained for about three weeks. In contrast, despite of sufficient dopaminergic insufficiency at striatum, activation of microglias was trivial, and distinguished 3 day later. Antegrade slow neuronal degeneration is major pathophysiology in striatal dopaminergic deficiency. So, the acuteness of neuronal damage and consequential degree of neuronal degeneration may be important factor for microglial activation in neurodegenerative diseases such as Parkinson's disease. Additionally, osteopontin may be a possible marker for several subsets of activated microglia, possibly the phagocytic form.

• Radiation Oncology Journal
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• v.9 no.1
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• pp.27-35
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• 1991

An interstitial radiofrequency needle electrode system was constructed for interstitial heating of brain tissue. Radiofrequency electrodes with Thermotron RF 8 were tested in an agar phantom and in a normal canine brain to determine how variations in physical factors affected temperature distributions. Temperature distributions were checked after heating with 1 mm diameter needle electrode implants on the corners of 1 and 2 cm squares in a phantom and plot isotherms for various electrodes arrangement. We observed that the 1 cm square array would heat a volume with a 1.25 cm radius circular field cross section to therapeutic temperatures ($90\%$ relative SAR using Tm) and the 2 cm square array with a 1.75 cm radius rectangular field with central inhomogeneity. With 2 cm long electrode implants, we observed that the 1 cm square array would heat a 3 cm long sagittal section to therapeutic temperature ($90\%$ relative SAR using Tm). We found that radiofrequency electrodes could be selected to match the length of the heating area without affecting its performance. The histopathological changes associated with RF heating of normal canine brains have been correlated with thermal distributions. RF needle electrode heating was applied for 50min to generate tissue temperatures of $43^{\circ}C$. We obtained a quarter of the heated tissue material immediately after heating and sacrificed at intervals from $7\sim30$days. The acute stage (immediately after heating) was demonstrated by liquefactive necrosis, pyknosis of neuronal element in the gray matter and by some polymer-phonuclear leukocytes infiltration. The appearance of lipid-laden macrophages surrounding the area of liquefaction necrosis was demonstrated in all three sacrificed dogs. Mild gliosis occurring around the necrosis was demonstrated in the last sacrificed (Days 30) canine brain.

• Radiation Oncology Journal
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• v.11 no.2
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• pp.249-258
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• 1993

Between March 1983 and December 1989, ninety-six patients with intracranial glioma were treated in the Department of Therapeutic Radiology, Kangnam St. Mary's Hospital, Catholic University Medical College. We retrospectively reviewed each case to evaluate variable factors influencing the treatment results and to develop an optimal therapy Policy. Median follow-up is 57 months (range: 31~133 months). Of the 96 patients, 60 $(63\%)$ were males and 36 $(37\%)$ were females. Ages ranged from 3 to 69 years (median 42 years). The most common presenting symtoms were headeche $(67\%)$ followed by cerebral motor and sensory discrepancy $(54\%),$ nausea and vomiting $(34\%),$ seizure $(19\%),$ mental change $(10\%)$ and memory and calculation impairment $(8\%).$ Eighty five $(88.5\%)$ patients all, except 11 $(11.5\%)$ brain stem lesions, were biopsy proven intracranial glioma. The distribution by histologic type was 64 astrocytomas $(75\%),$ 4 mixed oligoastrocytomas $(5\%),$ and 17 oligodendrogliomas $(20\%).$ Fourty nine patients $(58\%$ were grade I, II histology and 36 $(42\%)$ patients were grade III, IV histology. Of the 96 patients, 64 $(67\%)$ recieved postoperative RT and 32 $(33\%)$ were treated with primary radiotherapy. Gross total resection was peformed in 14 $(16\%)$ patients, subtotal resection En 29 $(34\%),$ partial resection in 21 $(25\%),$ and biopsy only in 21 $(25\%).$ Median survival time was 53 months (range 2~ 133 months), and 2- and, 5-year survival rate were $69\%,49\%$ respectively. 5-year survival rate by histologic grade was grade I, $70\%,$ grade II, $58\%,$ grade III, $28\%,$ and grade IV, $15\%.$ Multivariated analysis demonstrate that age at diagnosis (p=0.0121), Karnofsky performance Status (KPS) (p=0.0002), histologic grade (p=0.0001), postoperative radiation therapy (p=0.0278), surgical extent (p =0.024), cerebellar location of tumor (p=0.0095) were significant prognostic factors influencing on survival.