• Maxillofacial Plastic and Reconstructive Surgery
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• v.27 no.5
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• pp.415-423
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• 2005

Distraction osteogenesis (DO) is frequently used technique in reconstruction of bony defects resulted from tumor resection, congenital deformity, and trauma in the maxillofacial region. Although the histologic and ultrastructural changes associated with distraction osteogenesis have been extensively described, the exact changing of the surrounding tissues, such as nerve tissues, were still unclear. This study observed the histological changes and the expression of nerve growth factor (NGF) in the inferior alveolar nerve (IAN) after distraction osteogenesis. Unilateral mandibular distraction (0.5 mm twice per day for 10 days) was performed in eight mongrel dogs. Two animals were sacrificed at 7, 14, 28 and 56 days after completion of distraction, respectively. The distracted IAN and contralateral control nerve were harvested and processed for histological and innunohistochemical examinations. The signs of acute nerve injuries, such as demyelination and partial discontinuation of nerver fiber, were observed in the distracted IAN on 7 and 14 days after distraction. The initial remyelination and regeneration of distracted IAN were showed at 14 days after completion of distraction. At 56 days later, the histologic features of distracted IAN was similar to those of the normal control IAN. The expression of NGF was significantly increased in most distracted nerve tissues on 7, 14 and 28 days after distraction. On 56 days after distraction, the expression of NGF returned to the normal level. This study suggested that the acute IAN injury caused by mandibular distraction were mostly recovered during consolidation period. The NGF was seemed to be induced from Schwann cell and damaged nerve tissues, and it may have important roles in the initial healing of damaged nerves.

• Clinical and Experimental Pediatrics
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• v.54 no.6
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• pp.234-240
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• 2011

Acute disseminated encephalomyelitis (ADEM) is a demyelinating disease of the central nervous system (CNS) that typically presents as a monophasic disorder associated with multifocal neurologic symptoms and encephalopathy. ADEM is considered an autoimmune disorder that is triggered by an environmental stimulus in genetically susceptible individuals. The diagnosis of ADEM is based on clinical and radiological features. Most children with ADEM initially present with fever, meningeal signs, and acute encephalopathy. The level of consciousness ranges from lethargy to frank coma. Deep and subcortical white-matter lesions and gray-matter lesions such as thalami and basal ganglia on magnetic resonance imaging (MRI) are associated with ADEM. In a child who presents with signs of encephalitis, bacterial and viral meningitis or encephalitis must be ruled out. Sequential MRI is required to confirm the diagnosis of ADEM, as relapses with the appearance of new lesions on MRI may suggest either multiphasic ADEM or multiple sclerosis (MS). Pediatric MS, defined as onset of MS before the age of 16, is being increasingly recognized. MS is characterized by recurrent episodes of demyelination in the CNS separated in space and time. The McDonald criteria for diagnosis of MS include evidence from MRI and allow the clinician to make a diagnosis of clinically definite MS on the basis of the interval preceding the development of new white matter lesions, even in the absence of new clinical findings. The most important alternative diagnosis to MS is ADEM. At the initial presentation, the 2 disorders cannot be distinguished with certainty. Therefore, prolonged follow-up is needed to establish a diagnosis.

• Korean Journal of Veterinary Pathology
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• v.2 no.2
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• pp.139-145
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• 1998

A total of 5 animals including 3 raccoons, 1 badger, and 1 fennec fox kept in outdoor exhibits at the Everland Zoological Gardens showed depression, anorexia, dyspnea, serous oculonasal discharge, diarrhea, and convulsions. All the affected animals died within 10 days after the onset of clinical signs. This outbreak lasted about 4 months. On necropsy, major gross lesions were confined to the lungs. Red to grey sublobular to lobular consolidations with various sized tan to reddish spots were observed in the lungs. Histopathologically, the pulmonary lesions were characterized by acute to subacute bronchointerstitial pneumonia with secondary bacterial or adenoviral infections. Intracytoplasmic eosinophilic inclusion bodies compatible with canine distemper virus (CDV) were found in the lung, urinary bladder, kidney, intrahepatic bile duct, stomach, small and large intestines. Multifocal areas of severe demyelination and accumulation of gitter cells or nonsuppurative inflammation were seen in the brains of 2 raccoons. CDV -specific antigens were demonstrated in the lung sections on immunofluorescent assay. The present report describes an outbreak of CDV infection in a zoo and indicates the range of susceptible zoo animal species.

• Journal of Veterinary Clinics
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• v.36 no.6
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• pp.340-344
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• 2019

A 14-month-old Thoroughbred colt with hind limbs lameness was referred to Equine Hospital of Jeju National University. During physical examination, the patient could not walk in a straight line but wobbled especially with hind limbs. He hesitated when backing and crossed hind limbs while circling tightly by protracting the outer hind limb keeping the inner hind limb stationed. Stenosis was observed between the 2nd (C2) and 3rd (C3), and the C3 and 4th (C4) cervical vertebrae on radiographs. The colt diagnosed as cervical stenotic myelopathy (CSM) based on the clinical signs and radiological findings. To confirm the diagnosis, postmortem computed tomography (CT) and histopathologic examination were performed after the euthanasia. The CT images revealed severe compression of the spinal cavity and cord between C3 and C4 cervical vertebrae. Grossly, there was compression of the spinal cord between the C3 and C4 cervical vertebrae. Histopathologically, severe axonal swelling and demyelination characterized by vacuolation and cavity formation were observed in the white matter of the spinal cord, especially in C3 and C4. CSM is problematic in the horse racing industry because of abnormal walking. This case report of CSM may offer information for diagnosis of the disease in the equine veterinary fields in the Republic of Korea.

• Journal of Korean Academy of Nursing
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• v.49 no.3
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• pp.317-328
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• 2019

Purpose: The purpose of this study was to identify the effect of ghrelin on memory impairment in a rat model of vascular dementia induced by chronic cerebral hypoperfusion. Methods: Randomized controlled groups and the posttest design were used. We established the representative animal model of vascular dementia caused by bilateral common carotid artery occlusion and administered $80{\mu}g/kg$ ghrelin intraperitoneally for 4 weeks. First, behavioral studies were performed to evaluate spatial memory. Second, we used molecular biology techniques to determine whether ghrelin ameliorates the damage to the structure and function of the white matter and hippocampus, which are crucial to learning and memory. Results: Ghrelin improved the spatial memory impairment in the Y-maze and Morris water maze test. In the white matter, demyelination and atrophy of the corpus callosum were significantly decreased in the ghrelin-treated group. In the hippocampus, ghrelin increased the length of hippocampal microvessels and reduced the microvessels pathology. Further, we confirmed angiogenesis enhancement through the fact that ghrelin treatment increased vascular endothelial growth factor (VEGF)-related protein levels, which are the most powerful mediators of angiogenesis in the hippocampus. Conclusion: We found that ghrelin affected the damaged myelin sheaths and microvessels by increasing angiogenesis, which then led to neuroprotection and improved memory function. We suggest that further studies continue to accumulate evidence of the effect of ghrelin. Further, we believe that the development of therapeutic interventions that increase ghrelin may contribute to memory improvement in patients with vascular dementia.

• Journal of Korean Society of Health-System Pharmacists
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• v.35 no.4
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• pp.430-440
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• 2018

Background : Hyponatremia is the most common electrolyte disturbance in hospitalized patients and has been associated with increased morbidity and mortality. Tolvaptan, a vasopressin receptor antagonist, is increasingly used for the treatment of euvolemic and hypervolemic hyponatremia. The aim of this study was to evaluate the effectiveness and safety of tolvaptan for the management of hyponatremia. Methods : This study was a retrospective evaluation of 106 patients who received at least one dose of tolvaptan for hyponatremia at a single tertiary academic hospital between January 2014 and June 2015. The primary endpoint was the change in serum sodium concentration after tolvaptan administration within 24 hours, with secondary endpoints of overcorrection and adverse effects. Results : The mean initial dose of tolvaptan was $20.2{\pm}7.2mg$ and the median duration of treatment was 15 days (range, 1-261 days). The maximal changes in sodium levels at 24 and 48 hours were $8.2{\pm}4.7mmol/L$ and $10.5{\pm}15.3mmol/L$, respectively. Of 99 patients in whom sodium concentrations were followed up, sodium overcorrection was observed in 26 (26.3%) patients, which was associated with concomitant use of an enzyme inhibitor (odds ratio [OR] = 4.80, 95% Cl: 1.27-18.15). However, sex, body mass index (BMI), serum albumin, a daily dose of tolvaptan, and concomitant use of hypertonic saline did not show any significant difference in overcorrection. The most commonly reported adverse effects were mild and related to aquaresis, such as polyuria, thirst, and constipation. However, severe adverse effects such as hyperkalemia, hypotension, and one death related to osmotic demyelination were also reported. Conclusions : Tolvaptan is effective for treating hyponatremia. Nevertheless, the drug should be used cautiously due to serious adverse effects related to sodium overcorrection.

• Biomolecules & Therapeutics
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• v.29 no.1
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• pp.83-89
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• 2021

Multiple system atrophy (MSA) is a neurodegenerative disease characterized by presence of α-synuclein-positive inclusions in the cytoplasm of oligodendrocytes. These glial cytoplasmic inclusions (GCIs) are considered an integral part of the pathogenesis of MSA, leading to demyelination and neuronal demise. What is most puzzling in the research fields of GCIs is the origin of α-synuclein aggregates in GCIs, since adult oligodendrocytes do not express high levels of α-synuclein. The most recent leading hypothesis is that GCIs form via transfer and accumulation of α-synuclein from neurons to oligodendrocytes. However, studies regarding this subject are limited due to the absence of proper human cell models, to demonstrate the entry and accumulation of neuronal α-synuclein in human oligodendrocytes. Here, we generated mature human oligodendrocytes that can take up neuronderived α-synuclein and form GCI-like inclusions. Mature human oligodendrocytes are derived from neural stem cells via "oligosphere" formation and then into oligodendrocytes, treating the cells with the proper differentiation factors at each step. In the final cell preparations, oligodendrocytes consist of the majority population, while some astrocytes and unidentified stem cell-like cells were present as well. When these cells were exposed to α-synuclein proteins secreted from neuron-like human neuroblastoma cells, oligodendrocytes developed perinuclear inclusion bodies with α-synuclein immunoreactivity, resembling GCIs, while the stem cell-like cells showed α-synuclein-positive, scattered puncta in the cytoplasm. In conclusion, we have established a human oligodendrocyte model for the study of GCI formation, and the characterization and use of this model might pave the way for understanding the pathogenesis of MSA.

• Journal of Veterinary Clinics
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• v.10 no.1
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• pp.111-130
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• 1993

Lead toxicity was evaluated in forty-five cats on a balanced diet, Treated with 0(control), 10, 100(low), 1, 000, 2, 000, and 4, 000(high) ppm of lead acetate orally on a body weight basis. The objectives were to establish toxic dosage level of leaf in cats, to characterize changes in behavior and clinical pathology, and to demonstrate what blood lead concentrations correlate with the known dosages of lead. Some high dose cats showed projectile vomiting, hyperactivity, and seizures. The growth rates did not appear to be altered in any of the dosed groups. Normal blood lead concentration in cats were lower than that of humans, dogs, and cattle. Blood lead concentrations of 3 to 20$\mu\textrm{g}$/100$m\ell$ could be termed a 'subclinical' range in the cat. Clinical lead toxicity in cats may have blood lead concentrations ranging 20 to 120$\mu\textrm{g}$/100$m\ell$. Zinc protoporphyrin concentrations were proportional to lead dosages and a significant ZPP elevation, greater than 50$\mu\textrm{g}$/100$m\ell$, may be indicative of clinical lead toxicity. The enzyme aminolevulinic acid dehydratase showed an inverss dose response relationship for all lead dosages and a significant ZPP elevation, greater than 50$\mu\textrm{g}$/100$m\ell$, may be indicative of clinical lead toxicity. The enzyme aminolevulinic acid dehydratase showed an inverse dose response relationship for all lead dosages and appears to be a good indicator of lead exposure in cats. Urinary aminolevuliruc acid concentrations generally increased with lead dosage, but individual values varied. Hair lead concentrations rose proportionately to lead dosages. Lead at least in high doses appears to inhibit chemotactic activity of polymorphonuclear cells and monocytes. No consistent dose response relationships were observed in hemoglobin, RBC, WBC, neutrophil, lymphocyte, monocyte, and eosinophil counts. There were no consistent dose related changes in total protein, plasma protein, BUN, and ALT values. Reticulocyte counts did not increase significantly in most lead dosage levels, and are probably of little value in diagnosing lead toxicity in cats. The fact that no significant changes were found in nerve conduction velocities may support that there was no segmental demyelination resulting from lead ingestion. The lethal dose in cats appear to range from 60 to 150mg/kg body weight. A reliable diagnosis of lead poisoning can be made utilizing blood lead, ZPP, and ALAD, and hair lead.

• Journal of Korean Medicine Rehabilitation
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• v.20 no.2
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• pp.1-15
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• 2010

Objectives : This study was performed to evaluate the effects of root of Cibotii rhizoma(CR) ethanol extract on the tissue and neuronal damage of the spinal cord injury(SCI). Methods : SCI was induced by mechanical contusion following laminectomy of 10th thoracic vertebra in Sprague-Dawley rats. CR was orally given once a day for 7 days after SCI. Tissue damage and nerve fiber degeneration were examined with cresyl violet and luxol fast blue(LFS) histochemistry. HSP72(as neuronal damage marker), MAP2(as nerve fiber degeneration marker), c-Fos(immediate early gene), and Bax(pro-apoptotic molecule) expressions were examined using immuno-histochemistry. Individual immuno-positive cells expressing HSP72, MAP2, c-Fos and Bax were observed on the damaged level and the upper thoracic and lower lumbar spinal segments. Results : 1. CR reduced degeneration of nerve fibers and motor neuron shrinkage in the ventral horn of the lower lumbar spinal segment, but generally it did not seem to ameliorate the tissue injury following SCI. 2. CR reduced demyelination in the ventral and lateral funiculus of the lower lumbar spinal segment. 3. CR reduced HSP72 expression on the neurons in the peri-central canal gray matter adjacent to the damaged region. 4. CR strengthened MAP2 expression on the motor neurons in the ventral horn and on nerve fibers in the lateral funiculus of the lower lumbar spinal segment. 5. CR reduced c-Fos positive cells in the peri-lesion and the dorsal horn of the damaged level and in the ventral horn of the lower lumbar spinal segment. 6. CR reduced Bax positive cells in the peri-lesion and the dorsal horn of the damaged level and in the ventral horn of the lower lumbar spinal segment. Conclusions : These results suggest that CR plays an inhibitory role against secondary neuronal damage and nerve fiber degeneration. following SCI.

• The Journal of Korea Assosiation for Disability and Oral Health
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• v.12 no.2
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• pp.96-100
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• 2016

Metachromatic leukodystrophy (MLD) is a progressive and degenerative neurological disease caused by a deficiency of the catabolic enzyme arylsulfatase A. Deficiency of arylsulfatase A results in accumulation of sulfatide in the white matter of the peripheral and central nervous system and it occurs demyelination as a result. The patient gradually goes through mental and motor failure. General symptoms of MLD include gait disturbance, mental deterioration, muscle rigidity and impaired swallowing. Inheritance of the disease is autosomal recessive. We report a dental caries treatment of a 3-year old boy with MLD. The patient underwent hematopoietic stem cell transplantation (HSCT) to slow the progression of the disease. He was suffered from difficulties of mastication and swallowing from the degenerative neurological symptom. He was ingesting food by both oral feeding and tubal feeding after he took percutaneous endoscopic gastrostomy (PEG). The cause of multiple caries was mainly presumed as patient's prolonged time of meal. The treatment was performed under general anesthesia considering patient's incompliance. Severely affected lower primary molars were treated with pulp treatment and restored with stainless steel crown. Others were restored with composite resin. There were no postoperative complications. MLD is life threatening progressive disease and also has an impact on unfavorable condition for oral health. Routine home oral care and periodic professional dental care should be emphasized to the caregiver of patient considering the susceptibility of dental caries. Not only the medical care, but periodic dental office visit would benefit the quality of life of the patient.