• Journal of Pharmaceutical Investigation
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• v.35 no.6
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• pp.453-460
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• 2005

4-Aminopyridine (AP) is a potassium channel blocker used in the treatment of neurological disorders such as multiple sclerosis and Alzheimer disease. AP‘s window of therapeutic effect appears to correlate with its plasma halflife (3.5 hours). It demonstrates pH-dependent solubility because of a weakly basic drug. In addition, the resulting release from conventional matrix tablets decreases with increasing pH-milieu of the gastrointestinal tract. The aim of this study is to design sustained release matrix tablet containing AP, overcoming this problem. $Eudragit^{\circledR}$ L 100 (EuL) and sodium alginate were used in an effort to achieve pH independent drug release. The effect of sodium alginate and EuL on drug release from matrix tablet was investigated. The drug release behavior from the different tablets was analyzed by $t_{20%},\;t_{40%},\;t_{60%}$, The exponential diffusion coefficient n, kinetic constant K were calculated according to the Korsmeyer-Peppas equation. The drug release from matrix tablets prepared with sodium alginate was decreased with increasing the content of sodium alginate in pH 7.4 while there is no significant difference in pH 1.2. The exponent n values were determined to be approximately 0.5 and 0.8 respectively, in both pH 1.2 and 7.4. These values indicate diffusion-based anomalous mechanism and erosion-based anomalous mechanism, respectively. The drug release from sodium alginate matrix tablets prepared with solid dispersion of EuL containing drug showed a slow drug release in an acidic medium and a more fast drug release in phosphate medium, compared with sodium alginate matrix tablets prepared with physical mixture. These results may be attributed to the gel forming ability of sodium alginate and pH dependent solubility of EuL. Therefore, sustained-release AP matrix tablets using sodium alginate and EuL were successfully prepared.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.1
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• pp.43-48
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• 2012

Glutamate excitotoxicity is emerging as a contributor to degeneration of spinal cord motoneurons in amyotrophic lateral sclerosis (ALS). Recently, we have reported that ghrelin protects motoneurons against chronic glutamate excitotoxicity through the activation of extracellular signal-regulated kinase 1/2 and phosphatidylinositol-3-kinase/Akt/glycogen synthase kinase-$3{\beta}$ pathways. Previous studies suggest that activated microglia actively participate in the pathogenesis of ALS motoneuron degeneration. However, it is still unknown whether ghrelin exerts its protective effect on motoneurons via inhibition of microglial activation. In this study, we investigate organotypic spinal cord cultures (OSCCs) exposed to threohydroxyaspartate (THA), as a model of excitotoxic motoneuron degeneration, to determine if ghrelin prevents microglial activation. Exposure of OSCCs to THA for 3 weeks produced typical motoneuron death, and treatment of ghrelin significantly attenuated THA-induced motoneuron loss, as previously reported. Ghrelin prevented THA-induced microglial activation in the spinal cord and the expression of pro-inflammatory cytokines tumor necrosis factor-${\alpha}$ and interleukin-$1{\beta}$. Our data indicate that ghrelin may act as a survival factor for motoneurons by functioning as a microglia-deactivating factor and suggest that ghrelin may have therapeutic potential for the treatment of ALS and other neurodegenerative disorders where inflammatory responses play a critical role.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.40 no.3
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• pp.140-146
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• 2014

Pigmented villonodular synovitis (PVNS) is a benign but locally aggressive and destructive disease originating in the synovial membranes. It is a proliferative disorder of unknown etiology. Involvement of the temporomandibular joint (TMJ) is very rare. Computed tomography clearly reveals areas of lytic bone erosion and sclerosis, and also clearly defines the extent of the tumor which is the focal areas of hyperdensity within the soft-tissue mass. Magnetic resonance images invariably show profound hypointensity on both T1- and T2-weighted sequences due to hemosiderin pigmentation. Additionally, high signal intensity on T2-weighted images may indicate cystic loculation of the joint fluid. This case study describes a rare case of PVNS of the TMJ with bone destruction of the mandibular condyle. Complete surgical excision of the lesion was performed through a preauricular approach with temporal extension. During the 10-year follow-up, two more operations were performed due to local recurrence and the fracture of the reconstruction plate. Total joint reconstruction with Biomet was finally performed, and the absence of disease was confirmed with a biopsy report showing fibrosis with hyalinization and mild inflammation of the excised soft tissue from the old lesion.

• Advances in Traditional Medicine
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• v.10 no.4
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• pp.239-253
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• 2010

Coenzyme $Q_{10}$ ($CoQ_{10}$, or ubiquinone) is an electron carrier of the mitochondrial respiratory chain (electron transport chain) with antioxidant properties. In view of the involvement of $CoQ_{10}$ in oxidative phosphorylation and cellular antioxidant protection a deficiency in this quinone would be expected to contribute to disease pathophysiology by causing a failure in energy metabolism and antioxidant status. Indeed, a deficit in $CoQ_{10}$ status has been determined in a number of neuromuscular and neurodegenerative disorders. Primary disorders of $CoQ_{10}$ biosynthesis are potentially treatable conditions and therefore a high degree of clinical awareness about this condition is essential. A secondary loss of $CoQ_{10}$ status following HMG-CoA reductase inhibitor (statins) treatment has been implicated in the pathophysiology of the myotoxicity associated with this pharmacotherapy. $CoQ_{10}$ and its analogue, idebenone, have been widely used in the treatment of neurodegenerative and neuromuscular disorders. These compounds could potentially play a role in the treatment of mitochondrial disorders, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, Friedreich's ataxia, and other conditions which have been linked to mitochondrial dysfunction. This article reviews the physiological roles of $CoQ_{10}$, as well as the rationale and the role in clinical practice of $CoQ_{10}$ supplementation in different neurological diseases, from primary $CoQ_{10}$ deficiency to neurodegenerative disorders. These will help in future for treatment of patients suffering from neurodegenerative disease.

• Tuberculosis and Respiratory Diseases
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• v.39 no.3
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• pp.261-265
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• 1992

Pleural effusion due to hepatic cirrhosis and ascites is well known. But rarely a pleural effusion may develop in a cirrhotic patient in the absence of detectable ascites. The differential diagnosis of a right-sided transudative pleural effusion in a patient with chronic liver disease with or without ascites includes congestive heart failure and nephrotic syndrome. These diseases are usually ruled out with standard clinical tests. Patients with hepatic hydrothorax should be treated with fluid restriction, diuretics and the correction of hypoalbuminemia. Patients with severe symptoms due to refractory hepatic hydrothorax might benefit from pleural sclerosis and surgical closure of diaphragmatic defect. We experienced a case of right-sided pleural effusion in liver cirrhosis without ascites.

• The Journal of the Korean bone and joint tumor society
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• v.7 no.2
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• pp.68-72
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• 2001

Adamantinoma is a rare malignant tumor and approximately 85% of cases occur in the tibia. In 1985, Moon and Mori reviewed the world literature and identified 195 cases. A 59-year-old woman was presented with nonspecific pain on left leg after trauma. Radiographic finding showed well-circumscribed soap bubble appearance with areas of sclerosis in diaphyseal region of the tibia. Magnetic resonance imaging and biopsy was performed for diagnosis. Histologically, the lesion was compatible with adamantinoma. Wide resection with bone graft was performed. There was no recurrence at 3 years follow-up. We report a case of adimantinoma that arose in diaphyseal region of the tibia with review of literature.

• Preventive Nutrition and Food Science
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• v.7 no.4
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• pp.454-460
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• 2002

While atherosclerosis is a major killer, there is now concern that mortality from the disease will increase due to the rising incidence of type II diabetes. Because diet can potentially influence both diseases, it is important to elucidate the role of diet in the progression of atherosclerosis. In addition, the mechanisms involved in dietary-related alterations of the disease need to be defined to guide public health recommendations to reduce athero-sclerosis incidence and limiting unwanted side effects. Since diet is thought to play a role in atherosclerosis even without added complications due to type II diabetes, reducing the incidence of that metabolic disease will not be enough. While evidence is increasing that high intake of carbohydrate can lead to type II diabetes and atherosclerosis, the preponderance of existing evidence indicates that intake of specific fats as a major dietary causal factor. It has recently been hypothesized that a dietary fat link to atherosclerosis may depend partly on the activity of a transcriptional regulator, the peroxisome proliferator activated receptors (PPAR). Thusfar, PPAR $\alpha$, $\beta$/$\delta$ and ${\gamma}$, have been shown to play a major role in metabolism, inflammation, and cancer. Furthermore, PPAR may regulate specific processes associated with atherosclerosis such as triglyceride and low density lipoprotein (LDL) metabolism; the reverse cholesterol transport pathway; lipid accumulation within plaques; the local inflammatory response and plaque stability. Synthetic ligands for PPAR have been developed; however, natural ligands include specific fatty acids and their metabolites. Though the role of PPAR in atherosclerosis has been reported with respect to synthetic ligands, additional studies need to be done with established and possible natural ligands. In this review, we will focus on the relation of dietary fat to PPAR alteration of atherosclerosis.

• The korean journal of orthodontics
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• v.23 no.4 s.43
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• pp.645-660
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• 1993

In this study, effects of incision of retrodiscal tissue and unilateral occlusal reduction on temporomandibular joint of rabbit were investigated. Twenty-seven adult New Zealand White Rabbits, weighing over 3.5kg, were utilized in this study. Temporomandibular joint surgery was performed in left temporomandibular joint of 24 rabbits to displace disc anteriorly through incising the retrodiscal tissue 1-2mm posterior to the disc. They were divided into two groups : twelve were left untreated after surgery, occlusal reduction was performed on left posterior teeth every 2 weeks in the other twelve rabbits, The remaining three served as the control group. The sample were sacrificed by 8, 12, and 16 weeks after surgery. Histologic examinations were performed after sacrificing them. The results were as follows : 1. Histologic findings which were manifested by flat articular fossa, broad articular surface, generalized recession of articular cartilage and sclerosis of subchondral bone were observed. These findings were similar to internal derangement. 2. In the rabbits untreated after surgery, thin cartilagenous layer and necrotic tissue were observed in 8 weeks group, calcifying cartilagenous layer was observed in 12 weeks group, and cartilagenous layer on anterior portion was observed in 16 weeks group. So, it showed gradual healing pattern into the normal tissue except displaced disc. 3. Occlusal trauma after surgery resulted in generalized recession of upper and lower articular surface. Necrosis and vertical split on condylar process of mandible were observed in 8 weeks group. Osteoclasts, exposure of subchondral bone due to erosion on upper and lower articular surface, and degenerative changes on retrodiscal tissue were observed in 16 weeks group. So, it showed continuous prowess pattern of osteoarthrosis.

• Journal of Korean Academy of Oral and Maxillofacial Radiology
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• v.19 no.1
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• pp.7-18
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• 1989

The authors analyzed the clinical findings, radiological findings and their correlations in the temporomandibular joint disorders. The results were as follows: 1. The most prevalent age group was in the first decade, then the second decade and the third decade. Female were more common with a ratio of 3.4:1. 2. The most common clinical findings was the pain on open mouth position (42.3%), then came the clicking and limitation of mouth opening. 3. The most common bone change on the condyle side was the erosion, then came the flattening, the osteopyte and the sclerosis in that orders. 4. In the case of the crepitus, the coarse crepitus showed more radiological change than the fine crepitus. The 27% of the patients with crepitus showed the bone change and the patients with crepitus showed more bone change than any other clinical symptoms. 5. In the case of the mouth opening limitation, the evaluation of the translatory movement by transcranial projection was in accordance with the clinical evaluation. 6. The correlation between the clinical symptom and the condylar position within the mandibular fossa was not present and in the case of diagnosis of disc displacement, the transcranial projection seemed not to be able to substitute for the arthrography. Radiographically, the most prevalent age group which showed the bone change was in the first, the second and the third decade. And the bone change seemed to have no relationship with aging.

• Korean Journal of Biological Psychiatry
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• v.24 no.1
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• pp.1-9
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• 2017

The proton magnetic resonance spectroscopy ($^1H-MRS$) is a tool used to detect concentrations of brain metabolites such as N-acetyl aspartate, choline, creatine, glutamate, and gamma-amino butyric acid (GABA). It has been widely used because it does not require additional devices other than the conventional magnetic resonance scanner and coils. Demyelination, or the neuronal damage due to loss of myelin sheath, is one of the common pathologic processes in many diseases including multiple sclerosis, leukodystrophy, encephalomyelitis, and other forms of autoimmune diseases. Rodent models mimicking human demyelinating diseases have been induced by using virus (e.g., Theiler's murine encephalomyelitis virus) or toxins (e.g., cuprizon or lysophosphatidyl choline). This review is an overview of the MRS findings on brain metabolites in demyelination with a specific focus on rodent models.