• Asian-Australasian Journal of Animal Sciences
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• v.22 no.6
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• pp.788-795
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• 2009

Vascular endothelial growth factor (VEGF) is a key regulator of angiogenesis under various physiological and pathological conditions. We found that the VEGF isoforms VEGF120, VEGF164, and VEGF188 were expressed in the bovine mammary gland and bovine mammary epithelial cells (bMECs). Expression of VEGF in the mammary gland was significantly higher during the lactation period than during the dry period. Although dexamethasone or prolactin alone had little effect on the expression of VEGF, that in dexamethasone-treated cells was significantly induced after additional treatment with prolactin. Furthermore, the VEGF expression induced by the combination of dexamethasone and prolactin was reduced by PD98059 in a dose-dependent manner. This combination also stimulated the phosphorylation of p44/p42 MAP kinase in these cells. These results strongly suggest that the combination of dexamethasone and prolactin stimulates VEGF expression in bMECs via p44/p42 MAP kinase.

• BMB Reports
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• v.43 no.4
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• pp.233-244
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• 2010

Parkinson's disease (PD) is the second most common neurodegenerative disease, and 5-10% of the PD cases are genetically inherited as familial PD (FPD). LRRK2 (leucine-rich repeat kinase 2) was first reported in 2004 as a gene corresponding to PARK8, an autosomal gene whose dominant mutations cause familial PD. LRRK2 contains both active kinase and GTPase domains as well as protein-protein interaction motifs such as LRR (leucine-rich repeat) and WD40. Most pathogenic LRRK2 mutations are located in either the GTPase or kinase domain, implying important roles for the enzymatic activities in PD pathogenic mechanisms. In comparison to other PD causative genes such as parkin and PINK1, LRRK2 exhibits two important features. One is that LRRK2's mutations (especially the G2019S mutation) were observed in sporadic as well as familial PD patients. Another is that, among the various PD-causing genes, pathological characteristics observed in patients carrying LRRK2 mutations are the most similar to patients with sporadic PD. Because of these two observations, LRRK2 has been intensively investigated for its pathogenic mechanism (s) and as a target gene for PD therapeutics. In this review, the general biochemical and molecular features of LRRK2, the recent results of LRRK2 studies and LRRK2's therapeutic potential as a PD target gene will be discussed.

• Transactions of the Korean Society of Mechanical Engineers B
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• v.33 no.6
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• pp.461-467
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• 2009

Knowledge of airflow characteristics in nasal cavities is essential to understand the physiological and pathological aspects of nasal breathing. Several studies have utilized physical models of the healthy nasal cavity to investigate the relationship between nasal anatomy and airflow. In our laboratory, there have been a series of experimental investigations on the nasal airflow in normal, abnormal, and deformed nasal cavity models by PIV under both constant and periodic flow conditions. In this time normal and several deformed nasal cavity models, which simulate surgical operation, Turbinectomy, are investigated numerically by the FVM general purpose code and PIV analysis. The comparisons of these results are appreciated. Dense CT data and careful treatment of model surface under the ENT doctor's advice provide more sophisticated cavity models. The Davis (LaVision Co.) code is used for PIV flow analysis. Average and RMS distributions have been obtained for inspirational and expirational nasal airflows in the normal and deformed nasal cavities.

• Korean Journal of Head & Neck Oncology
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• v.33 no.2
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• pp.43-47
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• 2017

Epithelial-myoepithelial carcinoma (EMC) is a rare type of low-grade malignant tumor that account for approximately 0.5% to 1% of salivary gland neoplasm and arises most commonly in the parotid gland (80%). We introduce three cases of parotid EMC arose as painless cystic mass in male patients over 70 years old. All patients were diagnosed as benign tumors (pleomorphic adenoma) by image and pathologic study (fine needle aspiration) before surgery, but the final histopathologic results were EMC. All three patients underwent parotidectomy without adjuvant radiotherapy. There were no complications such as facial paralysis. No complications or recurrences were observed during follow-up for 6 to 9 months. Since the reports of EMC are still relatively few, we report our three cases with the clinical and pathological review.

• Korean Journal of Acupuncture
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• v.33 no.3
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• pp.95-101
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• 2016

Objectives : This study aims to overview the therapeutic mechanism of back-shu points in terms of sympathetic visceral motor nervous system. Methods : Studies about autonomic nervous system, and studies and ancient texts about back-shu points were reviewed. We interpreted possible mechanism of back-shu points considering similarities of anatomical and physiological characteristics of back-shu points and visceral motor nervous system. Results : Afferent signals for organ lesions that can develop the symptoms of autonomic neurological symptoms, pain, hyperalgesia through the skin segment. Through a physical examination of the myotome and dermatome, it is possible to diagnose segmental disorders. Treatment stimulation of the thick fibers of the disorder segment skin can reduce abnormal autonomic influence over the sympathetic reflex mechanism. In addition, if spinal muscles are relaxed, the pressure on the nerve roots could be reduced and consequently the hyperactivity of the sympathetic visceral motor signal would be suppressed. Conclusions : The back-shu points treatments work through the mechanism of the sympathetic nervous reflex. Moreover, segmental acupuncture can reduce tension of the spinal muscles, thereby improving pathological conditions of the sympathetic nervous system.

• Korean Journal of Acupuncture
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• v.26 no.1
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• pp.111-123
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• 2009

Objective : The purpose of this study is to observe the effect of high frequency electro-acupuncture (hf-EA) at Yanglingquan(GB34) on $CCl_4$-induced liver damage in rats. Methods : The author performed several experimental items, including measurements of body weight and liver weight, hematological analysis for RBC, WBC, PLT, hemoglobin, lymphocytes, neutrophils, monocytes and biochemical assays for ALT, AST, ALP and total cholesterol in serum, and histological analysis of liver tissue. Results & Conclusion : 1. WBC level in blood was slightly reduced by acupuncture and hf-EA at GB34. 2. Lymphocyte level in blood was decreased by $CCl_4$-intoxication and significantly increased by acupuncture and hf-EA at GB34. 3. Neutrophils level in blood was slightly reduced by acupuncture and hf-EA at GB34. 4. ALT and AST in serum were reduced significantly by acupuncture and hf-EA at GB34. 5. The pathological changes of liver tissue induced by $CCl_4$ was reduced by hf-EA at GB34. 6. No significant difference was found between the effects of acupuncture and hf-EA on CCl4-induced liver damage in rats.

• Molecules and Cells
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• v.25 no.1
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• pp.99-104
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• 2008

Gangliosides, sialic acid-containing glycosphingolipids, are implicated in many neuronal diseases, but the precise molecular mechanisms underlying their pathological activities are poorly understood. Here we report that TLR2 participates in the initiation of ganglioside-triggered inflammatory signaling responses. Using FACS analysis and immunofluorescence microscopy, we found that gangliosides rapidly enhanced the cell surface expression of TLR2 in microglia, while reducing that of TLR4. The ganglioside-dependent increase of TLR2 expression was also observed at the messenger and protein levels. We also showed that gangliosides stimulate the interaction of TLR2 with Myd88, an adaptor for TLRs, and obtained evidence that lipid raft formation is closely associated with the ganglioside-induced activation of TLR2 and subsequent inflammatory signaling. These results collectively suggest that TLR2 contributes to the ability of gangliosides to cause inflammatory conditions in the brain.

• Molecules and Cells
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• v.25 no.1
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• pp.124-130
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• 2008

Astrocyte ion channels participate in ionic homeostasis in the brain. Inward rectifying potassium channels (Kir channels) in astrocytes have been particularly implicated in $K^+$ homeostasis because of their high open probability at resting potential and their increased conductance at high concentrations of extracellular $K^+$. We examined the expression of the Kir2.1 subunit, one of the Kir channel subunits, in the mouse brain by immunohistochemistry. Kir2.1 channels were widely distributed throughout the brain, with high expression in the olfactory bulb and the cerebellum. Interestingly, they were abundantly expressed in astrocytes of the olfactory bulb, while astrocytes in other brain regions including the hippocampus did not show any detectable expression. However, Kir2.1 channel-expressing cells were dramatically increased in the hippocampus by kainic acid-induced seizure and the cells were glial fibrillary acidic protein (GFAP)-positive, which confirms that astrocytes in the hippocampus express Kir2.1 channels under pathological conditions. Our results imply that Kir2.1 channels in astrocyte may be involved in buffering $K^+$ against accumulated extracellular $K^+$ caused by neuronal hyperexcitability under phathophysiological conditions.

• Molecules and Cells
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• v.43 no.5
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• pp.431-437
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• 2020

The hypothalamus is a crucial organ for the maintenance of appropriate body fat storage. Neurons in the hypothalamic arcuate nucleus (ARH) detect energy shortage or surplus via the circulating concentrations of metabolic hormones and nutrients, and then coordinate energy intake and expenditure to maintain energy homeostasis. Malfunction or loss of hypothalamic ARH neurons results in obesity. Accumulated evidence suggests that hypothalamic inflammation is a key pathological mechanism that links chronic overconsumption of a high-fat diet (HFD) with the development of obesity and related metabolic complications. Interestingly, overnutrition-induced hypothalamic inflammation occurs specifically in the ARH, where microglia initiate an inflammatory response by releasing proinflammatory cytokines and chemokines in response to excessive fatty acid flux. Upon more prolonged HFD consumption, astrocytes and perivascular macrophages become involved and sustain hypothalamic inflammation. ARH neurons are victims of hypothalamic inflammation, but they may actively participate in hypothalamic inflammation by sending quiescence or stress signals to surrounding glia. In this mini-review, we describe the current state of knowledge regarding the contributions of neurons and glia, and their interactions, to HFD-induced hypothalamic inflammation.

• Journal of Oriental Neuropsychiatry
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• v.10 no.2
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• pp.59-70
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• 1999

We investigated whether an aqueous extract of Rehmannia glutinosa steamed root (RGAE) inhibits secretion of inflammatory cytolanes from primary cultures of mouse astrocytes. RGAE dose-dependently inhibited the $TNF-{\alpha}$ secretion by astrocytes stimulated with substance P (SP) and lipopolysaccharide (LPS). Interleukin-1 (IL-1) has been shown to elevate $TNF-{\alpha}$ secretion from LPS-stimulated astrocytes while having no effect on astrocytes in the absence of LPS. We therefore also investigated whether IL-1 mediated inhibition of $TNF-{\alpha}$ secretion from primary astrocytes by RGAE. Treatment of RGAE to astrocytes stimulated with both LPS and SP decreased IL-1 secretion to the level observed with LPS alone. Moreover, incubation of astrocytes with IL-1 antibody abolished the synergistic cooperative effect of LPS and SP. These results suggest that RGAE has an antiinflammatory activity on the central nervous system curing some pathological disease states.