• 대한치과의사협회지
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• 제54권11호
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• pp.874-879
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• 2016

Damage to the inferior alveolar nerve(IAN) is a relatively infrequent complication in endodontic treatment. However, endodontic overfilling involving the mandibular canal may cause an injury of the inferior alveolar nerve resulting in sensory disturbances such as pain, dysesthesia, paresthesia or anesthesia. Two mechanism(chemical neurotoxicity and mechanical compression) are responsible for the IAN injury. When absorbent materials overfilled, it can be treated as a non-surgical procedure. But early surgical intervention required when mechanical, chemical nerve damage expected. We report surgical removal of overfilled gutta-percha and IAN decompression through sagittal split osteotomy in case of dysesthesia after overfilling of endodontic material into the mandibular canal. Dysesthesia recovered 3 months after surgical treatment.

• 한국환경보건학회지
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• 제24권3호
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• pp.35-40
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• 1998

This study was conducted to examine the pathological changes of rat peripheral nervous system during exposure to tellurium known to be a demyelinating agent by using teasing nerve fiber method and quantitative light microscopic analysis by image analyzer. The pellet containing 1.2% of tellurium were fed for 3, 5, 7, 9, 13 days to male wistar rats (21 days old) and then neurologic symptom and the feature of nerve fiber myelination were studied. From this study, following results were obtained. In 3 days treated group, it showed various neurologic symptom and teased nerve fiber showed slight irregularity of the myeline sheath. In 5 days and 7 days treated groups, it showed the segmental demyetination in larger size fiber and widening of nodes of ranvier. In 9 days and 13 days treated groups, the remyelinated fibers were observed and it was generally small in size. We consequently suggest that teasing nerve fiber method and quantitative analysis of nerve fiber were useful pathologic screening method of neurotoxicity of the peripheral nervous system.

• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2003년도 생물공학의 동향(XII)
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• pp.743-746
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• 2003

The major pathological lesion in Parkinson's disease(PD) is selective degeneration and loss of pigmented dopaminergic neurons in substantia nigra (SN). Although the initial cause and subsequent molecular signaling mechanisms leading to the dopaminergic cell death underlying the PD process is elusive, the potent neurotrophic factors (NTFs), brain derived neurotrophic factor (BDNF) and glial cell line derived neurotrophic factor (GDNF), are known to exert dopaminergic neuroprotection both in vivo and in vitro models of PD employing the neurotoxin, MPTP. BDNF and its receptor, trkB are expressed in SN dopaminergic neurons and their innervation target. Thus, neurotrophins may have autocrine, paracrine and retrograde transport effects on the SN dopaminergic neurons. This study determined the BDNF secretion from SN dopaminergic neurons by ELISA. Regulation of BDNF synthesis/release and changes in signaling pathways are monitored in the presence of free radical donor, NO donor and mitochondrial inhibitors. Also, this study shows that BDNF is able to promote survival and phenotypic differentiation of SN dopaminergic neurons in culture and protect them against MPTP-induced neurotoxicity via MAP kinase pathway.

• 한국약용작물학회:학술대회논문집
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• 한국약용작물학회 2008년도 추계학술발표회
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• pp.314-315
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• 2008

• 한국환경보건학회:학술대회논문집
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• 한국환경보건학회 2005년도 국제학술대회
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• pp.303-305
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• 2005

3-Monochloro-1,2-propanediol (3-MCPD) is a contaminant of acid-hydrolyzed vegetable protein. Several reports have suggested that chronic exposure to 3-MCPD could produce neurotoxicity in vitro or neurobehavioral effects inaspects of experimental animals. Disturbance of the nitric oxide signaling pathway by chronic exposure to 3-MCPD may be a causal factor of neurological disorders in rats. In order to investigate the relationship between 3-MCPD administration and expression of inducibal nitric oxide synthase (iNOS), the numbers and distribution patterns of iNOS-immunoreactive neurons were examined. At the all three bregma level examined, the optical density of iNOS-postive neurons was significantly increased following exposure to 3-MCPD. The change was more severe in the upper layer than in deep layer of the cortex. These data suggest that 3-MCPD toxicity may be mediated through disturbances to the nitric oxide signaling pathway.

• 대한한의학회지
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• 제26권4호
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• pp.152-161
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• 2005

The excessive release of proinflammatory products by activated microglia causes neurotoxicity, and this has been implicated in the pathogenesis of neurodegenerative diseases. Harpagophytum procumbens (Pedaliaceae) has been widely used for the treatment of pain and arthritis in the clinical field. In this study, we investigated the effect of Harpagophytum procumbens against lipopolysaccharide-induced inflammation. From the present results, the aqueous extract of Harpagophytum procumbens was shown to suppress prostaglandin-E2 synthesis and nitric oxide production by inhibiting the lipopolysaccharide-stimulated enhancement of cyclooxygenase-2 and inducible nitric oxide synthase expressions in mouse BV2 microglial cells. These results suggest that Harpagophytum procumbens may offer a valuable means of therapy for the treatment of brain inflammatory diseases by attenuating lipopolysaccharide-induced prostaglandin-E2 synthesis and nitric oxide production.

• 한국발생생물학회지:발생과생식
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• 제15권2호
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• pp.173-178
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• 2011

The amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA) is a potent monoaminergic neurotoxin with the potential to cause serotonergic neurotoxicity, but has become a popular recreational drug. Little has been known about the cellular effects induced by MDMA. This report shows that MDMA inhibits neuronal cell growth and differentiation. MDMA suppressed neuronal cell growth. The results of quantitative real-time PCR analysis showed that Egr-1 expression is elevated in mouse embryo and neuroblastoma cells after MDMA treatment. Transiently transfected Egr-1 interfered with the neuronal differentiation of neuroblastoma cells such as SH-SY5Y and PC12 cells. These findings provide evidence that the abuse of MDMA during pregnancy may impair neuronal development via an induction of Egr-1 over-expression.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.214-217
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• 2002

Cyclosporin A (CSA) is a poorly water-soluble cyclic peptide comprising 11 amino acids. It inhibits T-lymphocyte function that plays an important role in the induction of immune response. The potent immunosuppressive activity of CSA has been used for the prevention of rejection following transplantation of liver, kidney and bone marrow, etc. The use of CSA has been often limited by several disadvantages including low bioavailability, narrow therapeutic window, nephrotoxicity, hepatotoxicity and neurotoxicity. Moreover, CSA injection is limited to patients who are unable to take the oral preparations, because it has a risk of anaphylactic shock and nephrotoxicity due to Cremophor EL$\textregistered$, a solubilizing agent used in the commercial intravenous formulation. Owing to above mentioned disadvantages of commercial products, there is a great interest in the development of the alternative dosage forms. (omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.228.2-229
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• 2002

Methylmercury (MeHg). a potent neurotoxicant. produces neuronal death that may be partially mediated by glutamate. Glutamine synthetase (GS), a glial-specific enzyme. catalyzes the synthesis of glutamine from glutamate and ammonia and is associated with ischemic injury and neurological diseases. Objectives of this experiment are to investigate whether in vivo and in vitro MeHg exposure have adverse effects on GS and whether duration of exposure to MeHg and glutamate co-treatment playa role in MeHg-induced toxicity. (omitted)

• 한국식품저장유통학회:학술대회논문집
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• 한국식품저장유통학회 2003년도 춘계총회 및 제22차 학술발표회
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• pp.109.2-110
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• 2003

The neuroprotective effect of solvent fraction of native edible plant MK-104 in the mice administered with kainate was evaluated using behavioral sign, neuronal injuries and biomarkers of oxidative stress. Mice, ICR male, were administered with the BFME through a gavage for 4 days consecutively, and on the 3rd day, kainate (450 mg/kg) was i.p. administered. The fraction(400 mg/kg) delayed the onset time of neurobehavioral change (p<0.01), reduced the severity of convulsion and lethality (p<0.05), and restored the level of GSH and lipid peroxidation in brain to control value. A similar protective action was also expressed by fraction-I (200 mg/kg), which showed a prominent protection against the neuronal damage in hippocampal CA1 and CA2 regions (p<0.01) caused by kainate injection. of TBARS value. Based on these results, BFME-I is suggested to contain a functional agent to prevent against oxidative stress in the brain of mice.