• Korean Journal of Audiology
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• v.24 no.3
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• pp.113-118
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• 2020

Tinnitus is a prevalent disorder that has no cure currently. Within the last two decades, neuroscientific research has facilitated a better understanding of the pathophysiological mechanisms that underlie the generation and maintenance of tinnitus, and the brain and nerves have been identified as potential targets for its treatment using non-invasive brain stimulation methods. This article reviews studies on tinnitus patients using transcranial magnetic stimulation, transcranial electrical stimulation, such as transcranial direct current stimulation, alternating current stimulation, transcranial random noise stimulation as well as transcutaneous vagus nerve stimulation and bimodal combined auditory and somatosensory stimulation. Although none of these approaches has demonstrated effects that would justify its use in routine treatment, the studies have provided important insights into tinnitus pathophysiology. Moreover bimodal stimulation, which has only been developed recently, has shown promising results in pilot trials and is a candidate for further development into a valuable treatment procedure.

• Journal of Audiology & Otology
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• v.24 no.3
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• pp.113-118
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• 2020

Tinnitus is a prevalent disorder that has no cure currently. Within the last two decades, neuroscientific research has facilitated a better understanding of the pathophysiological mechanisms that underlie the generation and maintenance of tinnitus, and the brain and nerves have been identified as potential targets for its treatment using non-invasive brain stimulation methods. This article reviews studies on tinnitus patients using transcranial magnetic stimulation, transcranial electrical stimulation, such as transcranial direct current stimulation, alternating current stimulation, transcranial random noise stimulation as well as transcutaneous vagus nerve stimulation and bimodal combined auditory and somatosensory stimulation. Although none of these approaches has demonstrated effects that would justify its use in routine treatment, the studies have provided important insights into tinnitus pathophysiology. Moreover bimodal stimulation, which has only been developed recently, has shown promising results in pilot trials and is a candidate for further development into a valuable treatment procedure.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.83-85
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• 2002

Over the last 5 years or so, there has been a significant increase in the molecular characterization of transport proteins in animals and man. This has led to a better understanding of the importance of such transport proteins in the disposition of endogenous compounds, drugs and other xenobiotics in many organs such as the intestine, liver, kidney and brain. (omitted)

• Proceedings of the Ginseng society Conference
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• 2002.10a
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• pp.84-95
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• 2002

• Clinical and Experimental Pediatrics
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• v.60 no.1
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• pp.1-9
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• 2017

Malformations of cortical development are rare congenital anomalies of the cerebral cortex, wherein patients present with intractable epilepsy and various degrees of developmental delay. Cases show a spectrum of anomalous cortical formations with diverse anatomic and morphological abnormalities, a variety of genetic causes, and different clinical presentations. Brain magnetic resonance imaging has been of great help in determining the exact morphologies of cortical malformations. The hypothetical mechanisms of malformation include interruptions during the formation of cerebral cortex in the form of viral infection, genetic causes, and vascular events. Recent remarkable developments in genetic analysis methods have improved our understanding of these pathological mechanisms. The present review will discuss normal cortical development, the current proposed malformation classifications, and the diagnostic approach for malformations of cortical development.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.19 no.1
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• pp.477-485
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• 2018

The aim of this study was to improve the 'self-directed learning ability and attitudeselementary school students by applying a brain education-based learning program based on brain science in the form of a short term camp in consideration of the elementary school students' brain characteristics and mechanisms. For this purpose, this study was conducted on 4, 5, and 6 elementary school students in Korea. The brain training based learning camp program was conducted for two nights and three days. The camps were conducted twice from February 3 to 5, 2017 with 45 students from grade 6 and from February 22 to July 24, 2017, with 56 students from grades 4 and 5, 101 students in total. The conclusions of this study are as follows. The brain education-based learning camp program was found to be effective in improving the elementary school students' self-directed learning ability and learning attitude. First, the brain education-based learning camp program can increase the learning concentration through brain gymnastics, breathing, and meditation. Second, brain training called 'Brain Screen' among the brain education-based learning camp program can improve the brain ability of memory. Third, it can establish a self - directed learning philosophy of 'My study is done by me' by giving reason and motivation to study through the brain education-based learning camp program.

• Journal of Yeungnam Medical Science
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• v.30 no.1
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• pp.4-9
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• 2013

Leptin, a 16-kDa cytokine, is secreted by adipose tissue in response to the surplus of fat store. Thereby, the brain is informed about the body's energy status. In the hypothalamus, leptin triggers specific neuronal subpopulations (e.g., POMC and NPY neurons) and activates several intracellular signaling events, including the JAK/STAT, MAPK, PI3K, and mTOR pathway, which eventually translates into decreased food intake and increased energy expenditure. Leptin signal is inhibited by a feedback inhibitory pathway mediated by SOCS3. PTP1B involves another inhibitory pathway of leptin. Leptin potently promotes fat mass loss and body weight reduction in lean subjects. However, it is not widely used in the clinical field because of leptin resistance, which is a common feature of obesity characterized by hyperleptinemia and the failure of exogenous leptin administration to provide therapeutic benefit in rodents and humans. The potential mechanisms of leptin resistance include the following: 1) increases in circulating leptin-binding proteins, 2) reduced transport of leptin across the blood-brain barrier, 3) decreased leptin receptor-B (LRB), and/or 4) the provocation of processes that diminish cellular leptin signaling (inflammation, endoplasmic reticulum stress, feedback inhibition, etc.). Thus, interference of the cellular mechanisms that attenuate leptin signaling improves leptin action in cells and animal models, suggesting the potential utility of these processes as points of therapeutic intervention. Various experimental trials and compounds that improve leptin resistance are introduced in this paper.

• Psychiatry investigation
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• v.15 no.11
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• pp.1094-1097
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• 2018

Objective Patients with acute coronary syndrome (ACS) are at an increased risk of suicide. It is well known that epigenetic mechanisms may explain the pathophysiology of suicidal behavior including suicidal ideation (SI), but no study has explored these mechanisms in ACS populations. Methods In total, 969 patients were initially recruited within 2 weeks of the acute coronary event and, 711 patients were successfully followed up 1 year after ACS. SI was evaluated using the relevant items on the Montgomery-${\AA}sberg$ Depression Rating Scale and covariates potentially affecting SI were estimated. Results Brain-derived neurotrophic factor (BDNF) hypermethylation was associated with SI in both the acute and chronic phases of ACS, although the association was not statistically significant in the acute phase after applying Bonferroni's correction. Conclusion These results suggested that BDNF hypermethylation may have played a role in an epigenetic predisposition for SI in ACS patients, particularly during the chronic phase.

• International Journal of Oral Biology
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• v.34 no.1
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• pp.7-14
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• 2009

Nitric oxide (NO) acts as an intracellular messenger at the physiological level but can be cytotoxic at high concentrations. The cells within periodontal tissues, such as gingival and periodontal fibroblasts, contain nitric oxide syntheses and produce high concentrations of NO when exposed to bacterial lipopolysaccharides and cytokines. However, the cellular mechanisms underlying NO-induced cytotoxicity in periodontal tissues are unclear at present. In our current study, we examined the NO-induced cytotoxic mechanisms in human gingival fibroblasts (HGF). Cell viability and the levels of reactive oxygen species (ROS) were determined using a MTT assay and a fluorescent spectrometer, respectively. The morphological changes in the cells were examined by Diff-Quick staining. Expression of the Bcl-2 family and Fas was determined by RT-PCR or western blotting. The activity of caspase-3, -8 and -9 was assessed using a spectrophotometer. Sodium nitroprusside (SNP), a NO donor, decreased the cell viability of the HGF cells in a dose- and time-dependent manner. SNP enhanced the production of ROS, which was ameliorated by NAC, a free radical scavenger. ODQ, a soluble guanylate cyclase inhibitor, did not block the SNP-induced decrease in cell viability. SNP also caused apoptotic morphological changes, including cell shrinkage, chromatin condensation, and DNA fragmentation. The expression of Bax, a member of the proapoptotic Bcl-2 family, was upregulated in the SNP-treated HGF cells, whereas the expression of Bcl-2, a member of the anti-apoptotic Bcl-2 family, was downregulated. SNP augmented the release of cytochrome c from the mitochondria into the cytosol and enhanced the activity of caspase-8, -9, and -3. SNP also upregulated Fas, a component of the death receptor assembly. These results suggest that NO induces apoptosis in human gingival fibroblast via ROS and the Bcl-2 family through both mitochondrial- and death receptor-mediated pathways. Our data also indicate that the cyclic GMP pathway is not involved in NO-induced apoptosis.

• Investigative Magnetic Resonance Imaging
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• v.22 no.1
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• pp.56-60
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• 2018

Therapeutic hypothermia in cardiac arrest patients is associated with favorable outcomes mediated via neuroprotective mechanisms. We report a rare case of a 32-year-old male who demonstrated complete recovery of signal changes on perfusion-weighted imaging after therapeutic hypothermia due to cardiac arrest. Brain MRI with perfusion-weighted imaging, performed three days after ending the hypothermia therapy, showed a marked decrease in relative cerebral blood flow (rCBF) and delay in mean transit time (MTT) in the bilateral basal ganglia, thalami, brain stem, cerebellum, occipitoparietal cortex, and frontotemporal cortex. However, no cerebral ischemia was not noted on diffusion-weighted imaging (DWI) or fluid-attenuated inversion recovery (FLAIR) sequences. A follow-up brain MRI after one week showed complete resolution of the perfusion deficit and the patient was discharged without any neurologic sequelae. The mechanism and interpretation of the perfusion changes in cardiac arrest patients treated with therapeutic hypothermia are discussed.