2.The Role of Transient Receptor Potential Channel in Pain.
Hanyang Medical Reviews 2011;31(2):116-122
Transient receptor potential (TRP) channels, a large family of receptor channel proteins, initially attracted researchers in the pain field as key molecules in nociception, but later they became known as more general transducer molecules for various physical stresses. In this review, I will discuss their roles in thermal and mechanical sensation, and then consider their contribution to physiological pain.
Humans
;
Nociception
;
Proteins
;
Sensation
;
Transducers
;
Transient Receptor Potential Channels
4.Study on the Mitochondrial Dysfunction by p53 Regulation in Ceramide-induced Neuronal Cell Death.
Do Yeon LEE ; Hyun Jung LEE ; Yoo Hun NOH ; Ji Young YUN ; In Sook HAN ; Yoon Hee CHUNG ; Kyung Yong KIM ; Sung Su KIM ; Won Bok LEE
Korean Journal of Physical Anthropology 2006;19(1):49-59
Ceramide induces cell death in a dose- and time-dependent manner in neuroblastoma SK-N-SH cells. To investigate the mechanism of SK-N-SH cell death by C2-ceramide, morphological features and Hoechst 33258 staining were analyzed. In these morphlogic study the cell death by ceramide showed typical apoptotic features, nuclear condensation, fragmentation, and membrane blebbing. Ceramide-induced apoptosis was accompanied by nuclear accumulation of p53. Inhibition of p53 expression with p53 antisense oligonucleotides inhibited apoptosis evoked by ceramide. Also, ceramide induced mitochondrial event, collapse of mitochondrial membrane potential (delta psi m) and interestingly, inhibition of p53 attenuated collapse of mitochondrial membrane potential, suggests that ceramide induces mitochondrial dysfunction through upregulation of p53 expression. These results suggest that ceramide-induced apoptosis is dependent upon increase in cellular p53 levels which play a critical role in the regulation of apoptotic cell death and p53 modulates mitochondrial function such as mitochondrial membrane potential level.
Apoptosis
;
Bisbenzimidazole
;
Blister
;
Cell Death*
;
Membrane Potential, Mitochondrial
;
Membranes
;
Neuroblastoma
;
Neurons*
;
Oligonucleotides, Antisense
;
Up-Regulation
5.Fucodiphlorethol G Purified from Ecklonia cava Suppresses Ultraviolet B Radiation-Induced Oxidative Stress and Cellular Damage.
Ki Cheon KIM ; Mei Jing PIAO ; Jian ZHENG ; Cheng Wen YAO ; Ji Won CHA ; Madduma Hewage Susara Ruwan KUMARA ; Xia HAN ; Hee Kyoung KANG ; Nam Ho LEE ; Jin Won HYUN
Biomolecules & Therapeutics 2014;22(4):301-307
Fucodiphlorethol G (6'-[2,4-dihydroxy-6-(2,4,6-trihydroxyphenoxy)phenoxy]biphenyl-2,2',4,4',6-pentol) is a compound purified from Ecklonia cava, a brown alga that is widely distributed offshore of Jeju Island. This study investigated the protective effects of fucodiphlorethol G against oxidative damage-mediated apoptosis induced by ultraviolet B (UVB) irradiation. Fucodiphlorethol G attenuated the generation of 2, 2-diphenyl-1-picrylhydrazyl radicals and intracellular reactive oxygen species in response to UVB irradiation. Fucodiphlorethol G suppressed the inhibition of human keratinocyte growth by UVB irradiation. Additionally, the wavelength of light absorbed by fucodiphlorethol G was close to the UVB spectrum. Fucodiphlorethol G reduced UVB radiation-induced 8-isoprostane generation and DNA fragmentation in human keratinocytes. Moreover, fucodiphlorethol G reduced UVB radiation-induced loss of mitochondrial membrane potential, generation of apoptotic cells, and active caspase-9 expression. Taken together, fucodiphlorethol G protected human keratinocytes against UVB radiation-induced cell damage and apoptosis by absorbing UVB radiation and scavenging reactive oxygen species.
Apoptosis
;
Caspase 9
;
DNA Fragmentation
;
Humans
;
Keratinocytes
;
Membrane Potential, Mitochondrial
;
Oxidative Stress*
;
Reactive Oxygen Species
6.Synthesis of (4-18FFluorophenyl)triphenylphosphonium as a Mitochondrial Voltage Sensor for PET.
Dong Yeon KIM ; Kook Hyun YU ; Hee Seung BOM ; Jung Joon MIN
Nuclear Medicine and Molecular Imaging 2007;41(6):561-565
PURPOSE: Lipophilic cations including tetraphenylphosphonium (TPP) salts penetrate the hydrophobic barriers of the plasma and mitochondrial membranes, resulting in accumulation in mitochondria in response to the negative inner transmembrane potentials. The development of radiolabeled phosphonium cations as a noninvasive imaging agent may serve as a new molecular "voltage sensor" probe to investigate the role of mitochondria in the pathophysiology and diagnosis of cancer. MATERIALS AND METHODS: We have synthesized a reference compound (4-fluorophenyl)triphenylphosphonium (TPP) and a labeled compound [18F]TPP via two step nucleophilic substitution of no-carrier-added [18F]fluoride with the precursor, 4-iodophenyltrimethylammonium iodide, in the presence of Kryptofix-2.2.2 and K2CO3. RESULT: The reference compound (4-fluorophenyl)triphenylphosphonium (TPP) was synthesized in 60% yield. The radiolabeled compound [18F]TPP was synthesized in 10~15% yield. The radiochemical purity of the [18F]TPP was 95.57+/-0.51% (n=11). CONCLUSION: [18F]TPP was successfully synthesized that might have a potential to be utilized as a novel myocardial or cancer imaging agent for PET. However, it is required to improve the radiochemical yield to apply [18F]TPP in preclinical or clinical researches.
Cations
;
Diagnosis
;
Membrane Potential, Mitochondrial
;
Membrane Potentials
;
Mitochondria
;
Mitochondrial Membranes
;
Plasma
;
Salts
7.Studies on Signal Transduction Mechanism of Alcohol-induced Neuronal Cell Death and Protective Effect.
Do Yeon LEE ; Sung Su KIM ; Kyung Yong KIM ; Won Bok LEE ; Dae Kyong KIM ; Kyung Hwan KIM ; Hee Youn JUNG ; Sang Hyung LEE
Korean Journal of Physical Anthropology 2004;17(1):31-43
Excessive use of alcohol is a serious problem in our society and induces various, severe alcohol related diseases. The cytotoxicities of ethanol are still largely unknown. We studied the molecular mechanisms of EtOH-induced SK-N-SH neuronal cell death and protective effects of baicalein and gramineus against EtOH-induced cytotoxicities. In our results, the cell death by EtOH showed morphologic features of apoptosis like as membrane blebbing, nuclear condensation and fragmentation. Furthermore, pretreated baicalein attenuated EtOH-induced neuronal cell death effectively. EtOH increased expression levels of p53 and both p53 antisense oligonucleotide and Pifithrin protected the cell death against EtOH. Also, EtOH induced mitochondrial event, collapse of mitochondrial membrane potential ( delta psi m ) and caspase cascade as a downstream of mitochondria. Interestingly, baicalein decreased expression levels of p53 and inhibited collapse of mitochondrial membrane potential. These results suggest that baicalein reduces mitochondrial dysfunction induced by EtOH through down-regulation of p53 expression levels. Also, baicalein attenuated activation of caspase, which was triggered by mitochondrial malfunction. But gramineus didn't have any protective effect. These results imply that baicalein significantly protects EtOH-induced neuronal cell death through regulating p53, mitochondrial dysfunction and caspase activation.
Apoptosis
;
Blister
;
Cell Death*
;
Down-Regulation
;
Ethanol
;
Membrane Potential, Mitochondrial
;
Membranes
;
Mitochondria
;
Neurons*
;
Signal Transduction*
8.Studies on Signal Transduction Mechanism of Alcohol-induced Neuronal Cell Death and Protective Effect.
Do Yeon LEE ; Sung Su KIM ; Kyung Yong KIM ; Won Bok LEE ; Dae Kyong KIM ; Kyung Hwan KIM ; Hee Youn JUNG ; Sang Hyung LEE
Korean Journal of Physical Anthropology 2004;17(1):31-43
Excessive use of alcohol is a serious problem in our society and induces various, severe alcohol related diseases. The cytotoxicities of ethanol are still largely unknown. We studied the molecular mechanisms of EtOH-induced SK-N-SH neuronal cell death and protective effects of baicalein and gramineus against EtOH-induced cytotoxicities. In our results, the cell death by EtOH showed morphologic features of apoptosis like as membrane blebbing, nuclear condensation and fragmentation. Furthermore, pretreated baicalein attenuated EtOH-induced neuronal cell death effectively. EtOH increased expression levels of p53 and both p53 antisense oligonucleotide and Pifithrin protected the cell death against EtOH. Also, EtOH induced mitochondrial event, collapse of mitochondrial membrane potential ( delta psi m ) and caspase cascade as a downstream of mitochondria. Interestingly, baicalein decreased expression levels of p53 and inhibited collapse of mitochondrial membrane potential. These results suggest that baicalein reduces mitochondrial dysfunction induced by EtOH through down-regulation of p53 expression levels. Also, baicalein attenuated activation of caspase, which was triggered by mitochondrial malfunction. But gramineus didn't have any protective effect. These results imply that baicalein significantly protects EtOH-induced neuronal cell death through regulating p53, mitochondrial dysfunction and caspase activation.
Apoptosis
;
Blister
;
Cell Death*
;
Down-Regulation
;
Ethanol
;
Membrane Potential, Mitochondrial
;
Membranes
;
Mitochondria
;
Neurons*
;
Signal Transduction*
9.Measurement of body surface Laplacian ECG and its signal processing.
Yuzhen CAO ; Shijiu JIN ; Min CHEN ; Gang LI
Journal of Biomedical Engineering 2007;24(4):768-771
Surface Laplacian of the body surface potential (Laplacian ECG--LECG) is a new approach to resolve spatially distributed bioelectrical source. In this paper, we discussed an LECG sensor which integrated triple concentric ring electrodes and signal adjustor on a printed board. The LECG is measured directly by this sensor. The frequency, amplitude and phase of the power line interference were detected by a nonlinear adaptive filter so that interference was eliminated. The wavelet shrinking technique was used to eliminate the rest of random noise. And we got the high quality LECG signal. It laid the foundation for heart disease diagnosis.
Algorithms
;
Body Surface Potential Mapping
;
methods
;
Electrocardiography
;
methods
;
Electrodes
;
Humans
;
Signal Processing, Computer-Assisted
10.Parameter optimization of body surface laplacian electrodes in bioelectricity detection.
Journal of Biomedical Engineering 2007;24(3):671-677
In this article, some details about the parameter optimization of body surface Laplacian electrodes are presented theoretically and practically. The influence of these parameters on the performance of the electrodes is studied to derive some rules which have to be obeyed during the design. An evaluation routine based on relative error analysis and the noise level of amplifier is prompted. Furthermore, the paper particularly indicates that, it would be helpful to reduce the relative error when assuming that the effective radius b is equal to the inner radius r(i) of the ring electrode. Finally, we suggest that in the presence of weak bioelectrical signals, the effective radius of the electrodes should be reasonably increased in order to improve signal-to-noise ratio (SNR).
Body Surface Potential Mapping
;
methods
;
Electric Impedance
;
Electrodes
;
Humans
;
Signal Processing, Computer-Assisted