The purpose of this study was to investigate the antibacterial effect of the low temperature atmospheric plasma device with needle tip designed for easy approach to the oral cavity and root canal against Streptococcus mutans, Enterococcus faecalis and Candida albicans. The antibacterial activities evaluated by measuring clear zone of agar plate smeared with each bacteria after plasma treatment. To quantify antibacterial effects, dilution plate method was used. In addition, scanning electron microscope (SEM) was used for observation of changes in bacterial morphology. As treatment time of plasma increased, the clear zone was enlarged. The death rate was more than 99%. The SEM results showed that the globular shape of bacteria was distorted. These results suggest that needle tip plasma could be an innovative device for prevention of dental caries, and treatment of apical infection and soft tissue diseases.

The nitric oxide(NO) is a major factor contri buting to t he loss of neurons in ischemic st roke. demyelina t ing diseases, and other neurodegenerative di sorders . But it is known that NO is not function ing as a direct neurotoxin. NO combined with superoxide(02-) by the diffusion-contl'O ll ed reaction, formed a peroxin it ri te anion (ONOO-)‘ which this s pecies has been shown to contribute to oxidative s igna ling and damage. ONOO stimuJates apoptosis in many cell types. whether ONOO acts direct ly as an ox idant 0 1' the induction of apoptosis is because of the radicals derived from ONOO- decompositi on . But. the mecha ni sm by which ONOO- induces apoptosis is un clear although subsequent forrnation 0 1' reactive oxygen s pecies(ROS) has been suggested in a few reports The aim of this study is to investigate the a nti -apoptotic pathway by inhibi tion 0 1' ONOO synthesis t hrough scavenging of ROS us ing s pecific wavelength 0 1' light irradiation . The present study investi gated the a nti -apop totic effect of the specific wavelength 0 1' irradi ation in Sodium Nitroprusside(SNP) t reated SJ-I-SY5Y ceJls, by MTT, DNA fragmentation, and flow cytometric assay and th rough western blot and caspase-3, -9 activity assay for confirmation of caspase pathway. Also. NO reJease and ROS leveJ was measured in order to observe the changes of NO involved in radical by Griess reaction analysis and DCF'-DH. Results showed that the cell viability were r educed by about 50% of control group by SNP treatment, but re covered to about 80% by 590nm irradiation . The apoptotic cells were observed by flow cytomet ry and DNA fra g mentation assay in SNP-treated group‘ but 590nm irradiation led apoptotic feature to be reduced . Released NO a nd ROS level were increased after SNP treatment but ROS level was dec reased in 590nm irradi at ion - treated group, in spite of high NO concentration fo llowing SNP treatment Also. SNP t reatment led cytochrom C release but 590nm irraidiation inhibit it, hence the expression 0 1' caspase-3 and -9 was dec reased sign ificantly‘ These results showed that 590nm irradiation protect neuronal death thl'Ough bl ocking of NO-induced mi tochondri al apoptotic pathway. Also, it suggests that specific wavelength of irradi ation was used for prevent ion from neurodegenerative disordcr progression

It has been reported that light-emitting diodes(LED) can be used in the treatment of oral diseases. Although bio-stimulatory effects of LED irradiation such as promotes stimulation of wound healing have been well known, there are few reports about molecular mechanism associated with cell cycle by LED irradiation. The purpose of present study was to examine the molecular event in cell cycle of LED irradiation on primary human gingival fibroblast(hGF) in vitro. The source of light for irradiation was a continuous-wave LED emitting at a wavelength of 635nm, and manufactured that energy density was 5mW/cm2 on sample surface. The hGF were irradiated for 1 hour at 37℃ in 5% CO2 humidified chamber. Experimental samples were acquired at 0 (right after irradiation), 8 and 24 hour after irradiation. To investigate the molecular mechanisms associated with cell cycle, growth phase was determined by flow cytometry and mRNA expression of cyclin A, cyclin B, cyclin D1, cyclin E, cdc2, PCNA, p18, p27, p21, and p53 were determined by real time RT-PCR. Flow cytometric analysis demonstrated the percentage of cells in the G1 and S phase were decreased, but the G2 phase increased, which showed cells irradiated by LED were transitioned from S to G2 phase. For mRNA expression, cyclin B, cdc2, PCNA and p53 were increased at 0 hour after irradiation, and most of cell cycle molecules were increased at 8 hour after irradiation. At 24 hour after irradiation, cyclin A, cyclin E, PCNA and p18 were increased. Taken together, LED irradiation induced proliferation of hGF cells through transition from S to G2 phase.

The purpose 01' pl'esent study was to examine the molecular events in apoptosis by CoCl2, mimicking hypoxic cond ition and recovering effects by LED ir l'adiation on Human SH-SY5Y neuroblastoma cells The SOUl'ce 0 1' light for ir l'adiation was a continuous-wave LED emitting at a wavelenl양h of 590 nm, and manufactured that ene rgy density was 5 mW!cm2 on sample surface, After ir l'adiation, cell viabi lity was measured with BrdU , cell morphol ogy was examined with Diff- Quik staining, cell signaling was monitored with various apoptosis-related molecules using RNase Pl'otection Assay(RPA) , W11en treated with CoC12, apoptotic induction was found in the SH-SY5Y cells in a concentration-dependent and time-dependent manner , Diff-Quik s taining was revealed that DNA fragmentation re presented apoptosis was examined in CoC12-tl'eated group, Moreover, RPA assay of SH-SY5Y cclls lIs ing val'iolls apoptosis-related molecllles showed that the apoptotic cell population was mcreased J-loweve. there was sorne signifïcant change in LED irradiatied cells aftel' treatement of CoC12 The main mechanism for Lhese a poptosis appearecl to be mito c hondriεt - m ecliated pathway, such as cytochrome- c‘ caspase-9, caspase-3, pro-apototic protein ßax, anti-apototic protein Bcl-2, and death receptor• mediated pathway, such as Fas, cas pase- 8, a ncl TNFRl These results demonstrate that CoCI2 induce apoptosis in SH-SY5Y via different dual apop tosis pathway through death receptor pathway as well as mitochondria- dependent pathway and LED irradiation can recl llces the CoCl2-induced apoptosis by blocking their internal signaling pathway