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      • KCI등재

        시판되는 생수 내 무기물 함량에 관한 연구

        소유려,백병주,김재곤,양연미,김하나 大韓小兒齒科學會 2009 大韓小兒齒科學會誌 Vol.36 No.3

        생수 내에는 많은 미네랄이 포함하고 있으며, 이 중 칼슘, 나트륨, 칼륨, 마그네슘, 불소는 생수통에 반드시 표기해야 할 무기물이다. 칼슘, 마그네슘, 불소와 같은 무기물은 치아형성에 관여하며, 적절하게 섭취시 치아우식증을 예방할 수 있다. 현행 먹는 샘물 수질기준에 따르면 무해무기물질인 칼슘과 마그네슘에 대한 기준치는 없으며, 유해무기물질인 불소와 같은 무기물은 2 mgF/L 이하로 규정하고 있다. 본 연구는 국내에서 판매되고 있는 생수 15종을 대상으로 칼슘, 마그네슘, 불소의 농도를 측정하였고, 생수 내 무기물 함량의 표기 여부 및 무기물 농도를 비교, 검토하여 다음과 같은 결론을 얻었다. 1. 15개의 생수 중 1개의 생수를 제외하고 모두 칼슘함량을 표기하였다. 평균 칼슘농도는 34.68±31.84 mg/L, 최대 12.891±1.85 mg/L, 최소 2.0±0.02 mg/L이었다. 2. 15개의 생수 중 2개의 생수를 제외하고 모두 마그네슘 함량을 표기하였다. 평균 마그네슘 농도는 9.22±11.06 mg/L, 최대 30.43±0.75 mg/L, 최소 0.0 mg/L이었다. 3. 15개의 생수 중 4개의 생수를 제외하고 모두 불소 함량을 표기하였다. 평균 불소 농도는 0.25±0.33 mg/L, 최대 1.13±0.04 mg/L, 최소 0.01±0.03 mg/L이었다. 모두 생수는 현행 먹는 샘물 기준치인 2 mgF/L 이하에는 만족시켰다. Drinking water has lots of minerals, especially calcium, sodium, kalium, magnesium, and fluoride must be labelled on the bottle about their contents. Minerals like calcium, magnesium, and fluoride have influence to the tooth development. Appropriately taking some minerals, dental caries can be prevented somewhat degree. There is no guide line about innoxious minerals like calcium and magnesium, however, noxious mineral like fluoride, should be contained less than 2 mgF/L according to the current drinking water standard. Hereupon, it is necessary to recognize the concentration of fluoride in drinking water, so I studied 15 samples of domestic drinking water on sale about the concentration of calcium and magnesium, fluoride. The results obtained were as follows ; 1. 14 drinking waters in 15 samples showed various Ca concentration. The average Ca concentration is 34.68±31.84 mg/L. the highest is 128.91±1.85 mg/L and the lowest is 2.0±0.02 mg/L. 2. 13 drinking waters in 15 samples indicate the Mg concentration. The average concentration is 9.22±11.06 mg/L. the highest is 30.43±0.75 mg/L and the lowest is 0.0 mg/L. 3. 11 drinking waters in 15 samples indicate the F concentration. The average concentration is 0.25±0.33 mg/L, the highest is 1.13±0.04 mg/L and the lowest is 0.01±0.03 mg/L. All samples are satisfied the current drinking water standard, 2 mg F/L.

      • KCI등재후보

        사용자 수술명과 수술분류 code(ICD-9-CM) 일치율 향상에 관한 연구 : 수술실 OCS program 사용 활성화를 통하여

        최향하,김미영,김도진,유지원,장정화,박수정,박재성 한국의료QA학회 2005 한국의료질향상학회지 Vol.12 No.1

        Background : The necessity of unify and standardize codes used at hospital has been emphasized since OCS (Order Communicating System) was adopted. Therefore, the purpose of this study were to standardize operation code by continuous training of the ICD-9-CM code that is used as standard code in OCS program at operating room. Method : In 400 operation data, operation code entered in OCS program at operating room was compared to operation name recorded in medical record. In addition, a matching rate between input data of operation code by medical record department and computing input data of operation code in 3,710 cases was compared for each department. User operation name and operation code were matched and major diagnosis by operation department and operation name were also matched. Results : User operation name was reflected in operation classification code in detail, and operation code entered on user was registered. Input rate and matching rate of operation code were gradually improved after improvement activity. In particular, a matching rate was high at ophthalmology where operation name is segmented. Plastic surgery and orthopedics with a lot of emergency operation and comprehensive operation name show low input rates. Conclusions : As the medical field makes progress in computerlization, awareness of information exchange and sharing becomes higher. Among codes to classified medical institution, codes related to surgical operation are all different by user of hospital and department. Computerlization and standardization is essential. And when efforts of standardization continue in alliance with individual hospital and institution, initiative of preparing medical policy data at a national level will be accelerated.

      • 부산 일부 대학교 학생들의 니코틴 의존도와 구취의 연관성

        김유린(외 5명) 신라대학교 자연과학연구소 2012 自然科學論文集 Vol.22 No.-

        The purpose of this study is to examine the association of bad breath and nicotine dependency. By use of the findings from this study, This study conducted the survey of 53 smoker who visited dental hygiene lab for delivery from October to November 2012 with structured questionnaires(Fagerstrom Tolerance Questionnaire FTQ) and equipment(CO measuring instrument, Oral Chroma etc). The data were analyzed by using SPSS 20.0 program for χ2-test, ANOVA. Smokers' average age was 23 years old. The more higher nicotine dependence the more the average age was higher. The more higher nicotine dependence the less to nque brushing. No association of nicotine dependence and self-bad breath level. CO State was Significant differences(ND1(M=2.58), ND2(M=3.98), ND3(M=7.41), ND4(M=4.19), ND5(M=13.14))(F=2.616, p=.047). Dimethyl Sulfide was Significant differences(F=3.026, p=.026).

      • KCI등재후보

        지각과민억제제 적용이 수종 접착제의 미세인장결합강도에 미치는 영향

        황성연,이경하,유미경,이광원 大韓齒科保存學會 2003 Restorative Dentistry & Endodontics Vol.28 No.5

        This study evaluated the influence of a desensitizer(MS coat) on microtensile bond strength of different adhesives:a three step adhesive(All Bond 2), a two step adhesive(Single Bond), a one step adhesive(One up Bond F). Non-caries extracted human molars were used. Dentin surface was obtained by horizontal section on mid-portion of crown using a water cooled low speed diamond saw. Teeth were randomly divided into 6 group. AMO(MS coat + All Bond), SMO(MS coat + Single Bond) and OMO(MS coat + One up Bond F) dentin surface were treated with 17% EDTA before bonded adhesive. AMX, SMX and OMX dentin surface were bonded with All-Bond 2, Single Bond and One-up Bond F, respectively. with no previous treatment with MS coat and 17% EDTA. About 1cm high resin composite(Z 250) were incrementally build-up on the treated surface. The specimens for the microtensile test were serially sectioned perpendicular to the adhesive layer to obtain 0.7 × 0.7 mm sticks. 30 sticks were prepared from each group. After that, tensile bond strength for each stick was measured with Microtensile Tester at a 1mm/min crosshead speed. Fractured dentin surfaces were observed under the SEM. The results were statistically analysed by using a One way ANOVA and Tukey's test(p<0.05). Value in MPa were: AMO 44.35±13.21; SMO 39.35±13.32; OMO 31.07±1O.25; AMX 49.22± 16.38; SMX 56.02±13.35; OMX 72.93±16.19. Application of MS coat reduced microtensile bond strengths of both Single Bond and One up Bond F, whereas microtensile bond strengths of All Bond 2 were not affected significantly.

      • KCI등재

        다양한 치근단공 크기와 근관단면의 형태를 가지는 치아에서 taper의 정도가 미세누출에 미치는 영향

        김정희,이경하,이세준,유미경,이광원 大韓齒科保存學會 2005 Restorative Dentistry & Endodontics Vol.30 No.2

        The aim of this study was to evaluate the microleakage of teeth according to root canal preparation with & without apical enlargement in various size of apical foramen. 60 extracted one canal roots were cross-cutted at 5 mm from root apex and divided into two groups according to their apical foramen size of large (L) and small (S). Each group was subdivided into two groups accordance with their cross-sectional configuration at 5 mm from apex, round (R) and ovoid (O); SR Group, SO Group LR Group, LO Group. Each group was shaped in .02 taper by Quantec series Nickel-Titanium (NiTi) rotary file, obturated by lateral condensation method. Leakage was measured using a fluid transport model under 40cmH₂O pressure. After the leakage test, blocks which had showed the leakage retreated with .04 taper and ,06 taper and evaluated the degree of fluid filtration in each group. The data was analysed statistically using chi-square test and fisher's exact test. The results obtained were as follows : 1. Significant difference in leakage was found in groups which had different apical foramen size in .02 taper instrumentation (p < 0.05), but not in .04 taper instrumentation (p > 0.05) 2. The difference in microleakage according to the shape of canal was not evident at 5 mm from apex (p > 0.05). 3. There was correlation between .02 taper instrumentation and .04 taper instrumentation in LR group, LO group (p < 0.05). 이 연구의 목적은 근단공의 크기가 다양한 치아에서 근단공 확대의 유무에 따른 근관성형시 치아의 미세누출을 평가하기 위함이다. 1근관 치아 60개를 치근첨 상방 5mm에서 절단후 각 치아의 근단공 크기에 따라 큰 근단공 (L) 작은 근단공 (S)으로 나누었다 이 두 군을 치근첨 상방 5mm의 횡단면상 근관의 형태로 원형 (R)과 난형 (O)으로 나누었다(SR, SO, LR, LO). 각 군은 Quantec series Nickel-Titanium (Ni-Ti) rotary file을 이용하여 .02 taper로 성형 후 측방가압법으로 충전하였다. 누출은 40cmH₂O 압력하에 fluid transport method로 측정하였다. 측정 후 누출이 있는 시편은 .04 taper와 .06 taper로 재근관치료 하여 다세 미세누출을 평가하였다. 통계학적으로 chi-square test와 fisher's exact test를 이용하였다. 결과는 다음과 같다. 1. .02 taper로 성형한 군에서는 근단공의 크기에 따른 미세누출은 통계적으로 유의성이 있었고 (p < 0.05) .04 taper로 성형한 군에서는 통계적으로 유의한 차이를 보이지 않았다 (p > 0.05). 2.근첨 상방 5 mm에서 근관단면의 형태에 따른 미세누출은 통계적으로 유의하지 않았다 (p > 0.05). 3. LR group과 LO group에서는 .02 taper로 성형한 군과 .04 taper로 성형한 군사이에 유의한 차이를 보였다 (p < 0.05).

      • SCIESCOPUSKCI등재

        Pitavastatin Regulates Ang II Induced Proliferation and Migration via IGFBP-5 in VSMC

        Yu Mi Ha,Ju-Ock Nam,Young Jin Kang 대한생리학회-대한약리학회 2015 The Korean Journal of Physiology & Pharmacology Vol.19 No.6

        Angiotensin II (Ang II), a key mediator of hypertensive, causes structural changes in the arteries (vascular remodeling), which involve alterations in cell growth, vascular smooth muscle cell (VSMC) hypertrophy. Ang II promotes fibrotic factor like IGFBP5, which mediates the profibrotic effects of Ang II in the heart and kidneys, lung and so on. The purpose of this study was to identify the signaling pathway of IGFBP5 on cell proliferation and migration of Ang II-stimulated VSMC. We have been interested in Ang II-induced IGFBP5 and were curious to determine whether a Pitavastatin would ameliorate the effects. Herein, we investigated the question of whether Ang II induced the levels of IGFBP5 protein followed by proliferation and migration in VSMC. Pretreatment with the specific Angiotensin receptor type 1 (AT1) inhibitor (Losartan), Angiotensin receptor type 2 (AT2) inhibitor (PD123319), MAPK inhibitor (U0126), ERK1/2 inhibitor (PD98059), P38 inhibitor (SB600125) and PI3K inhibitor (LY294002) resulted in significantly inhibited IGFBP5 production, proliferation, and migration in Ang II-stimulated VSMC. In addition, IGFBP5 knockdown resulted in modulation of Ang II induced proliferation and migration via IGFBP5 induction. In addition, Pitavastatin modulated Ang II induced proliferation and migration in VSMC. Taken together, our results indicated that Ang II induces IGFBP5 through AT1, ERK1/2, P38, and PI3K signaling pathways, which were inhibited by Pitavastatin. These findings may suggest that Pitavastatin has an effect on vascular disease including hypertension.

      • SCIESCOPUSKCI등재

        Pitavastatin Regulates Ang II Induced Proliferation and Migration via IGFBP-5 in VSMC

        Ha, Yu Mi,Nam, Ju-Ock,Kang, Young Jin The Korean Society of Pharmacology 2015 The Korean Journal of Physiology & Pharmacology Vol.19 No.6

        Angiotensin II (Ang II), a key mediator of hypertensive, causes structural changes in the arteries (vascular remodeling), which involve alterations in cell growth, vascular smooth muscle cell (VSMC) hypertrophy. Ang II promotes fibrotic factor like IGFBP5, which mediates the profibrotic effects of Ang II in the heart and kidneys, lung and so on. The purpose of this study was to identify the signaling pathway of IGFBP5 on cell proliferation and migration of Ang II-stimulated VSMC. We have been interested in Ang II-induced IGFBP5 and were curious to determine whether a Pitavastatin would ameliorate the effects. Herein, we investigated the question of whether Ang II induced the levels of IGFBP5 protein followed by proliferation and migration in VSMC. Pretreatment with the specific Angiotensin receptor type 1 (AT1) inhibitor (Losartan), Angiotensin receptor type 2 (AT2) inhibitor (PD123319), MAPK inhibitor (U0126), ERK1/2 inhibitor (PD98059), P38 inhibitor (SB600125) and PI3K inhibitor (LY294002) resulted in significantly inhibited IGFBP5 production, proliferation, and migration in Ang II-stimulated VSMC. In addition, IGFBP5 knockdown resulted in modulation of Ang II induced proliferation and migration via IGFBP5 induction. In addition, Pitavastatin modulated Ang II induced proliferation and migration in VSMC. Taken together, our results indicated that Ang II induces IGFBP5 through AT1, ERK1/2, P38, and PI3K signaling pathways, which were inhibited by Pitavastatin. These findings may suggest that Pitavastatin has an effect on vascular disease including hypertension.

      • SCIESCOPUSKCI등재

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