• 대한치과보철학회지
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• 제41권2호
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• pp.207-222
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• 2003

As a material of metal-ceramic prosthesis, nickel as a form of Ni-Cr alloy has been used for many dental prostheses in many cases. However, several problems in use of the alloy have been revealed (ex ; tissue stimulation, skin allergy, hypersensitivity cytotoxicity and carcinogenecity). Little is known about nickel with respect to the relationship between Ni-prosthesis and gaining of Niresistance in oral microorganisms. The present study was undertaken to check whether use of Ni-prosthesis leads to occurrence of Ni-resistant microorganisms. So this study may suggest the possible relationships between the oral microorganisms and nickel-resistance in oral environment. Bacteria were isolated from the gingival crevicular fluid on the patients wearing Ni-Cr prosthesis. The isolated bacteria were tested fir their Ni-resistance in nickel containing media at different concentration from 3mM to 110mM. E. coli HB101 was used as control. The Ni-resistant bacteria were isolated and biochemically identified. The Ni-resistant bacteria were tested several biochemical, molecular-biological tests. Performed tests were : measuring the growth curve, antibiotic test, growth ability test in liquid media, isolation of the chromosome and plasmid, digestion of DNA by restriction enzyme, electrophoresis of chromosome and plasmid DNA, identification of Ni-resistant genes by the DNA hybridization. The results were as follows 1) The bacteria isolated from gingival crevicular fluid on the patients wearing Ni-Cr alloy prosthesis showed nickel-resistance. 2) The isolated microorganisms grew at nickel containing media of high concentrations (60mM-110mM). 3) Based on the biochemical tests, the isolated microorganisms were identified as Enterococcus faecalis(13 cases), Klebsiella pneumoniae(1 case) and Enterobacter gergoviae(1 case). 4) Enterococcus faecalis expressed not only nickel resistance but also the multi-drug resistance to several antibiotics ; chloramphenicol, kanamicin, streptomycin, lincomycin, clindamycin, However, all strain showed the sensitivity against the tetracycline. 5) DNA hybridization result suggests that there is no homology between the previously known gene of nickel resistance in Klebsiella pneumoniae and chromosomal DNA of Enterococcus faecalis.

• 한방안이비인후피부과학회지
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• 제15권2호
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• pp.271-288
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• 2002

Authors investigated the pathogenesis and treatment of dennatosurgical diseases in the ImJeungJiNamUiAn(臨證指南醫案). 1. The symptoms and diseases of dermatosurgery were as follows; 1) BanSaJinRa(반사진라) : eczema, atopic dermatitis, seborrheic dermatitis, psoriasis, lichen planus, pityriasis rosea, hives, dermographism, angioedema, cholinergic urticaria, urticaria pigmentosa, acne, milium, syringoma, keratosis pilaris, discoid lupus erythematosus, hypersensitivity vasculitis, drug eruption, polymorphic light eruption, rheumatic fever, juvenile rheumatoid arthritis(Still's disease), acute febrile neutrophilic dermatosis(Sweet's syndrome), Paget's disease, folliculitis, viral exanthems, molluscum contagiosum, tinea, tinea versicolor, lymphoma, lymphadenitis, lymphangitis, granuloma annulare, cherry angioma 2) ChangYang(瘡瘍) : acute stage eczema, seborrheic dermatitis, stasis ulcer, intertrigo, xerosis, psoriasis, lichen planus, ichthyosis, pityriasis rosea, rosacea, acne, keratosis pilaris, dyshidrosis, dermatitis herpetiformis, herpes gestationis, bullae in diabetics, pemphigus, lupus erythematosus, fixed drug eruption, erythema multiforme, toxic epidermal necrolysis, toxic shock syndrome, staphylococcal scaled skin syndrome, scarlet fever, folliculitis, impetigo, pyoderma gangrenosum, tinea, candidiasis, scabies, herpes simplex, herpes zoster, chicken pox, Kawasaki syndrome, lipoma, goiter, thyroid nodule, thyroiditis, hyperthyroidism, thyroid cancer, benign breast disorder, breast carcinoma, hepatic abscess, appendicitis, hemorrhoid 3) Yeok(疫) : scarlet fever, chicken pox, measles, rubella, exanthem subitum, erythema infectiosum, Epstein-Barr virus infection, cytomegalovirus infection, hand-foot-mouth disease, Kawasaki disease 4) Han(汗) : hyperhidrosis 2. The pathogenesis and treatment of dermatosurgery were as follows; 1) When the pathogenesis of BalSa(발사), BalJin(發疹), BalLa(발라) and HangJong(項腫) are wind-warm(風溫), exogenous cold with endogenous heat(外寒內熱), wind-damp(風濕), the treatment of evaporation(解表) with Menthae Herba(薄荷), Arctii Fructus(牛蒡子), Forsythiae Fructus(連翹) Mori Cortex(桑白皮), Fritillariae Cirrhosae Bulbus(貝母), Armeniaoae Amarum Semen(杏仁), Ephedrae Herba(麻黃), Cinnamomi Ramulus(桂枝), Curcumae Longae Rhizoma(薑黃), etc can be applied. 2) When the pathogenesis of BuYang(부양), ChangI(瘡痍) and ChangJilGaeSeon(瘡疾疥癬) are wind-heat(風熱), blood fever with wind transformation(血熱風動), wind-damp(風濕), the treatment of wind-dispelling(疏風) with Arctii Fructus(牛蒡子), Schizonepetae Herba(荊芥), Ledebouriellae Radix(防風), Dictamni Radicis Cortex(白鮮皮), Bombyx Batrytioatus(白？?), etc can be applied. 3) When the pathogenesis of SaHuHaeSu(사후해수), SaJin(사진), BalJin(發疹), EunJin(은진) and BuYang(부양) are wind-heat(風熱), exogenous cold with endogenous heat(外寒內熱), exogenous warm pathogen with endogenous damp-heat(溫邪外感 濕熱內蘊), warm pathogen's penetration(溫邪內陷), insidious heat's penetration of pericardium(伏熱入包絡), the treatment of Ki-cooling(淸氣) with TongSeongHwan(通聖丸), Praeparatum(豆？), Phyllostachys Folium(竹葉), Mori Cortex(桑白皮), Tetrapanacis Medulla(通草), etc can be applied. 4) When the pathogenesis of JeokBan(적반), BalLa(발라), GuChang(久瘡), GyeolHaek(結核), DamHaek(痰核), Yeong(？), YuJu(流注), Breast Diseases(乳房疾患) and DoHan(盜汗) are stagnancy's injury of Ki and blood(鬱傷氣血), gallbladder fire with stomach damp(膽火胃濕), deficiency of Yin in stomach with Kwolum's check (胃陰虛 厥陰乘), heat's penetration of blood collaterals with disharmony of liver and stomach(熱入血絡 肝胃不和), insidious pathogen in Kwolum(邪伏厥陰), the treatment of mediation(和解) with Prunellae Spica(夏枯草), Chrysanthemi Flos(菊花), Mori Folium (桑葉), Bupleuri Radix(柴胡), Coptidis Rhizoma(黃連), Scutellariae Radix(黃芩), Gardeniae Fructus(梔子), Cyperi Rhizoma(香附子), Toosendan Fructus(川？子), Curcumae Radix(鬱金), Moutan Cortex(牧丹皮), Paeoniae Radix Rubra(赤芍藥), Unoariae Ramulus Et Uncus(釣鉤藤), Cinnamorni Ramulus(桂枝), Paeoniae Radix Alba(白芍藥), Polygoni Multiflori Radix (何首烏), Cannabis Fructus (胡麻子), Ostreae Concha(牡蠣), Zizyphi Spinosae Semen(酸棗仁), Pinelliae Rhizoma(半夏), Poria(백복령). etc can be applied. 5) When the pathogenesis of BanJin(반진), BalLa(발라), ChangI(瘡痍), NamgChang(膿瘡). ChangJilGaeSeon(瘡疾疥癬), ChangYang(瘡瘍), SeoYang(署瘍), NongYang(膿瘍) and GweYang(潰瘍) are wind-damp(風濕), summer heat-damp(暑濕), damp-warm(濕溫), downward flow of damp-heat(濕熱下垂), damp-heat with phlegm transformation(濕熱化痰), gallbladder fire with stomach damp(膽火胃濕), overdose of cold herbs(寒凉之樂 過服), the treatment of damp-resolving(化濕) with Pinelliae Rhizoma(半夏), armeniacae Amarum Semen(杏仁), Arecae Pericarpium(大腹皮), Poria(백복령), Coicis Semen(薏苡仁), Talcum(滑石), Glauberitum(寒水石), Dioscoreae Tokoro Rhizoma(？？), Alismatis Rhizoma(澤瀉), Phellodendri Cortex(黃柏), Phaseoli Radiati Semen(？豆皮), Bombycis Excrementum(?沙), Bombyx Batryticatus(白？?), Stephaniae Tetrandrae Radix(防己), etc can be applied. 6) When the pathogenesis of ChangPo(瘡泡), hepatic abscess(肝癰) and appendicitis(腸癰) are food poisoning(食物中毒), Ki obstruction & blood stasis in the interior(기비혈어재과), damp-heat stagnation with six Bu organs suspension(濕熱結聚 六腑不通), the treatment of purgation(通下) with DaeHwangMokDanPiTang(大黃牧丹皮湯), Manitis Squama(穿山甲), Curcumae Radix(鬱金), Curcumae Longae Rhizoma(薑黃), Tetrapanacis Medulla(通草), etc can be applied. 7) When the pathogenesis of JeokBan(적반), BanJin(반진), EunJin(은진). BuYang(부양), ChangI(瘡痍), ChangPo(瘡泡), GuChang(久瘡), NongYang(膿瘍), GweYang(潰瘍), Jeong(정), Jeol(癤), YeokRyeo(疫？) and YeokRyeolpDan(疫？入？) are wind-heat stagnation(風熱久未解), blood fever in Yangmyong(陽明血熱), blood fever with transformation(血熱風動), heat's penetration of blood collaterals(熱入血絡). fever in blood(血分有熱), insidious heat in triple energizer(三焦伏熱), pathogen's penetration of pericardium(心包受邪), deficiency of Yong(營虛), epidemic pathogen(感受穢濁), the treatment of Yong & blood-cooling(淸營凉血) with SeoGakJiHwangTang(犀角地黃湯), Scrophulariae Radix(玄參), Salviae Miltiorrhizae Radix(丹參), Angelicae Gigantis Radix(當歸), Polygoni Multiflori Radix(何首烏), Cannabis Fructus(胡麻子), Biotae Semen(柏子仁), Liriopis Tuber(麥門冬), Phaseoli Semen(赤豆皮), Forsythiae Fructus(連翹), SaJin(사진), YangDok(瘍毒) and YeokRyeoIpDan(역려입단) are insidious heat's penetration of pericardium(伏熱入包絡), damp-warm's penetration of blood collaterals(濕溫入血絡), epidemic pathogen's penetration of pericardium(심포감수역려), the treatment of resuscitation(開竅) with JiBoDan(至寶丹), UHwangHwan(牛黃丸), Forsythiae Fructus(連翹), Curcumae Radix(鬱金), Tetrapanacis Medulla(通草), Acori Graminei Rhizoma(石菖蒲), etc can be applied. 9) When the pathogenesis of SaHuSinTong(사후신통), SaHuYeolBuJi(사후열부지), ChangI(瘡痍), YangSon(瘍損) and DoHan(盜汗) are deficiency of Yin in Yangmyong stomach(陽明胃陰虛), deficiency of Yin(陰虛), the treatment of Yin-replenishing(滋陰) with MaekMunDongTang(麥門冬湯), GyeongOkGo(瓊玉膏), Schizandrae Fructus(五味子), Adenophorae Radix(沙參), Lycii Radicis Cortex (地骨皮), Polygonati Odorati Rhizoma(玉竹), Dindrobii Herba(石斛), Paeoniae Radix Alba(白芍藥), Ligustri Lucidi Fructus (女貞子), etc can be applied. 10) When the pathogenesis of RuYang(漏瘍) is endogenous wind in Yang collaterals(陽絡內風), the treatment of endogenous wind-calming(息風) with Mume Fructus(烏梅), Paeoniae Radix Alba (白芍藥), etc be applied. 11) When the pathogenesis of GuChang(久瘡), GweYang(潰瘍), RuYang(漏瘍), ChiChang(痔瘡), JaHan(自汗) and OSimHan(五心汗) are consumption of stomach(胃損), consumption of Ki & blood(氣血耗盡), overexertion of heart vitality(勞傷心神), deficiency of Yong(營虛), deficiency of Wi(衛虛), deficiency of Yang(陽虛), the treatment of Yang-restoring & exhaustion-arresting(回陽固脫) with RijungTang(理中湯), jinMuTang(眞武湯), SaengMaekSaGunjaTang(生脈四君子湯), Astragali Radix (황기), Ledebouriellae Radix(防風), Cinnamomi Ramulus(桂枝), Angelicae Gigantis Radix(當歸), Ostreae Concha(牡蠣), Zanthoxyli Fructus(川椒), Cuscutae Semen(兎絲子), etc can be applied.

• Pediatric Infection and Vaccine
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• 제8권2호
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• pp.206-212
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• 2001

최근 소아의 인두염 및 인두편도염에서 EM-resistant group A streptococci가 15~40%까지 보고가 되고 있으며, 같은 계통의 macrolide제제들의 대한 내성도 점차 증가하고 있는 양상이 나타나고 있다. 따라서 세균성 인두편도염이 의심되는 환아의 치료에 있어서 경구용 항생제를 선택할 때는 항생제에 대한 내성과 경제성 및 환아의 순응도를 고려하여 항생제를 선택하여야 하겠다.

• 대한미생물학회지
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• 제21권3호
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• pp.311-329
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• 1986

The experimental exposure of animals to sources of ultraviolet radiation (UVR) which emit their energy primarily in the UVB region (280-320nm) is known to result in a number of well-described changes in the recipient's immune competence. Two such changes include a depressed capacity to effectively respond immunologically to transplants of syngeneic UVR tumors and a markedly reduced responsiveness to known inducers of delayedtype (DTH) and contact hypersensitivity (CH) reactions. The results of experiments that were designed to elucidate the mechanisms responsible for UVR-induced immunomodulation have implicated: 1) an altered pattern of lymphocyte recirculation, 2) suppressor T cells(Ts), 3) deviations in systemic antigen presenting cell (APC) potential. 4) changes in the production of interleukin-1-like molecules, and 5) the functional inactivation of epidermal Langerhans cells in this process. The exposure of skin to UVR, therefore, causes a number of both local and systemic alterations to the normal host immune system. In spite of this seeming complexity and diversity of responses, our recent studies have established that each of the UVR-mediated changes is probably of equal importance to creating the UVR-induced immunocompromised state. Normal animals were exposed to low dose UVR radiation on their dorsal surfaces under conditions where a $3.0\;cm^2$ area of skin was physically protected from the light energy. Contact sensitization of these animals with DNFB, to either the irradiated or protected back skin, resulted in markedly reduced CH responses. This was observed in spite of a normal responsiveness following the skin sensitization to ventral surfaces of the UVR-exposed animals. Systemic treatment of the low dose UVR recipients with the drug indomethacin (1-3 micrograms/day) during the UVR exposures resulted in a complete reversal of the depressions observed following DNFB sensitization to "protected" dorsal skin while the altered responsiveness found in the group exposed to the skin reactive chemical through directly UVR-exposed sites was maintained. These studies implicate the importance of EC as effective APC in the skin and also suggest that some of the systemic influences caused by UVR exposure involve the production of prostaglandins. This concept was further supported by finding that indomethacin treatment was also capable of totally reversing the systemic depressions in CH responsiveness caused by high dose UVR exposure (30K joules/$m^2$) of mice. Attempts to analyze the cellular mechanisms responsible established that the spleens of all animals which demonstrated altered CH responses, regardless of whether sensitization was through a normal or an irradiated skin site, contained suppressor cells. Interestingly, we also found normal levels of T effector cells in the peripheral lymph nodes of the UVR-exposed mice that were contact sensitized through normal skin. No effector cells were found when skin sensitization took place through irradiated skin sites. In spite of such an apparent paradox, insight into the probable mechanisms responsible for these observations was provided by establishing that UVR exposure of skin results in a striking and dose-dependent blockade of the efferent lymphatic vessels in all peripheral lymph nodes. Therefore, the afferent phases of immune responses can apparently take place normally in UVR exposed animals when antigen is applied to normal skin. The final effector responses, however, appear to be inhibited in the UVR-exposed animals by an apparent block of effector cell mobility. This contrasts with findings in the normal animals. Following contact sensitization, normal animals were also found to simultaneously contain both antigen specific suppressor T cells and lymph node effector cells. However, these normal animals were fully capable of mobilizing their effector cells into the systemic circulation, thereby allowing a localization of these cells to peripheral sites of antigen challenge. Our results suggest that UVR is probably not a significant inducer of suppressor T-cell activity to topically applied antigens. Rather, UVR exposure appears to modify the normal relationship which exists between effector and regulatory immune responses in vivo. It does so by either causing a direct reduction in the skin's APC function, a situation which results in an absence of effector cell generation to antigens applied to UVR-exposed skin sites, inhibiting the capacity of effector cells to gain access to skin sites of antigen challenge or by sequestering the lymphocytes with effector cell potential into the draining peripheral lymph nodes. Each of these situations result in a similar effect on the UVR-exposed host, that being a reduced capacity to elicit a CH response. We hypothesize that altered DTH responses, altered alloresponses, and altered graft-versus-host responses, all of which have been observed in UVR exposed animals, may result from similar mechanisms.