• Asian Pacific Journal of Cancer Prevention
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• 제17권8호
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• pp.4107-4111
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• 2016

Background: Oral cancers account for approximately 2% of all cancers diagnosed each year; however, the vast majority (80%) of the affected individuals are smokers whose risk of developing a lesion is five to nine times greater than that of non-smokers. Tobacco smoke contains numerous carcinogens that cause DNA damage, including oxidative lesions that are removed effectively by the base-excision repair (BER) pathway, in which poly (ADP-ribose) polymerase 1 (PARP-1), plays key roles. Genetic variations in the genes encoding DNA repair enzymes may alter their functions. Several studies reported mixed effects on the association between PARP-1 variants and the risk of cancer development. Till now no reported studies have investigated the association between PARP-1 variants and oral squamous cell carcinoma (OSCC) risk in an Indian population. Materials and Methods: In the present case control study 100 OSCC patients and 100 matched controls were genotyped using PARP1 single nucleotide peptides (SNP's) rs1136410 and rs3219090 using TaqMan assays. Results: The results indicated significantly higher risk with PARP1 rs1136410 minor allele "C" (OR=1.909; p=0.02942; CI, 1.060-3.439). SNP rs1136410 also showed significantly increased risk in patients with smoking habit at C/C genotype and at minor allele C. Conclusions: The PAPR-1 Ala762Val polymorphism may play a role in progression of OSCC. Larger studies with a greater number of samples are needed to verify these findings.

• 한국식품위생안전성학회지
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• 제34권3호
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• pp.303-308
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• 2019

L-carnitine은 라이신과 메티오닌으로 생합성되며 골격근과 심근을 포함한 다양한 동물조직에서 발견된다. L-carnitine이 포함된 식품으로는 양고기, 소고기, 돼지고기 등이 있고 근육발달에 도움을 주며 뼈를 강화하거나 대사작용을 도와주는 기능을 하여 영양 보조제로 많이 섭취하는 것으로 알려져 있다. 최근 L-carnitine은 제 2형 당뇨병, 골다공증, 대사성 신경증후군 등의 다양한 질병의 약물로도 연구 되고 있으며 암에서는 치료 보조제로 개발되어있다. 하지만 대장암에서의 L-carnitine에 대한 효과 및 기전에 대해서는 명확하지 않고 연구된 바가 없기 때문에 본 연구에서 저자들은 L-carnitine의 효능을 인간대장암세포주 HCT116에서 규명하고자 하였다. L-carnitine은 세포 내 활성산소종 (ROS)를 높은 수준으로 증가시켜 세포 증식을 억제하였다. 또한, 세포 증식과 죽음에 관련한 단백질 ERK1/2와 p38을 유의적으로 활성화 시킨다는 것을 입증하였다. 이때, ERK1/2 억제제(PD98059)를 처치하여 ERK1/2의 활성화가 활성산소종 발생 및 세포사멸에 중요하다는 것을 밝혔다. 따라서, 본 연구 결과는 L-carnitine이 대장암세포주의 증식을 억제 할 수 있고 이는 대장암의 치료에 있어 잠재적인 치료 물질이 될 수 있음을 시사하며 이 과정에 관여하는 신호전달기전을 조사하여 항암의 치료기전에서 활성산소종이나 ERK1/2, p38 단백질의 활성화의 중요성을 제시하였다.

• Korean Journal of Acupuncture
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• 제22권2호
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• pp.9-24
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• 2005

Objective: We have studied the effects of acupuncture and low level He-Ne laser therapy(LLLT) at $SI_3$, $BL_{40}$ on the tibial, sural nerve injury due to sports-damage or traffic accident and L5 spinal nerve ligature model like general herniation of nucleus pulposus(HNP) in a rat of neuopathic pain. Methods: A model of neuropathic pain was made by injuring tibial nerve and sural nerve while common peroneal nerve was maintained. Also, it was made by isolating left 5th lumbar spinal nerve. Three weeks after the neuropathic surgery, acupuncture and LLLT was injected at $SI_3$,$BL_{40}$ one time a day for one week. LLLT was divided three groups, that is LLLT-1(5mW), LLLT-2(10mW) and LLLT-3(30mW). After that, we examined the withdrawal response of neuropathic rats' legs by Von frey filament and acetone stimulation. And also we examined c-Fos, Nocieptin and KOR-3 in the midbrain central gray of neuropathic rats. Results: As we have observed the effect of mechanical allodynia, LLLT-3 group were diminished on 4 day, 5 day, 6 day and 7 day in the resection model compared with control model, LLLT-1 group were diminished on 5 day, LLLT-2 group were diminished on 3 day and 6 day, LLLT-3 group were diminished on 3 day, 4 day, 5 day, 6 day and 7 day in connected model compared with control group. As we have observed the effect of cold allodynia, LLLT-3 group were diminished on 7 day in the resection model compared with control model, LLLT-1 group were diminished on 6 day, 7 day, LLLT-3 group were diminished on 7 day in connected model compared with control group. As we have observed the effect of activity of c-Fos in the central gray part, LLLT-3 were diminished in resection model compared with control group, LLLT-1 group were diminished in connected model compared with control group. As we have observed the effect of activity of Nociceptin in the central gray part, resection model were not increased compared with control group, LLLT-1 group and LLLT-3 group were increased in connected model compared with control model. As we have observed the effect of activity of KOR-3 in the central gray part, resection model were not increased compared with control group, LLLT-3 group were increased in connected model compared with control model. Conclusions: We have noticed that LLLT-1 and LLLT-3 group have more controllable effect than acupuncture group. This study can be used in clinical therapy for neuropathic pain. But it is not reliability that Nociceptin and KOR-3 have effectively to control pain. Therefore We have to follow up about that.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제27권5호
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• pp.373-384
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• 2001

Cellular proliferation is an intricately regulated process mediated by the coordinated interactions of critical growth control genes. Two of these factors in mammalian cells are the p53 and mdm-2 genes. A protein product of the mem-2 oncogene has been recently shown to associate with the protein encoded by the tumor suppressor gene p53. The p53 tumor suppressor protein is stabilized in response to DNA damage and other stress signals and causes the cell to undergo growth arrest or apoptosis, thus preventing the establishment of mutations in future cellular generations. Mutation or loss of p53 is a very common event in tumor progression. It occurs in about 50% of all tumors analysed including of colon, lung, breast and liver. The cellular mdm-2 gene, which has potential transforming activity that can be activated by overexpression, is amplified in a significant percentage of human sarcoma and in other mammalian tumors. Proteins encoded by the mdm-2 gene are able to bind to the p53 protein and, when overexpressed, can inhibit p53's transcriptional activation function, thus mdm-2 can act as a negative regulator of p53 function. Experimental study was performed to observe the relationship between p53 gene mutation and mdm-2 protein expression and apply the results to the clinical activity. 36 golden syrian hamster each weighing $60{\sim}80g$ were used and painted with 0.5% DMBA by 3 times weekly on the right buccal cheek(experimental side) for 6, 8, 10, 12, 14 and 16 weeks. Left buccal cheek(control side) was treated with mineral oil as the same manner to the right side. The hamsters were sacrificed on the 6, 8, 10, 12, 14 & 16 weeks. Normal and tumor tissues from paraffin block were examined for histology and immunohistochemistry observation, and were completely dissected by microdissection and DNA from both tissue were isolated by proteins K/phenol/chloroform extraction. Segments of the hamster p53 exons 5, 6, 7 and 8 were amplified by PCR using the oligonucleotide primers, and then confirmational change was observed by SSCP respectively. The results were as follows : 1. Dysplasia at 6 weeks, carcinoma in situ at 8 weeks and invasive carcinoma from 10 weeks could be observed in experimental groups. 2. p53 mutations were detected in 10 of the 36(28%) and the exons 6(6 of the 10 : 60%) was the most hot spot area among the highy conserved region(exons 5, 6, 7 & 8). 3. Immunohistochemical study confirmed 22 of the 36(61%) of p53 expression involving 10 of p53 mutations. 4. mdm-2 expression of was showed in 3 of the 36(8%) involving 1 of the 22 of p53 expression and 2 of the 14 of p53 non-expression. From the above results, mutation of p53 gene or expression of p53 protein may have the influence of the DMBA induced carcinoma of hamster buccal pouch but the expression of mdm-2 protein may not have relationship with tumorigenesis.

• 대한소아치과학회지
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• 제35권2호
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• pp.351-356
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• 2008

뇌성마비(cerebral palsy)는 비진행성의 정신, 운동 장애를 총칭하는 용어로, 소아 장애의 흔한 원인이 된다. 자해 행위란(self-injurious behavior) 자살 의도없이 자신의 신체 일부를 고의적으로 손상시키는 것으로, 종종 반복적인 행동으로 나타난다. 소아에서의 이러한 자해 습관은 정상적인 어린이에서는 드물며, 증후군, 유전질환, 정신지체 어린이 등에서 그 발생률이 높게 보고된다. 구강 내 자해 행위의 가장 흔한 유형은 혀나 입술 혹은 구강 점막을 물어뜯는 것이다. 이러한 자해 행위를 조절하기 위하여 행동 수정법, 약물 치료, 신체 속박술, 치과적 장치의 적용, 외과적 수술 또는 치아 발치술 등의 다양한 방법들이 제시되었다. 이 중 마우스가드 등의 치과적 장치를 이용한 방법은 구강 내 자해 행위의 감소와 조직의 보호를 위해 가장 보존적이며 적합한 방법이라고 사료된다. 본 증례에서는 자해 습관에 의해 하순과 협점막에 궤양성 병소를 가진 뇌성마비 환아에 있어서, 변형된 마우스가드를 이용하여 자해에 의한 손상을 방지하고 만족할 만한 치유 양상을 보였기에 이를 보고하는 바이다.

• Journal of Chest Surgery
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• 제37권2호
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• pp.131-138
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• 2004

이공심폐기를 사용하지 않는 관상동맥 우회술에서 출혈로부터 수술시야를 확보하기 위해 사용하는 고유량의 가스 통기는 관상동맥 내피세포에 나쁜 영향을 미칠 수 있다. 본 연구에서는 이산화탄소 가스 통기가 유량에 따라서 관상동맥 내피세포에 다른 영향을 미치는가를 규명하고, 가습의 추가가 관상동맥 내피세포에 보호효과를 나타내는지를 평가하고자 하였다. 대상 및 방법: 돼지(n=9)를 이용하여 정중흉골 절개 후 좌전하 관상동맥을 노출한 후 4개의 분절로 나누어, 심박동 상태에서 각각의 관상동맥 분절에 절개를 가한 후, 가장 원위부 분절은 가스통기 없이 10분간 노출하였고(대조군), 다음 원위부 분절은 가습 없이 5 L/min의 유량으로(I군), 중앙 분절은 가습하면서 5 L/min의 유량으로 (II군), 근위부 분절은 가습하면서 10 L/min의 유량으로(III군) 각각 10분간 절개부위에 이산화탄소를 통기하였다. 관상동맥 분절들을 적출 후 내피세포층의 손상 정도를 평가하기 위해 hematoxyline-eosin 염색, 특수염색인 탄력섬유 염색, CD34 monoclonal antibody를 이용한 면역염색 등을 시행하고 전자현미경을 통하여 관상동맥 내막의 미세구조를 관찰하였다. 결과: I, II, III군 모두에서 내탄력판은 손상없이 온전하였으나 관상동맥 내피세포층은 모두에서 유의한 손상이 관찰되었다. 내피세포의 평균 잔존비율은 각각 I군이 20.9$\pm$16.7%, II군이 39.3$\pm$19.6%, III군이 6.8$\pm$5.3%로, II군이 다른 군들에 비해서 통계적으로 유의하게 높았으며(p=0.008), I군은 III군보다 유의하게 높았다. 결론: 이상의 결과로 이산화탄소 가스 통기로 인한 관상동맥 손상의 정도는 주로 통기 가스의 유량에 달려있으며, 10 L/min 이상의 고유량의 이산화탄소 가스 통기 시에는 가습을 하더라도 관상동맥 내피세포층의 보호효과를 기대하기 힘들다고 할 수 있다.

• Journal of Chest Surgery
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• 제33권9호
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• pp.697-706
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• 2000

Background: Isolated lung perfusion(ILP) was developed as a new treatment approach to non-resectable primary or metastatic lung cancer, because of its ability to reduce systemic toxicity while delivering high-dose chemotherapeutic agents to the target organs. This research was planned to evaluate the direct toxic effect of high-dose cisplatin to the lung tissue during isolated lung perfusion. Material and Method: Fifteen mongrel dogs were divided in the perfusate for 40 minutes. The second group was composed of 5 mongrel dogs which underwent ILP with cisplatin 2.5 mg/Kg added to the perfusate for 30 minutes and 10 minutes with washing solution without cisplatin. The third group underwent the same procedure as the second group except cisplatin 5.0 mg/Kg in the perfusate. Activities of serum angiotensin converting enzyme(ACE), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and concentration of serum lactate dehydrogenase(LDH) and blood urea nitrogen/creatinine (BUN/Cr) were analyzed in each groups at the time of pre-perfusion, 1 hour, 1 day, 1 week, and 2 weeks after ILP. Result: Serum ACE activities before and 1 hour, 1 day, 1 week, and 2 weeks after ILP in control group were 45.1$\pm$6.3, 44.6$\pm$9.3, 46.7$\pm$9.5, 50.8$\pm$9.1, 46.1$\pm$4.3 U/L. Those in cisplatin 2.5 and 5.0 mg/Kg groups were 49.4$\pm$12.6, 39.0$\pm$8.6, 42.3$\pm$15.9, 50.0$\pm$2.6, 53.8$\pm$8.3 and 55.5$\pm$12.3, 47.0$\pm$6.3, 45.1$\pm$6.9, 74.8$\pm$19.5, 60.2$\pm$12.0 U/L, respectively. Serum TNF-$\alpha$ activities in each group before and after ILP were 5.0$\pm$1.5 / 7.7$\pm$2.2 / 6.6$\pm$2.5 / 4.3$\pm$1.3 / 5.2$\pm$1.1(control), 8.7$\pm$1.6 / 9.9$\pm$2.2 / 7.9$\pm$1.5 / 6.3$\pm$2.2 / 7.4$\pm$2.4 (cisplatin 2.5 mg/Kg), and 6.9$\pm$0.7 / 8.9$\pm$3.4 / 7.9$\pm$4.0 / 3.3$\pm$0.9 / 5.8$\pm$1.3 pg/ml(cisplatin 5.0 mg/Kg). Mean LDH levels of each group were 225.7 / 271.3 / 328.9 / 350.8 / 255.7(control), 235.7 / 265.7 / 336.0 / 379.5 / 299.2 (cisplatin 2.5 mg/Kg), and 259.6 / 285.2 / 340.6 / 433.4 / 292.4 IU/L(cisplatin 5.0 mg/Kg). So there was no significant difference in serum ACE, TNF-$\alpha$, and LDH activity changes after ILP between the 3 groups. And, there was no significant changes in BUN/Cr in each groups, which was independent of ILP and perfused concentration of cisplatin. In addition, all dogs survived the ILP and there was no significant evidence of pulmonary vascular injury after 2 weeks of ILP with cisplatin. Conclusion: There was no harmful effect of cisplatin to the lund tissue of the mongrel dog up to 5.0 mg/Kg in perfusate. Therefore, it is perceived to be safe and effective to deliver high-dose cisplatin to the lung without pulmonary toxicity and renal damage with ILP.

• 한국방사선학회논문지
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• 제15권2호
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• pp.265-271
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• 2021

수목의 내부 부후의 양상은 많은 원인에 의존한다. 이런 다양한 부후의 원인은 일반적인 방법으로는 탐지가 어렵기 때문에 장기간 부후 상태를 확인할 수 없다면 부후 부위의 확대로 인해 수목의 심각한 피해가 발생할 수 있다. 수목 단층 영상을 획득하는 방식은 센서를 고무망치로 두드려 수목을 통과하는 임펄스가 생성되어 이동하는 속도를 기록한다. 본 논문에서는 물리적 손상에 의한 균열, 공동, 부후를 측정할 수 있도록 Arbotom에서 획득한 수목 단면 영상을 이용하여 수목의 내부 상태를 알 수 있는 3D 뷰어를 개발하여 수목 내부의 부후가 진행된 정도를 파악하고 이를 바탕으로 수목의 외과적 수술이 필요한 경우 참고할 수 있는 데이터를 제시하고자 하였다. 수목의 단층 영상을 획득하기 위해 세 그루의 양버즘 나무와 단풍 나무에 6개의 센서를 부착하여 1m 길이의 나무를 Arbotom 프로그램을 이용하여 측정하였으며 MATLAB을 이용하여 제작한 3D Viewer를 통하여 3D 영상을 구현하였다. 단순히 영상의 획득 뿐만 아니라 수목의 단면 길이와 부피를 측정하였으며 실제로 제작한 3D Viewer에서 단풍 나무의 부후가 발생된 부분 길이는 33.12 cm, 양버즘 나무의 부후는 21.41 cm로 측정되었으며 단풍 나무의 부후의 부피는 78.832 ㎤로 측정되었다. Arbotom의 단면 영상과 3D 영상을 비교한 결과 수목의 실제 양상과 같은 결과를 획득하였기 때문에 제작된 소프트웨어 신뢰성 또한 확보된 것으로 판단할 수 있으며 제작된 Viewer를 통하여 외과적 수목 수술에 적용할 데이터를 제공해 수목의 피해를 최소화 할 것으로 사료된다.

• 대한치과마취과학회지
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• 제14권1호
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• pp.49-56
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• 2014

Background: Propofol (2.6-diisopropylphenol) is a widely used intravenous anesthetic agent for the induction and maintenance of anesthesia during surgeries and sedation for ICU patients. Propofol has a structural similarity to the endogenous antioxidant vitamin E and exhibits antioxidant activities.13) However, the mechanism of propofol on hypoxia/reoxygenation (H/R) injury has yet to be fully elucidated. We investigated how P-PostC influences the autophagy and cell death, a cellular damage occurring during the H/R injury. Methods: The groups were randomly divided into the following groups: Control: cells were incubated in normoxia (5% CO2, 21% O2, and 74% N2) without propofol treatment. H/R: cells were exposed to 24 h of hypoxia (5% CO2, 1% O2, and 94% N2) followed by 12 h of reoxygenation (5% CO2, 21% O2, and 74% N2). H/R + P-PostC: cells post-treated with propofol were exposed to 24 h of hypoxia followed by 12 h of reoxygenation. 3-MA + P-PostC: cells pretreated with 3-MA and post-treated propofol were exposed to 24 h of hypoxia followed by 12 h of reoxygenation Results: The results of our present study provides a new direction of research on mechanisms of propofol-mediated cytoprotection. There are three principal findings of these studies. First, the application of P-PostC at the onset of reoxygenation after hypoxia significantly increased COS-7 cell viability. Second, the cellular protective effect of P-PostC in H/R induced COS-7 cells was probably related to activation of intra-cellular autophagy. And third, the autophagy pathway inhibitor 3-MA blocked the protective effect of P-PostC on cell viability, suggesting a key role of autophagy in cellular protective effect of P-PostC. Conclusions: These data provided evidence that P-PostC reduced cell death in H/R model of COS-7 cells, which was in agreement with the protection by P-PostC demonstrated in isolated COS-7 cells exposed to H/R injury. Although the this study could not represent the protection by P-PostC in vivo, the data demonstrate another model in which endogenous mechanisms evoked by P-PostC protected the COS-7 cells exposed to H/R injury from cell death.

• 대한한의학회지
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• 제26권2호
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• pp.217-230
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• 2005

Objectives: Chungpaesagan-tang (CPSGT), which is frequently used for treating patients of cerebrovascular disease, has not been reported by clinical doctors concerning the effect of neuronal aptosis caused by brain ischemia. To study the effect of CPSGT on focal cerebral ischemia in normal and diabetic rats and SHR, focal cerebral ischemia was induced by transient MCAO, and after onset CPSGT was administrated. Methods: Rats (Sprague-Dawley) were divided into four groups: sham-operated group, MCA-occluded group, CPSGT­administrated group after MCA occlusion, and normal group. The MCA was occluded by intraluminal method. CPSGT was administrated orally twice (l and 4 hours) after middle cerebral artery occlusion. All groups were sacrificed at 24 hours after the surgery. The brain tissue Was stained with $2\%$ triphenyl tetrazolium chloride (TTC) or $1\%$ cresyl violet solution, to examine effect of CPSGT on ischemic brain tissue. The blood samples were obtained from the heart.~. Tumor necrosis $factor-\alpha$ level and interleukin-6 level of serum was measured from sera using enzyme-linked immunoabsorbent assay (ELISA). Then changes of immunohistochemical expression of $TNF-\alpha$ in ischemic damaged areas were observed. Results: In NC+MCAO+CP and DM+MCAO+CP, CPSGT significantly (p<0.01) decreased the number of neuron cells compared to the control group. CPSGT markedly reduced (p<0.01) the infarct size of the forebrain in distance from the interaural line on cerebral ischemia in diabetic rats. CPSGT significantly reduced the $TNF-\alpha$ expression in penumbra region of damaged hemisphere in diabetic rats. Conclusions: CPSGT had a protective effect on cerebral ischemia in SD rats, especially in diabetic rats compared with normal SD rats.