• 제목/요약/키워드: induction therapy

검색결과 406건 처리시간 0.024초

식도암의 다원적 치료 (Multimodal Treatment of Esophageal Cancer)

  • 조건현
    • Journal of Chest Surgery
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    • 제23권4호
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    • pp.707-714
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    • 1990
  • Despite of mortality and morbidity rates that are higher than other forms of therapy, surgical resection has been mainstay for the treatment of esophageal cancer because of a prompt completeness as well as a high possibility of cure. But a substantial numbers of patients are unsuitable for surgical treatment and those undergoing resection have still poor long term survival rate. With hopes of improving long term survival, we have attempted multimodal approach, composed of preoperative induction chemotherapy utilizing Cisplatin and 5 \ulcornerFU, surgery and postoperative loco-regional radiotherapy for the treatment of esophageal cancer since 1985. During the period of 1967 \ulcorner1985, 27 patients[group A] were treated by surgery only and during recent 5 years 28 patients[group B] by multimodal treatment, Clinical review and comparison between the two groups were as follows: l. Applied surgical procedures were hand-sewn esophagogastrostomy, esophagocologastrostomy and esophagojejunostomy in group A. In group B, only esophagogastrostomy was underwent using stapler mainly. 2. Incidence of peri and postoperative complication showed no remarkable differences between the two groups, but the occurrences of leakage from the anastomotic site were 5[19% ] out of group A and 1[4%] out of group B. 3. The response rate to induction chemotherapy was 36% in group B, 4. The number of local cancer recurrence at the site of anastomosis was 6[22%] out of group A, whereas 2[7%] out of group B. 5. Postoperative I year and 2 year survival were 61%, 15% in group A and 75%, 42% in group B.

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Induction of Prostaglandin E2 by Porphyromonas gingivalis in Human Dental Pulp Cells

  • Kim, So-Hee;Paek, Yun-Woong;Kang, In-Chol
    • International Journal of Oral Biology
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    • 제42권4호
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    • pp.149-153
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    • 2017
  • Cyclooxygenase-2 (COX-2)-mediated prostaglandin $E_2$ ($PGE_2$) plays a key role in development and progression of inflammatory responses and Porphyromonas gingivalis is a common endodontic pathogen. In this study, we investigated induction of COX-2 and $PGE_2$ by P. gingivalis in human dental pulp cells (HDPCs). P. gingivalis increased expression of COX-2, but not that of COX-1. Increased levels of $PGE_2$ were released from P. gingivalis-infected HDPCs and this $PGE_2$ increase was blocked by celecoxib, a selective COX-2 inhibitor. P. gingivalis activated all three types of mitogen-activated protein kinases (MAPKs). P. gingivalis-induced activation of nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) was demonstrated by the results of phosphorylation of $NF-{\kappa}B$ p65 and degradation of inhibitor of ${\kappa}B-{\alpha}$ ($I{\kappa}B-{\alpha}$). Pharmacological inhibition of each of the three types of MAPKs and $NF-{\kappa}B$ substantially attenuated P. gingivalis-induced $PGE_2$ production. These results suggest that P. gingivalis should promote endodontic inflammation by stimulating dental pulp cells to produce $PGE_2$.

The Association of Increased Lung Resistance Protein Expression with Acquired Etoposide Resistance in Human H460 Lung Cancer Cell Lines

  • Lee, Eun-Myong;Lim, Soo-Jeong
    • Archives of Pharmacal Research
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    • 제29권11호
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    • pp.1018-1023
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    • 2006
  • Chemoresistance remains the major obstacle to successful therapy of cancer. In order to understand the mechanism of multidrug resistance (MDR) that is frequently observed in lung cancer patients, here we studied the contribution of MDR-related proteins by establishing lung cancer cell lines with acquired resistance against etoposide. We found that human H460 lung cancer cells responded to etoposide more sensitively than A549 cells. Among MDR-related proteins, the expression of p-glycoprotein (Pgp) and lung resistance protein (LRP) were much higher in A549 cells compared with that in H460 cells. When we established H460-R1 and -R2 cell lines by progressive exposure of H460 cells to increasing doses of etoposide, the response against etopbside as well as doxorubicin was greatly reduced in R1 and R2 cells, suggesting MDR induction. Induction of MDR was not accompanied by a decrease in the intracellular accumulation of etoposide and the expression of MDR-related proteins that function as drug efflux pumps such as Pgp and MRP1 was not changed. We found that the acquired resistance paralleled an increased expression of LRP in H460 cells. Taken together, our data suggest the implicative role of LRP in mediating MDR in lung cancer.

봉독요법(蜂毒療法)의 항염증(抗炎症) 기전(機轉) 연구(硏究)에 관(關)한 고찰(考察) (The Review on the Study related to Anti-inflammatory Mechanism of Bee Venom Therapy)

  • 최정식;박장우;오민석
    • 혜화의학회지
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    • 제15권1호
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    • pp.141-160
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    • 2006
  • The obtained results are summarized as follows 1. New findings are reporting year by year as for the study related to Anti-inflammatory mechanism of Bee Venom therapy. 2. The Anti-inflammatory effect of Bee Venom therapy is achieved through counterirritation, stimulations to adrenal cortex, immuno-regulation, antioxidation, removal of free radicals, modulation of AGP gene induction. 3. The chief components of Bee Venom related to Anti-inflammatory effect are Melittin, MCD peptide, Apamin, Adolapin etc. 4. Melittin binds to secretory phospholipase A2 and inhibits its enzymatic activity. 5. Melittin blocks neutophil O2-production. 6. MCD peptide(Peptide 401) stimulates the mast cell secrets histamine, Anti-inflammatory effect caused by this is 'conterirritation'. 7. Melittin & Apamin have an anti-inflammatory effect by inducing cortisone secretion. 8. MCD peptide & Apamin increase immunologic fuction by stimulating hypophysis & adrenal cortex and have an anti-inflammatory effect by inhibiting synthesis of prostaglandin from arachidonic acid. 9. Adolapin have an anti-inflammatory effect by inhibiting COX. 10. Bee Venom have an anti-inflammatory effect by suppressing AGP($\alpha$-acid glycoprotein). 11. Bee Venom have an anti-inflammatory effect by inhibiting NO, iNOS, PLA2, COX-2, TNF-$\alpha$, IL-1, NF-${\kappa}B$, MAP kinase.

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테이핑 요법으로 호전된 요통환자의 요추전만도 변화 1례 (Change of Lumbar Lordotic angle by Taping Therapy on Low Back Pain Patient with Lumbar Hyperlordosis ; A Case Report)

  • 윤유석;이종수;문상현
    • 대한추나의학회지
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    • 제4권1호
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    • pp.157-165
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    • 2003
  • Low back pain (LBP) is a significant in today's society, with lifetime include factors associated with LBP ar reporter. Among the causes, aberration of posture may play a role in the development of LBP. Many investigators have assessed the curvature of spine in standing posture. But LBP is associated with Lumber Hyperlordosis of Hyperlordosis is controversial Subjects: In conservative treatment(acupuncture, herb med, manipulation & TENS. exercise, potural correction) for a 40 years old woman who had low back pain(V AS) be caused by decrease lumbar lordotic angie. Objectives: The object is change of lumbar lordotic angle of a 40 years old woman who had low back pain with Lumbar hyperlordosis, In conservative treatment. Method: In conservative treatment, We added taping therapy(mechanical correction taping of Kinesio Taping) about Lumbar Lordosis. Conclusion: We experienced a 40 years old woman who had love pack pain with Lumbar hyperlordosis. In conservative treatment, Her pain was Improved by additional taping therapy In company with decrease of Lumbar Lordosis. 1. abnormal spinal curvature, specially lumbar hyperlordosis act on induction & perpetuation agent for low back pain 2. In a patient had low back pain with lumbar hyperlordosis, change of lumbar lordotic angle is of utility value for the effect of treatment and assessment of prognosis. 3. pain control is more relative with change of lumbosacral angle than lumbar lordotic angle, in patient had low back pain with lumbar hyperlordosis. 4. mechanical taping therapy with elastic adhesive tape is effective for patient had low back pain with lumbar hyperlordosis

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Mouse Air Pouch Model에서 침전극 저주파치료로 유도된 소염 작용에 관한 연구 (Study for Related Mechanism of Anti-Inflammatory Effect Induced by Neddle electrode electrical stimulation in Mouse Air Pouch Model.)

  • 정진우;황현숙;임종수
    • 대한물리치료과학회지
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    • 제9권2호
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    • pp.111-122
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    • 2002
  • In oriental medicine, manual-acupuncture and electroacupuncture (EA) have been widely utilized to cure several inflammatory diseases such as arthritis. We designed this experiment to find neurochemical mechanism related to electroacupuncture induced anti-inflammatory effect on mouse air pouch model. EA with both low frequency (1 Hz) and high frequency (120 Hz) was treated after induction of inflammation in air pouch using injection of zymosan. To verify the role of opioid system in electroacupuncture-induced anti-inflammatory effect, naloxone (10 mg/kg) was pretreated. In addition, idazoxan (5 mg/kg) was pre-treated to evaluate the possible effect of endogenous adrenergic system in autonomic system on EA induced anti-inflammatory effect. As results of this study, naloxone pretreatment did not change the anti-inflammatory effect evoked by high frequency EA, while low frequency EA(1 Hz) induced anti-inflammatory effect was dramatically suppressed by naloxone pretreatment. These data indicated that endogenous opioid system might be extensively involve in anti-inflammatory effect evoked by not high frequency, but low frequency EA. However, idazoxan pretreatment did not produce any modulatory effect on both low and high frequency EA induced anti-inflammatory effect, suggesting that EA induced anti-inflammatory effect was not mediated by endogenous adrenergic system. In conclusion, these data strongly suggested that EA induced anti-inflammatory effect is mediated by endogenous opioid system, not endogenous adrenergic system.

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기계판막을 갖고있는 임산부에서 항응고요법 (Anticoagulant Therapy in Pregnant Women with Mechanical Cardiac valve Prostheses)

  • 최순호;고광표;한재오;최종범;김경호
    • Journal of Chest Surgery
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    • 제33권6호
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    • pp.502-506
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    • 2000
  • Background: Anticoagulant therapy can be required during pregnancy with prosthetic heart valves. Warfarin and heparin provide real protection against thromboembolic phenomena, but they also carry serious risks for the fetus and the mother. In an attempt to identify the best treatment for pregnant women with cardiac valve prostheses who are receiving anticoagulant, we studied 19 pregnancies, the warfarin was discontinued and heparin was administered every 12 hours by subcutaneous injection in doses adjusted to keep the midinterval aPTT in the therapeutic range(at least 2-2.5 control) from the conception to the 12th week of gestation and oral antiocagulant was then administered until the middle of the third trimester in the therapeutic range(at least 2 INR), and heparin therapy was restared until delivery. Also in order to avoid an anticoagulant effect during delivery, it has been our practice to instruct women to either discontinue their heparin injections with the onset of labur or to stop heparin injections 12 hours prior to the elective induction of labour. Result: The outcome of 19 pregnancies managed with above protocol was spontaneous abortion in 3 cases, voluntary termination in 2 cases, premature delivery at 35 weeks in 1 case and delivery at full-term in 14 cases. There was no maternal morbidity and moratality and fetopathy. Conclusion: We conclude that in the second and third trimester of pregnancy, warfarin provide effective protection against thromboembolism, Oral antiocagulant therapy should be avoided in 2 weeks before delivery because of the risk of serious perinatal bleeding caused by the trauma of delivery to the anticoagulated fetus. However, the substitution of heparin at first trimester and 2 weeks before delivery reduce the incidence of complications.

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Extracellular ATP Induces Apoptotic Signaling in Human Monocyte Leukemic Cells, HL-60 and F-36P

  • Yoon, Mi-Jung;Lee, Hae-Jin;Kim, Jae-Hwan;Kim, Dong-Ku
    • Archives of Pharmacal Research
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    • 제29권11호
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    • pp.1032-1041
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    • 2006
  • Extracellular adenosine 5'-triphosphate (ATP) affects the function of many tissues and cells. To confirm the biological activity of ATP on human myeloid leukemic cells, F-36P and HL-60, cells were treated with a variety of concentrations of ATP. The stimulation with extracellular ATP induced the arrest of cell proliferation and cell death. from the analysis of Annexin-V staining and caspase activity by flow cytometry. The Annexin-V positive cells in both cell lines were dramatically increased following ATP stimulation. The expression of P2 purinergic receptor genes was confirmed, such as P2X1, P2X4, P2X5, P2X7 and P2Y1, P2Y2, P2Y4, P2Y5, P2Y6, P2Y11 in both leukemic cell lines. Interestingly, ATP induced intracellular calcium flux in HL-60 cells but not in F-36P cells, as determined by Fluo-3 AM staining. Cell cycle analysis revealed that ATP treatment arrested both F-36P and HL-60 cells at G1/G0. Taken together, these data showed that extracellular ATP via P2 receptor genes was involved in the cell proliferation and survival in human myeloid leukemic cells, HL-60 and F-36P cells by the induction of apoptosis and control of cell cycle. Our data suggest that treatment with extracellular nucleotides may be a novel and powerful therapeutic avenue for myeloid leukemic disease.

The maintenance mechanism of hematopoietic stem cell dormancy: role for a subset of macrophages

  • Cheong-Whan Chae;Gun Choi;You Ji Kim;Mingug Cho;Yoo-Wook Kwon;Hyo-Soo Kim
    • BMB Reports
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    • 제56권9호
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    • pp.482-487
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    • 2023
  • Hematopoiesis is regulated by crosstalk between long-term repopulating hematopoietic stem cells (LT-HSCs) and supporting niche cells in the bone marrow (BM). Here, we describe the role of KAI1, which is mainly expressed on LT-HSCs and rarely on other hematopoietic stem-progenitor cells (HSPCs), in niche-mediated LT-HSC maintenance. KAI1 activates TGF-β1/Smad3 signal in LT-HSCs, leading to the induction of CDK inhibitors and inhibition of the cell cycle. The KAI1-binding partner DARC is expressed on macrophages and stabilizes KAI1 on LT-HSCs, promoting their quiescence. Conversely, when DARC+ BM macrophages were absent, the level of surface KAI1 on LT-HSCs decreases, leading to cell-cycle entry, proliferation, and differentiation. Thus, KAI1 acts as a functional surface marker of LT-HSCs that regulates dormancy through interaction with DARC-expressing macrophages in the BM stem cell niche. Recently, we showed very special and rare macrophages expressing α-SMA+ COX2+ & DARC+ induce not only dormancy of LT-HSC through interaction of KAI1-DARC but also protect HSCs by down-regulating ROS through COX2 signaling. In the near future, the strategy to combine KAI1-positive LT-HSCs and α-SMA/Cox2/DARC triple-positive macrophages will improve the efficacy of stem cell transplantation after the ablative chemo-therapy for hematological disorders including leukemia.

Vitexicarpin Induces Apoptosis in Human Prostate Carcinoma PC-3 Cells through G2/M Phase Arrest

  • Meng, Fan-Min;Yang, Jing-Bo;Yang, Chun-Hui;Jiang, Yu;Zhou, Yong-Feng;Yu, Bo;Yang, Hong
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권12호
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    • pp.6369-6374
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    • 2012
  • Vitexicarpin (3', 5-dihydroxy-3, 4', 6, 7-tetramethoxyflavone), a polymethoxyflavone isolated from Viticis Fructus (Vitex rotundifolia Linne fil.), has long been used as an anti-inflammatory herb in traditional Chinese medicine. It has also been reported that vitexicarpin can inhibit the growth of various cancer cells. However, there is no report elucidating its effect on human prostate carcinoma cells. The aim of the present study was to examine the apoptotic induction activity of vitexicarpin on PC-3 cells and molecular mechanisms involved. MTT studies showed that vitexicarpin dose-dependently inhibited growth of PC-3 cells with an $IC_{50}{\sim}28.8{\mu}M$. Hoechst 33258 staining further revealed that vitexicarpin induced apoptotic cell death. The effect of vitexicarpin on PC-3 cells apoptosis was tested using prodium iodide (PI)/Annexin V-FITC double staining and flow cytometry. The results indicated that vitexicarpin induction of apoptotic cell death in PC-3 cells was accompanied by cell cycle arrest in the G2/M phase. Furthermore, our study demonstrated that vitexicarpin induction of PC-3 cell apoptosis was associated with upregulation of the proapoptotic protein Bax, and downregulation of antiapoptotic protein Bcl-2, release of Cytochrome c from mitochondria and decrease in mitochondrial membrane potential. Our findings suggested that vitexicarpin may become a potential leading drug in the therapy of prostate carcinoma.