Search

Background. The purpose of this study was to evaluate the efficacy and safety of Panax ginseng extract (GS-KG9) in the treatment of hepatic dysfunction. Methods. A randomized, double-blind, placebo-controlled clinical trial was conducted from December 2017 to January 2019. The trial included 60 subjects between the ages of 19 and 70 who had higher alanine transaminase (ALT) levels than the normal upper limit. The subjects were randomly divided into two groups: GS-KG9 (n = 30) and placebo (n = 30). The former was administered three GS-KG9 capsules (3 g/day) and the latter three placebo capsules (3 g/day) twice each day orally after meals in the morning and evening for 12 weeks. The primary goal was to observe the changes in ALT and gamma-glutamyl transferase (GGT) levels. The safety of the treatment was assessed and adverse events (AEs) were recorded. Results. Out of 60 subjects, nine were excluded from the efficacy analysis because they met the exclusion criteria. Therefore, a total of 51 subjects were evaluated for the effectiveness of the treatment (26 in the GS-KG9 group and 25 in the placebo group). After 12 weeks of treatment, the ALT levels were significantly reduced in the GS-KG9 group compared to the placebo group (p=0.009). The GGT level of the GS-KG9 group was significantly lower than that of the placebo group (p=0.036). Mild AEs, such as diarrhea, occurred during the study. There were no significant differences between the two groups. Conclusion. The results of this trial suggest that GS-KG9 might be an effective and safe option for mild hepatic dysfunction. This trial is registered with KCT0004080.

From 25% to 50% of adults are affected by prehypertension. Prehypertension increases the risk of hypertension and affects the heart and systemic vascular system. Food mixed tree essence of Dendropa...

Background The purpose of this study was to evaluate the efficacy and safety of Panax ginseng extract (GS-KG9) in the treatment of hepatic dysfunction. Methods A randomized, double-blind, placebo-controlled clinical trial was conducted from December 2017 to January 2019. The trial included 60 subjects between the ages of 19 and 70 who had higher alanine transaminase (ALT) levels than the normal upper limit. The subjects were randomly divided into two groups: GS-KG9 (n = 30) and placebo (n = 30). The former was administered three GS-KG9 capsules (3 g/day) and the latter three placebo capsules (3 g/day) twice each day orally after meals in the morning and evening for 12 weeks. The primary goal was to observe the changes in ALT and gamma-glutamyl transferase (GGT) levels. The safety of the treatment was assessed and adverse events (AEs) were recorded. Results Out of 60 subjects, nine were excluded from the efficacy analysis because they met the exclusion criteria. Therefore, a total of 51 subjects were evaluated for the effectiveness of the treatment (26 in the GS-KG9 group and 25 in the placebo group). After 12 weeks of treatment, the ALT levels were significantly reduced in the GS-KG9 group compared to the placebo group (p=0.009). The GGT level of the GS-KG9 group was significantly lower than that of the placebo group (p=0.036). Mild AEs, such as diarrhea, occurred during the study. There were no significant differences between the two groups. Conclusion The results of this trial suggest that GS-KG9 might be an effective and safe option for mild hepatic dysfunction. This trial is registered with KCT0004080.

Sonography is conventionally used to diagnose fractures by identifying cortical discontinuity of the bone. In this study, fracture sonography in addition to color Doppler and dynamic scanning was performed in settings with limited or no access to radiography. We describe 5 cases of ankle and foot fractures with the use of sonography to identify changes in the fractured site. The width of the fracture space increased on dynamic scanning, and the Doppler signals were generated inside the fracture space on dynamic scanning. In conclusion, color Doppler sonography accompanied by dynamic scanning is a useful adjunctive diagnostic tool in addition to previously described sonographic fracture findings.

// Jong Cheon Joo 1, * , Jung Hoo Hwang 2, * , Eunbi Jo 3 , Young-Rang Kim 3 , Dae Joon Kim 4 , Kyung-Bok Lee 3 , Soo Jung Park 5 , Ik-Soon Jang 3 1 Department of Sasang Constitutional Medicine, Wonkwang University, Iksan, 54538, Republic of Korea 2 College of Medicine, Chung-Ang University, Seoul 156-756, Republic of Korea 3 Division of Bioconvergence Analysis, Korea Basic Science Institute, Daejeon 305-333, Republic of Korea 4 Department of Biomedical Sciences, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX 78539, USA 5 Department of Sasang Constitutional Medicine, Woosuk University, Wanju, Jeonbuk, 55338, Republic of Korea * These authors have contributed equally to this work Correspondence to: Ik-Soon Jang, email: jangiksn@kbsi.re.kr Soo Jung Park, email: taorgi@hanmail.net Keywords: cordycepin, CAV1, JNK, Foxo3a, apoptosis Received: June 13, 2016 Accepted: December 27, 2016 Published: January 14, 2017 ABSTRACT Forkhead transcription factor (Foxo3a) is a downstream effector of JNK-induced tumor suppression. However, it is not clear whether the caveolin-1 (CAV1)-mediated JNK/Foxo3a pathway is involved in cancer cell apoptosis. We found that cordycepin upregulates CAV1 expression, which was accompanied by JNK phosphorylation (p-JNK) and subsequent Foxo3a translocation into the nucleus, resulting in the upregulation of Bax protein expression. Furthermore, we found that CAV1 overexpression upregulated p-JNK, whereas CAV1 siRNA downregulated p-JNK. Additionally, SP600125, a specific JNK inhibitor, significantly increased Foxo3a phosphorylation, which downregulated Foxo3a translocation into the nucleus, indicating that CAV1 mediates JNK regulation of Foxo3a. Foxo3a siRNA downregulated Bax protein and attenuated A549 apoptosis, indicating that the CAV1-mediated JNK/Foxo3a pathway induces the apoptosis of A549 lung cancer cells. Cordycepin significantly decreased tumor volume in nude mice. Taken together, these results indicate that cordycepin promotes CAV1 upregulation to enhance JNK/Foxo3a signaling pathway activation, inducing apoptosis in lung cancer cells, and support its potential as a therapeutic agent for lung cancer.

Tongue of Fatigue by Classification of Sasang Constitution and Qi Blood Pattern Identification Na-Rae Choi ＊ , Soo-Jung Park ＊ , Jong-Cheon Joo ＊ , Young-Mi Kwon †＊ Dept. of Sasang Constitutional Medicine, College of Korean Medicine, Wonkwang University † Dept. of Radiology, College of Korean Medicine, Wonkwang UniversityObjectivesThe purpose of this study was to investigate the relevance of Sasang constitution, Qi Blood pattern identification, and tongue diagnosis in subjects complaining of fatigue.Methods Seventy-three subjects who complained of fatigue were assessed using the Chalder Fatigue Scale, tongue diagnosis, pattern identification questionnaire and Sasang constitution diagnosis. The association of tongue diagnosis with Qi Blood pattern identification and Sasang constitution was evaluated. Results1. There was no significant association between tongue diagnosis and Sasang constitution.2. Tongue color, which is one of the diagnostic indicators in tongue diagnosis, was redder in the Qi stagnation group than in the Qi deficiency and Blood deficiency groups. ConclusionsTongue diagnosis can be utilized in future if proper research regarding Sasang constitution and Sasang constitution pattern identification is conducted.Key Words

Cellular FLICE inhibitory protein (c-FLIP) is a key anti-apoptotic regulator that associates with the signaling complex downstream of NF-κB, negatively interfering with apoptotic signaling. The role of c-FLIP downregulation by negative regulation of NF-κB signaling during apoptosis is poorly understood. Here, we demonstrate that NF-κB-mediated c-FLIPL negatively regulates the JNK signaling pathway, and that cordycepin treatment of human renal cancer cells leads to apoptosis induction through c-FLIPL inhibition. TNF-α-induced inflammatory microenvironments stimulated NF-κB signaling and the c-FLIP long form (c-FLIPL) in TK-10 cells. Specifically, cordycepin inhibited TNF-α-mediated NF-κB activation, which induced renal cancer cell apoptosis. Cordycepin downregulated GADD45B and c-FLIPL, but upregulated MKK7 and phospho-JNK, by preventing nuclear mobilization of NF-κB. Furthermore, siRNA-mediated knockdown of GADD45B in cordycepin-treated TK-10 cells considerably increased MKK7 compared to cordycepin alone. siRNA-mediated knockdown of c-FLIPL prevented TNF-α-induced JNK inactivation, whereas c-FLIPL overexpression inhibited cordycepin-mediated JNK activation. The JNK inhibitor SP600125 strongly inhibited Bax expression. In nude mice, cordycepin significantly decreased tumor volume. Taken together, the results indicate that cordycepin inhibits TNF-α-mediated NF-κB/GADD45B signaling, which activates the MKK7-JNK signaling pathway through inhibition of c-FLIPL expression, thus inducing TK-10 cell apoptosis.

Sasang Constitutional Characteristic of Amyotrophic Lateral Sclerosis Soo-Jung Park, Ho-Hyun Jeong * , Eun-Su Jang † , Sang-Hyuk Kim † , Sung-Chul Kim, Jong-Cheon JooDept. of Sasang Constitutional Medicine, Wonkwang University Jeonju Korean Medicine Hospital, * Dept. of Acupuncture and Moxibustional Medicine, Wonkwang University Gwangju Korean Medicine Hospital, † KM Health Technology Research Group, Korea Institute of Oriental MedicineObjectivesThe purpose of this study was to analyze the Sasang constitution and psychological traits of amyotrophic lateral sclerosis (ALS) patients and to utilize the results in treatment and management. MethodsThe differences of Sasang Constitution distribution, psychological characteristics, comorbid disorders between ALS group of 26 patients and general group of 1132 persons were investigated and analyzed.ResultsThere was no significant different distribution of Sasang Constitution between ALS group and general group but there was Yang-like personality tendency in ALS group than general group. In overall constitution, ALS group had the high prevalence rate of musculoskeletal disorders and diabetes than general group. In Soyangin constitution, ALS group had a high prevalence rate of musculoskeletal disorders than genral group. In Taeeumin constitution, ALS group had a high prevalence rate of diabetes and hypertension than general group.ConclusionALS patients have the Yang-like personality. It is due to the adaptation of personality on the environmental changeor coping strategy on diseases rather than the characteristics of congenital Sasang Constitution.Key Words: Amyotrophic lateral sclerosis, Sasang Constitution, Personality, Comorbid disorder

Objectives This research was proposed to present Clinical Practice Guideline(CPG) for Soeumin Disease of Sasang Constitutional Medicine(SCM): Yang Depletion Symptomatology. Methods This CPG was developed by the national-wide experts committee consisting of the society of Sasang Constitutional Medicine. it was performed by search and collection of literature related SCM, opinion of SCM experts and journal search. And it was followed by CPG`s guideline. Results & Conclusions No article was selected and included in CPG for Yang Depletion Symptomatology of Kidney Heat-based Exterior Heat disease in Soeumin disease. CPG of Yang Depletion symptomatology in Soeumin Disease include classification, definition and standard symptoms of each pattern. Yang Depletion symptomatology is classified into severe and critical pattern by severity. Yang Depletion Symptomatology severe pattern is classified into initial phase pattern and intermediate phase pattern. And Yang Depletion Symptomatology critical pattern is classified into advanced phase pattern.

Objectives: This study was designed to investigate the effects of Calculus Bovis-Fel Uris-Moschus pharmacopuncture (BUM) on the regional cerebral blood flow (rCBF) and the mean arterial blood pressure (MABP) in normal and cerebral ischemic rats and to investigate a possible pathway involved in the effects of BUM. Methods: The changes in the rCBF and the MABP fol lowing BUM into Fengfu (GV16) were determined by using a laser-Doppler flow meter and a pressure trans ducer, respectively. Results: BUM significantly increased the rCBF and de creased the MABP in normal rats in a dose-dependent manner. The effect on the rCBF was significantly inhib ited by pretreatment with methylene blue (0.01 mg/kg, intraperitoneal), an inhibitor of guanylate cyclase, but was not affected by pretreatment with indomethacin (1 mg/kg, intraperitoneal), an inhibitor of cyclooxygenase. The BUM-induced decrease of the MABP was changed neither by methylene blue nor by indomethacin pretreatment. In the cerebral ischemic rats, the rCBF was stably increased upon cerebral reperfusion in the BUM group in contrast to the rapid and marked increase in the control group. Conclusion: This study demonstrated that BUM into Fengbu (GV16) increased the rCBF in a dose-dependent manner in the normal state; furthermore, it improved the stability of the rCBF in the ischemic state upon reperfusion. Also, the effects of BUM on the rCBF were attenuated by inhibition of guanylate cyclase, suggesting that the effects involved the guanylate cy clase pathway.

Houttuynia cordata Thunb ( H cordata), a medicinal plant, has anticancer activity, as it inhibits cell growth and induces cell apoptosis in cancer. However, the potential anti-cancer activity and mechanism of H cordata for human liver cancer cells is not well understood. Recently, we identified hypoxia-inducible factor (HIF)-1A, Forkhead box (FOX)O3, and MEF2A as proapoptotic factors induced by H cordata, suggesting that HIF-1A, FOXO3, and MEF2A contribute to the apoptosis of HepG2 hepatocellular carcinoma cells. FOXO3 transcription factors regulate target genes involved in apoptosis. H cordata significantly increased the mRNA and protein expression of HIF-1A and FOXO3 and stimulated MEF2A expression in addition to increased apoptosis in HepG2 cells within 24 hours. Therefore, we determined the potential role of FOXO3 on apoptosis and on H cordata–induced MEF2A in HepG2 cells. HIF-1A silencing by siRNA attenuated MEF2A and H cordata–mediated FOXO3 upregulation in HepG2 cells. Furthermore, H cordata–mediated MEF2A expression enhanced caspase-3 and caspase-7, which were abolished on silencing FOXO3 with siRNA. In addition, H cordata inhibited growth of human hepatocellular carcinoma xenografts in nude mice. Taken together, our results demonstrate that H cordata enhances HIF-1A/FOXO3 signaling, leading to MEF2A upregulation in HepG2 cells, and in parallel, it disturbs the expression of Bcl-2 family proteins (Bax, Bcl-2, and Bcl-xL), which results in apoptosis. Taken together, these findings demonstrate that H cordata promotes the activation of HIF-1A–FOXO3 and MEF2A pathways to induce apoptosis in human HepG2 hepatocellular carcinoma cells and is, therefore, a promising candidate for antitumor drug development.

Urokinase receptor (uPAR) is enhanced in many human cancer cells and is frequently an indicator of poor prognosis. Activation of [Formula: see text]1-integrin requires caveolin-1 and is regulated by uPAR. However, the underlying molecular mechanism responsible for the interaction between uPAR and [Formula: see text]1-integrin remains obscure. We found that modified regular Panax ginseng extract (MRGX) had a negative modulating effect on the uPAR/[Formula: see text]1-integrin interaction, disrupted the uPAR/integrin interaction by modulating caveoline-1, and caused early apoptosis in cancer cells. Additionally, we found that siRNA-mediated caveoline-1 downregulation inhibited uPAR-mediated [Formula: see text]1-integrin signaling, whereas caveoline-1 up-regulation stimulated the signaling, which suppressed p53 expression, thereby indicating negative crosstalk exists between the integrin [Formula: see text]1 and the p53 pathways. Thus, these findings identify a novel mechanism whereby the inhibition of [Formula: see text]1 integrin and the activation of p53 modulate the expression of the anti-apoptotic proteins that are crucially involved in inducing apoptosis in A549 lung cancer cells. Furthermore, MRGX causes changes in the expressions of members of the Bcl-2 family (Bax and Bcl-2) in a pro-apoptotic manner. In addition, MGRX-mediated inhibition of [Formula: see text]1 integrin attenuates ERK phosphorylation (p-ERK), which up-regulates caspase-8 and Bax. Therefore, ERK may affect mitochondria through a negative regulation of caspase-8 and Bax. Taken together, these findings reveal that MRGX is involved in uPAR-[Formula: see text]1-integrin signaling by modulating caveolin-1 signaling to induce early apoptosis in A549 lung-cancer cells and strongly indicate that MRGX might be useful as a herbal medicine and may lead to the development of new herbal medicine that would suppress the growth of lung-cancer cells.

Constitutive activation of extracellular signal regulated kinase (ERK)-Jun NH2-terminal kinase (JNK) signaling commonly occurs in tumors. The activation of ERK promotes cell proliferation, whereas that of JNK induces cell apoptosis. However, the apoptotic mechanism of ERK-JNK signaling in cancer is not well understood. Recently, we identified that apoptosis and activation of the JNK signaling pathway were induced after cordycepin treatment in human renal cancer, suggesting that JNK signaling might contribute to TK-10 cell apoptosis. We investigated the apoptotic effects of cordycepin by evaluating the activation of the ERK-JNK signaling pathway in renal cancer TK-10 cells. We found that cordycepin downregulated ERK and DUSP5, upregulated phosphorylated-JNK (p-JNK), and induced apoptosis. Moreover, we showed that siRNA-mediated inhibition of ERK downregulated DUSP5, whereas ERK overexpression upregulated DUSP5, and that DUSP5 knockdown by siRNA upregulated p-JNK. The JNK-specific inhibitor SP600125 upregulated nuclear translocation of β-catenin, and downregulated Dickkopf-1 (Dkk1), which has been shown to be a potent inhibitor of Wnt signaling. Dkk1 knockdown by siRNA upregulated nuclear β-catenin, suggesting the involvement of the Wnt/β-catenin signaling pathway. DUSP5 overexpression in TK-10 cells decreased p-JNK and increased nuclear β-catenin. The decreased Bax activation markedly protected against cordycepin-induced apoptosis. Bax subfamily proteins induced apoptosis through caspase-3. Taken together, we show that JNK signaling activation by cordycepin mediated ERK inhibition, which might have induced Bax translocation and caspase-3 activation via regulation of DUSP5 in TK-10 cells, thereby promoting the apoptosis of TK-10 cells. Targeting ERK-JNK signaling via the apoptotic effects of cordycepin could be a potential therapeutic strategy to treat renal cancer.

Objectives : The purpose of this study was to validate the Sasang Personality Questionnaire (SPQ), based on the diagnosis of Sasang constitutional medicine clinical specialist.

1. Objectives : In this study we derived constitutional characteristics both by using questionnaire on character and symptom and by collecting objective measurement data through face, body shape. Furthermore, by developing a program, we intend to help one`s diagnosis of Sasang constitution. 2. Methods : Through November 2007 to July 2009, we obtained questionnaire, face, and body shape data of 958 constitution confirmed subjects within the age range of 10-80 from 19 oriental medical facilities in the country. According to sex, we divided the subjects into two groups as real constitution and non-constitution group respectively. We analyzed the questionnaire through chi-square test (p

The ubiquitous transcription factor, NF-κB, has been reported to inhibit apoptosis and induce drug resistance in cancer cells. Cordyceps militaris extract (CME) is involved in the regulation of the NF-κB signaling pathway. However, the detailed role of CME in the suppression of the NF-κB signaling pathway is unclear. We found that CME dose-dependently inhibited tumor necrosis factor-α (TNF-α)-induced NF-κB activation in TK-10 human renal cell carcinoma. CME prevented NF-κB from translocating to the nucleus, which resulted in the downregulation of GADD45B, upregulation of MKK7, and phosphorylation of JNK (p-JNK). The increased activation of Bax led to pronounced CME-induced apoptosis, which occurred through caspase-3. Furthermore, the siRNA-mediated knockdown of GADD45B inhibited MKK7 expression, whereas the siRNA-mediated inhibition of MKK7 downregulated p-JNK and the JNK inhibitor, SP600125, inhibited Bax expression. Thus, these results indicated that CME inhibited the activation of GADD45B via the inhibition of NF-κB activation, which upregulated the MKK7-JNK signaling pathway to induce apoptosis in TK-10 cells. Thus, this study reveals a novel anticancer function of CME.

Multidrug resistance 1 (MDR1) is a gene that expresses P-glycoprotein (P-gp), a drug transporter protein. Genetic polymorphisms ofMDR1can be associated with Sasang constitutions because Sasang constitutional medicine (SCM) prescribes different drugs according to different constitutions. A Questionnaire for Sasang Constitution Classification II (QSCC II) was used to diagnose Sasang constitutions. Two hundred and seven healthy people whose Sasang constitutions had been identified were tested. Genotype analyses, restriction fragment length polymorphism (RFLP) and pyrosequencing were used in MDR1 C1236T, and in MDR1 G2677T/A and C3435T, respectively. Significant differences inMDR1 C1236Tgenotypes were found between So-yangin and So-eumin.MDR1 G2677T/Agenotype also showed significant differences in allele distribution between So-yangin and Tae-eumin. So-yangin and So-eumin showed significant differences in the distribution of both 1236C-2677G-3435C and 1236T-2677G-3435T, haplotypes ofMDR1. The genetic polymorphism of theMDR1gene was thus shown to be an indicator that could distinguish So-yangin from other constitutions.

This study was performed to determine whether a pulse analyzer was useful 1) to characterize the variables of pulse wave of cerebral infarction patieno (CI), compared with those of healthy subjects, as well as 2) to determine Sasang Constitution in CI and healthy subjects. 1. Calibrated in Gwan, the amount of energy(Energy), height of main peak(H1), height of aorticvalley(H2), height of aortic peak(H3), total area of pulse wave(At), and area of main peak width(Aw) of the CI group were higher than those of the healthy group. 2. Calibrated in Cheek, Energy, H1, H2, H3, height of valve valley(H4), At, Aw, and main peak angle(MPA) of the CI group were higher than those of the healthy group. 3. Among the healthy (subjects) group, Taeumin showed the highest contact pressure(CP) and height of valve peak(H5) calibrated in Chon. The main peak width divided by whole time of pulse wave(MPW/T) calibrated in Gwan and Cheok, was highest in Soyangin and was lowest in Taeumin. The H3 divided by H1(H3/H1) and the time to valve valley minus the time to main peak and divided by T[(T4-T1)/T] calibrated in Cheek were highest in Soyangin. The time to main peak(T1) was longest in Soumin. 4. Among the CI group, At calibrated in Chon was widest in Taeumin and was narrowest in Soumin The time to aortic peak(T3) calibrated in Cheek was longest in Soumin and was shortest in Soyangin. The time to valve peak(T5) was shortest in Soyangin. 5. There were main effects of cerebral infarction in the area of systolic period(As) and area of diastolic period(Ad) calibrated in Chon, Energy calibrated in Cwan, and Energy, H1, H2, H3, (H4+H5)/Hl, and MPA calibrated in Cheek. 6. There were main effects of Sasang Constitution in (T4-T1)/T, area of systolic period(As), and Ad calibrated in Chon. 7. The interactions between the cerebral infarction and Sasang Constitution were observed in H5/H1 , T, At, As, Ad, and MPA calibrated in Chon, H4, T4, (T4-T1)/T, As, and Ad calibrated in Cwan, and 74,75, and MPW calibrated in Cheok. Therefore, we concluded that pulse analyzer was useful to determine the risk degree of cerebral infarction and Sasang Constitution.

Sasang constitutional medicine is a major branch of Korean traditional Oriental medicine. The differences of disease susceptibility to be shown in Sasang constitution may be due to genetic factors. Therefore, the authors examined relationship between candidate genes of cerebral infarction (CI) and Sasang constitution. The homozygous deletion allele of the angiotensin converting enzyme gene (ACE/DD), homozygous threonine allele of the angiotensinogen gene (AGN/TT), and the e4 allele of the apolipoprotein E gene (ApoE/e4) are reported to be associated with ischemic heart disease. CI is another atherosclerotic disease; and the effects of these polymorphisms on CI have been confusing. This study investigated whether ACE/DD, AGN/TT, and ApoE/e4 genotypes are associated with CI and whether genetic risk is enhanced by Sasang constitutional classification. The authors ascertained these genotypes in patients with CI (N=211), diagnosed by brain computed tomography. Control subjects for the infarction group were randomly selected from 319 subjects matched for age, sex, and history of hypertension with patients. The ACE/DD genotype was not associated with CI. However, there was significant association between ApoE polymorphism and CI (chi2=15.089, p

태음인의 辛丑本 新定方 처방과 약재는 甲午本과 辛丑本을 거 치면서 表病과 裏病의 구분을 비롯한 생리, 병리의 인식과 병증 적 용에 있어서 많은 변화가 있었으며, 辛丑本에서도 주치증이 생략된 처방이 있어 辛丑本만으로는 모든 처방들의 病證論적 근거를 밝히 기가 어렵다. 辛丑本의 病證 분류도 사상의학 연구자에 따라 분류 기준이나 연구 의도에 따라 다르게 구분되어 다양한 각도의 체계적 인 연구가 필요하다1-6). 사상의학에서는 병증을 기존 證治醫學과는 달리 陰陽虛實로 논하지 않고 각 체질의 保命之主가 어떤 상황에 처하느냐에 따라 升降緩束에 따라 논한 것이 기존 證治醫學의 八綱辨證, 氣血辨證, 臟腑辨證의 개념과 두드러진 차이점이라고 볼 수 있다7). 東醫壽世保元의 처방과 약재에 관한 연구는 東醫壽世保元 新 定方과 東醫四象新編을 비교한 연구8), 東醫壽世保元과 藥徵을 비 교한 연구9), 기존의학의 歸經, 性味, 效能을 사상의학적으로 재해 석한 연구10,11), 傷寒論과 金匱要略과의 비교를 통한 연구12), 八綱 의 개념에서 사상의학 처방을 분석한 연구13) 등 다수가 있으나 사 상의학적 생리, 병리를 고려한 관점에서의 연구는 비교적 적은 편 이다. 또한 東醫四象新編을 비롯한 사상의학 처방 서적은 이제마가 저술한 서적과는 달리 四象醫學의 證治醫學的 응용을 위해 실용성 과 활용성에 중심을 두어 편찬되어 四象體質 病證 運用精神과는 차이가 있다14). 이제마의 저서로는 北韓 保健省 간행 東武遺稿, 藏書閣 所藏 東武遺稿, 格致藁, 東醫壽世保元四象草本卷(이하 草本卷), 東醫壽 世保元 甲午本(이하 甲午本), 東醫壽世保元 辛丑本(이하 辛丑本)이 있으나 처방과 약재에 관한 내용은 北韓 保健省 東武遺稿, 草本卷, 甲午本, 辛丑本의 네 서적에 주로 기재되어 있다15-17). 본 연구에서 는 이제마가 저술한 네 서적에서 태음인의 생리, 병리, 병증, 처방 에 관한 내용을 수집, 정리, 요약, 분석하여 태음인의 처방을 사상 의학적으로 설명하고자 시도하여 병리와 처방에 관한 내용을 정리 하여 보고하는 바이다. 태음인 처방의 사상의학적 병리 연구

During the last decade, a growing corpus of evidence has indicated an important role of cytokines in the development of brain damage following cerebral ischemia. Tumor necrosis factor-alpha (TNF-alpha), a potent immunomodulator and pro-inflammatory cytokine, has been implicated in many pathological processes. In this study, we examined whether promoter region polymorphism in the TNF-alpha gene at position -308 affects the odds of cerebral infarction (CI) and whether genetic risk is enhanced by Sasang constitutional classification. Two hundred and twelve CI patients and 610 healthy controls were genotyped and determined according to Sasang constitutional classification. A significant decrease was found for the TNF-alpha A allele in CI patients compared with controls (p = 0.033, odds ratio, OR: 0.622). However, there was no significant association between TNF-alpha polymorphism and Sasang constitution in CI patients. Our finding suggests that TNF-alpha promoter region polymorphism is responsible for susceptibility to CI in Koreans.

Sasang constitutional medicine is a major branch of Korean traditional oriental medicine. Constitutions of Sasang medicine refer to Taeyangin, Taeumin, Soyangin, and Soumin. The differences of disease severity to be shown in the constitution may be due to genetic factors. Therefore, we examined interrelationship among cerebral infarction, CI, angiotensin converting enzyme (ACE) gene polymorphism, and Sasang constitutional classification. We investigated the association between ACE genotype and CI by case-control study in a Korean population. We also classified CI patients and control group into groups according to Sasang constitutional medicine. 208 CI patients and 643 controls without CI were examined. ACE genotype was determined by 7.5 % polyacrylamide gel separation after DNA amplification. The ACE/DD genotype was not associated with CI. The frequency of Taeumin of Sasang constitutional medicine in patients with CI was significantly higher than that in controls (chi2=41.202, p0.001). However, the Taeumin constitution did not enhance the relative risk for CI in the subjects with ACE/DD genotype. Although we did not find any association between ACE gene polymorphism and CI in Koreans, there were significant differences in allele frequencies between Koreans and Europeans, but not Japanese and Chinese populations. Furthermore, we first attempted to evaluate the efficacy of Sasang constitutional medicine, and to find an association with CI.