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        • KCI등재

          정신분열증 환자에서 혈장 HVA 및 5-HIAA 농도와 정신병리와의 상관성

          김용구,박성근,김인,이민수,Kim, Yong-Ku,Park, Sung-Geun,Kim, Leen,Lee, Min-Soo 대한생물정신의학회 1997 생물정신의학 Vol.4 No.1

          The recent hypothesis about the pathophysiology of schizophrenia has been centered mainly on two theories, i.e. dopamine hypothesis and serotonin hypothesis. We investigate the correlations between plasma monoamine metabolite concentrations and clinical symptoms in schizophrenic patients. The first purpose of our study was to examine whether the plasma levels of HVA(homovanillic acid) and 5-HIAA(hydroxyindoleacetic acid) are significantly different in schizophrenics, compared to normal controls. And, with the intention of clarifying the interaction between dopaminergic system and serotoninergic system, the ratio of HVA/5-HIAA also was measured. The second purpose was whether the basal(pre-treatment) levels of these metabolites show the correlation with clinical symptoms. Finally, third purpose was whether basal HVA and 5-HIAA levels can be held as a predictor of treatment response. We used Scale for the Assessment of Positive Symptoms(SAPS) and Scale for the Assessment of Negative Symptoms(SANS) as the clinical symptom rating scales. Our results were as followed, 1) only the level of basal plasma HVA was significantly differ in schizophrenics. 5-HIAA and HVA/5-HIAA were not. 2) basal HVA showed significant correlation with SAPS score, especially delusion subscale. 3) the higher was the basal HVA level, the more improvement in clinical symptoms was observed. The basal 5-HIAA level and the HVA/5-HIAA ratio did not show any significant findings. These results support the dopamine hypothesis of schizophrenia, but fail to examine on the possible involvement of serotonin in schizophrenia.

        • KCI등재

          자살을 시도한 주요우울증 환자에서 혈청 콜레스테롤 농도의 저하

          김용구,이헌정,곽동일,Kim, Yong Ku,Lee, Heon Jeong,Kwak, Dong II 대한생물정신의학회 1996 생물정신의학 Vol.3 No.2

          Objective : Several studies hove suggested that reduction of cholesterol concentration and low cholesterol level increases suicide, homicide, and depression. The authors sought to determine whether low cholesterol is associated with a history of suicidal attempts among major depression patients. Method : The subjects were 105 patients with major depression, diagnosed according to the DSM-III-R criteria, and 105 age, sex matched healthy controls. Blood was token following overnight fast and serum cholesterol concentration were measured by a enzymatic method Results : The serum cholesterol level was significantly lower in the patients with major depression than in healthy controls($180.4{\pm}43.4mg/dl$ vs $199.7{\pm}35.8mg/dl$). And the serum cholesterol level was significantly lower in major depression patients with suicidal attempt than in major depression patients without suicidal attempt($156.7{\pm}38.2mg/dl$ vs $ 187.8{\pm}42.5mg/dl$) Conclusion : It is hypothesized that low cholesterol level is associated with depression by modifying the serotonin metabolism and the production of interleukin-2, low cholesterol concentration should be further investigated as a potential biological marker of suicidal risk in major depression. Prospective study with serial cholesterol determinations should be done.

        • KCI등재

          주요우울증환자에서 Acute Phase Proteins 농도 변화에 관한 연구

          김용구,김사준,이민수,Kim, Yong-Ku,Kim, Sa-Jun,Lee, Min-Soo 대한생물정신의학회 1995 생물정신의학 Vol.2 No.1

          A few researchers have reported that major depression may be associated with higher levels of positive acute phase proteins(APPs), such as haptoglobin(Hp), ${\alpha}1$-antitrypsin(${\alpha}1AT$), ceruloplasmin(Cp) and lower levels of negative APPs(visceral proteins), such as albumin(Alb) and transferrin(Tf). Elevated levels of positive APPs and a drop in negative APPs constitute important indicators of immune activation. This study was designed to investigate whether altered serum concentrations of positive APPs and of negative APPs reflect the state of depression. Twenty patients who fulfilled DSM-III-R criteria for major depressive disorder and for dysthymic disorder and twelve normal healthy controls were included. The authors measured positive APPs(Hp, ${\alpha}1AT$, Cp) and negative APPs(Alb, Tf) using rate nephelometry and bromcresol green method. 1) There were significant increases of ${\alpha}1AT$, Cp in major depressed patients as compared with normal controls. Trends towards higher Hp and lower Alb, Tf in major depressed patients were observed. 2) No significant difference of APPs concentrations between dysthymic patients and normal controls was found. 3) Severity of depression(HDRS, BDI score) was related to Hp, Cp, ${\alpha}1AT$ value positively. Our findings are partially compatible with the hypothesis that major depression may be accompanied by acute phase response with higher levels of positive APPs and lower levels of negative APPs.

        • KCI등재

          남자 정신분열증 환자에서 혈청 Interlenkin-2 농도의 증가

          김용구,김사준,이민수,Kim, Yong-Ku,Kim, Sa-Jun,Lee, Min-Soo 대한생물정신의학회 1996 생물정신의학 Vol.3 No.1

          We have previously reported that Korean schizophrenic patients hove low production of IL-2 in vitro suggestive of autoimmunity to the pathogenesis of the disorder. In an attempt to further explore this issue, we measured in vivo serum levels of interleukins(IL-$1{\beta}$, IL-2, and IL-6) using a quantitative "sandwich" enzyme immunoassay(ELISA) in 26 male schizophrenic patients and in 26 age-matched normal controls. Patients met DSM-IV criteria for schizophrenia and were drug free for at least six months. The severity of symptoms was assessed by SANS and SAPS. We found a significant increase of IL-2 level(p<0.05) in schizophrenic patients as compared with normal controls. There were significant positive correlations between IL-2, IL-6 levels and negative symptom scores. There were no correlations between age, age at onset, duration of illness and interleukin levels. Our results may support the hypothesis of viral-autoimmune dysfunction in schizophrenia. IL-2 or IL-6 may be associated with specific clinical feature in schizophrenic syndrome, especially negative symptom. 정신분열증에서 interleukin의 변화는 그 질환에서의 면역학적 가설의 부가적인 증거로 제시되어 왔다. 본 연구에서는 quantitative "sandwich" ELISA 법을 이용하여 26명의 정신분열증 환자를 대상으로 연령을 상응시킨 정상대조군과 비교해 IL-$1{\beta}$, IL-2, IL-6 농도의 차이가 있는지 알아보았다. 또한 정신분열증 환자에서 IL농도와 양성증상 및 음성증상, 연령, 유병기간 등의 임상변인과의 상관관계를 조사하여 다음과 같은 결론을 얻었다. 1) 정신분열증군이 정상대조군보다 IL-2 농도의 유의한 중가를 나타내었으며, IL-$1{\beta}$와 IL-6는 유의한 차이가 없었다. 2) 정신분열증군에서 IL-2, IL-6와 음성증상간의 유의한 상관관계가 있었다. 본 연구는 정신분열증의 연역학적 가설을 지지하고 있으며, IL은 정신분열증의 음성증상에 관련된다고 생각된다. 앞으로 국내에서도 이러한 환자들의 임상적 특징, 진단, 치료에 관심을 갖아야 할 것으로 사료된다.

        • KCI등재

          정신분열병 환자에서 인지기능 및 정신병적 증상의 상관관계

          김용구,이정애,이소연,이분희,한창수,Kim, Yong-Ku,Lee, Jung-Ae,Lee, So-Youn,Lee, Bun-Hee,Han, Chang-Su 대한생물정신의학회 2006 생물정신의학 Vol.13 No.3

          Objectives : The purpose of this study was to investigate whether the cognitive functions would be correlated with psychotic symptoms and whether antipsychotic treatments would affect the cognitive functions after 8 weeks. Methods : The thirty-five schizophrenic patients were conducted in this study. The psychopathology was measured using PANSS. The memory function, executive function, and sustained attention were measured using Memory Assessment Scale(MAS), Wisconsin Card Sorting Test(WCST), and Vigilance(VIG) and Cognitrone(COG) in Vienna Test System. After 8 weeks of antipsychotic treatment, we retested the cognitive tests. Results : 1) The cognitive tests after the 8 week's treatment showed significant improvements in memory and executive function in the schizophrenic patients. On the other side, sustained attention did not show improvement. 2) The change of PANSS were correlated with perseverative response, perseverative error and total correct in WCST at baseline. WCST scores at baseline were correlated with negative symptoms, but not positive ones. Conclusion : These study suggests that 1) the impaired sustained attention could be a vulnerability marker in schizophrenia, 2) memory & executive function deficit could be reversible after treatment, and 3) medication might have a benefit in improving the cognitive functions in schizophrenia. Furthermore, the data supports that the better premorbid executive function was, the more favorable was the treatment response in schizophrenic patients. Finally, this study indicates that executive function might be an index of treatment improvement.

        • KCI등재

          주요우울증에서 스트레스, 염증반응, 신경조직발생

          김용구,Kim, Yong-Ku 대한생물정신의학회 2011 생물정신의학 Vol.18 No.4

          Stress, a risk factor of major depression induces cytokine mediated inflammation and decreased neurogenesis. In patients with major depression, significant increases of pro-inflammatory cytokines have been consistently reported. The pro-inflammatory cytokines can stimulate the hypothalamic-pituitary-adrenal (HPA) axis to release glucocorticoids. In the brain, microglia and play a role of immune activation in response to stress. Increased pro-inflammatory cytokine play a role in restricting neurogenesis in the brain. Although neurogenesis may not be essential for the development of depression, it may be required for clinically effective antidepressant treatment. Hence, stimulation of neurogenesis is regarded as a promising strategy for new antidepressant targets. This review introduces changes in neurotransmitter, cytokine and neurogenesis in major depression and explores the possible relationship between pro-inflammatory cytokines and neurogenesis related to stress in major depression.

        • KCI등재

          사이토카인과 우울증

          김용구,Kim, Yong-Ku 대한생물정신의학회 2008 생물정신의학 Vol.15 No.3

          Accumulating evidence has suggested the existence of reciprocal communication between immune, endocrine, and neurotransmitter system. Cytokine hypothesis of depression implies that increased pro-inflammatory cytokine such as -1, IL-6, IL-12, TNF-${\alpha}$, and IFN-${\gamma}$ in major depression, acting neuromodulators, play a key role in the mediation of behavioral, neuroendocrine, and neurochemical disturbances in depression. Concerning the relation between cytokines and serotonin metabolism, pro-inflammatory cytokines have profound effects on the metabolism of brain serotonin through the enzyme indoleamine-2,3-dioxygenase(IDO) that metabolizes tryptophan, the precursor of 5-HT to neurodegenerative quinolinate and neuroprotective kynurenate. The neurodegeneration process is reinforced by the neurotoxic effect of the hypercortisolemia during depression. From this perspective, it is possible that efficacy of antidepressants in the treatment of depression may, at least in part, rely on downregulation of pro-inflammatory cytokine synthesis. So, the use of cytokine synthesis inhibitors or cytokine antagonists may be a new treatment approach in depression. However, at present the question whether cytokines play a causal role in the onset of depression or are mere epiphenomena sustaining depressive symptoms remains to be elucidated. Nevertheless, cytokine hypothesis has created new perspectives in the study of psychological and pathophysiological mechanism that are associated with major depression, as well as the prospect for developing a new generation antidepressants.

        • KCI등재

          자살 : 유전자-환경 상호작용

          김용구,Kim, Yong-Ku 대한생물정신의학회 2010 생물정신의학 Vol.17 No.2

          Gene-environment interactions are important in pathogenesis of suicide or suicidal behavior. Twin and adoption studies and family studies show that genetic factors play a critical role in suicide or suicidal behavior. Given the strong association between serotonergic neurotransmission and suicide, recent molecular genetic studies have focused on polymorphisms of serotonin genes, especially on serotonin transporter and tryptophan hydroxylase genes. Some studies have revealed a significant interaction between s allele of the serotonin transporter gene and the risk of suicide attempt associated with childhood trauma. In addition, the polymorphism of brain-derived neurotrophic factor gene also may influence the effect of childhood trauma in relation to the risk of attempting suicide. Future studies should explore genetic and environmental factors in suicide or suicidal behavior and examine for gene and environment interaction.

        • KCI등재

          치료저항성 우울증의 연구에서 패러다임의 전환

          김용구,Kim, Yong-Ku 대한생물정신의학회 2016 생물정신의학 Vol.23 No.2

          Treatment-resistant depression (TRD) is a major public health problem. It is estimated that about 30% of patients with major depressive disorder do not show substantial clinical improvement to somatic or psychosocial treatment. Most of studies for TRD have focused on the subjects already known as TRD. Patients with unipolar depressive episodes that do not respond satisfactorily to numerous sequential treatment regimens were included in the TRD studies. Such post hoc experimental design can be regarded only as consequences of having TRD, rather than as causal risk factors for it. Although informative, data derived from such studies often do not allow a distinction to be made between cause and effect. So, we should shift paradigm toward examining the risk for developing TRD in untreated depressed patients. To deal with this problem, untreated depressed patients should be enrolled in the study to identify biological markers for treatment resistance. The peripheral or central biological markers should be explored before starting treatment. Subsequent systematic administration of treatments with appropriate monitoring in the subjects can determine the risk for developing treatment resistance in untreated individuals. Such information could give a cue to improve the initial diagnosis and provide more effective treatment for TRD.

        • KCI등재

          정신분열증 환자에서 Interleukin-$1{\beta}$, -2, -6 생산능과 혈청농도 변화에 관한 연구

          김용구,이민수,서광윤,Kim, Yong-Ku,Lee, Min-Soo,Suh, Kwang-Yoon 대한생물정신의학회 1994 생물정신의학 Vol.1 No.1

          The etiology and pathophysiology of schizophrenia remain unknown. It has been postulated that infectious-autoimmune process may play a role in the pathogenesis of symptoms in some schizophrenic patients. Findings of altered interleukin(IL) regulation have been regarded as additional proof that schzophrenia has an infectious-autoimmune background. In the present study, we measured mitogen-stimulated production of and serum level of IL-$1{\beta}$, IL-2, IL-6 using ELISA in 16 neuroleptic-free schizophrenic patients and in 16 age, sex matched healthy controls. The results were as follows : 1) There was a significant decrease of IL-2 production in schizophrenic patients than in normal controls(respectively $1.90{\pm}0.13ng/m{\ell}$, $2.79{\pm}0.14ng/m{\ell}$, p<0.001). But there was no significant difference of IL-$1{\beta}$ production and IL-6 production between schizophrenic patients and normal controls. 2) There was a significant increase of serum level of IL-2 in schizophrenic pateitns than in normal controls(respectively $184.8{\pm}12.8pg/m{\ell}$, $104.2{\pm}34.2pg/m{\ell}$, p<0.01). Serum level of IL-$1{\beta}$ was partially detected in both groups and serum level of IL-6 was not detected in both groups. 3) There was no significant differences of IL-$1{\beta}$, -2, -6 production & serum level of IL-2 according to male vs female, paranoid type vs undifferentiated type, drug-naive group vs drug-free group in schizophrenic patients. 4) There was significant correlation between IL-$1{\beta}$ and IL-6 production(r=0.86, p<0.001). No correlation between IL-$1{\beta}$, -2, -6 production, serum level of IL-2 and age, duration of illness, and BPRS score was found. It has been suggested that the low lymphocyte production of IL-2 in the patients with autoimmune disease occurs because the T cells are activated and lymphocyte-derived IL-2 has been released into the serum. The authors suggest that decreased IL-2 production in our schizophrenic patients is due to increased IL-2 serum level in those patients. Thus our finding of low IL-2 production and high serum level of IL-2 in our schizophrenic patients is compatible with the possibility that our patients have an autoimmune process. Further study on relationship between IL alteration and other immunological abnormalities(the presence of serum autoantibody and of anti-brain antibody, $CD4^+$, $CD8^+$ cell index, etc) in schizophrenic patients will be warranted.

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