Quality of medical research reports should be evaluated before they are applied to clinical practice. Since 1990s, several guidelines on research reports were suggested. Most recently published Consolidated Standards of Reporting Trials statement 2010 consists of 25 checklists and flow diagram for reporting an randomized controlled trial. Strengthening the reporting of observational studies in epidemiology statement is a checklist of items that should be addressed in articles reporting on the observational studies in epidemiology. TREND statement for the reporting of nonrandomized designs consists of 22 checklists. The Quality of Reporting of Meta-analyses checklist proposes to provide checklist and flow diagram for reporting of meta-analyses. The Meta-analysis of Observational Studies in Epidemiology statement proposes a checklist for compensating the study errors about observational studies in epidemiology. After development of reporting guidelines, improvements in the quality of reports are continuously reported, so using guidelines in the medical research will be expected to be more generalized.
Checklist ; Meta-Analysis as Topic ; Research Report

The purposes of this study were to compare the difference of prolactin responses to risperidone and haloperidol, the sex difference in prolactin responses to each drug and the difference of prolactin responses to both drug in each sex. METHODS: The patients with schizophrenia, schizophreniform disorder, schizoaffective disorder, delusional disorder, brief psychotic disorder diagnosed by the criteria of DSM-IV were randomly assigned to risperidone group (n=18) or haloperidol group (n=15). Prolactin levels were measured before drug administration and at week 1, 2, 3, 4, 6 after drug administration by immunoradiometric assay. RESULTS: Prolactin levels after risperidone administration were significantly (p<0.05) higher than those after haloperidol. There was no sex difference in the prolactin responses to haloperidol administration. As for risperidone administration, female showed significantly (p<0.05) higher prolcatin levels than male. There was no difference of prolactin responses to both drugs in male, but in female, prolactin levels after risperidone administration were significantly (p<0.05) higher than those after haloperidol. CONCLUSION: Compared to haloperidol, risperidone can cause significantly higher prolactin response in female than male. Therefore one should consider whether there is a sexual side effects related to the elevated prolactin level especially in female during risperidone administration.
Diagnostic and Statistical Manual of Mental Disorders ; Female ; Haloperidol* ; Humans ; Immunoradiometric Assay ; Male ; Prolactin* ; Psychotic Disorders* ; Risperidone* ; Schizophrenia* ; Schizophrenia, Paranoid ; Sex Characteristics

The purpose of this study is to compare weight gain by risperidone, clozapine and olanzapine which are atypical antipsychotic drugs with that by haloperidol which is typical antipsychotic drug. METHODS: We performed a retrospective chart review of 278 schizophrenic patients who were treated longer than 12 weeks with 4 different drugs. We measure weight gain weekly until 12th week and weight change curve over 12 weeks was drawn. Additionally, we examined any correlations of weight change with some factors. RESULTS: 1) The highest weight gains were observed in the olanzapine and clozapine groups, followed by the risperidone and haloperidol groups. 2) The haloperidol group showed a main weight gain within first 3 weeks, and patients ingested 3 atypical drugs gained weight steadily during 12 weeks. 3) The initial underweight group showed the largest weight gain. CONCLUSION: This study shows that the atypical antipsychotic drugs induced more weight gain than haloperidol. And we can expect that long-term treatment with clozapine and olanzapine would induce more severe weight gain, particularly in underweight patients.
Antipsychotic Agents* ; Clozapine ; Haloperidol ; Humans ; Retrospective Studies ; Risperidone ; Thinness ; Weight Gain*

This study aims to examine the effect of methylphenidate, which is the most extensively prescribed medicine treating children with Attention Deficit Hyperactivity Disorder (ADHD), on the children's neuropsychiatric functions by comparing the symptomatic differences before and after its medication. MEHTODS: The subjects of this study were 48 children who corresponded to the diagnostic criteria for ADHD of DSM-IV, did not have any problem in vision or hearing, did not have neurologic disorder such as epilepsy and brain damage, and did not have other long term medication. To evaluate the effects of behavioral response and medication, after stopping medication over a week we handed out questionnaires to the parents and conducted CPT to the subjects. A dose of 0.3-0.7 mg/kg (bid or tid) was medicated at 8AM and 1PM everyday. After 4 weeks of medication, the same tests were conducted. RESULTS: Average age of the subjects was 8.88+/-1.55. There were 44 boys (91.7%) and 4 girls (8.3%). Mean intelligence was 96.60+/-18.12 and mental processing was 102.90+/-16.51. On ADDES-HV, after medication attention, impulsivity and hyperactivity were significantly improved (p<0.05). On AcTeRS, after medication attention, impulsivity and social skill were significantly improved (p<0.05). On CAPs, after medication inattention and hyperactivity were significantly improved (p<0.05). On SNAP, after medication inattention impulsivity and hyperactivity were significantly improved (p<0.05). On the academic performance rating scale, after medication total score, learning ability, impulse control and social withdrawal were significantly improved (p<0.05). On performing CPT, after medication commissions error, hit reaction time standard error, variability of standard error and attentiveness were significantly improved (p<0.05). CONCLUSIONS: With these results, we recognized methy-lphenidate is more effective in children's impulsivity and hyperactivity than attention, contrary to the clinical observation.
Attention Deficit Disorder with Hyperactivity* ; Brain ; Child* ; Diagnostic and Statistical Manual of Mental Disorders ; Epilepsy ; Female ; Hand ; Hearing ; Humans ; Impulsive Behavior ; Intelligence ; Learning ; Methylphenidate* ; Nervous System Diseases ; Parents ; Surveys and Questionnaires ; Reaction Time

No abstract available.
Adolescent* ; Child* ; Humans ; Psychopharmacology*

The aims of this article is to review the current knowledge on the role of cytokines in depression by discussing the brain action of cytokines, their role in the stress response, their relationship to depression, and their sensitivity of antidepressant treatment. From the data that are reviewed, several important points emerge: 1) Cytokines administered to patients and laboratory animals induce symptoms of depression, including, depressed mood, anhedonia, reduced food intake, sleep disorder, hyperactivity of HPA axis, and glucocorticoid resistance; 2) Stress-induced cytokine secretion may be responsible for the induction of depressive symptoms. 3) Antidepressants have anti-inflammatory properties and interfere with cytokine production and action. 4) Cytokine antagoinists may attenuate the symptoms of depression. The cytokine model in depression may play a crucial role in the etiology and psychopathology of depression.
Anhedonia ; Animals, Laboratory ; Antidepressive Agents ; Axis, Cervical Vertebra ; Brain ; Cytokines* ; Depression ; Eating ; Humans ; Neurotransmitter Agents ; Psychopathology

Depression is one of the most common disease, but the pathophysiologic mechanism of depression remains elusive. To elucidate the cellular and molecular mechanisms of depression, animal models of depression have been developed, and these models were used successfully to predict the clinical efficacy of new antidepressant drugs. However, it is not likely that current animal models imitate all aspects of depression and are reliable, because we can not evaluate emotional state of rodents verbally and rodents have very different behavioral responses compared with ours. Despite these difficulties, understanding the benefits and limitations of animal models is very important for an advance in basic and clinical research of depression. The first part of the review evaluates animal models of depression in relation with stress that may contribute, in part, to development of depression: chronic mild stress, chronic unpredictable stress, maternal separation. The second part describes the most widely used animal models to screen for potential antidepressant: learned helplessness model and forced swimming test.
Animals* ; Antidepressive Agents* ; Depression ; Helplessness, Learned ; Mass Screening* ; Models, Animal* ; Physical Exertion ; Rodentia

OBJECTIVE: The abnormality of mismatch negativity (MMN) in schizophrenia is thought to be associated with perceptional disturbance and cognitive dysfunction. And the antagonists of the N-methyl-D-aspartate (NMDA) receptors, ketamine, can induce anomalies of psychophysiology and cognitive function as those of schizophrenia. In order to explore the role of NMDA receptors on echoic memory system, MMN under ketamine administration was analyzed. METHODS: MMNs of Healthy 12 subjects under sub-anesthetic dose (0.65 mg/kg/hr) of ketamine administration in placebo-controlled design were recorded by 128 channel EEG. Brief Psychiatric Rating Scale (BPRS) change was also evaluated. RESULTS: BPRS score was significantly increased by ketamine administration (t=-6.655, p<0.001). Ketamine induced significant decrease in MMN amplitudes (Fz, t=-2.572, p=0.026). Neither MMN amplitude under placebo administration nor MMN latencies under ketamine administration and placebo was changed significantly. CONCLUSION: Ketamine induced echoic memory dysfunction in healthy subjects, which is usually found in schizophrenic patients. Consequently, reduced glutamatergic activity in brain could be involved some early processes of the memory dysfunction in schizophrenia.
Brain ; Brief Psychiatric Rating Scale ; Electroencephalography ; Glutamic Acid* ; Humans ; Ketamine* ; Memory* ; N-Methylaspartate ; Psychophysiology ; Receptors, Glutamate* ; Receptors, N-Methyl-D-Aspartate ; Schizophrenia*

OBJECTIVE: The purpose of this study was to evaluate how risperidone, a new atypical antipsychotics, affect the quality of life in schizophrenics on their maintenance treatment. METHODS: The authors selected 39 schizophrenic patients diagnosed by the criteria of DSM-IV. We investigated their sociodemographic data, clinical characteristics, laboratory examination, PANSS for psychopathology evaluation, and UKU side effect rating scale. Also the subjects were asked the KmSWN scale, which consists of 18 items and a 6-point score, three times for studying the effect on the quality of life in schizophrenics over 26-week period. For the assessment, the authors conducted repeated measures ANOVA to evaluate the differences of mean dose of risperidone, vital sign, weight, PANSS scores, and UKU side effect rating scores at period of baseline, 2-week, 14-week, and 26-week respectively. Also We used Pearson correlation coefficients to assess the relationship between KmSWN and PANSS scores, KmSWN and UKU side effect rating scores. RESULTS: The results were shown as follows : first, in clinical evaluation, we observed mild systolic pressure diminution and 2.3 kg of mean weight gain at 26-week period but did not detected abnormal blood glucose level ; second, we observed the significant reduction in PANSS and UKU side effect rating scores on risperidone treatment, but the change of subjective evaluation on quality of life did not reported ; third, the schizophrenic symptoms, particularly negative and general psychopathology symptoms, and side effects were correlated negatively with the subjective evaluation on quality of life in schizophrenic patients at 26-week period after risperidone treatment in the Pearson correlation analysis. CONCLUSION: The authors observed the significant reduction in PANSS and UKU side effect rating scores at 26-week compared to baseline period. As the negative and general psychopathology symptoms, and the side effects reduced, the subjective evaluation on the quality of life improved in schizophrenic patients.
Antipsychotic Agents ; Blood Glucose ; Blood Pressure ; Diagnostic and Statistical Manual of Mental Disorders ; Humans ; Psychopathology ; Quality of Life* ; Risperidone* ; Schizophrenia ; Vital Signs ; Weight Gain

OBJECTIVE: This study is to explore the effects on specific bindings between [ 3H]RX821002, alpha-2 adrenergic receptor antagonist and alpha-2 adrenergic receptor in rat brain by G-protein modulation. METHODS: The radioligand binding receptor study was conducted with [ 3H]RX821002, a new alpha-2 adrenergic receptor antagonist, in the presence or absence of Gpp(NH)p and pertussis toxin. RESULTS: The alpha-2 adrenergic receptors were saturated with [ 3H]RX821002 in the fashion of the single binding site. The dissociation constant (Kd) was 0.70+/-0.30 nM, and maximum binding (Bmax) was 599.9+/-283.4 fmol/mg protein. The saturation study showed that the maximum binding (B max ; 668.0+/-50.1 fmol/mg protein) was increased and the dissociation constant (Kd ; 0.61+/-0.14 nM) was decreased significantly in the presence of Gpp (NH)p compared to those (B max ; 559.8+/-81.9 fmol/mg protein, Kd ; 0.87+/-0.14 nM) in the absence of Gpp (NH)p (by paired t-test ; B max, p=0.023, Kd, p=0.005). In the presence of pertussis toxin, the maximum binding (B max ; 617.0+/-58.5 fmol/mg protein) was increased significantly (by paired t-test ; B max, p=0.001) but the issociation constant (Kd ; 0.92+/-0.24 nM) was not decreased compared to those (B max ; 554.1+/-66.1 fmol/mg protein, Kd ; 0.89+/-0.24 nM) in the absence of pertussis toxin. CONCLUSION: These results confirm that the binding profiles between [ 3H]RX821002 and alpha-2 adrenergic receptors be modified by G-protein modulation. This suggests that the drug effects on receptors be influenced by various conditions such as G-protein modulation.
Animals ; Binding Sites ; Brain* ; GTP-Binding Proteins* ; Guanylyl Imidodiphosphate ; Pertussis Toxin ; Rats* ; Receptors, Adrenergic, alpha-2