No abstract available.
Humans ; Radiography* ; Spine*

OBJECTIVES: To evaluate an association between depression and altered immunity, we examined peripheral T lymphocyte or natural killer (NK) cell measures plasma ACTH and cortisol using the flow cytometry in acute and unmedicated patients with major depressive disorder (MDD). METHODS: Forty-two patients with MDD from the outpatient clinic and forty normal controls from the hospital staff were recruited. We applied Hamilton Rating Scale for Depression (HAM-D) and Hamilton Rating Scale for Anxiety (HAM-A) for depressed subjects. Peripheral T lymphocyte or NK cell measures (CD3, CD4, CD8, or CD56) and plasma hormones (ACTH and cortisol) were obtained from all subjects. RESULTS: There were no statistical differences in CD3, CD4, CD8, or CD56 between the two subjects. The number of CD56 cells negatively correlated with HAM-D scores (r=-0.42, p<0.01), but did not correlate with HAM-A scores in patients with MDD. The number of CD56 cells showed strong negative correlation with CD4/CD8 (r=-0.47, p<0.01) in the control group, but not in the depressed group. Patients with MDD had higher cortisol level than controls within the normal range. CONCLUSION: The trait of immunological imbalance and HPA axis abnormality were shown in patients with MDD. Especially, the severity of depression, but not the anxiety, could be reflected as decreased number of CD56 (NK T) cells in acute and unmedicated state.
Adrenocorticotropic Hormone ; Ambulatory Care Facilities ; Anxiety ; Axis, Cervical Vertebra ; Depression ; Depressive Disorder, Major* ; Flow Cytometry ; Humans ; Hydrocortisone ; Killer Cells, Natural ; Lymphocytes ; Natural Killer T-Cells* ; Plasma ; Reference Values

Protective effect of human cerebrospinal fluid antioxidants against enzyme inactivation caused by metal-catalyzed oxidation systems were investigated. When purified glutamine synthetase(GS) was incubated with human cerebrospinal fluid(CSF), the enzyme was progressively inactivated. Catalase and EDTA could inhibit the enzyme inactivation by 50-80%. Small-molecular(Mr<-10,000) fraction of CSF inactivated the exogenous GS, but large-molecular(Mr>-10,000) fraction did not. The GS inactivation by the small-molecular fraction was also markedly inhibited by catalase and EDTA. These results suggested that metal-catalyzed oxidation is involved in the GS inactivation by the small-molecular fraction of CSF. Dithiothreitol(DTT)was shown to inhibit almost completely the oxidative inactivation of GS by CSF. However, DTT inhibited only partially the oxidative inactivation of GS caused by small-molecular fraction of CSF. When large-molecular fraction of CSF was separated by anion-exchange HPLC chromatography, there was a peak of antioxidant activity inhibiting the small-molecular fraction-induced GS inactivation in the presence of DTT. The antioxidant activity was neutralized by monoclonal antibodies to transthyretin. Purified transthyretin was found to efficiently inhibit ascorbate/Cu2+-induced GS inactivation in the presence of DTT. Uric acid and glucose did not shoe any protective effect on the GS inactivation in the same condition. The above results suggest that metal-catalyzed oxidation occurs normally in human CSF, and the transthyretin may play an important role as a CSF antioxidant in protecting proteins from metal-catalyzed oxidation.
Antibodies, Monoclonal ; Antioxidants ; Catalase ; Cerebrospinal Fluid* ; Chromatography ; Chromatography, High Pressure Liquid ; Edetic Acid ; Glucose ; Glutamine ; Humans* ; Prealbumin* ; Shoes ; Uric Acid

BACKGROUND: Reactive Oxygen Species (ROS) have been implicated in the pathophysiology of brain injury after ischemia/reperfusion. Recently, it has been reported that endonuclease G (EndoG), a mitochondrial protein, is activated by neuronal excitotoxicity and translocated into nucleus inducing apoptosis. However, it is not elucidated whether ROS are involved in the nuclear translocation of EndoG in focal cerebral ischemia/reperfusion in mice. We investigated whether treatment of manganese tetrakis (4-benzoic acid) porphyrin (MnTBAP) protects against early nuclear translocation of EndoG and reduces cerebral infarction after ischemia/reperfusion in mice METHODS: Adult male mice were subjected to middle cerebral artery occlusion (MCAO) for 60 min, followed by reperfusion. Immunohistochemistry and Western blot analysis for EndoG were performed at various time points after ischemia/reperfusion. Double staining with EndoG and Terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end-labeling (TUNEL) was also performed. MnTBAP was used to determine whether the production of ROS could inhibit translocation of EndoG into the nucleus. RESULTS: Western blot analysis and Immunohistochemistry of EndoG showed that nuclear EndoG was detected as early as 4 hrs after reperfusion, and mitochondrial EndoG was significantly reduced at the same time. Double staining with EndoG and TUNEL showed a spatial relationship between EndoG expression and DNA fragmentation. MnTBAP-treated mice showed that the translocation of EndoG was attenuated in comparison with the vehicle- treated mice and decreased infarction volume after ischemia/reperfusion. CONCLUSIONS: MnTBAP reduced the generation of ROS, and inhibited the early translocation of EndoG, which was followed by the reduction of infarction volume in the ischemic brain after ischemia/reperfusion.
Adult ; Animals ; Apoptosis ; Blotting, Western ; Brain ; Brain Injuries ; Cerebral Infarction* ; DNA Fragmentation ; Humans ; Immunohistochemistry ; In Situ Nick-End Labeling ; Infarction ; Infarction, Middle Cerebral Artery ; Male ; Manganese ; Mice* ; Mitochondrial Proteins ; Neurons ; Reactive Oxygen Species ; Reperfusion ; Uridine Triphosphate

PURPOSE: Despite current acceptance of its neuroprotective property, whether the minocycline affords neuroprotection or how it protects neurons against seizures in the animal model of epilepsy is not clear. This prompts us to investigate whether minocycline is neuroprotective against kainic acid (KA)-induced seizure in mice through inhibition of caspase-dependent mitochondrial apoptotic pathways. METHODS: Adult male ICR mice were subjected to seizures by intrahippocampal KA injection with treatment of vehicle or minocycline. For cell death analysis, histological analysis using cresyl-violet staining, TdT-mediated dUTP-biotin nick end labeling (TUNEL), and histone-associated DNA fragmentation analysis were performed. Evaluation of cytochrome c, cleaved caspase-3, and caspase-3 activity were also performed. RESULTS: Hippocampal neuronal death was evident by cresyl violet staining, TUNEL, and cell death assay in vehicle-treated mice after KA injection; however, there was significant reduction of cell death in the minocycline-treated group. Significant decrease of both cytosolic translocation of cytochrome c and subsequent activation of caspase-3 after treatment of minocycline were demonstrated by Western blot analysis, immunohistochemical staining, and caspase-3 activity assay. CONCLUSION: This study suggests that minocycline may be neuroprotective against hippocampal damage after KA-induced seizure through inhibition of caspase-dependent cell death pathways.
Adult ; Animals ; Apoptosis ; Blotting, Western ; Caspase 3 ; Cell Death* ; Cytochromes c ; Cytosol ; DNA Fragmentation ; Epilepsy ; Humans ; In Situ Nick-End Labeling ; Kainic Acid ; Male ; Mice* ; Mice, Inbred ICR ; Minocycline* ; Models, Animal ; Neurons ; Seizures* ; Viola

Rheumatoid meningitis, one of the most severe complications of rheumatoid arthritis, presents various symptoms such as headache, confusion, loss of consciousness, seizure, fever, and focal neurological deficits. A 63-year-old man with the history of rheumatoid arthritis presented with intermittent left leg weakness, seizures and later developed fever and confusion. Brain MRI demonstrated leptomeningeal enhancement in right fronto-parietal area. Brain biopsy revealed multifocal suppurative inflammation. After aggressive immunosuppressive treatment, he had gradually recovered and the lesion was reduced on a follow-up MRI.
Arthritis, Rheumatoid ; Biopsy ; Brain ; Fever ; Follow-Up Studies ; Headache ; Humans ; Inflammation ; Leg ; Meningitis ; Middle Aged ; Neurologic Manifestations ; Seizures ; Seizures, Febrile ; Unconsciousness

Idiopathic retroperitoneal fibrosis is a fibrotic process of the retroperitoneum that frequently produces ureteral obstruction. We report a case of idiopathic retroperitoneal fibrosis in a 22 year-old male patient with brief review of literatures.
Humans ; Male ; Retroperitoneal Fibrosis* ; Ureteral Obstruction ; Young Adult

PURPOSE: Matrix metalloproteinases (MMPs) have been known to participate in various pathologic situations by modulating extracellular matrix. Although MMP-9 upregulation has been reported in some experimental seizure models, the exact role of MMP-9 in hippocampal cell death during epileptogenesis and subsequent mossy fiber sprouting (MFS) is not clear. Here, we investigated the role of MMP-9 on hippocampal cell death and MFS after pilocarpine-induced status epilepticus (SE) in mice, using highly specific hydroxamic MMP-9 inhibitor. METHODS: SE was induced by intraperitoneal pilocarpine administration in adult male C57BL/6 mice. MMP-9 specific inhibitor was administered intracerebroventrically 3 h after pilocarpine-induced SE. Expression and activation of MMP-9 were assessed by zymography and Western blot analysis. TdT-mediated UTP-biotin nick end labeling (TUNEL) and caspase-3 activity assay were also performed. MFS was investigated using Timm staining. RESULTS: Increased expression and activation of MMP-9 after pilocarpine-induced SE were observed in zymography and Western blot analysis. MMP-9 specific inhibitor decreased MMP-9 activity in in situ zymography and hippocampal cell death in cresyl violet staining. DNA fragmentation and caspase-3 activity were also attenuated by MMP-9 specific inhibitor. Four months after pilocarpine-induced SE, MFS was evident in vehicle-treated mice; in contrast, MFS was barely observed in MMP-9 specific inhibitor-treated mice. CONCLUSIONS: This study suggests MMP-9 is associated with hippocampal cell death and MFS after pilocarpine-induced SE. Furthermore, the findings that MMP-9 specific inhibitor ameliorates cell death and MFS offers the possibility of MMP-9 specific hydroxamic inhibitor as novel therapeutic strategy to reduce hippocampal damage and epileptogenesis.
Adult ; Animals ; Apoptosis ; Blotting, Western ; Caspase 3 ; Cell Death* ; DNA Fragmentation ; Extracellular Matrix ; Humans ; Male ; Matrix Metalloproteinase 9 ; Matrix Metalloproteinases ; Mice* ; Mossy Fibers, Hippocampal ; Neurons* ; Pilocarpine ; Seizures ; Status Epilepticus* ; Up-Regulation ; Viola

PURPOSE: To investigate the pathogenesis of articular prosthesis osteolysis, and to clarify the role of OPG, RANKL and RANK on osteolysis in aseptic loosening of hip prostheses. MATERIALS AND METHODS: We examined the mRNAs of OPG, RANKL and RANK from cultured peripheral mononuclear cells and the tissue surrounding failed hip prostheses by RT-PCR and gel electrophoresis and performed immunohistochemistry for RANKL and RANK in the periprosthetic tissue of revised hip replacement therapy. RESULTS: RANKL was detected in 32% and RANK was detected in 20% of the periprosthetic tissues of failed hip prostheses. Proliferative responses of cultured PBMCs occurred in cells with the titanium, cobalt and LPS, and highest response was observed in cells with cobalt particles. The mRNAs of RANKL and OPG were expressed in the periprosthetic tissues of loosened hip prostheses, but RANK mRNA was not detected. OPG mRNA was not detected in cultured PBMCs with any particles, RANKL mRNA was detected in cultured PBMCs with titanium and cobalt particles by RT-PCR, and RANK mRNA was detected in PBMCs with cobalt particles, but not with titanium. CONCLUSION: Osteolysis around the failed hip prosthesis may be related to activation of the OPG-ANKLRANK system. It is suggested that OPG, RANKL and RANK are major mediators of osteolysis in failed hip prosthesis.
Cobalt ; Electrophoresis ; Hip Prosthesis* ; Hip* ; Immunohistochemistry ; Osteolysis ; Osteoprotegerin* ; Prostheses and Implants ; RANK Ligand* ; RNA, Messenger ; Titanium

Somatics refers to body work and movement study that emphasize internal perception and experience. Recently, a new perspective has emerged that views somatics-based techniques as a kind of mindful movement. Somatic techniques as contemplative movement can improve emotional regulation ability through improvement of body awareness or interoception. Based on this background, the present study attempts to develop a somatics based program suitable for a group of clinical patients suffering from emotional dysregulation. This study plans to collect quantitative and qualitative data in order to clarify how interoception and the related emotional regulation ability change after the program. These findings will help to explore whether the somatics technique has potential as an emotion regulation program in the future. In addition, the results are expected to contribute to finding an alternative treatment modality for patients who have not achieved a sufficient effect with conventional psychotherapy.