No abstract available.
Animals ; Cell Adhesion* ; Female ; Leiomyoma* ; Mice ; Myometrium* ; Neural Cell Adhesion Molecules*

OBJECTIVE: The treatment with low-dose aspirin in the patients with unexplained infertility has been reported to improve the pregnancy rate and implantation rate via increasing the blood flow in the endometrium. But there are little known about the relationships between low-dose aspirin and cell adhesion molecules, NCAM. The aim of this study was to evaluate the effect of low-dose aspirin and clomiphene citrate treatment on the expression of NCAM in the endometrium. METHODS: The patients with unexplained infertility (N=37) were grouped into 3 groups: clomiphene citrate and low-dose aspirin treated group (N=8), clomiphene citrate treated group (N=10), and natural cycle group (N=10, no treatment). As control group, the proliferative and menopausal endometrium was used. Each endometium was obtained by endometrial biopsy performed in late luteal phase and immunohistochemical staining with NCAM was performed. RESULTS: In the stromal cells, the staining intensity of NCAM expression and the number of vessels were significantly increased in the endomterium treated with clomiphene citrate and low-dose aspirin compared with other groups (p<0.05). And the expression of NCAM in the prolifertive and menopausal endometrium showed very weak staining. CONCLUSION: The expression of NCAM in the stromal cells and the number of vessels were increased in the endometrium of unexplained infertility patients treated with clomiphene citrate and low-dose aspirin. These findings may suggest low-dose aspirin has an important role during the secretory phase of endometrium to improve the implantation via increasing the expression of cell adhesion molecules, especially NCAM and increasing the number of vessels.
Aspirin* ; Biopsy ; Cell Adhesion Molecules ; Clomiphene* ; Endometrium* ; Female ; Humans* ; Infertility ; Luteal Phase ; Neural Cell Adhesion Molecules* ; Pregnancy Rate ; Stromal Cells

Dehydroevodiamine.HCl (DHED) has been reported to prevent memory impairment and neuronal cell loss in a rat model with cognitive disturbance. We investigated the effect of DHED on memory impairment and behavioral abnormality caused by stress. We demonstrated that DHED can improve stress-induced memory impairments and depression-like behaviors by using open-field test, Y-maze test and forced swimming test. DHED treatment significantly recovered the decreases in the levels of neural cell adhesion molecule (NCAM) proteins caused by stress and the decreases in cell viability. Our results suggested that DHED is a potential drug candidate for neuronal death, memory impairment and depression induced by stress.
Animals ; Cell Survival ; Depression* ; Fluoxetine ; Memory* ; Models, Animal ; Neural Cell Adhesion Molecules ; Neurons ; Physical Exertion ; Rats*

PURPOSE: This study was performed to examine the histopathologic changes of muscles and the expression patterns of ubiquitin and N-CAM (neural cell adhesion molecule) in accordance with cerebral palsy patient's spasticity. MATERIALS AND METHODS: We studied thirteen specimens from seven patients with spastic cerebral palsy, five patients suspected to have neuromuscular diseases, and one normal person. We performed the routine histologic procedures, the reverse transcriptional polymerase chain reaction (RT-PCR), and immunostaining. RESULTS: There were no disease-specific abnormalities related with the degree of spasticity on histopathologic evaluation. However, in the cerebral palsy patients, the degree of spasticity seems to have positive correlations with the expression of ubiquitin gene and negative correlations with the expression of N-CAM gene. On the other hand, in the immunostaining procedures, the reactions to ubiquitin protein were all negative and reactions to N-CAM protein were strongly positive only in two hereditary motor sensory neuropathy patients. CONCLUSION: The results of our study seem to be caused by multiple mechanisms. If more studies about the changes after the transcription of ubiquitin and N-CAM genes are performed, these results can be applied to the research and treatment of cerebral palsy on molecular biologic aspects.
Cell Adhesion ; Cerebral Palsy* ; Hand ; Humans ; Muscle Spasticity* ; Muscles* ; Neural Cell Adhesion Molecules* ; Neuromuscular Diseases ; Polymerase Chain Reaction ; Ubiquitin*

P19, murine embryonal carcinoma (EC) cells can be induced to differentiate into neurons in the presence of retinoic acid (RA). To investigate neuronal differentiation of P19 cells in details, P19 aggregates were obtained in the presence or absence of RA, ascorbic acid (AA) and 2-mercaptoethanol (2-ME) in bacteriological Petri dishes. When the aggregates were transferred into the serum depleted medium, P19 cells exhibited dramatic morphological changes. Cells contained long and thin processes as detected in differentiated neurons. Western blot analysis showed that treatment of RA and AA induced expression of neuron-specific markers such as NCAM, NSE and Tuj1. Expression of GFAP was not detected, suggesting that P19 cells differentiate into neurons under our experimental condition. Immunocytochemical studies also revealed that treatment of RA and AA increased expression of NCAM and Tuj1. On the contrary, 2-ME was ineffective in the neuronal differentiation of P19 cells, which is consistent the results from the western blot analysis. These results suggest that differentiated P19 cells have similar characteristics to those of typically differentiated neurons. This study also suggests that P19 cells may provide useful tools to study neuronal differentiation in vitro.
Ascorbic Acid ; Blotting, Western ; Carcinoma, Embryonal ; Mercaptoethanol ; Neural Cell Adhesion Molecules ; Neurons* ; Tretinoin

OBJECTIVE: Dysfunction of neural plasticity in the brain is known to alter neural networks, resulting in depression. To understand how fluoxetine regulates molecules involved in neural plasticity, the expression levels of NCAM, NCAM140, CREB and pCREB, in rat C6 glioma cells after fluoxetine treatment were examined. METHODS: C6 cells were cultured after 20 min or after 6, 24 or 72 h treatments with 10 microM fluoxetine. Immunocytochemistry was used to determine the effect of fluoxetine on the expression of NCAM. Western blot analysis was used to measure the expression levels of NCAM140 and CREB and the induction of pCREB after fluoxetine treatment. RESULTS: NCAM expression following 72-h fluoxetine treatment was significantly increased around cell membranes compared to control cells. Cells treated with fluoxetine for 6 and 72 h showed a significant increase in NCAM140 expression compared to cells treated for 20 min. The level of pCREB in the cells treated with fluoxetine for 72 h not only increased more than 60%, but was also significantly different when compared with the other treatment times. The 72-h fluoxetine treatment led to the increase of NCAM140 and the phosphorylation of CREB in C6 cells. CONCLUSION: Our findings indicate that fluoxetine treatment regulates neuronal plasticity and neurite outgrowth by phosphorylating and activating CREB via the NCAM140 homophilic interaction-induced activation of the Ras-MAPK pathway.
Animals ; Blotting, Western ; Brain ; Cell Membrane ; Depression ; Fluoxetine ; Glioma ; Immunohistochemistry ; Neural Cell Adhesion Molecules ; Neurites ; Neuronal Plasticity ; Phosphorylation ; Plastics ; Rats

Altitude ; Animals ; CA1 Region, Hippocampal ; metabolism ; physiology ; Male ; Neural Cell Adhesion Molecules ; metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors

OBJECTIVE: Repair of sensorial nerve defect is an important issue on peripheric nerve surgery. The aim of the present study was to determine the effects of sensory-motor nerve bridging on the denervated dermatomal area, in rats with sensory nerve defects, using a neural cell adhesion molecule (NCAM). METHODS: We compared the efficacy of end-to-side (ETS) coaptation of the tibial nerve for sural nerve defect repair, in 32 Sprague-Dawley rats. Rats were assigned to 1 of 4 groups: group A was the sham operated group, group B rats had sural nerves sectioned and buried in neighboring muscles, group C experienced nerve sectioning and end-to-end (ETE) anastomosis, and group D had sural nerves sectioned and ETS anastomosis was performed using atibial nerve bridge. Neurological evaluation included the skin pinch test and histological evaluation was performed by assessing NCAM expression in nerve terminals. RESULTS: Rats in the denervated group yielded negative results for the skin pinch tests, while animals in the surgical intervention groups (group C and D) demonstrated positive results. As predicted, there were no positively stained skin specimens in the denervated group (group B); however, the surgery groups demonstrated significant staining. NCAM expression was also significantly higher in the surgery groups. However, the mean NCAM values were not significantly different between group C and group D. CONCLUSION: Previous research indicates that ETE nerve repair is the gold standard for peripheral nerve defect repair. However, ETS repair is an effective alternative method in cases of sensorial nerve defect when ETE repair is not possible.
Animals ; Methods ; Muscles ; Neural Cell Adhesion Molecules ; Peripheral Nerves ; Rats ; Rats, Sprague-Dawley ; Skin ; Sural Nerve* ; Tibial Nerve*

We herein report a case of nasal type T/natural killer(NK)-cell lymphoma(TNKCL). This lymphoma is characterized by the expression of CD2, CD43 and NCAM(CD56) antigen, an aggressive clinical course, frequent extranodal spreading, a strong association with Epstein-Barr virus(EBV), and the absence of T-cell receptor(TCR) gene rearrangement. NCAM antigen is known to be a possible determinant of extranodal dissemination of peripheral T-cell lymphoma(PTCL). The patient is a 70-year-old male with skin lesion on his forearm. Histopathological and immunohistochemical studies were diagnostic of EBV-associated TNKCL. Untill now, he has failed to respond to anticancer therapy.
Aged ; Forearm ; Gene Rearrangement ; Herpesvirus 4, Human ; Humans ; Lymphoma* ; Male ; Neural Cell Adhesion Molecules ; Skin ; T-Lymphocytes

OBJECTIVES: Most of the mechanisms reported for antidepressant drugs are the enhancement of neurite outgrowth and neuronal survival in the rat hippocampus. Neural cell adhesion molecule 140(NCAM140) has been implicated as having a role in cell-cell adhesion, neurite outgrowth, and synaptic plasticity. In this report, we have performed to elucidate a correlation among chronic antidepressant treatments, NCAM140 expression, and activation of phosphorylated cyclicAMP responsive element binding protein(pCREB) which is a downstream molecule of NCAM140-mediated intracellular signaling pathway in the rat hippocampus. METHODS: Fluoxetine(10mg/kg) was injected acutely(daily injection for 5days) or chronically(daily injection for 14days) in adult rats. RNA and protein were extracted from the rat hippocampus, respectively. Real-time RTPCR was performed to analyze the expression pattern of NCAM140 gene and western blot analyses for the activation of the phosphorylation ratio of CREB. RESULTS: Chronic fluoxetine treatments increased NCAM140 expression 1.3 times higher than control in rat hippocampus. pCREB immunoreactivity in the rat hippocampus with chronic fluoxetine treatment was increased 4.0 times higher than that of control. CONCLUSION: Chronic fluoxetine treatment increased NCAM140 expression and pCREB activity in the rat hippo-campus. Our data suggest that NCAM140 and pCREB may play a role in the clinical efficacy of antidepressants promoting the neurite outgrowth and neuronal survival.
Adult ; Animals ; Antidepressive Agents ; Blotting, Western ; Fluoxetine ; Hippocampus ; Humans ; Neural Cell Adhesion Molecules ; Neurites ; Neurons ; Phosphorylation ; Plastics ; Rats ; RNA