Expression and correlation of β-Catenin and neural cell adhesion molecule in thyroid carcinoma / 中华内分泌外科杂志

Objective To investigate the expression level and correlation of β-catenin and neural cell adhesion molecule(NCAM) in thyroid carcinoma.Methods In this study,the expression levels of NCAM and β-catenin in thyroid carcinoma tissues (n=62) and thyroid adenoma tissues (n=44) collected from patients treated in Wenzhou Integrated Traditional Chinese and Western Medicine Hospital Affiliated to Zhejiang Chinese Medical University from Dec.2012 to Dec.2017 were detected by immunohistochemical staining,then its correlation with clinicopathological features was analyzed.Results The positive expression rate of NCAM in thyroid carcinoma tissues was significantly lower than that in thyroid adenoma tissues (12.90％ vs 90.91％,t=63.203,P=0.000).The positive expression rate of β-catenin protein in thyroid carcinoma tissues was significantly higher than that in thyroid adenoma tissues (82.26％ vs 6.82％,t=58.608,P=0.000).NCAM and β-catenin were negatively correlated in thyroid carcinoma tissues (r=-0.220,P=0.024).The difference of NCAM expression level was not significant among thyroid carcinoma patients with different gender,age,tumor diameter,histological type or pathological stage (t=1.960,0.054,3.335,0.807,0.218;P=0.162,0.816,0.069,0.848,0.641).The expression of NCAM in cancer tissues was significantly different in patients with different lymph node metastasis (t=8.373,P=0.004).The expression of β-catenin in cancer tissues was not significant in thyroid carcinoma patients with different gender,histological type,tumor diameter,age,lymph node metastasis or pathological stage (t=0.258,2.307,0.424,0.741,2.570,0.126;P=0.612,0.511,0.515,0.389,0.109,0.722).Conclusions In thyroid carcinoma patients,NCAM is down-regulated,and β-catenin is highly expressed.Moreover,the two indicators are negatively correlated.Additionally,NCAM expression is correlated with lymph node metastasis in thyroid carcinoma patients.

Loss of expression of the Neural Cell Adhesion Molecule 1 (NCAM1) in atypical teratoid/rhabdoid tumors: a new diagnostic marker?

Background: Atypical teratoid/rhabdoid tumors (AT/RT) are aggressive embryonal tumors of the central nervous system. They are largely characterized by inactivating mutations of the SMARCB1 tumor suppressor gene. AT/RT patients have a very poor prognosis and no standard therapeutic protocol has been defined yet. Recently, multimodal therapy with multiple drug combinations has slightly improved the overall survival, however drug toxicity remains high. In this scenario, a better understanding of the pathophysiology of the disease is needed. Methods: We evaluated the gene expression profile of AT/RT samples to find new genetic factors contributing to the pathophysiology of the disease. We found target genes significantly differentially expressed between AT/RT and medulloblastoma (MB), the most common embryonal brain tumor. The mRNA expression was validated by quantitative real-time PCR and, at the protein level, expression was validated by immunohistochemistry in an independent set of tumors. Results: The Neural cell adhesion molecule 1 (NCAM1) gene was found to be consistently downregulated in AT/RT samples when compared to MB and normal brain tissue. Immunohistochemistry showed that the expression of NCAM1 in AT/RT was significantly lower than that of MB. Conclusion: NCAM1 is an important molecule involved in neuron-to-neuron and neuron-to-muscle adhesion during development. Downregulation of NCAM1 has been implicated in several human cancers suggesting that it might have a tumor repressor role. In this study we found a significantly reduced expression of NCAM1 in AT/RT when compared to MB and we suggest that this feature can be used as a diagnostic marker, along with demonstration of SMARCB1 (INI1) or SMARCA4 (BRG1) inactivation. The roles of NCAM1 in the pathophysiology of AT/RT are still to be determined (AU)

Cancer stem cells in hepatocellular carcinoma - an immuno- histochemical study with histopathological association.

Background & objectives: Cancer stem cells (CSCs) may be responsible for tumour recurrence and resistance to chemotherapy in hepatocellular carcinoma (HCC). This study was carried out to evaluate the association between histological parameters and liver CSCs (LCSC) in HCC, and to compare distribution of liver CSCs in HCC associated with and without hepatitis B virus (HBV) infection. Methods: Seventy nine tumours (49 surgical resections from 46 patients, and 30 from autopsy) were reviewed. Immunohistochemical staining for the LCSC marker EpCAM (epithelial cell adhesion molecule), liver progenitor cell (LPC) markers CK19 (cytokeratin 19) and neural cell adhesion molecule (NCAM) were performed and were associated with histological features of tumour behaviour. Results: Thirty three tumours (41.8%) showed positive staining for EpCAM. CK19 and NCAM expression were seen in 26 (32.9%) and four (5.1%) tumours, respectively. The expression of EpCAM and CK19 was significantly associated with each other (P<0.001). EpCAM expression was significantly associated with clinical and histological features indicating aggressive tumour behaviour, including younger age of onset, higher serum alpha foetoprotein (AFP) levels, tumour cell dedifferentiation, increased mitotic activity, and vascular invasiveness. There was no significant difference in expression of EpCAM, CK19 and NCAM between HBV positive and negative HCC. Interpretation & conclusions: The LCSC marker EpCAM was expressed in less than half of HCC, was independent of HBV aetiology, and was strongly associated with clinical and histological features of aggressive tumour behaviour. Positive staining for CK19 suggests a possible LPC origin of the EpCAM positive HCCs.

NCAM140 and pCREB Expression after Tianeptine Treatment of SH-SY5Y Cells

OBJECTIVE: Antidepressants Modulate Neuronal Plasticity. Tianeptine, An Atypical Antidepressant, Might Be Involved In The Restoration Of Neuronal Plasticity; It Primarily Enhances The Synaptic Reuptake Of Serotonin. Ncam140 Is Involved In Neuronal Development Processes, Synaptogenesis And Synaptic Plasticity. We Investigated The Effect Of Tianeptine On The Expression Of Ncam140 And Its Downstream Signaling Molecule In The Human Neuroblastoma Cell Line Sh-sy5y. METHODS: NCAM protein expression was measured in human neuroblastoma SH-SY5Y cells that were cultivated in serum-free media and treated with 0, 10, or 20 microM tianeptine for 6, 24, or 72 hours. NCAM140 expression in the tianeptine treatment group was confirmed by Western blot, and quantified through measurement of band intensity by absorbance. CREB and pCREB expression was identified after treatment with 20 microM tianeptine for 6, 24, and 72 hours by Western blot. RESULTS: Compared to cells treated for 6 hours, cells treated with 0 or 10 microM tianeptine for 72 hours showed a significant increase in NCAM140 expression and cells treated with 20 microM tianeptine showed a significant increase after 24 and 72 hours. The pCREB level in cells treated with 20 microM tianeptine increased in time-dependent manner. CONCLUSION: Our findings indicated that the tianeptine antidepressant effect may occur by induction of NCAM140 expression and CREB phosphorylation.

The expression of collagen fibers,NCAM1 and RUNX1 in blood-supply myocardium of myocardial bridge / 重庆医学

Objective To investigate the express of collagen fibers ,NCAM11 and RUNX1 in blood-supply myocardium of myo-cardial bridge(MB) .Methods The Massion′s staining were conducted to reveal the morphology of collagen fibers in blood-supply myocardium among MB without artherosclerosis(group A) ,MB with artherosclerosis(group B) ,coronary artery disease(group C) , and non-cardiogenic instantly death(group D) .The expression level of NCAM1 and RUNX1 were detected among four groups using immunohistochemistry(IHC) and Western bolt ,respectively .Results There were a lot of collagen fibers in myocardium interstitial substance and/or heart muscle necrosis between group B and C ,but not almost collagen fibers between group A and D .The expres-sion of NCAM1 was positive in group B ,and mainly expressed on the cytoplasm and membranes of cardiac myocytes by IHC .group C was similar to results in vicinal myocardium with myocardial scar .However ,there was quite lowness or negative expression of NCAM1 in group A and D .Significant difference was found between group B as well as C and group A as well as D (P<0 .05) .The expression level of RUNX1 in blood-supply myocardium was almost like to the results of NCAM 1 .Conclusion MB with arthero-sclerosis might be lead to chronic myocardial ischemia .

Effect of anti-epileptic, nootropic drugs on the expression of ERK2 and NCAM1 in the hippocampus changes on the epileptic rats with cognitive dysfunction / 中华行为医学与脑科学杂志

Objective To study the effect of anti-epileptic,nootropic drugs on the expression of NCAM and ERK2 in the hippocampus changes on the epileptic rats with cognitive dysfunction.Methods A total of 120Wistar rats were used.20 controls and 100 in which epilepticus with cognitive dysfunction were randomly assigned to 5 groups (n =20/group) that received daily treatments for 30 days with either (1) saline (epilepsy),(2) carbamazine (traditional anti-epileptic),(3) oxcarbazine (new anti-epileptic),(4) aniracetam (brain protective),or (5) donepezil (nootopic).Spatial learning and memory were assessed with a Morris Water Maze (MWM).Hippocampus tissue was assessed for NCAM1 and ERK-2 mRNAs by RT-PCR and proteins by immunochemistry.Results The mean escape latency of the place navigation test:EP group ((67.14 ± 7.37)s)was all higher than NS group (35.78 ± 4.84 s)and there was statistical significance (P ＜ 0.01),carbamazepine group ((81.23 ± 9.46)s) ＞ EP group((67.14 ±7.37)s) ＞ donepezi group((53.75 ±6.74) s) (P＜0.01).Immunohistochemical and RT-PCR result:carbamazepine ＜ oxcarbazepine ＜ epilepsy ＜ aniracetam ＜ donepezi group.Compared with control group,donepezil group ＞ control group (P ＜ 0.01),aniracetam group ＞ control group (P ＜ 0.05).Conclusion ERK-2 expression is decreased and NCAM 1 expression is increased in the hippocampus in the epileptic rats.Thus,both are involved in cognitive dysfunction.Carbamazepine aggravates cognitive dysfunction,whereas donepezil improves cognitive dysfunction associated with epilepsy.

Fluoxetine Increases the Expression of NCAM140 and pCREB in Rat C6 Glioma Cells

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.

The effect of exposure to low intensity infrasound on the expression of PSA-NCAM in the rat hippocampus / 中华物理医学与康复杂志

Objective To observe the expression of the polysialic acid neural cell adhesion molecule ( PSA-NCAM) in the hippocampus of rats after exposure to low intensity ( 16 Hz,90 dB) infrasound for different periods.Methods One hundred and twenty male Sprague-Dawley rats were randomly divided into infrasound exposure and normal groups.The exposure group was tjem further divided into 1 day,7 days,14 days and 21 days exposure groups.After exposure,the rats' brains were removed and an immunohistochemical technique was used to observe the expression of PSA-NCAM in the hippocampus after 1,7,14 or 21 days of exposure. Methods The expression of PSA-NCAM had increased significantly after exposure for 7 days. It peaked at 14 days,then had decreased by 21 days,but always remaining higher than in the normal group.After the infrasound exposure had ended,the expression of PSA-NCAM demonstrated a tendency of decrease over time,and the least was on the 21st day.The largest decrease was observed in the 14 days exposure groups. Conclusion 16 Hz,90 dB infrasound can increase the expression of PSA-NCAM in the hippocampus,at least in rats.This suggests that low intensity infrasound might initiate recovery of an injured central nervous system.Migration of neural stem cells may aid in the repair of neural injuries resulted from infrasound exposure.

Effects of intermedin pretreatment on associated repairing genes in the kidney of rats with renal ischemia-reperfusion injury / 中华肾脏病杂志

Objective To investigate the effects of intermedin (IMD) pretreatment on associated repairing genes of the rats with injured kidneys by ischemia reperfusion injury (IRI)during the repair and regeneration process.Methods A total of 144 healthy male Wistar rats were randomly divided into 4 gourps:sham opration group,IRI group,empty plasmid group (EP)and IMD group.After resection of right kidneys of the rats,plasmid was transfected into the left kidneys by using ultrasonic microbubble technology.After one week,the renal IRI models were programmed.The samples of renal tissues after 1 d,2 d,3 d,4 d,7 d and 14 d of reperfusion were harvested respectively,then the mRNA expressions of the Pax-2,ZO-1,Ncam,Wt-1 and vimentin in renal tissues were detected by RT-PCR; the protein expressions of Pax-2,Wt-1 and vimentin were analyzed by Western blotting and the protein expressions of ZO-1 and Ncam were measured by ELISIA.Results (1) Compared with the sham group,the mRNA and protein expression of Pax-2,ZO-1,Ncam,Wt-1 and vimentin of the rats in IRI group increased significantly from day 1 to day 3 (P＜0.05),which peaked at day 2.After day 4,the above expressions in IRI group returned to normal level.(2) In IMD group,the mRNA and protein expressions of Pax-2,Zo-1,Ncam,Wt-1 and vimentin were significantly higher than those in other 3 groups (P＜0.05) at the same time after IRI day 1 to day 4,with a maximum in day 2.(3) The above expressions in IRI group,EP group,IMD group had no significant differences compared with sham group after day 7 or day 14 respectively (P＞0.05),and either between IRI group and EP group,though the expressions of the genes in IRI group and EP group increased compared with sham group after day 4.(4) The above expressions between IRI group and EP group also had no significant difference (P＞0.05).(5) Changes of ZO-1 and Ncam protein expression detected by ELISA were similar to those abore mRNA and protein expression by RT-PCR and Western blotting.Conclusion IMD pretreatment plays an important role in up-regulation of the expressions of associated repair genes during the process of repair and regeneration after renal ischemia reperfusion injury.

Chronic Treatment of Fluoxetine Increases Expression of NCAM140 in the Rat Hippocampus

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.

Expeiment study on the proliferation and plasticity of ependymal cells in situ in the injuried spinal cord of adult rats / 中国矫形外科杂志

[Objective]To observe the proliferation and plasticity of neural stem cells in sim in adult rats after spinal cord injury.[Method]Spinal cord injury models were made in 60 wistar rats and the dynamic expression of bromodeoxyuridine(BrDU) and polysialylated ependymal cells adhesion molecule(PSA-NCAM) were determined by immuno-histochemisty.[Result]Compared with the controls,the number of Brdupositive cells in the injured spinal cord increased strikingly on the 1 st day (P

Characterization of Differentially Expressed Genes upon Chronic Fluoxetine Treatment in Rat C6 Glioma Cells / 대한정신약물학회지

OBJECTIVE: The aim of this study was to identify diffrentially regulated genes after the treatment of fluoxetine in rat C6 glioma cells using cDNA microarray chip techniques and real-time RT-PCR. METHODS: Cells were incubated for 24 hours, and for 72 hours with or without 10 uM fluoxetine. Total RNAs extracted from cells were reversely transcribed to cDNA. These cDNA were used to carry out cDNA microarray chip. A part of the up-/down-regulated genes in cDNA microarray result were confirmed by real-time RT-PCR. RESULTS: 1) Genes in fluoxetinetreated cells for 72 hours (chronic treatment) were more regulated than that in fluoxetine-treated cells for 24 hours (acute treatment). 2) The expression level of Gs gene in fluoxetine-treated cells for 24 hours hardly altered, but that of Gs in fluoxetine-treated cells for 72 hours significantly increased. The expression of Gi2 also decreased in 72 hours in relation to 24 hours after the administration of fluoxetine. 3) The expression level of NCAM140 gene in fluoxetine-treated cells was higher than that in control cells. CONCLUSION: We identified genes (Gs, Gi2 and NCAM140) related to neural plasticity and intracellular signal transduction cascade from our result. This implies that fluoxetine may inhibit atrophy or death of impaired neural cells by promoting neurite outgrowth.

Construction of PSA and NCAM differently expressing COS-7 cell line and the effects of PSA on migration and invasion of the diverse COS-7 cell / 中国药理学通报

Aim To construct a polysialic acid(PSA)and neural cell adhesion molecule(NCAM)differently expressing COS-7 cell line,and investigate the effects of PSA on the cell adhesion,migration and invasion,aiming to establish the base for further investigation of the signaling passway of the diverse celluar migration and invasion,and elucidate the molecular mechanism of PSA promoting cancer cell metastasis.Methods A polysialic acid and neural cell adhesion molecule differently expressing COS-7 cell line was constructed by transient cotransfection,and the cotransfection efficiency was determined by Western blot and flow cytometry.Adhesion assay was used to investigate the effect of PSA on cell adhesion ability;transwell assay was used to measure migration and invasion ability.Results The PSA and NCAM differently expressing COS-7 cell line was successfully constructed,which demonstrated PSA inhibited the cell adhesion to basement membrane,and promoted the migration and invasion ability.Conclusions The constructed polysialic acid and neural cell adhesion molecule differently expressing COS-7 cell line can be used to investigate molecular mechanism of promoting cancer cell metastasis induced by PSA in the future.

THE EFFECT OF PRENATAL NICOTINE EXPOSURE ON DEVELOPMENT OF CEREBRAL CORTEX AND HIPPOCAMPUS IN THE OFFSPRINGS OF PREGNANT MICE AND EXPRESSIONS OF NEURAL CELL ADHESION MOLECULES / 解剖学报

Objective Our aim was to observe the effects of prenatal nicotine exposure on development of cerebral cortex and hippocampus in the offsprings of pregnant mice and expressions of NCAM proteins. Methods We established prenatally nicotine exposed(PNE) animal models.We investigated the offspring's structural changes of cerebral cortex and hippocampus with HE staining.Using immunohistochemistry and Western blotting we observed the changes of expressions of NCAM proteins in the neonatal mice. Results Cerebral cortex and hippocampus as well as hippocampal cell layers of the PNE offsprings were thinner than that of the control group.The expressions of PSA-NCAM in cerebral cortex and hippocampus of the PNE offsprings were higher than the control group while the expressions of NCAM-180,140 and 120 weaker.Conclusion Prenatally nicotine exposure can prevent normal morphogenesis of cerebral cortex and hippocampus of mice and can change the expressions of NCAM proteins in cerebral cortex and hippocampus of neonatal mice.

Immunohistochemical Study of the Expression of NCAM in the Fungiform Papilla of the Young Rat Tongue Following Single Dose Radiation / 대한해부학회지

Radiotherapy in the treatment of head and neck cancers is often used either alone or in addition to surgery. Radiation disrupts the proliferative capacity of the cancer while doing as little damage as possible to the normal tissue. Nevertheless, conventional radiotherapy of advanced head and neck tumors is frequently associated with severe oropharyngeal mucositis. The fungiform papillae are found on the dorsal surface of the anterior 2/3 of the tongue and have one taste bud which always located on the superior side. In recent years, many study have demonstrated the location of neuropeptides in the intragemmal cells of the taste buds. We used neural cell adhesion molecule (NCAM) in this study. NCAM is a membrane surface glycoprotein found in neural tissue that functions in cell -cell interactions such as adhesion and recognition and may contribute to neuronal and receptoneural synaptogenesis. However, to the best of our knowledge, there is no study about NCAM in relation to dysgeusia, especially after radiotherapy. Therefore, we studied the change of the expression of NCAM in the fungiform papilla of the young rat tongue following single dose radiation. Twenty days old 18 Sprague -Dawley rats were used. Twelve rats were irradiated with a single dose of 17 Gy gamma radiation. We sacrificed rats 1, 7, 20 days after radiation. The anterior part of tongues were removed and cut into at 30 micro gram on a cryocut. Using the free floating method, we immunostained sections. In control group, NCAM is expressed on some intragemmal cells which were located in the center of the bud and intragemmal nerve fibers. NCAM -immunoreactive (ir) perigemmal nerve fibers were rare, however basal plexus fibers and subpapillary nerve bundle showed strong immunoreactivity. One day after radiation, taste buds had no detectable changes of the expression of NCAM. However, seven days after radiation, the number of NCAM -ir intragemmal cells was reduced and the shape of ir cells was deformed. Immunoreactivity of basal plexus fibers and subpapillary nerve bundle was also decreased. The surface of the papilla was transformed into dome shape. Twenty days after radiation, overall forms of buds were recovered except a few deformed NCAM -ir intragemmal cells. NCAM was expressed in the intragemmal cells which are thought to be related with taste sensation, and we speculate that NCAM participate synaptogenesis. However, more studies using immunoelectron microscopic method are required.

Morphometric Evaluation of PGP9.5 and NCAM Expressing Nerve Fibers in Colonic Muscle of Patients with Hirschsprung's Disease

A quantitative assessment of the density of the protein gene product 9.5 (PGP9.5), the neural cell adhesion molecule (NCAM), and the low-affinity nerve growth factor receptor (NGFR) expressing nerve fibers in the circular muscle layer in the colon was carried out by morphometric analyses from 13 patients with Hirschsprung's disease (HD). The difference in the nerve fiber density between the ganglionic and aganglionic segments was compared by calculating the ratio of the sum of the areas occupied by positively stained nerve fibers per unit area of the muscle after immunohistochemical staining on paraffin embedded tissue sections using computer software. There was an obvious difference in the density of the PGP9.5 stained nerve fibers between the ganglionic (0.0380 +/- 0.0171) and aganglionic segments (0.0143 +/- 0.01661). The NCAM-positive nerve fibers were fewer in number than those of both the PGP9.5-positive fibers and NCAM-positive fibers, which were also markedly lower in number in the aganglionic segment (0.0066 +/- 0.0076) than in the ganglionic segment (0.0230 +/- 0.0195). Immunostaining for low-affinity NGFR revealed much fainter staining in the ganglionic and aganglionic segment without a statistically significant difference in their density. Considering the fact that PGP9.5 is a very sensitive marker for nerve fibers, the results of this study reaffirm the innervation failure of the proper muscle in HD. The decreased NCAM expression level in the aganglionic segment appears to be caused not by the selective down-regulation of NCAM expression among the nerve fibers but by a markedly reduced number of nerve fibers.

The Effect of low-dose Aspirin and Clomiphene Citrate on the Expression of Neural Cell Adhesion Molecules (NCAM) in the Human Endometrium / 대한산부인과학회잡지

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.

Effect of Schwann cell-derived neural cell adhesion molecule L_1 on axon regeneration of injured spinal cord / 中华骨科杂志

Objective To study the effect of Schwann cell enclosed by antibody of neural cell adhesion molecule L1 on injured spinal cord. Methods Over 98% of the purity of Schwann cells obtained from bilateral sciatic nerves of 2 days newborn SD rats, the concentration of Schwann cells was about 2.5?104 /?l. The Schwann cells were enclosed by the antibody of neural cell adhesion molecule L1 using co-culture. The adult SD rats (weight 200-250 g) were used to establish the model of spinal cord injury by hemi-transection at the left side of T10 level. The animals were divided into three groups; the SC group was transplanted with 20 ?l suspension Schwann cells; the anti-L1 group with 20 ?l Schwann cells enclosed by antibody of neural cell adhesion molecule L1; and the control group was injected solely with normal saline to the injured cord. Eight weeks later regenerated neural axons were investigated through horseradish peroxiase HRP retrograde trace immunohistochemistry of neurofilament and Western blot. Results Few regenerated neural axons appeared in the control group; some of regenerated neural axons could be observed in anti-L1 group; plentiful and bulky regenerated neural axons were found in SC group. The group with antibody had significant less HRP positive neurons and neural axons than the group without antibody. Western blot showed that the quantity of neurofilament in the anti-L1 group was only two thirds of the SC group. Conclusion Schwann cell-derived neural cell adhesion molecule L1 is able to enhance the neural axon regeneration of injured spinal cord.

An Morphological Study on the Alteration of Immunoreactivity of the Neural Cell Adhesion molecule ( NCAM ) in Rat Spinal Cord after Unilateral Sciatic Neurotomy and Reconnection

BACKGROUND: NCAM plays an important role in the peripheral innervation of the spinal neurons as well as in the development of the CNS. Although expression of NCAM is down-regulated in most areas of adult brain and spinal cord, it could be reexpressed after neuronal damages induced by various physical or chemical insults including peripheral nerve transection. METHOD: To investigate alterations of the NCAM immunoreactivity in the dorsal and ventral horns of the spinal cord induced by peripheral neurotomy and reconnection, the unilateral sciatic nerve of the rats were transected and immediately reconnected. Experimental animals were sacrificed at 1 week and 3 weeks after operation, and the alteration of NCAM immunoreactivity in the ventral and the dorsal horns of the lower lumbar spinal cord were examined. RESULTS: NCAM-immunoreactive astrocytes in the ipsilateral dorsal horn was increased at 1 week after operation. Neurons with NCAM?immunoreactive membranes and processes were increased in ipsilateral dorsal horns, and in large motor neurons of ventral horns of both sides at 3 weeks after unilateral sciatic neurotomy and reconnection. CONCLUSIONS: It is consequently suggested that unilateral sciatic neurotomy and reconnection induce the increase of the NCAM-immunoreactive neurons and glial cells in the spinal cord, and increase of NCAM immunoreactivity in the spinal cord may reflect the neuronal damage and healing process induced by peripheral nerve injury.

A Case of NCAM-positive Nasal Type T/NK-Cell Lymphoma

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.