BACKGROUND: Neuropathic pain produced by nerve injury has the characteristics of enhanced pain responses - allodynia. To understand the pathophysiology of the neuropathic pain, We evaluated the effect of NMDA antagonists and chemical sympathectomy on the c-fos mRNA expression. METHODS: We have divided rats(Sprague-Dawley, N=24) that their left L5 and L6 nerve were tightly ligated into two groups. In NMDA antagonist group(N=17), We injected 10 g MK801 and 10 g 5-amino-phosphonovalerate in three ways, intrathecally before the ligation, after ligation and subcutaneous continuously. Then behavioral tests for mechanical allodynia and cold allodynia were performed. After the test of allodynia,the expression of c-fos were assessed by Northern blot hybridization. In chemical sympathectomy group(N=7), We injected 70 mg/kg guanethidine into the peritoneum in two ways, before the ligation and after ligation. Then same methods were performed in NMDA antagonist group as well. RESULTS: Intrathecal NMDA antagonists before the ligation supressed the elevation of c-fos mRNA expression. Intrathecal NMDA antagonists on the 7 days after the ligation reduced the c-fos mRNA expression and neuropathic pain. Continuous treatment of subcutaneous NMDA antagonists supressed the development of neuropathic pain and the elevation of c-fos mRNA expression. Chemical sympathectomy before the ligation did not supress the elevation of c-fos mRNA expression. Chemical sympathectomy on the 7 days after the ligation reduced neuropathic pain and the elevation of c-fos mRNA expression. CONCLUSIONS: NMDA receptor is related to the induction and maitenance of neuropatic pain, and sympathetic nervous system has a main role in the already induced neuropathic pain.
Animals ; Blotting, Northern ; Dizocilpine Maleate ; Guanethidine ; Hyperalgesia ; Ligation ; N-Methylaspartate* ; Neuralgia ; Peritoneum ; Rats* ; RNA, Messenger* ; Sympathectomy* ; Sympathectomy, Chemical ; Sympathetic Nervous System

Anesthesia and surgery in patients with untreated or inadequately treated hypothyroidism carries the risk of potential complications such as prolonged unconsciousness, hypotension, hypoventilation, hyponatremia, precipitation of congestive heart failure, cardiopulmonary arrest and myxedema coma. In addition, these patients have an impaired ability to excrete free water. Therefore, careful attention must be devoted to fluid and electrolyte management to prevent fluid retention and edema. We experienced a case of acute pulmonary edema during emergence from anesthesia in a patient with cured hypothyroidism. The pulmonary edema was completely resolved with ICU care on the 5th postoperative day. We conclude that surgery in the patient with hypothyroidism require thyroid hormone replacement therapy, careful monitoring and management for the cardiovascular status.
Anesthesia ; Anesthesia, General* ; Coma ; Edema ; Heart Arrest ; Heart Failure ; Hormone Replacement Therapy ; Humans ; Hyponatremia ; Hypotension ; Hypothyroidism* ; Hypoventilation ; Myxedema ; Pulmonary Edema* ; Thyroid Gland ; Unconsciousness ; Water

OBJECTIVE: The transfection efficiencies of gynecologic cancer cell lines were investigated by different mediated transfection methods using recombinant LacZ plasmid (pRcCMVLacZ and pAAVCMVLacZ). METHODS: In this study, the gynecologic cancer cell lines were used CaSki, SiHa (cervical, HPV16+, wild type p53 gene), HeLa, HeLa S3 (cervical, HPV18+, wild type p53 gene), C33A, HT3 (cervical, HPV-, p53 mutant), HckE6/E7 (cervical, HPV16 immortalized keratocyte), PA-1 (ovary, wild type p53), SKOV-3, A2774 (ovary, p53del) and OVCAR-3 (ovary, p53 mutant). The pRcCMVLacZ and pAAVCMVLacZ plasmid transfection were performed by using liposome system such as Ca2+-phosphate, Fugen6(TM), Lipofection(TM), Lipogen(TM) and N-stearyl lactobionamide (N-SLBA) with X-gal staining. The LacZ gene was used the reporter gene for the transfection efficiencies evaluation. RESULTS: Each of cell lines were showed different transfection efficiencies by Ca2+-phosphate, Fugen6(TM), Lipofectin(TM), Lipogen(TM) and N-SLBA. Each of cell were revealed that HeLa S3, HT3 and A2774 were high transfection efficiency using the pRcCMVLacZ by the Lipogen(TM), SiHa, HeLa, QGU, OVCAR-3 and PA-1 were high efficiency using the pAAVCMVLacZ by Lipofectin(TM), CaSki was high efficiency using the pRcCMVLacZ by the Lipogen(TM), A2774 and Cx16.2 were high efficiency using the pRcCMVLacZ by the Lipofectin(TM), SKOV-3 and HkcE6/E7 were high efficiency using pAAVCMVLacZ by the Lipogen(TM). CONCLUSION: As a result, We proved that each of cell lines differed trasnfection efficiencies according to mediated transfection and recombinant LacZ plasmid style. Above all, Lipofectin(TM) mediated transfection was showed high efficiency at the most of cell lines.
Cell Line* ; Genes, Reporter ; Humans* ; Lac Operon* ; Liposomes ; Plasmids* ; Transfection*

PURPOSE: The tumor suppressor gene, p53, has been established as an essential component for the suppression of tumor cell growth. In this study, we investigated the time-course anticancer effects of adenoviral p53 (Adp53) infection on human ovarian cancer cells to provide insight into the molecular-level understanding of the growth suppression mechanisms involved in Adp53-mediated apoptosis and cell cycle arrest. MATERIALS AND METHODS: Three human cervical cancer cell lines (SiHa, CaSki, HeLa and HT3) were used. The effect of Adp53 infection was studied via cell count assay, cell cycle analysis, FACS, Western blot and macroarray assay. RESULTS: Adp53 exerts a significant role in suppressing cervical cancer cell growth. Adp53 also showed growth inhibitory effects in each cell line, and it induced apoptosis and cell cycle arrest. Adp53 differentially regulated the expression of genes and proteins, and the gene expression profiles in the SiHa cells revealed that the p21, p53 and mdm2 expressions were significantly up-regulated at 24 and 48 hr. Western blot shows that the p21 and p53 expressionlevels were significantly increased after Adp53 infection. In addition, in all cell lines, both the CDK4 and PCNA protein expression levels were decreased 48 h after Adp53 infection. Cell cycle arrest at the G1 phase was induced only in the SiHa and HeLa cells, suggesting that exogenous infection of Adp53 in cancer cells was significantly different from the other HPV-associated cervical cancer cells. CONCLUSION: Adp53 can inhibit cervical cancer cell growth through induction of apoptosis and cell cycle arrest, as well as through the regulation of the cell cycle-related proteins. The Adp53-mediated apoptosis can be employed as an advanced strategy for developing preferential tumor cell-specific delivery.
Adenoviridae* ; Apoptosis ; Blotting, Western ; Cell Count ; Cell Cycle Checkpoints ; Cell Cycle* ; Cell Line ; G1 Phase ; Genes, Tumor Suppressor ; Genetic Therapy ; HeLa Cells ; Humans* ; Ovarian Neoplasms ; Papilloma* ; Proliferating Cell Nuclear Antigen ; Transcriptome ; Uterine Cervical Neoplasms*