Whether there exists a Sympathetic neural mechanism regulating the expression of aquaporin (AQP) water channels in the kidney was investigated. Male Sprague-Dawley rats were treated with reserpine (1 mg/kg, IP), and the expression of AQP1-4 proteins was determined in the kidney one day thereafter. Following the treatment with reserpine, the systolic blood pressure measured in a conscious state was significantly decreased in the experimental group compared with that in the control (83+/-8 vs 124+/-6 mmHg n=6 each, P<0.05). The expression of AQP2 proteins was decreased in the cortex, outer medulla, and inner medulla. The decrease of AQP2 proteins was in parallel in the membrane and the cytoplasmic fractions, suggesting a preserved AQP2 targeting. No significant changes were observed in the expression of AQP1, AQP3, or AQP4. Neither basal nor AVP-stimulated formation of cAMP was significantly altered. These results suggest that the sympathetic nervous system has a tonic stimulatory effect specifically on the expression of AQP2 water channels in the kidney.
Animals ; Aquaporin 2* ; Aquaporins* ; Blood Pressure ; Cytoplasm ; Humans ; Kidney* ; Male ; Membranes ; Rats* ; Rats, Sprague-Dawley ; Reserpine* ; Sympathetic Nervous System

The present study was aimed to examine whether the expression of renin is associated with that of cyclooxygenase-2 (COX-2) in the kidney. Male Sprague-Dawley rats were made two-kidney, one clip (2K1C) or deoxycorticosterone acetate (DOCA)-salt hypertensive, to stimulate or to inhibit the endogenous renin-angiotensin system, respectively. The expression of renin and COX-2 mRNA was determined in the cortex of the kidney by reverse transcription-polymerase chain reaction. 2K1C hypertensive rats showed an increased expression of renin as well as of COX-2 in the clipped kidney. The expression of renin was decreased in parallel with that of COX-2 in the contralateral non-clipped kidney. Removal of the renal arterial clip reversed the expression of both genes, along with the blood pressure, to the control level. On the other hand, DOCA-salt hypertension was associated with parallel decreases of renin and COX-2 expression. These results indicate that renin and COX-2 genes are coordinately expressed in the kidney.
Animals ; Blood Pressure ; Cyclooxygenase 2* ; Desoxycorticosterone* ; Hand ; Humans ; Hypertension* ; Kidney ; Male ; Rats* ; Rats, Sprague-Dawley ; Renin* ; Renin-Angiotensin System ; RNA, Messenger

PURPOSE: Gastrointestinal stromal tumors (GISTs) are the most common form of mesenchymal tumor of the gastrointestinal tract. Recently, tyrosine kinase inhibitors have improved the treatment of GISTs, and their diagnosis facilitated by immunohistochemical markers. The aim of this paper was to study the clinicopathological features of GISTs of the stomach and determine the accuracy of a new grading system and the prognostic factors. METHODS: Patients with mesenchymal tumors of the stomach, operated on between 1982 and 2004, were identified using medical and pathological files. Immunohistochemical staining for KIT (CD117), CD34, smooth muscle actin (SMA), desmin and s-100 protein were performed, and the diagnoses reviewed. Cases were classified into either the very low, low, intermediate or high risk groups according to National Institutes of Health (NIH) consensus symposium. RESULTS: 78 mesenchymal tumors were reanalyzed, and with the supportive use of immunohistochemical markers, 71 (91%) of the gastrointestinal mesenchymal tumors were shown to be GISTs. The tumors often coexpressed KIT and CD34 (90%) and were variably positive for SMA (18%), s-100 protein (11%) and desmin (23%). With a median follow-up of 73.9 months (range 1~228 months), a recurrence occurred in 10 (14%) patients. Analyses demonstrated that the mitotic index (P<0.001) and tumor size (P<0.001) were significant prognostic factors for survival. The new grading system showed a significant difference between the risk groups and the survival rates (P<0.001). CONCLUSION: Immunohistochemical staining is needed to distinguish GISTs from other mesenchymal tumors. The tumor size and mitotic count are significant prognostic factors for GISTs. The new grading system (2001 NIH) for classifying the 4 risk groups of GISTs, according to the tumor size and the mitotic count, is useful in the evaluation of the tumor behavior.
Actins ; Consensus ; Desmin ; Diagnosis* ; Follow-Up Studies ; Gastrointestinal Stromal Tumors* ; Gastrointestinal Tract ; Humans ; Mitotic Index ; Muscle, Smooth ; National Institutes of Health (U.S.) ; Prognosis* ; Protein-Tyrosine Kinases ; Recurrence ; S100 Proteins ; Stomach* ; Survival Rate

BACKGROUND: One of the most important prognostic factors in colorectal cancer is lymph node metastasis, which predicts a reduced survival time. Although lymph node metastases were not detected by a conventional hematoxylin-eosin stain technique, 20 to 30 percent of patients fail long-term survival on account of a local or systemic recurrence. Recurrent disease in these patients is believed to develop from occult tumor in lymph nodes. PURPOSE: The authors have conducted an immunohistochemical study with two different antibodies against cytokeratin to identify occult micrometastases in lymph nodes which were diagnosed as tumor negative by conventional histopathology. METHODS: Paraffin blocks of sixty-five patients with colorectal cancer (T2/3, N0, M0) after a curative resection between January 1991 and December 1993 at Kyung-Hee University Hospital were stained with avidin-biotin-peroxidase complex technique using two monoclonal antibodies (anti-cytokeratin AE1/AE3 and anti-cytokeratin No. 20, DAKO, Hamburg, Germany). To assess the clinical correlation between micrometastasis in lymph node and patients survial, 5-year disease-free survival rates were calculated by Kaplan-Meier method and the significance of the differences was estimated by the log-rank test. P values <0.05 were taken to be significant. RESULTS: Of the sixty-five patients with 1133 lymph nodes, tumor cells detected by anti-cytokeratin AE1/AE3 and anti-cytokeratin No. 20, were 2.4 percent (27/1133) and 3.4 percent (38/1133), respectively. Micrometastases were detected in twenty-six patients (40.0 percent). The histologic stage of four cytokeratin positive cases was upstaged from T2, N0, M0 to T2, N1/2, M0, and twenty-two of T3, N0, M0 to T3, N1/2, M0. Cytokeratin-positive cases showed statistically significant recurrence rate (42.3 percent) compared to that of cytokeratin -negative cases (17.9 percent)(x2 test, p=0.032). With the median follow-up of 62 months, 5-year disease-free survival rates of the micrometastses negative and positive cases were 81.7 percent and 61.3 percent, respectively (p=0.0438). CONCLUSIONS: In conclusion, immunohistochemical technique to identify the occult micrometastases in lymph nodes overlooked in conventional histopathology is a useful staging method to anticipate a recurrence and a prognosis more precisely.
Antibodies ; Antibodies, Monoclonal ; Colorectal Neoplasms* ; Disease-Free Survival ; Follow-Up Studies ; Humans ; Keratins ; Lymph Nodes ; Neoplasm Metastasis ; Neoplasm Micrometastasis* ; Paraffin ; Prognosis ; Recurrence

PURPOSE: The primary metabolic characteristic of malignant cells is an increased uptake of glucose and its anaerobic glycolysis. Recent studies have demonstrated that facilitative glucose transport across the plasma membrane is mediated by a family of proteins, i.e., glucose transporters. PURPOSE: In order to evaluate the clinicopathologic correlations of glucose transporter genes expressed in colorectal cancer, the author studied the expression of glucose transporter genes in human colorectal cancer and analyzed their expression in normal and malignant colorectal tissues. METHODS: A reverse transcriptase-polymerase chain reaction (RT-PCR) was applied to quantitatively determine the levels of the glucose transporter genes, GLUT1 and GLUT3, from Crohnes diseases (N=2), adenomatous polyps (N=4), and colorectal cancers (N=40) and their normal counterparts. RESULTS: The expresssion of the GLUT1 gene was detected in 50% of the inflammatory colonic mucosae and adenomatous polyp tissues, but the levels of expression were not significantly different from their normal counterparts. Among the 40 colorectal cancer patients, 23 patients (57.5%) showed GLUT1 gene expression and the levels of expression were increaed by 1.8 as compared to their normal counterparts (p<0.05). The expression of the GLUT3 gene was detected in almost all tissues examined, and the levels of expression were not significantly different from their normal counterparts. In colorectal cancers, there was correlation between GLUT1 expression, the extent of lymph node involvement and the stage of colorectal cancers (p<0.05). But, the correlation between the expressions of the GLUT3 gene and the clinicopathologic prognostic factors of colorectal cancers could not be determined because almost all tissues showed a GLUT3 gene expression. CONCLUSIONS: In conclusion, the GLUT1 glucose transporter expression in colorectal cancer was associated with high possibilities of lymph node metastases and poorer prognosis, and the assessment of GLUT1 expression in colorectal cancer would be useful in identifying high risk patients.
Adenomatous Polyps ; Cell Membrane ; Colon ; Colorectal Neoplasms* ; Gene Expression ; Glucose Transport Proteins, Facilitative* ; Glucose* ; Glycolysis ; Humans ; Lymph Nodes ; Mucous Membrane ; Neoplasm Metastasis ; Prognosis

PURPOSE: Estrogens control the development and cell proliferation of various tissues including the normal mammary epithelial cells, where they induce the expression of the immediate and delayed hormone-responsive genes. The proliferative effects of estrogen have been attributed to its ability to increase the expression of the key cell cycle regulatory genes responsible for cell cycle progression. However, the regulation of cell proliferation is only one aspect of estrogen function. It has also been well documented that estrogen plays a critical role in the etiology and progression of human breast and gynecological cancers. This tumorigenic effect of estrogen might be associated with its anti- apoptotic activities such as of Bcl-2 induction. The aim of this study was to clarify the role of E2IG5, which is an estrogen-induced downstream effector molecule, in breast cancer cell lines. RESULTS: This study shows that E2IG5 is a pro-apoptotic protein that is localized to the mitochondrial membrane via two distinct transmembrane domains. When over-expressed, it induces a mitochondrial permeability transition with the resultant of release cytochrome c and caspase activation. However, three out of four breast cancer cell lines lost their estrogen dependence of E2IG5 expression, which suggests the possible involvement of E2IG5 in the development of breast cancer. CONCLUSION: These results suggest that breast cancer cells may loose their pro-apoptotic signals and selectively use the proliferative mechanism of estrogen, which drives the normal mammary epithelial cells to transform into cancer cells. Further studies using breast cancer tissues will be needed.
Breast Neoplasms* ; Breast* ; Cell Cycle ; Cell Line* ; Cell Proliferation ; Cytochromes c ; Epithelial Cells ; Estradiol ; Estrogens ; Genes, Regulator ; Humans ; Mitochondrial Membranes ; Permeability

No abstract available.
Leukemia*

No abstract available.
Endometriosis* ; Exons* ; Female ; Humans ; Polycystic Ovary Syndrome*

The present study was aimed at examining the regulation of aquaporin (AQP)-2 water channels in the kidney in two-kidney, one clip (2K1C) hypertension. Rats were made 2K1C hypertensive for 6 weeks, and their expression of AQP2 channel proteins was determined in the clipped and contralateral kidneys. To examine the upstream affecting AQP2 channels, adenylyl cyclase activity was also determined. Along with the hypertension, in the clipped kidney, the abundance of AQP2 proteins was significantly decreased in the cortex, outer and inner medulla, while their trafficking remained unaltered. Concomitantly with the reversal of the blood pressure at 24 hours following removal of the clip, the AQP2 abundance also returned to the control level. The arginine vasopressin-evoked generation of cAMP was decreased in the clipped kidney, which again was reversed to the control level following removal of the clip. In contrast, the expression of AQP2 channels as well as the activity of adenylyl cyclase remained unaltered in the contralateral kidney. These results indicate an altered regulation of AQP2 water channels in the clipped kidney in 2K1C hypertension.
Adenylate Cyclase/metabolism ; Animal ; Aquaporins/*analysis ; Blood Pressure ; Cyclic AMP/biosynthesis ; Hypertension, Renovascular/*metabolism ; Kidney/*chemistry ; Male ; Rats ; Rats, Sprague-Dawley

PURPOSE: To evaluate histopathologic change in the liver after injection of various kinds of sclerosants, andto thus determine whether 50% acetic acid, a new sclerosant, is suitable for percutaneous intrahepatic injection. MATERIALS AND METHODS: Four kinds of clinically available sclerosants were used : 50% acetic acid, 99% ethanol,10% phenol, and hot saline. Each group consisted of ten rats, and 0.1ml of each sclerosant was directly injectedinto the liver. After two days and one week, gross and histopathologic findings of resected liver in the area oftissue necrosis, as well as the degree of extrahepatic peritoneal adhesion, were assessed in each group. RESULTS:In all groups, the main pathologic changes were acute necrosis with inflammation after two days and secondaryregenerative fibrosis after week. In the 50% acetic acid injection group, the degree of necrosis was more severeand the mean diameter of the necrotic area was greater ; this latter was not, however, significantly wider than inthe 99% ethanol injection group, though was significantly wider than in the 10% phenol and hot saline injectiongroup. CONCLUSION: When used for percutaneous injection, 50% acetic acid, caused more tissue necrosis than 99%ethanol, 10% phenol, or hot saline. We therefore conclude that this acid may be useful for percutaneousintrahepatic injection of a hepatic tumor.
Acetic Acid* ; Animals ; Ethanol ; Fibrosis ; Inflammation ; Liver ; Necrosis ; Phenol ; Rats ; Sclerosing Solutions*