Basic fibroblast growth factor (bFGF) is a potent mitogen and angiogenic protein that may function as an autocrine growth regulator in a variety of malignancies. However, the prognostic value of bFGF expression in bladder cancer has not been adequately studied. We examined tumor tissues of 22 superficial and 25 invasive bladder cancers to define the prognostic value of bFGF expression. We performed immunohistochemical staining of bFGF in formalin-fixed and paraffin-embedded bladder tissue sections using rabbit polyclonal antibody. Microvessels were identified by immunohistochemistry using antibodies to endothelial marker, factor VIII-related antigen. The staining of bFGF were significantly correlated with grade and T stage (p<0.05). The elevated expression of bFGF in patients with invasive bladder cancer was significant correlated with recurrence and 2 year survival (p<0.05). However, no significantly correlation was observed between level of bFGF and vascular counts in frozen sections derived from bladder cancers. These results suggest that the bFGF expression has an important prognostic value in patients with bladder cancer. Immunohistochemical study for bFGF may become a valuable method to predict long-term survival and necessity for adjuvant therapy in patients with bladder cancer.
Antibodies ; Fibroblast Growth Factor 2* ; Frozen Sections ; Humans ; Immunohistochemistry ; Microvessels ; Recurrence ; Urinary Bladder Neoplasms* ; Urinary Bladder* ; von Willebrand Factor

No abstract available.
Hepacivirus* ; Hepatitis C* ; Hepatitis*

We studied to investigate the predictive values of gated SPECT for the improvement of wall motion after bypass surgery. As we compared postoperative SPECT with preoperative ones, we defined viability as wall motion improvement. We performed rest T1-20l/stress Tc-99m-MIBI gated SPECT in 25 patients before and 3 months after bypass surgery. Myocardial wall motion was graded as normal, hypokinesia, a kinesia, and dyskinesia by pair-wise visual analysis of gated pre and postoperative SPECT's on the same monitor wall motion abnormalities before operation, 69 (75%) improved and 23 did not. Before operation, we could find segments with good systolic thickenining 64 segments among total 92. Thickening of the remaining 28 was poor. Wall motion improved postoperatively in 45 segments (70%) among 64 with good thickening, Twenty four(86%) among 28 segments with poor thickening had also improved. We grouped segments into mild(hypokinetic) and severe(akinetic/dyskinetic) ones. Among 33 segments with severe motion abnormalities, 14 had good thickening and 19 did not. Nine(60%) improved out of 14 segments having severe abnormality with good thickening. However, 16(84%) segments out of 19 having severe abnormality with poor thickening also improved. Neither degree of perfusion decrease nor severity of wall motion abnormalities could explain the high rate of false negatives. In conclusion, as we defined viability as wall motion improvement by comparing pre and postoperative SPECT, systolic thickening observed by gated Tc-99m-MIBI SPECT in myocardial segments with wall motion abnormalities predicted wall motion improvement after bypass surgery. However, poor thickening could not be referred as evidence of nonviable myocardium both in mild and severe contractile dysfunction, so that we might need stimulation study such as dobutamine echocardiography or dobutamine gated SPECT.
Coronary Artery Disease* ; Coronary Vessels* ; Dobutamine ; Dyskinesias ; Echocardiography ; Humans ; Hypokinesia ; Myocardium ; Perfusion* ; Tomography, Emission-Computed, Single-Photon*

PURPOSE: This study was designed to investigate the role of NO in cisplatin induced nephrotoxicity of rats, especially in association with expressions of inducible nitric oxide synthase(iNOS) and the effects of iNOS inhibitor. MATERIALS AND METHODS: Male, Sprague-Dawley rats weighing 170-190gm were used. Nephrotoxicity was induced by single intraperitoneal administration of cisplatin(10mg/kg). Aminoguanidine sulfate (300mg/kg), a relatively specific iNOS inhibitor, was administrated 30 minutes prior to cisplatin administration. Individual kidneys were obtained from control, cisplatin single treated and cisplatin combined with aminoguanidine treated rats at 6, 12, 24, 48, 72hours and 7days after cisplatin administration. Serum BUN/creatinine(mg/dl), the unit weight of rat kidney (kidney wet weight/body weight) were estimated. HE stain was performed for histologic evaluation of nephrotoxicity. The expressions of iNOS were assessed by Western blotting and RT-PCR. RESULTS: Serum BUN/creatinine levels in aminoguanidine treated groups were suppressed its increment significantly at 12, 24 and 48 hours compared with cisplatin single treated groups (p<0.05). The unit weight of kidneys in aminoguanidine treated groups were decreased significantly at 24 and 48hours compared with cisplatin single treated groups (p<0.05). Western blotting represents intense iNOS protein bands (117KDa) at 24,48 and 72hours in cisplatin single treated groups. RT-PCR assay for iNOS mRNA (429bp) were weakly expressed in control groups and intense expressions were identified cisplatin single treated and cisplatin combined with aminoguanidine treated groups at 6, 12, 24 and 72hours. CONCLUSIONS: From these results, it is suggested that cisplatin induced nephrotoxicity may be partly mediated by NO. Aminoguanidine may delay or suppress the cisplatin induced nephrotoxicity of rat kidney.
Animals ; Blotting, Western ; Cisplatin* ; Humans ; Kidney ; Male ; Nitric Oxide ; Rats* ; Rats, Sprague-Dawley ; RNA, Messenger

PURPOSE: A sensitive, specific blood test to detect cancer would be of great value but the search for such a test has been fruitless so far. In actual practice, there is often a considerable interval between the point at which a tumor could have been detected and the point at which it produces symptoms as a result of tumor growth. The research has been largely directed toward the identification of tumor-specific subtances that are liberated into body fluid. These tumor markers will not only indicate the presence of a cancer but also identify its site of origin and morphology. The available tumor markers, including the oncofetal antigen, placental hormones and enzymes, do not have enough tumor specificity or sensitivity to be used in diagnosis, but they do have a selective role monitoring the progression of tumor growth and assessing the response to treatment. Plasma lipid abnormality occurs regularly in many experimental animal tumor system. In some cases, their pattern and pathogenesis as well as their correlation with tumor volume and histologic features have been well characterized. Since both in vivo and in vitro celluar lipid alterations have been studied most intensively and found most commonly in lymphoproliferative and myeloproliferative disease, these form a particularly interesting group of malignancies for further investigation. In this study, we prospectively evaluated 26 patients with leukemia and 10 patients with solid tumor with full plasma lipid profiles. METHODS: Plasma lipids and lipoproteins were studied in 36 patients with acute leukemia and solid tumor at initial presentation or relapse and lipid studies were regularly repeated during a period of clinical remission. Patients were admitted to the department of pediatrics Eulji general hospital between March 1988 and June 1992 and they had no drugs known to alter lipid metabolism. No patient had a history of thyroid disease or diabetes and none had evidence of hepatic or renal dysfunction. Full serum chemistry analysis was performed utilizing Automated Analyzer and total serum lactic acid dehydrogenase was used as an additional parameter of tumor burden in all patients. Lipoprotein concentrations in plasma were measured b electrophoresis, and total lipid, phospholipid and free fatty acid by enzyme immunoassay. RESULTS: A consistent and predictable pattern of alterations in plasma lipid and lipoproteins were found. This pattern consisted of a marked decrease in aloha-lipoprotein(p=0.0001) and total cholesterol(p=0.0066), and increase in beta-lipoprotein(p=0.0001). Changes in triglyceride, phospholipid, free fatty acid and pre-beta-lipoprotein levels were net significant. The degree of lipid abnormality was directly related to the underlying tumor burden in leukemia. Among the lipid and lipoprotein alteration, aloha-lipoprotein appeared to be most sensitive indicator for the presence of tumor. CONCLUSIONS: The result suggest that an abnormality in systemic lipid metabolism, possibly in cholesterol clearance, is present in cancer patient. There appeared to be a direct relationship between magnitude of lipid abnormality and the amount of tumor burden but at the present time the exact mechanism of tumor-host interaction and its possible clinical implications remain to be determined.
Animals ; Body Fluids ; Chemistry ; Cholesterol ; Diagnosis ; Electrophoresis ; Hematologic Tests ; Hospitals, General ; Humans ; Immunoenzyme Techniques ; Lactic Acid ; Leukemia* ; Lipid Metabolism ; Lipoproteins ; Oxidoreductases ; Pediatrics ; Placental Hormones ; Plasma* ; Prospective Studies ; Recurrence ; Sensitivity and Specificity ; Thyroid Diseases ; Triglycerides ; Tumor Burden ; Biomarkers, Tumor

No abstract available.
Humans ; Liver Cirrhosis* ; Liver* ; Sepsis* ; Vibrio cholerae* ; Vibrio*

OBJECTIVES: This study was conducted to validate a simple, rapid and sensitive reverse-phase high-performance liquid chromatographic method with UV detector (HPLC-UV) and present the plasma level of di(2-ethylhexyl)phthalate (DEHP) in some Korean male workers. METHODS: HPLC-UV for quantification of plasma DEHP was validated by the following guideline from the Center for Drug Evaluation and Research (CDER)-calibration/standard curve, precision, accuracy and recovery. Plasma DEHP from 255 healthy Korean male workers aged from 30 to 60 years was analyzed by validated HPLC-UV method. RESULTS: The calibration curve over the range 0~150 microgram/liter for the plasma DEHP standard solution showed linearity(r2=0.999). The limit of detection (LOD) and limit of quantification (LOQ) of plasma DEHP were 5.22 microgram/liter and 15.81 microgram/liter, respectively. The accuracy and precision for 2.5 microgram/liter of DEHP were acceptable in CDER guideline on the second and third day but not first day, and those for 50 microgram/liter and 150 microgram/liter of DEHP were acceptable on all three days(Ed-confirm this addition). The distribution of plasma DEHP level was skewed to the left and ranged from 0 to 18.9 microgram/liter. The plasma DEHP level was lower than 10 microgram/liter for 98 % of subjects and lower than 5 microgram/liter for 85 %. The geometric mean and standard deviation of plasma DEHP were 0.4 +/- 1.5 microgram/liter. CONCLUSIONS: The HPLC-UV method for quantification of plasma DEHP was acceptable by CDER guideline. The plasma DEHP of 255 Korean male workers ranged from 0 to 18.9 microgram/liter and the distribution was skewed to the left.
Calibration ; Diethylhexyl Phthalate ; Drug Evaluation ; Humans ; Limit of Detection ; Male* ; Plasma*

Pheochromocytoma is a rare, but an important cause of surgically curable hypertension. Pheochromocytoma is a highly vascular tumor and not infrequently undergoes hemorrhagic necrosis and pseudocyst formation. Such cystic pheochromocytoma may be accompanied by shock and sepsis and commonly invade adjacent organs, in which cases its diagnosis and management may be difficult. Herein we present a case of adrenal cystic pheochromocytoma which was accompanied by sepsis and hypertension and mimicked pararenal abscess with a review of literatures.
Abscess ; Diagnosis ; Hypertension ; Necrosis ; Pheochromocytoma* ; Sepsis ; Shock

PURPOSE: We evaluated the hypothesis that the telomerase expression is associated with c-Myc and peroxiredoxin I (Prx I) in patients with prostate cancer. The study determined the link between Prx I, c-Myc and human telomerase reverse transcriptase (hTERT) in prostate cancer cells. MATERIALS AND METHODS: The cDNA of the Prx I gene was obtained by reverse-transcriptase polymerase chain reaction (RT-PCR) amplification. Cotransfections were performed by using a hTERT luciferase reporter plasmid and each expression vector as indicated (c-Myc or Prx I). Empty vectors were used as controls for determining the basal promoter activity. RT-PCR was performed to evaluate the effect of the DEM-induced Prx I mRNA expression. Luciferase assay was performed to evaluate the inhibitory effect of transfected Prx I and the DEM induced Prx I on the transcriptional activity of hTERT in the human prostatic cancer cell lines PC-3 and DU-145. RESULTS: In this study, we found that Prx I could inhibit hTERT expression through direct interaction with c-Myc protein in the prostate cancer cell lines. In addition, it was obvious that Prx I could interact with c-Myc protein. We also found that DEM could induce upregulation of the Prx I mRNA expression and that the increased expression of Prx I could downregulate the expression of hTERT. CONCLUSIONS: Our results demonstrated a direct link between Prx I, c-Myc and hTERT, and we suggest that Prx I regulates cellular immortalization through c-Myc and hTERT, which is activation step in carcinogenesis.
Carcinogenesis ; Cell Line ; DNA, Complementary ; Humans* ; Luciferases ; Peroxiredoxins* ; Plasmids ; Polymerase Chain Reaction ; Prostatic Neoplasms* ; RNA, Messenger ; Telomerase* ; Up-Regulation

We performed 1st day Tc-99m-sestamibi gated SPECT with dipyridamole/rest T1-201 SPECT and 2nd day 24 hour delay T1-201 SPECT/rest Tc-99m-sestamibi gated SPECT in 27 patients with coronary artery disease(24) or having chest pain(3). Stress and rest Tc-99m- sestamibi gated SPECT was acquired at 60min post-injection. A 4-point scoring system(0 to 3 for normal to absent tracer uptake) for 17 segments was used. Wall motion was scored on another 4 point scale(0 to 3 for normal to dyskinesia) in the lst day post-stress gated and the 2nd day rest gated SPECT. Post-stress gated SPECT showed wall motion abnormality in 94 segments(20%). Fifty-five segments among these 94 showed the same wall motion between post-stress and rest gated SPECT:i.e. 1-1: 23 segments, 2-2: 29 segments, 3-3: 3 segments. Re-maining 39 segments (41.5%) showed different wall motion between post-stress and rest Tc-99m-sestamibi gated SFECT. Twenty one segments with wall motion abnormality had normal perfusion(rest:15 segments, 24 hour delay: 6 segments) at either rest or 24 hour delay. Fifteen among these 21 segments showed persistent post-stress and the 2nd day rest wall motion abnormality(persistent stunning). However, in 6 segments with prolonged (1 hour after stress) stunning, abnormal wall motion did improve in the 2nd day rest Tc-99m-sestamibi gated SPECT(transient prolonged stunning). These 6 segments had normal perfusion at rest(n=4) or at 24 hour delay(n=2). Post stress wall motions showed significantly higher scores in persistent stunning than in prolonged transient stunning(P value<0.05). It was concluded that we could find stunned myocardium with gated Tc-99m-sestamibi SPECT at either post-stress or rest and that some myocardial walls of post-stress 1 hour gated SPECT did not show truly rest wall motion. So, we should be cautious if we use post-stress Tc-99m-sestamibi wall motion to assess rest wall motion.
Coronary Vessels ; Dipyridamole* ; Humans ; Myocardial Stunning ; Perfusion ; Thorax ; Tomography, Emission-Computed, Single-Photon*