No abstract available.
HL-60 Cells* ; Humans ; Mass Screening* ; Protein Kinases*

No abstract available.
Microbubbles* ; Respiratory Distress Syndrome, Newborn*

Cyclins are proteins that activate different cyclin-dependent kinases(CDKs) and promote the cell cycles. Their correlations with several human cancers have been identified. Cyclin E, as one of G1 cylins, produces DNA replication through the progression of cell cycle G1 --> S phase. In contrast, cyclin-dependent kinase inhibitors(CDKI) bound with cyclin E-cdk2 complex control the cell cycle and inhibit the cell proliferation. P21(WAF1) proteins, which are CDKIs, are transcripted by a p53 gene and participate in the cell cycle inhibition. Variant p53 proteins produced by a mutated p53 gene lose the ability to control of the cell cycle resulting in cell proliferation. This study is aimed to reveal the expressions of cyclin E, p21(WAF1) protein, p53 variant protein in colorectal adenomas and carcinomas, and also reveal their correlations in the process of carcinogenesis. Twenty-one colorectal adenomas or adenomatous polyps, and thirty colorectal carcinoma tissues were obtained by operative resections or endoscopic polypectomies. Immuno histochemical stains of the above-mentioned three proteins and a statistical analysis of their correlations were made. The results were as follows: 1. P21 proteins were expressed in the upper-one third layer of all normal colonic mucosa, but cyclin E and variant p53 protein were not identified. 2. Cyclin E was expressed in 23.8% of adenomas and 76.7% of carcinomas. Variant p53 protein was expressed in 71.4% of adenomas and 83.3% in carcinomas. The degree of positivity of variant p53 expression was correlated with cancer staging. P21 protein was expressed in all adenomas, similar to normal mucosa, but was not expressed in 43.3% of carcinomas. 3. Expression of cyclin E was increased as to the positivity of variant p53 proteins but the correlations of p21 proteins and cyclin E, and p21 proteins and variant p53 proteins were not identified. Cancer staging was not correlated with the expressions of the three proteins. In conclusion, it can be thought that the overexpression of cyclin E and variant p53 proteins, and the loss of p21 proteins are related with the colorectal carcinogenesis. We can also identify the relationship of cyclin E and variant p53 proteins.
Adenoma* ; Adenomatous Polyps ; Carcinogenesis ; Cell Cycle ; Cell Proliferation ; Colon ; Colorectal Neoplasms ; Coloring Agents ; Cyclin E* ; Cyclins* ; DNA Replication ; Genes, p53 ; Humans ; Mucous Membrane ; Neoplasm Staging ; Phosphotransferases ; S Phase

No abstract available.
Antibodies, Monoclonal* ; Brain* ; Epitopes* ; Humans*

Colorectal cancer is one of the malignant tumours of which molecular genetic alterations have been much unveiled among the human cancers. In the multi-stepwise process to the carcinogenesis, it has been recently revealed that the neoplastic growth is originated either from the activiation of oncogene through its mutation, rearragement and amplification, or from the inactivation of the tumour suppression gene through its mutation and deletion. DCC(Deleted in colon cancer) protein is the product of DCC gene, the representative of tumor suppressor genes. The alteration of DCC protein may be related with the aggressiveness of carcinoma and metastasis. As a result, the prognosis of the cancer may be also thought to be affected. Now the prognosis of colorectal cancer mainly depends on pathologic staging, but there are some variations of survival and recurrence among the patients in same stage. Then this study is aimed to reveal the significance of alteration of DCC protein as an independent factor related to prognosis. Twenty three cancer tissues were obtained from the rejected specimens of colorectal carcinomas. We exacted the DCC gene products in the cancer tissues by the methods of immunohistochemical stains and Western blots. We also analyzed the relationships between the alteration of DCC proteins and the status of regional lymph node metastasis or the serum levels of CEA's(carcinoembryonic antigen). As results, we found the abscence or very scanty stains of DCC protein by Western lot in 14 cancer tissues of available 19 cases, but there were all negative responses in immunohistochemical stains. In contrast with above results, there were all positively stains of DCC proteins in corresponding 23 normal colorectal tissues by both the methods. There was no significantly statistical relation between the alteration of DCC proteins and the status of regional lymph node metastasis or the serum level of CEA. In conclusion, we can confirm that the DCC proteins are abscent or very scanty in colorectal cancer tissues and that may be related with the process of carcinogenesis. But the role of DCC protein loss as an independent prognostic factor was not found in this study.
Blotting, Western ; Carcinogenesis ; Colon ; Colorectal Neoplasms* ; Coloring Agents ; Genes, DCC ; Genes, Tumor Suppressor ; Humans ; Lymph Nodes ; Molecular Biology ; Neoplasm Metastasis ; Oncogenes ; Prognosis ; Recurrence ; Staphylococcal Protein A

To identify the role of the myocardial beta-adrenergic pathway in congestive heart failure, we examined beta-adrenergic receptor density and C-AMP by receptor assay with mononuclrear cell and polymorphonuclear cell in 7 cases of normal control and 7 cases of congestive heart failure. The results were as follows: 1)The mean serum concerntrations of norepinephrine(566.00+/-48.12 pg/ml)and epinephrine(353.14+/-44.24 pg/ml) in congestive heart failure group were significantly higher than those(218.12+/-17.08 pg/ml, 187.23+/-24.62 pg/ml)in normal contral group(P<0.05 for each comparison). 2) In normal control group, the receptor concentration of mononuclear cell was 35.51+/-19.19 fmol/mg and that of polymorphonuclrear cell was 35.53+/-15.05 fmol/mg. The affinity constant of mononuclear cell was(2.47+/-0.42)x10(9)/m and that of polymorphonuclear cell was(2.24+/-0.58)x10(9)/m. 3) In congestive heart failure group, the receptor concentration of mononuclear cell(29.31+/-5.41 fmol/mg) was significantly lower than that in normal control group(p<0.05). And the affinity constant(3.57+/-1.02)x10(9)/m) was significantly higher than that in normal control group(p<0.05). 4) In congestive heart failue group, the receptor concentration of polymorphonuclear cell(33.15+/-10.46 fmol/mg) was not significantly different from that in normal control group. And the affinity constant(2.66+/-0.43)x109/m) was not significantly different from that in normal control group. 5) In congestive heart failure group, the C-AMP concentrations of mononuclear cell(basal 119.9+/-17.2 pmol/min/mg, isoproterenol stimulation 137.2+/-23.2 pmol/min/mg) were significantly lower than those(basal 205.2+/-21.1 pmol/min/mg, isoproterenol stimulation 267.5+/-34.3 pmol/min/mg) in normal control group(p<0.05 for each comparison). 6) In congestive heart failure group, the C-AMP concentrations of polymorphonuclear cell(basal 115.2+/-34.3 pmol/min/mg, isoproterenol stimulation 142.5+/-20.5 pmol/min/mg) were significantly lower thatn those(basal 186.3+/-24.2 pmol/min/mg, isoproterenol stimulation 233.4+/-32.2 pmol/min/mg) in normal control group(P<0.05 for each comparison). In conclusion, a decrease in beta-adrenergic density in congestive heart failure leads to subsensitivity of the beta-adrenergic pathway and decreased beta-agonist-stimulated contraction. However, other factors may be important in adenylate cyclase activation, and so further research is needed.
Adenylyl Cyclases ; Estrogens, Conjugated (USP)* ; Heart ; Heart Failure* ; Isoproterenol ; Plasma*

When reduced glutathione(GSH) was incubated at neutral pH and at 37degrees, its concentration decteased slowly with formation of oxidized glutathione(GSSG). Autooxidation of GSH was accelerated by Cu2+ and Hg2+, but not by other common mono-, di-, and tri-valent cations. Tranthyretin was found to stimulate autooxidation of GSH in the presence or absence of Cu2+ and Hg2+. EDTA inhibited perfectly the autooxidation of GSH regardless of the presence of transthyretin. The stimulating activity of transthyretin was maximal at pH 7.0, declining progressively with increase or decrease of pH from 7.0. Sulfhydryl-blocking agents such as p-hydroxymercuribenzoic acid and N-ethylmaleimide markedly inhibited the stimulating activity of transthyretin. Transthyretin stimulated autooxidation of other sulfhydryl compounds such as dithiothreitol and cysteine. However, it did not show a significant effect on autooxidation of sulfhydryl group of egg albumin and eye lens proteins. And transthyretin did not cause any oxidative change to thyroxine(T4), 3, 5, 3'-tri iodo thyronine(T3) and 3, 3', 5'-triiodothyronine(rT3) bound to it in the presence of GSH and Cu2+. The above results suggest that transthyretin may play a role in regulation of oxidized status of sulfhydryl groups in blood plasma and cerebrospinal fluid.
Cations ; Cerebrospinal Fluid ; Crystallins ; Cysteine ; Dithiothreitol ; Edetic Acid ; Ethylmaleimide ; Glutathione* ; Hydrogen-Ion Concentration ; Ovum ; Plasma ; Prealbumin* ; Sulfhydryl Compounds

Carotid body tumor is relatively rare neoplasm of the extra-adrenal paraganglion system. We have experienced two cases of carotid body tumors and successfully resected without any complication. Pre-operative intravascular embolization of the major arterial feeders was used. The cases and literatures were briefly reviewed.
Carotid Body Tumor ; Carotid Body

Arthritis is the most common disease of joint in old age and almost all the old human are suffering from arthritis. Arthritis gives so severe pain hard to endure that it can devastate human. But we still do not know where the arthritic pain comes from and the generation mechanism of it. For the study of effects of anti-inflammatory drugs on the c-fos immunoreactive neurons, substance P-and CGRPimmunoreactive neurons in dorsal horn and DRG, cyclooxygenase (COX) inhibitors indomethacin (0.5 mg/kg), piroxicam (0.5 mg/kg), NMDA receptor antagonist MK 801 (2 mg/kg), and capsaicin (50 mg/kg) were administered to the experimental arthritis model. Male Sprague-Dawley rats were used for this study. Arthritis was induced by injection of 4% kaolin followed by 2% carrageenan into the articular capsule of left knee. Two hours, 24 hours and 7 days after injection, animals were sacrificed and processed for imunohistochemical staining for c-fos in spinal dorsal horn, for substance P (SP) and CGRP in DRG. The results were as follows; 1. The number of c-fos immunoreactive neurons were significantly decreased at 2 h after piroxicam and MK-801 administration and 1 week after indomethacin, MK-801 and capsaicin treatment in the inflamed side of dorsal horn. 2. There were the significant decrease of SP-and CGRP-immunoreactive area 2 h after indomethacin administration and 1week after capsaicin treatment in the inflamed side of dorsal horn. 3. The number of SP- and CGRP-immunoreactive neurons in DRG were decreased after drugs administration and no difference is in the degree of effectiveness between drugs. Indomethacin and piroxicam which is an inhibitors of COX, significantly reduced the expression of c-fos proteins and desensitized nociceptive primary afferents at the early time, and capsaicin, a pungent algesic substance, decreased the level of c-fos protein, SP and CGRP over a wider time in dorsal horn and DRG.
Animals ; Arthritis* ; Capsaicin ; Carrageenan ; Diagnosis-Related Groups ; Dizocilpine Maleate ; Ganglia, Spinal ; Horns ; Humans ; Indomethacin ; Joint Capsule ; Joints ; Kaolin ; Knee ; Male ; N-Methylaspartate ; Neurons ; Piroxicam ; Prostaglandin-Endoperoxide Synthases ; Proto-Oncogene Proteins c-fos ; Rats, Sprague-Dawley ; Substance P

BACKGROUND AND OBJECTIVES: We investigated whether prehypertensives (PHs) exhibit more prevalent electrocardiographic and echocardiographic left ventricular hypertrophy (ECG LVH) and if they are are more associated with impaired left ventricular (LV) diastolic function than are normotensives (NTs). SUBJECTS AND METHODS: A total of 608 subjects> or = 40 years of age with normal BP (SBP<120 mmHg and DBP<80 mmHg, n=335) and PH (n=273) and who were without a history of hypertension, diabetes and any other known cardiovascular diseases underwent blood sampling for obtaining the lipid profile, and they also underwent 12-lead electrocardiography and echocardiography. RESULTS: Compared with the NTs, the PHs had significantly higher Sokolow-Lyon and Cornell voltage for ECG LVH, and they ahd a higher prevalence of ECG LVH (men: 16.9% vs 5.9%, women: 2.0% vs 1.0%, respectively). The PHs had a more increased left ventricular mass index (LVMI, Men: 118.1+/-24.4 g/m2 vs 102.0+/-19.1 g/m2, p=0.02; Women: 117.5+/-26.4 g/m2 vs 101.9+/-30.7 g/m2, p=0.02) and a more decreased LV diastolic function (E/A, Men: 1.14+/-0.6 vs 1.30+/-0.4, p=0.03; Wemen: 1.11+/-0.6 vs 1.25+/-0.5, p=0.03) on echocardiography than the NTs. CONCLUSION: The PHs were associated with a higher prevalence of ECG LVH and a more increased LVMI on echocardiography than that of the NTs. Therefore, we should pay earlier attention to diagnose and screen the pre-hypertensive group.
Cardiovascular Diseases ; Echocardiography ; Electrocardiography ; Female ; Humans ; Hydrogen-Ion Concentration ; Hypertension ; Hypertrophy, Left Ventricular* ; Male ; Prevalence