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Biomedical subjects

M Tada

Publications and source records attributed to M Tada.

At least 451 records · Page 25Linked to original sources
PubMed1989

[Detection of ras gene mutations of pancreatic tumors by polymerase chain reaction and direct sequencing method].

Ras genes (H-,K-,N-ras) are converted to active oncogenes by point mutations occurring in either codon 12, 13 or 61. We analyzed 19 pancreatic tumors (formalin fixed paraffin embedded tissue) of these codons by a method to directly sequence nucleotides around codons 12/13 and 61 of the three ras genes, using polymerase chain reaction and direct sequencing method. Of 19 pancreatic tumors, all 17 duct cell carcinomas involving 2 mucous producing pancreatic cancers had point mutations of the K-ras codon 12, but 2 islet cell tumors had ano point mutation around codons 12, 13, 61 of the three ras genes. Extremely high incidence of ras gene mutation may be relevant to certain pathogenesis of pancreatic cancers.

Base Sequence↗
PubMed1989

[A case of cavernous hemangioma of the testis].

A 4-month-old boy was admitted with the chief complaint of painless mass in the right scrotum. A right testicular tumor complicated with hydrocele was diagnosed preoperatively by physical examination and ultrasonography. Right high orchiectomy was performed and the pathological diagnosis was cavernous hemangioma of the right testis. This disease is very rare, and our case is the 13th in the domestic and foreign literature.

Hemangioma, Cavernous↗
PubMed1989

[Recent problems in colonoscopy for the diagnosis of colorectal cancer].

Colonoscopy is valuable for the correct diagnosis of colorectal cancers and polyps, and it is widely utilized as the routine examination. One of our recent interests in colonoscopy has been how to diagnose minute lesions accurately. For the purpose, magnifying endoscopy using the magnifying colonoscope (type CF-HM and CF-UHM, Olympus), videoendoscopy, endoscopic ultrasonography, and so on, have been evaluated as a future colonoscopy.

Colonic Polyps↗
PubMed1988

Polymorphonuclear leukocyte activity and ventricular arrhythmia in acute myocardial infarction.

Polymorphonuclear leukocyte activity was compared with the incidence and severity of ventricular arrhythmia evaluated by Holter electrocardiographic monitoring in 21 patients with acute myocardial infarction. A positive correlation (r = 0.706) was seen between peripheral polymorphonuclear leukocyte count and the amount of leukotriene B4 produced by A23187 (20 microM)-stimulated polymorphonuclear leukocytes on the first hospital day (p less than 0.01). Patients were divided into 3 groups according to the severity of ventricular arrhythmia: no or mild (unifocal, maximal hourly ventricular premature complex rate less than 30, n = 6), moderate (maximal hourly ventricular premature complex rate greater than or equal to 30 or multifocal, n = 6) or severe (R on T, greater than or equal to 2 consecutive ventricular premature complexes or ventricular fibrillation, n = 9). Polymorphonuclear leukocyte count and its leukotriene B4 production were increased with the increase in severity of ventricular arrhythmia among 3 groups. Polymorphonuclear leukocyte count (13,300 +/- 900/microliter, mean +/- standard error of the mean) and its leukotriene B4 production (194 +/- 24 ng/10(7) cells) in patients exhibiting severe ventricular arrhythmia were significantly increased compared with those in patients exhibiting no or mild ventricular arrhythmia (10,300 +/- 1,000/microliter, p less than 0.05 and 120 +/- 21 ng/10(7) cells, p less than 0.05, respectively). Enzymatically estimated infarct size in the latter patient group was significantly smaller than those of the other 2 groups, between which there was no difference in infarct size. These results suggest that polymorphonuclear leukocyte activity is closely related to the incidence and severity of ventricular arrhythmia during the early phase of myocardial infarction.

Arrhythmias, Cardiac↗
PubMed1988

Immunohistochemical detection of 4-hydroxyaminoquinoline 1-oxide-DNA adducts in mouse tissues in vivo.

4-Hydroxyaminoquinoline 1-oxide (4HAQO)-DNA adducts were immunohistochemically demonstrated in the nuclei of various organs of mice with the use of an antibody directed against 4HAQO-modified DNA. Specificity of the immunostaining was confirmed by several tests, including preincubation of the antibody with 4HAQO-modified DNA or related molecules and digestion of the sections with DNase. 4HAQO dissolved in isotonic solution and injected sc into an isolated portion of the mouse skin clamped off with ring-shaped forceps resulted in dose-dependent generation of DNA adducts in the nuclei of epithelial cells, fibroblasts, and panniculus carnosus cells. Nuclear staining was absent in animals given injections of isotonic solution only, and the intensity of staining correlated well with the level of unscheduled DNA synthesis demonstrated autoradiographically. 4HAQO-DNA adducts were observed in all target organs of 4HAQO tumorigenesis (i.e., lung, trachea, pancreas, uterus, vagina, skin, and colon) after injection of the carcinogen. Nuclear staining was absent or low in nontarget organs, including the liver and brain. Considerable variation was found in staining levels between cell types and different anatomic locations of cells within each target organ. The intensity of immunohistochemical staining correlated well with numbers of 4HAQO-DNA adducts measured by the radiolabeling technique.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1988

Rabbit cardiac and slow-twitch muscle express the same phospholamban gene.

The nucleotide sequences of cDNAs encoding phospholamban were found to be virtually identical when the cDNA clones were isolated from rabbit slow-twitch (soleus) and rabbit cardiac muscle libraries. These findings demonstrate that both types of muscle express the same phospholamban gene. The deduced amino acid sequences of rabbit and dog phospholamban were identical except for a change from Asp (dog) to Glu (rabbit) at position 2. The nucleotide sequences of the 5'- and the very long 3'-untranslated regions of rabbit and dog phospholamban cDNAs also exhibited a high percentage of identity.

Amino Acid Sequence↗
PubMed1988

The effect of CV-4151, a selective inhibitor of thromboxane synthetase, on prostanoid formation and platelet aggregation in humans.

The pharmacokinetics and pharmacologic effects of a potent, selective inhibitor of thromboxane synthetase, CV-4151 [(E)-7-phenyl-7-(3-pyridyl)-6-heptenoic acid] on prostanoid formation and platelet aggregation were studied in 42 healthy male volunteers. The drug was well tolerated. After oral administration of 10 to 100 mg of CV-4151, peak plasma levels of 1-6 micrograms/mL were reached in a dose-dependent manner within 1 hour. Elimination followed first-order fashion with elimination half-life of about 1 hour. Serum levels of thromboxane B2 reduced to 4% to 15% of control at 2 hours after drug ingestion dose-dependently. Serum levels of 6-keto-prostaglandin F1 alpha increased to about four to six times basal levels. Platelet aggregation induced by collagen and arachidonate was inhibited in most cases. Such pharmacologic effects outlasted serum drug levels. In repeated administration, stable inhibition of serum thromboxane B2 production and platelet aggregation in proportion to the enhancement of serum 6-keto-prostaglandin F1 alpha production was observed although no drug accumulation was found. These results indicate that CV-4151 may be suitable for clinical trials in cardiovascular diseases in which imbalance between thromboxane and prostacyclin may be involved in the pathogenesis.

Adult↗
PubMed1988

Arachidonate metabolism in myocardial ischemia and reperfusion.

Circulatory blood corpuscles have enzymes catalyzing arachidonic acid. Platelets have cyclo-oxygenase system which produce highly vasoconstrictive and thrombogenic thromboxane A2 (TXA2). Neutrophils have another type of arachidonate metabolism system, lipoxygenase enzymes, which produce hydroxyeicosatetraenoic acids (HETE) and leukotrienes (LT), mediating inflammatory reactions. These arachidonate metabolites were found to play important roles in the evolution of myocardial ischemia. Thromboxane B2 (TXB2) a stable metabolite of TXA2, was elevated in peripheral blood of patients with angina pectoris. This elevation of TXB2 was supposed to be derived from platelet activation in coronary circulation due to altered production of TXA2 and prostacyclin (PGI2). Augmentation of TXA2 was also observed in patients with acute myocardial infarction. TXA2 synthetase inhibitors decreased plasma levels of TXB2 in these patients accompanied by attenuation of infarct size. Neutrophils were found to accumulate in ischemic myocardium and were augmented at reperfusion phase especially at interface between infarcted and risk zone. These infiltrated neutrophils may also provide deleterious effects on myocardial cells by producing lipoxygenase metabolites. In fact, a chemotactic and vasoconstrictive lipoxygenase product, 12-HETE, was produced selectively in ischemic myocardial tissue of an occlusion-reperfusion model. During evolution of myocardial cell damage, platelets and neutrophils, accumulated in ischemic tissue, may contribute to the exacerbation of microcirculatory disorders by producing vasoactive prostanoids, leading to expansion of myocardial necrosis. We should gain insights into these cellular interactions through arachidonate metabolism under normal and catastrophic conditions of coronary circulation.

Arachidonic Acids↗
PubMed1988

Accumulation of 2-deoxy-2-[18F]fluoro-D-galactose in the liver by phosphate and uridylate trapping.

To investigate the highest accumulation of 2-deoxy-2-[18F]fluoro-D-galactose ([18F]FdGal) in the liver, metabolic studies with [18F]FdGal were carried out in Wistar rats for 120 min after i.v. injection. As main metabolites 2-deoxy-2-[18F]fluoro-D-galactose 1-phosphate ([18F]FdGal-1-P) and UDP-2-deoxy-2-[18F]-fluoro-D-galactose (UDP-[18F]FdGal) were identified in the liver and other tissues. The [18F]FdGal was phosphorylated by galactokinase. The phosphorylation rate was very rapid in the liver, in which at 5 min after injection 81% of 18F was detected as [18F]FdGal-1-P. After this time the phosphate form decreased with time, which was explained by conversion of [18F]FdGal-1-P to UDP-[18F]FdGal by UDP-glucose: galactose-1-phosphate uridyltransferase. At 120 min after injection 77% of the 18F was measured in the UDP-[18F]FdGal. In the brain both reaction rates were slower than in the liver. Both phosphate and uridylate derivates were also observed as main metabolites in the heart, lung, spleen and small intestine. On the other hand, a small amount of [18F]FdGal-1-P was detected in the plasma, in which the percentage of phosphate increased gradually and was 6% at 120 min. These results show that the [18F]FdGal metabolism in tissue results in phosphate and uridylate trapping and that the [18F]FdGal has potential for measuring in vivo galactose metabolism with positron emission tomography.

Animals↗
PubMed1988

Polyclonal antibodies to DNA modified with 4-nitroquinoline 1-oxide: application for the detection of 4-nitroquinoline 1-oxide-DNA adducts in vivo.

Antibodies against 4-nitroquinoline 1-oxide (4NQO) adducts were elicited in rabbits immunized with 4NQO-modified DNA complexed with methylated bovine serum albumin. In enzyme-linked immunosorbent assay (ELISA), the antibodies could recognize either denatured or native 4NQO-modified DNA, but not unmodified DNA, DNA modified with other carcinogens or free 4NQO derivative. Modification levels as low as 5 mumol of adduct per one mole DNA nucleotide (5 adducts/10(6) nucleotides) can be easily detected by the competitive ELISA. Indirect immunofluorescence staining by anti 4NQO-DNA antibody indicated that the antibodies bound specifically to the nuclei of normal human skin fibroblast cells treated with 4NQO. The intensity of fluorescence was proportional to the dose of 4NQO used to treat the cells, and the fluorescence-positive cells could be detected after treatment with 0.25 microM 4NQO (which resulted in the formation of 10(4) adducts per cell). Applying the competitive ELISA to the quantitation of DNA-adducts in rats treated with 4NQO, it was confirmed that the sensitivity of immunochemical assays was equivalent to that of isotopic assays. These methods should be helpful in studies on the formation of adducts and their removal in cells and tissues.

4-Nitroquinoline-1-oxide↗