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Biomedical subjects

T Kitagawa

Publications and source records attributed to T Kitagawa.

At least 631 records · Page 35Linked to original sources
PubMed1983

[Sequential histological studies of prostatic adenocarcinoma after treatment].

Serially obtained needle biopsy specimens of 30 prostatic adenocarcinoma patients were examined to clarify the therapeutic effect on histology. Histology of the tumours after radiotherapy (Linac, 6,440 rad on average) revealed gradual degeneration without the formation of massive necrosis. The rates of cancer-free cases were 22.2% and 41.2% less and more than 1 year after radiation therapy, respectively. The 5-year survival rate was 53.3%. Of 10 patients who survived 5 years, all died of recurrence within 10 years. This indicates the necessity for longterm follow up in prostatic cancer patients.

Adenocarcinoma↗
PubMed1983

[Visceral metastasis in 135 cases of breast cancer: evaluation at autopsy].

We examined the distribution and frequency of metastasis in 135 breast carcinoma cases autopsied between 1946 and 1981 at the Cancer Institute, Tokyo, and studied the relationship between the results and various factors such as histological type, patient age, therapy and clinical course. Breast carcinoma metastasizes more widely and more frequently than other malignant tumors; there is a high rate of metastasis to the bone, adrenals, opposite breast, and thyroid. Medullary tubular carcinoma metastasizes more highly than other histological types. The frequency of metastasis is higher in the younger age group and in patients irradiated to the primary sites. There is little correlation between the frequency of metastasis and total duration.

Adult↗
PubMed1983

[Submucosal invasion in gastric carcinoma of the fundic area].

Gastric carcinoma of the undifferentiated type in the fundic gland area has a higher tendency for submucosal invasion than carcinoma located in the pyloric gland area. To investigate whether a similar tendency is present also in a cancerous focus, we studied 147 patients with early gastric carcinomas with submucosal invasion. Out of 27 undifferentiated carcinomas located in the intermediate zone, 20 (54%) showed peripheral submucosal invasion; in 16(80%) of these, the invasion was located near or in the fundic gland area. These results indicate that submucosal invasion is more likely to occur towards the fundic area.

Adult↗
PubMed1982

Evidence for hydrogen bonding of bound dioxygen to the distal histidine of oxycobalt myoglobin and haemoglobin.

The origin of the differences in oxygen binding energy in various haemoglobins and myoglobins has long been debated. Perutz proposed that the haem-coordinated histidine (proximal histidine) strains the haem iron in low affinity globins but relaxes it in high affinity globins. The existence of such tension in T-structure deoxyhaemoglobin (deoxyHb) was recently confirmed by electron paramagnetic resonance (EPR), resonance Raman and NRM spectroscopy. Although its contribution to the free energy of cooperativity is insignificant in the deoxy state, the tension at the haem is considered to be approximately 1 kcal mol-1 for the ligated form in which the haem iron moves into the porphyrin plane. The remaining free energy is probably stored in other parts of the molecule. Therefore, a study of the stabilization mechanisms of the oxygenated form became increasingly important. A hydrogen bond between the bound oxygen and the distal histidine has been proposed by Pauling; this would be expected to stabilize the oxy form of the protein and could contribute to the regulation of the oxygen affinity through the oxygen dissociation rate. A series of EPR and functional studies on various cobalt-substituted monomeric haemoglobins and myoglobins suggested the presence of such hydrogen bonding and it has recently been established in crystals of oxy iron myoglobin (oxyFeMb) and in oxyhaemoglobin. Here we present resonance Raman spectra of the oxy forms of cobalt--porphyrin-substituted myoglobin and haemoglobin (CoMb and CoHb) recorded in buffered H2O and D2O solutions at 406.7 nm excitation. Only the Raman lines corresponding to the O-O stretching mode of the bound oxygen, appearing near 1,130 cm-1, are shifted (2-5 cm-1) replacement of H2O by D2O; no other vibrations, including the Co--O2 stretching mode, exhibit any frequency shifts. This indicated that the bound oxygen in oxyCoMb and in both subunits of oxyCoHb interacts with the adjacent exchangeable proton, and confirms the formation of a hydrogen bond between the bound oxygen and the distal histidine.

Histidine↗
PubMed1982

N-alpha-carbobenzoxy pyroglutamyl diazomethyl ketone as active-site-directed inhibitor for pyroglutamyl peptidase.

Pyroglutamyl-peptidase (L-pyroglutamyl-peptide hydrolase, EC 3.4.19.3) from Bacillus amyloliquefaciens was covalently labeled with a newly synthesized N-carbobenzoxy-L-pyroglutamyl diazomethyl ketone (Z-PGDK) and was completely inactivated. The inactivation reaction proceeded in pseudo-first order. The kinetic studies demonstrated a rate-limiting step in the inhibition reaction, resulting in the formation of a reversible (enzyme.reagent) complex. The calculated KI,app is 0.12 mM at pH 7.58. The rate of inactivation was pH dependent with an extrapolated pK value of approx. 8.6. The enzyme could be protected against inactivation by a poor substrate, pyroglutamyl-valine. The PCMB-inactivated enzyme, that could be reversibly reactivated by mercaptoethanol, failed to react with Z-PGDK. The enzyme was insensitive toward the D-isomer of Z-PGDK and other diazomethyl ketone derivatives of carbobenzoxy amino acids such as Z-L-proline and Z-L-phenylalanine. These results strongly suggest that the Z-PGDK reacts as an affinity label, presumably with a cysteine residue as the site of alkylation in pyroglutamyl-peptidase, as was reported for chloromethyl ketone derivatives of pyroglutamic acid and its N-carbobenzoxy derivative.

Affinity Labels↗
PubMed1982

Neuraminidase activities in sialidosis and mucolipidosis.

Defects of neuraminidase activities towards sialyloligosaccharides in fibroblasts and leucocytes and enhanced excretion of sialyloligosaccharides in urine were shown in patients with adult type sialidosis with partial deficiency of beta-galactosidase and cherry red spot-myoclonus syndrome. No differences in their neuraminidase residual levels and urinary excretion patterns on thin-layer chromatography were found between these two disorders. In mucolipidosis II and III patients, the neuraminidase activities towards sialyloligosaccharides were almost normal in leucocytes, although decreased in fibroblasts. The discrepancy of neuraminidase activities towards 2 leads to 3 and 2 leads to 6 sialyloligosaccharide isomers was not noticed in all cases.

Chromatography, Thin Layer↗
PubMed1982

Induction of drug-metabolizing enzymes in the rat liver by 3'-methyl-4-(dimethylamino)azobenzene.

The influence of 3-methyl-4-(dimethylamino)azobenzene(3'-Me-DAB) on the drug-metabolizing system in the liver was investigated. Feeding of 3-Me-DAB for 3 weeks at 10, 20 and 600 ppm increased the content of hepatic microsomal cytochrome P-450 slightly (up to 27% raise) but significantly. The feeding effects were also demonstrated in S-9 activity (up to 91% raise) when the mutagenicity of 3-methylcholanthrene (3-MC) and 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2) was assayed in Ames system using S-9 fraction from 3'-Me-DAB-treated rat livers.

Animals↗
PubMed1982

Effect of diazepam on hepatocarcinogenesis in the rat.

The promotion effect of diazepam on the hepatocarcinogenesis initiated by 3'-methyl-4-(dimethyl-amino)azobenzene(3'-Me-DAB) in the rat was studied. Weanling rats were fed a diet containing 0.06% 3'-Me-DAB for 3 weeks, followed by either the basal diet or a diet containing 0.05% diazepam. The number and the size of enzyme-altered islands greater than 50 micrometers in diamter were scored at week 16. The feeding of diazepam did not increase the number and the size of enzyme-altered islands significantly, in comparison with those scored in animals fed 3'-Me-DAB alone. It was concluded that diazepam is not a promoter like phenobarbital in hepatocarcinogenesis.

Animals↗