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Biomedical subjects

H Kudo

Publications and source records attributed to H Kudo.

At least 271 records · Page 15Linked to original sources
PubMed1984

Cervical cord compression due to extradural granulation tissue in rheumatoid arthritis. A review of five cases.

Five patients with long-standing, severe rheumatoid arthritis who developed cervical myelopathy at the subaxial levels are presented. In each patient the myelopathy occurred in the absence of major subluxation. At laminectomy the cause of the cord compression was found to be a band-like mass of ligamentous and granulation tissue in the posterior half of the extradural space, extending to the underlying portion of the dura and forming a constricting ring. In three patients this constricting ring was released by longitudinal division of the dura followed by application of a fascial patch graft. This release seems to be essential for effective decompression of the cord and good neurological recovery was achieved in these three patients. Of the other two patients, the result was fair in one and poor in the other, this latter result being due to severe intra-operative bleeding with a massive wound haematoma.

Aged↗
PubMed1984

Flow cytometric analysis of deoxyribonucleic acid (DNA) content in adult leukemia.

Flow cytometric analysis of the bone marrow cellular DNA content was performed in 40 adult patients with acute leukemia. Twenty-eight had AML (29 previously untreated and 9 relapse) and 12 ALL (8 previously untreated and 4 relapse). For the whole series, the mean G1/0-phase compartment was 82 +/- 1.3%, the mean S-phase compartment 14 +/- 1%, and the mean G2 +M-phase compartment 4 +/- 0.7%. The percentage of cells in the S-phase had a positive correlation with the LDH level, but not with other parameters. Patients at relapse had significantly lower percentages of cells in the S-phase in AML and significantly higher in ALL. The changes of the S-phase size of the same patients at the first and relapse phases varied. Patients who obtained complete remission had significantly higher percent S phase than patients who did not. This difference was more significant in ALL. Percent cytoreduction had no correlation with the remission rate or S-phase size. Therefore, we analyzed changes of cells in the S-phase of patients with untreated AML during chemotherapy. The reduction rate of cells in the S-phase of patients who obtained complete remission was significantly higher than that of patients who did not.

Adolescent↗
PubMed1983

Effects of estrogen and progesterone on thymidine kinase activity in the immature rat uterus.

The effects of progesterone and/or 17 beta-estradiol on thymidine kinase activity and autoradiograms were investigated in immature rats. Thymidine kinase activity increased more than thirtyfold above the control level 30 hours after 17 beta-estradiol injection. The enzyme activity induced by 17 beta-estradiol was suppressed by progesterone, the dose of which was approximately 1,000-fold that of 17 beta-estradiol. The specific thymidine kinase isozyme, which was separated from 17 beta-estradiol-induced uterine thymidine kinase by diethylaminoethyl (DEAE) cellulose column chromatography and not affected by deoxycytidine triphosphate, was involved in the DNA replication and inhibited by progesterone. The autoradiogram revealed many grains due to 3H-thymidine in the endometrial epithelium, stroma, and the myometrium in the immature rat 30 hours after 17 beta-estradiol injection, whereas progesterone reduced remarkably the number of grains induced by 17 beta-estradiol in the epithelium. Progesterone seems to inhibit the increment of the specific thymidine kinase isozyme induced by 17 beta-estradiol in the endometrial epithelium.

Animals↗
PubMed1983

Mitochondrial abnormalities in Menkes' kinky hair disease (MKHD). Electron-microscopic study of the brain from an autopsy case.

The brain of an autopsy case of Menkes' kinky hair disease (MKHD), after routine histological examination, was studied extensively by electron microscopy, particularly the mitochondrial alteration. There were widespread mitochondrial abnormalities, including enlargement with tubulo-vesiculated cristae, swelling, and dense body formation and occasional accumulation of glycogen within mitochondria, in addition to increased numbers of mitochondria in some neurons. These abnormalities of mitochondria were present in decreasing severity in the following: Purkinje cells, neurons of the molecular and granule cell layers of the cerebellum, and neurons of the cerebral cortex, globus pallidus, lateral nuclei of the thalamus, caudate nucleus, and the myelinated axons in the white matter. This distribution and the degree of mitochondrial abnormalities in the various structures of the brain were compared with those of degenerative lesions in the respective structures. The comparison disclosed that there was a positive correlation between the two. The mitochondrial enlargement and swelling as in the present study had been well documented in the brain of the brindled mouse; mitochondrial dense bodies had also been reported in previous case reports of MKHD by other authors. The present study strongly suggests that the mitochondrial disease is an essential abnormality and may be responsible for the progressive degeneration of the CNS in MKHD.

Brain↗