[DNA synthetic cell analysis by monoclonal antibody of bromodeoxyuridine in patients with endometrial carcinoma].
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Biomedical subjects
Publications and source records attributed to M Matsuda.
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Effects of cadmium (Cd) on in vitro and in vivo erythropoiesis in rats were studied by methylcellulose colony assay. Cd suppressed the in vitro growth of late erythroid progenitors (CFU-E) in a dose-dependent fashion and did not lose its inhibitory potency with increasing doses of erythropoietin (EPO). In addition, in marrow suspension cultures, Cd did not significantly influence 59Fe incorporation into both the cells and heme, and the Cd dose-responsive inhibition curve of the number of living cells was similar to that of CFU-E. These results suggest that the suppression of CFU-E colony formation by Cd is not due to the blocking of either EPO action to stimulate the growth of CFU-E or the iron incorporation into the cells ahd heme, but due to its direct cytotoxic effect. The colony suppression by Cd could be prevented by adding metallothionein to the cultures. On the other hand, oral administration of Cd to animals (100 mg/liter in drinking water) induced an iron deficiency anemia characterized by microcytic hypochromic red cells, decreased plasma iron, and increased total iron binding capacity. Marrow CFU-E density steadily increased as plasma iron decreased due to Cd administration and reached a plateau after 50 days. Plasma EPO titers were also found to be elevated in such a Cd-induced anemia. Parenteral iron administration during the Cd drinking period could completely prevent the development of iron deficiency anemia and the increase of both CFU-E and plasma EPO. There was a hyperbolic correlation between CFU-E and plasma iron or transferrin saturation. These results demonstrate that oral CD administration produces bone marrow hyperplasia at the CFU-E level due to iron deficiency.
This study concerns 16 cases with spontaneous subarachnoid hemorrhage (SAH) of unknown etiology experienced in our department during a period from September 1979 through August 1986. SAH was confirmed by computed tomographic scanning (CT) or lumbar puncture. All cases were studied by four or three-vessel study. In the case of three-vessel study, adequate opacification of the posterior inferior cerebellar artery contralateral to the injected vertebral artery was considered as a necessary condition. Panangiography was repeated in all patients one to two weeks after the initial study and was negative. The severity of SAH in these patients on admission was relatively mild (Hunt and Kosnik grade I + II = 75%), and the degree of subarachnoid bleeding on CT was also mild. Medium to long-term outcome was excellent or good in 81% of cases, and none of them experienced rebleeding. Only one patient died of severe vasospasm on the 20th hospital day, but no aneurysm was found at autopsy. Illustrative 3 patients in whom the cause of SAH had been finally found was briefly reported. In the first patient, SAH was secondary to a paraventricular cryptic angioma. In the second patient, a microaneurysm had been concealed at the initial angiography by the parent arteries or intra-aneurysmal clot. In the third case of a fusiform aneurysm of the vertebral artery, the aneurysm proximal to the posterior inferior cerebellar artery could not be found at the first three-vessel angiography. Importance of CT and the necessity of repeat panangiography including magnification or oblique views so as not to over-look the causative vascular abnormalities were emphasized.
Diagnosis of hydrocephalus after aneurysmal subarachnoid hemorrhage has been facilitated by CT, but the true incidence and pathogenesis of the condition remain to be clarified. Extent of ventricular dilatation does not necessarily correlate with clinical symptoms and the indication of shunting operation is by no means definite. Consecutive 117 patients with ruptured aneurysm were retrospectively studied for possible factor(s) for development of hydrocephalus in the chronic stage. The incidence of chronic hydrocephalus was found to be high in those patients with aneurysm of the anterior communicating artery, those harboring acute hydrocephalus, those admitted with higher clinical grades, those showing thick clots and gyral enhancement on initial CT, and those who received tranexamic acid in excess of 30 g.
Wide-field specular microscopy was performed on both eyes of 33 patients with unilateral herpetic stromal keratitis. Endothelial changes were quantitated by computerized morphometric analysis of individual cells. In the 16 patients with disciform keratitis, the corneal endothelium of the affected eyes showed no difference in cell density but demonstrated significant increases of variation in cell size (polymegathism) and shape (pleomorphism) when compared to the cells in the fellow unaffected eyes. The eyes with keratouveitis (17 patients), however, had marked polymegathism and pleomorphism of the endothelium and a distinctly lower endothelial cell density (mean, 19%) than the healthy fellow eyes.
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Human poly(ADP-ribose) synthetase consists of three proteolytically separable domains, the first for binding of DNA, the second for automodification, and the third for binding of the substrate, NAD (Ushiro, H., Yokoyama, Y., and Shizuta, Y. (1987) J. Biol. Chem. 262, 2352-2357). We have isolated and sequenced cDNA clones for the enzyme using synthesized oligodeoxyribonucleotide probes based on the partial amino acid sequence of the protein. The open reading frame determined encodes a protein of 1,013 amino acid residues with a molecular weight of 113,203. The deduced amino acid sequence is consistent with the partial amino acid sequences of tryptic or alpha-chymotryptic peptides and the total amino acid composition of the purified enzyme. The native enzyme is relatively hydrophilic as judged from the hydrophilicity profile of the total amino acid sequence. The net charge of the NAD binding domain is neutral but the DNA binding domain and the automodification domain are considerably rich in lysine residue and quite basic. The DNA binding domain involves a homologous repeat in the sequence and exhibits a sequence homology with localized regions of transforming proteins such as c-fos and v-fos. Furthermore, this domain contains a unique sequence element which resembles the essential peptide sequences for nuclear location of SV40 and polyoma virus large T antigens. These facts suggest the possibility that the physiological function of poly(ADP-ribose) synthetase lies in its ability to bind to DNA and to control transformation of living eukaryotic cells like the cases of those oncogene products.
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We have developed a simple method for the evaluation of the association constant (Ka) between cortisol binding globulin (CBG) and cortisol using immunoadsorbent and a small amount of serum. Immunoadsorbent was prepared as follows; gamma-globulin fraction was obtained from goat anti-human CBG antiserum by salting out using 50% ammonium sulfate, followed by coupling to CNBr-activated Sepharose 4B. Immunoadsorbent thus prepared was used for the evaluation of Ka value between cortisol and CBG. Sera obtained from 5 healthy subjects (3 males and 2 females) were treated with charcoal (Norit A) to remove endogenous cortisol. Each of 10 microliter of serum was incubated with a constant amount of 125I-cortisol and different concentrations of unlabelled cortisol for 12 hours at 25 degrees C, pH 7.4. Then, 50 microliter of anti-CBG-Sepharose 4B (immunoadsorbent) was added to each incubation mixture, followed by incubation for another 4 hours at 25 degrees C. After centrifugation, radioactivity of the precipitate was counted and the results were analyzed using Scatchard plot. The Ka value between serum CBG and cortisol in 5 healthy subjects was 1.70 X 10(8)M-1 (SD = 0.24), which is comparable with that of a previously reported value using purified CBG from a large amount of serum. Interassay variation of this method was satisfactory with CV value of 10.1%. Our present method is considered to be clinically relevant, since it does not require purification of CBG from serum, and a relatively small amount (total amount, less than 200 microliter) of serum is enough to evaluate Ka value between CBG and cortisol.
Clostridium perfringens type A enterotoxin(500 ng/ml) induced extensive release of noradrenaline (1/3-2/3 of the total cell content) from PC12 cells in 2-4 min in the presence, but not the absence of extracellular Ca2+. Cells treated with toxin in the absence of Ca2+ released noradrenaline promptly on subsequent addition of Ca2+ to the medium. The amount of noradrenaline released depended on the concentrations of both Ca2+ and toxin in the medium (ED50, 0.3 mM and 420 ng/ml respectively). Ca2+ could be replaced by Ba2+ or Sr2+, and Mn2+ or Co2+, which are Ca2+ channel blockers, did not inhibit the release of the transmitter. These findings are discussed in relation to the systemic effects of enterotoxin.
The influence of exercise on left ventricular diastolic filling was evaluated in 14 patients with hypertrophic cardiomyopathy (HCM) and 14 normal controls (NC) by dynamic exercise echocardiography. Using X-Y digitizer and computer, normalized peak rate of change of the left ventricular dimension during systole (pVs) and the rapid filling phase (pVd) were determined from the left ventricular echocardiograms at rest and during exercise when heart rate reached 100 beats/min. At rest and during exercise, pVs was significantly higher in HCM (3.2 +/- 0.4/s at rest, 4.3 +/- 1.4/s during exercise) than in NC (2.4 +/- 0.5/s at rest, 3.0 +/- 0.4s during exercise) (p less than 0.001, p less than 0.001, respectively), but pVd in HCM (4.2 +/- 1.0/s at rest, 5.8 +/- 1.0/s during exercise) was not significantly different from that in NC (4.1 +/- 1.0/s at rest, 6.0 +/- 0.7/s during exercise). The ratio of pVd to pVs (pVd/pVs) in HCM did not show significant increment during exercise (1.35 +/- 0.38 to 1.43 +/- 0.35), though that ratio in NC was significantly increased by exercise (1.67 +/- 0.22/s to 1.97 +/- 0.19/s, p less than 0.001). There was no correlation between pVd and the degree of left ventricular hypertrophy. These results suggest that diastolic reserve to exercise is depressed in HCM and that other factors besides left ventricular hypertrophy may account for diastolic abnormality.
Our experience with fine-needle aspiration cytology in five cases of malignant lymphoma of the thyroid is reported. Only one case was correctly diagnosed as malignant lymphoma from the original cytologic reports. Three cases were misdiagnosed as anaplastic carcinoma of small-cell type and two of these three cases were subsequently revised as malignant lymphoma after a second aspiration. The final case was misdiagnosed as chronic thyroiditis at both the first and second aspirations; following a third aspiration, 8 mo later, it was correctly diagnosed as malignant lymphoma. Cytological findings of malignant lymphoma are as follows: many malignant cells are distributed as isolated cells and show monotonous features. Malignant cells are slightly larger than normal lymphocytes. Sometimes cleaved cells or large nucleoli are visible. The differential diagnosis of cytologic findings of malignant lymphoma and the other thyroid diseases is discussed in detail.
The midbrains of pups with congenital hydrocephalus spontaneously occurring in MT/HokIdr mice were histologically examined. The subcommissural organ (SCO) and the posterior commissure were completely absent in the hydrocephalic brain. The cerebral aqueduct in the hydrocephalic brain was never completely stenosed, though it was somewhat narrowed in its middle region as compared with that in the normal brain. A possible interrelationship between an absence of SCO and a cause of congenital hydrocephalus is discussed.
Left ventricular ejection fractions and regional ejection changes obtained from left ventriculograms at rest were analyzed in 15 normal subjects, in 17 patients with isolated, organic left anterior descending coronary artery disease, and in 11 patients with isolated left anterior descending coronary artery spasm. Patients with coronary artery spasm did not have significant organic lesions at the site of spasm. All patients with organic coronary artery disease and coronary artery spasm had a history of angina pectoris without myocardial infarction. No significant differences in ejection fraction were observed among the three groups. The regional ejection change of the anterolateral and apical wall supplied by the left anterior descending coronary artery was significantly decreased in patients with organic coronary artery disease compared with those in normal subjects (anterolateral 39.5 +/- 10.3% vs 48.4 +/- 7.7%, p less than 0.05; apical 48.4 +/- 8.8% vs 55.6 +/- 7.8%, p less than 0.05). However, the anterolateral and apical wall motion was not impaired in patients with coronary artery spasm. Thus, patients with organic coronary artery disease had impairment of left ventricular wall motion, while those with coronary artery spasm did not, although both groups of patients had symptoms of angina. These results suggest that patients with organic coronary artery disease may have had coronary blood flow disturbances through stenosed vessels and chronic active ischemia that produced left ventricular impairment.
Serum lipid and apolipoprotein concentrations were measured in 37 male survivors of cerebral infarction (CI) and in 30 healthy controls. Both groups had similar total cholesterol levels, but the HDL-cholesterol level was significantly lower and the serum triglyceride level was significantly higher in the CI patients than in the controls. The ApoB level was significantly higher in the CI patients but there was no significant difference between the 2 groups in the levels of the other apolipoproteins (ApoA-I, A-II, C-II, C-III, and E). The HDL-cholesterol/ApoA-I ratio was significantly lower in the CI patients. Both the VLDL-triglyceride and VLDL-cholesterol levels were higher in the CI patients but the VLDL-cholesterol especially its cholesterol ester level was conspicuously high. A population of VLDL particles that bound to heparin on heparin-Sepharose columns was increased in the CI patients. We suggest that cholesterol ester is excessively transferred from HDL to VLDL during the disturbed catabolism of VLDL in CI patients.
Somatosensory-evoked potentials were recorded during and after 31 operations for intracranial aneurysms, and the changes in the central conduction times, namely, the interpeak latencies between the N14 and N20 peaks in response to bipolar stimulation of the median nerve, were studied. Neuroleptanalgesia and routine intracranial operative procedures such as opening the dura mater, drainage of the cerebrospinal fluid, gentle retraction of the brain, and microsurgical dissection of the circle of Willis, were found to have no significant adverse effect on the evoked responses, whereas the temporary clipping of the major cerebral artery or premature rupture of the aneurysm associated with hypotension or both, often caused significant prolongation of the central conduction time. Prolongation of the central conduction time exceeding 1.2 ms or disappearance of the N20 peak adversely affected the postoperative conditions in 8 of 13 patients (62%).