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Biomedical subjects

M Usami

Publications and source records attributed to M Usami.

At least 127 records · Page 7Linked to original sources
PubMed1995

[Assessment of left ventricular contraction kinetics by ECG-gated myocardial SPECT with 99mTc-MIBI: a new attempt with multi-plane long axial tomography].

To investigate left ventricular (LV) contraction kinetics, we performed ECG gated myocardial tomography (gated-SPECT) with 99mTc-MIBI (99mTc methoxy-2-isobutyl isonitrile) at rest. Data were obtained from 32 views and R-R interval was divided into 16. To clarify whether myocardial count change during systole (%CC) reflected LV wall thickening (%WT), we compared septal and posterior %CC in short axis image with %WT which were obtained by echocardiography. And %CC correlated well with %WT (r = 0.86, p < 0.01). In order to assess myocardial contraction kinetics in various parts of LV, multi-plane long axial tomograms were constructed in 10 normal subjects and 9 patients with myocardial infarction (MI). By multi-plane long axial tomography, LV was divided into 17 segments. In each segment %CC was calculated from time activity curves of myocardial count of 99mTc-MIBI. And the disparity of the appearance of peak count in each segment was also observed. In normal subjects %CC was greatest at apex and they decreased from apex to cardiac base. Besides %CC at lateral segments was greater than that in septal segments. Normal range of %CC was determined segment by segment. In normal subjects the intervals from ECG R-wave to peak count were not different in each segment. But in patients with MI they distributed in wide range and prolonged intervals were observed in segments with rest perfusion defect (infarcted segment). In patients with MI decreased %CC was observed in 91% of infarcted segments, in 83% of the segments with exercise induced ischemia and in 89% of the segments with 123I-BMIPP defects. These results indicated decreased %CC represented viable but compromised myocardium as well as necrotic myocardium. In gated-SPECT we obtained useful informations in addition to myocardial perfusion. But it took more than 30 minutes to perform. More experience will be necessary to ascertain the value of this technique.

Adult↗
PubMed1995

[Teratogenicity study of stevioside in rats].

Teratogenicity of stevioside was examined in rats. Stevioside dissolved in distilled water was given to pregnant Wistar rats by gavage once a day from day 6 through 15 of pregnancy at doses of 0, 250, 500 and 1000 mg/kg/day. The pregnant rats were sacrificed on day 20 of pregnancy and their fetuses were examined for malformation. Stevioside caused no increased incidences of fetal malformation, and no toxic signs in the pregnant rats and the fetuses. It was concluded that stevioside has no teratogenicity in rats when given by gavage. The no observable adverse effect level was estimated to be over 1000 mg/kg/day for both pregnant rats and rat fetuses.

Abnormalities, Drug-Induced↗
PubMed1994

APP717 missense mutation affects the ratio of amyloid beta protein species (A beta 1-42/43 and a beta 1-40) in familial Alzheimer's disease brain.

We have biochemically purified A beta from brains of two unrelated familial Alzheimer's disease (FAD) pedigrees with the APP717 mutation (Val-->Ile) and from two sporadic Alzheimer's disease (AD) brains and characterized them by means of mass spectrometry and enzyme-linked immunosorbent assay. We observed two types of amyloid beta protein (A beta), the short-tail form (A beta 1-40) and the long-tail form (A beta 1-42/43), in sporadic AD and FAD brains, and found that the ratio of the long-tail form of A beta (A beta 1-42/43) to total A beta was increased in FAD brains. These in vivo results were confirmed in vitro using cultured cells transfected with three kinds of APP cDNAs bearing the APP717 mutations (Val-->Ile, Gly, or Phe). Taken together with the hypothesis that A beta 1-42/43 functions as a "seed" that increases the kinetics of amyloid fibril formation (Jarrett, J. T., and Lansbury, P. T., Jr. (1993) Cell 73, 1055-1058), we conclude that the APP717 missense mutation does not create new A beta species but promotes the increased accumulation of A beta 1-42/43 in the brain, which results in the enhancement of amyloid fibril formation from soluble A beta. These findings provide a causal relationship between this FAD genotype and the pathological phenotype of A beta deposition and senile plaque formation.

Adult↗
PubMed1994

Effect of repeated portal-triad cross-clamping during partial hepatectomy on hepatic regeneration in normal and cirrhotic rats.

The effects of ischemia/reperfusion during 70% partial hepatectomy on hepatic regeneration was evaluated in normal rats and thioacetamide-induced cirrhotic rats. Total hepatic ischemia and reperfusion (15 min each) by portal-triad cross-clamping was repeated two times in normal rats and four times in cirrhotic rats during hepatectomy. The labeling index of hepatocytes on Day 1 after operation (POD) and hepatic regeneration ratio on POD 28 were measured. In normal rats, the repeated ischemia/reperfusion decreased the survival rate from 100 to 77% (P < 0.05), lowered the hepatocyte labeling index from 33.5 +/- 2.5 to 16.7 +/- 6.5%, and diminished the hepatic regeneration ratio from 199 +/- 17 to 137 +/- 12% (P < 0.01). However, portal-systemic shunt improved those levels to 100, 30.6 +/- 13.7, and 169 +/- 19%, respectively (P < 0.01). In cirrhotic rats, no portal congestion was observed and hepatic regeneration was not suppressed by ischemia/reperfusion. Thus, portal pooling and the reperfusion of pooled portal blood may be the cause of inhibition on hepatic regeneration and not ischemia/reperfusion of the liver itself. Therefore, repeated portal-triad cross-clamping for short periods of time during the resection of cirrhotic liver is not harmful for hepatic regeneration.

Animals↗
PubMed1994

Adjuvant and neoadjuvant chemotherapy for invasive bladder cancer.

A total of 20 patients with primary invasive bladder cancer who underwent radical cystectomy received postoperative adjuvant chemotherapy using a CAP (cyclophosphamide, doxorubicin, and cisplatin) or modified M-VAC (methotrexate, vinblastine, pirarubicin, and cisplatin) regimen. In all, 16 of the patients were treated with CAP and 4 received the modified M-VAC regimen. Of the 20 patients, 17 had transitional-cell carcinoma with or without non-transitional-cell elements. All of the patients had tumors with a histological grade of G2 (6 cases) or G3 (14 cases). As for lymph-node metastasis, there were ten N0 cases, three N1 cases, six N2 cases, and one N3 case. Adjuvant chemotherapy was usually commenced 2 weeks after the surgery and was given every 3-4 weeks for two or three cycles. The 5-year survival rate of these 20 patients was 65.9%, whereas that of 49 patients who did not receive any adjuvant chemotherapy was 30.2%. Regarding toxicity, both of the adjuvant chemotherapy regimens used in this study were generally well tolerated. The most common toxic effects were gastrointestinal symptoms, alopecia, and myelosuppression. Another 19 patients with invasive transitional-cell carcinoma of the bladder received 2 or 3 cycles of neoadjuvant chemotherapy using the modified M-VAC or MEC (methotrexate, epirubicin, and cisplatin) regimen. Of 18 pathologically evaluable patients who underwent radical cystectomy or partial cystectomy, the stage was pT0 in 3 cases (17%), pTis in 3 (17%), pT1 in 3 (17%), and pT2 or higher in 9 (50%). The 4-year survival rate of 18 patients who received neoadjuvant chemotherapy was 71.5%. Regarding toxicity, one patient died of a bowel complication after surgery, and the complication was suggested to be drug-induced.

Adenocarcinoma↗
PubMed1994

The toxic effect of Alzheimer amyloid protein precursor overexpressed in the neuroblastoma cell line NB-1 on neurite outgrowth.

The neuroblastoma cell line NB-1 is induced to start neurite outgrowth by dibutyryl cyclic AMP (Bt2cAMP). To study the function of Alzheimer amyloid protein precursor (APP), a stable cell line overexpressing APP was established by cDNA transfection. The APP cDNA was driven by the cytomegalovirus early gene promoter. The transformant underwent degeneration as well as neurite outgrowth in the presence of Bt2cAMP, which also increased the amount of APP mRNA and protein. The expressed APP was mainly processed in the secretory pathway and few amyloidogenic fragments were observed. Hence, not only the beta/A4 protein but also the overexpressed APP itself might be neurotoxic.

Amyloid beta-Protein Precursor↗
PubMed1994

Confirmation study, using nitrobenzene, of the Combined Repeat Dose and Reproductive/Developmental Toxicity Test protocol proposed by the Organization for Economic Cooperation and Development (OECD).

A confirmatory familiarization study of the Combined Repeat Dose and Reproductive/Developmental Toxicity Screening (ReproTox) test protocol proposed by the Organization for Economic Cooperation and Development (OECD) was performed using nitrobenzene, a testicular toxicant. The agent was given daily by gavage to groups of 10 male and 10 female Sprague-Dawley rats at doses of 100, 60, 20 and 0 mg/kg body weight. Some of the high dose animals exhibited neurological signs, and two males and 9 females died. Hemolytic anemia due to methemoglobin formation was evident in treated males. Histopathologically, treated males showed atrophy of seminiferous tubules of the testis, reactive changes secondary to hemolytic anemia in the hematopoietic organs, and hepatocellular swelling. Cerebral gliosis was observed in middle and high dose males. Male fertility was not affected. The body weights of pups from treated dams were lowered, and their postnatal loss was increased. Most of the known toxicological properties of this chemical was demonstrated in the present study, with the exception of reduced fertility. Therefore, the ReproTox protocol was concluded as being useful as a screening test of existing high production volume chemicals. It should be noted that while the reproductive toxicity test alone is insensitive for detection of male fertility disturbances associated with testicular toxicity, the latter easily be distinguished on morphological grounds.

Animals↗
PubMed1994

Effect of nucleosides and a nucleotide mixture on proliferation of human gastric cancer cells (KATO III).

The effect of the nucleotides and a nucleotide mixture (OG-VI), consisting of inosine, guanosine 5'-monophosphate (5'-GMP), cytidine, uridine, thymidine (TdR) (4:4:4:3:1 in molar ratio), and TdR co-administration on proliferation of KATO III human gastric cancer cells in culture was evaluated. Consumption of purine and pyrimidine by cancer cells and changes in cell number with OG-VI or TdR were compared with the control culture medium (Williams E) after 72 hour-culture. Addition of OG-VI or TdR did not enhance the cellular proliferation, but inhibited growth when given in higher concentrations (0.3-3 mM inosine, 0.3-3 mM 5'-GMP, 0.22-2.2 mM uridine, 74-740 microM TdR). Consumption rate of TdR in the medium was less in the TdR group, 33.7%, than in the OG-VI group, 72.2% (p < 0.05). This suggests that TdR metabolism is modulated by other nucleosides and nucleotide included in OG-VI. Under the coadministration of 5-fluorouracil (FUra), addition of OG-VI or TdR suppressed cellular proliferation (p < 0.05). The inhibition rate of cellular proliferation in the OG-VI group was slightly higher than the TdR group, but there was no statistically significant difference between the two groups. The combination of FUra with OG-VI or TdR enhances the antitumor effect of FUra. It is concluded that the OG-VI does not enhance the tumor cell proliferation and it is a potential biochemical modulator of FUra metabolism in human cancer cells.

Cell Division↗
PubMed1994

[Is myocardial fatty acid metabolism different between hypertrophic cardiomyopathy and hypertensive hypertrophy?].

To investigate the characteristics of fatty acid metabolism in hypertrophic cardiomyopathy (HCM), we performed myocardial imaging with 123I-iodophenyl-3-methylpentadecanoic acid (BMIPP) in 24 patients with HCM, 13 patients with hypertensive hypertrophy (HT) and 10 normal subjects. Rest myocardial imaging with 123I-BMIPP was obtained at 20 minutes and 3 hours after 123I-BMIPP injection. Rest 201Tl imaging was also performed. In addition to ordinary tomography, whole body imaging was performed to calculate % Uptake (percentage of cardiac uptake of the isotope to total injected dose). As global indexes of fatty acid metabolism, we calculated two parameters; 1) Uptake Ratio (%Uptake of 123I-BMIPP normalized by myocardial perfusion) and 2) WOR (percent reduction of myocardial 123I-BMIPP within 3 hours). Regional abnormality was evaluated by visual assessment of ordinary tomograms and by BMIPP/T1 map. BMIPP/T1 map was made from Bull's-eye maps of 123I-BMIPP and 201Tl, and it represented 123I-BMIPP uptake normalized by myocardial perfusion of each pixel which constructed the image. %Uptake of 123I-BMIPP was not different among three groups. But Uptake Ratio was significantly (p < 0.001) different among three groups; normal (1.13 +/- 0.08) > HT (1.03 +/- 0.08) > HCM (0.87 +/- 0.09). WOR of 123I-BMIPP was accelerated in HCM (12.7 +/- 4.7%) and HT (10.2 +/- 2.9%) comparing with that in normal (5.1 +/- 3.1%) (p < 0.01). In patients with HCM, by visual assessment, regional abnormality of 123I-BMIPP distribution was found in 17 of 24 patients (71%) including 3 patients with equivocal abnormality. But in patients with HT, only equivocal abnormality was observed in 23%. In BMIPP/T1 map, abnormality was observed in 92% of HCM and 8% of HT. Although global myocardial fatty acid metabolism was equally disturbed both in HCM and HT, regional abnormality of fatty acid metabolism was observed preferentially in HCM. This indicated myocardial fatty acid metabolism was not identical between HCM and HT.

Adult↗
PubMed1994

[Myocardial imaging with 123I-metaiodobenzylguanidine (123I-MIBG) in essential hypertension: does the 123I-MIBG imaging have the ability to predict its prognosis?].

To study myocardial norepinephrine (NE) activity in essential Hypertension 9HT) and to clarify its prognostic significance, we performed myocardial imaging with 123I-metaiodobenzylguanidine (123I-MIBG) and 201Tl at rest in 16 patients with HT and 9 normal subjects. In addition to ordinary tomograms, whole body images were obtained in both 123I-MIBG and 201Tl imaging. From the whole body image, a ratio of myocardial radionuclide accumulation to total injected dose was calculated (%Uptake). And Uptake Ratio (%Uptake of 123I-MIBG/%Uptake of 201Tl) was used as an index of myocardial 123I-MIBG uptake. Reduction of myocardial 123I-MIBG during 3 hours was calculated and expressed as washout rate (WOR). From the Bull's-eye map, the extent of defect was quantitatively assessed (Defect Score) and the homogeneity of the radionuclide distribution within the myocardium (CV) was calculated. In 123I-MIBG imaging, defect appeared in 12 patients with HT (75%), but in normal subject no one showed defect. Patients with HT were divided into two groups according to left ventricular ejection fraction (EF) responses to exercise stress which were obtained by 99mTc blood pool imaging. Group 1 consisted of 8 patients who showed EF elevation (5-10%) by exercise and group 2 consisted of 6 patients with depression of EF (-4-6%) by exercise. Rest EF, peak filling rate, exercise heart rate, exercise blood pressure and left ventricular mass were identical between two groups. Uptake Ratio in Group 2 (0.67 +/- 0.04) was significantly smaller (p < 0.05) than those in Group 1 (0.75 +/- 0.05) and normal subject (0.75 +/- 0.06). And in Group 2, WOR of 123I-MIBG was greater than that of Group 1. In Group 2, defect of 123I-MIBG appeared in all patients, but in Group 1 defect developed in 50%, besides Defect Score was significantly greater in Group 2 than in Group 1 (3.8 +/- 1.4 vs. 1.5 +/- 1.8, p < 0.05). The unhomogeneity of 123I-MIBG distribution was significantly greater in Group 2 (CV; 30 +/- 5%) than in Group 1 (21 +/- 4%) and in normal subjects (18 +/- 4%). These results suggested that quantitative analysis of 123I-MIBG imaging may be helpful for assessing the prognosis of HT.

3-Iodobenzylguanidine↗
PubMed1994

A prospective randomized trial for treating stages B2 and C prostate cancer: radical surgery or irradiation with neoadjuvant endocrine therapy.

A randomized clinical trial of neoadjuvant endocrine therapy followed by either surgery or irradiation and a resumption of endocrine therapy for stages B2 and C prostate cancer has been in progress since 1989. A hundred patients entered the trial between 1989 and 1993, and 95 cases were evaluated. Forty-six patients received surgery and 49 were treated with irradiation. Neoadjuvant endocrine therapy for two months resulted in prostate shrinkage and prostate specific antigen lowering. Except for two patients, one dying of a progression of disease and the other of another concurrent cancer, all are alive with an average follow-up term of 25 (range 3-53) months. The good prognostic results obtained from both treatment groups at present seem to be due in part to the neoadjuvant endocrine therapy; but in order to reach a final conclusion further comparisons need to be made.

Aged↗
PubMed1994

[Quantitative analysis of 123I-metaiodobenzylguanidine myocardial imaging: assessment of its usefulness in patients with congestive heart failure].

To investigate the usefulness of the quantitative analysis of 123I-metaiodobenzylguanidine (123I-MIBG) myocardial uptake, we studied 9 normal subjects and 18 patients with congestive heart failure (CHF). Rest myocardial imaging with 123I-MIBG was performed at 20 minutes and 3 hours (delayed image) after 123I-MIBG injection. Rest 201Tl imaging was obtained at 20 minutes after 201Tl injection. In addition to ordinary tomograms, a planar anterior image and a whole body image were supplemented in each imaging. In patients with CHF fractional shortening (%FS) was calculated from echocardiography and left ventricular ejection fraction was obtained from cardiac blood pool imaging with 99mTc at rest. We calculated H/M (heart to mediastinum count ratio) from the anterior planar image and %Uptake (percentage of cardiac uptake of the isotope to total injected dose) from the whole body image. H/M of 123I-MIBG in delayed images separated patients with CHF from normal subjects (2.00 +/- 0.19 vs. 2.56 +/- 0.13, p < 0.01). H/M Ratio (H/M of 123I-MIBG divided by H/M of 201Tl) in delayed image could distinguish these two groups poorly (0.72 +/- 0.12 vs. 0.88 +/- 0.14, p < 0.05). On the other hand, %Uptake of 123I-MIBG was not different between two groups (3.49 +/- 0.60% in CHF, 3.54 +/- 0.34% in normal). But %Uptake of 201Tl was greater in CHF than in normal (5.96 +/- 1.09% vs. 4.70 +/- 0.30%, p < 0.05). When myocardial 123I-MIBG uptake was normalized by myocardial perfusion (%Uptake of 123I-MIBG divided by %Uptake of 201Tl, Uptake Ratio), Uptake Ratio in delayed image could distinguish theses two groups as same as H/M (0.60 +/- 0.05 in CHF, 0.75 +/- 0.05 in normal, p < 0.01). In patients with CHF, H/M of 123I-MIBG did not reflect LV function and serum norepinephrine (NE) level. But Uptake Ratio and H/M Ratio in delayed image correlated well with %FS (r = 0.88, r = 0.65), EF (r = 0.80, r = 0.68) and NE level (r = -0.77, r = -0.75). Although the calculation of Uptake Ratio is time consuming and expensive, it was assumed that Uptake Ratio is an useful index to quantitate myocardial 123I-MIBG uptake.

3-Iodobenzylguanidine↗
PubMed1993

Prognostic significance of bone metastases in patients with metastatic prostate cancer.

BACKGROUND: The distribution of bone metastases on a bone scan has not been duly considered when assessing the prognosis of metastatic prostate cancer. METHODS: The medical records of 76 patients with newly diagnosed, untreated metastatic prostate cancer were reviewed. According to the distribution of bone metastases on the initial bone scan, we divided the patients into three groups: Group I (having bone metastases exclusively within the pelvis and the lumbar spine), Group II (having bone metastases exclusively outside these bones), and Group III (having bone metastases in both areas). RESULTS: Among the responders to androgen deprivation, those in Group I survived significantly longer than did those in Groups II or III. Because the extent of the disease and the distribution of histologic differentiation in Groups I and II were similar, the results indicate that the presence of bone metastases outside the pelvis and the lumbar spine is predictive of short survival time. This prediction was not possible when the extent of disease (EOD) grading system was used. CONCLUSION: The distribution of bone metastases on the initial bone scan should be considered as a variable for the prognostic stratification of patients with metastatic prostate cancer.

Adenocarcinoma↗