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Biomedical subjects

M Akimoto

Publications and source records attributed to M Akimoto.

At least 55 records · Page 3Linked to original sources
PubMed2000

[Usefulness of rapid bedside cardiac troponin T assay for the diagnosis of acute myocardial infarction].

Cardiac troponin T(cTnT) is one of the most myocardial-specific markers for the diagnosis of acute myocardial infarction(AMI). Recently, the rapid bedside cTnT assay(Trop T rapid assay sensitive version), which can provide qualitative determinations within 15 min, has been developed for the emergency clinical setting. To evaluate the usefulness of rapid bedside cTnT assay, we performed the Trop T test and measured serum levels of myoglobin(Mb), creatine kinase MB isoenzyme(CK-MB) and cTnT in 256 consecutive emergency patients with suspected AMI(65 found to have AMI and 191 without AMI). The diagnostic sensitivities for AMI of Trop T, Mb and CK-MB measurements were 66%, 92% and 52%, respectively, whereas the specificities were 80%, 18% and 74%, respectively. The diagnostic accuracy for AMI of Trop T(77%) was significantly higher than that of Mb(37%, p < 0.001) and CK-MB(69%, p < 0.05). The sensitivity for AMI of Mb(86%) was significantly(p < 0.001) higher than that of Trop T (31%) and CK-MB(31%) in patients admitted < or = 3 hr after the onset of AMI. In contrast, the sensitivities of Trop T(80% and 100%) in patients admitted at 3-6 hr and > 6 hr showed no significant differences from those of Mb(100% and 96%). Furthermore, Trop T in patients admitted > 6 hr had significantly(p < 0.01) higher sensitivity compared with CK-MB(69%). The mortality rate in the non-AMI group during hospitalization in patients with positive Trop T test(39%) was significantly(p < 0.001) higher than that in patients with negative test(9%). When the positive Trop T test was regarded as > or = 0.10 ng/ml of serum cTnT, Trop T test had the best concordance of 92% with a quantitative of cTnT assay.

Aged↗
PubMed2000

Population pharmacokinetics and pharmacodynamics of TS-943 for selective nonpeptide platelet glycoprotein IIb/IIIa receptor antagonist in normal healthy subjects.

The pharmacokinetics and pharmacodynamics of TS-943 were evaluated with use of NONMEM in 36 healthy male subjects after constant infusion of five different single-dose regimens. Population analysis showed the plasma concentration-time profiles of TS-943 to be best-fit characterized by a two-compartment open model with constant infusion and first-order elimination. The pharmacodynamic model that best fitted the platelet aggregation was a sigmoid Emax model. The final estimates for baseline effect, 50% inhibitory concentration (IC50), and the Hill coefficient were 79.4%, 23.4 ng/mL and 1.63, respectively. The maximum effect (Emax) was fixed at 80% (submaximal aggregation response). In addition, correlations between TS-943 plasma concentration and extension of template bleeding time were examined by fitting with an exponential model. The model estimates that the TS-943 plasma concentration necessary to double template bleeding time is approximately 63 ng/mL (ie, 2.7-fold greater than the IC50). The population approaches for pharmacokinetic-pharmacodynamic investigation can be useful for the analysis of concentration-effect relationships and concentration-adverse event relationships for a platelet glycoprotein IIb/IIIa receptor antagonist.

Adult↗
PubMed2000

Myocardial scintigraphy using iodine-123 15-(p-iodophenyl)-3-R, S-methylpentadecanoic acid predicts the response to beta-blocker therapy in patients with dilated cardiomyopathy but does not reflect therapeutic effect.

Myocardial fatty acid metabolism is disturbed in patients with idiopathic dilated cardiomyopathy. Myocardial scintigraphy using iodine-123 15-(p-iodophenyl)-3-R, S-methylpentadecanoic acid(BMIPP) was used to assess the response to beta-blocker therapy in 19 patients with dilated cardiomyopathy. BMIPP myocardial scintigraphy was performed before and 6 months after initiating beta-blocker therapy with metoprolol. Cardiac BMIPP uptake was assessed as the total defect score (TDS) and heart-to-mediastinum activity (H/M) ratio. Patients were classified retrospectively as responders with an improvement of at least one functional class (New York Heart Association) or an increase in ejection fraction of > or = 0.10 at 6 months, or as nonresponders meeting neither criterion. Responders had a significantly better pretreatment TDS (p < 0.005) and H/M ratio (p < 0.0001) than nonresponders. TDS exhibited no significant changes over 6 months in either group (responders: 13.2 +/- 3.7 vs 12.5 +/- 3.3; nonresponders: 20.8 +/- 6.5 vs 20.5 +/- 3.0). Responders showed no significant changes in H/M ratio (2.47 +/- 0.28 vs 2.43 +/- 0.42); paradoxically, nonresponders showed a significant increase from 1.82 +/- 0.11 to 2.10 +/- 0.19 (p < 0.05), suggesting that beta-blocker therapy protected the myocardial fatty acid metabolism even in the absence of clinical improvement. BMIPP myocardial scintigraphy provides a prediction of response to beta-blocker treatment, but does not reflect the therapeutic effect in responders at 6 months.

Adrenergic beta-Antagonists↗
PubMed2000

[Delayed posttraumatic high flow priapism: a case report].

A 21-year-old male complained of persisting erection. A urethral balloon catheter had been for 3 weeks after indwelt urethral injury by a skateboard, and he was hospitalized because of penile erection persisting after removing the catheter. High flow priapism was suspected by intracavernous blood gas study and color Doppler ultrasound study. Selective internal pudendal arteriography revealed a leakage of contrast medium at the base of penis. He was treated with selective embolization of bilateral internal genital arteries using gelatin sponges and achieved detumescence. Normal potency was evident 3 months later by examining nocturnal penile tumescence.

Adult↗
PubMed2000

[A case of prostatic small cell carcinoma].

A 66-year-old man was referred to our hospital with a complaint of lumbago. Digital rectal examination showed an enlarged, irregular prostate with stony hardness. The serum level of prostate specific antigen (PSA) was elevated. Abdominal computed tomography showed enlarged common iliac and paraaortic lymph nodes, and multiple liver metastases. Bone scintigraphy showed multiple bone metastases. Histological and immunohistochemical examinations indicated small cell carcinoma and adenocarcinoma of the prostate. Chemotherapy could not be performed due to acute hepatic failure. The patient died 1 month after his first visit.

Adenocarcinoma↗
PubMed2000

[A case of tuberculous epididymitis which was difficult to distinguish from a testicular tumor].

A 70-year-old man complaining of painless right scrotal swelling was referred to our hospital. He had a past history of left nephrectomy for renal tuberculosis at the age of 28. Power Doppler ultrasonography revealed a hypoechoic and hypovascular tumor with septa in the scrotum. We suspected a right testicular tumor and therefore, performed a right high inguinal orchiectomy. On macroscopic findings, the fluid of the tumor was yellowish and mucinous and the ipsilateral testis was remarkably atrophic. The pathological diagnosis was tuberculous epididymitis with central necrosis. In recent years, tuberculous epididymitis is rare, and this case was considered to be the first report of power Doppler ultrasonographic findings in tuberculous epididymitis.

Aged↗
PubMed1999

Adenovirus-mediated gene transfer of Bcl-xL prevents cell death in primary neuronal culture of the rat.

Bcl-xL is a Bcl-2-related gene that regulates programmed cell death in a bcl-2-independent fashion. It is expressed in tissues containing long-surviving postmitotic cells, such as neurons in adult brains. To investigate the possibility of gene therapy for transferring this anti-apoptotic gene into the neuron for the treatment of vascular occlusive or neurodegenerative diseases, we examined the effect of a replication-deficient recombinant adenovirus vector coding human Bcl-xL gene on the augmentation of the survival of primarily-cultured rat neuronal cells in vitro. Immunoblot analysis revealed that primarily-cultured neuronal cells were successfully infected and transferred with this gene by recombinant adenovirus vector with high transduction efficiency. Bcl-xL gene transfer to the primarily-cultured neurons could prevent these cells from cell death.

Adenoviridae↗
PubMed1999

Histologic effects of ruby laser hair removal in Japanese patients.

BACKGROUND AND OBJECTIVE: Hair removal by lasers has recently become a popular method to remove unwanted hair. However, histologic changes in human skin before and after exposure to lasers have not been thoroughly investigated. The aim of this study was to clarify the differences that occur immediately after laser exposure and 1 month after laser exposure. STUDY DESIGN/MATERIALS AND METHODS: Eight adult Japanese volunteers were recruited for this study. They were treated with a long pulsed ruby laser at 20 J/cm(2). A single 3-mm punch biopsy of the laser-treated sites was obtained immediately after laser irradiation and at the 1-month follow-up visit, and they were analyzed using hematoxylin and eosin, PAM, and immunohistological staining. RESULTS: Immediately after laser exposure, hair follicles were very damaged and had extensive eosinophilic degeneration. One month after laser therapy, one type of hair follicle showed cystlike formations with negative proliferating cell nuclear antigen reactions (PCNA). Another type of hair follicle showed follicular mitotic figures with cytoplasmic halos. Early anagen hair follicles were apparently not treated effectively by ruby laser. CONCLUSION: Ruby laser leads to extensive follicular damage, and hair follicles considered to be at early anagen phase were not effectively treated. This may be the reason several courses of laser therapy are required to obtain satisfactory results.

Adult↗
PubMed1999

Localization of tumor suppressor gene associated with distant metastasis of urinary bladder cancer to a 1-Mb interval on 8p22.

To identify the location of one or more putative tumor suppressor genes that may be involved in urinary bladder cancer, we examined 82 such tumors for allelic losses at 19 microsatellite loci on 8p. Loss of heterozygosity was observed in 31 of the cases. Deletion mapping identified a commonly deleted region at 8p22, within the 1-Mb interval flanked by D8S1135 and AFM177XB10. Allelic loss at 8p22 was associated with higher tumor grade (17/31, 55%, vs. 12/51, 23%; P = 0.0013). Furthermore, no tumor that retained heterozygosity for markers at 8p22 had metastasized to distant organs, whereas a substantial portion of tumors that lost alleles in that region had done so (0/51, 0%, vs. 6/31, 20%; P = 0.001). These data imply that loss or inactivation of tumor-suppressing activity encoded on 8p contributes to malignancy and to the metastatic potential of bladder cancers.

Chromosome Deletion↗
PubMed1999

Simian virus 40-transformed metallothionein null cells showed increased sensitivity to cadmium but not to zinc, copper, mercury or nickel.

Primary cultured embryonic cells derived from mice with disrupted metallothionein (MT) I and II genes and from control mice were transformed with a plasmid encoding the simian virus 40 (SV40) large T antigen. The resulting MT-/- and MT+/+ cell strains showed similar cell morphology, cell cycle and no significant differences in glutathione levels or in the activities of glutathione-related enzymes and antioxidant enzymes. The MT-/- cells were more sensitive to Cd than MT+/+ cells, though no increase in the sensitivity to Zn, Cu, Hg or Ni were observed in MT-/- cells. MT+/+ cells accumulated more Cd than MT-/- cells but showed less lesion, suggesting the role of MT induced by Cd in MT+/+ cells as a scavenger of toxic Cd ion. These results suggest a dominant protective role of MT against Cd compared with other metals. SV40-transformed MT-/- cells seem to be a useful tool for the investigation of cellular function of MT.

Animals↗
PubMed1999

Existence of acyl-CoA hydrolase-mediated pathway supplying arachidonic acid for prostaglandin synthesis in microsomes from rabbit kidney medulla.

We have previously shown that acyl-coenzyme A (CoA) hydrolase that hydrolyzes arachidonoyl-CoA (AA-CoA) to arachidonic acid (AA) and CoA is present in the cytosol of rabbit kidney medulla and that this enzyme can supply AA for prostaglandin (PG) synthesis in this region. In the present study, the existence of the acyl-CoA hydrolase-mediated pathway that supplies AA available for PG synthesis in microsomes from the kidney medulla was examined. AA-CoA (20 microM) was preincubated with the 105,000 g pellet (microsomes, 0.5 mg of protein) from the medulla for 5 min at 37 degrees C followed by incubation with the medulla microsomes (0.5 mg of protein) (the source of PG synthesizing enzymes) in the presence of hydroquinone and reduced glutathione for 5 min at 37 degrees C. The PGs formed were measured by high-pressure liquid chromatography using 9-anthryldiazomethane for derivatization. The addition of the microsomal fraction from the medulla in the preincubation mixture increased total PG formation from 3.86 to 8.70 nmol, and this stimulatory effect was somewhat weaker than that of the cytosolic fraction. On the other hand, the microsomal fraction in the kidney cortex has an extremely lower capacity to supply AA for PG synthesis than do medulla microsomes. These results suggest that, in kidney medulla, the microsomes as well as the cytosol have the potential route that supplies AA from AA-CoA for PG synthesis and that this pathway is mediated by acyl-CoA hydrolase.

Acyl Coenzyme A↗
PubMed1999

Antitumour effects of the angiogenesis inhibitor AGM-1470 on rat urinary bladder tumours induced by N-butyl-N-(4-hydroxybutyl) nitrosamine.

OBJECTIVE: To examine the antitumour effects of the angiogenesis inhibitor AGM-1470 (TNP-470) on rat urinary bladder tumours induced by N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN). MATERIALS AND METHODS: Fischer-344 rats were allocated to one of four groups of 15 rats each; in group 1, rats were administered AGM-1470 intraperitoneally, with group 2 acting as the control and given only saline; in group 3, AGM-1470 was instillation intravesically and group 4 acting as control (intravesical saline). All rats were given 0.05% BBN in their drinking water for 8 weeks and then given water with no BBN. AGM-1470 was administered at a dose of 30 mg/kg every other day for 6 weeks in group 1 and at 15 mg/kg once a week for 6 weeks in group 3. This treatment was commenced at 21 weeks after the start of BBN treatment, when tumorigenesis was apparent in all rat bladders; approximately 70-80% of the tumours were carcinomas. All rats were killed in the 27th week. The antitumour effects of AGM-1470 on the BBN-induced bladder tumours were evaluated macroscopically and histologically. The inhibitory effect of AGM-1470 on endothelial cell proliferation was assessed in groups 1 and 2 by immunohistochemical staining for Factor VIII-related antigen and by counting the microvessels. RESULTS: The number and volume of bladder tumours were significantly less in group 1 than group 2. In the latter, at least one bladder tumour developed in each of the 15 rats. Histologically, transitional cell carcinoma (TCC) was found in 13 rats and papilloma in two, with invasive cancer in three of the 13 TCCs. Bladder tumours developed in only four of the 15 rats in group 1. Carcinomas were found in three of these four rats and no invasive cancer was detected. The rats in group 1 had significantly fewer microvessels than the controls. The rats in group 4 also showed slightly but insignificantly less tumour growth and fewer carcinomas. In neither experiment were any major side-effects seen except for mild weight loss after AGM-1470 treatment. CONCLUSION: AGM-1470 inhibited the growth and malignant progression of BBN-induced bladder tumours in rats, apparently mainly by the inhibition of tumour vessel development. The intraperitoneal administration of AGM-1470 produced better results than did intravesical instillation. These results suggest that the angiogenesis inhibitor AGM-1470 is a promising agent for the treatment of human bladder cancer.

Animals↗
PubMed1999

Mutant herpes simplex virus-mediated suppression of retinoblastoma.

PURPOSE: To test the ability of a mutant herpes simplex virus (HSV) hrR3 to inhibit growth of Y79 human retinoblastoma in vitro and in vivo. METHODS: Cultured Y79 cells were infected with multiplicities of infection (MOI) ranging from 0.004 to 0.1 of hrR3. Surviving cells were counted using trypan blue dye exclusion. Using X-gal staining, expression of the lacZ gene was examined in vitro on day 3 postinfection to evaluate viral replication. Nude mice harboring Y79 tumors subcutaneously received an intraneoplasmic injection of 5 x 10(7) plaque-forming units of hrR3. The tumor sizes were measured weekly. Expression of the lacZ gene was also examined on one week postinfection. RESULTS: There are 31% and 13% cells surviving in cultured Y79 cells infected by hrR3 at an MOI of 0.1 on days 3 and 5 postinfection respectively compared to those of mock-infected cells. Also more than 70% of Y79 cells were stained with X-gal at an MOI of 0.1 which demonstrated active viral replication in vitro. Virus-treated subcutaneous tumors were smaller than control tumors (p<<0.05, Student's t-test) on days 14, 21, and 28 postinfection. Positive X-gal staining was also observed in the tumor nodule which was challenged with this viral vector. CONCLUSIONS: We have demonstrated that hrR3 is capable of inhibiting Y79 tumor growth both in cell culture and in nude mice. These data suggest that gene therapy using this mutant HSV vector can be a new supplementary therapeutic modality for retinoblastoma.

Animals↗
PubMed1999

Effect of 13-hydroperoxyoctadecadienoic acid on the supply of arachidonic acid for prostaglandin synthesis from arachidonoyl-CoA mediated by the cytosolic or microsomal acyl-CoA hydrolase in rabbit kidney medulla.

The effects of 13-hydroperoxyoctadecadienoic acid (13-HPODE) on the cytosolic or microsomal acyl-CoA hydrolase (ACH) activity in rabbit kidney medulla and on the ACH-mediated prostaglandin (PG) formation from arachidonoyl-CoA (AA-CoA) were examined. 13-HPODE (10, 20, and 50 microM) had no effect on the cytosolic ACH activity but significantly inhibited the activity of the microsomal enzyme (43-57% inhibition). PG formation was measured as follows: AA-CoA (20 nmol) was preincubated with the cytosolic or microsomal fraction (as the source of ACH) in the presence or absence of 13-HPODE for 5 min at 37 degrees C, followed by incubation with the microsomal fraction (as the source of PG-synthesizing enzymes), hydroquinone and reduced glutathione for 5 min at 37 degrees C, and the PGs formed were measured by HPLC, with use of 9-anthryldiazomethane for derivatization. 13-HPODE reduced the PG formation when the microsomal fraction, but not the cytosolic fraction, was used as the source of ACH (10, 20, and 50 microM; 28-55% inhibition). These results suggest that 13-HPODE may modulate PG levels in rabbit kidney medulla by inhibiting the microsomal ACH activity.

Acyl Coenzyme A↗
PubMed1999

Metallothionein modulates the carcinogenicity of N-butyl-N-(4-hydroxybutyl)nitrosamine in mice.

We examined the carcinogenicity of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in transgenic mice deficient in the metallothionein (MT) I and II genes and in control (129/Sv) mice. Both strains of mice were given BBN for 8 weeks with or without Zn treatment. All mice were killed at 12 weeks after the cessation of BBN administration. BBN induced bladder tumors in 75% of MT null mice and in 43% of 129/Sv mice. The average number of bladder tumors per mouse was significantly higher in MT null mice (1. 18 +/- 0.27) than in 129/Sv mice (0.43 +/- 0.20). Zn treatment suppressed the carcinogenicity of BBN in 129/Sv mice but not in MT null mice. Histopathological examination of the tumors revealed that the malignant potential of bladder tumors in 129/Sv mice was greater than that in MT null mice. These results indicate that MT is an important modulator of carcinogenicity of BBN in the bladder of mice.

Animals↗
PubMed1999

Two target regions of allelic loss on chromosome 9 in urinary-bladder cancer.

Allelic losses on chromosome 9 are common in a wide variety of human tumors; moreover, two predisposing loci for some inherited cancer syndromes, i.e., familial malignant melanoma and Gorlin syndrome, have been identified on this chromosome. To define the location of putative tumor suppressor genes involved in cancer of the urinary bladder, 85 bladder cancers were examined for allelic loss at 18 microsatellite loci on chromosome 9. Correlations were also sought between loss of heterozygosity on chromosome 9 and several clinicopathological parameters. Allelic loss was observed in 54 of the tumors (64%) and deletion mapping identified two target regions; one at an interval on 9p21 flanked by D9S736 and D9S165, and the other at an interval on 9q31-34 flanked by D9S58 and D9S61. No subtle mutation was detected in the PTCH gene which lies in the latter interval. Allelic loss on chromosome 9 was observed frequently in low grade and non-invasive tumors as well as in tumors of more advanced phenotype. Inactivation of tumor suppressor genes lying in either of two regions of common deletion identified on chromosome 9 might affect carcinogenic mechanisms at an early stage of tumor development in the urinary bladder.

Chromosome Mapping↗
PubMed1999

Elimination of non-ionic contrast medium by hemodialysis in patients with impaired renal function.

The elimination rate of iohexol, a non-ionic contrast medium, from the blood by hemodialysis, and the elimination rate of iohexol by a dialyzer were studied in 15 patients with chronic renal dysfunction who required angiography or enhanced CT. The elimination rate of iohexol was 19.8% at 15 min after the start of hemodialysis, 30.6% after 30 min, 44.2% after 1 hour, 62.1% after 2 hours and 72.9% after 3 hours. The dialyzer elimination rate was maintained at about 75% from 1 to 3 hours after the start of hemodialysis. If only about 70% of iohexol in the blood needs to be eliminated, hemodialysis for 3 hours with a blood flow rate of 120 ml/min and a dialysate flow of 500 ml/min using a 0.7 m2 cellulose triacetate membrane is sufficient.

Contrast Media↗