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Biomedical subjects

T Nishitani

Publications and source records attributed to T Nishitani.

At least 19 recordsLinked to original sources
PubMed2005

Shielding design of the ITER NBI duct for nuclear and bremsstrahlung radiation.

Three-dimensional Monte Carlo shielding analyses are conducted on the ITER Neutral Beam Injection (NBI) duct for the nuclear and bremsstrahlung radiation. The detailed distribution is evaluated about the nuclear heating rate and surface heat load of the NBI duct wall by the neutron and photon transport calculation. The analytical representations of these nuclear responses are established as a function of the distance from the blanket surface. It is clarified that these representations are different between the duct wall facing the plasma and that hidden from the plasma, and also between the duct wall in the blanket region and that in the vacuum vessel region. These results are very useful for the shielding design of the NBI duct wall in the nuclear fusion reactor.

Computer Simulation↗
PubMed2005

Experiment and analyses for 14 MeV neutron streaming through a dogleg duct.

There are several vacant channels for diagnosis, RF heating and so on through the shielding structure in fusion reactors. Some of them consist of dogleg ducts, through which neutrons stream in a complex manner. An experiment was conducted with the Fusion Neutronics Source (FNS) facility at JAERI to study the behaviour of neutrons in the duct and assess the reliability of calculation methods for the design of fusion reactors such as ITER. The assembly was an iron slab 180 cm in thickness with a doubly bent duct 30 x 30 cm2 in cross section. The experiment was analysed using a simple design code for radiation streaming, DUCT-III, and the Monte Carlo code MCNP. The results indicate that the simple design code is reliable enough to be used for shielding design analyses as well as the Monte Carlo method, which showed excellent agreement between calculated and measured values.

Algorithms↗
PubMed1997

Two isoforms of orthodenticle-related proteins (HpOtx) bind to the enhancer element of sea urchin arylsulfatase gene.

The sea urchin (Hemicentrotus pulcherrimus) arylsulfatase (HpArs) gene, expressed specifically in aboral ectoderm, contains a 229-bp enhancer in its first intron that is required for the activation of HpArs gene expression. Deletion analysis shows that a tandem repeat of orthodenticle-related protein (Otx) binding sites are responsible for the activity of this enhancer. Gel mobility shift analysis reveals that three types of Otx-proteins, which show different mobilities in gel shift assays, form complexes with the enhancer. Band I appears before hatching and gradually decreases by the gastrula stage. Band III appears at the blastula stage and Band II appears at the mesenchyme blastula stage; the levels of Band II and III remain constant until the gastrula stage. Two distinct types of HpOtx cDNA clones have been isolated from cDNA libraries of unfertilized eggs and gastrulae. Nucleotide sequences of the homeobox and downstream regions are well conserved in the two types of HpOtx cDNAs, while the region upstream from the homeobox has different nucleotide sequences. By genomic Southern blot analysis, only a single copy of HpOtx gene is detectable in the Hp genome, making it likely that two HpOtx isoforms are generated from the same gene. Results from Northern blot analysis confirm the presence of two types of HpOtx transcripts. Transcriptional regulation of the HpArs gene may, in part, be carried out through switching of Otx isoforms.

Amino Acid Sequence↗
PubMed1992

Syntheses and antiulcer activities of 2-aminonorbornene derivatives.

2,2,-Disubstituted norbornenes (1, 2), 2,2-Disubstituted norbornane (3), 2,2,3-trisubstituted norbornenes (4, 5), oxanorbornenes (6) and azanorbornenes (7) were synthesized by the Diels-Alder reaction using alpha, beta-dehydroamino acids as a key step, and their antiulcer activities were examined. The oxazolidine derivative (1h) exhibited the most potent activities against several ulcer-models in rat.

Animals↗
PubMed1992

A synthesis of 2-substituted 2-aminoethanol derivatives having inhibitory activity against protein kinase C.

A series of 2-aminoethanol derivatives was synthesized and their inhibitory activities against protein kinase C were investigated. Among these compounds, 2-endo-hexadecylamino-5-norbornene-2- exo-methanol (4h) and 2-endo-hexadecylamino-5-norbornene-2,3-exo-dimethanol (4i) inhibited protein kinase C at the IC50 values of 2 x 10(-5) and 1 x 10(-5) M, respectively, but not protein kinase A at a concentration of 1 x 10(-3) M. The structure-activity relationships are discussed.

Animals↗
PubMed1991

A synthesis of 2-endo-amino-2-exo-hydroxymethylnorbornenes having inhibitory activity against protein kinase C.

2-endo-Hexadecylamino-2-exo-hydroxymethylnorbornene (1a) was synthesized from 2-acetamidonorbornene-2-carboxylic acid methyl ester (2) in a good overall yield. 2-endo-Hexadecylamino-2,3-exo-bis(hydroxymethyl)norbornene (1b) was synthesized starting from dimethyl acetamidofumarate based on Diels-Alder strategy. 1a and 1b inhibited protein kinase C at the IC51 values of 2 x 10(-5) and 1 x 10(-5) M, respectively, but not protein kinase A at a concentration of 1 x 10(-3) M. The structure-activity relationships are discussed.

Norbornanes↗
PubMed1987

Interrelation between plasma kinin and the sympathetic nervous system in normal subjects.

To investigate the relationship between plasma kinin and the sympathetic nervous system, we measured plasma kinin, norepinephrine, and angiotensin-I-converting enzyme (ACE:kininase II) activity in normal subjects. In six normal subjects, subpressor and pressor doses of norepinephrine (10 ng/kg/min and 50 ng/kg/min, respectively) were infused for 1 hour. In five normal subjects, 60-degree head-up tilting was performed for 20 minutes. After norepinephrine infusion, plasma kinin levels were decreased significantly (p less than 0.01) with the subpressor dose of norepinephrine and were further decreased (p less than 0.01) with the pressor dose. Plasma ACE activity, however, showed no significant changes following these infusions. During the tilting, plasma kinin levels decreased significantly (p less than 0.01), whereas plasma norepinephrine levels increased significantly (p less than 0.01). From these results, the assumption of elevated levels in plasma endogenous or exogenous norepinephrine leads to a decrease in plasma kinin levels; this suggests that these two systems may be closely interrelated.

Adult↗
PubMed1987

The role of plasma angiotensin I converting enzyme in regulation of renin-angiotensin system activity in patients with essential hypertension.

In order to investigate the role of plasma angiotensin I (pAI) converting enzyme on the activity of the renin-angiotensin system, we measured plasma renin activity (PRA), plasma angiotensin II (pAII), and plasma angiotensin I converting enzyme (pACE) activity in fourteen patients with essential hypertension before and after two hours of ambulation combined with intravenous furosemide administration. Significant increases were observed in the values of PRA (p less than 0.005), pAII (p less than 0.005) and ACE activity (p less than 0.05) after ambulation. The ratios of log pAII/log PRA were increased significantly after ambulation (p less than 0.005), and a significantly positive correlation was observed between log pAII/log PRA and ACE activity (p less than 0.01). These results suggested that not only PRA but also ACE activity contributed to the activity of renin-angiotensin system through the generation of AII.

Adult↗
PubMed1986

Interrelation between the renin-angiotensin system and kallikrein-kinin system in patients with essential hypertension.

In order to investigate the relationship between the kallikrein-kinin (K-K) system and renin-angiotensin (R-A) system, plasma kinin (pKIN), plasma angiotensin II (pAII), plasma renin activity (PRA) and angiotensin converting enzyme activity (ACEA) were determined in 19 essential hypertensives (EHT). pKIN and pATII measurements were performed by highly sensitive radioimmunoassay (RIA), both of which were established in our laboratory. The assay sensitivity of pKIN and pAII were 0.5 pg/tube and 0.1 pg/tube, respectively. In pKIN RIA, pKIN was extracted by ethanol from 0.8 ml of plasma obtained with a syringe containing kinin generating and destroying enzyme inhibitors. In pAII RIA, pAII was measured directly in small amounts of 50-100 microliter, unextracted plasma samples. The level in pAII was significantly higher (p less than 0.05) in the normal renin group (NRH: n = 13) as compared with low renin group of EHT (LRH: n = 6). However, no significant difference was found in pKIN and ACEA between these two groups. Although a significantly positive correlation was observed between pAII and PRA (p less than 0.001) in EHT, the ratio of pAII/PRA tended to be higher in LHR than in NRH. ACEA correlated positively with pAII (p less than 0.01) or PRA (p less than 0.02), respectively. On the other hand, a significant negative correlation was also found between pKIN and pAII (p less than 0.05). From these findings, it was assumed that there was a closed relationship between R-A and K-K systems, and that angiotensin converting enzyme (kininase II) might play some role in the interrelation between both systems.

Adult↗
PubMed1986

The method of urinary total kallikrein and prekallikrein measurement, and their urinary excretions in the patients with essential hypertension.

The method of measurement for urinary total kallikrein (KAL) and preKAL in human was developed, and daily excretions of urinary total KAL, KAL and preKAL were investigated in patients with essential hypertension. Forty microliter of urine samples were incubated with or without 120 micrograms of chymotrypsin-free trypsin for total KAL or KAL, respectively. KAL was measured with direct radioimmunoassay and kininogenase assay. PreKAL was calculated by the subtraction of KAL from total KAL. The subjects of this study included 7 normotensives (NT) and 8 essential hypertensives (EHT). Daily excretions of total KAL, KAL and preKAL were significantly lower in EHT than those in NT. KAL/total KAL ratio, which reflects the conversion rate from preKAL to KAL in the kidney, was not significantly different between EHT and NT. From these results, it is suggested that decreased urinary KAL excretion in EHT is mainly caused by reduced preKAL production rather than the impaired conversion from preKAL to KAL in the kidney. It is emphasized that this method of measurement for urinary total KAL and preKAL may be a very useful tool for research of the renal kallikrein-kinin system.

Adult↗
PubMed1986

Comprehensive studies on the renal kallikrein-kinin system in essential hypertension.

In order to investigate the role of the renal kallikrein-kinin (K-K) system in normal (NRH) and low renin (LRH) subgroups of essential hypertension (EHT), daily urinary excretions of renal K-K system components including kallikrein (KAL), total KAL, pre-KAL, kinin (KIN) and kininase (total, I and II), were measured in 21 normotensives (NT) and 45 patients with EHT (NRH: 29, LRH: 16). Urinary KAL and KIN quantities, KAL activity, total and pre-KAL, and kininase (total, I and II) were measured by direct RIA, kininogenase assay, direct RIA of KAL after trypsin treatment, and KIN destroying capacity, respectively. The daily excretions of KAL quantity and activity, total and pre-KAL, and KIN were significantly lower in EHT than in NT. That of total kininase and kininase I were significantly higher in EHT than in NT while no significant difference was found in kininase I between EHT and NT. In comparing NRH and LRH, the urinary KAL activity and KIN were lower in LRH than in NRH, and kininase I was higher in LRH than in NRH. No significant difference, however, was found in total and pre-KAL, KAL quantity and kininase II between NRH and LRH. The ratio of KAL quantity/total KAL which reflects the conversion rate from pre-KAL in the kidney, did not show any significant difference among NT, NRH and LRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1986

Purification of human low molecular weight kininogen and its application for a simple ND sensitive method for determination of human urinary kallikrein activity.

Human plasma low molecular weight kininogen was purified with ammonium sulfate fractionation, DEAE-cellulose, CM-Sephadex C-50 and aprotinin-agarose affinity column chromatography, after which this was further purified with Sephadex G-150 and DEAE-Sephadex A-50 column chromatographies. Kallikrein activity was measured as the kininogenase activity reflecting the kinin-producing capacity from kininogen. The purification factor from crude plasma to purified substrate was 44-fold, and the recovery was 18%. The purified human substrate did not contain kinin-generating or destroying enzymes which would interfere with kininogenase activity, and showed a cross-reactivity of less than 0.1% against kinin antiserum. In the kininogenase assay, all kininogen was removed by adding ethanol to terminate the enzyme reaction. Because of the high sensitivity of kinin radioimmunoassay, the kinin levels in urine could be determined in very small amounts of samples (0.5 to 2.0 nl of the original urine). These findings indicated that kinin levels in incubation solution could be measured directly, and the control tubes are unnecessary in this assay procedure. In a comparison among human, dog and bovine low molecular weight kininogen as the substrate for human urinary kallikrein, the enzyme activity was 5 and 80 fold higher in the human low molecular weight kininogen, respectively, suggesting that a human substrate is the best for human enzymes. This simple, specific, sensitive and homologous kininogenase assay system seems to be very useful investigating the physiological or pathophysiological role of the renal kallikrein-kinin system in hypertensive and renal diseases.

Animals↗
PubMed1986

The mechanism of the hypotensive effect of captopril (converting enzyme inhibitor) with special reference to the kallikrein-kinin and renin-angiotensin systems.

In order to clarify the mechanism of the hypotensive action of captopril, the acute and chronic effects of this drug on the kallikrein-kinin and renin-angiotensin systems were investigated respectively in 14 and 19 patients with hypertension. To determine the acute effect, a dose of 50 mg of captopril was administered once orally. For the chronic effect, 75-300 mg of the drug was administered daily for 14 days. In observations of the acute effect, blood pressure decreased significantly at 30 min. and maximally at 60-180 min. after administration with no change in heart rate. Significant increases in blood kinin levels and plasma renin activity (PRA), and a decrease in plasma angiotensin II levels were also observed. A marked augmentation was also found in urinary kinin excretion, but not in urinary kallikrein excretion. Moreover, the changes in blood pressure significantly correlated negatively with basal PRA, basal plasma angiotensin II and the changes in blood kinin levels, and positively with the changes in plasma angiotensin II. In our study of the chronic effect of captopril, similar changes in blood kinin levels, PRA, plasma angiotensin II levels, blood pressure and heart rate to the acute effect study were observed. Significant correlations of the changes in blood pressure were found negatively with basal PRA, basal plasma angiotensin II levels and the changes in blood kinin levels and positively with the changes in plasma angiotensin II levels. In addition, significant increases in urine volume and urinary sodium excretion occurred following administration of captopril for 14 days, and both increases negatively correlated with the changes in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗