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T Ishimatsu

Publications and source records attributed to T Ishimatsu.

At least 19 recordsLinked to original sources
PubMed2001

Development of a magnetic sensing device for tooth displacement under orthodontic forces.

We have developed a system for measuring tooth displacement from orthodontic force. Eight small magnetic sensors and a magnet are combined to measure three-dimensional displacement. Sensors, arranged cubically in the three planes of space, are placed in the mouth and fixed to the posterior teeth by a splint. A magnet is placed in the center of the eight sensors and attached to a front tooth that is subjected to orthodontic force. Sensors detect the magnet's movement as target tooth displacement. The system was designed to achieve displacement resolution of 1 microm. The mean percentage of measurement errors was determined to be less than 1% in a 600-cubic-microm volume from calibration. The system was tested clinically on human teeth. Although the oral environment, with high temperature and humidity, was not agreeable with the sensors, this system was stable and accurate enough for quantitative measurement of tooth displacement. The advantage of this system is the ability to detect tooth trajectories by decomposing displacement into translation and rotation and to determine the position of the center of rotation from these parameters.

Calibration↗
PubMed2000

Preserving normal ventricular activation versus atrioventricular delay optimization during pacing: the role of intrinsic atrioventricular conduction and pacing rate.

The purpose of the study was to compare the effects of DDD pacing with optimal AV delay and AAI pacing on the systolic and diastolic performance at rest in patients with prolonged intrinsic AV conduction (first-degree AV block). We studied 17 patients (8 men, aged 69 +/- 9 years) with dual chamber pacemakers implanted for sick sinus syndrome in 15 patients and paroxysmal high degree AV block in 2 patients. Aortic flow and mitral flow were evaluated using Doppler echocardiography. Study protocol included the determination of the optimal AV delay in the DDD mode and comparison between AAI and DDD with optimal AV delay for pacing rate 70/min and 90/min. Stimulus-R interval during AAI (ARI) was 282 +/- 68 ms for rate 70/min and 330 +/- 98 ms for rate 90/min (P < 0.01). The optimal AV delay was 159 +/- 22 ms. AV delay optimization resulted in an increase of an aortic flow time velocity integral (AFTVI) of 16% +/- 9%. At rate 70/min the patients with ARI < or = 270 ms had higher AFTVI in AAI than in DDD (0.214 +/- 0.05 m vs 0.196 +/- 0.05 m, P < 0.01), while the patients with ARI > 270 ms demonstrated greater AFTVI under DDD compared to AAI (0.192 +/- 0.03 m vs 0.166 +/- 0.02 m, P < 0.01). At rate 90/min AFTVI was higher during DDD than AAI (0.183 +/- 0.03 m vs 0.162 +/- 0.03 m, P < 0.01). Mitral flow time velocity integral (MFTVI) at rate 70/min was higher in DDD than in AAI (0.189 +/- 0.05 m vs 0.173 +/- 0.05 m, P < 0.01), while at rate 90/min the difference was not significant in favor of DDD (0.149 +/- 0.05 m vs 0.158 +/- 0.04 m). The results suggest that in patients with first-degree AV block the relative impact of DDD and AAI pacing modes on the systolic performance depends on the intrinsic AV conduction time and on pacing rate.

Aged↗
PubMed1999

Electrophysiological properties of the left atrium evaluated by coronary sinus pacing in patients with atrial fibrillation.

Repetitive atrial firing (RAF), marked fragmentation of atrial activity (FAA), and interatrial conduction delay (CD) have been shown to be electrophysiological features of the atrium in patients with atrial fibrillation (AF). Moreover, it has been observed that atrial extrastimuli are more likely to induce AF when delivered from the right atrial appendage (RAA) than from the distal coronary sinus (CSd). We examined the electrophysiological properties of the atrial muscle by CS and RAA stimulation in patients with paroxysmal AF. Patients were divided into two groups: group I, consisting of 18 patients with clinical paroxysmal AF; and group II, consisting of 22 patients with various cardiac arrhythmias in which the substrate does not exist in the atrium. In group I, the following values of electrophysiological parameters of the atrium indicated that AF was more likely to be induced during RAA pacing than CSd pacing: atrial effective refractory period (RAA vs CSd: 201 +/- 28 ms vs 240 +/- 35 ms, P < 0.001), RAF zone (16 +/- 25 ms vs 0 +/- 0 ms, P < 0.03), FAA zone (38 +/- 37 ms vs 5 +/- 19 ms, P < 0.01), maximum interatrial conduction time (144 +/- 19 ms vs 93 +/- 19 ms, P < 0.0001) and CD zone (53 +/- 21 ms vs 9 +/- 18 ms, P < 0.0001). The values of the electrophysiological parameters of the atrium evaluated by CSd pacing in group I patients were not significantly different from those in group II patients. In conclusion, when coronary sinus stimulation is performed, electrophysiological properties of the atrium in patients with AF show a significant decrease in atrial vulnerability compared to stimulation from RAA and also show similar values to those in patients without AF. It might be suggested that the left posterior or posterolateral atrium is electrophysiologically stable even in patients with paroxysmal AF.

Adult↗
PubMed1998

Abnormalities of electrocardiographic P wave morphology and their relation to electrophysiological parameters of the atrium in patients with sick sinus syndrome.

We examined the incidence of long P wave duration in lead II and increased P terminal force in lead V1 (PTFV1), and their relationship to electrophysiological findings of atrial muscle in 34 patients with sick sinus syndrome (SSS). Patients were divided into three groups: Group I, consisting of 20 patients with various cardiac arrhythmias other than SSS and paroxysmal atrial fibrillation (PAF) who served as controls; Group II, consisting of 18 patients with SSS but without PAF; and Group III consisted of 16 patients with SSS and PAF. P wave duration was significantly longer in Group III (122 +/- 11 ms, mean +/- SD, P < 0.0001) and Group II (111 +/- 15 ms, P < 0.002) than in Group I (98 +/- 10 ms). PTFV1 was greater in Group III (0.052 +/- 0.025 ms) than in Group I (0.028 +/- 0.011 ms, P < 0.05). P wave duration and PTFV1 had significantly and/or borderline correlations with longest duration of right atrial electrograms (r = 0.84, P < 0.0001 and 0.47, P < 0.02, respectively), maximal number of fragmented deflections of atrial electrograms (r = 0.69, P < 0.0001 and r = 0.51, P < 0.02, respectively), repetitive atrial firing zone (RAFZ) (r = 0.81, P < 0.0001 and 0.48, P < 0.05, respectively) and fragmented atrial activity zone (FAAZ)(r = 0.53, P < 0.01 and r = 0.45, P = 0.06, respectively). We concluded that long P wave duration and increased PTFV1 are electrocardiographic indicators for coexistence of electrophysiological abnormalities in the atria in SSS without recognizable heart disease.

Adult↗
PubMed1998

Atrial conduction curves in patients with and without atrial fibrillation.

In order to quantify underlying atrial conduction properties in patients with atrial fibrillation (AF) using clinical electrophysiology techniques, atrial conduction curves relating intra-atrial conduction times to extrastimulus prematurities during programmed atrial stimulation were drawn. Based on the presence or absence of AF episodes, 95 subjects were divided into 2 groups: control (n=42); and AF (n=53). During programmed stimulation introduced from the right atrial appendage, an atrial conduction curve was drawn for each patient. For most of the control subjects, when the extrastimulus prematurity was increased by 10-ms steps, the intra-atrial conduction times also increased gradually; the maximum stepwise prolongation in intra-atrial conduction time was 11.0+/-3.4 msec. For patients with AF, a 10-msec increase in extrastimulus prematurity often produced a sudden marked prolongation in the intra-atrial conduction time; the maximum stepwise prolongation of intra-atrial conduction time was 21.4+/-5.9 msec. In contrast to the gradual atrial conduction curves recorded in control subjects, the sudden prolongation of intra-atrial conduction time was remarkable on the curves obtained in patients with AF. Statistical significance was clearly established (p<0.0001). This difference could be related to differences in the underlying conduction properties in patients with and without AF.

Adult↗
PubMed1998

[Abnormalities of electrocardiographic P wave morphology and the relationship to electrophysiological parameters of the atrium in patients with idiopathic paroxysmal atrial fibrillation].

In 39 patients with idiopathic paroxysmal atrial fibrillation (PAF group), the incidence of the abnormal P wave morphology (prolonged P wave and mitral P in lead II and increased P terminal force in lead V1: PTF V1) was examined, and the relationships to the electrophysiologic findings of the atrial muscle were investigated. The control group consisted of 42 patients with various cardiac arrhythmias other than sick sinus syndrome. P wave duration was significantly longer in the PAF group than in the control group (112 +/- 12 vs 98 +/- 10 msec, p < 0.0001). PTF V1 was greater in the PAF group than in the control group (0.051 +/- 0.018 vs 0.028 +/- 0.010 msec, p < 0.0001). P mitrale occurred in only 5 patients (12%) in the control group as compared to 25 patients in the PAF group (64%, p < 0.0001). The longest duration of the right atrial electrograms was longer in the PAF group than in the control group (101 +/- 17 vs 85 +/- 10 msec, p < 0.0001), as was the maximal number of the fragmented deflections (8.0 +/- 2.5 vs 5.8 +/- 1.4, p < 0.0001). Repetitive atrial firing zone and also fragmented atrial activity zone were longer in the PAF group than in the control group (34 +/- 24 vs 12 +/- 19 msec, p < 0.02 and 47 +/- 27 vs 24 +/- 19 msec, p < 0.001, respectively). Interatrial conduction delay zone was longer in the PAF group than in the control group (55 +/- 25 vs 38 +/- 18 msec, p < 0.001). P wave duration and PTF V1 had significant and/or borderline correlations with the longest duration of the right atrial electrocardiograms (r = 0.75, p < 0.0001 and r = 0.68, p < 0.0001, respectively), and the maximal number of its fragmented defections (r = 0.50, p < 0.002 and r = 0.40, p < 0.05, respectively). Furthermore, P wave duration had a correlation with the repetitive atrial firing zone (r = 0.55, p < 0.01). Prolonged P wave duration and increased PTF V1 are electrocardiographic indicators for the coexistence of electrophysiologic abnormalities in patients with idiopathic paroxysmal atrial fibrillation.

Adult↗
PubMed1991

Synthetic inositol 1,3,4,5-tetrakisphosphate analogues.

Inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4] analogues were synthesized and their effects on [3H]Ins(1,3,4,5)P4 5-phosphatase, [3H]Ins(1,3,4,5)P4 3-phosphatase and [3H]inositol 1,4,5-trisphosphate [3H]Ins(1,4,5)P3] 5-phosphatase activities were examined. The Ins(1,3,4,5)P4 analogue with the aminobenzoyl group at the 2-position of Ins(1,3,4,5)P4 inhibited the hydrolysis of 5-phosphate of [3H]Ins(1,3,4,5)P4 catalysed by erythrocyte ghosts, with a lower Ki value than seen with Ins(1,3,4,5)P4, whereas the analogue with the aminocyclohexanecarbonyl group at the same position had a higher Ki value. The Ins(1,4,5)P3 analogues that we had previously synthesized were also capable of inhibiting this process, with the same tendency as Ins(1,3,4,5)P4 analogues. Such differences in the potency among Ins(1,3,4,5)P4 and Ins(1,4,5)P3 analogues were applicable to other phosphatase activities, namely [3H]Ins(1,3,4,5)P4 3-phosphatase and [3H]Ins(1,4,5)P3 5-phosphatase. These results suggest that the active sites of these enzymes may catalyse the dephosphorylation in a similar fashion.

Erythrocyte Membrane↗
PubMed1991

Determination of urinary Tamm-Horsfall protein by ELISA using a maleimide method for enzyme-antibody conjugation.

A method for enzyme-antibody conjugation using a new maleimide derivative as coupling reagent has been developed. Since a monomeric conjugate of horseradish peroxidase and Fab' antibody could be readily prepared with high efficiency and reproducibility, the enzyme activity and antigen-binding activity were well preserved and nonspecific staining was greatly reduced. The conjugate is suitable for use in both ELISA procedures and immunohistochemistry. Using both methods we examined the pathophysiological significance of Tamm-Horsfall protein (THP) and the present study describes the ELISA method to quantify urinary THP using the new method with rabbit anti-THP antibody. A low concentration (0.04 M) of urea added to the urine samples increased the linearity of the standard curve and the sensitivity of the assay, permitting the detection of as little as 20 ng/ml THP. Freezing and thawing the urine resulted in variable or lower values of THP concentration. THP concentrations in urine as determined by ELISA were stable for at least one month after -70 degrees C storage, but not after -30 degrees C storage. There was no correlation between THP concentrations in 24 h urine samples and the morning urine of the same patient. These results suggest that it is essential to use fresh or -70 degrees C stored 24 h urine samples with added urea (0.04 M) for the determination of THP concentrations in urine by the present enzyme-antibody conjugation method. The THP concentration in normal 24 h urine of young children was found to be less than 51.8 mg/g Cr.

Adult↗
PubMed1991

Urinary Tamm-Horsfall protein excretion in patients with primary vesicoureteral reflux.

The excretion of urinary Tamm-Horsefall protein (THP) was determined by enzyme-linked immunosorbent assay and glomerular filtration rate (GFR) was calculated with technetium-99m diethylenetriamine pentacetic acid (99mTc-DTPA) renal scintigraphy in 26 consecutive patients with primary vesicoureteral reflux (VUR) before and after antireflux surgery. Wide variations of urinary THP excretion and GFR were seen in all grades of VUR. On the basis of the relationship between urinary THP excretion and GFR before the surgery, patients were divided into three groups. The first group (group A, n = 8) had normal urinary THP values and normal values of GFR. The second group (group B, n = 11) had high THP excretion and moderately decreased GFR, the third group (group C, n = 7) had normal urinary THP excretion and severely decreased GFR. In group A, urinary THP values remained normal and GFR improved in all patients after surgery. In group B, GFR improved when urinary THP dropped immediately, but GFR did not improve when urinary THP remained high after surgery. In group C, GFR did not improve and urinary THP continued to be low or tended to drop again after the surgery. The results suggested that serial measurements of urinary THP excretion and GFR by 99mTc-DTPA renal scintigraphy before and after antireflux surgery are useful for the evaluation of renal function in patients with primary VUR.

Child↗
PubMed1991

[Pulsatile administration of LH-RH for hypogonadotropic hypogonadism].

A case of hypothalamic-pituitary failure is reported. A 28-year-old man who had been treated with testosterone for hypogonadism for two years was admitted to our hospital with the chief complaint of sexual problems. The serum level of gonadotropins was very low and hypophysial responses to luteinizing hormone-releasing hormone (LH-RH) were good. Treatment was started with subcutaneous pulses of 10 micrograms LH-RH every 120 minutes using a portable infusion pump. Gradually, his potency improved and ejaculation returned. The serum concentration of FSH, LH and testosterone increased to the normal range of adult males and the testicular volume increased rapidly from 5 ml to 14 ml after 13 weeks of treatment. Sperms appeared in the ejaculated fluid after 25 weeks and, after following 16 weeks, the concentration of sperms increased up to 20 x 10(6)/ml. Prolonged pulsatile subcutaneous administration of a low-dose of LH-RH at a physiologic frequency was an effective therapy for pubertal induction and maturation in hypogonadotropic hypogonadism due to hypothalamic-pituitary failure.

Adult↗
PubMed1990

Inositol 1,4,5-trisphosphate affinity chromatography.

Inositol 1,4,5-trisphosphate (IP3) affinity columns were made by coupling IP3 analogs to a supporting matrix. Sepharose 4B. IP3 5-phosphatase activity. IP3 3-kinase activity and IP3 binding activity from rat brain were absorbed on the IP3 columns. and were eluted by increasing KC1 concentration. This purification procedure increased the specific activities of these parameters 5-200-fold. Thus Sepharose 4B immobilized IP3 analogs can specifically interact with IP3-binding proteins, demonstrating that IP3 affinity columns are a good method for purifying such proteins. Furthermore, our results suggest that IP3 analogs can be linked to other molecules to make useful derivatives without loss of their biological activities.

Animals↗
PubMed1989

Synthetic inositol trisphosphate analogs and their effects on phosphatase, kinase, and the release of Ca2+.

A series of inositol 1,4,5-trisphosphate (IP3) analogs and positional isomers was examined to explore the structure-activity relationships among IP3 5-phosphatase, IP3 3-kinase, and the release of Ca2+. All analogs with additional groups on the 2nd position of IP3 inhibited the hydrolysis of [5-32P]IP3 catalyzed by erythrocyte ghosts, with a lower Ki value than seen with IP3. IP3 dehydroxylated at the 2nd position also had a lower Ki, while 2,4,5-IP3 or cyclic(1:2), 4,5-IP3 had higher Ki values. Among these compounds 2-deoxy-IP3 was as potent as IP3 in inhibiting the phosphorylation by [3H] IP3-3-kinase in rat brain cytosol. The other compounds, except for 2,4,5-IP3 inhibited the phosphorylation, however, 2-30 times higher concentrations were required. By lowering free Ca2+, the concentrations required for half-maximal inhibition were low, while those of IP3, 2-deoxy-IP3, and positional isomers remained unchanged. These compounds acted as full agonists in releasing Ca2+ from permeabilized macrophages, although 1.6-50-fold higher concentrations than IP3 were required. These compounds also inhibited the binding of [3H]IP3 to rat cerebellum and bovine adrenal cortex microsomes, but the potencies were 2.9-33 times less than that of IP3. Thus, the 2nd position of IP3 can be modified with only a slight loss of biological activity.

Animals↗
PubMed1989

Hageman factor dependent kinin generation system in guinea pig skin: extravascular localization of the components, and prolonged vascular reaction in inhibitor-depleted animal of this system.

1. Monospecific antibodies against components of the guinea pig Hageman factor-dependent system, such as Hageman factor, prekallikrein and high-molecular-weight (HMW) kininogen were prepared. These antibodies demonstrated the presence of all of these components in the normal guinea pig skin extract with the properties identical to them in plasma on western immunoblotting analysis. 2. Guinea pig macroalbumin which is a major circulating inhibitor of activated Hageman factor was immunologically depleted from three animals. Duration of a vascular permeability reaction caused by an intradermal injection of activated Hageman factor was prolonged in all of these guinea pigs approximately twice as long as the control, indicating a presence of negative feedback regulation of the Hageman factor-dependent kinin generation cascade in dermal tissue via the circulating protease inhibitor.

Animals↗
PubMed1989

Ca2+ dependence of inositol 1,4,5-trisphosphate 3-kinase activity in the cytosol fraction of pig coronary artery.

1. The activity of inositol 1,4,5-trisphosphate 3-kinase in subcellular fractions of smooth muscles of the pig coronary artery was examined. 2. Incubation of [3H]inositol 1,4,5-trisphosphate (IP3) with muscle homogenates produced more polar 3H-radioactivity (probably as inositol 1,3,4,5-tetrakisphosphate, IP4) than IP3, in the Mg2+- and ATP-dependent manner, thereby indicating the presence of IP3 3-kinase activity in homogenates of the muscle. 3. Most of the kinase activity was present in the cytosol fraction. The enzyme activity was reversibly activated by Ca2+ with a half-maximal effective concentration of 2.5 x 10(-7) M. 4. The calmodulin antagonists, W-7 and chlorpromazine inhibited the Ca2+-activated enzyme activity.

Animals↗
PubMed1989

Induction of peroxidase and thyroglobulin by TSH in cultured thyroid cells from patients with Basedow's disease and its inhibition by actinomycin D.

The effects of TSH on peroxidase activity (PO) and thyroglobulin (TG) production were investigated using primary cultures of thyroid cells obtained from patients with Basedow's disease (Basedow's cells). PO activity of cultured cells and TG concentration in the culture medium were measured by biochemical and sandwich enzyme immunoassays, respectively. The addition of TSH (10 mU/ml/day) to the medium did not increase the cell number but did increase the PO activity and TG concentration. It took more than 3 days for the PO activity of cells cultured with TSH (stimulated group) to reach a level twice that of cells cultured without TSH (control group), whereas 2 days of incubation with TSH was sufficient for increasing the TG concentration. When actinomycin D (AD) was added to the medium on the first day of 3-day incubation with TSH, the stimulatory effect of TSH on PO was completely blocked and the TG concentration was reduced to half that of the control group. AD given to the stimulated group on the last day of induction produced no inhibitory effect on the induction of PO activity by TSH, but reduced the TG concentration to almost half that in the stimulated group. An electron microscopic study of Basedow's cells cultured with AD and TSH failed to reveal any cytopathic change. The findings of the present study suggested that in cultured Basedow's cells TSH induces PO activity and TG production through the synthesis of new messenger RNA.

Cell Count↗
PubMed1989

[An autopsied case of double carcinomata consisting of hepatocellular and renal cell carcinoma associated with adrenocortical adenoma].

Reported is an autopsied case of a double carcinomata associated with an adrenocortical adenoma in a 68-year-old Japanese female. The hepatocellular carcinoma was classified as being type II, according to Edmondson's classification, and showed massive necrosis caused by TAE and metastases to both lungs the diaphragm, the portal veins, the hepatic veins, and the inferior vena cava. The renal cell carcinoma was latent and diagnosed as being a mixed-cell type, with clear and granular cells also present. Double carcinomata of hepatocellular and a renal cell carcinoma are extremely rate and such a combination occupies merely 0.27-1.04% of the total double carcinomata reported in the Japanese literature. The adrenocortical adenoma in the present case was considered to be a non-functioning adenoma, based on no specific clinical symptoms during the woman's hospitalization.

Adenoma↗
PubMed1989

Possible binding sites for inositol 1,4,5-trisphosphate in canine tracheal smooth muscle cells and rat liver cells.

To search for binding site of inositol 1,4,5-trisphosphate (InsP3) in relation to the release of Ca2+ from smooth muscle cells of the canine trachea, InsP3 coupled with p-azidobenzoyl beta-alanine (AB beta A) was synthesized for photoaffinity labelling, using N,N'-carbonyldiimidazole. With subsequent photolysis of the smooth muscle cells following incubation with this derivative (InsP3-AB beta A), the InsP3-induced Ca2+ release from saponin-permeabilized dispersed smooth muscle cells no longer occurred. The irreversible release of Ca2+ induced by InsP3-AB beta A was prevented by adding 10-fold excess amounts of InsP3. These observations strongly suggest that there is a covalent binding of InsP3-AB beta A to a specific "receptor" on the sarcoplasmic reticulum in tracheal smooth muscle cells. To determine the specific binding sites on the endoplasmic reticulum, I synthesized an isotope-labelled arylazide derivative of InsP3; InsP3 was coupled with p-[125I]azidosalicyl beta-alanine, using carbonyldiimidazole as a catalyst. I obtained three proteins with molecular weights of 44K-Da, 27K-Da and 22K-Da, which were preferentially labelled with the [125I]arylazide derivative of InsP3 (InsP3-[125I]AS beta A) in photoirradiated microsomal fractions of canine tracheal smooth muscle cells. The labelling of these proteins was partially blocked by an excess amount of unlabelled InsP3 but not by inositol 1,4-bisphosphate (Ins(1,4)P2). Similar binding proteins with molecular weights of 48K-Da, 32K-Da and 18K-Da were also labelled in the endoplasmic reticulum fraction of the rat liver, but such proteins were not evidenced in the plasma membrane fraction.

Animals↗