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Biomedical subjects

K Suyama

Publications and source records attributed to K Suyama.

At least 19 recordsLinked to original sources
PubMed1995

Genomic instability of microsatellite repeats in prostate cancer: relationship to clinicopathological variables.

Sixty-six patients with prostatic adenocarcinoma were screened for somatic instability at 8 microsatellite marker loci on 5 chromosomes. Differences in unrelated microsatellites for tumor and normal DNA were detected in 13 (19.7%) patients. Only extraglandular spread (nodal involvement and distant metastasis) was found to show significant association with somatic instability after controlling for other clinicopathological variables (P < 0.05). Microsatellite instability may possibly occur during the early stages of neoplastic transformation in a subset of prostate cancer rather than as a late event. This may be related to a phenotype with growth advantage. The frequency of this mutator phenotype is much higher in the United States than Japan, reflecting racial differences in the molecular tumorigenesis of this malignancy.

Adenocarcinoma↗
PubMed1995

A case of septal Wolff-Parkinson-White syndrome associated with newly developed delta waves due to disappearance of impedance mismatch.

A 65-year-old woman who had shown no delta waves or atrioventricular block when seen in February 1989, suddenly developed advanced atrioventricular block in April 1990. The first electrophysiologic study revealed that atrioventricular block was caused by His ventricular block, and only weak retrograde conduction was documented. A DDD-type permanent pacemaker was implanted. One month after implantation, delta waves developed. The second electrophysiologic study, performed in February 1993, disclosed that a Kent bundle with bidirectional conduction capacity was located at the posterior septum and that the normal conduction system remained blocked at the His ventricular site. The etiology of the newly developed delta waves seems to be the disappearance of impedance mismatch at the ventricular insertion site of the Kent bundle.

Aged↗
PubMed1995

Alterations in cyclic AMP generation and G protein subunits following transient ischemia in gerbil hippocampus.

We examined alterations in the cyclic AMP generating system and G protein subunits in gerbil hippocampus following 10 min of transient ischemia. In hippocampal slices, basal and isoproterenol- and forskolin-stimulated cyclic AMP accumulations were markedly increased at 6 and 24 h after ischemia. Interestingly, both the inhibition of forskolin-stimulated cyclic AMP and the potentiation of beta-adrenoceptor-stimulated cyclic AMP by a gamma-aminobutyric acidB receptor agonist were attenuated at these time points. Ischemia did not affect the immunolabeling of any of the G protein alpha subunits; only that of beta subunits was significantly decreased, by 28.2%, 4 days after ischemia. In contrast, pertussis toxin-catalyzed [32P]ADP ribosylation declined progressively during the late recirculation period, reaching a significant reduction (25.4%) at 6 h after ischemia. These results suggest that ischemia affects the heterotrimeric conformation (alpha beta gamma) of Gi/Go during the recirculation period, thereby leading to increased cyclic AMP production. Because cyclic AMP-dependent protein kinase A modulates the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-kainate receptor channels, postischemic sensitization of the cyclic AMP generating system may contribute to neuronal degeneration in the hippocampus.

Adenosine Diphosphate Ribose↗
PubMed1995

Red cell surface cysteine residue (285) of D polypeptide is not essential for D antigenicity.

BACKGROUND: Only one surface cysteine residue (285) has been thought to be involved in D antigenicity, according to studies using lyophilized or nonlyophilized red cell membranes. However, it has been reported that a 17-kDa chymotryptic fragment containing the N-terminus but not this cysteine residue is associated with D antigenicity. STUDY DESIGN AND METHODS: The role of the sulfhydryl (SH) group in D, c, and E antigenicity is assessed by using intact red cells treated with the reagents N-ethylmaleimide, 5,5'-dithiobis(2-nitrobenzoic acid), and 2-(4'-maleimidylanilino)- naphthalene-6-sulfonic acid. Antigenicity was appraised by hemagglutination titers and immunoprecipitation using human anti-D, -c, and -E. RESULTS: Treatment with N-ethylmaleimide or 5,5'-dithiobis(2-nitrobenzoic acid) at various concentrations (< or = 5 mM) or for various times (< or = 120 min) did not cause significant decrease in hemagglutination titers as compared to untreated intact red cells. Moreover, immunoprecipitation of Rh antigen-carrying peptides by human anti-D was not affected by prior treatment with N-ethylmaleimide or 2-(4'maleimidylanilino)-naphthalene-6-sulfonic acid. Efficacy of blockage of SH groups was demonstrated by inhibition of palmitic acid uptake by the Rh polypeptides for prior treatment with N-ethylmaleimide and by the presence of fluorescent Rh polypeptides for prior treatment with 2-(4'maleimidylanilino)-naphthalene-6-sulfonic acid. CONCLUSION: SH group involvement is not essential for D, c, or E antigenic expression in intact red cells.

Antibodies, Monoclonal↗
PubMed1995

Endocardial fragmented electrogram and prediction of ventricular tachycardia by body surface signal-averaged electrocardiographic mapping.

Signal-averaged (SA) electrocardiography and SA electrocardiographic mapping were performed in 50 patients with old myocardial infarction, 19 of whom had left ventricular aneurysm and 11 of whom had clinical sustained ventricular tachycardia. The SA electrocardiogram and SA electrocardiographic mapping data were then compared with those obtained by endocardial catheter mapping in patients with or without fragmented electrograms, sustained ventricular tachycardia, and ventricular aneurysm. Compared to SA electrocardiography, the SA map correlates with sustained VT with improved sensitivity but decreased specificity. However, SA electrocardiographic mapping had the advantage of displaying the extent of the body surface area that was positive for late potentials. In addition, the site of the longest endocardial fragmented electrogram could be predicted by SA electrocardiographic mapping, suggesting that this technique deserves wider clinical application.

Action Potentials↗
PubMed1995

[Agents preventing decrease in ultrafiltration in a rat model with peritoneal hyperpermeability].

Ultrafiltration failure has been one of the major causes of drop out from CAPD treatment. The present study was designed to develop an ultrafiltration failure model in the rat and to assess whether various agents could prevent a decrease in ultrafiltration capacity in this rat model. Peritoneal hyperpermeability was induced by repeated intraperitoneal injection of 15 ml of 4.25% dextrose dialysate for 7 days. Some of the rats received agents, such as phosphatidylcholine, chondroitin sulfate, siliac acid, heparan sulfate, keratan sulfate, sodium sulfate, sodium phosphate, and heparin sodium, simultaneously administered with 4.25 % dextrose dialysate for the same duration. Ultrafiltration volume, D4/D0 ratio of glucose and peritoneal net fluid absorption were evaluated by 4-hour dwelling of 30 ml of 2.5% dextrose dialysate. Sodium phosphate and heparan sulfate prevented peritoneal hyperpermeability due to repeated injection of hypertonic dialysate. Sodium phosphate, sodium sulfate, heparin and heparan sulfate suppressed peritoneal net fluid absorption, resulting in an increase in ultrafiltration. These findings may be applicable to CAPD patients with ultrafiltration loss.

Absorption↗
PubMed1994

Analysis of aldosine, an amino acid derived from aldol crosslink of elastin and collagen by high-performance liquid chromatography.

An ion-paired high-performance liquid chromatographic method for the determination of aldosine, which is derived from the aldol crosslink of both elastin and collagen, is described. Aldosine was determined as the pyridine derivative 6-(3-pyridyl) piperidine-2-carboxylic acid, which was synthesized by oxidative decarboxylation of aldosine using iron(III). This method does not require radioisotopes to label the aldol crosslink. In addition, pyridinium crosslinks such as desmosines can also be measured.

Amino Acids↗
PubMed1994

Rh(D) antigen expression and isolation of a new Rh(D) cDNA isoform in human erythroleukemic K562 cells.

Human erythroleukemic K562 cells are known to have several erythroid properties. K562 cells possess Rh mRNAs, but expression of Rh proteins has not previously been reported. We immunoprecipitated Rh protein from K562 cell lysate using rabbit anti-Rh and detected Rh(D) antigens on K562 cells using fluorescence-activated cell sorting (FACS). These results suggest that K562 cells will be useful as an expression model for most Rh antigens. We also cloned a new Rh(D) cDNA isoform (RhK562-II), from a K562 cDNA library using polymerase chain reaction (PCR) with 5' and 3' end oligonucleotides of the published Rh(e/E) antigen encoding cDNA sequence as primers. Sequence analysis showed that RhK562-II is composed of 951 nucleotides (316 amino acids), identical to the first 939 nucleotides (exons 1 to 6) of one of the Rh(D) cDNAs (RhXIII), except for nucleotide 654 (C-->G exchange). However, this exchange is the same as that of another published Rh(D) cDNA (RhPII cDNA). RhK562-II is deprived of exons 7 and 8 (nucleotides 940 to 1,153), followed by an identical sequence up to the 3' end of the open-reading frame of the RhXIII cDNA, which causes a frame-shift mutation and produces a premature stop codon. In vitro expression of RhK562-II using the transcription and translation rabbit reticulocyte lysate system produced two major Rh-related proteins (30 kD and 25 kD), which were immunoprecipitated by rabbit polyclonal anti-Rh and separated on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE).

Amino Acid Sequence↗
PubMed1994

[Diffuse slow washout pattern (DSWO) on exercise stress thallium-201 myocardial SPECT: correlative study with coronary arteriography and the related clinical factors].

DSWO was shown on bull's eye images of 98 of 1234 patients suspected of having coronary artery disease and examined with thallium-201 myocardial SPECT imaging. Fifty-eight of these 98 patients underwent coronary arteriography, and comparison studies were performed between the bull's eye SPECT images, the results of coronary arteriography and the laboratory data. DSWO was found in 11 of 58 cases (19.0%) of single vessel disease (1VD), 18 of 58 cases (31.0%) of double vessel disease (2VD) and 21 of 58 cases (36.2%) of triple vessel disease (3VD). Three of 58 cases (5.2%) of stenosis of a coronary artery less than 75% of its normal diameter (N group) also showed DSWO. DSWO was closely related with multiple vessel disease, as has been indicated by previous reports, but we also found another patient group that showed minor coronary arterial change (1VD and N group) and manifested DSWO. Based on the study of laboratory data, we clarified that this group of patients tended to show accompanying hypertension and hyperlipidemia as factors influencing the appearance of DSWO. DSWO was accompanied by hypertension and hyperlipidemia in 54.5% and 45.5% in 1VD. These values were higher than those in the 2VD and 3VD cases, which were 33.3% and 38.9% in 2VD, and 19.0% and 28.6% in 3VD, respectively. Hypertension and hyperlipidemia appeared to play an important role in causing DSWO by interfering with coronary circulation.

Adolescent↗
PubMed1994

A new biomaterial, hen egg shell membrane, to eliminate heavy metal ion from their dilute waste solution.

The egg shell membrane (ESM) is an intricate lattice network of stable and water-insoluble fibers with high surface area. ESM accumulates and eliminates various heavy metal ions from dilute aqueous solution with high affinity and in short contact time, depending on pH and characteristics of the individual ion. Under certain conditions, the level of precious ions, Au, Pt, and Pd accumulation approaches 55, 25, and 22% of dry wt of ESM, respectively. Also uranium uptake 30% of that of ESM. Experiments suggested that ESM is promising to use for the purpose of removal/recovery of metals and water pollution control.

Adsorption↗
PubMed1994

In vivo evidence that nonneuronal beta-adrenoceptors as well as dopamine receptors contribute to cyclic AMP efflux in rat striatum.

We applied in vivo microdialysis to assess the effects of dopaminergic and beta-adrenergic receptor stimulation on cyclic AMP efflux in rat striatum under chloral hydrate anesthesia. Dopamine (up to 1 mM) infused for 20 min through the probe did not increase cyclic AMP, whereas both the selective dopamine D1 agonist SKF 38393 and D2 antagonist sulpiride produced modest increases. It is interesting that the beta-adrenoceptor agonist isoproterenol produced a marked increase (204.7% of basal level at 1 mM) which was antagonized by the beta-adrenoceptor antagonist propranolol. Pretreatment with a glial selective metabolic inhibitor, fluorocitrate (1 mM), by a 5-h infusion through the probe attenuated basal cyclic AMP efflux by 30.3% and significantly blocked the response to isoproterenol. By contrast, striatal injection of a neurotoxin, kainic acid (2.5 micrograms), 2 days before the dialysis experiment did not affect basal cyclic AMP or the response to isoproterenol, but blocked the response to SKF 38393. These data demonstrate the beta-adrenoceptors as well as dopamine receptors contribute to cyclic AMP efflux in rat striatum in vivo. They also suggest that basal and beta-adrenoceptor-stimulated cyclic AMP efflux are substantially dependent on intact glial cells.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1994

Correlation of the endocardial fragmented electrogram with body surface signal-averaged electrocardiographic mapping.

We compared signal-averaged electrocardiography (SAE), SAE mapping, and left ventricular catheter mapping in 60 patients with ischemic heart disease. Using the data obtained in patients with no fragmented electrograms (FE) in the left ventricle, the late potential was defined by SAE as a filtered QRS duration > 131 msec or a root mean square voltage < 16 microV for the last 40 msec of the QRS complex. SAE mapping was performed by recording the signal-averaged electrocardiogram at 48 sites on the body surface. With SAE mapping, the filtered QRS duration and the area in the last 20 msec of the QRS complex were significantly different between the patients with and without FEs. The late potential was defined by SAE mapping as a filtered QRS duration > 136 msec or an area < 28 microV.msec for the last 20 msec of the QRS complex. The sensitivity and specificity of detecting FEs were 46% and 88%, respectively, by the SAE filtered QRS criterion, while they were 66% and 88% by the root mean square criterion. In contrast, SAE mapping gave values of 66% and 92% by the filtered QRS criterion, as well as values of 100% and 92% by the area criterion. Thus, SAE mapping provided better detection of the FE and was more closely correlated with the results of catheter mapping, suggesting its potential for clinical application.

Action Potentials↗
PubMed1994

[Experimental studies for immunoscintigraphy of adenocarcinoma of the prostate with 125I-labeled monoclonal antibody to gamma-seminoprotein].

We established LNCaP tumor in male nude mice after inoculation of LNCaP cells. The tumor produces the organ-specific glycoproteins in the human prostate, gamma-seminoprotein (gamma-Sm), which has been verified by immunohistochemistry and enzyme immuno assay. The LNCaP tumor is composed of 2 distinct portions, namely GEL/FLUID portion and SOLID portion. The GEL/FLUID portion contains much more gamma-Sm than the SOLID portion does. The monoclonal antibody against gamma-Sm (murine IgG1, K) was radio-labeled with iodine-125 by lactoperoxidase method followed by passage over column chromatography. Finally the conjugates with specific activity of 49.8-56.6 KBq/micrograms were obtained. Biodistribution of 125I-labeled monoclonal antibody to gamma-Sm (125I-gamma MAb) was evaluated by whole-body autoradiography (ARG) and by determination of label uptake (DLU) by the LNCaP tumor using the well type gamma counter. The ARG were obtained 1-9 days after intravenous administrations of 32-38 micrograms of 125I-gamma MAb to 12 nude mice bearing LNCaP tumor. The DLU were evaluated 3, 4 and 7 days after intravenous administrations of 18-25 micrograms of 125I-gamma MAb to 9 nude mice bearing LNCaP tumor. The DLU by organs (GEL/FLUID portion, SOLID portion, liver, kidney, spleen, lung, etc.) were expressed as F-values (%) which were calculated by the following formula: F = radioactivity per gram of tissue (dpm/g) divided by injected dose per gram of animal (dpm/g) x 100 and tissue-to-blood ratios (T/B). The specific uptake by the LNCaP tumors, especially in the GEL/FLUID portion, was observed on ARG, with optimal images of the tumor evaluated 4-7 days after administrations. The F-values and T/B of the LNCaP tumors were always higher than those of other organs. Especially T/B of GEL/FLUID portion were of 6.7 and 6.3, evaluated 4 and 7 days after administration of 125I-gamma MAb respectively. These results suggest that the radio-labeled gamma MAb is applicable for immunoscintigraphy of adenocarcinoma of the prostate.

Adenocarcinoma↗
PubMed1994

[Ultrafiltration failure in a peritoneal dialysis patient due to a marked increase in lymphatic absorption a case report].

A peritoneal dialysis patient was reported who had ultrafiltration loss due to a marked increase in lymphatic absorption and peritoneal membrane permeability. A 33-year-old male was transferred from hemodialysis to peritoneal dialysis because of acute subdural hematoma. His complicated history included left testicular tumor with retroperitoneal lymph node metastasis in 1982. He was treated with CDDP, Etoposide, Bleomycin, Vinblastine sulfate and Vincristine and received operation of retroperitoneal lymph node dissection in 1982. He had been on hemodialysis since 1983 due to cisplatinum nephropaty. Ultrafiltration failure was found immediately following the insertion of Tenckhoff catheter without malfunction of peritoneal catheter. Peritoneal equilibrate test and lymphatic absorption measurement showed a high permeability peritoneum with a marked increase in lymphatic absorption rate (3.7 ml/min). These two factors were thought to result in ultrafiltration loss. CAPD with 4-6 times exchange daily did not maintain ultrafiltration, because it gave approximately 2000 ml negative water balance every day. He was well maintained on a short time exchange intermittent peritoneal dialysis (IPD) with cycler using 18 L for 8 hours. We concluded that increased lymphatic absorption is one of the important factors for ultrafiltration fafilure and IPD with frequent exchange by cycler is suitable for the patient with ultrafiltration loss.

Absorption↗
PubMed1993

Increased growth rate and tumor burden of spontaneously metastatic Walker 256 cancer cells in the skeleton of bisphosphonate-treated rats.

We have studied the effect of 3-amino-1-hydroxypropylidene-1,1-bisphosphonate (APD) on the morphology of rat bone and the metastatic behavior of Walker 256 (W256) cancer cells in the rat skeleton. Male Fischer rats (150-175 g) received s.c. injections for 7 days with APD (0.5 mg/kg body weight/day) (+ APD; n = 20) or with vehicle (-APD; n = 20). Subsequently, 10 + PD and 10 -APD rats received i.m. injections with W256 cells (+ W256), and the remaining rats received injections of vehicle (-W256). All rats were killed 14 days later. Trabecular bone volume was increased by 46 +/- 3% by APD treatment alone and was decreased by 56 +/- 7% (SEM) by W256 tumor burden alone. After 14 days of tumor burden, + APD/+ W256 rats had 3-fold more trabecular bone than did -APD/+W256 rats. Despite this bone-sparing effect, APD treatment of +W256 rats was associated with a 2.6-fold increase in skeletal tumor burden, while metastatic tumor burden in the liver, lungs, and kidneys was unaffected. The increased skeletal tumor burden in + APD/+ W256 rats was accompanied by an increase in the growth rate of W256 cells located in bone. Independent of APD treatment, W256 cells located adjacent to trabecular bone surfaces had greater growth rates than did W256 cells in the marrow, located > 50 microns from trabecular bone. In summary, the APD-induced increase in trabecular bone volume in rats is associated with a selective increase in skeletal tumor burden and an increased growth rate of W256 cells in the skeleton.

Acid Phosphatase↗
PubMed1993

Expression of the 32-Kd polypeptide of the Rh antigen.

To develop procedures for the expression of Rh antigen-containing proteins, we prepared a previously cloned Rh cDNA by isolation from a human bone marrow library using polymerase chain reaction (PCR). The cDNA that encodes either Rh(E) or (e) antigens was inserted into a vector (pGEM7ZRh) and transcription/translation performed in a reticulocyte lysate system. This produced a major (32 Kd) and minor (30 Kd) protein band in the region of sodium dodecyl sulfate (SDS) gels where Rh proteins are known to migrate. These same two proteins were immunoprecipitated by a rabbit anti-Rh antibody preparation that reacts with all Rh proteins, confirming that Rh protein was expressed in this cell-free system. Transient expression of Rh protein in COS-1 cells was also accomplished using a transfection vector (pBC12BIPLRh) containing inserted Rh cDNA. COS-1 cells transfected with this vector also produced a 32-Kd protein band that formed an immune complex with rabbit anti-Rh, while cells transfected with the same vector minus the Rh cDNA insert did not yield any detectable Rh immune-complexed protein. This system should prove useful for studying the transport of Rh proteins within the cell and the expression of Rh antigenicity at the cell surface.

Animals↗
PubMed1993

Immunochemical characterization of rhesus proteins with antibodies raised against synthetic peptides.

Rabbit polyclonal antibodies were raised against synthetic peptides corresponding to hydrophilic regions of the human Rhesus (Rh) IX cDNA-encoded polypeptide predicted to be extracellularly or intracellularly exposed in the topologic model of the Rh blood group protein. Four antibodies encompassing residues 33-45 (MPC1), 224-233 (MPC4), 390-404 (MPC6), and 408-416 (MPC8) were characterized and compared with a polyclonal anti-Rh protein obtained by immunization with purified Rh proteins. All antibodies had specificity for authentic Rh polypeptides and reacted on Western blot with Rh proteins immunoprecipitated with human monoclonal anti-RhD, -c, and -E. MPC1, but not the other antibodies, agglutinated all human erythrocytes except Rhnull and Rhmod cells, which either lack totally or are severely deficient in Rh proteins, respectively. Immunoblotting analysis with membrane proteins from common and rare variants showed that MPC1 and MPC8 reacted in Western blot with 32-Kd Rh polypeptides from all common red blood cells except those from Rhnull and Rhmod, indicating that peptide regions 33-45 and 408-416 may be common to several if not all Rh proteins, whatever the Rh blood group specificity. MPC4 reacted only with membrane preparations from cells carrying the E antigen, whereas MPC6 recognized preferentially the Rh proteins from E and Ee preparations, suggesting that the protein encoded by the RhIXb cDNA carries the E and/or e antigen(s). Immunoadsorption experiments using inside-out or right-side-out sealed vesicules from DccEE red blood cells as competing antigen showed that the MPC6 and MPC8 antibodies bound only to the cytoplasmic side of the erythrocyte membrane, thus providing evidence for the intracellular orientation of the C-terminal 27 residues of the Rh polypeptides. Attempts to transiently or stably express the Rh polypeptides. Attempts to transiently or stably express the Rh cDNA in eukaryotic cells were largely unsuccessful, suggesting that Rh antigen expression at the cell surface requires correct transport and/or folding of the Rh proteins, possibly as a complex with one-membrane proteins of the Rh cluster that are lacking in Rhnull cells.

Animals↗