Biomedical subjects

Y Katayama

Publications and source records attributed to Y Katayama.

At least 505 records · Page 28Linked to original sources

PubMed1992

Comparison of imaging methods for localization of parathyroid tumors.

Preoperative localization of parathyroid tumors by computed tomography (CT), thallium-201/technetium-99m pertechnetate subtraction scintigraphy (Tl-201/Tc-99m), ultrasonography (US), and magnetic resonance imaging (MRI) was compared in patients with hyperparathyroidism (HPT) to examine the characteristics of each method. A total of 87 patients with HPT were divided into two groups according to the time when they were examined. Patients in group I were examined before MRI had been introduced in our hospital, and a 2.5-MHz transducer probe was used for US. Those in group II were examined by MRI and US using a 7.5-MHz transducer probe. Group I included 45 patients (36 with primary hyperparathyroidism [PHPT] and 9 with secondary hyperparathyroidism [SHPT]), and group II included 42 patients (15 with PHPT and 27 with SHPT). In both PHPT and SHPT and SHPT of group I and PHPT of group II, there was no significant difference in detection rates between all diagnostic methods. In patients with SHPT in group II, the detection rate was significantly higher for CT than for Tl-201/Tc-99m and MRI (both p less than 0.01), and for US than for Tl-201/Tc-99m (p less than 0.01). In both groups I and II, the detection rate of each study method was significantly higher in patients with PHPT than in those with SHPT (all p less than 0.01). Compared with group I, the rate was significantly improved in group II, in both types of patients. Regarding the location of the parathyroid tumor, the detection rate of CT was significantly higher for upper parathyroid glands than for lower glands, whereas that of US and Tl-201/Tc-99m was significantly higher for lower glands. The detection rate sharply increased when the tumor weight reached 250 mg (CT, US) or 1,000 mg (Tl-201/Tc-99m, MRI).

Adult↗

PubMed1992

Hippocampal CA3 lesion prevents postconcussive metabolic dysfunction in CA1.

Immediately following fluid-percussion (F-P) brain injury, the hippocampus exhibits a marked increase in its local CMRglc (LCMRglc; mumol/100 g/min) as determined using [14C]2-deoxy-D-glucose autoradiography. This injury-induced increase in metabolism is followed in 6 h by a subsequent decrease in LCMRglc. These two postinjury metabolic states may be the result of ionic disruptions following trauma via stimulation of glutamate-gated ion channels. To determine if endogenous glutamate innervation to the CA1 region of the hippocampus can provide an anatomical basis for this proposed mechanism, it was removed by kainic-acid-induced destruction of CA3, and the effect on CA1 metabolism following concussive injury was studied. Five days before a lateral F-P injury (3.5-4.5 atm), kainic acid (0.5 microgram) or vehicle was stereotaxically injected into the left ventricle of 65 rats. Histological inspection indicated that kainic acid produced severe cell loss primarily in the CA3 region of the hippocampus ipsilateral to the injection. The metabolic results indicated that immediately following injury, animals with an intact hippocampus exhibited an increase in LCMRglc to 84.6 +/- 5 within the CA1 region, representing a 81.5% increase over controls. However, in the CA3-lesioned animals, CA1 showed no evidence of an injury-induced hypermetabolism, with LCMRglc remaining at control levels (51.4 +/- 3.9). At 6 h postinjury, the intact hippocampus exhibited a reduction of LCMRglc to rates of 40.7 +/- 4.7 within the CA1 region, representing a 17.9% reduction compared with controls. In contrast, CA3-lesioned animals exhibited less of an injury-induced decrease in LCMRglc within the CA1 region, exhibiting a mean rate of 43.4 +/- 4.5, representing only a 12.5% reduction compared with controls. These results indicate that the removal of the CA3 projection to CA1 protects the CA1 cells from the metabolic dysfunction typically seen following injury. This supports our previous work indicating the important role glutamate plays in the ionic flux and subsequent metabolic changes that follow traumatic brain injury.

Animals↗

PubMed1992

Administration of excitatory amino acid antagonists via microdialysis attenuates the increase in glucose utilization seen following concussive brain injury.

Immediately following concussive brain injury, cells exhibit an increase of energy demand represented by the activation of glucose utilization. We have proposed that this trauma-induced hypermetabolism reflects the effort of cells to restore normal ionic balance disrupted by massive ionic fluxes through transmitter-gated ion channels. In the present study, changes in local CMRglc following fluid-percussion concussive injury were determined using [14C]2-deoxy-D-glucose autoradiography, and the effects of in situ administration (via microdialysis) of excitatory amino acid (EAA) antagonists [kynurenic acid (KYN), 2-amino-5-phosphonovaleric acid (APV; 100 microM, 1 mM, and 10 mM), and 6-cyano-7-nitroquinoxaline-2,3-dine (CNQX; 300 microM, 1 mM, and 10 mM] on glucose utilization were investigated. Animals that did not receive dialysis showed a remarkable increase (up to 181% of normal control) in cortical glucose utilization following injury. In contrast, this high demand for glucose was reduced in areas infiltrated with KYN, APV, and CNQX. These results indicate that EAA-activated ion channels are involved in the posttraumatic increase in glucose utilization, reflecting the energy demand of cells required to drive pumping mechanisms against an ionic perturbation seen immediately following the concussive injury. The effects of KYN, APV, and CNQX suggest that although all subtypes of the glutamate receptor appear to be involved in this phenomenon, N-methyl-D-aspartate-activated channels may play a major role.

2-Amino-5-phosphonovalerate↗

PubMed1992

Substance P inhibits activation of calcium-dependent potassium conductances in guinea-pig myenteric neurones.

1. Intracellular recordings were made from myenteric AH neurones of the guinea-pig ileum in vitro. Some experiments were done with a single-electrode voltage clamp to measure membrane currents. 2. Substance P (SP) applied by superfusion (10 nM-300 nM), pressure ejection (100 nM-10 microM, 760 mmHg, for 10-20 ms) or ionophoresis (1 mM, 100 nA, for 0.2 s) caused a membrane depolarization and an inward current, associated with a decrease in potassium conductance. 3. The SP-induced depolarization was abolished within 15 min by superfusion with calcium-free/high-magnesium (10 mM) solution or solutions containing cobalt, manganese or nickel at 1-3 mM. The response persisted even after 40-60 min of superfusion with calcium-free/normal-magnesium (1.2 mM) solution. In all these solutions, synaptic potentials were abolished within 5 min. 4. SP inhibited a slowly developing outward current and an outward tail current during and after a long depolarizing command pulse (2-10 s), and an outward after-current following single or multiple brief depolarizing command pulses (10-50 ms). These outward currents were suppressed in calcium-free/high-magnesium solution. 5. SP depressed both a calcium-dependent slow after-hyperpolarization following the action potential and an outward after-current preceded by a brief depolarizing command. Both the SP-induced depolarization and the SP-induced inward current were augmented when the peptide was pressure-ejected during the recovery phase of the slow after-hyperpolarization and during that of the slow outward after-current, but both of them were inhibited or almost abolished when SP was applied immediately after spike initiation or a brief depolarizing command. 6. The SP-induced response was depressed by barium (1-2 mM). The SP response was not inhibited by tetraethylammonium at low concentrations (5-10 mM), but was depressed at high concentration (20 mM). 7. Superfusion (1-10 nM) or pressure application of a calcium ionophore, A23187, inhibited or even reversed the SP depolarization and the SP-induced inward current. 8. These results indicate that SP inhibits activation of a calcium-dependent potassium conductance which contributes to both the slow after-hyperpolarization and the resting membrane potential. SP may affect the process by which calcium activates this potassium conductance.

Action Potentials↗

PubMed1992

Influence of morphologic factors on calcium-containing stone formation.

Pathogenesis of urolithiasis cannot be explained only by metabolic disorder. In the present study, morphologic differences of the renal pelvic-caliceal system (PCS) were examined on both the stone and normal sides in calcium-containing stone formers. The results indicated that as compared to the normal side, the urine flow in the PCS was stagnant or not straight on the stone side even in the same individual, showing unfavorable conditions for stone formation. It is therefore considered that morphologic disorders of the urinary tract may be one of the causes for stone formation.

Adult↗

PubMed1992

Primary localized amyloidosis of the bladder: a case of AL (lambda) amyloid protein and combination therapy using dimethyl sulfoxide and cepharanthin.

We report a case of primary localized amyloidosis of the bladder with amyloid deposits which was characterized as being of immunoglobulin light chain origin (AL) including lambda type (A lambda) and P component (AP) using the KMnO4 pretreatment method and immunohistochemical procedures. The patient was treated successfully with intravesical dimethyl sulfoxide instillation and oral administration of high-dose cepharanthin after transurethral resection. Combination therapy with dimethyl sulfoxide and cepharanthin was shown to be useful for primary localized amyloidosis of the bladder.

Aged↗

PubMed1992

Application of flexible renoureteroscope for antegrade urethroscopy in the treatment of congenital anterior urethral valve.

Antegrade urethroscopy was performed through a cystostomy using a 10.8-fr caliber flexible renoureteroscope in 4 children (aged 2 years and 8 months, 2 months, 14 years and 1 month) with anterior urethral valve. The anatomy of the valves as well as their destruction after transurethral resection (TUR) were well visualized by antegrade urethroscopy. This technique was helpful in performing TUR-valve, after which the findings of voiding cystourethrography in every case and the findings of uroflowmetry in the elder 2 cases showed remarkable improvement. This technique is relatively simple to perform and is thought to be one of the best methods to treat anterior urethral valve. This technique is also applicable to other lower urinary tract lesions in children.

Adolescent↗

PubMed1992

Inhibitory effect of bis(2-aminohexyl) disulfide and bis(2-amino-3-phenylpropyl) disulfide on several mouse inflammations.

The anti-inflammatory profile of the analogues of bis(2-aminopropyl) disulfide dihydrochloride with butyl (compd. II) and phenyl (compd. III) instead of the methyl group was studied in several mouse models related to phagocyte functions. The test samples were administered 2-3 h before the inflammatory stimulation or the peak of inflammation. Subcutaneously administered, compds. II and III significantly inhibited serotonin-induced paw edema in a dose-dependent manner (50% inhibitory dose values: 10 and 5 mg/kg, respectively), when orally administered at 25 mg/kg, these compounds were significantly effective, but their potencies were weaker. Neither compound had any irritant activity when administered at a dose of 12.5 micrograms/5 microliters/paw into the paw. In a sheep red blood cells (SRBC)-induced delayed-type hypersensitivity (DTH) reaction model, compd. II (25 mg/kg, s.c.) significantly inhibited the DTH responses when administered at two different times in relation to the time of challenge. However, there was only slight inhibition by compd. III (25 mg/kg, s.c.) on paw edema formation when administered 14 h after secondary immune response. In a model of experimental acute hepatic failure induced by successive injections of Propionibacterium acnes and lipopolysaccharide, both compounds increased mouse survived, compared with the control mice, and kept the serum levels of components involved in hepatic failure to nearly normal levels. These results demonstrate that compds. II and III possess an inhibitory effect on inflammation related to phagocytes.

Amines↗

PubMed1992

Inhibitory effects of bis(2-aminohexyl)disulfide and its analogues on polymorphonuclear leukocyte functions in vitro.

Water soluble analogues of the anti-inflammatory compound, bis(2-aminopropyl)disulfide dihydrochloride (compd. I) with a butyl (II), phenyl (III), benzyl (IV) or pyrrolidinyl group (V) instead of the methyl group were synthesized, and their effects on the functions of cells related to inflammation were studied in vitro. Compounds II, III and IV showed much higher inhibitory activity than compd. I on formyl Met-Leu-Phe (FMLP)-induced O2(-)-generation of polymorphonuclear leukocytes (PMNs) and platelet aggregation. Compound II showed the strongest activity among the compounds (IC50 values: 2.6 microM). The inhibition of O2(-)-generation of PMNs by compd. II was the most effective when FMLP was used as a stimulant rather than when phorbol myristate acetate, A-23187 and opsonized zymosan were used. However, compd. II was not an O2(-)-scavenger. Compounds II, III and IV significantly inhibited a series of activation processes in PMNs, chemotaxis, phagocytosis and lysosomal enzyme release at doses ranging from 10 to 100 microM. Under these doses, compds II, III and IV did not affect the histamine release from mast cells or the hemolysis of erythrocytes. These results strongly suggest that the anti-inflammatory action caused by compd. II and its analogues was at least partly due to inhibition of several functions of PMNs and platelets.

Amines↗

PubMed1992

Effect of a prostacyclin derivative (OP-41483) and a hyperosmotic agent (glycerol) on brain edema and metabolism in cerebral ischemia.

A PGI2 derivative, OP-41483, and a hyperosmotic agent, glycerol, were tested for possible beneficial effects on brain edema, metabolism and pathological changes in cerebral ischemia. Combination treatment with these agents was also tested. Cerebral ischemia was produced in spontaneously hypertensive rats, using bilateral common carotid artery ligation (BLCL). OP-41483 was administered four times, hourly (500 ng/kg x 4, i.p.). Ten percent glycerol was administered intravenously (6.6 ml/kg). And, for the combination treatment, OP-41483 was administered three times, hourly (500 ng/kg x 3, i.p.), and 10% glycerol was administered intravenously (6.6 ml/kg) in the same manner as the glycerol treated group. In ischemic controls, saline was administered intravenously (6.6 ml/kg). After 3 h of ischemia, brain water content and metabolites were determined and pathological observation was conducted using electron microscopy. OP-41483 treated animals maintained higher levels of ATP concentration and reduced accumulation of lactate, but showed no difference in brain water content compared to saline treated controls. Glycerol treated animals showed significance in terms of reduction of brain water content and accumulation of lactate. Glycerol abated the depletion of ATP concentration. OP-41483+glycerol treated animals showed the most significant effect on the reduction of brain water content and accumulation of lactate. The combination treatment also maintained higher levels of ATP concentration. Additionally, swelling of astrocytic foot processes and mitochondria with destroyed crista were not observed pathologically in the combination treated animals. These results show that OP-41483, glycerol and combination treatment are beneficial in the treatment of cerebral ischemia. They also indicate that the combination treatment significantly enhances the protective effects compared to individual treatment.

Animals↗

PubMed1992

[Effect of indomethacin on delayed neuronal death of hippocampal CA1 sector in gerbil under different levels of controlled cranial temperatures].

Effect of indomethacin on post-ischemic changes of CA1 neurons was studied in the hippocampus of the Mongolian gerbil. The gerbil was employed because due to poor development of posterior communicating artery ischemia could be easily induced in the forebrain simply by occluding bilateral common carotid arteries. Indomethacin (5 mg/kg, i.p.) was administered 30 min before the occlusion. The occlusion lasted for 5 divided into four groups. In one group, the temperature was not controlled. In the remaining three groups, the temperature was kept at 35.5 degrees C, 37.5 degrees C, and 39.5 degrees C, respectively. Seven days after the occlusion neuronal density was assessed on histological sections stained with hematoxylin eosin. It was found that in all groups indomethacin was effective in preventing delayed neuronal death regardless of the difference in the cranial temperature. However, delayed neuronal death was the least in the lowest temperature group. The drug also prevented the post-ischemic hyperthermia observed in the temperature non-controlled group. These results indicate that indomethacin has its own pharmacological action to prevent delayed neuronal death.

Animals↗

PubMed1992

Parathyroid hormone-related protein as a cause of hypercalcemia in a B-cell type malignant lymphoma.

Hypercalcemia occurred in a patient with non-Hodgkin's (B-cell type) lymphoma when generalized lymphadenopathy developed. Despite low normal plasma parathyroid hormone (PTH), nephrogenous cAMP (NcAMP) was not suppressed, and serum and urine PTH-related protein (PTH-rP) levels were elevated. The plasma level of 1,25(OH)2D was within normal range. The combined chemotherapies successfully reduced the tumor size, serum Ca, PTH-rP, and lactic dehydrogenase. Serum osteocalcin was suppressed while the patient was hypercalcemic, and increased after chemotherapy. In the extract of the tumor tissue obtained post mortem, bioactivity stimulating the production of cAMP in osteoblasts was demonstrated along with the immunoreactive PTH-rP. This is the first report of a B-cell lymphoma producing PTH-rP and its association with humoral hypercalcemia of malignancy.

Aclarubicin↗

PubMed1992

[Endoscopic operation of congenital anterior urethral valve. Application of flexible renoureteroscope for antegrade urethroscopy].

4 children with anterior urethral valve were treated by TUR-Valve. Before TUR, valve anatomy could be easily seen by antegrade urethroscopy through cystostomy using a 10.8Fr caliber flexible renoureteroscope and destruction of the valve could be recognized after TUR. Antegrade urethroscopy with a flexible fiberscope was so helpful to TUR-Valve and the findings of voiding cystourethrography and micturition have remarkably improved. This technique is not so difficult to apply and thought to be one of the best methods to recognize valve anatomy and degree of resection. This technique is also applicable to other lower urinary tract lesions in children.

Adolescent↗

PubMed1992

[MRI of pheochromocytoma--comparison with CT, 131I-MIBG, urinary catecholamine level and operative findings].

16 patients (7 male, 9 female) ranging in age from 13 to 71 (44.1 +/- 18.4) years old with clinically diagnosed pheochromocytoma were prospectively evaluated with CT (N = 16), MRI (N = 16), 131I-MIBG (N = 10) and operative findings in order to evaluate their diagnostic efficacy. 1. Normal adrenal glands appeared less intense than the liver on T1-weighted image (T1WI), less intense than or isointense with the liver on both proton density image (PDI) and T2-weighted image (T2WI). 2. Pheochromocytomas with high urinary noradrenaline level appeared less intense than the liver on T1WI, more intense on T2W1 and showed accumulation of radioisotope on 131I-MIBG scintigraphy. In cases with normal urinary noradrenaline level, they appeared less intense than or isointense with the liver on all pulse sequences (T1WI, PDI and T2WI). 3. Although diagnostic accuracy of localization was 81.3% (13/16) by CT, 93.8% (15/16) by MRI and 90% (9/10) by 131I-MIBG scintigraphy, MIBG scintigraphy showed higher diagnostic ability in cases with multiple lesions or recurrent tumors.

3-Iodobenzylguanidine↗

PubMed1992

[Sequential methotrexate and 5-fluorouracil, doxorubicin, and cisplatin for advanced urothelial cancer].

Twenty cases (fourteen males, six females, mean age 66.0) with locally advanced (T2-4 N0, M0, n = 9) or metastatic (N2-3 or M1, n = 11) urothelial cancer were treated sequentially with methotrexate (MTX) and 5-fluorouracil (5-FU), Doxorubicin (ADM), and cisplatin (CDDP) since August, 1988. Primary tumors were in the bladder in fifteen patients and in the renal pelvis or ureter in five cases. Histological findings were adenocarcinoma in one and transitional cell carcinoma in the other cases. Histological grades were grade 2 in four, grade 3 in fifteen, poorly differentiated adenocarcinoma in one. Seven patients were treated by neoadjuvant chemotherapy. Three were treated for recurrent lesions. Ten were treated for the unresectable disease. The patients received one to four cycles of this regimen (average: 2.8 cycles). Complete clinical response was observed in seven of twenty patients (35%) with measurable indicator lesions. Seven patients (35%) had a partial clinical response. Significant tumor regression was noted in fourteen of twenty patients (70%) in total, in eight of ten (80%) treated with full dose chemotherapy. The group of full dose chemotherapy showed an improved trend in survival rate as compared with the group treated by 80% and less dose chemotherapy. Toxicity was relatively mild, with anemia, leukopenia, thrombocytopenia, and no drug related death. The results suggest that the combined chemotherapy with sequential MTX and 5-FU, ADM, and CDDP is remarkably effective on advanced urothelial cancer.

Adenocarcinoma↗

PubMed1992

Enzymatic assay of inorganic phosphate with use of sucrose phosphorylase and phosphoglucomutase.

We developed a new enzymatic method for the assay of inorganic phosphate (Pi) by using sucrose phosphorylase (SP; EC 2.4.1.7) and phosphoglucomutase (PGM; EC 5.4.2.2). Pi is transferred to sucrose by SP, producing alpha-D-glucose 1-phosphate (G1P) and alpha-D-fructose. G1P is transphosphorylated by PGM in the presence of alpha-D-glucose 1,6-bisphosphate to form alpha-D-glucose 6-phosphate, which is oxidized by NAD+ and glucose-6-phosphate dehydrogenase (EC 1.1.1.49) to form 6-phosphogluconate (6PG) and NADH. Finally, the oxidation of 6PG by NAD+, catalyzed by 6-phosphogluconic dehydrogenase (EC 1.1.1.44), yields D-ribulose 5-phosphate and NADH. Thus two molecules of NADH are formed for each molecule of Pi, and the reaction is monitored at 340 nm. The Km values of SP for Pi and sucrose were 4.44 and 5.31 mmol/L, respectively. The best buffer was 1,4-piperazinediethanesulfonic acid (PIPES) at 50 mmol/L and pH 6-7. Implementing this method with a Cobas-Bio centrifugal analyzer allowed us to measure Pi accurately and precisely.

Buffers↗

PubMed1992

[Reconstructive surgery for mitral regurgitation caused by degenerative disease--indications for expansion and early clinical outcomes].

Between January 1983 and June 1990, there were 48 patients who underwent surgery for mitral regurgitation due to degenerative diseases. Among these, 20 patients received mitral valve repair. Overall operative mortality was 5% for patients who underwent valve repair, and 7.1% for those who underwent valve replacement. We standardized a maneuver for valve repair in August 1988 in an attempt to expand its indications. There were 35 patients who underwent surgery prior to that date (group 1), and 13 patients after that date (group 2). There were nine patients (25.7%) in group 1 and 2 patients (84.6%) in group 2 who underwent valve repair. Among these, one patient (11%) in group 1 died within 30 days after the operation, but there were no surgical deaths for any patients in group 2. In addition, one patient (11%) in group 1 and one (9%) in group 2 required another operation for valve replacement. Doppler echocardiographic studies performed postoperatively in 18 patients who had undergone valve repair showed that 13 (72.2%) had no regurgitation, 4 (22.2%) had trivial regurgitation, and 1 (5.6%) had mild regurgitation. Postoperative valve area as determined by continuous-wave Doppler echocardiography was 3.7 +/- 1.1 cm2 (mean +/- SD) for patients who had undergone reconstruction and 3.1 +/- 0.7 cm2 for those who had undergone replacement.

Adolescent↗

PubMed1992

Secondary injury and acidosis.

Following traumatic brain injury, cells that are not directly, and thereby irreversibly damaged are subjected to ionic fluxes including potassium and calcium. This injury-induced ionic flux is a result of both neuronal firing via direct mechanical stimulation of the neurons as well as the activation of ligand-gated ion channels primarily associated with excitatory amino acids (e.g. glutamate). This ionic destabilization places enormous energy demands on these cells in order to activate pumping mechanisms to reinstate normal ionic balance. The primary fuel used to acquire this energy is glucose, which results in a period of hyperglycolysis leading to the accumulation of lactate. This acute period of increased glucose metabolism lasts only during the acute period, after which these same cells exhibit a state of chronic metabolic depression for both glucose and oxygen. This metabolic derangement may prevent the necessary energy production for maintaining cellular protein synthesis which is inhibited following traumatic brain injury. This injury-induced metabolic derangement is not uniform throughout all regions. Some structures are more or less affected presumably due to their proximity to the site of trauma and/or to the extent to which they have a preponderance to being more vulnerable to insult. Within these affected regions, the metabolic dysfunction indicates that cells are functionally compromised in their ability to respond to both normal physiologic and pathophysiologic challenges. This results in the expression of neurological deficits and an enhanced vulnerability of these cells to a second insult, both of which dissipate as normal metabolic function returns over time.

Acidosis↗