Biomedical subjects

Y Katayama

Publications and source records attributed to Y Katayama.

At least 19 recordsLinked to original sources

PubMed1992

Functioning ovarian carcinoids induce severe constipation.

Five patients with ovarian carcinoid who had severe constipation for a long period preoperatively showed marked reduction of this symptom postoperatively. Because this phenomenon was believed to be caused by some biologically active substance rather than a mechanical effect of the tumor, reactivity to 17 amine and peptide hormones was studied immunohistochemically in these patients. Numerous peptide YY (PYY)-positive cells were detected, with PYY-positive cells representing more than 50% of all carcinoid tumor cells in each patient. PYY, which has a pharmacologic inhibitory action on intestinal motility, was presumably the cause of the constipation in these patients.

Adult↗

PubMed1992

Enduring suppression of hippocampal long-term potentiation following traumatic brain injury in rat.

This study investigated changes in synaptic responses (population spike and population EPSP) of CA1 pyramidal cells of the rat hippocampus to stimulation of the Schaffer collateral/commissural pathways 2-3 h after traumatic brain injury (TBI). TBI was induced by a fluid percussion pulse delivered to the parietal epidural space resulting in loss of righting responses for 4.90-8.98 min. Prior to tetanic stimulation, changes observed after the injury included: (1) decreases in population spikes threshold but not EPSP thresholds; (2) decreases in maximal amplitude of population spikes as well as EPSPs. TBI also suppressed long-term potentiation (LTP), as evidenced by reductions in post-tetanic increases in population spikes as well as EPSPs. Since LTP may reflect processes involved in memory formation, the observed suppression of LTP may be an electrophysiological correlate of enduring memory deficits previously demonstrated in the same injury model.

Animals↗

PubMed1992

Excitatory amino acid antagonist administered via microdialysis attenuates lactate accumulation during cerebral ischemia and subsequent hippocampal damage.

Our previous studies have shown that kynurenic acid (KYN), a broad-spectrum antagonist of excitatory amino acids (EAAs), administered in situ through a dialysis probe can delay the massive ionic fluxes in the rat hippocampus during cerebral ischemia. The present experiments demonstrated that the same procedure attenuates the increase in extracellular concentration of lactate ([lactate]e) during ischemia as measured by microdialysis. This finding suggests that the lactate accumulation is partially caused by a sudden increase in energy demand due to the rapid ionic fluxes through EAA-coupled ion channels. This inference is consistent with the hypothesis that the earlier ionic event during ischemia is a cause of energy depletion, rather than the result merely of energy failure. The present experiments also revealed that KYN administered by the same procedure attenuates death of hippocampal CA1 pyramidal cells after 5-min transient ischemia in gerbils. Since lactate accumulation is likely to be an important factor affecting cell viability, the protective effect of KYN may be attributable, in part, to inhibition of lactate accumulation.

Amino Acids↗

PubMed1992

A thiocyanate hydrolase of Thiobacillus thioparus. A novel enzyme catalyzing the formation of carbonyl sulfide from thiocyanate.

A thiocyanate hydrolase that catalyzes the first step in thiocyanate degradation was purified to homogeneity from Thiobacillus thioparus, an obligate chemolithotrophic eubacterium metabolizing thiocyanate to sulfate as an energy source. The thiocyanate hydrolase was purified 52-fold by steps involving ammonium sulfate precipitation, DEAE-Sephacel column chromatography, and hydroxylapatite column chromatography. The enzyme hydrolyzed 1 mol of thiocyanate to form 1 mol of carbonyl sulfide and 1 mol of ammonia as follows: SCN- + 2H2O----COS + NH3 + OH-. This is the first report describing the hydrolysis of thiocyanate to carbonyl sulfide by an enzyme. The enzyme had a molecular mass of 126 kDa and was composed of three different subunits: alpha (19 kDa), beta (23 kDa), and gamma (32 kDa). The enzyme exhibited optimal activities at pH 7.5-8.0 and at temperatures ranging from 30 to 40 degrees C. The Km value for thiocyanate was approximately 11 mM. Immunoblot analysis with polyclonal antibodies against the purified enzyme suggested that it was induced in T. thioparus cells when the cells were grown with thiocyanate.

Blotting, Western↗

PubMed1992

Early cellular swelling during cerebral ischemia in vivo is mediated by excitatory amino acids released from nerve terminals.

This study demonstrates ischemic cellular swelling in vivo detected as changes in the concentration of 14C-sucrose pre-perfused into the extracellular space (ECS) as an ECS marker. Microdialysis was utilized as a means of perfusion and measurement of the extracellular concentration of 14C-sucrose ([14C-sucrose]e). Concomitant with an abrupt increase in [K+]e at 1-3 min following the ischemia induction, [14C-sucrose]e was also rapidly elevated. Since sucrose is not taken up by either cells or capillaries, the absolute amount of 14C-sucrose in the ECS must be unchanged. The increase therefore appears to represent a relative decrease in water volume in the ECS resulting from a movement of water into the cells, i.e. cellular swelling. Ca(2+)-free perfusate containing Co2+, which has been shown to block excitatory amino acid release during cerebral ischemia, significantly delayed the increase in [14C-sucrose]e and [K+]e. Kynurenic acid, a broad-spectrum antagonist of excitatory amino acids, administered in situ through the dialysis probe also significantly delayed the increase in [14C-sucrose]e and [K+]e. These findings indicate that the early cellular swelling occurring during cerebral ischemia is a result of massive ionic fluxes mediated by excitatory amino acids which are released by a Ca(2+)-dependent exocytotic process from the nerve terminals.

Amino Acids↗

PubMed1992

A homogeneous assay system of aspartate aminotransferase iso-enzymes using proteases and application for clinical evaluation of myocardial infarction.

We designed a rapid, homogeneous assay for human aspartate aminotransferase (AST) isoenzymes, by a selective proteolysis of soluble AST (s-AST), using chymotrypsin and protease 401. The linearity of mitochondrial (m-AST) was elongated up to 4000 U/l. m-AST values from the human liver, and determined by a homogeneous assay using protease 401 or chymotrypsin, were relative to those obtained using an immunoprecipitation method. In perioperative patients or those with an acute myocardial infarction, the peaks of s-AST and m-AST values were noted 13 h and at 57 h after ictus, respectively, whereas the peak of ratio between was seen 6 h after ictus. In the case of Budd-Chiari syndrome, the maximum levels of the two AST activities were evident 14 days after hospitalization and the peak of ratio between them was seen after 7 days. We propose that this homogeneous assay can serve as a diagnostic tool for early phase detection of myocardial infarction and of Budd-Chiari syndrome.

Adult↗

PubMed1992

A new method for determination of urinary citrate.

We have developed a new assay technique using high-performance liquid chromatography. The assay was performed at a flow rate of 0.7 ml/min, a temperature of 60 degrees C and an ultraviolet absorption of 214 nm. Comparison of the results of the new assay with the results obtained for identical samples using the conventional fluorometric method demonstrated a very high correlation coefficient of 0.931.

Adult↗

PubMed1992

Intraparenchymal blood-fluid levels in traumatic intracerebral haematomas.

Blood-fluid levels within the cerebral parenchyma are observed more frequently on CT and MRI in traumatic intracerebral haematomas than in those of other aetiologies. The intraparenchymal blood-fluid interface can be formed without a fluid cavity. It is suggested that the blood-fluid levels represent layering of red blood cells within areas of contusion necrosis as well as extensive contusion oedema. The more extensive the damage to brain tissue, the more often blood-fluid levels formed. A poorer outcome can be therefore predicted when an intraparenchymal blood-fluid interface is seen.

Arteriovenous Malformations↗

PubMed1992

Differential diagnosis of adrenal tumour and upper pole renal tumour by I-131 cholesterol adrenocortical scintigraphy.

A 27-year-old housewife with right hypochondralgia was admitted for treatment of a huge right adrenal or upper pole renal tumour. The tumour measured 10 x 8 x 8 cm and was hypovascular. The main blood supply derived from the right adrenal artery which originated from the abdominal aorta just proximal to the right renal artery. Although several diagnostic imaging studies suggested that the tumour arose from the right adrenal gland, the bilateral adrenal glands were equally visualized on I-131 cholesterol adrenocortical scintigraphy. After surgery and pathological examination, the tumour proved to be a renal cell cancer, while the right adrenal gland was intact. This case demonstrates that adrenocortical scintigraphy is useful in the differentiation of adrenal and renal tumours when a large tumour occupies the upper pole of the kidney or adrenal gland.

Adrenal Gland Neoplasms↗

PubMed1992

Growth of a giant aneurysm following complete thrombosis by detachable balloon occlusion.

A giant basilar artery aneurysm demonstrating growth and causing neurological deterioration even after complete detachable balloon occlusion is reported. Autopsy revealed total thrombosis of the aneurysm and a hemiconcentric, onion skin-like, laminated structure. Numerous vascular channels and multiple fresh intramural hemorrhages were noted within the outer margin of the aneurysmal wall. Repeated intramural hemorrhages appeared to have been responsible for the aneurysmal laminated structure and contributed to progressive aneurysmal growth. This case demonstrates that the growth of some giant aneurysms is not dependent upon the continuity with the parent artery, and progressive enlargement cannot always be prevented by balloon occlusion.

Basilar Artery↗

PubMed1992

Primary Ewing's sarcoma of the temporal bone.

Primary cranial Ewing's sarcoma is exceptionally rare. Only ten cases of such a tumor had been reported heretofore in the literature. We describe a case of primary Ewing's sarcoma occurring in the temporal bone. The tumor was surgically excised, and the patient underwent radiation and chemotherapy. Neither recurrence nor distant metastasis was noted at 12 months after surgery. Although the prognosis of Ewing's sarcoma in general is often poor because of early metastasis to the lungs and/or to other bones, a review of the literature suggested that the same tumor occurring in the cranium can often be successfully managed by intensive therapy with radical excision and radiochemotherapy. This inference was supported by the case reported here.

Adult↗

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↗