Biomedical subjects

S Miyazaki

Publications and source records attributed to S Miyazaki.

At least 541 records · Page 30Linked to original sources

PubMed1991

[Blind ending bifid ureter with stone in the blind branch: report of a case].

Blind ending bifid ureter is a rare anomaly in the urinary tract. This anomaly may result from failure of a premature branch of the ureteral bud to join with the metanephric blastema. A 21-year-old man was admitted with macroscopic hematuria and colic pain in the left flank region. Urinalysis demonstrated hematopyuria and excretory urography suggested bifid ending accessory ureter with a stone on the left side. Surgical exploration showed that the accessory ureter was bifurcated from the left ureter at about 5 mm from the bladder wall and ran parallel with the left ureter. Although dense adhesions to the surrounding tissue existed, the accessory ureter was resected at the site of the junction. It measured 3 cm in length and 1 cm in greatest diameter. The stone found at the tip of the accessory ureter was composed of calcium oxalate (24%) and calcium phosphate (76%). Histological examination revealed that the ureter had all layers of normal ureteral structure and no renal tissue was identified in the specimen resected. During a follow-up period of 22 months after the operation, he was free of urinary tract infection and abdominal pain. Of 77 cases with blind ending bifid ureter reported in the Japanese literature, a ureteral stone was found in the blind branch in only 5 cases.

Adult↗

PubMed1991

Monoclonal anti-A and anti-A,B antibodies from a mouse immunized with A secretor saliva.

Using spleen cells from a mouse immunized with blood group A secretor saliva, we obtained 3 monoclonal anti-A antibodies (3H9, 5C6, 4D8) and 1 monoclonal anti-A,B antibody (2D10). In agglutination tests against red cells of A subgroups, 3H9 gave similar results to human anti-A serum, and 2D10 reacted with both A and B cells. 5C6 agglutinated especially A1 cells, while 4D8 showed stronger agglutination of A2 cells than the other antibodies. Using these antibodies, it is possible to distinguish the subgroups of A. The 4 antibodies had no reactivity with the red cells of 6 animal species and nonhuman primates except for group A anthropoid apes. All 4 antibodies were negative with Cad-positive, sheep and papain-treated O red cells that are agglutinated by the A-cell-reactive lectins. The activity of 3H9 was inhibited by A secretor saliva and that of 2D10 by both A and B secretor salivas. 4D8 showed a weak reaction with A secretor saliva. Antibody 5C6 was inhibited rather strongly even by A nonsecretor saliva. Thus, 5C6 is useful for application to test specimens in legal medicine, such as examination of blood or salivary stains for A antigens.

ABO Blood-Group System↗

PubMed1991

[Ultrastructural findings of arachnoid cysts and epithelial cysts].

There may be several kinds of pathological conditions in the cystic lesion which are clinically diagnosed as benign intracranial cysts on CT scan. Light and electron microscopic studies on cyst walls were important in the differential diagnosis of benign intracranial cysts. We have studied 5 cases of intracranial arachnoid cysts and two epithelial cysts using the light and electron microscopy. Five cases of intracranial arachnoid cysts included two children and three adults (three females and two males). Three cases of them were localized in the middle cranial fossa, one case in the anterior and middle cranial fossa and one case in the lateral ventricle, giving headache and convulsion as the initial complaints. As for the epithelial cysts, one was localized at the para-collicular area complaining enlarged head and swollen anterior fontanelle and the other of four years was located in the fourth ventricle with headache and ataxic gait. On CT all of them demonstrated diffuse low density areas in both the arachnoid and the epithelial cysts without communicating findings between the cystic cavities and subarachnoid space on metrizamide CT cisternography. The arachnoid cyst walls were basically similar in structure to the normal arachnoid membrane and composed of elongated epithelial cells like the arachnoid cell and the connective tissues with lamellar collagen fiber bundles. However, 3 of the 5 cases had only fibrous tissues without epithelial cells. The inner sheath of the arachnoid cyst walls was composed of one or several layers of the arachnoid cells with flattened and relatively electron-dense cytoplasm on electron micrograph. They had a lot of elongated process and were tangled with each other, making large extracellular spaces between them. Below the electron dense arachnoid cells, compact packed cells with interdigitation partly demonstrated intercellular contacts such as numerous desmosomes and tight junctions. In those intercellular spaces collagen fibers and microfibrils were observed. The cells contained abundant cytoplasmic microfibrils and numerous organelles. They were separated from numerous collagen fibers and fibroblasts by non continuous basal lamina under the epithelial cells. Epithelial cyst wall had a layer of cuboidal or columnal epithelium in the inner layer of cyst wall. Those epithelial cells demonstrated granules having positive in PAS and mucicarmine stain in their cytoplasm. On electron microscopical study epithelial cells revealed a lot of microvilli and coating materials on the surface of them without cilia. The basement membranes were well developed under the epithelial cells separated from the connective tissues. In the intercellular clefts of the epithelial cells tight junctions and interdigitations were recognized.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1991

[Diagnosis of adrenal diseases focusing on morphological and endocrinological viewpoints].

The recent advances in the diagnosis of adrenal diseases owe much to the rapid progress in radiological and endocrinological areas. The former is ascribed to the progress of medical electronics. The latter has been realized by the development, improvement and spread of the measurement of a very small amount of hormones or hormone-like substances in blood, urine or tissues, supported by the improvement of measurement instruments as well as the immunoassay or chemical assay techniques. This paper reviews approaches to diagnosis of adrenal diseases causing hypertension and asymptomatic, incidentally discovered adrenal tumors. Incidentally discovered adrenal tumors have increased owing to the spread of medical electronic instruments such as abdominal ultrasonography (US), computed tomography (CT) and magnetic resonance imaging (MRI). Discrimination of malignancy is an important clinical concern. More than 90% of the tumors reported in the Japanese were larger than 3 cm in diameter. The diagnosis of primary aldosteronism has been made by the measurement of plasma renin and aldosterone, CT and 131I-cholesterol scintigraphy. However the differential diagnosis of adrenal adenoma from bilateral adrenal hyperplasia has remained as a problem. There were a few patients in whom adrenal adenomas appeared after 2-3 years' follow-up period. In Cushing's syndrome, tumors are found with ease by US, CT and MRI. The diagnosis of pheochromocytoma is made mainly by urinary catecholamines and metabolites including metanephrine, normetanephrine and VMA. US, CT and MRI are very useful. Diagnosis and discovery of metastasis will be more reliably made when 131I-MIBG comes to the clinical stage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Gland Diseases↗

PubMed1991

[Studies on retroperitoneal lymph node dissection concerning postoperative ejaculatory function in patients with testicular cancer].

This study was done to explore the appropriate procedure of retroperitoneal lymph node dissection (RLND) to preserve ejaculatory function. The relation between postoperative ejaculatory function and area dissected at RLND was investigated in 47 patients with testicular cancer. The patients were divided into 5 groups according to the retroperitoneal area dissected. Group 1 (38 patients) underwent bilateral RLND, group 2 (3 patients) and 3 (2 patients) right unilateral RLND, and group 4 (2 patients) and 5 (2 patients) left unilateral RLND. The vertical limits of the dissected area were similar in all groups, namely renal pedicle and bifurcation of common iliac artery. The lateral limits were bilateral ureters in group 1, right border of aorta and right ureter in group 2, left border of aorta and left ureter in group 4, and vena cava and left ureter in group 5. Group 3 was similar to group 2, but the paraaortic region at the root of inferior mesenteric artery was also dissected. All patients in group 1 had dry ejaculation. Thirty patients in this group were examined for seminal emission and none of them could demonstrate seminal emission. Normal antegrade ejaculation was seen in group 2 and 4 patients, but retrograde ejaculation was recognized in group 3. Inability of seminal emission ws confirmed in group 5 patients. When consideration is given to the function of retroperitoneal sympathetic nerves, our results suggest that unilateral RLND without impairing superior hypogastric plexus should be adopted to preserve ejaculatory function.

Adolescent↗

PubMed1990

[Release mechanisms of inactive renin from rat renal cortical slices: role of the submandibular gland].

In our previous studies, we showed an in vivo stimulating effect of the extract of the rat submandibular gland on plasma inactive renin release. In this study, we evaluated the effects of the rat submandibular gland extract and of some plasma active renin stimulants on inactive renin release from rat renal cortical slices. Adult male Wistar rats (250-350g) were kept on a regular diet (Na 260mg/100g) and nephrectomized under pentobarbital anesthesia (50mg/kg, i.p.). Five thin renal cortical slices were obtained from each kidney by using a razor blade. These renal cortical slices were incubated in Earle's buffer (pH7.4, Difco) at 37 degrees C for 30 min (preincubation), then transferred into 10ml fresh Earle's buffer with or without some agents and incubated at 37 degrees C for 1 hour (experimental incubation). For each experiment, 6 groups of 5 renal cortical slices were employed. The agents used in this study were as follows: isoproterenol (10(-5)M), furosemide (50 micrograms/ml), prostaglandin E1 (10(-5)M), prostaglandin I2 (10(-5)M) and the rat submandibular gland extract (100 microliters) which was obtained after homogenation with 10 x (w/v) 0.01M pyrophosphate buffer (pH6.5) including 0.1M NaCl. One ml of samples of this Earle's buffer were withdrawn every 20 min. Active renin in the samples was assayed by the commercial RIA-kit (Dainabot), and total renin was assayed after trypsin (Worthington) treatment (30 micrograms/300 microliters sample) at 4 degrees C for 10 min. Inactive renin was determined as the difference between total renin and active renin. Active and inactive renins increased linearly in the buffer without any agents (control) during the observation period (60 min). Isoproterenol (10(-5)M) stimulated the release of active renin significantly (p less than 0.01 vs. control) but did not affect the release of inactive renin. Furosemide (50 micrograms/ml) stimulated the release of active and inactive renins significantly at 20 and 40 min (p less than 0.05 vs. control) but did not affect the release of either renin at 60 min. Both prostaglandins E1 and I2 (10(-5)M) stimulated the release of active renin significantly (p less than 0.01 vs. control) but inhibited, on the other hand, the release of inactive renin significantly (p less than 0.01 vs. control). The rat submandibular gland extract (100 microliters) did not affect the release of active renin but stimulated the release of inactive renin significantly (p less than 0.05 vs. control).(ABSTRACT TRUNCATED AT 400 WORDS)

Alprostadil↗

PubMed1990

[Roles of the kidney in activation and release of plasma inactive renin in the rat].

Plasma inactive as well as active renin is supposed to originate from the kidney, though there is little direct evidence. As we have previously reported (Sakanaka et al., Folia Endocrinol. Jap., 63: 961-977, 1987; Miyazaki et al., J. Hypertension 4 (Suppl 6): S453-S455, 1986; Miyazaki et al., J. Hypertension 6: 33-40, 1988), the submandibular gland, but not the kidney, is thought to play an crucial role in releasing plasma inactive renin in the rat. In the present acute studies, we attempted to elucidate the roles of the kidney in the release mechanisms of plasma inactive renin. Adult male rats maintained on a regular rat chow (Na: 260 mg/100g) were uninephrectomized, and vessel clips were placed on the renal pedicles of the contralateral kidneys to make completely ischemic and non-filtered kidneys. In the first protocol, the renal pedicles were occluded for 2 h, followed by the removal of the vessel clips. During the occlusion for 2 h, plasma active renin concentration (PAC) in the peripheral blood obtained from the femoral cannulae decreased, while plasma inactive renin concentration (PIC) along with plasma total renin concentration (PTC) increased as in the case of total nephrectomy, which supports our previous studies. Then, declipping resulted in the rapid rise in PAC with the peak values at 2 min, which was followed by its gradual decrease with time during the experimental period (30 min). On the other hand, PIC decreased gradually toward control levels with no rise after declipping. In the second protocol, blood trapped in the kidney was collected through the renal venous cannulae at 0, 60, 120 and 240 min after the pedicle occlusion in the different groups of rats. The renal blood levels of PAC increased by more than three times at 240 min compared to the control values, while PIC decreased to one third of the control values. PTC increased at 120 and 240 min. Renal tissue levels of renin were also measured at 0 and 120 min in the second protocol in the kidneys of rats which were maintained on a regular rat chow. Inactive renin concentration increased, while active renin concentration decreased. These were compatible with the results obtained in plasma. In the last protocol, the second protocol was in part repeated in salt-depleted rats which were kept on a low salt diet (Na: 11.3 mg/100g) for 2 weeks.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1990

[Role of the submandibular glands in in vivo mechanisms of plasma inactive renin release in the rat].

In our present studies, we evaluated the role of the submandibular glands (SMG) on plasma inactive renin (PIR) releasing mechanisms in rats using some agents which are known to stimulate plasma active renin (PAR) release. The results were analyzed between sialoadenectomized (SX) and sham-operated (control: C) rats. Twenty-four h after the operation, PAR releasing agents, furosemide (FRO) 2.5 mg/rat/h with prior iv bolus 5 mg, captopril (CAP) 5 mg/rat/h with prior iv bolus 10 mg, 1-Sar-8-Ile-angiotensin II (Ang II A) 300 ng/kg/min, prostaglandin E1 (PGE1) 100 ng/kg/min, and prostaglandin I2 (PGI2) 100 ng/kg/min, were infused through femoral venous cannulae. Blood samples were taken through femoral arterial cannulae into test tubes containing 2 mg EDTA-2Na. PAR was assayed by RIA, and total renin was obtained after tryptic activation. According to the responses of PIR, the agents used were categorized into three patterns: FRO increased PIR, both PGs lowered PIR, and, CAP and Ang II A had no effect on PIR release. The PIR release mechanisms by FRO were further investigated by 20 mg FRO ip injection in totally nephrectomized rats. PIR increased even in nephrectomized rats, but the increase was totally canceled by the following SX. In conclusion, FRO alone among some agents studied is able to stimulate PIR release only under the existence of SMG.

Angiotensin II↗

PubMed1990

[Combination chemotherapy with methotrexate, vincristine, cis-platinum, cyclophosphamide, adriamycin, and bleomycin: MVP-CAB for disseminated urological cancer].

Twenty-eight evaluable patients with disseminated measurable malignancies of the genitourinary organs except testicular cancer were treated with MVP-CAB, between May 1985 and June 1988. Chemotherapy was given at 3 to 4 week intervals, as follows. On day 1, methotrexate 20 mg/m2, vincristine 0.6 mg/m2, cyclophosphamide 500 mg/m2, adriamycin 20 mg/m2, and bleomycin 30 mg/body were administered. On day 2, cis-platinum 50 mg/m2, on day 1 to 3, prednisolone 20 mg/body were also administered. The administration of bleomycin and adriamycin were limited to 90 mg/body and 400 mg/m2. The median age was 59 years. The median follow-up duration was 11 months. The primary lesions were urothelial tract cancer (19 patients), malignant lymphoma (1 patient), renal cell adenocarcinoma, penile cancer, prostatic adenocarcinoma, and leiomyosarcoma (2 patients each). CR was observed in 2 patients, and PR in 11 patients with urothelial tract cancer. The overall response rate was 68% (13/19). The response rates in primary and metastatic lesions were 56% (5/9) in primary, 73% (8/11) in lymph node, 71% (5/7) in lung, 67% (2/3) in liver, and 20% (1/5) in bone. The median duration of survival in the responders was 13.5 months, and in the non-responders was 5 months. The 1 year survival rate by Kaplan-Meier method was 70% in responders. On the other hand, the longest survival time in non-responders was 9 months. Marked improvement of survival time was noted in the responders. PR was observed in 1 patient with malignant lymphoma, prostatic adenocarcinoma, and leiomyosarcoma in each. The main toxic effect of MVP-CAB was bone marrow suppression. Leucopenia (WBC less than 4,000/mm3) was noted in 24 patients (86%), and 16 patients (57%) had a WBC count nadir below 2,000/mm3. Thrombocytopenia (plt less than 10 x 10(4)/mm3) was noted in 10 patients (36%). However, there were no deaths due to the bone marrow suppression.

Adult↗

PubMed1990

Oedema fluid formation within contused brain tissue as a cause of medically uncontrollable elevation of intracranial pressure: the role of surgical therapy.

In patients with focal cerebral contusions, medical therapies have generally been advocated unless haemorrhages significantly contributing to the elevated intracranial pressure (ICP) exist. We report here several lines of clinical evidence which indicate that (1) enormous amount of extracellular oedema fluid is formed within contused brain tissue, (2) the formation of extracellular oedema fluid within contused brain tissue alone can be a cause of medically uncontrollable elevation of ICP and (3) surgical excision of the contused brain tissue provides excellent control of the elevated ICP in such patients. The excision of contused brain tissue appears to be the only therapy currently available to alleviate the formation of extracellular oedema fluid in cerebral contusions. We believe that, if ICP is elevated primarily by extracellular oedema due to cerebral contusions and the elevated ICP is medically uncontrollable, surgical excision of contused brain tissue should be carried out without delay regardless of the size of associated haemorrhages.

Body Fluids↗

PubMed1990

Survival and fibre outgrowth of neuronal cells transplanted into brain areas associated with interstitial oedema.

The influence of interstitial oedema on the survival of fetal raphe cells transplanted into serotonin (5-HT)-denervated rats and the fibre outgrowth from these cells was investigated. Fetal raphe cells were transplanted into the corpus callosum in which long-lasting interstitial oedema had been induced by intracisternal kaolin injection. The 5-HT and 5HIAA levels in the corpus callosum were restored to their maximum within 5-6 weeks post-transplantation regardless of whether interstitial oedema was induced or not. Furthermore, it was appeared that the presence of interstitial oedema even facilitated fibre growth as demonstrated by the 5-HT immunohistochemistry and the restoration of the 5-HT and 5-HIAA levels in brain areas distant from the transplantation sites. These results imply favourable effects of interstitial oedema on the survival of transplanted raphe cells and their fibre outgrowth.

Animals↗

PubMed1990

Hyperammonemia caused by impaired mitochondrial ornithine transport in a patient with partial quantitative deficiency of ornithine carbamoyltransferase.

Late-onset hyperammonemia was observed in a male patient with partial quantitative deficiency of ornithine carbamoyltransferase (OCT). His liver contained 10% of the normal level of OCT, but with normal kinetics. This reduced enzyme activity alone, however, could not explain the hyperammonemia. Therefore, the effects of impaired ornithine transport into mitochondria, which seemed to be a possible precipitating factor, were examined by numerical simulation of the urea cycle. The results were as follows: (a) On the assumption that the ornithine concentrations in the cytosol and mitochondrial matrix were always equal, the ammonia handling efficiency would be unchanged by decrease in the OCT concentration to 10% of normal; (b) Under conditions of impaired mitochondrial ornithine transport that had no effects on ureagenesis with a normal amount of enzyme, 10% of the normal concentration of enzyme would impair ammonia handling efficiency. Thus, impaired mitochondrial ornithine transport seemed to cause hyperammonemia in the state of partial quantitative deficiency of OCT in this case.

Adolescent↗

PubMed1990

Facilitated growth of transplanted raphe cells in hydrocephalic interstitial edema.

Fetal raphe cells were transplanted into the anterior corpus callosum (CC) of serotonin (5-HT)-denervated hydrocephalic rats. The levels of 5-HT and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), were measured in the anterior and posterior parts of the CC at 1-2, 5-6, and 7-8 weeks posttransplantation. The 5-HT and 5-HIAA levels in the anterior part were restored to their maximum within 5-6 weeks posttransplantation in both hydrocephalic and nonhydrocephalic rats. In contrast, the 5-HT and 5-HIAA levels in the posterior part continued to increase for the period beyond 5-6 weeks posttransplantation. The longer time course of the restoration in the posterior part may reflect the time for fiber growth from the site of transplantation to remote brain areas. Hydrocephalic rats showed slightly higher levels of 5-HT (154.4%) and 5-HIAA (159.5%) in the anterior part, and markedly higher levels of 5-HT (254.8%) and 5-HIAA (388.7%) in the posterior part at 5-6 weeks posttransplantation, compared with nonhydrocephalic rats. These results imply favorable effects of interstitial edema associated with hydrocephalus on the survival of transplanted raphe cells and fiber outgrowth.

Animals↗

PubMed1990

A nicked beta-subunit of human chorionic gonadotropin purified from pregnancy urine.

Human chorionic gonadotropin (hCG) is a glycoprotein hormone composed of two dissimilar subunits (alpha and beta) and normally excreted in urine of pregnant women. An uncommon beta-subunit of hCG was purified from fresh early normal pregnancy urine by Sepralyte C8, resin adsorption. Sephadex G-100 column chromatography, and reverse-phase HPLC. SDS-PAGE under non-reducing conditions showed that the apparent molecular weight (39,000) of this beta-subunit was extremely similar to that of the native beta-subunit, which is known to consist of 145 amino acid residues and carbohydrates. However, SDS-PAGE, under reducing conditions, resulted in two bands with apparent molecular weights of 22,000 and 18,000, indicating that it consisted of two peptide fragments connected with disulfide bridge(s). These two peptide fragments, separated and purified from the reduced and carboxymethylated protein, were subjected to amino acid and N-terminal sequence analyses. It was found that this beta-subunit consisted of two polypeptide chains composed of residues 1-47 disulfide-bridged to residues 48-145 of the beta-subunit, which may be produced by nicking of the beta-subunit at the one site (Gly47-Val48). This beta-subunit was termed a nicked beta-subunit of hCG (N-hCG beta). It was also found that N-hCG beta was present in urine as an alpha beta dimer, indicating that an intrachain nicking of this site in the beta-subunit does not inhibit alpha beta dimer formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMed1990

Clinical value of magnetic resonance imaging for cervical myelopathy.

The magnetic resonance imaging (MRI) findings in 115 cases of cervical myelopathy, 121 cases of cervical radiculopathy, and 64 cases of neck pain with no neurologic deficit were prospectively studied to investigate the clinical value of MRI for cervical myelopathy. The MRI findings in the T1-weighted sagittal projection were classified into four groups according to the degree of the compressed deformities of the cervical cord. The degree of compression of the cervical cord on MRI findings showed a significant correlation with the severity of myelopathy, the anteroposterior diameter of the spinal column, and the degree of compression of the dural tube in the myelograms (P less than 0.01). Fifty-one patients of cervical myelopathy had undergone both preoperative and postoperative MRI. Of these, the spinal canal of 47 patients that was well decompressed was recognized according to plain computed tomography (CT). However, 24 (51%) of these 47 patients showed on MRI a deformity in the spinal cord amounting to cord atrophy. The correlation between the clinical function of the spinal cord and the recovery of the cord deformity on MRI at the operative levels was accurately investigated in 34 patients who had no cord deformities in the adjacent intervertebral levels. Twenty patients with cord atrophy had slightly poor clinical results, although no significant difference was found between these 20 and 14 patients with recovery in the cord deformities. From these results, it was evident that T1-weighted MRI is useful in the accurate diagnosis of compression myelopathy, in accurately deciding the level of the disease focus, and in the accurate assessment of the surgical results.

Cervical Vertebrae↗

PubMed1990

Treatment of pediatric malignant tumors with VP-16. West Japan Pediatric Oncology Group.

The West Japan Pediatric Oncology Group studied the treatment of pediatric malignant tumors with VP-16 from December 1984 to March 1988. Study subjects were divided into two groups. One group received only VP-16, while the other received VP-16 combined with other anti-tumor agents. VP-16 evaluation was possible in a total of 116 cases. The efficacy rate was calculated by considering both complete and partial remission as effective. The efficacy rate for VP-16 alone was 87.5% for primary cases of ANLL and 100% for primary cases of histiocytosis. The efficacy rates for combination therapy were as follows: 92.6% for primary cases of ANLL, 66.7% for primary cases of histiocytosis, 45.5% for relapsed cases of ANLL and 66.7% for relapsed cases of ALL. Bone marrow suppression was seen in the form of leukopenia and thrombocytopenia for 2 to 3 weeks after VP-16 administration. Alopecia, mucositis and gastrointestinal symptoms were also observed, but they presented no significant problem. From our results, we believe that chemotherapy including VP-16 is effective for remission induction therapy in primary cases of ANLL and for salvage therapy in relapsed leukemia. Additionally, VP-16 is considered to be effective for the treatment of histiocytosis.

Adolescent↗

PubMed1990

Synergistic activation by serotonin and GTP analogue and inhibition by phorbol ester of cyclic Ca2+ rises in hamster eggs.

1. Synergistic activation of a GTP-binding protein (G protein) by external serotonin (5-hydroxytryptamine, 5-HT) and internally applied guanosine-5'-O-(3-thiotriphosphate (GTP gamma S) in hamster eggs was demonstrated by the facilitation of repetitive increases in cytoplasmic Ca2+ as measured by their associated hyperpolarizing responses (HRs) and by aequorin luminescence. 2. Rapid application of 70 nM-5-HT caused a single HR of 10-12 s duration and with a delay of 80 s. The critical concentration of 5-HT to cause an HR was 50 nM. 3. With 10 microM-5-HT four to six HRs were often elicited with a delay to the first HR of 8-30 s. HRs disappeared after prolonged or repeated application of 5-HT, indicating an apparent desensitization. 4. 5-HT-induced HRs were completely inhibited by the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (TPA) (100 nM). Conversely, the PKC inhibitor sphingosine (2 microM) enhanced the series of HRs by shortening the delay to the first HR (3-9 s) and by causing more HRs. 5. Ionophoretic injection of GTP gamma S into the egg usually produced a large HR with a delay of 120-240 s followed by a series of much smaller HRs. When 5-HT was applied within 1 min of injection of GTP gamma S. 70 nM-5-HT induced a number of large HRs and even 1 nM-5-HT could induce HR(s). In contrast, when 5-HT was applied after the size of GTP gamma S-induced HRs had declined, as much as 10 microM-5-HT could only elicit a single large HR. Thus, GTP gamma S apparently caused a sensitization and then a desensitization of the action of 5-HT. 6. GTP gamma S-induced Ca2+ transients were facilitated when injected in the presence of 5-HT concentrations as low as 0.1 nM. The time delay to the first HR was 65 s in 0.1 nM-5-HT or 4 s in 100 nM-5-HT whereas it was 170 s without 5-HT (mean values). The magnitude as well as frequency of HRs succeeding the first HR was enhanced by 5-HT at concentrations above 0.01 nM. 7. TPA (100 nM) blocked the GTP gamma S-plus-5-HT-potentiated HRs after the first four to five HRs. Sphingosine (2 microM) augmented the series of HRs.(ABSTRACT TRUNCATED AT 400 WORDS)

Aequorin↗

PubMed1990

Effects of interstitial edema on brain cell transplantation.

Fetal raphe cells were transplanted into the anterior part of the corpus callosum of serotonin denervated hydrocephalic rats using a cell suspension method. Hydrocephalus was induced by intracisternal injection of kaolin. The survival of the transplanted cells and fiber outgrowth were evaluated according to the level of serotonin and its metabolite, hydroxyindoleacetic acid, using high-performance liquid chromatography with electrochemical detection in the anterior and posterior parts of the corpus callosum 1-2, 5-6, and 7-8 weeks after transplantation. The results suggest favorable effects of interstitial edema associated with hydrocephalus on the survival of transplanted raphe cells and fiber outgrowth.

Animals↗