Respiratory syncytial virus.
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Antiviral Agents↗
Biomedical subjects
T Yamauchi
Publications and source records attributed to T Yamauchi.
Delayed neuropathy and inhibition of soluble neuropathy target esterase following the administration of organophosphorus compounds to hens.
Delayed neuropathy and inhibition of soluble neuropathy target esterase (NTE) and acetylcholinesterase (AChE) activities in different regions of brain and spinal cord of adult hens were studied after the intravenous administration of leptophos (30 mg/kg), tri-o-cresyl phosphate (TOCP 40 mg/kg) or dipterex (200 mg/kg). The level of NTE activity varied according to the regions of the central nervous system (CNS) of the control (normal) hen, being higher in the cerebrum (74.1 micromol of phenyl valerate hydrolyzed/10 minutes/mg protein) and in the cerebellum (68.7), and lower in the spinal cord (44.5 in cervical, 55.6 in thoracic and 50.0 in lumbar cord). Hens given leptophos and TOCP demonstrated delayed neuropathy with obvious inhibition of NTE, but the times of onset and the degrees of peak inhibition of NTE activity were different: 6-24 hours after dosing and 73-82% of normal activity for leptophos, and 24-48 hours and 45-80% for TOCP, respectively. Furthermore, the average inhibition of NTE during 6-48 hours after dosing, (called here 'period average inhibition') was also significantly different between the leptophos group (63-73%) and TOCP group (40-64%). Hens given dipterex did not demonstrate delayed neuropathy, and had the least peak inhibition and period average inhibition of NTE activity among the 3 groups. Ratios of NTE inhibition/AChE inhibition were higher in the leptophos group (0.91-1.24) and TOCP group (1.13-2.45) than in the dipterex group (0.25-0.79). These results indicate that the distribution of NTE in the soluble fraction of membrane proteins is different in different regions of the CNS, and that the degree of peak inhibition of NTE activity and the time of onset of peak inhibition induced by organophosphorus compounds (OPs) also differ for different OPs. Thus, practical and useful NTE measurements should identify the peak inhibition and period inhibition in several nervous tissue regions.
Acetylcholinesterase↗
Pharmacokinetics and neurotoxicity of dipterex in hens. A comparative study of administration methods.
We compared the tissue concentration of dipterex and the inhibition of the neuropathy target esterase (NTE) activity among groups of hens (n = 8 each) which were intravenously (i.v.), subcutaneously (s.c.) or orally (p.o.) administered the insecticide dipterex. The tissue concentrations of dipterex in the s.c. group were higher than those in the i.v. and p.o. groups. When dosed subcutaneously, the tissue concentration of dipterex was high in the brain, spinal cord and muscle at 3 hr after dosing and then concentrated in the spinal cord and muscle for the subsequent 3 hr. When dosed intravenously or orally, dipterex was evenly dispersed in various tissues. All hens treated with dipterex showed acute neurotoxic signs within 15 min after dosing. The hens dosed intravenously recovered from this acute poisoning within 3 hr, and the hens dosed orally recovered within 6 hr, while the hens dosed subcutaneously recovered within 24 hr after dosing. One hen in the s.c. group exhibited acute neurological sequelae following the acute poisoning. In addition, the loss of body weight was the largest in the s.c. group (157 +/- 49 g), moderate in the i.v. group (133 +/- 91 g), small in the p.o. group (96 +/- 54 g) and the smallest in the PMSF (phenylmethanesulfonyl fluoride, which was dosed to promote delayed neuropathy) group (80 +/- 49 g). In the untreated hens, the activity of NTE in both the cerebrum and cerebellum was higher than that in the midbrain (p < 0.01). There was no difference in NTE activity between the cerebrum and cerebellum. In both the cerebrum and midbrain, the inhibition of NTE activity in the p.o. group was less than that in the i.v. and s.c. groups, and no difference was found between the i.v. and s.c. groups. In the cerebellum, the inhibition of NTE activity in the s.c. group was larger than that in the i.v. and p.o. groups. These results indicate that the s.c. dosing of dipterex results in a stronger neurotoxicity compared to i.v. and p.o. dosing. However, it was difficult to induce the clinical signs of delayed neuropathy with any administration of dipterex in hens, even when the promotion of delayed neurotoxicity of dipterex was attempted with PMSF or double doses of dipterex itself.
Administration, Oral↗
Cushing's syndrome due to unilateral adrenocortical hyperplasia.
A 49-year-old woman with Cushing's syndrome due to unilateral adrenal hyperplasia is presented. She had developed obesity and menopause for 2 years, but no hypertension or hypertrichosis was observed. Although plasma adrenocorticotropin and serum cortisol levels were within normal ranges, the circadian rhythm has completely disappeared. Free thyroxine and triiodothyronine levels were decreased. Adrenocorticotropin did not respond to corticotropin-releasing hormone, and urinary excretion of 17-hydroxycorticosteroids was not suppressed by dexamethasone. Abdominal computed tomography and 131I-Adosterol scintigraphy demonstrated a unilateral functioning mass in the left adrenal gland. The resected left adrenal mass was pathologically diagnosed as the rare condition of adrenocortical nodular hyperplasia.
17-Hydroxycorticosteroids↗
[Renal hemangiopericytoma: report of a case].
A 34-year-old house wife presented with a right renal mass detected by work-up for epigastralgia. The mass located in the right renal sinus was round and approximately 3 cm in diameter. Although the tumor was well enhanced with contrast medium on CT scan, it was hypovascular on the early arterial phase of renal angiography. Translumbar radical nephrectomy was performed on suspicion of the right renal cell carcinoma. The tumor was solid and hard and, the cut surface of the tumor was homogenously colored pale pink. Microscopically it was hemangiopericytoma arising in the renal sinus, composed of well-developed pericytes and capillaries with so-called staghorn configuration, with invasion of hilar renal vein. Immunohistochemically, the hemangiopericytes were strongly positive for CD34, but negative for factor VIII associated antibodies. To our knowledge, the present patient is the 6th case in the Japanese literature and the first case with incidentally detected renal hemangiopericytoma.
Adult↗
[The results of a long-term follow-up for patients with stage Ta bladder cancer, especially regarding those with multiple recurrences].
OBJECTIVE: We reviewed our series of stage Ta bladder cancer patients with a long-term follow-up in order to clarify the prognosis of these patients, especially those who have repeated recurrences. MATERIALS AND METHODS: A retrospective study was done on 88 patients with stage Ta bladder cancer who were treated between 1971 and 1990 at our hospital. All patients reviewed were followed up for at least 5 years. RESULTS: Fifty-three patients out of 88 had recurrence, and the number of recurrences ranged from one to eleven. In the first recurrence, the 5- and 10-year recurrence-free rates were 53.4% and 37.1%, respectively. In the second recurrence, those rates were 25.7% and 15.9%, respectively. Comparisons of the recurrence-free rates between the first recurrence and that of more than 2 times yielded statistically significance (p < 0.01). On the other hand, when the recurrence-free rates of those patients showing recurrence more than 2 times were compared no statistical significance was observed among them. In addition, most patients with multiple recurrences also tended to show a long tumor-free period at some point. In eight patients a stage-up of > or = T1 developed during the study period. No characteristics of the tumors, including the multiplicity of the recurrence, was found to correlate with the stage-up. CONCLUSIONS: Most patients with multiple recurrences demonstrated a long tumor-free period at some point, and, moreover, in some of those patients there was also a possibility that no further recurrence occurred. In addition, frequent recurrence was not associated with increased incidence of stage-up. Based on these findings, multiple recurrence is not thought to be an especially ominous sign, and therefore bladder-preserving therapy is indicated for such patients.
Adult↗
[Rapid ACTH test to judge recovery of adrenal function in patients with Cushing's syndrome].
BACKGROUND: Steroid hormone replacement and recovery of adrenal function after unilateral adrenalectomy were studied in 12 patients with Cushing's syndrome due to adenocortical adenoma. PATIENTS AND METHOD: The patients were 3 males and 9 females aged 19 to 61 years old (mean 34.3 years old). Recovery of adrenal function was judged by plasma cortisol level and rapid ACTH test peridocally. RESULTS: Plasma cortisol level was 13.7 to 20.8 micrograms/dl without diurnal rythme before adrenalectomy. Average replacement period with low dose hydrocortisone was 15 +/- 9.2 months after adrenalectomy. Plasma ACTH and cortisol concentration was recovered to normal range after 3.4 +/- 2.9 months and 12.2 +/- 8.2 after adrenalectomy, respectively. Plasma ACTH concentration was recovered to normal range earlier than plasma cortisol level in all patients. Sufficient response of plasma cortisol concentration in rapid ACTH test was seen a little later than recovery of plasma cortisol level. CONCLUSION: Present data suggest that it is insufficient to judge recovery of adrenal function only by the rise of plasma ACTH and/or cortisol concentrations. Therefore rapid ACTH test is useful to judge sufficient recovery of adrenal function during and after steroid hormone replacement.
Adenoma↗
K1115 A, a new anthraquinone derivative that inhibits the binding of activator protein-1 (AP-1) to its recognition sites. I. Biological activities.
K1115 A, a new anthraquinone derivative, was isolated from the culture broth of Streptomyces griseorubiginosus (Mer-K1115). K1115A inhibited the direct binding of activator protein-1 (AP-1) to AP-1 oligonucleotide (IC50 = 100 microM), and the production of collagenase in IL-1 alpha-stimulated rat synovial cells (IC50 = 60 microM). In vivo, the application of K1115 A decreased phorbol myristate acetate (PMA)-induced mouse ornithine decarboxylase (ODC) activity. These results indicated that K1115 A is able to attenuate the inflammatory response mediated by AP-1.
Animals↗
[Metastatic renal tumor originating from lung cancer: a case report].
A 45-year-old house-wife, who had undergone surgical treatment for lung adenocarcinoma 2 years previously, presented with a left renal mass detected by follow-up CT. During 7 months of observation, it rapidly enlarged from 1 cm to 3 cm in maximum diameter. Although the short doubling time (40 days) suggested that the tumor was metastatic, abdominal urtrasonography, angiography and CT scan did not exclude primary renal cell carcinoma. Left nephrectomy was performed. Histologically, the tumor proved to be metastasis from the previous lung adenocarcinoma. She has been alive with pulmonary recurrence 13 months after nephrectomy. The doubling time of the tumor may be one of the key factors in differentiating a metastatic renal tumor from a primary carcinoma.
Adenocarcinoma↗
Renal AT1 receptor: autoradiographic localization and quantification in rat.
To elucidate the precise localization of angiotensin II (Ang II) type 1 (AT1) receptors in the kidney, we utilized in vitro macro- and micro-autoradiography (ARG) of [3H]-Ang II bindings to the Wistar rat kidney in the presence of L-158,809, a specific non-peptide AT1 receptor antagonist. Besides, we estimated the density of renal AT1 receptors using the quantification of macro-ARG. The density of [3H]-Ang II binding to renal tissue was concentration-dependent in both renal cortex and medulla. Although the addition with 500 nM arginine vasopressin and 500 nM atrial natriuretic peptide had no effect on [3H]-Ang II, the total binding of [3H] Ang II completely displaced by the addition with 500 nM unlabeled Ang II or L-158,809. Macro-ARG revealed that the amount of both Ang II and AT1 receptors in the renal medulla greatly exceeded those in the renal cortex. In the medulla, the density of these receptors was not localized on the outer medulla but was confirmed mainly to the inner medulla, especially to the inner zone and longitudinal bands. Since the density and localization of AT1 receptors was consistent with that of total Ang II receptors, it appears that AT1 receptors comprise most of the Ang II receptors in the kidney. Micro-ARG revealed that Ang II receptors were mainly located in the glomerulus and proximal tubules of the renal cortex, as well as on the circumferences of vessels and the vasa recta of the renal medulla. The present study established a method for ARG of AT1 receptors in the kidney as well as a method for quantifying the macro-ARG.
Angiotensin I↗
Renal AT1 receptor: computerized quantification in spontaneously hypertensive rats and DOCA-salt rats.
To assess the involvement of angiotensin II (Ang II) in the regulation of blood pressure, we investigated the alterations of renal Ang II type 1 (AT1) receptors in two different models of hypertension; i.e., in spontaneously hypertensive rats (SHR) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats by using the method for quantification of in vitro macro-autoradiography (ARG). In the SHR model, although the number of cortical AT1 receptors equaled that of Wistar Kyoto (WKY) rats at 4 and 12 weeks of age, the number of medullary AT1 receptors in the 4-week-old SHR animals was significantly lower than that in age-matched WKY rats, and increased by 12 weeks of age. The renal AT1 receptor number in DOCA-salt hypertensive rats was significantly higher than that in control rats. The amount of these receptors also increased with age in both DOCA-salt hypertensive rats and control rats. These findings indicate that the development of medullary AT1 receptors in early stages of hypertension in the SHR model differs from that in WKY rats or DOCA-salt hypertensive rats. This suggests that renal AT1 receptors may contribute to the hypertension seen in the SHR group. The renal AT1 receptors appear to be up-regulated in early stages of DOCA-salt-induced hypertension as well.
Age Factors↗
[Clinical studies on the prognostic factors in prostate cancer].
To evaluate the prognostic factors and the outcome of treatment, a retrospective study was done on 141 patients with prostate cancer who were newly diagnosed at Kitano Hospital between January 1985 and November 1996. In recent years, the number of patients and the ratio of low stage cancer have increased. The overall 5-year crude survival rate was 49.9%. The 5-year crude survival rate for clinical stage A, B, C and D was 67%, 70%, 62% and 30% respectively. The overall 5-year disease-specific survival rate was 65.6%. The 5-year disease-specific survival rate for clinical stage A, B, C and D was 100%, 89%, 72% and 42%, respectively. By univariate analysis, clinical stage, Gleason score, prostate specific antigen (PSA) level, and patient age were prognostic factors for disease-specific survival of prostate cancer. According to Cox's regression analysis by the stepwise forward regression method, clinical stage and Gleason score were selected as more valuable prognostic factors than PSA level, patient age, comorbidity, and initial treatment. In Gleason score 2 to 8, the prognosis became significantly worse as clinical stage advanced, but in Gleason score 9 and 10 the prognosis was poor regardless of clinical stage.
Aged↗
Tyrosine phosphorylation of the EGF receptor by the kinase Jak2 is induced by growth hormone.
When growth hormone binds to its receptor, which belongs to the cytokine receptor superfamily, it activates the Janus kinase Jak2 which has tyrosine-kinase activity and initiates an activation of several key intracellular proteins (for example, mitogen-activated protein (MAP) kinases) that eventually execute the biological actions induced by growth hormone, including the expression of particular genes. In contrast to receptors that themselves have tyrosine kinase activity, the signalling pathways leading to MAP kinase activation that are triggered by growth hormone are poorly understood, but appear to be mediated by the proteins Grb2 and Shc. We now show that growth hormone stimulates tyrosine phosphorylation of the receptor for epidermal growth factor (EGFR) and its association with Grb2 and at the same time stimulates MAP kinase activity in liver, an important target tissue of growth hormone. Expression of EGFR and its mutants revealed that growth-hormone-induced activation of MAP kinase and expression of the transcription factor c-fos requires phosphorylation of tyrosines on EGFR, but not its own intrinsic tyrosine-kinase activity. Moreover, tyrosine at residue 1,068 of the EGFR is proposed to be one of the principal phosphorylation sites and Grb2-binding sites stimulated by growth hormone via Jak2. Our results indicate that the role of EGFR in signalling by growth hormone is to be phosphorylated by Jak2, thereby providing docking sites for Grb2 and activating MAP kinases and gene expression, independently of the intrinsic tyrosine kinase activity of EGFR. This may represent a novel cross-talk pathway between the cytokine receptor superfamily and growth factor receptor.
Adaptor Proteins, Signal Transducing↗
Effects of OPC-21268, a vasopressin V1-receptor antagonist, on expression of growth factors from glomeruli in spontaneously hypertensive rats.
To assess the chronic in vivo effects of OPC-21268, a vasopressin-V1 receptor antagonist, on renal injury, we investigated the mRNA expressions of platelet-derived growth factor (PDGF) B-chain, transforming growth factor (TGF)-beta1 and proliferating cell nuclear antigen (PCNA) in the glomeruli of spontaneously hypertensive rats (SHR) treated with OPC-21268 for 3 weeks. SHR aged 10 weeks were given 2% NaCl in drinking water for 3 weeks. The OPC group was fed a 0.5% OPC-21268-containing diet for 3 weeks and the control group was given a normal diet. There were no significant changes in the time course of systolic blood pressure, heart rate, urine volume, or urinary sodium, protein and N-acetyl-beta-glucosaminidase (NAG) excretion between the two groups. Serum electrolytes, protein and creatinine levels also did not differ between the groups. The mRNA expressions of PDGF B-chain, TGF-beta1 and PCNA in the glomerulus were examined using reverse transcriptase-polymerase chain reaction (RT-PCR) methods. The mRNA expressions of PDGF B-chain and PCNA among these were significantly suppressed in the OPC group. No significant differences in renal histology including the organ weights were found between the two groups; however, the glomerular size tended to be enlarged in the OPC group. These findings suggest that chronic V1-receptor blockade directly inhibits the glomerular proliferative injury of salt-loaded SHR at the established hypertension stage.
Acetylglucosaminidase↗
Phosphorylation-dependent reversible association of Ca2+/calmodulin-dependent protein kinase II with the postsynaptic densities.
The association of soluble Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) with postsynaptic densities (PSDs) was determined by activity assay, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and immunoblotting of the enzyme. Soluble CaM kinase II was autophosphorylated with ATP in the presence of Ca2+ and calmodulin, and then it was incubated with PSDs. Autophosphorylated CaM kinase II was precipitated with PSDs by centrifugation. The kinase that was not autophosphorylated did not precipitate with PSDs. These results indicate that the soluble previously autophosphorylated CaM kinase II associates with PSDs and forms PSD-CaM kinase II complex. A maximum of about 60 microg of soluble CaM kinase II bound to 1 mg of PSD protein under the experimental conditions. Ca2+-independent activity generated by autophosphorylation of the kinase was retained in the PSD-CaM kinase II complex. The CaM kinase II thus associated with PSDs phosphorylated a number of PSD proteins in both the absence and presence of Ca2+. When the CaM kinase II-PSD complex was incubated at 30 degrees C, its Ca2+-independent activity was gradually decreased. This decrease was correlated with dephosphorylation of the kinase and its release from PSD-CaM kinase II complex. These results indicate that CaM kinase II reversibly translocates to PSDs in a phosphorylation-dependent manner.
Animals↗
Role of insulin receptor substrate-1 and pp60 in the regulation of insulin-induced glucose transport and GLUT4 translocation in primary adipocytes.
In muscle and fat, glucose transport occurs through the translocation of GLUT4 from an intracellular pool to the cell surface. Phosphatidylinositol (PI) 3-kinase has been shown to be required in this process. Insulin is thought to activate this enzyme by stimulating its association with tyrosine-phosphorylated proteins such as insulin receptor substrate (IRS)-1, IRS-2, Grb2-associated binder-1, and pp60. To study the role of these endogenous substrates in glucose transport, we analyzed adipocytes from IRS-1 null mice that we previously generated (Tamemoto, H., Kadowaki, T., Tobe, K., Yagi, T., Sakura, H., Hayakawa, T., Terauchi, Y., Ueki, K., Kaburagi, Y., Satoh, S., Sekihara, H., Yoshioka, S., Horikoshi, H., Furuta, Y. , Ikawa, Y., Kasuga, M., Yazaki Y., and Aizawa S. (1994) Nature 372, 182-186). In adipocytes from these mice, we showed that: 1) insulin-induced PI 3-kinase activity in the antiphosphotyrosine immunoprecipitates was 54% of wild-type; 2) pp60 was the major tyrosine-phosphorylated protein that associated with PI 3-kinase, whereas tyrosine phosphorylaion of IRS-2 as well as its association with this enzyme was almost undetectable; and 3) glucose transport and GLUT4 translocation at maximal insulin stimulation were decreased to 52 and 68% of those from wild-type. These data suggest that both IRS-1 and pp60 play a major role in insulin-induced glucose transport in adipocytes, and that pp60 is predominantly involved in regulating this process in the absence of IRS-1.
Adipocytes↗
Insulin resistance syndrome in mice deficient in insulin receptor substrate-1.
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Animals↗
Overexpression of alpha and beta isoforms of Ca2+/calmodulin-dependent protein kinase II in neuroblastoma cells -- H-7 promotes neurite outgrowth.
Since the alpha and beta isoforms of CaM kinase II are known to be expressed almost exclusively in the brain, we compared the effect of overexpression of the beta isoform of CaM kinase II with that of the alpha isoform. The subcellular distribution of the alpha isoform was different from that of the beta isoform, although the catalytic properties of the alpha and beta isoforms expressed in transfected cells were similar to those of brain CaM kinase II. The alpha isoform was found in the soluble fraction more than in the particulate fraction, whereas most of the beta isoform bound to subcellular structures. In the cell overexpressing alpha and beta isoforms of CaM kinase II, neurite extension was promoted when compared with the morphology of neo transfectants. Neurite outgrowth of cells overexpressing CaM kinase II was further stimulated by the treatment of 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), a selective but not absolutely specific inhibitor of protein kinase C. The morphological change was rapid and observed within 1 h followed by H-7 treatment. Morphological changes, such as the number of cells with neurites and length of neurites were greater in the beta cells than in the alpha cells. Chelerythrine, a specific inhibitor of protein kinase C, also stimulated the neurite outgrowth of these cells. Some substrates of CaM kinase II related to neurite outgrowth were detected in cells overexpressing CaM kinase II stimulated with H-7. These results suggest that CaM kinase H and protein kinase C play an important role in the control of cell change, and that the subcellular distribution of CaM kinase II is important for regulating cellular functions efficiently.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗