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Osamu Saito

Publications and source records attributed to Osamu Saito.

At least 19 recordsLinked to original sources

A case of recurrent renal failure associated with metabolic alkalosis induced by protracted vomiting.

We describe a case of recurrent deterioration of renal function in a 54-year-old man who was found to have metabolic alkalosis, with a maximum PaCO(2) of 73.9 mmHg and a bicarbonate concentration of 55.3 mmol/l. He had a gradual exacerbation of nausea and vomiting due to atrophic gastritis, with a scarred, deformed pyloric part of the stomach and a duodenal bulb secondary to chronic peptic ulcer. His metabolic alkalosis and deteriorated renal function were corrected by intravenous saline with or without potassium chloride. However, his recovered creatinine clearance was at most 60 l/day (41.6 ml/min). A renal biopsy revealed cellular infiltration of mononuclear cells and atrophic change in the tubulointerstitium, suggesting chronic interstitial nephritis. Latent renal insufficiency and dehydration induced by protracted vomiting may easily induce a rapid and recurrent deterioration of renal function, and control of vomiting seemed to be the cardinal measure. Initially, his nausea and vomiting seemed to be successfully controlled by medication, however, they later became persistent and surgical correction of the stomach was carried out. Postoperative recovery was smooth, and the patient's vomiting and recurrent deterioration of renal function finally settled.

Acid-Base Equilibrium↗

Ketamine and N-acetylaspartylglutamate peptidase inhibitor exert analgesia in bone cancer pain.

PURPOSE: Not all bone cancer pain can be effectively treated with current therapies. In the present study, the effects of ip administration of alpha-2 agonists (dexmedetomidine and clonidine), N-methyl-D-aspartate (NMDA) antagonists (MK-801 and ketamine), an N-acetylaspartylglutamate peptidase inhibitor (ZJ-43), and morphine were examined in a mouse bone cancer pain model. METHODS: A bone cancer pain model was produced by injection of murine sarcoma cells into the medullary cavity of the distal femur. To estimate the level of bone cancer pain, the number of pain-related behaviours induced by repeated applications of a von Frey monofilament (0.166 g) to the site of tumour cells implantation was counted. Drugs were administered two weeks after the implantation. RESULTS: Morphine produced a significant analgesic effect (P < 0.001). The alpha-2 agonists produced analgesic effects (P < 0.001) with an efficacy similar to that of morphine, but only at doses that produced severe sedation. MK-801 had only limited analgesic effects, while ketamine produced an analgesic effect (P < 0.001) with the same efficacy as morphine. ZJ-43 (100 mg.kg(-1)) had a significant analgesic effect (P < 0.05) and the effect of ZJ-43 was antagonized by the selective group II metabotropic glutamate receptor (mGluR) antagonist. CONCLUSION: These data suggest that alpha-2 agonists produce an analgesic effect only at a sedative dose and that ketamine, but not MK-801, is associated with an analgesic response without overt side effects. The effect of ZJ-43 is mediated by activating group II mGluRs.

Adrenergic alpha-Agonists↗

Complex behavioral automatism arising from insular cortex.

We describe two cases of complex partial seizures with ictal violent movements arising from the insular cortex. The first patient, a 14-year-old girl, presented with hyperkinetic behavior such as rolling, thrashing, and pedaling, and the second case, a 38-year-old woman, had been suffering from frequent daytime hyperkinetic seizures characterized by bizarre vocalization, jumping, and violent bimanual movements. Both patients showed a slight high signal change in the right posterior ventral insular cortex in fluid-attenuated inversion recovery (FLAIR) studies involving magnetic resonance imaging, and extensive subdural electroencephalographic monitoring revealed EEG seizure onset from the temporal lobe. The posterior ventral insular and lateral temporal cortices were resected, resulting in complete seizure freedom in both cases. The histological diagnoses were focal cortical dysplasia in the first case and gliosis in the second case. There may exist a group of patients with complex partial seizures with ictal violent automatism that can be ameliorated by the resection of epileptogenic lesions in the insular cortex. Careful inspection of the insular cortex is necessary to diagnose this type of epileptic seizure.

Adolescent↗

Characterization of a rabbit kidney prostaglandin F(2{alpha}) receptor exhibiting G(i)-restricted signaling that inhibits water absorption in the collecting duct.

PGF(2alpha) is the most abundant prostaglandin detected in urine; however, its renal effects are poorly characterized. The present study cloned a PGF-prostanoid receptor (FP) from the rabbit kidney and determined the functional consequences of its activation. Nuclease protection assay showed that FP mRNA expression predominates in rabbit ovary and kidney. In situ hybridization revealed that renal FP expression predominates in the cortical collecting duct (CCD). Although FP receptor activation failed to increase intracellular Ca(2+), it potently inhibited vasopressin-stimulated osmotic water permeability (L(p), 10(-7) cm/(atm.s)) in in vitro microperfused rabbit CCDs. Inhibition of L(p) by the FP selective agonist latanoprost was additive to inhibition of vasopressin action by the EP selective agonist sulprostone. Inhibition of L(p) by latanoprost was completely blocked by pertussis toxin, consistent with a G(i)-coupled mechanism. Heterologous transfection of the rabbit FPr into HEK293 cells also showed that latanoprost inhibited cAMP generation via a pertussis toxin-sensitive mechanism but did not increase cell Ca(2+). These studies demonstrate a functional FP receptor on the basolateral membrane of rabbit CCDs. In contrast to the Ca(2+) signal transduced by other FP receptors, this renal FP receptor signals via a PT-sensitive mechanism that is not coupled to cell Ca(2+).

Amino Acid Sequence↗

Anti-hyperalgesic effects of intrathecally administered neuropeptide W-23, and neuropeptide B, in tests of inflammatory pain in rats.

Neuropeptide W-23 (NPW23) is an endogenous ligand of both GPR7 and GPR8, and neuropeptide B (NPB) is an endogenous ligand of GPR7. GPR7 mRNA has been detected in regions of the cortex, the hippocampus, the hypothalamus, and the spinal cord in the rat, but GPR8 has not been found in rodents. GPR7 and GPR8 receptors have structural features in common with both opioid and somatostatin receptors. The effects of intrathecal (i.t.) application of NPW23 and NPB were tested in two inflammatory pain models (plantar injection of formalin or carrageenan) and two thermal nociceptive tests (52.5 degrees C and 50.5 degrees C hot plates) and one mechanical nociceptive test in the rat. I.t. injection of either NPW23 or NPB decreased the number of agitation behaviors induced by paw formalin injection and attenuated the level of mechanical allodynia, but not the level of thermal hyperalgesia, induced by paw carrageenan injection in a dose-dependent manner at a dose between 0.1 and 10 microg, significantly. The effects of either 10 microg of NPW23 or 10 microg of NPB were not antagonized by 10 microg of naloxone. I.t. injection of either NPW23 or NPB had no effect in both the 52.5 degrees C hot plate test or in the 50.5 degrees C hot plate tests at a dose between 1 and 100 microg. I.t. injection of either 10 microg of NPW23 or 10 microg of NPB had no effect in the mechanical nociceptive test. I.t. injection of either 10 microg of NPW23 or 10 microg of NPB significantly suppressed the expression of Fos-like immunoreactivity of the L4-5 spinal dorsal horn induced by paw formalin injection. These data suggest that both spinally-applied NPW23 and NPB suppressed the input of nociceptive information to the spinal dorsal horn, produced an analgesic effect in the formalin test, and attenuated the level of mechanical allodynia in the carrageenan test, and that either spinally applied NPW23 or spinally applied NPB had no effect in the physiological condition.

Animals↗

Analgesic effects of nonsteroidal antiinflammatory drugs, acetaminophen, and morphine in a mouse model of bone cancer pain.

PURPOSE: Bone metastasis is one of the major causes of cancer-related pain, and not all bone cancer pain can be effectively treated. Recently, a mouse model of bone cancer pain was introduced. To test the analgesic effects of nonsteroidal antiinflammatory drugs on bone cancer pain, the authors examined the effects of oral administration of a cyclooxygenase-1 (COX-1) selective inhibitor (SC560), a COX-2 selective inhibitor (celecoxib), and a nonselective COX inhibitor (indomethacin) on bone cancer pain and compared these effects to the effect of orally administered acetaminophen and morphine. METHODS: An animal model of bone cancer pain was induced by injecting osteolytic murine sarcoma cells in the mouse femur. Drugs were administered orally 2 weeks after tumor-cell implantation, and the level of bone cancer pain was assessed 30, 60, 90, 120, and 180 min after drug administration. RESULTS: Oral administration of acetaminophen, indomethacin, and morphine, but not of SC560 or celecoxib, produced an analgesic effect on bone cancer pain. Co-administration of a subanalgesic does of morphine with acetaminophen enhanced the analgesic effect of acetaminophen. CONCLUSION: These data suggest that bone cancer pain is effectively treated by oral administration of indomethacin, acetaminophen, and morphine and that the co-administration of acetaminophen and an opioid provides a beneficial effect when treating of bone cancer pain.

Acetaminophen↗

A case of thoracic hemorrhage due to ectopic parathyroid hyperplasia with chronic renal failure.

We report a case of secondary hyperparathyroidism in a 53-year-old man who had thoracic hemorrhage originating from an ectopic thymic parathyroid gland tumor. He was on long-term hemodialysis treatment and had persistent secondary hyperparathyroidism caused by 3 swollen parathyroid glands around the thyroid gland and a mediastinal ectopic parathyroid gland tumor. Parathyroidectomy and removal of the mediastinal tumor were planned. Preoperative chest x-ray and a computed tomographic scan obtained just before surgery showed left pleural effusion. Furthermore, diagnostic thoracentesis yielded hemorrhagic exudative fluid. Thoracoscopy confirmed the presence of a mediastinal tumor lesion that was bleeding into the thoracic cavity. The tumor was resected using thoracoscopic surgery, and ectopic thymic parathyroid gland hyperplasia associated with hemorrhage was pathologically diagnosed. A postoperative diagnostic chest computed tomographic scan and technetium 99m 2-methoxyisobutyl isonitrile scintigraphy showed successful removal of the ectopic parathyroid gland tumor. Subsequently, the secondary hyperparathyroidism could be clinically controlled by medical treatment, and total parathyroidectomy has been postponed indefinitely. We consider that hemorrhage from the ectopic parathyroid gland tumor resulted in thoracic bleeding. To our knowledge, this is the first case report of secondary hyperparathyroidism with thoracic hemorrhage originating from an ectopic mediastinal parathyroid gland.

Adenoma↗

Ligand-induced rearrangement of the dimeric metabotropic glutamate receptor 1alpha.

The extracellular domain of the metabotropic glutamate receptor 1alpha (mGluR1alpha) forms a dimer and the ligand, glutamate, induces a structural rearrangement in this domain. However, the conformational change in the cytoplasmic domain, which is critical for mGluR1alpha's interaction with G proteins, remains unclear. Here we investigated the ligand-induced conformational changes in the cytoplasmic domain by fluorescence resonance energy transfer (FRET) analysis of mGluR1alpha labeled with fluorescent protein(s) under total internal reflection field microscopy. Upon ligand binding, the intersubunit FRET efficiency between the second loops increased, whereas that between first loops decreased. In contrast, the intrasubunit FRET did not change clearly. These results show that ligand binding does not change the structure of each subunit, but does change the dimeric allocation of the cytoplasmic regions, which may underlie downstream signaling.

Dimerization↗

Activation of spinal orexin-1 receptor produces anti-allodynic effect in the rat carrageenan test.

Orexin-A and orexin-1 receptors are found in the dorsal root ganglion cells and the spinal dorsal horn and this suggests that orexin-A is involved in the spinal nociceptive transmission. The authors examined the effect of intrathecally administered orexin-A on the level of mechanical allodynia and thermal hyperalgesia induced by paw carrageenan injection in the rat. Intrathecal injection of 0.3 and 3 nmol of orexin-A suppressed the level of mechanical allodynia, but not that of thermal hyperalgesia, and the effect of orexin-A on mechanical allodynia was antagonized by the pretreatment of 1-(2-methylbenzoxazol-6-yl)-3-[1,5]naphthyridin-4-yl urea hydrochloride, SB-334867, a selective orexin-1 receptor antagonist. These data suggest that the activation of spinal orexin-1 receptor modulates the mechanical information transmission, but not thermal information transmission, in the spinal cord during carrageenan test.

Animals↗

Anti-mechanical allodynic effect of intrathecal and intracerebroventricular injection of orexin-A in the rat neuropathic pain model.

Orexin-A has been reported to produce an analgesic effect in the hot plate test and in the inflammatory pain models. In the present study, the authors examined the effect of orexin-A on the mechanical allodynia induced by partial sciatic nerve ligation (a model of neuropathic pain) in the rat. Partial sciatic nerve ligation is created by tight ligation of one-third or one-half of the right sciatic nerve. Orexin-A was administered intrathecally or intracerebroventricularly 7 days after a partial sciatic nerve injury. Either intrathecal or intracerebroventricular injection of orexin-A attenuated the level of mechanical allodynia induced by partial sciatic nerve ligation. These data suggest that either intrathecal or intracerebroventricular injection of orexin-A is a new therapeutic approach to treating mechanical allodynia caused by nerve injury.

Animals↗

Analgesic effect of intrathecally administered matrix metalloproteinase 2 (MMP-2) in the rat formalin test.

Matrix metalloproteinases (MMPs) are a family of extracellular endopeptidases that selectively degrade components of the extracellular matrix. In the present study, the authors examined the effect of intrathecal injection of MMP-2 on the nociceptive transmission during the rat formalin test (a model of inflammatory pain). The paw formalin injection induces biphasic flinching (phase 1: 0-6 min; phase 2: 10-60 min) of the injected paw. Intrathecal injection of 1 microg of MMP-2 depressed the phase 1 agitation behavior, but not the phase 2 agitation behavior, and this effect of MMP-2 was antagonized by ONO-4817, an MMP inhibitor. ONO-4817 itself had no effect on the formalin test. These data suggest that exogenously applied MMP-2 to the spinal cord produces analgesic effects in the rat formalin test.

Analgesics↗

Expression of the prostaglandin F receptor (FP) gene along the mouse genitourinary tract.

PGF(2alpha) is one of the major prostanoids produced by the kidney. The cellular effects of PGF(2alpha) are mediated by a G protein-coupled transmembrane receptor designated the FP receptor. Both in situ hybridization and beta-galactosidase knocked into the endogenous FP locus were used to determine the cellular distribution of the mouse FP receptor. Specific labeling was detected in the kidney, ovary, and uterus. Abundant FP expression in ovarian follicles and uterus is consistent with previous reports of failed parturition in FP-/- mice. In the kidney, coexpression of the mFP mRNA with the thiazide-sensitive cotransporter defined its expression in the distal convoluted tubule (DCT). FP receptor was also present in aquaporin-2-positive cortical collecting ducts (CCD). No FP mRNA was detected in glomeruli, proximal tubules, or thick ascending limbs. Intrarenal expression of the FP receptor in the DCT and CCD suggests an important role for the FP receptor regulating water and solute transport in these segments of the nephron.

Animals↗

[Effect of oral intake of an enteric capsule preparation containing Bifidobacterium longum on the progression of chronic renal failure].

Since the accumulation of intestinal putrefactive products, such as indole and phenol, is known to play a role in the exacerbation of chronic renal failure, reduction of these intestinal putrefactive products can be expected to retard the progression of renal failure. In the present study, an enteric capsule preparation containing Bifidobacterium longum(Bifidus HD) was administered orally to 27 patients with chronic renal failure(CRF) for 6 months. Though no significant effect was found in the whole group, a significant retardation of the progression of renal failure was found in patients with an initial serum creatinine level > or = 4.0 mg/dl or those with an initial serum inorganic phosphate level > or = 4.0 mg/dl. There was no adverse effect observed in any case. Bifidus HD is considered a useful tool for suppressing the progression of chronic renal failure(CRF) in the conservative period.

Administration, Oral↗

Cloning and expression of the rabbit prostaglandin EP2 receptor.

BACKGROUND: Prostaglandin E2 (PGE2) has multiple physiologic roles mediated by G protein coupled receptors designated E-prostanoid, or "EP" receptors. Evidence supports an important role for the EP2 receptor in regulating fertility, vascular tone and renal function. RESULTS: The full-length rabbit EP2 receptor cDNA was cloned. The encoded polypeptide contains 361 amino acid residues with seven hydrophobic domains. COS-1 cells expressing the cloned rabbit EP2 exhibited specific [3H]PGE2 binding with a Kd of 19.1 +/- 1.7 nM. [3H]PGE2 was displaced by unlabeled ligands in the following order: PGE2>>PGD2=PGF2alpha=iloprost. Binding of [3H]PGE2 was also displaced by EP receptor subtype selective agonists with a rank order of affinity consistent with the EP2 receptor (butaprost>AH13205>misoprostol>sulprostone). Butaprost free acid produced a concentration-dependent increase in cAMP accumulation in rabbit EP2 transfected COS-1 cells with a half-maximal effective concentration of 480 nM. RNase protection assay revealed high expression in the ileum, spleen, and liver with lower expression in the kidney, lung, heart, uterus, adrenal gland and skeletal muscle. In situ hybridization localized EP2 mRNA to the uterine endometrium, but showed no distinct localization in the kidney. EP2 mRNA expression along the nephron was determined by RT-PCR and its expression was present in glomeruli, MCD, tDL and CCD. In cultured cells EP2 receptor was not detected in collecting ducts but was detected in renal interstitial cells and vascular smooth muscle cells. EP2 mRNA was also detected in arteries, veins, and preglomerular vessels of the kidney. CONCLUSION: EP2 expression pattern is consistent with the known functional roles for cAMP coupled PGE2 effects in reproductive and vascular tissues and renal interstitial cells. It remains uncertain whether it is also expressed in renal tubules.

Amino Acid Sequence↗

Simultaneous analyses of hypoglycemic agents and C-peptide are essential in a homicide case with the combined dosing insulin and insulin-releasing drug.

A 5-year-old girl was given a sulfonylurea hypoglycemic agent, 25 mg of glibenclamide (ten tablets of Euglucon) with two benzodiazepine drugs, 2 mg of estazoram and 0.75 mg of triazolam (one tablet of Eurodin and three tablets of Halcion), by her 37-year-old pharmacist father and then injected with 70 units of insulin (NovoLet 40R). She died several hours after the injection of insulin. Autopsy was carried out 12 h after the death. A glibenclamide level of 103 ng/ml was detected in the serum collected from the heart at autopsy. The serum insulin and C-peptide concentrations were 295 microU/ml and 0.5 ng/ml, respectively. The high level of insulin and the low level of C-peptide indicated that most of the serum insulin was exogenous. The determination of the serum C-peptide concentration was useful to the diagnosis of hypoglycemia caused by exogenous insulin even in the case of co-administration with an endogenous-insulin-releasing agent.

Journal Article↗

Identification of the sex pheromone components secreted by female moths of Peridroma saucia (Noctuidae: Noctuinae).

The variegated cutworm, Peridroma saucia Hübner, is a lepidopteran pest to a large number of crops in Canada, the United States, and Europe. It was probably naturalized in Japan in the 1970s. The pheromone glands of the female moth include two components with electroantennographic activity in a ratio of 3:1. GC-MS analyses of pheromone extracts untreated and treated with dimethyl disulfide revealed the major component to be (Z)-11-hexadecenyl acetate and the minor component to be (Z)-9-tetradecenyl acetate. The synthetic pheromone was used to attract a large number of males in a vegetable field in Tokyo, which suggests that this species has already become a harmful pest in Japan.

Acetates↗

Determinants of chronic hypercapnia in Japanese men with obstructive sleep apnea syndrome.

STUDY OBJECTIVE: To identify the determinants of chronic hypercapnia (ie, PaCO(2), > or = 45 mm Hg) in men with obstructive sleep apnea syndrome (OSAS) without airflow obstruction. DESIGN: An analysis was conducted of 143 male patients with OSAS, which had been diagnosed by polysomnography (PSG), who had been referred to a university hospital. Patients were classified as hypercapnic (ie, PaCO(2), > or = 45 mm Hg) and normocapnic (ie, PaCO(2), < 45 mm Hg), and obese (ie, body mass index [BMI], > or = 30 kg/m(2)) or nonobese (ie, BMI, < 30 kg/m(2)). Patients with airflow obstruction (ie, FEV(1)/FVC ratio, < 70%) were excluded from the study. Baseline clinical characteristics, pulmonary function, PSG data, and blood gas data were compared between hypercapnic and normocapnic patients. Correlations between PaCO(2) and several anthropometric, respiratory, and polysomnographic variables were determined by stepwise multiple regression analysis. RESULTS: Fifty-five patients (38%) were hypercapnic. Hypercapnic patients were younger and heavier, and had more abnormalities on pulmonary and PSG testing. Stepwise multiple regression analysis revealed that the PaCO(2) level was influenced significantly by the mean level of arterial oxygen saturation (SaO(2)) during sleep and by the percent of vital capacity (%VC) (R(2) = 0.430; p < 0.0001), indicating that 43% of the total variance in the PaCO(2) could be explained by the mean SaO(2) and %VC in hypercapnic patients. In contrast, only 13% of the total variance in the PaCO(2) was accounted for by the mean SaO(2) and BMI in normocapnic patients (R(2) = 0.134; p = 0.0034). The mean SaO(2), %VC, and PaO(2) were selected as independent variables for predicting the PaCO(2) in obese patients. These variables explained 41% of the total variance in the PaCO(2) (R(2) = 0.407; p < 0.0001), whereas the mean SaO(2) only accounted for 13% of the total variance in PaCO(2) levels in nonobese patients (R(2) = 0.134; p = 0.0064). CONCLUSION: Nocturnal desaturation and restrictive pulmonary impairment play major roles in determining the PaCO(2) in hypercapnic and obese OSAS patients without airflow obstruction.

Adult↗