PubMed Health⌕ Search

Biomedical subjects

Kazuo Watanabe

Publications and source records attributed to Kazuo Watanabe.

At least 55 records · Page 3Linked to original sources

Successful treatment of lymph node metastases recurring from gallbladder cancer.

A 66-year-old woman who had undergone cholecystectomy for the treatment of gallbladder cancer 5 years and 10 months previously was referred to our center due to increased carbohydrate antigen (CA)19-9. Increased CA19-9 (136U/ml) was the only abnormality detected on initial examination, and, despite various tests, clear signs of recurrence could not be detected. Subsequently, the patient was followed. Six months after the initial examination, dynamic computerized tomography confirmed lymphadenopathy. The results of fluoro-deoxy-glucose positron emission tomography suggested lymph node metastasis of the gallbladder cancer, and after consideration of the site of recurrence and the length of time between the primary surgery and detection of recurrence, the patient underwent extrahepatic bile duct resection and lymphadenectomy. Levels of CA19-9 normalized postoperatively, and, at the time of writing (26 months postoperatively), blood tests and diagnostic imaging revealed no signs of recurrence.

Adenocarcinoma↗

Involvement of glutamate and gamma-amino-butyric acid receptor systems on gastric acid secretion induced by activation of kappa-opioid receptors in the central nervous system in rats.

1. Various neurotransmitters in the brain regulate gastric acid secretion. Previously, we reported that the central injection of kappa-opioid receptor agonists stimulated this secretion in rats. Although the existence of kappa(1)-kappa(3)-opioid receptor subtypes has been proposed, the character is not defined. We investigated the interactions between kappa-opioid receptor subtypes and glutamate, gamma-amino-butyric acid (GABA) or 5-hydroxy tryptamine (5-HT) receptors in the rat brain. 2. Gastric acid secretion induced by the injection of U69593 (8.41 nmol, a putative kappa(1)-opioid receptor agonist) into the lateral cerebroventricle was completely inhibited by the central injection of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10.9 nmol, an antagonist for non-N-methyl-D-aspartate (non-NMDA) receptors) and by bicuculline infusion (222 micro g kg(-1) per 10 min, i.v., GABA(A) receptor antagonist). The secretion induced by bremazocine (8.52 nmol, a putative kappa(2)-opioid receptor agonist) was inhibited by bicuculline infusion, but not by CNQX. The secretion induced by naloxone benzoylhydrazone (224 nmol, a putative kappa(3)-opioid receptor agonist) was slightly and partially inhibited by CNQX and bicuculline. 3. Treatment with CNQX and bicuculline inhibited gastric acid secretion induced by the injection of dynorphin A-(1-17) into the lateral, but not the fourth, cerebroventricle. Antagonists for NMDA, GABA(B) and 5-HT(2/1C) receptors did not inhibit the secretions by kappa-opioid receptor agonists. 4. In rat brain regions close to the lateral cerebroventricle, kappa-opioid receptor systems (kappa(1)>kappa(3)>>kappa(2)) are regulated by the non-NMDA type of glutamate receptor system, and kappa(1)- and kappa(2)-opioid receptor systems are regulated by the GABA(A) receptor system. The present findings show pharmacological evidence for kappa-opioid receptor subtypes that regulate gastric acid secretion in the rat brain.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

Intra-epithelial neuroendocrine carcinoma of the nasal cavity.

We describe a distinctive neuroendocrine carcinoma (NEC) that proliferated intra-epithelially. The tumor was 35 mm in diameter and arose from the right superior turbinate of a 46-year-old woman. Histologically, the tumor exhibited papillary growth and the tumor cells were localized in the thickened mucosal epithelium. The tumor cells had round to oval and vesicular or hyperchromatic nuclei, and cohered without any specific structure such as a fibrillary background, rosette or glandular structure. No stromal invasion by the tumor was observed. Immunohistochemically, the tumor cells were positive for neuron-specific enolase focally. In addition, many tumor cells expressed cytokeratin (AE1/AE3 and CAM 5.2), mostly with characteristic perinuclear dot-like patterns. Electron microscopy revealed focal but well-eveloped cytoplasmic processes containing arrays of microtubules and a few dense core granules. The tumor was considered to be a poorly differentiated neuroendocrine carcinomas (NEC) that exhibited exceptional intra-epithelial proliferation. The tumor completely disappeared after the stereotactic radiosurgery and has not recurred for 40 months. It might be difficult to distinguish a poorly differentiated NEC in the sinonasal region from other neuroectodermal tumors, including olfactory neuroblastoma, but the differential diagnosis is important because each tumor has different clinicopathological characteristics.

Biomarkers, Tumor↗

Polyangitis overlap syndrome: a fatal case combined with adult Henoch-Schönlein purpura and polyarteritis nodosa.

Henoch-Schönlein purpura (HSP) is a rather common disease characterized by systemic hypersensitivity vasculitis in the skin and other visceral organs. It has a favorable prognosis unless it is complicated by severe glomerular disease. We report a distinctive fatal case of systemic vasculitis combined with HSP and polyarteritis nodosa (PN) in a 56-year-old man who died of progressive renal failure one month after the onset of the disease. He complained of arthralgia, purpura of both lower extremities, nasal bleeding and tarry stool, and acute renal failure was noted at the time of admission to hospital. A skin biopsy from the purpura lesion exhibited leucocytoclastic vasculitis with IgA deposition, and HSP was considered. However, renal failure progressed rapidly and subsequently was complicated by acute myocardial infarction. Postmortem examination revealed PN type necrotizing vasculitis in the kidneys, heart and mesentery resulting in acute multiple infarctions of these organs. We think the current case was a polyangitis overlap syndrome. It is important to suspect the polyangitis overlap syndrome positively when progressive acute renal failure is seen in a patient with HSP and to begin appropriate therapy immediately.

Fatal Outcome↗

Steroid therapy reduces mesangial matrix accumulation in advanced IgA nephropathy.

BACKGROUND: Steroid therapy for IgA nephropathy (IgAN) has been reported to ameliorate the long-term prognosis of IgAN, but its mode of action has not been fully elucidated. In this study, we examined the effect of steroids on glomerular morphological changes in IgAN. METHODS: We examined 16 patients with biopsy-proven IgAN (male/female =11/5, mean age 32.1 years) who were divided into prognosis groups according to criteria set by the Japanese Society of Nephrology. Initially, they received a loading dose of steroids, followed by a daily dose of 10-15 mg prednisolone. After 12 months, they underwent a second biopsy, and their histological and clinical features were examined. RESULTS: Before and after therapy, systolic blood pressure, diastolic blood pressure, serum creatinine and creatinine clearance all remained unchanged. However, urinary protein excretion decreased dramatically, from 1.6+/-1.7 to 0.4+/-0.2 g/day (P<0.005). Furthermore, computerized imaging revealed a significant reduction of the mesangial matrix index (MMI) from 14.5+/-5.2 to 9.5+/-3.6% (P<0.001). The numbers of sclerosing glomeruli did not change. CONCLUSIONS: Steroid therapy reduces mesangial matrix accumulation and reduces urinary protein excretion in advanced IgAN.

Adult↗

Stimulatory effects of nitric oxide donors on histamine release in isolated rat gastric mucosal cells.

We previously reported stimulatory effects of endogenous and exogenous nitric oxide (NO) on gastric acid secretion. In the present study, we investigated effects of NO donors on release of histamine, which is related to acid secretion, in isolated rat gastric mucosal cells. NO donors such as (+/-)-(E)-4-methyl-2-[(E)-hydroxyimino]-5-nitro-6-methoxy-3-hexanamide (NOR 1) and sodium nitroprusside significantly augmented the histamine release. It was inhibited by 2-(4-carboxyphenyl)-4,4,5,5,-tetramethylimidazoline-1-oxyl-3-amide (carboxy-PTIO), a NO scavenger, and 6-(phenylamino)-5,8-quinolinedione (LY83583), a soluble guanylate cyclase inhibitor. Dibutyryl cyclic GMP also stimulated histamine release. These results suggest that NO donors act on cyclic GMP pathway in isolated gastric mucosal cells, resulting in facilitation of histamine release. NO may stimulate gastric acid secretion through histamine release from the histamine-containing cells, possibly enterochromaffin-like cells.

Animals↗

[Traumatic dislocation of the testis: report of five cases].

Five cases of traumatic dislocation of the testis are described. Dislocation of the testis is a rare injury, with only 93 cases having been reported in Japan. Recent reports have revealed an increased number of motor cycle accidents involving teenage patients. Early surgical management is required, since closed reduction is difficult. We discuss its classification, diagnosis and treatment.

Accidents, Traffic↗

Developmental changes in KCC1, KCC2, and NKCC1 mRNA expressions in the rat brain.

We investigated the expressions of KCC1, KCC2 and NKCC1 mRNAs in the developing rat brain. The neuroepithelium showed abundant KCC1 and NKCC1 mRNA expressions, while KCC2 mRNA was not detected there. In contrast, KCC2 mRNA was preferentially expressed in postmitotic mature neurons. These results suggest that the appearance of KCC2 expression mainly depends on the maturation of individual neurons.

Animals↗

Antisecretory effect of somatostatin on gastric acid via inhibition of histamine release in isolated mouse stomach.

Somatostatin is known to inhibit gastric acid secretion via both inhibition of histamine release from gastric enterochromaffin-like cells and direct inhibition of parietal cell function. We tried to clarify which of these two mechanisms plays a more important role in the inhibition of gastric acid section by somatostatin using isolated mouse stomach preparations. The gastric acid secretion stimulated by histamine was not inhibited by pretreatment with somatostatin (1 micro M), but somatostatin abolished acid secretion induced by 4-[[[(3-chlorophenyl)amino]carbonyl]oxy]-N,N,N,-trimethyl-2-butynyl-1-aminium chloride (McN-A-343), a muscarinic M(1) receptor agonist. In addition, the histamine-H(2) receptor antagonist famotidine also completely inhibited the secretion stimulated by McN-A-343. Similarly, pretreatment with both somatostatin and famotidine completely abolished pentagastrin-induced acid secretion. Somatostatin partially inhibited the acid secretion stimulated by bethanechol. The late sustained acid secretion induced by bethanechol was reduced more strongly by somatostatin than the initial peak secretion. In addition, somatostatin had no effect on the transient increase in bethanechol-induced acid secretion in famotidine-pretreated preparations. Somatostatin had no effect on basal histamine secretion in isolated mouse stomach preparations, but markedly reduced histamine release induced by McN-A-343 and bethanechol. The present study showed that the acid secretory response via the endogenous histamine-mediated pathway was inhibited by somatostatin, but the response to a direct activation of gastric parietal cells was not. These results suggest that the inhibition of histamine release from enterochromaffin-like cells plays a more important role in the inhibition of gastric acid secretion by somatostatin than the direct inhibition of parietal cells. In addition, somatostatin inhibited the sustained acid secretion more strongly than the initial peak secretion after the cholinergic stimulation.

Animals↗

Effect of mitragynine, derived from Thai folk medicine, on gastric acid secretion through opioid receptor in anesthetized rats.

Mitragynine, an indole alkaloid from Thai folk medicine Mitragyna speciosa, exerts agonistic effects on opioid receptors. Gastric acid secretion is proposed to be regulated by opioid receptors in the central nervous system (CNS). Previously, we reported the dual roles (inhibition via micro-opioid receptors and stimulation via kappa-opioid receptors) of the opioid system in the central control of gastric acid secretion. We investigated whether mitragynine affects gastric acid secretion via opioid receptors in the CNS. Injection of mitragynine (30 microg) alone into the lateral cerebroventricle did not have a significant effect on basal gastric acid secretion in the perfused stomach of anesthetized rats. Injection of mitragynine (3-30 microg) into the fourth cerebroventricle, like morphine, inhibited 2-deoxy-D-glucose-stimulated gastric acid secretion. The inhibitory effect of mitragynine (30 microg) was reversed by naloxone (100 microg). These results suggest that mitragynine has a morphine-like action on gastric acid secretion in the CNS.

Animals↗

Studies on the synthesis and opioid agonistic activities of mitragynine-related indole alkaloids: discovery of opioid agonists structurally different from other opioid ligands.

Mitragynine (1) is a major alkaloidal component in the Thai traditional medicinal herb, Mitragyna speciosa, and has been proven to exhibit analgesic activity mediated by opioid receptors. By utilizing this natural product as a lead compound, synthesis of some derivatives, evaluations of the structure-activity relationship, and surveys of the intrinsic activities and potencies on opioid receptors were performed with guinea pig ileum. The affinities of some compounds for mu-, delta-, and kappa-receptors were determined in a receptor binding assay. The essential structural moieties in the Corynanthe type indole alkaloids for inducing the opioid agonistic activity were also clarified. The oxidative derivatives of mitragynine, i.e., mitragynine pseudoindoxyl (2) and 7-hydroxymitragynine (12), were found as opioid agonists with higher potency than morphine in the experiment with guinea pig ileum. In addition, 2 induced an analgesic activity in the tail flick test in mice.

Analgesics↗

Gastric acid secretion stimulated by centrally injected nociceptin in urethane-anesthetized rats.

Nociceptin is a preferred endogenous ligand for the orphan opioid receptor-like 1 (ORL1) receptor. Central administration of nociceptin showed various pharmacological effects on analgesia, cardiovascular and renal responses, food intake, and so on. In the present study, we investigated the effect of nociceptin injected into the central nervous system (CNS) on gastric acid secretion in the perfused stomach of urethane-anesthetized rats. Injection of nociceptin (0.55-5.52 nmol per rat) into the fourth cerebroventricle stimulated gastric acid secretion and the secretion was inhibited in atropine-treated (1 mg/kg, i.v.) and vagotomized rats. The secretion induced by nociceptin (1.65 nmol) was not inhibited by the central injection of naloxone (275 nmol, a non-selective antagonist of opioid receptors). The secretion was significantly inhibited by the central injection of [Phe(1)psi(CH(2)-NH)Gly(2)]nociceptin-(1-13)-NH(2) ([F/G]nociceptin-(1-13), 0.21 nmol, an antagonist of ORL1 receptor), although [F/G]nociceptin-(1-13) alone at higher doses (2.10 and 7.31 nmol) markedly stimulated gastric acid secretion. In the 0-40 min period, the secretion induced by nociceptin was inhibited at least partially by CompB (68.8 nmol, a nonpeptidic antagonist of ORL1 receptor). Injection of nociceptin (5.52 nmol) into the lateral cerebroventricle also stimulated the secretion. Injection of nociceptin did not modify gastric acid secretion stimulated by 2-deoxy-D-glucose (200 mg/kg, i.v.). In conclusion, nociceptin injected into the CNS stimulated gastric acid secretion in rats via the ORL1 receptors and through mechanisms involving the vagus nerve.

Anesthesia↗

Mesaconitine-induced relaxation in rat aorta: involvement of Ca2+ influx and nitric-oxide synthase in the endothelium.

Aconiti tuber, roots of aconite (Aconitum japonicum), is an oriental herbal medicine used for centuries in Japan and China to improve the health of persons with a weak constitution and poor metabolism. We investigated the effects of mesaconitine, one of the aconite alkaloids in Aconiti tuber, on the contraction and free intracellular Ca2+ concentration ([Ca2+]i) level in isolated rat thoracic aorta. Mesaconitine at 30 microM inhibited 3 microM phenylephrine-induced contraction in the endothelium-intact, but not endothelium-denuded, aortic rings. The effect of mesaconitine was dependent on external Ca2+ concentrations. The relaxation induced by mesaconitine was abolished by N(omega)-nitro-L-arginine methyl ester (0.1 mM, an inhibitor of nitric-oxide synthase), as well as the relaxation induced by acetylcholine. Acetylcholine induced relaxation in two phases in our conditions; the initial phase was transient and external Ca2+ -independent, and the second phase was sustained and external Ca2+ -dependent. Treatment with 100 nM thapsigargin, which depleted intracellular Ca2+ stores, inhibited acetylcholine-induced, but not mesaconitine-induced, relaxation. Mesaconitine increased the [Ca2+]i level in endothelial cells by influx of Ca2+ from extracellular spaces. These findings suggest that mesaconitine-induced Ca2+ influx and activation of nitric-oxide synthase in endothelial cells and, thus, induced vasorelaxation in rat aorta.

Aconitine↗

Determination of 41Ca in biological-shield concrete by low-energy X-ray spectrometry.

An X-ray spectrometric method has been developed for the determination of 41Ca in the biological-shield concrete of nuclear reactors. The concrete sample was first decomposed with nitric, hydrofluoric, and perchloric acids. Calcium was then separated from other radionuclides by ion-exchange chromatography and recovered as an oxalate precipitate. X-rays at 3.3 keV from 41Ca in the calcium oxalate pellet were measured. The detection efficiency of the X-ray measurement at 3.3 keV was calculated from those obtained by measuring 55Fe standard pellets at 5.9 keV using mass-absorption coefficients of the calcium oxalate pellet at each X-ray energy. A lower limit of determination of 8 Bq g(-1) was obtained for a sample weight of 1 g.

Journal Article↗

Inflammatory myofibroblastic tumor (IMT) of the pancreas.

Inflammatory myofibroblastic tumor (IMT) is an uncommon mass lesion composed of a variety of inflammatory and other mesenchymal cells. Although IMT was originally reported in the lung, it is now recognized that IMT can occur in a variety of organs. The occurrence of IMT in the pancreas, however, is rare. Here, we report a case of IMT arising from the head of the pancreas in a 55-year-old man. He underwent pancreaticoduodenectomy, with the diagnosis of carcinoma of the pancreas; the pathological diagnosis of the tumor was IMT. By referring to previously reported cases, we conclude that, in the management of IMT in the pancreas, surgical excision is the primary choice, in order to obtain a definitive diagnosis as well as to relieve symptoms, and strict follow-up after surgery is required.

Cholangiopancreatography, Endoscopic Retrograde↗