Treatment of multiple rectal carcinoids by endoscopic mucosal resection using a device for esophageal variceal ligation.
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Biomedical subjects
Publications and source records attributed to K Oshiro.
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INTRODUCTION: Infantile hypertrophic pyloric stenosis (IHPS) consists of hypertrophy of the muscular layer of the pylorus. Its etiology is still unknown. In the last years only few jobs that studied the extracellular matrix (ECM) in the muscular layer in the IHPS have been reported. Our aim was to investigate the expression of two ECM molecules: chondroitin-sulfate proteoglycan (CSPG) and fibronectin (FN), and fibroblasts. MATERIAL AND METHODS: Full-thickness muscle biopsy specimens were obtained from 33 IHPS patients at pyloromyotomy and 12 controls. Indirect immunohistochemistry was performed using CSPG, FN and fibroblasts monoclonal antibodies. The results were showed by a semiquantitative scale as follows: strong (++), moderate (+), weak (+/-), and absent (-). RESULTS: We demonstrated that the CSPG immunoreactivity was localized in the connective tissue septa and the expression of FN molecules in the pericellular space. Both molecules were significantly the increased in the muscle layer of the pylorus with IHPS in relation to control pylorus. We also demonstrated a marked increased expression in the number of fibroblasts in the muscle layer of the pylorus with IHPS. Even-though the most striking increase was localized in the septa, we also observed great number of fibroblasts amongst the smooth muscle cells. CONCLUSIONS: We suggest that IHPS is characterized, not only by the muscle layer hypertrophy, but also by the increase of several ECM molecules, such as CSPG and FN. We also think that the increase of fibroblast could explain the higher expression of both ECM molecules in the muscle layer of pylorus in IHPS.
OBJECTIVE: Hypertrophic nerves have long been considered a histopathologic feature of the aganglionic segment in Hirschsprung disease, but they remain incompletely explained. The purpose of this study was to define the nature and diagnostic importance of hypertrophic nerves in Hirschsprung disease and to clarify their relation to nearby smaller nerve fibers. METHODS: We used an immunoperoxidase staining technique to compare the distribution of 2 nerve markers-erythrocyte-type glucose transporter (GLUT-1), a marker of perineurium, and nerve growth factor receptor, a marker of both nerve fibers and perineurium-in aganglionic tissue (12 resected specimens and 4 rectal biopsies) and control tissue (6 autopsy specimens and 17 rectal biopsies) of children. RESULTS: In control ganglionic tissue, the myenteric and submucosal areas contained only occasional GLUT-1-positive nerves (usually less than 50 microm in diameter), but extramural extrinsic (serosal) nerves were invariably positive for GLUT-1. In aganglionic tissue, GLUT-1-positive nerves in the myenteric and submucosal areas were frequent and included both large (50-150 microm) and small (<50 microm) diameter nerves. Nerve growth factor receptor-positive fibers were frequent in all layers of all tissue studied. In aganglionic bowel, a distinct perineurium could be identified in the largest nerves, but nerve growth factor receptor had poor discrimination for small perineurium-sheathed nerves. CONCLUSION: Most nerves, of both large and small diameter, in the myenteric and submucosal plexus of aganglionic bowel are GLUT-1 positive. Serosal extrinsic nerves stain identically, supporting the interpretation that the mural nerves are of extrinsic origin. Mural GLUT-1-positive nerves, when they are multiple and especially when they are greater than 50 microm in diameter (a figure which may be used as a threshold for hypertrophic nerves), are suggestive of Hirschsprung disease.
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A 55-year-old male patient underwent CABG for triple-vessel disease using the minimal access approach. The procedure was performed through a limited (10 cm) left para-sternal thoracotomy using extracorporeal circulation established with a usual aortic cannula, and pulmonary arterial and right atrial drainage. The myocardium was protected by antegrade administration of cold cardioplegic solution while the aorta was being cross-clampled. The saphenous vein graft was connected sequentially to the 4 PD and OM branches, and the left internal thoracic artery was grafted to the LAD. The postoperative course was uneventful and coronary angiography showed that all three grafts were patent. The patient was discharged one week postoperatively.
The methanol extract from Machilus thunbergii showed a suppressive effect on umu gene expression of the SOS response in Salmonella typhimurium TA1535/pSK1002 against the mutagen, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1), which requires liver metabolizing enzymes. The methanol extract from M. thunbergii was successively re-extracted with chloroform, butanol and water. A suppressive compound in the chloroform extract fraction was isolated by SiO2 column chromatography and identified as meso-dihydroguaiaretic acid by GC-MS, and 1H- and 13C-NMR spectroscopy. Meso-dihydroguaiaretic acid inhibited of the SOS-inducing activity of Trp-P-1 in the umu test. Gene expression was suppressed by 62% at less than 0.18 mumol/ml, the ID50 value being 0.08 mumol/ml. Compound 1 was also assayed with aflatoxin B1 (AfB1) and showed a suppressive effect.
1. A 6-week gliclazide treatment improved left ventricular developed pressure and left ventricular end-diastolic pressure, left ventricular pressure-rate products in isolated working hearts from streptozotocin-induced diabetic rats. 2. Post-ischemic recovery in heart rate, left ventricular developed pressure, left ventricular end-diastolic pressure, left ventricular pressure-rate products and cardiac work were also shown in gliclazide-treated diabetic rats. 3. Gliclazide treatment did not modify the degree of insulinopenia and hyperglycemia, nor the myocardial energy metabolism during ischemia-reperfusion. 4. The results suggest that the gliclazide treatment has a cardioprotective effect on basal and post-ischemic cardiac functions of chronic diabetes.
We modified Studer's bladder substitute technique and constructed continent urinary reservoir for 7 patients with bladder tumors after transprostatic cystoprostatectomy. Studer's bladder substitute technique is characterized by both a tubular isoperistatic proximal limb of 20 cm of the ileum in continuity with the pouch constructed using the detubularized ileum and the ureters reimplanted into the proximal part of the limb using a simple lateral anastomosis of the ureters to the end of the limb. Our modifications, transprostatic resection, was that distal one third or fourth of the prostate was left after cystoprostatectomy followed by either enucleation of the whole residual prostatic tissue including the urethra (type II) or sharp resection of the tissue leaving the urethra (type III). A small hole in the lowest part of the pouch was anastomosed either to the residual prostatic capsule (type II) or to the residual prostatic urethra (type III). Our modified Studer's technique was simple, easy to perform, and had low risk of massive bleeding especially from the central vein overlying the appex of the prostate. Clinical results were as follows; 1) all patients were satisfied with the passing of their urine per urethra without any cutaneous stoma, 2) no patients had clinical signs of pyelonephritis after discharge, 3) urine was not infected.(ABSTRACT TRUNCATED AT 250 WORDS)
A 16-year-old boy was admitted to the hospital because of chest pain, dyspnea, and syncope. Physical examination revealed blood pressure of 100/60 mmHg, regular pulse of 120 beats/min, and respiratory rate of 30/min. Pulsation of the right ventricle was palpable in the left margin of the parasternum. An increased second sound was audible in the second inter-costal lesion of the left subclavicle mid-line. Results of blood tests were close to normal limits, except for slight leukocytosis and elevation of the LDH value. Analysis of artery blood gas showed hypoxia. The chest x-ray film showed cardiac enlargement. The value of systolic pulmonary artery pressure was estimated to be 47 mmHg by the cardiac echogram, which revealed enlargement of the right ventricle. Pulmonary embolism was suspected from the above findings. The value of pulmonary artery pressure was found to be 49/19 mmHg by Swan-Ganz catheter. Angiography of the pulmonary artery revealed filling defects of right in the right pulmonary artery. Tissue plasminogen activator was injected directly to the right pulmonary artery. After that, chest pain and dyspnea were relieved. In addition, arterial oxygen improved and pulmonary artery pressure decreased. At the 6th day after admission, the defect in the pulmonary artery angiography disappeared. Deep vein thrombosis of both femoral veins was recognized as a cause of pulmonary embolism by angiography of the femoral vein.
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To find predictive parameters for development and progression of adult T-cell leukemia (ATL) in human T-cell leukemia virus type-I (HTLV-I) carriers, we investigated cellular immune responses such as mitogenic responses and natural killer activity of the peripheral blood mononuclear cells (PBMC). And serum or plasma levels of cytokines, including tumor-necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and immunosuppressive acidic protein (IAP), were also measured in patients with ATL, healthy HTLV-I carriers and healthy HTLV-I non-carriers as controls. Results are as follows: (1) increased spontaneous proliferation and decreased mitogenic responses of PBMC already existed in HTLV-I carriers; (2) IAP was significantly higher in patients with acute/lymphoma type ATL than in those with chronic/smoldering type, HTLV-I carriers and HTLV-I non-carriers. These results suggest that spontaneous proliferation or mitogenic responses and IAP may be useful parameters for the development and progression of ATL from the carriers. Since HTLV-I carriers already have various grades of immunosuppression, we should seriously try to prevent further HTLV-I transmission.
The chronic effects of tolbutamide on myocardial contractility of the diabetic heart during ischemia and reperfusion were evaluated in perfused, isolated rat hearts. Five experimental groups were used: (1) control rats (C), (2) insulin dependent diabetic rats (IDDM, single intravenous injection of 60 mg/kg streptozotocin (STZ) in male Sprague-Dawley rats), (3) non insulin dependent diabetic rats (NIDDM; single subcutaneous injection of 90 mg/kg STZ in 5 day neonates), (4) tolbutamide-treated IDDM and (5) NIDDM (T-IDDM, T-NIDDM; giving tolbutamide 100 mg/kg/day for 6 weeks via an orogastric tube every day, respectively). At 14 weeks of age, experiments were performed using a Langendorff perfused heart preparation. After equilibration, T (myocardial developed tension), +dT/dt (contraction velocity), -dT/dt (relaxation velocity) and RT (resting tension) were measured during a 15 min period of global ischemia, followed by reperfusion for 20 min. Basal values of T increased in both T-IDDM and T-NIDDM, compared to IDDM and NIDDM, respectively. The percent recovery rate of +dT/dt in T-IDDM increased significantly during both ischemia and reperfusion, but the change in T-NIDDM was not significant. The recovery rates of -dT/dt in T-IDDM and T-NIDDM were significantly higher throughout reperfusion than in IDDM and NIDDM, respectively. On the other hand, that of T in T-IDDM and T-NIDDM were significantly higher than IDDM and NIDDM throughout ischemia and reperfusion, respectively. The RT was significantly higher in IDDM than in C and NIDDM throughout ischemia and reperfusion. The RT was significantly lower during ischemia in IDDM, but it did not differ significantly from IDDM during reperfusion. These results indicate that chronic oral administration of tolbutamide directly improved myocardial contractility throughout ischemia and reperfusion regardless of the improvement of glycemia. The improvement was also greater in IDDM than in NIDDM.
An elderly case of idiopathic retroperitoneal fibrosis (IRPF) with bilateral ureteral obstruction was reported. A 74-year-old man was admitted with complaints of general fatigue and loss of appetite. An elastic hard mass with a smooth surface was palpated in the left upper quadrant of the abdomen. Abnormal ESR and CRP were noticed. Abdominal ultrasonography showed both a homoechoic mass which surrounded the aorta in the retroperitoneal space and bilateral hydronephrosis. Computed tomography revealed a retroperitoneal mass involving bilateral ureters. Magnetic resonance imaging demonstrated a mass with a sharp image and signal intensity. Furthermore the morphological relationship between the mass and the ureters and major vessels clearly indicated the characteristics of benign retroperitoneal fibrosis. Based upon the above findings, a diagnosis of IRPF was made. After confirming the histological diagnosis by biopsy, treatment consisting of bilateral ureterolysis, intra-abdominal transposition of ureters and oral administration of prednisolone was performed, resulting in a normalization of laboratory findings. Analysis of 86 previously cases of IRPF reported up to 1990 in Japan, revealed the peak age to be in the 7th decade with predominance in males (males: females = 57:29).
Acute hemodynamic and coronary vasodilating effects of nicorandol (SG-75, Sigmat; CAS 65141-46-0) and glyceryl trinitrate (GTN, nitroglycerin) were examined in 20 subjects under cardiac catheterization and coronary arteriography. Nicorandil 4 mg i.v. produced significant increases in heart rate, cardiac index and stroke volume index and significant decreases in systolic, diastolic and mean blood pressure, pulmonary capillary wedge pressure, left ventricular enddiastolic pressure, systemic vascular resistance and total pulmonary resistance. Degree of percent changes in these parameters by nicorandil were similar to that by GTN 0.3 mg i.v. Coronary vasodilating effects of both drugs were also at the same degree. Results indicate that nicorandil has cardiovascular and coronary vasodilating effects similar to those of GTN when administered intravenously.
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In order to test the safety of glucagon (GG), the immunogenicity of GG was studied in rabbits and guinea pigs. Any sensitization, as revealed by anaphylactic shock, Arthus reaction, passive cutaneous anaphylaxis (PCA) or radioimmunoassay, was not demonstrated in animals immunized with GG alone. The anti-GG antibodies were detected by PCA and radioimmunoassay in two of the five animals immunized with GG mixed with Freund's complete adjuvant. Anti-GG IgE antibody production in mice was found in one of the ten mice given 570 micrograms and three of the six mice given 1,000 micrograms of GG with aluminum hydroxide gel (Alum), but other doses of GG with Alum produced no IgE antibody. These results indicate that the antigenicity of GG is very weak.
No consensus about the antigenicity of monocomponent insulin has yet been reached. We have therefore administered different insulin preparations to rabbits and rats to determine IgG and IgE antibody production. The preparations used were porcine monocomponent insulin, conventional bovine and porcine insulin powders, porcine b-component and synthesized porcine mono-desamido-insulin and hexa-desamido-insulin. In rabbits, porcine b-component was the most antigenic preparation, followed by conventional bovine and porcine insulins. No antibody production was observed with the other preparations. In rats the 60 h passive cutaneous anaphylaxis test showed virtually no insulin IgE antibody production in response to porcine monocomponent insulin. However, if porcine b-component or porcine hexa-desamido-insulin was employed both for sensitisation and as the challenging antigen, positive skin reactions were observed with demonstration of insulin IgE antibodies. Our results confirm the low antigenicity of the pharmaceutical preparation of porcine monocomponent insulin and suggest that porcine hexa-desamido-insulin and porcine b-component administration may result in the production of reagin-type antibodies.