Disclosure of results of gastric-cancer operations in Japan.
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Humans↗
Biomedical subjects
H Yamauchi
Publications and source records attributed to H Yamauchi.
Long-term changes of hemodynamics and metabolism after carotid artery occlusion.
OBJECTIVE: To investigate whether in selected patients with internal carotid artery (ICA) occlusion and initially normal oxygen extraction fraction (OEF) measured with PET, subsequent changes of cerebral hemodynamics and metabolism occur during long-term follow-up and, if so, whether the changes are associated with atrophy of the corpus callosum or subsequent ischemic strokes. BACKGROUND: The course of the changes in cerebral hemodynamics and metabolism after ICA occlusion remain unclear. After ICA occlusion, an increase in OEF may increase the risk of cerebral ischemia, and an increase in cortical ischemia would cause progression of callosal atrophy. METHODS: The authors used PET and MRI to examine twice seven medically treated patients with unilateral ICA occlusion and initially normal OEF at intervals ranging from 24 to 64 (mean +/- SD, 42 +/- 17) months. No intervening ischemic attacks occurred between the two examinations. RESULTS: In the hemisphere with ICA occlusion, OEF increased and blood flow decreased during follow-up. At the follow-up evaluation, abnormally increased OEF values were found in three patients, in whom ipsilateral ischemic strokes occurred during subsequent follow-up (18 +/- 6 months). A decrease in oxygen metabolism also occurred and was significantly correlated with the decrease of callosal size. CONCLUSIONS: These preliminary findings in a small, selected patient sample suggest that in patients with ICA occlusion and initially normal OEF, deteriorations of cerebral hemodynamics and metabolism during long-term follow-up may be associated with callosal atrophy or subsequent ischemic strokes.
Aged↗
Decreased serum concentrations of nitric oxide metabolites among Chinese in an endemic area of chronic arsenic poisoning in inner Mongolia.
Prolonged exposure to arsenic results in peripheral and cardiovascular manifestations, as does impaired production of endothelial nitric oxide (NO). In vitro studies have indicated that endothelial cells undergo damage by arsenic. However, no information has been available on the relationship between NO synthesis and chronic arsenic poisoning in humans. The present study was designed to reveal this question. The subjects were 33 habitants who continued to drink well water containing high concentrations of inorganic arsenic (mean value = 0.41 microg/ml) for about 18 years in Inner Mongolia, China, and 10 other people who lived in this area but exposed to minimal concentrations of arsenic (mean value = 0.02 microg/ml) were employed as controls. Mean blood concentration of total arsenic was six times higher in exposed subjects than controls; 42.1 vs. 7.3 ng/ml, p <.001. Mean serum concentration of nitrite/nitrate, stable metabolites of endogenous NO, was lower in arsenic-exposed subjects than in controls: 24.7 vs. 51.6 microM, p<.001. In total samples, an inverse correlation with serum nitrite/nitrate levels was strong for blood inorganic arsenic (r = -0.52, p <.001) and less strong for its metabolites, monomethyl arsenic (r = -0.45, p<.005) and dimethyl arsenic (r = -0.37, p<.05). Furthermore, serum nitrite/nitrate concentration was significantly correlated with nonprotein sulfhydryl level in whole blood (r = 0.58, p<.001). In an in vitro study, we demonstrated that inorganic arsenite or arsenate suppresses the activity of endothelial NO synthase in human umbilical vein endothelial cells. These results suggest that long-term exposure to arsenic by drinking well water possibly reduces NO production in endothelial cells, resulting in a decrease in reduced nitrite/nitrate concentrations. Peripheral vascular disorders caused by arsenic may be attributable in part to impairment of NO production in vivo.
Adolescent↗
Glucose metabolism in the rat frontal cortex recovered without the recovery of choline acetyltransferase activity after lesioning of the nucleus basalis magnocellularis.
We measured the cerebral metabolic rate of glucose (CMRglc) by using positron emission tomography (PET) with [18F]fluorodeoxyglucose (FDG) and the choline acetyltransferase (ChAT) activity at 3 days and 3 months after destruction of the nucleus basalis magnocellularis (NBM). Although the frontal ChAT activity remained 20% lower than that of controls even at 3 months post-lesioning, the frontal CMRglc, which was reduced by 40% at 3 days, returned to normal at 3 months, namely CMRglc recovered with time without the recovery of ChAT activity with time. Since glucose metabolism reflects mainly presynaptic neuronal activity, we speculate that presynaptic rearrangement may have some relation to the recovery of CMRglc.
Animals↗
Pregnancy in a woman with a Y chromosome after removal of an ovarian dysgerminoma.
BACKGROUND: It appears to be a general belief that pregnancy might be impossible in women with the XY karyotype. Therefore, it is recommended that patients with dysgerminoma of the ovary associated with the XY karyotype should undergo a bilateral salpingo-oophorectomy. CASE: We report an extremely rare case of a true hermaphrodite with a 20% 46,XX/80% 46,XY karyotype who became pregnant after removal of an ovarian dysgerminoma. The patient had a completely normal female phenotype. A dysgerminoma with ovotestis was found in the right ovary. Two courses of chemotherapy following a right salpingo-oophorectomy were carried out. Nine months later she became pregnant and delivered a healthy male infant. CONCLUSION: A unilateral salpingo-oophorectomy followed by combination chemotherapy can be the treatment of choice for any woman who wishes to preserve her capacity for conception at the time of operation for dysgerminoma of the ovary.
Adolescent↗
Efficacy of leukocyte-depleted terminal blood cardioplegia in congenital heart disease.
OBJECTIVE: Activated leukocytes and their products play a significant role in reperfusion injury and cause microvascular occlusion--the 'no-reflow phenomenon'--which decreases coronary blood flow after the release of the aortic cross-clamp during open-heart surgery. This study was designed to evaluate the efficacy of leukocyte-depleted terminal blood cardioplegia in patients with right ventricular pressure or volume overloaded congenital heart disease undergoing intracardiac repair. SUBJECTS AND METHODS: Fourteen infants and children undergoing intracardiac repair for congenital heart defects were the subjects in this study. Leukocyte-depleted terminal blood cardioplegia was employed in seven patients (Group I). For the control, terminal blood cardioplegia with leukocytes was employed in seven patients (Group II). In order to evaluate the myocardial anaerobic metabolism, the arteriovenous difference in the pyruvate and lactate levels was compared between both groups. Blood samples were taken simultaneously from both the arterial limb of the bypass circuit and the coronary sinus immediately after, and at 5, 10, and at 20 minutes after, the release of the aortic cross-clamp. RESULTS: The coronary arteriovenous difference in the pyruvate and lactate levels demonstrated that the myocardial anaerobic metabolism in Group II was significantly higher than in Group I. The delta excess lactate demonstrated that myocardial hypoxia in Group II persisted significantly longer than in Group I. There was a tendency for the creatine kinase-MB level at 6 hr after surgery to be lower in Group I than in Group II. CONCLUSION: Leukocyte-depleted terminal blood cardioplegia may reduce the myocardial anaerobic metabolism in patients with right ventricular pressure or volume overloaded congenital heart disease undergoing intracardiac repair.
Blood↗
Acquired ileal diverticulum: an unusual bleeding source.
Acquired ileal diverticulum is an uncommon condition and diagnosis is often difficult when bleeding occurs from this source. Here we describe two cases of ileal diverticulum with massive bleeding. Both patients presented with anal bleeding, but upper and lower gastrointestinal endoscopy did not reveal the source. Selective visceral angiography finally detected bleeding lesions in the terminal ileum. Surgical resection was performed in both patients, confirming that the bleeding arose from diverticula less than 1 cm in size. In patients with obscure gastrointestinal bleeding, an ileal diverticulum should be considered, and selective visceral angiography should be performed for precise diagnosis.
Aged↗
Enprostil, a prostaglandin-E(2) analogue, inhibits interleukin-8 production of human colonic epithelial cell lines.
We previously reported that intracolonic administration of enprostil, a prostaglandin-E(2) (PGE(2)) analogue, had therapeutic effects on acute colitis induced in rodents by dextran sulfate sodium (DSS). In addition, production of growth-regulated gene product/cytokine-induced neutrophil chemoattractant-1 [GRO/CINC-1; an interleukin(IL)-8 like cytokine] was suppressed in the inflamed tissues. In the present study we used a human colon cancer cell line (HT-29) to investigate enprostil effects on the IL-8 production of intestinal epithelial cells stimulated by various stimulants. In a MTT assay, concentrations of enprostil >10(-5)M had cytotoxitic effects on HT-29 cells. Furthermore, 10(-6) M enprostil suppressed IL-8 production in HT-29 cells, SW620 and CaCo2 stimulated with interleukin-1 beta (IL-1 beta) or lipopolysaccharide (LPS), but did not suppress this response when cells were stimulated with tumour necrosis factor (TNF)-alpha. These results suggest that enprostil affects a point in the pathway between the IL-1 receptor or LPS receptor and nuclear factor-kappa B(NF-kappa B), without affecting the pathway between the TNF receptor and NF-kappa B, with the latter factor being required for the IL-8 gene transcription. The therapeutic effect of exogenous enprostil on DSS colitis may involve the inhibition of IL-8 production in colonic epithelial cells stimulated by IL-1 beta or LPS.
Colitis, Ulcerative↗
Thoracoscopic major lung resection for primary lung cancer by a single surgeon with a voice-controlled robot and an instrument retraction system.
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Adenocarcinoma↗
New agents for the treatment of infarcted myocardium.
Local delivery of angiogenic growth factors for the treatment of myocardial ischemia has been well documented in various animal models, and clinical trials are now in progress. Our strategy was radically different, based on selective protection of some of the growth factors naturally present within the injured tissue. This protection was obtained by applying a chemically defined substitute for Dextran called RGTA11 (for ReGeneraTing Agent). RGTA is a family of agents, which has properties mimicking those of heparan sulfates toward heparin-binding growth factors (HBGF) and which stimulate tissue repair and protection. Indeed, we have previously shown that RGTA prevents most of the damage resulting from acute skeletal muscle ischemia [FASEB J. (1999) 13, 761-766]. We now show that the same agent can be used for the treatment of myocardial infarction. Acute myocardial infarction was induced in pigs by ligation of the left circumflex artery. One hour later, a single injection of 10 mg of RGTA11 was made in the center of the infarcted area. Three weeks later we observed 1) recovery of 84% of the initial left ventricular ejection fraction (only 55% in saline-treated controls), 2) an almost 50% reduction in the infarct size, 3) a reduction in fibrotic tissue formation, 4) significant preservation of myocytes, and 5) an increase in the number of blood vessels. The treatment of ischemic heart disease with RGTA would have clear advantages over other therapies such as growth factor, gene, or cell transplants, based on a stable, simple, and easy-to-develop chemical product.
Actins↗
Metastatic breast carcinoma masquerading as primary colon cancer.
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Barium Sulfate↗
Atrophy of the corpus callosum associated with a decrease in cortical benzodiazepine receptor in large cerebral arterial occlusive diseases.
OBJECTIVES: It remains controversial whether selective neuronal ischaemic change develops in patients with occlusion of the large cerebral arteries. Previous studies have shown atrophy of the corpus callosum with reduced cortical oxygen metabolism in large cerebral arterial occlusive diseases, which might be indirect evidence of loss of the neurons in cortical layer 3. Recent studies of patients with ischaemic cerebrovascular diseases have demonstrated reduced central benzodiazepine receptor (BZR) binding in the normal appearing cortical areas, which might be more direct evidence of changes of the neurons. Although pathophysiology of the decreased BZR is unclear, a decrease in the cortical BZR binding with neuronal loss would cause atrophy of the corpus callosum. The purpose of this study was to determine whether atrophy of the corpus callosum is associated with a decrease in cortical BZR binding in large cerebral arterial occlusive diseases. METHODS: Seven patients with occlusive diseases of the middle cerebral or internal carotid artery and only minor subcortical infarctions were studied. Single photon emission tomographic images of (123)I labelled iomazenil (IMZ) obtained 180 minutes after injection were analysed for BZR binding. The midsagittal corpus callosum area/skull area ratio (on T1 weighted magnetic resonance images) was compared with the cerebral IMZ uptake/cerebellar IMZ uptake ratio. RESULTS: Compared with 23 age and sex matched control subjects, the patients had significantly decreased callosal area/skull area ratio. The degree of corpus callosum atrophy was significantly and strongly (rho=0.99, p<0.02) correlated with that of the decreases in the mean cerebral cortical IMZ uptake ratio. CONCLUSION: Corpus callosum atrophy may occur in association with a decrease in cortical BZR binding in large cerebral arterial occlusive diseases. Corpus callosum atrophy with decreased cortical BZR binding might reflect cortical neuronal damage in large cerebral arterial occlusive diseases.
Aged↗
Comparison of the pattern of atrophy of the corpus callosum in frontotemporal dementia, progressive supranuclear palsy, and Alzheimer's disease.
OBJECTIVES: The loss of the neurons in layer 3, one of the groups of cortical neurons most vulnerable in various degenerative brain diseases, results in axonal degeneration leading to atrophy of the corpus callosum. Previous studies showed callosal atrophy in three degenerative dementias: frontotemporal dementia (FTD), progressive supranuclear palsy (PSP), and Alzheimer's disease (AD). However, it is unclear whether a characteristic pattern of atrophy is present in each. The objective of this study was to investigate whether the pattern of the callosal atrophy was different among patients with FTD, PSP, or early onset AD. METHODS: Eleven patients with FTD, nine patients with PSP, 16 patients with early onset AD, and 23 normal controls, all age and sex matched, were studied using MRI. The ratios of midsagittal corpus callosum areas to the midline internal skull surface area on T1 weighted images were analyzed. The corpus callosum was divided into quarters: the anterior, middle-anterior, middle-posterior, and posterior portions. RESULTS: Compared with controls, all three patient groups had significantly decreased total callosal/skull area ratio. An analysis of covariance adjusted for the total callosal area/skull area ratio showed that the anterior quarter callosal/skull area ratio in FTD, the middle-anterior quarter area ratio in PSP, and the posterior quarter area ratio in AD were significantly smaller than those in the other three groups. CONCLUSION: Although atrophy of the corpus callosum is not specific to any degenerative dementia, the patterns of the atrophy are different among patients with FTD, PSP, or early onset AD. Differential patterns of callosal atrophy might reflect characteristic patterns of neocortical involvement in each degenerative dementia.
Aged↗
Sensitivity to interferon-alpha and interferon-stimulated gene factor 3 binding activity in human chronic myelogenous leukemia cell line KT-1.
The mechanism of responsiveness of chronic myelogenous leukemia (CML) cells to interferon (IFN)-alpha was examined by using two subclones of CML cell line KT-1 which exhibited significantly different sensitivities to the antiproliferative and apoptosis-inducing effects of IFN-alpha. IFN-stimulated gene factor 3 (ISGF3) formation by IFN-alpha was reduced in the IFN-alpha-resistant subclone compared to the IFN-alpha-sensitive subclone. We conclude that the level of ISGF3 formation is responsible for the difference in IFN-alpha responses between these subclones.
Antineoplastic Agents↗
Corpus callosum atrophy in patients with leukoaraiosis may indicate global cognitive impairment.
BACKGROUND AND PURPOSE: The extent of white matter high-intensity lesions (WMLs) on T2-weighted MR images may be an indicator of cognitive impairment, especially impairment related to frontal lobe dysfunction. However, it is unclear whether the extent of WMLs is an independent predictor of cognitive impairment. In patients with extensive WMLs, atrophy of the corpus callosum may be an important predictor of global cognitive impairment. The purpose of this study was to investigate the relation of the extent of WMLs and callosal size with cognitive functions in a patient population with a wide range of extent of WMLs. METHODS: We studied 62 patients, aged 49 to 86 years, who underwent MRI because of neurological symptoms and were diagnosed as having lacunar stroke or no specific neurological disease: 28 with lacunar infarcts and 34 without. Multivariate analysis was used to test the independent predictive value of patient age, sex, educational level, other medical illness, lacunar infarct, corpus callosum area, and extent of WMLs with respect to scores of Mini-Mental State Examination or verbal fluency task. RESULTS: Only callosal size and age were significant independent predictors of the scores of the Mini-Mental State Examination, while only the extent of WMLs was an independent predictor of the score of the verbal fluency task. CONCLUSIONS: Callosal atrophy may be an important predictor of global cognitive impairment in patients with WMLs, whereas the extent of WMLs per se may be related to impairment of frontal lobe function independent of callosal atrophy.
Aged↗
Phase II evaluation of thalidomide in patients with metastatic breast cancer.
PURPOSE: To determine the efficacy, safety, pharmacokinetics, and effect on serum angiogenic growth factors of two dose levels of thalidomide in patients with metastatic breast cancer. PATIENTS AND METHODS: Twenty-eight patients with progressive metastatic breast cancer were randomized to receive either daily 200 mg of thalidomide or 800 mg to be escalated to 1,200 mg. Fourteen heavily pretreated patients were assigned to each dose level. Each cycle consisted of 8 weeks of treatment. Pharmacokinetics and growth factor serum levels were evaluated. RESULTS: No patient had a true partial or complete response. On the 800-mg arm, 13 patients had progressive disease at or before 8 weeks of treatment and one refused to continue treatment. The dose was reduced because of somnolence to 600 mg for five patients and to 400 mg for two and was increased for one to 1,000 mg and for four to 1,200 mg. On the 200-mg arm, 12 patients had progressive disease at or before 8 weeks and two had stable disease at 8 weeks, of whom one was removed from study at week 11 because of grade 3 neuropathy and the other had progressive disease at week 16. Dose-limiting toxicities included somnolence and neuropathy. Adverse events that did not require dose or schedule modifications included constipation, fatigue, dry mouth, dizziness, nausea, anorexia, arrhythmia, headaches, skin rash, hypotension, and neutropenia. Evaluation of circulating angiogenic factors and pharmacokinetic studies failed to provide insight into the reason for the lack of efficacy. CONCLUSION: Single-agent thalidomide has little or no activity in patients with heavily pretreated breast cancer. Further studies that include different patient populations and/or combinations with other agents might be performed at the lower dose levels.
Adult↗
Surgical treatment of coarctation complex in neonates and infants.
BACKGROUND: There remains controversy regarding the appropriate surgical treatment of coarctation of the aorta associated with intracardiac anomalies in neonates and infants. Furthermore, the relative benefits of one versus two-stage repair, and subclavian flap aortoplasty versus end-to-end anastomosis for some of these lesions, remain controversial. The purpose of this paper is to review our experience with two-stage repair using subclavian flap aortoplasty and to seek an appropriate procedure. METHODS AND RESULT: From June 1996 to November 1999, thirteen patients underwent subclavian flap aortoplasty in our department. The age range was 16 to 101 days (mean 52 days), and the body weight range was 1.9 to 4.5 kg (mean 3.0 kg). Anatomic diagnosis was coarctation with ventricular septal defect (six patients), double outlet right ventricle (two patients), atrioventricular canal defect (one patient), tricuspid atresia (two patients), mitral atresia (one patient), and single atrium and subaortic stenosis (one patient). There was one hospital death in our series due to the progression of pulmonary hypertension 3 months after the operation. The mean follow up for remaining twelve patients was 28 months (range 7 approximately 48 months). There was one reoperation for recurrent coarctation. Three patients underwent pulmonary artery plasty in a second operation because of right pulmonary artery stenosis. We performed the definitive operation for six patients with coarctation with ventricular septal defect and two patients with double outlet right ventricle, and we performed a bidirectional cavopulmonary shunt for four univentricular hearts who are candidates for the Fontan operation. Two patients required Damus-Kaye-Stansel procedure to release restrictive bulboventricular foramen. Three patients underwent a modified Fontan operation after these palliations. In our series, the intraoperative mortality rate for subclavian flap aortoplasty was 0% and the post operative mortality rate was 7.7% (1/13). Ten patients underwent the final operation successfully, and further two patients are considered good candidates for the final operation. The overall mortality was 7.7% (1/13). CONCLUSION: Two-stage repair appears to offer a good prognosis for neonates and infants with a coarctation complex. Subclavian flap aortoplasty showed the lowest rate of restenosis. However, late mortality may be associated with the progression of pulmonary vascular disease and the presence of associated severe cardiac anomalies. Although Fontan candidates need staged operations, if biventricular repair is feasible, one-stage repair would be a reasonable procedure considering the progression of the pulmonary vascular disease and the distortion of the pulmonary artery due to pulmonary artery banding. It would appear to improve the quality of life of those children if a one-stage operation can be performed with reasonable risk and good midterm outcome.
Aorta↗
Bile acid metabolism, bacterial bowel flora and intestinal function following ileal pouch-anal anastomosis in dogs, with reference to the influence of administration of ursodeoxycholic acid.
The pathophysiology following a total colectomy with ileal pouch-anal anastomosis (IPAA) has not been sufficiently clarified yet. We investigated bile acid metabolism, bacterial bowel flora and transit of the alimentary tract after IPAA, with reference to administration of ursodeoxycholic acid (UDCA) in dogs undergoing IPAA. Ten adult beagle dogs underwent IPAA at one stage, and were observed for 12 months. UDCA (100 mg/day) was administered orally to five dogs, and the other five did not. In the UDCA(+) group, UDCA replaced other bile acids, especially cholic acid, accounting for 16.5% of gallbladder bile at 12 months after surgery. Both plasma levels and postprandial increase of total bile acids remained unchanged in the UDCA(+) group, but decreased in the UDCA(-) group at 12 months. Fecal excretion of bile acids tended to be smaller in the UDCA(+) group, and the ratio of secondary to primary bile acids was larger in the UDCA(-) group. Almost all the bile acids were in free form in stool, and UDCA constituted 19% in the UDCA(+) group. The transit time of the whole alimentary tract was elongated by administering UDCA, especially at an early period after IPAA. Although both anaerobic and aerobic bacteria decreased after IPAA, the latter decreased more in stool, resulting in an increase in the ratio of total anaerobes/total aerobes, especially in the UDCA(-) group. The decrease in Bacteroidaceae and Lactobacillus after IPAA was slightly smaller in the UDCA(+) group. Administration of UDCA following IPAA was efficient to induce rapid intestinal adaptation and also to keep the bile acid fraction in the ileal pouch less harmful.
Administration, Oral↗