[Clinical symptoms of gastric ulcer in the aged].
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Biomedical subjects
Publications and source records attributed to F Yamaguchi.
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The immunopharmacological behavior of DMG, an antitumor polysaccharide, was studied in mice. DMG administered ip or sc stimulated peritoneal macrophages to produce high levels of interleukin-1 activity, which can amplify successive immune responses. DMG dose-dependently and schedule-dependently increased the cellular immune response against allogeneic tumor cells and the humoral immune response to sheep erythrocytes. DMG also enhanced nonspecific antitumor effector functions, such as natural killer activity of spleen and peritoneal cells, and the cytostatic activity of peritoneal macrophages. Peritoneal macrophages activated by ip or sc injection of DMG exhibited high cytostatic activity, especially after exposure in vitro to lymphokine supernatants containing macrophage activation factor. Moreover, granulocyte/macrophage colony-stimulating activity in the serum increased 2-10 hr after DMG administration. Thus, DMG potentiated antigen-specific immunological functions and nonspecific functions of host defense systems against cancer both qualitatively and quantitatively.
Levan fructotransferase of the bacterium Arthrobacter ureafaciens, which produces di-D-fructose 2,6':6,2' dianhydride (difructose anhydride IV) from levan by an intramolecular transfructosylation reaction, was purified to give a single protein band of pI 4.5-4.7 on isoelectric focusing. It had a molecular weight of 128,000 on gel-filtration on Sephadex G-200 and 60,000 on SDS-polyacrylamide disc gel-electrophoresis, suggesting that the enzyme is composed of two identical subunits. The shortest levanoligosaccharide chain required for the difructose anhydride IV formation was determined to be tetraose. TLC of the enzymic digest of a modified levanhexaose derived from levanhexaose by the reduction of the reducing end to an alditol residue with sodium borohydride gave the difructose anhydride IV spot, suggesting that the enzyme attacks the modified levanhexaose molecule from the direction of the non-reducing fructose end. The enzymic digests of levantetraose, -pentaose, and -hexaose as the substrate gave, in addition to the difructose anhydride IV spot, spots of oligofructans of lower mobility than the original substrate on TLC. From the digest of levantetraose, a hexaoligofructan and a smaller amount of a pentaoligofructan but no fructose were separated, indicating enzymic intermolecular levanbiosyl and fructosyl transfer reactions.
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Regional cerebral blood flow measured in patients with dementias (N = 60) using xenon Xe 133 inhalation was compared with measurements in health volunteers (N = 70). Volunteers were age-matched (N = 15); another group was younger. In normal aging, there is progressive, diffuse reduction of weight and flow of gray matter (F1) but not of white matter. Therefore, age-matched control subjects are necessary in studies of dementia. In Alzheimer's disease (AD), F1 shows bilateral and symmetrical reduction. The F1 reduction correlated with atrophy estimated by computerized tomography, and duration and severity of dementia. In multi-infarct dementia (MID), bilateral hemispheric F1 was patchily reduced. Cerebral vasodilator response to 5 percent carbon dioxide inhalation was reduced in patients with MID but was normal in patients with AD. Patients with Wernicke-Korsakoff's dementia showed normal values. Patients with dementia due to multiple sclerosis showed significant F1 reduction compared with normal subjects. Standard behavioral activation in all patients with moderate to severe dementia failed to produce normal F1 increases.
Cerebral vasodilator responses to hypercarbia were tested during inhalation of 5% CO2 in air by normal volunteers with and without risk factors for cerebral atherosclerosis. The results were compared with those of patients with hemispheric infarction or ischemia or vertebrobasilar arterial insufficiency (VBI). Regional cerebral blood flow was measured by the 133Xe inhalation method before and during hypercarbia. Responsiveness to CO2 was expressed as the percentage increase of gray matter flow per mm Hg of end-tidal CO2 tension. Cerebral vasodilator responsiveness is mildly impaired by the atherosclerosis of normal aging, is moderately impaired in normal subjects with risk factors for cerebral atherosclerosis, and is greatly impaired in patients with symptomatic hemispheric ischemia and VBI. Testing regional cerebral blood flow with CO2 appears to be a useful, harmless screening test for cerebral atherosclerosis.
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Regional cerebral blood flow (rCBF) was measured by 133Xe inhalation in 46 normal volunteers, aged 21 to 63 years, and 14 neurologically asymptomatic subjects above age 40 with risk factors for atherothrombotic stroke, including hypertension, diabetes mellitus, and hyperlipidemia. In normal volunteers, there was diffuse and progresive reduction of gray matter flow and weight as well as increases of cerebrovascular resistance (CVR) with advancing age. Reduction of gray matter flow with advancing age appears to be attributed in part to neuronal atrophy and in part to cerebral arteriosclerosis. Regional increases of CVR and reduction of gray matter flow with advancing age were most evident in the middle cerebral arterial (MCA) distribution and were enhanced by the association of risk factors. Development of cerebral arteriosclerosis with age and/or risk factors appears to be most evident in MCA distribution.
The question of contamination of cerebral clearance curves utilized for measuring regional cerebral blood flow by radioactivity derived from the nasopharyngeal air passages following inhalation of 133Xe was tested in patients with chronic tracheostomy. The peak counts for head curves were 5--9% higher when 133Xe was inhaled via a face mask than when inhaled via the tracheal stoma. Calculated flow values using standard recommended start-fit-times were not significantly different between these two different methods. Present results indicate that neither overestimation of fast flow values due to contamination from rapid 133Xe washout recorded from the air passages nor the underestimation of slow flow due to contamination from 133Xe trapped in the air sinuses produced significant measurement errors. However, if earlier start-fit-times were used, flow values were artificially high, particularly for brain stem/cerebellar probes because of an initial rapid decline in the head desaturation curves due to an arterial peak believed to be derived from the basilar artery.
Regional cerebral blood flow (rCBF) was measured as fast flow clearance (F1) and the initial slope index (ISI2) after inhalation of 133Xe in 30 patients with subarachnoid hemorrhage (SAH). Vasomotor responsiveness to reduction in end-tibal PECO2 was examined in those patients who could carry out this procedure satisfactorily as a test for the presence or absence of vasospasm. F1 and ISI2 were significantly reduced in patients with recent SAH compared to 35 age-matched normal volunteers. The degree of reduction of F1 and ISI2 correlated directly with severity of the neurological deficit graded according to the Hunt and Hess rating scale. Topographic reductions of rCBF correlated with angiographically demonstrated vasospasm or intracerebral hematoma. The degree of impairment of cerebral vasomotor responsiveness to reduction of PECO2 by hyperventilation also correlated with the severity of vasospasm demonstrated angiographically in 16 patients. The reductions of rCBF values were maximal during the first week after SAH but returned gradually toward normal by the 5th week. Individual patients with SAH whose lowest F1 values were above 50 ml/100 g brain/min tolerated surgical intervention best. Non-invasive measurements of rCBF after SAH appear to be helpful in estimating the presence and time course of vasospasm, in recognizing the development of normal pressure hydrocephalus, and in planning medical and surgical management.
Cerebral vasoconstrictive capacitance was measured during voluntary hyperventilation hypocapnia in 22 healthly normal volunteers aged 21--65 years by serial 133Xe inhalation estimates of rCBF by the initial slope index method of Risberg (ISI2) in the steady state followed by the hypocapnic state. End-tidal PCO2 was monitored by a capnograph. There was significant linear correlation between reduction of PECO2 and the ISI2 values. Significant reduction of cerebral vasoconstrictive response to hypocapnia was found with normal advancing age which is attributed to (1) minor atherosclerosis or loss of elasticity of cerebral vessels with advancing age, (2) the presence of an ischemic threshold during hyperventilation at which CBF tends to stabilize.
Serial measurements of regional cerebral blood flow were made by the 135Xe inhalation method during the early stages of sleep and wakefulness in eight normal volunteers and 12 patients with narcolepsy. Electroencephalogram, electro-oculogram, and submental electromyogram were recorded simultaneously. In normals, mean hemispheric gray matter blood flow (Fg) during stages I and II sleep was significantly less (-9.2 percent) than waking values (84.3 +/- 13 ml per 100 gm brain per minute). Maximum regional blood flow decreases during sleep occurred in the brainstem-cerebellar (-25.1 percent), right inferior temporal (-23.1 percent) and bilateral frontal (-18.9 percent) regions (p less than 0.05). In patients with narcolepsy, mean hemispheric Fg while awake was 80.5 +/- 13 ml per 100 gm brain per minute. During REM sleep (n = 2), mean hemispheric Fg increased by 9.8 percent concurrently with large increases (+34.6 percent) in brainstem-cerebellar region flow. During stages I and II sleep without REM (n = 6), there were significant increases in mean hemispheric Fg of +/-20.2 percent (p less than 0.01) and brainstem-cerebellar Fg of 38.0 percent (p less than 0.01), just the opposite of changes in normals. In narcolepsy, there appears to be a reversal of normal cerebral deactivation patterns, particularly involving the brainstem, during stages I and II sleep.
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