Ultraviolet inverse-photoemission and photoemission spectroscopy studies of diluted magnetic semiconductors Cd1-xMnxTe (0 <= x <= 0.7).
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Biomedical subjects
Publications and source records attributed to K Mimura.
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Macrophage scavenger receptors mediate the recognition of a wide range of negatively charged macromolecules including acetylated low density lipoproteins (AcLDL). Chinese hamster ovary (CHO) cells were cultured in the presence of increasing concentrations of simvastatin, a cholesterol biosynthesis inhibitor, and AcLDL as the sole source of exogenous lipoproteins. The cells surviving under these conditions specifically bound 125I-labeled AcLDL with high affinity and degraded them via an endocytic pathway. Unexpectedly, the association and degradation of 125I-labeled AcLDL by these CHO cells were not inhibited by dextran sulfate, fucoidan, and polyinosinic acid, competitors of macrophage scavenger receptors, but were completely inhibited by maleylated bovine serum albumin. Furthermore, these cells effectively took up negatively charged liposomes containing acidic phospholipids such as phosphatidylserine and phosphatidic acid, whereas CHO cells expressing macrophage scavenger receptors did not. AcLDL and negatively charged liposomes were cross-competed with each other. Northern blot analysis using the cDNA for the macrophage scavenger receptor revealed that these CHO cells did not express this receptor. From these observations, we conclude that the isolated CHO cells express a novel type of AcLDL receptor, which is distinct from macrophage scavenger receptors with respect to ligand specificity and competitor sensitivity.
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Pseudomonas aeruginosa septicemia rarely occurs in non-immunocompromised adults. We present a case of septic shock following Pseudomonas aeruginosa pneumonia in a previously healthy 48-year-old woman. The onset was sudden, with back pain, pyrexia and shock. Chest radiographs revealed pneumonia, and Pseudomonas aeruginosa was identified from blood and sputum cultures. Therapy with dopamine, piperacillin and fluid replacement led to a prompt recovery. Laboratory tests failed to reveal any immunological deficits. Including this case, only five cases of Pseudomonas aeruginosa septicemia in patients though to be non-immunocompromised have been reported. Two remarkable features of this type of Pseudomonas infection are apparent: i) it commonly develops from pneumonia and ii) it has a better prognosis than that in immunocompromised hosts.
A neutral lipid class was isolated by thin-layer chromatography from the skin surface lipids of the hairless mouse. The fraction migrated faster than triglycerides and had a migration rate similar to that of diacyl alkanediols (diester wax). Upon deacylation, however, the long-chain diols were identified as 1-alkylglycerol ethers based on their chromatographic properties and on the mass spectra of their nicotinylidene derivatives. Thus, the skin lipid fraction was identified as 1-O-alkyl-diacylglycerol. The alkyl moieties were all saturated and even-numbered and ranged in chainlength from C16 to C22 with 1-O-hexadecylglycerol amounting to 34% of the total glycerol ether moieties. The fatty acids derived from this lipid fraction were mostly monoenoic with chainlengths ranging from C16 to C24. The major acyl component was eicosenoic acid (20:1) representing 61% of the total fatty acids.
Vascular endothelial cells, which are polyfunctional, play an important role in the pathogenesis of diabetic complications. The increase in vascular permeability, ie, regulated by vascular endothelial cells, has been reported in patients with diabetes mellitus complicated by angiopathy. To determine the role of hyperglycemia in endothelial cell permeability, we examined the effect of high concentrations of glucose on the permeability of cultured bovine aortic endothelial cells. The permeations of albumin and fluorescein-labeled dextran (FD) across endothelial cell monolayers were increased when cultured with a high concentration of glucose (400 mg/dL). This increased permeation of albumin but not FD was temperature-dependent and was partially reduced by adding 100 mumol/L ponalrestat (ICI 128,436, Statil; ICI, Cheshire, UK), which is an aldose reductase inhibitor. Stimulation or inhibition of Na,K-adenosine triphosphatase (ATPase) in bovine aortic endothelial cells failed to alter their permeability. These findings suggest that high concentrations of glucose enhance transendothelial permeability of albumin in part by activating the polyol pathway, but independently of Na,K-ATPase activity.
The effects of high glucose concentrations on the selective permeability of a layer of cultured bovine vascular endothelial cells (ECs) were investigated. ECs were derived from the intima of the thoracic aorta and permeability to nonglycated albumin, glycated albumin, and fluorescein dextrans (FDs) of molecular mass to albumin was measured. ECs were cultured on a filter coated with type I collagen and preincubated in the presence of various glucose concentrations for 96 h. Human serum albumin was glycated by incubation with glucose in vitro. Nonglycated and glycated albumin were separated by affinity column chromatography. The permeation rates of nonglycated and glycated albumin as well as those of neutral and anionic FD through the EC layer were increased by preincubation of cells with high glucose concentrations (22.2 and 44.4 mmol/l). The permeation rate of glycated albumin was significantly less than that of nonglycated albumin at all glucose concentrations tested, whereas the permeation rate of anionic FD was significantly lower than that of neutral FD only at a physiological glucose concentration (5.6 mmol/l). The aldose reductase inhibitor ponalrestat partially inhibited the high glucose-induced increase in trans-endothelial permeation of albumin (both nonglycated and glycated), but had no effect on the increased permeation of FD. These results indicate that high glucose concentrations enhance trans-endothelial permeability to albumin and FD and may disturb the barrier function of vascular ECs. Furthermore, metabolism of glucose via the polyol pathway may contribute to abnormalities in trans-endothelial permeability.
It has been reported that some modified low-density lipoproteins (LDLs) such as glycated LDL and malondialdehyde-rich LDL (MDA-LDL) probably exist in the circulation. The present study was undertaken to investigate the in vitro and in vivo metabolism of MDA-LDL occurring in chronic haemodialysis patients and the effects of alpha-tocopherol on these abnormalities. MDA-LDL from haemodialysis patients was degraded more rapidly by human monocyte-derived macrophages and disappeared more slowly from the circulation when compared with LDL from healthy controls. Treatment with alpha-tocopherol at doses of 600 mg/day for 2 weeks resulted in improvement of these metabolic abnormalities depending upon the degree of return to normal MDA concentrations in LDL.
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By means of the euglycemic three step hyperinsulinemic clamp technique, suppression of endogenous C-peptide secretion by exogenous insulin infusion was evaluated in patients with insulinoma (n = 8) and healthy controls (n = 20). Euglycemic hyperinsulinemic clamp studies were performed with an artificial pancreas (STG-22 NIKKISO, Tokyo, Japan). Insulin (Actrapid human insulin) was infused at the rate of 1.12, 3, and 10 mU/kg/min. Plasma glucose levels were clamped at 80 mg/dl, and high insulin levels were maintained in all subjects (833 +/- 78 microU/ml at the rate of 10 mU/kg/min insulin infusion). During the clamp studies, plasma C-peptide levels in normal subjects declined from 2.0 +/- 0.2 to 0.9 +/- 0.2 ng/ml, indicating suppression of endogenous insulin secretion by exogenous insulin infusion. In patients with insulinoma, plasma C-peptide levels were 3.1 +/- 1.6 ng/ml in the basal state, and were not suppressed even during exogenous hyperinsulinemia. We concluded that the feedback inhibition of insulin secretion by exogenous insulin infusion is attenuated in patients with insulinoma, and that the hyperinsulinemic clamp technique may be a useful method for the diagnosis of insulinoma.
To evaluate the efficacy of the schedule currently recommended for immunization with trivalent oral poliovirus vaccine (TOPV) (i.e., at birth, 6 weeks, 10 weeks, and 14 weeks after birth), we randomly assigned 452 infants into test (231 infants) and control (221 infants) groups. The test group received TOPV as currently recommended, and the dose at birth was omitted for the control group. At 10, 14, and 18 weeks of age, the levels of poliovirus neutralizing antibodies as well as seroconversion rates were consistently higher for the test group than for the control group. The final seroconversion rates against poliovirus types 1, 2, and 3 were 83.5%, 91% and 83%, respectively, for the test group and 75%, 83.2%, and 79.1%, respectively, for the control group. The TOPV immunization schedule starting at birth therefore produced better results. Seroconversion rates as well as antibody levels were highest in infants with low maternal antibodies.
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A 37-yr-old woman was admitted to our hospital for evaluation of diabetes mellitus, liver cirrhosis and primary amenorrhea. Serological and hematological examinations revealed that she suffered from hemochromatosis secondary to congenital dyserythropoietic anemia (CDA), characterized by ineffective hematopoiesis and erythropoietic dysplasia. Iron deposition was suggested by MRI on the pancreas, liver and pituitary gland. Endocrinological examinations demonstrated that she had isolated gonadotropin deficiency and ovarian failure, resulting in hypogonadotropic hypogonadism. In addition, despite normal responses of serum cortisol and plasma aldosterone to ACTH and furosemide-standing tests, respectively, serum dehydroepiandrosterone (DHEA) responded poorly to ACTH test, suggesting selective damage of zona reticularis in adrenocortical steroidogenesis in association with hemochromatosis.
To determine if wound excision and superoxide dismutase (SOD) treatment prevent ongoing lipid peroxidation after burn injury, the plasma, kidney, and lung lipid peroxide (LPO) levels in 25% total body surface area (TBSA) burned rats was studied. The animals were given intraperitoneal bovine copper-, zinc-SOD (Cu/Zn-SOD) (50,000 U/kg dissolved in saline) or saline immediately after burns and were operated by wound debridement and allograft 2 hours after the burn. We measured LPO levels of 6-hour postburn plasma and tissues by the thiobarbituric acid (TBA) method, and measured the manganese SOD (Mn-SOD) by an enzyme-linked immunosorbent assay. Wound excision alone prevented the increase of plasma LPO levels but could not prevent the increase in tissues. The combination of wound excision and Cu/Zn-SOD treatment markedly inhibited the increase in both plasma and tissue LPO levels after the burn, but did not prevent the increase in Mn-SOD. Wound excision in conjunction with SOD-treatment might be therapeutic in the management of severe burns.
Ultrasoundcardiogram (UCG) was measured to evaluate the effects of 2 years of endurance training on left ventricular dimensions and function in 3 female collegiate runners (mean age 19.7 years). All subjects had had an experience in endurance training as athletes and underwent the endurance training at the college for two years. Training consisted mainly of about 2 hours of running, 3 to 4 days a week. Training effects were found as measured by a 5000m-run pretraining (mean 19: 40.3 min) and post-training (mean 18: 49.3 min). The average increase in maximal oxygen uptake (VO2max/kg) after training was 9.4% (P < 0.05). UCG's dimensional variables such as LVDd, LVPWT and IVST in the post-training period did not reveal any increase. However, LVDs as a cardiac dimension showed a tendency to decrease, and functional variables such as SV, EF, FS showed a tendency to increase. This functional improvement appeared to be due to a decrease in LVDs. From these results, it is likely that the endurance training prior to this study might have helped an effective adaptation in their cardiac dimensions. Thus, we suggest that prior to this study cardiac dimensions had extended and enlarged to a certain extent, and then cardiac function might be improved as the subsequent physiological phenomenon.
A 48-year-old female who had general fatigue was admitted to our hospital. She had swelling of the axillary, inguinal, and paraaortic lymph nodes and mediastinal lesions. Laboratory examinations showed anemia, polyclonal hyperimmunoglobulinemia with IgG 5570 mg/dl, renal dysfunction and interstitial changes of the lungs. Microscopic findings of hematoxylin-eosin staining in biopsy specimens of the left inguinal and axillary lymph nodes revealed increased levels of infiltration of mature plasma cells without evidence of malignancy. Immunoperoxidase staining showed intracytoplasmic polyclonal immunoglobulin. These findings were identical to those of idiopathic plasmacytic lymphadenopathy with polyclonal hyperimmunoglobulinemia (IPL) described by Mori et al. (1980). The specimens also showed evidence of chronic nephritis with infiltration of lymph cells and a slight invasion of plasma cells. Accordingly this case was diagnosed as IPL with renal involvement, which is associated with chronic nephritis. Recently, five cases of IPL with renal dysfunction have been reported. In particular, two cases of IPL with renal dysfunction, which included our case, revealed an increased level of IL6. These findings suggest that the occurrence of renal involvement with IPL may be related to changes in IL6, which is an important factor in the pathogenesis of IPL.
A 60-year-old man was admitted to the Kyushu University Hospital because of poor glycemic control of diabetes mellitus. Although he had been treated with glicrazide and nifedipine for his diabetes and hypertension, the controls of the diseases were unsatisfactory. Plasma triglyceride level was 186 mg/dl. Furthermore, extreme insulin resistance was found by measuring glucose infusion rate with an euglycemic hyperinsulinemic clamp method. These findings were compatible to those seen in syndrome X. After admission, diet therapy of 1,800 Cal was started and his metabolic disorders such as hyperglycemia, hyperlipidemia, and hypertension were all improved. Moreover, euglycemic hyperinsulinemic clamp study also revealed a decreased insulin resistance after diet therapy. Our experience from the case suggested that insulin resistance may closely related with the metabolic disorders of the disease "syndrome X".
Membrane-bound Na+/K(+)-ATPase purified from dog kidney was solubilized with octaethylene glycol dodecyl ether (C12E8), and the resultant solubilized enzyme was chromatographed on a TSKgel G4000SWXL or G3000SWXL column equilibrated with elution buffers containing various ligands affecting oligomerization of the enzyme. Weight-averaged molecular weight (Mw) values for the main protein components eluted were estimated by low-angle laser light-scattering photometry. With increasing concentration of C12E8 included in the elution buffer from 0.1 to 5 mg/ml, the Mw decreased from 230,000 to 153,000, indicating that C12E8 induced dissociation of the enzyme. In contrast, the Mw of the protein component increased up to 1.44.10(6) as the concentration of phosphatidylserine (PS) added to the elution buffer containing a fixed concentration of 0.3 mg/ml C12E8 was increased to 120 micrograms/ml. The association and/or aggregation were reversible by removal of the PS by rechromatography. Addition of PS to the elution buffer also allowed the solubilized enzyme to exhibit ATPase activity comparable to that of the membrane-bound enzyme during passage through the column. This was also the case with phosphatidylglycerol (PG) and phosphatidylinositol, but not with phosphatidylcholine or phosphatidylethanolamine. The specific refractive index increment (dn/dcp) of the solubilized enzyme was increased by addition of exogenous PG or PS, strongly suggesting that the phospholipid became bound to the enzyme, and that it induced association of the enzyme. The association induced by PS was inhibited by ATP and ADP, but not AMP. The concentrations for half-maximal inhibition were 0.44 mM for ATP and 0.88 mM for ADP. The PS-induced associated enzyme isolated by chromatography in the presence of 120 micrograms/ml PS was dissociated by ATP with K0.5 of 0.16 mM. The dissociating effect of C12E8, ATP and ADP and the associating effect of PS on the solubilized enzyme are consistent with the reports that C12E8 mimics the effect of regulatory ATP at the low-affinity site on the conformational transition from E2 to E1, and that phospholipids are essential for the reverse transition from E1 to E2. The results can be explained by assuming that the enzyme takes the form of a loosely associated diprotomer in the E1 state and a tightly associated one in the E2 state.