Platelet transfusion refractoriness associated with plasma proteins.
Explore the source record for details and available documents.
Blood Component Transfusion↗
Biomedical subjects
H Yasuda
Publications and source records attributed to H Yasuda.
A combined occurrence of neuroendocrine carcinoma of the skin and a benign appendageal neoplasm.
A 76-year-old Japanese male presented with a subcutaneous nodule in the dorsal cubital region of the right arm. The center of the nodule showed typical features of neuroendocrine carcinoma of the skin. The peripheral portion showed epithelial islands of squamoid cells with horn cysts suggestive of benign appendageal tumor with pilar differentiation. The coexistence of two skin neoplasms in the same lesion would suggest that both tumors developed from common pluripotential stem cell.
Aged↗
Activity of the carbapenem panipenem and role of the OprD (D2) protein in its diffusion through the Pseudomonas aeruginosa outer membrane.
Evidence of permeation of panipenem through the OprD (D2) channel of Pseudomonas aeruginosa outer membrane was shown by using OprD protein-producing and -nonproducing strains which contained plasmid pHN4, which codes for L-1 beta-lactamase of Xanthomonas maltophilia. Permeation by panipenem was determined by measuring hydrolysis of the carbapenem by beta-lactamase in the periplasmic space. Permeation by panipenem was also determined by counting uptake of [14C]panipenem into P. aeruginosa PAO1 and its OprD protein-deficient mutant, and this permeation of PAO1 was inhibited by L-lysine. These results indicate that panipenem, as well as imipenem, uses the OprD channel, which functions as a specific channel for diffusion of basic amino acids. Panipenem and imipenem showed stronger activities against PAO1 and clinical isolates in human serum than in Mueller-Hinton broth, which contains more amino acids than human serum does. The activities of the carbapenems were reduced by addition of L-lysine to human serum. Similar results were obtained with mouse serum and ascitic fluid. In contrast, such a change in the activities of carbapenems was not observed with an OprD protein-deficient mutant, suggesting that the main reason for the strong activities of carbapenems in biological fluids is a decrease in competition between the antibiotics and basic amino acids for permeation through the OprD channel. Panipenem and imipenem showed much stronger therapeutic efficacies against experimental infections with P. aeruginosa in mice than did the reference antibiotics. Their in vivo activities were more consistent with their MICs in biological fluids than with those in Mueller-Hinton broth.
Animals↗
Interaction between biofilms formed by Pseudomonas aeruginosa and clarithromycin.
Interactions between bacterial biofilms formed by Pseudomonas aeruginosa and clarithromycin, a macrolide having no anti-P. aeruginosa activity, were investigated. P. aeruginosa incubated for 10 days on membrane filters formed biofilms on the surfaces of the filters. The biofilms were characterized by dense colonizations of bacteria and thick membranous structures that covered the colonies. Treatment of the biofilms with a relatively low concentration of clarithromycin for 5 days resulted in an eradication of the membranous structures. Quantitative analysis of alginate and hexose was done to evaluate the quantity of polysaccharides in or on the biofilms. Treatment of the biofilms with clarithromycin decreased the quantity of alginate and hexose and therefore perhaps the quantity of polysaccharides as well. Eradication of the membranous structures of biofilms, or the decrease in the quantity of polysaccharides, resulted in an increase in the rate of penetration of antibiotics through bacterial biofilms. In vivo therapeutic effects of ofloxacin in the rat infection model, in which the biofilm mode of growth of P. aeruginosa is characteristic, were enhanced by oral coadministration of clarithromycin. It is suggested that clarithromycin eradicated glycocalyx produced by P. aeruginosa, or suppressed the production of glycocalyx, by unknown mechanisms and thereby enhanced the therapeutic efficacies of other antimicrobial agents against infections caused by P. aeruginosa.
Alginates↗
Activin A: an autocrine inhibitor of initiation of DNA synthesis in rat hepatocytes.
The present study was conducted to examine the effect of activin A on growth of rat hepatocytes. EGF induced a 10-fold increase in DNA synthesis as assessed by [3H]thymidine incorporation in cultured hepatocytes. When activin A was added together with EGF, DNA synthesis induced by EGF was markedly inhibited. Inhibition was detected at a concentration of 10(-10) M, and 5 x 10(-9) M activin A almost completely blocked EGF-mediated DNA synthesis. Similarly, activin A completely blocked DNA synthesis induced by hepatocyte growth factor/scatter factor. Activin A was capable of inhibiting EGF-mediated DNA synthesis, even when added 36 h after the addition of EGF. With the same time interval, TGF-beta also blocked EGF-induced DNA synthesis. Although both activin A and TGF-beta inhibited growth of hepatocytes in a similar manner, either activin A or TGF-beta did not compete with each other in their binding when assessed by competitive binding using an iodinated ligand. When hepatocytes were incubated with EGF, release of bioactivity of activin A into culture medium was detected after 48 h or later. Activity of activin A was released from parenchymal cells but not from nonparenchymal cells. mRNA for beta A subunit of activin was detected only slightly in unstimulated hepatocytes, but markedly increased at 48 h after the addition of EGF. To determine whether endogenously produced activin A affects DNA synthesis, we examined the effect of follistatin, an activin-binding protein that blocks the action of activin A. An addition of follistatin significantly enhanced EGF-induced DNA synthesis. Finally, in partial hepatectomized rat, expression of mRNA for beta A subunit in liver was markedly increased 24 h after the partial hepatectomy. These results indicate that activin A inhibits initiation of DNA synthesis in hepatocytes by acting on its own receptor and that activin A acts as an autocrine inhibitor of DNA synthesis in rat hepatocytes.
Activins↗
Existence of activin-A in A- and D-cells of rat pancreatic islet.
Activin-A, a member of the transforming growth factor-beta supergene family, stimulates insulin secretion in rat pancreatic islets and causes glycogenolysis in isolated rat hepatocytes. These observations prompted us to determine whether activin-A existed in rat pancreas by using an immunocytochemical method. Cells in pancreatic islets were stained by antibody against activin-A, whereas no immunoreactivity was observed in exocrine pancreas. Cells localized in the mantle of the islets were densely stained by the antibody. Immunoelectron microscopic study showed that activin-A existed in secretory granules in both A- and D-cells. Furthermore, studies using a double labeling method revealed that activin-A coexisted with glucagon in secretory granules in A-cells and with somatostatin in D-cells. Antibody against inhibin-A weakly stained cells in both the core and mantle of the islets only when the rat was pretreated with colchicine. Subtypes of activin subunit in islets were identified to be beta A by a reverse transcription-polymerase chain reaction method. In addition, mRNA for inhibin alpha-subunit was expressed in islets. However, mRNA for these inhibin subunits was not detected in exocrine pancreas. To further examine the action of activin-A on insulin secretion, we examined the effect of activin-A in a flow-through perifusion system. Activin-A induced a biphasic insulin secretory response in the presence of 2.8 mM glucose, and a low concentration of activin-A, which does not stimulate insulin secretion by itself, markedly enhanced glucose-mediated insulin secretion at concentrations above 2.8 mM glucose. Inhibin-A did not affect insulin secretion. These results suggest the existence of activin-A in A- and D-cells of rat pancreatic islets and raise the possibility that activin-A acts as a physiological regulator of carbohydrate metabolism.
Activins↗
[The characterization of human cdc2 kinase and CDK2].
p34cdc2 kinase plays a key role in the initiation of mitosis. The activity of this kinase requires the binding of a protein, named cyclin, to it. The kinase forms a heterodimer with cyclin. Cyclin A or B is the counterpart of this complex. The differences in the activity between cyclin A/cdc2 kinase and cyclin B/cdc2 kinase have not been cleared. In recent years, the other cdc2-like kinases were identified. One of them was CDK2 (cyclin dependent kinase 2). CDK2 could rescue the defect of the budding yeast CDC28 mutation, which arrested the cells at a point named START, in G1 phase. Then, CDK2 was thought to be worked at G1 through S phase in a cell cycle, but the details on the role of this kinase has not been cleared so far. In this study, we separated the human cyclin A/cdc2 kinase, cyclin B/cdc2 kinase and CDK2, each other by use of column chromatography, and characterized the each kinase. These kinases had the same substrate specificities when the synthesized peptides were tested. They phosphorylated the threonine residue in the sequence -Thr-Pro-Lys-Lys-Ala- but hardly phosphorylated threonine residue the sequence -Thr-Pro-Lys-Ala-Lys-. They had some differences in the substrate-preference when the native proteins were tested. In a cell cycle of human cells, the activity of cdc2 kinase increased at G2/M phase and the activity of CDK2 was high from S through M phase. These data suggested that cdc2 kinase works at the transition from G2 to M phase and that CDK2 works from G1 through G2/M phase. They could phosphorylate different protein-substrates having the common phosphorylated sequence -Thr-Pro-X-Lys-.
Amino Acid Sequence↗
Ventilatory anaerobic threshold before and after cardiac valve surgery.
The purpose of this study was to objectively assess exercise tolerance before and after cardiac valve surgery by using an objectively determined ventilatory anaerobic threshold (AT). Nine patients (mean age: 38.2 +/- 8.1 years) with predominantly mitral regurgitant lesions were studied by a symptomatic maximal treadmill exercise test which included a determination of AT. The mean lengths of time from preoperative exercise testing to cardiac surgery, and from surgery to postoperative exercise testing were 5.9 +/- 4.0 and 12.1 +/- 8.3 months, respectively. The determination of AT on data plots was performed after blinding to patient identification and pre- vs postoperative status. After surgery, the clinical symptoms and NYHA class improved significantly with a decrease in the cardio-thoracic ratio and echocardiographic diastolic dimensions. The mean peak VO2 (ml/kg/min) increased significantly from 20.2 +/- 7.1 to 29.7 +/- 7.9 (p < 0.01). Together with these changes, AT (ml/kg/min in VO2) increased from a mean of 14.8 +/- 4.8 to 22.8 +/- 5.5 (p < 0.01). In conclusion, symptomatic improvement and an increase in peak oxygen uptake after cardiac valve surgery were accompanied by a significant increase in the objectively determined AT. AT determined in a blind manner provides an objective means of evaluating exercise tolerance when a double-blind intervention cannot be performed.
Adult↗
[Left ventricular relaxation and systolic contractile state in aortic regurgitation before and after aortic valve replacement].
Explore the source record for details and available documents.
Aortic Valve↗
[Indication for cardiac transplantation and recipient selection from the medical viewpoint].
Explore the source record for details and available documents.
Adult↗
Isolation of reovirus type 3 from dogs with diarrhea.
Three virus strains were isolated in DK cell cultures inoculated with fecal specimens of dogs manifesting diarrhea. The isolates were identified as reoviruses on the basis of their biological and physico- chemical properties. They possessed reovirus type 3 antigenic specificity revealed by hemagglutination-inhibition and neutrarization tests with the reovirus prototype strains. It was suspected that the isolates were participated in this diarrheic cases.
Animals↗
Mechanism of transfusion-associated graft-versus-host disease.
Recent investigations have revealed that transfusion-associated graft-versus-host disease (TA-GVHD) occurs in patients whose immune system is immature or impaired, but also in immunocompetents. The mechanism of TA-GVHD in immunocompromised patients is that donor's viable lymphocytes can not be rejected by the recipient because of defects in cellular immunity. While, even in immunocompetent patients, TA-GVHD may occur when an HLA-heterozygous recipient receives blood from a donor who is homozygous for one of the patient's haplotypes. Engraftment of donor's lymphocytes may be established without rejection, as the donor's homozygous lymphocytes are identical with one of the patient's haplotypes in HLA. Our calculations show that the Japanese have a greatest risk of TA-GVHD than other populations among relatives and unrelated donors.
Graft vs Host Disease↗
Successful surgical management of thoracic aortic aneurysm in a right-sided aortic arch.
A 24-year-old woman with a multilocular sacciform aneurysm in a right-sided aortic arch was successfully treated by aneurysmorrhaphy. Although the cause of the aneurysm could be attributed to congenital factors, its growth was considered to be related to the features of the right-sided aortic arch; strong haemodynamic forces were caused by sharp curving of the aorta which started from an unusually high position and subsequently had a decreased radius.
Adult↗
Brain protection against ischemic injury by nizofenone.
Ischemic brain injury is induced in a complex and multifactorial pathogenic cascade; but the fundamental mechanism is the imbalance between energy demand and supply in ischemic brain tissue. Nizofenone is a potent neuroprotective drug which ameliorates this imbalance and also various pathophysiologic events during ischemia, such as ATP depletion, lactate accumulation, glutamate release, free fatty acid liberation, edema, and neuronal degeneration; in particular, ischemia-induced excessive glutamate release has been completely blocked by this drug. This drug has also radical-scavenging action, comparable to vitamin E, and inhibits oxygen radical-induced lipid peroxidation. The potent cerebroprotective effect of nizofenone has been demonstrated in various experimental models of cerebral hypoxia, ischemia (focal and global), ischemia-reperfusion, and infarction. The clinical efficacy of nizofenone has been proved by pioneering double-blind studies in acute subarachnoid hemorrhage patients. Nizofenone is clinically used for preventing the delayed ischemic neurologic deficits due to late vasospasm following subarachnoid hemorrhage. In this report, the property of the cerebroprotective effect and the clinical efficacy of nizofenone is reviewed.
Animals↗
Regulation of Na+/glucose cotransport in LLC-PK1 cells by glucose in culture medium: involvement of Gi protein.
The reduction of the glucose concentrations in the culture medium results in an increase in Na+/glucose cotransport activity in the epithelial cells. To study this regulation of Na+/glucose cotransport in LLC-PK1 cells, we have attempted to examine the involvement of Gi protein. The immunoblotting with an antibody for the carboxy-terminal of alpha subunit of Gi protein (Gi alpha) revealed no significant change in the level of Gi alpha in cells cultured with low (5 mM) or high (25 mM) glucose concentrations. In contrast, the cultured with low glucose concentrations induced the increases of both islet activating protein (IAP)-catalyzed ADP-ribosylation of Gi alpha and Na+/glucose cotransport activity. Furthermore, this increase in the transport activity was blocked by the presence of IAP in a dose dependent manner. These results suggest that there is a close relationship between the concentration of the heterotrimeric form of Gi protein (Gi alpha beta gamma) and the activity of Na+/glucose cotransport in LLC-PK1 cells.
Adenosine Diphosphate Ribose↗
[Regulation of mammalian cell cycle progression by cdc 2 kinase and cdk].
Explore the source record for details and available documents.
Animals↗
[Effect of enalapril on left ventricular hypertrophy and left ventricular function in patients with hypertension].
The aim of this study was to study the effect of enalapril (E) on left ventricular (LV) mass, LV function and blood renin-angiotensin (RA) in patients with hypertension. Sixteen hypertensives were included in this study (WHO I 8, WHO II 8, 49.5 +/- 10.5 yrs). They were examined for blood pressure and heart rate. Chest X-ray film, echocardiography (echo), X-ray computed tomography (CT) and RA before and after about 6 months of E administration were studied. The LV mass was calculated by CT. The LV function was measured by echo. RAS was unchanged during this study. LV mass was significantly reduced after E (121.4 +/- 25.6 vs 104.6 +/- 13.7 g/cm2). The LV systolic function was unchanged after E, but LV diastolic function improved. It was shown that the long-term administration of E improves LV hypertrophy and LV diastolic function without any change of RAS.
Adult↗
Butyrolactone I, a selective inhibitor of cdk2 and cdc2 kinase.
We screened cdc2 kinase inhibitors from cultured mediums of micro organisms using purified mouse cyclin B-cdc2 kinase and a specific substrate peptide for cdc2 kinase. A selective inhibitor of cdc2 kinase was isolated from the cultured medium of Aspergillus species F-25799, and identified as butyrolactone I. Butyrolactone I inhibited cdc2 and cdk2 kinases but it had little effect on mitogen-activated protein kinase, protein kinase C, cyclic-AMP dependent kinase, casein kinase II, casein kinase I or epidermal growth factor-receptor tyrosine kinase. Its inhibitory effect was found to be due to competition with ATP. Butyrolactone I selectively inhibited the H1 histone phosphorylation in nuclear extracts. It also inhibited the phosphorylation of the product of retinoblastoma susceptibility gene in nuclear extracts and intact cells. Thus butyrolactone I should be very useful for elucidating the function of cdc2 and cdk2 kinases in cell cycle regulation.
4-Butyrolactone↗