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Biomedical subjects

S Konno

Publications and source records attributed to S Konno.

At least 181 records · Page 10Linked to original sources
PubMed1989

[Adrenomedullary epinephrine excretion and myocardial norepinephrine release during cardiopulmonary bypass].

It has long been known that shock or surgical stress promotes an epinephrine (E) excretion from the adrenomedullary glands. In fourteen adult cardiac patients, plasma E values in both superior vena cava (SVC) cannula and inferior vena cava (IVC) cannula during total cardiopulmonary bypass (CPB) are studied at three stages, before aortic cross clamp (pre AXC), after release of aortic cross clamp (post AXC) and at 34 degrees C rectal temperature in rewarming (34 degrees C RT). Although E values in both SVC and IVC are slightly higher values than normal in pre AXC, they increase sharply to peaked values at post AXC and decline uniformly close to normal at 34 degrees C RT. IVC-E is constantly significantly higher (statistically) than SVC-E at each of all three stages. It is strongly suggested that E response to CPB is mainly originated from the adrenomedullary glands, and cardiac reflex which has sympathetic efferent limbs triggered by myocardial ischemia can indicate the increase in E during AXC. Myocardial norepinephrine (NE) release in heart ischemia such as acute myocardial infarction has been generally accepted. To examine whether myocardial NE release occurs during AXC, if there is the association of NE release with any clinical parameters, the second investigation is done in twenty-six adult cardiac patients. Plasma NE values in both the radial artery (A) and the coronary sinus (CS) are measured at six stages, pre AXC (stage 1), post AXC (stage 2), post CPB (stage 3), three hours after off CPB (stage 4), six hours off CPB (stage 5) and twelve hours off CPB (stage 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1988

Analysis of the secondary structure of hirudin and the mechanism of its interaction with thrombin.

Highly purified hirudin with a specific activity of 13,950 antithrombin units/mg was isolated from a commercial preparation by reversed-phase chromatography. The circular dichroism (CD) spectrum of hirudin was investigated and it was found that the spectrum cannot be accounted for solely in terms of the traditional three components of peptide backbone. It was also found that the CD spectrum of the thrombin-hirudin complex was not additive with respect to the individual spectra of thrombin and hirudin. This deviation from additivity was significant between 210 and 225 nm, indicating alterations in the secondary structures of the proteins during complex formation. When thrombin was titrated with hirudin, the spectral deviation from additivity was sigmoidal, suggesting the cooperative nature of the binding process. Gel filtration of the thrombin-hirudin mixture showed no molecular species greater than a 1:1 complex (Mr 45,500), but gel filtration of free hirudin showed a multimeric form (Mr 51,300) under the same experimental conditions. It is concluded that the cooperative nature of the binding process is due to the binding of thrombin molecules to the multimeric form of hirudin. This initial binding occurs with little or no change in the CD spectrum. In the second step, the multiple complex dissociates to form 1:1 complexes, resulting in larger conformational changes and a considerable increase in binding affinity.

Binding Sites↗
PubMed1988

Myopathy and encephalopathy in chick embryos experimentally infected with Akabane virus.

Chick embryos infected with Akabane virus by the yolk sac route at 6 days of incubation developed polymyositis and encephalitis. At 3 to 7 days after inoculation, skeletal muscles had myotubule degeneration, clumping of muscle cell nuclei, and infiltration of heterophils; dysplasia and aplasia were evident at 9 to 15 days after inoculation. Changes in the cerebral neostriatum and optic lobes at 2 to 11 days after inoculation included necrosis of primordial nervous tissue, hemorrhages, and hyperplasia of the vascular endothelial cells. Cavities were in nervous tissue subsequent to encephalitis. Hydranencephaly and vascular wall thickening were found 13 and 15 days after inoculation. Embryos infected intravenously at 15 days incubation had foci of encephalitis 3 to 6 days after inoculation, including neuronal degeneration, neuroglial hyperplasia, vascular endothelial proliferation, and heterophil infiltration.

Anencephaly↗
PubMed1987

[Neuronal and adrenomedullary catecholamine response to cardiopulmonary bypass: with special reference to comparative studies based on functional classification].

Plasma epinephrine (E) and norepinephrine (NE) levels during cardiopulmonary bypass (CPB) were studied in thirty-eight cardiac patients with various grades of NYHA classification. Striking increases of both E and NE levels after release of aortic cross clamp (stage 4) were noted. A thirteen fold increase in E (from 0.05 +/- 0.05 ng/ml to 0.62 +/- 0.48 ng/ml) and sixfold increase in NE (from 0.21 +/- 0.18 ng/ml to 1.26 +/- 0.78 ng/ml) occurred from prebypass (stage 1) to stage 4. The values of E and NE were peaked at stage 4 and rapidly decreased after heart beating (stage 5). At chest closure (stage 7), E returned to close to prebypass control (stage 1) value, however NE remained still in moderately high level. Patients were divided into three groups: The mild group (NYHA class I and II, fourteen patients), the ill group (NYHA class III and IV, nineteen patients) and the IABP group (IABP support since prior to CPB due to unstable angina and ventricular septal perforation, five patients). Whereas E value at either stage 4 or stage 5 in the mild group was statistically significantly higher (p less than 0.05) than each E value at corresponding stages in the ill group. NE value at each stage 3 (prior to aortic cross clamp), stage 4 or stage 5 in ill group significantly higher than each NE value at same stages in the mild group respectively. These data suggest that depletion of E and compensatory increase of NE in the ill group may be occurred during CPB.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[A case of myonephropathic metabolic syndrome treated with limb washout using a roller pump and cell saver].

We operated on a 65 year old male for the saddle embolism presenting the signs of MNMS. Before the reperfusion of the ischemic limbs which were successfully embolectomized with the use of Fogarty catheter, we performed limb washout using roller pump and cell saver. The washout was done in the high flow and large volume by the roller pump. The red blood cells in the efflux were saved using cell saver and retransfused to the patient. The patient recovered without deterioration of MNMS. The limb washout was effective for the prevention of the deterioration of MNMS.

Acute Disease↗
PubMed1986

Partial purification and characterization of phorbol ester-regulated translational inhibitor(s) in human HL-60 leukemic cells.

Addition of nanomolar concentration of the phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA) to the human promyelocytic HL-60 leukemia cells is associated with a cessation of cellular proliferation and a subsequent differentiation into macrophage-like cells. Because the growth rate of mammalian cells is tightly coupled to the functions of the protein synthetic machinery, we have examined whether TPA induces a change in HL-60 translational functions. Addition of control HL-60 cell extracts to rabbit reticulocyte lysates results in a pronounced inhibition of protein synthesis, while TPA-treated HL-60 cell extracts are significantly less inhibitory. The reduction in TPA-induced translational inhibitory activity can be observed after a 3-6-h treatment and reaches a maximum after 24 h. Fractionation of control cell extracts on DEAE-cellulose columns reveals two inhibitory activities, eluting at 100 and 350 mM KCl, respectively. The DEAE-100 inhibitor(s) is further resolved into two activities by heparin-agarose column chromatography (HEP-100 and HEP-250). TPA treatment of HL-60 cells for 48 h completely eliminates the HEP-250 inhibitory activity and reduces the HEP-100 and the DEAE-350 inhibitory activities by 50 and 25%. Inhibition of protein synthesis in rabbit reticulocyte lysates by DEAE-100 inhibitory activities can be partially reversed by the addition of globin mRNA while translational inhibition by DEAE-350 inhibitor(s) can be reversed by addition of eukaryotic initiation factor (eIF) 2 or fructose 6-phosphate. The DEAE-100 inhibitor(s) causes extensive degradation of radioactive polynucleotides while the DEAE-350 inhibitor(s) is capable of phosphorylating both the alpha- and the beta-subunits of the highly purified rabbit reticulocyte initiation factor eIF-2. These data show that the DEAE-100 inhibitor(s) contains a nuclease while the DEAE-350 inhibitor(s) is associated with eIF-2 alpha and eIF-2 beta protein kinases.

Animals↗
PubMed1986

Microdosimetric considerations of effects of heavy ions on microorganisms.

An estimation of dose around the trajectory of an ion has been made by use of Tabata and Ito's energy deposition algorithm for electrons which takes into account transmission coefficient. The result of the calculation, as well as Butts and Katz's dose, is successfully applied to the interpretation of inactivation cross sections of vegetative cells of E. coli Bs-1, and E. coli B/r and of B. subtilis spores for He, C and N ions.

Algorithms↗
PubMed1986

Effects of nicotine on cellular proliferation, cell cycle phase distribution, and macromolecular synthesis in human promyelocytic HL-60 leukemia cells.

Addition of nicotine causes a dose- and time-dependent inhibition of cell growth in the human promyelocytic HL-60 leukemia cells, with 4 mM nicotine resulting in a 50% inhibition of cellular proliferation after 48-50 h. Accompanying the anticellular effect of nicotine is a significant change in the cell cycle distribution of HL-60 cells. For example, treatment with 4 mM nicotine for 20 h causes an increase in the proportion of G1-phase cells (from 49% to 57%) and a significant decrease in the proportion of S-phase cells (from 41% to 32%). These results suggest that nicotine causes partial cell arrest in the G1-phase which may in part account for its effects on cell growth. To determine whether nicotine changes the cellular uptake/transport to macromolecular precursors, HL-60 cells were treated with 2-6 mM nicotine for 30 h, at the end of which time cells were labeled with [3H]-thymidine, [3H]uridine, [14C]lysine and [35S]methionine, the trichloroacetic acid soluble and insoluble radioactivities from each of the labeling conditions were determined. These studies show that nicotine mainly affects the de novo synthesis of proteins.

Cell Cycle↗
PubMed1986

The heterotopically transplanted rat urinary bladder as a model for detection of tumor-promoting urinary growth factor(s).

The heterotopically transplanted rat urinary bladder (HTB) was developed in our laboratory as a model to study the role of urine in urinary bladder carcinogenesis. With this model, normal urine was found to enhance urinary bladder carcinogenesis initiated by N-methyl-N-nitrosourea or N-butyl-N-(4-hydroxybutyl)nitrosamine. Two crude urinary components (Fractions I and II) were obtained by gel filtration chromatography; they stimulated ornithine decarboxylase (ODC) in a test bladder carcinoma cell line 804G, and promoted carcinogenesis in the HTB system. Fraction I was found to stimulate growth of 804G cells in vitro. Preliminary data indicate that Fraction I contains at least one, and possibly two heat-stable ODC-inducible and mitogenic components. Further characterization of these components is in progress. The HTB system has been demonstrated to be useful for other investigations; for example, alpha-difluoromethylornithine, an enzyme-activated irreversible inhibitor of ODC, when instilled repeatedly to the bladder lumen, inhibited tumorigenesis in HTBs.

Animals↗
PubMed1986

Effects of temperature, aurintricarboxylic acid and cibacron blue on 2',5'-oligoadenylate binding protein (RNase L) activity in rabbit reticulocyte lysates.

The binding of p3A4,3'-32P [pCp] to rabbit reticulocyte RNase L can be displaced by the trimer and tetramer triphosphates of 2',5'-oligoadenylates (2-5A). Using assay conditions of protein synthesis, 2-5A trimer or tetramer triphosphates are shown to be equally effective when the displacement is done at 4 degrees C (on ice). In contrast, at 30 degrees C, the tetramer triphosphates still displace whereas the trimer triphosphates become ineffective. When lysates are preincubated at temperature ranging from 4 degrees-37 degrees C, the same results are obtained even when the subsequent displacement is done on ice. Incubation temperature also significantly affects the ability of metabolically stable dyes cibacron blue and aurintricarboxylic acid to inhibit RNase L binding activity. Taken together, these results suggest that rabbit reticulocyte RNase L may assume multiple conformations which are differentially affected by various forms of 2-5A or other compounds.

Animals↗
PubMed1985

Effects of K+ concentration on inhibition of protein synthesis by trimer and tetramer triphosphates of 2',5'-oligoadenylates in rabbit reticulocyte lysates.

The inhibition of protein synthesis by trimer or tetramer triphosphates of 2',5'-oligoadenylates (2-5A) in rabbit reticulocyte lysates is dependent on the concentration of K+ in the assay mixture. Based on studies using mRNA-dependent rabbit reticulocyte lysates and the degradation of [3H] polyadenylated mRNA, the greater inhibitory effects of trimer or tetramer triphosphates at the higher K+ is shown to be due to a more active 2-5A-dependent endoribonuclease (RNase L).

Adenine Nucleotides↗