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Biomedical subjects

K Konno

Publications and source records attributed to K Konno.

At least 325 records · Page 18Linked to original sources
PubMed1988

Abnormal breathing patterns in patients with mitral stenosis: a possible compensatory role.

The breathing patterns of 37 patients with mitral stenosis were investigated in standing position by Konno-Mead analysis. Hemodynamic parameters were measured by cardiac catheterization, pulmonary function variables by pulmonary function testings and distribution of pulmonary perfusion by Tc-99m-MAA scintigraphy. Seventeen patients displayed rib cage dominant breathing patterns, and 6 patients displayed paradoxical breathing patterns, whereas 14 patients displayed normal breathing patterns. None of these patients exhibited an abdomen dominant breathing pattern. The patients with abnormal breathing patterns (rib cage dominant or paradoxical) displayed significantly higher values of pulmonary arterial pressure (p less than 0.01), capillary wedge pressure (p less than 0.01), total pulmonary vascular resistance (p less than 0.01) and mitral valve gradient (p less than 0.05) as well as smaller mitral valve area (p less than 0.05) and lower values of both in PaO2 (p less than 0.05) and diffusing capacity (p less than 0.05) than patients with normal breathing patterns. Abnormal distribution of pulmonary perfusion with hyperperfusion in the upper zone of the lung were found to be associated with the abnormal breathing patterns. Since rib cage dominant and paradoxical breathing patterns are known to increase ventilation in the upper zone of the lung, these abnormal breathing patterns may represent a compensatory mechanism serving to match ventilation and perfusion.

Adult↗
PubMed1987

Deprotonation of tyrosines in bacteriorhodopsin as studied by Fourier transform infrared spectroscopy with deuterium and nitrate labeling.

Fourier transform infrared (FTIR) difference spectra are presented for bacteriorhodopsin (BR) at low temperature. Previous FTIR measurements have identified several tyrosine residues that change their absorption characteristics between light-adapted BR and dark-adapted BR, or between intermediates K and M [Dollinger, G., Eisenstein, L., Lin, S.-L., Nakanishi, K., Odashima, K., & Termini, J. (1986) Methods Enzymol. 127, 649-662]. These changes were explained by protonation/deprotonation of tyrosine moieties and perturbation of the protein environment surrounding tyrosines. A tyrosine deprotonation was observed to occur between intermediates K and M. The present studies confine the deprotonation to being between intermediates L and M and show that no tyrosines undergo changes between the K and the L states. Evidence is presented that none of the tyrosines undergoing changes at low temperature can be assigned to tyrosine-64. The environmental changes of these tyrosines are discussed in relation to the proton pumping mechanism. Their spatial relation to the chromophore is also discussed. At least two tyrosines are suggested to reside close to the retinal binding site. The reactive groups of the nitrated tyrosine-64 are speculated to be remote from the Schiff base and the active tyrosines but can possibly interact sterically with the ionone ring of the retinal.

Bacteriorhodopsins↗
PubMed1987

Functional, chymotryptically split actin and its interaction with myosin subfragment 1.

We have prepared chymotryptically split actin that retains the characteristic properties of intact actin. Chymotryptic digestion of G-actin produces an intermediate 35-kilodalton (kDa) fragment and from this a final product of 33 kDa known as the C-terminal "core". These fragments remain attached to an N-terminal 10-kDa fragment. The 35-kDa-10-kDa complex is able to polymerize upon addition of KCl and MgCl2, like intact actin, whereas the 33-kDa-10-kDa complex is not. The 35-kDa-10-kDa complex is here termed "split actin". In the rigor state, split actin binds to myosin subfragment 1 (S-1) strongly, with the same stoichiometry as intact actin. In the rigor state, split actin forms a carbodiimide-induced cross-linked product with S-1; the cross-linking sites on the split actin and on S-1 were proved to be the N-terminal 10-kDa fragment of split actin and the 20-kDa domain of S-1. There was no cross-linking between the 50-kDa domain of S-1 and the 10 kDa of actin. Therefore, the structure of the split actin-S-1 complex differs somewhat from that of the complex with intact actin. The cross-linking of split actin to S-1 causes superactivation of S-1 ATPase to approximately the same extent as does cross-linking of intact actin, whereas non-cross-linked split actin activates S-1 ATPase to a lesser extent. The N-terminus of the 35-kDa fragment was found to be residue 45 (Val-45) by amino acid sequence analysis; so there is no residue missing in split actin.

Actins↗
PubMed1987

Synergism of tumor necrosis factor and interferon-gamma in induction of differentiation of human myeloblastic leukemic ML-1 cells.

Natural or recombinant human tumor necrosis factor (TNF) induced NBT-reducing activity of ML-1 cells in a dose-dependent manner. Interferon-gamma (IFN-gamma) induced NBT-reducing activity only marginally. However, when IFN-gamma was combined with TNF, induction of NBT-reducing activity was remarkably increased. IFN-alpha or -beta had almost no effect on the induction of NBT-reducing activity of ML-1 cells, either alone or in combination with TNF. Treatment with both TNF and IFN-gamma synergistically enhanced morphological changes, growth inhibition and activity of Fc receptors, and NBT reduction in ML-1 cells, but not phagocytic activity. The TNF treated cells were classified as macrophage-like by morphology, and by lineage-specific alpha-naphthyl acetate esterase stain. The results indicate that combinations of TNF and IFN-gamma act synergistically in the induction of differentiation of human myeloblastic ML-1 cells.

Cell Differentiation↗
PubMed1987

Treatment of acute leukemia and malignant lymphoma with (2"R)-4'-O-tetrahydropyranyladriamycin.

Eighty-four previously treated adult patients with acute leukemia and malignant lymphoma were treated with (2"R)-4'-O-tetrahydropyranyladriamycin (THP). THP (10-55 mg/m2) was administered by i.v. bolus injection daily for acute leukemia, and according to three different schedules for malignant lymphoma: daily, weekly or once every 3-4 weeks. Complete and partial remission (CR and PR) were achieved by 1 (5%) and 3 of 19 patients with acute myelogenous leukemia and by 2 (13%) and 3 of 15 patients with acute lymphoblastic leukemia, respectively. All CRs were in the groups receiving 25 mg/m2 THP daily. CR and PR were achieved by 6 (14%) and 8 of 42 patients with non-Hodgkin lymphoma (NHL) and by 4 (50%) and 2 of 8 patients with Hodgkin's disease (HD), respectively. No particular sensitivity was found among the subtypes of NHL and HD. Response (CR + PR) was noted in 10 (40%) of 25 patients treated every 3-4 weeks, in 1 (17%) of 6 treated weekly, and in 9 (47%) of 19 treated daily. The major side effects were myelosuppression and gastrointestinal toxicities. Alopecia was observed in only 10 (12%) patients. ECG abnormalities were observed in 7 (10%) patients, all of whom had previously been treated with other anthracyclines. No severe cardiotoxicity was observed.

Adult↗
PubMed1987

Effect of theophylline on respiratory neuromuscular drive.

To investigate the possible mechanisms by which theophylline affects the control of ventilation, neuromuscular drive and ventilatory function were examined in 7 healthy men receiving an incremental intravenous aminophylline dosing schedule to achieve plasma theophylline concentrations of 5, 10, and 15 micrograms/ml. As compared with the baseline (predose) values, the 3 incremental aminophylline doses significantly (p less than 0.05 to 0.01) increased occlusion pressure (P0.1) and maximum inspiratory pressure static (MIPS) at functional residual capacity (FRC). This was not observed for ventilatory flow (V), tidal volume (VT), inspiratory time to total breathing cycle time ratio (Ti/Ttot) VT/Ti, and effective impedance [P0.1/VT/Ti)]. When maximum electrical activity of diaphragm (Edimax) and transdiaphragmatic pressure (Pdimax) were examined in 3 of the 7 subjects, Pdi/Edi tended to increase with increasing theophylline concentrations, while Edimax did not. Our results suggest that the increase in P0.1 during the increase in aminophylline dose is caused by an improvement in respiratory muscle contractility, rather than by a central effect or by an increase in neural drive.

Adult↗
PubMed1987

In vitro activity of (S)-9-(3-hydroxy-2-phosphonylmethoxypropyl)adenine against newly isolated clinical varicella-zoster virus strains.

The highly potent and selective anti-DNA virus agent (S)-9-(3-hydroxy-2-phosphonylmethoxypropyl)adenine [(S)-HPMPA] was found to inhibit in vitro the replication of a number of clinical varicella-zoster virus strains within the concentration range of 0.63-5.7 ng/ml. With a mean 50% inhibitory concentration of 1.8 ng/ml and selectivity index of 29000, (S)-HPMPA is one of the most potent and most selective varicella-zoster virus inhibitors discovered to date.

Adenine↗
PubMed1987

Acid glycosaminoglycans in experimental pleural effusions.

Acid glycosaminoglycans (GAG) were quantitated and partially characterized in pleural effusions in guinea pigs with experimental allergic pleurisy. Increase of GAG in the pleural effusion preceded the increase of effusion volume. Effusion was associated with the presence of cuboidal mesothelial cells on visceral pleura, and hemorrhage, infiltration of neutrophils, and destruction of the alveolar structure of the lung. A significant difference was found in the relative percentage of GAG subtypes in the effusion, serum, and the lung tissue of guinea pigs with experimental pleurisy. There was a difference in molecular size of hyaluronic acid in pleural effusion between the early and late stages of pleurisy. Presumably GAGs found in pleural effusion were released from the pleural tissue.

Animals↗
PubMed1987

Electropalatographic analysis of apraxia of speech in a left hander and in a right hander.

Two cases with 'pure' apraxia of speech are reported. The articulatory disturbances were quite similar. One of the two cases was a left-handed male with a subcortical haemorrhage and the other a right-handed male with a cerebral infarct. The MRI and CT scans showed that the first case had a lesion that mainly involved the right precentral gyrus and its deep white matter, and that the second had a lesion mainly affecting the lower parts of the left precentral and postcentral gyri and their deep white matter. These findings and a literature review suggest that a corticosubcortical lesion of the lower part of the left precentral gyrus in most right handers and a lesion of the symmetric region in the right hemisphere in some left handers cause apraxia of speech. The omission errors for sounds articulated by the tongue and the hard palate were analysed using electropalatography, which records visually the dynamics of the palatolingual contact. The results demonstrated that there were three kinds of omission errors: true omissions (no palatolingual contact); omissions with incorrect contact (palatolingual contact for a different sound or undifferentiated sound); and omissions with correct contact (correct palatolingual contact for a target sound). The latter two types of omission error were observed for initial consonants and they were probably caused by a delay in air flow. The patients also showed a tendency to substitute one of the two consonants/t, t/for other sounds, which suggested that they had difficulty in the inhibition of tongue activity.

Adult↗
PubMed1987

Amino acid sequence of the essential light chain of adductor muscle myosin from Ezo giant scallop, Patinopecten yessoensis.

The amino acid sequence of the essential light chain (abbreviated as SHLC) of adductor muscle myosin from Ezo giant scallop (Patinopecten yessoensis) was determined by conventional methods. The light chain was composed of 156 amino acid residues with proline and lysine as its amino and carboxyl termini, respectively. Comparing this sequence with that of the SHLC from bay scallop (Aquipecten irradians), only 5 amino acid substitutions were recognized. The sequence homology between scallop and squid SHLCs was 53.7%. On the other hand, a partially fragmented SHLC "modified SHLC" reported by Konno and Watanabe (J. Biochem. 98, 141-148 (1985) was prepared by chymotryptic digestion of the scallop myosin in the presence of EDTA, and was assigned as the carboxyl-terminal 106-residue peptide of the SHLC. This may suggest that the regulatory light chain covers the amino-terminal region of the SHLC in the myosin molecule.

Amino Acid Sequence↗
PubMed1987

Amino acid sequence of the regulatory light chain of squid mantle muscle myosin.

The amino acid sequence of the regulatory light chain of mantle muscle myosin from squid (Todarodes pacificus) was determined by conventional methods. It was: xA-E-E-A-P-R-R-V-K-L-S-Q-R-Q-M-Q-E-L-K-E-A-F-T-M-I-D-Q-D-R-D-G-F-I-G-M- E-D-L-K-D-M-F-S-S-L-G-R-V-P-P-D-D-E-L-N-A-M-L-K-E-C-P-G-Q-L-N-F-T- A-F-L-T-L-F-G-E-K-V-S-G-T-D-P-E-D-A-L-R-N-A-F-S-M-F-D-E-D-G-Q-G-F-I-P- E-D-Y-L-K-D-L-L-E-N-M-G-D-N-F-S-K-E-E-I-K-N-V-W-K-D-A-P-L-K-N-K-Q-F- N-Y-N-K-M-V-D-I-K-G-K-A-E-D-E-D. The alpha-amino group of this light chain was blocked, and a typical calcium-binding structure was recognized at the sequence of residue 26 to residue 37, like those in other myosin regulatory light chains.

Amino Acid Sequence↗
PubMed1987

Electron microscopy of Pseudomonas aeruginosa treated with sulbenicillin and dibekacin.

A possible mechanism responsible for the combined effects of sulbenicillin and dibekacin on Pseudomonas aeruginosa IAM 1007 was investigated. The bactericidal activity of the above two drugs in combination was very strong. The regrowth of test strains after removal of the drugs was suppressed markedly, even when they were exposed to sulbenicillin plus dibekacin at a subinhibitory concentration of individual drugs. Sulbenicillin caused elongation of the bacterial cells. At the early stage of elongation, no demonstrable changes of ultrastructure of the cell wall were observed. At the late stage, lysis of the peptidoglycan layer occurred and spheroplast was formed. However, most of the outer membrane of the cell wall remained intact. Sulbenicillin acts upon the peptidoglycan layer, but not on the outer membrane. Thus it is difficult for sulbenicillin alone to cause cell lysis. On the other hand, dibekacin caused destruction of ribosomes and lysis of the outer membrane of the cell wall. Both sulbenicillin and dibekacin act on the cell wall, the former on the peptidoglycan layer (the inner membrane) and the latter on the outer membrane. The combined use of sulbenicillin and dibekacin caused elongation of bacilli and severe destruction of the inner and outer membranes of the cell wall. These morphological changes occurred even when the concentration of the individual drug was lower than its minimum inhibitory concentration (MIC). Furthermore, the cells elongated by sulbenicillin were ruptured easily when treated with dibekacin subsequently. The bacilli treated with dibekacin at a concentration lower than MIC and then treated with sulbenicillin at a concentration lower than MIC showed a marked elongation of the cells, which indicated that the effects of sulbenicillin was enhanced by dibekacin. These findings suggested strongly that sulbenicillin and dibekacin act on cell wall constituents and that their effects were complementary and synergistic.

Cell Wall↗
PubMed1987

Antitumor activity of cyclophosphamide and lipopolysaccharide in tumor-bearing mice pretreated with BCG.

Antitumor effects of cyclophosphamide (CY) and lipopolysaccharide (LPS) were investigated in BCG-treated mice. C3H/He mice and CDF1 mice were injected with BCG and were inoculated subcutaneously with syngeneic mouse hepatoma and mastocytoma P815 respectively. A subsequent injection of LPS caused hemorrhagic necrosis and retarded growth of tumor. When mice were treated with LPS plus suboptimal dose of CY, tumor growth was retarded and survival time was prolonged. The antitumor effects were more remarkable when mice were treated with CY prior to the injection of LPS. Without BCG pretreatment, LPS showed no antitumor activity in mice. Sera from mice treated with BCG plus LPS was cytotoxic for cultured tumor cells. However treatment of mice with CY did not increase the in vitro cytotoxicity. In this experimental condition, CY had no effect on delayed type hypersensitivity when evaluated by the footpad reaction to purified protein derivative (PPD). These results seem to indicate that the antitumor effects of the treatment with CY and LPS in BCG-treated mice are mediated by the reduction of tumor burden by CY and a serum factor induced by LPS.

Animals↗
PubMed1987

Incorporation of (E)-5-(2-iodovinyl)-2'-deoxyuridine into deoxyribonucleic acids of varicella-zoster virus (TK+ and TK- strains)-infected cells.

The incorporation of (E)-5-(2-iodovinyl)-2'-deoxyuridine (IVDU) into DNA of varicella-zoster virus (VZV)-infected human embryo fibroblasts was studied, using thymidine kinase-positive (TK+) and thymidine kinase-negative (TK-) VZV strains. [125I]IVDU was taken up by cells infected with TK+ VZV-, but not by TK- VZV- or mock-infected cells. [125I]IVDU was incorporated into both VZV DNA and cellular DNA of TK+ VZV-infected cells. When the cells were exposed to 0.3 microM IVDU, a more marked shift was noted in the buoyant density of viral DNA than of host DNA. In contrast, the DNAs isolated from TK- VZV- or mock-infected cells did not exhibit a detectable incorporation of [125I]IVDU. [125I] IVDU-labeled VZV DNA was purified from the viral nucleocapsids of TK+ VZV-infected cells. Substitution of no more than 0.1-1% of the thymidine residues in the VZV DNA by IVDU seemed to suffice to inhibit the replication of VZV.

Autoradiography↗