Search PubMed⌕ Search

Biomedical subjects

A Saeki

Publications and source records attributed to A Saeki.

At least 55 records · Page 3Linked to original sources
PubMed1995

[Acute myelomonocytic leukemia complicated with syndrome of inappropriate secretion of antidiuretic hormone, nephrotic syndrome, and hemophagocytic syndrome].

A 59-year-old man was admitted to our hospital because of fever in August 1991. Bone marrow showed normocellularity with 41.5% of CD13, 14, 33 positive blasts, and a diagnosis of AMMoL was made. Laboratory investigation revealed hyponatremia and elevated serum ADH level, indicating the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Intensive chemotherapy successfully induced hematological complete remission and his serum sodium level became normal. In February 1992, he developed proteinuria and findings were consistent with nephrotic syndrome (NS). Renal biopsy specimen showed membranous proliferative glomerulonephritis and massive infiltration of macrophages, and his serum interleukin 6 level was elevated. Five months later, he suffered from pancytopenia and elevation of biliary enzymes with increase of hemophagocytic histiocytes in his bone marrow (hemophagocytic syndrome). He transiently responded to low dose chemotherapy but he died due to severe infection. It is interesting that association between macrophages and/or cytokines with these various complications was suggested in AMMoL.

Fatal Outcome↗
PubMed1995

[Aplastic anemia with giant splenomegaly and myelofibrosis successfully treated with antilymphocyte globulin].

Severe aplastic anemia was diagnosed in a 58-year-old female because of pancytopenia with leukocyte count 700/microliters, hemoglobin 3.4 g/dl, platelet count 4.2 x 10(4)/microliters and fatty hypoplastic bone marrow in August 1992. In January 1993, she was admitted with an abdominal skin infection caused by pseudomonas aeruginosa. After treatment of the infection, antilymphocyte globulin was given at a dose of 2,000 mg/day for four consecutive days in July 1993. This resulted in a gradual but steady improvement in her hematological data. In February 1995, her leukocyte count increased to 2,000/microliters, hemoglobin to 15.2 g/dl and platelet count to 11.0 x 10(4)/microliters. Although no splenomegaly or myelofibrosis was found previously, from April 1993, the spleen enlarged and was palpable 10 cm below the costal margin. Her bone marrow biopsy in June 1993 revealed prominent myelofibrosis. Thereafter no changes were found in these features. Splenomegaly and myelofibrosis are characteristic of primary myelofibrosis and although the relationship is uncertain, there is no previous report on aplastic anemia with splenomegaly and myelofibrosis.

Anemia, Aplastic↗
PubMed1995

[A clinical experience of DNA probe method for identifying Mycobacterium avium and Mycobacterium intracellulare].

In Japan the number of patient infected with M. avium complex (MAC) has been increasing in contrast to a decrease of pulmonary tuberculosis. DNA probe method enabled us be able to differentiate an isolated MAC into M. avium and M. intracellulare. From 1991 to 1992, we performed an investigation to apply this new technique of the DNA probe method on 52 patients of atypical mycobacteriosis diagnosed as infected with MAC by the ordinary method at the Higashi Nagoya National Hospital. The group consisted of 27 males and 25 females. M. avium infection was found in 39 patients (M. avium group) and M. intracellulare in 16 patients (M. intracellulare group). No significant gender difference was found between two groups. The M. avium group showed more complications in contrast to the M. intracellulare group. As complications in the M. avium group, pulmonary aspergillus infection, bacterial pneumonia and bronchiectasis were found in 4, 3 and 2 cases, respectively. The rate of drug resistance to antituberculosis drugs was high in the both groups. Chemotherapy with isoniazid (INH) rifampin (RFP) and streptomycin (SM) in five patients, that with INH, RFP and ethambutol (EB) in three were found to be effective after 4 months treatment. Three patients in M. avium group died of respiratory failure, aspergillus infection and renal failure. In contrast the prognosis of patients in the M. intracellulare group seemed to be better as there was no fatal case. We conclude that DNA probe method is useful to differentiate between M. avium and M. intracellulare, and enable us to select more appropriate selection of the chemotherapy and to assess of the prognosis.

Aged↗
PubMed1995

[Bilateral ankle ulcers associated with hydroxyurea therapy for chronic myelogenous leukemia].

Bilateral ankle skin ulcers developed in a 61-year-old man in the chronic phase of chronic myelogenous leukemia receiving hydroxyurea therapy. The circulating immune complex (anti-C3d antibody) was high in this case, but vasculitis was not observed in the pathological findings of biopsied skin materials. This association has been reported in patients who had chronic myelogenous leukemia or other myeloproliferative disorders and were treated with hydroxyurea. It is likely that skin ulcers are caused by hydroxyurea.

Foot Ulcer↗
PubMed1994

Genetic analysis of Escherichia coli O9 rfb: identification and DNA sequence of phosphomannomutase and GDP-mannose pyrophosphorylase genes.

Subcloning, transposon insertion, and deletion analysis revealed that the Escherichia coli O9 rfb region is about 12 kb in size. The region encodes at least seven polypeptides of 89, 74, 55, 50, 44, 41 and 39.5 kDa. Southern hybridization analysis of rfb regions of E. coli O8 and O9, and Klebsiella O3 and O5 serotypes (all of these O polysaccharides are mannose homopolymers and the structures of the repeating unit of E. coli O9 and Klebsiella O3 are identical) showed that a central region specific for E. coli O9 and Klebsiella O3 is flanked by two regions common to all four. Complementation experiments using strains with known defects and specific tests for the enzymic activity showed that the 50 and 55 kDa polypeptides, encoded by the common region, are phosphomannomutase (PMM) and GDP-mannose pyrophosphorylase (GMP), respectively. Nucleotide sequencing of the region revealed the presence of two genes, rfbK and rfbM, analogous to the corresponding genes of Salmonella typhimurium. In E. coli O9, rfbK and rfbM encode proteins of 460 amino acids (50,809 Da) and 471 amino acids (52,789 Da). The amino acid sequence of GMP was conserved in RfbMs of E. coli O7 and Salmonella groups B, C1 and C2, CpsB of S. typhimurium, AlgA of Pseudomonas aeruginosa, and XanB of Xanthomonas campestris. The phylogenetic trees of PMM and GMP were different in topology and in the evolutionary distances from ancestors.

Amino Acid Sequence↗
PubMed1994

Hypercapnic acidosis increases oxygen cost of contractility in the dog left ventricle.

The effect of acidosis on left ventricular (LV) mechanoenergetics was assessed in seven excised, cross-circulated dog hearts with the use of the frameworks of the contractility index (Emax) and the relationship between myocardial oxygen consumption (VO2) and pressure-volume area (PVA; a measure of the LV total mechanical energy). Acidosis was stably maintained without hypoxia by appropriately mixing CO2 and air in a membrane oxygenator in the coronary arterial perfusion circuit. Acidosis [pH: 6.98 +/- 0.09 (SD), PCO2: 91 +/- 25 mmHg in the coronary arterial blood] decreased Emax by 45 +/- 12% (P < 0.01) and PVA by 47 +/- 12% (P < 0.01) at a fixed LV volume. When the preacidosis Emax level was restored by Ca2+ infusion during acidosis, unloaded VO2 (the VO2 intercept of the VO2-PVA relation) exceeded the control value by 19 +/- 17% (P < 0.05), indicating that acidosis required higher VO2 for nonmechanical activities at a matched Emax. Moreover, the oxygen cost of enhanced contractility (the incremental ratio of unloaded VO2 to Emax) was 1.53 +/- 0.40 times higher (P < 0.01) during acidosis than preacidosis. We conclude that acidosis results in LV contractile dysfunction accompanied by an increased oxygen cost of contractility. This increased energy cost of the excitation-contraction coupling can be accounted for by a decreased Ca2+ sensitivity of the contractile proteins during acidosis.

Acidosis↗
PubMed1994

Stunned myocardium after rapid correction of acidosis. Increased oxygen cost of contractility and the role of the Na(+)-H+ exchange system.

Left ventricular (LV) contractile dysfunction during acidosis has been reported to be almost reversible in crystalloid-perfused hearts after correction of acidosis. In contrast, we have found that, in blood-perfused hearts, contractile function is paradoxically depressed after correction of acidosis with a transient overshoot of contractility during the recovery of pH. To clarify the mechanism of this phenomenon, we measured the LV contractility index (Emax) and the relation between myocardial oxygen consumption (VO2) and systolic pressure-volume area (PVA, a measure of the LV total mechanical energy) before and after induction and rapid correction of acidosis by CO2 loading (pH 7.00) and unloading in 13 excised cross-circulated canine hearts. During the rapid correction of acidosis in six control hearts, a severe transient overshoot of Emax (404% of acidosis) occurred. However, after correction of acidosis, Emax and PVA were lower than the preacidosis values by 46% (P < .01) and 44% (P < .01) at the same LV volume. When the preacidosis Emax level was restored by Ca2+ infusion, the VO2 intercept (PVA-independent VO2) of the linear VO2-PVA relation exceeded the control value by 18% (P < .05) with an unchanged slope. In addition, the oxygen cost of contractility, defined as the slope of the relation between PVA-independent VO2 and Emax, increased by 83% (P < .01) after correction of acidosis, indicating that postacidosis myocardium requires higher VO2 for nonmechanical activities for a unit increase in Emax. Then, we hypothesized that these mechanoenergetic disorders after rapid correction of acidosis would result from Ca2+ overload via accelerated Na(+)-Ca2+ exchange due to the heavily operating Na(+)-H+ exchange system at the time of rapid pH recovery. To examine this hypothesis, dimethylamiloride, a selective Na(+)-H+ exchange inhibitor, was administered just before the correction of acidosis in the other seven hearts. The administration of dimethylamiloride completely prevented both the mechanical and energetic disorders after correction of acidosis. We conclude that rapid recovery of pH paradoxically depresses myocardial contractility and increases the oxygen cost of contractility through an activation of the Na(+)-H+ exchange system.

Acidosis↗
PubMed1993

Comparison of the cardiac force-time integral with energetics using a cardiac muscle model.

Several investigators have found experimentally that the force-time integral varies non-linearly with energy expenditure over the course of a cardiac contraction. Also, recent research findings have indicated that the crossbridge cycle to ATP hydrolysis ratio in muscle fiber systems may not be coupled with a one-to-one ratio. In order to investigate these findings, Huxley's sliding filament crossbridge muscle model coupled with parallel and series elastic components was simulated to examine the behavior of the crossbridge energy utilization and force-time integral vs time. Crossbridge (CB) energy utilization was determined by considering the ATP hydrolysis for the crossbridge cycling, and this CB energy was compared with the force-length energy in a contraction. This CB energy was calculated in both isometric and isotonic contractions as a function of contraction time and compared to the force-time integral. Simulation results demonstrated that the ratio of the force-time integral to CB energy varies strongly throughout the cardiac cycle for both isometric and isotonic cases, as has been observed experimentally. Simulations also showed that using the force-length energy component of energy vs the CB energy gave a better correlation between the total energetic predictions and the force-time integral, agreeing with recent finding that the crossbridge cycle to ATP hydrolysis ratio may not be coupled one-to-one, especially at lower force levels.

Actins↗
PubMed1993

Coupling between regional myocardial oxygen consumption and contraction under altered preload and afterload.

OBJECTIVES: This study was designed to assess the relation between left ventricular regional myocardial oxygen consumption (VO2) and variables of regional myocardial contractile function under various loading conditions. BACKGROUND: Although the relation between global VO2 and global ventricular function has been extensively studied, the relation between regional VO2 and regional myocardial contraction is not fully understood. METHODS: Myocardial shortening (regional area shrinkage), regional work, regional total mechanical energy index and regional VO2 were measured under variously altered loading conditions in the isolated, blood-perfused dog left ventricle. Regional total mechanical energy per beat was quantified by wall tension-regional area area (TAA) by the analogy of left ventricular pressure-volume area. Left ventricular loading conditions were altered by changing end-diastolic volume and stroke volume with a servo pump as follows: 1) increased preload (increased end-diastolic volume and stroke volume at a constant ejection fraction), 2) decreased afterload (increased stroke volume at a constant end-diastolic volume), 3) increased preload and afterload (increased end-diastolic volume at a constant stroke volume), and 4) altered mode of contraction (ejecting vs. isovolumetric contractions). RESULTS: During increased preload, all three variables correlated positively with regional VO2 (r = 0.78 to 1.00). During decreased afterload, the correlation was negative for area shrinkage (r = -0.65 to -0.91) and variable for regional work (r = -0.55 to 0.98) but positive and highly linear for TAA (r = 0.80 to 0.99). During increased preload and afterload, the correlation was again negative for area shrinkage (r = -0.77 to -0.97) but positive for regional work (r = 0.83 to 0.93) and TAA (r = 0.95 to 0.99). During altered mode of contraction, the correlation was insignificant for area shrinkage (r = 0.24 to 0.57) and moderate for regional work (r = 0.50 to 0.79), whereas again highly linear for TAA (r = 0.95 to 0.98). Thus, only TAA correlated closely with regional VO2 under any loading conditions. Furthermore, the slope and regional VO2 intercept of the regional VO2-TAA relation was remarkably consistent among the different hearts and loading conditions. CONCLUSIONS: We conclude that there is a tight coupling between regional VO2 and regional total mechanical energy represented by TAA regardless of left ventricular afterload and preload conditions.

Animals↗
PubMed1993

Isolation of rfb gene clusters directing the synthesis of O polysaccharides consisting of mannose homopolymers and serological analysis of lipopolysaccharides.

Four serotypes of two genera, Escherichia coli O8 and O9 and Klebsiella O3 and O5, produce the O polysaccharides consisting of mannose homopolymers. Previously, we reported the isolation and expression of E. coli O9 rfb in E. coli K-12 strains (Kido et al, J. Bacteriol., 171: 3629-3633, 1989). In this study, R' plasmids carrying his-rfb region of the other three strains were isolated and expressed in E. coli K-12 strain. Serological study of lipopolysaccharides (LPS) synthesized in E. coli K-12 strain was carried out. His-linked rfb genes from E. coli O9 and Klebsiella O3 directed the synthesis of O polysaccharides with the same antigenicity as those of the parental strains in E. coli K-12 strain. On the other hand, rfb genes from E. coli O8 and Klebsiella O5 directed the synthesis of O polysaccharides which were antigenically not identical but partially common to those of the parental strains. A rough strain derived from E. coli O8 synthesized LPS which showed the identical antigenicity as the wild strain when the his-rfb region of E. coli O8 was introduced. The results suggest that some genes located distantly from his are additionally required to complete the synthesis of O polysaccharides of E. coli O8 and Klebsiella O5.

Carbohydrate Conformation↗
PubMed1993

Ejecting deactivation does not affect O2 consumption-pressure-volume area relation in dog hearts.

We studied the effects of ejection velocity and resistive properties of the left ventricle (LV) on myocardial oxygen consumption (VO2) in 13 excised cross-circulated dog hearts. Increases in peak ejection velocity (-dV/dt) from 4.0 +/- 1.3 (SD) end-diastolic volume (EDV)/s to 12.7 +/- 5.3 EDV/s with constant EDV and end-systolic volume (velocity run) induced systolic pressure deficit. This decreased pressure-volume area (PVA; a measure of ventricular mechanical energy) and LV end-systolic elastance (Emax) by 47 +/- 14 and 38 +/- 15%, respectively. Unchanged maximum rate of left ventricular pressure rise and time-varying elastance during the isovolumic contraction period at the same EDV indicated that these contractions started with the same contractile state although the quicker ejection caused the greater deactivation. If the PVA deficit due to systolic pressure deficit is attributable to an internal energy-dissipating resistive element, VO2 in the velocity run will not as much decrease in proportion to PVA as in the isovolumic or slowly ejecting control run. However, the decreases in PVA due to increased -dV/dt decreased VO2 to the same extent as in the control run. This result negated the possibility that the pressure and PVA deficits would be caused by a mechanical energy-losing process. The same results were obtained whether or not Emax was decreased by quick ejection. We conclude that the pressure and PVA deficits and the proportionally decreased VO2 during quick ejection are mainly attributable to suppression of a ventricular mechanical energy generation process, but not of mechanical energy-losing process, by ejecting deactivation.

Animals↗
PubMed1993

Ryanodine wastes oxygen consumption for Ca2+ handling in the dog heart. A new pathological heart model.

Ryanodine (RYA) at a low concentration (several tens of nM) is known to selectively bind to Ca2+ release channels in sarcoplasmic reticulum (SR) and to fix them open. The present study was designed to investigate the effects of the selective change in Ca2+ release channel activity on cardiac mechanoenergetics as a model of Ca(2+)-leaky SR observed in pathological hearts. We analyzed the negative inotropic effect of RYA at a low concentration (up to 30 +/- 13 nM) on left ventricular (LV) mechanoenergetics using frameworks of LV Emax (a contractility index) and the myocardial oxygen consumption (LV VO2)-systolic pressure-volume area (PVA) (a measure of total mechanical energy) relation in 11 isolated, blood-perfused dog hearts. RYA significantly decreased Emax by 42%, whereas PVA-independent VO2 remained disproportionately high (93% of control). This oxygen-wasting effect of RYA was quite different from ordinary inotropic drugs, which alter Emax and PVA-independent VO2 proportionally. The present result suggests that RYA suppresses force generation of cardiac muscle for a given amount of total sequestered Ca2+ by SR in a similar way to myocardial ischemia and stunning. We speculate about the underlying mechanism that RYA makes SR leaky for Ca2+ and thereby wastes energy for Ca2+ handling by SR.

Analysis of Variance↗
PubMed1993

Ventricular perspective on efficiency.

The heart has many efficiencies of different definitions, of which mechanical work efficiency is the most popular and conventional. We have proposed a method to quantify the total mechanical energy generated by ventricular contraction. This energy can be quantified as a specific area called "systolic pressure-volume area" or "PVA" in the ventricular pressure-volume diagram. In the left ventricle of excised, cross-circulated dog heart preparations, we found a closely linear relation between PVA and oxygen consumption (VO2) under various loading conditions in a stable contractile state (Emax). An enhanced contractility was accompanied by an elevation of the load-independent VO2-PVA relation in a parallel manner, where the elevation was proportional to Emax. The slope of the VO2-PVA relation represents the "oxygen cost of mechanical energy (or PVA)" and its reciprocal indicates the "contractile efficiency", i.e., the energy conversion efficiency from PVA-dependent VO2 to PVA. This efficiency was 40% on the average, independent of various inotropic interventions. The slope of the PVA-independent VO2-Emax relation represents the "oxygen cost of contractility (or Emax)". This cost was relatively constant for different inotropic interventions except for myocardial cooling and stunning. We considered the discrepancy between the stable contractile efficiency and the variable thermal economy of force generation and maintenance.

Animals↗
PubMed1993

[Pure red cell aplasia complicated with polyarthritis, angitis, and acute renal failure].

A case of pure red cell aplasia (PRCA) with various complications polyarthritis, angitis, acute renal failure and DIC was successfully treated with steroid pulse therapy was described. A 55-year-old woman was hospitalized with a 9-month of intermittent but progressive joint pain, morning stiffness, general fatigue, and fever. Her initial laboratory evaluation revealed a hemoglobin of 4.4 g/dl and absence of reticulocyte. Her bone marrow aspirate showed no erythroblast which was compatible with a diagnosis of PRCA. Marked leukocytosis and thrombocytosis, positive antinuclear antigen, elevation of gammaglobulin and C-reactive protein and the presence of polyarthritis and angitis which was confirmed by renal angiography, indicated an underlying autoimmune disorders. Steroid pulse therapy was administered at 500 mg/day for 3 days, resulting in the complete response in both red cell aplasia and above findings. PRCA is known to be associated with systemic lupus erythematosus and rheumatoid arthritis very rarely, but this case did not fulfill the criteria of known collagen diseases, and there is no previous report representing PRCA with various complications such as polyarthritis, angitis and acute renal failure. This case may help us to understand more about the relationship between PRCA and autoimmune disorders.

Acute Kidney Injury↗
PubMed1992

Ejecting volume, filling volume and stroke volume gains: new indexes of inotropism and lusitropism.

We propose new indexes to evaluate the effects of ventricular inotropism and lusitropism on stroke volume. The end-systolic pressure-volume relationship (ESPVR) or its slope (Emax) has been employed to assess ventricular inotropism. The end-diastolic pressure-volume relationship (EDPVR) or compliance has been used to express ventricular diastolic properties or lusitropism. However, their net effect on stroke volume under a given set of preload and afterload pressures has not quantitatively been evaluated. Ejecting volume gain (Ge) was proposed to quantify the inotropic effect on stroke volume by the change in end-systolic volume between the two ESPVR curves obtained before and during an inotropic intervention at a specified ejecting pressure. Ge is a function of afterload pressure. Filling volume gain (Gf) was proposed to quantify the lusitropic effect on stroke volume by the change in end-diastolic volume between the two EDPVR curves before and during a lusitropic intervention at a specified filling pressure. Gf is a function of preload pressure. The net effect of these inotropic and lusitropic effects on stroke volume at these specified preload and afterload pressures can be expressed by the sum of Ge and Gf. We call this sum stroke volume gain (Gsv). Gsv is a function of preload and afterload pressures. Using representative examples, we demonstrate that these new indexes are conceptually useful to quantitatively understand changes in the pumping ability of the heart under simultaneous inotropic and lusitropic effects as a function of ejecting and filling pressures.

Animals↗
PubMed1992

Mechanoenergetic effects of pimobendan in canine left ventricles. Comparison with dobutamine.

BACKGROUND: We hypothesized that the effect of pimobendan (UD-CG 115 BS) to increase calcium sensitivity of contractile protein might result in less myocardial oxygen consumption (VO2) in comparison with dobutamine when they enhance ventricular contractility to the same extent. To examine this hypothesis, we compared the effects of pimobendan and dobutamine on left ventricular contractility and energetics using the frameworks of Emax (contractility index) and the relation between VO2 and PVA (systolic pressure-volume area, a measure of left ventricular total mechanical energy). METHODS AND RESULTS: We measured VO2, Emax, PVA, and force-time integral (FTI) in excised, cross-circulated, nonfailing dog hearts. The slope of the VO2-PVA relation reciprocally indicates the efficiency from PVA-dependent VO2 to the total mechanical energy (contractile efficiency). The VO2 intercept of the VO2-PVA relation, i.e., PVA-independent VO2, reflects energy utilization for excitation-contraction coupling. The ratio of FTI to PVA-dependent VO2 can be called contractile economy. Both drugs comparably enhanced Emax. Although the contractile economy was greater by 14 +/- 19% (p less than 0.05) for pimobendan than for dobutamine, the contractile efficiency was similar between the two drugs. Oxygen cost of contractility, defined as the slope of the relation between the PVA-independent VO2 and Emax, was the same between the two drugs. Other mechanoenergetic effects of both drugs were similar except for a greater coronary vasodilating effect of pimobendan. CONCLUSIONS: Pimobendan has almost the same mechanoenergetic effects as dobutamine but slightly greater contractile economy and coronary vasodilation. The calcium-sensitizing effect of pimobendan did not save the oxygen cost of contractility.

Animals↗
PubMed1992

Left ventricular contractility and energetic cost in disease models--an approach from the pressure-volume diagram.

Left ventricular contractility and the energetic cost of contraction were assessed in various disease models in experimental animals utilizing frameworks of Emax (left ventricular contractility index) and pressure-volume area (PVA, a measure of total left ventricular mechanical energy expenditure) derived from the pressure-volume (P-V) diagram. Under various contractile conditions, PVA linearly correlates with myocardial oxygen consumption per beat (VO2) in a load-independent manner. The reciprocal of the slope of the linear VO2-PVA relation indicates "contractile efficiency" (the energy transduction efficiency from oxygen to total mechanical energy). It was similar between dog and rabbit hearts (about 40%) and was not significantly affected by enhanced contractility with calcium, epinephrine, or cardiac cooling, or by depressed contractility with propranolol, decreased coronary perfusion pressure, or stunned myocardium. However, in thyrotoxic rabbit hearts contractile efficiency was significantly depressed compared to normal hearts. On the other hand, the VO2 intercept of the VO2-PVA relation (PVA-independent VO2), which reflects VO2 for non-mechanical activities such as excitation-contraction coupling and basal metabolism, positively correlates with Emax. Therefore, the ratio of an increase in PVA-independent VO2 to an increase in Emax indicates "oxygen cost of contractility". Oxygen cost of contractility was higher in stunned myocardium than in normal hearts, suggesting that the energy cost of calcium handling is elevated in stunned myocardium. Thus, using the frameworks of Emax and PVA, we can interconnect cardiac mechanics and energetics. Further, using the concepts of contractile efficiency and oxygen cost of contractility, we can approach the pathogenesis of variously altered contractile conditions.

Animals↗