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Biomedical subjects

Atsushi Baba

Publications and source records attributed to Atsushi Baba.

At least 19 recordsLinked to original sources

Psychiatric problems of heart transplant candidates with left ventricular assist devices.

Most heart transplant candidates are equipped with left ventricular assist devices (LVADs). LVAD therapy is associated with characteristic psychiatric and psychosocial problems. To investigate the mental states of heart transplant candidates, psychiatric diagnosis, psychological or behavioral problems, and the need for treatment were evaluated around the time of registration to the waiting list and during follow-up. Saitama Medical University Hospital has been designated a hospital for heart transplantation since October 2002. The subjects were 14 heart transplant candidates (9 male candidates and 5 female candidates, mean age 29 years) at the hospital from September 1997 to October 2005. These 14 candidates were equipped with LVADs. The waiting periods on LVAD support were from 119 days to 1028 days, and the average waiting period was 313 days. Six candidates among the 14 had more than one DSM-IV diagnosis. Seven candidates were diagnosed with adjustment disorder, which was the most frequent diagnosis. Three candidates had depressive disorder, one had psychotic disorder, and one had dissociative disorder. Three candidates had acute cognitive dysfunction (delirium) due to their general medical condition. All three had other disorders with mainly psychological elements. Nine candidates (64%) were diagnosed with disorders with mainly psychological elements. Antipsychotics were used for the candidates in psychotic states and with delirium, and there was a need for crisis intervention. Antidepressants and antianxiety drugs were used for the candidates with depressive disorder; they needed intensive observation. Four candidates (28%) needed some attention and some antianxiety drugs or hypnotics. Psychiatric interventions were not necessary in five candidates (36%).

Adjustment Disorders↗

Neonatal management of trisomy 18: clinical details of 24 patients receiving intensive treatment.

Management of neonates with trisomy 18 is controversial, supposedly due to the prognosis and the lack of precise clinical information concerning efficacy of treatment. To delineate the natural history of trisomy 18 managed under intensive treatment, we reviewed detailed clinical data of 24 patients with full trisomy 18 admitted to the neonatal intensive care unit of Nagano Children's Hospital, providing intensive treatment to those with trisomy 18, from 1994 to 2003. Cesarean, resuscitation by intubation, and surgical operations were performed on 16 (67%), 15 (63%), and 10 (42%) of the patients, respectively. Mechanical ventilation was required by 21 (88%), and 6 (29%) of them were extubated. Survival rate at age 1 week, 1 month, and 1 year was 88%, 83%, and 25%, respectively. Median survival time was 152.5 days. Respiration was not stabilized in two patients with left diaphragmatic eventration and hypoplasia accompanied by lung hypoplasia, even with maximal ventilation. The common underlying factors associated with death were congenital heart defects and heart failure (96%), followed by pulmonary hypertension (78%). The common final modes of death were sudden cardiac or cardiopulmonary arrest (26%) and possible progressive pulmonary hypertension-related events (26%). These data of improved survival, through neonatal intensive treatment, are helpful for clinicians to offer the best information on treatment options to families of patients with trisomy 18.

Birth Weight↗

Liquid incubator with perfluorochemicals for extremely premature infants.

OBJECTIVES: Maintenance of appropriate body temperature, humidification and prevention of skin injury are very important in the management of extremely premature infants with immature skin. We have developed a new closed liquid incubator, utilising the characteristics of perfluorochemical (PFC) liquids, i.e., high specific gravity and chemical and biological inertness. The potential of this incubator to control body temperature was evaluated in rats. METHODS: PFC liquid (FC43; 3M Company, Tokyo, Japan) within the incubator was heated or cooled and the rectal temperature of each rat and the PFC temperature were monitored. RESULTS: The rectal temperature of rats floating on the PFC liquid surface changed almost in parallel to the temperature of PFC within the incubator, indicating that this technique can be used to warm or cool adults rats in a stable manner. The relative humidity of air within the incubator was maintained constant at 100%. CONCLUSIONS: The liquid incubator used in the present study maintained an environment with a relative humidity of 100% and allowed stable maintenance of temperature in adult rats. We also demonstrated that heating and cooling the PFC liquid allowed control of body temperature. Although further studies are required, this new incubator may be useful for the clinical management of extremely premature infants.

Animals↗

Influence of flow design on microcirculation in conditions of undulation pump-left ventricle assist device testing.

To study the microvessels in bulbar conjunctiva, we conducted an experiment in goat with a pneumatically driven left heart bypass pump, which was replaced with an undulation pump-left ventricle assist device for 9 days. Three flow patterns were tested: complete pulsatile, continuous, and percentage of pulsatile. We studied the morphology of arterioles and venules of the bulbar conjunctiva using photograph records. The setting up of continuous flow caused global vasoconstriction (significant in venules-P < 0.05). During the pumping in the pulsatile and percentage of pulsatile modes, no significant changes of microvessel morphology were observed. The findings described could point to some disturbances in the microcirculatory bed in conditions of continuous flow.

Animals↗

Differential effects of short-acting beta2-agonists on human granulocyte functions.

BACKGROUND: beta2-Adrenergic agonists play a pivotal role in the management of bronchial asthma. Although the major effect of short-acting beta2-agonists on the airway is relaxation of smooth muscles, they may also have several effects on surrounding immunomodulatory cells. METHODS: We examined whether widely used short-acting beta2-agonists differ in their ability to modulate granulocyte functions, such as superoxide anion (O2-) production and degranulation. RESULTS: Procaterol (PC), a full agonist, significantly inhibited both O2- production by granulocytes (neutrophils and eosinophils) and their degranulation at the clinically relevant concentrations, whereas salbutamol and tulobuterol (partial agonists) showed smaller effects. PC inhibited N-formyl methionyl-leucyl-phenylalanine-induced O2- production and peroxidase release, but failed to inhibit responses induced by phorbol 12-myristate 13-acetate and/or opsonized zymosan. Exposure to 5 x 10(-8)M PC for 120 min resulted in approximately 50% inhibition of O2- production and degranulation of neutrophils. The effects of beta2-agonists were more obvious in neutrophils than in eosinophils. A selective beta2-receptor antagonist, ICI-118551, reversed the inhibitory effect of beta2-agonists (PC, salbutamol, tulobuterol B) on N-formyl methionyl-leucyl-phenylalanine-induced O2- production. CONCLUSIONS: These results suggest that beta2-agonists had an inhibitory effect on granulocyte functions, mainly mediated viareceptors and their efficacy. Our observations support that beta2-agonists with a rapid onset of action and high intrinsic efficacy (short-acting and full agonists) may be optimal for the rescue therapy against acute asthma attack and sedation of its airway inflammation in an early phase.

Adrenergic beta-Agonists↗

Degradation of oxidative stress-induced denatured albumin in rat liver endothelial cells.

We previously identified conformationally denatured albumin (D2 and D3 albumin) in rats with endotoxicosis (Bito R, Shikano T, and Kawabata H. Biochim Biophys Acta 1646: 100-111, 2003). In the present study, we attempted first to confirm whether the denatured albumins generally increase in conditions of oxidative stress and second to characterize the degradative process of the denatured albumin using primary cultured rat liver endothelial cells. We used five models of oxidative stress, including endotoxicosis, ischemic heart disease, diabetes, acute inflammation, and aging, and found that serum concentrations of D3 albumin correlate with the serum levels of thiobarbituric acid-reactive substance (R = 0.87), whereas the concentrations of D2 albumin are 0.52. Ligand blot analysis showed that the D3 albumin binds to gp18 and gp30, which are known endothelial scavenger receptors for chemically denatured albumin. Primary cultured rat liver endothelial cells degraded the FITC-D3 albumin, and the degradation rate decreased to approximately 60% of control levels in response to anti-gp18 and anti-gp30 antibodies, respectively. An equimolar mixture of these antibodies produced an additive inhibitory effect on both uptake and degradation, resulting in levels approximately 20% those of the control. Furthermore, filipin and digitonin, inhibitors of the caveolae-related endocytic pathway, reduced the FITC-D3 albumin uptake and degradation to <20%. Laser-scanning confocal microscopic observation supported these data regarding the uptake and degradation of D3 albumin. These results indicate that conformationally denatured D3 albumin occurs generally under oxidative stress and is degraded primarily via gp18- and gp30-mediated and caveolae-related endocytosis in liver endothelial cells.

Animals↗

TRRAP as a hepatic coactivator of LXR and FXR function.

TBP-free TAF II-containing-type HAT complex subclasses, which contain hGCN5 HAT and TRRAP, appear to act as common coactivator complexes for nuclear receptors. However, their physiological significance with respect to each nuclear receptor remains to be established. To address this issue, we used hepatic cell lines (HepG2) with reduced endogenous TRRAP expression through antisense RNA expression or with overexpressed TRRAP or other major coactivators. The ligand-induced transactivation function of liver X receptor alpha (LXRalpha) and farnesoid X receptor/bile acid receptor reflected TRRAP expression levels, while that of PPARgamma did not. A GST pull-down assay indicated that TRRAP contains two potential LXRalpha-interacting domains in the C-terminal and central domains. Expression of antisense TRRAP RNA in HepG2 cells abolished the ligand-induced expression of LXRalpha target genes. These results suggested that TRRAP plays an important role as a coactivator, presumably part of a complex, in lipid metabolism through regulation of the LXRalpha-mediated gene cascade in hepatic cells.

Adaptor Proteins, Signal Transducing↗

Superoxide dismutase (SOD) as a potential inhibitory mediator of inflammation via neutrophil apoptosis.

Superoxide dismutase (SOD) is supposed to be an effective agent for neutrophil-mediated inflammation in the area of critical medicine. We investigated the involvement of SOD in the regulation of neutrophil apoptosis. Exogenously added SOD effectively induced neutrophil apoptosis, and the fluorescence patterns determined using annexin-V and the 7-AAD were similar to those seen in Fas-mediated neutrophil apoptosis. Neutrophils are short-lived leukocytes that need to be removed safely by apoptosis. The clearance of apoptotic neutrophils from sites of inflammation is a crucial determinant of the resolution of inflammation. Catalase inhibited the neutrophil apoptosis and caspase-3 activation. Spontaneous apoptosis, hydrogen peroxide and anti-Fas antibody-induced apoptosis of neutrophils were accelerated in Down's syndrome patients, in whom the SOD gene is overexpressed. Hydrogen peroxide was thought to be a possible major mediator of ROS-induced neutrophil apoptosis in caspase-dependent manner. Neutrophil apoptosis represents a crucial step in the mechanism governing the resolution of inflammation and has been suggested as a possible target for the control of neutrophil-mediated tissue injury. SOD may be a potential inhibitory mediator of neutrophil-mediated inflammation.

Adult↗

Neutrophil-mediated inflammation in respiratory syncytial viral bronchiolitis.

BACKGROUND: The involvement of neutrophil-mediated inflammation may play an important role in the pathogenesis of acute respiratory syncytial virus bronchiolitis. However, no measurable marker is sensitive enough to assess neutrophil-mediated inflammation in the airways. Released neutrophil elastase (NE) in intraluminal airways has been reported to induce pulmonary inflammation. The aim of this study was to determine whether the amount of urinary trypsin inhibitor (UTI) in serum, a degenerate induced by NE, reflects the degree of airway inflammation in children with respiratory syncytial viral (RSV) bronchiolitis and whether the severity of inflammation is evaluated. The pre-alpha-/inter-alpha-trypsin inhibitor is assumed to be precursors of the UTI. When NE degrades these inhibitors, UTI is liberated. METHODS: Serum UTI concentrations in infants admitted with RSV bronchiolitis, other viral infections, bacterial pneumonia and control subjects were measured by means of one-step sandwich-type enzyme immunoassay. RESULTS: Serum UTI concentrations in 25 patients on admission were significantly higher than the 15 infantile control values (mean +/- SEM, 22.126 +/- 2.317 and 6.701 +/- 0.719 U/mL, respectively; P < 0.0001). The elevated levels returned to baseline values with improvement in the respiratory symptoms. Higher levels of serum UTI with RSV infection were consistently associated with clinical symptoms and artificial ventilation. Serum NE concentrations of patients were elevated in some patients but not significantly different from controls in the patients who showed only upper respiratory symptoms with RSV infections. CONCLUSION: The findings strongly suggested that neutrophil-mediated events are involved in the pathogenesis of RSV bronchiolitis, and the monitoring of UTI concentrations might be useful for evaluating the neutrophil-mediated airway inflammation.

Bronchiolitis↗

Beta-amyloid prevents excitotoxicity via recruitment of glial glutamate transporters.

Amyloid beta-protein (Abeta), a putative pathogenic endotoxin involved in Alzheimer's disease, induces redistribution of glutamate transporters in astrocytes and promotes their pump activity. Because the transporters are assumed to protect neurons against excitotoxicity by removing extracellular glutamate, we hypothesized that Abeta alters the vulnerability of neurons to glutamate. Cerebrocortical neuron-astroglial co-cultures were exposed to glutamate, the concentration of which was selected so that only 20% of the neurons exhibited degeneration. When cultures were pre-treated with Abeta, exposure to the same "mild" glutamate concentration failed to damage neurons. The Abeta-induced protection was abolished by a glial glutamate transporter inhibitor. Thus, Abeta can alleviate excitotoxicity through glutamate transporter activity. The present results may challenge prevailing concepts that Abeta-induced neuron loss causes Alzheimer's dementia and also provide practical insights into neuro-glial interactions in glutamate toxicity.

Amino Acid Transport System X-AG↗

Activity-evoked capacitative Ca2+ entry: implications in synaptic plasticity.

The Ca2+ influx controlled by intracellular Ca2+ stores, called store-operated Ca2+ entry (SOC), occurs in various eukaryotic cells, but whether CNS neurons are endowed with SOC capability and how they may operate have been contentious issues. Using Ca2+ imaging, we present evidence for the presence of SOC in cultured hippocampal pyramidal neurons. Depletion of internal Ca2+ stores by thapsigargin caused intracellular Ca2+ elevation, which was prevented by SOC channel inhibitors 2-aminoethoxydiphenyl borate (2-APB), SKF96365, and La3+. Interestingly, these inhibitors also accelerated the decay of NMDA-induced Ca2+ transients without affecting their peak amplitude. In addition, SOC channel inhibitors attenuated tetanus-induced dendritic Ca2+ accumulation and long-term potentiation at Schaffer collateral-CA1 synapses in hippocampal slice preparations. These data suggest a novel link between ionotropic receptor-activated SOC and neuroplasticity.

Animals↗

Preliminary study of a new type of energy transmission system for artificial hearts.

A transcutaneous energy transmission (TET) system is the most common way to power artificial hearts and ventricular assist devices. However, an external battery used with a TET system poses several problems, such as its heavy mass, small charge capacity, and long recharging time. The battery is indispensable when patients want to be ambulatory. This article proposes a new type of TET system that does not require an external battery because electrical energy is supplied remotely by using electromagnetic waves. For this system to operate, multiple transmitting antennas have to be mounted in a room or facility that has been shielded from electromagnetic waves, and a receiving antenna is attached to the patient. Electromagnetic waves transmit electrical power from the transmitting antennas to the receiving antenna. The received electrical power is sent to an implanted device through the TET system. The total power efficiency was plotted against the transmitter-receiver distance by measuring the power that was input to the transmitting antennas, and the final direct current (DC) power that was received by the receiving antenna. A 430-MHz frequency was applied in the experiments. The obtained efficiency was around 10% within a transmitter-receiver distance of 1 m when Yagi-Uda antennas were used for the transmitting antennas and two other types of antenna were used for the receiving antennas: a folded dipole with a reflector and a single loop with a reflector. The results suggested that the proposed system is worth considering. The proposed system would go a long way toward enhancing the patient's quality of life compared with the currently used conventional TET system.

Computer Simulation↗

Evaluation of pulsatile and nonpulsatile flow in microvessels of the bulbar conjunctiva in the goat with an undulation pump artificial heart.

This study has three purposes, as follows. The first is to develop a microscopic system to observe the microcirculation of animals implanted with an artificial heart. The second is to investigate the influence of flow pattern change from pulsatile to nonpulsatile on the microcirculation. The third is to study the effects of pulsatility in blood flow on endothelium-derived nitric oxide release in the microvasculature. When the flow pattern was changed from pulsatile to nonpulsatile, the velocity of erythrocytes in many capillaries dropped and remained at a low level, and the number of perfused capillaries decreased. After the flow pattern was returned to pulsatile, the velocity of erythrocytes recovered to the initial level. In many cases, the flow of nonperfused capillaries recovered to the initial level as well. Also, the pulsatile flow enhances the basal and flow-stimulated endothelium-derived nitric oxide release in microvessels.

Animals↗

Progress in the control system of the undulation pump total artificial heart.

The undulation pump total artificial heart (UPTAH) is a small implantable total artificial heart. As the UPTAH generates outflow and inflow at the same time, control of the UPTAH is very difficult. Therefore suitable control methods specifically for the UPTAH should be established. Various motor control, left-right flow balance control, and physiological control methods were examined and tried for the UPTAH control in this study. The control system is divided into seven categories. It has a hierarchical structure and all control modes work at the same time. The UPTAH with the newly developed control method has been implanted into the chest cavities of 48 goats. Until now, six goats survived for more than one month, including 63 days in the longest case. The good condition of the UPTAH implanted animal could be maintained with the newly developed control scheme, consisting of the 1/R control and several other additional controls.

Animals↗

A study on an energy supply method for a transcutaneous energy transmission system.

This study proposes a new type of a transcutaneous energy transmission system (TETS) that can supply electrical power for an implanted device without an external battery. In this system, the power is supplied from the floor to the shoes of the patients through coils that are set beneath the floor and the bottom of the shoes. If the patients wear the special shoes, they will be able to move freely on the specially designed floor without an external battery. Direct current (DC)-DC power efficiency was measured in the experiments, and the results showed that it varies with relative positions between the shoe and the floor coils. The results suggested that three-layered floor coils would enable the system to meet the demand for providing the required power anywhere on the floor without intermission. DC-DC power efficiency could be kept over 60% under the practical condition. It can then be concluded that the proposed system has a potential to provide better quality of life for the patients using a TETS.

Electromagnetic Fields↗

Global analysis of shear stress-responsive genes in vascular endothelial cells.

DNA microarray gene expression analysis was conducted in human umbilical vein endothelial cells (HUVECs) and coronary artery endothelial cells (HCAECs) exposed to laminar or turbulent shear stress. Approximately 3% of the total 5600 gene in HUVECs and HCAECs increased their expression more than two-fold or decreased it to less than half the static control in response to an arterial level of laminar shear stress (15 dynes/cm(2) for 24 hours). The proportions of shear-stress-responsive genes decreased to around 2% under the venous level of laminar shear stress (1.5 dynes/cm(2)) in both cell lines. Turbulent shear stress of 1.5 dynes/cm(2) altered the expression of 1.1% of all genes in the HCAECs. Laminar shear stress, but not turbulent shear stress, decreased the expression of a number of genes involved in DNA synthesis and the cell cycle in both HUVECs and HCAECs. Clustering analysis showed a variety of temporal profiles of gene expression in HUVECs exposed to laminar shear stress of 15 dynes/cm(2) for 3, 6, 12, 24, and 48 hours. Turbulent shear stress affected expression of many genes that play a role in vascular remodeling, including genes encoding plasminogen activators and their inhibitor, endothelin-1, transforming growth factor-beta, collagen type IV, and ephrin A1.

Arteriosclerosis↗

Beta-amyloid enhances glial glutamate uptake activity and attenuates synaptic efficacy.

Although amyloid beta-protein (A beta) has long been implicated in the pathogenesis of Alzheimer's disease, little is known about the mechanism by which A beta causes dementia. A beta leads to neuronal cell death in vivo and in vitro, but recent evidence suggests that the property of the amnesic characteristic of Alzheimer's disease can be explained by a malfunction of synapses rather than a loss of neurons. Here we show that prolonged treatment with A beta augments the glutamate clearance ability of cultured astrocytes and induces a dramatic decrease in glutamatergic synaptic activity of neurons cocultured with the astrocytes. Biotinylation assay revealed that the enhancement of glutamate uptake activity was associated with an increase in cell-surface expression of GLAST, a subtype of glial glutamate transporters, without apparent changes in the total amount of GLAST. This phenomenon was blocked efficiently by actin-disrupting agents. Thus, A beta-induced actin-dependent GLAST redistribution and relevant synaptic malfunction may be a cellular basis for the amnesia of Alzheimer's disease.

Amino Acid Transport System X-AG↗