Yasuko Baba

The University of Tokyo, Tokyo, Tokyo-to, Japan

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Publications (14)34.63 Total impact

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    ABSTRACT: Perioperative complications are prevalent among current smokers. Smoking cessation program is covered by national insurance for patients who meet certain criteria in Japan. We established a smoking cessation program in a preoperative clinic of our anesthesia department in July 2010. We pick up patients who meet the following criteria; Brinkman index of over 200, tobacco dependence screener test of 5 or higher, and having a will to quit smoking, and encourage them to enroll in the program. The program consists of counseling, prescription of varenicline, and an examination of carbon monoxide fraction in exhaled breath. Patients who lose impulse to smoke and actually quit smoking when 12 weeks' program is completed are considered as successes. As of December 2012, 24 patients were enrolled in the program. Eighteen succeeded, 2 failed, and 4 discontinued the program. The discontinuers of the program were patients who had side effects (2) and patients who lost will to quit smoking (2). The success rate was 75%. Varenicline is one of the first-line medications for smoking cessation aid in the U.S.A. and is also approved in Japan. It is also well documented that counseling in addition to medication results in higher smoking abstinence rate than either counseling or medication alone. Anesthesiologists usually have better knowledge about perioperative complications related to smoking than physicians of other specialties. Therefore, there is an advantage in anesthesiologists being the counselor of the smoking cessation program. In addition, patients may be well motivated for quitting smoking right before receiving a surgery. Smoking cessation program is effective when offered to patients right before surgery. Preoperative anesthesia clinic may be one of the most suitable opportunities for the program.
    Masui. The Japanese journal of anesthesiology 11/2013; 62(11):1372-4.
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    ABSTRACT: Pulmonary fibrosis has high rates of mortality and morbidity, but there is no established therapy at present. We demonstrate here that bleomycin-induced pulmonary fibrosis in mice is ameliorated by intratracheal administration of keratinocyte growth factor (KGF)-expressing adenovirus vector. Progressive pulmonary fibrosis was created by continuous subcutaneous administration of 120 mg/kg of bleomycin subcutaneously using an osmotic pump twice from Day 1 to 7 and Day 29 to 35. The mice initially exhibited subpleural fibrosis and then exhibited advanced fibrosis in the parenchyma of the lungs. These histopathological changes were accompanied by reduced lung compliance (0.041 ± 0.011 versus 0.097 ± 0.004; P < 0.001), reduced messenger expression of surfactant proteins, and reduced KGF messenger expression in the lungs at 4 weeks compared with naive group. Intratracheal instillation of Ad-KGF at 1 week after the first administration of bleomycin increased KGF mRNA expression in the lungs compared with the fibrosis-induced mice that received saline alone. The phenotype was associated with alveolar epithelial cell proliferation, increased pulmonary compliance (0.062 ± 0.005 versus 0.041 ± 0.011; P = 0.023), and decreased mortality (survival rate on Day 56: 68.8% versus 0%; P = 0.002), compared with mice receiving only the saline vehicle. These observations suggest the therapeutic utility of a KGF-expressing adenoviral vector for pulmonary fibrosis.
    American Journal of Respiratory Cell and Molecular Biology 12/2010; 45(3):489-97. · 4.15 Impact Factor
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    ABSTRACT: Ischemia-reperfusion not only damages the affected organ but also leads to remote organ injuries. Hepatic inflow interruption usually occurs during hepatic surgery. To investigate the influence of liver ischemia-reperfusion on lung injury and to determine the contribution of tidal volume settings on liver ischemia-reperfusion-induced lung injury, we studied anesthetized and mechanically ventilated rats in which the hepatic inflow was transiently interrupted twice for 15 min. Two tidal volumes, 6 ml/kg as a low tidal volume (IR-LT) and 24 ml/kg as a high tidal volume (IR-HT), were assessed after liver ischemia-reperfusion, as well as after a sham operation, 6 ml/kg (NC-LT) and 24 ml/kg (NC-HT). Both the IR-HT and IR-LT groups had a gradual decline in the systemic blood pressure and a significant increase in plasma TNF-alpha concentrations. Of the four groups, only the IR-HT group developed lung injury, as assessed by an increase in the lung wet-to-dry weight ratio, the presence of significant histopathological changes, such as perivascular edema and intravascular leukocyte aggregation, and an increase in the bronchoalveolar lavage fluid TNF-alpha concentration. Furthermore, only in the IR-HT group was airway pressure increased significantly during the 6-h reperfusion period. These findings suggest that liver ischemia-reperfusion caused systemic inflammation and that lung injury is triggered when high tidal volume ventilation follows liver ischemia-reperfusion.
    AJP Lung Cellular and Molecular Physiology 04/2007; 292(3):L625-31. · 3.52 Impact Factor
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    ABSTRACT: At present there is no known effective pharmacological therapy for acute lung injury (ALI). Because keratinocyte growth factor (KGF) promotes epithelial cell growth, intratracheal administration of KGF has the possibility of restoring lung tissue integrity in injured lungs and improving patient outcomes. However, treatment using recombinant KGF protein is limited by its short effective duration. Thus, we investigated the effectiveness of intratracheal KGF gene transduction using adenoviral vector in ALI. We constructed an adenoviral vector expressing mouse KGF (mKGF), and 1.0 x 10(9 ) plaque-forming units of mKGF cDNA-expressing (Ad-KGF) and control (Ad-1w1) adenoviral vector was intratracheally instilled, using a MicroSprayer, into anesthetized BALB/c mice. Three days later, the mice were exposed to >90% oxygen for 72 hr, and the effect of KGF on hyperoxia-induced lung injury was examined. In the Ad-KGF group, KGF was strongly expressed in the airway epithelial cells, while peribronchiolar and alveolar inflammation caused by adenoviral vector instillation was minimal. The KGF overexpression not only induced proliferation of surfactant protein C-positive cuboidal cells, especially in the terminal bronchiolar and alveolar walls, but also prevented lung injury including intraalveolar exudation/hemorrhage, albumin permeability increase, and pulmonary edema. The arterial oxygen tension and the survival rate were significantly higher in the KGF-transfected group. These findings suggest that KGF gene transduction into the airway epithelium is a promising potential treatment for ALI.
    Human Gene Therapy 02/2007; 18(2):130-41. · 4.02 Impact Factor
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    ABSTRACT: Rare cases of thymic granulomatous lesions were found in pigs. The lesions consisted of epithelioid cells, multinucleated giant cells, and lymphocytes. Such lesions also were observed in the mesenteric lymph nodes, spleen, kidney, and stomach. The cytoplasm of the majority of giant cells and some epithlioid cells was periodic acid-Schiff (PAS) positive. All cells were positive for vimentin, lysozyme, and desmin. Ultrastructurally, the giant cells were rich in organella and attached to adjacent epithelioid cells by membrane interdigitation. The cells included numerous coated vesicles and granules. No etiologic pathogen, including porcine circovirus type 2, was detected in the lesions. This is the rare case of idiopathic thymic granulomatous lesion in pigs.
    Veterinary Pathology 12/2006; 43(6):1037-40. · 1.93 Impact Factor
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    Y Baba, K Saeki, T Onodera, K Doi
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    ABSTRACT: We previously reported that the strain difference in the development of porcine-serum (PS)-induced rat hepatic fibrosis was closely related to the difference in the mode of MHC class-II-related genes expression. This study was carried out to clarify the serological and immunohistochemical changes in this hepatic fibrosis model. Six-week-old male Brown Norway (BN) and Wistar rats were injected with 0.5 ml of sterile PS twice a week for up to 8 weeks. The serum levels of PS-specific IgG1, IgG2a, and IgM were elevated more prominently in BN rats than Wistar rats. In the liver, significant increases in the numbers of PS-, OX-6 (RT1.B)-, CD4-, CD8, ED1-, and ED2-positive cells occurred earlier in BN rats than Wistar rats. At 8 weeks, deposition of PS and immunoglobulins was observed in hepatic fibrous septa and renal glomerular mesangium, and IgG1- and IgG2a-positive cells were found in the white pulp of the spleen. The present results suggest that humoral immunity probably regulated by MHC class II molecules and inflammatory cells may be involved in PS-induced hepatic fibrosis in rats.
    Experimental and Molecular Pathology 01/2006; 79(3):229-35. · 2.13 Impact Factor
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    ABSTRACT: We previously reported the expression profiles of 9 cytochrome P450 isozymes (CYPs) proteins and those of 40 CYPs genes in pregnant rat's liver, placenta and fetal liver after treatment with pregnenolone-16alpha-carbonitrile (PCN) or phenobarbital (PB). This study was carried out focusing on the gene expression profiles of Phase II drug metabolizing enzymes, Glutathione S-transferase isozymes (GSTs) and UDP-glycosyltransferase isozymes (UDPGTs). Fischer 344 (F344) pregnant rats were daily treated intraperitoneally with 50 mg/kg of PCN or 80 mg/kg of PB from 13 to 16 days of gestation (DG). They were sacrificed on 17 DG, and microarray analysis using Affymetrix Rat Expression Array 230 A was performed. Among 16 GSTs genes examined in this study, 7 genes were significantly induced in dam's liver and 3 genes in fetal liver, respectively, in the PCN-group, while 8 genes were significantly induced in dam's liver and 1 gene in fetal liver, respectively, in the PB-group. On the other hand, among 11 UDPGTs genes examined, 5 genes were significantly induced in dam's liver and 3 genes in fetal liver, respectively, in the PCN-group, while 5 genes were significantly induced in dam's liver and 1 gene in fetal liver, respectively, in the PB-group. There were no significant changes in the placenta of all groups. This is the first report of the gene expression profiles of Phase II drug metabolizing enzymes in pregnant rat and fetal livers and placenta after treatment with typical inducers of drug metabolizing enzymes.
    Experimental and Molecular Pathology 01/2006; 79(3):272-7. · 2.13 Impact Factor
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    ABSTRACT: We previously reported the protein expression profiles of nine cytochrome P450 isozymes (CYPs) in pregnant rat's liver, fetal liver, and placenta after treatment with pregnenolone-16alpha-carbonitrile (PCN), dexamethasone (DEX), or phenobarbital (PB). In this study, the gene expression of 40 CYPs and 2 orphan nuclear receptors for CYP inducers, that is, Nr1i2 (CYP3A subfamily inducible by PCN) and Nr1i3 (CYP2B subfamily inducible by PB), in pregnant rat's liver, fetal liver, and placenta was investigated at one time. Fischer 344 (F344) pregnant rats were daily treated intraperitoneally with 50 mg/kg of PCN or 80 mg/kg of PB from 13 to 16 days of gestation (DG). They were sacrificed on 17 DG, and microarray analysis using Affymetrix Rat Expression Array 230A was performed. Ten genes expression significantly increased in dam's liver in PCN group, and seven genes expression in PB group. On the other hand, four genes expression increased in fetal liver in PCN group, and three genes expression increased in PB group. Being common to dam's and fetal livers, the gene expression of Cyp3A1 (CYP3A subfamily) and cytochrome P-450e (CYP2B subfamily) increased in both PCN and PB groups. In placenta, the expression of Cyp3A1 gene was significantly induced in PB group, and it also showed a tendency to increase in PCN group. The expression of Nr1i2 gene was significantly elevated only in dam's liver of PCN group, while the expression of Nr1i3 gene showed no changes in all groups. The results of the present study of 40 CYPs gene expression mostly corresponded to our previous reports on 9 CYPs protein expression.
    Experimental and Molecular Pathology 03/2005; 78(1):71-7. · 2.13 Impact Factor
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    ABSTRACT: The site-specific recombinase Cre is valuable for regulation of gene expression not only in vitro but also in vivo. We previously reported that replication-deficient recombinant adenovirus (rAd) expressing Cre can mediate efficient and strict regulation in 100% of cultured cells. Recently, the constitutive-expression of Cre using retrovirus or lentivirus vector reportedly inhibited cell-growth, but the effect of transient Cre expression have not yet been examined. Here we showed that an excess amount of Cre produced from Cre-expressing rAd caused a deleterious effect in cells even when Cre was transiently expressed. We used three rAds carrying promoters with different activities: the SV40 early promoter (AxSVENCre), the SR alpha promoter (AxSRCre) and the CAG promoter (AxCANCre). Cell toxicity was clearly caused by Cre itself and was distinguishable from that caused by rAd virions when the cytopathic effects of these rAds were compared with that of a control virus lacking the Cre expression unit. Cre toxicity was strongly correlated with the expression level of Cre. Importantly, AxSRCre and AxCANCre gave a 60-fold range of effective MOIs ("effective range") sufficient for gene activation without causing cell toxicity from either the rAd particles or Cre itself, while AxSVENCre failed to give such a range because the expression level of Cre was too low. When Cre was tagged with a nuclear localization signal (NLS), not only its activity but also Cre toxicity was increased fourfold, and the effective range was unchanged. Therefore, AxSRNCre might be more useful to control cell toxicity from the rAd virions than AxSRCre. Cre-induced cell toxicity can be avoided by pre-examining the "effective range" using the purpose cell lines before starting experiments utilizing the experiment of Cre-expressing rAd.
    Microbiology and Immunology 02/2005; 49(6):559-70. · 1.55 Impact Factor
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    ABSTRACT: A five-month-old, female Japanese domestic shorthair cat with proportionate dwarfism developed neurological disorders, including ataxia, decreased postural responses and generalised body and head tremors, at between two and five months of age. Leucocytosis due to lymphocytosis with abnormal cytoplasmic vacuolations was observed. The concentration of G(M2)-ganglioside in its cerebrospinal fluid was markedly higher than in normal cats, and the activities of beta-hexosaminidases A and B in its leucocytes were markedly reduced. On the basis of these biochemical data, the cat was diagnosed antemortem with G(M2)-gangliosidosis variant 0 (Sandhoff-like disease). The neurological signs became more severe and the cat died at 10 months of age. Histopathologically, neurons throughout the central nervous system were distended, and an ultrastructural study revealed membranous cytoplasmic bodies in these distended neurons. The compound which accumulated in the brain was identified as G(M2)-ganglioside, confirming G(M2)-gangliosidosis. A family study revealed that there were probable heterozygous carriers in which the activities of leucocyte beta-hexosaminidases A and B were less than half the normal value. The Sandhoff-like disease observed in this family of Japanese domestic cats is the first occurrence reported in Japan.
    The Veterinary record 01/2005; 155(23):739-44. · 1.80 Impact Factor
  • Yasuko Baba, Kunio Doi
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    ABSTRACT: Genes, especially MHC class II-related genes, expression was examined in porcine-serum (PS)-induced hepatic fibrosis model. Brown-Norway (BN) and Wistar rats were injected intraperitoneally with 0.5 ml sterile porcine serum twice a week for 1, 2, 3, 4, and 8 weeks. Histopathologically, inflammation started at 2 weeks in BN and at 4 weeks in Wistar rats, and hepatic fibrosis developed at 4 weeks in BN rats and at 8 weeks in Wistar rats. Microarray analysis done at 2 and 4 weeks revealed that the expression of MHC class II-related genes and acute phase inflammation-related genes significantly increased at 2 weeks in BN and at 4 weeks in Wistar rats. On the other hand, the expression of some transcription-related genes was down-regulated in both strains. In BN rats, the results of semiquantitative RT-PCR analysis done on four MHC class II-related genes mRNAs corresponded well with those of microarray analysis. MHC class II is considered to be involved in the initiation of PS-induced hepatic fibrosis in rats.
    Experimental and Molecular Pathology 01/2005; 77(3):214-21. · 2.13 Impact Factor
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    ABSTRACT: To examine morphological and gene expression changes induced by T-2 toxin in the fetal brain in detail, pregnant rats on day 13 of gestation were treated orally with a single dose of T-2 toxin (2 mg/kg) and sacrificed at 1, 3, 6, 9, 12 and 24 h after treatment (HAT). Histopathologically, the number of apoptotic neuroepithelial cells in the telencephalon increased from 1 HAT and peaked at 12 HAT. Based on the histopathological examinations, microarray analysis was performed at 6, 12 and 24 HAT. Microarray analysis showed that the expression of oxidative stress-related genes (heat shock protein 70 (HSP70) and heme oxygenase (HO)) was strongly induced by T-2 toxin at 12 HAT, the peak time point of apoptosis induction. The expression of mitogen-activated protein kinase (MAPK)-related genes (MEKK1 and c-jun) and other apoptosis-related genes (caspase-2 and insulin-like growth factor-binding protein-3 (IGF-BP3)) was also induced by the T-2 toxin treatment. The changes observed by microarray analysis were confirmed for four up-regulated genes (HSP70, HO, IGF-BP3 and VEGF-A) using real-time RT-PCR. Our results suggest that the T-2 toxin-induced apoptosis in the fetal brain is due to oxidative stress, and that the MAPK pathway may be involved in T-2 toxin-induced toxicity.
    Food and Chemical Toxicology 12/2004; 42(11):1727-36. · 3.01 Impact Factor
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    ABSTRACT: Pneumonia caused by Pseudomonas aeruginosa carries a high rate of morbidity and mortality. A lung-protective strategy using low tidal volume (V(T)) ventilation for acute lung injury improves patient outcomes. The goal of this study was to determine whether low V(T) ventilation has similar utility in severe P. aeruginosa infection. A cytotoxic P. aeruginosa strain, PA103, was instilled into the left lung of rats anesthetized with pentobarbital. The lung-protective effect of low V(T) (6 ml/kg) with or without high positive end-expiratory pressure (PEEP, 10 or 3 cmH(2)O) was then compared with high V(T) with low PEEP ventilation (V(T) 12 ml/kg, PEEP 3 cmH(2)O). Severe lung injury and septic shock was induced. Although ventilatory mode had little effect on the involved lung or septic physiology, injury to noninvolved regions was attenuated by low V(T) ventilation as indicated by the wet-to-dry weight ratio (W/D; 6.13 +/- 0.78 vs. 3.78 +/- 0.26, respectively) and confirmed by histopathological examinations. High PEEP did not yield a significant protective effect (W/D, 4.03 +/- 0.32) but, rather, caused overdistension of noninvolved lungs. Bronchoalveolar lavage revealed higher concentrations of TNF-alpha in the fluid of noninvolved lung undergoing high V(T) ventilation compared with those animals receiving low V(T). We conclude that low V(T) ventilation is protective in noninvolved regions and that the application of high PEEP attenuated the beneficial effects of low V(T) ventilation, at least short term. Furthermore, low V(T) ventilation cannot protect the involved lung, and high PEEP did not significantly alter lung injury over a short time course.
    AJP Lung Cellular and Molecular Physiology 09/2004; 287(2):L402-10. · 3.52 Impact Factor
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    ABSTRACT: Rat strain differences in the early development of porcine serum (PS)-induced hepatic fibrosis were histologically and immunohistochemically examined using Brown Norway (BN), Sprague Dawley (SD) and Wistar rats. They were injected i.p. with 0.5 ml sterile PS twice a week for 4 and 8 weeks. In addition, rats treated with physiological saline in the same way served as controls. At 4 weeks, hepatic fibrosis accompanying fibrous septa mainly composed of type III collagens developed in BN and SD rats but not in Wistar rats. In addition, the numbers of eosinophils, CD3-positive cells and ED-1-positive cells significantly increased in BN and SD rats, that of CD45RA-positive cells in BN rats, and that of alpha-smooth muscle actin (SMA)-positive cells in SD rats, respectively. Such differences in the number of inflammatory cells may be related with the absence of hepatic fibrosis in Wistar rats at 4 weeks. At 8 weeks, hepatic fibrosis with formation of many small-sized pseudolobules was observed in all strains at almost similar degree, and the numbers of infiltrating cells increased in all strains of rats with some exception. In addition, the main location of inflammatory cells was different, suggesting a different role of each inflammatory cell in the process of hepatic fibrosis.
    Experimental and Toxicologic Pathology 04/2004; 55(5):325-30. · 2.62 Impact Factor