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Biomedical subjects

Yuji Murata

Publications and source records attributed to Yuji Murata.

At least 55 records · Page 3Linked to original sources
PubMed2005

Occurrence of fetal choroid plexus cysts in siblings: concerns regarding recurrence and chromosomal abnormality.

Choroid plexus cysts (CPC) are a well-known ultrasound aneuploidy marker easily detectable at second-trimester ultrasound examination. However, their genetic etiology is totally unknown. We report two cases of Japanese mothers who carried two and three siblings respectively; all the fetuses that had CPC were noticed at second trimester. Genetic amniocentesis revealed that each fetus had different karyotypes, that is, trisomy 18 and 46,XX in the case of one mother, and trisomy 18, 46,XY and trisomy 21 in the case of the other. These observations indicate that the genetic basis of the cysts is not linked to abnormal chromosomes. We propose that careful ultrasound observation and genetic counseling of the siblings should be offered to patients who have previously had a baby with CPC, despite that baby having a normal karyotype.

Adult↗
PubMed2005

Changes of plasma vascular endothelial growth factor level after uterine artery embolisation for leiomyomata.

Uterine artery embolisation (UAE) has become an alternative treatment for symptomatic uterine leiomyomata. Most reports suggest that it is well tolerated and effective, although there have been no reports of studies of biological parameters after UAE. In this study, we analysed the plasma level of vascular endothelial growth factor (VEGF) and the pulsatility index (PI) of uterine arteries before and after UAE. The level of plasma VEGF increased significantly after UAE (on day 1 and day 3) and decreased on day 7, and then increased again on day 30. The level of VEGF reached a peak value within three days after UAE. A significant inverse correlation was found between uterine artery PI and the level of VEGF on day 30, suggesting that VEGF may have negative effect on the efficacy of treatment of uterine leiomyomata by UAE.

Adult↗
PubMed2005

Effect of Lo Han Kuo (Siraitia grosvenori Swingle) on nasal rubbing and scratching behavior in ICR mice.

We studied the effect of Lo Han Kuo (Siraitia grosvenori Swingle) on histamine-induced nasal rubbing and compound 48/80-induced skin scratching behavior in ICR mice. An extract and glycoside (a complex of sweet components) of Lo Han Kuo were used in the study. Both the extract and glycoside caused no significant effect on nasal rubbing or scratching behavior, even at a dose of 1000 mg/kg when administered in a single dose. However, the effect of Lo Han Kuo became clear after repeated administration, and 300 and 1000 mg/kg of both extract and glycoside significantly inhibited nasal rubbing and skin scratching behavior after consecutive treatment for 4 weeks. Both the extract and glycoside inhibited the histamine release induced by compound 48/80 at concentrations of 300 and 1000 microg/ml. From these results, it is assumed that the inhibition of nasal rubbing and skin scratching behavior induced by Lo Han Kuo occurs through a mast cell-dependent mechanism.

Animals↗
PubMed2005

Abnormal regional cerebral blood flow in systemic lupus erythematosus patients with psychiatric symptoms.

OBJECTIVE: Single-photon emission computed tomography (SPECT) studies have demonstrated decreased regional cerebral blood flow (rCBF) in systemic lupus erythematosus (SLE) patients. However, no study has done voxel-based analysis using statistical parametric mapping (SPM) that can evaluate rCBF objectively, and the relationship between rCBF and psychiatric symptoms has not been well investigated. Using L,L-ethyl cysteinate dimer (99mTc ECD) SPECT and SPM, we aimed to clarify the association of rCBF changes with psychiatric symptoms in SLE patients whose magnetic resonance imaging (MRI) showed no morphological abnormalities. METHOD: Twenty SLE patients and 19 healthy volunteers underwent 99mTc ECD SPECT. Data were collected from August 2000 to March 2003. SLE was diagnosed according to American College of Rheumatology criteria, and psychiatric symptoms were diagnosed according to ICD-10 criteria. On the basis of the modified Carbotte, Denburg, and Denburg method, the patients were classified into 3 groups: a group with major psychiatric symptoms (hallucinosis, delusional disorder, and mood disorder), a group with minor psychiatric symptoms (anxiety disorder, dissociative disorder, and emotionally labile disorder), and a group without psychiatric symptoms. Gross organic lesions were ruled out by brain MRI. Group comparisons of rCBF were performed with analysis using SPM99. RESULTS: SLE patients without MRI lesions showed decreased rCBF in the posterior cingulate gyrus and thalamus. The reduction in rCBF was overt in patients with major psychiatric symptoms. CONCLUSION: Our study indicated that SLE patients may have dysfunction in the posterior cingulate gyrus and thalamus and that this may be associated with the severity of psychiatric symptoms.

Adolescent↗
PubMed2004

Hypoxia up-regulates hypoxia-inducible factor-1alpha expression through RhoA activation in trophoblast cells.

During early pregnancy, trophoblast cells are exposed to relatively low-oxygen tension. Recently, the Rho GTPase family has been shown to play a key role in hypoxia-inducible factor-1 (HIF-1) alpha induction in renal cell carcinoma. The present study was designed to investigate the effect of low-oxygen conditions on RhoA expression in trophoblast cells isolated from early stages of human placenta and in trophoblast-derived BeWo cells and JAR cells. Immunoblot and RT-PCR analyses showed that low-oxygen conditions (1% O(2) or 250 mum CoCl(2)) stimulated expression of RhoA protein and mRNA. Pull-down assays demonstrated that these low-oxygen conditions increased RhoA activity. Preincubation of BeWo cells with Clostridium botulinum C3 exoenzyme, a specific inhibitor of Rho, inhibited hypoxia-induced HIF-1alpha expression. Under 1% O(2) or 250 mum CoCl(2), BeWo cells, transfected with a dominant-negative RhoA, exhibited decreased levels of HIF-1alpha protein and mRNA compared with the control vector transfectants. BeWo cells expressing constitutively active RhoA showed enhanced protein levels of not only HIF-1alpha but also vascular endothelial growth factor (VEGF) and glucose transporter 1, which are target gene products of HIF-1alpha. These findings suggest that up-regulation of RhoA induced by low-oxygen conditions may play an important role in regulation of HIF-1alpha expression in trophoblast cells.

ADP Ribose Transferases↗
PubMed2004

Inhibition of inhibitor of nuclear factor-kappaB phosphorylation increases the efficacy of paclitaxel in in vitro and in vivo ovarian cancer models.

We investigated whether inhibition of nuclear factor-kappaB (NFkappaB) increases the efficacy of paclitaxel in in vitro and in vivo ovarian cancer models. Treatment of paclitaxel-sensitive Caov-3 cells with paclitaxel transiently activated the phosphorylation of Akt, the phosphorylation of IkappaB kinase (IKK), and the phosphorylation of inhibitor of NFkappaB (IkappaBalpha). Paclitaxel also caused a transient increase in NFkappaB activity, followed by a decrease in NFkappaB activity. We show an association between Akt and IKK and show that the phosphorylation of IKK induced by paclitaxel is blocked by treatment with a phosphatidylinositol 3-kinase inhibitor (wortmannin or LY294002). Furthermore, interference of the Akt signaling cascade inhibits the transient induction of IkappaBalpha phosphorylation and NFkappaB activity by paclitaxel. Inhibition of NFkappaB activity by treatment with an IkappaBalpha phosphorylation inhibitor (BAY 11-7085) attenuated both basal and transient induction of IkappaBalpha phosphorylation by paclitaxel. Treatment with BAY 11-7085 also enhanced the inhibition of NFkappaB activity by paclitaxel for up to 24 hours. In addition, treatment with BAY 11-7085 decreased the viability of cells treated with paclitaxel. Moreover, treatment with BAY 11-7085 increased the efficacy of paclitaxel-induced inhibition of intraabdominal dissemination and production of ascites in athymic nude mice inoculated intraperitoneally with Caov-3 cells. These results suggest that paclitaxel transiently induces NFkappaB activity via the phosphatidylinositol 3-kinase/Akt cascade and that combination therapy with paclitaxel and an NFkappaB inhibitor would increase the therapeutic efficacy of paclitaxel.

Androstadienes↗
PubMed2004

Surgical reinforcement of support for the vagina in pelvic organ prolapse: concurrent iliococcygeus fascia colpopexy (Inmon technique).

To reinforce the support of the vagina, concurrent use of iliococcygeus fascia colpopexy with the McCall culdeplasty was scheduled for primary uterine prolapse. Forty-five women with primary uterine prolapse without stress urinary incontinence were treated by McCall culdeplasty alone or McCall culdeplasty plus iliococcygeus fascia colpopexy for suspension of the upper portion of the vagina. Recurrence of vaginal support defects were carefully followed for 15-50 months. Additional iliococcygeus fascia colpopexy did not change with the axis of the vagina obtained by McCall culdeplasty, although it prolonged total operation time by 32 min and increased blood loss by 94 ml. Two cases (8.3%) had postoperative vaginal defects in the group undergoing combined procedures and seven recurrent cases (33.3%) were observed in the group undergoing McCall culdeplasty alone. The durability of the combined procedures was superior to that of the modified McCall culdeplasty alone by Kaplan-Meier analysis. These results suggest that iliococcygeus fascia colpopexy is reasonably safe and strengthens not only the attachment of the upper part of the vagina but also that of the anterolateral vaginal wall.

Aged↗
PubMed2004

Correlation between p14(ARF)/p16(INK4A) expression and HPV infection in uterine cervical cancer.

The CDKN2A locus on human chromosome 9p21 encodes two tumor suppressors, p14(ARF) and p16(INK4A), which enhance the growth-suppressive functions of the retinoblastoma (Rb) and the p53 proteins, respectively. Conversely, the E6 and E7 oncoproteins of the high-risk human papillomaviruses (HPVs) causally associated with carcinogenesis of the uterine cervix contributes to tumor development by inactivating p53 and Rb. Nevertheless, a correlation between expression of p14(ARF)/p16(INK4A) and HPV infection in uterine cervix is less clear. To clarify this, we examined 25 cervical cancers and 11 normal uterine cervixes. HPV was detected in 21 of 25 cervical cancers (84%) and their subtype was determined by PCR-RFLP. Quantitative real-time RT-PCR assays showed overexpression of p14(ARF) mRNA in all 21 HPV-positive cases (100%). p16(INK4A) mRNA was overexpressed in 17 cases of the HPV-positive cases (81%). In four HPV-negative cancers, reduced expression of p14(ARF) mRNA was detected in two cases (50%) and reduced p16(INK4A) mRNA in three cases (75%). Our data indicate that the overexpression of p14(ARF) and p16(INK4A) strongly associates with HPV-positive cervical cancers and that reduced expression of p14(ARF) and p16(INK4A) correlates with HPV-negative cervical cancers. These findings may indicate that impaired p14(ARF) and p16(INK4A) mRNA expression contribute to tumor development in HPV-negative cervical cancers by failure to support p53 and Rb instead of their inactivation by HPV E6 and E7.

Carcinoma, Squamous Cell↗
PubMed2004

Alteration of the timing of implantation by in vivo gene transfer: delay of implantation by suppression of nuclear factor kappaB activity and partial rescue by leukemia inhibitory factor.

Nuclear factor kappaB (NF-kappaB) is activated in the murine endometrium during implantation period [Am. J. Reprod. Immunol. 51 (2004) 16]. Transient transfection of IkappaBalpha mutant (IkappaBalphaM) cDNA into the mouse uterine cavity using hemagglutinating virus of Japan envelope vector suppressed uterine NF-kappaB activity less than half of that observed in control on days 3.5 and 4.5 p.c. IkappaBalphaM cDNA transfection led to significant delay of implantation. After IkappaBalphaM cDNA transfection, LIF mRNA expression in the uterus was significantly suppressed on days 3.5 and 4.5 p.c. Co-transfection of LIF cDNA with IkappaBalphaM cDNA in the uterus partially rescued the delay of implantation induced by suppression of NF-kappaB activity. Taken together, these findings indicate that NF-kappaB activation determines the timing of the implantation, at least in part, via control of LIF expression.

Animals↗
PubMed2004

Na+ / H+ exchanger-3 is involved in mouse blastocyst formation.

The mouse blastocyst consists of the trophectoderm, the inner cell mass, and a fluid-filled cavity, the blastocoel. Formation and subsequent expansion of this cavity is important for further differentiation of the inner cell mass and successful implantation. Previous work provided evidence that vectorial transport of Na+ and CL- ions through the trophectoderm into the blastocoel generates an osmotic gradient that drives fluid across this epithelium. As the activity of the Na+ / H+ exchanger (NHE) has been implicated as the exchanger responsible for facilitating the transtrophectodermal Na+ flux, the functional role of NHE in mouse blastocoel development was determined. Embryos were cultured in the presence of subtype-specific NHE inhibitors to examine the role of NHEs in blastocoel development. When 2-cell stage embryos were treated continuously with a specific inhibitor of NHE-1, cariporide, the embryos passed beyond the 8-cell stage and became blastocysts. However, in the presence of a specific inhibitor of NHE-3, S3226, the 2-cell stage embryos developed to the morula stage but formation of the blastocyst were inhibited in a dose-dependent manner. Cariporide did not inhibit the formation of the blastocoel cavity from the morula stage whereas S3226 did inhibit that process. S3226 also reduced the rate of re-expansion of blastocysts collapsed by cytochalasin D upon transfer to the control medium. An immunofluorescence study showed that NHE-3 was detected in the vicinity of the cell membrane of the trophectoderm, especially in the apical cell margins of the trophectoderm. These results suggest that NHE-3 is likely involved in blastocyst formation.

Analysis of Variance↗
PubMed2004

Correlation of neuron-specific enolase and S100B with histological cerebral damage in fetal sheep after severe asphyxia.

Experimental brain damage was induced in 16 fetal sheep by umbilical cord occlusion, and the correlation of neuron-specific enolase (NSE) or S100B with the damage grade was investigated in seven fetuses. Significant correlations of damage degree with NSE (p = 0.016) and S100B (p = 0.018) in serum 2 h after insult were shown by Spearman's test. These findings suggest that they represent potentially useful markers for detecting brain damage at early stage after ischemic insult.

Animals↗
PubMed2004

Idarubicin administered during pregnancy: its effects on the fetus.

Acute myeloblastic leukemia, subtype M1, was diagnosed in a 39-year-old G2P1 Japanese woman at 21 weeks' gestation. Remission-induction polychemotherapy, including daunorubicin, performed for one cycle, did not lead to remission. Second-line chemotherapy, including idarubicin, performed for one cycle, was administrated during the early third trimester of pregnancy. Septic shock occurred due to severe myelosuppression. An emergent cesarean section was performed in response to a nonreassuring pattern of the fetal heart rate and a rapid decrease in fetal amniotic fluid. The neonate delivered at 32 weeks' gestation showed no signs of cardiac failure but did show signs of transient myelosuppression, hepatopathy, and elevated creatine kinase. Complete remission was established with idarubicin including chemotherapy.

Adult↗
PubMed2004

Human breast milk suppresses the transcriptional regulation of IL-1beta-induced NF-kappaB signaling in human intestinal cells.

Neonatal necrotizing enterocolitis (NEC), which is a disease with a poor prognosis, is considered to be caused by the coincidence of intestinal ischemia-reperfusion injury and systemic inflammation due to the colonization of pathogenic bacteria. Interleukin (IL)-8, a proinflammatory cytokine, plays an important role in the pathophysiology of NEC. It was recently reported that IL-1beta activates the IL-8 gene by regulating the transcriptional nuclear factor kappaB (NF-kappaB) signaling pathways in intestinal cells. The protective role of maternal milk in NEC pathogenesis has been reported in both human and animal studies. In this study, we show that human breast milk dramatically suppressed the IL-1beta-induced activation of the IL-8 gene promoter by inhibiting the activation pathway of NF-kappaB. Moreover, we also show that human breast milk induced the production of IkappaBalpha. These results suggest that human breast milk could be protective and therapeutic in neonates with NEC by inhibiting the activation pathway of NF-kappaB.

Blotting, Western↗
PubMed2004

Rho-kinase is involved in mouse blastocyst cavity formation.

During mammalian embryonic development, the formation and subsequent expansion of a fluid-filled cavity, the blastocoel, is crucial for successful implantation. Our present experiments were aimed at exploring the contribution of Rho-kinase, a downstream effector of the small GTP-binding protein RhoA, to mouse blastocoel formation. RT-PCR analysis showed that Rho-kinase mRNA is present throughout mouse preimplantation development. When 2-cell embryos were cultured in the presence of a specific inhibitor of Rho-kinase, Y-27632, they developed to the morula stage but failed to develop to the blastocyst stage. Y-27632 inhibited the formation of the blastocoel cavity from the morula stage, and this inhibitory effect was reversible when embryos were returned to medium without Y-27632. Moreover, Y-27632 reduced the rate of re-expansion of blastocysts collapsed by cytochalasin D upon transfer to the control medium. These results suggest that Rho-kinase is likely involved in blastocyst formation.

Amides↗
PubMed2004

Induction of hTERT expression and phosphorylation by estrogen via Akt cascade in human ovarian cancer cell lines.

We examined the mechanism by which estrogen regulates telomerase activity in Caov-3 human ovarian cancer cell lines, which express ER, to determine whether the regulation affects the expression and/or phosphorylation of the telomerase catalytic subunit (hTERT). 17beta-Estradiol (E(2)) induced telomerase activity and hTERT expression. Transient expression assays using luciferase reporter plasmids containing various fragments of hTERT promoter showed that the estrogen-responsive element appeared to be partially responsible for the E(2)-induced activation of the hTERT promoter. Either pretreatment with a phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, or transfection with a dominant-negative Akt attenuated the E(2)-induced activation of the hTERT promoter. In addition, estrogen induced the phosphorylation of IkappaB inhibitor protein via the Akt cascade, and cotransfection with a dominant-negative subunit of NFkappaB attenuated the response of the ERE-deleted hTERT promoter to E(2). Moreover, E(2) induced the phosphorylation of hTERT, the association of 14-3-3 protein and NFkappaB with hTERT, and nuclear accumulation of hTERT in an Akt-dependent manner. These results indicate that E(2) induces telomerase activity not only by transcriptional regulation of hTERT via an ERE-dependent mechanism and a PI3K/Akt/NFkappaB cascade, but also by post-transcriptional regulation via Akt-dependent phosphorylation of hTERT. Thus, the phosphorylation of Akt is a key event in the induction of telomerase activity by E(2) in human ovarian cancer cells.

14-3-3 Proteins↗
PubMed2004

Long-term change in size of cerebral infarction: predictive value of brain perfusion SPECT using statistical parametric mapping.

A focus of infarction is surrounded by hypoperfused areas. The present study was undertaken to examine the long-term changes in the size of infarcts, the relationship between the size of an infarct and the extent of the surrounding hypoperfused areas, and the background of such changes. The subjects of this study were 11 patients with ischemic lesions of the brain who had undergone brain SPECT ((99m)Tc-ethyl cysteinate dimer) within 1 week after initial MRI, and who underwent MRI again more than half a year later. Statistical parametric mapping (SPM) was conducted to detect significantly hypoperfused areas on the SPECT images. Relative size of significantly hypoperfused areas on SPM and infarcts on T(2)-weighted MR images were measured. The patients were divided into two groups based on the percentage of the infarct's size relative to the size of the surrounding hypoperfused areas (75-125 and 0-39%). Infarcts in the '75-125%' group showed little change in size, while in the '0-39%' group infarcts increased slowly until it reached the same rate as the former group. All patients with infarct in the '0-39%' group were noted to have severe stenosis of the internal carotid arteries bilaterally. Patients having severe stenosis of the internal carotid artery often had a slowly enlarging infarct. SPM seems to be useful in predicting the ultimate size of the infarct.

Adult↗
PubMed2004

Inhibition of NFkappaB increases the efficacy of cisplatin in in vitro and in vivo ovarian cancer models.

Whether or not inhibition of NFkappaB increases the efficacy of cisplatin in in vitro and in vivo ovarian cancer models was investigated. We compared the basal levels of phosphorylation of IkappaBalpha and activity of NFkappaB between cisplatin-sensitive A2780 cells and cisplatin-resistant Caov-3 cells. The basal levels of phosphorylation of IkappaBalpha and activity of NFkappaB in Caov-3 cells were significantly higher than those in A2780 cells. Cisplatin caused a more marked decrease in the phosphorylation of IkappaBalpha and activity of NFkappaB in A2780 cells than in Caov-3 cells. Thus, high basal levels of phosphorylation of IkappaBalpha and activation of NFkappaB and less marked inhibition of the phosphorylation of IkappaBalpha and activation of NFkappaB by cisplatin seem to reduce the sensitivity of cells to cisplatin. Inhibition of NFkappaB activity either by treatment with the IkappaBalpha phosphorylation inhibitor (BAY 11-7085) or a specific NFkappaB nuclear translocation inhibitor (SN-50) or by transfection of p50DeltaNLS (which lacks the nuclear localization signal domain) increased the efficacy of both the cisplatin-induced attenuation of IkappaBalpha phosphorylation and NFkappaB activity and the cisplatin-induced apoptosis. In addition, treatment with BAY 11-7085 increased the efficacy of the cisplatin-induced attenuation of both the expression of X-linked inhibitor of apoptosis protein (XIAP) and cell invasion through Matrigel. Moreover, treatment with BAY 11-7085 increased the efficacy of the cisplatin-induced inhibition of the intra-abdominal dissemination and production of ascites using athymic nude mice inoculated intraperitoneally with Caov-3 cells. These results suggest that combination therapy of cisplatin with the NFkappaB inhibitor should increase the therapeutic efficacy of cisplatin.

Animals↗