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Y Imai

Publications and source records attributed to Y Imai.

At least 37 records · Page 2Linked to original sources

Measurement of strange-quark contributions to the nucleon's form factors at Q(2) = 0.230 (GeV/c)(2).

We report on a measurement of the parity-violating asymmetry in the scattering of longitudinally polarized electrons on unpolarized protons at a Q2 of 0.230 (GeV/c)(2) and a scattering angle of theta (e) = 30 degrees - 40 degrees. Using a large acceptance fast PbF2 calorimeter with a solid angle of delta omega = 0.62 sr, the A4 experiment is the first parity violation experiment to count individual scattering events. The measured asymmetry is A(phys)=(-5.44+/-0.54(stat)+/-0.26(sys))x10(-6). The standard model expectation assuming no strangeness contributions to the vector form factors is A(0) = (-6.30+/-0.43) x 10(-6). The difference is a direct measurement of the strangeness contribution to the vector form factors of the proton. The extracted value is G(s)(E) + 0.225G(s)(M) = 0.039+/-0.034 or F(s)(1) + 0.130F(s)(2) = 0.032+/-0.028.

Journal Article↗

New proposal for T classification of gingival carcinomas arising in the maxilla.

When the current T classification of the UICC (1987 and 1997) is used to stage carcinomas arising the upper alveolus and gingival and hard palate, most cases are classified as T4 because of their anatomic characteristics, similar to carcinomas arising in the lower alveolus and gingiva. This study compared the following two methods for classifying the T stage of maxillary carcinomas: (1) the original T classification criteria proposed by the UICC (1987 and 1997), and (2) a new T classification criteria, called the sinus and nasal floor (SNF) criteria. We found that the SNF criteria were more closely related to tumor control and survival than were the UICC criteria in patients with carcinomas arising in the upper alveolus and gingival and hard palate. Increased use of the SNF criteria is expected to improve staging of gingival tumors arising in the maxilla and increase the accuracy of diagnosis, especially of T4 tumors.

Adenocarcinoma↗

Increased incidence of acute graft-versus-host disease with the continuous infusion of cyclosporine A compared to twice-daily infusion.

We retrospectively compared the incidence of acute graft-versus-host disease (GVHD) before and after September 1999, when we changed the mode of cyclosporine A (CsA) administration from twice-daily infusions (TD) (n=58) to continuous infusion (CIF) (n=71). The incidence of grade II-IV acute GVHD in the CIF group (56%) was significantly higher than that in the TD group (27%, P=0.00022). Multivariate analysis identified only two independent significant risk factors for the development of grade II-IV acute GVHD; CIF of CsA (relative risk 2.59, 95% CI 1.46-4.60, P=0.0011) and the presence of HLA mismatch (2.01, 95% CI 1.15-3.53, P=0.014). The incidence of relapse was significantly lower in the CIF group when adjusted for disease status before transplantation (0.41, 95% CI 0.18-0.95, P=0.038), which resulted in better disease-free survival in high-risk patients (43 vs 16% at 2 years, P=0.039), but not in standard-risk patients (72 vs 80%, P=0.45). CIF of CsA with a target level of 250-400 ng/ml may not be appropriate for GVHD prophylaxis in standard-risk patients.

Acute Disease↗

Predictors for severe cardiac complications after hematopoietic stem cell transplantation.

The value of pre-transplant factors for predicting the development of cardiac complications after transplantation has been inconsistent among studies. We analyzed the impact of pre-transplant factors on the incidence of severe cardiac complications in 164 hematopoietic stem cell transplant recipients. We identified eight patients (4.8%) who experienced grade III or IV cardiac complications according to the Bearman criteria. Seven died of cardiac causes a median of 3 days after the onset of cardiac complications. On univariate analysis, both the cumulative dose of anthracyclines and the use of anthracyclines within 60 days before transplantation affected the incidence of severe cardiac complications (P=0.0091 and 0.011). The dissociation of heart rate and body temperature, which reflects "relative tachycardia", was also associated with a higher incidence of cardiac complications (P=0.024). None of the variables obtained by electrocardiography or echocardiography were useful for predicting cardiac complications after transplantation, although the statistical power might not be sufficient to detect the usefulness of ejection fraction. On a multivariate analysis, the cumulative dose of anthracyclines was the only independent significant risk factor for severe cardiac complications. We conclude that the cumulative dose of anthracyclines is the most potent predictor of cardiac complications and the administration of anthracyclines should be avoided within two months before transplantation.

Adult↗

Transbronchial administration of adenoviral-mediated interleukin-10 gene to the donor improves function in a pig lung transplant model.

Interleukin-10 (IL-10) gene transfection of donor lungs prior to transplantation is an attractive strategy to reduce ischemia-reperfusion induced lung injury. However, experimental data with gene therapy in large animal models of lung transplantation are generally lacking. We have developed a simple clinically applicable technique for adenoviral-mediated gene delivery of human IL-10 to the lung of large animals that provides homogenous gene expression after 12-24 h of transfection. Using this technique of gene delivery, we have studied the dynamics of adenoviral gene delivery to the lung in the setting of lung transplantation. Although there is a persistent inflammatory response to the adenoviral vector, we achieved significant expression of human IL-10 in lung tissue before lung retrieval to obviate the deleterious impact of the adenoviral vector on the donor lung. The administration of adenoviral-mediated human IL-10 to the donor lung reduced ischemia-reperfusion injury and improved graft function after lung transplantation in this pig lung transplantation model. Transfection of adenoviral-mediated human IL-10 to the donor lung prevented the release of inflammatory cytokines such as IL-6 in lung tissue and plasma. We have demonstrated that IL-10 gene therapy has significant potential to prevent or treat the inflammatory response associated with ischemia-reperfusion injury in lung transplantation. In the future, IL-10 gene therapy could also be used for immunomodulation or tolerance induction.

Adenoviridae↗

Interferon treatment improves survival in chronic hepatitis C patients showing biochemical as well as virological responses by preventing liver-related death.

Interferon therapy for chronic hepatitis C reduces the risk of hepatocellular carcinoma, especially among virological and biochemical responders. However, little is known about the effect of interferon therapy on mortality. We studied the long-term effect of interferon therapy on mortality in patients with chronic hepatitis C. For this retrospective cohort study, 2954 patients with chronic hepatitis C were recruited, of whom 2698 received interferon therapy and 256 did not. The effect of interferon therapy on survival was assessed by standardized mortality ratio (SMR) based on published mortality data for the general Japanese population and by risk ratio calculated by proportional hazard regression. Over 6.0 +/- 2.2 years follow-up, death from liver-related diseases was observed in 69 (68%) of 101 deaths among interferon-treated patients and in 42 (81%) of 52 deaths among untreated patients. Compared with the general population, overall mortality was high among untreated patients (SMR: 2.7; 95% CI: 2.0-3.6) but not among interferon-treated patients (SMR: 0.9; 95% CI: 0.7-1.1). Liver-related mortality was extremely high among untreated patients (SMR: 22.2; 95% CI: 16.0-30.0) and less among interferon-treated patients (SMR: 5.5; 95% CI: 4.3-6.9). The risk of death from all causes was lower for interferon-treated than untreated patients (risk ratio: 0.47; 95% CI: 0.261-0.836; P = 0.01). The risk of death from liver-related diseases was significantly lower for sustained virological responders (risk ratio: 0.04; 95% CI: 0.005-0.301; P = 0.002) compared with untreated patients, but not for nonsustained virological responders. Sustained biochemical responders (risk ratio: 0.03; 95% CI: 0.004-0.230; P < 0.001) and transient biochemical responders (risk ratio: 0.18; 95% CI: 0.063-0.532; P = 0.002) showed a significantly reduced risk of death from liver-related death, whereas biochemical nonresponders did not. Hence interferon treatment improved survival in chronic hepatitis C patients showing a biochemical as well as a virological response by preventing liver-related deaths.

Adult↗

Haemostatic management of intraoral bleeding in patients with congenital deficiency of alpha2-plasmin inhibitor or plasminogen activator inhibitor-1.

Haemostatic management of intraoral bleeding was investigated in patients with congenital alpha2-plasmin inhibitor (alpha2-PI) deficiency or congenital plasminogen activator inhibitor- 1 (PAI-1) deficiency. When extracting teeth from patients with congenital alpha2-PI deficiency, we advocate that 7.5-10 mg kg(-1) of tranexamic acid be administered orally every 6 h, starting 3 h before surgery and continuing for about 7 days. For the treatment of continuous bleeding, such as post-extraction bleeding, 20 mg kg(-1) of tranexamic acid should be administered intravenously, and after achieving local haemostasis 7.5 mg kg(-1) of tranexamic acid should be administered orally every 6 h for several days. In addition, when treating haematoma caused by labial or gingival laceration or buccal or mandibular contusion, haemostasis should be achieved by administering 7.5-10 mg kg(-1) of tranexamic acid every 6 h. Tranexamic acid can also be used for haemostatic management of intraoral bleeding in patients with congenital PAI-1 deficiency, but is less effective when compared with use in patients with congenital alpha2-PI deficiency. Continuous infusion of 1.5 mg kg(-1) h(-1) of tranexamic acid is necessary for impacted tooth extraction requiring gingival incision or removal of local bone.

Adult↗

FT-Raman spectroscopy of calcium hydroxide medicament in root canals.

AIM: To investigate chemical changes in calcium hydroxide introduced into human root canals as a medicament using Fourier transform-(FT) Raman spectroscopy. METHODOLOGY: Ten necrotic maxillary anterior teeth were selected in 10 patients. The teeth were divided into five treatment groups, according to the survey time. Root canal instrumentation was performed with hand instruments until the master apical file was size 40. Calcium hydroxide paste, in a 1 : 1.25 mixture by weight of powder and distilled water, was introduced directly into the root canal with a lentulo-spiral filler and then condensed with a finger plugger. The access cavity was sealed with a temporary dressing. After 2 and 4 days, then 2, 4 and 6 weeks, the calcium hydroxide paste was sampled with a K-file and then analysed using FT-Raman spectroscopy. The excitation source was an Nd : YAG laser with an excitation wavelength of 1064 nm. All spectra were taken with a laser power of 200 mW, 275-1185 scans, and 4 cm(-1) resolution. The conversion of calcium hydroxide to calcium carbonate was calculated on the basis of the spectral data obtained from the mixtures of both compounds. RESULTS: The calcium hydroxide paste in the apical region showed weak bands at 1088 and 284 cm(-1), in addition to bands associated with calcium hydroxide. The weak bands, assigned to calcium carbonate, became stronger with time. Calcium carbonate content increased rapidly in the first 2 days and then tended to increase slowly. Approximately 11% of the calcium hydroxide at the apical portion of the canal was converted to calcium carbonate after 6 weeks. However, little alteration of the paste was noticed in the samples from the middle portion of the canal. CONCLUSIONS: Calcium hydroxide medicament in root canals became transformed into calcium carbonate in the apical region within 2 days. Although the transformation continued with time, approximately 90% of the calcium hydroxide remained unchanged after 6 weeks.

Calcium Carbonate↗

Neuroprotective effect of the angiotensin-converting enzyme inhibitor perindopril in MPTP-treated mice.

The angiotensin -converting enzyme (ACE) inhibitor perindopril has been shown to exert beneficial effects on the dopaminergic system. Here, we investigated the effects of perindopril on the dopaminergic system in mice after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment, in comparison with a Ca(2+) antagonist, amlodipine. Administration of perindopril showed dose-dependent neuroprotective effects against MPTP-induced striatal dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) depletion. However, administration of amlodipine showed no significant effects on striatal dopamine depletion after MPTP treatment. In our immunohistochemical studies with antibodies against tyrosine hydroxylase (TH), microtubule-associated protein 2a, b (MAP2), dopamine transporter (DAT), parvalbumin (PV), glial fibrillary acidic protein (GFAP) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD), the administration of perindopril significantly attenuated MPTP-induced substantia nigra and striatal damage. This drug also blocked the increases in GFAP-positive astrocytes in the striatum and substantia nigra after MPTP treatment. Furthermore, the administration of perindopril showed a protective effect against the intense Cu/Zn-SOD immunoreactivity in the neurons and glial cells in both the striatum and substantia nigra after MPTP treatment. These results indicated that the ACE inhibitor perindopril can protect against MPTP-induced striatal dopamine and DOPAC depletion in mice. The protective effect may be, at least in part, caused by the reduction of free radicals caused by MPTP. The present study also demonstrated that perindopril is effective against MPTP-induced neurodegeneration of the nigro-striatal dopaminergic pathway. Furthermore, our results provided further evidence that free radical scavengers may be effective in the treatment of neurodegenerative diseases such as Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

TSC-22 (TGF-beta stimulated clone-22): a novel molecular target for differentiation-inducing therapy in salivary gland cancer.

TSC-22 (Transforming growth factor-beta stimulated clone-22) was originally isolated as a TGF-beta-inducible gene in mouse osteoblastic cells. TSC-22 encodes a putative transcriptional regulator containing a leucine zipper-like structure. Several differentiation-inducing stimuli up-regulate the TSC-22 gene. Furthermore, TSC-22 acts as an effector that integrates multiple extracellular signals during embryogenesis of Drosophila and mouse. Separately, we identified TSC-22 cDNA as an anti-cancer drug (vesnarinone)-inducible gene in a human salivary gland cancer cell line, TYS. Vesnarinone is known to have a differentiation-inducing activity in several cell types. We showed that TSC-22 negatively regulated the growth of TYS cells, and that down-regulation of TSC-22 played a major role in the salivary gland tumorigenesis. Subsequently, we found that artificial overexpression of TSC-22 enhanced chemosensitivity and radiation-sensitivity by inducing apoptosis in TYS cells. Recently, we isolated TSC-22 genomic DNA and analyzed the transcriptional and post-transcriptional regulation of the TSC-22 gene. Then, we confirmed by the luciferase reporter assay that several differentiation-inducing stimuli directly activated the promoter region of TSC-22 gene. Now we are investigating the chemical compounds, which could enhance the transcription of the TSC-22 gene. Thus, because TSC-22 is a key molecule for differentiation of several cells, it can be used as a molecular target for cancer differentiation therapy in salivary gland cancer.

Amino Acid Sequence↗

Cerebral alterations in a MPTP-mouse model of Parkinson's disease--an immunocytochemical study.

We investigated the immunohistochemical alterations of neuronal nitric oxide synthase (nNOS), endothelial NOS (eNOS), tyrosine hydroxylase (TH), microtubule-associated protein 2a,b (MAP 2), glial fibrillary acidic protein (GFAP), parvalbumin (PV), and dopamine transporter (DAT) in the striatum and substantia nigra following the application of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mice. TH-, MAP 2- and DAT-immunoreactive cells were decreased gradually in the striatum and substantia nigra from 1 day up to 7 days after MPTP treatment, as well as the reduction of the striatal dopamine, DOPAC and HVA content. The number of GFAP-immunoreactive astrocytes increased gradually in the striatum and substantia nigra from 1 day up to 7 days after MPTP treatment. Striatal nNOS-immunoreactive cells were unchanged in MPTP-treated mice. In the substantia nigra, intense immunoreactivity of nNOS-positive cells increased 5 hr after MPTP treatment. Thereafter, the immunoreactivity of nNOS-positive cells decreased gradually from 1 day up to 7 days after MPTP treatment. eNOS-immunopositive cells were unchanged in the striatum and substantia nigra. These results demonstrate that nNOS may play a key role in the development of MPTP neurotoxicity. Our findings also indicate that MPTP can cause the functional damage of interneurons in the substantia nigra, but not in the striatum.

Animals↗

Role of dopamine transporter against MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) neurotoxicity in mice.

We investigated the alterations of dopamine transporter (DAT)-immunopositive cells against MPTP neurotoxicity, in comparison with tyrosine hydroxylase (TH)-immunopositive neurons and glial fibrillary acidic protein (GFAP)-immunopositive cells. This study showed that DAT and TH immunoreactivity was decreased gradually in the striatum and substantia nigra of mice after MPTP treatment. The patterns of the intense TH-immunoreactive fibers and cell bodies were similar to those of DAT-immunoreactive fibers and cell bodies in the striatum and substantia nigra of mice after MPTP treatment. In contrast, GFAP immunoreactivity was increased gradually in the striatum and substantia nigra after MPTP treatment. In our double-labeled immunostaining with anti-DAT and anti-GFAP antibodies, DAT immunoreactivity was observed only in the nigral dopaminergic neurons, but not in the reactive astrocytes. The present results provide further evidence that the functional damage of DAT may precede dopaminergic neuronal death after MPTP treatment, although the decrease in the number of TH-immunopositive neurons was more pronounced than that in the number of DAT-immunopositive neurons. Furthermore, our findings demonstrate that MPTP can selectively injure the dopaminergic neurons which DAT proteins are predominantly distributed on the striatum and substantia nigra. The results provide beneficial information for MPTP-induced neurodegeneration of the nigrostriatal dopaminergic neuronal pathway.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

Male predominance among Japanese adult patients with late-onset hemorrhagic cystitis after hematopoietic stem cell transplantation.

Late-onset hemorrhagic cystitis (LHC) after hematopoietic stem cell transplantation (HSCT) is mainly caused by viral infections. We retrospectively analyzed the records of 141 Japanese adult patients who underwent a first allogeneic HSCT from 1995 to 2002. In all, 19 patients developed LHC a median of 51 days after HSCT. Adenovirus (AdV) was detected in the urine of 10 LHC patients, of whom eight had AdV type 11. Five of the six available serum samples from these patients were also positive for AdV type 11, but the detection of AdV in serum was not associated with a worse outcome. Male sex and the development of grade II-IV acute graft-versus-host disease were identified as independent significant risk factors for LHC. Male predominance was detected in LHC after HSCT, as has been previously shown in children with AdV-induced acute HC. The detection of AdV DNA in serum did not predict a poor outcome.

Adenoviridae Infections↗

Identification of a novel fusion gene, TTL, fused to ETV6 in acute lymphoblastic leukemia with t(12;13)(p13;q14), and its implication in leukemogenesis.

ETS variant gene 6 (ETV6)/translocation, ETS, leukemia (TEL)-involving chromosomal translocations are frequently observed in various hematologic neoplasms. We describe here a novel ETV6-involving translocation, t(12;13)(p13;q14), found in the case of acute lymphoblastic leukemia, in which ETV6 fused with a previously unknown gene, named Twelve-thirteen Translocation Leukemia gene (TTL), at 13q14. TTL was weakly but ubiquitously expressed in normal human tissues as detected by reverse transcribed-PCR. Three TTL splicing forms were identified, TTL-T from a human testis cDNA library, with an open-reading frame of 402 bp encoding 133 amino acids (aa), and TTL-B1 and -B2 from a human brain cDNA library. These proteins have no homology to known proteins. In leukemic cells from the patient, both reciprocal fusion transcripts, ETV6/TTL and TTL/ETV6, were expressed. The predominant fusion transcript, TTL/ETV6-1, encodes a predicted 530 aa fusion protein containing 89 aa of the N-terminal TTL fusing to the helix-loop-helix domain and ETS-binding domain of ETV6. Although the function of TTL is yet to be elucidated, our findings will provide another insight into the molecular pathogenesis of leukemia having ETV6-involving translocations.

Alternative Splicing↗

Adenoviral gizzard erosion in commercial broiler chickens.

Pathologic and immunohistochemical changes caused by group I of the fowl adenovirus (FAV) serotype-1 99ZH strain, isolated from broiler chickens exhibiting gizzard erosion, were investigated in commercial broiler chickens. One hundred twenty-two chickens were inoculated with the strain by both oral and ocular routes at 1, 3, or 5 weeks of age and euthanatized for necropsy within 4-18 days of inoculation. Focal gizzard erosions were observed in the inoculated chickens of each age group. A histologically degenerative koilin layer, necrotic mucosa, intranuclear inclusion bodies in the glandular epithelial cells, inflammatory cell infiltrations in the lamina propria, submucosa, and a muscle layer were seen in the gizzards. Immunohistochemical staining showed evidence of FAV antigens in the intranuclear inclusion bodies. These findings were recognized regardless of their maternal antibody levels for FAV serotype-1. Gizzard lesions appeared later in the lower-dose-inoculated chickens than in the higher-dose-inoculated chickens. Numerous CD3-positive cells and IgY-positive plasma cells were seen in the gizzard lesions. In 5-week-old chickens the heterophil infiltrations in the lesions were milder than in younger chickens. Intranuclear inclusion bodies also were observed in the epithelial cells of the ileum or cecal tonsils of some chickens. Thus, this study shows that FAV-99ZH causes adenoviral gizzard erosion in broiler chickens without hepatic or pancreatic lesions and that cell infiltration is more severe than in dietary gizzard erosions.

Adenoviridae Infections↗

[Repair for atrioventricular valve regurgitation using autologous pericardium: report of a case].

A 13-year-old boy with [SLL] single left ventricle first underwent ventricular septation using a dacron patch at 3 years of age. Eight years after the first surgery, he presented with general fatigue on exertion as the chief complaint. Right-sided atrioventricular valve regurgitation, and dilatation of the right heart were diagnosed. Eleven years after surgery, right heart failure was uncontrollable by medicine, and 2nd surgery was performed. At operation, the right-sided heart valve leaflet was tightly adherent to the dacron septation patch, and valve plasty was judged impossible. We repaired the right-sided atrioventricular valve using an autologous pericardial valve leaflet and sub-valvular tissue. The postoperative course was uneventful, and he has been free from any complication for 33 months.

Adolescent↗