Search PubMed⌕ Search

Biomedical subjects

T Taki

Publications and source records attributed to T Taki.

At least 37 records · Page 2Linked to original sources

Holmium:YAG laser endoureterotomy in the treatment of ureteroenteric stricture following Indiana urinary diversion.

A 57-year-old man who had received radical urethrocystectomy and Indiana urinary diversion 6 months earlier was treated for ureteroenteric anastomosis stricture (left side) using a Holmium:YAG laser via antegrade approach. The availability of small (6.9 Fr) flexible ureteroscope, as well as the use of the Holmium:YAG laser has facilitated the ability to precisely incise the stricture under direct endoscopic visualization. The technique is described for laser endoureterotomy in a patient with ureteroenteric stricture following Indiana urinary diversion.

Anastomosis, Surgical↗

Endoscopic ureteral incision using the holmium:YAG laser.

BACKGROUND: We reviewed the results of endoscopic ureteral incision for benign ureteral stricture, ureteropelvic junction obstruction and ureteroenteroanastomotic stricture using the holmium laser. METHODS: We carried out endoscopic ureteral incision using the holmium laser through an 8-Fr semirigid or 6.9-Fr flexible ureteroscope on 17 ureters in 15 patients. Balloon dilatation was not necessary before insertion of the ureteroscope. The stricture was incised with the holmium laser using a 200-365 microm fiber through the working channel of the ureteroscope. After completion of the incision, a 12-Fr double-J catheter was left for 6 weeks. Thereafter patients were followed by renal scan and/or ultrasound and excretory urography at 3-6 month intervals. RESULTS: The mean operative time was 65 min (18-135 min). The stricture resolved completely in 86.7% of cases at an average follow up of 20.5 months (11-32 months). CONCLUSIONS: The holmium laser endoscopic ureteral incision was associated with a good outcome in our series. We recommend this procedure to be employed initially because it is less invasive and has a favorable outcome.

Adult↗

Clinical study of transitional cell carcinoma of the prostate associated with bladder transitional cell carcinoma.

BACKGROUND: Transitional cell carcinoma of the prostate in patients with bladder cancer appears to influence the prognosis and affects the decision about therapeutic modality. Therefore, it is important to characterize transitional cell carcinoma associated with bladder cancer. METHODS: From April 1980 to December 1998, 81 male patients underwent total cystoprostatectomies for transitional cell carcinoma of the bladder. The 81 cystoprostatectomy specimens were examined to clarify the characteristics of prostatic involvement by transitional cell carcinoma. The extent, origin, mode of spread and risk factor of prostatic involvement as well as the prognosis were investigated. In 13 of 15 patients with prostatic involvement the prostate was examined by sequential step sections. RESULTS: Prostatic involvement was observed in 15 of 81 patients (18.5%). Prostatic urethral involvement, invasion to prostatic duct/acinus, prostatic stromal invasion and extraprostatic extension and/or seminal vesicle involvement were recognized in 12 (80%), 14 (93.3%), six (40%), and five (33.3%) of the 15 patients, respectively. Twelve of the 15 patients (80%) with prostatic involvement had papillary or non-papillary tumors (i.e. carcinoma in situ) both in the prostatic urethra and prostatic duct. In 10 of these 12 patients (88.3%), there was contiguity between prostatic urethral and ductal tumors. Seven of the 23 patients (30.4%) with carcinoma in situ of the bladder showed prostatic involvement, which increased to 50% in the presence of carcinoma in situ of the trigone or bladder neck. CONCLUSIONS: Eighty per cent of the patients with prostatic involvement showed papillary or non-papillary tumors both in the prostatic urethra and prostatic duct. There was a high level of contiguity between both tumors. Patients with carcinoma in situ of the trigone or bladder neck revealed significantly higher incidence of prostatic involvement.

Carcinoma in Situ↗

CA19-9-producing transitional cell carcinoma of the renal pelvis: a case report.

We report a case of CA19-9-producing transitional cell carcinoma of the renal pelvis. A 59-year-old male patient with left hydronephrosis was referred to us from a local physician. Retrograde pyelogram revealed irregular filling defects involving calices, pelvis and proximal ureter. The serum CA19-9 level was elevated. Under the diagnosis of renal pelvic tumor, we performed radical left nephroureterectomy. The tumor was histologically diagnosed as transitional cell carcinoma. The tumor cells showed positive immunostaining for CA19-9. The serum CA19-9 level was normalized after the operation. To our knowledge, this is the 28th case of a CA19-9-producing tumor in the Japanese literature.

CA-19-9 Antigen↗

Ureteral fibroepithelial polyp associated with urolithiasis induced by steroid therapy in a child: a case report.

A 14-year-old boy complained of left flank pain. He had been given high-dose corticosteroid therapy for chronic inflammatory demyelinating polyneuropathy (CIDP). Retrograde pyelography revealed irregular defects at the left ureteropelvic junction (UPJ), and ureteroscopy demonstrated ureteral polyp. The polyp was removed and histologically diagnosed as fibroepithelial polyp. Hypercalciuria due to the corticosteroids and bedridden was assumed to have been a causative factor in the stone formation. To our knowledge, this is the first report of a ureteral fibroepithelial polyp in children associated with urolithiasis, and associated with CIDP.

Adolescent↗

Clinical significance of CD151 gene expression in non-small cell lung cancer.

Transmembrane 4 superfamily (TM4SF) is a recently described gene family, and TM4SF members are known to play roles in the signal transduction pathways and to regulate cell activation, development, proliferation, and motility. MRP-1/CD9, KAI1/CD82, and ME491/CD63, members of the TM4SF, have been reported to suppress tumor progression or metastasis. Previously, we showed that MRP-1/CD9 suppressed cell motility and metastatic potential to lungs. Moreover, reduction of MRP-1/CD9 and KAI1/CD82 gene expression was found to be a factor in a poor prognosis for patients with non-small cell lung cancer. However, among TM4SF, CD151 is identical to an existing gene, PETA-3, which may promote tumor metastasis of malignant cells, and its expression may be involved in the malignant progression of cancer. The function of CD151 is opposite that of the metastasis suppressor genes, MRP-1/CD9 and KAI1/CD82. On the basis of these results, we used reverse transcription-PCR and immunohistochemical techniques for a retrospective study of CD151 gene expression in tumor tissues from 145 lung cancer patients; 72 tumors were stage I, 29 stage II, 27 stage IIIA, and 17 stage IIIB. Whereas 86 patients had tumors positive for the CD151 gene, 59 had tumors that were negative for the CD151 gene. The overall survival rate of patients with CD151-positive tumors was much lower than that of CD151-negative patients (51.9% versus 73.1%; P = 0.013). Our findings suggest that high CD151 gene expression in lung cancer may be associated with a poor prognosis. Assessment of CD151 could be instrumental for improvements in lung cancer diagnosis and therapies.

Antigens, CD↗

[Long-term outcome after extracorporeal shock wave lithotripsy for gallstones].

We retrospectively reviewed 289 cases followed for a long time after extracorporeal shock wave lithotripy (ESWL) for gallstones. Follow-up periods ranged from 0.5 years to 9.2 years, with a median of 4.1 years. The complete resolution rate was 45.6%. A solitary gallstone, non-calcified gallstones on CT, and Tsuchiya's sonographic type Ia and Ib gallstones were found to be statistically significant variable for resolution of the disease. With a maximum follow-up period of 9 years, the cumulative recurrence rate was 30.7%. Among the 156 patients whose gallstones did not resolve, 70 were symptomatic and the other 86 were asymptomatic. Thirty-eight of the symptomatic patients (54.3%) became symptom-free, while 23 asymptomatic patients (29.1%) became symptomatic. The cumulative rate of occurrence of colic attacks and/or acute cholecystitis was significantly higher in the cases with lithotripsy fragments 4 mm or more in size than in the cases wih fragments 3 mm or less in size (51.8% vs. 16.7%; p < 0.05). ESWL was followed by surgery in 23.1% because symptoms developed or became aggravated after ESWL in 58.3% of them. Gallbladder cancer was discovered in one case. Patients undergoing ESWL should be followed by focusing on postoperative recurrence, symptoms, and gallbladder cancer.

Adult↗

Detection of antibody to sialyl-i, a possible antigen in patients with Meniere's disease.

An autoimmune hypothesis for the etiology of Meniere's disease has been proposed. In this study, we focused on gangliosides as potential antigens for autoantibodies in Meniere's disease patients. In an attempt to investigate ganglioside antigens which respond to the serum of patients with Meniere's disease, we analyzed gangliosides of human acoustic neurinomas, and used them as antigens to broadly explore gangliosides that react to serum. All the acoustic neurinoma samples used in the present study showed a similar ganglioside profile on TLC (thin-layer chromatography). For the microscale ganglioside analysis, a newly developed TLC blotting/secondary ion mass spectrometry (SIMS) system together with TLC immunostaining method was employed. Most of the ganglioside bands could be analyzed, and they were identified as GM3, GM2, SPG, GM1a, GD3, S-i (sialyl-i ganglioside) and GD1a. GD1a was the predominant ganglioside and many neolactoseries gangliosides were recognized by immunological analysis. Next, the immune reactivity of serum samples, from patients with Meniere's disease, with the acoustic neurinoma gangliosides was studied by TLC immunostaining. The result showed that five of 11 patients with Meniere's disease and one of eight normal subjects reacted with a specific band, which was identified as S-i by the TLC blotting/SIMS system. The findings of the present study indicate that S-i ganglioside is an autoantigen and possibly involved in the pathogenesis of Meniere's disease.

Autoantibodies↗

Identification and characterization of cell lines with a defect in a post-adsorption stage of Sendai virus-mediated membrane fusion.

In the early stage of infection, Sendai virus delivers its genome into the cytoplasm by fusing the viral envelope with the cell membrane. Although the adsorption of virus particles to cell surface receptors has been characterized in detail, the ensuing complex process that leads to the fusion between the lipid bilayers remains mostly obscure. In the present study, we identified and characterized cell lines with a defect in the Sendai virus-mediated membrane fusion, using fusion-mediated delivery of fragment A of diphtheria toxin as an index. These cells, persistently infected with the temperature-sensitive variant Sendai virus, had primary viral receptors indistinguishable in number and affinity from those of parental susceptible cells. However, they proved to be thoroughly defective in the Sendai virus-mediated membrane fusion. We also found that viral HN protein expressed in the defective cells was responsible for the interference with membrane fusion. These results suggested the presence of a previously uncharacterized, HN-dependent intermediate stage in the Sendai virus-mediated membrane fusion.

Animals↗

SN-1, a novel leukemic cell line with t(11;16)(q23;p13): myeloid characteristics and resistance to retinoids and vitamin D3.

The MLL gene is fused with the cAMP-responsive element binding protein-binding protein (CBP) gene in t(11;16)(q23;p13), which has been reported to be associated with therapy-related acute leukemia. We established a novel myeloid cell line, SN-1, from a patient with T-cell acute lymphoblastic leukemia with t(11;16)(q23;p13) having in-frame MLL-CBP fusion transcripts. The majority of the SN-1 cells were positive for myeloperoxidase when examined using an electron microscope and expressed CD13, CD33, CD56, and HLA-DR antigens, but not CD7, CD10, CD19, CD34, or CD41 antigens, suggesting that these cells are of myeloid origin. SN-1 cells underwent functional and morphological differentiation when treated with actinomycin D or sodium butyrate, but not with all-trans-retinoic acid (ATRA) or 1alpha,25-dihydroxyvitamin D3 (VD3). Exposure of SN-1 cells to ATRA hardly affected cell growth and differentiation, whereas the growth of HL-60 and NB4 cells treated with ATRA was effectively inhibited, and differentiation into mature granulocytes was induced. SN-1 cells were relatively insensitive to VD3 with respect to inhibiting the cell growth and inducing the ability to reduce nitroblue tetrazolium, lysozyme activity, and morphological differentiation, although the expression of CD11b was slightly induced by VD3. These results suggest that the cell line was impaired in the signal transduction systems of ATRA and VD3. This cell line should be useful for the study of the role of CBP as a transcriptional regulator in leukemia differentiation and for the functional analysis of the MLL-CBP fusion gene, which will provide new insights into leukemogenesis caused by 11q23 translocations.

Amino Acid Sequence↗

Suppression of GD1alpha ganglioside-mediated tumor metastasis by liposomalized WHW-peptide.

GD1alpha ganglioside-replica peptides were recently isolated from a phage-displayed random pentadecapeptide library by assaying for inhibition of adhesion of RAW117-H10 lymphosarcoma cells to hepatic sinusoidal microvessel endothelial (HSE) cells. We show here that the Trp-His-Trp (WHW) peptide was identified as a minimal sequence of the GD1alpha-replica peptide WHWRHRIPLQLAAGR. The addition of WHW peptide-attached liposomes displayed efficient inhibition of liver metastasis of RAW117-H10 cells as well as of GD1alpha-mediated adhesion of RAW117-H10 cells to HSE cells in vitro. These results suggest that engineered liposomes for peptide delivery are applicable to treatment for metastasis.

Amino Acid Sequence↗

Down's syndrome with myelodysplastic syndrome showing t(7;11)(p13;p14).

We report a boy with Down's syndrome (DS) who developed myelodysplastic syndrome (MDS) after spontaneous remission of transient myeloproliferative disorder (TMD) at birth. Chromosomal analysis of the blasts in the MDS phase demonstrated t(7;11)(p13;p14) which had not been detected in the TMD phase. NUP98-HOXA9 chimera mRNA, which is known to be involved in t(7;11)(p15;p15) translocation in acute myeloid leukemia (AML), was not detected by reverse transcriptase-polymerase chain reaction, and NUP98 rearrangement was not detected by Southern blot analysis of the blasts in the MDS phase. Reciprocal translocation is very rare in AML/MDS in DS, and the t(7;11)(p13;p14) found in our patient was different from the recurrent translocation t(7;11)(p15;p15) previously reported.

Blotting, Southern↗

Transpapillary biopsy in gallbladder disease.

BACKGROUND: Endoscopic biopsy is routine in gastrointestinal disease; similarly, histopathologic diagnosis is desirable in gallbladder disease. In this study we examined the clinical usefulness and the problems associated with transpapillary gallbladder biopsy. METHODS: Transpapillary gallbladder biopsy was attempted in 9 patients with gallbladder disease. After inserting a catheter sheath into the gallbladder using a guidewire via the transpapillary route without sphincterotomy, we inserted a biopsy forceps into the lumen of the sheath up to the gallbladder lumen and obtained specimens. RESULTS: We could obtain sufficient specimens for histopathologic diagnosis in 8 of 9 cases (88.9%). Of the 8 successful cases, targeted specimens were obtained in 7 (87.5%). Diagnostic accuracy with respect to malignant versus benign disease was 100% (2 of 2) and 83.3% (5 of 6), respectively. There were no complications. CONCLUSION: Transpapillary gallbladder biopsy is a clinically useful technique because it facilitates histopathologic diagnosis and therefore guides the choice of therapy.

Biopsy↗

Novel missense mutations in the glutamate dehydrogenase gene in the congenital hyperinsulinism-hyperammonemia syndrome.

OBJECTIVES: The objectives of this study were to clarify the involvement of the glutamate dehydrogenase gene in congenital hyperinsulinemia-hyperammonemia syndrome (CHHS) and the relationships between the mutation of the gene and clinical severity. STUDY DESIGN: Five unrelated Japanese patients (3 girls and 2 boys) with CHHS were investigated. All patients had convulsions or loss of consciousness resulting from hypoglycemia at less than 1 year of age. We examined mutations of the glutamate dehydrogenase gene using genomic or reverse-transcriptase polymerase chain reactions, followed by direct sequencing. RESULTS: We identified heterozygous missense mutations in all patients. Three patients had a previously identified mutation (C-->T at nt 1506) at codon 445 in the allosteric domain. Two novel missense mutations were identified in the other patients. These mutations included a change of A-->C at nt 1059 and a change of G-->A at nt 966, within the catalytic domain of the glutamate dehydrogenase gene. The locus of the mutations was not associated with the severity of hypoglycemia. CONCLUSIONS: Our results suggest that structural aberrations of not only the allosteric domain but also the catalytic domain of the glutamate dehydrogenase protein, caused by missense mutations, can result in the development of CHHS.

Adenine↗

Triterpenoids from Tripterygium wilfordii.

The extract (T(II)) of Tripterygium wilfordii Hook f. afforded four triterpenoids: wilforic acid D (3beta,24-epoxy-2alpha-hydroxy-24R*-ethoxy-29-friedelanoic acid); (E) 3beta,24-epoxy-2-oxo-3alpha-hydroxy-29-friedelanoic acid; (F) 2beta-hydroxy-3-oxo-friedelan-29-oic acid; 29-hydroxy-3-oxo-olean-12-en-28-oic acid and 17 known triterpenoids. Their structures were established on the basis of spectroscopic studies. In a bioactivity analysis, only the known dulcioic acid compound showed a significant inhibitory effect on cytokine production.

Immunosuppressive Agents↗

Hypermethylation of p16 and p15 genes and RB protein expression in acute leukemia.

Both p16 and p15, encoded by genes located on chromosome 9p21, are inhibitors of cyclin-dependent kinases 4/6 (CDK4/6) and upstream regulators of RB function, and set up the RB/p16 tumor suppressive pathway, which is abrogated frequently in human neoplasms, either through inactivation of the RB or p16 tumor-suppressor protein, or alteration of the cyclin D1 or CDK4 oncoproteins. In hematological malignancies, deletion of p16/p15 locus has been shown to be highly specific to lymphoid malignancies, and more particularly to T-cell acute lymphoblastic leukemia (T-ALL). However, in the other subsets of ALL, deletions of p16 and p15 are relatively rare events. To investigate whether these genes are inactivated by methylation of the 5' CpG islands, we examined 35 leukemia cell lines and 29 childhood acute myeloid leukemia (AML) patients by Southern blot, polymerase chain reaction (PCR) and Western blot analyses. We found methylation of p16 in 12 (50%) of 24 ALL cell lines, 5 (50%) of 10 AML cell lines without homozygous deletion of p16, and 11 (38%) of 29 AML patients. Those leukemia cell lines subjected to p16 methylation were found to have lost p16 protein expression. The p15 gene was methylated in 10 (34%) of 29 ALL cell lines, 6 (60%) of 10 AML cell lines without homozygous deletion of p15, and 15 (52%) of 29 AML patients. These results revealed the frequent methylation of p16 and p15 genes in B-ALL and AML despite a low frequency of p16 and p15 deletions and mutations in these leukemias. In the study for expression of RB protein, we found no expression of RB in 4 of 16 leukemia cell lines. Inactivation of the p16 gene was found in all the cell lines with expression of RB. Neither amplification nor rearrangement of cyclin D1 gene was found in any cell lines. These results suggest that inactivation of p16 and p15 genes is one of the most common genetic events in acute leukemia, and plays an important role for the RB/p16 pathway in the pathogenesis of acute leukemia.

Acute Disease↗