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M Tada

Publications and source records attributed to M Tada.

At least 91 records · Page 5Linked to original sources
PubMed1999

DNA-binding specificity and embryological function of Xom (Xvent-2).

Xom (also known as Xvent-2) is a homeobox-containing gene expressed throughout the early gastrula of the Xenopus embryo with the exception of the organizer. Activation of Xom is an immediate-early response to BMP signaling, and overexpression of Xom, like overexpression of BMP family members, causes ventralization of the embryo. In this paper we first show that Xom is a transcriptional repressor and we then define its preferred DNA-binding site. Overexpression of wild-type Xom and a dominant-negative form suggests that Xom functions by repressing transcription of goosecoid, and analysis of the goosecoid promoter reveals a site which is required for Xom-mediated repression of goosecoid promoter reporter constructs. Together, these results suggest that Xom causes down-regulation of goosecoid in a direct fashion and that this accounts, at least in part, for the ability of Xom to cause ventralization of the Xenopus embryo.

Activins↗
PubMed1999

Deletion of the COOH-terminal region of p73alpha enhances both its transactivation function and DNA-binding activity but inhibits induction of apoptosis in mammalian cells.

The candidate tumor suppressor p73 has a high sequence homology with p53 within the NH2-terminal transactivation domain, the sequence-specific DNA-binding region, and the oligomerization domain. However, p73alpha, which is most abundantly expressed in many tissues and cells among the alternatively spliced forms of p73, has an additional long COOH-terminal tail that might distinguish the function of p53 and p73alpha or other p73 splicing variants. To examine the functional role of the p73alpha COOH-terminal region, we generated a series of p73alpha truncation mutants including p73alpha(1-247) (retaining only a transactivation domain), p73alpha(1-427) (lacking the most COOH-terminal region including a SAM domain), and p73alpha(1-548) (deleting an extreme COOH-terminal region except a SAM domain). When transfected into COS cells, all of p73alpha, p73alpha(1-548), and p73alpha(1-427) localized in the cellular nucleus, whereas p73alpha(1-247) localized in both nucleus and cytoplasm. Intriguingly, when compared with p73alpha, both p73alpha(1-427) and p73alpha(1-548) showed a significant stimulation of the transcription of luciferase reporters harboring three p53-responsive promoters (p21(Waf1), Mdm2, and Bax) in p53-deficient SAOS-2 cells. Gel retardation assays showed that DNA-binding activity of p73alpha(1-427) and p73alpha(1-548) was increased as compared with that of the full-length p73alpha. However, the colony formation assays using SAOS-2 cells demonstrated that, contrary to p73alpha, transfection of p73alpha(1-427) or p73alpha(1-548) resulted in no significant reduction of the number of colonies. These suggest that the distal COOH-terminal region of p73alpha is a cis- or trans-acting regulatory domain and regulates its functions diversely.

Alternative Splicing↗
PubMed1999

A functional and quantitative mutational analysis of p53 mutations in yeast indicates strand biases and different roles of mutations in DMBA- and BBN-induced tumors in rats.

In order to analyze the mutational events and to understand the biological significance of the p53 gene in chemical carcinogenesis, we applied a new yeast-based p53 functional assay to ovarian tumors induced by 7, 12-dimethylbenz[a]anthracene (DMBA), as well as to transitional cell carcinomas of the urinary bladder induced by N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) in rats. The assay demonstrated that 15 of 19 DMBA induced tumors harbored clonal p53 mutations, which is consistent with the expectations of the "clonal expansion" hypothesis. The majority of the mutations were purine (AG) to pyrimidine (CT) transversions (12/19) on the non-transcribed (sense) strand (NTS), which is likely to be due to depurination created by DMBA adduct formation on the NTS. In contrast, we found no pyrimidine to purine [corrected] transversion on the NTS. After cessation of BBN treatment, BBN-induced multifocal lesions in the bladder contained heterogeneous p53 mutations at an early stage. In the later stage, however, clonal p53 mutations were identified in 4 out of 7 bladders analyzed, conforming with the concept of "field cancerization". The observed base substitutions were G-->A (1/6) or C -->T transitions (2/6), and mutations at T (3/6) on the NTS in clonal mutations, together with non-clonal mutations, showing a preference of C-->T to G-->A (17 vs. 0). Thus, preferential repair was found in the transcribed strand of the p53 gene, whether modified by DMBA or by BBN carcinogens. Very similar mutation patterns were observed between clonal and non-clonal mutations in the DMBA- and BBN-induced tumors, indicating that the rat yeast p53 functional assay can be a potential tool for the characterization of in vivo mutation patterns of p53, when modified by chemical carcinogens.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1999

Transmembrane helix M6 in sarco(endo)plasmic reticulum Ca(2+)-ATPase forms a functional interaction site with phospholamban. Evidence for physical interactions at other sites.

In an earlier study (Kimura, Y., Kurzydlowski, K., Tada, M., and MacLennan, D. H. (1997) J. Biol. Chem. 272, 15061-15064), mutation of amino acids on one face of the phospholamban (PLN) transmembrane helix led to loss of PLN inhibition of sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) molecules. This helical face was proposed to form a site of PLN interaction with a transmembrane helix in SERCA molecules. To determine whether predicted transmembrane helices M4, M5, M6, or M8 in SERCA1a interact with PLN, SERCA1a mutants were co-expressed with wild-type PLN and effects on Ca(2+) dependence of Ca(2+) transport were measured. Wild-type inhibitory interactions shifted apparent Ca(2+) affinity of SERCA1a by an average of -0.34 pCa units, but four of the seven mutations in M4 led to a more inhibitory shift in apparent Ca(2+) affinity, averaging -0.53 pCa units. Seven mutations in M5 led to an average shift of -0.32 pCa units and seven mutations in M8 led to an average shift of -0.30 pCa units. Among 11 mutations in M6, 1, Q791A, increased the inhibitory shift (-0.59 pCa units) and 5, V795A (-0.11), L802A (-0.07), L802V (-0.04), T805A (-0.11), and F809A (-0.12), reduced the inhibitory shift, consistent with the view that Val(795), Leu(802), Thr(805), and Phe(809), located on one face of a predicted M6 helix, form a site in SERCA1a for interaction with PLN. Those mutations in M4, M6, or M8 of SERCA1a that enhanced PLN inhibitory function did not enhance PLN physical association with SERCA1a, but mutants V795A and L802A in M6, which decreased PLN inhibitory function, decreased physical association, as measured by co-immunoprecipitation. In related studies, those PLN mutants that gained inhibitory function also increased levels of co-immunoprecipitation of wild-type SERCA1a and those that lost inhibitory function also reduced association, correlating functional interaction sites with physical interaction sites. Thus, both functional and physical data confirm that PLN interacts with M6 SERCA1a.

Biological Transport↗
PubMed1999

A point mutation of human p53, which was not detected as a mutation by a yeast functional assay, led to apoptosis but not p21Waf1/Cip1/Sdi1 expression in response to ionizing radiation in a human osteosarcoma cell line, Saos-2.

PURPOSE: The 123A point mutation of p53 showed increased radiosensitivity, whereas other mutations (143A, 175H, and 273H) were not affected. To determine the reason for increased radiosensitivity of the 123A mutation, the response of the transformant of 123A mutation to ionizing radiation (IR) was examined and compared to those of transformants with the wild type p53 or other point mutations (143A, 175H, and 273H). METHODS AND MATERIALS: Stable transformants with a mutant or wild type p53 made by introducing cDNA into the human osteosarcoma cell line, Saos-2, which lacks an endogenous p53 were used. The transcriptional activity of mutant p53 was examined using a yeast functional assay. The transformants were examined for the accumulation of p53, the induction of p21Waf1/Cip1/Sdi1 (hereafter referred to as p21), and the other response of p53-responsive genes (MDM2, Bax, and Bcl-2) by Western blotting. Apoptosis was analyzed by detection of DNA fragmentation. RESULTS: The 123A point mutation of p53 was detected as a wild type in the yeast functional assay. The 123A mutant accumulated p53 in response to IR. The 123A mutant did not induce p21, but normally responded to MDM2, Bax, and Bcl-2. The 123A mutant entered apoptosis earlier than the wild type p53 transformant, and induced Fas at earlier in response to IR. CONCLUSION: The 123A mutant led to apoptosis, but not p21 expression in response to IR. The occurrence of apoptosis, but not induction of p21, corresponded to the radiosensitivity in the transformant. The early occurrence of apoptosis in 123A transformants may depend on the early induction of Fas.

Apoptosis↗
PubMed1999

Cells with TP53 mutations in low grade astrocytic tumors evolve clonally to malignancy and are an unfavorable prognostic factor.

It is important to understand how low grade tumors recur and progress to malignant lesions since this dramatically shortens patient survival. Here, we evaluated the concept that malignant progression and poor prognosis of low grade astrocytic tumors are TP53 dependent through clonal expansion of mutated cells. TP53 status was established in primary and recurrent tumors from 36 patients with WHO grade II astrocytic tumors and two tumor types were found. Tumors from 14 patients (39%; type 1) had TP53 mutated cells, and 92% of these recurred with 57% progressing to malignancy. The evolution of TP53 mutated cells before and after progression was examined using a clonal analysis procedure in yeast. Malignant progression was accompanied by an increased percentage of mutant TP53 (red) yeast colonies resulting from monoclonal expansion of cells with mutated TP53. The presence of TP53 mutations in WHO grade II astrocytic tumors was associated with malignant progression (P=0. 034, chi2 test) and shorter progression-free survival (PFS; 47.6+/-9. 6 months for TP53-mutated tumors vs 67.8+/-8.2 months for TP53-wild type tumors, P<0.05, log-rank test). Tumors from 22 patients (61%; type 2) were without TP53 mutations, and 64% of these recurred without a change in TP53 status, although 41% progressed to malignancy. This suggests that TP53 mutation is not an initiating or progression event in the majority of low grade astrocytic tumors. Our study also indicates that irradiation for WHO grade II astrocytic tumors might be associated with poor outcome (P<0.0001) and this was independent of TP53 status. These findings have important implications in the clinical management of patients with low grade astocytoma and provide new support to the clonal evolution model for tumor progression.

Adolescent↗
PubMed1999

Functional role of c-Src in gap junctions of the cardiomyopathic heart.

Given the essential role played by gap junctions in the coordination of cardiac muscle contraction, it is plausible that down-regulation of gap junctional conduction is in part responsible for the contractile dysfunction observed in hypertrophied and failing hearts. In the present study, we analyzed the expression and function of the gap junction protein, connexin43, in the ventricular myocardium of hereditary cardiomyopathic, Syrian BIO 14.6 hamsters. Immunoprecipitation and immunoblot analyses revealed that levels of tyrosine phosphorylated connexin43 were increased in BIO 14.6 hamsters at the late stage of congestive heart failure. Furthermore, the increased tyrosine phosphorylation was correlated with increased c-Src activity. The functional consequences of tyrosine phosphorylation of connexin43 in gap junction were assessed using transfected cells expressing constitutively active c-Src. It was found that constitutively active c-Src diminished propagation of Ca(2+) waves in HEK293 cells and reduced gap junctional conductance between pairs of cardiac myocytes. We, therefore, conclude that during the progression of cardiac dysfunction in the cardiomyopathic heart, gap junctional communication is reduced via c-Src-mediated tyrosine phosphorylation of connexin43.

Animals↗
PubMed1999

Dominant-negative mutations of the tumor suppressor p53 relating to early onset of glioblastoma multiforme.

Previous experiments have suggested that some mutant forms of p53 are able to inactivate the endogenous wild-type p53 protein in a dominant-negative fashion. However, it remains unknown whether tumors with such dominant-negative (transdominant) p53 mutants have a biological significance that is different from that of recessive p53 mutants. In this study, we examined the dominant-negative potential of various p53 mutants using a yeast-based assay in which both wild-type and mutant p53 were efficiently expressed. We tested a total of 106 p53 mutants, which were identified in brain tumors, glioblastoma multiforme-derived cell lines, breast cancers, or premalignant lesions and squamous cell carcinomas of oral epithelium or were otherwise created by mutagenesis. In agreement with the previous studies, our results demonstrated that transdominant mutations affected amino acid residues that are essential for the stabilization of the DNA-binding surface in the p53 core domain and for the direct interaction of p53 with its DNA-binding sequence. Among 40 patients with sporadic glioblastomas, the average age at diagnosis was significantly younger in the patients with tumors harboring dominant-negative mutations (30.4 +/- 14.7 years, n = 7) than it was in those with recessive mutations (55.2 +/- 18.6 years, n = 9, P < 0.012) and in those without mutations (54.7 +/- 17.1 years, n = 24, P < 0.003). Our data suggest that dominant-negative p53 mutants accelerate development and/or growth of glioblastoma anlagen.

Age of Onset↗
PubMed1999

Protection against the bacterial mutagenicity of heterocyclic amines by purpurin, a natural anthraquinone pigment.

Purpurin (1,2,4-trihydroxy-9,10-anthraquinone) is a naturally occurring anthraquinone pigment found in species of madder root. We have found that the presence of purpurin in bacterial mutagenicity assays is responsible for a marked inhibition of mutagenicity induced by food-derived heterocyclic amines. Purpurin was found to be a better inhibitor of Trp-P-2-dependent mutagenicity than either epigallocatechin gallate or chlorophyllin both of which are well-established anti-mutagenic components of diet. Inhibition of Trp-P-2(NHOH) mutagenicity by purpurin was dependent upon pH. It was a better inhibitor in neutral than acidic conditions. Purpurin was protective against the direct mutagen Trp-P-2(NHOH) in both the presence and the absence of hepatic S9 but required pre-incubation. Finally, purpurin was responsible for the inhibition of human CYP1A2 and human NADPH-cytochrome P450 reductase and a decrease in the bioactivation of Trp-P-2 by these enzymes when they were expressed in Salmonella typhimurium TA1538ARO. However, inhibition of Trp-P-2(NHOH)-dependent mutations suggests purpurin also has a direct effect on this mutagen in addition to inhibiting its formation by CYP1A2.

Animals↗
PubMed1999

Specific p53 gene mutations in urinary bladder epithelium after the Chernobyl accident.

After the Chernobyl accident, the incidence of urinary bladder cancers in the Ukraine population increased gradually from 26.2 to 36.1 per 100,000 between 1986 and 1996. Urinary bladder epithelium biopsied from 45 male patients with benign prostatic hyperplasia living in radiocontaminated areas of Ukraine demonstrated frequent severe urothelial dysplasia, carcinoma in situ, and a single invasive transitional cell carcinoma, combined with irradiation cystitis in 42 cases (93%). No neoplastic changes (carcinoma in situ or transitional cell carcinoma) were found in 10 patients from clean areas (areas without radiocontamination). DNA was extracted from the altered urothelium of selected paraffin-embedded specimens that showed obviously abnormal histology (3 cases) or intense p53 immunoreactivity (15 cases), and mutational analysis of exons 5-8 of the p53 gene was performed by PCR-single-strand conformational polymorphism analysis followed by DNA sequencing. Nine of 17 patients (53%) had one or more mutations in the altered urothelium. Urine sediment samples were also collected from the patients at 4-27 months after biopsy and analyzed by PCR-single-strand conformational polymorphism analysis or yeast functional assay, and identical or additional p53 mutations were found in four of five cases. Interestingly, a relative hot spot at codon 245 was found in five of nine (56%) cases with mutations, and 11 of the 13 mutations determined (73%) were G:C to A:T transitions at CpG dinucleotides, reported to be relatively infrequent (approximately 18%) in human urinary bladder cancers. Therefore, the frequent and specific p53 mutations found in these male patients may alert us to a future elevated occurrence of urinary bladder cancers in the radiocontaminated areas.

Aged↗
PubMed1999

In vitro sonographic evaluation of common bile duct stones and fragments with a high-frequency microprobe.

PURPOSE: This study was conducted to evaluate the sonographic characteristics of common bile duct (CBD) stones and stone fragments scanned in vitro with a high-frequency (20-MHz) microprobe. METHODS: We sonographically examined 4 whole CBD stones (1 cholesterol stone with radiant cross section, 1 cholesterol stone with lamellar cross section, 1 black pigment stone, and 1 brown pigment stone), 44 fragments of a cholesterol stone (diameter range, 1.1-3.0 mm; mean diameter, 2.0 mm), and 75 fragments of a black pigment stone (diameter range, 1.1-3.0 mm; mean diameter, 2.0 mm). The chemical composition of all stones was analyzed by infrared absorption spectroscopy. All stones and fragments were placed in a plastic box filled with physiologic saline solution for scanning with a 20-MHz microprobe and a 5-MHz probe. Echogenic foci and acoustic shadows revealed at each frequency were compared. RESULTS: At 5 MHz, the 4 CBD stones showed different sonographic characteristics. The cholesterol stone with radiant cross section showed an echogenic focus but no definite acoustic shadow, whereas the cholesterol stone with lamellar cross section showed an echogenic line, several echogenic spots, and a definite acoustic shadow. The black pigment stone showed an echogenic line with a vague acoustic shadow, and the brown pigment stone showed echogenicity of the whole stone and a definite acoustic shadow. At 20 MHz, the 4 stones showed an echogenic line with a definite acoustic shadow. All fragments appeared as echogenic foci at 20 and 5 MHz. Seventy-seven percent (34) and 5% (2) of 44 cholesterol stone fragments cast a definite acoustic shadow at 20 and 5 MHz, respectively. Sixty-nine percent (52) and 15% (11) of 75 black pigment stone fragments cast a definite acoustic shadow at 20 and 5 MHz, respectively. Among fragments 1.5 mm in diameter and smaller, only 45% (5 of 11) from a cholesterol stone and 30% (6 of 20) from a black pigment stone showed a definite acoustic shadow at 20 MHz. CONCLUSIONS: High-frequency (20-MHz) sonography demonstrates a definite acoustic shadow more frequently among CBD stones and fragments 1.6 mm in diameter or larger than does low-frequency (5-MHz) sonography, but it does not discriminate the chemical composition.

Adult↗
PubMed1999

Development of plasma kallikrein selective inhibitors.

During the course of the development of active center-directed plasmin inhibitors, it was found that N-(trans-4-aminomethylcyclohexanecarbonyl)-lysine-4-methoxycarb onylanilide inhibited plasma kallikrein more potently than other enzymes such as plasmin, urokinase, and thrombin, although the inhibitory activity was not as potent and enzyme selectivity not as high. Based on studies of structure-activity relationship, we designed and synthesized the plasma kallikrein selective inhibitor, N-(trans-4-aminomethylcyclohexanecarbonyl)-phenylalanine-4-carboxy methyl- anilide (Tra-Phe-APAA). Tra-Phe-APAA inhibited plasma kallikrein with a Ki value of 0.81 microM, while it inhibited glandular kallikrein, plasmin, urokinase, tissue plasminogen activator, factor Xa, factor XIIa, and thrombin with Ki values of > 500, 390, 200, > 500, > 500 > 500, and > 500 microM, respectively. We designated Tra-Phe-APAA as PKSI-527. Using PKSI-527 as an affinity ligand, we synthesized a new affinity gel (PKSI-Toyopearl) and employed it for the rapid purification of plasma kallikrein from human plasma. Human plasma activated with kaolin after acid treatment was applied to a PKSI-527-Toyopearl column. Adsorbed protein was eluted with 50 mM glycinehydrochloric acid buffer (pH 3.0). Plasma kallikrein was purified 181-fold with a yield of 85% from the kaolin-activated plasma.

Binding Sites↗
PubMed1999

A new simple technique for performing intraoperative endoscopic resection of small-bowel polyps in patients with Peutz-Jeghers syndrome.

We describe herein a simple method for performing intraoperative endoscopic resection of small-bowel polyps associated with Peutz-Jeghers syndrome, using a corrugated anesthetic tube. A 34-year-old man with Peutz-Jeghers syndrome underwent emergency surgery for an ileo-ileo-colic intussusception. A sterile corrugated anesthetic tube was inserted into the small-bowel, proximal to the affected lesion. The small bowel was then telescoped sequentially over the tube using a pleating technique. Consequently, a colonoscope inserted through the tube was easily able to reach the duodeno-jejunal junction, and ten small-bowel polyps were removed using a wire snare and electrocauterization. All resected specimens were washed out by the instillation of saline through a nasogastric tube, then collected on gauze placed near the outlet of the tube. Our technique has the following merits: it is feasible even in emergency surgery; it prevents contamination of the surgical field; and it facilitates the easy collection of polypectomized specimens.

Adult↗
PubMed1999

Comparison of the distribution of fluorine-18 fluoromisonidazole, deoxyglucose and methionine in tumour tissue.

To evaluate the tumour imaging potential of fluorine-18 fluoromisonidazole (FMISO), we studied FMISO uptake in an experimental tumour model and examined the correlation between intratumoral distributions of FMISO, 14C-2-deoxyglucose (2DG) and 14C-methionine (Met). The study was performed using control rats with the AH109A tumour and rats with the same tumour under local hypoxia. Tumour uptake of FMISO was constant between 30 min and 2 h after injection, and the tumour to muscle ratio was 2 from 2 to 4 h. A tumour study with FMISO was scheduled at 2 h. Double-tracer autoradiography of the tumour demonstrated that in the areas of high FMISO uptake, there was low uptake of Met, while areas of low FMISO uptake showed high Met uptake. FMISO showed high grain density in the rim of the tumour surrounding the necrotic area. 2DG showed a more uniform distribution over the entire section of viable cells. The mean uptake of FMISO by hypoxic, radioresistant tumours was significantly higher than that by the control tumours (P<0.05), while both 2DG and Met uptake by the control tumours was higher than uptake by hypoxic tumours. When individual tumours were examined, the uptake of FMISO was inversely correlated with that of Met (r = -0.507, P<0.02), while 2DG showed almost uniform uptake with no significant correlation to FMISO. In conclusion, hypoxic and radioresistant tumours could be identified by increased FMISO uptake in our model, consistent with findings reported by others. We found a large overlap in the distribution of FMISO and 2DG within the tumour, but only a small overlap in the distribution of FMISO and Met. A combination of FMISO and other tracers in positron emission tomography or single-photon emission tomography studies might be more helpful than single-tracer studies in predicting the response of tumour tissues to radiotherapy.

Animals↗
PubMed1999

Endosonography during endoscopic mucosal resection to enhance its safety: a new technique.

BACKGROUND: We have performed endoscopic mucosal resection of the esophagus (172 cases), stomach (102 cases), and colon (28 cases) using a transparent plastic cap. Because the lesion-bearing mucosa is suctioned up inside the cap under endoscopic suction, the mucosa should be dissected sufficiently from the proper muscle layer to prevent perforation. METHODS: To avert the risk of perforation, we introduced endosonographic assessment of submucosal dissection (47 cases). In all cases, just keeping the ultrasonic probe on the surface of the mucosa allowed us to evaluate whether the mucosal lesion was lifted up sufficiently from the proper muscle layer after local saline injection. RESULTS: It was possible to confirm that the muscle layer was kept outside the strangulating snare by the same procedure (32 of 37 cases, 86.5%). CONCLUSIONS: We experienced five muscular resections in cases without the ultrasonic probe and no muscular resection with the ultrasonic probe. Thus we recommend endosonographic assessment during endoscopic mucosal resection to enhance its safety.

Colonic Neoplasms↗
PubMed1999

Immunohistological study to determine the presence of pericryptal myofibroblasts and basement membrane in colorectal epithelial tumors.

Pericryptal myofibroblasts (PMFs) are thought to be involved in the production of the basement membrane (BM) of the colonic epithelium. To clarify the involvement of PMFs in the formation of the BM during the growth of colon cancer, we conducted an immunohistological study of tumor specimens from 85 patients with colorectal epithelial tumor to detect the presence of PMFs. The tumor specimens were classified as adenoma with low-grade dysplasia, adenoma with high-grade dysplasia, or colon cancer. PMFs were detected in 66.6% of the specimens from patients with adenoma with low-grade dysplasia; 20% of specimens of adenoma with high-grade dysplasia; and 3.2% of specimens of colon cancer. As the degree of dysplasia of the tumor increased, the probability that PMFs existed decreased. We also tested 49 of the tumor specimens for the presence of laminin, a component of the BM, and found that in most of these 49 cases, the BM and PMFs co-existed. This provides further evidence that PMFs are involved in the production of the BM. These findings are important in gaining an understanding of the cause and growth of colorectal epithelial tumors.

Actins↗
PubMed1999

Washout of small stones in the bile duct by saline infusion using a side-holed balloon catheter in patients undergoing endoscopic papillary balloon dilation.

BACKGROUND: Complete bile duct clearance of stones should be achieved in patients managed with endoscopic papillary balloon dilation. However, complete retrieval of small stones or tiny fragments sometimes proves difficult using conventional devices. METHODS: We attempted the removal of fine stone fragments by saline infusion using a specially designed retrieval balloon catheter with a blind tip and a side hole located proximal to the balloon in 14 patients. RESULTS: Using this technique, bile duct clearance was achieved in a single attempt in 13 of 14 patients; 2 attempts were required in 1 patient. Cholecystitis occurred in 2 patients with gallstones in situ after the procedure. CONCLUSIONS: Saline washout using a side-holed retrieval balloon catheter effectively cleans stones and stone fragments from the bile duct in patients treated with endoscopic papillary balloon dilation.

Aged↗