Biomedical subjects

H Kawamata

Publications and source records attributed to H Kawamata.

At least 37 records · Page 2Linked to original sources

PubMed2001

Inhibitory effect of (+)-catechin on the growth of influenza A/PR/8 virus in MDCK cells.

We investigated whether (+)-catechin, a building block of tannins contained in the extract of Ephedrae herba (EHext), exerts an inhibitory effect on the acidification of intracellular compartments such as endosomes and lysosomes (referred to as ELS), and thereby inhibits the growth of influenza A PR/8/34 (PR8) virus (H1N1 subtype) in Madin-Darby canine kidney cells. The vital fluorescence microscopic study with acridine orange showed that 1-h treatment with (+)-catechin inhibited the acidification of ELS in a concentration-dependent manner (1.0-10.0 mM). Moreover, the growth of PR8 virus was inhibited markedly when the cells were treated with (+)-catechin (1.25-10.0 mM) for 1 h immediately after infection, or treated within as little as 5 to 10 min after infection. Conversely, virus growth resumed within 3 h concomitantly with the reappearance of acidified ELS after removal of (+)-catechin. Similar to EHext, (+)-catechin inhibited both the acidification of ELS and the influenza virus growth. It suggests that (+)-catechin is one of the active components in EHext.

Animals↗

PubMed2001

Enhanced production of macrophage inflammatory protein 2 (MIP-2) by in vitro and in vivo infections with encephalomyocarditis virus and modulation of myocarditis with an antibody against MIP-2.

Interleukin-8 (IL-8) is a chemotactic cytokine for neutrophils and lymphocytes. Macrophage inflammatory protein 2 (MIP-2) is a murine counterpart of IL-8. The present study was performed to determine whether MIP-2 aggravates murine myocarditis. We examined (i) the MIP-2-producing activity of encephalomyocarditis (EMC) virus-infected cultured macrophages, (ii) serial plasma MIP-2 levels in EMC virus-induced mice by enzyme-linked immunosorbent assay, and (iii) the effects of antimouse MIP-2 monoclonal antibody (MAb) in vivo upon myocarditis. The production of MIP-2 increased in an infection dose- and time-dependent manner in virus-infected RAW 264. 7 macrophages. Five-week-old C(3)H/He mice were inoculated with EMC virus. Plasma MIP-2 levels were significantly elevated in mice on days 7 and 14 postinfection. Mice were injected subcutaneously with anti-MIP-2 MAb at 10 microg/day (group 2) or 100 microg/day (group 3) on days 0 to 5 and were observed until day 21. Uninfected control mice (group 1) were prepared. The survival rate was higher in the anti-MIP-2-treated group (group 3), but not in group 2, than in the control group. Histopathological analysis revealed that cellular infiltration and myocardial necrosis with macrophage and T-cell accumulation were less prominent in the anti-MIP-2 MAb-treated group, but not in group 2, compared to the level in the controls. MIP-2 is an important naturally occurring inflammatory cytokine in myocarditis, and anti-MIP-2 MAb treatment may prevent the inflammatory response.

Animals↗

PubMed2001

Concurrent occurrence of gastric adenocarcinoma and duodenal neuroendocrine cell carcinoma: a composite tumour or collision tumours ?

BACKGROUND: Neuroendocrine cell (NEC) carcinoma is occasionally accompanied by adenocarcinoma but the relationship between these two morphologically distinct tumours is unclear. Two hypotheses have arisen regarding the mechanism for the association of adenocarcinoma and NEC carcinoma. One is that both are derived from a common multipotential epithelial stem cell. The second hypothesis is that adenocarcinoma and NEC carcinoma arise from a multipotential epithelial stem cell and a primitive NEC, respectively. AIMS: To elucidate the relationship between the two histologically distinct tumours, adenocarcinoma of the stomach and NEC carcinoma of the duodenum. PATIENT/METHODS: We present a case in which the tumour extended across the pyloric ring, the gastric portion of which revealed adenocarcinoma while the duodenal portion showed argyrophil NEC carcinoma. The two histologically distinct lesions of the tumour were examined by immunohistochemistry and genetic analysis of p53. RESULTS: The gastric region was negative for chromogranin A staining but positive for carcinoembryonic antigen (CEA) staining. In contrast, the duodenal region was positive for chromogranin A but negative for CEA. All tumour regions showed a point mutation in p53 gene at exon 7 (GGC (glycine)-->GTC (valine) at codon 245). The distal portion of the duodenal tumour showed an additional point mutation in p53 gene at exon 5 (GCC (alanine)-->GTC (valine) at codon 129). CONCLUSIONS: The two histologically distinct tumours, adenocarcinoma of the stomach and NEC carcinoma of the duodenum, appear to be derived from a common epithelial cell.

Adenocarcinoma↗

PubMed2001

Decreased expression of E-cadherin and Yamamoto-Kohama's mode of invasion highly correlates with lymph node metastasis in esophageal squamous cell carcinoma.

OBJECTIVES: A reduction in cell-cell adhesion in cancer cells is an essential step in the progression from localized malignancy to metastatic disease. E-Cadherin is an important component of cell-cell adhesion molecules and may be a crucial determinant of tumor invasion and metastasis. E-Cadherin expression is reported to be correlated with lymph node metastasis in esophageal squamous cell carcinoma (SCC). The objective of this experiment is to examine the factors that are associated with invasion and metastasis of esophageal SCC. METHODS: Forty-six cases of esophageal SCC were examined by immunohistochemical staining for E-cadherin. The relationship between E-cadherin-staining patterns, conventional clinicopathological parameters and Yamamoto-Kohama's (Y-K's) mode of invasion were examined. RESULTS: The expression of E-cadherin on the cell membrane was reduced or lost in some of the esophageal SCC. Lymph node metastasis was highly correlated with the expression pattern of E-cadherin (p = 0.0002) and also highly correlated with Y-K's mode of invasion (p = 0.0078). However, lymph node metastasis was not correlated with any conventional clinicopathological parameters for invasion. CONCLUSIONS: These results indicate that E-cadherin plays a crucial role in invasion and metastasis in esophageal SCC, and that Y-K's mode of invasion highly reflects the invasiveness and metastatic potentials of esophageal SCC cells. Therefore, examination of the expression of E-cadherin and Y-K's mode of invasion would be helpful in predicting lymph node metastasis in esophageal SCC.

Aged↗

PubMed2001

A new in vivo model for studying invasion and metastasis of esophageal squamous cell carcinoma.

The aim of our current study was to establish an orthotopic inoculation model for studying invasion and metastasis of esophageal squamous cell carcinoma (SCC). Male BALB/c nude mice were used for the experiment. A midline incision was made from the upper to middle abdomen. The abdominal esophagus was carefully exposed. Human esophageal T.Tn SCC cells or human cervical HeLa SCC cells, were injected into the submucosa of the lower esophagus. One of the mice injected with T.Tn cells was sacrificed at 5 weeks, and the remaining five sacrificed at 13 weeks after inoculation. The mice injected with HeLa cells were sacrificed at 3-4 weeks after inoculation. T.Tn cells and HeLa cells formed tumors at the esophagus, but did not metastasize to lymph nodes or lungs. HeLa cells produced peritoneal implants, and directly invaded the stomach and the liver. In the present study, we established a novel orthotopic inoculation model of esophageal SCC. This system is an appropriate and a useful model for studying invasion and metastasis of esophageal SCC, and can also be used as a model for developing therapeutic strategies for esophageal cancer in vivo.

Animals↗

PubMed2001

Dihydropyrimidine dehydrogenase mRNA level correlates with the response to 5-fluorouracil-based chemo-immuno-radiation therapy in human oral squamous cell cancer.

The measurement of the intra-tumoral level of thymidylate synthetase (TS), and dihydropyrimidine dehydrogenase (DPD), may be useful in predicting tumor sensitivity to 5-fluorouracil (5-FU). In this study, we examined the mRNA levels of DPD and TS in 28 oral squamous cell carcinomas (SCC), and 22 salivary gland tumors by semi-quantitative reverse transcription polymerase chain reaction. Then we examined the correlation of the responsiveness of the patients with oral SCC to 5-FU with the intra-tumoral levels of DPD and TS mRNA. All specimens were obtained at the biopsy before treatment, and then the patients were treated by oral administration of a 5-FU compound (UFT), the irradiation of cobalt-60 (upto 60 Gy) and injection of an immuno-potentiator (OK-432). Intra-tumoral levels of DPD mRNA in the patients who showed CR (complete response) and PR (partial response) were significantly lower than those in the patients who showed NC (no change). However, intra-tumoral levels of DPD mRNA did not correlate with the local recurrence of the tumor during the observation period after initial treatment with or without surgical resection of the residual tumors. On the other hand, TS mRNA levels in the tumors did not correlate with any clinico-pathological parameters. These observations suggest that intra-tumoral levels of DPD mRNA may predict the tumor response to 5-FU-based chemo-immuno-radiation therapy in the patients with oral SCC.

Antimetabolites, Antineoplastic↗

PubMed2001

[Colitis enhances the colorectal carcinogenesis in rats: correlation between the incidence of aberrant crypt foci and the incidence of tumors].

We examined the implication of colitis on the colorectal carcinogenesis in rats. We used 1, 2-dimethylhydrazine (DMH) as a carcinogen and trinitrobenzenesulfonic acid (TNB) as a colitis-inducing agent on F344 rats. After treating the rats with DMH, TNB markedly enhanced the incidence of aberrant crypt foci (ACF), putative preneoplastic lesions, as well as colon cancers in the rats (p < 0.01). There was positive correlation between the incidence of ACF and the incidence of tumors. Furthermore, we treated the rats with two different anti-inflammatory drugs (a non-steroidal anti-inflammatory drug: Fenbufen and a platelet activating factor-receptor antagonist: PAF-RA) after pre-treatment with DMH and TNB. Only PAF-RA significantly decreased the incidence of ACF in the rats (p < 0.05).

1,2-Dimethylhydrazine↗

PubMed2001

Immunoglobulin treatment prevents congestive heart failure in murine encephalomyocarditis viral myocarditis associated with reduction of inflammatory cytokines.

We have previously shown that immunoglobulin therapy suppressed murine coxsackievirus B3 myocarditis. In the present study, we examined the effects of immunoglobulin upon murine myocarditis induced by encephalomyocarditis virus, which is not pathogenic to humans. Antiviral activity of immunoglobulin (Venilon) against encephalomyocarditis virus could not be detected in vitro. The production of cytokines was decreased in virus-infected macrophages by the treatment of immunoglobulin in vitro. Immunoglobulin (1 g/kg/day) was administered intraperitoneally to the virus-infected C3H/He mice daily for 2 weeks, beginning simultaneously with virus inoculation in experiment I and on day 14 after virus inoculation in experiment II. In experiment I, survival rate did not differ significantly between immunoglobulin-treated and untreated groups. In experiment II, survival rate was higher in immunoglobulin compared with control groups. Immunoglobulin administration suppressed the development of myocardial necrosis with T-lymphocyte infiltrates in mice not only in the acute viremic but in the chronic aviremic stages concomitantly associated with the reduction of inflammatory cytokines, i.e., tumor necrosis factor-alpha, interferon-gamma, macrophage inflammatory protein-2, and interleukin-6. Taken together, immunoglobulin therapy could have the potential to prevent congestive heart failure.

Animals↗

PubMed2000

Nuclear translocation of TSC-22 (TGF-beta-stimulated clone-22) concomitant with apoptosis: TSC-22 as a putative transcriptional regulator.

We examined the alteration of the subcellular localization of TSC-22 (TGF-beta-stimulated clone-22) after induction of apoptosis and the transcription-regulatory activity of TSC-22. In the living cells, TSC-22-green fluorescent protein (GFP) fusion protein was clearly localized to the cytoplasm, however, in the apoptotic cells, the TSC-22-GFP fusion protein was translocated from the cytoplasm to the nucleus. TSC-22 fused to GAL4-DNA binding domain (GAL4BD) did not show the transcriptional activity on the reporter genes in yeast and in HSG (salivary gland cancer cells) and Hela. However, in CHO cells, TSC-22-GAL4BD fusion protein strongly activated the reporter gene. The transcriptional activity of the leucine zipper structure of TSC-22 is greater than that of the full-length TSC-22. These findings suggest that after receiving the apoptotic stimuli, TSC-22 translocates from the cytoplasm to the nucleus and shows the transcription-regulatory activity.

Animals↗

PubMed2000

Immunoglobulin treatment ameliorates murine myocarditis associated with reduction of neurohumoral activity and improvement of extracellular matrix change.

OBJECTIVES: We examined effects of immunoglobulin on murine myocarditis induced by encephalomyocarditis virus, not pathogenic to humans, and analyzed the plasma cytokine and catecholamine levels and the changes of the extracellular matrix with or without the treatment. BACKGROUND: We have previously shown that immunoglobulin therapy suppressed murine coxsackievirus B3 myocarditis by an antiviral effect. However, it is not yet determined whether beneficial effects of immunoglobulin for myocarditis are due to antiviral effects or to other unknown effects. METHODS: Antiviral activity of human immunoglobulin (Polyglobin-N) against encephalomyocarditis virus was determined in vitro. Immunoglobulin (1 g/kg/day) was administered intraperitoneally to the virus-infected mice daily for two weeks, beginning simultaneously with virus inoculation in experiment I and on day 14 after virus inoculation in experiment II. RESULTS: Antiviral activity of immunoglobulin could not be detected in the assay of a plaque-reduction method in vitro. The in vivo study showed that immunoglobulin administration ameliorated both myocardial necrosis with interstitial fibrin deposition in experiment I and interstitial fibrosis with the improvement of ventricular remodeling in experiment II by the reduction of plasma catecholamines, interferon-alpha, and soluble intercellular adhesion molecule-1. CONCLUSIONS: Immunoglobulin therapy could suppress myocarditis associated with the improvement of extracellular matrix changes by the reduction of neurohumoral activity.

Animals↗

PubMed2000

Membrane association and protein conformation of alpha-synuclein in intact neurons. Effect of Parkinson's disease-linked mutations.

Two missense mutations (Ala-30 --> Pro and Ala-53 --> Thr) in the gene encoding alpha-synuclein are associated with rare autosomal dominant forms of familial Parkinson's disease. In addition, alpha-synuclein is an abundant component of Lewy bodies in sporadic Parkinson's disease and diffuse Lewy body disease. However, the normal conformation of alpha-synuclein, its cellular localization in neurons, and the effects of the mutations remain to be determined. In the present study, we examine these questions using sensitive fluorescence resonance energy transfer techniques. Transient transfection of alpha-synuclein expression constructs into primary cortical neurons and counterstaining with the lipophilic fluorescent marker, DiI, demonstrates a close association between alpha-synuclein and cellular membranes. Both the N- and C-terminal regions of alpha-synuclein are tightly associated with membranes. A weak interaction also occurs between the N and C termini themselves. The Parkinson's disease-associated mutations have no effect on membrane interaction; however, the Ala-30 --> Pro mutation alters the three-dimensional conformation of alpha-synuclein, as measured by significantly increased fluorescence resonance energy transfer between the N and C termini.

Animals↗

PubMed2000

Role of MIP-2 in coxsackievirus B3 myocarditis.

Interleukin-8 (IL-8) is a chemotactic cytokine for neutrophils and lymphocytes. Macrophage inflammatory protein-2 (MIP-2) is a murine counterpart of IL-8. The present study was performed to determine the role of MIP-2 in murine myocarditis. We examined (1) the MIP-2 producing activity of Coxsackievirus B3 (CB3)-infected cultured macrophages, (2) serial plasma MIP-2 levels in CB3-induced mice by enzyme-linked immunosorbent assay (ELISA), and (3) the effects of anti-mouse MIP-2 monoclonal antibody (mAb) in vivo upon myocarditis. The production of MIP-2 increased in an infection dose- and time-dependent manner in virus-infected RAW 264.7 macrophages. Three-week-old C(3)H/He mice were inoculated with CB3. Plasma MIP-2 levels were significantly elevated in mice on days 7, 10 and 14 post-infection. Mice were injected subcutaneously with anti-MIP-2 mAb at 10 microg/day (Group 2) or 100 microg/day (Group 3) on days 0-7, and were observed until day 14. Uninfected control mice (Group 1) were injected with saline. Survival rate was higher in the anti-MIP-2-treated group (Group 3), but not in Group 2, than in the control group. Histopathological analysis revealed that cellular infiltration and myocardial necrosis with macrophage and T cell accumulation were less prominent in the anti-MIP-2 mAb-treated groups as compared to the controls. MIP-2 is an important naturally occurring inflammatory cytokine in CB3 myocarditis, and anti-MIP-2 mAb treatment may prevent the inflammatory response.

Animals↗

PubMed2000

Over-expression of TSC-22 (TGF-beta stimulated clone-22) markedly enhances 5-fluorouracil-induced apoptosis in a human salivary gland cancer cell line.

We have recently isolated TSC-22 (transforming growth factor-beta-stimulated clone-22) cDNA as an anticancer, drug-inducible (with vesnarinone) gene in a human salivary gland cancer cell line, TYS. We have also reported that TSC-22 negatively regulates the growth of TYS cells and that down-regulation of TSC-22 in TYS cells plays a major role in salivary gland tumorigenesis (Nakashiro et al, 1998). In this study, we transfected TYS cells with an expression vector encoding the TSC-22-GFP (green fluorescent protein) fusion protein, and we established TSC-22-GFP-expressing TYS cell clones. Next, we examined (a) the subcellular localization of the fusion protein, (b) the sensitivity of the transfectants to several anticancer drugs (5-fluorouracil, cis-diaminedichloroplatinum, peplomycin), and (c) induction of apoptotic cell death in the transfectants by 5-fluorouracil treatment. The TSC-22-GFP fusion protein was clearly localized to the cytoplasm, but not to the nucleus. Over-expression of the TSC-22-GFP fusion protein did not affect cell growth, but significantly increased the sensitivity of the cells to the anticancer drugs (p < 0.01; one-way ANOVA). Furthermore, over-expression of the TSC-22-GFP fusion protein markedly enhanced 5-fluorouracil-induced apoptosis. These findings suggest that over-expression of TSC-22-GFP protein in TYS cells enhances the chemosensitivity of the cells via induction of apoptosis.

Antineoplastic Agents↗

PubMed2000

Endoscopic characteristics of low-grade gastric mucosa-associated lymphoid tissue lymphoma after eradication of Helicobacter pylori.

BACKGROUND AND AIMS: It was recently reported that low-grade gastric lymphoma of mucosa-associated lymphoid tissue (MALT) was regressed by the eradication of Helicobacter pylori. The aim of this study was to confirm the effect of H. pylori eradication on low-grade gastric MALT lymphoma and to investigate the whitish mucosa that appeared with regression of the lesions. METHODS: Forty-seven H. pylori-positive patients with low-grade gastric MALT lymphoma were treated by using triple therapy. Biopsy specimens were histologically graded and B cell clonality was examined by using reverse transcription-polymerase chain reaction before and after eradication treatment. The relationship between the appearance of whitish mucosa and the degree of gastric gland loss was evaluated. RESULTS: Histologic regression was observed 2 months after eradication therapy in 42 of 47 patients. However, B cell monoclonality changed to polyclonality in only 23 patients during the follow-up period. The appearance of whitish mucosa in patients who showed histologic regression became more frequent as the degree of gastric gland loss increased (P< 0.001). CONCLUSIONS: Most low-grade gastric MALT lymphoma histologically regressed after H. pylori eradication. The appearance of whitish mucosa after histologic regression reflected the degree of gastric gland loss. Whitish mucosa is an endoscopic characteristic and may be an endoscopic marker for regression of low-grade gastric MALT lymphoma.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed2000

Effects of heart rate and right ventricular pressure on right coronary arterial flow and its systolic versus diastolic distribution in a variety of congenital heart diseases in children.

BACKGROUND AND METHODS: In order to elucidate the underlying adjusting mechanism of human right coronary arterial (RCA) flow to increased right ventricular pressure (RVP) in children, we recorded RCA flow velocity in 24 pediatric cardiac patients at the orifice of its main trunk at the time of heart catheterization using the Doppler guidewire. RESULTS: The ratio of diastolic flow (DF)/total flow (TF), or the proportion of the DF time integral over a total of one cardiac cycle, had a negative correlation with heart rate (HR; r = -0.58, n = 11) in children with normal right ventricular systolic pressure (RVSP; RVSP < 35 mmHg). In contrast, the DF/TF ratio had a good correlation (r = 0.88, n = 24) with RVSP in all patients under study. The ratio of diastolic area (DA)/total area (TA), defined as the ratio of an area encircled by the aortic pressure curve above and the RVP curve below for diastole, over a total of one cardiac cycle, representing the overall effect of both HR and transcoronary pressure difference, also correlated well (r = 0.89, n = 24) with DF/TF. Total volume flow of the RCA also increased (r= 0.76, n = 24) with increases in RVSP, first by an increase in flow velocity through the RCA, during both systole and diastole, then by widening of the RCA lumen at very high pressures. These changes were initially more dependent on diastole with increasing RVSP because: (i) of a more marked augmentation of flow velocity in diastole compared with systole; and then (ii) of a significant decrease in flow velocity in systole at very high pressures. CONCLUSIONS: We clarify how the RCA manages to increase flow through it at different HR as a function of chronic RVP overload in pediatric cardiac patients.

Adolescent↗

PubMed2000

Therapeutic effect of anti-macrophage inflammatory protein 2 antibody on influenza virus-induced pneumonia in mice.

We investigated the effect of anti-macrophage inflammatory protein 2 immunoglobulin G (aMIP-2 IgG) on the progression of influenza virus-induced pneumonia in mice. When mice were infected with a mouse lung-adapted strain of influenza A/PR/8/34 virus by intranasal inoculation, neutrophil counts in the bronchoalveolar lavage fluid (BALF) increased in parallel with the kinetics of MIP-2 production, which peaked 2 days after infection. After intracutaneous injection of a dose of 10 or 100 microg of aMIP-2 IgG once a day on days 0 and 1, neutrophil counts in BALF on day 2 were reduced to 49 or 37%, respectively, of the value in the control infected mice administered anti-protein A IgG. The antibody administration also improved lung pathology without affecting virus replication. Furthermore, by prolonged administration with a higher or lower dose for up to 5 days, body weight loss became slower and finally 40% of mice in both treatment groups survived potentially lethal pneumonia. These findings suggest that MIP-2-mediated neutrophil infiltration during the early phase of infection might play an important role in lung pathology. Thus, MIP-2 was considered to be a novel target for intervention therapy in potentially lethal influenza virus pneumonia in mice.

Animals↗

PubMed2000

Enhanced expression of inducible nitric oxide synthase by Juzen-taiho-to in LPS-activated RAW264.7 cells, a murine macrophage cell line.

We have investigated the effect of Juzen-taiho-to (TJ-48) on inducible NO synthase (iNOS) expression and nitric oxide (NO) production in RAW264.7 cells, a murine macrophage cell line. TJ-48-lipopolysaccharide (LPS) combination induced iNOS mRNA expression earlier, stronger and remained longer that paralleled but with a higher NO production compared to LPS stimulation. TJ-48 itself showed no inducible effect either on NO production or iNOS mRNA expression. This phenomenon could be considered to contribute, at least in part, to the beneficial effects of TJ-48 through the iNOS-mediated activation of biodefense mechanism.

Animals↗

PubMed2000

Peripheral directional atherectomy evaluated with a rotational digital angiography system.

BACKGROUND: One of the factors that affect the recurrence rate after peripheral directional atherectomy (DA) is the degree of residual stenosis. A new method of peripheral DA to reduce residual stenoses was evaluated with a rotational digital angiography (RDA) system that provides both angiography and fluoroscopy at multiple projections within 360 degrees. PATIENTS AND METHODS: Between March 1995 and July 1999, severe short segmental stenoses of six iliac arteries and two superficial femoral arteries (SFA) in eight patients were treated with the Simpson DA catheter under RDA system guidance. After pre-procedural RDA evaluation, the first series of DA were performed under ordinary PA fluoroscopic guidance. The residual stenoses were evaluated with RDA. If the residual stenoses exceeded 30%, a second series of DA were performed covering the residual plaque with the cutter window of the DA catheter. To this purpose the fluoroscopy of the RDA system was fixed in the direction in which the residual stenoses were largest and most eccentric. The end point was defined to be a residual stenosis of less than 30% evaluated with the RDA system, and the procedures were repeated until the end point was achieved. RESULTS: Five of six iliac artery lesions were curved at the pre-procedural RDA evaluation. After the first series of DA, only two of six iliac lesions but all SFA lesions achieved the end point. Among the four other iliac lesions, three achieved the end point with one or two additional series of DA using the RDA system guidance to control the selective cuts of the residual plaques. One patient had a residual stenosis of 50% because the procedure could not be completed by balloon rupture of the DA catheter. In the patients with iliac stenoses, there was no final residual stenosis in one, and the range was from 20% to 25% in the four patients. The residual stenoses were located on the greater curvature side of the curved artery in three of these four patients. CONCLUSION: The RDA system is a valuable tool in aiding reduction of the residual stenoses during peripheral DA. Minimal stenoses often remain on the greater curvature side of the wall because the rigid and straight metallic capsule (cylindrical housing) of the Simpson DA catheter does not completely fit the curved wall. This phenomenon was thought to be a mechanical limitation of this device.

Aged↗