Biomedical subjects
Mitsuo Iida
Publications and source records attributed to Mitsuo Iida.
Fatal colorectal cancer in juvenile polyposis syndrome.
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Progressive duodenal adenomatosis in a familial adenomatous polyposis pedigree with APC mutation at codon 1556.
PURPOSE: In familial adenomatous polyposis, genotype-duodenal phenotype correlations have not been clearly understood. We identified the adenomatous polyposis coli gene mutation in a family pedigree with severe duodenal adenomatosis. METHODS: Among 53 familial adenomatous polyposis families, we found a pedigree composed of five affected members with severe duodenal adenomatosis. Clinical manifestations of the family members were reviewed. The adenomatous polyposis coli gene of four members were screened by polymerase chain reaction-based single strand conformation polymorphism or protein truncation test. RESULTS: The family was characterized by sparse colorectal polyposis, osteomas, and epidermal cysts. However, there were intrafamilial variabilities in the occurrence of fundic gland polyposis, congenital hypertrophy of the retinal pigment epithelium, and desmoids. All the members had duodenal adenomatosis in their second or third decades, and the adenomatosis in three members progressed during surveillance. A frameshift mutation was found at codon 1556 of the adenomatous polyposis coli gene in two members, and the equivalent mutation was confirmed by protein truncation test in another two. CONCLUSIONS: Distal 3' mutation of the adenomatous polyposis coli gene seems to contribute to severe duodenal adenomatosis in familial adenomatous polyposis. Specification of the adenomatous polyposis coli gene mutation may be a clue for surveillance strategy for duodenal adenomatosis in patients with familial adenomatous polyposis.
Effect of sulindac treatment for attenuated familial adenomatous polyposis with a new germline APC mutation at codon 161: report of a case.
INTRODUCTION: Patients with familial adenomatous polyposis develop colorectal cancers if left untreated. As indicated in patients with familial adenomatous polyposis, prophylactic colectomy has been recommended even in a milder colonic phenotype referred to as attenuated familial adenomatous polyposis. However, therapeutic strategies in attenuated familial adenomatous polyposis are still controversial. METHODS: We report a patient with attenuated familial adenomatous polyposis who has been treated with sulindac for five years. During the period of observation, she has been carefully followed up by chromoscopic and radiographic surveillance. Immunohistochemical study for cyclooxygenase-2 and genetic analysis in the adenomatous polyposis coli gene was also performed. RESULTS: Continuous administration of sulindac resulted in obvious regression of both colorectal adenomatous polyps and gastric fundic gland polyps, and no cancers developed during the observation period. Immunohistochemical study showed the decrease of cyclooxygenase-2-positive epithelial cells in colorectal polyps by the treatment. The genetic analysis revealed a C to A substitution at nucleotide 481 of her germline adenomatous polyposis coli gene, which resulted in a nonsense mutation at codon 161. CONCLUSIONS: Our case suggests that treatment with sulindac accompanied by intensive colonoscopic surveillance may be a choice of management for attenuated familial adenomatous polyposis.
Comparison of EUS and magnifying colonoscopy for assessment of small colorectal cancers.
BACKGROUND: Prediction of invasion depth and lymph node metastasis is mandatory when local treatment is considered for small colorectal cancer. The aim of this study was to compare the accuracy of EUS with a catheter probe (probe-EUS) and magnifying colonoscopy for prediction of invasion depth and lymph node metastasis for small colorectal cancer. METHODS: Small colorectal cancers were imaged by both probe-EUS and magnifying colonoscopy. Invasion depth by probe-EUS was determined by the presence or absence of distortion of the third sonographic layer. Findings by magnifying colonoscopy were divided into regular, distorted, and amorphous patterns. Histopathologically, depth of invasion was classified as intramucosa/slight or deep invasion. Findings by probe-EUS and magnifying colonoscopy were compared with respect to deep invasion and lymph node metastasis. RESULTS: There were 22 small colorectal cancers with intramucosa/slight invasion and 28 with deep invasion. Four of 30 cancers had associated lymph node metastasis. Accuracy for depth of invasion was 91.8% for probe-EUS and 63.3% in magnifying colonoscopy, the difference being statistically significant (p = 0.0013). Negative predictive value of probe-EUS for deep invasion was higher than that for magnifying colonoscopy (respectively, 90.9% vs. 54.1%) in the population studied (prevalence deep invasion 56%). The accuracy for lymph node metastasis was 24.1% for probe-EUS and 72.4% for magnifying colonoscopy, the difference being statistically significant (p < 0.001). Positive predictive value for lymph node metastasis was higher when the amorphous pattern was noted by magnifying colonoscopy compared with the positive predictive value for deep invasion by probe-EUS (respectively, 33.3% vs. 8.7%) in the population studied (prevalence lymph node metastasis 13.3%). CONCLUSIONS: Probe-EUS is superior to magnifying colonoscopy for determination of invasion depth in small colorectal cancer. Magnifying colonoscopy may be predictive of lymph node metastasis, thereby suggesting that the procedures provide complementary information with respect to the decision for local versus surgical therapy.
Does metronidazole cure cap polyposis by its antiinflammatory actions instead of by its antibiotic action? A case study.
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Critical role of gap junctions in endothelium-dependent hyperpolarization in rat mesenteric arteries.
1. Acetylcholine (ACh) evokes endothelium-dependent hyperpolarization in arterial cells, presumably through endothelium-derived hyperpolarizing factor (EDHF). The identity of EDHF is still elusive; however, several recent studies suggest the possible involvement of myoendothelial gap junctions in the EDHF response. 2. To elucidate the role of gap junctions in endothelium-dependent hyperpolarization, we examined the effects of the gap junction inhibitors 18 alpha-glycyrrhetinic acid (18 alpha-GA; 10(-4) mol/L) and carbenoxolone (3 x 10(-4) mol/L), a water-soluble form of 18 beta-GA, on hyperpolarization and relaxation to ACh in rat proximal and distal mesenteric arteries. Experiments were performed in the presence of indomethacin (10(-5) mol/L) and N(G)-nitro-L-arginine (10(-4) mol/L). 3. In both proximal and distal mesenteric arteries, ACh-induced hyperpolarization and relaxation were partially inhibited by 18 alpha-GA and abolished by carbenoxolone. 4. Endothelium-independent hyperpolarization to levcromakalim, an ATP-sensitive K+ channel opener, were unaffected by 18 alpha-GA or carbenoxolone in both arteries. 5. Relaxations to levcromakalim were unaffected by 18 alpha-GA, but were inhibited somewhat by carbenoxolone in proximal mesenteric arteries. 6. These findings suggest that myoendothelial gap junctions play a critical role in EDHF-mediated responses in both proximal and distal mesenteric arteries of the rat.
Glycoxidized low-density lipoprotein enhances monocyte chemoattractant protein-1 mRNA expression in human umbilical vein endothelial cells: relation to lysophosphatidylcholine contents and inhibition by nitric oxide donor.
Low-density lipoprotein (LDL) may undergo more glycation or oxidation in patients with diabetes mellitus than in nondiabetic subjects. We investigated whether glycoxidized LDL (goLDL) induces monocyte chemoattractant protein-1 (MCP-1) mRNA expression through activation of nuclear factor-kappaB (NFkappaB), and determined the effect of nitric oxide (NO) on MCP-1 mRNA expression in human umbilical vein endothelial cells (HUVEC). Oxidized (oxLDL) or goLDL enhanced MCP-1 mRNA expression in HUVEC, and preincubation with NOR3, a NO donor, abrogated such stimulation. goLDL increased NFkappaB-DNA binding activity in HUVEC and this effect was also suppressed by NOR3. We measured lysophosphatidylcholine (lyso-PC) contents in modified LDL using electrospray ionization liquid chromatography/mass spectrometry (LC/MS) to identify its molecular species. MCP-1 mRNA expression and NFkappaB activation correlated significantly with palmitoyl- and stearoyl-lyso-PC contents in LDL. Our results suggest that LDL modified by glycation and oxidation may contribute to the development of accelerated atherosclerosis in the presence of diabetes, a process that may be prevented by increased vascular NO availability.
Significance of appendiceal involvement in patients with ulcerative colitis.
BACKGROUND: The appendix is occasionally involved in patients with distal ulcerative colitis. This study investigated the clinical significance of patchy involvement at the appendiceal orifice in ulcerative colitis. METHODS: Colonoscopy was performed in 40 patients with active distal ulcerative colitis of mild to moderate severity. Patients were divided into 2 groups based on the presence or absence (positive or negative) of involvement at the appendiceal orifice at colonoscopy. Clinical activity, histologic grade of inflammation, and subsequent clinical course were compared between patients who were positive (appe(+)) and negative (appe(-)). RESULTS: Twenty-three patients had involvement at the appendiceal orifice (reddish mucosa with mucinous exudate). The proximal-most extent of involvement by ulcerative colitis, the endoscopic grade, and clinical activity were not different between appe(+) and appe(-) groups. However, histologic grade of inflammation in the ascending colon was higher in the appe(+) group than in the appe(-) group. The endoscopic remission rate at 12 months was higher in the appe(+) group than in the appe(-) group (84% vs. 40%, p < 0.05). CONCLUSIONS: In patients with distal ulcerative colitis, involvement at the appendiceal orifice may be indicative of histologically active disease, which responds reasonably well to pharmacotherapy.
Colonic aphthoid erosions as the only manifestation of tuberculosis: case report.
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EUS in the diagnosis of diffuse esophageal leiomyomatosis.
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GI involvement in Henoch-Schönlein purpura.
BACKGROUND: The diagnosis of Henoch-Schönlein purpura is difficult, especially when abdominal symptoms precede cutaneous lesions. The aim of this study was to determine the distribution of GI involvement in Henoch-Schönlein purpura. METHODS: Endoscopic or radiographic findings throughout the entire GI tract were retrospectively reviewed for 7 patients with Henoch-Schönlein purpura. Histopathologic findings were analyzed and correlated with findings at EGD and colonoscopy. OBSERVATIONS: The duodenum and small intestine were most frequently involved (6 patients, each site). Contrast radiography of the small intestine demonstrated thickened mucosal folds or small barium flecks. Findings at EGD were multiple irregular ulcers, mucosal redness and petechiae in the duodenum. In 4 patients, the second part of the duodenum was predominantly affected. Ulcerating lesions accompanied by hematoma-like protrusions were detected in 4 patients in whom leukocytoclastic vasculitis was proven histopathologically. CONCLUSIONS: EGD appears to have the greatest diagnostic utility in patients suspected to have Henoch-Schönlein purpura with GI involvement.
A rare case of ulcerative colitis complicating Wilson's disease: possible association between the two diseases.
A case of ulcerative colitis complicated by Wilson's disease is described. In this case, ulcerative colitis occurred 12 years after the diagnosis of Wilson's disease, and the colitis was intractable to prednisolone and salazosulfapyridine. Because copper is one of the trace elements necessary for antioxidant defenses during inflammatory process, altered copper metabolism may have contributed to the intractability of the ulcerative colitis in this case.
Angiotensin II receptor antagonist improves age-related endothelial dysfunction.
BACKGROUND: We previously demonstrated that the angiotensin converting enzyme (ACE) inhibitor, enalapril, prevents the age-related impairment of endothelium-dependent hyperpolarization and relaxation mediated by endothelium-derived hyperpolarizing factor (EDHF). OBJECTIVE: To test whether angiotensin II type 1 (AT1) receptor antagonists would also improve age-related endothelial dysfunction. METHODS: Normotensive Wistar-Kyoto (WKY) rats were treated for 3 months with either the AT1 receptor antagonist, candesartan cilexetil (3.5 mg/kg per day; candesartan group), or the ACE inhibitor, enalapril (20 mg/kg per day; enalapril group), from 9 to 12 months of age. Untreated 12-month-old WKY rats (old group) served as controls (n = 7-12). RESULTS: The two treatments decreased systolic blood pressure comparably. EDHF-mediated hyperpolarization in response to acetylcholine (ACh; 10(-5) mol/l) in the presence of norepinephrine in mesenteric arteries was improved in both the candesartan and enalapril groups to a similar extent compared with the old group (candesartan group, -24 +/- 3 mV; enalapril group, -21 +/- 2 mV; old group, -13 +/- 2 mV). EDHF-mediated relaxation was similarly improved in the candesartan and enalapril groups (maximum relaxation: candesartan group, 70 +/- 7%; enalapril group, 63 +/- 8%; old group, 33 +/- 9%). Hyperpolarization and relaxation responses to levcromakalim, an ATP-sensitive K+-channel opener, were similar in all groups. CONCLUSIONS: These findings suggest that the AT1 receptor antagonist is as effective as the ACE inhibitor in improving the age-related decline in EDHF-mediated hyperpolarization and relaxation in normotensive rats. Thus AT1 receptor antagonists might serve as novel tools with which to prevent endothelial dysfunction associated with aging.
The diagnostic yield of colonoscopy and the therapeutic value of intraduodenal amidotrizoic acid injection in intestinal Diphyllobothrium latum infection: report of a case.
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Central ghrelin modulates sympathetic activity in conscious rabbits.
Ghrelin is an orexigenic peptide originally isolated from the stomach. Intravenous administration of ghrelin has been shown to elicit a decrease in arterial pressure without a significant change in heart rate (HR), suggesting that ghrelin may act on the central nervous system to modulate sympathetic activity. The aim of the present study was to determine the central effects of ghrelin on cardiovascular and sympathetic responses in conscious rabbits. Intravenous injection of ghrelin elicited dose-related decreases in arterial pressure and HR, without a significant change in renal sympathetic nerve activity. On the other hand, intracerebroventricular injection of 1 nmol of ghrelin decreased arterial pressure, HR, and renal sympathetic nerve activity. Peak depressor or sympathoinhibitory responses of mean arterial pressure and renal sympathetic nerve activity (-19.0+/-1.5 mm Hg and -43.3+/-5.4%) were observed at 50 and 40 minutes, respectively, after intracerebroventricular injection of 1 nmol of ghrelin. Furthermore, a subdepressor dose of intracerebroventricular infusion of ghrelin (0.3 nmol/150 micro L per hour) significantly augmented the baroreflex sensitivities assessed by renal sympathetic nerve activity and HR compared with those of vehicle infusion (G(max); -17.8+/-3.1 versus -9.4+/-1.6%/mm Hg, P<0.05; -12.5+/-1.8 versus -6.6+/-1.2 bpm/mm Hg, P<0.05; respectively). These results suggest that intravenous injection of ghrelin acts, at least in part, on the central nervous system to decrease arterial pressure and renal sympathetic nerve activity, and that central ghrelin participates in the regulations of the sympathetic nerve activity to the kidney and the baroreceptor reflex in conscious rabbits.
Intracellular angiotensin II stimulates voltage-operated Ca(2+) channels in arterial myocytes.
Although the presence of intracellular angiotensin II (Ang II) and of Ang II-binding sites has been reported, their roles in cell function have not been fully clarified. The purpose of the present study was to test the hypothesis that intracellular Ang II modifies voltage-operated Ca(2+) channels in vascular smooth muscle. Ca(2+) channel currents were recorded in guinea pig mesenteric arterial myocytes with the whole-cell patch-clamp method. Intracellular dialysis of Ang II increased the amplitudes of Ca(2+) channel current (133 +/- 9% of the control with 10 nmol/L Ang II, n=16). Concomitant dialysis of the Ang II type 1 receptor antagonist, CV-11974 (1 micromol/L, n=11), but not the bath application of this drug, suppressed this Ang II action. In contrast, the dialysis of the Ang II type 2 receptor antagonist, PD123319 (1 micromol/L, n=5), failed to affect the Ang II action. Dialysis of either a phospholipase C inhibitor (U-73122, 10 micromol/L, n=5) or protein kinase C inhibitors (calphostin C, 100 nmol/L, n=5; protein kinase C inhibitor peptide-[19-36], 1 micromol/L, n=5) suppressed the Ang II action. Dialysis of KT5720 (100 nmol/L, n=5), an inhibitor of cAMP-dependent protein kinase, did not affect the Ang II action. Intracellular dialysis of angiotensin I (10 nmol/L) enhanced Ca(2+) channel currents (13 3 +/- 8%, n=6), which were sensitive to intracellular enalaprilat (1 micromol/L, n=5) or CV-11974 (n=5). These results suggest that intracellular Ang II has a stimulating action on voltage-operated Ca(2+) channels in vascular smooth muscle, possibly through intracellular binding sites similar to the Ang II type 1 receptor, which are associated with phospholipase C and protein kinase C.
Detection of angiotensin-converting enzyme gene insertion/deletion polymorphism from paraffin-embedded tissues: the Hisayama study.
Previous studies have suggested that archival materials from formalin-fixed paraffin-embedded blocks are unsuitable for most molecular techniques because the extracted DNA can be severely degraded. Therefore, the present study was designed to investigate the accuracy of genotyping for the insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene from paraffin-embedded tissues of autopsy cases from Hisayama Town, Japan. The genotype was determined using the double polymerase chain reaction method and to test the accuracy of the method, the polymorphism was investigated using paraffin-embedded tissues from 18 cases whose ACE genotypes (6 cases for each genotype) were known in advance from analysis of fresh-frozen tissue samples. Genotyping using paraffin-embedded tissues was then determined for 968 autopsy subjects. The genotype could be determined in 16 of the 18 test samples (88.9%) and there was no discrepancy with the results obtained from the fresh-frozen tissues. Of the 968 autopsy cases, the frequency of the DD, ID, and II genotypes was 12.4%, 47.3%, and 40.3%, respectively, a distribution that did not deviate from the Hardy-Weinberg equilibrium (chi(22df )= 0.67, p=0.72). These findings suggest the accuracy of the present method of ACE genotyping from paraffin-embedded tissues.