BACKGROUND:Helicobacter pylori stool antigen (HpSA) test is a new tool for evaluating the H. pylori infection. The present study was carried out to investigate the clinical usefulness of the HpSA test in the evaluation of eradication therapy by comparing it with the (13)C-urea breath test (UBT). METHODS:One hundred and five patients received eradication therapy for H. pylori. After more than 8 weeks, the success of the therapy was evaluated by the HpSA test and the UBT. Concordant results were regarded as a final diagnosis, but when the results were discordant, histological examination was carried out. RESULTS:Of the 105 patients receiving eradication therapy for H. pylori, 25 patients were regarded as H. pylori positive by the UBT and and 20 patients were regarded as H. pylori positive by the the HpSA test. Nine patients (8.6%) showed discordant results (seven cases with UBT(+) and HpSA(-), and two with UBT(-) and HpSA(+)). Five cases out of nine were ultimately judged as having a false-positive result of the UBT, and in these cases the UBT values were relatively low (below 10 per thousand). The final diagnostic accuracies of the UBT and the HpSA test were 94.3% (88.0-97.9%; 95% CI) and 97.1% (91.9-99.4%), respectively. When we used the HpSA test in cases with weakly positive UBT values, we were able to diagnose the correct status of H. pylori infection after eradication in 99% of all patients (94.8-100.0%). CONCLUSION:The HpSA test is a useful tool for the evaluation of eradication therapy and a combination of the HpSA test and UBT is clinically recommended.

BACKGROUND:We have previously shown BTEB2, a Krüppel-like zinc finger transcription factor, to regulate expression of the SMemb/NMHC-B gene, which has been implicated in phenotypic modulation of smooth muscle cells (SMCs). The present study was done to assess the developmental and pathological expression profiles of BTEB2 and to further evaluate the clinical relevance of BTEB2 expression in human coronary artery disease.METHODS AND RESULTS:Immunohistochemistry showed developmentally regulated expression of BTEB2 with abundant expression in fetal but not in adult aortic SMCs of humans and rabbits. In balloon-injured aortas, predominant expression of BTEB2 was seen in neointimal SMCs. Atherectomy specimens obtained from primary and restenotic lesions showed predominant expression of BTEB2 to stellate SMCs. The incidence of restenosis in primary lesions was significantly higher in lesions containing BTEB2-positive cells than in lesions without (55.6% versus 25.0%, P:=0.01).CONCLUSIONS:The present study shows that BTEB2 expression is developmentally and pathologically regulated. BTEB2 is preferentially expressed in dedifferentiated or activated SMCs. Examination of human coronary artery specimens suggests that primary lesions containing BTEB2-positive cells are associated with higher risk of restenosis than BTEB2-negative lesions. These results suggest that BTEB2 can serve as a molecular marker for phenotypic modulation of vascular SMCs.

A coronary stent was made radioactive by implantation of 133Xe ions for the purpose of suppressing the renarrowing of the part of blood vessel in which the stent is implanted. Electrons of relatively low energies emitted in the decay of 133Xe may give an antiproliferative effect of ionizing radiation to the intimal cells within a limited range of 1 mm. A 133Xe+ beam accelerated at 40 or 60 keV was directed to several stainless steel stents mounted on a target-holder table that could revolve and move up and down to distribute the 133Xe+ ions within a stent as well as among the stents. The radioactive stents produced contained up to 100 kBq of 133Xe and were implanted into the abdominal aortas of rabbits. Neointimal thickening was analyzed by histomorphometry for samples taken 4 weeks after stent implantation. The results indicate that the radioactive stents have a potential to suppress neointimal hyperplasia in rabbits.

A 23-year-old woman with heterozygous Fabry's disease who had acroparesthesia was admitted to hospital for precise examination of the disease before childbearing. She had no cardiac-related symptoms and no abnormality on physical examination. The alpha-galactosidase A activity in her leukocytes was present, but lower than normal. However, the endomyocardial biopsy showed specific changes for Fabry's disease. As Fabry's disease is a rare X-linked recessive inborn error of glycosphingolipid metabolism, heterozygous females are usually asymptomatic, but rarely can be affected as severely as hemizygous males. This is an isolated case of heterozygous Fabry's disease in a female in whom cardiac involvement was detected by endomyocardial biopsy, although she had no cardiac abnormality on physiological examinations. In conclusion, endomyocardial biopsy is useful for evaluation of the cardiac involvement of Fabry's disease even in an asymptomatic case.

We describe the novel karyotype of a 33-year-old woman with severe mental retardation and multiple cardiac anomalies, including patent ductus arteriosus, a ventricular septal defect, pulmonary atresia, and an overriding aorta. Her karyotype was 46, XX, add(17)(p13). The short arm of chromosome 17 was slightly elongated owing to the deletion of the distal portion of that chromosome and the addition of extra material from another chromosome. Miller-Dieker syndrome is characterized by a patent ductus arteriosus, lissencephaly, and the deletion of chromosome 17p13.3; however, as the patient's brain surface appeared normal on computed tomography, Miller-Dieker syndrome was excluded. The breakpoint in her chromosome 17 was probably located distal to band 17p13.3. In fact, fluorescence in situ hybridization analysis demonstrated that band 17p13.3 was intact. To date, genes distal to 17p13.3 have not been implicated in cardiac anomalies. This patient probably carries a novel deletion on the short arm of chromosome 17.

Vascular smooth muscles contain at least three types of developmentally regulated myosin heavy-chain (MHC) isoforms; SM1, SM2, and SMemb. By investigating the expression of the three MHC isoforms, we previously demonstrated in rabbits that smooth muscles proliferating in the neointima of arterio- and atherosclerotic lesions regain an "embryonic" phenotype. In the present study, we examined if neointimal cells are morphologically similar to embryonal smooth muscles and if dedifferentiation of neointimal smooth muscles is a reversible process. Vascular injury was produced in rabbits either by endothelial cell denudation of the aorta or by poststenotic dilation of the carotid artery. We have demonstrated in this study that the proliferating neointimal cells expressed SM1 and SMemb, but not SM2, indicating smooth muscles of an "embryonic" phenotype. The dedifferentiation of neointimal smooth muscles was found to be reversible; at 4 to 8 weeks after injury, a majority of the cells reexpressed both SM1 and SM2, but not SMemb. By electron microscopy, we have revealed smooth-muscle phenotypes determined by MHC isoforms to correspond to the morphologic phenotypes as an increase in membranous organelles, and a decrease in myofilaments was associated with the reexpression of SMemb. Interestingly, we also found that in the medial wall at 4 to 8 weeks after ballooning injury, a number of SM1-negative cells proliferated rapidly, replacing normal smooth muscles. These cells were negative against SM1 and SM2 but positive for SMemb. These SM1-negative cells contained abundant membranous organelles and few myofilaments. These cells did not express SM1 or SM2 even after 8 weeks postinjury. We conclude from these results that the proliferating synthetic-type smooth muscles after vascular injury are composed of SM1-positive cells that are morphologically similar to embryonal smooth muscle and that maintain ability to redifferentiate, and SM1-negative cells that contain few myofilaments and remain dedifferentiated.

The angiotensin-converting enzyme (ACE) inhibitor enalapril was administered to 13 patients with chronic heart failure (New York Heart Association class II or III) for 12 weeks, and its effects on resting cardiac function (shown by echocardiogram), exercise capacity, and biochemical factors were investigated. Left ventricular end-diastolic and end-systolic diameters improved significantly from 60.3 ± 5.4 mm at baseline to 57.2 ± 5.7 mm after 12 weeks of treatment and from 50.2 ± 5.9 mm to 46.8 ± 5.6 mm, respectively; however left atrial dimension did not change significantly after treatment. Peak oxygen uptake also improved significantly after enalapril treatment (20.0 ± 6.9 mL/kg/min at baseline to 22.4 ± 7.6 mL/kg/min after treatment), as did anaerobic threshold by gas exchange (17.1 ± 6.4 mL/kg/min vs 18.4 ± 5.8 mL/kg/min). The serum levels of atrial natriuretic peptide and beta-endorphin decreased significantly after treatment (47.6 ± 42.1 pg/mL before vs 31.6 ± 29.2 pg/mL after treatment and 11.6 ± 3.6 pg/mL vs 5.9 ± 2.8 pg/mL, respectively). These results indicated that enalapril is useful for improving resting cardiac function, exercise capacity, and biochemical factors in patients with chronic heart failure.

The association between the lack of adrenergic symptoms during hypoglycemia and myocardial I-123-metaiodobenzylguanidine (MIBG) accumulation was investigated in 12 insulin-treated non-insulin-dependent diabetes mellitus (NIDDM) patients who had no evidence of heart disease, These patients were divided into 2 groups according to the presence (group A) or absence (group B) of adrenergic symptoms during hypoglycemia. Autonomic function tests revealed significantly severe autonomic dysfunction in group B compared to that in group A, Insulin infusion test indicated no significant difference in the catecholamine response between the two groups. I-123-MIBG scintigraphy showed that the heart/mediastinum ratio of MIBG uptake was significantly lower, and scintigraphic defect was greater in group B than in group A. There were no significant differences in the washout rate between the two groups, These results suggested that the lack of adrenergic symptoms during hypoglycemia may be associated with cardiac sympathetic nervous dysfunction in insulin-treated NIDDM patients, and this dysfunction is mainly due to cardiac sympathetic denervation.

For the purpose of achieving emergency hemostasis of a ruptured hepatocellular carcinoma (HCC) or prevention of such rupture, we applied a new method of transcatheter therapy: intra-arterial alcoholization. Five patients with a ruptured HCC and 42 with an impending rupture were treated by intra-arterial injection of absolute ethanol mixed with an equal volume of iodized oil, Lipiodol (EtOH-Lp). The tumor size ranged from 4 to 26 cm (mean 7.8 cm) in diameter. The catheter tip was placed in the segmental branch or a more distal position of the hepatic artery, and 2–40 (mean 10.6) ml of EtOH-Lp was infused under fluoroscopic guidance. Infiltration of ethanol into the HCC mass was recognized as a dense deposition of Lipiodol on plain abdominal X-rays and computed-tomography. In all five cases of ruptured HCC, hemostasis was achieved. In all 42 cases of impending rupture, tumor rupture was prevented, and all except 3 patients could be discharged. No significant complication of the gastrointestinal tract or biliary tract was seen. The incidence and severity of postembolization syndrome were markedly lower than those seen in cases treated with Gelfoam embolization.