Search PubMed⌕ Search

Biomedical subjects

A Takagi

Publications and source records attributed to A Takagi.

At least 127 records · Page 7Linked to original sources

Prevention of Helicobacter pylori infection by lactobacilli in a gnotobiotic murine model.

BACKGROUND: Helicobacter pylori is a bacterium which causes gastric inflammatory diseases. Oral inoculation of H pylori usually results in only a temporary colonisation without a successful infection in the stomach of conventional mice in which lactobacilli are the predominant indigenous bacteria. AIM: To determine whether lactobacilli exert an inhibitory effect on colonisation by H pylori in the stomach. METHODS: The effects of H pylori on attachment to murine and human gastric epithelial cells and the H pylori mediated release of interleukin-8 (IL-8) by these cells were examined in vitro. Lactobacillus salivarius infected gnotobiotic BALB/c mice and control germ free mice were inoculated orally with H pylori to examine whether L salivarius can inhibit colonisation by H pylori. RESULTS: L salivarius inhibited both the attachment and IL-8 release in vitro. H pylori could not colonise the stomach of L salivarius infected gnotobiotic BALB/c mice, but colonised in large numbers and subsequently caused active gastritis in germ free mice. In addition, L salivarius given after H pylori implantation could eliminate colonisation by H pylori. CONCLUSION: These findings suggest the possibility of lactobacilli being used as probiotic agents against H pylori.

Animals↗

Clinical analysis of abdominal aortic aneurysms associated with iliofemoral occlusive disease.

Patients with abdominal aortic aneurysm (AAA) associated with iliofemoral occlusive disease due to arteriosclerosis obliterans (ASO) are often encountered clinically, but their clinical characteristics remain poorly defined. We divided 275 patients undergoing aneurysmectomy into 2 groups: 58 patients with both AAA and ASO (Group A) and 217 patients with AAA only (Group B). General characteristics, morphological features of the aneurysms, surgical procedures and operative results were then compared between the groups. In Group A, ruptured aneurysms were significantly less common (p = 0.005) and the aneurysms were smaller (p = 0.0009). The most common cause of death in Group A was acute myocardial infarction (3/7), in contrast to aneurysmal rupture of another arterial segment and malignancy (6/27, each) in Group B. These findings indicate that patients with AAA and ASO represent a subgroup of patients with particular clinical features.

Aged↗

Perforin-secreting killer cell infiltration in the aortic tissue of patients with atherosclerotic aortic aneurysm.

Cell-mediated immunity has been implicated in the pathogenesis of vascular cell injury in patients with atherosclerotic aortic aneurysms. To clarify the immunologic mechanisms involved, we examined the expression of a cytolytic factor, perforin, in infiltrating cells from aortic tissue samples taken from 6 patients with atherosclerotic aortic aneurysms. Immunohistochemical studies showed that the infiltrating cells consisted mainly of macrophages, natural killer (NK) cells, cytotoxic T lymphocytes (CTLs), and T helper cells, and that perforin was expressed in NK cells and CTLs. Immunoelectron microscopic studies demonstrated that the infiltrating cells released massive amounts of perforin directly on to the surface of arterial vascular cells. These findings provide the first direct evidence that some of the infiltrating cells in the aortic tissue consist of killer cells, and strongly suggest that these killer cells, especially NK cells and CTLs, may play a critical role in the vascular cell injury caused by atherosclerotic aortic aneurysm by releasing perforin.

Aged↗

Flagellin gene diversity among Helicobacter pylori strains and IL-8 secretion from gastric epithelial cells.

BACKGROUND: To clarify the pathological functions of the virulence factors of Helicobacter pylori, a comparative analysis was carried out on the relationship between motility, flagellar gene polymorphism, vacuolating cytotoxin (VT) production and interleukin-8 (IL-8) induction. METHODS: Twenty-five strains were examined for restriction fragment length polymorphism (RFLP) of the flagellin gene. Motility was measured using semisolid agar plates. Cytotoxicity was assayed using RK-13 cells. IL-8 secretion was assessed by the enzyme-linked immunosorbent assay (ELISA) methods. RESULTS: H. pylori was classified into four groups according to their flagellar RFLP. No differences were noted in motility or VT production among the four groups, but a significant difference was noted in IL-8 induction. In addition, highly motile strains produced more IL-8. CONCLUSION: This flagellar genetic polymorphism may be associated with IL-8 induction.

Animals↗

[Autosomal dominant distal myopathy with rimmed vacuoles and cytoplasmic inclusions: report of a family].

We reported four patients with distal myopathy in the same family. Muscle weakness and atrophy started in the lower extremities, especially in the calf muscle, and it extended to the upper extremities and pelvic muscles to a variable extent. Facial and bulbar muscles were slightly involved in one case. The anterior tibial muscle tended to be better preserved than the calf muscle. Cardiac abnormalities were absent in any case. Serum creatine kinase activity was normal or mildly elevated. Skeletal muscle biopsies revealed myopathic process presenting rimmed vacuoles, eosinophilic cytoplasmic inclusions and/or subsarcolemmal mass. Ultrastructurally, cytoplasmic inclusions were composed of electron dense granular material and intermediate-sized filaments. There were membranous whorls and myelin-like figures which were the characteristic findings of rimmed vacuoles. Immunohistochemistry revealed accumulation of desmin, dystrophin and vimentin in the cytoplasm of degenerating muscle fibers and in the inclusion. In present patients, cardiac function was normal and the tibialis anterior muscle was relatively spared. These features were different from the autosomal dominant rimmed-vacuolar myopathy with desmin storage described in previous reports.

Adult↗

[Two cases of adenosquamous cell carcinoma of advanced cervical cancer treated by carboplatin-based chemotherapy with peripheral blood stem cell autotransplant].

In two cases with adenosquamous cell carcinoma of advanced cervical cancer, carboplatin-based chemotherapy was given intraarterially from the internal iliac artery as neoadjuvant chemotherapy, and peripheral blood stem cells (PBSCs) were harvested. After the operation, conventional intravenous chemotherapy with PBSC autotransplant was performed. PBSCs were mobilized by neoadjuvant chemotherapy and G-CSF administration. By the apheresis procedures, 0.7-2.6 x 10(6)/kg CD34 positive cells were obtained. They had no severe side effects from intravenous chemotherapy with PBSCT, and they were free of disease 20 months. Neoadjuvant chemotherapy and G-CSF administration may be capable of mobilization of PBSCs, and chemotherapy with PBSCT may be useful in radioresistant advanced adenosquamous carcinoma of the cervical cancer.

Adult↗

[Molecular pathology of malignant hyperthermia and central core disease].

Recent advances of research on malignant hyperthermia(MH) were reviewed. The rate of Ca-induced Ca release(CICR) from the sarcoplasmic reticulum(SR) was measured on the skinned muscle fiber preparation of porcine and human MH. The rate of CICR was significantly increased both in porcine and human MH. These observations supported conclusion obtained by genetical studies that the ryanodine receptor (RYR1) was site of abnormality in most of porcine and part of human MH. The RYR1 is Ca release channel of skeletal muscle SR and CICR is one of main function of the channel. Subsequently, point mutation of RYR1 gene was found in the foot domain of the molecule. Heretofore, 9 kind of mutations were described in association of MH-susceptible(MHS) trait. 4 of them were accompanied by a form of congenital myopathy, central core disease(CCD). CCD is considered as an allelic disease of MH. But pathogenesis of peculiar morphological abnormality of CCD is mostly unknown. Mutations are identified only in half of familial MH cases, suggesting MH is heterogeneous. Recently, it was reported that mutation of the dihydropyridine receptor gene was associated with MHS in a french family. The dihydropyridine receptor is distributed on the transverse tubule membrane and constitutes the triad structure with RYR1.

Alleles↗

Restricted usage of T-cell receptor Valpha-Vbeta genes in infiltrating cells in aortic tissue of patients with Takayasu's arteritis.

BACKGROUND: Infiltration by perforin-secreting killer lymphocytes, such as T cells and natural killer cells, has been shown to be involved in the pathogenesis of vascular cell damage in Takayasu's arteritis. METHODS AND RESULTS: To investigate the immunological mechanisms involved, especially the nature of T-cell infiltration in Takayasu's arteritis as well as atherosclerosis, we analyzed the expression of T-cell receptor (TCR) Valpha and Vbeta genes in infiltrating cells in the aortic tissue of patients with Takayasu's arteritis and the atherosclerotic aortic aneurysm by polymerase chain reaction (PCR). We also analyzed the expression of cytokine genes by PCR. We found that the repertoires of TCR Valpha as well as Vbeta gene transcripts in Takayasu's arteritis were restricted. The infiltrating cells expressing Valpha2, Valpha16, Valpha17, Vbeta7, and Vbeta13.1 were found in 3 of 4 patients. In contrast, TCR Valpha-Vbeta repertoires in atherosclerotic aortic aneurysm were polyclonal. There was no significant difference in the pattern of cytokine gene expression between the two diseases. CONCLUSIONS: The restricted usage of TCR Valpha as well as Vbeta genes by infiltrating T cells in Takayasu's arteritis may indicate that a specific antigen in the aortic tissue was targeted. Our findings provide the evidence that distinct immunological mechanisms are involved in the pathogenesis of Takayasu's arteritis and atherosclerotic aortic aneurysm.

Aged↗

Oxidative DNA damage and cell proliferation in the livers of B6C3F1 mice exposed to pentachlorophenol in their diet.

Pentachlorophenol (PCP), which has been used as a wood preservative, was reported to be a liver carcinogen in mice. To investigate the initial effects of PCP administration under the same conditions of exposure as in the carcinogenic study, we examined oxidative stress and cell proliferation, along with other hepatotoxicological parameters, in the livers of B6C3F1 mice fed PCP in their diet at doses of 0.03, 0.06, and 0.12% for up to 4 weeks. We observed significant increases of 8-OHdG levels in hepatic nuclear DNA at doses of 0.03% and above at 2 and 4 weeks. Likewise, dose-dependent increases in the labeling index of cells were detected by counting those that had incorporated 5-bromo-2'-deoxyuridine throughout the experimental period. Also, we found significant elevations of the liver weights, concurrent with increases in hepatic DNA content in the treated mice, which again were dose-related. Serum aspartic transferase activity at doses of 0.06% and above were significantly increased despite these changes being slight. Also, histopathological examination provided no evidence of necrotic changes, but severe hepatocyte swelling in the treated mouse livers. These data indicate that PCP might be able to induce cell proliferation in the mouse liver, as well as induce oxidative DNA damage, suggesting both changes may play an important role in hepatocarcinogenesis.

Animals↗

Isomer-specific acute toxicity and cell proliferation in livers of B6C3F1 mice exposed to dichlorobenzene.

The acute hepatotoxicity of isomers of dichlorobenzene (o-, m-, and p-DCB) was compared in livers of male B6C3F1 mice at different time points after a single intragastric administration. The highest doses of o-, m-, and p-DCB administered, 300, 300, and 1800 mg/kg, respectively, are below the lethal range. Acute hepatic injury was assessed by serum alanine aminotransferase (ALT) activity and hepatic histology. Hepatocyte replication was estimated by means of immunohistochemical demonstration of BrdU-labeled cells. Both o-DCB and m-DCB at a dose of 300 mg/kg produced significant elevations of liver weight and ALT activity as well as extensive liver cell necrosis. In contrast, p-DCB at a highest dose of 1800 mg/kg induced slight hepatocyte injury. Dose-response studies indicated that the rank order for acute hepatotoxicity of the isomers was m-DCB > o-DCB > or = p-DCB. However, p-DCB induced hepatocyte cell proliferation in spite of the lack of manifest hepatotoxicity. In contrast, increases of cell proliferation due to o- or m-DCB exposure occurred only after dosages that caused hepatic injury. These data suggest the hepatocyte proliferation induced by o- or m-DCB is compensatory regeneration while that induced by p-DCB is a response to mitogenic stimulation.

Acute Disease↗

Magnetic resonance imaging of patients with large vestibular aqueducts.

The vestibular aqueduct (VA) and endolymphatic sac (ES) were examined by magnetic resonance imaging in eight patients (14 ears) with large VAs, and the results were compared with those obtained in five normal volunteers (10 ears). It was not possible to identify either the VA or ES in any of the control ears. However, in all the 14 ears with a large VA, the VA was detected as a fluid-filled structure. In 12 ears the ES was seen to be markedly enlarged and also filled with fluid. In one ear, the volume of the fluid-filled space within the VA and ES was measured as 912 mm3 on serial images. Five patients (ten ears) were observed to have a fluid-filled VA and enlarged ES without cochlear anomalies and reported frequent episodes of sudden hearing loss and vertigo following exercise, long exposure to sunshine, minor trauma and the like. Two other patients (three ears) also had enlarged VA and ES as well as cochlear anomalies, but did not have episodes of sudden hearing loss and vertigo. These findings suggest that direct transmission of intracranial pressure changes to the inner ear or subsequent movement of endolymph in patients with a large VA may adversely influence a seemingly normal cochlea and vestibule.

Adult↗

Fine structural changes of muscle spindles in the gracile axonal dystrophy mutant mouse.

Fine structural changes of muscle spindles in the extensor digitorum longus of the gracile axonal dystrophy mutant mouse were studied from 20 to 120 postnatal days. Degenerative nerve endings in muscle spindles were first recognized at 20 postnatal days. The sensory nerve endings were usually swollen with decrease of cell organelles, and the cytoplasm was electron-lucent. At 50 postnatal days, atrophic nerve endings were frequently observed in the narrow spaces between the indented cell membrane of intrafusal muscle cells and the basement membrane. In addition to degenerative and atrophic changes, regenerative axons showing fine sprouts (with or without Schwann cell projections) appeared in the sensory nerve endings at this time. At 80 postnatal days, sensory nerve endings frequently showed dystrophic changes characterized by axonal dilatation with accumulations of neurofilaments, tubulovesicular structures, mitochondria and myelin-like figures. These findings suggest that axonal transport in the sensory nerve endings is impaired in this mutant mouse. Motor nerve endings were usually well preserved and normal structures even at 80 postnatal days. Intrafusal fibrosis, decrease in number of sensory nerve endings and atrophy of intrafusal muscle fibres were clearly recognized by 100 days of age.

Aging↗

Use of a nondissection method in lower extremity revascularization: a report on our 12-year experience of autogenous vein bypass surgery.

We report herein on our 12-year experience of performing autogenous vein grafting in the lower extremity using a nondissection method. This method involves limiting preparation for the distal anastomosis to exposure of the anterior surface of the vascular sheath, and substituting an Esmarch's rubber bandage or a pneumatic tourniquet for vascular clamps. A series of 86 consecutive patients who received 101 autogenous vein grafts employing this method were retrospectively analyzed. The causes of arterial occlusion were atherosclerosis in 55 patients, Buerger's disease in 23, and other causes in 9. There was one operative death, and 12 late deaths were recorded within a follow-up period extending to 12 years. Of four early occlusions and two stenoses, three were successfully revised within 30 days of surgery. A total of 11 revision operations were required for 10 grafts during the follow-up period, and late graft closure occurred in 9 bypasses. The primary, primary revised, and secondary patency rates at 5 years for the entire series (n = 101) were 65%, 85%, and 86%, respectively, with 42 bypasses to the tibial or peroneal artery having 84% primary revised and 86% secondary patency rates. These findings led us to conclude that minimization of the surgical injury at the distal anastomosis contributed to the long-term patency of the distal bypass.

Adult↗

Bleeding gastric varices as a result of splenic vein compression by a celiac arterial aneurysm.

Celiac arterial aneurysms are very unusual and often lack clinical manifestations. According to our review of the literature, this is the first report of a patient with a large celiac arterial aneurysm who exhibited hematemesis from gastric varices. Arteriography, as well as color Doppler ultrasonography and enhanced computed tomography, contributed to the diagnosis of this aneurysm, which was best exposed by a left thoracoabdominal approach. In this patient the lesion was a false aneurysm with perforation of the celiac artery, so simple closure of the orifice was carried out and the revascularization of the celiac artery was not necessary, but we should take care not to ignore the possible recurrence of vascular lesions. The risk of celiac arterial aneurysm rupture is relatively high, but the operative mortality of unruptured aneurysms is now so low that operation is strongly recommended for all patients with this type of aneurysm.

Aneurysm↗

Structural organization and promoter activity of the human ryudocan gene.

To better understand the regulation of ryudocan (syndecan-4) expression, we have determined the structural organization of the human ryudocan gene. The human ryudocan gene extends approximately 24 kilobases and is divided into five exons, which appear to be conserved in syndecan family members. Exon I encodes the signal peptide; exons II-IV, the extracellular domain; and exon V, the transmembrane and cytoplasmic domains, which are highly homologous among syndecan family members. Primer extension analysis showed that human ryudocan gene had a single transcription initiation site, located 3 bases upstream from the described cDNA [Kojima et al. (1993) BBRC 190, 814-822]. The 5'-flanking sequences of human ryudocan gene contain a TATA-like sequence as well as a variety of other potential binding sites for transcription factors, including Sp1, Ap-2, NF-kB, E-alpha H box, H4TF-2, and LBP-1, and were capable of functioning as a promoter. The determination of the human ryudocan gene structure will allow elucidation of constitutive, cell-specific, tissue-specific, and developmentally regulated expression.

Animals↗