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Biomedical subjects

M Ueno

Publications and source records attributed to M Ueno.

At least 19 recordsLinked to original sources
PubMed2001

Structural characterization of heparan sulfate and chondroitin sulfate of syndecan-1 purified from normal murine mammary gland epithelial cells. Common phosphorylation of xylose and differential sulfation of galactose in the protein linkage region tetrasaccharide sequence.

Syndecan-1, present on the surfaces of normal murine mammary gland epithelial cells, is a transmembrane hybrid proteoglycan, which bears glycosaminoglycan (GAG) side chains of heparan sulfate (HS) and chondroitin sulfate (CS). Purified syndecan-1 ectodomains were analyzed for disaccharide composition and the GAG-protein linkage region after digestion with bacterial lyases. The HS chains contained predominantly a nonsulfated unit with smaller proportions of two monosulfated, two disulfated, and a trisulfated unit, whereas CS chains were demonstrated for the first time to bear GlcUA-GalNAc(4-O-sulfate) as a major component as well as GlcUA-GalNAc, GlcUA-GalNAc(6-O-sulfate), and an E disaccharide unit GlcUA-GalNAc(4,6-O-disulfate) as minor yet appreciable components. Two kinds of linkage region tetrasaccharides, GlcUA-Gal-Gal-Xyl and GlcUA-Gal-Gal-Xyl(2-O-phosphate), were found for the HS chains in a molar ratio of 55:45. In marked contrast, an additional sulfated tetrasaccharide, GlcUA-Gal(4-O-sulfate)-Gal-Xyl, was demonstrated only for the CS chains, and the unmodified phosphorylated and sulfated components were present at a molar ratio of 55:26:19. The present study thus provided conclusive evidence for the hypothesis that 4-O-sulfation of Gal is peculiar to CS chains in contrast to the phosphorylation of Xyl, which is common to both HS and CS chains. These modifications may be required for biosynthetic maturation of the linkage region tetrasaccharide sequence, which is a prerequisite for creating the repeating disaccharide region of GAG chains and/or biosynthetic selective chain assembly of CS and HS chains.

Animals↗
PubMed2001

Delayed functional recovery by vincristine after sciatic nerve crush injury: a mouse model of vincristine neurotoxicity.

Neuropathy is the dose-limiting side effect of vincristine (VCR) in cancer therapy. However, no simple experimental model has yet been reported. Here, we present a simple experimental model of VCR neurotoxicity using a mouse sciatic nerve crush model, which allows evaluation within a few weeks. VCR administered intravenously once on the day after the crush lesion caused a dose-dependent delay of the recovery of motor and sensory functions. The minimal dose required to cause the delay was 0.25 mg/kg, which corresponded to five times the usual clinical dose for man and was far less than the reported doses required to cause functional impairment in intact animals. The model would be useful not only for the development of new drugs but also for the estimation of the drug interactions in combination cancer therapy.

Animals↗
PubMed2001

Ultrastructural and permeability features of microvessels in the periventricular area of senescence-accelerated mice (SAM).

Brain transfer of intravenously injected horseradish peroxidase (HRP) and the ultrastructural features of the vessels were examined in periventricular areas in senescence-accelerated mice (SAMP8), which show age-related deficits in learning and memory, and senescence-accelerated resistant mice (SAMR1), which do not show age-related deficits. In all mice examined with light microscopy, staining reaction for HRP was seen in the periventricular area adjacent to the medial side of the lateral ventricle. Electron microscopic examination in the periventricular area of young and old mice of both strains showed that the staining reaction for HRP appeared in the vesicular profiles of the endothelial cytoplasm, the cytoplasm of the perivascular cells, the basal lamina, and the adjoining extracellular spaces of the white matter, suggesting an incomplete blood-brain barrier (BBB) in the periventricular white matter. In addition, irregularly thickened endothelial cell cytoplasm, membranous inclusions within the basal lamina, and electron-dense endothelial cell cytoplasm were occasionally seen in aged SAMP8 mice. These findings were not observed in 3-month-old SAMP8 mice and 3- and 13-month-old SAMR1 mice. Perivascular collagen deposits were also frequently seen in aged SAMP8 mice. These findings indicate that the endothelial cells and pericytes in the periventricular white matter in aged SAMP8 mice have an ultrastructure with damaged BBB function. Intravascular substances can easily penetrate the periventricular white matter and the BBB of the vessels in the area can be deteriorated with aging in SAMP8 mice.

Aging↗
PubMed2001

Microemulsion formed by alkyl polyglucoside and an alkyl glycerol ether with weakly charged films.

We have studied the effects on phase equilibria of a nonionic surfactant mixture-water-oil system when replacing small amount of surfactant molecules by ionic surfactant, sodium dodecyl sulfate (SDS). The nonionic surfactant system contains dodecyl-beta-D-maltoside (C(12)AG2) and iso-octyl glyceryl ether (i-C(8)GE) as cosurfactant, water and cyclohexane at constant water to oil ratio of 60/40 (w/w). Adding a small amount of SDS has large impact on the phase behavior. Clear liquid crystalline phase and upper microemulsion phase are added to the phase sequence at high i-C(8)GE/(C(12)AG2+i-C(8)GE) ratio. We also compare the phase equilibria of pure dodecyl maltoside system with polyglucosides mixture system.

Journal Article↗
PubMed2001

Schizosaccharomyces pombe taf1+ is required for nitrogen starvation-induced sexual development and for entering the dormant GO state.

Environmental change, such as nutritional starvation, induces physiological and morphological alterations that enable fission yeast cells to survive. We isolated a novel gene, taf1+, required for the response to nitrogen starvation in the fission yeast Schizosaccharomyces pombe. taf1 disruptants could not mate upon nitrogen starvation, but could upon carbon starvation. taf1 disruptants had a defect in inducing stell+ expression under nitrogen starvation conditions. Furthermore, they lost viability quickly in nitrogen-depleted medium. Unlike wild-type cells, starved taf1-cells had nuclear chromatin that were flat and adhered to the cell periphery. These results indicate that tqf1+ is required for nitrogen starvation-induced sexual development and entering the dormant G0 state.

Amino Acid Sequence↗
PubMed2001

alpha-1-Antichymotrypsin gene A1252G variant (ACT Isehara-1) is associated with a lacunar type of ischemic cerebrovascular disease.

alpha-1-Antichymotrypsin (ACT) is a plasma protease inhibitor belonging to the serpine superfamily; it has many functions. and thus qualitative change in ACT is likely to result in specific diseases. We previously reported a variant AACT (ACT Isehara-1, Met389Val, A1252G) in patients with ischemic cerebrovascular disease (CVD). The present study was designed to examine the association of the variant with ischemic CVD, in 87 patients and 397 age-matched controls. We found that the frequency of the A1252G variant (ACT Isehara-1) was higher in the group with ischemic CVD than in the control group (P = 0.0397), which appeared to be independent of known risk factors. We subdivided the CVD group into lacunar and atherothrombotic subgroups. Further analysis by subtype of ischemic CVD showed an association of ACT Isehara-1 with lacunar infarction (P = 0.0036). These results suggest that ACT lsehara-1 is a new genetic risk factor for ischemic CVD, especially lacunar-type infarction, in Japan.

Adult↗
PubMed2001

Effects of aging and blood pressure on the structure of the thoracic aorta in SAM mice: a model of age-associated degenerative vascular changes.

The effects of aging and blood pressure on the structural alterations of the thoracic aorta were examined using male, accelerated senescence-prone, short-lived SAMP11 mice or accelerated senescence-resistant, long-lived SAMR1 mice. The aortic wall thickness increased significantly by 34% in SAMR1 and by 62% in SAMP11 with advanced age. We observed branching, breakage and disorganization of the elastic lamellae, an increase in thin collagen fibrils between the medial smooth muscle cells and hypertrophy but a significant decrease in the number of medial smooth muscle cells with aging in both strains. These alterations observed in SAMP11 occurred earlier and were more exaggerated with advanced age than in SAMR1. The aortic lumen dilated gradually in SAMR1, but narrowed significantly in SAMP11 with aging. The systolic blood pressure did not differ significantly among SAMP11s aged 3-9months, or among all ages of SAMR1. However, it was elevated in SAMP11 at the terminal stage of their life. Our results suggest that the aorta in SAMR1 might reflect the physiological process of aging, whereas SAMP11 showed earlier changes due to the senescence acceleration of the vascular cells, which were exaggerated by the elevated blood pressure.

Aging↗
PubMed2001

Characterization of a newly established cell line derived from human adrenocortical carcinoma.

BACKGROUND: ACT-1, a new cell line of human adrenocortical carcinoma, has been established and successfully maintained in culture. This study examined the biological characteristics of the cells. METHODS: The tumor cells were isolated from a surgical specimen of the tumor thrombus and cultured in monolayer. RESULTS: Histologically, the primary tumor was composed of a solid proliferation of large polygonal cells. A part of the atrophic adrenal cortex remained at the periphery of the tumor. The cultured ACT-1 cells were spindle-shaped in morphology and grew exponentially with an approximate population doubling time of 24 h. A chromosomal analysis revealed a modal number of 61 with consistent structural abnormalities of add(3)(q11), add(9)(p11), and add(16)(ql1). The expression of 3beta-hydroxysteroid dehydrogenase was observed in the ACT-1 cells as well as in normal human adrenal glands. CONCLUSIONS: The ACT-1 cell line provides a reproducible model system which gives good insight into the oncogenesis of adrenocortical carcinoma.

Adrenal Cortex Neoplasms↗
PubMed2001

Expression of osteopontin in gentamicin-induced acute tubular necrosis and its recovery process.

BACKGROUND: There is controversy regarding the exact localization and roles of osteopontin (OPN), a multipotential chemokine, in renal injury. There is little information on the expression and role of OPN in gentamicin-induced acute tubular necrosis (ATN) and its recovery process. METHODS: A severe ATN model was made using male Wistar rats by injecting gentamicin (150 mg/kg/day) for five days and limiting the provision of water. The expression and localization of OPN mRNA and protein, ED1 as a macrophage marker, proliferating cellular nuclear antigen (PCNA), CD44 as an OPN receptor, megalin as a proximal tubule marker, and their relationships to each other were examined from the early tubular necrotic period to the late recovery period by Northern blotting, in situ hybridization, and double immunohistochemical staining. RESULTS: In the gentamicin group, OPN mRNA and protein were expressed in only the PCNA-positive proliferating cortical distal tubules, not in the necrotic proximal tubules, until day 6 after the first administration, but were found markedly in PCNA-positive regenerative proximal and distal tubules on days 10, 15, and 30. The localization of PCNA-positive cells was almost always accompanied with the up-regulated expression of OPN using quantitative analysis (P < 0.01). CD44 expression was markedly up-regulated in the renal cortical tubular epithelium from days 6 to 30. In the control group, no expression of OPN and CD44 in the cortical area was found throughout the experimental period. CONCLUSIONS: These results suggested that OPN is related to the proliferation and regeneration of tubular epithelial cells after tubular damage.

Animals↗
PubMed2001

Novel glomerular lipoprotein deposits associated with apolipoprotein E2 homozygosity.

BACKGROUND: Hyperlipoproteinemia is occasionally associated with severe glomerular injury caused by abnormal accumulation of lipid in glomeruli, which occurs in conditions such as lipoprotein glomerulopathy (LPG). This study investigates the cases of two siblings with homozygous apolipoprotein (apo) E2 who show unique histologic features, massive proteinuria, and dysbetalipoproteinemia. METHODS: Histologic studies were performed using renal biopsy specimens. Plasma lipoproteins were extensively characterized. The exons of the apo E genes were sequenced to avoid missing any mutations. RESULTS: Histologically, the siblings' condition resembled LPG by light microscopy studies. Electron microscopy studies revealed large lipoid deposits in the paramesangium, subendothelium, and subepithelium of the glomeruli, which were different from LPG in terms of not forming the layered structure resembling a fingerprint even in large lipoprotein thrombi, and mesangial foam cells. Immunohistochemically, the lipoid deposits contained apo E and apo B. These patients did not have either diabetic nephropathy or other known forms of glomerulonephritis. The sequence of exons of the apo E genes revealed homozygosity for apo E2 in both cases. CONCLUSION: The extensive lipoprotein deposition in glomeruli, which resembles LPG, can also occur in apo E2 homozygous individuals, but in a distinct fashion. Because the two cases were siblings, they may have other shared alleles, in addition to the apo E2 allele, that negatively affect processing of lipoproteins and lead to abnormal accumulation of lipoprotein deposits in glomeruli.

Amino Acid Sequence↗
PubMed2001

Therapeutic time-window of a group IIA phospholipase A2 inhibitor in rabbit acute lung injury: correlation with lung surfactant protection.

OBJECTIVE: We attempted to determine whether group IIA secretory phospholipase A2 (sPLA2-IIA) blockade after the onset of lung injury exerted therapeutic efficacy in the treatment of oleic acid (OA)-induced acute lung injury by using S-5920/LY315920Na, a novel specific inhibitor of sPLA2-IIA, with special interest in the changes of lung surfactant. DESIGN: Prospective animal study. SETTING: University laboratory. SUBJECTS: Forty Japanese white rabbits. INTERVENTIONS: The rabbits, under anesthesia, were endotracheally intubated and mechanically ventilated and then were divided into the following groups: OA + vehicle groups, intravenous infusion of OA for the first 2 hrs (0.1 mL x kg(-1) x hr(-1)) with the addition of vehicle (1 or 2 hrs after OA administration, each n = 9, total 18 rabbits); OA + S-5920/LY315920Na groups, treated identically to the OA control with the addition of S-5920/LY315920Na (1 mg/kg bolus followed by infusion at 0.5 mg x kg(-1) x hr(-1)) after OA (1 or 2 hrs after OA administration, each n = 9, total 18 rabbits); saline control groups, treated with saline instead of OA with the addition of vehicle (1 hr after OA administration, 4 rabbits). Arterial blood gas, lung mechanics, lung inflammation, lung surfactant phospholipids, and production of inflammatory mediators in the lung were measured. MEASUREMENTS AND MAIN RESULTS: Treatment with S-5920/LY315920Na 1 hr after OA infusion, but not 2 hrs after infusion, significantly attenuated the lung injury, as estimated by hypoxemia, decreased lung compliance, pulmonary edema, and vascular permeability. The therapeutic efficacy was similar to that found in our previous pretreatment study. The treatment after 1 hr dramatically inhibited OA-induced surfactant degradation in the bronchoalveolar lavage fluid (BALF), without affecting the concentrations of thromboxane A2, leukotriene B4, and interleukin-8 in BALF. The degree of surfactant degradation in BALF paralleled well with the severity of the lung injury. Furthermore, recombinant human sPLA2-IIA reproduced the similar hydrolysis pattern of isolated surfactant in vitro, which was inhibited by S-5920/LY315920Na. CONCLUSIONS: Our results indicate that therapeutic blockade of sPLA2-IIA ameliorated lung dysfunction via protection of surfactant degradation in an animal model of acute lung injury, and they suggest a new strategy in treating clinical acute lung injury.

Acetates↗
PubMed2001

Determination of optimal blood pressure for patients with IgA nephropathy based on renal histology.

To evaluate the optimal BP control for patients with IgA nephropathy (IgAN) based on the histologic severity of the nephropathy and the degree of renal dysfunction. We analyzed 332 consecutive renal biopsy specimens and clinical data from patients with IgAN. Patients were divided into three groups based on their BP at the time of biopsy: an optimal BP (SBP<120 mmHg and DBP<80 mmHg), a hypertensive BP (SBP > or = 140 mmHg and/or DBP > or = 90 mmHg), and an intermediate BP group. Each biopsy specimen was evaluated for mesangial proliferation, degree of sclerosis and/or hyalinosis of the arterioles and the interlobular artery using a semiquantitative method. Creatinine clearance and the percentage of sclerosed glomeruli were also determined. Both the degree of renal dysfunction and the histologic changes correlated significantly with BP, even in patients with a BP <140/90 mmHg. The patients with an optimal BP at the time of biopsy had significantly less histologic damage with respect to mesangial proliferation and vessel changes than those with an intermediate or hypertensive BP. In the patients with a hypertensive BP, the percentage of sclerotic glomeruli was significantly higher and the creatinine clearance was significantly lower. The optimal BP proposed by the WHO in 1999 prevents histologic evidence of renal damage for patients with IgAN.

Adult↗
PubMed2001

Rhabdomyolysis triggered by an asthmatic attack in a patient with McArdle disease.

We describe a patient with McArdle disease who developed rhabdomyolysis triggered by a bronchial asthmatic attack. A 64-year-old man had chronic pulmonary emphysema with asthma, and an asthmatic attack led to severe rhabdomyolysis that required continuous hemodiafiltration. After 2 years, a physical examination revealed atrophy of the extremities compared with previous examinations, especially of the intercostal muscles. During that time, he suffered two severe bronchial asthmatic attacks. His serum level of creatinine kinase remained between 4,000 and 7,000 IU/l when he did not suffer from asthmatic attacks and rhabdomyolysis had abated. Therefore, we suspected that his recent muscle atrophy was caused by asthmatic attacks, and discussed the possibility of his respiratory muscle weakness due to McArdle disease in relation to his severe bronchial asthmatic attacks as well as chronic obstructive pulmonary disease.

Asthma↗
PubMed2001

[Left adrenocortical cancer with inferior vena cava tumor thrombus--a case report].

An 62-year-old male was admitted to our hospital for an evaluation of high grade fever, body weight loss and lumbago. He was diagnosed as having a left adrenal tumor with intracaval extension and underwent a radical surgery, including resection of the tumor, left kidney, spleen and IVC tumor thrombus. Histopathological diagnosis was adrenocortical carcinoma with tumor thrombus. To our knowledge, our case seems to be the 8th case report of left adrenocortical cancer with tumor thrombus extension into IVC. Average survival of reported cases was about 15 months. At 4 months after surgery, the patient died due to lung metastasis.

Adrenal Cortex Neoplasms↗
PubMed2000

The delivery of protein into living cells by use of membrane fusible erythrocyte ghosts.

We examined the effects of pretreatment of monkey kidney normal cells (CV-1) and human cervical tumor cells (HeLa) with membrane fusible erythrocyte ghosts (MFEG) encapsulating superoxide dismutase (SOD-MFEG) on adriamycin (ADM) cytotoxicity. The decrease in CV-1 cells with ADM was inhibited markedly, and the initiation of decrease in HeLa cells was delayed for 2 days by the pretreatment with SOD-MFEG, indicating that the delivered SOD held the activity in the cells.

Animals↗
PubMed2000

Possible association of thioredoxin and p53 in breast cancer.

Expression of thioredoxin (TRX), a dithiol-reducing enzyme, and mutations of p53 have been detected in various cancer tissues. We recently reported that TRX-dependent redox regulation plays a crucial role in DNA binding activity of p53. In this study, we investigated the possibility of functional association between TRX and p53 in breast cancer. First, we examined the expression of TRX and mutated p53 in 100 primary breast cancer tissues by immunohistochemistry. Expression of TRX was detected in cases of 84/100 (84%) and expression of p53, which means existence of mutated p53, in cases of 63/100 (63%). TRX positive cases was 89% (56/63) in mutant p53 positive cases. Next, we examined the expression of TRX and p53 in breast cancer cell line MCF-7 cells after CDDP treatment or irradiation. CDDP treatment or irradiation augmented expression of TRX and p53 in MCF-7 cells by western blotting. Immunofluorescence cell analysis by confocal microscopy showed that CDDP treatment induced translocation of TRX into nuclei. These results suggest the possible association of TRX with p53-dependent function including DNA repair in breast cancer.

Adult↗
PubMed2000

Dendritic cell-like immunoreactivity in the glomerulus of the olfactory bulb and olfactory nerves of mice.

Dendritic cell-like immunoreactivity was examined in the mouse brain. The glomerulus of the olfactory bulb and the olfactory nerves were stained by antibodies against the dendritic cells, NLDC-145 and MIDC-8, while these structures were not stained by antibodies against microglia or macrophages, F4/80, Mac1 or CD45. Immunoelectron microscopy showed that the immunoreaction for NLDC-145 was localized to the sheath and presynaptic terminals of the olfactory nerves. These findings suggest that the sheath and presynaptic terminals of the primary olfactory nerves have some degree of the antigenicity in common with dendritic cells.

Animals↗