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Biomedical subjects

Y Ando

Publications and source records attributed to Y Ando.

At least 37 records · Page 2Linked to original sources
PubMed2004

Near-infrared spectrophotoscopy of finger venules in assessment of autonomic dysfunction.

The authors evaluated morphologic changes in the venules of the finger using near-infrared spectrophotoscopy in patients with autonomic dysfunction, such as familial amyloidotic polyneuropathy and multiple-system atrophy. Abnormalities of the venules, such as tortuosity, irregular venous caliber, and microaneurysm-like change, and a linear negative correlation between the degree of orthostatic hypotension and the degree of vasoconstriction of the venules were observed.

Adult↗
PubMed2004

Smallest carbon nanotube is 3 a in diameter.

Previous energetic considerations have led to the belief that carbon nanotubes (CNTs) of 4 A in diameter are the smallest stable CNTs. Using high-resolution transmission electron microscopy, we find that a stable 3 A CNT can be grown inside a multiwalled carbon nanotube. Density functional calculations indicate that the 3 A CNT is the armchair CNT(2,2) with a radial breathing mode at 787 cm(-1). Each end can be capped by half of a C12 cage (hexagonal prism) containing tetragons.

Journal Article↗
PubMed2004

Physical and functional interaction between BH3-only protein Hrk and mitochondrial pore-forming protein p32.

Bcl-2 homology domain (BH) 3-only proteins of the proapoptotic Bcl-2 subfamily play a key role as initiators of mitochondria-dependent apoptosis. To date, at least 10 mammalian BH3-only proteins have been identified, and it is now being realized that they have different roles and mechanisms of regulation in the transduction of apoptotic signals to mitochondria. Hrk/DP5 is one of the mammalian BH3-only proteins implicated in a variety of physiological and pathological apoptosis, yet the molecular mechanism involved in Hrk-mediated apoptosis remains poorly understood. In an attempt to identify cellular proteins participating in Hrk-mediated apoptosis, we have conducted yeast two-hybrid screening for Hrk-interacting proteins and isolated p32, a mitochondrial protein that has been shown to form a channel consisting of its homotrimer. In vitro binding, co-immunoprecipitation, as well as immunocytochemical analyses verified specific interaction and colocalization of Hrk and p32, both of which depended on the presence of the highly conserved C-terminal region of p32. Importantly, Hrk-induced apoptosis was suppressed by the expression of p32 mutants lacking the N-terminal mitochondrial signal sequence (p32(74-282)) and the conserved C-terminal region (p32 (1-221)), which are expected to inhibit binding of Hrk competitively to the endogenous p32 protein and to disrupt the channel function of p32, respectively. Furthermore, small interfering RNA-mediated knockdown of p32 conferred protection against Hrk-induced apoptosis. Altogether, these results suggest that p32 may be a key molecule that links Hrk to mitochondria and is critically involved in the regulation of Hrk-mediated apoptosis.

Amino Acid Sequence↗
PubMed2004

Targeted conversion of the transthyretin gene in vitro and in vivo.

Familial amyloidotic polyneuropathy (FAP) is the common form of hereditary generalized amyloidosis and is characterized by the accumulation of amyloid fibrils in the peripheral nerves and other organs. Liver transplantation has been utilized as a therapy for FAP, because the variant transthyretin (TTR) is predominantly synthesized by the liver, but this therapy is associated with several problems. Thus, we need to develop a new treatment that prevents the production of the variant TTR in the liver. In this study, we used HepG2 cells to show in vitro conversion of the TTR gene by single-stranded oligonucleotides (SSOs), embedded in atelocollagen, designed to promote endogenous repair of genomic DNA. For the in vivo portion of the study, we used liver from transgenic mice whose intrinsic wild-type TTR gene was replaced by the murine TTR Val30Met gene. The level of gene conversion was determined by real-time RCR combined with mutant-allele-specific amplification. Our results indicated that the level of gene conversion was approximately 11 and 9% of the total TTR gene in HepG2 cells and liver from transgenic mice, respectively. Gene therapy via this method may therefore be a promising alternative to liver transplantation for treatment of FAP.

Amyloid Neuropathies↗
PubMed2003

Long-term follow-up study of HTLV-I infection in bottle-fed children born to seropositive mothers.

Human T-lymphotropic virus Type-I (HTLV-I) infects children via mother's milk. Infection of Human T-lymphotropic virus Type-I (HTLV-I) was investigated by long-term follow-up surveys of modified milk-fed children. Our observations of modified milk-fed infants revealed that: 1 of 154 (0.6%) at year 1, 5 of 129 (3.9%) at 1.5 years, and 5 of 108 (4.6%) at year 2 were anti-HTLV-I antibody-positive. No infants or children became newly antibody-positive thereafter. Modified milk feeding could prevent the HTLV-I infection of infants from mothers in many cases, however the infants who had became anti-HTLV-I antibody-positive due to established infection by the age 2 remained positive at age 11-12 with persistent infections. Modified milk-fed infants who had been born from HTLV-I seropositive mothers did not show that they had complete protection from HTLV-I infection, but a low infection rate was seen, showing that modified milk feeding is useful to protect from HTLV-I infection.

Animals↗
PubMed2003

Long-term follow up study of vertical HTLV-I infection in children breast-fed by seropositive mothers.

Infection of Human T-lymphotropic virus type-I (HTLV-I) was investigated by long-term follow up surveys of mother's milk-fed infants. HTLV-I infections of infants via seropositive mother's milk, that is, anti-HTLV-I antibody-positive infants, increased in number up to the age 2, but no infants became antibody-positive thereafter. Infants who had became antibody positive by age 2 remained so at age 11-12. HTLV-I infection via feeding with mother's milk was established by the age 2. While in epidemiologic surveys an increase of the anti-HTLV-I antibody-positive rate has been reported, this survey revealed that after acquisition of HTLV-I from breast feeding, there was no further horizontal transmission prior to puberty.

Breast Feeding↗
PubMed2003

Relapse of neonatal herpes simplex virus infection.

BACKGROUND: Neonatal herpes simplex virus (HSV) infection is a severe disease with high mortality and morbidity. Recurrence of skin vesicles is common. OBJECTIVE: To determine the features of relapse and identify the factors related to relapse. DESIGN: Thirty two surviving patients with neonatal herpes virus infections were enrolled. All patients received acyclovir treatment. Clinical and virological data were analysed and compared between relapsed and non-relapsed cases. RESULTS: Thirteen (41%) had either local skin or central nervous system relapse between 4 and 63 days after completing the initial antiviral treatment. Nine patients exhibited local skin relapses, and four developed central nervous system relapses. In one skin and two central nervous system relapse cases, neurological impairment later developed. Type 2 virus infection was significantly related to relapse (odds ratio 10.4, 95% confidence interval 1.1 to 99.0). Patients with relapse had worse outcomes than those without relapse. CONCLUSION: Neonates with HSV type 2 infections have a greater risk of relapse. Relapsed patients have poorer prognoses.

Acyclovir↗
PubMed2002

ABO-incompatible auxiliary partial orthotopic liver transplant for late-onset familial amyloid polyneuropathy.

A 60-year-old Japanese man with late-onset familial amyloid polyneuropathy type I (FAP transthyretin Met30) showed clinical improvement following auxiliary partial orthotopic liver transplantation (APOLT) from an ABO-incompatible living related donor. Preoperatively, plasmapheresis and immunosuppressant drugs were used to reduce serum antibodies against the donor's ABO type. APOLT was chosen so the residual liver could sustain the patient in the event of hyperacute rejection. OLT is applicable to late-onset FAP transthyretin Met30, and APOLT can be considered in ABO-incompatible cases.

ABO Blood-Group System↗
PubMed2002

Changes in osteoprotegerin and markers of bone metabolism during glucocorticoid treatment in patients with chronic glomerulonephritis.

It is well known that long-term glucocorticoid treatment causes osteoporosis, but the precise mechanism remains unclear. Recently, osteoprotegerin (OPG) has been identified as a cytokine that inhibits osteoclast differentiation. We have previously demonstrated that serum OPG is suppressed by glucocorticoids. Therefore, the present study was carried out to clarify the interrelationships between OPG and other markers of bone metabolism during glucocorticoid treatment. Thirteen patients (7 men, 6 women; 44.1 +/- 5.9 years old) with chronic glomerulonephritis who were to be treated with glucocorticoids for the first time were chosen for this study. Markers of bone metabolism, including serum OPG, osteocalcin (OC), bone-specific alkaline phosphatase activity (bAP), parathyroid hormone (PTH), tartrate-resistant acid phosphatase (TRAP), and bone mineral density (BMD), were measured before and during the treatment period. Glucocorticoids significantly reduced BMD of the lumbar spine in the 6 month treatment period (p < 0.01). Serum OPG was decreased significantly by glucocorticoids within 2 weeks (p < 0.001), and serum TRAP, a marker of bone resorption, was markedly increased (p < 0.001). On the other hand, there were no remarkable changes in serum PTH. Serum OC and bAP, markers of bone formation, were transiently reduced during the treatment period (p < 0.01). Furthermore, only serum OPG was positively and independently correlated with percentage BMD of age-matched reference (%AMR). These findings imply that glucocorticoid-induced bone loss develops rapidly via enhanced bone resorption and suppressed bone formation. Moreover, the increased bone resorption caused by glucocorticoids may be, at least in part, mediated by inhibition of OPG, not increment of PTH.

Adult↗
PubMed2002

Reduction of free radical activity in amyloid deposits following liver transplantation for familial amyloidotic polyneuropathy.

OBJECTIVES: Liver transplantation halt the progress of familial amyloidotic polyneuropathy (FAP). Oxidative stress has been implicated in amyloid toxicity and formation. The objective of this study was to establish whether markers for oxidant stress and antioxidant capacity change following liver transplantation in patients with FAP. DESIGN: Morphometric and biochemical study. SETTING: Tertiary referral centre. SUBJECTS: Duodenal biopsy samples from 16 patients, taken before and after liver transplantation were used for morphometry. Serum samples from 14 patients, seven of whom had received transplants, were analysed regarding antioxidant capacity. INTERVENTION: Liver transplantation. MAIN OUTCOME MEASURES: Immunohistochemistry was used to stain for the lipid peroxidation product 4-hydroxynonenal (HNE), and Congo red staining was used for amyloid detection. Positive areas were quantified by point counting. Total antioxidant capacity (TAC) was measured with a colourimetric assay. RESULTS: In tissue, a decrease of HNE was noted after liver transplantation, whereas no significant changes were detected for amyloid deposits. No difference between transplanted and not transplanted patients was noted for total antioxidant capacity measured in serum. CONCLUSION: To our knowledge, this is the first description of a reduction of markers for free radical activity after cessation of amyloid formation. The findings implicate that amyloid formation in transthyretin (TTR) amyloidosis generates oxidative stress, whereas amyloid deposits as such are less toxic to sourrounding tissues.

Adult↗
PubMed2002

Effect of ticlopidine hydrochloride on erythropoietin-induced rise in blood pressure in patients on maintenance hemodialysis.

BACKGROUND/AIMS: A recent observation that antiplatelet-aggregation drugs, including ticlopidine hydrochloride, may prevent erythropoietin (EPO)-induced rise in blood pressure in hemodialysis (HD) patients remains a subject of particular interest. The aim of the present study was to determine the effect of ticlopidine hydrochloride on EPO-induced rise in blood pressure of HD patients with special reference to blood levels of vasoactive substances. METHODS: HD patients who showed hypertension or aggravation of preceding hypertension with EPO treatment were selected for this study. Ticlopidine hydrochloride was administered at a dose of 200 mg daily for 4 weeks. Blood pressure and serum levels of nitric oxide (NO), atrial natriuretic peptide (ANP) and endothelin (ET) were determined before and after drug administration. Patients were divided into two groups, one of which showed a drop in mean blood pressure (MBP) of >10 mm Hg (group I) and one which did not (group II), and a comparison was made between them with respect to the blood parameters. RESULTS: Five of 15 patients showed a drop of MBP of >10 mm Hg (group I), and 10 patients did not show any change in MBP (group II). In group I, there was a significant increase in blood NO levels compared to the concentrations before ticlopidine administration, while there was no change in group II. With respect to ANP and ET, there was no significant change in either of the groups. CONCLUSION: The findings suggest that the preventive effect of ticlopidine hydrochloride on EPO-induced rise in blood pressure may partly be related to the enhancement of NO production in patients on maintenance HD.

Adult↗
PubMed2002

[Platelet activation in obstructive sleep apnea syndrome].

The incidences of cardiovascular and cerebrovascular diseases are reportedly higher in patients with obstructive sleep apnea (OSA) than in OSA-free subjects, though the mechanism remains unknown. Recently, the contribution of activated platelets to a number of pathological conditions such as stroke or ischemic heart disease has been suggested. We hypothesized that the expression of activated platelet markers resulting from OSA might be higher than in healthy subjects. By flow cytometry using monoclonal antibodies, we measured two such markers, PAC-1 and CD 62 P, in OSA patients and healthy subjects. Twelve healthy men (age, 52.7 +/- 12.8 y/o; and body mass index (BMI), 22.2 +/- 16.1 kg/m2; mean +/- S.D.) and 20 male patients with OSA (age, 50 +/- 7.96 y/o; BMI, 28.1 +/- 3.3 kg/m2; apnea hypopnea index (AHI), 38.2 +/- 21.2 times/hr; and lowest SpO2, 75.6 +/- 11.3%) were enrolled in this study. PAC-1 expression was significantly higher in OSA patients (65.1 +/- 17.8%) than in healthy subjects (16.8 +/- 7.4%), as was CD 62 P expression (8.5 +/- 8.8% vs. 0.88 +/- 0.57%). The increase in PAC-1 expression was correlated with AHI and the arousal index. These findings suggest that activated platelet markers could be good indicators for untreated OSA.

Adult↗
PubMed2001

Gene expression analysis in human monocytes, monocyte-derived dendritic cells, and alpha-galactosylceramide-pulsed monocyte-derived dendritic cells.

In vitro proliferation and functional activation of V alpha 24NKT cells following stimulation with alpha-galactosylceramide (alpha-GalCer)-pulsed dendritic cells (DCs) have been observed. Because little is known about the molecular events on DCs following interaction with alpha-GalCer, we performed gene expression profiling of 2400 genes in monocytes and monocyte-derived immature DCs pulsed with alpha-GalCer (alpha-GalCer-imDCs). Overall, the expression levels of 48 genes were up-regulated and 28 were down-regulated in alpha-GalCer-imDCs. Semiquantitative RT-PCR analysis on monocytes, imDCs, alpha-GalCer-imDCs, and mature DCs confirmed the up- and down-regulation of the mRNA expression levels of 28 selected genes. Notably, we identified the specific up-regulation of mRNA expression levels of ribonuclease A and collapsin response mediator protein upon the stimulation of imDC with alpha-GalCer, suggesting a novel immunomodulating effect of alpha-GalCer on imDCs. In this study, we used imDCs prepared by culturing of monocytes with GM-CSF and IL-4 for 5 days and mDCs prepared by further culturing of imDCs with TNF alpha for two extra days.

Cell Differentiation↗
PubMed2001

Prognostic value of performance status assessed by patients themselves, nurses, and oncologists in advanced non-small cell lung cancer.

Accuracy in the assessment of performance status by oncologists has not been well evaluated. We investigated possible discrepancies in the assessment of performance status among patients, nurses, and oncologists, and evaluated the prognostic importance of each assessment. Two hundred and six inpatients with inoperable, advanced non-small cell lung cancer were investigated prospectively. Weighted Kappa statistics for inter-observer agreement were 0.53 between oncologists and patients and 0.63 between oncologists and nurses. There was a significant difference among the assessments by the three groups (P < 0.001). Oncologists gave the healthiest performance status assessment, nurses an intermediate assessment, and patients the poorest. When included separately in the Cox model, the assessment by each group was significantly correlated with survival. However, the assessment by the patients themselves failed to distinguish survival of patients with performance status 1 and 2. Among the three models including patient-, nurse-, and oncologist-assessed PS, that including oncologist-assessed PS best fitted to the observed survival data. These results showed that the assessment by the patients themselves is different from those by the nurses and the oncologists and provided additional support for the use of the assessment by oncologists in clinical oncology.

Aged↗