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Biomedical subjects

Takako Saito

Publications and source records attributed to Takako Saito.

18 recordsLinked to original sources
PubMed2006

Prospective assessment of proliferative diabetic retinopathy with observations of posterior vitreous detachment.

PURPOSE: To study the relation between posterior vitreous detachment (PVD) and progression of diabetic retinopathy (DR), based on our observation that proliferative DR is rare in patients with complete PVD. METHODS: The medical records of 403 patients with diabetes were reviewed for the relation between progressive DR and the status of PVD and HbA(1c) over 3 years. PVD was classified into none, complete PVD with collapse, complete PVD without collapse, partial PVD with a thickened posterior vitreous cortex, and partial PVD without a thickened posterior vitreous cortex. DR was classified into none, simple, preproliferative, or proliferative. When it became more extensive or when laser treatment or vitreous surgery was performed, the DR was considered progressive. RESULTS: Progression of DR over 3 years occurred in 128/292 (43.8%) eyes with no PVD, 0/14 (0%) eyes with complete PVD with collapse, 2/8 (25%) eyes with complete PVD without collapse, 15/15 (100%) eyes with partial PVD with a thickened posterior vitreous cortex, and 19/74 (25.7%) eyes with partial PVD without a thickened posterior vitreous cortex. Progression of DR occurred significantly more frequently in eyes with partial PVD with a thickened posterior vitreous cortex compared to eyes with complete PVD with collapse (p<0.0001). HbA(1c), did not differ significantly between these two groups (6.9 +/- 0.9% and 7.5 +/- 0.9%, respectively; p = 0.14), although HbA(1c) was significantly higher (p = 0.04) in patients with progressive DR (78 +/- 1.8%) than in patients without progressive DR (7.5 +/- 1.5%). CONCLUSION: Complete PVD is a strong negative risk factor for DR. The PVD status in patients with diabetes should be evaluated.

Diabetic Retinopathy↗
PubMed2005

Human parvovirus B19 infection of monocytic cell line U937 and antibody-dependent enhancement.

Human parvovirus B19 (B19) infects human erythroid lineage cells. Accumulating evidence also shows that B19 is detectable in nonerythroid lineage cells in vivo, but the mechanism of infection is still not clear. In this study, we explored the mode of B19 infection of human monocytic cell line U937. An in vitro infection study demonstrated B19 binding of U937 and slow replication of B19-DNA with B19-NS1 mRNA transcription. B19-DNA replication in U937 was accompanied by undetectable level of B19-VP1 mRNA transcription, indicating that B19 infection of U937 cells may be abortive. Levels of B19-DNA and B19-NS1 mRNA transcription increased in the presence of anti-B19 IgG antibodies, but this effect decreased in the presence of anti-Fc receptor antibodies, showing antibody-dependent enhancement by B19 infection. Antibody-dependent enhancement also caused the increased production of TNFalpha in U937. This study is the first to suggest B19 infection of nonerythroid lineage cells with antibody-dependent enhancement.

Antibodies, Viral↗
PubMed2005

Alteration in risk factor accumulations of acute myocardial infarction during the last one decade: analysis of patients admitted in Coronary Care Unit.

The present study was undertaken to determine accumulation of risk factors in acute myocardial infarction during two periods of 2002 and 1990-1991. We collected 173 and 153 patients with acute myocardial infarction in 2002 and 1990-1991, respectively, and analyzed the history of multiple risk factors, including diabetes mellitus, impaired glucose tolerance, hyperlipidemia, hypertension and obesity, and laboratory findings. The numbers and their percentages of all the risk factors increased in 2002 compared with 1990-1991. According to plasma glucose level, the patients who had type 2 diabetes mellitus, and impaired fasting glucose or impaired glucose tolerance had increased markedly from 41 to 65%. Multiple accumulation of risk factors had increased during the last one decade, and only one or no risk factor per se was not the case in the patients with acute myocardial infarction. Hyperlipidemia and hypertension became fairly controlled in the patients, but not hyperglycemia in type 2 diabetes mellitus in the period of 2002. These findings may indicate that increased multiple accumulation of risk factors accelerates the occurrence of acute myocardial infarction in 2002 as compared to 1990-1991.

Blood Glucose↗
PubMed2005

Hypertonicity regulates the aquaporin-2 promoter independently of arginine vasopressin.

BACKGROUND: Aquaporin-2 (AQP-2) is an arginine vasopressin (AVP)-regulated water channel in kidney collecting duct cells. The present study was undertaken to determine whether a change in tonicity could directly regulate the AQP-2 gene in an in vitro experiment. METHODS: Various fragments of the 5'-flanking region of the murine AQP-2 gene up to -9.5 kb were cloned into a luciferase (Luc) reporter plasmid, and they were transiently transfected into Madin-Darby canine kidney cells. RESULTS: Hypertonicity significantly increased the Luc activity of the constructs containing >6.1 kb of the 5'-flanking region of the AQP-2 gene (-6.1AQP2). However, promoter regions <4.3 kb in length containing the tonicity-responsive enhancer (TonE) at bp -570 to -560 were not stimulated by hypertonicity. The TonE-deleted construct which contains -9.5 to -1.1 kb of the 5' side of the AQP-2 gene, 8.4AQP2, was also stimulated by hypertonicity. Mitogen-activated protein (MAP) kinase inhibitors SB203580 and U0126 did not affect the Luc activity of -6.1AQP2 induced by hypertonicity. In addition, the vector expressing dominant-negative TonE-binding protein (TonEBP) did not affect the hypertonicity-induced Luc activity of -6.1AQP2. The Luc activity of -6.1AQP2 was stimulated by the overexpression of TonEBP. Hypertonicity further increased the Luc activity of -6.1AQP2 under the overexpression of TonEBP. CONCLUSION: These findings indicate that hypertonicity regulates AQP-2 promoter activity via an AVP-independent mechanism, and that the tonicity-responsive element resides between the -6.1 and -4.3 kb 5'-flanking region of the AQP-2 gene, in which the structure and mechanism of response to hypertonicity could be distinct from those of TonE.

5' Flanking Region↗
PubMed2005

Tetracycline protects myocardium against ischemic injury.

Stress pretreatments protect myocardium from ischemic injury. We hypothesized that tetracycline, an antibiotic, may induce a stress response via the inhibition of mitochondrial translation as it induces the cold stress response by translational inhibition in E. coli. If so, tetracycline may protect myocardium from ischemic injury as stress pretreatments do. Thus, we investigated the effects of tetracycline on myocardial ischemia and its association with stress response. In a dog model of acute ischemia, 4mg/kg tetracycline injected 30 min prior to the occlusion improved the functional recovery from stunning of myocardium caused by ischemia. The same dosage of tetracycline dramatically reduced the size of infarct area in murine hearts analyzed by tetrazolium staining. In HeLa cells, tetracycline induced molecules that were increased by cold stress, which suggests that tetracycline may induce a cold stress-like response in mammalian cells. These molecules were also induced by ischemic stress in murine hearts, suggesting that the stress response caused by translational inhibition in mitochondria may be associated with the cardioprotection by tetracycline. Our results suggest that a subclinical dosage of tetracycline may protect heart from ischemic injury. Therefore, tetracycline may be of great use in suppressing the development of infarction caused by myocardial ischemia. This study is also important for providing new insights into the non-antimicrobial effects of tetracycline and its derivatives.

Animals↗
PubMed2005

Close association of hypoadiponectinemia with arteriosclerosis obliterans and ischemic heart disease.

Adiponectin is an adipose-derived cytokine, and it is suggested that hypoadiponectinemia increases the prevalence of ischemic heart disease (IHD). The present study was undertaken to determine serum adiponectin levels in patients with arteriosclerosis obliterans (ASO) and IHD. Forty-nine patients with ASO and 49 age-, sex-, and body mass index-matched control subjects were examined. The diagnosis of ASO was derived from an ankle brachial index of less than 0.90 and stenotic or obstructive change in angiogram. Ischemic heart disease was diagnosed by ischemic or stenotic change in ECG, treadmill, or coronary angiogram. Serum adiponectin level was 8.6 +/- 0.9 microg/mL in the patients with ASO, a value significantly less than that of 12.4 +/- 1.0 microg/mL in the control subjects ( P < .01). Next, we subgrouped the subjects into 4 groups according to the presence of ASO and IHD. Serum adiponectin levels were 9.4 +/- 1.5 and 10.2 +/- 1.6 microg/mL in the subjects with ASO (n =23) and those with IHD (n = 13), respectively. It was further reduced to 7.9 +/- 1.2 microg/mL in the subjects having both ASO and IHD (n = 26), a value significantly less than that of 13.2 +/- 1.4 microg/mL in the control subjects (n = 36; P < .05). Serum high-density lipoprotein cholesterol was significantly less in the subjects with ASO than in the control subjects (42.1 +/- 1.7 vs 48.5 +/- 2.0 mg/dL; P < .05), but there were no differences in blood pressure, total cholesterol, low-density lipoprotein cholesterol, triglyceride, and uric acid levels. The present results indicate that a reduction in serum adiponectin level is associated with the prevalence and magnitude of systemic atherosclerosis including IHD and ASO.

Adiponectin↗
PubMed2005

Elevation of serum adiponectin levels in Basedow disease.

The present study was undertaken to determine whether thyroid hormone affects serum adiponectin levels in the patients with Basedow disease. Sixty-four patients with Basedow disease were examined; 32 patients had hyperthyroid state and 32 patients had euthyroid state who had been treated with antithyroid drugs. In addition, 30 age- and sex-matched subjects served as a control. Serum adiponectin, free T4, free T3, thyroid-stimulating hormone, and thyroid-stimulating hormone receptor antibody (TRAb) were measured. Serum adiponectin levels were 12.9+/-1.6 microg/mL in the hyperthyroid state, a value significantly greater than that of 8.2 +/- 0.5 microg/mL in the euthyroid state (P<.05) and that of 8.6+/-0.7 microg/mL in the control subjects (P<.05). Serum adiponectin levels had positive correlations with either of serum free T4 (r=0.453, P<.001), free T3 (r=0.47, P< .001), or TRAb (r= 0.491, P<.001), but not with body mass index. Multiple regression analysis showed TRAb had the strongest contribution to serum adiponectin concentration in the patients with Basedow disease. The present findings indicate that hyper-adiponectinemia is closely associated with increases in serum thyroid hormone levels and TRAb in Basedow disease.

Adiponectin↗
PubMed2005

[Big five personality factors related to face recognition].

The present study examined whether scores on big five personality factors correlated with face-recognition response time in visual search paradigm. Sixty adjectives were used to measure personality scores of 60 participants along the five factors of Extroversion, Neuroticism, Openness to Experience, Agreeableness, and Conscientiousness. Picture of human faces or geometrical figures in a 4 x 4 array were used as stimuli. The sixteen faces or figures were either identical (absent condition) or one randomly placed target with 15 identical distracters (present condition). Participants were asked to respond 'present' or 'absent' as fast and accurately as possible. Results showed that the response time differed significantly between high and low groups of each personality factor except Agreeableness. For Extroversion, Neuroticism, and Conscientiousness, the response time difference was observed only for human face recognition. The results suggested that personality differences and face recognition were related.

Adult↗
PubMed2004

Human parvovirus B19 transgenic mice become susceptible to polyarthritis.

Human parvovirus B19 (B19) often causes acute polyarthritis in adults. In this paper, we analyzed nucleotide sequences of the B19 genome of patients with rheumatoid arthritis (RA), and then introduced the nonstructural protein 1 (NS1) gene of B19 into C57BL/6 mice that had a genetic origin not susceptible to arthritis. The transgenic mice developed no lesions spontaneously, but were susceptible to type II collagen (CII)-induced arthritis. B19 NS1 was expressed in synovial cells on the articular lesions that were histologically characteristic of granulomatous synovitis and pannus formation in cartilage and bone. Serum levels of anti-CII Abs and TNF-alpha increased in NS1 transgenic mice to the same levels as those of DBA/1 mice, which were susceptible to polyarthritis. Stimulation with CII increased secretion of Th1-type- and Th2-type cytokines in NS1 transgenic mice, indicating that a nonpermissive H-2(b) haplotype in the wild type of C57BL/6 mice can be made susceptible to polyarthritis through the expression of NS1. This study is the first to show that a viral agent from the joints in humans can cause CII-induced arthritis resembling RA.

Animals↗
PubMed2004

Urinary excretion of aquaporin-2 water channel exaggerated dependent upon vasopressin in congestive heart failure.

BACKGROUND: Impaired water excretion occurs in patients with congestive heart failure. The present study was undertaken to determine whether urinary excretion of aquaporin-2 (AQP-2) water channel is exaggerated in patients with congestive heart failure dependent upon arginine vasopressin (AVP). METHODS: Sixty-five patients with congestive heart failure and eight age- and gender-matched control subjects were examined. The patients were divided into four groups according to the criteria of New York Heart Association (NYHA). Plasma AVP levels, urinary excretion of AQP-2, and cardiac index were determined. RESULTS: Plasma AVP levels were progressively increased following the severity of NYHA class in the patients with congestive heart failure. Cardiac index was inversely decreased, and there was a negative correlation between plasma AVP levels and cardiac index (r=-0.430, P < 0.02). Urinary excretion of AQP-2 was 187.3 +/- 50.2 fmol/mg creatinine in the control subjects. It was markedly increased in the patients. Urinary excretion of AQP-2 was elevated to 1144.4 +/- 257.5 and 990.5 +/- 176.0 fmol/mg creatinine in the patients with NYHA class III and class IV, respectively, values significantly greater than the control subjects (P < 0.05). Urinary excretion of AQP-2 had a positive correlation with plasma AVP levels (r= 0.280, P < 0.02). CONCLUSION: The present study indicates that exaggerated urinary excretion of AQP-2 is dependent on baroreceptor-mediated release of AVP in patients with congestive heart failure.

Adult↗
PubMed2004

Unilateral active adrenal tuberculosis featuring persistent intermittent fever.

The adrenal gland is one of the organs which tuberculosis infects. In most clinical settings bilateral adrenal tuberculosis has been clarified after adrenal insufficiency is overt. On the contrary, active adrenal tuberculosis is rarely detected during the survey of infectious disease. A 68-year-old man was admitted because of intermittent fever. The fever had continued for the last 3 months. The intermittent fever was accompanied with leukocytosis and elevation of C-reactive protein. Serum soluble interleukin-2 receptor was 1920 U/ml, and beta2-microglobulin was 4.0 mg/l. Bacterial cultures of blood, sputa, urine, bone marrow and cerebrospinal fluid did not show any particular bacteria. Mycobacterium tuberculosis was negative in culture of sputa, and there was no tuberculin reaction. Plasma ACTH and serum cortisol were 18.5 pmol/l and 527.0 nmol/l, respectively. Abdominal CT scan showed right adrenal mass with a size of 28 x 20 mm, which was low density and had a well-encapsulated homogenous appearance. After the adrenalectomy, histology verified active adrenal tuberculosis. The intermittent fever disappeared, and white blood cells and C-reactive protein normalized. These findings indicate an atypical, rare case of unilateral, active adrenal tuberculosis closely linked to intermittent fever, and without any other organ involvement.

Acute Disease↗
PubMed2003

A novel angiotensin II type 2 receptor signaling pathway: possible role in cardiac hypertrophy.

We describe a novel signaling mechanism mediated by the G-protein-coupled receptor (GPCR) angiotensin II (Ang II) type 2 receptor (AT(2)). Yeast two-hybrid studies and affinity column binding assay show that the isolated AT(2) C-terminus binds to the transcription factor promyelocytic zinc finger protein (PLZF). Cellular studies employing confocal microscopy show that Ang II stimulation induces cytosolic PLZF to co-localize with AT(2) at the plasma membrane, then drives AT(2) and PLZF to internalize. PLZF slowly emerges in the nucleus whereas AT(2) accumulates in the perinuclear region. Nuclear PLZF binds to a consensus sequence of the phosphatidylinositol-3 kinase p85 alpha subunit (p85 alpha PI3K) gene. AT(2) enhances expression of p85 alpha PI3K followed by enhanced p70(S6) kinase, essential to protein synthesis. An inactive mutant of PLZF abolishes this effect. PLZF is expressed robustly in the heart in contrast to many other tissues. This cardiac selective pathway involving AT(2), PLZF and p85 alpha PI3K may explain the absence of a cardiac hypertrophic response in AT(2) gene-deleted mice.

Amino Acid Sequence↗
PubMed2003

Evaluation of anti-parvovirus B19 activity in sera by assay using quantitative polymerase chain reaction.

Human parvovirus B19 (B19) infects cells of erythroid lineage. Production of neutralizing antibodies (Abs) is indispensable for recovery from B19-related disease state. In this study, we used a convenient method to measure neutralizing activities in human sera by using a real-time quantitative PCR based assay. Erythroid cell line KU812Ep6 was incubated with test sera before infection with B19 virus. The copy number of B19-DNA in cultures was decreased in the presence of the sera from patients who recovered from acute B19 infection, whereas no decrease in B19-DNA was in cultures incubated with sera from healthy volunteers who had no B19 infection. The decrease in B19-DNA copy number was calculated and the inhibition percentage was expressed as neutralizing activity to B19. A clinical study showed that the levels of neutralizing ability were high in patients who recovered soon after acute B19 infection, but were low in some patients with a prolonged clinical course for recovery from B19 infection. This method is simple and convenient compared with methods described previously, showing its usefulness to evaluate the neutralizing activity to B19.

Animals↗
PubMed2003

Lessons learned as a research assistant studying ambulatory blood pressure in elderly Japanese stroke patients.

The research assistant plays a critical part in research projects, yet there is little structured information about the role. The present paper describes the research assistant"s role and provides an example of the research assistant"s activities in nursing research. In this pilot study, 24 h ambulatory blood pressure monitoring was conducted on 15 elderly Japanese stroke patients in a hospital rehabilitation unit. The research assistant's involvement is described along the course of the study: pre-data collection; data collection and data processing. A research assistant needs to have good communication skills, a detail-oriented focus and an inquisitive nature.

Aged↗
PubMed2002

Urinary excretion of aquaporin-2 water channel in diabetic ketoacidosis.

We studied the changes in plasma arginine vasopressin (AVP) and urinary excretion of aquaporin-2 (UAQP-2) water channel in 3 patients with diabetic ketoacidosis. They had marked hyperglycemia of 27.9 +/- 2.8 mmol/l (mean +/- SEM), and elevated hemoglobin A1c of 8.8 +/- 1.4%. Circulatory blood volume was decreased by approximately 25%, which was determined by the changes in hematocrit. Plasma AVP levels were elevated to 10.3 +/- 3.0 pmol/l and UAQP-2, 578 +/- 200 fmol/mg creatinine (normal, 153 +/- 28) at the hospitalization. When hyperglycemia was improved by the intravenous infusion of a small dose of insulin plus fluid administration, both plasma AVP and UAQP-2 promptly decreased to 1.2 +/- 0.2 pmol/l and 252 +/- 29 fmol/mg creatinine on day 7, respectively. These alterations were concomitant with the recovery of circulatory blood volume. In the present study, UAQP-2, in addition to plasma AVP, indicates circulatory blood volume depletion, and the changes in UAQP-2 estimates the AVP-dependent recovery of circulatory blood volume during the therapeutic period in the patients with diabetic ketoacidosis.

Adult↗
PubMed2002

Decrease in urinary excretion of aquaporin-2 associated with impaired urinary concentrating ability in diabetic nephropathy.

Aquaporin-2 (AQP-2) is known to be expressed in the renal collecting duct cells and participates in urinary concentration in response to arginine vasopressin (AVP). The present study was undertaken to determine whether progression of renal dysfunction affects urinary excretion of AQP-2 in diabetic nephropathy. The study was composed of 8 control subjects and 14 patients with type 2 diabetes classified into two groups according to serum creatinine level (cut-off point; 1.5 mg/dl). After an 8-hour water deprivation, both urinary osmolality (U(osm)) and urinary excretion of AQP-2 significantly decreased in the diabetic patients with chronic renal failure as compared to the control subjects (p < 0.0001, p < 0.05, respectively). After a water load (10 ml/kg), no differences were found in plasma osmolality (P(osm)), AVP levels and U(osm), whereas urinary excretion of AQP-2 significantly decreased in the patients with chronic renal failure as compared to the control subjects (p < 0.05). These results indicate that the decreased urinary excretion of AQP-2 in diabetic nephropathy is due to the impaired cellular signaling of AVP in collecting duct cells, which may be partly involved in the urinary concentrating defect in renal failure.

Aquaporin 2↗