ELISA for soluble form of lectin-like oxidized LDL receptor-1, a novel marker of acute coronary syndrome.
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Acute Disease↗
Biomedical subjects
Toru Kita
Publications and source records attributed to Toru Kita.
Thoracoabdominal-aortoiliac MDCT angiography using reduced dose of contrast material.
OBJECTIVE: The objective of our study was to compare the image quality of MDCT angiography studies obtained by injection of low doses of contrast medium with saline flush versus conventional doses of contrast medium. MATERIALS AND METHODS: Seventy-one patients with pre- or postoperative aortic aneurysms underwent MDCT angiography throughout the thoracoabdominal-aortoiliac system using an 8-MDCT scanner. In 37 patients, 100 mL of contrast medium was injected at a flow rate of 3.0 mL/s (hereafter referred to as the 100-mL group). In 34 patients, 50 mL of contrast medium followed by a 20-mL saline flush was injected at a flow rate of 2.5 mL/s (the 50-mL group). For each group, quantitative analysis involved calculating the mean aortoiliac enhancement, plateau deviation, and contrast enhancement in the pulmonary trunk and superior vena cava (SVC). Qualitative analysis involved assessing the 3D postprocessing images. RESULTS: Significant differences between the groups in mean aortoiliac enhancement (100-mL group vs 50-mL group, 337 +/- 6 H vs 319 +/- 5 H, p < 0.0001) and mean plateau deviation (51 +/- 4 H vs 58 +/- 4 H, p < 0.0001) were found. However, adequate arterial enhancement (>or= 200 H) was observed in 31 of 34 patients in the 50-mL group and uniform aortoiliac enhancement (< 50 H) was seen in 26 patients. Visual analysis showed no difference in contrast material magnitude and homogeneity between the groups. Furthermore, in the 50-mL group, the thoracic aorta was more clearly visualized because of a reduction in the opacity of the main pulmonary artery and SVC. CONCLUSION: In our experience, administration of 50 mL of contrast medium followed by a 20-mL saline flush produces thoracoabdominal-aortoiliac MDCT angiographic examinations of effective quality in most cases.
Adult↗
[Behavioral and psychological symptoms, cognitive impairment and caregiver burden related to Alzheimer's disease patients treated in an outpatient memory clinic].
AIM: The relationships among behavioral and psychological symptoms of dementia (BPSD), cognitive impairment of Alzheimer's disease (AD) patients and the caregiver burden of their caregivers were investigated in an outpatient memory clinic. METHODS: Forty-six pairs of AD patients and their family caregivers were involved in this study. Neuropsychiatry Inventory (NPI) was used to estimate BPSD, to which memory symptoms were added as a subcategory of BPSD. MMSE, word fluency, clock drawing test and category-cued memory test were used for cognitive measurement. Zarit burden interview (ZBI) and CES-D were used to assess caregiver burden. RESULTS: Among 11 BPSD subcategories, memory symptoms, apathy, depression, delusion, aggression and anxiety were prevalent BPSD was a strong determinant of caregiver burden. Among BPSD symptoms, anxiety, aggression and aberrant motor behavior were significantly related to ZBL In terms of the relationship between BPSD and cognitive impairment, the scores for delusion and apathy were significantly related to the cognitive decline. On the other hand, patients who showed symptoms related to memory and depression had higher cognitive function than those who did not. CONCLUSION: These analyses will contribute to better assessment of AD patients and their caregivers, hopefully resulting in better support for them.
Aged↗
Prevalence of metabolic syndrome in the general Japanese population in 2000.
To determine the prevalence of metabolic syndrome in the Japanese general population, we analyzed data from a nationwide survey conducted in 2000. According to the Japanese new diagnostic criteria for metabolic syndrome in 2005, we analyzed 3,264 people aged from 20 to 79 (men, 1,917; women, 1,347) from the total participants. The incidence of metabolic syndrome was 7.8%. Men had a higher incidence (12.1%) than women (1.7%). Most of the women satisfying the criteria were 50 years old or over, while the incidence in men started to rise from their 30s. When we applied the criteria of Adult Treatment Panel III, the incidence was about 3-fold higher. In this population visceral obesity was associated with metabolic abnormalities, such as higher LDL-cholesterol, triglyceride, glucose, and blood pressure and lower HDL-cholesterol. Thus we determined the incidence of metabolic syndrome and each metabolic abnormality in the Japanese general population in 2000 and found an association of visceral obesity with metabolic abnormalities. Intervention to reduce the incidence of metabolic syndrome in Japan is necessary to reduce the risk of cardiovascular disease.
Adult↗
A catheter-based intravascular radiation detector of vulnerable plaques.
UNLABELLED: Detection of vulnerable plaques before rupture is important in preventing acute coronary events such as myocardial infarction. Although therapeutic strategies such as percutaneous transluminal coronary angioplasty appear to prevent coronary occlusion and consequently may lead to improved prognosis in these patients, a method of detecting vulnerable plaques has not been established. A nuclear method that uses an intravascular radiation detector (IVRD) with the plaque-avid tracer (18)F-FDG is one of the most promising methods. The catheter-based IVRD consists of a catheter probe (a scintillator and flexible optic fibers), photomultipliers, a controller, and an automatic pullback unit and personal computer. A phantom study demonstrated that this detector was highly sensitive to (18)F and enabled the detection of (18)F point sources. However, details of the detection system in vivo remain unclear. METHODS: To evaluate vulnerable plaques in vivo, we investigated a canine femoral artery and coronary artery using this detector system. Our goal was to estimate the ability of this device to navigate through these arteries and to detect (18)F point sources fixed on their adventitia. RESULTS: In the study using a canine femoral artery, the IVRD could detect the point sources with good repeatability. In the study using an open-chest canine model, the catheter probe could easily be advanced into the left descending coronary artery, and the IVRD could detect target sources attached externally to the coronary artery (7- to 15-mm intervals) with good resolution. CONCLUSION: This newly developed catheter-based IVRD was able to detect, with good resolution, the slight radioactivity from (18)F point sources attached to the femoral artery and the coronary adventitia. These results show that catheter-based detection of coronary vulnerable plaques may be feasible.
Animals↗
Endothelin-1 activates Homer 1alpha expression via mitogen-activated protein kinase in cardiac myocytes.
Homer proteins are a family of scaffolding proteins which may play an important role in calcium signaling by facilitating the assembly of signaling complexes in neuronal cells. Among the three splice variants of Homer 1, Homer 1alpha is rapidly up-regulated by neural stimulation and may regulate the disassembly of signaling complexes mediated by Homer proteins. In spite of its potential importance in calcium signaling, the regulation of Homer 1alpha expression in cardiac myocytes has never been investigated. In this study, we examined the regulation of Homer 1alpha expression in cardiac myocytes. Homer 1alpha was significantly up-regulated by several hypertrophic agonists, including endothelin-1 (ET-1), phenylephrine, isoprotenerol and angiotensin-II, and ET-1 most strikingly induced Homer 1alpha expression. The induction of Homer 1alpha expression by ET-1 peaked at 2 h and inhibitors for mitogen-activated/extracellular signal regulated kinase (MEK) significantly suppressed the induction of Homer 1alpha. This study first clarified the regulation of Homer 1alpha expression in cardiac myocytes and demonstrated that ET-1 induced Homer 1alpha expression through the mitogen-activated protein kinase pathway.
Angiotensin II↗
[Immunoglobulin stabilizes plaque formation in experimental atherosclerosis].
OBJECTIVES: Immunoglobulin treatment is known to suppress atherosclerosis in apolipoprotein E-deficient mice. In addition, immunoglobulin inhibits atherosclerosis via the Fc receptors. However, the effect of immunoglobulin treatment at the advanced stage of atherosclerosis is still unclear. This study examined the effects of immunoglobulin on apolipoprotein E-deficient mice at the advanced stage of the disease. METHODS: Atherosclerosis was induced in mice fed a high-fat diet containing 0.3% cholesterol. After confirming the presence of atherosclerotic lesions at 11 weeks, mice were intraperitoneally treated with injections of either intact type of immunoglobulin (1 g/kg/day) or F (ab') 2 fragments of immunoglobulin (1 g/kg/day) on alternate days over 4 weeks. Oil red-O staining and immunohistochemical staining with CD4+ cells were performed of the aorta, and atherosclerotic lesions was evaluated and compared between the groups. RESULTS: Fatty streak lesion was significantly suppressed by intact immunoglobulin compared with saline, and inflammatory cell infiltration and expression of CD4+ cells were less in mice treated with intact immunoglobulin compared with the control. CONCLUSIONS: Immunoglobulin treatment even at the advanced stage of atherosclerosis suppressed the development of fatty lesions and may stabilize atherosclerotic plaques by inhibiting inflammatory cell expression. Immunoglobulin suppression of atherosclerosis was confirmed to act via the Fc receptors.
Animals↗
Current understanding of biochemical markers in heart failure.
Chronic heart failure (CHF) is a major cause of morbidity and mortality in industrialized countries. As societies are aging, efforts are directed toward early interventions to preserve quality of life as well as lower mortality. However, because of the paucity of specific symptoms, an early diagnosis and management of CHF might be challenging. In contrast, biochemical markers, which can be measured easily and without inter-observer variability, are now being carefully examined. Since CHF is a complex syndrome, a single biochemical marker cannot reflect its multiple manifestations. An ideal biochemical marker should 1) be a prognostic indicator, 2) reflect the therapeutic response, 3) be heart specific 4) be independent from other markers 5) reflect the pathophysiology of CHF, 6) assist in the early diagnosis of CHF, and 7) be reliable throughout the various phases of the syndrome, from before the onset of its clinical manifestations through its end-stage. This review summarizes our current understanding of biochemical markers of CHF based on its pathophysiology.
Biomarkers↗
WTC deafness Kyoto (dfk): a rat model for extensive investigations of Kcnq1 functions.
KCNQ1 forms K+ channels by assembly with regulatory subunit KCNE proteins and plays a key role in the K+ homeostasis in a variety of tissues. In the heart, KCNQ1 is coassembled with KCNE1 to produce a cardiac delayed rectifier K+ current. In the inner ear, the KCNQ1/KCNE1 complex maintains the high concentration of K+ in the endolymph. In the stomach, KCNQ1 is coassembled with KCNE2 to form the K+ exflux channel that is essential for gastric acid secretion. In the colon and small intestine, KCNQ1 is coassembled with KCNE3 to play an important role in transepithelial cAMP-stimulated Cl- secretion. For further understanding of Kcnq1 function in vivo, an animal model has been required. Here we reported the identification of a coisogenic Kcnq1 mutant rat, named deafness Kyoto (dfk), and the characterization of its phenotypes. WTC-dfk rats carried intragenic deletion at the Kcnq1 gene and showed impaired gain of weight, deafness, and imbalance resulting from the marked reduction of endolymph, prolonged QT interval in the electrocardiogram (ECG), and gastric achlorhydria associated with hypertrophic gastric mucosa. Surprisingly, WTC-dfk rats showed hypertension, which suggested that Kcnq1 might be involved in the regulation of blood pressure. These findings suggest that WTC-dfk rats could represent a powerful tool for studying the physiological functions of KCNQ1 and for the establishment of new therapeutic procedures for Kcnq1-related diseases.
Alleles↗
Uterine sensitization-associated gene-1 (USAG-1), a novel BMP antagonist expressed in the kidney, accelerates tubular injury.
Dialysis dependency is one of the leading causes of morbidity and mortality in the world, and once end-stage renal disease develops, it cannot be reversed by currently available therapy. Although administration of large doses of bone morphogenetic protein-7 (BMP-7) has been shown to repair established renal injury and improve renal function, the pathophysiological role of endogenous BMP-7 and regulatory mechanism of its activities remain elusive. Here we show that the product of uterine sensitization-associated gene-1 (USAG1), a novel BMP antagonist abundantly expressed in the kidney, is the central negative regulator of BMP function in the kidney and that mice lacking USAG-1 (USAG1 mice) are resistant to renal injury. USAG1 mice exhibited prolonged survival and preserved renal function in acute and chronic renal injury models. Renal BMP signaling, assessed by phosphorylation of Smad proteins, was significantly enhanced in USAG1 mice with renal injury, indicating that the preservation of renal function is attributable to enhancement of endogenous BMP signaling. Furthermore, the administration of neutralizing antibody against BMP-7 abolished renoprotection in USAG1 mice, indicating that USAG-1 plays a critical role in the modulation of renoprotective action of BMP and that inhibition of USAG-1 is a promising means of development of novel treatment for renal diseases.
Adaptor Proteins, Signal Transducing↗
High risk for bradyarrhythmic complications in patients with Brugada syndrome caused by SCN5A gene mutations.
OBJECTIVES: We carried out a complete screening of the SCN5A gene in 38 Japanese patients with Brugada syndrome to investigate the genotype-phenotype relationship. BACKGROUND: The gene SCN5A encodes the pore-forming alpha-subunit of voltage-gated cardiac sodium (Na) channel, which plays an important role in heart excitation/contraction. Mutations of SCN5A have been identified in 15% of patients with Brugada syndrome. METHODS: In 38 unrelated patients with clinically diagnosed Brugada syndrome, we screened for SCN5A gene mutations using denaturing high-performance liquid chromatography and direct sequencing, and conducted a functional assay for identified mutations using whole-cell patch-clamp in heterologous expression system. RESULTS: Four heterozygous mutations were identified (T187I, D356N, K1578fs/52, and R1623X) in 4 of the 38 patients. All of them had bradyarrhythmic complications: three with sick sinus syndrome (SSS) and the other (D356N) with paroxysmal complete atrioventricular block. SCN5A-linked Brugada patients were associated with a higher incidence of bradyarrhythmia (4 of 4) than non-SCN5A-linked Brugada patients (2 of 34). Families with T187I and K1578fs/52 had widespread penetrance of SSS. Notably, the patient with K1578fs/52, who had been diagnosed as having familial SSS without any clinical signs of Brugada syndrome, showed a Brugada-type ST-segment elevation after intravenous administration of pilsicainide and programmed electrical stimulation-induced ventricular tachycardia. All of the mutations encoded non-functional Na channels, and thus were suggested to cause impulse propagation defect underlying bradyarrhythmias. CONCLUSIONS: Our findings suggest that loss-of-function SCN5A mutations resulting in Brugada syndrome are distinguished by profound bradyarrhythmias.
Adult↗
Activation of TGF-beta1-TAK1-p38 MAPK pathway in spared cardiomyocytes is involved in left ventricular remodeling after myocardial infarction in rats.
Transforming growth factor-beta1 (TGF-beta1) alters myocardial gene expression, resulting in myocyte hypertrophy, through activation of TGF-beta-activated kinase (TAK1), a member of the mitogen-activated protein kinase kinase kinase (MAPKKK) family. We hypothesized that the TGF-beta1-TAK1-p38 MAPK pathway might be activated during ventricular remodeling after myocardial infarction (MI). One, 3, 7, and 14 days after ligation of the left anterior descending coronary artery, noninfarcted left ventricular tissue samples were obtained. Protein levels as well as mRNA levels of the signaling pathway, TGF-beta1, TGF-beta-receptors, and TAK1 increased in the noninfarcted myocardium in MI rats compared with sham-operated animals. Phosphorylation of MAPKK 3/6 (MKK3/6) and p38 MAPK, the downstream targets of TAK1, was also increased in the noninfarcted region. Moreover, an in vitro kinase assay revealed that the activated TAK1 in the noninfarcted myocardium was capable of activating recombinant MKK3/6, suggesting a causative role of TAK1 in the remodeling process. The activation of the TGF-beta1-TAK1-p38 MAPK pathway paralleled the transcriptional upregulation of cardiac markers for ventricular hypertrophy, beta-myosin heavy chain and atrial natriuretic peptide. TAK1 was mainly localized to cardiomyocytes, whereas TGF-beta1 receptors were observed in vascular smooth muscle cells and fibroblasts as well as cardiomyocytes. Thus the TGF-beta1-TAK1-MKK3/6-p38 MAPK pathway in the cardiomyocytes of noninfarcted spared myocardium is activated after acute MI and may play an important role in ventricular hypertrophy and post-MI remodeling in rats.
Animals↗
Images in cardiovascular medicine. Endovascular treatment of a giant aortic arch aneurysm with a triple-branched stent graft.
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Aged, 80 and over↗
Clinical efficacy of intravenous immunoglobulin for patients with MPO-ANCA-associated rapidly progressive glomerulonephritis.
BACKGROUND: To determine whether intravenous immunoglobulin (IVIg) can control disease activity in patients with myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA)-associated rapidly progressive glomerulonephritis (RPGN). METHODS: Twelve patients with serologically and histologically confirmed MPO-ANCA-associated RPGN (7 men, 5 women; mean age 71 +/- 3 years) received IVIg (400 mg/kg/day) alone for 5 days. The effects of IVIg were evaluated by white blood cell counts, serum C-reactive protein levels, Birmingham Vasculitis Activity Score, rate of change in reciprocal creatinine (1/Cre), and plasma tumor necrosis factor-alpha levels after IVIg administration. Corticosteroids with or without cyclophosphamide were commenced after IVIg. RESULTS: After IVIg treatment, a significant decrease was observed in white blood cell count (p < 0.05), C-reactive protein values (p < 0.001), and Birmingham Vasculitis Activity Score (p < 0.001) concomitant with the amelioration of systemic symptoms. The rate of change in 1/Cre significantly improved (p < 0.05). Plasma tumor necrosis factor-alpha levels that were significantly elevated in patients before IVIg compared with normal controls (p < 0.0001), rapidly declined after IVIg with a significant reduction (p < 0.05). Three months post-treatment with IVIg, all patients showed improvement of disease without serious infectious complications. CONCLUSION: IVIg is a potential component of remission induction therapy for patients with MPO-ANCA-associated RPGN.
Aged↗
Mechanism of impairment of long-term potentiation by amyloid beta is independent of NMDA receptors or voltage-dependent calcium channels in hippocampal CA1 pyramidal neurons.
beta-Amyloid peptide (Abeta) is known to be involved in Alzheimer's disease (AD). Although the fibril form of Abeta is known to have neurotoxicity, it has been shown that not only the fibril form but also the oligomer form of Abeta may be related to the neuropathophysiology of AD, specifically to memory loss. Some studies have demonstrated that low concentrations of the Abeta oligomer impair long-term potentiation (LTP), a cellular model for learning and memory, after short exposure times in vivo and in vitro, although little is known about the mechanism involved in Abeta-mediated inhibition of LTP. In this study, we used the patch clamp whole-cell technique in rat hippocampal CA1 pyramidal neurons to study more precisely how the Abeta oligomer affects synaptic plasticity. The brief perfusion of slices with a low concentration (1microM) of Abeta(1-42) significantly impaired LTP induction of the excitatory input. The same concentration of Abeta did not affect basal transmission or paired-pulse facilitation. We also demonstrated that neither NMDAR-EPSCs nor the voltage-depended calcium channel (VDCC) currents were affected by the same concentration of Abeta(1-42) as used in the LTP experiments. These data suggest that Abeta mediated impairment of LTP induction is independent of NMDARs or VDCCs.
Amyloid beta-Peptides↗
Serum soluble lectin-like oxidized low-density lipoprotein receptor-1 levels are elevated in acute coronary syndrome: a novel marker for early diagnosis.
BACKGROUND: Markers of cardiac injury, including troponin-T (TnT), are used to diagnose acute coronary syndrome (ACS); however, markers for plaque instability may be more useful for diagnosing ACS at the earliest stage. Lectin-like oxidized LDL receptor-1 (LOX-1) appears to play crucial roles in the pathogenesis of atherosclerotic plaque rupture and ACS onset. LOX-1 is released in part as soluble LOX-1 (sLOX-1) by proteolytic cleavage. METHODS AND RESULTS: We examined serum sLOX-1 levels in 521 patients, consisting of 427 consecutive patients undergoing coronary angiography, including 80 ACS patients, 173 symptomatic coronary heart disease patients, 122 patients with significant coronary stenosis without ischemia, and 52 patients without apparent coronary atherosclerosis plus 34 patients with noncardiac acute illness and 60 patients with noncardiac chronic illness. Time-dependent changes in sLOX-1 and TnT levels were analyzed in an additional 40 ACS patients. Serum sLOX-1 levels were significantly higher in ACS than the other groups and were associated with ACS as shown by multivariable logistic regression analyses. Given a cutoff value of 1.0 ng/mL, sLOX-1 can discriminate ACS from other groups with 81% and 75% of sensitivity and specificity, respectively. sLOX-1 can also discriminate ACS without ST elevation or abnormal Q waves and ACS without TnT elevation from non-ACS with 91% and 83% of sensitivity, respectively. Peak values of sLOX-1 in ACS were observed earlier than those of TnT. CONCLUSIONS: sLOX-1 appears to be a useful marker for early diagnosis of ACS.
Acute Disease↗
Depression, activities of daily living, and quality of life of community-dwelling elderly in three Asian countries: Indonesia, Vietnam, and Japan.
The purpose of this study was to examine the prevalence of screening-based depression and the association of depression with activities of daily living (ADL) and quality of life (QOL) of community-dwelling elderly in the developing and developed countries. A total of 2,695 community-dwelling elderly subjects aged 60 years or older living in five rural Asian towns (Indonesia: 411, Vietnam: 379, Japan: 1,905) participated in this cross-sectional study. Depressive symptoms were assessed using a 15-item geriatric depression scale (GDS-15). ADL, higher daily activities, and medical and social history were assessed by interviews or self-report questionnaires. For the assessment of subjective QOL, a 100mm visual analogue scale was used. Using a cut-point of 5/6 for the GDS-15, 782 participants (29.0%) appeared to have depression (Indonesia: 33.8%, Vietnam: 17.2%, Japan: 30.3%). Subjects with depression had significantly lower scores for both ADL and QOL than those without depression in all the three countries. In all the three countries, 17.2-33.8% of community-dwelling elderly subjects had screening-based depression, which was commonly associated with both lower quantitative ADL and lower QOL.
Activities of Daily Living↗
CXCL16 is a novel angiogenic factor for human umbilical vein endothelial cells.
CXCL16 is a unique chemokine with characteristics as a receptor for phosphatidylserine and oxidized low density lipoproteins in macrophages, and is involved in the accumulation of cellular cholesterol during atherosclerotic lesion development. In this study, we report a new function of CXCL16 as a novel angiogenic factor in human umbilical vein endothelial cells (HUVEC). CXCL16 stimulated proliferation and chemotaxis of HUVEC in a dose-dependent manner, reaching a maximum at 1 nM. CXCL16 also significantly induced tube formation of HUVEC on Matrigel. Further, exposure of HUVEC to CXCL16 led to a time- and dose-dependent activation of mitogen-activated protein kinase (ERK1/2), which was completely inhibited by a mitogen-activated protein kinase kinase inhibitor, PD98059. Proliferation and tube formation in response to CXCL16 were also blocked by the pretreatment with PD98059, but not CXCL16-induced chemotaxis. Thus, our data indicate that CXCL16 may act as a novel angiogenic factor for HUVEC and that ERK is involved as an important signaling molecule to mediate its angiogenic effects.
Cell Movement↗