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Toru Kita

Publications and source records attributed to Toru Kita.

At least 19 recordsLinked to original sources
PubMed2007

Leptin induces elongation of cardiac myocytes and causes eccentric left ventricular dilatation with compensation.

One of the major manifestations of obesity is an increased production of the adipocyte-derived 16-kDa peptide leptin, which acts mainly on hypothalamic leptin receptors. Leptin receptors are widely distributed in various tissues, including the heart. Whereas increased plasma leptin levels have been reported in patients with congestive heart failure, systemic alterations induced by obesity can affect cardiac hypertrophy, and the direct effects of leptin on cardiac structure and function still remain to be determined. We first exposed primary cardiac myocytes from neonatal rats to leptin for 48 h. This resulted in a significant increase in myocyte long-axis length (P < 0.05 at 50 ng/ml) but not in the short-axis width. Leptin induced the rapid phosphorylation of STAT3 and its DNA binding in cardiac myocytes. Administration of a JAK2 inhibitor, AG-490, completely inhibited all of these effects by leptin. Furthermore, we examined the effect of continuous infusion of leptin for 4 wk following myocardial infarction in mice. Echocardiography demonstrated that left ventricular fractional shortening in the leptin-infused group (28.4 +/- 2.8%) was significantly higher than that in the PBS-infused group (18.4 +/- 2.2%) following myocardial infarction. Interestingly, left ventricular diastolic dimension in the leptin-infused group (4.56 +/- 0.12 mm) was also higher than that in the PBS-infused group (4.13 +/- 0.09 mm). These results demonstrate that leptin induces the elongation of cardiac myocytes via a JAK/STAT pathway and chronic leptin infusion causes eccentric dilatation with augmented systolic function after myocardial infarction.

Animals↗
PubMed2007

Genotype-phenotype correlations of KCNJ2 mutations in Japanese patients with Andersen-Tawil syndrome.

Andersen-Tawil syndrome (ATS) is a rare inherited disorder characterized by periodic paralysis, mild dysmorphic features, and QT or QU prolongation with ventricular arrhythmias in electrocardiograms (ECGs). Mutations of KCNJ2, encoding the human inward rectifying potassium channel Kir 2.1, have been identified in patients with ATS. We aimed to clarify the genotype-phenotype correlations in ATS patients. We screened 23 clinically diagnosed ATS patients from 13 unrelated Japanese families. Ten different forms of KCNJ2 mutations were identified in the 23 ATS patients included in this study. Their ECGs showed normal QTc intervals and abnormal U waves with QUc prolongation and a variety of ventricular arrhythmias. Especially, bidirectional ventricular tachycardia (VT) was observed in 13 of 23 patients (57%). Periodic paralysis was seen in 13 of 23 carriers (57%), dysmorphic features in 17 (74%), and seizures during infancy in 4 (17%). Functional assays for the two novel KCNJ2 mutations (c. 200G>A (p. R67Q) and c. 436G>A (p. G146S)) displayed no functional inward rectifying currents in a heterologous expression system and showed strong dominant negative effects when co-expressed with wild-type KCNJ2 channels (91% and 84% reduction at -50 mV respectively compared to wild-type alone). Immunocytochemistry and confocal imaging revealed normal trafficking for mutant channels. In our study, all of the clinically diagnosed ATS patients had KCNJ2 mutations and showed a high penetrance with regard to the typical cardiac phenotypes: predominant U wave and ventricular arrhythmias, typically bidirectional VT.

Adolescent↗
PubMed2007

Serum levels of S-glutathionylated proteins as a risk-marker for arteriosclerosis obliterans.

BACKGROUND: Oxidative stress plays a role in the development of chronic peripheral arterial disease (PAD) because under these conditions redox regulation is impaired, inducing the S-glutathionylation of proteins. A method of estimating the levels of S-glutathionylated proteins has been developed using biotinylated glutathione S-transferase, which allows the study of their crucial role in the oxidative stress-related progression of PAD. METHODS AND RESULTS: The serum levels of S-glutathionylated proteins were examined in 41 patients with arteriosclerosis obliterans (ASO) and 38 age-matched non-ASO patients using biotinylated glutathione S-transferase. The levels were higher in the patients with ASO, even early on, and positively correlated with the ankle/brachial index. In vitro, the levels of S-glutathionylated proteins were reduced in the presence of glutathione and glutaredoxin. CONCLUSIONS: Serum levels of S-glutathionylated proteins are a sensitive risk-marker for ASO at an early stage.

Aged↗
PubMed2006

Angiotensin II receptor blockade ameliorates mesangioproliferative glomerulonephritis in rats through suppression of CTGF and PAI-1, independently of the coagulation system.

BACKGROUND: Previously we observed that the coagulation system promotes matrix protein accumulation through transforming growth factor (TGF)-beta and connective tissue growth factor (CTGF) expression in rat mesangioproliferative glomerulonephritis (MsPGN). Angiotensin II receptor blockers (ARBs) are known to suppress matrix accumulation in experimental MsPGN. In the present study, we investigated whether ARB suppresses MsPGN through inhibition of these profibrotic cytokines, and in relation to coagulation and fibrinolytic systems. METHODS: MsPGN was induced in Wistar rats by intravenous injection of anti-Thy-1.1 monoclonal antibody, OX-7. As an ARB, olmesartan was orally administered in rat feed from the day of OX-7 injection (day 0) to day 8, when rats were sacrificed and kidney specimens were collected. The degrees of cellular proliferation, matrix production, coagulation factors, and inhibitory factor of fibrinolysis were evaluated. RESULTS: Although blood pressure did not change in the normal, disease control, or treatment groups, the amount of urinary protein was significantly decreased in the ARB-treated groups, compared with the disease control group (p < 0.05). alpha-Smooth muscle actin expression was suppressed significantly in the treatment groups (p < 0.001). Blue-staining areas of trichrome, the number of proliferating cell nuclear antigen (PCNA)- or ED-1-positive cells, fibronectin and plasminogen activator inhibitor type 1 in glomeruli significantly decreased in the treatment groups (p < 0.05, respectively); however, fibrin-related antigen and factor V depositions were not suppressed in the treatment groups. CONCLUSIONS: These results suggest that the ARB drug would ameliorate MsPGN in vivo, at least partly through CTGF and plasminogen activator inhibitor type 1 suppression, and independently of the local coagulation system in glomeruli.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

Roles of coagulation pathway and factor Xa in rat mesangioproliferative glomerulonephritis.

Tissue factor initiates the extrinsic coagulation pathway by activating coagulation factor X to factor Xa, and factor V is a cofactor for the prothrombin activation by factor Xa. As factor Xa is known to promote the proliferation of mesangial cells in culture, the roles of the coagulation pathway and factor Xa were studied in an animal model of mesangioproliferative glomerulonephritis (MsPGN). MsPGN was induced in Wistar rats by an intravenous injection of anti-Thy 1.1 monoclonal antibody, OX-7. To clarify the role of factor Xa in MsPGN, a specific factor Xa inhibitor, DX-9065a, was injected intravenously at 2.5 or 10 mg/kg at the same time as OX-7, and kidney involvement was assessed by immunohistological analyses. We also examined p44/42 mitogen-activated protein (MAP) kinase activation. Time-course study revealed that expressions of tissue factor, factor V, and protease-activated receptor 2 (PAR2) were peaked on day 3, followed by factor X accumulation and mesangial proliferation. DX-9065a treatment significantly ameliorated proteinuria in a dose-dependent manner on day 8. Histological analyses showed a significant reduction in the size of glomeruli, the total number of glomerular cells, and crescent formation by DX-9065a treatment. Macrophage infiltration, which was rapidly observed on day 1 in disease control rats was not inhibited on days 1-3 by DX-9065a treatment, however it was suppressed on days 5-8. The deposition of fibrin, the number of PCNA-positive cells, and phosphorylation of p44/42 MAP kinase were markedly increased in the disease control group, whereas they were significantly reduced in the treatment group. Tissue factor and factor V induction may accelerate MsPGN through the activation and accumulation of factor X via proinflammatory and procoagulant mechanisms, and the inhibition of factor Xa would be a promising method to regulate the disease process.

Analysis of Variance↗
PubMed2006

Measurements of baseline and follow-up concentrations of cardiac troponin-T and brain natriuretic peptide in patients with heart failure from various etiologies.

Since chronic heart failure (CHF) is a complex clinical syndrome, a single biomarker may not reflect all of its characteristics. In this study, the clinical significance of combination and serial measurement of biochemical markers of myocyte injury and myocardial load in patients with CHF from various etiologies was examined. Serum concentrations of cardiac troponin-T (cTnT) and plasma concentrations of brain natriuretic peptide (BNP) were measured simultaneously in 190 patients with CHF, including dilated cardiomyopathy (DCM) (n = 41), ischemic heart disease (n = 40), valvular or congenital disease (n = 53), hypertensive heart disease (n = 16), and hypertrophic cardiomyopathy (HCM) (n = 22). Serum cTnT concentrations >or=0.01 ng/ml were found in 46/190 patients (24%) at baseline (20% in DCM, 42% in ischemic heart disease, 21% in valvular or congenital disease, 43% in hypertensive heart disease, and 9% in HCM). Follow-up samples were obtained in 137 patients after a mean treatment period of 31.8 days. Although BNP decreased significantly in each disease category (P < 0.0001: DCM; P < 0.005: ischemic heart disease; P < 0.05: valvular or congenital disease; P < 0.005: hypertensive heart disease; P < 0.05: HCM), cTnT remained high in 36/137 patients (26%) (19% in DCM, 39% in ischemic heart disease, 25% in valvular or congenital disease, 38% in hypertensive heart disease, and 19% in HCM). The rate of adverse cardiac events was significantly higher in patients with high cTnT than in patients with low cTnT concentrations (P < 0.0001) (P < 0.05: DCM; P < 0.05: ischemic heart disease; P < 0.01: valvular or congenital disease). Multivariate analysis showed that both cTnT and BNP are independent prognostic factors, and patients with elevations of both cTnT and BNP had the poorest prognosis (P < 0.0001). In patients with CHF, the evolution and prognostic value of cTnT and BNP are different. The combined measurements of these markers should refine our understanding of the state and evolution of CHF.

Aged↗
PubMed2006

Structural and functional assessment of arrhythmogenic right ventricular dysplasia/cardiomyopathy by multi-slice computed tomography: comparison with cardiovascular magnetic resonance.

Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an uncommon inheritable cardiomyopathy involving predominant right ventricle with progressive fibrofatty tissue replacement. An integrated assessment of electrical, functional and anatomic abnormalities, in addition to personal and family history would be used to diagnose this disease entity. We present the case of a 69-year-old man with a history of sustained ventricular tachycardia. Fatty infiltration and regional wall motion abnormalities over biventricular myocardium were clearly demonstrated by cardiac 64-slice computed tomography (CT), as consistent with magnetic resonance imaging. Thus, multi-slice CT may have a significant role in the assessment and follow-up of patients with ARVD/C by providing excellent structural, functional assessment and tissue characterization.

Aged↗
PubMed2006

Protection of atherogenesis in thromboxane A2 receptor-deficient mice is not associated with thromboxane A2 receptor in bone marrow-derived cells.

In the previous study, we generated mice lacking thromboxane A2 receptor (TP) and apolipoprotein E, apoE(-/-)TP(-/-) mice, and reported that the double knockout mice developed markedly smaller atherosclerotic lesions than those in apoE(-/-) mice. To investigate the mechanism responsible for reduced atherosclerosis in apoE(-/-)TP(-/-) mice, we examined the role of TP in bone marrow (BM)-derived cells in the development of the atherosclerotic lesions. When we compared the function of macrophages in apoE(-/-) and in apoE(-/-)TP(-/-) mouse in vitro, there was no difference in the expression levels of cytokines and chemokines after stimulation with lipopolysaccharide. We then transplanted the BM from either apoE(-/-) or apoE(-/-)TP(-/-) mice to either apoE(-/-) or apoE(-/-)TP(-/-) mice after sublethal irradiation. After 12 weeks with high fat diet, we analyzed the atherosclerotic lesion of aortic sinus. When the BM from apoE(-/-) or apoE(-/-)TP(-/-) mice was transplanted to apoE(-/-) mice, the lesion size was almost the same as that of apoE(-/-) mice without BM transplantation. In contrast, when the BM from apoE(-/-) or apoE(-/-)TP(-/-) mice was transplanted to apoE(-/-)TP(-/-) mice, the lesion size was markedly reduced. These results indicate that the protection of atherogenesis in TP(-/-) mice is not associated with TP in BM-derived cells.

Animals↗
PubMed2006

Mulberry leaf aqueous fractions inhibit TNF-alpha-induced nuclear factor kappaB (NF-kappaB) activation and lectin-like oxidized LDL receptor-1 (LOX-1) expression in vascular endothelial cells.

Mulberry (Morus Alba L., family Moraceae) leaf extracts have various biological effects including inhibition of oxidative modification of low-density lipoprotein (LDL), which is the major cause of atherosclerosis. Endothelial dysfunction elicited by oxidized LDL (Ox-LDL) has been implicated in atherogenesis. Lectin-like Ox-LDL receptor-1 (LOX-1), a cell-surface receptor for atherogenic Ox-LDL, appears to mediate Ox-LDL-induced inflammation, which may be crucial in atherogenesis. Previous studies revealed that expression of LOX-1 is highly inducible by proinflammatory stimuli, including tumor necrosis factor-alpha (TNF-alpha), lipopolysaccharide (LPS), and transforming growth factor-beta (TGF-beta). Therefore, we examined whether mulberry leaf aqueous fractions inhibit LOX-1 expression induced by proinflammatory stimuli. Pretreatment of cultured bovine aortic endothelial cells (BAECs) with mulberry leaf aqueous fractions inhibited TNF-alpha- and LPS-induced expression of LOX-1 at both protein and mRNA levels in a time- and concentration-dependent manner. In contrast, mulberry leaf aqueous fractions did not affect TGF-beta-induced LOX-1 expression. Furthermore, mulberry leaf aqueous fractions inhibited TNF-alpha-induced activation of nuclear factor-kappaB (NF-kappaB) and phosphorylation of inhibitory factor of NF-kappaB-alpha (IkappaB-alpha) in a time- and concentration-dependent fashion. Thus, mulberry leaf aqueous fractions suppress TNF-alpha- and LPS-induced LOX-1 gene expression, by inhibiting NF-kappaB activation.

Animals↗
PubMed2006

Identification of lipomatous metaplasia in old infarcted myocardium by cardiovascular magnetic resonance and computed tomography.

Lipomatous metaplasia of myocardium after myocardial infarction (MI) is less reported, and the exact prevalence and clinical implications of this phenomenon are unclear. A case of lipomatous metaplasia after MI evaluated with cardiovascular magnetic resonance (CMR) and computed tomography (CT) is presented. The presence of lipomatous metaplasia could not be easily differentiated from scar simply by the delayed-enhanced images. Loss of signal on TrueFISP cine MRI can be a hint. A pre-contrast T1-weighted image with or without frequency-selective fat suppression is useful in order to verify the existence of lipomatous metaplasia on CMR.

Humans↗
PubMed2006

Real-time 2-photon imaging of mitochondrial function in perfused rat hearts subjected to ischemia/reperfusion.

BACKGROUND: Mitochondria play pivotal roles in cell death; the loss of mitochondrial membrane potential (delta psi(m)) is the earliest event that commits the cell to death. Here, we report novel real-time imaging of delta psi(m) in individual cardiomyocytes within perfused rat hearts using 2-photon laser-scanning microscopy, which has unique advantages over conventional confocal microscopy: greater tissue penetration and lower tissue toxicity. METHODS AND RESULTS: The Langendorff-perfused rat heart was loaded with a fluorescent indicator of delta psi(m), tetramethylrhodamine ethyl ester. Tetramethylrhodamine ethyl ester was excited with an 810-nm line of a Ti:sapphire laser, and its fluorescence in the heart cells was successfully visualized up to approximately 50 microm from the epicardial surface. Taking advantage of this system, we monitored the spatiotemporal changes of delta psi(m) in response to ischemia/reperfusion at the subcellular level. No-flow ischemia caused progressive delta psi(m) loss and a more prominent delta psi(m) loss on reperfusion. During ischemia/reperfusion, cells maintained a constant delta psi(m) for the cell-to-cell specific period of latency, followed by a rapid, complete, and irreversible delta psi(m) loss, and this process did not affect the neighboring cells. Within a cell, delta psi(m) loss was initiated in a particular area of mitochondria and rapidly propagated along the longitudinal axis. These spatiotemporal changes in delta psi(m) resulted in marked cellular and subcellular heterogeneity of mitochondrial function. Ischemic preconditioning reduced the number of cells undergoing delta psi(m) loss, whereas cyclosporin A partially inhibited delta psi(m) loss in each cell. CONCLUSIONS: Investigation of cellular responses in the natural environment will increase knowledge of ischemia/reperfusion injury and provide deeper insights into antiischemia/reperfusion therapy that targets mitochondria.

Animals↗
PubMed2006

Angiotensin II, oxidative stress, and extracellular matrix degradation during transition to LV failure in rats with hypertension.

Angiotensin II (Ang-II) plays pivotal roles in the progression of left ventricular (LV) remodeling in diseased hearts; it remains to be elucidated how Ang-II links to degradation of the extracellular matrix (ECM). Using hypertensive Dahl salt-sensitive rats that show the distinctive transition from concentric LV hypertrophy to LV remodeling, we chronically treated them with an angiotensin type-1 receptor blocker (telmisartan 5 mg/kg/day, ARB group) or vehicle (0.5% CMC, CHF group). During the process of LV remodeling, we assessed, (1) in-vivo LV shape and function; (2) animal survival; (3) amounts of ECM in LV using a scanning electron microscope (SEM); (4) mRNA (by real time RT-PCR) and protein (by immunoblotting) levels in LV of NADPH oxidase, glutathione peroxidase-1 (GPX-1), and matrix metalloproteinase (MMP)-2, -9, and -13; (5) immunohistochemical staining of myocardial 4-hydroxy-2-nonenal and 8-hydroxy-2'-deoxyguanosine; (6) nuclear factor kappa-B (NFkappaB) protein levels in the nuclear extract; and (7) endogenous activities of MMP-2 and -9 by an antibody capture method. Compared with CHF, ARB group showed an improvement of survival and preserved LV shape and function, and ECM density in SEM that was accompanied by decreases in oxidative stress-mediated protein degenerations, activities of GPX-1, NADPH oxidase, NFkappaB, and MMP-2, -9, and -13. Local activation of Ang-II in hypertrophic LV triggers MMP-mediated ECM degradation, namely LV remodeling, at least in part, through NADPH oxidase-induced oxidative stress and the subsequent NFkappaB activation.

Angiotensin II↗
PubMed2006

Cognitive impairment and frontal-subcortical geriatric syndrome are associated with metabolic syndrome in a stroke-free population.

BACKGROUND: Metabolic syndrome (Met.S) consists of a conglomeration of obesity, hypertension, glucose intolerance, and dislipidemia. Frontal-subcortical geriatric syndrome (FSCS) is caused by ischemic disruption of the frontal-subcortical network. It is unknown if Met.S is associated with FSCS. METHODS: We evaluated 422 community-dwelling elderly (> or =60) in Brazil. FSCS was defined as the presence of at least one frontal release sign (grasping, palmomental, snout, or glabellar) plus coexistence of > or =3 the following criteria: (1) cognitive impairment, (2) late-onset depression, (3) neuromotor dysfunction, and (4) urgency incontinence. All values were adjusted to age and gender. RESULTS: Met.S was present in 39.3% of all subjects. Cases without any of the FSCS components represented 37.2% ('successful neuroaging' group). People with 1-3 of the FSCS components ('borderline pathological neuroaging' group) were majority (52.6%), whereas those with 4-5 of these components (FSCS group) were minority (10.2%). Met.S was significantly associated with FSCS (OR=5.9; CI: 1.5-23.4) and cognitive impairment (OR=2.2; CI: 1.1-4.6) among stroke-free subjects. Number of Met.S components explained 30.7% of the variance on the number of FSCS criteria (P<0.001). If Met.S were theoretically removed from this population, prevalence of FSCS would decline by 31.6% and that of cognitive impairment by 21.4%. CONCLUSIONS: Met.S was significantly associated with a 5.9 and 2.2 times higher chance of FSCS and cognitive impairment, respectively. Met.S might be a major determinant of 'successful' or 'pathological' neuroaging in western societies.

Aged↗
PubMed2006

Nardilysin enhances ectodomain shedding of heparin-binding epidermal growth factor-like growth factor through activation of tumor necrosis factor-alpha-converting enzyme.

Like other members of the epidermal growth factor family, heparin-binding epidermal growth factor-like growth factor (HB-EGF) is synthesized as a transmembrane protein that can be shed enzymatically to release a soluble growth factor. Ectodomain shedding is essential to the biological functions of HB-EGF and is strictly regulated. However, the mechanism that induces the shedding remains unclear. We have recently identified nardilysin (N-arginine dibasic convertase (NRDc)), a metalloendopeptidase of the M16 family, as a protein that specifically binds HB-EGF (Nishi, E., Prat, A., Hospital, V., Elenius, K., and Klagsbrun, M. (2001) EMBO J. 20, 3342-3350). Here, we show that NRDc enhances ectodomain shedding of HB-EGF. When expressed in cells, NRDc enhanced the shedding in cooperation with tumor necrosis factor-alpha-converting enzyme (TACE; ADAM17). NRDc formed a complex with TACE, a process promoted by phorbol esters, general activators of ectodomain shedding. NRDc enhanced TACE-induced HB-EGF cleavage in a peptide cleavage assay, indicating that the interaction with NRDc potentiates the catalytic activity of TACE. The metalloendopeptidase activity of NRDc was not required for the enhancement of HB-EGF shedding. Notably, a reduction in the expression of NRDc caused by RNA interference was accompanied by a decrease in ectodomain shedding of HB-EGF. These results indicate the essential role of NRDc in HB-EGF ectodomain shedding and reveal how the shedding is regulated by the modulation of sheddase activity.

ADAM Proteins↗
PubMed2006

Down-regulation of cardiac apelin system in hypertrophied and failing hearts: Possible role of angiotensin II-angiotensin type 1 receptor system.

Cardiac apelin has recently been suggested to contribute to the pathophysiology of heart failure (HF) in humans. In animal experiments, its infusion acutely improved systolic as well as diastolic LV function. Although its deficit could critically determine the cardiac dysfunction, its regulatory mechanism is unknown. Accordingly, we investigated the role and regulation of the cardiac apelin system in the diseased heart using Dahl salt-sensitive rats, which show a distinctive transition from compensatory LV hypertrophy (LVH) to HF. In the compensatory LVH stage, apelin and its receptor APJ mRNA showed no change compared with control animals, while these were markedly down-regulated in the HF stage (72% and 57% decrease, respectively). The rats were chronically treated with telmisartan (angiotensin type 1 receptor blocker [ARB], 5 mg/kg/day, n=9), ONO-4817 (matrix metalloproteinase [MMP] inhibitor, 200 mg/kg/day, n=9), bisoprolol (beta blocker, 3 mg/kg/day, n=6) or vehicle (0.5%CMC, n=9) from the LVH stage. Although the functional improvements were similar among the three treated groups 6 weeks after treatment, restoration of cardiac apelin and APJ expression was observed only in the ARB group. Furthermore, in angiotensin II-infused rats, cardiac apelin mRNA was decreased after 24 h of treatment and its restoration was achieved by treatment with ARB. These results indicate that the cardiac apelin system is markedly down-regulated in experimental HF and may be regulated by the angiotensin II-angiotensin type 1 receptor system directly. Inhibition of the renin-angiotensin system may have beneficial effects, at least in part, through restoration of the cardiac apelin system in the treatment of HF.

Angiotensin II↗
PubMed2006

Constitutive GDP/GTP exchange and secretion-dependent GTP hydrolysis activity for Rab27 in platelets.

We have previously demonstrated that Rab27 regulates dense granule secretion in platelets. Here, we analyzed the activation status of Rab27 using the thin layer chromatography method analyzing nucleotides bound to immunoprecipitated Rab27 and the pull-down method quantifying Rab27 bound to the GTP-Rab27-binding domain (synaptotagmin-like protein (Slp)-homology domain) of its specific effector, Slac2-b. We found that Rab27 was predominantly present in the GTP-bound form in unstimulated platelets due to constitutive GDP/GTP exchange activity. The GTP-bound Rab27 level drastically decreased due to enhanced GTP hydrolysis activity upon granule secretion. In permeabilized platelets, increase of Ca(2+) concentration induced dense granule secretion with concomitant decrease of GTP-Rab27, whereas in non-hydrolyzable GTP analogue GppNHp (beta-gamma-imidoguanosine 5'-triphosphate)-loaded permeabilized platelets, the GTP (GppNHp)-Rab27 level did not decrease upon the Ca(2+)-induced secretion. These data suggested that GTP hydrolysis of Rab27 was not necessary for inducing the secretion. Taken together, Rab27 is maintained in the active status in unstimulated platelets, which could function to keep dense granules in a preparative status for secretion.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Complementary appearance of glucose and lipid metabolism in cardiac sarcoidosis.

Sarcoidosis is a non-caseating granulomatous systemic disease of unknown pathogenesis, and cardiac involvement is the most important prognostic factor. We have evaluated the value of the combined study of F-18 fluoro-2-deoxyglucose positron emission tomography and iodine-123 labeled 15-(p-iodophenyl)-3R,S-methylpentadecanoic acid single-photon emission tomography for the assessment of cardiac involvement of sarcoidosis, by comparing the findings with gadolinium magnetic resonance in a patient with histologically-proven cardiac sarcoidosis.

Aged↗