尾崎 行男

In-stent thrombosis (IST) after carotid artery stenting (CAS) is a rare but potentially devastating complication. We present a case of early IST after CAS despite sufficient antiplatelet therapy in a patient with bladder cancer. A 77-year-old man under preventive triple antiplatelet therapy underwent CAS without any intra-or periprocedural complications. However, the patient developed a large asymptomatic IST 6 days after CAS. Anticoagulant therapy with argatroban was reintroduced to treat IST concomitant with antiplatelet agents. Subsequently, the IST shrank and disappeared without any thrombotic symptoms. Malignancy is regarded as an acquired thrombophilic condition associated with a significant risk of thrombosis. In the field of coronary stents, cancer is associated with a significant increasing risk of IST. The cause of IST in our case was possibly related in hypercoagulable state because of the patient's cancer. Attention for IST should be paid in CAS cases with these risk factors, and repeated examination is recommended.

Background: The prevalence and clinical sequelae of optical frequency domain imaging (OFDI)-detected intimal flaps caused by vessel trauma or plaque rupture in the proximal native coronary arteries have not been described. Methods and Results: OFDI investigation was performed following stent implantation in patients with ST-segment elevation myocardial infarction (STEMI). We defined a flap-like structure (FS) as a disruption or discontinuation of the endoluminal vessel surface, and classified as actual flap or artifact. FS in the left main stem, or maximally 20mm distal to the guiding catheter in the proximal right coronary artery were assessed. A total of 8,931 frames in 97 patients were analyzed in a frame-by-frame fashion (0.125-mm interval). OFDI identified 8 FS in 7 patients, none of which was evident angiographically. All FS were left untreated because the operators per protocol were blinded to the OFDI images. A total of 5 FS in 5 patients (5.1%) appeared to be actual flaps in which only the intima was involved (mean distance from guiding catheter: 4.8 +/- 2.7 mm). The remaining 3 FS in 3 patients were artifacts; namely, residual blood and interface light reflectivity. There were no adverse cardiac events during 6-months follow-up. Conclusions: In 5.1% of STEM patients, post-procedural OFDI identified flaps with minimal involvement of the intima in the proximal coronary arteries. A precise interpretation of FS may help decision making to avoid unnecessary procedures. (Clinical Trial Registration Information: ClinicalTrials.gov identifier: NCT01271361.)

First generation drug-eluting stents have considerably reduced in-stent restenosis and broadened the applications of percutaneous coronary interventions for the treatment of coronary artery disease. The polymer is an integral part of drug-eluting stents in that, it controls the release of an antiproliferative drug. The main safety concern of first generation drug-eluting stents with permanent polymers-stent thrombosis-has been caused by local hypersensitivity, delayed vessel healing, and endothelial dysfunction. This has prompted the development of newer generation drug-eluting stents with biodegradable polymers or even polymer-free drug-eluting stents. Recent clinical trials have shown the safety and efficacy of drug-eluting stents with biodegradable polymer, with proven reductions in very late stent thrombosis as compared to first generation drug-eluting stents. However, the concept of using a permanent metallic prosthesis implies major drawbacks, such as the presence of a foreign material within the native coronary artery that causes vascular inflammation and neoatherosclerosis, and also impedes the restoration of the vasomotor function of the stented segment. Bioresorbable scaffolds have been introduced to overcome these limitations, since they provide temporary scaffolding and then disappear, liberating the treated vessel from its cage. This update article presents the current status of these new technologies and highlights their future perspectives in interventional cardiology. (C) 2012 Sociedad Espanola de Cardiologia. Published by Elsevier Espana, S. L. All rights reserved.

Platelets play a pivotal role in thrombosis and hemostasis; however, a series of recent research has demonstrated that platelets also play roles other than in clotting. We discovered that a platelet receptor, C-type lectin-like receptor 2 (CLEC-2), facilitates lymph/blood vessel separation in the developmental stage by binding to its ligand, podoplanin, on lymphatic endothelial cells. We have previously reported that CLEC-2-deficient mice showed blood-filled lymphatic vessels and severe edema, suggesting that CLEC-2 is essential for lymph/blood vessel separation; however, its mechanism has not been elucidated to date. Although CLEC-2 is mainly expressed in platelets and megakaryocytes, marginal expression is observed in other blood cells in mice. We found that specific deletion of CLEC-2 from platelets/megakaryocytes also impaired blood/lymphatic vessel separation, suggesting that CLEC-2 in platelets is required for separation. Based on several in vitro experiments, we proposed the mechanism of blood/lymphatic vessel separation as follows: In the developmental stage, when lymphatic vessels separate from cardinal veins, CLEC-2 in platelets binds to podoplanin in lymphatic endothelial cells. Subsequent platelet activation results in the release of platelet granule contents, including the transforming growth factor 8 family. These platelet contents inhibit migration, proliferation, and tube formation of lymphatic endothelial cells, which facilitates blood/lymphatic vessel separation. We also found that soluble CLEC-2 is released upon platelet activation. We hypothesized that plasma soluble CLEC-2 could be a marker of thrombosis and established an ELISA system to measure soluble CLEC-2. Although current tests for in vivo platelet activation require special methods for blood sampling, soluble CLEC-2 can be measured with ordinary blood sampling. We are now investigating the potential of soluble CLEC-2 as a useful marker for in vivo platelet activation.

Background: The role of combined evaluation of myocardial perfusion imaging (MPI; by single-photon emission computed tomography) and computed tomography angiography (CTA) for risk stratification of coronary artery disease was evaluated. For CTA, the extent of luminal stenosis, and also the features of high-risk plaques (HRP, including positive remodeling and low attenuation) were evaluated. Methods and Results: A total of 304 patients (65 +/- 11 years, male 72%, median follow-up: 24 months) who underwent CTA and MPI were enrolled in the study. Summed stress scores and summed difference scores (SDS) for MPI, stenosis, and HRP were evaluated, and event rates were compared. Cardiac events were defined as acute coronary event including cardiac death or non-fatal acute myocardial infarction, and unstable angina requiring revascularization. Of 304 patients, 51 (16.8%) underwent early revascularization. In the remaining 253 patients, an event occurred in 11 (4.3%). HRP (hazard ratio [HR], 4.75, P=0.00171) and stenosis (+) with SDS >0 (HR, 4.58, P=0.0461) were). HRP (hazard ratio [HR], 4.75, P=0.00171) and stenosis (+) with SDS >0 (HR, 4.58, P=0.0461) were significant independent predictors of cardiac event. The event rate for stenosis (+) with SDS >0 was significantly higher than others (log-rank P=0.0490). The event rates were significantly different between HRP(+) and HRP(-) (16.1% vs. 2.7%, log-rank P=0.0013). Conclusions: HRP on CTA was an independent predictor of acute coronary events, as was stenosis (+) with SDS >0, and HRP had increased prognostic value over stenosis and abnormal MPI findings. (Circ J 2013; 77: 411-417)

Background: The JAPAN-ACS (Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome) trial showed that intensive statin therapy could induce significant coronary plaque regression in acute coronary syndrome (ACS). We evaluated the impact of metabolic syndrome (MetS) and its components on coronary plaque regression in the JAPAN-ACS patients. Methods and Results: Serial intravascular ultrasound measurements over 8-12 months were performed in 242 ACS patients receiving pitavastatin or atorvastatin. Patients were divided into groups according to the presence of MetS or the number of MetS components. Although the percent change in plaque volume (%PV) was not significantly different between the MetS (n=119) and non-MetS (n=123) groups (P=0.50), it was significantly associated with an increasing number of MetS components (component 0: -24.0%, n=7; components 1: -20.8%, n=31; components 2: -16.1%, n=69; components 3: -18.7%, n=83; components 4: -13.5%, n=52; P=0.037 for trend). The percent change in body mass index (%BMI) significantly correlated with %PV (r=0.15, P=0.021), especially in the MetS components 4 group (r=0.35, P=0.017). In addition, %BMI was an independent predictor of plaque regression after adjustment for the changes of low- and high-density lipoprotein cholesterol, triglycerides and HbA1c. Conclusions: The clustering of MetS components, but not the presence of MetS itself, could attenuate coronary plaque regression during intensive statin therapy in ACS patients. Therefore, to achieve a greater degree of plaque regression, it is necessary to treat to each MetS component and use lifestyle modification. (Circ J 2012; 76: 2840-2847)

Introduction: Cilostazol has been shown to be effective for prevention and treatment of cerebral infarction. However, there appears to be no widely accepted method appropriate for monitoring cilostazol. We attempted to establish an assay system for cilostazol monitoring, using platelet aggregation induced by arachidonic acid (AA) in the presence of PGE(1) which upregulates intracellular cyclic AMP. Methods: Blood was drawn from stroke patients before and after cilostazol intake. AA-induced platelet aggregation after pretreatment with 0 similar to 30 nM PGE(1) for 2 minutes was measured by light transmittance aggregometry. Results: AA-induced platelet aggregation was 73.1 +/- 2.2% in the absence of PGE(1), and pretreatment with 30 nM PGE(1) had virtually no inhibitory effect on platelet aggregation prior to cilostazol intake. In contrast, after cilostazol intake, 30 nM PGE(1) significantly inhibited platelet aggregation to 12.7 +/- 4.5% (p=7.8x10(-11)), while in the absence of PGE(1) platelet aggregation remained similar to that of prior-to-cilostazol value (70.6 +/- 3.5%). The plasma concentration of cilostazol ranged from 0.55 to 3.51 mu M. In the presence of 30 nM PGE(1), all the patients with cilostazol concentrations exceeding 1 mu M had their platelet aggregation inhibited almost completely. ROC analysis suggests that AA-induced platelet aggregation in the presence of 30 nM PGE(1) had the excellent sensitivity (90.5%) and specificity (88.4%) for monitoring cilostazol. Conclusions: AA-induced platelet aggregation in the presence of 30 nM PGE(1) could give good estimate on plasma concentrations of cilostazol. It is suggested that this system is a good tool for monitoring cilostazol. (c) 2012 Published by Elsevier Ltd.

While human platelets release endogenous brain-derived neurotrophic factor (BDNF) upon activation, a previous report on MEG-01, a megakaryocytic cell line, found no trace of BDNF production, and the pathophysiological function of platelet BDNF has remained elusive. In the present study, we demonstrate that MEG-01 produces BDNF in the presence of TPO and that this serves to potentiate cell proliferation. Our in vitro findings suggest that BDNF regulates MEG-01 proliferation in an autocrine manner, and we suggest that BDNF may be a physiological autocrine regulator of megakaryocyte progenitors. (C) 2012 Elsevier Inc. All rights reserved.

Background: The incidence, risk factors, and outcome of contrast-induced acute kidney injury (CI-AKI) in 730 patients with acute coronary syndrome (ACS) undergoing emergency percutaneous coronary intervention (PCI), whose contrast volume was below maximum allowable contrast dose (MACD) was prospectively investigated. Methods and Results: MACD was defined as (5 mlxbody weight [kW/baseline creatinine [mg/dl]). CI-AKI was defined as a greater than 25% increase in creatinine from the baseline or an absolute increase of >= 0.5 mg/dl within 48 h after the procedure. CI-AKI occurred in 212 (29%) patients. Patients with CI-AKI had a higher risk for in-hospital mortality (9.4% vs. 1.5%, P<0.001) and a longer stay in the coronary care unit (median, 4.0 vs. 3.0 days, P<0.001) compared with those without CI-AKI. In a multivariate logistic analysis including 20 clinical variables, elevated glucose levels as variables categorized into quartiles were independently (P<0.001) associated with the development of CI-AKI. In addition, this relationship was seen in both the subgroup of patients with known diabetes and that of those without known diabetes. Conclusions: CI-AKI might occur commonly and could be be associated with a more complicated clinical course in ACS patients undergoing emergency PCI whose contrast volume does not exceed MACD. Elevated pre-procedural glucose might be a powerful and independent risk factor for the development of CI-AKI in this population. (Circ J 2012; 76: 1848-1855)

Background: While the utilization of integrated backscatter intravascular ultrasound (IB-IVUS) for the quantitative in vivo assessment of coronary plaque continues to grow, the validity of IB-IVUS images obtained from newly developed and conventional systems remains uncertain. Methods and Results: To assess the accuracy and reliability of a newly developed IB-IVUS system (VISIWAVE) as compared to the conventional system (Clearview), we compared quantitative IB-IVUS plaque characteristics in the 2 systems using 125 post-mortem specimens from 26 coronary arteries in 11 cadavers, as well as using 200 clinical plaques in 32 patients undergoing coronary intervention. The overall agreement between the histological and IB-IVUS diagnoses using VISIWAVE (Cohen's kappa=0.82, 95%CI: 0.73-0.90) was similar to that using Clearview (Cohen's kappa=0.80, 95%Cl: 0.71-0.89). The 2 systems also demonstrated comparably high sensitivity and specificity. In the direct comparison, the overall agreement between IB-IVUS diagnoses using VISIWAVE and Clearview was also excellent (Cohen's kappa=0.87, 95%Cl: 0.78-0.95). In the clinical comparison, measured plaque dimensions were similar (VISIWAVE: 8.27 +/- 3.46 mm(2) vs. Clearview; 8.31 +/- 3.46 mm(2), P=0.44) and there was strong concordance between both greyscale and IB-IVUS parameters. Conclusions: There was close agreement of analyzed results in both systems when compared with the gold standard of histology. Both systems are able to reliably and accurately characterize coronary plaque and thereby make a valuable contribution to our understanding of atherosclerosis. (Circ J 2012; 76: 1678-1686)

We have previously shown that a single nucleotide polymorphism rs11536889 in the 3'-untranslated region (UTR) of TLR4 was associated with periodontitis. In this study the effects of this single nucleotide polymorphism on Toll-like receptor (TLR) 4 expression were investigated. Monocytes from subjects with the C/C genotype expressed higher levels of TLR4 on their surfaces than those from subjects with the other genotypes. Peripheral blood mononuclear cells (PBMCs) from the C/C and G/C subjects secreted higher levels of IL-8 in response to lipopolysaccharide (LPS), a TLR4 ligand, than the cells from the G/G subjects. However, there was no significant difference in TLR4 mRNA levels in PBMCs from the subjects with each genotype. After stimulation with tripalmitoylated CSK4 (Pam(3)CSK(4)), TLR4 mRNA levels increased in PBMCs from both the C/C and G/G subjects, whereas TLR4 protein levels increased in PBMCs from the C/C but not G/G subjects. Transient transfection of a series of chimeric luciferase constructs revealed that a fragment of 3'-UTR containing rs11536889 G allele, but not C allele, suppressed luciferase activity induced by LPS or IL-6. Two microRNAs, hsa-miR-1236 and hsa-miR-642a, were predicted to bind to rs11536889 G allele. Inhibition of these microRNAs reversed the suppressed luciferase activity. These microRNA inhibitors also up-regulated endogenous TLR4 protein on THP-1 cells (the G/G genotype) after LPS stimulation. Furthermore, mutant microRNAs that bind to the C allele inhibited the luciferase activity of the construct containing the C allele. These results indicate that genetic variation of rs11536889 contributes to translational regulation of TLR4, possibly by binding to microRNAs.

INTRODUCTION Myocardial scintigraphy with I-123-15-(p-iodophenyl)-3-methyl pentadecanoic acid (I-123-BMIPP) is used to evaluate impaired fatty acid metabolism. B-type natriuretic peptide (BNP), which is secreted by the ventricular myocardium on stretching and/or pressure overload, is a useful cardiac biomarker. This study aimed to evaluate the usefulness of I-123-BMIPP imaging and serum BNP levels in patients with heart failure (HF). METHODS 113 patients with HF were enrolled. There were 68 patients with ischaemic heart disease (IHD) and 22 with overt HF. Cardiac scintigraphy was performed 7 +/- 3 days after admission, and heart-to-mediastinum (H/M) count ratios on early and delayed images and washout rates (WR) of I-123-BMIPP were recorded. Serum BNP levels were recorded on the day of I-123-BMIPP imaging. The ejection fraction (EF) was calculated just before cardiac scintigraphy using conventional echocardiography. RESULTS The mean BNP level and EF were 282 pg/mL and 47%, respectively, with significant correlation between them. The mean H/M count ratios on early and delayed images were 2.29 and 1.93, respectively, showing significant positive correlations with EF (r = 0.31, p = 0.0006). The WR was significantly correlated with EF (r = -0.36, p < 0.0001) and BNP levels (r = 0.33, p = 0.003), and mean WR was significantly higher in patients with overt HF compared to those without (p < 0.001). Patients with IHD had significantly higher EFs than those with non-IHD (p = 0.03). CONCLUSION The evaluation of impaired myocardial metabolism using I-123-BMIPP scintigraphy and serum BNP levels appears to be useful for the evaluation of severity of HF.

Background: The differences in the coronary plaque characteristics between patients with mild chronic kidney disease (CKD) (estimated glomerular filtration rate [eGFR] 30-59 ml . min(-1) . 1.73 m(-2)) and those without CKD (eGFR >= 60) by 320-row area detector computed tomography (CT) have not been studied. Methods and Results: We enrolled 487 patients undergoing coronary CT angiography with suspected stable coronary artery disease (mean age: 66.6 +/- 10.8 years, 131 with mild CKD) and analyzed 6,352 segments. All coronary plaques were characterized for the presence of vessel remodeling, plaque consistency and the disposition of coronary calcification, and a plaque with positive vessel remodeling and/or low-attenuation was defined as high risk. The number of diseased segments per patient was higher in mild CKD patients than in those without CKD (4.61 +/- 3.83 vs. 2.95 +/- 3.11, P<0.0001). The prevalence of severe stenosis (>= 70% luminal diameter) was significantly higher in cases of mild CKD than in no CKD (35.1% vs. 19.4%, P=0.0003), but there was no significant difference in the prevalence of high-risk plaque (13.0% vs. 9.8%, P=0.3189). Conclusions: The severity of coronary artery stenosis was higher in the patients with mild CKD, though there was no significant difference in the prevalence of high-risk plaque. We suggest that the high risk of coronary events in patients with CKD is related to the severity of stenosis rather than to the characteristics of plaque. (Circ J 2012; 76: 1436-1441)

The platelet activation receptor CLEC-2 plays crucial roles in thrombosis/hemostasis, tumor metastasis, and lymphangiogenesis, although its role in thrombosis/hemostasis remains controversial. An endogenous ligand for CLEC-2, podoplanin, is expressed in lymphatic endothelial cells (LECs). We and others have reported that CLEC-2-deficiency is lethal at mouse embryonic/neonatal stages associated with blood-filled lymphatics, indicating that CLEC-2 is essential for blood/lymphatic vessel separation. However, its mechanism, and whether CLEC-2 in platelets is necessary for this separation, remains unknown. We found that specific deletion of CLEC-2 from platelets leads to the misconnection of blood/lymphatic vessels. CLEC-2(+/+) platelets platelets, but not by CLEC-2(-/-) platelets, inhibited LEC migration, proliferation, and tube formation but had no effect on human umbilical vein endothelial cells. Additionally, supernatants from activated platelets significantly inhibited these three functions in LECs, suggesting that released granule contents regulate blood/lymphatic vessel separation. Bone morphologic protein-9 (BMP-9), which we found to be present in platelets and released upon activation, appears to play a key role in regulating LEC functions. Only BMP-9 inhibited tube formation, although other releasates including transforming growth factor-beta and platelet factor 4 inhibited proliferation and/or migration. We propose that platelets regulate blood/lymphatic vessel separation by inhibiting the proliferation, migration, and tube formation of LECs, mainly because of the release of BMP-9 upon activation by CLEC-2/podoplanin interaction.

Thrombosis and hemostasis related disease have a heavy burden in cardiovascular disease and it is important to have a journal where research into this can be accessed by all. © 2012 ten Cate and Ozaki licensee BioMed Central Ltd.

We retrospectively studied 89 patients with chronic hepatitis C virus (HCV) infection, including 50 chronic hepatitis (CH) cases, 18 liver cirrhosis (LC) cases, and 21 LC with hepatocellular carcinoma (LC + HCC) cases, with regard to various factors related with thrombocytopenia. The platelet count decreased with the stage advancement of liver diseases. Multiple regression analysis revealed that splenomegaly and von Willebrand factor (vWF) were explanatory variables that correlated with thrombocytopenia. Splenomegaly appears to be the most responsible factor, although there are a considerable number of thrombocytopenic cases without splenomegaly, suggesting other factors may also be responsible. The vWF level is inversely correlated with the platelet count. Soluble thrombomodulin, a marker of endothelial dysfunction, increases with the advancement of liver fibrosis. It is positively correlated with vWF and inversely with the platelet count. Our present results imply that vascular endothelial dysfunction is also involved in thrombocytopenia during chronic HCV infection.

Thrombus formation on disrupted atherosclerotic lesion is a key mechanism of cardiovascular events. Podoplanin (Aggrus), expressed on the surface of several tumor cells, is an endogenous ligand for C-type lectin-like receptor 2 (CLEC-2), and is involved in tumor cell-induced platelet aggregation and itsmalignant potency. Podoplanin, which is also expressed in lymphatic endothelial cells, facilitates blood/lymphatic vessel separation. However, podoplanin expression in atherosclerotic lesion has not been investigated. To clarify podoplanin expression in atherosclerotic lesion and to assess its importance for the onset of cardiovascular events, we examined podoplanin expression in abdominal aortas obtained from 31 autopsy cases. Immunohistochemical analysis indicated that podoplanin was localized to smooth muscle cells and macrophages. Moreover, podoplanin immunoreactivity was increased in advanced atherosclerotic lesions containing necrotic core, many macrophages and smooth muscle cells, compared with early lesions composed of smooth muscle cells and small numbers of macrophages. Furthermore, Western-blot and real time-PCR analyses showed that podoplanin expression was significantly enhanced in advanced atherosclerotic lesions, compared with early lesions. These results suggest that podoplanin contributes to thrombotic property of advanced stages of atherosclerosis and that it might be a novel molecular target for an anti-thrombus drug. (C) 2012 Elsevier Ltd. All rights reserved.

Background: The JAPAN-ACS study demonstrated that statins significantly reduced coronary plaque volume in patients with acute coronary syndrome (ACS). The clinical implications of plaque regression for clinical outcomes in ACS patients has not been established. The Extended JAPAN-ACS study was conducted to evaluate the relationship between coronary plaque regression and long-term clinical outcome, and to explore the factors associated with cardiovascular events. Methods and Results: Patients with intravascular ultrasound (IVUS) data at both enrollment and follow-up in the JAPAN-ACS study were enrolled and observed for at least 3 years. Patients were divided into lesser and greater coronary plaque regression groups. The primary endpoint was defined as a composite of the following events: cardiovascular death, nonfatal myocardial infarction, nonfatal cerebral infarction, and unstable angina. The median value of the percent change in plaque volume, -18.0%, was used as a cutoff point. There were 4 primary events (3.4%) in the lesser regression group, and 2 events (1.7%) in the greater regression group (P=0.4). Cumulative secondary cardiovascular events did not differ between the 2 groups. Multivariate analysis identified the high-density lipoprotein cholesterol (HDL-C) at baseline and the % change of the external elastic membrane volume as independent risk factors of cardiovascular events. Conclusions: Coronary plaque regression induced by an intensive statin regimen did not predict future cardiovascular events in ACS patients. Rather, the baseline HDL-C level and reverse vessel remodeling might serve as predictors for cardiovascular events. (Circ J 2012; 76: 825-832)

Effects of exogenous gibberellin (GA), gibberellin biosynthesis inhibitors, and abscisic acid (ABA) on rhizome morphogenesis (transition to storage organ) were examined in seed-derived lotus (Nelumbo nucifera Gaertn.) plants. Exogenous 1 mg.L-1 GA(3) promoted rhizome elongation without swelling under short-day conditions, whereas uniconazole with 0.1 mg.L-1 and paclobutrazole with 0.1, 1, and 10 mg.L-1 stimulated rhizome enlargement under long-day conditions. Rhizomes of the plants grown with 10 and 25 mg.L-1 ABA also enlarged under long-day conditions. Rhizome enlargement was closely related to cell enlargement and starch grain accumulation. In all the experiments, starch grain accumulation in expanded cells was recognized in the enlarged rhizomes, but not in the elongated rhizomes. It was suggested that rhizome transition to the storage organ was regulated via biosynthesis of GA and/or ABA.

Kakrol (Momordica dioica Roxb.) is a cucurbitaceous vegetable native to India and Bangladesh. Bitter gourd (Momordica charantia Linn.), a species related to kakrol, has been shown to have pharmacological properties including antidiabetic and antisteatotic effects. In this study, we investigated the effect of dietary kakrol on lipid metabolism in rats. Sprague-Dawley rats were fed AIN-76 formula diets containing 3% freeze-dried powders of whole kakrol or bitter gourd for two weeks. Results showed significantly lowered liver cholesterol and triacylglycerol levels in rats fed on both diets. Fecal lipid excretion increased in rats fed the kakrol diet, and lymphatic transport of triacylglycerol and phospholipids decreased in rats fed the kakrol diet after permanent lymph cannulation. Furthermore, n-butanol extract from kakrol caused a significant concentration-dependent decrease in the pancreatic lipase activity in vitro. These results indicate that the mechanisms of action on lipid metabolism in kakrol and bitter gourd are different and that dietary kakrol reduces liver lipids by inhibiting lipid absorption.

The c-type lectin-like receptor 2 (CLEC-2) was first identified from a bio-informatic screen for c-type lectin-like receptors. However, neither its function nor its ligand(s) had been elucidated for several years. In 2006, we reported that the receptor is expressed on the surface of platelets and serves as a receptor for the snake venom rhodocytin, which potently stimulates platelet aggregation. Since then CLEC-2 has been intensively investigated, and its endogenous/exogenous ligands and several physiological/pathological roles have been clarified. In this article and its accompanying poster, we outline the structure, distribution, signal transduction mechanism and functions of CLEC-2.