Angiographic coronary lesion complexity has been reported to predict plaque vulnerability. It is important to develop a noninvasive blood biomarker for accurate prognostication of angiographically complex lesions in patients with coronary artery disease CAD.

Coronary lesions were classified as simple or complex lesions based on coronary plaque morphology. The authors have no other funding, financial relationships, or conflicts of interest to disclose. We prospectively asked consecutive patients undergoing coronary angiography for the evaluation of CAD in our hospital from September to February to participate in this study.

The exclusion criteria were patients with a history of coronary intervention or coronary artery bypass graft surgery, suspected myocarditis or pericarditis, diabetes mellitus DMmalignant disease, active inflammatory disease, and advanced renal disease. In total, consecutive patients with CAD were enrolled in this study.

Patients with ACS included 34 with acute myocardial infarction and 24 with unstable angina. Written informed consents were obtained from all patients for their participation. This study was approved by the Ethics Committee of Fujian Medical University and conducted in accordance with the principles outlined in the Declaration of Helsinki. Conventional invasive coronary angiography was performed according to standard protocols.

Two experienced interventional cardiologists, blind to the patients' clinical characteristics and biochemical results, reviewed all the angiographic images. Coronary lesion morphology was assessed as previously reported Briefly, complex lesions were defined according to the presence of at least 1 of the following features: 1 irregular morphology or scalloped borders, or both; 2 overhanging or abrupt edges perpendicular to the vessel wall; 3 plaque ulceration; and 4 the presence of filling defects consistent with intracoronary thrombus.

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Venous blood was drawn from all patients just before the angiographic procedure. All of the statistical analyses were performed using SPSS version The baseline clinical characteristics of each group are listed in Table S1. The baseline clinical characteristics of each group are listed in Table S2.

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Associations between the presence of complex lesions and all other parameters were first analyzed by univariate logistic regression analysis Table S3.

Associations between the presence of multiple complex lesions and all other parameters were first analyzed by univariate logistic regression analysis Table S4.

circulating levels of lectin

Rupture of vulnerable plaques with subsequent thrombus formation has been implicated as the most common pathogenic mechanism responsible for the development of ACS. As the angiographic hallmark of plaque vulnerability, angiographically complex lesions correlate with pathologic plaque rupture and thrombus 29 and have been shown to provide prognostic information.

Therefore, it is important to develop a noninvasive blood biomarker to provide incremental predictive value for accurate prognostication of angiographically complex lesions in patients with CAD when added to other traditional risk factors. Although vulnerable plaques are more common in ACS patients than in stable CAD patients, the incidence of the presence of vulnerable plaques is also high in the latter. There are still some important limitations needed to be considered in this study.

First, coronary angiography provides insufficient information regarding true lesion complexity and coronary thrombus, which can be evaluated in humans by updated vascular imaging modalities including virtual histology intravascular ultrasound, optical coherence tomography, and magnetic resonance imaging. Therefore, it is necessary to validate our data in prospective studies with a larger sample size.

Last, we excluded diabetic patients to avoid the contribution of DM as a potential confounder, which might include some bias because complex lesions appear to be more prominent in patients with DM than in patients without DM. However, further studies are needed to define more clearly the significance of these findings.Lectin-like oxidized low density lipoprotein receptor-1 LOX-1the main oxidized low-density lipoprotein OxLDL in endothelial cells, is upregulated in atherosclerotic lesions and is involved in several cellular processes that regulate the pathogenesis of atherosclerosis.

The LOX-1 expressed on the cell surface can be proteolytically cleaved and released in a soluble form sLOX-1 in the circulation under pathological conditions. Serum levels of sLOX-1, in fact, are elevated at the early stages of acute coronary syndrome and are associated with coronary plaque vulnerability and with the presence of multiple complex coronary lesions.

Moreover, in subjects with stable CAD, levels of serum sLOX-1 are associated with the presence of lesions in the proximal and mid-segments of the left anterior descending artery that are the most prone to rupture; in subjects undergoing percutaneous coronary intervention, baseline preprocedural serum sLOX-1 levels are associated with the incidence of periprocedural myocardial infarction. Altogether, these findings suggest that circulating levels of sLOX-1 might be a diagnostic and prognostic marker for atherosclerotic-related events.

High levels of low density lipoprotein LDL represent a major risk factor for atherosclerosis, since the oxidation of LDL is a key process in the initiation and progression of atherosclerotic lesion development.

Oxidized LDL OxLDL acts through the interaction with several scavenger receptors, expressed differentially on the surface of the cells of the arterial wall and inflammatory circulating cells involved in the atherosclerotic process. Through the interaction with LOX-1, OxLDL activates endothelial cells and induces endothelial dysfunction, SMC proliferation, and apoptosis; participates in the transformation of macrophages into foam cells, and induces platelet activation [ 3 ].

LOX-1 is undetectable in healthy vessels but overexpressed in atherosclerotic lesions [ 2 ], where it actively participates in the initiation and progression of the disease, as demonstrated by LOX-1 deletion or overexpression studies in animal models [ 45 ]. It contains 4 domains: a short N-terminal cytoplasmic domain, a transmembrane domain, a neck domain, and a lectin-like extracellular C-terminal domain which interacts with OxLDL [ 6 ].

The extracellular domain can be proteolytically cleaved and released as a soluble form sLOX-1 [ 7 ]. In addition, the inflammatory factor IL stimulates sLOX-1 cleavage from cell membrane, and ADAM10 a disintegrin and metalloproteinase domain-containing protein 10 appears to be one of the proteases involved in this process [ 10 ] Figure 1. Schematic illustration of sLOX-1 release from cell membrane. Under acute inflammatory conditions, such as acute coronary syndrome ACSthe increase of proinflammatory cytokines leads to protease activation and to subsequent sLOX-1 release.

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As elevated plasma levels of soluble receptors may reflect the increased expression of membrane-bound receptors and disease activities, circulating sLOX-1 has been suggested as a potential cardiovascular disease biomarker. Acute coronary syndrome ACSwhich derives from the rupture of atheromatous plaques followed by thrombus formation, is one of the major causes of death and morbidity in developed countries.

Atherosclerotic plaques with abundant lipid-rich macrophages and activated SMCs appear to be more prone to rupture [ 11 ]; within these plaques, LOX-1 is highly expressed mainly by SMCs and macrophages [ 2 ], and participates in the induction of SMC apoptosis and the production of metalloproteases from endothelial cells [ 12 ], suggesting the involvement of LOX-1 in lesion destabilization.

In addition, an enhanced protease activity within atherosclerotic lesions may increase sLOX-1 production. These observations suggest the possibility that, although LOX-1 expression is higher in atherosclerotic-related diseases and is increased by proinflammatory stimuli, sLOX-1 levels do not reflect only the presence of an atherosclerotic disease or an inflammatory status but rather the instability of an atherosclerotic plaque, thus discriminating ACS from other CAG groups.

Interestingly, peak levels of sLOX-1 were observed on admission of or after percutaneous coronary intervention PCIwhile troponin T, a marker of cardiac injury, peaked around day 1 [ 13 ]; again, no correlation was found between sLOX-1 and troponin T [ 13 ], reinforcing the hypothesis that sLOX-1 is not a marker of cardiac damage but is an early diagnostic marker of ACS, as suggested by the finding that sLOX-1 level on admission showed almost the peak values in ACS patients.

For patients who have no chance to undergo coronary angiography, sLOX-1 level measurement might thus help in identifying the presence of vulnerable atherosclerotic lesions. Multiple complex lesions are often associated with adverse clinical outcomes in ACS patients [ 15 ]; as sLOX-1 levels correlate with the presence of multiple complex lesions, it was hypothesized that sLOX-1 levels might predict the prognosis after ACS [ 16 ].

These observations reinforce the hypothesis that serum sLOX-1 levels may be a biomarker for the vulnerability of atherosclerotic plaque and predict ACS recurrence in ACS patients. The diagnostic accuracy for ACS is essential to identify high-risk patients and differentiate them from non-ACS with similar chest pain and electrocardiogram anomalies; the evaluation of serum cardiac markers, which include cardiac troponins, cardiac kinase-MB CK-MBmyoglobin, and heart-type fatty acid-binding protein H-FABPplays a crucial role in the diagnosis of ACS.

Acute aortic dissection AAD is the most common life-threatening disorder affecting the aorta and it has a high mortality rate if not correctly and rapidly diagnosed. D-dimer evaluation is the standard method to diagnose AAD [ 21 ], but it is not specific, as it is elevated also in acute ischemic events [ 22 ]. Atherosclerotic plaques of the proximal and mid segments of the left anterior descending LAD artery are the most prone to rupture.

Percutaneous coronary intervention PCI is a common procedure for coronary revascularization in patients with stable CAD. In addition, sLOX-1 levels were evaluated before and after the procedure to verify whether it could predict in-stent restenosis ISR during the followup of patients with stable CAD who underwent successful primary PCI [ 28 ]. However, the increase was more robust in patients with ISR at 6-month followup Table 2and postprocedural levels are significantly associated with the risk and severity of ISR after stent implantation [ 28 ].

This suggests that stent implantation induces plaque disruption and upregulation of LOX-1 in several cell types, including platelets, resulting in SMC migration, platelet aggregation, and inflammatory cell recruitment leading to restenosis. Circulating levels of sLOX-1 are significantly higher in metabolic disorders including obesity [ 29 ] and type 2 diabetes mellitus [ 30 ]. The metabolic syndrome MetS constitutes a complex disorder combining obesity, dyslipidemia, hyperglycemia, and hypertension, associated with an increased risk of cardiovascular diseases, especially CAD.Lectin-like oxidized-low-density lipoprotein receptor-1 LOX-1 is increasingly linked to atherosclerotic plaque formation and the soluble form of this receptor may reflect activities of disease.

We investigated the associations among levels of sLOX-1, oxidized-low-density lipoprotein ox-LDLcytokines and the extension of atherosclerosis in patients with coronary artery disease CAD. These findings suggest that sLOX-1 levels are up-regulated during CAD progression and are associated with inflammatory markers.

The measurement of the circulating soluble form of this receptor may be potentially useful in predicting CAD progression in humans.

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This is a preview of subscription content, log in to check access. Nature — Yoshida H, Kondratenko N, Green S, Steinberg D, Quehenberger O Identification of the lectin-like receptor for oxidized low-density lipoprotein in human macrophages and its potential role as a scavenger receptor. Biochem J Pt 1 :9— Khan BV, Parthasarathy SS, Alexander RW, Medford RM Modified low density lipoprotein and its constituents augment cytokine-activated vascular cell adhesion molecule-1 gene expression in human vascular endothelial cells.

J Clin Invest — Arterioscler Thromb Vasc Biol — Circ Res — Biochem J — Circulation — Int J Cardiol. J Lipid Res 49 7 — FEBS Lett — Aderka D The potential biological and clinical significance of the soluble tumor necrosis factor receptors. Cytokine Growth Factor Rev — J Biol Chem — Download references. Monasterio foundation, Via Moruzzi, 1,Pisa, Italy. Correspondence to Giuseppina Basta. Lubrano, V. Lipids 43, — Download citation.

Received : 03 June Accepted : 29 July Published : 10 September Issue Date : October Search SpringerLink Search. Abstract Lectin-like oxidized-low-density lipoprotein receptor-1 LOX-1 is increasingly linked to atherosclerotic plaque formation and the soluble form of this receptor may reflect activities of disease.

circulating levels of lectin

References 1. Acknowledgments The authors thank Manuela Walker for the reviewing of the English language.

Circulating levels of leptin, adiponectin, resistin, and ghrelin in inflammatory bowel disease

View author publications. About this article Cite this article Lubrano, V.Background: There is evidence that adipocytokines play an important role in metabolism and in inflammation. Because human metabolism dramatically changes in inflammatory bowel disease IBD and chronic inflammation is the hallmark of the disease, we studied serum levels of leptin, adiponectin, resistin, and ghrelin in patients with ulcerative colitis UC and Crohn's disease CD in comparison with healthy controls HC.

circulating levels of lectin

Methods: Leptin, adiponectin, resistin, and active ghrelin serum levels were measured in IBD patients 46 UC and 54 CD and in 60 matched HC using commercially available enzyme-linked immunosorbent assays. Leptin, adiponectin, resistin, and ghrelin levels were correlated with disease activity, type, localization, and treatment.

Results: Mean serum leptin levels were Mean serum adiponectin levels were Mean serum resistin levels were Mean serum ghrelin levels were Serum levels of these adipocytokines were not correlated with either C-reactive protein levels or the clinical indices of activity. No association between serum adipocytokines levels and disease localization in both UC and CD patients was found.

Conclusions: Serum levels of adiponectin, resistin, and active ghrelin are increased whereas serum levels of leptin are decreased in patients with IBD. Further studies are needed to elucidate the role of adipocytokines in IBD. Abstract Background: There is evidence that adipocytokines play an important role in metabolism and in inflammation. Publication types Comparative Study.The development of type 1 and type 2 diabetes mellitus has a substantial negative impact on morbidity and mortality and is responsible for substantial individual and socioeconomic costs worldwide.

One of the most serious consequences of diabetes mellitus is the development of diabetic angiopathy, which manifests clinically as microvascular and macrovascular complications.

One microvascular complication, diabetic nephropathy, is the most common cause of end-stage renal disease in developed countries. Although several available therapeutic interventions can delay the onset and progression of diabetic nephropathy, morbidity associated with this disease remains high and new therapeutic approaches are needed.

In addition, not all patients with diabetes mellitus will develop diabetic nephropathy and thus new biomarkers are needed to identify individuals who will develop this life-threatening disease. An increasing body of evidence points toward a role of the complement system in the pathogenesis of diabetic nephropathy. For example, circulating levels of mannose-binding lectin MBLa pattern recognition molecule of the innate immune system, have emerged as a robust biomarker for the development and progression of this disease, and evidence suggests that MBL, H-ficolin, complement component C3 and the membrane attack complex might contribute to renal injury in the hyperglycaemic mileu.

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New approaches to modulate the complement system might lead to the development of new agents to prevent or slow the progression of diabetic nephropathy. Abstract The development of type 1 and type 2 diabetes mellitus has a substantial negative impact on morbidity and mortality and is responsible for substantial individual and socioeconomic costs worldwide.

Publication types Review.The levels of circulating leptin promptly increase in response to an increase in calorie intake. However, leptin is insufficient for preventing weight gain and restraining feeding behavior.

A study led by Gerald I.

circulating levels of lectin

Shulma, professor of physiological chemistry, cellular and molecular physiology and medicine at Yale University found that when there is a drop in the levels of leptin and insulin, the body moves from using glucose to burning fat for fulfilling the energy requirements of the body. The research builds a basis of understanding of how to lose weight if you have diabetes.

Earlier it was known that mammals can switch from burning carbohydrates, such as glucose to instead burning fat. This allows for mammals to get energy without the process of breaking down muscle mass.

Therefore, it was assumed that a decrease in the levels of insulin is what is needed to help burn fat. However, new studies have found that a decrease in the levels of leptin is also needed. Insulin and leptin are both hormones.

While leptin is responsible for curbing appetite, insulin works to decrease the levels of blood sugar by moving glucose out of the body and into the neighboring cells where it is directed stored as fat in the body or used as fuel. If the level of insulin is high, it also prevents fat from being broken down for energy.

Whereas, leptin is linked with appetite and plays an important role in the regulation of energy. In the study, researchers studied the rate of fat and carbohydrate metabolism in a fed and fasted state. It was observed that as the rats fasted, the levels of leptin decreased, activating a pathway that led to fat burning instead of carbohydrate burning.

As a result, the rats use of stored glucose and sugar levels decreased during fasting. The bodies of the rats then broke down the body fat for it to be converted to ketones for energy2. The study further concluded that while the levels of insulin needed to decrease for the process of fat burning to start, a decrease in the levels of leptin was also needed for the fat burning process.

The role of the complement system in diabetic nephropathy

The findings helped researchers understand how different changes in lifestyle have an impact on the success in weight loss.

References Wang, T. Relationships between changes in leptin and insulin resistance levels in obese individuals following weight loss.

Lectin Shield - Intestinal Health Support - Gundry MD

Perry, R. The role of leptin in maintaining plasma glucose during starvation. Necessary cookies are absolutely essential for the website to function properly. This category only includes cookies that ensures basic functionalities and security features of the website.

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Kaspersky 2020

Patients with multiple myeloma MM who undergo autologous stem cell transplantation ASCT are susceptible to severe infections. Low levels of circulating mannan-binding lectin MBL are associated with increased risk of infection. In this prospective study, we evaluated patients who underwent ASCT regarding the effect of MBL on the incidence and severity of febrile episodes.

Although there was no statistical difference regarding the development of febrile episodes between patients with low and normal MBL, among 17 patients with low MBL levels, six out of eleven patients who received antibiotic prophylaxis developed a febrile episode compared with six out of six patients who did not receive antibiotic prophylaxis and developed a febrile episode.

Patients with low MBL levels who responded less frequently to first line antibiotic therapy required more frequent administration of a second more advanced line of antibiotics, independently of receiving or not prophylaxis, and required prolonged hospitalization.

Our results suggest that patient with low MBL levels should receive antibiotic prophylaxis to reduce the number of febrile episodes and raise the issue of MBL replacement for these patients. Recurrent infections are a common symptom of multiple myeloma. The mannan-binding lectin MBL pathway of the complement system is part of the innate immune system 67 and seems to affect the risk of infections not only for healthy individuals, 89 but also of cancer patients during treatment.

MBL is a protein that belongs to the collectin family and is produced by hepatocytes. MBL acts via binding to the surface of bacteria and other pathogen factors, thus facilitating complement activation with formation of the membrane attack complex, leading to microbial lysis. The serum level of MBL is dependent on various factors such as polymorphisms, ethnicity and age. The participation of the patients in another clinical trial was not an exclusion criterion for participation in the study.

The primary endpoint of the study was the evaluation of febrile episodes among MM patients with low or normal MBL levels during their hospitalization for the administration of high dose melphalan and ASCT. Secondary endpoints included differences among patients with low and normal MBL levels during the same time period regarding: i number and type of infectious episodes; ii severity of infectious episodes; iii incidence of bacteremia; iv number of days of hospitalization; v number of days with fever; vi in case of febrile episode response to first line antibiotics therapy; vii transplantation related morbidity and mortality; viii PFS and overall survival OS.

The enrollment period was between June and January Patients were informed of the objectives and the details of the study before giving their approval and signing the informed consent forms. The study was conducted according to the principles defined by the 18th World Medical Association Assembly Declaration of Helsinki, and all its future amendments. The study protocol was designed and executed according to the guidelines and regulations pertaining to studies in Greece, as well as the Good Clinical Practice Guidelines as defined by the International Conference of Harmonization.

The study was approved by the local ethics committee. Data were collected from the medical files of the enrolled patients.