Multi-center, randomized, double-blind, placebo-controlled, cross-over Phase II study to evaluate the safety and efficacy of inhaled Bimosiamose for the treatment of patients with moderate to severe Chronic Obstructive Pulmonary Disease (COPD)

开始日期2010-02-25

申办/合作机构

Revotar Biopharmaceuticals AG

EUCTR2009-013163-18-DE / Not yet recruitingN/A

A double-blind, placebo controlled, randomized, cross-over Phase IIa study to evaluate the effect of Bimosiamose on ozone induced sputum neutrophilia in healthy subjects.

开始日期2009-08-11

申办/合作机构

Revotar Biopharmaceuticals AG

EUCTR2008-000197-20-DE / Not yet recruitingN/A

Multi-center, randomized, double-blind, placebo-controlled Phase 2 study to evaluate the safety and efficacy of Bimosiamose 5% Cream for the treatment of patients with chronic plaque type psoriasis - Psoriasis POC

开始日期2008-11-28

申办/合作机构

Revotar Biopharmaceuticals AG

100 项与 E-sel x P-sel x L-sel 相关的临床结果

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100 项与 E-sel x P-sel x L-sel 相关的转化医学

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0 项与 E-sel x P-sel x L-sel 相关的专利（医药）

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341

项与 E-sel x P-sel x L-sel 相关的文献（医药）

2024-11-01·Journal of Surgical Research

Amitriptyline Decreases Mouse Lung Endothelial Cell Inflammatory Responses to Packed Red Blood Cell Microparticles

Article

作者: Chae, Ryan ; Nguyen, Christopher ; Wattley, Lindsey ; Schuster, Rebecca ; Caldwell, Charles ; Goodman, Michael ; Pritts, Timothy A ; Lentsch, Alex

INTRODUCTIONLarge-volume packed red blood cell (pRBC) transfusion is associated with lung injury and worsened outcomes. Amitriptyline reduces lung injury and inflammation in a murine sepsis model. We hypothesized that red cell microparticles (MP) activate endothelial cells, leading to lung injury and that treatment with amitriptyline would blunt the inflammatory response MPs through inhibition of acid sphingomyelinase (ASM).METHODSMurine pRBCs were obtained from C57Bl/6 mice and stored in AS3 for 14 d. The MPs were isolated from pRBCs by serial centrifugation. Mouse lung endothelial cells (MLECs) were pretreated with amitriptyline (0, 2.5, 25, 27 μM, n = 5) for 30 min prior to MP treatment. Chemokine secretion and adhesion molecule shedding was assessed. ASM activity was measured from cell lysates.RESULTSMPs increased the secretion of chemokines and shedding of adhesion molecules in MLECs at both four and 24 h. Amitriptyline treatment of MLECs decreased ASM activity in the setting of MPs. Amitriptyline pretreatment decreased the secretion of chemokines and shedding of adhesion molecules in response to MPs at 4 h but did not decrease adhesion molecule shedding at 24 h CONCLUSIONS: Endothelial cell treatment with MPs induces secretion of chemokines responsible for chemotaxis (keratinocyte chemoattractant, regulated upon activation normal T cell expressed and presumably secreted, and G-granulocyte colony-stimulating factor) as well as many downstream proinflammatory effects (interleukin-6). Additionally, MPs induce adhesion molecule shedding (vascular cell adhesion molecule-1, intracellular adhesion molecule-1, P-selectin, and E-selectin), which has been shown to be associated with endothelial cell activation. Amitriptyline pretreatment decreases MLEC inflammatory response and ASM activity is decreased. These data suggest that ASM inhibition in MLECs is a potential strategy to blunt the inflammatory response to the red blood cell storage lesion.

2024-09-19·International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience

Decreased levels of L-selectin and platelet-endothelial cell adhesion molecule-1 in children with autism spectrum disorder.

Article

作者: Altun, Hatice ; Seyithanoğlu, Muhammed ; Arslan, Semiha Cömertoğlu ; Taş, Dilan ; Doğaner, Adem ; Arslan, Feyzullah Necati ; Islah, Elif Milhan

OBJECTIVEThis study aimed to ascertain the serum levels of selectins (E, L, P) and platelet-endothelial adhesion molecule-1 (PECAM-1) in preschool children with autism spectrum disorder (ASD) and to establish a comparison with the levels observed in healthy controls.METHODSThe study included 34 children aged 2-7 years diagnosed with ASD (ASD group) and 34 randomly selected healthy children matched for age and sex to the ASD group. The children were free of any genetic or physical disease, clinically active infection, or medication use. The sociodemographic data form was completed by all parents. The Childhood Autism Rating Scale (CARS) and the Autism Behavior Checklist (ABC) were administered to the patient group, and the Aberrant Behavior Checklist (AbBC) was completed by the families of all children. Serum selectin (E, L, P) and PECAM-1 levels were measured using enzyme-linked immunosorbent assay (ELISA) kits.RESULTSThe results showed that the levels of both L-selectin (p = 0.007) and PECAM-1 (p = 0.019) were significantly lower in the ASD group than in the control group. No significant difference was observed between the groups concerning E-selectin and P-selectin levels (p > 0.05). It was observed that P-selectin variables were statistically significant in predicting the presence of ASD (p = 0.019). A remarkable inverse correlation was found between the AbBC irritability subscale score and L-selectin (r = -0.296, p = 0.014) and PECAM-1 (r = -0.276, p = 0. 023); the AbBC Lethargy-Social Withdrawal subscale score and E-Selectin (r = -0.239, p = 0.049), L-Selectin (r = -0.297, p = 0.014) and PECAM-1 (r = -0.264, p = 0.029); L-Selectin levels and the AbBC stereotypic behavior subscale (r = -0.248, p = 0.042). No statistically significant relationship was observed between selectins (E, L, P) and PECAM-1 levels and CARS scale, ABC subscale or total scores and age variables (p > 0.05).CONCLUSIONSThese study results suggest that L-selectin, P-selectin and PECAM-1 may play a role in the pathophysiology of ASD.

2024-09-01·Osteoporosis International

The association of microvascular disease and endothelial dysfunction with vertebral trabecular bone mineral density

Article

作者: Carbone, Laura ; Buzkova, Petra ; Kestenbaum, Bryan ; Budoff, Matthew J ; Mukamal, Kenneth J ; Cotch, Mary Frances ; Bielinski, Suzette J ; Barzilay, Joshua I ; Austin, Thomas R

Retinopathy and albuminuria are associated with hip fracture risk. We investigated whether these disorders and endothelial dysfunction (which underlies microvascular diseases) were associated with low trabecular bone density. No significant associations were found, suggesting that microvascular diseases are not related to fracture risk through low trabecular bone density.PURPOSEMicrovascular diseases of the eye, kidney, and brain are associated with endothelial dysfunction and increased hip fracture risk. To explore the basis for higher hip fracture risk, we comprehensively examined whether markers of microvascular disease and/or endothelial dysfunction are related to trabecular bone mineral density (BMD), a proximate risk factor for osteoporotic fractures.METHODSAmong 6814 participants in the Multi-Ethnic Study of Atherosclerosis study (MESA), we derived thoracic vertebral trabecular BMD from computed tomography of the chest and measured urine albumin to creatinine ratios (UACR), retinal arteriolar and venular widths, flow mediated dilation (FMD) of the brachial artery after 5 min of ischemia; and levels of five soluble endothelial adhesion markers (ICAM-1, VCAM-1, L-selectin, P-selectin, and E-selectin). Linear regression models were used to examine the association of trabecular BMD with markers of microvascular disease and with markers of endothelial dysfunction.RESULTSWe observed no significant associations of UACR, retinal arteriolar or venular widths, or FMD with BMD. We also observed no statistically significant association of spine trabecular BMD with levels of endothelial adhesion markers. Men and women had largely similar results.CONCLUSIONWe conclude that there is little evidence to connect thoracic spine trabecular BMD to microvascular disorders or to endothelial dysfunction among multi-ethnic middle-aged and older adults. Other factors beyond trabecular BMD (e.g., bone quality or predisposition to falling) may be responsible for the associations of microvascular disease with osteoporotic fractures.