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42 results on '"Kaluzhny, Yulia"'

5. Comparison of In VitroCorneal Permeation and In VivoOcular Bioavailability in Rabbits of Three Marketed Latanoprost Formulations

Author

Chauchat, Laure, Guerin, Camille, Kaluzhny, Yulia, and Renard, Jean-Paul

Abstract

Background and Objective: All latanoprost formulations currently available for the treatment of glaucoma or ocular hypertension contain the same concentration of latanoprost (0.005%) but differ in excipients, which may affect corneal drug permeability or stability. This study aimed at comparing corneal penetration of three marketed latanoprost solutions with different excipient formulations in in vitroand in vivodrug permeability studies. Methods: Three latanoprost formulations were tested under good laboratory practice conditions: a formulation containing benzalkonium chloride (BAK) but no surfactant (Preserved latanoprost); the same formulation except preservative-free (PF) without BAK or surfactant (SF) (PF SF latanoprost); and a different formulation without BAK but containing a non-ionic surfactant (MGHS 40 at 5%) combined with thickening agents (Carbomer 974P, Macrogol 4000) (PF latanoprost). Corneal permeation of latanoprost acid (LAT) was first determined in vitrousing a reconstructed human corneal epithelium tissue. Then, in vivopharmacokinetic studies were performed on pigmented rabbits, for which LAT concentration was measured in the aqueous humour (AH) and iris–ciliary body (ICB). Results: In vitro, the cumulative transport of LAT was linear between 1 h and 4 h for preserved latanoprost and PF SF latanoprost, and LAT concentrations matched exactly at each timepoint. By contrast, the permeation of PF latanoprost was linear between 2 h and 12 h and was significantly lower than that of preserved latanoprost and PF SF latanoprost at 4 and 8 h (p< 0.001). In rabbits, the concentrations of LAT in AH and ICB were not statistically different between preserved latanoprost and PF SF latanoprost at each timepoint, except at 1 h in ICB (p= 0.005). By comparison, the LAT concentration of PF latanoprost was statistically (p< 0.05) lower than that of preserved latanoprost and PF SF latanoprost in AH and ICB from 0.5 to 3 h. Conclusion: BAK did not influence the corneal penetration of latanoprost in in vitroand in vivostudies. The formulation containing a non-ionic surfactant resulted in lower and slower ocular penetration compared with preserved or PF SF formulations. This raises questions about the relevance of BAK and some surfactants in enhancing corneal penetration of ocular formulations.

Published
2023
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8. Pretreatment of adult bone marrow mesenchymal stem cells with cardiomyogenic growth factors and repair of the chronically infarcted myocardium

Author

Bartunek, Jozef, Croissant, Jeffrey D., Wijns, William, Gofflot, Stephanie, de Lavareille, Aurore, Vanderheyden, Marc, Kaluzhny, Yulia, Mazouz, Naima, Willemsen, Philippe, Penicka, Martin, Mathieu, Myrielle, Homsy, Christian, De Bruyne, Bernard, McEntee, Kathleen, Lee, Ike W., and Heyndrickx, Guy R.

Subjects
Hematopoietic stem cells -- Research, Heart attack -- Research, Biological sciences
Abstract

The in vivo cardiac differentiation and functional effects of unmodified adult bone marrow mesenchymal stem cells (MSCs) after myocardial infarction (MI) is controversial. We postulated that ex vivo pretreatment of autologous MSCs using cardiomyogenic growth factors will lead to cardiomyogenic specification and will result in superior biological and functional effects on cardiac regeneration of chronically infarcted myocardium. We used a chronic dog MI model generated by ligation of the coronary artery (n = 30). Autologous dog bone marrow MSCs were isolated, culture expanded, and specified into a cardiac lineage by adding growth factors, including basic FGF, IGF-1, and bone morphogenetic protein-2. Dogs underwent cell injection >8 wk after the infarction and were randomized into two groups. Group A dogs (n = 20) received MSCs specified with growth factors (147 [+ or -] 96 x [10.sup.6]), and group B (n = 10) received unmodified MSCs (168 [+ or -] 24 x [10.sup.6]). After the growth factor treatment, MSCs stained positive for the early muscle and cardiac markers desmin, antimyocyte enhancer factor-2, and Nkx2-5. In group A dogs, prespecified MSCs colocalized with troponin I and cardiac myosin. At 12 wk, group A dogs showed a significantly larger increase in regional wall thickening of the infarcted territory (from 22 [+ or -] 8 to 32 [+ or -] 6% in group A; P < 0.05 vs. baseline and group B, and from 19 [+ or -] 7 to 21 [+ or -] 7% in group B, respectively) and a decrease in the wall motion score index (from 1.60 [+ or -] 0.05 to 1.35 [+ or -] 0.03 in group A; P < 0.05 vs. baseline and group B, and from 1.58 [+ or -] 0.07 vs. 1.56 [+ or -] 0.08 in group B, respectively). The biological ex vivo cardiomyogenic specification of adult MSCs before their transplantation is feasible and appears to improve their in vivo cardiac differentiation as well as the functional recovery in a dog model of the chronically infarcted myocardium. cardiac repair; myogenesis; chronic myocardial infarction; heart failure

Published
2007

16. The EpiOcular Eye Irritation Test (EIT) for Hazard Identification and Labelling of Eye Irritating Chemicals: Protocol Optimisation for Solid Materials and the Results after Extended Shipment

Author

Kaluzhny, Yulia, primary, Kandárová, Helena, additional, Handa, Yuki, additional, DeLuca, Jane, additional, Truong, Thoa, additional, Hunter, Amy, additional, Kearney, Paul, additional, d'Argembeau-Thornton, Laurence, additional, and Klausner, Mitchell, additional

Published
2015
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41. Role of Apoptotic Processes in Platelet Biogenesis.

Author

Kaluzhny, Yulia and Ravid, Katya

Subjects
*APOPTOSIS, *MEGAKARYOCYTES, *BONE marrow cells, *BLOOD platelets, *CYTOSKELETON
Abstract

Platelets are anucleate cells that fragment from mature megakaryocytes and play an essential role in thrombosis and hemostasis. Platelets are among the first cell types to be recruited to an injured blood vessel, assisting in endothelial repair. Platelet hyperactivation contributes to the development of atherosclerosis, myocardial infarction, and ischemia of peripheral limbs. A fall in platelet counts, due to a variety of conditions, including disseminated intravascular coagulation, chemotherapy or genetic disorders, may lead, in most severe cases, to death from hemorrhage. This review focuses on the late stages of megakaryocyte differentiation and platelet fragmentation, including associated cytoskeletal changes, and on the importance of apoptotic events for these processes. Studies point to a unique biological system in which programmed cell death may be linked with biogenesis of new cells.Copyright © 2004 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2004
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42. Signaling by the Mpl receptor involves IKK and NF-kappaB.

Author

Zhang Y, Sun S, Wang Z, Thompson A, Kaluzhny Y, Zimmet J, and Ravid K

Subjects
Animals, Apoptosis physiology, Bone Marrow Cells cytology, Bone Marrow Cells drug effects, Bone Marrow Cells metabolism, Cell Division, Cells, Cultured, DNA metabolism, Dimerization, Down-Regulation, I-kappa B Kinase, Megakaryocytes cytology, Megakaryocytes drug effects, Megakaryocytes physiology, Mice, NF-kappa B drug effects, NF-kappa B genetics, Polyploidy, Promoter Regions, Genetic, Protein Serine-Threonine Kinases drug effects, Protein Serine-Threonine Kinases genetics, Rats, Receptors, Thrombopoietin, Thrombopoietin genetics, Thrombopoietin pharmacology, Transcriptional Activation, NF-kappa B metabolism, Neoplasm Proteins metabolism, Protein Serine-Threonine Kinases metabolism, Proto-Oncogene Proteins metabolism, Receptors, Cytokine metabolism, Signal Transduction physiology, Thrombopoietin metabolism
Abstract

Binding of tumor necrosis factor-alpha (TNF-alpha) to its receptor activates IKK complex, which leads to inducement of NF-kappaB activity. Here we report that activation of Mpl ligand is also linked to IKK and NF-kappaB activity. Mpl ligand, also known as thrombopoietin (TPO) or megakaryocyte growth and development factor (MGDF), induces megakaryocyte differentiation and inhibition of mitotic proliferation, followed by induction of polyploidization and fragmentation into platelets. The latter process is often observed in megakaryocytes undergoing apoptosis. Treatment of a Mpl ligand-responding megakaryocytic cell line with this cytokine led to an immediate, transient increase in IKK activity followed by a profound decrease in this kinase activity over time. This decrease was not due to an effect on the levels of the IKK regulatory components IKKalpha and IKKbeta. Proliferating megakaryocytes displayed a constitutive DNA-binding activity of NF-kappaB p50 homodimers and of NF-kappaB p50-p65 heterodimers. As expected, reduced IKK activity in Mpl ligand-treated cells was associated with a significant reduction in NF-kappaB DNA binding activity and in the activity of a NF-kappaB-dependent promoter. Our study is thus the first to identify a constitutive NF-kappaB activity in proliferating megakaryocytes as well as to describe a link between Mpl receptor signaling and IKK and NF-kappaB activities. Since a variety of proliferation-promoting genes and anti-apoptotic mechanisms are activated by NF-kappaB, retaining its low levels would be one potential mechanism by which inhibition of mitotic proliferation is maintained and apoptosis is promoted during late megakaryopoiesis., (Copyright 2002 Wiley-Liss, Inc.)

Published
2002
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