scholarly journals Experimental Hemolytic Anemia in Rabbits. Protective Role of Sensitization to the Species-specific Protein of the Heteroimmune Hemolytic Serum

Blood ◽  
1957 ◽  
Vol 12 (8) ◽  
pp. 710-725 ◽  
Author(s):  
ISRAEL DAVIDSOHN ◽  
DAVID HERMONI ◽  
ELEANOR G. HANAWALT
1998 ◽  
Vol 126 (5) ◽  
pp. 1149-1151
Author(s):  
A. Yu. Karyagina ◽  
V. M. Chesnokova ◽  
A. N. Ivanova ◽  
A. A. Tinnikov ◽  
L. N. Ivanova

2006 ◽  
Vol 291 (3) ◽  
pp. H1395-H1401 ◽  
Author(s):  
Francisco R. González-Pacheco ◽  
Juan J. P. Deudero ◽  
María C. Castellanos ◽  
María Angeles Castilla ◽  
María Victoria Álvarez-Arroyo ◽  
...  

The defense mechanisms of endothelial cells (EC) against reactive oxygen species (ROS) are insufficiently characterized. We have addressed the hypothesis that vascular endothelial growth factor (VEGF) and its receptors are relevant elements in this response. Cell viability, VEGF and VEGF receptor (VEGFR1 and VEGFR2) expression, and transcription factor activation were studied on transient exposure of monolayer EC to H2O2. Wild-type and mutant inhibitors of κBα (IκBα) constructions were used to further assess the role of NF-κB in the induction of VEGFR2 expression. A concentration of H2O2 ≥60 μM elicited clear-cut damaging effects on EC, whereas lower concentrations (2–4 μM) were cytoprotective. The cytoprotective effect was shifted to an EC-damaging pattern by means of specific VEGF blockade, therefore revealing a major role of autologous VEGF. Exposure to H2O2 increased VEGF and VEGFR2 mRNA and protein in EC, without affecting VEGFR1 expression. Also, H2O2 challenge was accompanied by increased NF-κB, activator protein-1, and specific protein-1 nuclear binding. A role of NF-κB as the mediator of the H2O2 induction of VEGFR2 mRNA expression was supported by inhibition by the ROS scavenger pyrrolidine dithiocarbamate and by the blocking effect of transfected IκBα. Exposure to exogenous VEGF also increased VEGFR2 and induced NF-κB in EC. In summary, autologous VEGF is instrumental for EC protection induced by low concentrations of ROS. ROS induce expression not only of VEGF but also of VEGFR2. VEGFR2 increase by ROS is mainly driven through a NF-κB-dependent pathway.


2010 ◽  
Vol 11 (2) ◽  
pp. 41-42
Author(s):  
Z. Guo ◽  
T. Tang ◽  
X. Lin ◽  
H. Yang

2018 ◽  
Vol 189 (2) ◽  
pp. 490-500 ◽  
Author(s):  
Rankaljeet Kaur ◽  
Preety Ghanghas ◽  
Pulkit Rastogi ◽  
Naveen Kaushal

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.


2015 ◽  
Vol 36 (3) ◽  
pp. 170-176 ◽  
Author(s):  
Erin N. Stevens ◽  
Joseph R. Bardeen ◽  
Kyle W. Murdock

Parenting behaviors – specifically behaviors characterized by high control, intrusiveness, rejection, and overprotection – and effortful control have each been implicated in the development of anxiety pathology. However, little research has examined the protective role of effortful control in the relation between parenting and anxiety symptoms, specifically among adults. Thus, we sought to explore the unique and interactive effects of parenting and effortful control on anxiety among adults (N = 162). Results suggest that effortful control uniquely contributes to anxiety symptoms above and beyond that of any parenting behavior. Furthermore, effortful control acted as a moderator of the relationship between parental overprotection and anxiety, such that overprotection is associated with anxiety only in individuals with lower levels of effortful control. Implications for potential prevention and intervention efforts which specifically target effortful control are discussed. These findings underscore the importance of considering individual differences in self-regulatory abilities when examining associations between putative early-life risk factors, such as parenting, and anxiety symptoms.


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