scholarly journals Activation of Cellular Defense Mechanism by Organic-Inorganic Hybrid Molecules

2014 ◽  
Vol 134 (7) ◽  
pp. 813-815
Author(s):  
Tomoya Fujie ◽  
Hiroshi Naka ◽  
Chika Yamamoto ◽  
Yasuhiro Shinkai ◽  
Yoshito Kumagai ◽  
...  
1956 ◽  
Vol 184 (2) ◽  
pp. 296-300 ◽  
Author(s):  
László Kátó ◽  
Béla Gözsy

Experiments are presented to the effect that in an inflammatory process histamine and leucotaxin appear successively at different and orderly time intervals, thus assuring an increased fluid flow through the capillary wall. Histamine is released not only in the inflammatory process but also by intradermal administration of such substances (volatile oils or their components) which induce neither the triple response of Th. Lewis nor any tissue damage. This could be explained by the fact that in the tissues histamine is ‘present’ but leucotaxin is ‘formed.’


Author(s):  
Shubhangi H. Pawar ◽  
Vishal S. Gulecha ◽  
Manoj S. Mahajan ◽  
Aman B Upaganiawar ◽  
Chandrashekhar D. Upasani

Oxidative stress is strongly linked to neurodegeneration and oxidative species can modify many amino acids and proteins in the brain. Cysteine amino acid is most susceptible to oxidative post-translational modifications (PTMs). Reversible or irreversible cysteine PTMs can cause dyshomeostasis, which further continued to cellular damage. Many cysteine dependent proteins and many non-proteins using cysteine as their structural components are affected by oxidative stress. Several cysteine dependent enzymes are acting as antioxidants. Cysteine is a major contributor to glutathione (GSH) and superoxide dismutase (SOD) synthesis. Cysteine precursor N-acetylcysteine (NAC) supplementation is proven as a potent free radical scavenger and increase brain antioxidants and subsequently potentiates the natural antioxidant cellular defense mechanism. Thus, in this chapter, the authors explore the linkage of cellular cysteine networks and neurodegenerative disorders.


1956 ◽  
Vol 34 (1) ◽  
pp. 571-579
Author(s):  
Béla Gözsy ◽  
László Kátó

Monocytes were obtained by the washing of the peritoneal cavity of guinea pigs with Hanks' solution six days after intraperitoneal administration of a saline solution containing glycogen. Phagocytosis of tubercle bacilli (BCG strain) was studied after a one hour incubation at 37 °C. under the influence of histamine and 1,4-dimethyl-7-isopropyl-bicyclo-decapentane, which latter substance had shown a beneficial influence on the outcome of experimental tuberculosis. Histamine increased the phagocytic activity of monocytes, within the limits of 1 μgm. to 10 μgm per ml. This stimulation was inhibited in vitro by a synthetic antihistamine substance. Fifty and 100 μgm. per ml. histamine decreased the phagocytosis of tubercle bacilli (BCG) by the monocytes. Monocytes withdrawn from histamine treated guinea pigs showed no stimulated activity. From 0.5 to 100 μgm. per ml. of 1,4-dimethyl-7-isopropylbicyclo-decapentane stimulated the phagocytic activity of monocytes against tubercle bacilli (BCG) in vitro and monocytes withdrawn from animals treated with the same substance showed equally a stimulated activity. This increased phagocytosis was equally inhibited in vitro by the antihistamine, but to a lesser degree than the inhibition of the histamine stimulated phagocytosis. The above observations suggest that the stimulating action of the 1,4-dimethyl-7-isopropyl-bicyclo-decapentane is a direct action on the monocytes rather than an indirect one caused by activation of latent histamine. Experiments also show the possibility of stimulation of the cellular defense mechanism, by appropriate treatment.


2021 ◽  
Vol 22 (17) ◽  
pp. 9624
Author(s):  
Elena Muscolino ◽  
Laura-Marie Luoto ◽  
Wolfram Brune

Various intrinsic and extrinsic factors can interfere with the process of protein folding, resulting in protein aggregates. Usually, cells prevent the formation of aggregates or degrade them to prevent the cytotoxic effects they may cause. However, during viral infection, the formation of aggregates may serve as a cellular defense mechanism. On the other hand, some viruses are able to exploit the process of aggregate formation and removal to promote their replication or evade the immune response. This review article summarizes the process of cellular protein aggregation and gives examples of how different viruses exploit it. Particular emphasis is placed on the ribonucleotide reductases of herpesviruses and how their additional non-canonical functions in viral immune evasion are closely linked to protein aggregation.


Viruses ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 293 ◽  
Author(s):  
Nicolas Baillet ◽  
Sophie Krieger ◽  
Alexandra Journeaux ◽  
Valérie Caro ◽  
Frédéric Tangy ◽  
...  

Lassa virus (LASV) and Mopeia virus (MOPV) are two closely related Old-World mammarenaviruses. LASV causes severe hemorrhagic fever with high mortality in humans, whereas no case of MOPV infection has been reported. Comparing MOPV and LASV is a powerful strategy to unravel pathogenic mechanisms that occur during the course of pathogenic arenavirus infection. We used a yeast two-hybrid approach to identify cell partners of MOPV and LASV Z matrix protein in which two autophagy adaptors were identified, NDP52 and TAX1BP1. Autophagy has emerged as an important cellular defense mechanism against viral infections but its role during arenavirus infection has not been shown. Here, we demonstrate that autophagy is transiently induced by MOPV, but not LASV, in infected cells two days after infection. Impairment of the early steps of autophagy significantly decreased the production of MOPV and LASV infectious particles, whereas a blockade of the degradative steps impaired only MOPV infectious particle production. Our study provides insights into the role played by autophagy during MOPV and LASV infection and suggests that this process could partially explain their different pathogenicity.


Blood ◽  
1969 ◽  
Vol 34 (5) ◽  
pp. 712-716 ◽  
Author(s):  
MINORU OKUMA ◽  
MANFRED STEINER ◽  
MARIO BALDINI

Abstract Blood platelets showed an age dependent accumulation of lipid peroxides. Lipid peroxidation stimulated by heavy metal also increased with platelet age and rose at a much faster rate than the spontaneous peroxide formation. This suggests the loss of a cellular defense mechanism against lipid peroxidation in aging blood platelets.


Langmuir ◽  
2011 ◽  
Vol 27 (7) ◽  
pp. 3982-3990 ◽  
Author(s):  
Shu-Zheng Liu ◽  
Xiong Wu ◽  
Ai-Qing Zhang ◽  
Jin-Jun Qiu ◽  
Cheng-Mei Liu

2014 ◽  
Vol 26 (8) ◽  
pp. 1753-1763 ◽  
Author(s):  
Valluri V. Satyavathi ◽  
Asha Minz ◽  
Javaregowda Nagaraju

BMB Reports ◽  
2004 ◽  
Vol 37 (2) ◽  
pp. 139-143 ◽  
Author(s):  
Jong-Min Lee ◽  
Jeffrey A. Johnson

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