GENOMIC ANALYSES OF THE MOLECULAR BASES FOR TOXIC RESPONSES

2000 ◽  
Vol 28 (5) ◽  
pp. A141-A141
Author(s):  
I. Kimber ◽  
G. Orphanides ◽  
W. D. Pennie
Author(s):  
S.S. Poolsawat ◽  
C.A. Huerta ◽  
S.TY. Lae ◽  
G.A. Miranda

Introduction. Experimental induction of altered histology by chemical toxins is of particular importance if its outcome resembles histopathological phenomena. Hepatotoxic drugs and chemicals are agents that can be converted by the liver into various metabolites which consequently evoke toxic responses. Very often, these drugs are intentionally administered to resolve an illness unrelated to liver function. Because of hepatic detoxification, the resulting metabolites are suggested to be integrated into the macromolecular processes of liver function and cause an array of cellular and tissue alterations, such as increased cytoplasmic lysis, centrilobular and localized necroses, chronic inflammation and “foam cell” proliferation of the hepatic sinusoids (1-4).Most experimentally drug-induced toxicity studies have concentrated primarily on the hepatic response, frequently overlooking other physiological phenomena which are directly related to liver function. Categorically, many studies have been short-term effect investigations which seldom have followed up the complications to other tissues and organs when the liver has failed to function normally.


2007 ◽  
Vol 27 (4) ◽  
pp. 319-341 ◽  
Author(s):  
M. Zouhair Atassi ◽  
Behzod Z. Dolimbek ◽  
Lance E. Steward ◽  
K. Roger Aoki

2011 ◽  
Vol 33 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Xing-Hua PAN ◽  
Hai-Ying ZHU ◽  
Sadie L MARJANI

2020 ◽  
Author(s):  
Shilin Tian ◽  
Xuming Zhou ◽  
Dejing Zhang ◽  
Chunyou Ning ◽  
Diyan Li ◽  
...  

2012 ◽  
Vol 11 (1) ◽  
pp. 25-32 ◽  
Author(s):  
James West ◽  
James E. Loyd ◽  
Rizwan Hamid

For more than 60 years, researchers have sought to understand the molecular basis of idiopathic pulmonary arterial hypertension (PAH). Recognition of the heritable form of the disease led to the creation of patient registries in the 1980s and 1990s, and discovery of BMPR2 as the cause of roughly 80% of heritable PAH in 2000. With discovery of the disease gene came opportunity for intervention, with focus on 2 alternative approaches. First, it may be possible to correct the effects of BMPR2 mutation directly through interventions targeted at correction of trafficking defects, increasing expression of the unmutated allele, and correction of splicing defects. Second, therapeutic interventions are being targeted at the signaling consequences of BMPR2 mutation. In particular, therapies targeting cytoskeletal and metabolic defects caused by BMPR2 mutation are currently in trials, or will be ready for human trials in the near future. Translation of these findings into therapies is the culmination of decades of research, and holds great promise for treatment of the underlying molecular bases of disease.


1963 ◽  
Vol 27 (3) ◽  
pp. 305-324 ◽  
Author(s):  
Walter J. Nickerson
Keyword(s):  

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