This finding indicates the presence of receptor reserve (spare ..

92. Fourches D, Barnes JC, Day NC, Bradley P, Reed JZ, Tropsha A. Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species. 2010;23:171-83

 95. Sietsema WK. The absolute oral bioavailability of selected drugs.  1989;27:179-211

219. Suggitt M, Bibby MC. 50 years of preclinical anticancer drug screening: empirical to target-driven approaches. 2005;11:971-81


Langley challenged the dominant hypothesis that drugs ..

87. Igarashi T, Nakane S, Kitagawa T. Predictability of clinical adverse reactions of drugs by general pharmacology studies. 1995;20:77-92


The Ketogenic Diet: Does it live up to the hype? The …

Many genetic changes in the MC1R gene increase the risk of developing skin cancer, including a common, serious form of skin cancer that begins in melanocytes (melanoma). Alterations in the MC1R gene disrupt the ability of the melanocortin 1 receptor to trigger eumelanin production in melanocytes. Because eumelanin normally protects skin from the harmful effects of UV radiation, a lack of this pigment leaves fair skin more vulnerable to damage from sun exposure. Skin damage caused by UV radiation from the sun is a major risk factor for developing melanoma and other forms of skin cancer.

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Common variations (polymorphisms) in the MC1R gene are associated with normal differences in skin and hair color. Certain genetic variations are most common in people with red hair, fair skin, freckles, and an increased sensitivity to sun exposure. These MC1R polymorphisms reduce the ability of the melanocortin 1 receptor to stimulate eumelanin production, causing melanocytes to make mostly pheomelanin. Although MC1R is a key gene in normal human pigmentation, researchers believe that the effects of other genes also contribute to a person's hair and skin coloring. The melanocortin 1 receptor is also active in cells other than melanocytes, including cells involved in the body's immune and inflammatory responses. The receptor's function in these cells is unknown.

Thyroid Cancer - Thyroid Disease Manager

There are several claims here for the value of SRs. While we do not dispute the value of SRs to improve the quality of research and perhaps increase acceptance of the 3Rs, we strongly contest the notion that SRs will allow scientists to develop animal models that are predictive modalities for human responses to drugs and disease. Claims such as those above by Bracken and the organizers of the Symposium (and more we will cite below) regarding the benefit of using animal models in translational research however, directly assumes predictive ability. We will discuss this further when describing table .

How to cite this article: Greek R, Menache A

Because nonhuman animal models (hereafter referred to as animal models or animals) have on multiple occasions been unsuccessful in predicting human response to drugs and disease (we will address this claim in depth), many have called for SRs in order to improve the models [-]. An example of this predicament would be the animal models used to determine which drugs to develop in an attempt to diminish neurological damage from ischemia events of the central nervous system (CNS) [, -]. By analyzing animal-based research with SRs, flaws in the methodology would also become apparent thus leading to eventual standardization of such studies. This would ostensibly also lead to better predictive values for humans (see table for calculating such values). Bracken supports this, stating: