Nasal allergen challenge and environmental exposure chamber challenge: A randomized trial comparing clinical and biological responses to cat allergen.

Background: The direct-instillation nasal allergen challenge (NAC) and the environmental exposure chamber (EEC) are 2 methods of conducting controlled allergen provocations. The clinical and biological comparability of these methods has not been thoroughly investigated.

Objective: We sought to compare clinical and immunologic responses to cat allergen in NAC versus EEC.

Product Development Under FDA's Animal Rule: Understanding FDA's Expectations and Potential Implications for Traditional Development Programs.

In 2002 the US Food and Drug Administration (FDA) established a regulatory pathway for drug and biological products targeting indications for which human efficacy studies are not feasible or ethical. These regulations (21 CFR 314.600 for drugs and 21 CFR 601.

The Mouse Tumor Biology Database: integrated access to mouse cancer biology data.

Mice have long been used as models for the study of human cancer. The National Cancer Institute has included among its research areas of extraordinary opportunity the development of new mouse genetic models of human cancer and the exploration of cancer imaging as a research tool. Because of the volume and interconnectedness of relevant data, the creation and maintenance of bioinformatics resources of mouse tumor biology is necessary to facilitate current and future cancer research.

Ribosomal protein L11 negatively regulates oncoprotein MDM2 and mediates a p53-dependent ribosomal-stress checkpoint pathway.

The gene encoding p53 mediates a major tumor suppression pathway that is frequently altered in human cancers. p53 function is kept at a low level during normal cell growth and is activated in response to various cellular stresses. The MDM2 oncoprotein plays a key role in negatively regulating p53 activity by either direct repression of p53 transactivation activity in the nucleus or promotion of p53 degradation in the cytoplasm.

2,5-hexanedione-induced testicular injury.

Now in its third decade of mechanistic investigation, testicular injury caused by 2,5-hexanedione (2,5-HD) exposure is a well-studied model with a rich database. The development of this model reflects the larger changes that have moved biology from a branch of chemistry into the molecular age. Critically examined in this review is the proposed mechanism for 2,5-HD-induced testicular injury in which germ cell maturation is disrupted owing to alterations in Sertoli cell microtubule-mediated functions.