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A cornerstone of modern biomedical research is the use of mouse models to explore basic pathophysiological mechanisms, evaluate new therapeutic approaches, and make go or no-go decisions to carry new drug candidates forward into clinical trials. Systematic studies evaluating how well murine models mimic human inflammatory diseases are nonexistent. Here, we show that, although acute inflammatory stresses from different etiologies result in highly similar genomic responses in humans, the responses in corresponding mouse models correlate poorly with the human conditions and also, one another.

The mouse is a common model used in research as a way of studying human biology and diseases, but a new study questions whether this is an accurate approach considering some stark differences - aside from many similarities - between the two species.

The mouse is the leading organism for disease research. A rich resource of genetic variation occurs naturally in inbred and special strains owing to spontaneous mutations. However, one can also obtain desired gene mutations by using the following processes: targeted mutations that eliminate function in the whole organism or in a specific tissue; forward genetic screens using chemicals or transposons; or the introduction of exogenous transgenes as DNAs, bacterial artificial chromosomes (BACs) or reporter constructs. The mouse is the only mammal that provides such a rich resource of genetic diversity coupled with the potential for extensive genome manipulation, and is therefore a powerful application for modeling human disease.

Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever, neither delayed blood coagulation and disseminated intravascular coagulation, nor death from shock, thus restricting pathogenesis studies to non-human primates. Here we show that mice from the Collaborative Cross exhibit distinct disease phenotypes following mouse-adapted Ebola virus infection. Phenotypes range from complete resistance to lethal disease to severe hemorrhagic fever characterized by prolonged coagulation times and 100% mortality. Inflammatory signaling was associated with vascular permeability and endothelial activation, and resistance to lethal infection arose by induction of lymphocyte differentiation and cellular adhesion, likely mediated by the susceptibility allele Tek. These data indicate that genetic background determines susceptibility to Ebola hemorrhagic fever.

Species like yeast, flies, fish and mice have many genes in common with humans and are therefore considered 'model organisms' and are widely used in research to study human genes and human diseases. Mouse research has lead to major advances in our ability to treat a number of serious diseases and conditions.

Mouse study fingers potential cause of fertility problems, proposing obesity and egg quality link.

While humans and mice look and act very differently, 85 to 90 percent of our genes are the same or similar. So if scientists can understand the instructions in every mouse gene, people will get a good idea of the instructions in virtually every human gene as well.

" An anti-cancer drug reverses memory deficits in an Alzheimer's disease mouse model, University of Pittsburgh Graduate School of Public Health researchers confirm in the journal Science."

A new study from the Monell Center, the U.S. Department of Agriculture (USDA), and collaborating institutions reports a uniquely identifiable odor signature from mouse models of Alzheimer's disease. The odor signature appears in urine before significant development of Alzheimer-related brain pathology, suggesting that it may be possible to develop a non-invasive tool for early diagnosis of Alzheimer's disease.

Biologists at the Massachusetts Institute of Technology have created a genetically modified version of a common bacteria found in the gut that can sense the environment there and fight disease. And when this designer bacteria works, the proof is in the poop - glowing poop. (In this case, mouse poop.)

In the Oct. 30 edition of Science, scientists describe strains of laboratory mice bred to test the role of an individual's genetic makeup in the course of Ebola disease. Systems biologists and virologists Angela Rasmussen and Michael Katze from the Katze Laboratory at the University of Washington Department of Microbiology led the study in collaboration with the National Institutes of Health's Rocky Mountain Laboratories in Montana and University of North Carolina at Chapel Hill.

Researchers have designed a nanoparticle-based therapy that is effective in treating mice with multiple myeloma, a cancer of immune cells in the bone marrow.

The number of new Ebola cases is tapering off, but the search for new treatments continues. Now, one research team has found potential drug candidates that successfully treated up to 90 percent of mice exposed to the Ebola virus. They report their findings in the journal ACS Infectious Diseases.

Now, University of Missouri researchers have determined that a compound found in green tea, and voluntary exercise, slows the progression of the disease in mice and may reverse its effects. Further study of the commonly found extract could lead to advancements in the treatment and prevention of Alzheimer's disease in humans.

de Villena and his colleagues counted the RNA molecules produced and found that genes from the father produced on average more RNA than genes from the mother. (And remember, RNA directs the production of proteins, which are the workhorses of the body's development and function.) The implication? "It's not only what you inherit, but from whom you inherit," he said.

Researchers have made dramatic inroads into the study of polygenic and other complex human diseases, due in large part to knowledge of the human genome sequence, the generation of widespread markers of genetic variation, and the development of new technologies that allow investigators to associate disease phenotypes with genetic loci. Although polygenic diseases are more common than single-gene disorders, studies of monogenic diseases provide an invaluable opportunity to learn about underlying molecular mechanisms, thereby contributing a great deal to our understanding of all forms of genetic disease.

Immune cells in mice with lupus symptoms have overactive metabolisms, so scientists inhibited two metabolic pathways and succeeded in reversing lupus symptoms in mice

A new study by Duke University researchers helps clarify the matter by showing how a sugar habit changes specific brain circuits, and how those changes produce cravings that reinforce the habit. The research team began by getting a group of healthy mice hooked on sugar. Similar to classic studies on drug addiction, the mice in this study were trained to press a tiny lever to receive doses of sweets. Once the mice were hooked, they continued pressing the lever even when the sweets were removed. So that was step one, establishing a behavioral pattern to get the goods.

The team, led by senior authors Qi Zhou and Xiao-Yang Zhao, both from the Institute of Zoology at the Chinese Academy of Sciences, took embryonic stem cells from mice and treated them to a series of carefully worked out steps that included first exposing the stem cells to testicular cells in newly born male mice. The scientists then recreated the chemical environment that sperm cells need to grow, including early development factors and sex hormones including testosterone, follicle stimulating hormone and a growth factor from the pituitary gland.