Lactose, found in dairy products and other foods, is comprised of two simple sugars, glucose and galactose. In galactosemia, where galactose is not properly metabolized, build-up of toxic compounds, such as galactose-1-phosphate, can lead to liver disease, renal failure, cataracts, brain damage, and even death if this disorder is left untreated. Currently, the only treatment for galactosemia is elimination of lactose and galactose from the diet, but in some cases this is not sufficient to avoid long-term complications from the disorder.

Attempts to manage body weight are often unsuccessful or only temporary. This is, in part, due to antiquated dieting methods that attempt to address calorie consumption while ignoring metabolic and physical changes. Personalized and more comprehensive methods to track and manage body weight may be more effective.

Systemic lupus erythematosus (SLE) is a multi-organ inflammatory disease characterized by a significant morbidity and mortality related to both disease evolution as well as therapeutic side effects. At least half of SLE patients develop lupus nephritis.

The National Institutes of Health announces polyclonal antibodies against mouse cytochrome P450s CYP2J and CYP2C. Cytochrome P450s catalyze the metabolism of a wide range of exogenous compounds, including drugs, industrial chemicals, environmental pollutants, and carcinogens. The 2C family of cytochrome P450 metabolizes an extensive number of drugs which include tolbutamide, S-Warfarin, mephenytoin, diazepam and taxol. Many of the P450 enzymes are also active in the NADPH-dependent oxidation of arachidonic acid to various eicosanoids found in several species.

Available for licensing are monoclonal antibodies targeting human DNA polymerase beta (Pol B). Pol B is a constitutively expressed "housekeeping" enzyme that plays a role in base excision repair (BER), a cellular defense mechanism that repairs DNA base damage and loss. Aberrant Pol B expression is associated with genomic instability indicating that Pol B is required for DNA maintenance, replication and recombination.

Smad4 knockout: Smad4 is essential for epiblast proliferation, egg cylinder formation and mesoderm induction in early embryogenesis.

FGFR4 knockout: Lung alveoli fail to develop normally in double mutant with FGFR4 and FGFR3 knockouts.

mEpoR-/- hEpoR+: The mouse Erythropoietin Receptor knockout that contains a human Erythropoietin Receptor transgene can be used to define the potency of recombinant erythropoietin preparations used to treat anemia associated with chronic kidney disease.

M5 muscarinic receptor knockout: Deficiency of M5Rs reduces drug-seeking behavior.

The five Muscarinic Acetylcholine (ACh) receptors are G-protein coupled receptors (M1R-M5R). M1R, M3R and M5R selectively couple to Gq/G11; M2R and M4R selectively couple to Gi/Go. M5R knockout mice are viable and fertile, and have no major morphological abnormalities.

Selective inactivation of Stat1 in mammary cells indicates that its effect as a tumor suppressor in breast is direct.

STAT1 is considered a tumor suppressor, but it is not known if this effect occurs directly in mammary cells or secondarily by disrupting interferon signaling through the JAK/STAT1 pathway to induce immune responses. ERBB2/neu-induced breast cancer appeared sooner in mice lacking STAT1 only in mammary cells than in wild-type mice, indicating that STAT1 tumor suppression was intrinsic to mammary cells and not secondary to an induced immune response.