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Available for licensing and commercial development are intellectual property rights covering a method of imaging a biological specimen (e.g., human tissue) using fluorescent nanodiamonds implanted into the subject of interest, applying a magnetic field to said subject and producing a resultant image by a net juxtaposition of a second acquired image. This process suppresses the background and permits selective imaging of the nanodiamonds in the presence of background fluorescence that exceeds the signal from the nanodiamonds.

Available for licensing are inhibitors that target the USP1/ UAF1 deubiquitinating enzyme (DUB) complex. The FDA approval and commercial success of Velcade®, a small molecule proteasome inhibitor, has established the ubiquitin-proteasome system (UPS) as a valid target for anticancer treatment. However, proteasome inhibitors in general suffer from a narrow therapeutic index and acquired resistance. A promising alternative to proteasome inhibition has been to target the enzymes upstream of proteasome-mediated protein degradation, i.e.

The invention relates to systems and methods for localization microscopy for superresolution imaging of fluorescent molecules. The method utilizes intrinsic bleaching/blinking properties of fluorophores in which superresolution is achieved by capturing successive images and subtracting from each either the subsequent image. The location of a single fluorescent molecule can be identified when the molecules either photobleach, blink off, or blink between successive images using a higher magnification lens to achieve a smaller pixel size.

The present invention is directed to a transgenic rat model of Alzheimer's Disease (AD) termed TgF344-19+/-. The invention rat overexpresses two human genes (APPswe and PS1deltaE9 genes), each of which are believed to be independent dominant causes of early-onset AD. The hemizygote exhibits major features of AD pathology (i.e., dense and diffuse amyloid plaques, neurofibrillary tangles, cerebral amyloid angiopathy, hyperphosphorylated tau, paired-helical filaments, Hirano bodies, granulovacuolar degeneration, cognitive impairment, and cortical neuronal loss).

Q490L point mutation was introduced into the rat M3 muscarinic receptor cDNA to confer persistent, constitutive (ligand-independent) activity. Expression of the M3 receptor mutant was placed under the control of a 650 bp fragment of the rat insulin promoter II (RIP II) to limit expression to the islet beta cell.

Researchers at NIH have developed islet beta cell M3 muscarinic acetylcholine receptor knockout mouse. The mice were generated by crossing floxed mouse M3 muscarinic acetylcholine receptor mice with mice in which Cre recombinase was controlled by the beta-cell specific rat insulin promoter (RIP-Cre mice).

Researchers at NIH have generated transgenic mice in which the M3 muscarinic receptor is overexpressed in pancreatic beta cells. This was done by placing the receptor gene under the control of the 650 bp rat insulin promoter II (RIP II). The resulting mice show a pronounced increase in glucose tolerance and enhanced plasma insulin levels. Strikingly, these mutant mice were resistant to diet-induced glucose intolerance and hyperglycemia.

Legionnaires' disease is caused by a type of bacteria called Legionella. CDC scientists have developed a real-time multiplex PCR assay for diagnosis and identification of Legionella strains. The assay consists of five sets of primers (targeting L. bozemanii, L. dumoffii, L. feeleii, L. longbeachae, or L. micdadei) and corresponding probes. Each probe is labeled with a different fluorophore which allows the detection of a particular strain in a single tube reaction.

Two isoforms of sphingosine kinase, sphingosine kinase 1 (SphK1) and sphingosine kinase 2 (SphK2), convert sphingosine to sphingosine 1-phosphate (S1P) in mammalian cells. While the importance of SphK1 has been known for some time, information about SphK2 is still being revealed. Therefore, researchers at NIH have developed an antibody against mouse SphK2, which can be used to further understand the role of this enzyme.

The cleavage of sphingoid base phosphates by sphingosine-1-phosphate (S1P) lyase to produce phosphoethanolamine and a fatty aldehyde is the final degradative step in the sphingolipid metabolic pathway. Researchers at NIH injected rabbits with the C-terminal peptide of the mouse S1P lyase — 551-TTDPVTQGNQMNGSPKPR-568 — to develop an antibody that can be used in western blotting to study this pathway.