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This technology includes (N)-methanocarba derivatives that are selective agonists of the A3 receptor to be used for the treatment of chronic neuropathic pain. This class of compounds produced full agonists of the human A3AR of nanomolar affinity that were consistently highly selective (>1000-fold vs. A1AR and A2AAR). The selectivity at mouse A3 receptors is smaller, but the compounds are still effective in vivo in reducing or preventing development of neuropathic pain.

This technology includes novel hyperactive Hermes Transposase mutants and their encoding genes. These transposases are easily purified in large quantity after expression in bacteria. The modified Hermes Transposases are soluble and stable and exist as smaller active complexes compared to the native enzyme. The consensus target DNA recognition sequence is the same as the native enzyme and shows minimal insertional sequence bias.

This technology includes the discovery that two specific microRNAs are not required for the development and function of brown fat in mice. Effects of inactivating microRNAs in cell culture in vitro have not always been reproduced in vivo. The paper tests the effect of inactivating two microRNAs, miR-193b and miR-365-1 on the differentiation, function and development of brown adipose tissue. In contrast to positive results previously observed in vitro, the mouse in vivo studies failed to demonstrate significant effects.

This technology includes a transgenic mouse model which can be used to study perinatal oocyte dynamics. In the first two days after birth, the number of primordial ovarian follicles and their germ cells undergo a major decrease. The mechanism for this decrease was studied. Ablation of FIGLA (Factor in the germline, alpha), a basic helix-loop-transcription factor, results in massive perinatal oocyte loss. A transgenic mouse line was established, Figla-EGFP /Cre, in which EGFP and Cre recombinase are expressed just before birth in germ cells.

This technology includes new nucleoside inhibitors containing rigid rings that provide high potency for use as antiepileptic drugs. Adenosine kinase (AdK) inhibitors raise the level of endogenous adenosine, particularly in disease states, and are of interest for the potential treatment of seizures and neurodegenerative and inflammatory conditions.

This technology includes a model for providing a patient-specific diagnosis of disease using clinical data. Specifically, the present invention relates to a fully unsupervised, machine-learned, cross-validated, and dynamic Bayesian Belief Network model that utilizes clinical parameters for determining a patient-specific probability of transplant glomerulopathy. Kidney failure is a growing problem worldwide, in part related to the increase incidence of diabetes and hypertension. Renal replacement therapy includes dialysis or renal transplantation.

This technology includes lentivirus vectors to be used to treat sickle cell disease and beta thalassemia. (i) Lin28A or Lin28B vectors designed for erythroid-specific expression using EKLF1, SPTA1, or similar erythroid-specific regulatory elements will be used to transduce hematopoietic stem cells isolated from humans with sickle cell disease or beta-thalassemia syndromes.

This technology includes adenosine receptor binding compounds which could potentially be used for development of more selective and safe treatment of cardiovascular, psychiatric and neurodegenerative disorders. Though adenosine has been extensively studied as a primary chemical scaffold for adenosine receptor agonists, very little structure activity data exist for C5' substitution. This technology presents novel rationally designed small molecule compounds capable of selective binding to adenosine receptor (subtypes A2a, A1, A2b and A3) and inducing effector-biased downstream signaling.

This technology includes transgenic mice in which designer rat M3 muscarinic receptor mutants were expressed only in islet 13-cells (directed by rat insulin promoter II), were unable to bind acetylcholine (the endogenous ligand) but could be selectively activated by an otherwise pharmacologically inert compound (clozapine-N-oxide (CNO)). The R-q receptor contained a Y148C point mutation, which enabled CNO to selectively activate G proteins of the Gq/11 family. The R-5 receptor contained an A238G mutation, which enabled CNO to selectively activate G proteins of the G5 family.

This technology includes identification of the wild mouse microbiome as a method to increase resistance to lethal viral infection. We establish that the gut microbiome of barrier-raised C57BL/6 mice is dysbiotic compared to that of their outbred, wild-living progenitors, Mus musculus domesticus. We find that the multigenerational offspring of pregnant germfree C57BL/6 mice reconstituted with the gut microbiome of wild mice exhibit a less inflammatory response and increased survival following influenza A virus infection.