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Dengue hemorrhagic fever (DHF) is a severe, potentially deadly infection spread by mosquitos. CDC scientists have identified vitronectin as an important biomarker of DHF. They have shown vitronectin is significantly reduced in DHF and severe dengue infections when compared to dengue non-hemorrhagic fever patients. Presently, DHF is established by assessing antibody concentrations and other rule-of-thumb criteria, but often these assays can be difficult to interpret and lead to false conclusions.

Dengue virus (DENV) is the cause of dengue illness (dengue fever, dengue hemorrhagic fever, and dengue shock syndrome). CDC researchers have developed a RT-PCR multiplex assay that, prior to sero-conversion, selectively detects dengue virus in biological or other fluid media, such as whole blood, plasma, or serum. The primers and probes from this assay are sufficiently specific to amplify and detect all four DENV serotypes. This FDA-approved technology may provide an improved method for rapid and accurate serotyping of dengue virus in clinical and research settings.

The invention provides for a full-length cloned cDNA copy of the RNA genome of a predominant norovirus strain (Genogroup II.4) designated MD145-12 that was associated with human gastrointestinal illness. The noroviruses, which were formerly known as "Norwalk-like" viruses are estimated to cause 23 million cases of acute gastroenteritis in the USA each year. The virus has been designated into category B of the CDC biodefense-related priority pathogens because it can be used as an agent of bioterrorism.

Biological materials are important research tools that can be used for diagnostic as well as therapeutic purposes. Antibodies have become viable drugs in the market today and there is a general market need for systems that may facilitate production of efficient and effective antibodies. In recent years, monoclonal antibodies have gained significant importance in their use, both as diagnostics and therapeutics, to intervene and combat diseases such as cancer, cardiovascular diseases, and infections.

This technology is directed to the discovery of specific microRNAs that target and downregulate enzymes within the cholesterol biosynthetic pathway and is currently being tested in vivo.

Recently-developed protein tags enable the specific covalent attachment of synthetic ligands, incorporating fluorophores or other substituted groups, to fusion proteins containing these tags. For example, SNAP and CLIP tags bind O⁶-benzylguanine-containing and O²-benzylcytosine containing ligands respectively, which can be derivatized with a wide variety of labels, including fluorescent dyes, affinity probes, and cross-linkers.

A method of detecting DNase I hypersensitive sites ((DHS) in a single cell or very small number of cells, including cells recovered from formalin-fixed paraffin-embedded (FFPE) tissue slides of patient samples. DHS has revealed a large number of potential regulatory elements for transcriptional regulation in various cell types. The application of DNase-Seq techniques to patient samples can elucidate pathophysiological mechanisms of gene function in a variety of diseases as well as provide potentially important diagnostic and prognostic information.

PTEN is a tumor suppressor gene that is frequently deleted or mutated in a variety of human cancers, including prostate, breast, endometrial, lung, and ovarian cancers. In prostate cancer cells, PTEN deletion is the most common event observed. The loss of PTEN is thought to play and important role in tumor cell proliferation and metastasis due to a lack of control of the signaling pathways that mediate cellular processes such as apoptosis and migration.

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

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.