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The invention relates to recombinant chimeric rabbit/human monoclonal antibody fragments (Fabs) against hepatitis B Virus e-antigen (HBeAg), notably Fab me6. Viral hepatitis is the seventh leading cause of death worldwide. Hepatitis B core antigen (HBcAg) forms an icosahedral structure containing the viral genome. Both the HBcAg and the HBeAg of interest here are expressed by two different start codons of the viral C gene. Unlike the related HBcAg which activates type 1 T helper (Th1) cells leading to immune attack, the HBeAg activates Th2 cells which promote immune tolerance.

This technology includes a product for local delivery of alkaline phosphatase for the treatment of periodontal disease. Our laboratory has discovered that factors regulating phosphate metabolism and specifically the appropriate balance between phosphate (Pi) and pyrophosphate (PPi) at local sites are needed for formation (development), maintenance and regeneration of the tooth root surface (cementum), periodontal ligament (PDL) and surrounding alveolar bone, i.e., the periodontal apparatus.

This invention relates to improved methods of preparing Bacillus anthracis protective antigen (PA) for use in vaccines. PA is a secreted, non-toxic protein with a molecular weight of 83 KDa. PA is a major component of the currently licensed human vaccine (Anthrax Vaccine Adsorbed, AVA).

This technology provides a novel method of treating or preventing pruritis (itch) using natriuretic polypeptide b (Nppb) blocking agents. Itch (also known as pruritis) is a sensation that may be perceived as an unpleasant skin irritation and may drive an urge to scratch. Conditions such as, for example, psoriasis, atopic dermatitis, renal failure, liver cirrhosis and some cancers may cause persistent itch. Itch is triggered by somatosensory neurons expressing the ion channel TRPV1 (transient receptor potential cation channel subfamily V member 1).

Rapid point-of-care, antibody-based testing is not available for the diagnosis of autoimmune and most infectious diseases. For detecting autoantibodies associated with most autoimmune conditions, fluid-phase immunoprecipitation assays are required. However, these assays usually involve radioactivity and are not feasible for point-of-care applications. The subject invention describes methods of using neodymium magnet for diagnosis of infectious and autoimmune diseases including lupus, Sjögren's syndrome, type I diabetes, HIV and Lyme disease.

NIH scientists have identified new compositions that could potentially be used to treat or prevent pruritus (itchiness). The newly discovered compounds can block a newly identified itch pathway and might be effective for persistent itch caused by psoriasis, atopic dermatitis, renal failure, liver cirrhosis and chemotherapy. These compounds are different from commonly used antihistamines which induce drowsiness and sedation. These compounds have the potential to be used for human and animals.

This technology includes mice which are intended to be bred with mice that have the tetracycline-response element promoter driving a gene of interest, for the study of kidney diseases. When the dual transgenic mice are fed tetracycline or doxycycline, the transgene is activated in glomerular podocytes.

This technology includes antibodies to apolipoprotein L1 (ApoL 1) to be used in basic science laboratory studies. ApoL 1 is a protein that is present within cells and circulates as component of high-density lipoprotein. Its functions are not well understood. Recently APOL 1 genetic variants have been shown to be highly associated with kidney disease in African Americans.

Available for licensing are monoclonal antibodies against HIV-1 viral protein R (Vpr) and the respective hybridoma cell lines expressing the same. The antibodies provide a means for detecting HIV-1 Vpr. Currently, the mechanism of HIV pathogenesis believed to involve viral replication inside immune cells and other cells. At present, there are no clinical assays for detecting HIV-1 Vpr. Vpr circulates at detectable levels in the blood and is likely derived from degraded virions or released from infected cells. Vpr facilitates viral replication and disrupt normal cell function.