Abstract: A hole-jetting type mixer-reactor, comprises the following parts: a first feeding port, a second feeding port, an outer casing, an inner casing, jet holes and a mixing reaction zone. The inner casing is inside the outer casing, and the lower portion of the outer casing forms a buffer chamber with the inner casing. The first feeding port connects with the inner casing to constitute one flow channel, and the second feeding port connects with the buffer chamber to form the other flow channel. The jet holes are on the wall of the inner casing situated at lower portion of the buffer chamber. The mixing reaction zone is inside the inner casing below the jet holes. The cross section of the inner casing is rectangular or rectangle-like. The mixer-reactor can achieve a fast mixing of two reactant streams which reacts with instantaneous, complicated parallel or consecutive competing reactions. The time scale of the mixing process is several milliseconds.

Abstract: Compounds according to formula (I) wherein Z is S, SO, or SO2, may be prepared by a process that includes charging to a reactor hydrogen sulfide and an alkyl glycidyl ether according to formula (III), in the presence of a base. The compounds may also be prepared by contacting an alkoxychlorohydrin according to formula (II) with a sulfide source.

Abstract: Computer system for controlled creation, processing, administration and display of quality information within an enterprise. Linkages may be defined among enterprise entities, process/product development attributes, strategies, goals, process improvement opportunities, etc. Visual analysis of data associated with the linkages is provided in an interactive fashion. Linkages may also be defined among online quality-related documentation throughout an enterprise such that information is automatically propagated/reconciled through the enterprise in a controlled and efficient fashion. The creation of process documentation for new products is facilitated based on a concept of content/document inheritance.

Abstract: Compounds according to formula (I) wherein Z is S, SO, or SO2, may be prepared by a process that includes charging to a reactor hydrogen sulfide and an alkyl glycidyl ether according to formula (III), in the presence of a base. The compounds may also be prepared by contacting an alkoxychlorohydrin according to formula (II) with a sulfide source.

Abstract: The administration of an Akt inhibitor in a suitable carrier to a rheumatoid arthritis synovial fibroblast affords a process for inducing rheumatoid arthritis synovial fibroblast apoptosis. The Akt inhibitor is administered either as an active molecule or as a gene sequence expressible within rheumatoid arthritis synovial fibroblast cells. The gene sequence can be encompassed within a gene vector such as an adenovirus. A process for assaying rheumatoid arthritis drug candidates for apoptosis affect includes exposing a culture of rheumatoid arthritis synovial fibroblast cells to a drug candidate and monitoring apoptosis in the culture in the presence of the drug candidate. Apoptosis in the culture is compared to apoptosis induced in a duplicate culture in the presence of a known Akt inhibitor.

Abstract: One major problem with adenovirus gene therapy has been the T-cell mediated immune response elicited by inoculation of adenovirus, which leads to rapid clearance of the virus and loss of transgene expression. In the instant invention, the immune response to a virus is prevented by pre-treatment with adenovirus, adenoassociated virus or herpes virus infected antigen-presenting cell (APC) expressing Fas ligand with induced T-cell tolerance. Administration of AdCMVLacZ after tolerance resulted in prolonged expression of LacZ in tolerized animals compared to control treated animals. In control, but not tolerized animals, there was proliferation of CD3+T-cell in the spleen in response to AdCMVLacZ treatment. Tolerance induction is also indicated by decreased production of interferon-&ggr; and IL-2 by peripheral T-cells isolated from treated animals after stimulation with the adenovirus infected APCs.

Abstract: One major problem with adenovirus gene therapy has been the T-cell mediated immune response elicited by inoculation of adenovirus, which leads to rapid clearance of the virus and loss of transgene expression. In the instant invention, the immune response to a virus is prevented by pre-treatment with adenovirus, adenoassociated virus or herpes virus infected antigen-presenting cell (APC) expressing Fas ligand with induced T-cell tolerance. Administration of AdCMVLacZ after tolerance resulted in prolonged expression of LacZ in tolerized animals compared to control treated animals. In control, but not tolerized animals, there was proliferation of CD3+ T-cell in the spleen in response to AdCMVLacZ treatment. Tolerance induction is also indicated by decreased production of interferon-&ggr; and IL-2 by peripheral T-cells isolated from treated animals after stimulation with the adenovirus infected APCs.

Abstract: The present invention provides a method of increasing adenoviral gene expression in a tissue of an animal, comprising the step of administering to said animal a pharmacologically effective dose of tumor necrosis factor binding protein. Also provided is a various method of method of reducing an inflammatory response associated with adenoviral administration in a tissue of an animal, comprising the step of administering to said animal a pharmacologically effective dose of tumor necrosis factor binding protein.

Abstract: The present invention discloses a method of producing large-scale recombinant adeno-associated virus stocks by infection of cells with at least one recombinant adenovirus vector(s). The vector(s) encode a therapeutic gene flanked by the terminal repeat ends of adeno-associated virus and the adeno-associated virus rep and cap genes. Transfection with two recombinant adenovirus vector(s) instead of two plasmids plus adenovirus results in the large scale, high titer production of recombinant adeno-associated virus with little to no contaminating adenovirus present.

Abstract: The present invention provides a method of increasing adenoviral gene expression in a tissue of an animal, comprising the step of administering to said animal a pharmacologically effective dose of tumor necrosis factor binding protein. Also provided is a various method of method of reducing an inflammatory response associated with adenoviral administration in a tissue of an animal, comprising the step of administering to said animal a pharmacologically effective dose of tumor necrosis factor binding protein.