Philip Murphy

Bio: Philip Murphy is an academic researcher from Murphy Oil. The author has contributed to research in topics: Antenna (radio) & Transponder. The author has an hindex of 14, co-authored 19 publications receiving 4018 citations. Previous affiliations of Philip Murphy include IBM.

CC CKR5: A RANTES, MIP-1α, MIP-1β Receptor as a Fusion Cofactor for Macrophage-Tropic HIV-1

Abstract: Human immunodeficiency virus-type 1 (HIV-1) entry requires fusion cofactors on the CD4 + target cell. Fusin, a heterotrimeric GTP-binding protein (G protein)-coupled receptor, serves as a cofactor for T cell line-tropic isolates. The chemokines RANTES, MIP-1α, and MIP-1β, which suppress infection by macrophage-tropic isolates, selectively inhibited cell fusion mediated by the corresponding envelope glycoproteins (Envs). Recombinant CC CKR5, a G protein-coupled receptor for these chemokines, rendered CD4-expressing nonhuman cells fusion-competent preferentially with macrophage-tropic Envs. CC CKR5 messenger RNA was detected selectively in cell types susceptible to macrophage-tropic isolates. CC CKR5 is thus a fusion cofactor for macrophage-tropic HIV-1 strains.

Thin radio frequency transponder with leadframe antenna structure

Abstract: A novel radio frequency transponder (tag) with a minimum of components and connects is thin and flexible because these components and connects can be unsupported by a substrate layer. This is accomplished by using a conducting leadframe structure not only as a connection medium but also as a circuit element, i.e., the transponder antenna. In various preferred embodiments, the leadframe is mechanically positioned and fixably attached to a circuit chip so that the leadframe (antenna) is self supporting. A protective coating can be added where the leadframe is attached to the circuit chip. Further a protective surrounding can envelops the entire leadframe antenna, circuit chip, and, if provided, the protective coating.

Method and apparatus for testing RFID tags

Abstract: The present invention provides a method and apparatus for testing RFID tags using wireless radio frequency (RF) communication. The method and apparatus allow RFID tags to be tested individually or in groups while they are in close proximity to each other (e.g., within the read range of the tag).

Radio frequency identification transponder having a high gain antenna configuration

Abstract: A radio frequency identification transponder has a high gain antenna for increased range. In an embodiment, the radio frequency transponder has a reflector to increase its operative range. A system of one or more reflectors is operatively associated with a transponder and may be formed out of any sort of radio frequency reflective material. The reflector system can enhance reception or transmission of radio waves by or from the transponder. The reflector system may also be used to provide for selective coupling of the radio frequency transponder with a base station, user- or vehicle-supported reader, or the like based on relative orientation. In addition, the reflector system may be used to selectively reflect particular radio waves. In another embodiment, the radio frequency transponder has a horn antenna providing increased gain and directivity. In yet another embodiment, the radio frequency transponder has a patch antenna providing increased gain and circular polarization. The patch antenna may further comprise a patch antenna array, a multi-layer patch or a dipole comprised of patch elements.

Stepped electronic device package

Abstract: An electronic device packaging structure is described wherein an electronic device (40) is electrically connected to a substrate (44) wherein the electronic device subtends a non-normal angle with respect to the substrate. In a more specific embodiment, a plurality of electronic devices (40) are stacked at offset with respect to each other to expose contact locations on the surface of each electronic device at an edge of each electronic device to form a stepped surface exposing a plurality of electronic device contact locations. This surface is disposed against a substrate having a plurality of contact locations (46) thereon. The electronic device contact locations can be electrically interconnected to the substrate contact locations by solder mounds (48) or alternatively by a cylindrical shaped elastomeric body having metallization bands with a spacing corresponding to the electronic device contact locations. The elastomeric body is pressed between the edge of the stacked electronic devices having the contact locations thereon and substrate surface to form electrical interconnections between electronic device contact locations and substrate contact locations through the electrically conducting bands. The stacked electronic devices can be thermally connected to a heat dissipation means. The stacked electronic devices can have a stepped surface (34) embodying an enhanced area for transfer of heat from the electronic device stack to the heat dissipation means (50).

Chemokines — Chemotactic Cytokines That Mediate Inflammation

Abstract: The attraction of leukocytes to tissues is essential for inflammation and the host response to infection. The process is controlled by chemokines, which are chemotactic cytokines. This review introduces the burgeoning family of cytokines, with special emphasis on their role in the pathophysiology of disease and their potential as targets for therapy. Structure and Function of Chemokines Over 40 chemokines have been identified to date, most of them in the past few years. The relations among chemokines were not initially appreciated, which led to an idiosyncratic nomenclature consisting of many acronyms. When initially identified, these proteins had no known biologic . . .

Resistance to HIV-1 infection in caucasian individuals bearing mutant alleles of the CCR-5 chemokine receptor gene.

Abstract: HIV-1 and related viruses require co-receptors, in addition to CD4, to infect target cells. The chemokine receptor CCR-5 (ref.1) was recently demonstrated to be a co-receptor for macrophage-tropic (M-tropic) HIV-1 strains, and the orphan receptor LESTR (also called fusin) allows infection by strains adapted for growth in transformed T-cell lines (T-tropic strains). Here we show that a mutant allele of CCR-5 is present at a high frequency in caucasian populations (allele frequency, 0.092), but is absent in black populations from Western and Central Africa and Japanese populations. A 32-base-pair deletion within the coding region results in a frame shift, and generates a non-functional receptor that does not support membrane fusion or infection by macrophage- and dual-tropic HIV-1 strains. In a cohort of HIV-1 infected caucasian subjects, no individual homozygous for the mutation was found, and the frequency of heterozygotes was 35% lower than in the general population. White blood cells from an individual homozygous for the null allele were found to be highly resistant to infection by M-tropic HIV-1 viruses, confirming that CCR-5 is the major co-receptor for primary HIV-1 strains. The lower frequency of heterozygotes in seropositive patients may indicate partial resistance.

Genetic Restriction of HIV-1 Infection and Progression to AIDS by a Deletion Allele of the CKR5 Structural Gene

Abstract: The chemokine receptor 5 (CKR5) protein serves as a secondary receptor on CD4 + T lymphocytes for certain strains of human immunodeficiency virus-type 1 (HIV-1). The CKR5 structural gene was mapped to human chromosome 3p21, and a 32-base pair deletion allele ( CKR5Δ32 ) was identified that is present at a frequency of ∼0.10 in the Caucasian population of the United States. An examination of 1955 patients included among six well-characterized acquired immunodeficiency syndrome (AIDS) cohort studies revealed that 17 deletion homozygotes occurred exclusively among 612 exposed HIV-1 antibody-negative individuals (2.8 percent) and not at all in 1343 HIV-1-infected individuals. The frequency of CKR5 deletion heterozygotes was significantly elevated in groups of individuals that had survived HIV-1 infection for more than 10 years, and, in some risk groups, twice as frequent as their occurrence in rapid progressors to AIDS. Survival analysis clearly shows that disease progression is slower in CKR5 deletion heterozygotes than in individuals homozygous for the normal CKR5 gene. The CKR5Δ32 deletion may act as a recessive restriction gene against HIV-1 infection and may exert a dominant phenotype of delaying progression to AIDS among infected individuals.

Human chemokines: an update.

Abstract: Interleukin 8, the first chemokine to be characterized, was discovered nearly ten years ago. Today, more than 30 human chemokines are known. They are often upregulated in inflammation and act mainly on leukocytes inducing migration and release responses. The present review deals largely with the new developments of the last three years. Several structural studies have shown that most chemokines form dimers. The dimers, however, dissociate upon dilution, and the monomers constitute the biologically active form. Chemokine activities are mediated by seven-transmembrane-domain, G protein coupled receptors, five of which were discovered in the past three years. The primary receptor-binding domain of all chemokines is near the NH2 terminus, and antagonists can be obtained by truncation or substitutions in this region. Major progress has been made in the understanding of chemokine actions on T lymphocytes that respond to several CC chemokines but also to IP10 and Mig, two CXC chemokines that selectively attract ...