DreamPharm Products:
J Immunol. 2002 Sep 15;169(6):2892-9.
Surfactant protein D reduces alveolar macrophage apoptosis in vivo.
Clark H, Palaniyar N, Strong P, Edmondson J, Hawgood S, Reid KB.
Medical Research Council Immunochemistry Unit, Department of Biochemistry, University of Oxford, Oxford, United Kingdom. howard.clarioch.ox.ac.uk
Surfactant protein D (SP-D) is a molecule of the innate immune system that recognizes the patterns of surface carbohydrate on pathogens and targets them for phagocytosis and killing. SP-D-deficient mice show an increased number of macrophages in the alveolar space, excess surfactant phospholipid, overproduction of reactive oxygen species, and the development of emphysema. We report here that SP-D-deficient mice have a 5- to 10-fold increase in the number of apoptotic and necrotic alveolar macrophages, as defined by annexin V and propidium iodine staining, respectively. Intrapulmonary administration of a truncated 60-kDa fragment of human recombinant SP-D reduces the number of apoptotic and necrotic alveolar macrophages and partially corrects the lipid accumulation in SP-D-deficient mice. The same SP-D fragment binds preferentially to apoptotic and necrotic alveolar macrophages in vitro, suggesting that SP-D contributes to immune homeostasis in the lung by recognizing and promoting removal of necrotic and apoptotic cells.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12218102&dopt=Abstract
J Immunol. 2002 Sep 15;169(6):2915-24.
Effects of nicotine exposure on T cell development in fetal thymus organ culture: arrest of T cell maturation.
Middlebrook AJ, Martina C, Chang Y, Lukas RJ, DeLuca D.
Department of Microbiology and Immunology, University of Arizona College of Medicine, Tucson, AZ 85274, USA.
There is evidence for both physiological functions of the natural neurotransmitter, acetylcholine, and pharmacological actions of the plant alkaloid, nicotine, on the development and function of the immune system. The effects of continuous exposure to nicotine over a 12-day course of fetal thymus organ culture (FTOC) were studied, and thymocytes were analyzed by flow cytometry. In the presence of very low concentrations of nicotine many more immature T cells (defined by low or negative TCR expression) and fewer mature T cells (intermediate or high expression of TCR) were produced. In addition, the numbers of cells expressing CD69 and, to a lesser extent, CD95 (Fas) were increased. These effects took place when fetal thymus lobes from younger (13-14 days gestation) pups were used for FTOC. If FTOC were set up using tissue from older (15-16 days gestation pups), nicotine had little effect, suggesting that it may act only on immature T cell precursors. Consistent with an increase in immature cells, the expression of recombinase-activating genes was found to be elevated. Nicotine effects were partially blocked by the simultaneous addition of the nicotinic antagonist d-tubocurarine. Furthermore, d-tubocurarine alone blocked the development of both immature and mature murine thymocytes, suggesting the presence of an endogenous ligand that may engage nicotinic acetylcholine receptors on developing thymocytes and influence the course of normal thymic ontogeny.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12218105&dopt=Abstract
Proc Natl Acad Sci U S A. 2002 Sep 17;99(19):12293-7. Epub 2002 Sep 06.
Involvement of PD-L1 on tumor cells in the escape from host immune system and tumor immunotherapy by PD-L1 blockade.
Iwai Y, Ishida M, Tanaka Y, Okazaki T, Honjo T, Minato N.
Department of Medical Chemistry, Graduate School of Medicine, Japan Science and Technology Corporation, Kyoto 606-8501, Japan.
PD-1 is a receptor of the Ig superfamily that negatively regulates T cell antigen receptor signaling by interacting with the specific ligands (PD-L) and is suggested to play a role in the maintenance of self-tolerance. In the present study, we examined possible roles of the PD-1/PD-L system in tumor immunity. Transgenic expression of PD-L1, one of the PD-L, in P815 tumor cells rendered them less susceptible to the specific T cell antigen receptor-mediated lysis by cytotoxic T cells in vitro, and markedly enhanced their tumorigenesis and invasiveness in vivo in the syngeneic hosts as compared with the parental tumor cells that lacked endogenous PD-L. Both effects could be reversed by anti-PD-L1 Ab. Survey of murine tumor lines revealed that all of the myeloma cell lines examined naturally expressed PD-L1. Growth of the myeloma cells in normal syngeneic mice was inhibited significantly albeit transiently by the administration of anti-PD-L1 Ab in vivo and was suppressed completely in the syngeneic PD-1-deficient mice. These results suggest that the expression of PD-L1 can serve as a potent mechanism for potentially immunogenic tumors to escape from host immune responses and that blockade of interaction between PD-1 and PD-L may provide a promising strategy for specific tumor immunotherapy.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12218188&dopt=Abstract
Tumour Biol. 2002 May-Jun;23(3):123-9.
Production of macrophage migration inhibitory factor by human and murine neuroblastoma.
Bin Q, Johnson BD, Schauer DW, Casper JT, Orentas RJ.
Department of Pediatrics, Section of Hematology-Oncology, Medical College of Wisconsin, Milwaukee, Wisc 53226, USA.
Tumor cells avoid immune recognition by subverting the ability of the immune system to mount an inflammatory response that generates cytotoxic effector cells. This can be achieved through cytokine production by the tumor itself. Our objective was to determine the cytokine profile of neuroblastoma (NB) lesions in tumor vaccine models. We found that the murine NB cell line, Neuro2a, secretes macrophage migration inhibitory factor, MIF, a multifunctional cytokine with the potential to block effective immune responses to a tumor. Patient-derived NB cell lines were also found to produce MIF. MIF production by NB was documented at the level of RNA by RNAse protection, soluble cytokine production by ELISA, and in a macrophage migration assay. Our studies also confirmed reports of IL-6 production by human NB cell lines. NB culture-derived MIF was also shown to activate tumor cell migration. This supports the hypothesis that MIF is a tumor-derived cytokine that may play a role in NB aggressiveness and evasion of immune recognition. 2002 S. Karger AG, Basel
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12218292&dopt=Abstract
AIDS. 2002 Sep 6;16(13):1755-60.
Dynamics of spontaneous HIV-1 specific and non-specific B-cell responses in patients receiving antiretroviral therapy.
Fournier AM, Baillat V, Alix-Panabieres C, Fondere JM, Merle C, Segondy M, Huguet MF, Reynes J, Vendrell JP.
From the Departement de Virologie Clinique, Hopitaux Lapeyronie et Saint Eloi, 34295 Montpellier Cedex 5, France.
OBJECTIVES: As spontaneous anti-HIV-1 antibody and IgG secretion by peripheral blood mononuclear cells (PBMC) reflect immune system activation by HIV-1 antigens, we evaluated the impact of antiretroviral therapies on HIV-1 specific and non-specific B cell responses. METHODS: Anti-HIV-1 antibody and non-specific IgG were measured by ELISA in supernatants of PBMC cultured during 7 day from 30 patients initiating an antiretroviral therapy at baseline, 8, 16, 24, 36 and 48 weeks. RESULTS: An early and sustained fall in plasma viral load to below the detection limit (20 copies/ml) was observed in 17 sustained responder patients (SR), whereas HIV-1 RNA remained detectable in 13 others incomplete responders. In both groups, HIV-1 specific antibody secretion decreased significantly in parallel with plasma viral load and polyclonal immunoglobulin production became similar to that of PBMC controls. However, HIV-1 specific antibody production became negative in only six SR, exhibiting a greater increase of CD4 T-cell counts and higher levels of the spontaneous HIV-1 specific IgA secretion at baseline than the other SR. CONCLUSIONS: Antiretroviral therapy induced a rapid and dramatic decrease of spontaneous HIV-1 specific and non-specific B cell responses. These results pointed out that HIV-1 specific antibody secretion persisted in 11 out of 17 SR patients, suggesting persistent immune system activation by residual HIV-1 antigens. 2002 Lippincott Williams & Wilkins
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12218386&dopt=Abstract
Natural Herbal Supplement: Hair Million
The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer a biologically essential part of our body, just
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