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Blood. 2003 Feb 1;101(3):1063-70. Epub 2002 Oct 03.
Leukemia-associated monoclonal and oligoclonal TCR-BV use in patients with B-cell chronic lymphocytic leukemia.
Rezvany MR, Jeddi-Tehrani M, Wigzell H, Osterborg A, Mellstedt H.
Immune and Gene Therapy Laboratory, Cancer Center Karolinska, the Department of Oncology (Radiumhemmet), Karolinska Hospital, Stockholm, Sweden.
T-cell receptor-B-variable (TCR-BV) gene usage and the CDR3 size distribution pattern were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) in patients with B-cell chronic lymphocytic leukemia (B-CLL) to assess the T-cell repertoire. The use of TCR-BV families in CD4 and CD8 T cells stimulated with autologous activated leukemic cells was compared with that of freshly obtained blood T cells. Overexpression of individual TCR-BV families was found in freshly isolated CD4 and CD8 T cells. Polyclonal, oligoclonal, and monoclonal TCR-CDR3 patterns were seen within such overexpressed native CD4 and CD8 TCR-BV families. In nonoverexpressed TCR-BV families, monoclonal and oligoclonal populations were noted only within the CD8 subset. After in vitro stimulation of T cells with autologous leukemic B cells, analyses of the CDR3 length patterns showed that in expanded TCR-BV populations, polyclonal patterns frequently shifted toward a monoclonal/oligoclonal profile, whereas largely monoclonal patterns in native overexpressed TCR-BV subsets remained monoclonal. Seventy-five percent of CD8 expansions found in freshly obtained CD8 T cells further expanded on in vitro stimulation with autologous leukemic B cells. This suggests a memory status of such cells. In contrast, the unusually high frequency of CD4 T-cell expansions found in freshly isolated peripheral blood cells did not correlate positively to in vitro stimulation as only 1 of 9 expansions continued to expand. Our data suggest that leukemia cell-specific memory CD4 and CD8 T cells are present in vivo of patients with CLL and that several leukemia cell-associated antigens/epitopes are recognized by the patients' immune system, indicating that whole leukemia cells might be of preference for vaccine development.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12393705&dopt=Abstract
Bioelectromagnetics. 2002 Dec;23(8):614-21.
Effect of millimeter waves on cyclophosphamide induced suppression of the immune system.
Logani MK, Anga A, Szabo I, Agelan A, Irizarry AR, Ziskin MC.
Richard J. Fox Center for Biomedical Physics, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA. mkloganotmail.com
The effect of millimeter electromagnetic waves (MWs) on cyclophosphamide (CPA) induced toxicity to leukocytes, bone marrow cells, and T-cell-mediated immunity was examined. For studying the effect of MWs on CPA induced leukopenia and myelosuppression, BALB/C mice were irradiated for 3 days, 30 min each day, prior to administration of CPA (200 mg/kg). MWs were produced with a Russian made YAV-1 generator. The device produced 42.2 +/- 0.2 GHz modulated wave radiation through a 10 mm x 20 mm rectangular output horn. The animals were irradiated on the nose area. Peak SAR and incident power density were measured as 622 +/- 100 W/kg and 31 +/- 5 mW/cm(2), respectively. For studying the effect of MWs on CPA induced suppression of T-cell mediated immunity, a delayed type hypersensitivity (DTH) assay in mouse skin was used. The DTH reaction in mouse skin was induced by topical application of dinitrochlorobenzene (DNCB) and quantified by measuring the increase in ear thickness and by histological examination. Treatment of animals with CPA significantly (P < 0.05) reduced leukocyte and bone marrow cell population, but MW irradiation did not show any significant protection from the immunosuppressive effects of CPA. Furthermore, MW irradiation did not protect the animals from CPA induced suppression of T-cell mediated immunity. 2002 Wiley-Liss, Inc.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12395417&dopt=Abstract
Dig Dis Sci. 2002 Oct;47(10):2154-62.
Relationship between response to interferon-alpha and function of peripheral blood mononuclear cells in chronic hepatitis C patients.
Esquivel F, Albillos A, Carrion F, Prieto A, Reyes E, Martinez-Martin B, Calleja JL, Cacho G, Alvarez-Mon M.
Department of Medicine, Hospital Principe de Asturias, University of Alcala, Madrid, Spain.
The factors responsible for the low response of chronic hepatitis C patients to interferon-a treatment are not fully understood, although it is known that interferon requires an efficient host immune response to achieve viral clearance. This study was designed to test the hypothesis that hepatitis C virus infection is associated with functional impairment of peripheral blood mononuclear cells, which influence the response to interferon. The proliferative and apoptotic responses of peripheral blood mononuclear cells and purified T cells stimulated with polyclonal mitogenic signals were assessed in 35 chronic hepatitis C patients and 30 healthy controls. Patients were divided into responders and nonresponders according to their sustained response to a course of alpha-interferon-a (3 MU three times weekly for 12 months). The proliferative response to polyclonal mitogens (PHA, TPA) was significantly decreased in nonresponders compared to responders and controls. The defective response was partially normalized by the exogenous addition of interleukin-2 or interleukin-4, and cannot be ascribed to increased apoptosis. Interestingly, the proliferative response of enriched T cells to the same signals was normal. In conclusion, the clinical response to interferon-a defines two different patterns of proliferation by mononuclear cells in chronic hepatitis C patients. This suggests that an alteration of the immune system in these patients may underlie their inadequate response to antiviral therapy.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12395886&dopt=Abstract
Immunobiology. 2002 Sep;205(4-5):446-54.
Assays for the functional activity of the mannan-binding lectin pathway of complement activation.
Thiel S, Moller-Kristensen M, Jensen L, Jensenius JC.
Department of Medical Microbiology and Immunology, University of Aarhus, Denmark. steffen.thieicrobiology.au.dk
Mannan-binding lectin (MBL) activates complement independently of the adaptive, clonal immune system and thus presents an innate anti-microbial defence mechanism. Events in the MBL pathway of complement activation involve the binding of MBL to patterns of carbohydrate structures presented by the surface of micro-organisms. For the activation of complement to occur MBL must be associated with serine proteases (MBL-associated serine proteases, MASPs) in an MBL/MASP complex. When bound to micro-organisms, the MBL complex mediates the activation of C4 and C2, generating the C3 convertase, C4bC2b. The C4/C2 cleaving activity of the MBL complex is shared with the C1 complex of the classical pathway of complement activation. Different assays that allow for determination of the activity of the MBL complex in serum samples have been developed and are discussed in this report. We present data from one such assay (MBL/MASP activity test), which we have found useful for the routine evaluation of clinical samples. In this assay any influence of the classical pathway has been eliminated by using a hypertonic buffer, which inhibits the binding of C1q to immuncomplexes and disrupt the C1 complex, while leaving the function of the MBL complex intact. In parallel we determine the MBL concentration in the sample. As predicted a very high correlation is observed between the results of the two assays.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12396006&dopt=Abstract
Mediators Inflamm. 2002 Aug;11(4):245-50.
Influence of opioid peptides on human neutrophil apoptosis and activation in vitro.
Sulowska Z, Majewska E, Krawczyk K, Klink M, Tchorzewski H.
Microbiology and Virology Center, Polish Academy of Sciences, Lodz, Poland.
BACKGROUND: It has been shown that cells of the immune system release opioid peptides and possess receptors for them. The concentrations of opioid peptides in the peripheral circulation rapidly increase during inflammation and acute stress response. AIMS: The effect of opioid peptides Met-enkephalin (M-ENK) and beta-endorphin (beta-END) on the oxidative metabolism of normal human neutrophils and their death by apoptosis in vitro was investigated. METHODS: Isolated from peripheral blood, neutrophils were incubated in the presence or absence of 10(-6) to 10(-10) M of M-ENK and beta-END for 12 and 18 h. Apoptosis of neutrophils was determined in vitro by flow cytometric analysis of cellular DNA content and Annexin V-FITC protein binding to the cell surface. The MTT-reduction assay was employed to estimate the oxidative metabolism of neutrophils. RESULTS: Treatment with M-ENK caused a significant increase in apoptotic cells after 18 h of culture: *0 M (control) versus 10(-10) M, p < or = 0.02; **10(-10) M versus 10(-10) M, p < or = 0.02. Treatment with beta-END caused a significant increase in apoptotic cells after 12 h of culture: 0 M versus 10(-8) M, p < or = 0.03; **0 M versus 10(-10) M, p < or = 0.04. We found the significant increase in MTT reduction by neutrophils in the presence of M-ENK and beta-END both before and after the culture. However, the ability of neutrophils to reduce the MTT salt to formazan decreased significantly after the culture. CONCLUSIONS: We observed that the in vitro effect of opioid peptides on the neutrophil survival and their functional state was time and dose dependent. The presence of antioxidants in the culture medium modifies neutrophil survival.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12396476&dopt=Abstract
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