DreamPharm Products:
Lutein-20||Herbs for headache, fever, and migraine ||
Milk thistle||Saw palmetto||
Triple B Super Vision||Garlic, Ginger, and Grapeseed Extract||
Ginseng and Ginkgo||Hair Million||
DHEA||Coenzyme Q10||
Sleep Aid herbal formula - natural sleep aid||Herbal Breath - herbs for bad breath problems.||
Weight loss herbal formula for menopause and pms||Ginkgo biloba||
Colon cleansing, Laxative||ViaVita, Lecithin for healthy liver
Fatty acids resources:
Fatty acids research abs 1 || Fatty acids research abs 2 || Fatty acids research abs 3 || Fatty acids research abs 4 || Fatty acids research abs 5
Immunol Rev. 2003 Jun;193(1):93-100.
Transducing signals from antigen receptors to nuclear factor kappaB.
Ruland J, Mak TW.
Advanced Medical Discovery Institute, Ontario Cancer Institute and University of Toronto, Toronto, ON, Canada.
Signaling leading to the survival or apoptosis of immune system cells must be balanced to ensure the normal mounting and extinguishing of immune responses. One of the essential regulators of immune cell survival is the transcription factor nuclear factor kappaB (NF-kappaB). NF-kappaB is critical for the activation of T and B lymphocytes and is a central coordinator of innate and adaptive immunity. Pathogen recognition, whether mediated via the Toll-like receptors or via the antigen-specific T- and B-cell receptors, initiates the activation of distinct signal transduction pathways that activate NF-kappaB. Activation of NF-kappaB by these pathways is necessary for lymphocyte activation, expansion, and effector function in response to infection. In addition, recent work has shown that the aberrant activation of NF-kappaB by these pathways can contribute to the development of autoimmunity, chronic inflammation, or lymphoid malignancy. There is thus an urgent need to understand the exact molecular details of these signal transduction cascades so that we may develop novel therapeutics. This article will review the specific signal transduction pathways that mediate NF-kappaB activation in response to antigen receptor ligation in T and B lymphocytes. These newly defined pathways, which are essential for adaptive immune responses, are built around the key adapter protein, Bcl-10. Bcl-10 is known to participate in chromosomal translocations in human mucosa-associated lymphoid tissue lymphomas.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12752674&dopt=Abstract [PubMed - in process]
J Biol Chem. 2003 Mar 14;278(11):9928-37. Epub 2003 Jan 02.
A novel fluorescent toxin to detect and investigate Kv1.3 channel up-regulation in chronically activated T lymphocytes.
Beeton C, Wulff H, Singh S, Botsko S, Crossley G, Gutman GA, Cahalan MD, Pennington M, Chandy KG.
Department of Physiology and Biophysics, University of California, Irvine, California 92697, USA.
T lymphocytes with unusually high expression of the voltage-gated Kv1.3 channel (Kv1.3(high) cells) have been implicated in the pathogenesis of experimental autoimmune encephalomyelitis, an animal model for multiple sclerosis. We have developed a fluoresceinated analog of ShK (ShK-F6CA), the most potent known inhibitor of Kv1.3, for detection of Kv1.3(high) cells by flow cytometry. ShK-F6CA blocked Kv1.3 at picomolar concentrations with a Hill coefficient of 1 and exhibited >80-fold specificity for Kv1.3 over Kv1.1 and other K(V) channels. In flow cytometry experiments, ShK-F6CA specifically stained Kv1.3-expressing cells with a detection limit of approximately 600 channels per cell. Rat and human T cells that had been repeatedly stimulated 7-10 times with antigen were readily distinguished on the basis of their high levels of Kv1.3 channels (>600 channels/cell) and ShK-F6CA staining from resting T cells or cells that had undergone 1-3 rounds of activation. Functional Kv1.3 expression levels increased substantially in a myelin-specific rat T cell line following myelin antigen stimulation, peaking at 15-20 h and then declining to baseline over the next 7 days, in parallel with the acquisition and loss of encephalitogenicity. Both calcium- and protein kinase C-dependent pathways were required for the antigen-induced Kv1.3 up-regulation. ShK-F6CA might be useful for rapid and quantitative detection of Kv1.3(high) expressing cells in normal and diseased tissues, and to visualize the distribution of functional channels in intact cells.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12511563&dopt=Abstract
Immunol Cell Biol. 2003 Jun;81(3):196-206.
Evasion of innate and adaptive immunity by flaviviruses.
Diamond MS.
Department of Medicine, Washington University School of Medicine, Saint Louis, Missouri 63110, United States of America. diamonorcim.wustl.edu
After a virus infects an animal, antiviral responses are generated that attempt to prevent dissemination. Interferons, antibody, complement, T and natural killer cells all contribute to the control and eradication of viral infections. Most flaviviruses, with the exception of some of the encephalitic viruses, cause acute disease and do not establish persistent infection. The outcome of flavivirus infection in an animal is determined by a balance between the speed of viral replication and spread, and the immune system response. Although many of the mechanistic details require further elucidation, flaviviruses have evolved specific tactics to evade the innate and adaptive immune response. A more thorough understanding of these principles could lead to improved models for viral pathogenesis and to strategies for the development of novel antiviral agents.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12752684&dopt=Abstract [PubMed - in process]
Immunol Cell Biol. 2003 Jun;81(3):217-23.
MHC class I up-regulation by flaviviruses: Immune interaction with unknown advantage to host or pathogen.
Lobigs M, Mullbacher A, Regner M.
Division of Immunology and Genetics, John Curtin School of Medical Research, Australian National University, Canberra, Australian Capital Territory, Australia. Mario.Lobignu.edu.au
In contrast to many other viruses that escape from cytotoxic T cell recognition by down-regulating major histocompatibility complex class I-restricted antigen presentation, flavivirus infection of mammalian cells up-regulates cell surface expression of major histocompatibility complex class I molecules. Two putative mechanisms for flavivirus-induced major histocompatibility complex class I up-regulation, one via activation of the transcription factor NF-kappaB, the second by augmentation of peptide import into the lumen of the endoplasmic reticulum, are reviewed, and the biological effect of the flavivirus-mediated phenomenon on target cell recognition by natural killer and cytotoxic T cells is addressed. Finally, we speculate on the physiological role of flavivirus-mediated modulation of major histocompatibility complex class I antigen presentation in the context of the biology of flavivirus transmission between the vertebrate host and arthropod vector and suggest that it may represent a strategy for immune evasion from the natural killer cell response or, alternatively, that up-regulation of major histocompatibility complex class I is a by-product of flavivirus replication without significance for virus growth.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12752686&dopt=Abstract [PubMed - in process]
Immunol Cell Biol. 2003 Jun;81(3):230-6.
Infection of mouse neurones by West Nile virus is modulated by the interferon-inducible 2'-5' oligoadenylate synthetase 1b protein.
Lucas M, Mashimo T, Frenkiel MP, Simon-Chazottes D, Montagutelli X, Ceccaldi PE, Guenet JL, Despres P.
Unite des Interactions Moleculaires Flavivirus-Hotes, Institut Pasteur, Paris, France.
Over the past 7 years, West Nile zoonosis has been an emerging concern for public health in Europe, Middle East and more recently in North America. West Nile virus causes epidemic outbreaks in humans and infected patients may exhibit severe neurological symptoms. Because susceptibility and sensitivity to West Nile virus infections may depend on host genetic factors, a mouse model has been established to investigate the genetic determinism of host susceptibility to West Nile virus. A nonsense mutation in gene encoding the 1b isoform of the 2'-5'oligoadenylate synthetase (OAS1b) was constantly associated with the susceptibility of mouse strains to experimental West Nile virus infection. Oligoadenylate synthetase are interferon-inducible proteins playing a role in the endogeneous antiviral pathway. It was of interest to establish whether interferon-alpha and OAS 1B were sufficient to mediate resistance to West Nile virus infection. In the present study, we showed that interferon-alpha had the ability to modulate West Nile virus infection in mouse. In vitro, interferon-alpha protected mouse neuroblastoma cells against West Nile virus infection if cells have been pretreated with the cytokine for several hours. As a consequence of the presence of a stop codon, the Oas1b gene of the susceptible mice encodes a truncated and presumably inactive form, while resistant mice have a normal copy of the gene. Stable mouse neuroblastoma cell clones overexpressing mutant or wild-type OAS 1B were established. Replication of West Nile virus was less efficient in cells that produce the normal copy of OAS 1B as compared to those expressing the truncated form. Our data illustrate the notion that interferon-alpha and Oas genes may be critical for West Nile virus pathogenesis.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12752688&dopt=Abstract [PubMed - in process]
Concerned about losing hair? Hair loss and baldness is indeed a visible problem, and
could be more than just the matter of change in appearance.
Saw palmetto berry is a widely known herbal supplement for hair loss problems.
However, there are a number of great anecdotal herbs that people used for thousands of years stop hair loss and
start hair growth.
Numerous anecdotal cases have demonstrated that this herbal formula based on Chinese herbs actually improves the age-related hair thinning and hair loss
for a significant fraction of people who take it diligently. It is unknown how Hair Million herbs actually stop hair loss, and promote hair growth,
No scientific research or placebo controlled clinical trials have been conducted. Nonetheless, a number of people agree that it works.
DHEA is a natural hormone, and it is produced in our body by the adrenal glands.
DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones)
or estrogens (female hormones) in the cells.
Our bodies produce decreasing amount of DHEA as we get older.
various health benefits: To deter aging,
improve sexual function/erectile dysfunction, treat cognitive decline, enhance athletic performance,
facilitate weight loss, improve strength, prevent osteoporosis, enhance immunomodulation for rheumatic conditions,
and treat depression.
DreamPharm Online Healthy Supplements ||
Constipation relief, laxative, colon cleansing ||
Lutein ||
Progesterone Cream ||
Natural herbal formula for hair loss problems ||