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DHEA||Coenzyme Q10||
Sleep Aid herbal formula - natural sleep aid||Herbal Breath - herbs for bad breath problems.||
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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
J Virol. 2000 Dec;74(23):10930-8.
Tegument-specific, virus-reactive CD4 T cells localize to the cornea in herpes simplex virus interstitial keratitis in humans.
Koelle DM, Reymond SN, Chen H, Kwok WW, McClurkan C, Gyaltsong T, Petersdorf EW, Rotkis W, Talley AR, Harrison DA.
Department of Medicine, University of Washington, Seattle, Washington 98195, USA. viralim.washington.edu
Herpes stromal keratitis (HSK) is a prevalent and frequently vision-threatening disease associated with herpes simplex virus type 1 (HSV-1) infection. In mice, HSK progression occurs after viral clearance and requires T cells and neutrophils. One model implicates Th1-like CD4 T cells with cross-reactivity between the HSV-1 protein UL6 and a corneal autoantigen. HSK can be prevented by establishing specific immunological tolerance. However, HSK can also occur in T-cell receptor-transgenic X SCID mice lacking HSV-specific T cells. To study the pathogenesis of HSK in the natural host species, we measured local HSV-specific T-cell responses in HSK corneas removed at transplant surgery (n = 5) or control corneas (n = 2). HSV-1 DNA was detected by PCR in two specimens. HSV-specific CD4 T cells were enriched in three of the five HSK specimens and were not detectable in the control specimens. Reactivity with peptide epitopes within the tegument proteins UL21 and UL49 was documented. Responses to HSV-1 UL6 were not detected. Diverse HLA DR and DP alleles restricted these local responses. Most clones secreted gamma interferon, but not interleukin-5, in response to antigen. HSV-specific CD8 cells were also recovered. Some clones had cytotoxic-T-lymphocyte activity. The diverse specificities and HLA-restricting alleles of local virus-specific T cells in HSK are consistent with their contribution to HSK by a proinflammatory effect.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11069987&dopt=Abstract
J Infect Dis. 2000 Dec;182(6):1643-51. Epub 2000 Nov 08.
Human immunodeficiency virus transactivator protein (Tat) stimulates chemotaxis, calcium mobilization, and activation of human polymorphonuclear leukocytes: implications for Tat-mediated pathogenesis.
Benelli R, Barbero A, Ferrini S, Scapini P, Cassatella M, Bussolino F, Tacchetti C, Noonan DM, Albini A.
Tumor Progression Section, Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy.
The extracellular activities of the human immunodeficiency virus (HIV) transactivator protein (Tat) include induction of angiogenesis and stimulation of monocyte migration. Here it is shown that polymorphonuclear leukocytes (PMNL), mostly neutrophils, rapidly invade in response to Tat in vivo and initiate the formation of new vessels. In vitro, Tat was chemotactic for PMNL and induced calcium (Ca(2+)) mobilization. Tat proteins with inactivating substitutions in the arginine-glycine-aspartic acid or basic domain were still active in inducing PMNL migration, whereas Tat peptides mapped the migration and Ca(2+) mobilization activity to a cysteine-rich core domain, previously described as a Tat "chemokine-like" region (peptide CysL(24-51)). Tat and the CysL(24-51) peptide also induced PMNL superoxide production and the release of the angiogenic factors interleukin-8 and vascular endothelial growth factor from PMNL. CysL(24-51) did not induce endothelial cell migration but was angiogenic in vivo. These data indicate that the Tat activity on PMNL is mediated by its chemokine-like region and that PMNL recruitment by Tat is linked to angiogenesis.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11069235&dopt=Abstract
J Periodontol. 2000 Oct;71(10):1575-82.
Cyclooxygenase-2-dependent prostaglandin production by peripheral blood monocytes stimulated with lipopolysaccharides isolated from periodontopathogenic bacteria.
Noguchi K, Yanai M, Shitashige M, Nishihara T, Ishikawa I.
Department of Periodontology, Faculty of Dentistry, Tokyo Medical and Dental University, Japan. kazuyuki-noguchi.perent.tmd.ac.jp
BACKGROUND: Prostaglandin E2 (PGE2) plays important roles in the pathogenesis of periodontal disease. Recent studies have revealed the existence of 2 isozymes of cyclooxygenase (COX), called COX-1 and COX-2. The purpose of the present study was to investigate the contribution of COX-1 and COX-2 to PGE2 production by human peripheral blood monocytes that are stimulated with lipopolysaccharides (LPS) from periodontopathogenic bacteria. METHODS: LPS were isolated from Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) and Porphyromonas gingivalis (P. gingivalis) by the phenol-water method. Peripheral blood monocytes were stimulated with LPS for the indicated periods, and the levels of PGE2 or interleukin (IL)-1 beta in the culture media were measured by enzyme-linked immunosorbent assay. Expression of COX-1 and -2 proteins was studied by immunocytochemical staining, and COX-2 mRNA expression was examined by Northern blot analysis. RESULTS: Peripheral blood monocytes stimulated with A. actinomycetemcomitans- or P. gingivalis-LPS produced PGE2 in a time- and dose-dependent manner. Indomethacin, a non-selective COX-1/COX-2 inhibitor, and NS-398, a specific COX-2 inhibitor, completely inhibited PGE2 production. Immunocytochemical staining of COX-1 and COX-2 proteins showed that expression of COX-2 protein was increased in monocytes that were stimulated with A. actinomycetemcomitans- or P. gingivalis-LPS, compared with that in unstimulated monocytes, whereas expression of COX-1 protein was not altered. Northern blot analysis showed that monocytes stimulated with A. actinomycetemcomitans- or P. gingivalis-LPS expressed COX-2 mRNA, while COX-2 mRNA was not detectable in unstimulated cells. Treatment of A. actinomycetemcomitans-LPS-stimulated monocytes with NS-398 induced a significant increase of IL-1 beta production to the same extent as treatment with indomethacin. CONCLUSIONS: These results suggest that COX-2 is induced in monocytes stimulated with LPS derived from A. actinomycetemcomitans and P. gingivalis and that the COX-2 is primarily responsible for PGE2 production. COX-2 may be pivotal in PGE2 production in periodontal lesions and may be involved in inflammatory responses.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11063390&dopt=Abstract
Virology. 2000 Nov 10;277(1):178-83.
Autographa californica M nucleopolyhedrovirus chiA is required for processing of V-CATH.
Hom LG, Volkman LE.
Department of Molecular and Cell Biology, University of California, Berkeley, California, 94720, USA.
Infection of permissive insect hosts by the baculovirus Autographa californica M nucleopolyhedrovirus results in liquefaction, a pathogenic effect that enhances the dispersal of progeny virions. Two viral gene products-a protease, V-CATH, and a chitinase, chiA-have been shown to be required for liquefaction to occur. It has been generally accepted that the primary functions of these proteins is to degrade the proteinaceous and chitinous components of the host cadaver, respectively. We have generated suggestive evidence, however, that chiA may also serve as a molecular chaperone for proV-CATH, the precursor of V-CATH. When cells were infected with virus lacking a functional chiA gene, proV-CATH failed to undergo processing in vivo and in vitro and formed insoluble aggregates in the endoplasmic reticulum of infected cells. Thus, expression of chiA may be required for the proper folding of the nascent V-CATH polypeptide in the endoplasmic reticulum. Identical results were obtained when tunicamycin was used to block N-linked glycosylation in cells infected with wildtype virus, suggesting that the putative chiA/V-CATH interaction is mediated by N-linked oligosaccharides. 2000 Academic Press.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11062048&dopt=Abstract
Genetics. 2000 Nov;156(3):1083-96.
Caenorhabditis elegans lin-25: a study of its role in multiple cell fate specification events involving Ras and the identification and characterization of evolutionarily conserved domains.
Nilsson L, Tiensuu T, Tuck S.
Umea Center for Molecular Pathogenesis, Umea University, SE-901 87 Umea, Sweden.
Caenorhabditis elegans lin-25 functions downstream of let-60 ras in the genetic pathway for the induction of the 1 degrees cell fate during vulval development and encodes a novel 130-kD protein. The biochemical activity of LIN-25 is presently unknown, but the protein appears to function together with SUR-2, whose human homologue binds to Mediator, a protein complex required for transcriptional regulation. We describe here experiments that indicate that, besides its role in vulval development, lin-25 also participates in the fate specification of a number of other cells in the worm that are known to require Ras-mediated signaling. We also describe the cloning of a lin-25 orthologue from C. briggsae. Sequence comparisons suggest that the gene is evolving relatively rapidly. By characterizing the molecular lesions associated with 10 lin-25 mutant alleles and by assaying in vivo the activity of mutants lin-25 generated in vitro, we have identified three domains within LIN-25 that are required for activity or stability. We have also identified a sequence that is required for efficient nuclear translocation. We discuss how lin-25 might act in cell fate specification in C. elegans within the context of models for lin-25 function in cell identity and cell signaling.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11063686&dopt=Abstract
Hair growth is a sophisticated biological process, which is still not thoroughly understood. A multitude of therapeutic measures, including drugs, surgery, and suppelements have been made available, and used. However, due to the diversity of the problems underlying hair loss, there is no single solution for all hair loss cases. Most of chemical drugs and hair transplantation surgeries are not free from varying degrees of undesirable side effects on health.
Hair Million is an alternative solution to cope with hair loss problems. Anecdotally, it shows prositive results and improvement especially for age-related hair thinning and hair loss for a fraction of people who take it. We do not know the mechanisms of action as to how Hair Million works to help stop hair loss, and promote hair growth.
We only know by anecdotal observations. There has been no clinical trials nor placebo controlled statistical analysis on the efficacy of Hair Million on hair loss and hair growth.
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Natural herbal formula for hair loss problems ||