DreamPharm Products:
J Immunol. 2002 Nov 15;169(10):5555-63.
Retinoic acid stimulates the cell cycle machinery in normal T cells: involvement of retinoic acid receptor-mediated IL-2 secretion.
Ertesvag A, Engedal N, Naderi S, Blomhoff HK.
Department of Medical Biochemistry, Institute Group of Basic Medical Sciences, Faculty of Medicine, University of Oslo, N-0317 Oslo, Norway.
The mechanisms whereby vitamin A stimulates the immune system are poorly understood. In the current study, we attempted to elucidate the potential mechanisms of action of all-trans retinoic acid (atRA) on proliferation of human T lymphocytes. We found that physiological levels of atRA potently augmented T cell proliferation when added in combination with common T cell-stimulating agents. This was reflected in a time- and concentration-dependent stimulation of the cell cycle machinery. The presence of atRA led to elevated levels of cyclin D3, -E, and -A, decreased levels of p27(Kip1), increased activity of cyclin-dependent kinase 2, and enhanced phosphorylation of the retinoblastoma protein (pRB). The atRA-mediated changes in the cell cycle machinery were late events, appearing after 20 h of stimulation, indicating that the effects of atRA were indirect. atRA did not alter the expression of the high-affinity IL-2R. However, the level of IL-2 secreted by T cells was strongly enhanced by atRA. rIL-2 was able to substitute for the effects of atRA on the cell cycle machinery and on DNA synthesis, and blocking the IL-2R markedly inhibited atRA-induced cell proliferation and pRB phosphorylation. A retinoic acid receptor (RAR)-selective agonist and 9-cis-RA had the same potency as atRA on T cell proliferation and IL-2 secretion, whereas a retinoid X receptor-selective agonist had only marginal effects. Furthermore, a RAR-selective antagonist completely suppressed T cell proliferation and pRB phosphorylation induced by atRA. Taken together, these results suggest that atRA stimulates the cell cycle machinery and proliferation of normal human T cells by increasing IL-2 secretion through mechanisms involving RARs.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12421932&dopt=Abstract
J Immunol. 2002 Nov 15;169(10):6012-9.
Tobacco reduces membrane HLA class I that is restored by transfection with transporter associated with antigen processing 1 cDNA.
Fine CI, Han CD, Sun X, Liu Y, McCutcheon JA.
Department of Biological Sciences, College of Dentistry, New York University, New York, NY 10010, USA.
HLA class I molecules are recognized by CTL that eliminate virally infected and malignantly transformed cells presenting foreign peptide-a process termed immunosurveillance. Many tumors have reduced levels of membrane HLA class I. Tumor cells with mutations that reduce HLA class I avoid immunosurveillance and continue to proliferate. As tobacco use can induce tumors, we examined the effect of tobacco extracts on membrane HLA class I. These studies show that culture of cells in media containing tobacco extracts reduces membrane HLA class I, but not other proteins, on primary keratinocytes and other cell types. Culture in tobacco extracts, but not extracts of other substances, reduces TAP1 protein, but does not reduce expression of HLA class I H chain, L chain, or the housekeeping protein beta-actin. The reduction of TAP1 protein occurs within 4 h and is dose-dependent. Culture in tobacco extracts reduces TAP1 protein abundance, but not steady-state mRNA abundance. Tobacco-treated cells show defects in HLA class I biosynthesis similar to those found in TAP1-deficient cell lines. Transfection with TAP1 cDNA restores TAP1 protein abundance, HLA class I biosynthesis, and cell surface expression. Combined, these data show that culture in tobacco extracts reduces TAP1 protein abundance and membrane HLA class I levels. Reduction in membrane HLA class I could permit subsequent malignant transformation of cells to be undetected by the immune system.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12421988&dopt=Abstract
Presse Med. 2002 Oct 12;31(33):1551-3.
[Psychosis revealing a silent celiac disease in a young women with trisomy 21]
[Article in French]
Serratrice J, Disdier P, Kaladjian A, Granel B, Azorin JM, Laugier R, Berenguer M, Weiller PJ.
Service de medecine interne, Hopital de la Timone Marseille.
INTRODUCTION: Down's syndrome is characterized by an abnormal frequency of coeliac disease and by the frequent occurrence of neurological disorders such as Alzheimer-type dementia of early onset. However, psychosis is rare in Down's syndrome. OBSERVATION: We report the case of a 41-year-old woman, who presented with Down's syndrome. She was living with her parents and had a normal social life. She suddenly experienced some esthesic hallucinations, depression, anorexia, affective flattening and autistic behavior. Biological evaluation revealed macrocytosis, polyclonal IgA and IgG hypergammaglobulinemia and strong positivity for anti-gliadin antibodies of IgG and IgA isotypes. Brain CTscan was normal. Since digestive specimen biopsies did not evidence villous atrophy, we concluded in a silent coeliac disease. After 12 months of gluten-free diet a spectacular and lasting improvement of both psychotic and depressive symptoms was obtained. DISCUSSION: The effects of abnormal interaction between the immune system and gluten can be expressed not only in the gut (coeliac disease) but also in the brain (psychosis) in genetically predisposed patients, such as those suffering from Down's syndrome. There was evidence for brain disorder related to coeliac disease in our patient. CONCLUSION: Our case report shows that, before concluding in Alzheimer-type dementia in Down's syndrome, a biological search for coeliac disease is useful since a gluten-free diet may improve the psychiatric symptoms.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12422480&dopt=Abstract
Therapie. 2002 May-Jun;57(3):289-96.
[Characteristics of hypersensitivity syndrome to lamotrigine: review of one case reported in the Regional Center of Pharmacovigilance of Nantes]
[Article in French]
Veyrac G, Marcade G, Chiffoleau A, Bourin M, Jolliet P.
Centre Regional de Pharmacovigilance, CHU, Institut de Biologie, Nantes, France.
Drug-induced hypersensitivity syndrome is an uncommon but potentially life-threatening idiosyncratic drug reaction. In the literature, about five cases have been reported concerning hypersensitivity syndrome with lamotrigine. Most cases concern aromatic anticonvulsants but we report a case induced by lamotrigine which is a non aromatic anticonvulsant. A 73-year-old man was treated with lamotrigine for epilepsy due to a cerebrovascular stroke for 5 weeks. After 2 weeks with a single oral dose of 50 mg lamotrigine, the patient received 100 mg. Quickly thereafter fever, erythema and edema involving the periorbital area appeared. He was then admitted to hospital and lamotrigine was immediately discontinued. He developed acute hepatic and renal failure. During his hospital stay, he was treated with systemic and topical corticosteroids. After slow improvement, he was discharged 4 weeks later. Concerning this typical case, we review the characteristics of hypersensitivity syndrome and the different etiopathogenesis. The hypersensitivity syndrome typically develops two to six weeks after a drug is first administered, later than most other serious skin reactions. This syndrome manifests as rash, fever, tender lymphadenopathy, hepatitis and eosinophilia. The mechanism of hypersensitivity syndrome is unknown. Several theories have been proposed. The reaction is secondary to circulating antibodies or concerns toxic metabolities. On the other hand, association of human herpes virus 6 infection may play a role in the development of hypersensitivity syndrome. Hypersensitivity reactions to the aromatic antiepileptic drugs appear to have an immune etiology much like lamotrigine: bioactivation, detoxification, covalent adduct formation, processing and presentation of antigen to the immune system, and consequent formation of antibody and T-cell immune effectors. Another theory involves toxic metabolites; the aromatic antiepileptic agents are metabolised by cytochrome P-450 to an arene oxide metabolite. This is normally detoxified by epoxide hydrolase. This enzyme may be lacking or mutated in persons that develop the syndrome, and this is genetically determined. Lamotrigine is mainly metabolised by hepatic glucuronidation, but hypersensitivity may involve similar processes such aromatic antiepileptic drugs, except that the toxic metabolite has not yet been found. Because of slow evolution and clinical similarity to many infectious illnesses, the diagnosis of hypersensitivity syndrome may be delayed. Prompt recognition and withdrawal of the suspected drug is essential. The goal of research is to describe a "susceptibility profile" identifying individuals at risk for these forms of drug toxicity.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12422544&dopt=Abstract
J Gastroenterol Hepatol. 2002 Dec;17(12):1291-8.
Oral administration of lactoferrin reduces colitis in rats via modulation of the immune system and correction of cytokine imbalance.
Togawa J, Nagase H, Tanaka K, Inamori M, Nakajima A, Ueno N, Saito T, Sekihara H.
Third Department of Internal Medicine, Yokohama City University School of Medicine, Japan. j_togawed.yokohama-cu.ac.jp
BACKGROUND AND AIMS: The natural immunomodulator, lactoferrin, is widespread among various biological fluids and is known to exert an anti-inflammatory effect. However, there has been only one study that examined the mode of action of lactoferrin in reducing intestinal damage. We investigated the therapeutic role of lactoferrin and its effect on the levels of pro-inflammatory and anti-inflammatory cytokines, by using a rat model of dextran sulfate sodium (DSS) induced-colitis. METHODS: Male Sprague-Dawley rats were given distilled drinking water containing 2.5% (wt/vol) synthetic DSS ad libitum. Bovine lactoferrin was given once daily through gavage, starting 3 days before beginning the DSS administration, until death. The whole colon was removed to be examined macroscopically and histologically. Myeloperoxidase activity, and pro-inflammatory and anti-inflammatory cytokines in the colonic tissue were also measured. RESULTS: Dextran sulfate sodium-induced colitis was attenuated by oral administration of lactoferrin in a dose-dependent manner, as reflected by improvement in clinical disease activity index, white blood cell count and hemoglobin concentration, macroscopic and histological scores, and myeloperoxidase activity. Reduced inflammation in response to lactoferrin was correlated with the significant induction of the anti-inflammatory cytokines, interleukin-4 and interleukin-10, and with significant reductions in the pro-inflammatory cytokines, tumor necrosis factor alpha, interleukin-1beta, and interleukin-6. CONCLUSIONS: We concluded that oral administration of lactoferrin exerts a protective effect against the development of colitis in rats via modulation of the immune system and correction of cytokine imbalance. Lactoferrin has potential as a new therapeutic agent for inflammatory bowel disease. 2002 Blackwell Publishing Asia Pty Ltd
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12423274&dopt=Abstract
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