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Alopecia, hair loss abstracts ||

J Cell Biochem. 2003 Jun 1;89(3):440-9.
Vitamin D enhances mitogenesis mediated by keratinocyte growth factor receptor in keratinocytes.

Gamady A, Koren R, Ron D, Liberman UA, Ravid A.

The Basil and Gerald Felsenstein Medical Research Center, Sackler Faculty of Medicine, Tel-Aviv University, Petah-Tikva, Israel.

The hormonally active vitamin D metabolite, 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), and keratinocyte growth factor (KGF) belong to the network of autocrine and paracrine mediators in the skin. Both were shown to modulate keratinocyte proliferation, to reverse epidermal atrophy, to increase wound healing, and to reduce chemotherapy-induced alopecia. The overlap between their activities may suggest that vitamin D exerts some of its actions by modulation of KGF activities in the skin. This notion was examined by using HaCaT keratinocytes cultured in serum-free medium in the absence of exogenous growth factors and in the presence of the EGF receptor tyrosine kinase inhibitor AG 1478 that blocks their autonomous proliferation. These cells could be stimulated to proliferate by different fibroblast growth factors (FGFs). The relative mitogenic efficacy of basic FGF, acidic FGF, or KGF was in correlation with their affinities for the KGF receptor (KGFR). Forty-eight hour co-treatment with 1,25(OH)(2)D(3) enhanced KGFR-mediated cell proliferation in a dose dependent manner. Both ERK1/2 and c-Jun N-terminal kinase (JNK) were activated by the FGFs. Treatment with 1,25(OH)(2)D(3) increased the activation of ERK but reduced the activation of JNK. Treatment with 1,25(OH)(2)D(3) increased the levels of KGFR in the presence but not in the absence of KGF, probably due to inhibition of ligand-induced receptor degradation. Inhibition of protein kinase C with bisindolylmaleimide did not interfere with the effect of 1,25(OH)(2)D(3) on KGFR-mediated ERK activation. Our results support the notion that the paracrine KGF-KGFR system in the skin can act in concert with the autocrine vitamin D system in keratinocytes to promote keratinocyte proliferation and survival under situations of stress and injury. J. Cell. Biochem. 89: 440-449, 2003. 2003 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12761878&dopt=Abstract [PubMed - in process]

Am J Clin Dermatol. 2003;4(6):429-33.
Mycosis fungoides with follicular mucinosis displaying aggressive tumor-stage transformation : successful treatment using radiation therapy plus oral bexarotene combination therapy.

Apisarnthanarax N, Ha CS, Duvic M.

Department of Dermatology, University of Texas MD Anderson Cancer Center, Houston, Texas 77030-4095, USA.

Follicular mucinosis is a tissue reaction pattern characterized by mucin deposition with follicular sebaceous units and is found as an idiopathic, primary, benign process (alopecia mucinosa), or as a secondary process due to inflammatory and neoplastic disorders (mycosis fungoides). When associated with follicular mucinosis, mycosis fungoides commonly pursues an aggressive course, often undergoing large-cell transformation, which is associated with resistance to therapy and poor prognosis. We present a case of mycosis fungoides with follicular mucinosis that was treated with incomplete courses of interferon, isotretinoin, and polychemotherapy with subsequent rapid progression to tumor-stage mycosis fungoides with large cell transformation and nodal and bone marrow involvement. In this setting, the patient was treated with local radiation therapy, total-skin electron beam therapy, and therapy and maintenance with the oral retinoid-X-receptor retinoid bexarotene, and achieved a durable complete remission.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12762834&dopt=Abstract [PubMed - in process]

Cancer Chemother Pharmacol. 2003 Jul;52(1):86-8. Epub 2003 May 23.
Clinical effects of combination therapy with mitoxantrone, vincristine, and prednisolone in breast cancer.

Katsumata K, Tomioka H, Kusama M, Aoki T, Koyanagi Y.

Department of Surgery, Tokyo Medical University, 6-7-1 Nishi-Shinjuku, Shinjuku-ku, 160-0023 Tokyo, Japan. k.katsol.ne.jp

PURPOSE: We assessed the clinical efficacy and safety of mitoxantrone hydrochloride which has been used as an anticancer drug in our hospital to treat breast cancer patients since 1993. METHODS: A group of 23 patients with breast cancer were given one course of the following regimen every 3 weeks: mitoxantrone hydrochloride (8 mg/m(2) i.v. day 1), vincristine sulfate (1.2 mg/m(2) i.v. day 1), and prednisolone (30 mg orally days 1-7). RESULTS: The response rate was 52.2% including a complete response in four patients, and a partial response in eight patients. Adverse drug reactions included leukocytopenia (78.3%, 18/23 patients), alopecia (30.8%, 7/23), and peripheral neuropathy and generalized fatigue (26.1%, 6/23). In patients responding to the drug regimen, 50% survival was 29 months, and in those not responding it was 12 months. CONCLUSION: Combination treatment with mitoxantrone hydrochloride, vincristine sulfate and prednisolone is an effective treatment for breast cancer.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12764670&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.

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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.

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