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Arch Dermatol. 2000 Oct;136(10):1207-9.
Occult neurofibroma and increased S100 protein in the skin of patients with neurofibromatosis type 1: new insight to the etiopathomechanism of neurofibromas.
Karvonen SL, Kallioinen M, Yla-Outinen H, Poyhonen M, Oikarinen A, Peltonen J.
Department of Dermatology, University Hospital of Oulu, FIN-90220 Oulu, Finland. seija-liisa.karvoneulu.fi
BACKGROUND: Neurofibromas represent proliferation of the connective tissue cells of peripheral nerves and deposition of collagenous extracellular matrix. There is evidence that the appearance and growth of neurofibromas may be associated with prior or ongoing mechanical trauma in patients with neurofibromatosis type 1 (NF1). OBJECTIVE: To study the histologic characteristics of apparently healthy skin of patients with NF1. DESIGN: The histologic features of healthy-looking skin of patients with NF1 were analyzed. SETTING: University hospital. PATIENTS: Ten patients who fulfilled the criteria for NF1. INTERVENTIONS: Punch biopsy specimens of healthy-looking skin of the forearm from 9 volunteer patients and of the upper eyelid during cosmetic operation from 1 volunteer patient were obtained. MAIN OUTCOME MEASURES: The main outcomes were not predicted, and the hypothesis was formulated during data collection. RESULTS: Apparently unaffected skin of 5 patients with NF1 was studied by routine histologic testing with respect to expression of S100 protein. Unexpectedly, analysis of the samples revealed the presence of a small neurofibroma tumor in one of the samples. The tumor was located in deep dermis around a hair follicle. In addition, neurofibromatous tissue not large enough to be called a tumor was found on the same anatomical location in another patient. In further studies, 10 punch biopsy specimens of apparently healthy skin from patients with NF1 were similarly sectioned and analyzed. No tumors were found in these additional samples. In 4 patients, however, abundant S100 protein-positive cells were located within collagenous extracellular matrix surrounding hair follicles. CONCLUSIONS: The skin of patients with NF1 might be more widely affected than previously thought and occult neurofibromas are not rare.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11030766&dopt=Abstract
Arch Surg. 2000 Oct;135(10):1154-9.
Transforming growth factor beta3 promotes fascial wound healing in a new animal model.
Tyrone JW, Marcus JR, Bonomo SR, Mogford JE, Xia Y, Mustoe TA.
Division of Plastic and Reconstructive Surgery, Northwestern University Medical School, 675 N St Clair St, Suite 19-250, Chicago, IL 60611, USA.
HYPOTHESIS: Transforming growth factor beta(3) (TGF-beta(3)) promotes fascial wound healing in a new animal model, as measured by wound breaking strength, collagen deposition, and cellular proliferation. DESIGN/INTERVENTION: Bilateral, longitudinal incisions were made in the anterior rectus sheaths of 24 male New Zealand white rabbits. One incision was treated with 1 microg of TGF-beta(3); the contralateral incision served as a control. The wounds were harvested at 1, 2, 3, 4, 6, and 8 weeks after creation ("wounding"). MAIN OUTCOME MEASURES: Wound tissue was tested for breaking strength using a tensiometer and processed for histological examination of collagen deposition and cellular proliferation at all time points after wounding. Collagen deposition and cellular proliferation were measured in histological cross sections of wounds with Masson trichrome staining and proliferating cell nuclear antigen immunohistochemistry, respectively. RESULTS: At all time points after wounding, treatment with TGF-beta(3) significantly increased the wound breaking strength (up to 138%) and collagen deposition (up to 150%) over the control group. Cellular proliferation was increased during the first 3 weeks after wounding (up to 147%), but returned to baseline levels by the fourth week. CONCLUSIONS: Transforming growth factor beta(3) promotes fascial wound healing. In this new animal model of fascial wound healing, TGF-beta(3) increased fascia breaking strength, collagen deposition, and cellular proliferation. These results are similar to findings in cutaneous wound models and demonstrate, for the first time, a pharmacologic agent to accelerate fascial healing.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11030871&dopt=Abstract
Arterioscler Thromb Vasc Biol. 2000 Oct;20(10):2220-5.
Effect of fluid flow on smooth muscle cells in a 3-dimensional collagen gel model.
Wang S, Tarbell JM.
Biomolecular Transport Dynamics Laboratory, Departments of Chemical Engineering and Bioengineering, Pennsylvania State University, University Park, PA, USA.
A 3D collagen gel model was developed to simulate interstitial fluid flow and to assess the importance of this flow on the biochemical production rates of vascular smooth muscle cells (SMCs). Rat aortic SMCs were suspended in type I collagen, and the gel was supported by nylon fibers that allowed a 9-cm length of the SMC-gel model to withstand 90 cm H(2)O differential pressure over a 6-hour period without significant compaction. Up to 1 dyne/cm(2) shear stress on the suspended SMCs could be induced by the pressure-driven interstitial flow. The suspended SMCs were globular, had a diameter of approximately 10 microm, and were distributed uniformly throughout the gel. The collagen fibers formed a network that was connected randomly with the surface of SMCs and nylon fibers. The diameter of the collagen fibers was approximately 100 nm, and the concentration of collagen was 2.5 mg/mL. Using these parameters, fiber matrix theory predicted a Darcy permeability coefficient (K:(p)) of 1.22x10(-)(8) cm(2), which was close to the measured value of K:(p). The production rates of prostaglandin (PG) I(2) and PGE(2) were used as markers of biochemical responsiveness of SMCs to fluid shear stress. Both PGI(2) and PGE(2) production rates under 1 dyne/cm(2) shear stress were significantly elevated relative to static (no-flow) controls. The production rates, however, were approximately 10 times lower than observed when the same cells were plated on collagen-treated glass slides (2D model) and exposed to the same level of shear stress by use of a rotating disk apparatus. The results indicate that interstitial flow can affect SMC biology and that SMCs are more quiescent in 3D cultures than in 2D cultures. The 3D collagen gel model should be useful for future studies of interstitial flow effects on SMC function.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11031207&dopt=Abstract
Thromb Res. 2002 Aug 15;107(3-4):169-74.
Plasminogen activator-plasmin system potentiates the proliferation of hepatocytes in primary culture.
Akao M, Hasebe Y, Okumura N, Hagiwara H, Seki T, Ariga T.
Department of Nutrition and Physiology, Nihon University Graduate School of Applied Life Sciences, Kameino 1866, Kanagawa 252-8510, Fujisawa, Japan
Background/AIMS: Liver regeneration after partial hepatectomy is thought to be regulated by various molecules including the components of the plasminogen activator (PA)-plasmin system. We have examined the role of fibrinolytic factors, i.e., tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA), and their substrate, plasminogen, in the proliferation of hepatocytes in primary culture. METHODS: Hepatocyte and nonparenchymal liver cells were isolated from Wistar strain rat by a method perfusing the liver with collagenase. DNA synthesis was assessed by measuring the incorporation of [3H]-thymidine into cellular DNA fraction. tPA, uPA and type-1 plasminogen activator inhibitor (PAI-1) gene expressions were measured by Northern blotting. PA activity was measured by fibrin/agarose plate method. RESULTS: Cellular density-dependent DNA synthesis was observed in the primary cultured hepatocytes; DNA synthesis was lower at high cell density (1.0x10(5) cells/cm(2)) than that at low cell density (0.2x10(5) cells/cm(2)). DNA synthesis in the hepatocytes cultured at a low cell density was increased by co-culture with nonparenchymal liver cells. Under these growth-stimulated culture conditions, tPA and uPA mRNAs were induced and up-regulated. On the contrary, the PAI-1 mRNA level was decreased under these conditions, and total PA activity was augmented accordingly. The synthetic plasmin inhibitor tranexamic acid, a competitive inhibitor for the plasmin molecule, and PASI-535, a plasmin active center-directed inhibitor, both suppressed hepatocyte proliferation in a dose-dependent fashion. Anti-plasmin antibody also suppressed hepatocyte proliferation. CONCLUSIONS: The up-regulation of PA activity for ensuring plasmin activity should be an important mechanism in the proliferation of hepatocytes.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12431485&dopt=Abstract [PubMed - in process]
Arch Otolaryngol Head Neck Surg. 2000 Oct;126(10):1217-23.
Role of CD44 variant exon 6 in invasion of head and neck squamous cell carcinoma.
Kanke M, Fujii M, Kameyama K, Kanzaki J, Tokumaru Y, Imanishi Y, Tomita T, Matsumura Y.
Department of Otolaryngology-Head and Neck Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
OBJECTIVES: To determine the correlation between the expression of CD44 variant exon 6 (v6) and the clinicopathological features of head and neck squamous cell carcinomas (HNSCCs), and to study the role of CD44v6 in cell invasion using a human HNSCC cell line (HSC-2). DESIGN: The expression of CD44v6 was evaluated using immunohistochemical analysis in paraffin-embedded tissue specimens from 89 primary lesions. The concentration of CD44v6 protein in 37 cryopreserved tumor specimens was evaluated using the enzyme-linked immunosorbent assay. The HSC-2 cells were treated with 2F10, a monoclonal antibody against CD44v6. The effects of 2F10 on HSC-2 cell proliferation, migration, and invasion potential were evaluated. RESULTS: The down-regulation of CD44v6 expression or the concentration of cancer tissue significantly correlated with a lower degree of pathohistological differentiation and a higher rate of cervical metastasis. The invasion of HSC-2 cells into type I collagen gel and the expression of CD44v6 were decreased in invading cells released from the upper layer. Furthermore, the treatment of HSC-2 cells with 2F10 significantly enhanced cell invasion. However, 2F10 did not affect either the proliferation or migration properties of HSC-2 cells. CONCLUSIONS: The down-regulation of CD44v6 expression may be useful as a biological marker for the degree of malignancy in HNSCCs. We assume that the loss or dysfunction of CD44v6 is involved in the acquisition of invasion ability in HSC-2 cells. In addition, the potential existence of a CD44v6-mediated signal transduction pathway may play a role in inhibiting the invasion in HNSCCs.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11031408&dopt=Abstract
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