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Osteoarthritis Cartilage. 1996 Dec;4(4):275-85.
Sequestration of type VI collagen in the pericellular microenvironment of adult chrondrocytes cultured in agarose.
Chang J, Poole CA.
Department of Anatomy, School of Medicine, University of Auckland, New Zealand.
The chondron represents the chondrocyte and its pericellular microenvironment and plays an important role in the progression of osteoarthritis. Type VI collagen is preferentially localized in the pericellular microenvironment of adult articular cartilage and increases during osteoarthritis. In this study, we characterized the pericellular sequestration of type VI collagen in long-term chondrocyte-agarose cultures, and assessed the action of interleukin-1 on type VI collagen deposition and assembly. Immunohistochemical and biochemical analysis showed that cultured chondrocytes initiate type VI collagen sequestration immediately upon plating and continue pericellular matrix sequestration in a time dependent manner. Confocal microscopy confirmed the cell surface localization and pericellular accumulation of type VI collagen, while image analysis identified a 'cargo-net like' organization of type VI collagen around each chondrocyte. Quantitative analysis revealed a primary phase of rapid cell division and low levels of type VI collagen sequestration, followed by a secondary phase of relative growth stability and high levels of type VI collagen deposition. Interleukin-1 treated cultures showed increased sequestration and retention of type VI collagen in an expanded microenvironment surrounding the chondrocytes. The data suggests a role for type VI collagen in the differentiation of the pericellular microenvironment in vitro. The increased type VI collagen sequestration promoted by interleukin-1 was consistent with previous studies on osteoarthritic cartilage, and implies a functional role for type VI collagen in the chondron remodeling associated with cartilage degradation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11048624&dopt=Abstract
Mod Pathol. 2000 Oct;13(10):1128-33.
Tonsillar lymphangiomatous polyps: a clinicopathologic series of 26 cases.
Kardon DE, Wenig BM, Heffner DK, Thompson LD.
Department of Endocrine and Otorhinolaryngic-Head and Neck Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000, USA.
BACKGROUND: Lymphangiomatous polyps are uncommon benign tumors of the tonsils. METHODS: Twenty-six cases of lymphangiomatous polyps diagnosed between 1980 and 1999 were retrieved from the files of the Otorhinolaryngic-Head and Neck Tumor Registry of the Armed Forces Institute of Pathology. Hematoxylin and eosin-stained slides were reviewed to characterize the histologic features of these tumors. Immunohistochemical stains were performed on 15 cases. Clinical follow-up data were obtained. RESULTS: The patients included 13 males and 13 females, ages 3 to 63 years (mean, 25.2 years). Patients experienced dysphagia, sore throat, and the sensation of a mass in the throat. Symptoms were present from a few weeks to years. The tonsillar masses were unilateral in all cases. Clinically, the lesions were frequently mistaken for a neoplasm (n = 18 patients). Grossly, all of the lesions were polypoid and measured 0.5 to 3.8 cm (mean, 1.6 cm). Histologically, the polyps were covered by squamous epithelium showing variable epithelial hyperplasia, dyskeratosis, and lymphocytic epitheliotropism. The masses showed a characteristic submucosal proliferation of small to medium-sized, endothelial-lined, lymph-vascular channels lacking features of malignancy. Collagen, smooth muscle, and adipose tissue were present in the stroma. Intravascular proteinaceous fluid and lymphocytes were noted. Immunohistochemical findings confirmed the endothelial origin of the vascular proliferation and a mixed lymphoid population. The differential diagnosis included fibroepithelial polyp, lymphangioma, juvenile angiofibroma, and squamous papilloma. In all patients with follow-up, complete surgical excision was curative (mean follow-up, 5.4 years; range, 1 mo to 14 years). CONCLUSIONS: We detail the clinical and pathologic features of tonsillar lymphangiomatous polyps. These tumors are uncommon and may clinically be mistaken for a malignant neoplasm. The characteristic histologic features should allow for its correct diagnosis and differentiation from similar appearing tonsillar lesions.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11048808&dopt=Abstract
J Oral Pathol Med. 2000 Nov;29(10):483-90.
Enamel proteins and extracellular matrix molecules are co-localized in the pseudocystic stromal space of adenomatoid odontogenic tumor.
Murata M, Cheng J, Horino K, Hara K, Shimokawa H, Saku T.
Department of Pathology, Faculty of Dentistry, Niigata University, Japan.
In order to examine the functional differentiation of tumor cells of adenomatoid odontogenic tumor (AOT) as ameloblasts and to determine the participation of the extracellular matrix (ECM) in the formation of its characteristic histologic architecture, tissue samples from five cases of adenomatoid odontogenic tumor were examined by immunohistochemical staining for enamel proteins and ECM molecules. Amelogenin, enamelin, laminin, heparan sulfate proteoglycan, fibronectin, collagen type IV and type V were immunolocalized within the luminal space and along the inner rim of duct-like structures. Eosinophilic hyaline droplets within the whorled or rosette masses of tumor cells showed basically the same staining pattern as the luminal contents. High columnar tumor cells that formed duct-like structures were immunopositive for amelogenin, while the staining intensity decreased with flattening of the cells, which was a result of luminal growth. The findings suggest that the constituent cells of duct-like structures are differentiated once to ameloblasts but fail to mature further due instead to increased production of ECM molecules and due to their retention in the lumina. It is possible to regard these special structures in AOT as stromal pseudocysts.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11048964&dopt=Abstract
Blood. 2002 Dec 1;100(12):4001-10.
Transcriptional activation of endoglin and transforming growth factor-beta signaling components by cooperative interaction between Sp1 and KLF6: their potential role in the response to vascular injury.
Botella LM, Sanchez-Elsner T, Sanz-Rodriguez F, Kojima S, Shimada J, Guerrero-Esteo M, Cooreman MP, Ratziu V, Langa C, Vary CP, Ramirez JR, Friedman S, Bernabeu C.
Centro de Investigaciones Biologicas, Consejo Superior Investigaciones Cientificas (CSIC), Madrid, Spain. cibluisib.csic.es
Endoglin is an endothelial membrane glycoprotein involved in cardiovascular morphogenesis and vascular remodeling. It associates with transforming growth factor-beta (TGF-beta) signaling receptors to bind TGF-beta family members, forming a functional receptor complex. Arterial injury leads to up-regulation of endoglin, but the underlying regulatory events are unknown. The transcription factor KLF6, an immediate-early response gene induced in endothelial cells during vascular injury, transactivates TGF-beta, TGF-beta signaling receptors, and TGF-beta-stimulated genes. KLF6 and, subsequently, endoglin were colocalized to vascular endothelium (ie, expressed in the same cell type) following carotid balloon injury in rats. After endothelial denudation, KLF6 was induced and translocated to the nucleus; this was followed 6 hours later by increased endoglin expression. Transient overexpression of KLF6, but not Egr-1, stimulated endogenous endoglin mRNA and transactivated the endoglin promoter. This transactivation was dependent on a GC-rich tract required for basal activity of the endoglin promoter driven by the related GC box binding protein, Sp1. In cells lacking Sp1 and KLF6, transfected KLF6 and Sp1 cooperatively transactivated the endoglin promoter and those of collagen alpha1(I), urokinase-type plasminogen activator, TGF-beta1, and TGF-beta receptor type 1. Direct physical interaction between Sp1 and KLF6 was documented by coimmunoprecipitation, pull-down experiments, and the GAL4 one-hybrid system, mapping the KLF6 interaction to the C-terminal domain of Sp1. These data provide evidence that injury-induced KLF6 and preexisting Sp1 may cooperate in regulating the expression of endoglin and related members of the TGF-beta signaling complex in vascular repair.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12433697&dopt=Abstract
Shock. 2000 Oct;14(4):484-9.
Plasma concentration of biologically active fibronectin and fibronectin bound to gelatin-like material in a porcine model of hyperdynamic endotoxic shock.
Nagelschmidt M, Rink AD, Neugebauer E.
IInd Dept. of Surgery, University of Cologne, Germany.
Due to its opsonizing role, plasma fibronectin (pFN) binds to circulating degradation products deriving from collagenous structures and mediates their elimination by the reticuloendothelial system (RES). In septic shock, an overflow of this material may lead to a lack of pFN and an impaired RES activity. In fact, low pFN levels have been reported to correlate with unfavorable clinical outcome. However, dysfunction of the RES is also caused by other shock related factors, and death from septic shock also has been observed in the presence of normal FN levels. To investigate the involvement of opsonic FN in the progression of sepsis, we discriminated between biologically active FN and FN bound to gelatin-like material in pigs developing a hyperdynamic endotoxic shock. All FN determinations were performed with the immunochemical assay. Discrimination between free FN and complexed FN was achieved by separation on gelatin sepharose. A continuous decrease of total FN and free FN was observed in the septic group reaching 57% and 50% of the initial level at the end of the 5-h observation period, respectively. However, a significant difference was not detected before both the microcirculatory and macrocirculatory alterations indicative of hyperdynamic endotoxic shock were completely established. Complexed FN was increased slightly in both groups without any group specific differences. We conclude that the FN-mediated opsonization of circulating gelatine-like material does not play a critical role in early circulatory shock.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11049114&dopt=Abstract
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