keloid/برولين

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Inverse correlation between CD34 expression and proline-4-hydroxylase immunoreactivity on spindle cells noted in hypertrophic scars and keloids.

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The CD34 positive (CD34+) spindle cells constitute a special population of spindle cells which shows a unique distribution in the skin. So far, however, the functional role of CD34+ spindle cells and the regulation of CD34 expression on dermal spindle cells are totally unknown. We examined

Alteration of amino acid transport by hydrocortisone. Different effects in human fibroblasts derived from normal skin and keloid.

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The rate of proline transport increases significantly when human dermal fibroblasts are grown with 1.5 microM hydrocortisone. Fibroblasts derived from keloid tissue are significantly more stimulated than normal fibroblasts. An average increase of 41% is obtained with 8 normal strains, whereas uptake

[Response of keloid fibroblasts to the effect of tumor necrosis factor-alpha(TNF-alpha)].

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OBJECTIVE To investigate the biologic behavior of keloid fibroblasts and the pathogenesis of keloid. METHODS Human dermal fibroblasts cultured from normal skin and keloid were treated with tumor necrosis factor-alpha(TNF-alpha) for 48 hours at 10(3) U/ml and 10(4) U/ml. Collagen production by

[Effects of connective tissue growth factor antisense oligonucleotides on the cultured human keloid fibroblasts in vitro].

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OBJECTIVE To explore the effects of connective tissue growth factor (CTGF) on the pathogenesis of human keloid. METHODS CTGF antisense oligonucleotides (ASODN) conjugated with isothiocyanate fluorescence was encapsulated by liposome, and then added into the human keloid fibroblast (HKF) culturing

[Effects of antisense oligonucleotides on the expression of connective tissue growth factor gene and on the collagen synthesis in the cultured human keloid fibroblasts].

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OBJECTIVE To study the role of connective tissue growth factor (CTGF) in the pathogenesis of human keloid. METHODS Human keloid fibroblasts (HKF) were isolated from human keloid and cultured in vitro. The cells were then divided into 3 groups according to different processing, i.e. ASODN treatment

Differences in collagen production between normal and keloid-derived fibroblasts in serum-media co-culture with keloid-derived keratinocytes.

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Keloids are characterized by the deposition of excessive extracellular-matrix collagen by abnormal fibroblasts in response to cutaneous injury. Studies to date have largely concentrated on the role of the keloid fibroblast in the pathogenesis of this lesion. Recent studies have highlighted the

[Investigation of p53 polymorphism for genetic predisposition of keloid and hypertrophic scar].

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OBJECTIVE To investigate the codon-72 polymorphism of the tumor suppressor gene p53, codon-72 encodes arginine (Arg) or proline (Pro) for a genetic predisposition,to keloid or hypertrophic scar. METHODS The distribution of codon 72 polymorphism of p53 gene was analyzed from the 54 keloid and 30

The effect of suppressing discoidin domain receptor expression on keloid formation and proliferation .

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BACKGROUND Discoidin domain receptors (DDR) with tyrosine kinase activity have been identified as novel receptors for modulating collagen production and organization in scar tissue. The purpose of this study was to explore the effect of blocking discoidin domain receptor 1 (DDR1), signaling of

Analysis of p53 gene mutations in keloids using polymerase chain reaction-based single-strand conformational polymorphism and DNA sequencing.

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BACKGROUND Keloids are the result of a dysregulated wound healing process. They are characterized by the formation of excess scar tissue that proliferates beyond the boundaries of the original wound. Somatic mutations of p53 have been implicated as causal events in up to 50% of all human

Troglitazone suppresses transforming growth factor-beta1-induced collagen type I expression in keloid fibroblasts.

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BACKGROUND Peroxisome proliferator-activated receptor (PPAR)-gamma agonists are increasingly used in patients with diabetes and some studies have suggested a beneficial effect on organ fibrosis. However their effects on dermal fibrosis in keloids are unknown. OBJECTIVE To investigate the effect of

Collagen biosynthesis in normal human skin, normal and hypertrophic scar and keloid.

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A comparison of the rates of synthesis of collagen in normal skin, normal and hypertrophic scars, and keloids has been made by measuring the rate of incorporation of [14-C]-proline into peptide-bound [14-C]-hydroxyproline by tissue minces in vitro. The rate of synthesis of collagen, as measured by

Quantitative assay of types I and III collagen synthesized by keloid biopsyes and fibroblasts.

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Molecular sieve column chromatography was used to determine the amount of type I and III collagen synthesized by normal dermis and keloid biopsies and fibroblasts derived from these tissues. After incubation with radioactive proline, the collagen was extracted and separated into types I and III and

Hydrocortisone induction of system A amino acid transport in human fibroblasts from normal dermis and keloid.

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The rate of proline transport increases when human dermal fibroblasts are grown in physiological levels of hydrocortisone. This response to hydrocortisone is significantly greater in fibroblasts derived from keloids, benign dermal tumors caused by an inherited abnormality in wound healing (Russell,

Compound Astragalus and Salvia miltiorrhiza extract inhibits cell proliferation, invasion and collagen synthesis in keloid fibroblasts by mediating transforming growth factor-β / Smad pathway.

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BACKGROUND The transforming growth factor (TGF)-β/Smad pathway plays a key role in keloid development. We have previously demonstrated that compound Astragalus and Salvia miltiorrhiza extract (CASE) inhibits liver fibrosis and reduces invasion capacity of HepG2 cells by mediating the TGF-β/Smad

Vitamin D: a novel therapeutic approach for keloid, an in vitro analysis.

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BACKGROUND Vitamin D and its metabolites play an important role in calcium homeostasis, bone remodelling, hormone secretion, cell proliferation and differentiation. Recent studies also suggest a beneficial role of vitamin D in slowing the progression of tissue fibrosis. However, their effects on

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keloid/برولين

Inverse correlation between CD34 expression and proline-4-hydroxylase immunoreactivity on spindle cells noted in hypertrophic scars and keloids.

Alteration of amino acid transport by hydrocortisone. Different effects in human fibroblasts derived from normal skin and keloid.

[Response of keloid fibroblasts to the effect of tumor necrosis factor-alpha(TNF-alpha)].

[Effects of connective tissue growth factor antisense oligonucleotides on the cultured human keloid fibroblasts in vitro].

[Effects of antisense oligonucleotides on the expression of connective tissue growth factor gene and on the collagen synthesis in the cultured human keloid fibroblasts].

Differences in collagen production between normal and keloid-derived fibroblasts in serum-media co-culture with keloid-derived keratinocytes.

[Investigation of p53 polymorphism for genetic predisposition of keloid and hypertrophic scar].

﻿﻿﻿﻿﻿﻿﻿﻿﻿﻿﻿The effect of suppressing discoidin domain receptor expression on keloid formation and proliferation ﻿﻿﻿﻿﻿﻿﻿﻿.

Analysis of p53 gene mutations in keloids using polymerase chain reaction-based single-strand conformational polymorphism and DNA sequencing.

Troglitazone suppresses transforming growth factor-beta1-induced collagen type I expression in keloid fibroblasts.

Collagen biosynthesis in normal human skin, normal and hypertrophic scar and keloid.

Quantitative assay of types I and III collagen synthesized by keloid biopsyes and fibroblasts.

Hydrocortisone induction of system A amino acid transport in human fibroblasts from normal dermis and keloid.

Compound Astragalus and Salvia miltiorrhiza extract inhibits cell proliferation, invasion and collagen synthesis in keloid fibroblasts by mediating transforming growth factor-β / Smad pathway.

Vitamin D: a novel therapeutic approach for keloid, an in vitro analysis.

قاعدة بيانات الأعشاب الطبية الأكثر اكتمالا التي يدعمها العلم

The effect of suppressing discoidin domain receptor expression on keloid formation and proliferation .