| دانلود رایگان مقاله انگلیسی + خرید ترجمه فارسی
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| عنوان فارسی مقاله: |
راهبردهای جلوگیری از اسکار: آنچه می توان از پوست جنین آموخت؟ |
| عنوان انگلیسی مقاله: |
Strategies for prevention of scars: what can we learn from fetal skin? |
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| مشخصات مقاله انگلیسی (PDF) | |
| سال انتشار مقاله | 2011 |
| تعداد صفحات مقاله انگلیسی | 9 صفحه با فرمت pdf |
| رشته های مرتبط با این مقاله | زیست شناسی و پزشکی |
| گرایش های مرتبط با این مقاله | علوم سلولی و مولکولی، بیوتکنولوژی پزشکی، پوست و مو، آشناسی یا پاتولوژی، میکروبیولوژی و ژنتیک |
| مجله مربوطه | مجله بین المللی پوست (International Journal of Dermatology) |
| دانشگاه تهیه کننده | مرکز تحقیقات تکنولوژی سلول های بنیادی و تراریخت ایران، دانشگاه علوم پزشکی شیراز |
| لینک مقاله در سایت مرجع | لینک این مقاله در سایت wiley |
| نشریه | Wiley |
| مشخصات و وضعیت ترجمه فارسی این مقاله (Word) | |
| تعداد صفحات ترجمه تایپ شده با فرمت ورد با قابلیت ویرایش و فونت 14 B Nazanin | 20 صفحه |
| ترجمه عناوین جداول | ترجمه شده است |
| ترجمه متون داخل جداول | ترجمه شده است |
- فهرست مطالب:
چکیده
مقدمه
درمان اسکارلس
نسبت انواع كلاژن
اسيد هيالورونيك (هيالورونان،HA)
فيزيولوژي بهبود زخم بدون اسكار
فاكتور رشد تغييردهندۀ بتا(TGF-b)
دکورین، فیبرومودولین و لیزیل اکسیداز TGF-b
متالوپرتئینازهای ماتریکس (MMP) و TIMPها
عامل رشد پلاکت (PDGF) و عامل رشد فیبروبلاست(FGF)
هیپوکسی و VEGF
فیبروبلاست ها و میوفیبروبلاست ها
سلول های نقطه ایی(Dot cells)
التهاب و HA
ژن های هموباکس(Homeobox genes)
ارتباط ارتقای cosmesis اسکار با سن
راهبردهای مقبول، کارآمد و بحث برانگیز در کاهش اسکار
نتیجه گیری
- بخشی از ترجمه:
جلوگیری از تشکیل اسکار از مدت ها قبل اهمیت داشته است و در بسیاری از زمینه ها و اختلالات پزشکی به وضوح مشاهده ميشود.با توجه به این ارزش بالینی بسیار گسترده و پتانسیل بسیار بالای تجاری آن ، امید میرود که ارزش بالینی آن آشکار گردد. برای نیل به این هدف، پیشرفت های علمی و آزمایشات بالینی با کیفیت نیاز است. با توجه به داده های ارائه شده در این مقاله، می توان به آینده خوشبینانه نگریست.
- بخشی از مقاله انگلیسی:
Introduction Scar formation is a major clinical problem resulting in adverse cosmesis, loss of function, especially if over joints, and hindrance of growth in children. Scars also have a dramatic impact on the patient’s quality of life, and have been associated with anxiety, social avoidance, and depression.1 Therefore, prevention of scar formation has long been important. Scar reduction is not only important to dermatologists, but is also salient in many other conditions, such as adhesions and strictures resulting from surgical procedures in abdominal and pelvic cavities, spinal cord ruptures, scarification of hand tendons after injury, corneal abrasions, glomerulonephritis, cirrhosis, human vascular restenosis lesions, myocardial infarction, systemic sclerosis, and diffuse fasciitis. The principles of anti-scarring therapy based on modulation of pro-scarring vs. anti-scarring factors appear to be promising for all the above-mentioned conditions, indicating that studies in the skin could have a broader clinical application. Scarless healing Scar and fibrosis are the end result of surgical and nonsurgical skin injury. Aggressive wound healing may have once offered an evolutionary advantage for survival at the expense of scar formation. Amazingly, fetal cutaneous wounds, especially in the first 6 months of gestation, heal without scar formation.2 Many clinicians hope that understanding the remarkable reparative capabilities of the fetus may lead to the development of new woundhealing therapies that reduce or prevent scar formation and fibrosis. Fetal monkey lip incisional wounds heal with restoration of normal appendage and dermal collagen architecture in midgestation. At the start of the third trimester, these wounds do not restore appendage (hair follicle and sebaceous gland) architecture, but still heal with a normal collagen pattern. Thus, a ‘‘transition wound’’ phenotype occurs. By the mid-third trimester, the wounds heal with a typical scar pattern, i.e. no appendages and collagen scar.3 The transition point in a human fetal skin model also occurs after the second trimester of gestation.4 It is notable that not all fetal tissues share the anti-scarring properties of fetal skin; fetal wounds in the diaphragm and the gastrointestinal tract heal by fibrosis and contraction, as in the adults.5,6 Fetal cutaneous wound healing is not only scarless but also rapid. The rapid epithelialization of fetal wounds may occur in part because of early deposition of tenascin and fibronectin, which are thought to be necessary for migration and cell anchoring, respectively.7 As discussed below, overexpression of vascular endothelial growth factor (VEGF) may be another reason for rapid healing of fetal wounds. How is scarless wound healing different than the scarring wound healing? In scarless wounds, collagen is rapidly deposited in a fine reticular pattern indistinguishable from uninjured skin. In contrast, adult scarring wounds have disorganized and thick collagen bundles with more collagen cross-linking.7 Interestingly, amniotic fluid is neither essential nor suf- ficient for scarless repair. Fetal marsupials develop outside the uterus in a maternal pouch and heal cutaneous wounds without scar.8 Adult sheep skin transplanted onto the backs of fetal sheep bathed in the amniotic fluid of the intrauterine environment heal with scarring of incisional wounds.9 Structure of fetal vs. postnatal wounds Several structural and molecular differences between adult and fetal wounds exist. Ratio of collagen types Type I collagen is the predominant collagen of both adult and fetal extracellular matrix. However, fetal skin has a higher ratio of type III to type I collagen; with maturation, the relative amount of type III collagen decreases.10,11 Hyaluronic acid (hyaluronan, HA) A glycoprotein called HA-stimulating activity (HASA) is found in fetal skin and is absent in adult wounds. This glycoprotein is suggested to be responsible for an increase in HA and the resulting enhanced fluidity, which allows better influx of fibroblasts.12 By the nature of its hygroscopic properties, HA can occupy 10,000 times its own volume. Thus, HA allows proliferating cells to avoid inhibitory contacts.13 Hyaluronic acid synthesis precedes mitosis and dissociates the dividing cell from its substratum, permitting cell movement.13 Fetal fibroblasts have more surface receptors for HA than adult fibroblasts, enhancing fibroblast migration.2 Experimental tympanic membrane perforations in rats treated with HA not only close faster but also heal with much less scar tissue than the untreated controls.12 Scarless wound-healing physiology Transforming growth factor-b (TGF-b) Transforming growth factor-b is secreted by most cells involved in wound healing, including neutrophils, lymphocytes, macrophages, keratinocytes, and fibroblasts. Transforming growth factor-b is first released from degranulating platelets.14 Interestingly, TGF-b upregulates its own production in an autocrine pattern, leading to TGF-b overproduction and scar formation.14 Transforming growth factor-b is a potent chemoattractant of macrophages, neutrophils and fibroblasts, and stimulates extracellular matrix synthesis and prevents its degradation by upregulating the expression of tissue inhibitors of metalloproteinases (TIMPs) and downregulating the expression of proteases.
| دانلود رایگان مقاله انگلیسی + خرید ترجمه فارسی
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| عنوان فارسی مقاله: |
راهبردهای جلوگیری از اسکار: آنچه می توان از پوست جنین آموخت؟ |
| عنوان انگلیسی مقاله: |
Strategies for prevention of scars: what can we learn from fetal skin? |
|
|