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		<title>BMC Dermatology - Most viewed articles</title>
		<link>http://www.biomedcentral.com/bmcdermatol/mostviewed/</link>
		<description>Most viewed articles in last 30 days from BMC Dermatology (ISSN 1471-5945) published by 
				
				BioMed Central
		</description>
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				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/6/7"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/8/2"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/8/3"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/6/3"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/6/10"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/4/14"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/4/11"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/7/2"/>			    
            
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		<item rdf:about="http://www.biomedcentral.com/1471-5945/6/7">
            
            <title>Case report and summary of literature: giant perineal keloids treated with post-excisional radiotherapy</title>
			<description>Background:
Keloids are common benign tumors of the dermis, typically arising after insult to the skin. While typically only impinging on cosmesis, large or recurrent keloids may require therapeutic intervention. While no single standardized treatment course has been established, several series report excellent outcomes for keloids with post-surgery radiation therapy.Case presentationWe present a patient with a history of recurrent keloids arising in the absence of an ascribed trauma and a maternal familial history of keloid formation, whose physical examination several large perineal keloids of 6-20 cm in the largest dimension. The patient was treated with surgical extirpation and adjuvant radiation therapy. Radiotherapy was delivered to the scar bed to a total dose of 22 Gy over 11 daily fractions. Acute radiotherapy toxicity necessitated a treatment break due to RTOG Grade III acute toxicity (moderate ulceration and skin breakdown) which resolved rapidly during a 3-day treatment break. The patient demonstrated local control and has remained free of local recurrence for more than 2 years.
Conclusion:
Radiotherapy for keloids represents a safe and effective option for post-surgical keloid therapy, especially for patients with bulky or recurrent disease.</description>
			<link>http://www.biomedcentral.com/1471-5945/6/7</link>		
			<dc:creator>Kristin Jones, Clifton D Fuller, Join Y Luh, Craig C Childs, Alexander R Miller, Anthony W Tolcher, Terence S Herman and Charles R Thomas</dc:creator>
			<dc:source>BMC Dermatology 2006, 6:7</dc:source>
			<dc:subject>Number of accesses: 1259</dc:subject>
			<dc:date>2006-04-19</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-6-7</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>6</prism:volume>
					
			
							
					<prism:startingPage>7</prism:startingPage>
					
			
							
					<prism:publicationDate>2006-04-19</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/8/2">
            
            <title>A systematic review of natural health product treatment for vitiligo</title>
			<description>Background:
Vitiligo is a hypopigmentation disorder affecting 1 to 4% of the world population. Fifty percent of cases appear before the age of 20 years old, and the disfigurement results in psychiatric morbidity in 16 to 35% of those affected.
Methods:
Our objective was to complete a comprehensive, systematic review of the published scientific literature to identify natural health products (NHP) such as vitamins, herbs and other supplements that may have efficacy in the treatment of vitiligo. We searched eight databases including MEDLINE and EMBASE for vitiligo, leucoderma, and various NHP terms. Prospective controlled clinical human trials were identified and assessed for quality.
Results:
Fifteen clinical trials were identified, and organized into four categories based on the NHP used for treatment. 1) L-phenylalanine monotherapy was assessed in one trial, and as an adjuvant to phototherapy in three trials. All reported beneficial effects. 2) Three clinical trials utilized different traditional Chinese medicine products. Although each traditional Chinese medicine trial reported benefit in the active groups, the quality of the trials was poor. 3) Six trials investigated the use of plants in the treatment of vitiligo, four using plants as photosensitizing agents. The studies provide weak evidence that photosensitizing plants can be effective in conjunction with phototherapy, and moderate evidence that Ginkgo biloba monotherapy can be useful for vitiligo. 4) Two clinical trials investigated the use of vitamins in the therapy of vitiligo. One tested oral cobalamin with folic acid, and found no significant improvement over control. Another trial combined vitamin E with phototherapy and reported significantly better repigmentation over phototherapy only. It was not possible to pool the data from any studies for meta-analytic purposes due to the wide difference in outcome measures and poor quality ofreporting.
Conclusion:
Reports investigating the efficacy of NHPs for vitiligo exist, but are of poor methodological quality and contain significant reporting flaws. L-phenylalanine used with phototherapy, and oral Ginkgo biloba as monotherapy show promise and warrant further investigation.</description>
			<link>http://www.biomedcentral.com/1471-5945/8/2</link>		
			<dc:creator>Orest Szczurko and Heather S Boon</dc:creator>
			<dc:source>BMC Dermatology 2008, 8:2</dc:source>
			<dc:subject>Number of accesses: 678</dc:subject>
			<dc:date>2008-05-22</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-8-2</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>2</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-05-22</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/8/3">
            
            <title>Melasma and its association with different types of nevi in women: A case-control study</title>
			<description>Background:
Very little is known about possible association of nevi and melasma. The study objective was to determine if there is an association between melasma and existence of different kinds of nevi.
Methods:
In a case-control study, 120 female melasma patients referred to dermatology clinic of Ardabil and 120 patients referred to other specialty clinics who lacked melasma were enrolled after matching for age. Number of different types of nevi including lentigines and melanocytic nevi were compared between case and control group patients. Data were entered into the computer and analyzed by SPSS 13 statistical software.
Results:
Mean number of lentigines was 25.5 in melasma group compared to 8 in control group(P &lt; 0.01). Mean number of melanocytic nevi was 13.2 in cases compared to 2.8 in control group(P &lt; 0.001). Multivariate analysis showed that existence of freckles, lentigines and more than three melanocytic nevi were positively related to developing melasma. The chance of melasma increased up to 23 times for patients having more than three melanocytic nevi. Congenital nevi were observed among 10% both in case and control groups. Campbell de morgan angiomas were seen among 26 patients(21.8%) in case group compared to 6 patients(5%) in control group.
Conclusion:
Existence of lentigines and melanocytic nevi increases chance of having melasma</description>
			<link>http://www.biomedcentral.com/1471-5945/8/3</link>		
			<dc:creator>Hassan Adalatkhah, Homayoun Sadeghi-bazargani, Nayereh Amini-sani and Somayeh Zeynizadeh</dc:creator>
			<dc:source>BMC Dermatology 2008, 8:3</dc:source>
			<dc:subject>Number of accesses: 467</dc:subject>
			<dc:date>2008-08-05</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-8-3</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>3</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-05</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/6/3">
            
            <title>Anti-thyroid peroxidase antibody and vitiligo: a controlled study</title>
			<description>Background:
Vitiligo is an acquired depigmenting disorder due to destruction of melanocytes. Although many theories have been suggested for its pathogenesis, the role of autoimmunity is the most popular one. The association of vitiligo with autoimmune thyroid diseases and the increased prevalence of autoantibodies including thyroid autoantibodies in vitiligo favor this role. Our objective was to compare the frequency of thyroid peroxidase antibody (anti-TPO) in vitiligo patients with healthy subjects in Iran.
Methods:
Ninety-four cases of vitiligo (46 female and 48 male) and 96 control subjects (49 female and 47 male) were enrolled in this controlled study. Patients with known thyroid disease, history of thyroid surgery and those receiving thyroid medications were not included. The two groups were matched regarding gender and age. The demographic data, symptoms related to thyroid diseases and results of skin and thyroid examinations were recorded in a questionnaire for each subject. Thyroid function tests including free T3, free T4 and TSH-IRMA were performed. Anti-TPO levels were assessed as well. The collected data were analyzed by SPSS version-11 in vitiligo patients and subgroups according to gender, age, extent, and duration of the disease compared with the control group.
Results:
Anti-TPO was detected in 17 (18.1%) of patients affected by vitiligo, while this figure was 7 (7.3%) in the control group; the difference was significant with p-value &lt; 0.025 (Phi &amp; Cramer's V = 0.162). When analyzing subgroups, the difference in the frequency of anti-TPO remained significant only in females (p-value &lt; 0.044) (Phi &amp; Cramer's V = 0.207) and in patients in the age ranges of 18&#8211;25 (p-value &lt; 0.05) (Phi &amp; Cramer's V = 0.28) and 26&#8211;35 year-old (p-value &lt; 0.042) (Phi &amp; Cramer's V = 0.304).The difference of the frequency of anti-TPO was not significant regarding the duration and extent of vitiligo. In addition, there was no significant difference in the levels of free T3, free T4, and TSH in vitiligo patients compared with the control group.
Conclusion:
According to our study, anti-TPO was shown to be significantly more common in vitiligo patients especially in young women, compared with control group. As this antibody is a relatively sensitive and specific marker of autoimmune thyroid disorders including Hashimoto thyroiditis and Graves' disease, and considering the fact that vitiligo usually precedes the onset of thyroid dysfunction, periodic follow-up of vitiligo patients for detecting thyroid diseases is further emphasized especially in young women with increased level of anti-TPO.</description>
			<link>http://www.biomedcentral.com/1471-5945/6/3</link>		
			<dc:creator>Maryam Daneshpazhooh, Mahtab Mostofizadeh G , Javad Behjati, Maryam Akhyani and Reza Mahmoud Robati</dc:creator>
			<dc:source>BMC Dermatology 2006, 6:3</dc:source>
			<dc:subject>Number of accesses: 455</dc:subject>
			<dc:date>2006-03-10</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-6-3</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>6</prism:volume>
					
			
							
					<prism:startingPage>3</prism:startingPage>
					
			
							
					<prism:publicationDate>2006-03-10</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/6/10">
            
            <title>Mohs math &#8211; where the error hides</title>
			<description>Background:
Mohs surgical technique allows a full view of surgical margins and has a reported cure rate approaching 100%.MethodA survey amongst Mohs surgeons was performed to assess operator technique. In addition, an animated clay model was constructed to identify and quantify tissue movement seen during the processing of Mohs surgical specimens.
Results:
There is variability in technique used in Mohs surgery in regards to the thickness of layers, and the number of blocks layers are cut into. A mathematical model is described which assesses the clinical impact of this variability.
Conclusion:
Our mathematical model identifies key aspects of technique that may contribute to error. To keep the inherent error rate at a minimum, we advocate minimal division and minimal physical thickness of Mohs specimens.</description>
			<link>http://www.biomedcentral.com/1471-5945/6/10</link>		
			<dc:creator>Jeffrey I Ellis, Tatiana Khrom, Anthony Wong, Mario O Gentile and Daniel M Siegel</dc:creator>
			<dc:source>BMC Dermatology 2006, 6:10</dc:source>
			<dc:subject>Number of accesses: 333</dc:subject>
			<dc:date>2006-12-06</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-6-10</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>6</prism:volume>
					
			
							
					<prism:startingPage>10</prism:startingPage>
					
			
							
					<prism:publicationDate>2006-12-06</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/4/14">
            
            <title>Pimecrolimus 1% cream for anogenital lichen sclerosus in childhood</title>
			<description>Background:
Lichen sclerosus is a chronic inflammatory disease with a predilection of the anogenital region. Because of the potential side effects of repeated local application of potent glucocorticosteroids, equally-effective, safer therapeutic options are required, especially in the treatment of children.Case presentationsWe report on the efficacy of twice-daily application of pimecrolimus 1% cream in four prepubertal girls (range of age: 4 to 9 years) who suffered from anogenital lichen sclerosus. After three to four-month treatment, all patients had almost complete clinical remission including relief from itch, pain and inflammation. Only minor improvement was observed for the white sclerotic lesions. No significant side effects have been observed.
Conclusions:
Topical pimecrolimus appears to be an effective and safe treatment for children with anogenital lichen sclerosus. The clinical benefits observed in the four patient presented particularly include relief of pruritus, pain and inflammation. Vehicle-controlled studies on a larger number of patients are now warranted to substantiate our promising findings, and to investigate long-term efficacy and safety of topical pimecrolimus in anogenital lichen sclerosus.</description>
			<link>http://www.biomedcentral.com/1471-5945/4/14</link>		
			<dc:creator>Stefanie Boms, Thilo Gambichler, Marcus Freitag, Peter Altmeyer and Alexander Kreuter</dc:creator>
			<dc:source>BMC Dermatology 2004, 4:14</dc:source>
			<dc:subject>Number of accesses: 297</dc:subject>
			<dc:date>2004-10-14</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-4-14</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>4</prism:volume>
					
			
							
					<prism:startingPage>14</prism:startingPage>
					
			
							
					<prism:publicationDate>2004-10-14</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/4/11">
            
            <title>UVA/UVA1 phototherapy and PUVA photochemotherapy in connective tissue diseases and related disorders: a research based review</title>
			<description>Background:
Broad-band UVA, long-wave UVA1 and PUVA treatment have been described as an alternative/adjunct therapeutic option in a number of inflammatory and malignant skin diseases. Nevertheless, controlled studies investigating the efficacy of UVA irradiation in connective tissue diseases and related disorders are rare.
Methods:
Searching the PubMed database the current article systematically reviews established and innovative therapeutic approaches of broad-band UVA irradiation, UVA1 phototherapy and PUVA photochemotherapy in a variety of different connective tissue disorders.
Results:
Potential pathways include immunomodulation of inflammation, induction of collagenases and initiation of apoptosis. Even though holding the risk of carcinogenesis, photoaging or UV-induced exacerbation, UVA phototherapy seems to exhibit a tolerable risk/benefit ratio at least in systemic sclerosis, localized scleroderma, extragenital lichen sclerosus et atrophicus, sclerodermoid graft-versus-host disease, lupus erythematosus and a number of sclerotic rarities.
Conclusions:
Based on the data retrieved from the literature, therapeutic UVA exposure seems to be effective in connective tissue diseases and related disorders. However, more controlled investigations are needed in order to establish a clear-cut catalogue of indications.</description>
			<link>http://www.biomedcentral.com/1471-5945/4/11</link>		
			<dc:creator>Frank Breuckmann, Thilo Gambichler, Peter Altmeyer and Alexander Kreuter</dc:creator>
			<dc:source>BMC Dermatology 2004, 4:11</dc:source>
			<dc:subject>Number of accesses: 260</dc:subject>
			<dc:date>2004-09-20</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-4-11</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>4</prism:volume>
					
			
							
					<prism:startingPage>11</prism:startingPage>
					
			
							
					<prism:publicationDate>2004-09-20</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/7/2">
            
            <title>Eruptive papules during efalizumab (anti-CD11a) therapy of psoriasis vulgaris: a case series</title>
			<description>Background:
Newer biological therapies for moderate-to-severe psoriasis are being used more frequently, but unexpected effects may occur.Case presentationsWe present a group of 15 patients who developed inflammatory papules while on efalizumab therapy (Raptiva, Genentech Inc, anti-CD11a). Immunohistochemistry showed that there were increased CD11b+, CD11c+ and iNOS+ cells (myeloid leukocytes) in the papules, with relatively few CD3+ T cells. While efalizumab caused a decreased expression of CD11a on T cells, other circulating leukocytes from patients receiving this therapy often showed increased CD11b and CD11c. In the setting of an additional stimulus such as skin trauma, this may predispose to increased trafficking into the skin using these alternative &#946;2 integrins. In addition, there may be impaired immune synapse formation, limiting the development of these lesions to small papules. There is little evidence for these papular lesions being "allergic" in nature as there are few eosinophils on biopsy, and they respond to minimal or no therapy even if efalizumab is continued.
Conclusion:
We hypothesize that these papules may represent a unique type of "mechanistic" inflammatory reaction, seen only in the context of drug-induced CD11a blockade, and not during the natural disease process.</description>
			<link>http://www.biomedcentral.com/1471-5945/7/2</link>		
			<dc:creator>Michelle A Lowes, Francesca Chamian, Maria V Abello, Craig Leonardi, Wolfgang Dummer, Kim Papp and James G Krueger</dc:creator>
			<dc:source>BMC Dermatology 2007, 7:2</dc:source>
			<dc:subject>Number of accesses: 248</dc:subject>
			<dc:date>2007-02-26</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-7-2</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>2</prism:startingPage>
					
			
							
					<prism:publicationDate>2007-02-26</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/7/1">
            
            <title>Photostability of commercial sunscreens upon sun exposure and irradiation by ultraviolet lamps</title>
			<description>Background:
Sunscreens are being widely used to reduce exposure to harmful ultraviolet (UV) radiation. The fact that some sunscreens are photounstable has been known for many years. Since the UV-absorbing ingredients of sunscreens may be photounstable, especially in the long wavelength region, it is of great interest to determine their degradation during exposure to UV radiation. Our aim was to investigate the photostability of seven commercial sunscreen products after natural UV exposure (UVnat) and artificial UV exposure (UVart).
Methods:
Seven commercial sunscreens were studied with absorption spectroscopy. Sunscreen product, 0.5 mg/cm2, was placed between plates of silica. The area under the curve (AUC) in the spectrum was calculated for UVA (320&#8211;400 nm), UVA1 (340&#8211;400 nm), UVA2 (320&#8211;340 nm) and UVB (290&#8211;320 nm) before (AUCbefore) and after (AUCafter) UVart (980 kJ/m2 UVA and 12 kJ/m2 of UVB) and before and after UVnat. If theAUC Index (AUCI), defined as AUCI = AUCafter/AUCbefore, was > 0.80, the sunscreen was considered photostable.
Results:
Three sunscreens were unstable after 90 min of UVnat; in the UVA range the AUCI was between 0.41 and 0.76. In the UVB range one of these sunscreens was unstable with an AUCI of 0.75 after 90 min. Three sunscreens were photostable after 120 min of UVnat; in the UVA range the AUCI was between 0.85 and 0.99 and in the UVB range between 0.92 and 1.0. One sunscreen showed in the UVA range an AUCI of 0.87 after UVnat but an AUCI of 0.72 after UVart. Five of the sunscreens were stable in the UVB region.
Conclusion:
The present study shows that several sunscreens are photounstable in the UVA range after UVnat and UVart. There is a need for a standardized method to measure photostability, and the photostability should be marked on the sunscreen product.</description>
			<link>http://www.biomedcentral.com/1471-5945/7/1</link>		
			<dc:creator>Helena Gonzalez, Nils Tarras-Wahlberg, Birgitta Str&#246;mdahl, Asta Juzeniene, Johan Moan, Olle Lark&#246;, Arne Ros&#233;n and Ann-Marie Wennberg</dc:creator>
			<dc:source>BMC Dermatology 2007, 7:1</dc:source>
			<dc:subject>Number of accesses: 242</dc:subject>
			<dc:date>2007-02-26</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-7-1</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>1</prism:startingPage>
					
			
							
					<prism:publicationDate>2007-02-26</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/8/1">
            
            <title>Topical rapamycin inhibits tuberous sclerosis tumor growth in a nude mouse model</title>
			<description>Background:
Skin manifestations of Tuberous Sclerosis Complex (TSC) cause significant morbidity. The molecular mechanism underlying TSC is understood and there is evidence that systemic treatment with rapamycin or other mTOR inhibitors may be a useful approach to targeted therapy for the kidney and brain manifestations. Here we investigate topical rapamycin in a mouse model for TSC-related tumors.
Methods:
0.4% and 0.8% rapamycin ointments were applied to nude mice bearing subcutaneous, TSC-related tumors. Topical treatments were compared with injected rapamycin and topical vehicle. Rapamycin levels in blood and tumors were measured to assess systemic drug levels in all cohorts.
Results:
Treatment with topical rapamycin improved survival and reduced tumor growth. Topical rapamycin treatment resulted in systemic drug levels within the known therapeutic range and was not as effective as injected rapamycin.
Conclusion:
Topical rapamycin inhibits TSC-related tumor growth. These findings could lead to a novel treatment approach for facial angiofibromas and other TSC skin lesions.</description>
			<link>http://www.biomedcentral.com/1471-5945/8/1</link>		
			<dc:creator>Aubrey Rauktys, Nancy Lee, Laifong Lee and Sandra L Dabora</dc:creator>
			<dc:source>BMC Dermatology 2008, 8:1</dc:source>
			<dc:subject>Number of accesses: 241</dc:subject>
			<dc:date>2008-01-28</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-8-1</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>8</prism:volume>
					
			
							
					<prism:startingPage>1</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-01-28</prism:publicationDate>
					

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