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		<title>BMC Dermatology - Latest articles</title>
		<link>http://www.biomedcentral.com/bmcdermatol/</link>
		<description>The latest articles from BMC Dermatology (ISSN 1471-5945) published by 
				
				BioMed Central
		</description>
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				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/8/3"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/8/2"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/8/1"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/7/6"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/7/5"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/7/4"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/7/3"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/7/2"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-5945/7/1"/>			    
            
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		<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: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/1471-5945/8/2">
            
            <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: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/1471-5945/8/1">
            
            <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: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>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/7/6">
            
            <title>The establishment and utility of Sweha-Reg: a Swedish population-based registry to understand hereditary angioedema</title>
			<description>Background:
The importance of acquiring comprehensive epidemiological and clinical data on hereditary angioedema has increasingly caught the attention of physicians and scientists around the world. The development of networks and creation of comprehensive policies to improve care of people suffering from rare diseases, such as hereditary angioedema, is a stated top priority of the European Union.Hereditary angioedema is a rare disease, that it may be life-threatening. Although the exact prevalence is unknown, current estimates suggest that it is 1/10,000&#8211;1/150,000 individuals. The low prevalence requires combined efforts to gain accurate epidemiological data on the disease and so give us tools to reduce morbidity and mortality, and improve quality of life of sufferers.
Methods:
Sweha-Reg is a population-based registry of hereditary angioedema in Sweden with the objectives of providing epidemiological data, and so creates a framework for the study of this disease. The registry contains individual-based data on diagnoses, treatments and outcomes.
Conclusion:
The present manuscript seeks to raise awareness of the existence of Sweha-Reg to stimulate the international collaboration of registries. A synthesis of data from similar registries across several countries is required to approach an inclusive course understanding of HAE.</description>
			<link>http://www.biomedcentral.com/1471-5945/7/6</link>
			
			 	<dc:creator>Lotus Mallbris, Patrik Nordenfelt, Janne Bj&#246;rkander, Anders Lindfors, Sonja Werner and Carl-Fredrik Wahlgren</dc:creator>
			
			<dc:source>BMC Dermatology 2007, 7:6</dc:source>
			<dc:date>2007-11-30</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-7-6</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>6</prism:startingPage>
					
			
							
					<prism:publicationDate>2007-11-30</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/7/5">
            
            <title>Single nucleotide polymorphism-based genome-wide linkage analysis in Japanese atopic dermatitis families</title>
			<description>Background:
Atopic dermatitis develops as a result of complex interactions between several genetic and environmental factors. To date, 4 genome-wide linkage studies of atopic dermatitis have been performed in Caucasian populations, however, similar studies have not been done in Asian populations. The aim of this study was to identify chromosome regions linked to atopic dermatitis in a Japanese population.
Methods:
We used a high-density, single nucleotide polymorphism genotyping assay, the Illumina BeadArray Linkage Mapping Panel (version 4) comprising 5,861 single nucleotide polymorphisms, to perform a genome-wide linkage analysis of 77 Japanese families with 111 affected sib-pairs with atopic dermatitis.
Results:
We found suggestive evidence for linkage with 15q21 (LOD = 2.01, NPL = 2.87, P = .0012) and weak linkage to 1q24 (LOD = 1.26, NPL = 2.44, P = .008).
Conclusion:
We report the first genome-wide linkage study of atopic dermatitis in an Asian population, and novel loci on chromosomes 15q21 and 1q24 linked to atopic dermatitis. Identification of novel causative genes for atopic dermatitis will advance our understanding of the pathogenesis of atopic dermatitis.</description>
			<link>http://www.biomedcentral.com/1471-5945/7/5</link>
			
			 	<dc:creator>Hisako Enomoto, Emiko Noguchi, Shigeruko Iijima, Takenori Takahashi, Kazuhito Hayakawa, Mikako Ito, Toshiyuki Kano, Takeshi Aoki, Yoichi Suzuki, Minori Koga, Mayumi Tamari, Tetsuo Shiohara, Fujio Otsuka and Tadao Arinami</dc:creator>
			
			<dc:source>BMC Dermatology 2007, 7:5</dc:source>
			<dc:date>2007-09-28</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-7-5</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>5</prism:startingPage>
					
			
							
					<prism:publicationDate>2007-09-28</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/7/4">
            
            <title>Self reported skin morbidity and ethnicity: a population-based study in a Western community</title>
			<description>Background:
Recent studies have shown ethnic differences concerning cardio-vascular disease, diabetes and mental health. Little is known about ethnic differences in skin morbidity. The purpose of this study was to describe possible ethnic differences in self-reported skin morbidity in a Western urban community.
Methods:
The design was cross sectional. 40 888 adults in Oslo, Norway, received a postal questionnaire providing information on socio-demographic factors and self-reported health, including items on skin complaints.
Results:
18770 individuals answered the questionnaire. In the sample 84% were from Norway. The largest immigrant group was from Western countries (5%) and the Indian Subcontinent (3%). Itch was the most prevalent reported skin symptom (7%), and was significantly more reported by men from East Asia (18%) and Middle East/North Africa (13%). The same observations were seen for reported dry and sore skin. Hair loss was a dominating complaint for men from the Indian Subcontinent and the Middle East/North Africa (23% and 25%) and for women from the same ethnic groups. Women from Sub-Saharan Africa reported significantly more pimples than in the other groups (17%).
Conclusion:
The study showed that there were significant differences in self-reported skin complaints among ethnic groups. Issues concerning the cultural value of some skin symptoms should be examined further.</description>
			<link>http://www.biomedcentral.com/1471-5945/7/4</link>
			
			 	<dc:creator>Florence Dalgard, Jan &#216;ivind Holm, &#197;ke Svensson, Bernadette Kumar and Johanne Sundby</dc:creator>
			
			<dc:source>BMC Dermatology 2007, 7:4</dc:source>
			<dc:date>2007-06-29</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-7-4</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>4</prism:startingPage>
					
			
							
					<prism:publicationDate>2007-06-29</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-5945/7/3">
            
            <title>Association of toll-interacting protein gene polymorphisms with atopic dermatitis</title>
			<description>Background:
Atopic dermatitis (AD) is a common inflammatory skin disorder, affecting up to 15% of children in industrialized countries. Toll-interacting protein (TOLLIP) is an inhibitory adaptor protein within the toll-like receptor (TLR) pathway, a part of the innate immune system that recognizes structurally conserved molecular patterns of microbial pathogens, leading to an inflammatory immune response.
Methods:
In order to detect a possible role of TOLLIP variation in the pathogenesis of AD, we screened the entire coding sequence of the TOLLIP gene by SSCP in 50 AD patients. We identified an amino acid exchange in exon 6 (Ala222Ser) and a synonymous variation in exon 4 (Pro139Pro). Subsequently, these two variations and four additional non-coding polymorphisms (-526 C/G, two polymorphisms in intron 1 and one in the 3'UTR) were genotyped in 317 AD patients and 224 healthy controls.
Results:
The -526G allele showed borderline association with AD in our cohort (p = 0.012; significance level after correction for multiple testing 0.0102). Haplotype analysis did not yield additional information. Evaluation of mRNA expression by quantitative real-time polymerase chain reaction in six probands with the CC and six with the GG genotype at the -526 C/G locus did not reveal significant differences between genotypes.
Conclusion:
Variation in the TOLLIP gene may play a role in the pathogenesis of AD. Yet, replication studies in other cohorts and populations are warranted to confirm these association results.</description>
			<link>http://www.biomedcentral.com/1471-5945/7/3</link>
			
			 	<dc:creator>Tobias T Schimming, Qumar Parwez, Elisabeth Petrasch-Parwez, Michael Nothnagel, Joerg T Epplen and Sabine Hoffjan</dc:creator>
			
			<dc:source>BMC Dermatology 2007, 7:3</dc:source>
			<dc:date>2007-03-16</dc:date>
			<dc:identifier>doi:10.1186/1471-5945-7-3</dc:identifier>
			
			
							
					<prism:publicationName>BMC Dermatology</prism:publicationName>
					
			
							
					<prism:issn>1471-5945</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>3</prism:startingPage>
					
			
							
					<prism:publicationDate>2007-03-16</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: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: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/1471-5945/6/10">
            
            <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: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/"/>
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