215 results on '"Percy Lehmann"'
Search Results
202. Biochemical and clinical findings in 5 patients with congenital erythropoietic porphyria
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Thomas Ruzicka, Percy Lehmann, Klaus Bolsen, Clemens Fritsch, and Birgit Verwohlt
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medicine.medical_specialty ,business.industry ,Internal medicine ,Congenital erythropoietic porphyria ,medicine ,Dermatology ,business ,Molecular Biology ,Biochemistry ,Gastroenterology - Published
- 1998
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203. Association between Mspl polymorphism of the cytochrome P4501A1 gene and hereditary porphyria cutanea tarda
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Percy Lehmann, Clemens Fritsch, Ellen Fritsche, Sherko von Schmiedeberg, Josef Abel, and Thomas Ruzicka
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Genetics ,Cytochrome ,biology.protein ,Dermatology ,Biology ,Molecular Biology ,Biochemistry ,Gene ,Hereditary porphyria cutanea tarda - Published
- 1998
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204. Acknowledgments to Reviewers
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Jorge Frank, Hasan Mukhtar, S. von Schmiedeberg, Angela M. Christiano, Percy Lehmann, Valdir C. Colussi, Clemens Fritsch, Thomas Ruzicka, Petro E. Petrides, Klaus Bolsen, W. Neuse, H.F. Merk, Denise K. Feyes, and K. Lang
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Pharmacology ,Medical education ,Physiology ,business.industry ,Medicine ,Dermatology ,General Medicine ,business - Published
- 1998
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205. The History of Photography in Dermatology
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Gerd Plewig, Thomas Jansen, Norbert J. Neumann, Percy Lehmann, and W. Neuse
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medicine.medical_specialty ,business.industry ,Photography ,Daguerreotype ,History, 19th Century ,Dermatology ,General Medicine ,History, 20th Century ,Medical photography ,History, 18th Century ,Skin Diseases ,United States ,Europe ,visual_art ,Medical Illustration ,visual_art.visual_art_medium ,Humans ,History of photography ,Medicine ,Textbooks as Topic ,Periodicals as Topic ,business ,History, 15th Century - Abstract
From the Middle Ages to the 20th century, talented artists have created illustrations of signs of human diseases. Since the birth of photography in 1840, artists and physicians have used photographic techniques to illustrate the diseases of the skin; dermatology especially relies on these visual signs. In dermatology today, photography is still very important because of the need for adequate illustrations in medical textbooks and journals. From the early days of daguerreotypes to modern times, medical photography was developed in different stages and many physicians have taken part in the development of photographic techniques and chemistry. This historical survey describes the milestones in the development of medical photographic illustration from its beginning to the 20th century.
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- 1996
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206. PUVA Bath Photochemotherapy for Localized Scleroderma
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Martin Röcken, Michael Meurer, Martina Kerscher, Matthias Volkenandt, Christian A. Sander, Percy Lehmann, and Gerd Plewig
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Adult ,Male ,medicine.medical_specialty ,Adolescent ,medicine.medical_treatment ,Dermatology ,Scleroderma ,Scleroderma, Localized ,chemistry.chemical_compound ,Humans ,Medicine ,Child ,Localized Scleroderma ,PUVA Therapy ,Psoralen ,Aged ,Muscle contracture ,business.industry ,Ultrasound ,General Medicine ,Middle Aged ,medicine.disease ,Connective tissue disease ,Surgery ,chemistry ,PUVA therapy ,Warm water ,Female ,business - Abstract
REPORT OF A CASE A 42-year-old woman who suffered for more than 2 years from disseminated localized scleroderma (LS) (Figure 1) markedly improved during treatment with psoralen with UV-A (PUVA) bath photochemotherapy with 8-methoxy-psoralen (8-MOP).1The 8-MOP was applied to the skin during a warm water bath, which was immediately followed by UV-A exposure. Clinical, histological, and ultrasound indications of LS (Figure 2) regressed almost completely during PUVA bath photochemotherapy in this and 2 other patients, 1 with disseminated LS and 1 with contractures caused by linear LS of the dorsal aspects of the left thigh and entire left leg.1 THERAPEUTIC CHALLENGE No single therapy produces uniform disease remission in LS.2-6A safe and effective therapy associated with the least potential complications is required. SOLUTION Since clinical regression of sclerosis was confirmed by ultrasound and histological evaluations, we considered PUVA bath photochemotherapy a promising novel therapeutic approach
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- 1996
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207. Rapid Decrease of Phototoxicity After PUVA Bath Therapy With 8-Methoxypsoralen
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Percy Lehmann, Martina Kerscher, Thomas Ruzicka, and Norbert J. Neumann
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Photosensitizing Agents ,Time Factors ,business.industry ,medicine.medical_treatment ,Dermatology ,General Medicine ,Pharmacology ,Time optimal ,Bioavailability ,Photosensitivity ,PUVA therapy ,medicine ,Humans ,Methoxsalen ,Phototoxicity ,business ,PUVA Therapy ,Dermatitis, Phototoxic - Abstract
PUVA bath therapy has distinct advantages compared with systemic PUVA therapy, eg, lack of systemic side effects and better bioavailability of psoralen.1-6However, one astonishing drawback of the PUVA bath procedure is the lack of study-generated guidelines for the realization of the procedure. Therefore, we conducted 2 studies to determine the optimal time for irradiation and for how long photosensitivity persists after the bath. The biological activity of 8-methoxypsoralen (8-MOP) was evaluated by determination of the minimal phototoxicity dose (MPD). In a previous study7on PUVA bath phototoxicity, we demonstrate that irradiation immediately and 20 minutes after the bath induces a relatively uniform ).ototoxic response with low UV-A doses (0.5-1.0 J/cm2). Thereafter, a rapid increase of the MPD occurred, thus indicating a decrease of drug activity.7The aim of the present study was to evaluate the photosensitivity up to 4 hours after PUVA bath. Materials and Methods. Six
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- 1996
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208. PUVA-Bath Photochemotherapy of Lichen Planus
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Martina Kerscher, Gerd Plewig, Matthias Volkenandt, Percy Lehmann, and Martin Röcken
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medicine.medical_specialty ,business.industry ,medicine.medical_treatment ,Methoxsalen ,Inflammatory skin disease ,Dermatology ,General Medicine ,Acitretin ,Regimen ,chemistry.chemical_compound ,chemistry ,PUVA therapy ,medicine ,In patient ,business ,Psoralen ,medicine.drug - Abstract
Lichen planus (LP) is a common inflammatory skin disease, accounting for approximately 1% of all diagnoses seen in patients seeking dermatologic care. In some patients, therapy remains difficult, and systemic application of glucocorticosteroids, cyclosporine, systemic photochemotherapy with psoralen plus UV-A (PUVA), and acitretin have been used with limited success.1To circumvent the problems of oral PUVA therapy, methoxsalen (8-methoxypsoralen) in a dilute bathwater solution may be applied to the skin before UV-A.2A PUVA-bath photochemotherapy regimen has been shown to be an elegant alternative in the treatment of psoria- sis.2,3We describe our first four patients with LP who received PUVA-bath photochemotherapy. Patients and Methods. Four patients (age range, 42 to 76 years) with histopathologically proven LP received PUVA-bath photochemotherapy (Table). All had a history of LP for 14 to 24 months and had received topical or systemic glucocorticosteroids, oral PUVA (one patient), and acitretin (one patient)
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- 1995
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209. Ultraviolet radiation–induced injury, chemokines, and leukocyte recruitment: An amplification cycle triggering cutaneous lupus erythematosus.
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Stephan Meller, Franziska Winterberg, Michel Gilliet, Anja Müller, Ingrida Lauceviciute, Juliane Rieker, Norbert J. Neumann, Robert Kubitza, Michael Gombert, Erich Bünemann, Ulrike Wiesner, Petra Franken‐Kunkel, Holger Kanzler, Marie‐Caroline Dieu‐Nosjean, Ali Amara, Thomas Ruzicka, Percy Lehmann, Albert Zlotnik, and Bernhard Homey
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LUPUS erythematosus ,LEUCOCYTES ,APOPTOSIS ,CYTOKINES ,PEPTIDES ,CHEMOKINES ,IMMUNOHISTOCHEMISTRY ,ANTIVIRAL agents - Abstract
To investigate the activation and recruitment pathways of relevant leukocyte subsets during the initiation and amplification of cutaneous lupus erythematosus (LE).Quantitative real‐time polymerase chain reaction was used to perform a comprehensive analysis of all known chemokines and their receptors in cutaneous LE lesions, and the cellular origin of these chemokines and receptors was determined using immunohistochemistry. Furthermore, cytokine‐ and ultraviolet (UV) light–mediated activation pathways of relevant chemokines were investigated in vitro and in vivo.In the present study, we identified the CXCR3 ligands CXCL9 (interferon‐γ [IFNγ]–induced monokine), CXCL10 (IFNγ‐inducible protein 10), and CXCL11 (IFN‐inducible T cell α chemoattractant) as being the most abundantly expressed chemokine family members in cutaneous LE. Expression of these ligands corresponded with the presence of a marked inflammatory infiltrate consisting of mainly CXCR3‐expressing cells, including skin‐homing lymphocytes and blood dendritic cell antigen 2–positive plasmacytoid dendritic cells (PDCs). Within cutaneous LE lesions, PDCs accumulated within the dermis and were activated to produce type I IFN, as detected by the expression of the IFNα‐inducible genes IRF7 and MxA. IFNα, in turn, was a potent and rapid inducer of CXCR3 ligands in cellular constituents of the skin. Furthermore, we demonstrated that the inflammatory CXCR3 ligands cooperate with the homeostatic chemokine CXCL12 (stromal cell–derived factor 1) during the recruitment of pathogenically relevant leukocyte subsets. Moreover, we showed that UVB irradiation induces the release of CCL27 (cutaneous T cell–attracting chemokine) from epidermal compartments into dermal compartments and up‐regulates the expression of a distinct set of chemokines in keratinocytes. Taken together, our data suggest an amplification cycle in which UV light–induced injury induces apoptosis, necrosis, and chemokine production. These mechanisms, in turn, mediate the recruitment and activation of autoimmune T cells and IFNα‐producing PDCs, which subsequently release more effector cytokines, thus amplifying chemokine production and leukocyte recruitment, finally leading to the development of a cutaneous LE phenotype. [ABSTRACT FROM AUTHOR]
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- 2005
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210. Polymorphous light eruption
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Renate von Kries, Gerd Plewig, Percy Lehmann, and E. Hölzle
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Pathology ,medicine.medical_specialty ,Erythema ,medicine.medical_treatment ,Solar urticaria ,Provocation test ,Dermatology ,Biochemistry ,Perivascular Lymphocytic Infiltrate ,medicine ,Humans ,Polymorphic light eruption ,Photosensitivity Disorders ,Erythema multiforme ,Sunburn ,Molecular Biology ,Ultraviolet radiation ,Skin ,Immunity, Cellular ,Lupus erythematosus ,integumentary system ,business.industry ,Cell Biology ,medicine.disease ,Rash ,PUVA therapy ,Sunlight ,Phototesting ,Female ,medicine.symptom ,business ,Skin lesion ,Polymorphous light eruption ,Spongiosis - Abstract
Polymorphous light eruption (PLE) is a common photo-dermatosis of unknown etiology. It afflicts mainly fair-skinned patients, with a preponderance of young females. There is, however, no absolute restriction as to age, sex, or race. Clinical variants include the papular, vesiculo-bullous, and hemorrhagic variety, as well as plaque, erythema multiforme—like, and insect bite (strophulus)-like types. Skin lesions appear only in certain exposed areas hours or a few days after intense sunshine, and are nearly always mono-morphous in the same patient. The rash subsides spontaneously within several days without leaving scars. The histopathologic picture is characteristic and shows a perivascular lymphocytic infiltrate in the upper and middle corium with subepidermal edema, vacuolization of basal cells, and spongiosis in the lower epidermis. The most important differential diagnoses are solar urticaria, photosensitive erythema multiforme, and lupus erythematosus. The action spectrum of PLE is under debate. Reproduction of skin lesions has been reported with UVB, UVA, and, rarely, visible light, with UVA probably being the most effective part of the spectrum. More important than treatment of PLE is prophylaxis. UVA- and UVB-effective sunscreens are of some help. Phototherapy and especially photochemotherapy (psoralen + UVA; PUVA) offer effective ways to decrease light sensitivity. Systemic treatment with chloroquine or β -car-otene has been disappointing. J Invest Dermatol 88:32s—38s, 1987
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- 1982
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211. Corticosteroid Atrophy in Human Skin. A Study by Light, Scanning, and Transmission Electron Microscopy
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Percy Lehmann, Peishu Zheng, Robert M. Lavker, and Albert M. Kligman
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Adult ,Male ,Steroid atrophy ,Pathology ,medicine.medical_specialty ,Biopsy ,Human skin ,Dermatology ,Biochemistry ,Dermis ,Adrenal Cortex Hormones ,medicine ,Humans ,Molecular Biology ,Skin ,biology ,Chemistry ,Ground substance ,Cell Biology ,medicine.disease ,Elastin ,Resorption ,medicine.anatomical_structure ,Transmission electron microscopy ,Microscopy, Electron, Scanning ,biology.protein ,Collagen ,Atrophy ,Reticular Dermis - Abstract
Steroid atrophy was induced in 3 volunteers by the continuous, occlusive application of clobetasol propionate to the forearms for 6 weeks. The changes were followed sequentially by light, scanning, and transmission electron microscopy. A 59% decrease in viable epidermal thickness was noted after the sixth week of treatment, as well as a flattening of the dermal-epidermal junction. The 3-dimensional architecture of the dermis was strikingly reorganized. This was largely brought about by resorption of the ground substance as revealed by a progressive dimunition of Hale's stain for acid mucopolysaccharides. Loss of ground substance resulted in decreased spaces between collagen and elastic fibers as shown by scanning and transmission electron microscopy. The fibrous network consequently collapsed, yielding a more compact papillary and reticular dermis. This compression caused the reorientation of both collagen and elastic fibers. However, no differences in collagen and elastin fine structure were noted. Fibroblasts were shrunken but not reduced in density. A marked decrease in number of mast cells was noted in 3-week specimens and virtually no mast cells were observed after 6 weeks. We found that the primary effect of short-term steroid use was a rearrangement of the geometry of the denial fibrous network. This was not due to alterations in the fibers themselves but a secondary consequence of the loss of ground substance.
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- 1983
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212. Phototesting in Lupus Erythematosus
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Peter Kind, Percy Lehmann and Plewig, Gerd
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immune system diseases ,Cell Biology ,Dermatology ,skin and connective tissue diseases ,Molecular Biology ,Biochemistry - Abstract
Ultraviolet (UV) irradiation is a major factor in the pathogenesis of certain variants of cutaneous lupus erythematosus. Photosensitivity constitutes one of the criteria of the American Rheumatism Association for the diagnosis of systemic lupus erythematosus, which further emphasizes its importance. The pathomechanism of UV-induced lupus erythematosus remains unknown. The characterization of photosensitive subacute cutaneous lupus erythematosus (SCLE) by Gilliam and Sontheimer has Ied to a new approach. Through the development of standardized test methods it has became possible to reproduce cutaneous lesions in the UV-A and UV-B spectrum. These standardized test methods allow a better definition of photosensitivity than clinical history does. Recent clinical data show that besides SCLE another variant, lupus erythematosus tumidus, also reveals pronounced photosensitivity. In this review article phototest procedures, phototest results, and clinical correlations in different subgroups are discussed.
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213. Role of Integrin αE(CD103)β7 for Tissue-Specific Epidermal Localization of CD8+ T Lymphocytes
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Percy Lehmann, Katrin Pauls, Christina M. Parker, Margarete Schön, Michael P. Schön, Andrea Wiesenborn, Thomas Ruzicka, Robert Kubitza, and Bernhard Homey
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Cytotoxicity, Immunologic ,Pathology ,medicine.medical_specialty ,αEβ7 ,integrin ,T cell ,chemical and pharmacologic phenomena ,Dermatology ,Biology ,CD8-Positive T-Lymphocytes ,CD8+ T cells ,Biochemistry ,Antigen ,Antigens, CD ,TGF-β1 ,medicine ,Cytotoxic T cell ,Humans ,Molecular Biology ,Cells, Cultured ,Epidermis (botany) ,Lymphoblast ,hemic and immune systems ,T lymphocyte ,Cell Biology ,epidermotropism ,psoriasis ,Molecular biology ,medicine.anatomical_structure ,Epidermal Cells ,CD103 ,Epidermis ,Integrin alpha Chains ,CD8 ,Transforming growth factor - Abstract
Tissue-specific T cell localization is crucial for immune surveillance of normal tissues and the pathogenesis of inflammatory disorders. In psoriatic skin, CD8+ lymphocytes predominantly reside within the epidermis, whereas CD4+ T cells are most abundant within the dermis. Molecular mechanisms guiding this spatial compartmentalization are not completely understood, however. Here, we demonstrate that 55% (+/-9.7%, n = 14) of the epidermal T cells, predominantly of the CD8+ phenotype, expressed the integrin alphaE(CD103)beta7. In contrast, only 5% (+/-2.0%) of the dermal T cells were alphaE(CD103)beta7+. Integrin alphaE(CD103)beta7 was not detected in normal skin (n = 10), and less than 1% of peripheral blood lymphocytes derived from normal (n = 11) or psoriatic (n = 10) donors expressed alphaE(CD103). When cultured T lymphoblasts (n = 12 donors) were stimulated with transforming growth factor beta1, expression of integrin alphaE(CD103)beta7 was induced on 52.8% (+/-16.2%) of CD8+ cells, but only on 6.1% (+/-2.3%) of CD4+ cells, suggesting selective inducibility on CD8+ lymphocytes. Whereas similar overall expression of transforming-growth-factor-beta1-specific mRNA was detected in normal and psoriatic skin by real-time quantitative polymerase chain reaction, immunohistochemistry revealed focal overexpression of transforming growth factor beta1 underneath psoriatic, but not normal, epidermis. This heterogenous transforming growth factor beta1 expression may contribute to induction of alphaE(CD103) in vivo. Adhesion of transforming-growth-factor-beta1-stimulated CD8+, but not CD4+, T cells to cultured keratinocytes and psoriatic epidermis in frozen sections could be significantly inhibited by antibodies that blocked the alphaE(CD103)/E-cadherin interaction. Co-culture of lymphoblasts and keratinocytes resulted in marginal enhancement of alphaE(CD103)beta7 expression in some cases. Overall, integrin alphaE(CD103)beta7 appears to contribute to tissue-specific epidermal localization of CD8+ T lymphocytes.
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214. Lichtdiagnostische Verfahren bei Patienten mit Verdacht auf Photodermatosen
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Percy Lehmann, Gerd Plewig, E. Hölzle, and R. von Kries
- Abstract
Derzeit gibt es keine einheitliche, allgemein akzeptierte Empfehlung fur Lichttestungen zur Diagnostik bei Patienten mit Verdacht auf Lichtdermatosen. Vorliegend werden Testverfahren beschrieben, die es ermoglichen, die normalen Lichtreaktionen des Patienten zu prufen und pathologische Reaktionen festzustellen. Die Durchfuhrung von Lichttreppen zur Bestimmung von minimalen Erythemdosen (MED-UV-B, MED- UV-A) und Pigmentierungsfahigkeit werden erlautert und Methoden fur UV-Provokation, Photopatchtest und systemische Photoprovokation werden beschrieben. Die Aussagekraft der Testmethoden wird diskutiert.
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- 1987
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215. Bestrahlung Mit UV-A Oder UV-B wirkt protektiv gegenüber Irritantien
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Gerd Plewig, E. Hölzle, Percy Lehmann, and S. Helbig
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Untersuchungen uber den Einflus der UV-Strahlung auf die Hautreaktivitat gegen toxische Substanzen liegen bisher nicht vor. Anhand dreier unterschiedlicher Irritationsmodelle wurde der Einflus von UV-A und UV-B auf die Hautreaktivitat untersucht. Zwei seitengetrennte Testfelder am Rucken 26 freiwilliger Probanden wurden drei Wochen lang dreimal wochentlich mit UV-A und UV-B bestrahlt. Insgesamt wurden 9mal 100 J/cm2 UV-A und 9mal die 1,5fache MED-UV-B appliziert. Danach erfolgten auf den bestrahlten Feldern sowie auf normaler Haut folgende Testungen: 1. Alkaliresistenz-Test, 2. Dimethylsulfoxid-Test, 3. Natriumlaurylsulfat-Test.
- Published
- 1988
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