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Biomedical subjects

M Focke

Publications and source records attributed to M Focke.

47 records · Page 3Linked to original sources
PubMed1997

Diagnosis of trichothiodystrophy in 2 siblings.

Trichothiodystrophy (TTD) is a rare autosomal recessively inherited disorder which is characterized by sparse and brittle hair with low cystine content. It is often associated with physical and mental retardation. We report 2 cases of TTD in 2 sibs who were born to related parents. The children showed clinical features typical of TTD and in addition other symptoms such as epilepsy, ataxia, spasticity, strabismus, atopic dermatitis, dysarthria and hyperextensible fingerjoints. The sulfur content of hair was reduced to about 50% of normal values and scanning electron microscopy of hair showed trichorrhexis nodosa, trichoschisis, missing cuticle scales with weathering of hair shafts. Under polarizing microscopy an alternating dark and bright banding was found. The present cases show that the correct diagnosis of TTD in practice can be impeded for many years because of the heterogeneous clinical appearance and that the determination of the sulfur content in hair is a simple but indispensable method.

Ataxia↗
PubMed1997

Oilseed rape pollen is a potentially relevant allergen.

Oilseed rape (Brassica napus) (OSR) is a partly wind-pollinated crop which has been increasingly cultivated both in Europe and overseas. Allergological data about OSR is scarce and controversial. We evaluated the frequency of sensitization to OSR pollen by skin prick test and RAST over a period of 1 yr. Airborne OSR pollen load and the agricultural role of this crop were analysed. Furthermore, six patients were investigated by immunoblot. In 4468 patients with suspect inhalant allergy investigated between June 1994 and May 1995, routine skin prick testing revealed OSR sensitivity in 7.1% of pollen-allergic patients. In all, monovalent sensitization was detected in nine patients. Routine pollen counts showed daily maxima not exceeding 50 grains/m3/24 h, but airborne OSR pollen has continuously increased during the last decade correlating with the increasing acreage. Characterization of OSR allergens by immunoblot revealed major allergens of 6/8 kD, 12/14 kD and in the high molecular weight range at 33, 42, 51, 58/61 and 70 kD. Some OSR proteins may cross-react with birch pollen allergens. In summary, the results suggest that OSR pollen is a moderate but true source of allergy and may sensitize despite low pollen exposure.

Allergens↗
PubMed1996

Allergic contact dermatitis to artificial fingernails prepared from UV light-cured acrylates.

BACKGROUND: Contact dermatitis from artificial nails made from self-curing acrylic resins is occasionally reported. Recently, UV light-cured products introducing new acrylics have become available. OBJECTIVE: Our purpose was to identify relevant allergens in commercial light-curing products by patch tests and to evaluate the efficacy of "hypoallergenic" products by inclusion into the test series. METHODS: Patients wearing photobonded acrylic nails who had perionychial and subonychial eczema were patch tested with an acrylate battery and "hypoallergenic" commercial products. RESULTS: Triethyleneglycol dimethacrylate, hydroxyfunctional methacrylates, and (meth)-acrylated urethanes proved to be relevant allergens in photobonded nail preparations. Methacrylated epoxy resin sensitization was not observed. All "hypoallergenic" products provoked positive reactions. CONCLUSION: The omission of irritant methacrylic acid in UV-curable products does not reduce the high sensitizing potential of new acrylates. In contrast to the manufacturers' declarations, all "hypoallergenic" products continue to include acrylate functional monomers and therefore continue to cause allergic sensitization.

Acrylates↗
PubMed1996

Formaldehyde and phenol exposure during an anatomy dissection course: a possible source of IgE-mediated sensitization?

The sensitizing potency of formaldehyde and phenol exposure during 4 weeks of an anatomy dissection course was assessed in 45 medical students. Specific IgE against formaldehyde by RAST and by ELISA and specific IgE against phenol by ELISA were assessed before and after the course. At the start of the course, symptoms, type I allergy, respiratory diseases, and smoking habits were noted. At the end of the course, only symptoms experienced during the dissection lessons were assessed. Indoor formaldehyde levels were measured continuously. The mean indoor formaldehyde level was 0.124 +/- 0.05 ppm, with a minimum of 0.059 ppm and a maximum of 0.219 ppm. Specific IgE against formaldehyde or phenol was found in none of the subjects at the beginning of the course, and no student showed specific IgE against formaldehyde or phenol after the course. Assessment of primarily irritant symptoms during the lesson revealed itch and paraesthesia of hands in 33/45 students (P < 0.00005), headache in 15/45 students, burning eyes in 13/45 students (P < 0.02), dizziness in 8/45 students (P < 0.008), sneezing in 4/45 students, epistaxis in 2/45 students, and shortness of breath in 1/45 students. According to our data, 1-month exposure to formaldehyde and phenol during an anatomy dissection course does not induce specific IgE against formaldehyde or phenol.

Adolescent↗
PubMed1990

Allicin, a naturally occurring antibiotic from garlic, specifically inhibits acetyl-CoA synthetase.

Allicin is shown to be a specific inhibitor of the acetyl-CoA synthetases from plants, yeast and mammals. The bacterial acetyl-CoA-forming system, consisting of acetate kinase and phosphotransacetylase, was inhibited too. Non-specific interaction with sulfhydryl-groups could be excluded in experiments with dithioerythritol and p-hydroxymercuribenzoate. Binding of allicin to the enzyme is non-covalent and reversible. [14C]-Acetate incorporation into fatty acids of isolated plastids was inhibited by allicin with an I50-value lower than 10 microM. Other enzymes of the fatty acid synthesis sequence were not affected, as was shown using precursors other than acetate.

Acetate-CoA Ligase↗