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Biomedical subjects

B C Melnik

Publications and source records attributed to B C Melnik.

11 recordsLinked to original sources
PubMed1991

Disturbances of essential fatty acid- and prostaglandin E-mediated immunoregulation in atopy.

Impaired suppressor T lymphocyte maturation and function in atopic individuals are explained by an insufficient transmission of prostaglandin E (PGE) signals during thymic lymphocyte differentiation as well as an impaired ability of the atopic immune system to activate suppressor T-cells by PGE-mediated feed back mechanisms. We demonstrate that spontaneous in vitro immunoglobulin E synthesis of atopic peripheral blood mononuclear cells could be suppressed by the addition of 10(-6) M to 10(-5) M PGE1 or PGE2. Decreased plasma and breast milk levels of PGE-precursor fatty acids and reduced numbers of PGE2-receptors on atopic lymphocytes have been observed in atopic individuals. These insights might offer a novel approach for the prevention of atopic disease by substitution of the atopic pregnant and nursing woman and her newborn infant with long chain omega-6-fatty acids.

Adult↗
PubMed1991

Influence of UV irradiation on the composition of human stratum corneum lipids.

Irradiation with suberythemal doses of either UV-A or UV-B yielded an increase in the amount of stratum corneum lipids extracted from the lumbar skin area of 20 volunteers. These lipids were quantified after separation by high-performance thin-layer chromatography. Ten subfractions in the ceramide region were separated; two of them (fractions 7a and 7b) were only detectable after UV-A or UV-B irradiation. Improvement of barrier function after UV irradiation of human skin with suberythemal doses may be related to an increase in the stratum corneum ceramides.

Adult↗
PubMed1991

[Stratum corneum and nail lipids in patients with atopic dermatitis. Decrease in ceramides--a pathogenetic factor in atopic xerosis?].

Dry skin is seen in many patients with atopic dermatitis and correlates with a disturbed epidermal barrier function demonstrated by such features as increased transepidermal water loss and diminished stratum corneum hydration. With regard to the importance of stratum corneum lipids for the permeability barrier, we have analysed plantar (n = 8) and lumbar (n = 20) stratum corneum and nail lipids (n = 15) of atopic subjects by high-performance thin-layer chromatography (HPTLC). Compared with controls our investigations show a decrease in the ceramide fraction as a percentage of total lipid and a diminished ratio of ceramides and free sterols in atopic subjects. This implies that impaired ceramide synthesis may be a factor in the pathogenesis of atopic xerosis.

Dermatitis, Atopic↗
PubMed1990

[A chance for the prevention of atopic diseases].

The proposed concept links the alterations in cell-mediated and humoral immunity in atopy to impaired prostaglandin E (PGE)-mediated thymic maturation of T-suppressor lymphocytes and diminished activation of T-suppressor lymphocytes of the peripheral atopic immune system. The decreased sensitivity of atopic T lymphocytes to PGE, recently explained by a reduction of PGE2-receptors on atopic lymphocytes, is regarded as the common underlying defect in atopy. A second defect, the delta-6-desaturase deficiency, affects the regular supply of the PGE-precursors dihomo-gamma-linolenic acid and arachidonic acid and predisposes for atopic dermatitis. Furthermore, the composition of omega-6-fatty acids in breast milk of atopic mothers represents a delta-6-desaturase deficiency. Substitution of the delta-6-desaturase product gamma-linolenic acid to the atopic pregnant and nursing woman and her newborn infant at increased risk for atopy offers a chance for the prevention of atopic diseases.

Breast Feeding↗
PubMed1989

Is the origin of atopy linked to deficient conversion of omega-6-fatty acids to prostaglandin E1?

Our hypothesis on the origin of atopy links alterations in omega-6-fatty acid metabolism in atopic persons (i.e., reduced formation of delta-6-desaturase products) to deficient T cell differentiation and function. We suggest that a relative deficiency in dihomo-gamma-linolenic acid-derived prostaglandin E1 is the major etiologic factor for diminished T cell maturation postpartum. Its precursors, gamma-linolenic acid and dihomo-gamma-linolenic acid, are physiologically provided in colostrum and mature breast milk of healthy mothers. Depressed cell-mediated immunity and uncontrolled B-cell response with increased IgE synthesis are explained as prostaglandin E1-dependent defects of T cell differentiation caused by insufficient supply of prostaglandin E1 precursors during early infancy. Thus, in our opinion atopy is a metabolic disorder and the associated immunologic disturbances are epiphenomena.

Adjuvants, Immunologic↗
PubMed1989

Microanalytical screening of all major stratum corneum lipids by sequential high-performance thin-layer chromatography.

For rapid and sensitive screening of lipid biochemical abnormalities of scaling skin disorders a sequential, one-dimensional high-performance thin-layer chromatographic method (HPTLC) has been developed. All major human stratum corneum lipid classes, i.e., cholesterol sulfate, glucosylceramides, six major ceramide fractions, free sterols, free fatty acids, triglycerides, sterol esters, squalene, and n-alkanes, are separated and quantitated after a stepwise development of a single silica gel 60 HPTLC-plate using three consecutive solvent systems. Reproducible results have been obtained by degradative charring as well as fluorescence detection. By fluorescence detection the method is particularly suitable for the determination of minor amounts of cholesterol sulfate and other sterols.

Chromatography, High Pressure Liquid↗
PubMed1988

Analytical isoelectric focusing of apolipoprotein B of human plasma low-density lipoproteins in the presence of a nonionic and a zwitterionic detergent.

A method for the analytical isoelectric focusing of Nonidet-P40-delipidated apolipoprotein B of human plasma low-density lipoproteins has been developed. Isoelectric focusing was performed in the presence of the zwitterionic nondenaturing detergent Chaps, 3-[(3-cholamidopropyl)-dimethylammonio]-1-propane sulfonate, and the nonionic surfactant Nonidet-P40, polyoxyethyleneglycol p-t-octylphenol with a mean of 9.0 ethylene oxide units per molecule. Low-density lipoprotein (LDL) apolipoprotein B (apo-B) entered 3.75% polyacrylamide gels without precipitation at the sites of sample application, permitting apoprotein recoveries of greater than 90% in the migrating bands. LDL apo-B exhibited 10 distinguishable bands with apparent isoelectric points of 7.34 (band 1), 7.27 (band 2), 7.16 (band 3), 7.02 (band 4), 6.88 (band 5), 6.70 (band 6), 6.61 (band 7), 6.48 (band 8), 6.40 (band 9), and 6.24 (band 10), respectively. Bands 3 and 4, 6 and 7, as well as 8 and 9 could be identified as major double bands. When the focused apo-B was run in a second dimension by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the same relative molecular weight of B-100 was obtained for all focused bands. After electrotransfer to nitrocellulose paper, all bands reacted with polyclonal anti-human LDL antibody. Furthermore, the detergent-solubilized apo-B retained the immunological properties of native low-density lipoproteins when tested by double immunodiffusion against polyvalent anti-human LDL sera.

Apolipoproteins B↗
PubMed1987

Evaluation of the atherogenic risk of isotretinoin-induced and etretinate-induced alterations of lipoprotein cholesterol metabolism.

Inverse alterations in plasma levels of low-density lipoprotein cholesterol and high-density lipoprotein cholesterol are recognized side effects of systemic treatment with the synthetic retinoids isotretinoin and etretinate. The mass quotients of total plasma cholesterol and high-density lipoprotein cholesterol as well as low-density lipoprotein cholesterol and high-density lipoprotein cholesterol are well-established predictive risk factors of cardiovascular disease. We evaluated and compared these lipoprotein cholesterol ratios of 80 patients treated systemically with isotretinoin (13-cis-retinoic acid) and 81 patients treated with etretinate (aromatic retinoid). Lipoprotein cholesterol data were derived from 5 lipid studies on isotretinoin, including our own results, and 4 published lipid studies on etretinate. For all isotretinoin and etretinate lipid studies, significant increases in the mean plasma levels of total cholesterol and low-density lipoprotein cholesterol and significant decreases in the mean concentration of high-density lipoprotein cholesterol were demonstrated. In comparison with etretinate, oral isotretinoin gave rise to a nearly twofold percent increase of both lipoprotein cholesterol ratios from pretreatment levels. Furthermore, for isotretinoin, an approximately linear dose-related increase of the ratio of low-density lipoprotein cholesterol and high-density lipoprotein cholesterol could be observed. If sustained over long periods, the mean differential rise of the ratio of low-density lipoprotein cholesterol and high-density lipoprotein cholesterol of 0.92 +/- 0.51 for isotretinoin and 0.56 +/- 0.10 for etretinate indicates an increased risk of cardiovascular disease for both retinoids. Etretinate could be identified as the less harmful retinoid for prolonged oral therapy.

Arteriosclerosis↗