Search Results - (Author, Cooperation:D. Wegmann)

2018-07-18

The American Society for Microbiology (ASM)

0022-538X

1098-5514

Medicine

2012-05-19

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Computer Science

Medicine

Natural Sciences in General

Physics

African Americans/genetics ; Asian Continental Ancestry Group ; Disease/*genetics ; European Continental Ancestry Group/genetics ; Gene Frequency ; Genetic Association Studies ; Genetic Predisposition to Disease ; *Genetic Variation ; *Genome, Human ; Geography ; High-Throughput Nucleotide Sequencing ; Humans ; Molecular Targeted Therapy ; Multifactorial Inheritance ; Mutation Rate ; Pharmacogenetics ; Phenotype ; Polymorphism, Single Nucleotide ; Population Growth ; Sample Size ; Selection, Genetic

2018-06-01

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Geosciences

Computer Science

Medicine

Natural Sciences in General

Physics

Anthropology

0003-2670

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Chemistry and Pharmacology

Electronic Resource

0029-554X

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Energy, Environment Protection, Nuclear Power Engineering

Physics

Electronic Resource

1436-5073

Springer Online Journal Archives 1860-2000

Chemistry and Pharmacology

Zusammenfassung Eine Reihe von 15 anionenselektiven Membranen, beruhend auf unterschiedlichen quaternären Ammoniumionen und auf verschiedenen Weichmachern, führt auch bei voneinander abweichenden Membranzusammensetzungen durchwegs zur Selektivitätssequenz: $$ClO_4 - 〉 SCN - 〉 I - 〉 NO_3 - 〉 Br - 〉 Cl - 〉 HCO_3 - \sim OAc - \sim SO_4 ^2 - \sim HPO_4 ^2 - .$$ . Eine umfassende Analyse zeigt, daß das Selektivitätsmuster solcher Systeme nur dann grundlegend verändert werden kann, wenn a) mobile, positiv geladene Austauschzentren mit hinreichend starker, spezifischer Wechselwirkung mit Anionen eingesetzt werden und/oder b) elektrisch neutrale anionenselektive Membrankomponenten gewählt werden.

Summary A series of 15 anion-selective membranes, based on quaternary ammonium compounds of different constitution and on a variety of plasticizers in different compositions of the solvent polymeric membranes, lead throughout to the selectivity sequence $$ClO_4 - 〉 SCN - 〉 I - 〉 NO_3 - 〉 Br - 〉 Cl - 〉 HCO_3 - \sim OAc - \sim SO_4 ^2 - \sim HPO_4 ^2 - .$$ . A detailed analysis demonstrates that the selectivity pattern of such systems may be drastically modified only if a) a mobile, positively charged site with a sufficiently strong and specific interaction with anions is chosen and/or b) an electrically neutral anion-selective membrane component is used.

Electronic Resource

1432-0428

Keywords Autoreactivity ; autoimmunity ; human T-cells ; GAD65 ; GAD autoantibodies ; insulin-dependent diabetes ; molecular mimicry.

Springer Online Journal Archives 1860-2000

Medicine

Summary GAD65 is one of the major autoantigens associated with insulin-dependent diabetes mellitus (IDDM). The two peptides p17 and p18 of GAD65 that share sequence similarity with coxsackie virus (amino acid sequence identity: PEVKEK) appeared to be the major determinants of GAD65 recognized preferably by T cells from new-onset IDDM patients and their first degree relatives. In contrast, in our study unrelated control subjects frequently recognized the two GAD peptides (55 %, 16/29), similar to first degree relatives (41 %, 12/29) and IDDM patients post-onset (68 %, 15/22). However, recent-onset IDDM patients, responded less frequently (25 %, 4/16) compared with IDDM patients post-onset (p 〈 0.03) or unrelated control subjects (borderline significant) confirming previous observations in humans and NOD mice that T-cell reactivity to GADp17/p18 at diabetes onset is decreased. Moreover, this study demonstrated a positive correlation of T-cell proliferation to GAD p17 (amino acid 247–266) and p18 (amino acid 260–279) with simultaneous responses to both peptides in 13 % of all subjects tested (n = 97) (p 〈 0.001). T-cell proliferation to GAD p17 was higher than to p18 in recent-onset diabetic patients, first degree relatives and unrelated control subjects (p 〈 0.02, p 〈 0.004, p 〈 0.002, respectively). However, in post-onset IDDM patients, the two peptides were recognized equally well. Our results show that T-cell reactivity to GAD65 peptides homologous with coxsackie protein is very frequently observed, but not primarily associated with IDDM. The temporary decline of T-cell proliferation is not associated with the beta-cell destruction process, but with clinical manifestation. The positive correlation of reactivity to the two peptides in the viral motif implicates that PEVKEK is an immunogenic epitope. [Diabetologia (1997) 40: 332–338]

Electronic Resource

1432-0428

Keywords Insulin ; autoantibodies ; autoreactivity ; T-lymphocytes ; insulin-dependent diabetes mellitus.

Springer Online Journal Archives 1860-2000

Medicine

Summary Insulin-dependent diabetes mellitus (IDDM) is the result of a T-cell mediated autoimmune beta-cell destruction,which is accompanied by autoantibodies. We analysed the cellular and humoral immune response to insulin and insulin peptides in patients with recent-onset IDDM, IDDM patients treated with insulin, non-diabetic first degree relatives and unrelated control subjects. There were no differences in T-cell reactivity to whole insulin or insulin peptides in general between age-matched groups of IDDM patients, relatives or healthy control subjects. In contrast to investigations in NOD mice, no immunodominant or disease-specific insulin peptide could be identified. Surprisingly, a positive correlation of T-cell responses to insulin with age was noted (p 〈 0.005). This resulted in an inverse relation of insulin autoantibodies (IAA) and insulin reactive T-cells (p 〈 0.001) together with the well-described negative correlation of IAA with age. Interestingly, insulin-treated patients differed from age-matched recent-onset IDDM patients: first, simultaneous immune recognition of insulin with T-cells and IAA was only seen in patients treated for 6 months with insulin; second, insulin-treated patients rarely responded to whole insulin; third, they displayed less determinant spreading, and finally, recognition of multiple insulin peptides was not accompanied by crossreactivity to whole insulin. These distinct observations in insulin-treated IDDM patients, together with the inverse correlation between humoral and cellular responses to insulin, may result from activation or modulation of different T-cell subsets, and may be of relevance to insulin therapy trials, in which selective activation of non-destructive T-cell subsets may be a key to successful intervention. [Diabetologia (1997) 40: 564–572]

Electronic Resource