CSR-Handbuch : ein Ratgeber

Aus dem Projekt "Förderung angehender weiblicher Führungskräfte in kleinen und mittleren Unternehmen als CSR-Maßnahme"; ein Projekt der Hochschule Bonn-Rhein-Sieg im Rahmen des Programms "CSR-Gesellschaftliche Verantwortung im Mittelstand" gefördert durch das Bundesministerium für Arbeit und Soziales und durch den Europäischen Sozialfonds

Lack of experts as an ideal introduction to CSR

The Federal Ministry of Labour and Social Affairs (Bundesministerium für Arbeit und Soziales, BMA) is supporting 73 projects in Germany using European Union (EU) funds in the amount of € 26 million. By providing the subsidies, the European Commission and the German Federal Government are hoping to implement Corporate Social Responsibility (CSR) among German small and medium-sized businesses (SMBs). The project run by Bonn-Rhein-Sieg University is one of these CSR projects. It is aimed at providing comprehensive information on CSR to the businesses in question and at emphasizing their responsibility along the supply chain

Generation and characterization of mice with null mutation of the chloride intracellular channel 1 gene

Summary: CLIC1 belongs to a family of highly conserved and widely expressed intracellular chloride ion channel proteins existing in both soluble and membrane integrated forms. To study the physiological and biological role of CLIC1 in vivo, we undertook conditional gene targeting to engineer Clic1 gene knock-out mice. This represents creation of the first gene knock-out of a vertebrate CLIC protein family member. We first generated a Clic1 Knock-in (Clic1FN) allele, followed by Clic1 knockout (Clic1-/-) mice by crossing Clic1FN allele with TNAPcre mice, resulting in germline gene deletion through Cre-mediated recombination. Mice heterozygous or homozygous for these alleles are viable and fertile and appear normal. However, Clic1-/- mice show a mild platelet dysfunction characterized by prolonged bleeding times and decreased platelet activation in response to adenosine diphosphate stimulation linked to P2Y12 receptor signaling

Generation and characterization of mice with null mutation of the chloride intracellular channel 1 gene

CLIC1 belongs to a family of highly conserved and widely expressed intracellular chloride ion channel proteins existing in both soluble and membrane integrated forms. To study the physiological and biological role of CLIC1 in vivo, we undertook conditional gene targeting to engineer Clic1 gene knock-out mice. This represents creation of the first gene knock-out of a vertebrate CLIC protein family member. We first generated a Clic1 Knock-in (Clic1FN) allele, followed by Clic1 knock-out (Clic1−/−) mice by crossing Clic1FN allele with TNAP-cre mice, resulting in germline gene deletion through Cre-mediated recombination. Mice heterozygous or homozygous for these alleles are viable and fertile and appear normal. However, Clic1−/− mice show a mild platelet dysfunction characterized by prolonged bleeding times and decreased platelet activation in response to adenosine diphosphate stimulation linked to P2Y₁₂ receptor signaling.10 page(s