Modern Social Welfare in the Light of the Sustainability Model

The paper presents the analysis of interaction between the social welfare and sustainable development. The aim of this paper is to show that the social development mostly depends on community values that form the pathway of the social movement. It is shown that mankind can influence the future choosing the optimum way of its development. Therefore, it is necessary to appreciate personal aspects of sociogenesis and a mechanism of its functioning, differences between social and natural dynamics. From the authors’ viewpoint, a philosophical understanding of sustainability by means of welfare as a regulation mechanism, is one of approaches to the study of social life and social development. A model of socio-practical man's existence mostly oriented towards satisfaction of needs helps to analyze the relationship between the categories under review. The more so as an ordinary intake of consumer amenities transforms to the instrument of construction od social identity, the sociocultural integration of individual with society. Social welfare is presented as a multiple-factor construct represented by a synthesis of cause and effect. Explication technique, hermeneutical approach, and comparison study are used to clarify basic notions of this research

Klonierung und funktionelle Charakterisierung des 'long transient receptor channel 2', LTRPC2, einem Mitglied der Familie kalziumpermeabler TRP-Kationenkanäle

It has been proposed that transient receptor potential channels (TRP-channels) participate in ligand gated Ca^(2+) entry in non-excitable cells. To analyze the physiological relevance of TRP-channels human neutrophile granulocyte were chosen as a model for non-excitable cells. The activation of neutrophiles is accompanied by membrane depolarisation and by a rise of the [Ca^(2+)]i. Until now the identity of the proteins which initiate the activation of neutrophile granulocytes is not known. Among the TRP-channels, the LTRPC2 is predominantly expressed by neutrophile granulocytes. To investigate the relevance of LTRPC2 for the function of neutrophile granulocytes, LTRPC2 was cloned by the RT-PCR technique and was then heterologously transfected in CHO- and in HEK 293 cells for functional characterisation. Two splice variants of the LTRPC2 were identified in human neutrophile granulocytes. These splice forms were used to construct four alternative variants with deletions at the N-terminal and/or C-terminal domain (LTRPC2; LTRPC2-deltaC; LTRPC2-deltaN; LTRPC2-deltaN-deltaC) using an appropriate cloning strategy. Fluorometric measurments of the [Ca^(2+)]i and measurment of ionic currents of heterologously transfected cells with patch clamp revealed no activation of the LTRPC2 variants in dependence of an intracellular Ca^(2+) store depletion. This stands in contrast to the classical TRP-proteins. Since NAD^(+) and its metabolite ADP-ribose have recently been reported to activate LTRPC2, I analysed the response of LTRPC2 variants to NAD^(+) and ADP-ribose. Whereas no activation by NAD^(+) was observed in any LTRPC2 variant, ADP-ribose exerted a stimulating effect exclusively on the full-lenght LTRPC2. Since ADP-ribose can be formed from NAD^(+), and NAD^(+) is elevated during oxidative stress, it was tested wether the various LTRPC2 channel variants mediate cation influx in response to an oxidant. Therefore ion currents and the [Ca^(2+)]i were measured after stimulating transfected cells with H2O2 as a model of oxidative stress. A stimulation with H2O2 could be observed in cells transfected with full-length LTRPC2 or transfected with the variant LTRPC2-deltaC. Thus the activation of LTRPC2 by H2O2 is independent of ADP-ribose because the splice variant LTRPC2-deltaC was exclusively activated by H2O2, while full-length LTRPC2 could be activated by ADP-ribose as well. Since intracellular application of the antioxidant mannitol prevented a stimulation of LTRPC2 and LTRPC2-deltaC by H2O2, it can be concluded that H2O2 does not act directly on the channel but by intracellular oxidation reactions. It is possible that the activation of LTRPC2 plays a role for the stimulation of neutrophile granulocytes during inflammation, when neutrophiles become activated by H2O2

Klonierung und funktionelle Charakterisierung des 'long transient receptor channel 2', LTRPC2, einem Mitglied der Familie kalziumpermeabler TRP-Kationenkanäle

It has been proposed that transient receptor potential channels (TRP-channels) participate in ligand gated Ca^(2+) entry in non-excitable cells. To analyze the physiological relevance of TRP-channels human neutrophile granulocyte were chosen as a model for non-excitable cells. The activation of neutrophiles is accompanied by membrane depolarisation and by a rise of the [Ca^(2+)]i. Until now the identity of the proteins which initiate the activation of neutrophile granulocytes is not known. Among the TRP-channels, the LTRPC2 is predominantly expressed by neutrophile granulocytes. To investigate the relevance of LTRPC2 for the function of neutrophile granulocytes, LTRPC2 was cloned by the RT-PCR technique and was then heterologously transfected in CHO- and in HEK 293 cells for functional characterisation. Two splice variants of the LTRPC2 were identified in human neutrophile granulocytes. These splice forms were used to construct four alternative variants with deletions at the N-terminal and/or C-terminal domain (LTRPC2; LTRPC2-deltaC; LTRPC2-deltaN; LTRPC2-deltaN-deltaC) using an appropriate cloning strategy. Fluorometric measurments of the [Ca^(2+)]i and measurment of ionic currents of heterologously transfected cells with patch clamp revealed no activation of the LTRPC2 variants in dependence of an intracellular Ca^(2+) store depletion. This stands in contrast to the classical TRP-proteins. Since NAD^(+) and its metabolite ADP-ribose have recently been reported to activate LTRPC2, I analysed the response of LTRPC2 variants to NAD^(+) and ADP-ribose. Whereas no activation by NAD^(+) was observed in any LTRPC2 variant, ADP-ribose exerted a stimulating effect exclusively on the full-lenght LTRPC2. Since ADP-ribose can be formed from NAD^(+), and NAD^(+) is elevated during oxidative stress, it was tested wether the various LTRPC2 channel variants mediate cation influx in response to an oxidant. Therefore ion currents and the [Ca^(2+)]i were measured after stimulating transfected cells with H2O2 as a model of oxidative stress. A stimulation with H2O2 could be observed in cells transfected with full-length LTRPC2 or transfected with the variant LTRPC2-deltaC. Thus the activation of LTRPC2 by H2O2 is independent of ADP-ribose because the splice variant LTRPC2-deltaC was exclusively activated by H2O2, while full-length LTRPC2 could be activated by ADP-ribose as well. Since intracellular application of the antioxidant mannitol prevented a stimulation of LTRPC2 and LTRPC2-deltaC by H2O2, it can be concluded that H2O2 does not act directly on the channel but by intracellular oxidation reactions. It is possible that the activation of LTRPC2 plays a role for the stimulation of neutrophile granulocytes during inflammation, when neutrophiles become activated by H2O2

Expression profile of the transient receptor potential (TRP) family in neutrophil granulocytes: evidence for currents through long TRP channel 2 induced by ADP-ribose and NAD

An early key event in the activation of neutrophil granulocytes is Ca(2+) influx. Members of the transient receptor potential (TRP) channel family may be held responsible for this. The aim of the present study is to analyse the expression pattern of TRP mRNA and identify characteristic currents unambiguously attributable to particular TRP channels. mRNA was extracted from human neutrophils, isolated by gradient centrifugation and also by magnetically labelled CD15 antibodies. The presence of mRNA was demonstrated using reverse transcriptase-PCR in neutrophils (controlled to be CD5-negative) as well as in human leukaemic cell line 60 (HL-60) cells, for the following TRP species: the long TRPC2 (LTRPC2), the vanilloid receptor 1, the vanilloid receptor-like protein 1 and epithelial Ca(2+) channels 1 and 2. TRPC6 was specific for neutrophils, whereas only in HL-60 cells were TRPC1, TRPC2, TRPC3, melastatin 1 and melastatin-related 1 found. Patch-clamp measurements in neutrophils revealed non-selective cation currents evoked by intracellular ADP-ribose and by NAD(+). Both these modes of activation have been found to be characteristic of LTRPC2. Furthermore, single-channel activity was resolved in neutrophils and it was indistinguishable from that in LTRPC2-transfected HEK-293 cells. The results provide evidence that LTRPC2 in neutrophil granulocytes forms an entry pathway for Na(+) and Ca(2+), which is regulated by ADP-ribose and the redox state