A Study on Community Participation in Implementing Neighborhood Upgrading and Shelter Sector Project in Kelurahan Pontap, Palopo

City’s population growth will highly influence the increase of housing needs because housing is one of the basic necessities besides cloths and food. Apparently, this becomes serious problem when it is related to poor urban residents who are impelled to build squatter area close to working area even though they have to live in crowded living space. It is on this area that the infrastructures availability is limited. The residents’ low socio-economic condition prompts it to be a slum area. For this reason, one concrete and comprehensive alternative solution to handle urban slum settlement area is Neighborhood Upgrading and Shelter Sector Project (NUSSP) program. NUSSP program at Palopo city is started on 2006 to 2008. This program uses community participatory approach as the target of the policy and program. The implementation of NUSSP program at Kelurahan Pontap is the construction of slum area infrastructure such as environment path, alley, sanitation and clean water. This research aims to study the community’s participation in implementing the slum area development program at Kelurahan Pontap, Palopo city. The target research are the identification of slum area development program, the characteristic of the community at Kelurahan Pontap, the analysis of community participation in the slum settlement development program and to conclude the relation between the program implementation and community participation. The analysis method used in this research is descriptive analysis using qualitative approach in a form of words, not numbers. This research uses random sampling for the respondents of Kelurahan Pontap whose houses are categorized as slum. The conclusions are obtained from the targets through the infrastructure construction such as the building of environment path, MCK (public bathing, washing and toilet facilities) building and drainage. The community participation to support the infrastructure building is by contributing themselves such as their involvement on the program/ project planning and implementation that are carried out by the local community. The community participation is carried out in each RW (neighborhood), that is RW 1, RW 2, RW 3 and RW 4 which is supported by the influencing factors such as active involvement in meetings, giving idea or suggestion and involved in decision making at the planning phase. While the implementation phase is influenced by skill and power factor, the monitoring phase is influenced by the result and benefit. The recommendation given for the community at Kelurahan Pontap, Palopo city are a socialization and workshop for the community at RW 1, RW 2, RW 3 and RW 4 about the importance of education; community involvement to democratically make a decision in RW 3 and RW 4; socialization in each RW upon the importance of healthy living; other programs supporting community participation in creating environment quality, community-based sanitation quality improvement and so on; community encouragement to involve at their improvement of healthy life-style; community encouragement to involve in community organization in increasing community participation to upgrade and improve environment quality

Quantification of anandamide content in animal cells and tissues: the normalization makes the difference

Anandamide (N-arachidonoylethanolamine, AEA) is an endogenous lipid that binds to cannabinoid receptors in the central nervous system and in peripheral cells. Quantitative analysis of AEA is generally based on the normalization to the fresh weight of the samples. Here, we show that the normalization procedure of AEA content is such a critical factor, that it might introduce per se significant discrepancies in the quantification of AEA even in the same sample. We suggest that a rapid, accurate and most reliable reference to quantify AEA and congeners from different sources is the protein content, a common parameter to cells and tissues

Anandamide uptake by synaptosomes from human, mouse and rat brain: inhibition by glutamine and glutamate

Anandamide (N-arachidonoylethanolamine, AEA) belongs to an emerging class of endogenous lipids, called "endocannabinoids". A specific AEA membrane transporter (AMT) allows the import of this lipid and its degradation by the intracellular enzyme AEA hydrolase. Here, we show that synaptosomes from human, mouse and rat brain might be an ideal ex vivo system for the study of: i) the accumulation of AEA in brain, and ii) the pharmacological properties of AMT inhibitors. Using this ex vivo system, we demonstrate for the first time that glutamine and glutamate act as non-competitive inhibitors of AEA uptake by human, mouse and rat brain AMT

Anandamide induces apoptosis in human cells via vanilloid receptors. Evidence for a protective role of cannabinoid receptors.

The endocannabinoid anandamide (AEA) is shown to induce apoptotic bodies formation and DNA fragmentation, hallmarks of programmed cell death, in human neuroblastoma CHP100 and lymphoma U937 cells. RNA and protein synthesis inhibitors like actinomycin D and cycloheximide reduced to one-fifth the number of apoptotic bodies induced by AEA, whereas the AEA transporter inhibitor AM404 or the AEA hydrolase inhibitor ATFMK significantly increased the number of dying cells. Furthermore, specific antagonists of cannabinoid or vanilloid receptors potentiated or inhibited cell death induced by AEA, respectively. Other endocannabinoids such as 2-arachidonoylglycerol, linoleoylethanolamide, oleoylethanolamide, and palmitoylethanolamide did not promote cell death under the same experimental conditions. The formation of apoptotic bodies induced by AEA was paralleled by increases in intracellular calcium (3-fold over the controls), mitochondrial uncoupling (6-fold), and cytochrome c release (3-fold). The intracellular calcium chelator EGTA-AM reduced the number of apoptotic bodies to 40% of the controls, and electrotransferred anti-cytochrome c monoclonal antibodies fully prevented apoptosis induced by AEA. Moreover, 5-lipoxygenase inhibitors 5,8,11,14-eicosatetraynoic acid and MK886, cyclooxygenase inhibitor indomethacin, caspase-3 and caspase-9 inhibitors Z-DEVD-FMK and Z-LEHD-FMK, but not nitric oxide synthase inhibitor Nomega-nitro-l-arginine methyl ester, significantly reduced the cell death-inducing effect of AEA. The data presented indicate a protective role of cannabinoid receptors against apoptosis induced by AEA via vanilloid receptors

Progesterone activates fatty acid amide hydrolase (FAAH) promoter in human T lymphocytes through the transcription factor Ikaros. Evidence for a synergistic effect of leptin.

Physiological concentrations of progesterone stimulate the activity of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) in human T lymphocytes, up to a ∼270% over the untreated controls. Stimulation of FAAH occurred through up-regulation of gene expression at transcriptional and translational level and was specific. Indeed, neither the activity of the anandamide-synthesizing N-acyltransferase and phospholipase D, nor the activity of the anandamide transporter, nor the binding to cannabinoid receptors were affected by progesterone under the same experimental conditions. The activation of FAAH by progesterone was paralleled by a decrease (down to 60%) of the cellular levels of anandamide and involved increased nuclear levels of the transcription factor Ikaros. Analysis of the FAAH promoter showed an Ikaros binding site, and mutation of this site prevented FAAH activation by progesterone in transient expression assays. Electrophoretic mobility shift and supershift assays further corroborated the promoter activity data. Furthermore, the effect of progesterone on FAAH promoter was additive to that of physiological amounts of leptin, which binds to a cAMP response element-like site in the promoter region. Taken together, these results suggest that progesterone and leptin, by up-regulating the FAAH promoter at different sites, enhance FAAH expression, thus tuning the immunomodulatory effects of anandamide. These findings might also have critical implications for human fertility

Dear Feminist Press

Letter from Woman\u27s Role Group of East Hill School, 116 N Quarry St., Ithaca, N.Y. 14850

Anandamide Uptake by Human Endothelial Cells and Its Regulation by Nitric Oxide

Anandamide (AEA) has vasodilator activity, which can be terminated by cellular re-uptake and degradation. Here we investigated the presence and regulation of the AEA transporter in human umbelical vein endothelial cells (HUVECs). HUVECs take up AEA by facilitated transport (apparent K(m) = 190 +/- 10 nm and V(max) = 45 +/- 3 pmol. min(-1).mg(-1) protein), which is inhibited by alpha-linolenoyl-vanillyl-amide and N-(4-hydroxyphenyl)-arachidonoylamide, and stimulated up to 2.2-fold by nitric oxide (NO) donors. The NO scavenger hydroxocobalamin abolishes the latter effect, which is instead enhanced by superoxide anions but inhibited by superoxide dismutase and N-acetylcysteine, a precursor of glutathione synthesis. Peroxynitrite (ONOO(-)) causes a 4-fold activation of AEA transport into cells. The HUVEC AEA transporter contributes to the termination of a typical type 1 cannabinoid receptor (CB(1)) -mediated action of AEA, i.e. the inhibition of forskolin-stimulated adenylyl cyclase, because NO/ONOO(-) donors and alpha-linolenoyl-vanillyl-amide/N-(4-hydroxyphenyl)-arachidonoylamide were found to attenuate and enhance, respectively, this effect of AEA. Consistently, activation of CB(1) cannabinoid receptors by either AEA or the cannabinoid HU-210 caused a stimulation of HUVEC inducible NO synthase activity and expression up to 2.9- and 2. 6-fold, respectively. Also these effects are regulated by the AEA transporter. HU-210 enhanced AEA uptake by HUVECs in a fashion sensitive to the NO synthase inhibitor Nomega-nitro-l-arginine methyl ester. These findings suggest a NO-mediated regulatory loop between CB(1) cannabinoid receptors and AEA transporter

The histone deacetylase inhibitor romidepsin synergizes with lenalidomide and enhances tumor cell death in T-cell lymphoma cell lines

We investigated the cytotoxic interactions of romidepsin, a histone deacetylase inhibitor, and lenalidomide, an immunomodulatory agent, in a T-cell lymphoma preclinical model. Hut-78 and Karpas-299 cells were treated with romidepsin and lenalidomide alone and in combination. The interaction between romidepsin and lenalidomide was evaluated by the Chou–Talalay method, and cell viability and clonogenicity were also evaluated. Apoptosis, reactive oxygen species (ROS) levels, and cell cycle distribution were determined by flow cytometry. ER stress, caspase activation, and the AKT, MAPK/ERK, and STAT-3 pathways were analyzed by Western blot. Combination treatment with romidepsin and lenalidomide had a synergistic effect in Hut-78 cells and an additive effect in Karpas-299 cells at 24 hours and did not decrease the viability of normal peripheral blood mononuclear cells. This drug combination induced apoptosis, increased ROS production, and activated caspase-8, −9, −3 and PARP. Apoptosis was associated with increased hallmarks of ER stress and activation of UPR sensors and was mediated by dephosphorylation of the AKT, MAPK/ERK, and STAT3 pathways.The combination of romidepsin and lenalidomide shows promise as a possible treatment for T-cell lymphoma. This work provides a basis for further studies

Digital storytelling per l’infanzia

Proponiamo il racconto di un’esperienza condotta da alcune classi di scuola dell’infanzia della provincia di Trento, durante l’anno scolastico 2019/2020, il primo della pandemia. L’attività di formazione e la relativa sperimentazione nelle classi si è incentrata sull’utilizzo di un particolare strumento digitale, l’i-Theatre, che consente l'effettuazione di percorsi di Media Education nella scuola dei piccoli. Il percorso ci ha permesso di avviare con i docenti una riflessione su questo tema, partendo dalla domanda di fondo se l’introduzione della tecnologia in questo ordine di scuola sia auspicabile