Evaluation of Social Impact of Traffic Noice in Amman, Jordan

Few road traffic studies were conducted in Jordan, but the issue is drawing an increasing attention due to its growing magnitude and various impacts as a result of the high increase in vehicular traffic. This study further investigates the issue with the aim of providing an understanding of its social impact on residents of Amman, the capital of Jordan. Traffic noise levels were measured at selected locations along urban arterials and a social survey was performed to examine the reactions and attitudes of the neighboring residents towards these levels of traffic noise. The survey included social characteristics of individuals, and their attitudes towards traffic noise, and how it impacted their daily activities. A predesigned questionnaire was used for this purpose which included questions to evaluate the awareness of respondents of the problem and its environmental and health impacts. The financial impact that residents perceive of noise and the need for attenuation measures were also addressed. The results of the study also revealed that the impact of traffic noise on people can cause annoyance while performing daily activities were 24% of respondents reported that they get annoyed by traffic while working, 49% while resting, 34% while talking to others, 31% while talking on the phone, 39% while reading, 38% while watching TV and 53% of respondents get annoyed while sleeping. The respondents have also pointed out the following effects of noise: twist in mood (53%), headache (36%), and difficulty in concentration (40%). About 57% of respondents think traffic noise reduces the value of their properties and a total of 31% are willing to sell their house at reduced cost. About 59% of respondents consider attenuation measures necessary, and in order to reduce the noise, about 54% of respondents were willing to pay for attenuation measures which reflects the public awareness of the issue magnitude

Eps15 and Dap160 control synaptic vesicle membrane retrieval and synapse development

Epidermal growth factor receptor pathway substrate clone 15 (Eps15) is a protein implicated in endocytosis, endosomal protein sorting, and cytoskeletal organization. Its role is, however, still unclear, because of reasons including limitations of dominant-negative experiments and apparent redundancy with other endocytic proteins. We generated Drosophila eps15-null mutants and show that Eps15 is required for proper synaptic bouton development and normal levels of synaptic vesicle (SV) endocytosis. Consistent with a role in SV endocytosis, Eps15 moves from the center of synaptic boutons to the periphery in response to synaptic activity. The endocytic protein, Dap160/intersectin, is a major binding partner of Eps15, and eps15 mutants phenotypically resemble dap160 mutants. Analyses of eps15 dap160 double mutants suggest that Eps15 functions in concert with Dap160 during SV endocytosis. Based on these data, we hypothesize that Eps15 and Dap160 promote the efficiency of endocytosis from the plasma membrane by maintaining high concentrations of multiple endocytic proteins, including dynamin, at synapses

The novel endosomal membrane protein Ema interacts with the class C Vps–HOPS complex to promote endosomal maturation

Defective attenuation of BMP signaling causes synapses to overgrow in Drosophila Ema mutants due to impaired endosomal maturation

Tricornered Kinase Regulates Synapse Development by Regulating the Levels of Wiskott-Aldrich Syndrome Protein

<div><p>Precise regulation of synapses during development is essential to ensure accurate neural connectivity and function of nervous system. Many signaling pathways, including the mTOR (mechanical Target of Rapamycin) pathway operate in neurons to maintain genetically determined number of synapses during development. mTOR, a kinase, is shared between two functionally distinct multi-protein complexes- mTORC1 and mTORC2, that act downstream of Tuberous Sclerosis Complex (TSC). We and others have suggested an important role for TSC in synapse development at the <i>Drosophila</i> neuromuscular junction (NMJ) synapses. In addition, our data suggested that the regulation of the NMJ synapse numbers in <i>Drosophila</i> largely depends on signaling via mTORC2. In the present study, we further this observation by identifying Tricornered (Trc) kinase, a serine/threonine kinase as a likely mediator of TSC signaling. trc genetically interacts with Tsc2 to regulate the number of synapses. In addition, Tsc2 and trc mutants exhibit a dramatic reduction in synaptic levels of WASP, an important regulator of actin polymerization. We show that Trc regulates the WASP levels largely, by regulating the transcription of WASP. Finally, we show that overexpression of WASP (Wiskott-Aldrich Syndrome Protein) in trc mutants can suppress the increase in the number of synapses observed in trc mutants, suggesting that WASP regulates synapses downstream of Trc. Thus, our data provide a novel insight into how Trc may regulate the genetic program that controls the number of synapses during development.</p></div

Presynaptic, but not postsynaptic, overexpression of <i>wasp</i> rescues the increase in synaptic boutons observed in <i>trc</i>^<i>1</i> mutants and <i>trc</i>^<i>1</i>/Tsc2 transheterozygotes.

<p><b>A)</b> Representative confocal images of the wild type (WT), <i>trc</i>^<i>1</i> mutants and <i>trc</i>^<i>1</i> mutants overexpressing WASP either presynaptically (presyn <i>wsp</i>^OE) using BG380.Gal4 or postsynaptically (postsyn <i>wsp</i>^OE) using G7.Gal4 driver. <b>B</b>. Quantification of genotypes in A followed by One-way ANOVA plus Tukey post-hoc test. ***p<0.001 and n.s = not significant. <b>C</b>. Representative confocal images of the wild type (WT), <i>Tsc2</i>/<i>trc</i>^<i>1</i> transheterozygotes and <i>Tsc2</i>/<i>trc</i>^<i>1</i> transheterozygotes overexpressing UAS-<i>wasp</i> transgene either presynaptically (presyn <i>wasp</i>^OE; <i>Tsc2/trc</i>^<i>1</i>) when crossed to BG380.Gal4 driver or postsynaptically (postsyn <i>wasp</i>^OE) using G7.Gal4 driver, stained by anti-HRP antibody. <b>D</b>. Quantification of bouton numbers of genotypes in C. One-way ANOVA followed by Tukey’s post-hoc test was performed. ***p<0.001 and n.s indicates “not significant”.</p

Reduction in presynaptic but not postsynaptic, Trc kinase decreases synaptic WASP levels.

<p><b>A.</b> Representative confocal images of wild type (WT), presynaptically expressed <i>trc</i>^<i>RNAi</i> (<i>trc</i>^<i>RNAi</i> x BG380.Gal4) and postsynaptically expressed <i>trc</i>^<i>RNAi</i> (<i>trc</i>^<i>RNAi</i> x G7.Gal4) stained with anti-HRP and anti-WASP antibodies. <b>B</b>. Quantification of synaptic WASP levels in genotypes in A. n>10. One-way ANOVA plus Tukey post-hoc analysis was performed. ***p<0.001, n.s = not significant.</p

<i>trc</i> interacts genetically with <i>Tsc2</i>, <i>rictor</i> and <i>Akt1</i> to restrict the number of synaptic boutons.

<p><b>A.</b> Representative confocal images of muscle 4 NMJ synapses of heterozygotes of <i>trc</i>^<i>1</i>, <i>Tsc2</i>, <i>rictor</i>^<i>Δ42</i>, <i>Akt1</i> marked as <i>trc</i>¹/+, <i>gig</i>¹⁰⁹/+, <i>ric</i>^Δ42/+ and <i>Akt1</i>/+ respectively and transheterozygotes of <i>trc</i>^<i>1</i> with <i>Tsc2</i> (<i>gig</i>¹⁰⁹/<i>trc</i>¹), rictor (<i>ric</i>^∇42/<i>trc</i>¹) and Akt (<i>Akt1</i>/<i>trc</i>¹), stained with anti-HRP antibody. <b>B</b>) Quantification of synaptic bouton numbers from genotypes in A. n>10, One-way ANOVA followed by Tukey post-hoc test was performed. **p<0.01, ***p<0.001. Error bars represent S.E.M.</p

Schematic model of how Trc may regulate synapse development at <i>Drosophila</i> NMJ.

<p>Based on our data, Trc likely acts downstream of mTORC2 in the presynaptic compartment to regulate synaptic WASP, largely by regulating the transcription of WASP. Since WASP is known to regulate the polymerization of actin, we hypothesize that Trc ultimately regulates the actin cytoskeleton to regulate synapse development at the Drosophila NMJ synapses.</p

Synaptic WASP levels are reduced in <i>trc</i> and <i>Tsc2</i> mutant synaptic boutons.

<p><b>A</b>. Representative confocal images of wild type (WT) and <i>trc</i> mutant synapses (<i>trc</i>^<i>1</i>) stained with anti-HRP, anti-Discs-large (Dlg) and anti-WASP antibodies. <b>B</b>. Quantification of total synaptic WASP levels in WT, <i>trc</i>^<i>1</i> mutants and transheterozygote of <i>trc</i>^<i>1</i> crossed to an independent deficiency line that deletes the entire <i>trc</i> gene (<i>trc</i>^<i>1</i>/<i>trc</i>^<i>Df</i>). <b>C</b>. Representative confocal images showing NMJ synapses of wild type (WT) and <i>Tsc2</i> mutants and <i>Akt1</i> mutants stained with antibodies against DGluRIII and WASP. <b>D</b>. Quantification of the synaptic WASP levels measured in genotypes described in C. <b>E</b>. Quantification of the synaptic WASP levels in WT (CS), heterozygotes of <i>Tsc2</i> and <i>trc</i>^<i>1</i> (<i>Tsc2/+</i>, <i>trc1/+</i>) and in their respective transheterozygotes (<i>Tsc2/trc1</i>). One-Way ANOVA followed by Tukey’s post-hoc test was performed. *p<0.01, **p<0.001, ***p<0.0001. Error bars represent S.E.M. <b>F</b>. Representative gel showing <i>wasp</i> transcripts from ventral nerve cords (VNC) and muscles of WT and <i>trc</i>¹ mutants. Ribosomal protein 49 (RP49) is used as a control.</p