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Senato: Palazzo Madama aperto al pubblico per la Festa del Lavoro.

Venerdì 28 4 2017

Lunedì 1° maggio, Festa del Lavoro, e sabato 6 maggio, in occasione dell’iniziativa “Open House Roma”, il Senato della Repubblica apre le porte ai visitatori.
Ecco il quadro completo delle aperture dal 28 aprile al 6 maggio:

Venerdì 28 e sabato 29 aprile, lunedì 1° maggio e venerdì 5 maggio sarà possibile visitare Palazzo Madama e la mostra “Libri che hanno fatto l’Europa. Governo dell’economia e democrazia dal XV al XX secolo”, allestita in Sala Koch. La mostra è stata realizzata in occasione del 60° anniversario della firma dei Trattati di Roma e propone una selezione di 140 prime e rare edizioni, dal 1468 al 1950, di opere dei padri del pensiero economico, giuridico e politico europeo.
Le visite, gratuite e della durata di circa 40 minuti, sono curate da personale del Senato, che illustra i principali aspetti storici, artistici e istituzionali delle sale di rappresentanza e dei luoghi più suggestivi di Palazzo Madama. L’orario di accesso è dalle ore 10 alle ore 18 (ultimo ingresso alle ore 17.30). E’ necessario ritirare un biglietto di accesso presentandosi presso l’ingresso di Piazza Madama n. 11 il giorno stesso dell’apertura al pubblico, dalle ore 8.30 in poi. Ciascun visitatore potrà richiedere, fino a esaurimento, un massimo di quattro biglietti se adulto e un biglietto se minorenne, scegliendo un orario compreso tra le 10 e le 18, con intervalli di trenta minuti.
Lungo il percorso di visita, è possibile ammirare l’unico calco esistente a grandezza naturale del “Torso del Belvedere”. L’opera originale, attribuita allo scultore ateniese Apollonios e risalente al I secolo a.C., fa parte delle collezioni di scultura classica dei Musei Vaticani, ed è stata esposta in Senato, in via del tutto eccezionale, dal 18 al 26 marzo.

Sabato 6 maggio, in occasione di “Open House Roma”, sarà possibile visitare Palazzo Madama e Palazzo Giustiniani. I biglietti d’ingresso ai Palazzi sono gratuiti e potranno essere ritirati presso le portinerie, in Piazza Madama 11 e in Via della Dogana Vecchia 29, a partire dalle ore 8,30. Per Palazzo Giustiniani ciascun visitatore potrà richiedere, fino ad esaurimento, un massimo di due biglietti se adulto e un biglietto se minorenne, scegliendo un orario compreso tra le 10.00 e le 18.00, con intervalli di trenta minuti.

Tratto da www.senato.it.
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Structural diversity of <i>Burkholderia pseudomallei</i> lipopolysaccharides affects innate immune signaling

by Michael H. Norris, Herbert P. Schweizer, Apichai Tuanyok

Burkholderia pseudomallei (Bp) causes the disease melioidosis. The main cause of mortality in this disease is septic shock triggered by the host responding to lipopolysaccharide (LPS) components of the Gram-negative outer membrane. Bp LPS is thought to be a weak inducer of the host immune system. LPS from several strains of Bp were purified and their ability to induce the inflammatory mediators TNF-α and iNOS in murine macrophages at low concentrations was investigated. Innate and adaptive immunity qPCR arrays were used to profile expression patterns of 84 gene targets in response to the different LPS types. Additional qPCR validation confirmed large differences in macrophage response. LPS from a high-virulence serotype B strain 576a and a virulent rough central nervous system tropic strain MSHR435 greatly induced the innate immune response indicating that the immunopathogenesis of these strains is different than in infections with strains similar to the prototype strain 1026b. The accumulation of autophagic vesicles was also increased in macrophages challenged with highly immunogenic Bp LPS. Gene induction and concomitant cytokine secretion profiles of human PBMCs in response to the various LPS were also investigated. MALDI-TOF/TOF was used to probe the lipid A portions of the LPS, indicating substantial structural differences that likely play a role in host response to LPS. These findings add to the evolving knowledge of host-response to bacterial LPS, which can be used to better understand septic shock in melioidosis patients and in the rational design of vaccines.
Tratto da: www.plos.org.
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Risk factors and outcome of <i>Shigella</i> encephalopathy in Bangladeshi children

by Farzana Afroze, Tahmeed Ahmed, Monira Sarmin, Abu SMSB Shahid, K. M. Shahunja, Lubaba Shahrin, Mohammod Jobayer Chisti

Background

Although, Shigella encephalopathy, a serious extra-intestinal complication of shigellosis, significantly increases the risks of death, data are very limited on predicting factors particularly related to electrolyte profiles in children below five years of age with Shigella encephalopathy. Our objective was to determine the clinical as well as laboratory predicting factors and outcome of children with Shigella encephalopathy.

Methodology/Principal findings

In this unmatched case-control design, children aged 2–59 months having a positive stool culture for Shigella and who had their serum electrolytes been done from July 2012 to June 2015 were studied. Children with Shigella encephalopathy, defined as having abnormal mentation, constituted the cases, and those without encephalopathy constituted the controls. During the study period, we identified a total of 541 children less than five years of age, who had Shigella in their stool culture. Only 139 children fulfilled the study criteria and among them 69 were cases and 70 were controls. The cases more often had fatal outcome compared to the controls (7% vs. 0%, P = 0.02). In logistic regression analysis, the cases were independently associated with shorter duration (1.2 ± 0.4 days) of diarrhea prior to admission, dehydrating diarrhea, sepsis and hyponatremia (p<0.05 for all). Among 139 Shigella isolates, S. flexneri (88/139, 63%) and S. sonnei(34/139, 24%) were the dominant species. S. dysenteriae was not isolated throughout the study period. S.sonnei was more frequently isolated from the cases (24/69, 35%) than the controls (10/70, 14%), whereas the isolation of S. flexneri was comparable between the groups (40/69, 58% vs 48/70, 69%). A total of 94 (67.6%) isolates were resistant to trimethoprim-sulphamethoxazole, 84 (60.4%) to ciprofloxacin, 66/138 (48%) to ampicillin, 5 (3.5%) to ceftriaxone, 17 (12.2%) to mecillinum and 35 (25%) to azithromycin.

Conclusions/Significance

The case-fatality-rate was significantly higher among the children with Shigella encephalopathy compared to those without encephalopathy. Early identification and aggressive management of simple risk factors for Shigella encephalopathy may help to reduce morbidity and deaths in such children especially in resource-limited settings.


Tratto da: www.plos.org.
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Genetic diversity and population structure of the tsetse fly <i>Glossina fuscipes fuscipes</i> (Diptera: Glossinidae) in Northern Uganda: Implications for vector control

by Robert Opiro, Norah P. Saarman, Richard Echodu, Elizabeth A. Opiyo, Kirstin Dion, Alexis Halyard, Augustine W. Dunn, Serap Aksoy, Adalgisa Caccone

Uganda is the only country where the chronic and acute forms of human African Trypanosomiasis (HAT) or sleeping sickness both occur and are separated by < 100 km in areas north of Lake Kyoga. In Uganda, Glossina fuscipes fuscipes is the main vector of the Trypanosoma parasites responsible for these diseases as well for the animal African Trypanosomiasis (AAT), or Nagana. We used highly polymorphic microsatellite loci and a mitochondrial DNA (mtDNA) marker to provide fine scale spatial resolution of genetic structure of G. f. fuscipes from 42 sampling sites from the northern region of Uganda where a merger of the two disease belts is feared. Based on microsatellite analyses, we found that G. f. fuscipes in northern Uganda are structured into three distinct genetic clusters with varying degrees of interconnectivity among them. Based on genetic assignment and spatial location, we grouped the sampling sites into four genetic units corresponding to northwestern Uganda in the Albert Nile drainage, northeastern Uganda in the Lake Kyoga drainage, western Uganda in the Victoria Nile drainage, and a transition zone between the two northern genetic clusters characterized by high level of genetic admixture. An analysis using HYBRIDLAB supported a hybrid swarm model as most consistent with tsetse genotypes in these admixed samples. Results of mtDNA analyses revealed the presence of 30 haplotypes representing three main haplogroups, whose location broadly overlaps with the microsatellite defined clusters. Migration analyses based on microsatellites point to moderate migration among the northern units located in the Albert Nile, Achwa River, Okole River, and Lake Kyoga drainages, but not between the northern units and the Victoria Nile drainage in the west. Effective population size estimates were variable with low to moderate sizes in most populations and with evidence of recent population bottlenecks, especially in the northeast unit of the Lake Kyoga drainage. Our microsatellite and mtDNA based analyses indicate that G. f. fuscipes movement along the Achwa and Okole rivers may facilitate northwest expansion of the Rhodesiense disease belt in Uganda. We identified tsetse migration corridors and recommend a rolling carpet approach from south of Lake Kyoga northward to minimize disease dispersal and prevent vector re-colonization. Additionally, our findings highlight the need for continuing tsetse monitoring efforts during and after control.
Tratto da: www.plos.org.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution (CC BY) license.

Gut Check: The evolution of an educational board game

by David A. Coil, Cassandra L. Ettinger, Jonathan A. Eisen

The “gamification” of science has gained a lot of traction in recent years, and games that convey scientific concepts or themes are increasingly popular. While a number of existing games touch on microbiology, very few consider the beneficial (as opposed to the detrimental) aspects of microbes. We designed a board game called “Gut Check: The Microbiome Game” to fill this gap. The game is meant to be both educational as well as challenging and fun. Here we discuss the development of the game, some of the logistics of game development in this context, and offer suggestions for others thinking of similar projects.
Tratto da: www.plos.org.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution (CC BY) license.

The mismatch repair and meiotic recombination endonuclease Mlh1-Mlh3 is activated by polymer formation and can cleave DNA substrates in trans

by Carol M. Manhart, Xiaodan Ni, Martin A. White, Joaquin Ortega, Jennifer A. Surtees, Eric Alani

Crossing over between homologs is initiated in meiotic prophase by the formation of DNA double-strand breaks that occur throughout the genome. In the major interference-responsive crossover pathway in baker’s yeast, these breaks are resected to form 3′ single-strand tails that participate in a homology search, ultimately forming double Holliday junctions (dHJs) that primarily include both homologs. These dHJs are resolved by endonuclease activity to form exclusively crossovers, which are critical for proper homolog segregation in Meiosis I. Recent genetic, biochemical, and molecular studies in yeast are consistent with the hypothesis of Mlh1-Mlh3 DNA mismatch repair complex acting as the major endonuclease activity that resolves dHJs into crossovers. However, the mechanism by which the Mlh1-Mlh3 endonuclease is activated is unknown. Here, we provide evidence that Mlh1-Mlh3 does not behave like a structure-specific endonuclease but forms polymers required to generate nicks in DNA. This conclusion is supported by DNA binding studies performed with different-sized substrates that contain or lack polymerization barriers and endonuclease assays performed with varying ratios of endonuclease-deficient and endonuclease-proficient Mlh1-Mlh3. In addition, Mlh1-Mlh3 can generate religatable double-strand breaks and form an active nucleoprotein complex that can nick DNA substrates in trans. Together these observations argue that Mlh1-Mlh3 may not act like a canonical, RuvC-like Holliday junction resolvase and support a novel model in which Mlh1-Mlh3 is loaded onto DNA to form an activated polymer that cleaves DNA.
Tratto da: www.plos.org.
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WDR23 regulates NRF2 independently of KEAP1

by Jacqueline Y. Lo, Brett N. Spatola, Sean P. Curran

Cellular adaptation to stress is essential to ensure organismal survival. NRF2/NFE2L2 is a key determinant of xenobiotic stress responses, and loss of negative regulation by the KEAP1-CUL3 proteasome system is implicated in several chemo- and radiation-resistant cancers. Advantageously using C. elegans alongside human cell culture models, we establish a new WDR23-DDB1-CUL4 regulatory axis for NRF2 activity that operates independently of the canonical KEAP1-CUL3 system. WDR23 binds the DIDLID sequence within the Neh2 domain of NRF2 to regulate its stability; this regulation is not dependent on the KEAP1-binding DLG or ETGE motifs. The C-terminal domain of WDR23 is highly conserved and involved in regulation of NRF2 by the DDB1-CUL4 complex. The addition of WDR23 increases cellular sensitivity to cytotoxic chemotherapeutic drugs and suppresses NRF2 in KEAP1-negative cancer cell lines. Together, our results identify WDR23 as an alternative regulator of NRF2 proteostasis and uncover a cellular pathway that regulates NRF2 activity and capacity for cytoprotection independently of KEAP1.
Tratto da: www.plos.org.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution (CC BY) license.