C. elegans feeding defective mutants have shorter body lengths and increased autophagy

BACKGROUND: Mutations that cause feeding defects in the nematode C. elegans are known to increase life span. Here we show that feeding defective mutants also have a second general trait in common, namely that they are small. RESULTS: Our measurements of the body lengths of a variety of feeding defective mutants, or of a variety of double mutants affecting other pathways that regulate body length in C. elegans, i.e. the DBL-1/TGFβ, TAX-6/calcineurin and the SMA-1/β(H)-spectrin pathways, indicate that food uptake acts as a separate pathway regulating body length. In early stages, before eating begins, feeding defective worms have no defect in body length or, in some cases, have only slightly smaller body length compared to wild-type. A significant difference in body length is first noticeable at later larval stages, a difference that probably correlates with increasing starvation. We also show that autophagy is induced and that the quantity of fat is decreased in starved worms. CONCLUSION: Our results indicate that the long-term starvation seen in feeding-defective C. elegans mutants activates autophagy, and leads to depletion of fat deposits, small cell size and small body size

The Enigmatic Canal-Associated Neurons Regulate Caenorhabditis elegans Larval Development Through a cAMP Signaling Pathway.

Caenorhabditis elegans larval development requires the function of the two Canal-Associated Neurons (CANs): killing the CANs by laser microsurgery or disrupting their development by mutating the gene ceh-10 results in early larval arrest. How these cells promote larval development, however, remains a mystery. In screens for mutations that bypass CAN function, we identified the gene kin-29, which encodes a member of the Salt-Inducible Kinase (SIK) family and a component of a conserved pathway that regulates various C. elegans phenotypes. Like kin-29 loss, gain-of-function mutations in genes that may act upstream of kin-29 or growth in cyclic-AMP analogs bypassed ceh-10 larval arrest, suggesting that a conserved adenylyl cyclase/PKA pathway inhibits KIN-29 to promote larval development, and that loss of CAN function results in dysregulation of KIN-29 and larval arrest. The adenylyl cyclase ACY-2 mediates CAN-dependent larval development: acy-2 mutant larvae arrested development with a similar phenotype to ceh-10 mutants, and the arrest phenotype was suppressed by mutations in kin-29 ACY-2 is expressed predominantly in the CANs, and we provide evidence that the acy-2 functions in the CANs to promote larval development. By contrast, cell-specific expression experiments suggest that kin-29 acts in both the hypodermis and neurons, but not in the CANs. Based on our findings, we propose two models for how ACY-2 activity in the CANs regulates KIN-29 in target cells

Yksittäisen kuluttajan moraaliset velvoitteet pikamuodin kuluttamisen kontekstissa

Tämä tutkielma perehtyy kysymykseen yksittäisten kuluttajien moraalisista velvollisuuksista osana heidän kuluttamaansa pikamuotia. Muotiteollisuus hyödyntää tunnetusti kehitysmaiden alhaisempaa ympäristötietoisuutta ja väljempää ympäristön sääntelyjärjestelmää havitellessaan alhaisia tuotantokustannuksia tuotteilleen. Samanaikaisesti ihmiset ovat yhä kiinnostuneempia kestävästä kehityksestä ja tietoisempia vaateteollisuuden moraalisista epäkohdista. Vastauksena tälle kiinnostukselle on muotimarkkinoille ilmestynyt kestävinä vaihtoehtoina markkinoituja vaatteita. Samalla kun yhä useampi vaatteita valmistava yritys julistautuu vastuulliseksi, lupausten kriittinen tarkastelu jää kuluttajan vastuulle. Voimmeko jättää vastuun yksittäisille ihmisille, kun kyse on valtavasta globaalista ongelmasta? Lähestyn kysymystä yksilön vastuusta vahingon käsitteen kautta. Tutkielmani on luonteeltaan teoreettinen ja päälähteinäni käytän Walter Sinnott-Armstrongin artikkelia ”It’s Not My Fault: Global Warming and Individual Moral Obligations” ja sille vastaparina Simo Kyllösen artikkelia Climate Change, No-Harm Principle, and Moral Res-ponsibility of Individual Emitters”. Vertailen toisiinsa Sinnott-Armstrongin ja Kyllösen vastakkaisia ajatuksia siitä, olemmeko moraalisesti vastuussa aiheuttamastamme ilmastohaitasta soveltaen heidän argumenttejaan pikamuotiin ja muotiteollisuuteen. Tulen tutkielmassani johtopäätökseen, että yksilön pikamuodin kuluttaminen on moraalisesti moitittavaa toimintaa. Yksilöt ovat moraalisesti velvoitettuja olemaan aiheuttamatta vahinkoa siitä huolimatta, kuinka merkityksetön tai merkityksellinen teko on laajemmassa mittakaavassa. Totean, että teon merkityksellisyys ja moraalisuus ovat kaksi eri asiaa. Pikamuotiin sovellettuna väitteen mukaan olemme siis moraalisesti velvollisia pidättäytymään pikamuodin kuluttamisesta, vaikka yksittäisen kuluttajan ostopäätöksillä ei olisi suurta vaikutusta

C. elegans ten-1 is synthetic lethal with mutations in cytoskeleton regulators, and enhances many axon guidance defective mutants

<p>Abstract</p> <p>Background</p> <p>Teneurins are transmembrane proteins that assist morphogenetic processes in many organisms. <it>ten-1 </it>is the <it>C. elegans </it>teneurin homolog with two transcripts, <it>ten-1a </it>and <it>ten-1b</it>, that respectively encode a long (TEN-1L) and short (TEN-1S) form of the protein. We previously isolated a <it>C. elegans </it>mutant where one pharyngeal neuron was frequently misplaced, and now show that it corresponds to a novel allele of <it>ten-1</it>.</p> <p>Results</p> <p>The novel <it>ten-1(et5) </it>allele is a hypomorph since its post-embryonic phenotype is weaker than the null alleles <it>ten-1(ok641) </it>and <it>ten-1(tm651)</it>. <it>ten-1 </it>mutants have defects in all pharyngeal neurons that we examined, and in vivo reporters show that only the long form of the <it>ten-1 </it>gene is expressed in the pharynx, specifically in six marginal cells and the M2 neurons. Defects in the pharyngeal M2 neurons were enhanced when the <it>ten-1(ok641) </it>mutation was combined with mutations in the following genes: <it>mig-14</it>, <it>unc-5, unc-51, unc-52 </it>and <it>unc-129</it>. None of the body neurons examined show any defects in the <it>ten-1(ok641) </it>mutant, but genetic interaction studies reveal that <it>ten-1(ok641) </it>is synthetic lethal with <it>sax-3, unc-34 </it>and <it>unc-73</it>, and examination of the hypodermal cells in embryos of the <it>ten-1(ok641) </it>mutant point to a role of <it>ten-1 </it>during hypodermal cell morphogenesis.</p> <p>Conclusions</p> <p>Our results are consistent with <it>ten-1 </it>normally providing a function complementary to the cytoskeletal remodeling processes that occur in migrating cells or cells undergoing morphogenesis. It is possible that <it>ten-1 </it>influences the composition/distribution of extracellular matrix.</p

Reducing queues: demand and capacity variations

Purpose – The aim of this paper is to investigate how waiting lists or queues could be reduced without adding more resources; and to describe what factors sustain reduced waiting-times. Design/methodology/approach – Cases were selected according to successful and sustained queue reduction. The approach in this study is action research. Findings – Accessibility improved as out-patient waiting lists for two clinics were reduced. The main success was working towards matching demand and capacity. It has been possible to sustain the improvements. Research limitations/implications – Results should be viewed cautiously. Transferring and generalizing outcomes from this study is for readers to consider. However, accessible healthcare may be possible by paying more attention to existing solutions. Practical implications – The study indicates that queue reduction activities should include acquiring knowledge about theories and methods to improve accessibility, finding ways to monitor varying demand and capacity, and to improve patient processing by reducing variations. Originality/value – Accessibility is considered an important dimension when measuring service quality. However, there are few articles on how clinic staff sustain reduces waiting lists. This paper contributes accessible knowledge to the field

Den livsviktiga läsningen : en uppsats om litteracitet och bibliotekariers läsfrämjande arbete

The importance of reading : a Master’s Thesis about literacy and librarians’ motivational reading strategies towards children and teenagers. The public literacy debate has exploded all over Swedish media since PISA published their report at the end of 2013 with the result that politicians, teachers and parents suddenly have shown a lot more interest in what and how young people read. The report has also led to a new public interest in the research on young people’s reading habits. The idea for our master’s thesis came to us when we came across the Swedish debate about the PISA-report and how young people’s literacy is reported to steadily decrease. Our master’s thesis examines how school and public librarians work with motivational reading strategies towards children and teenagers. We believe that the work that the librarians do is the way to reach higher literacy. We have interviewed librarians to be able to understand their daily work. Our main theoretical approaches are the sociocultural perspectiv, with theorists like Lev Vygotskij and Roger Säljö, and literacy, we have used a number of different theorists within that field. We have concluded that both the school librarians and the public librarians are very qualified when it comes to the smaller children, but in the work towards teenagers we have noticed that they have difficulties to reach them, and that they work without clear strategies and methods for this target group. However, we do not look at these difficulties as a fault in the librarians’ daily work, we conclude that the problem comes from above, due to governmental regulations, strategies and funding

Distinct roles in autophagy and importance in infectivity of the two ATG4 cysteine peptidases of leishmania major

Macroautophagy in Leishmania, which is important for the cellular remodeling required during differentiation, relies upon the hydrolytic activity of two ATG4 cysteine peptidases (ATG4.1 and ATG4.2). We have investigated the individual contributions of each ATG4 to Leishmania major by generating individual gene deletion mutants (Δatg4.1 and Δatg4.2); double mutants could not be generated, indicating that ATG4 activity is required for parasite viability. Both mutants were viable as promastigotes and infected macrophages in vitro and mice, but Δatg4.2 survived poorly irrespective of infection with promastigotes or amastigotes, whereas this was the case only when promastigotes of Δatg4.1 were used. Promastigotes of Δatg4.2 but not Δatg4.1 were more susceptible than wild type promastigotes to starvation and oxidative stresses, which correlated with increased reactive oxygen species levels and oxidatively damaged proteins in the cells as well as impaired mitochondrial function. The antioxidant N-acetylcysteine reversed this phenotype, reducing both basal and induced autophagy and restoring mitochondrial function, indicating a relationship between reactive oxygen species levels and autophagy. Deletion of ATG4.2 had a more dramatic effect upon autophagy than did deletion of ATG4.1. This phenotype is consistent with a reduced efficiency in the autophagic process in Δatg4.2, possibly due to ATG4.2 having a key role in removal of ATG8 from mature autophagosomes and thus facilitating delivery to the lysosomal network. These findings show that there is a level of functional redundancy between the two ATG4s, and that ATG4.2 appears to be the more important. Moreover, the low infectivity of Δatg4.2 demonstrates that autophagy is important for the virulence of the parasite

Molecular Characteristics of Kraft-AQ Pulping Lignin Fractionated by Sequential Organic Solvent Extraction

Kraft-AQ pulping lignin was sequentially fractionated by organic solvent extractions and the molecular properties of each fraction were characterized by chemical degradation, GPC, UV, FT-IR, 13C-NMR and thermal analysis. The average molecular weight and polydispersity of each lignin fraction increased with its hydrogen-bonding capacity (Hildebrand solubility parameter). In addition, the ratio of the non-condensed guaiacyl/syringyl units and the content of β-O-4 linkages increased with the increment of the lignin fractions extracted successively with hexane, diethylether, methylene chloride, methanol, and dioxane. Furthermore, the presence of the condensation reaction products was contributed to the higher thermal stability of the larger molecules

Influence of production variables and starting material on charcoal stable isotopic and molecular characteristics

We present a systematic study on the effect of starting species, gas composition, temperature, particle size and duration of heating upon the molecular and stable isotope composition of high density (mangrove) and low density (pine) wood. In both pine and mangrove, charcoal was depleted in o13C relative to the starting wood by up to 1.6&#37; and 0.8&#37;, respectively. This is attributed predominantly to the progressive loss of isotopically heavier polysaccharides, and kinetic effects of aromatization during heating. However, the pattern of o13C change was dependant upon both starting species and atmosphere, with different structural changes associated with charcoal production from each wood type elucidated by Solid-State o13C Nuclear Magnetic Resonance Spectroscopy. These are particularly evident at lower temperatures, where variation in the oxygen content of the production atmosphere results in differences in the thermal degradation of cellulose and lignin. It is concluded that production of charcoal from separate species in identical conditions, or from a single sample exposed to different production variables, can result in significantly different o13C of the resulting material, relative to the initial wood. These results have implications for the use of charcoal isotope composition to infer past environmental change