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Please, Help Yourself: A Best Practice Model Analysis on the Self-Represented Litigants in America\u27s Legal System
No full textPlease, Help Yourself: A Best Practice Model Analysis on the Self-Represented Litigants in America\u27s Legal System
No full text
Effect on muscle building associated with alcohol intake after exercise
No full textSahlgrenska Academy
At University of Gothenburg
Department of Internal Medicine and Clinical Nutrition
Abstract:
Titel: Effect on muscle building associated with alcohol intake after exercise
Author: Frida Bond och Linnea Danielsson
Supervisor: Frode Slinde
Examminer: Anna Winkvist
Programme: Dietician study programme, 180/240 ECTS
Type of paper: Examination paper, 15 hp
Datum: May 26, 2014
Background: Drinking alcohol is often used as something to spice up weekdays as well as more festive occasions. The reverse aspect of alcohol consumption is that the body sees alcohol as toxic and therefore the basis for a number of diseases. Exercise and physical activity have been proven to be good for several welfare diseases such as diabetes and cardiovascular disease. Among people in general, opinion is divided as to how exercise combined with alcohol affects muscle building, but what do science say? Objective: The purpose of this review article is to analyze and summarize the existing scientific data about how the structure of muscles is affected in relation to alcohol intake after exercise. Search strategy: A systematic literature search was conducted in PubMed and Scopus with the keywords alcohol drinking, exercise, muscle strength, free testosterone, ethanol. Selection criteria: Inclusion criteria: RCT or crossover study design, written in English or Swedish, healthy adult (18 +) people. Exclusion criteria: Review articles, articles that are not available in full text, studies done on people with alcohol dependence. Studies that do not include measures outcomes for muscle building. Data collection and analysis: Seven studies remained after the selection. The study quality was graded according to quality assessment of randomized trials. Outcome was evidence graded according to the GRADE system.
Main Results: In these studies, alcohol doses varied between 0.5 g alcohol/kg body weight - 1g alcohol/kg body weight. The larger the volume of alcohol consumed the greater the reduction in muscle strength the succeeding hours. Regarding testosterone results show heterogeneity, where the testosterone level provides three different results from three studies. Creatinekinase increases after exercise independently of alcohol. Cortisol appears to increase in the intervention groups. The evidence for all outcomes are low (++) to moderate (+++) besides strength having low evidence (++).
Conclusions: Today's evidence is highly ambiguous about alcohol effects on muscle building after exercise, since all outcomes, except for creatine kinase are heterogeneous. The future needs to provide more research, where larger doses are tested and where blinding occurs in whenever it is possible.Sahlgrenska Akademin vid Göteborgs universitet Avdelningen för invärtesmedicin och klinisk nutrition
Sammanfattning:
Titel: Påverkan på muskeluppbyggnad i samband med alkoholintag efter träning
Författare: Frida Bond och Linnea Danielsson
Handledare: Frode Slinde
Examinator: Anna Winkvist
Linje: Dietistprogrammet, 180/240 hp
Typ av arbete: Examensarbete, 15 hp
Datum: 2014-05-26 Bakgrund: Drycken alkohol berikar och förgyller stämning i både vardagstid så som festligare sammanhang. Alkoholkonsumtion har även en baksida, då det för kroppen behandlas som ett gift och därmed ligger till grunden för ett flertal sjukdomar. Träning och fysisk belastning av kroppen är bevisligen bra för att förebygga flera välfärdssjukomar så som diabetes och hjärt- och kärlsjukdomar. Bland folk i allmänhet går åsikterna isär när det gäller hur träning i kombination med alkohol påverkar muskeluppbyggnad, men vad säger vetenskapen?
Syfte: Syftet med denna översiktsartikel är att analysera och sammanfatta det befintliga vetenskapliga underlaget kring hur uppbyggnaden av muskler påverkas i samband med alkoholintag efter träning.
Sökväg: En systematisk litteratursökning genomfördes i databaserna PubMed och Scopus med sökorden alcohol drinking, exercise, muscle strength, free testosterone, ethanol.
Urvalskriterier: Inklusionskriterier: RCT- eller crossover studiedesign, skrivna på engelska eller svenska, vuxna(18+), friska människor. Exklusionskriterier: Översiktsartiklar, artiklar som ej finns i full text, studier gjorda på personer med alkoholberoende. Studier som inte innefattar effektmåtten för muskeluppbyggnad.
Datainsamling och analys: Efter urvalet återstod sju studier. Samtliga kvalitetsgranskades enligt en mall för randomiserade studier. Aktuella effektmått evidensgraderades och betygsattes enligt GRADE.
Resultat: I studierna har alkoholdoser varierat mellan 0,5g alkohol/kg kroppsvikt - 1g alkohol/kg kroppsvikt. Ju större volym alkohol som konsumeras desto mer minskar muskelstyrkan de efterföljande timmarna. Gällande testosteron visar resultaten på heterogenitet, där testosteronhalten ger tre olika resultat utifrån tre studier. Kreatinkinas ökar efter träning oberoende av alkohol. Kortisol ger ett tecken av att öka i interventionsgrupperna. Evidensen för alla effektmått är låg (++) till måttlig (+++) förutom styrka som har låg (++).
Slutsats: Dagens underlag är ytterst mångtydigt kring alkoholeffekt på muskeluppbyggnad efter träning, då samtliga effektmått, förutom kreatinkinas är heterogena. Framtiden behöver ge oss mer forskning, där större doser prövas, där blindning sker i största möjliga utsträckning
Interactions of genetic variants and prenatal stress in relation to the risk for recurrent respiratory infections in children
No full textGenetic variants may predispose children to recurrent respiratory
infections (RRIs) but studies on genotype-environment interaction are
rare. We hypothesized that the risk for RRIs is elevated in children
with innate immune gene variants, and that prenatal exposure to maternal
psychological distress further increases the risk. In a birth cohort,
children with RRIs (n = 96) were identified by the age of 24 months and
compared with the remaining cohort children (n = 894). The risk for RRIs
in children with preselected genetic variants and the interaction
between maternal distress during pregnancy and child genotype were
assessed with logistic regression. The IL6 minor allele G was associated
with elevated risk for RRIs (OR 1.55; 95% CI 1.14–2.12). Overall, there
was no interaction between maternal psychological distress and child
genotype. Exploratory analyses showed that, the association between the
variant type of IL6 and the risk for RRIs was dependent on prenatal
exposure to maternal psychological distress in males (OR 1.96; 95% CI
1.04–3.67). Our study didn’t find genotype-environment interaction
between prenatal maternal distress and child genotype. Exploratory
analyses suggest sex differences in gene-environment interaction related
to susceptibility to RRIs. © 2021, The Author(s).</p
Regulation of Ahr signaling by Nrf2 during development : effects of Nrf2a deficiency on PCB126 embryotoxicity in zebrafish (Danio rerio)
No full textAuthor Posting. © The Author(s), 2015. This is the author's version of the work. It is posted here by permission of Elsevier for personal use, not for redistribution. The definitive version was published in Aquatic Toxicology 167 (2015): 157-171, doi:10.1016/j.aquatox.2015.08.002.The embryotoxicity of co-planar PCBs is regulated by the aryl hydrocarbon receptor (Ahr), and
has been reported to involve oxidative stress. Ahr participates in crosstalk with another
transcription factor, Nfe2l2, or Nrf2. Nrf2 binds to antioxidant response elements to regulate the
adaptive response to oxidative stress. To explore aspects of the crosstalk between Nrf2 and Ahr
and its impact on development, we used zebrafish (Danio rerio) with a mutated DNA binding
domain in Nrf2a (nrf2afh318/fh318), rendering these embryos more sensitive to oxidative stress.
Embryos were exposed to 2 nM or 5 nM PCB126 at 24 hours post fertilization (prim-5 stage of
pharyngula) and examined for gene expression and morphology at 4 days post fertilization (dpf;
protruding –mouth stage). Nrf2a mutant eleutheroembryos were more sensitive to PCB126
toxicity at 4 dpf, and in the absence of treatment also displayed some subtle developmental
differences from wildtype embryos, including delayed inflation of the swim bladder and smaller
yolk sacs. We used qPCR to measure changes in expression of the nrf gene family, keap1a,
keap1b, the ahr gene family, and known target genes. cyp1a induction by PCB126 was
enhanced in the Nrf2a mutants (156-fold in wildtypes vs. 228-fold in mutants exposed to 5 nM).
Decreased expression of heme oxygenase (decycling) 1 (hmox1) in the Nrf2a mutants was
accompanied by increased nrf2b expression. Target genes of Nrf2a and AhR2,
NAD(P)H:quinone oxidoreductase 1 (nqo1) and glutathione S-transferase, alpha-like (gsta1),
showed a 2-5-fold increase in expression in the Nrf2a mutants as compared to wildtype. This
study elucidates the interaction between two important transcription factor pathways in the
developmental toxicity of co-planar PCBs.University of Massachusetts Amherst Commonwealth Honors College Research grant (to M.R.),
National Institutes of Health grants R01ES016366 (MEH), R01ES006272 (MEH), and
F32ES017585 (ART-L)
Author Correction: Dose escalation and expansion cohorts in patients with advanced breast cancer in a Phase I study of the CDK7-inhibitor samuraciclib
No full textCorrection to: Nature Communicationshttps://doi.org/10.1038/s41467-023-40061-y, published online 24 July 2023 In the version of the article initially published, there was an error in the Table 3 rows reporting progression-free survival for patients without liver metastases, which, now reading “No liver metastases (N = 17); 13.8 (7.4, NC),” appeared originally as “No liver metastases (N = 17); 11.1 (1.7, NC),” while in the row now reading “Liver metastases (N = 14); 2.8 (1.8, 7.4)” the row originally read “Liver metastases (N = 14); 2.8 (1.8, 5.3)” The change is reflected in the HTML and PDF versions of the article
Author Correction: Dose escalation and expansion cohorts in patients with advanced breast cancer in a Phase I study of the CDK7-inhibitor samuraciclib
No full textWriting resistance together
No full textThis piece of writing is a joint initiative by the participants in the Gender, Work and Organization writing workshop organized in Helsinki, Finland, in June 2019. This is a particular form of writing differently. We engage in collective writing and embody what it means to write resistance to established academic practices and conventions together. This is a form of emancipatory initiative where we care for each other as writers and as human beings. There are many author voices and we aim to keep the text open and dialogical. As such, this piece of writing is about suppressed thoughts and feelings that our collective picket line allows us to express. In order to maintain the open‐ended nature of the text, and perhaps also to retain some ‘dirtiness’ that is essential to writing, the article has not been language checked throughout by a native speaker of English
Depression: Can we predict who will relapse?
No full textThis thesis addresses risk factors and proposed mechanisms to explain relapse to depression. Volume 1 comprises three parts: Part 1 is a literature review consisting of meta-reviews of systematic and non-systematic reviews of studies reporting on risk factors for relapse to depression, and a systematic-review of neuroimaging and experimental studies investigating risk factors for relapse and potential mechanisms of action of these risk factors. The reviews found that only residual symptoms of depression at the end of treatment and childhood maltreatment were sufficiently evidenced as predictors of relapse and neither have great clinical utility. A number of psychological and neuropsychological factors were suggested to play a role in conferring risk for relapse. Considering the inter-relationships between these factors the reviews were used to propose a conceptual framework which may be used to help guide future research into relapse to depression in adults. Part 2 is an empirical paper in which data were analysed from service users of a primary care mental health service to identify risk factors for relapse and for the presence of residual symptoms, and survival analysis methods were used to determine when relapses occur most often and what factors impact survival. In addition, a prospective cohort study was formed to investigate the relationship between cognitive control and depressive symptoms. The findings confirmed that cognitive control can be used to predict residual symptoms of depression post-treatment and therefore potentially to predict relapse. Part 3 is a critical appraisal focussing on the theoretical reasons as to why studying relapse in a manner as used in the prospective study is so important and discusses the logistical difficulties conducting such research in the current context of NHS services and of the D.Clin.Psy research project. Methodological decisions made that impacted upon the research process are discussed and reflective conclusions are offered
