An important challenge in interactive machine learning, particularly in subjective or ambiguous domains, is fostering bi-directional alignment between humans and models.
Any individual sentence that describes information designed to set the stage for the contribution of the paper.
In supervised and semi-supervised machine learning (ML) pipelines, labeled data is a vital component of training and validating models [46].
An individual sentence describing the setting in which this work was done.
In the context of co-adaptive learning, supporting the intertwined evolution of both the user's understanding and the model's learning is crucial [16].
An individual sentence describing the setting in which this work was done.
Machine teaching, a part of the human-in-the-loop approach, has been used as a process in which a human expert (the "teacher") provides guidance to a machine learning model to help it learn important and robust features for decision making [57].
An individual sentence describing the setting in which this work was done.
A targeted approach in IML is machine teaching (MT) [60], an interactive framework that allows users to devise and select useful data for labeling, with the goal of teaching the model relevant features during training [7, 18].
An individual sentence describing the setting in which this work was done.
Interactive ML (IML) methods, like active learning [3], continuously apply human feedback during model training to iteratively build and refine the model [35, 42, 43].
An individual sentence describing the setting in which this work was done.
https://youtu.be/ZXlYNEej9t0?si=gDN_6cDPn2N7fVB6&t=211
Ben Kingsley used a Continental typewriter in Schindler's List. It's housed at the Amblin Film Archive.
it slightly increased losses of soluble P
Yes - and what's going on behind the scenes here is that we assume that fertilizer contributes to the DP fraction only in the season of application, but with manure we account for DP contributions in the first season of application AND the second and third seasons after application (this is all based on work that Peter Vadas did). In the second season following application, 20% of the manure total P remaining on the soil surface is expected to become water soluble. In the third season following application, 5% of the total P remaining on the soil surface is expected to become water soluble.
Vadas, P.A., L.B. Owens, and A.N. Sharpley. 2008. An empirical model for dissolved phosphorus in runoff from surface-applied fertilizers. Agric. Ecosys. Environ. 127-59-65. Vadas, P.A., L.W. Good, P. A. Moore Jr., and N. Widman. 2009. Estimating phosphorus loss in runoff from manure and fertilizer for a phosphorus loss quantification tool. J. Environ. Qual. 38:1645-1653. Vadas, P. A. and P. J. A. Kleinman. 2006. Effect of methodology in estimating and interpreting water-extractable phosphorus in animal manures. J. Environ. Qual. 35: 1151-1159. Vadas, P.A., W.J. Gburek, A.N. Sharpley, P. J. Kleinamn, P. A. Morre, Jr., M. L. Cabrera, and R. D. Harmel. 2007. A model for phosphorus transformations and runoff loss for surface-applied manures. J. Environ. Qual. 36:324-332
Vadas, P.A., Gburek, W.J., Sharpley, A.N., Kleinman, P.J.A., Moore, P.A., and Cabrera, M.L. et al. 2007a. A model for phosphorus transformation and runoff loss for surface-applied manures. J. Environ. Qual. 36: 324–332. doi: https://doi.org/10.2134/jeq2006.0213
public data
Unjournal data
Logic map:
There's some text overlap in the diagram.
e possible costs of negative or mixed findings.
what 'costs of negative findings'? This is a bit of a vague sentence.
Request evaluation when:
also state and interpret the equation in terms of 'benefits vs cost' -- easier to interpret I think
+,- is
don't use "+" and "-" as variables ... we can do better
The Unjournal evaluates research; it does not publish papers as journal articles, and evaluators do not issue accept/reject decisions. This matters because many author co
links don't need to be bolded
Logic map: where public evaluation changes the author's payoff
overlapping text in diagram below
or policy relevance.
remove 'or policy relevance' perhaps -- The Unjournal prioritizes research with global impact potential (although that's not what we mainly rate the research on)
or the likely criticism is about taste, importance, novelty, or fit rather than checkable claims
not sure I understand the logic behind the latter part
or the likely criticism is correct
how would someone know this?
Author-Facing Guide
This is a possible set of considerations -- I don't want to state it as definitive
reader s
maybe the 'gatekeeper' or 'editor' instead of the 'reader'?
public signal is Y in +,-,
Is it a truly 'public' signal, or only one the evluator sees after reading the paper? Or should we have both?
r[qA - (1-q)L] + (1-r)[(1-q)A - qL] - k ≥ 0
notation needs improvement, and it should be explained more -- how derived, how to interpret it? Tooltips and expanding sections could help
Requesting a noisy public test is not the same as disclosing an already-known verifiable fact.
I suspect another paper has dealt with this question ... 'when noisy signals help the seller' or some such
e reader should not update from p0 after observing the evaluation res
this needs clarification, I don't quite see why this is the case. Isn't it possible that the author's signal is positive so they submit, but the evaluator reading the paper gets a negative signal?
he relevant prior
relevant to whom?
he reader acts when posterior belief exceeds threshold c.
what is 'acts' and what is 'c' -- underexplained
binary quality Q in {H,L}, w
is this 'binary' rhe relevant threshold? Where did it com from? is it sort of generalizable? Consider if it misses some important nuance
tive, the reader
who is the 'reader'? I think we mean the later journal evaluator, or career gatekeeper
Main
base
Single
simple
empirically import
why?
Public anonymity statistic. The anonymity choice is empirically important. Running python unjournal_anonymity_stats.py on the public data bundle gives 65 anonymous/generic public evaluator identifiers among 113 deduplicated evaluator-paper pairs with quantitative ratings: 57.5%. In the subset matched to published-evaluation status, the share is 63/105: 60.0%, with 7 unmatched title rows. This supports saying "a bit over half" choose anonymous/generic public identifiers, but the denominator should be stated. The wider evaluator_paper_level.csv denominator is not clean for this claim because survey-only rows are assigned generic Evaluator N labels.
this should be a fold or footnote -- give a quick statistic and footnote yow it was captured
are the right default
too strong. And takes the 'high dowside' idea for granted too much IMO
When the answer is unclear, the practical move is not immediate publicity. It is a fit-and-timing conversation, coauthor consen
too much 'not this but that' AI speak. And 'publicity' is vague here
downstream readers
more like 'editors and peer reviewers'
4. Are you or your coauthors especially exposed to a durable negative public signal?
This framing feels too negative and definitive for my taste. As some of the modeling and discussion gets at, a single 'negative public signal' should not be so damning as people seem to think.
bout conditional embargo.
too much use of bold within paragraphs and prose
Read these as sequential gates. Realization handles liquidity and legal availability; follow-through handles intent; allocation handles cause choice; deployment handles the timing of actual grants by the deadline.
where do the defaults come from? Explain, reference, link (maybe as tooltips)
This may leave legally awkward, politically controversial, or non-lab-compatible work underfunded.
this needs fleshing out -- not sure what this is about
People who could puncture the rumor may also be financially incentivized not to alienate future donors.
I don't see how this would 'alienate future donors'?
Glossaire
Faire un glossaire - vitrine linguistique du Québec. EPBE,
Adresser les questions clés
Revue de littérature globale (bref) > locale
Progrès vers les cibles du Plan Nature
Document à part?
Moteurs de changement
switch 2 and 3
egor.katkov@mcgill.ca
Remplacer par adresse CSBQ
A.1 Qui peut contribuer?
Contactez nous so vous voulez contribuer si vous avez des compétences à une large échelle ou large group taxonomique.
Le comité va prendre un décision.
Ouverture à la science citoyenne.
A.3 Quelles sont des connaissances utiles pour contribuer?
Mettre de l'avant les cométences scientifiques et non techniques
Explicit crux Which specific uncertainties — AGI timing, takeoff speed, power-seeking tendency, offense-defense balance, pause feasibility — most shift expert p(doom) estimates?Community solicitation for explicit AI-risk cruxes: uncertainties whose resolution would significantly shift p(doom), including AGI arrival year, takeoff speed, power-seekin
this is meta -- I don't want meta, or at least put that into an 'opt-in' list
ntes de llegar al Ministerio del Interior de la dictadura encabezada por Videla, Harguindeguy había sido jefe de la Policía Federal durante más de un año, nombrado por María Estela Martínez de Perón. Allí creó el Grupo de Tareas 2 (GT-2), encargado de la represión ilegal, en el ámbito de Coordinación Federal.
Grupo de Tareas 2
El Memo relata que el día miércoles 1° de octubre “los cinco generales que tienen los fierros, de Sur a Norte: Antonio Domingo Bussi (Cuerpo I); Juan Carlos Trimarco (Cuerpo II); Cristino Nicolaides (Cuerpo III) y José Rogelio Villarreal (Cuerpo V) informaron a Galtieri que su posición era que Viola no era negociable y que, si era necesario, se debía modificar la regla de unanimidad” en la Junta Militar. Pocos lo dicen: desde hacía tiempo Galtieri pretendía ser Presidente con retención de la comandancia en Jefe del Ejército, ambición que recién concretaría en diciembre del año siguiente, con el respaldo del almirante Jorge Anaya, tras nombrar nuevos jefes de Cuerpo a su antojo. Pasaron a retiro Villarreal y Bussi.
Important
A public dataset is not encountered in the same way by every actor. For one community, it may be a tool for language preservation, research or local innovation. For a large company, it may become one more input into a product that returns little value to the people represented in the data.
I am old enough, and have worked with enough organisations, to know that a written rule and an organisational behaviour are very often distant relatives who meet only at weddings.
Wikipedia looks effortless only if one has never watched the effort.
I notice that the AI I use currently actually broadcasts little joke "progress" messages, designed to further obscure the actual information-generating process. How different it would be if it even broadcast random facts about the training data set,,,
“True openness means participation with fairness and respect, not unchecked extraction.”
If AI systems use the commons while reducing the visibility of the commons, then the problem becomes sustainability of public knowledge itself.
A person reading an essay is one thing. A teacher using an article in class is one thing. A volunteer translating a public-interest resource is one thing. A crawler absorbing enormous amounts of human work into a commercial machine-learning system, with no meaningful conversation about permission, attribution, compensation or future use, is something else. Scale changes the nature of the act. When use becomes extraction at industrial speed, the old language starts to feel inadequate.
eLife Assessment
This important study examines the benefits of spatial cognition in a wild population of mountain chickadees. Using robust genetic analyses and experimental design, the authors show with compelling evidence that females seeking out extra-pair copulations prefer males with strong spatial cognition, and that these males have a reproductive advantage over other males. This work is of broad interest to evolutionary and behavioural biologists.
Reviewer #1 (Public review):
This manuscript presents compelling evidence from a wild chickadee population linking heritable spatial cognition to extra-pair paternity success, supporting sexual selection via good genes in a food-caching species. The integration of RFID cognition tests with ddRAD paternity assignment is methodologically strong and timely for behavioral ecology, though causal mechanisms and confounds warrant clarification.
Overall, a major revision of the manuscript is recommended, addressing the points below.
(1) Confirmation of manipulation and treatment effects. The central claim hinges on spatial cognition driving EP siring, but direct evidence that cognition predicts observed copulations (vs. post-copulatory mechanisms) is absent. While territories do not cluster by performance (Figure S4), quantify male aggression/movement data during fertile periods to rule out intrusion-based EPP. The authors should provide metrics like nearest-neighbor distances for EP sires or playback responses linking cognition to dominance, as in prior chickadee work. Without this, causal female preference remains correlational.
(2) Female cognition-EPY link inconsistency. Poor female cognition predicts more EPY (first-20-trials: offspring-level χ²=6.21, P=0.013; nests: χ²=6.79, P=0.009), but not for full-task (P>0.5). The authors should discuss why (e.g., learning speed vs. memory stability) and add exploratory correlations (female errors vs. EPY proportion). They should soften claims in the Discussion section of "female-driven" without consistent support and should frame this as a hypothesis.
(3) Cognitive task sensitivity and validity. Mean errors aggregate learning curves effectively, but single feeder-assignment (non-preferred) confounds neophobia/motivation with spatial ability. The authors should report trial-by-trial improvements (Figure S7 subset) or criterion-to-learn metrics. Justify excluding high-error birds (<3 mean); sensitivity analysis needed to check bias toward high performers.
(4) Paternity assignment robustness. ddRAD-CERVUS with bimodal LODs (Figure S8) is solid, but unassigned EPY (social-genotyped but no sire) implies missing sires (~?% of EPY?). Include all alive males as candidates yearly? Test power simulations for LOD thresholds. 2019 exclusion justified, but multi-year SNP alignment could boost resolution.
(5) Mechanistic speculation vs. data. Discussion invokes hippocampus genes (GWAS priors) and good genes, but no offspring cognition/survival data. Label as hypotheses; suggest tracking EPY recruitment. No brood size costs for EP sires is key, but monitor long-term nest investment (e.g., feeding rates).
Reviewer #2 (Public review):
Summary:
In this study, the authors ask whether spatial cognition is under sexual selection in mountain chickadees. To do so, the authors examined a large dataset that includes a) spatial cognition data for both males and females (obtained via use of a clever RFID-based feeder system) and b) social and extra-pair paternity nesting data. As predicted, males with higher spatial cognition sired more extra-pair offspring, and extra-pair sires had, on average, higher spatial cognition scores than the males they cuckolded. Interestingly, females with lower spatial cognition scores were more likely to seek extra-pair copulations, potentially to compensate for their own low spatial cognition. Surprisingly, there was no difference in spatial cognition scores between males that sired their own offspring and those that lost paternity at the nest. Also surprising was the fact that there were no differences in patterns of extra-pair paternity and spatial cognition between high- and low-elevation sites. The latter is particularly surprising in that spatial cognition should be under stronger selection at the high elevation site. Overall, this is a fascinating study that demonstrates that spatial cognition - a trait under natural selection as it directly impacts winter foraging and survival behaviour -is also under sexual selection.
Strengths:
The authors have a robust dataset (n = 732 offspring sampled over 3 years), high-quality spatial cognition data collected with a procedure that has been well-honed over the years, and couple the data with solid statistical procedures that address many potential covariates and potentially confounding factors. In addition, the authors are careful in the discussion to elaborate on the many potential alternative explanations from the results and questions that are likely to arise in the minds of readers (e.g., how are females assessing male spatial ability?)
Weaknesses:
Overall, no major weaknesses were identified in this study. As always, there are editorial issues that I would encourage the authors to consider, including presentation of data/results and clarification on some statistical issues. Overall, however, this is an excellent study that will make an important contribution to our understanding of the evolution of cognition and targets of sexual selection.
Reviewer #3 (Public review):
Summary:
The authors presented evidence that spatial cognition in this population is under sexual selection, with extra-pair males, primarily chosen by the females, having better spatial cognition than males they cuckolded and males with better spatial cognition having more extra-pair young.
Strengths:
This cognitive ecology study was conducted on a well-known long-term study population of free-ranging mountain chickadees. This strong base, alongside a thorough study design and extensive statistical analyses, enabled the authors to address research questions that few other labs can address, making this a potentially powerful study of broad general interest.
Weaknesses:
Throughout the manuscript, there is a focus on the "mean number of location errors per trial over the first 20 trials". Performance changes across trials, so why weren't learning vs peak performance analyzed separately? Similarly, authors also describe results in the context of the entire task, but sometimes in the context of the first 20 trials - why is one prioritised over the other, and why is the emphasis not always consistent? Are the results across the two generally the same? A more thorough explanation addressing all these points is necessary.
Lines 429-432: Why was a categorical (i.e., chi-square test) and not a numerical comparison implemented? A numerical statistical test would capture more of the variation (i.e., the number of years separating the social and EPY males).
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representa la curva guía para la presa i en la etapa m
supongo que en los preliminares se explicará que es una curva guía
Cderr,Cdef,CCG,Ccrit son constantes de penalización ajustadas empíricamente
en qué momento se dirá el valor específico de esas constantes?
as
hay que explicar 10⁶ y el 3600 10⁶
eficiencia de conversión hidráulica a eléctrica,
supongo se que explicará esto en los preliminares
volumen
falta explicar el 10
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M es 6?
2.3 Développement commercial, résidentiel et récréatif
Message clé!!
“经济上的显著生产力将提高生活水平，今天双职工家庭将变成单职工家庭。”
Prometheus融资120亿美元，估值达410亿美元，成为物理AI领域最大单笔投资之一。
贝索斯认为AI生产力提升将导致劳动力稀缺，与主流AI领袖预测的大规模失业观点相左。
“未来比我们预想的来得更快”，过去几年还只是假设的风险，现在已成为现实问题。
DeepMind联合多家机构设立1000万美元基金，专门研究多智能体系统的安全风险，但相比其内部研究预算仍显不足。
DeepMind认为学术界能比企业实验室看得更远，不受短期商业目标限制，这是推动多智能体安全研究的关键动力。
. Or use + Suggest entry above to open a GitHub issue.
the 'suggest entry' is now going to a dead GH page -- find a better approach and solution
Three explicit flags that would substantially revise the estimates: (1) better proxy validity research (reversal learning, parental care as welfare indicators); (2) new data on understudied invertebrates; (3) theoretical advances o
can these be restated as questions?
The load-bearing belief is that neuron counts are only a defensible proxy for moral weight if they reliably correlate with the welfare-relevant capacities organisms actually posse
Better stated as a question ... something like "Do neuron counts reliably correlate with the welfare-relevant capacities organisms actually possess?" (of course 'reliably' probably would need operationalization, and this elides the possibility that it may "reliably correlate" but the correlation may be low)
Three explicit cruxes structuring the entire cross-cause model: (1) animals' moral weights relative to humans; (2) expected value of the long-run future; (3) preference for making a difference vs. expected value. Cause rankings reve
these are good, but can they be separated out and flexhed out and made more explicit?
The load-bearing belief is that any significant moral weight for animals, combined with Rethink Priorities' finding that corporate animal welfare campaigns are ~1000x more cost-effective than top global health interventions (e.g. AMF), implies Open Phil should prioritize animal welfare in neartermism. The author's position would change if the moral weights / welfare-range estimates favoring animals were substantially lower, or if a defensible reason were given for valuing human welfare units far above animal welfare units purely on species membership. The author explicitly asks what would have to change in OP's views to NOT prioritize animal welfare.
Not sure this one is an actual crux, rather an attempt to draw out Open Phil (now CG) on their moral weighting
the moral-weighting framework for suffering: whether one prioritizes duration of welfare improvement or the intensity/severity of suffering averted.
'prioritizes' is not clear here. Do they better operationalize this ... how would it be decided/measured?
What belief changes would actually alter donations or work — and what are the poster's actual cruxes? Author foregrounds room for more funding and marginal value.
meta -- not an actual crix
The load-bearing belief is that no compelling cost-effectiveness case exists for the alternatives; a promising cost-effectiveness estimate for institutional meat reduction campaigns would make the author excited about (and supportive of reallocating funding toward) them. To me, to be excited about such campaigns I'd need to see a promising cost-effectiveness estimate. High Shortlist EA Forum Did corporate campaigns in the US have any counterfactual impact? A quantitative model verified No — published 2019, before 2024 window Karolina Sarek 2019-06-24 Key uncertainty
clarify -- hard to read this
The estimated counterfactual impact of US corporate cage-free campaigns (2.1-10%) is load-bearing on the price elasticity of egg demand, a parameter drawn from a literature review with only ~13 observations.
this is a fairly well-defined operationalized crux. It's old, but I guess 'we still are not confident'!
is load-bearing on the price elasti
'is load-bearing on' ... that's too jargony; state it more clearly
He would be persuaded toward global health if shown a defensible rationale for valuing one unit of human welfare so much more than animal welfare that it justifies Open Phil funding GH ~6x as much as AW —
this latter bit is closer to being a specific 'crux'. remember we want these stated as operationalizable questions,if possible. And try to find the single question crux that seems most important or most correlated to the others. You can have another column listing other cruxes raised.
The author's load-bearing claim
you don't need "the authors ... " ... just state their crux question ... obviously it's the author
y The author's recommendation hinges on whether furnished-cage advocacy is actually more cost-effective per unit welfare than cage-free advocacy. He remains skeptical despite his own estimate (2.84x), and his position would shift on whether advocacy costs scale linearly with producer costs, whether infrastructure lock-in blocks later cage-free transitions, and whether furnished-cage campaigns would undermine the cohesiveness of global laying-hen advocacy.
This one is getting good. It seems pretty relevant, but I want you to state it as an explicit opertionalizable question here.
What are the most important questions you'd want answered before deciding how, where, and when to give $20M?
too meta
The author's position that shrimp welfare rests on a weak evidentiary base
State the actual crux. Your description here is more about the implications of the crux.
You can state somewhat general grounds, but then give a specific instantiation if possible. E.g., something about whether one form of slaughter is more painful to shrimp than another, or whether analgesia is good evidence, etc.
Would update on: timelines, public/model concern for animals, indirect normativity, moral-circle expansion, and simulated-animal welfare.
this is too general/vague. I want explicit defined crixes. What is the specific question they are uncertain about, how would you measure it, and what decision would it change?
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citar de donde salió
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revisar todos los asterisos
Haier HBC-150
poner foto del refrigerador
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A simple kind of method that returns a value is what is formally called an accessor because it accesses a value in an object. In the real world everyone calls them getters.
A getter is a method whose job is to give you information about an object.
Now the newscast jumped to the Mathematicianswho'd discovered the equation for flight
Another science fiction part of the story "Equation for flight".
The motion-activated device had caught thelast fifty feet of the man's fall, the windmill panic offlailing arms, the spread of his body on the ground
Good description of what was seen in the footage and wow fifty feet is a long fall. I am pretty sure the man died.
It means twenty-four-hour news coverage. It meanspoliticians doing damage control, activists egging onprotests. It means Francisco Furcal's granddaughter ata press conference defending her family's legacy."My grandfather's formula is sound. Math is constant and absolute. Any problems that arise are thefault of those who miscalculate it."Bad move, lady. This could only put everyone onthe defensive, compelling them to trot out their transcripts and test results and every other thing thatproved their genius. Nneoma tried to think of whereshe'd put her own documents after the move, but that
This story seems to have some elements of science like mathematics. Overall this two paragraphs are funny and interesting.
Best instead to concentrate on the shaky footage captured by a securitycamera
Seems to me the cameras had poor quality videos.
It means twenty-four-hour news coverage. It meanspoliticians doing damage control
That was a very good way of introducing story. It makes sure reader gets interested in a story.
Typewriter repair people on r/typewriters:
Title : Installateur de pompe à chaleur RGE partout en France | Hello Watt Meta : "Hello Watt installe votre pompe à chaleur avec un professionnel certifié RGE. Devis gratuit, calcul des aides, suivi de A à Z. Plus de 3 000 installations en France."
FAQ : vos questions sur les installateurs de PAC
ajouter 2 questions ?
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Pourquoi installer une pompe à chaleur ?
réduire ou supprimer la section (très informationnel)
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suppr
Type de PAC Prix moyen (pose incluse) Air-air 6 000 à 9 000 € Air-eau 9 000 à 13 000 € Géothermique 12 000 à 20 000 € Hybride 10 000 à 15 000 €
ajouter "(tarifs 2026, pose incluse)" si prix à jour
Une pompe à chaleur représente un investissement de départ non négligeable. En général, l’installation représente en moyenne 10 à 15 % du coût total de la PAC. Voici les fourchettes moyennes observées pour l’achat et la pose d’une pompe à chaleur par un professionnel en 2026 :
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Pourquoi faire appel à un installateur pour sa pompe à chaleur ?
supprimer cette section
L’astuce Hello Watt Il est vivement recommandé de demander au moins 3 devis à des installateurs de pompes à chaleur différents pour comparer les prestations et les prix. Notez que la demande de devis est une démarche gratuite et sans engagement.
suppr ou remplacer par ""Hello Watt compare plusieurs installateurs certifiés pour vous proposer le meilleur rapport qualité/prix. Vous recevez un devis clair, sans démarchage."
Étape 3 : vérifier les références de l’installateur
Supprimer ou fusionner dans un encadré "Notre processus de sélection" :
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Étape 2 : choisir un installateur certifié RGE
Intégrer le contenu RGE/QualiPAC dans le bloc de réassurance Hello Watt :
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Un bon installateur de pompe à chaleur commencera toujours par réaliser un audit énergétique pour évaluer les déperditions thermiques de votre logement. Ce diagnostic permet de choisir une puissance adaptée et d’éviter les erreurs de dimensionnement : une PAC surdimensionnée gaspille de l’énergie, tandis qu’une PAC sous-dimensionnée ne fournit pas le confort attendu. Il peut même être judicieux de prévoir des travaux d’isolation avant d’installer une pompe à chaleur pour améliorer ses performances et réduire votre facture.
suppr ou reformuler nouvelle intention
Remplacer première image par chantier hello watt
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Reviewer #1 (Evidence, reproducibility and clarity (Required)): __ In this manuscript, the authors describe the discovery of a molecular regulator of the immune transcriptional program, which is activated by intestinal distension upon bacterial colonization of the C. elegans intestine. Taking advantage of the fact that inhibition of aex-5 is known to cause intestinal distension and a C-type lectin gene clec-60 as a marker for the immune response to intestinal distension (clec-60p::gfp), the authors performed a forward genetic screen for suppressors of the immune response activation. Of the two mutants isolated, they focused on the stronger suppressor, which corresponded to a cysteine-type DUB, the Ubiquitin Specific Peptidase-14 (usp-14). Through rescue experiments, phenocopy analyses, and quantitative RT-PCR, they validated usp-14 as the causal gene and initiated characterization of its role in immune response activation. To this end, the authors investigated the tissue of action, identifying the intestine as the tissue in which usp-14 mediates the regulation of the immune response. Through transcriptomic analyses, they found that the signalling pathway likely regulated by usp-14 in response to intestinal distension is the Wnt pathway, as they have observed reduction in the transcriptional level of some of the Wnt pathway components in usp-4(tm1481), in response to infection with S. aureus. Additionally, transcriptomic data indicate that usp-14 plays a role in immunity regulation even in the absence of infection. Based on these findings, the authors propose that usp-14 has a dual role in immune regulation: one in surveillance immunity, preventing overactivation of immune responses, and another as a mediator of pathogen-induced responses, such as those triggered by P. aeruginosa or S. aureus. The experiments are rigorous and the results robust; however, some points would benefit from further investigation or clarification. __Response: We thank the reviewer for an excellent summary of our work and for the valuable feedback.
Comment: The expression domain of usp-14 appears to be quite expanded based on single cell RNAseq data (e.g. PMID: 28818938) therefore it is likely that the transgenes used for expression analysis are lacking key regulatory information. Alternative methods like smFISH would be more appropriate to characterise the spatiotemporal pattern of usp-14 expression in more detail. Response: We thank the reviewer for this valuable suggestion. In the original version of the manuscript, we used a 714 bp region upstream of the usp-14 start codon to generate the transcriptional reporter. In the revised manuscript, we reconstructed the reporter using a longer 1924 bp upstream promoter region together with a portion of exon 1. Using this updated reporter, we observed substantially broader expression of usp-14, particularly during the early larval stages. These results are described on page 6, lines 148-153: “We next examined the spatiotemporal expression pattern of usp-14 in C. elegans. To this end, we generated transgenic worms expressing GFP under the control of the usp-14 promoter (usp-14p::gfp). During early larval development, usp-14 was broadly expressed across multiple tissues (Figure 3A). However, in L4 larvae and adult animals, expression became more restricted and was predominantly observed in the intestine and a subset of neuronal cells. Notably, both intestinal and neuronal expression persisted throughout development (Figure 3A).”
Comment: __The mutation mapped in usp-14(jsn19) is a missense mutation (E122K) that suppresses the immune response to a degree comparable to the usp-14(tm1481) deletion allele. However, the authors do not show the functional domains in Fig. 1E potentially affected by this missense mutation. __Response: We have now updated Figure 1E to include the functional domains of USP-14 and mapped both the usp-14(jsn19) missense allele and the usp-14(tm1481) deletion allele onto the protein schematic.
Comment: __How USP-14 regulates Wnt and how Wnt signalling relates to activation of immune responses is not fully supported. Are the Wnt components mentioned in the study induced specifically in the intestine upon infection and does USP-14 act in the intestine in the context of this regulation? How do the authors interpret that both Wnt ligands and receptors are induced ? Does Wnt signalling appear as a GO term in the transcriptomic analysis? The authors can include Wnt signalling components in the analysis of the transcriptomic results. __Response: We thank the reviewer for these insightful comments. Previous studies have shown that the Wnt pathway components examined in our study are induced in the intestine upon infection and function within the intestine to regulate host defense against bacterial pathogens (PMID: 29768179; PMID: 36323254).
We did not observe significant enrichment of Wnt signaling terms in the GO analysis of our transcriptomic dataset. We believe this is likely due to the stringent thresholds used for differential expression analysis (fold change > 2 and p At present, the precise mechanism by which USP-14 regulates Wnt pathway components remains unclear. One possibility is that USP-14 influences Wnt signaling indirectly through additional substrates or interacting proteins that regulate transcriptional outputs. We have now clarified this point in the Discussion (page 13, lines 344–349): “These observations raise the possibility that additional USP-14 substrates or interacting proteins modulate transcriptional outputs downstream of intestinal distension. Future studies aimed at identifying the direct substrates of USP-14 and defining how USP-14 interfaces with neuronal ACC-4 signaling and other distension-responsive pathways will provide important mechanistic insight into how intestinal distension is coupled to innate immune activation.”
Regarding the simultaneous induction of Wnt ligands and receptors, we interpret this as a potential amplification or reinforcement mechanism that enhances Wnt/β-catenin signaling during infection-induced intestinal distension. However, further studies will be required to determine the mechanistic significance of this coordinated transcriptional regulation.
Comment: __Overall, in most of the figures, the micrographs are in general quite dark and exhibit poor contrast between signal and background, particularly in Fig. 1, panels B and J, and Fig. 2, panels B and F (upper rows). Even though these panels are intended to show absence of response, the outlines of the worms are difficult to discern. __Response: We thank the reviewer for the feedback. We have now improved the image presentation throughout the manuscript by either increasing the intensity or adding dotted outlines to more clearly indicate worm positions.
Comment: __In Figure S3, panels A and B, the pmk-1(km25); usp-14(tm1481) animals subjected to aex-5 RNAi show some level of fluorescence/response induction comparable to pmk-1(km25) alone. This observation is not discussed in the text. __Response: We have now discussed this observation in the text. These results are described on page 9, lines 244-248: “Although pmk-1(km25);usp-14(tm1481) worms displayed relatively higher GFP levels than usp-14(tm1481) single mutants upon aex-5 RNAi treatment, this effect likely reflects the elevated basal GFP expression observed in pmk-1(km25) mutants (Figure S4B). Importantly, pmk-1(km25);usp-14(tm1481) animals still exhibited significantly lower GFP levels than pmk-1(km25) single mutants.”
Reviewer #1 (Significance (Required)): __ __Comment: __The work is interesting because it expands some previous work in the field demonstrating immune response induction as a consequence of intestinal distension even in the absence of bacterial infection. This is known to be mediated by the neuronal acetylcholine receptor ACC-4, which signals to the intestine where it regulates immune genes via the Wnt pathway. However, how USP-14 relates to ACC-4 is currently unclear and whether USP-14 function is really required in the intestine to control Wnt signalling is not demonstrated. The authors should include a model to describe how their findings relate to the previous literature and how USP-14 may link mechanistically to Wnt signalling pathway activation. __Response: We thank the reviewer for this insightful comment. We agree that the relationship between USP-14, ACC-4, and Wnt signaling requires further clarification. As suggested by the reviewer, we have now included a model summarizing the current understanding of intestinal distension-induced immune activation and integrating our findings with previous literature (Figure 6H).
Comment: __It remains also unclear whether usp-14 is the only deubiquitinase involved in intestinal distension-induced signalling via the Wnt pathway, or whether other paralog usp genes might also contribute to regulation of immune-responsive transcription. Notably, several mammalian deubiquitinases have established roles in cancer suppression and inflammatory response and innate immunity in other systems so this would increase the potential significance of the work. __Response: We thank the reviewer for this valuable suggestion. To systematically examine whether additional DUBs contribute to intestinal distension-induced immune activation, we performed an RNAi screen targeting all DUBs available in the Ahringer RNAi library using the aex-5(sa23);clec-60p::gfp reporter strain. Among the DUBs tested, knockdown of usp-14 produced the strongest suppression of clec-60p::gfp expression. Although knockdown of usp-5 also partially suppressed GFP induction, usp-5 RNAi did not affect survival during P. aeruginosa infection, suggesting that usp-5 is not required for host defense under these conditions. Together, these findings identify USP-14 as the major DUB required for intestinal distension-induced immune activation in our experimental system. These results are now included in Figure 1G, H, and Figure S2.
Reviewer #2 (Evidence, reproducibility and clarity (Required)): __ Summary C. elegans are soil-dwelling nematodes that feed on bacteria and fungi and thus must be able to distinguish between innocuous and pathogenic species of microbes to survive. Though they lack adaptive immunity, these animals have an ancient version of an innate immune system that has no circulating sentinel or phagocytic cells yet can still mount a response to pathogen exposure. A consequence of the mode of infection of some ingested bacterial pathogens is intestinal distension which by itself, even in the absence of pathogens, is sufficient to trigger the expression of genes encoding immune effectors, including proteins that are bactericidal. The complete mechanistic scheme connecting intestinal distension to the expression of immunity genes has not been resolved, motivating the authors to perform a forward genetic screen for additional components of this pathway. One mutant that the authors isolated was usp-14, encoding an evolutionarily conserved deubiqutinating enzyme. Functional analysis revealed that usp-14 confers protection from microbial pathogens and that the intestine is its primary site of action for its role in host defense. The authors' data indicate that while USP-14 regulates the expression of innate immunity genes that are induced by intestinal distension, surprisingly it functions independently of several canonical innate immune signaling pathways, including the pmk-1/p38 MAPK pathway. Instead, USP-14 appears to act through Wnt signaling to regulate immune effectors by upregulating the expression of several components of that pathway, including the C. elegans ß-catenin ortholog bar-1. This places usp-14 within a gut-brain axis previously shown to control the C. elegans innate immune response through acetylcholine-mediated activation of Wnt signaling. The authors' findings provide new mechanistic insight to this pathway and add to the understanding of ubiqutination as an immune regulatory module. __Response: We thank the reviewer for providing an excellent summary of our work.
Major comments __1. There are three types of experiments in which the authors use the same set of controls across several different figure panels, as stated in the legend to Figure 2. First, when quantifying GFP levels of clec-60::gfp in RNAi-treated animals, the authors use the same clec-60p::gfp and usp-14(jsn19);clec-60p::gfp controls for Fig. 1K, 2C, and 2G. For infection assays with S. aureus NCTC8325, the survival plots for the clec-60p::gfp and usp-14(jsn19);clec-60p::gfp controls shown in Fig. 2E are the same as the ones used in Fig. 1M. Similarly, for infection assays with P. aeruginosa PA14, the survival plots for the clec-60p::gfp and usp-14(jsn19);clec-60p::gfp controls shown in Fig. 2I is the same as was used for Fig 1I. In each case, if the authors in fact collected all of the data for each strain that they studied at the same time but then chose to parse larger datasets into separate figure panels to make it more clear to the reader, then this approach is valid but the authors need to explicitly state that this is what they did. However, if the data pertaining to the control strains were collected at a different time or if it comes from a separate biological replicate, then re-using data from the controls is not appropriate because it would not accurately reflect the specific conditions of the experiment to which the data are being compared. If this is indeed the scenario, then the authors will need to repeat these experiments and include the appropriate control in each iteration. __Response: While preparing the manuscript, these experiments were performed simultaneously. Therefore, all panels that share controls have results from experiments performed simultaneously and represent the same biological replicate. We have added this additional information in the relevant figure legends.
Comment: __2. From the legends describing figure panels that include data pertaining to clec-60p::gfp expression levels as assessed by fluorescence microscopy it seems that, in general, the authors measured GFP fluorescence in about 30 animals to produce quantitative data. How many biological replicates of these types of experiments were carried out? This is not explicitly stated in the section describing fluorescence imaging in the Methods section. Following the description of their methodology regarding statistical analysis of survival curves from microbial infection assays, however, the authors state that, "[a]ll experiments were performed independently at least three times unless otherwise noted." Does this statement apply to microscopy or only to experiments involving infection assays? If the data reporting quantitation of GFP signal is based on only 30 animals, then additional biological replicates are necessary, along with appropriate statistical analyses. __Response: The quantified GFP fluorescence data are derived from three independent biological replicates. In each experiment, we typically imaged and quantified approximately 10 worms per condition, yielding a total of ~30 worms analyzed per genotype or treatment across all replicates (except Figure S1B, where we had two independent replicates). We have added the number of experiments in the figure legends for these data.
Comment: __3. The authors have made all of the RNASeq data publicly available on the Sequence Read Archive, and they include data from several pairwise comparisons for differential gene expression analysis in their supplemental files. One of the most important facts to come out of the authors' Gene Ontology analyses of their RNASeq data is that the genes that are upregulated in a usp-14-dependent manner upon intestinal distension are enriched for those whose products play a role in innate immunity/host defense. The authors should say more about these genes. Are there any commonalities between them with regard to function? Are any of them targets of transcription factors that are known to function in C. elegans innate immunity? If so, this could provide clues as to what the substrates of USP-14 might be. Importantly, the specific identity of the genes assigned in the GO analyses to biological processes pertaining to innate immunity and host defense should be revealed in a supplemental file, and designated as being dependent on or independent of usp-14 for their expression during intestinal distension. __Response: We thank the reviewer for this insightful suggestion. We have now expanded the Results section to describe the functional categories enriched among the USP-14-dependent intestinal distension-induced immune genes, including C-type lectins, ShK toxin domain-containing proteins, and lysozymes (page 7, lines 194-196).
In addition, we compared our transcriptomic dataset with previously published transcription factor-regulated gene sets using WormExp analysis and identified a substantial overlap with genes regulated by the GATA transcription factor ELT-2. These new analyses are described on page 7, lines 197-210: “To identify transcription factors potentially involved in intestinal distension-induced immune activation, we performed transcription factor enrichment analysis using WormExp on genes upregulated in N2 worms following aex-5 RNAi treatment. This analysis revealed a substantial overlap between aex-5 RNAi-induced genes and genes regulated by the GATA transcription factor ELT-2 (Figure S3D). We next examined whether USP-14-dependent immune genes overlapped with ELT-2-dependent immunity genes induced by intestinal distension. To this end, we identified innate immune genes common to both ELT-2-regulated gene sets and aex-5 RNAi-induced genes. Strikingly, these ELT-2-dependent intestinal distension-induced immune genes showed substantial overlap with USP-14-dependent immune genes (Figure S3E and Table S5), suggesting that USP-14 may regulate distension-induced immunity, at least in part, through ELT-2-dependent transcriptional programs. Consistent with this possibility, RNAi-mediated knockdown of elt-2 did not further increase the susceptibility of usp-14(tm1481) worms to P. aeruginosa infection relative to wild-type worms (Figure S3F), supporting a model in which USP-14-mediated immune responses require ELT-2 activity.”
Finally, we have created a new table (Table S5) that specifies the identity of the genes assigned in the GO analyses to biological processes pertaining to innate immunity and host defense, for USP-14-dependent and independent genes.
Comment: __4. The authors' data suggest that in response to bacterial infection USP-14 upregulates the expression of bar-1, along with other components of the Wnt signaling pathway, which in turn upregulates innate immunity genes. This could be further substantiated by directly demonstrating that there are USP-14-regulated innate immunity genes whose induced expression in the presence of microbial pathogens also requires bar-1. Along those lines, an initial test would be to assess clec-60p::gfp expression in bar-1 animals versus bar-1;usp-14 double mutants, similar to the experiment whose results are reported in Fig. S4. If generating the bar-1;usp-14 double mutant is not feasible, then RNAi could be used to knockdown bar-1 expression in clec-60p::gfp;usp-14(tm1481) animals. To expand this analysis, the expression of the six innate immunity genes shown to be regulated upon intestinal distension in usp-14-dependent manner could be measured in the presence and absence of intestinal distension or microbial infection in bar-1 and bar-1;usp-14 animals by qRT-PCR. At a minimum, the authors should conduct a bioinformatics analysis to compare the USP-14-regulated innate immunity genes identified in their RNAseq studies to lists of known BAR-1 transcriptional targets to look for potential overlap. __Response: We agree that extending these analyses to qRT-PCR experiments examining additional immune genes would be informative. However, both bar-1 mutants and bar-1 RNAi-treated worms exhibited severe developmental and physiological defects, including sick and dead animals during development, likely reflecting the pleiotropic developmental roles of BAR-1. Although fluorescence imaging and survival assays could be performed by selectively transferring surviving adults, we were concerned that bulk collection of worms for qRT-PCR analyses would introduce confounding effects arising from developmental defects and reduced viability.
To further address the reviewer’s suggestion, we carried out a comparative analysis between USP-14-dependent intestinal distension-induced immune genes and previously identified BAR-1-dependent immune genes. Although transcriptome-wide datasets for BAR-1-dependent pathogen-induced immune genes are not currently available, an earlier study identified seven immune response genes regulated by BAR-1 during infection (PMID: 18981407). We found that six of these genes overlap with the USP-14-dependent intestinal distension-induced immune genes identified in our study. These analyses have now been added to the Results section and included in Table S5.
Comment: __5. While in their Discussion section the authors mention evolutionarily conserved roles for protein ubiquitination as means of immunomodulation, there are few if any comments regarding ubiqutination as a regulatory scheme in C. elegans innate immunity or how their findings enhance our understanding of this phenomenon. Ubiquitination affects C. elegans immunity at multiple levels, from avoidance behavior to gene regulation, and it seems appropriate for the authors to address this in order to more fully contextualize their findings. __Response: We thank the reviewer for the suggestion. We have now added a new paragraph to the Discussion that places our findings in the context of the existing literature on ubiquitination, deubiquitination, and innate immunity in C. elegans. The discussion is added on pages 11-12, lines 299-312: “Although ubiquitin-mediated signaling has emerged as a central regulator of innate immunity across metazoans (Jiang & Chen, 2011; Mello-Vieira & Dikic, 2026), the contribution of DUBs to host defense in C. elegans remains poorly understood. Previous studies in C. elegans have shown that ubiquitin-dependent processes regulate diverse aspects of immunity, including immune surveillance, xenophagy, and pathogen tolerance (Garcia-Sanchez et al, 2021). Perturbations in proteasome function have also been shown to activate surveillance immunity (Ghosh & Singh, 2026; Troemel et al, 2026), highlighting the importance of ubiquitin-associated pathways in sensing pathogen-induced cellular damage. However, most prior studies have focused on ubiquitin ligases, proteasome-associated pathways, or global ubiquitin signaling rather than on specific DUBs directly regulating antibacterial immune responses. To our knowledge, our study provides the first direct evidence that a specific DUB regulates antibacterial innate immunity in C. elegans. Thus, our findings establish USP-14 as a previously unrecognized regulator of host defense and identify deubiquitination as an important regulatory layer in intestinal distension-mediated immunity.”
__Minor comments __1. In the Results section, the authors state that "[k]nockdown of cec-10 led to only a marginal decrease in survival during P. aeruginosa infection" (lines 92 and 93) and that cec-10 "has minimal impact on C. elegans survival during infection" (lines 93 and 94). However, as reported in Supplemental Table 5 the magnitude of the calculated difference in mean survival time between animals treated with RNAi targeting cec-10 and untreated control animals (-20% to -24% and statistically significant in 3/3 replicates) closely approximates the difference in mean survival between usp-14 mutants and controls (-19% to -28% and statistically significant in 3/3 replicates), which the authors clearly find to be significant. If by this metric usp-14 is important for host defense, then so too is cec-10. In light of this, the authors should use different language to describe the impact of cec-10 knockdown on the susceptibility of C. elegans to microbial infection and the potential role of cec-10 in immunity.
Response: We chose not to pursue cec-10 further primarily because it lacks a clear human homolog and because the mutant exhibited reduced expression of the co-injection marker, raising the possibility of broader transgene-related effects. We have modified the text on page 4, lines 93-97: “Knockdown of cec-10 resulted in a significant reduction in survival during P. aeruginosa infection (Figure S1C). However, we did not pursue cec-10 further for two reasons: (i) cec-10(jsn20) mutants exhibited a modest but significant reduction in the myo-2p::mCherry co-injection marker (Figure 1D), raising the possibility of broader transgene-related defects, and (ii) cec-10 lacks a clear human homolog.”
Comment: __2. All of the micrographs in Fig. 1B appear very dark. The GFP expression in the control animals appears dim, making it difficult for the reader to compare the signal in those animals to the GFP expression levels in the mutants. I recommend adjusting the brightness level in an equivalent manner across all of the micrographs to account for this. __Response: We have increased the brightness of all the images, as suggested by the reviewer.
__Comment: __3. Fig. 1E depicts a gene structure diagram for usp-14 with the position of the point mutation in the jsn19 allele isolated in the authors' forward genetic screen indicated by the amino acid substitution symbol drawn over the second exon. Instead of mixing gene- and protein-level information about the jsn19 allele, I recommend replacing the gene structure diagram with a domain structure diagram of the USP-14 protein that depicts the conserved C19 peptidase and ubiquitin-like domains. The relative position of the E122K substitution should still be noted. __Response: __We have now updated Figure 1E to include the functional domains of USP-14 and mapped both the usp-14(jsn19) missense allele and the usp-14(tm1481) deletion allele onto the protein schematic.
Comment: __4. Since all of the information in Fig. 1F appears elsewhere in the text, I recommend eliminating this panel. __Response: We have removed it.
Comment: __5. Regarding the RNAseq analysis, the authors state that 1241 genes are upregulated upon aex-5 knockdown (line 162). The authors then ask which of these genes are regulated by usp-14 in the context of intestinal distension and find that 633 are upregulated a usp-14-dependent manner when aex-5 is targeted by RNAi and that 595 are upregulated even in the absence of usp-14 (Fig. 3D). This accounts for 1228 genes in total, not 1241. Can the authors explain this discrepancy? __Response: We thank the reviewer for carefully noting this discrepancy. The difference arises from the criteria used to classify genes into the categories shown in Figure 5D (previously Figure 3D). Specifically, genes uniquely upregulated in usp-14(tm1481) worms were defined as genes that were either exclusively induced in usp-14(tm1481) worms or expressed at levels more than 2-fold higher in usp-14(tm1481) worms compared to N2 worms. During this classification, 13 genes that were initially identified as upregulated in N2 worms following aex-5 RNAi were found to be expressed at levels more than 2-fold higher in usp-14(tm1481) worms than in N2 worms (Table S4). These genes were therefore reassigned to the “usp-14(tm1481)-specific” category in the Venn diagram. Consequently, the total number of genes represented in the Venn diagram becomes 1228 instead of 1241. To clarify this point, we have now added an explanation to the figure legend.
Comment: __6. For the sake of clarity, in the legend to Fig. 3D I recommend expanding the description of the categories of genes depicted in the Venn diagram by using the same language as in the first worksheet of Supplemental Table 4. __Response: We thank the reviewer for the suggestion. We have now added these details to the legend of Figure 5D (previously Figure 3D). The legend reads: “(D) Venn diagram showing the overlap between genes upregulated upon aex-5 RNAi in N2 and usp-14(tm1481) worms. The GO analyses for the biological processes of unique and common genes are shown. USP-14-dependent genes were defined as genes that were either exclusively upregulated in N2 worms or expressed at levels greater than 2-fold higher in N2 worms than in usp-14(tm1481) worms. USP-14-independent genes were defined as genes upregulated in both N2 and usp-14(tm1481) worms with expression differences of less than 2-fold between the two strains. Genes uniquely upregulated in usp-14(tm1481) worms were defined as genes that were either exclusively induced in usp-14(tm1481) worms or expressed at levels greater than 2-fold higher in usp-14(tm1481) worms than in N2 worms. Thirteen genes classified as upregulated in N2 worms were more than 2-fold higher in usp-14(tm1481) worms than in N2 worms (Table S4) and were therefore included in the usp-14(tm1481)-specific category.”
Comment: __7. In Fig. 4B, the authors' annotation indicates that there is a statistically significant difference (**, p __Comment: __8. In Fig. S5, the shade of blue used to represent the data from the nhr-49(nr2041);usp-14(tm1481);clec60p::gfp animals in panel E is different from that used to represent data from the same animals in panel B. This breaks the pattern of all of the other panels of this figure in which the data pertaining to a given phenotype are depicted in the same color. Also, in the symbol key in panel E there is an extra semi-colon before clec-60p::gfp that should be eliminated in the second genotype notation. __Response: We thank the reviewer for carefully examining the figure and for bringing these issues to our attention. We have made the changes.
Comment: __9. The authors' data show that USP-14 regulates bar-1 expression, and in the Discussion section they mention that in mammals beta-catenin is a substrate of USP14. Can the authors comment on the possibility of/evidence for BAR-1 autoregulation in C. elegans and the prospect of it being facilitated by USP-14? This could be a minor point to add to the Discussion. __Response: In both contexts, USP-14 appears to stabilize BAR-1 by regulating it at either the transcriptional or post-translational level. However, it is currently unknown whether BAR-1 regulates USP-14 expression and thereby participates in an autoregulatory mechanism. Nevertheless, we have added to the Discussion that USP14 may regulate the Wnt pathway through both transcriptional and post-translational mechanisms, depending on the biological context. __Reviewer #2 (Significance (Required)): __ The study described in this manuscript ties in to the findings from two prior genetic screens carried out in C. elegans that aimed to identify immune regulators (Ren et al., Cell Reports, 2022 and Labed et al., Immunity, 2018). Though their strategies differed, both of these previous studies uncovered a role for acetylcholine receptors in modulating the response to ingested microbial pathogens, especially when infection is associated with intestinal distension, indicating that a neuron-to-gut axis controls innate immunity in C. elegans. Labed and colleagues were the first to show that activation of this pathway results in the upregulation of genes encoding Wnt signaling pathway components, including the worm ortholog of beta-catenin called bar-1, which are necessary for the expression of immune effectors in the intestine. The Labed study also revealed that protein ubiquitination could contribute to regulating host defense gene induction because knockdown of lin-23, the substate binding subunit of a ubiquitin ligase complex that mediates BAR-1 degradation, results in constitutive expression of clec-60p::gfp, the same transcription reporter used by Ghosh and Singh as a readout for the expression of innate immunity genes. In their screen that revisits the Ren et al. approach, Ghosh and Singh find that another protein implicated in regulating protein stability via ubiquitination status, USP-14, also controls the expression of innate immunity genes in response to intestinal distension. Interestingly, their data indicate that it does so by upregulating bar-1. This discovery therefore adds an element of mechanistic detail regarding the regulation of Wnt signaling in immunity. While the Labed data suggest that ubiquitination may regulate BAR-1 at the post-translational level, Ghosh and Singhs' results indicate a second layer of regulation of bar-1 at the transcriptional level that also appears to involve ubiquitination. In this case, USP-14 is predicted to modulate the ubiquitination status of a yet-to-be-identified substrate that directly or indirectly governs bar-1 expression. The authors' findings thus bring the field closer to having a complete picture of the Ach-Wnt pathway in C. elegans. As they point out in the Discussion section of their manuscript, ubiquitination is an evolutionarily conserved yet complex means of tuning the immune system. The work described here helps to shed light on this important immune regulatory mode and could have implications for aspects of epithelial immunity that are in common to both invertebrates and vertebrates.
Response: We thank the reviewer for providing such a thoughtful overview of the field and for placing our findings in the context of previous studies on intestinal distension-induced immunity in C. elegans. We also sincerely appreciate the reviewer’s constructive feedback and insightful comments, which have helped us improve the quality and clarity of the manuscript.
My research interest and specific area of expertise pertains to evolutionarily conserved genetic pathways that control healthspan through affecting cellular resilience later in life. Using C. elegans as a surrogate for aging humans, my group studies age-dependent changes in the activity of regulatory modules that protect older animals from the molecular damage associated with intrinsic and extrinsic sources of cellular stress, with a particular emphasis on microbial infection and oxidative stress.
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Summary
C. elegans are soil-dwelling nematodes that feed on bacteria and fungi and thus must be able to distinguish between innocuous and pathogenic species of microbes to survive. Though they lack adaptive immunity, these animals have an ancient version of an innate immune system that has no circulating sentinel or phagocytic cells yet can still mount a response to pathogen exposure. A consequence of the mode of infection of some ingested bacterial pathogens is intestinal distension which by itself, even in the absence of pathogens, is sufficient to trigger the expression of genes encoding immune effectors, including proteins that are bactericidal. The complete mechanistic scheme connecting intestinal distension to the expression of immunity genes has not been resolved, motivating the authors to perform a forward genetic screen for additional components of this pathway. One mutant that the authors isolated was usp-14, encoding an evolutionarily conserved deubiqutinating enzyme. Functional analysis revealed that usp-14 confers protection from microbial pathogens and that the intestine is its primary site of action for its role in host defense. The authors' data indicate that while USP-14 regulates the expression of innate immunity genes that are induced by intestinal distension, surprisingly it functions independently of several canonical innate immune signaling pathways, including the pmk-1/p38 MAPK pathway. Instead, USP-14 appears to act through Wnt signaling to regulate immune effectors by upregulating the expression of several components of that pathway, including the C. elegans ß-catenin ortholog bar-1. This places usp-14 within a gut-brain axis previously shown to control the C. elegans innate immune response through acetylcholine-mediated activation of Wnt signaling. The authors' findings provide new mechanistic insight to this pathway and add to the understanding of ubiqutination as an immune regulatory module.
Major comments
Minor comments
The study described in this manuscript ties in to the findings from two prior genetic screens carried out in C. elegans that aimed to identify immune regulators (Ren et al., Cell Reports, 2022 and Labed et al., Immunity, 2018). Though their strategies differed, both of these previous studies uncovered a role for acetylcholine receptors in modulating the response to ingested microbial pathogens, especially when infection is associated with intestinal distension, indicating that a neuron-to-gut axis controls innate immunity in C. elegans. Labed and colleagues were the first to show that activation of this pathway results in the upregulation of genes encoding Wnt signaling pathway components, including the worm ortholog of beta-catenin called bar-1, which are necessary for the expression of immune effectors in the intestine. The Labed study also revealed that protein ubiquitination could contribute to regulating host defense gene induction because knockdown of lin-23, the substate binding subunit of a ubiquitin ligase complex that mediates BAR-1 degradation, results in constitutive expression of clec-60p::gfp, the same transcription reporter used by Ghosh and Singh as a readout for the expression of innate immunity genes. In their screen that revisits the Ren et al. approach, Ghosh and Singh find that another protein implicated in regulating protein stability via ubiquitination status, USP-14, also controls the expression of innate immunity genes in response to intestinal distension. Interestingly, their data indicate that it does so by upregulating bar-1. This discovery therefore adds an element of mechanistic detail regarding the regulation of Wnt signaling in immunity. While the Labed data suggest that ubiquitination may regulate BAR-1 at the post-translational level, Ghosh and Singhs' results indicate a second layer of regulation of bar-1 at the transcriptional level that also appears to involve ubiquitination. In this case, USP-14 is predicted to modulate the ubiquitination status of a yet-to-be-identified substrate that directly or indirectly governs bar-1 expression. The authors' findings thus bring the field closer to having a complete picture of the Ach-Wnt pathway in C. elegans. As they point out in the Discussion section of their manuscript, ubiquitination is an evolutionarily conserved yet complex means of tuning the immune system. The work described here helps to shed light on this important immune regulatory mode and could have implications for aspects of epithelial immunity that are in common to both invertebrates and vertebrates.
My research interest and specific area of expertise pertains to evolutionarily conserved genetic pathways that control healthspan through affecting cellular resilience later in life. Using C. elegans as a surrogate for aging humans, my group studies age-dependent changes in the activity of regulatory modules that protect older animals from the molecular damage associated with intrinsic and extrinsic sources of cellular stress, with a particular emphasis on microbial infection and oxidative stress.
Note: This preprint has been reviewed by subject experts for Review Commons. Content has not been altered except for formatting.
Learn more at Review Commons
In this manuscript, the authors describe the discovery of a molecular regulator of the immune transcriptional program, which is activated by intestinal distension upon bacterial colonization of the C. elegans intestine. Taking advantage of the fact that inhibition of aex-5 is known to cause intestinal distension and a C-type lectin gene clec-60 as a marker for the immune response to intestinal distension (clec-60p::gfp), the authors performed a forward genetic screen for suppressors of the immune response activation. Of the two mutants isolated, they focused on the stronger suppressor, which corresponded to a cysteine-type DUB, the Ubiquitin Specific Peptidase-14 (usp-14). Through rescue experiments, phenocopy analyses, and quantitative RT-PCR, they validated usp-14 as the causal gene and initiated characterization of its role in immune response activation. To this end, the authors investigated the tissue of action, identifying the intestine as the tissue in which usp-14 mediates the regulation of the immune response. Through transcriptomic analyses, they found that the signalling pathway likely regulated by usp-14 in response to intestinal distension is the Wnt pathway, as they have observed reduction in the transcriptional level of some of the Wnt pathway components in usp-4(tm1481), in response to infection with S. aureus. Additionally, transcriptomic data indicate that usp-14 plays a role in immunity regulation even in the absence of infection. Based on these findings, the authors propose that usp-14 has a dual role in immune regulation: one in surveillance immunity, preventing overactivation of immune responses, and another as a mediator of pathogen-induced responses, such as those triggered by P. aeruginosa or S. aureus. The experiments are rigorous and the results robust; however, some points would benefit from further investigation or clarification.
The expression domain of usp-14 appears to be quite expanded based on single cell RNAseq data (e.g. PMID: 28818938) therefore it is likely that the transgenes used for expression analysis are lacking key regulatory information. Alternative methods like smFISH would be more appropriate to characterise the spatiotemporal pattern of usp-14 expression in more detail.
The mutation mapped in usp-14(jsn19) is a missense mutation (E122K) that suppresses the immune response to a degree comparable to the usp-14(tm1481) deletion allele. However, the authors do not show the functional domains in Fig. 1E potentially affected by this missense mutation.
How USP-14 regulates Wnt and how Wnt signalling relates to activation of immune responses is not fully supported. Are the Wnt components mentioned in the study induced specifically in the intestine upon infection and does USP-14 act in the intestine in the context of this regulation? How do the authors interpret that both Wnt ligands and receptors are induced ? Does Wnt signalling appear as a GO term in the transcriptomic analysis? The authors can include Wnt signalling components in the analysis of the transcriptomic results.
Overall, in most of the figures, the micrographs are in general quite dark and exhibit poor contrast between signal and background, particularly in Fig. 1, panels B and J, and Fig. 2, panels B and F (upper rows). Even though these panels are intended to show absence of response, the outlines of the worms are difficult to discern.
In Figure S3, panels A and B, the pmk-1(km25); usp-14(tm1481) animals subjected to aex-5 RNAi show some level of fluorescence/response induction comparable to pmk-1(km25) alone. This observation is not discussed in the text.
The work is interesting because it expands some previous work in the field demonstrating immune response induction as a consequence of intestinal distension even in the absence of bacterial infection. This is known to be mediated by the neuronal acetylcholine receptor ACC-4, which signals to the intestine where it regulates immune genes via the Wnt pathway. However, how USP-14 relates to ACC-4 is currently unclear and whether USP-14 function is really required in the intestine to control Wnt signalling is not demonstrated. The authors should include a model to describe how their findings relate to the previous literature and how USP-14 may link mechanistically to Wnt signalling pathway activation.
It remains also unclear whether usp-14 is the only deubiquitinase involved in intestinal distension-induced signalling via the Wnt pathway, or whether other paralog usp genes might also contribute to regulation of immune-responsive transcription. Notably, several mammalian deubiquitinases have established roles in cancer suppression and inflammatory response and innate immunity in other systems so this would increase the potential significance of the work.
2.3 一人连续 @ 同一个 agent —— 运行中注入（Task Manager）
与产品讨论是否接任务中心，任务归属于谁?
Figure 1. Ptpn11E76K/+ mutation in Nestin+ MSPCs aberrantly activates neighbouring wild-type HSCs, inducing MPN in Ptpn11E76K/+Nestin-Cre+ mice.
OS2
tesis
falta
FALTA PONER LA TABLE DE LOS RESULTADOS Y LA EXPLICACION
falta
FALTA PONER LA TABLE DE LOS RESULTADOS Y LA EXPLICACION
falta
Harguindeguy venía de ser juzgado por el secuestro de los empresarios algodoneros Federico y Miguel Gutheim,
Look up
2.3 一人连续 @ 同一个 agent —— 运行中注入（Task Manager）
待与产品讨论: 产品侧是否需要任务中心，cancel标记? 任务归属问题?
Le Bien-être à l'École : Repenser l'Enjeu des Sanitaires Scolaires
La question des toilettes scolaires, bien que souvent reléguée au second plan, constitue un levier fondamental pour la santé, la sécurité et le climat scolaire.
Les données issues du contexte source révèlent une situation alarmante : 80 % des élèves se retiennent d'utiliser les sanitaires et 50 % n'y vont jamais, entraînant des pathologies physiques (infections urinaires) et une détresse psychologique.
L'analyse démontre que l'organisation binaire et non mixte des toilettes, instaurée dès l'âge de 6 ans, ne protège pas les élèves mais favorise au contraire l'impunité, le harcèlement et la cristallisation des stéréotypes de genre.
La transition vers des sanitaires repensés — privilégiant l'intimité individuelle (cabines fermées), la suppression des urinoirs, et une visibilité accrue des espaces communs (co-veillance) — s'avère être une solution efficace pour restaurer la civilité et le bien-être des élèves, de la maternelle au lycée.
Le sujet des toilettes est trop souvent ignoré ou considéré comme secondaire par les institutions.
Pourtant, il touche au quotidien et aux droits fondamentaux des enfants.
Impact sur la santé : L'infirmerie scolaire rapporte des cas fréquents d'infections urinaires, particulièrement chez les filles qui s'interdisent de boire pour éviter les sanitaires.
Obstacles à l'usage : Selon les baromètres d'usage (Harris Interactive/Programme « À nous les toilettes »), la fréquentation est entravée par trois facteurs majeurs :
Le manque de fournitures de base (papier toilette, savon, poubelles).
L'insécurité et le manque d'intimité.
Peur et renoncement : Un élève sur cinq en primaire rapporte avoir été gêné par des regards indiscrets.
Ce sentiment est directement corrélé à d'autres formes de violence (moqueries, menaces, racket).
La séparation stricte entre filles et garçons dans les blocs sanitaires est une construction sociale qui génère des effets contre-productifs.
Injonctions stéréotypées : L'aménagement diffère selon le sexe (présence systématique de miroirs chez les filles, urinoirs imposant l'absence de pudeur chez les garçons).
Fantasme de l'autre : La séparation crée un "monde" inconnu, favorisant les préjugés et les comportements sexistes ou homophobes.
L'entre-soi masculin : Les blocs garçons sont souvent des lieux de mise en scène de la virilité et de la "crapulerie", entraînant des dégradations rapides (souvent moins de deux ans après construction).
Absence de surveillance : Parce que les urinoirs exposent la nudité des garçons, les adultes s'interdisent d'entrer dans les blocs, créant des espaces hors de contrôle où le harcèlement peut s'exercer sans témoin.
Le refuge des filles : À l'inverse, les toilettes des filles deviennent parfois leur seul espace de visibilité ou de retrait social face à une cour de récréation dominée par les garçons.
L'expertise scientifique (L'AROBE) et les expérimentations (notamment en Gironde) proposent de transformer les sanitaires pour répondre aux besoins réels des élèves.
L'intimité ne doit pas être pensée par rapport au sexe, mais par rapport à l'individu.
Suppression des urinoirs : 87 % des garçons interrogés ne souhaitent pas d'urinoirs et préfèrent des cabines individuelles garantissant leur pudeur.
Cabines "pleines" : Les portes doivent être fermées du haut jusqu'au bas pour empêcher les regards (par-dessus/par-dessous) et l'usage de téléphones portables pour filmer à l'insu d'autrui.
Cette transparence permet aux adultes d'intervenir sans briser l'intimité des cabines.
La présence de l'autre corps social (fille ou garçon) incite à un meilleur "prendre soin" de l'espace.
| Problématique | Solution Préconisée par les Experts | | --- | --- | | Tabou des règles | Distribution de protections hygiéniques dans des lieux visibles et accessibles (pas seulement à l'infirmerie). | | Manque de fournitures | Équiper chaque cabine de papier toilette et d'une poubelle individuelle de manière systématique. | | Sentiment d'insécurité | Rendre les blocs "surveillables" sans être intrusifs ; supprimer les verrous défaillants. | | Invisibilité du personnel | Humaniser l'espace en nommant le personnel d'entretien et en impliquant les élèves dans la décoration (fresques). |
Le document souligne que les freins au changement sont principalement situés "dans la tête des adultes".
Ils sont légitimes pour interroger les municipalités (écoles) et les départements (collèges) sur l'état des bâtiments.
Les Élus et Techniciens : Lors de constructions neuves, il est impératif de ne plus reproduire les modèles obsolètes (urinoirs, cloisons partielles) et de privilégier des sanitaires neutres et sécurisés.
Les Élèves : Leur participation est cruciale.
Les impliquer dans la définition des règles et l'autorégulation de l'espace favorise la citoyenneté et le respect mutuel.
« L'école est le lieu de protection des enfants. Donc les adultes qui viennent doivent être surveillés pour ça aussi. »
« On ne fait pas d'économies, on ne fait pas d'écologie sur le papier toilette. »
« La mixité n'a pas résolu tous les problèmes [si elle n'est pas accompagnée], mais elle a permis d'apaiser certaines choses, notamment sur le tabou des règles. »
Ce document de synthèse est basé sur les interventions d'Edith Maruéjouls et les travaux de la FCPE nationale présentés lors du webinaire de juin 2026.
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La Littératie en Santé : Enjeux, Concepts et Leviers d'Action
Ce document de synthèse analyse les interventions et les données présentées lors du webinaire co-organisé par Promotion Santé Île-de-France et l’ARS Île-de-France.
Il définit le concept de littératie en santé, dresse un état des lieux de la situation en France et propose des pistes d'action concrètes pour les professionnels.
La littératie en santé est désormais reconnue comme un déterminant majeur de la santé, influençant les comportements, l'utilisation des services et les inégalités sociales et territoriales.
Les points clés identifiés sont :
Une urgence nationale : Selon l'OCDE (2024), près d'un adulte sur deux en France ne possède pas le niveau de littératie suffisant (niveau 3) pour fonctionner de manière autonome au quotidien.
Un obstacle systémique : 73 % des adultes éprouvent des difficultés à naviguer dans le système de santé.
La littératie ne dépend pas seulement des compétences individuelles, mais aussi de la complexité du système.
Le virage organisationnel : Il est impératif de passer d'une responsabilité individuelle à une approche "pro-littératie" où les organisations simplifient leurs processus et leur communication.
La fracture numérique : Le numérique est un facteur aggravant d'inégalités.
72 % des adultes rencontrent des difficultés avec les outils numériques en santé, nécessitant un maintien systématique de l'accompagnement humain.
La littératie est définie par l'OCDE comme l'aptitude à comprendre et à utiliser l'information écrite pour atteindre des buts personnels et étendre ses connaissances.
L'OCDE distingue cinq niveaux de littératie.
Le niveau 3 est considéré comme le seuil minimal pour être autonome dans un pays industrialisé.
En France :
48 % des 55-65 ans ont des difficultés de lecture et d'écriture.
17 % des 16-24 ans sont concernés.
Seuls 9 % des adultes atteignent le niveau 5 (maîtrise des textes complexes).
Les données soulignent une fracture sociale et géographique marquée :
Diplôme : 58 % des personnes sans diplôme ou de niveau CAP/BEP ont une faible littératie.
Origine : 60 % des personnes nées hors de France sont en situation de faible littératie, contre 22 % pour les natifs.
Numérique : 45 % des 55-65 ans peinent à utiliser les outils numériques, ce qui les exclut de services publics de plus en plus dématérialisés.
La littératie en santé n'est pas une caractéristique fixe de l'individu, mais le résultat de l'interaction entre les compétences d'une personne et la complexité du système de santé.
| Domaine de difficulté | Pourcentage d'adultes concernés | | --- | --- | | Accéder, comprendre, évaluer l'information de santé | 44 % | | Naviguer dans le système de santé | 73 % | | Communiquer avec les professionnels de santé | 29 % | | Utiliser des outils numériques en santé | 72 % |
L'Approche Organisationnelle (Pro-littératie)
Le concept de "littératie en santé organisationnelle" (Brach) définit la capacité des organisations à permettre aux individus de trouver et d'utiliser l'information de manière équitable.
Une organisation "pro-littératie" doit :
Intégrer la littératie dans ses missions et sa planification stratégique.
Former son personnel à une communication claire.
Inclure les usagers dans la conception des services et documents.
Simplifier l'accès et la signalisation dans les services.
Assurer la clarté des coûts et de la couverture santé.
L'analyse distingue les interventions simples des approches complexes pour améliorer l'intelligibilité du système.
Cela déplace la responsabilité de la compréhension sur le professionnel.
Le FALC (Facile à Lire et à Comprendre) : Utiliser des phrases courtes, des mots simples et une hiérarchisation visuelle claire de l'information.
Aménagement des salles d'attente : Limiter le nombre d'affiches, regrouper les thématiques et encourager explicitement les patients à poser des questions.
Le Diagnostic en marchant : Parcourir l'établissement avec des usagers pour identifier les obstacles à l'orientation et à la compréhension administrative.
La Décision partagée : Former les équipes à la négociation avec le patient pour adapter les recommandations médicales à son contexte de vie réel.
L'approche communautaire : Aller vers les lieux de vie (centres sociaux) plutôt que d'attendre que les usagers viennent vers les structures de soins.
L'ARS Île-de-France a fait de la périnatalité une priorité en raison d'indicateurs alarmants : la mortalité infantile en Île-de-France est de 4,3 pour 1000, contre 3,6 au niveau national.
Lancé en 2023, ce projet vise à améliorer le niveau de littératie des femmes enceintes via trois phases :
Diagnostic : Identification des profils de littératie via le questionnaire HLQ (Health Literacy Questionnaire).
Plan d'action : Élaboration d'outils pédagogiques avec des partenaires de terrain.
Mise en œuvre : Accompagnement de projets spécifiques sur le territoire.
Enseignements de la recherche en périnatalité
Savoirs expérientiels : Il est crucial de reconnaître la légitimité des connaissances des mères et de les confronter aux savoirs professionnels sans hiérarchie.
Cercle de grossesse : Sortir du cadre médical strict pour créer des espaces collectifs de suivi de grossesse dans les lieux de vie des femmes.
Universalité proportionnée : Agir pour tous les publics tout en intensifiant l'aide pour ceux qui en ont le plus besoin, afin de ne pas stigmatiser les populations vulnérables.
Le dossier "Comprendre et Agir" de Promotion Santé Île-de-France propose plusieurs outils pour les acteurs de terrain :
Le Guide LISA : Décliné en trois volumes (Comprendre, Agir, Dossier documentaire), spécifiquement axé sur la périnatalité mais adaptable à d'autres thématiques.
La formation en ligne : Un module d'auto-formation de 2 heures conçu par l'association belge "Culture et Santé" pour s'initier aux concepts.
Récits de capitalisation (CAPS) : Six exemples de projets concrets permettant d'identifier les leviers et les freins à la mise en œuvre d'actions de littératie.
Base de données d'outils : Accès à des outils d'animation, des bibliographies enrichies (notamment sur la littératie et les migrants) et des appels à projets.
Die Spanne ist groß und hängt vom Modell ab. JTL-Wawi bietet einen kostenlosen Einstiegstarif. Billbee startet bei 9 €/Monat plus einer mit dem Bestellvolumen sinkenden Transaktionsgebühr. PlentyONE beginnt bei 59 €/Monat (Edition Lite), wobei sich die Gesamtkosten aus dem gebuchten Tarif und dem abgewickelten Umsatzvolumen zusammensetzen. Xentral startet bei 349 €/Monat zuzüglich volumenabhängiger Bestellgebühren, weclapp bei 39 €/Nutzer/Monat, wobei E-Commerce-Funktionen erst ab dem Trade-Tarif (ab 163 €/Nutzer/Monat) verfügbar sind. Kalkulieren Sie deshalb immer mit mehr als der Grundgebühr: Implementierung, Zusatzmodule und mögliche Mehrkosten pro Bestellung kommen hinzu.
die spanne ist gross und haengt sehr vom beduerfniss ab...change something like this
Als Faustregel gilt: Ab etwa drei parallel betriebenen Verkaufskanälen kann sich eine Multichannel-Warenwirtschaft lohnen, ab rund fünf Kanälen wird sie praktisch unvermeidbar. Der Grund ist die Bestandssynchronisierung: Je mehr Kanäle denselben Lagerbestand verkaufen, desto höher das Risiko von Überverkäufen und desto größer der manuelle Pflegeaufwand. Bei zwei Kanälen und geringem Volumen reicht oft noch ein leichtgewichtiges Tool wie Billbee oder die kostenlose JTL-Wawi.
change a little. depends on the specific case. amount of channels, amount of orders and time lost coordinating and and managing operations. then go with 3 most of the times, 5 nearly always necesasry. and then the last sentence you made aoubt leichtgewichtige tools
Jahresabschluss/Bilanz teils weiterhin über DATEV/Steuerberater
cut this point
30 Tage kostenlos testen, keine Kreditkarte erforderlich
cut this point
Nur 7 Verkaufskanäle, schmaler als bei spezialisierten Multichannel-Tools
change to andere tools and not spezialisierte ...tools
20 native Verkaufskanäle, erweiterbar über Mirakl-/Tradebyte-Middleware
cut this point
Einstieg ab 59 €/Mo., 30 Tage kostenlos testen
cut this point
Einrichtung und Onboarding erfordern erheblichen Zeitaufwand
cut this point
Gegründet 2006 Kassel, Deutschland 150+ Verkaufskanäle nativ in einem System bis zu 85 % weniger Aufwand im E-Commerce 4,0/5 OMR Reviews
change 4,0/5 to simply 4/5
Non l'ho letto ma mi sembra che presenti le terapie tradizionali e i loro problemi e perché PCSK9 possa essere la soluzione
The too little interest is more involved than the too high
not clear
cover the cost
up front
charges
usually (there are 0% APR deals)
full cost in cash
funds to self-finance out of pocket
a loan
from a financial intermediary like a bank.
“Now I bid you, my beloved hero,that you reveal this vision to men,tell them in words that it is the tree of glory
The divine vision must be shared with others, highlighting the cross as a symbol of glory and the importance of spreading spiritual truth through words.
the true way of life for speech-bearers. Lo! the King of glory, Guardian of heaven’s kingdomhonored me over all the trees of the forest,
It emphasizes the spiritual truth of Christianity, showing the cross as honored above all creation by God.
I rise up under the heavens, and am able to healeach of those who is in awe of me.
The speaker shows a transformation from suffering to divine power, showing the healing and reverence inspired in others.
“Now you can hear, my dear hero,that I have endured the work of evil-doers,harsh sorrows.
The speaker reflects on the suffering caused by evil forces, emphasizing survival and testimony.
They began to sing a dirge for him,wretched at evening, when they wished to travel hence,
The passage shows mourners grieving Christ's death through a funeral song, emphasizing the ending of the crucifixion and the weight of the loss.
they watched the Lord of heaven there, who rested a while,weary from his mighty battle
The passage presents Christ as both human and divine, showing his suffering as "mighty battle" and showing the crucifixion as an event witnessed by all.
Shadows spreadgrey under the clouds; all creation wept,
The passage uses dark personification and imagery to show that all creation is mourning Christ's suffering.
I watched it all.I was all beset with sorrow, yet I sank into their hands,humbly, eagerly. There they took almighty God,
The speaker witnessed Christ's suffering with sorrow while still accepting the divine event with reverence and humility, highlighting the nature of the crucifixion.
They mocked us both together
The speaker relates to the shared suffering with Christ, showing how both are rejected and mocked.
I trembled when he embraced me, but I dared not bow to the ground,or fall to the earth’s corners––I had to stand fast.
The speaker shows that he experiences awe and fear when encountering the divine.
enemies enough fixed me fast. Then I saw the Lord of mankindhasten eagerly, when he wanted to ascend upon me.I did not dare to break or bow downagainst the Lord’s word,
The passage highlights Christ's suffering and the recognition of authority, showing obedience, sacrifice, and the power of God's will over fear.
And yet, lying there a long while,I beheld in sorrow the Savior’s tree
The speaker reflects on the cross, responding with sadness and devotion. as he recognizes its significance as the symbol of Christ's sacrifice.
I was all beset with sorrows,fearful for that fair vision; I saw that eager beacon
The speaker expresses their emotional conflict, feeling fear and sorrow while still recognizing the Cross as a powerful symbol of salvation and hope.
And yet beneath that gold I began to seean ancient wretched struggle
Beneath teh Cross's appearance lies a ancient and painful struggle, which shows the redemption and suffering in the Christian vision.
and I was stained by sins,wounded with guilt; I saw the tree of glory
The speaker reflects on personal sin and guilt while recognizing the cross as a symbol of salvation and glory.
. All the angels of the Lord looked on;fair through all eternity; that was no felon’s gallows,
It shows the cross as a eternal and holy symbol, not a place of punishment or shame, emphasizing its divine significance in Christian belief.
JTL, PlentyONE und weclapp bringen teils eigene Shop-Lösungen mit, während sich Shopify, WooCommerce und Shopware über native Schnittstellen oder Middleware koppeln lassen.
confusing sentence. its more about adding that these competitors allow you to connect to your online shop and even offer replacements, which you can choose or not choose. either way possible. i want to prevent that people think some erps integrate, some replace the shopsystem, since that might be a step to far. in fact, maybe its worth briefly stating that erps are the orchestration layer or similar, the backend to manage many different channels. thus its build to connect to the shopsystems. and then that some even offer their own shopsystem if needed. as a plus
please take the entire paragraph into consideration here.
Die Bandbreite ist groß. JTL-Wawi und Odoo Community (selbst gehostet) lassen sich kostenlos nutzen. PlentyONE beginnt bei 59 €/Monat für ein vollwertiges ERP, Xentral bei 349 €/Monat, weclapp ab 39 €/Nutzer/Monat im Basistarif, für E-Commerce erst ab dem Trade-Tarif (ab 163 €). Zusätzlich zu den Abogebühren sollten Sie Implementierung (bei Odoo 15.000 bis über 250.000 €), Zusatzmodule und mögliche Kosten je Bestellung einkalkulieren.
structure this differently. just start with listing prices for the classic cloud tools. and then even state that there are free tools but you need to host and maintain yourself which really depends on your specific case but can have costs in the 10s of thousands.
Implementierung oft deutlich teurer als die Lizenz (15.000 bis über 250.000 €)
maybe make two points out of this or not. but the key point is that you need to build and maintain yourself and eitehr you have your own team or you hire partners, wich can be very expensive. this is the downside of open source. not entirely clear yet
Schmalere Marktplatz-Integrationsbreite als Spezialtools
andere tools instead of spezialtools
150+ Vertriebskanäle, eine der breitesten Auswahlen im DACH-Raum Echtes All-in-one: PIM, OMS, WMS, CRM und POS in einer Plattform Cloud-nativ mit 99,99 % SLA, bewährt bis in den Enterprise-Bereich Günstiger Einstieg ab 59 €/Mo., 30 Tage kostenlos testen
add also compared to all the other tools more international sales channels native integrated, thats a strong thing. add it as a separate point of strenght if possible
Keine native doppelte Buchführung
write it the same way as at how we handle it at the new plenty one version. or is there any real difference in offering? in the intro it sounded like three of the competitors are all the same when it comes to bookkeeping (dateve exports) make that point consistently
Niedrige Tarife begrenzen Kanäle, SKUs und Workflows
replace with bookkeeping, only datev/export. phrase it the same way as in other places. keep it relativly neutral, its just something to be aware of
Umsatzbasierte GMV-Gebühr kann bei starkem Wachstum die Basiskosten deutlich übersteigen
get rid of the word "deutlich", no need to replace it
Aufwändige Ersteinrichtung und langes Onboarding Eingeschränkte technische SEO-Funktionen im integrierten Shop
delete these points, seem redundant
Welches System für welchen Bedarf? Die fünf Systeme gewinnen in unterschiedlichen Szenarien. Diese Übersicht zeigt, welche Plattformen für welche typischen Anforderungen besonders geeignet sind. Im Folgenden werden die Plattformen im Detail vorgestellt. PlattformIhr SchwerpunktWarum PlentyONESkalierender Multichannel-Verkauf, Commerce-Betrieb in einem System gebündelt150+ native Vertriebskanäle plus PIM, OMS, WMS und Shop in einer cloud-nativen Plattform JTLGünstiger Einstieg, einzelner Shop plus ein bis zwei Marktplätze im DACH-RaumKostenlose JTL-Wawi und tiefes, deutsches Shop- und Marktplatz-Ökosystem XentralE-Commerce und zugleich Produktion oder B2B-Großhandel in einem System200+ Integrationen, No-Code-Automatisierung sowie Einkauf und Fertigung weclappCRM, Projekte und Dienstleistung neben dem Verkauf, native Buchhaltung gewünschtNatives, GoBD-konformes Finanzmodul in einer vollständigen Business-Suite OdooMaximale Anpassung bzw. Open Source, E-Commerce als einer von mehreren Kanälen80+ Module, voller Quellcode-Zugriff und enge Backend-Integration
do not create a table here, just have little paragraphs or something similar, the table looks super weird.
power of the radar signal is proportional to the square of the electric field amplitude
I think, this talks about the power Pt...where it is deifned as P = v^2 divided by R