Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: -19 PreprintsProtocolsVideosJournalsTools & a 10. 21203/rs. 3. rs-1639546/v1This work is licensed under a CC BY 4. 0 LicenseStatus:PostedVersion 1posted You are reading this latest preprint versionAbstractBackground: Hormone levels can be determined according the prevalence of a balance between generation metabolism and clearance rates. High-Training (HIIT) can affect this balance through a variety of mechanisms, including competition-associated stress, diet, body composition, heat production and hypoxia. Aims: The present study aimed to evaluate the impact of HIIT on the Health hormones of femininity and fertility in young women. Methods: The study was comprised of Eighteen females aged 18. 06 ± 0. 128 years old. The participants were subjected to an eight-week training program (3 sessions/week, two hours (h) after lunch). Participants underwent basal pre-and post-exercise intervention tests, such as reproductive and trophic hormones. Results: The results revealed that 143. 16% increased estrogen levels and a 62. 12% reduction in testosterone levels. No significant differences were detected in Luteinizing hormone (LH) and Prolactin (PRL) between participants. Conclusions: HIIT exercise training in young women decreases testosterone levels and increases estrogen levels, with no effect on trophic hormones (LH, PRL). Trophic hormonesReproductive hormonesHigh-TrainingFiguresFigure 1Figure 2Figure 3IntroductionHigh-intensity interval training (HIIT) includes alternate bouts of high-intensity intensive exercise along with low-intensity recovery periods. It is considered one of the most effective methods to improve cardiorespiratory and metabolic health [1]. Women have avoided resistance training for many years out of fear of being masculinized due to heavyweights. However, researchers have demonstrated that significant female strength could be observed with only minor degrees of muscle hypertrophy [2, 3]. Currently, it is widely accepted that exercise training in young women is very beneficial, as it can lead to reduced adiposity and increased cardiovascular fitness. Nevertheless, even if the exercise volume exceeds the physiological limit, this causes adverse effects on the skeletal and reproductive system, one of which is primary/secondary amenorrhea, induced by many factors such as inadequate nutrition and low body weight [3]. [SEP] Justify:

Output: The text provided is irrelevant to the claim as it discusses a study on the effects of high-intensity interval training (HIIT) on hormone levels in young women and does not address urban living or its relation to stress levels. The concepts presented in the text focus on exercise, hormones, and health benefits rather than the effects of urban living.


Input: Task: corroborate the claim using the given text. Claim: Ocean acidification, caused by increased carbon dioxide, is threatening marine ecosystems globally. [SEP] Text: 5 ha/year (Prato and others 2016) for the present-state scenario based on current market value (Table 3). The SSF is subjected to a loss in economic revenue that is similar in the two scenarios. For example, FF4 and FM4 are both subjected to a reduction of the SSF economic income by 23% (V = 58, p-value = 0. 76). Table 3 Associated with the Species. Full size tableThe market-based indicator (the average price of each species belonging to the functional group: ISMEA database) suggested that the degradation cost associated with OA impacts, as represented in scenario FF4 and scenario FM4, was almost − 20% of the economic income of SSF (Table 3, Figure S4). SSF is of great importance in terms of job opportunities and the contribution to the economies of coastal communities in Europe, generating approximately half of all direct employment within the EU fishing sector and representing a quarter of the catch value (FAO 2018). DiscussionOur study highlights how OA-induced changes in HFSs such as P. oceanica and coralligenous habitat could have substantial ecological consequences due to complex food web interactions and how these changes adversely impact ecological indicators and fisheries catches chosen as proxies for related ecosystem services. We explored the potential effects of habitat loss due to OA by implementing a new parametrization within a mathematical food web model and describing the decrease in HFS biomass, the cascading potential trophic and non-trophic effects on other species, the related consequences in terms of ecosystem structure and functioning, and eventually the loss of ecosystem services. The modeling approaches can help the understanding and quantification of ecosystem trends in future scenarios, providing indications that could help both prevention and mitigation of climate change impacts. of OA through HFSOur results show that the habitat changes due to OA could threaten keystone species (that is, dusky groupers, amberjack & dentex+ and large-scale scorpionfish+, Prato and others 2016) by reducing both their foraging area and their habitat, thus decreasing the services that these habitats provide to these species (that is, the protection offered in nursery areas). A slight decrease in the biomass of medium and large dusky groupers will lead to large indirect effects on the food web that should favor cephalopods+, which are the groupers’ favorite prey. [SEP] Justify:

Output: The text corroborates the claim by highlighting the detrimental effects of ocean acidification (OA) on habitat-forming species (HFS) and the ecological consequences of these changes. It discusses the loss in economic revenue associated with OA impacts and how changes in habitats could threaten keystone species, which are crucial for maintaining the structure of marine ecosystems. The response emphasizes that OA could reduce the habitat and foraging areas for species such as dusky groupers, which are important for their ecological roles, thus supporting the claim that ocean acidification threatens marine ecosystems globally.


Input: Task: contrast the claim using the given text. Claim: AI translation can handle complex, culturally sensitive documents with absolute accuracy. [SEP] Text: By comparing how ChatGPT handles the same proverb in different languages, students can gain insights into the complexities of translation and the significance of context in conveying meanings accurately across languages. summary, integrating ChatGPT into the classroom for teaching Arabic proverbs has several benefits, including vocabulary enrichment, cultural awareness, and critical thinking development. However, it should be used alongside traditional teaching methods to ensure accuracy and context preservation. This study revealed that ChatGPT and struggle with translating proverbs due to their complex cultural implications and idiomatic expressions. Human oversight is crucial for contextually accurate translations. This work underscores the importance of context, cultural awareness, and language proficiency in achieving precise proverb translations and suggests the potential for future machine translation advancements. Classroom activities involving Arabic proverbs can include providing English equivalents, exploring equivalent sayings in students’ languages or cultures, and comparing meaning nuances across languages. Students can also be encouraged to create riddles based on Arabic proverbs, and ChatGPT can assist by generating riddles on their prompts. Additionally, students can prompt ChatGPT to generate original proverbs on specific topics, enhancing language skills and critical thinking while promoting cultural exchange. These activities enrich the learning experience and contribute to a deeper understanding of proverbs. [SEP] Justify:

Output: The text contrasts the claim by highlighting that ChatGPT struggles with translating proverbs due to their complex cultural implications and idiomatic expressions. It states that human oversight is crucial for contextually accurate translations, indicating that AI translation does not achieve absolute accuracy on its own.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: Primary and secondary amenorrhea are patterns of follicle-stimulating and luteinizing hormone suppression. Additionally, it may involve the hypothalamic-pituitary-adrenal axis and hypothalamic-pituitary-gonadal axis. Hypoestrogenism may have a negative effect on bone growth in athletes. Amenorrhea, eating disorders, and osteopenia are all symptoms of fatigue in female athletes. Women with delayed menarche demonstrate elevated stress features, osteopenia, and incidence of scoliosis compared with girls with average menarche [4, 5]. The balance of clearance rates, metabolism, and production is essential for maintaining hormonal blood levels. This balance may be affected by intensive physical exercises or through some mechanisms like dieting, production of heat and hypoxia, stress related to competition, and reduction of body fat mass [6]. Women who engage in high-intensity exercise on a regular basis may experience menstrual disturbances such as oligomenorrhea, amenorrhea, or delayed menarche due to hormonal changes. Among the exercise-induced menstrual disturbance is the impaired production of gonadotropins, which may lead to anovulation and luteal phase deficiency [7]. Previous literature illustrated that prolonged and high-intensity training has a disadvantageous effect on female reproductive hormones. The hypothalamus-ovarian axis and the circulation of feminine reproductive hormones are disrupted due to related fatigue associated with low energy, leptin levels, and high-stress hormone concentration following strenuous exercise. This imbalance could lead to miss menstrual cycle regulation associated with the luteal phase and anovulation deficiency. Consequently, this study aims to investigate further the potential interventions of HIIT, which may be beneficial to reduce or prevent the impacts on reproductive health among female athletes by assessing femininity and fertility hormones. The current study assessed eighteen females, as depicted in (Table 1). The participants completed a familiarization session before initiating the measurements, where participants were excluded if suffering from any metabolic disease or renal, pulmonary, or cardiovascular pathological conditions. Before the onset of any testing or training session, it was required to obtain all participants' oral and written informed signed consent. approved the Faculty of study, Mansoura University, Egypt. Table (1) illustrates the participants' physical characteristics. Table 1 The participants' Physical characteristics. [SEP] Justify:

Output: The text does not address the claim directly and focuses on hormonal changes and menstrual disturbances in female athletes due to physical exercise and does not mention urban living or its effects on stress levels.


Input: Task: corroborate the claim using the given text. Claim: Ocean acidification, caused by increased carbon dioxide, is threatening marine ecosystems globally. [SEP] Text: Preprints AbstractDiscussion © Author(s) 2022. This work is distributed under the Attribution 4. 0 License. © Author(s) 2022. This work is distributed under the Attribution 4. 0 License. Preprints AbstractDiscussionMetrics 26 Sep 2022 | 26 Sep 2022 Unifying biological field observations to detect and compare ocean acidification impacts across marine species and ecosystems: What to monitor and why án-Espitia, Claudine Hauri, Janet A. Newton, Mark Wells, and Abstract. Approximately one quarter of the CO2 emitted to the atmosphere annually from human activities is absorbed by the ocean, resulting in a reduction of seawater pH and shifts in seawater carbonate chemistry. This multi-decadal process, termed “anthropogenic ocean acidification” (OA) has been shown to have detrimental impacts on marine ecosystems. Recent years have seen a globally coordinated effort to measure the changes in seawater chemistry caused by OA, with best practices now available for these measurements. In contrast to these substantial advances in observing physico-chemical changes due to OA, quantifying their biological consequences remains challenging, especially from in-situ observations under real-world conditions. Results from two decades of controlled laboratory experiments on OA have given insight into the likely processes and mechanisms by which elevated CO2 levels affect biological process, but the manifestation of these process across a plethora of natural situations has yet to be explored fully. This challenge requires us to identify a set of fundamental biological and ecological indicators that are i) relevant across all marine ecosystems, ii) have a strongly demonstrated link to OA, and iii) have implications for ocean health and the provision of ecosystem services with impacts on local marine management strategies and economies. This paper draws on the understanding of biological impacts provided by the wealth of previous experiments, as well as the findings of recent meta-analyses, to propose five broad classes of biological indicators that, when coupled with environmental observations, including carbonate chemistry, would allow the rate and severity of biological change in response to OA to be observed and compared. These broad indicators are applicable to different ecological systems, and the methods for data analysis suggested here would allow researchers to combine biological response data across regional and global scales by correlating rates of biological change with the rate of change in carbonate chemistry parameters. [SEP] Justify:

Output: The text corroborates the claim by stating that approximately one quarter of the CO2 emitted annually is absorbed by the ocean, leading to a reduction in seawater pH and shifts in carbonate chemistry. This process, referred to as 'anthropogenic ocean acidification' (OA), has been shown to have detrimental impacts on marine ecosystems. Furthermore, the text discusses recent coordinated efforts to measure changes in seawater chemistry due to OA and highlights the challenges of quantifying biological consequences, indicating a strong link between increased CO2 levels and the threats posed to marine ecosystems.


Input: Task: contrast the claim using the given text. Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Please avert referring to tubular lysosomes as "reforming" or "pre-reforming" – this is strictly an assumption at this stage and the authors provide no evidence to support this. 2) The authors mention in the Discussion "the lysosomal tubules in aged adults are static and are not readily stained by LysoSensor Green" indicating that "the lysosomal tubules enriched in aged adults are probably catalytically inactive". This should be investigated and quantification of Lysostaining in tubular lysosomes should be presented. 3) Figure 4A-L should include quantification of tubular lysosome length. It is also unclear how the tubules for quantification were chosen (Materials and methods) and more details should be provided in the Materials and methods section. 4) The conclusions on the degradation capacity of lysosomes are mostly based on processing of protein substrate Nuc1-Cherry and CPL-1 processing. Thus, testing lysosomal degradative ability during aging by analysis of an endogenous cargo could be an important addition to the results. If probes such as and/or DQ-BSA permeate through C. elegans surface, they can be also used to analyze lysosomal degradation capacity. 5) The authors also need to be more careful about referring to lysosome changes as en block. The manuscript text describes the changes to lysosomes caused by aging, long-living mutants, and those driven by daf-16/SKN1 as if all aspects of lysosome function and identity changed. This is clearly not the case as indicated by the RNA expression data presented in the manuscript. While a large number of transcripts encoding lysosomal proteins are reduced with age, there is a substantial number that increase or is unchanged. This is also true for all conditions they examined. In the revised version, the authors should include all lysosomal transcripts that have been analyzed in the supplementary files (and not only the transcripts whose levels are reduced). The findings presented here suggest that lysosomes are remodelled in some way but do not necessarily indicate total disruption of lysosomal function. The authors are thus asked to discuss with greater nuance this issue and to reflect this in the Abstract. [SEP] Justify:

Output: The text contrasts the claim by discussing the complexities and nuances of lysosomal function in relation to aging rather than supporting the notion of biohacking as a guaranteed means to extend lifespan. It highlights the lack of conclusive evidence regarding lysosomal changes and the variability of lysosomal function, suggesting that while there may be remodeling of lysosomes, this does not imply a total disruption or a definitive method for enhancing longevity. Therefore, the discussion on lysosome changes and recommendations for further investigation undermine the assertion that biohacking can guarantee longevity.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: Values are represented as mean (± sem) (years) Height (m) Body mass (kg) BMI (kg/m2) Mean 18. 06 1. 65 63. 35 21. 35 sem. 128 2. 74 2. 68 0. 46 1. Hormonal Assay: Trained laboratory technicians performed blood sampling at standardized laboratory conditions. Before obtaining a blood sample, participants were required to fast for at least 4 hours. Subsequently, the venous blood sample was collected on the third day of the spontaneous cycle. The collected samples were allowed to clot at room temperature for one hour and were then subsequently centrifuged at 8000 rpm for 15 minutes at 4 oC. The serum samples were then stored at -20 oC until assayed. Clear non-hemolyzed sera were separated and used for the assay of testosterone, estrogen, follicle-stimulating (FSH), luteinizing hormone (LH), and prolactin (PRL) by solid-phase competitive chemiluminescent enzyme immunoassay through the utilisation of analyser purchased from DPC (). None of the participants had engaged in any form of an exercise training programme for at least two months prior to the study. The group carried out their HIIT exercise training program (3 sessions/week, 2 h after lunch) for eight weeks on alternate days (Sunday, Tuesday, and Thursday). Each participant's repetition maximum (1RM) was measured. Participants completed a warm-up set of 8–10 repetitions at 50% of their estimated 1RM, before moving to a warm-up set of 3–5 repetitions at 85% of their estimated 1RM. To determine squat 1RM, participants performed 1RM attempts over 4–5 trials separated by 3 min rest intervals. 1RM was measured again, and intensity was re-established after four weeks of HIIT training. The detailed exercise training programme is presented in Table 2. [SEP] Justify:

Output: The text is irrelevant to the claim about urban living and stress levels. It provides detailed information about a hormonal assay and exercise training protocol, with no mention of urban living or stress levels. Therefore, it does not support, contrast, or relate to the claim in any way.


Input: Task: corroborate the claim using the given text. Claim: Ocean acidification, caused by increased carbon dioxide, is threatening marine ecosystems globally. [SEP] Text: Moreover, a method using laboratory observation to design an optimal observing strategy (frequency and duration) and observe meaningful biological rates of change highlights the factors that need to be considered when applying our proposed observation strategy. This innovative observing methodology allows inclusion of a wide diversity of marine ecosystems in regional and global assessments and has the potential to increase the contribution of OA observations from countries with developing OA science capacity. How to cite. Widdicombe, S. , Isensee, K. , Artioli, Y. , Gaitán-Espitia, J. D. , Hauri, C. , Newton, J. A. , Wells, M. , and Dupont, S. : Unifying biological field observations to detect and compare ocean acidification impacts across marine species and ecosystems: What to monitor and why, EGUsphere [preprint], 2022. Received: 10 Sep 2022 – Discussion started: 26 Sep 2022 Publisher's note: remains neutral with regard to jurisdictional claims made in the text, published maps, institutional affiliations, or any other geographical representation in this preprint. The responsibility to include appropriate place names lies with the authors. Download & links Preprint (PDF, 1138 KB) Notice on discussion status The requested preprint has a corresponding peer-reviewed final revised paper. You are encouraged to refer to the final revised version. Preprint (1138 KB) Download & links The requested preprint has a corresponding peer-reviewed final revised paper. You are encouraged to refer to the final revised version. Preprint (1138 KB) revised paper 10. 5194/os-19-101-2023, 2023 Short summary Short summary Ocean acidification is a global perturbation of the ocean carbonate chemistry as a consequence of increased carbon dioxide concentration in the atmosphere. While great progress has been made over the last decade for chemical monitoring, ocean acidification biological monitoring remains anecdotal. This is a consequence of a lack of standards, general methodological framework, and overall methodology. This paper presents methodology focusing on sensitive traits and rates of change. án-Espitia, Claudine Hauri, Janet A. [SEP] Justify:

Output: The text corroborates the claim by stating that 'Ocean acidification is a global perturbation of the ocean carbonate chemistry as a consequence of increased carbon dioxide concentration in the atmosphere.' This supports the assertion that increased carbon dioxide is causing ocean acidification and suggests its implications for marine ecosystems.


Input: Task: contrast the claim using the given text. Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Supplementary file 5 includes data of the 43 down-regulated lysosomal genes in the long-lived mutants daf-2, eat-2 and isp-1. As suggested by the reviewer, we have revised the manuscript text including the Abstract to indicate clearly the lysosomal aspects that are altered in a certain condition and we have included the point about “lysosome remodeling” in the Discussion section. 6) The authors have employed mutants lacking CUP-5 and CPL-1 activity to conclude that lifespan extension in C. elegans requires lysosome function. However, whether decline in lysosomal function during aging is comparable to what is observed in the cup-5 and cpl-1 mutants is not clear. This can be addressed by functional assays such as cathepsin processing, LSG/LTR ratio tested in any one of the mutants (cup-5/cpl-1) and compared with worms at day 9. As suggested by the reviewer, we examined the acidity and degradation activity of lysosomes in cup-5 by LSG/LTR and CPL-1 processing assays. As shown in Figure 9—figure supplement 1P-X, the fluorescence intensity ratio of LSG vs. LTR was reduced significantly in cup-5 mutants at days 1, 3, 5, while the LSG/LTR ratio in cup-5 was similar to wild type at day 9. CPL-1 processing was also reduced significantly in cup-5 compared with wild type and the reduction was observed at all adult ages that were tested (days 1, 3, 5, 9) (Figure 9—figure supplement 1Y, Z). 7) The authors have shown that ratio of lysosensor to lysotracker is reduced in aging worms, indicating that lysosome become less acidic (Figure 2I). Further the pHTomato experiments also indicate that pH is less acidic in aged worms. It would be very informative if the authors can measure the actual pH of lysosomal compartments to understand the magnitude of pH change during aging. If the lysosomal pH measurement is not feasible in this model system, the findings with the pHTomato probe should be complemented with data that directly report pH change such the LSG/LTR ratio. The latter experiment can be added to Figure 6. [SEP] Justify:

Output: The text contrasts the claim by discussing specific research findings related to lifespan extension through lysosome function in C. elegans, rather than making any guarantees about biohacking or doubling human lifespan. It mentions that lifespan extension requires lysosome function but does not assert that biohacking mechanisms can or will guarantee such results. The text indicates that while there are mutations that impact lifespan, it does not directly support the idea that biohacking leads to a doubling of human lifespan.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: Table 2 High-Training (HIIT) 1,2 Week 3,4 Week 5,6 Week 7,8 (time× sets) rest (time× sets) rest (time× sets) rest (time× sets) rest 1 High knees (10×3) 10 (15×4) 30 (20×4) 20 (30×3) 30 Squats (10×3) 10 (15×4) 30 (20×4) 20 (30×3) 30 Basic burpees (10×3) 10 (15×4) 30 (20×4) 20 (30×3) 30 Elbow plank (10×3) 10 (15×4) 30 (20×4) 20 (30×3) 30 Flutter kicks (10×3) 10 (15×4) 30 (20×4) 20 (30×3) 30 2 Plank (10×4) 20 (15×3) 30 (20×5) 40 (30×5) 60 Elbow plank (10×4) 20 (15×3) 30 (20×5) 40 (30×5) 60 Body saw (10×4) 20 (15×3) 30 (20×5) 40 (30×5) 60 Side bridges (10×4) 20 (15×3) 30 (20×5) 40 (30×5) 60 Crunches (10×4) 20 (15×3) 30 (20×5) 40 (30×5) 60 3 Sit-ups (10×5) 30 (15×5) 45 (20×3) 40 (30×4) 60 Jumping jacks (10×5) 30 (15×5) 45 (20×3) 40 (30×4) 60 Scissors chops (10×5) 30 (15×5) 45 (20×3) 40 (30×4) 60 (10×5) 30 (15×5) 45 (20×3) 40 (30×4) 60 Climbers (10×5) 30 (15×5) 45 (20×3) 40 (30×4) 60 Session (S), Time, rest by seconds 2. for (SPSS) (version 23. 0. ) and Graph(version 8. 4. 2. Graph154 ) were used to perform all statistical analyses. [SEP] Justify:

Output: The text does not address the claim regarding urban living and stress levels. Instead, it focuses on a detailed exercise regimen, which is unrelated to the claim about stress in urban environments.


Input: Task: corroborate the claim using the given text. Claim: Ocean acidification, caused by increased carbon dioxide, is threatening marine ecosystems globally. [SEP] Text: , 2018b) which call for greater global connectivity between the collection of Variables (EOVs) through the (GOOS), and Variables (EBVs) from the Group on Network (). Although it should be noted that our inclusive approach encourages the collection of carbonate chemistry and biological data that goes beyond the defined set of observations that are recognised as either EOVs or EBVs. It should be further noted that several of the biological EOVs, remain to be further defined and the implemenaion of related observation alongside the physical and biogeochemical variables to be implemented (Miloslavich et al. , 2018). Even so, our paper does support the ambitions outlined by Muller-Karger et al. (2018b) by proposing a practical way in which observing the biological impacts of ocean acidification can embrace the huge variety of biological observations that could be performed. Such an approach would not only facilitate the creation of completely new observing activities that include both biological and biogeochemical observations from the start, but also would provide guidance on how existing biochemical ocean acidification monitoring can add relevant biological observations to their suite of observations, and vice versa, to better appreciate the biological consequences of OA across regional and global scales. ” Reviewer comment: Linear regressions, correlations and the comparison of dose-response curves (e. g. Fig. 4A) are not innovative methods. What is new is that they are applied in the context of OA to calculate monitoring durations in the field. There are a number of dose-response concepts in (eco)toxicology that can be instrumental to understanding and modelling OA effects (see e. g. species sensitivity distribution in Wittmann & Pörtner 2013). It would help the reader in understanding that using linear regression is a valid method to compare curves in Fig. 4A, if the authors would refer them to the respective literature in (eco)toxicology. Author response: We fully agree with the reviewer that pH dose-responses curves are not expected to be linear (as for other environmental drivers). With enough data (e. g. long time series and/or high rates of chemical changes), it must be possible to use non-linear regressions to calculate the rate of biological change. [SEP] Justify:

Output: The text corroborates the claim by discussing the monitoring of biological impacts of ocean acidification (OA) and emphasizing the need to collect both biogeochemical and biological data to understand the consequences of OA on marine ecosystems. It mentions that the approach proposed would aid in observing the effects of ocean acidification across regional and global scales, thus supporting the notion that OA threatens marine ecosystems.


Input: Task: contrast the claim using the given text. Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: The measurement of lysosomal pH is not feasible in live C. elegans. We performed the LSG/LTR staining assay as suggested by the reviewer to further support the pHTomato assay. These new data are presented in Figure 6L, Figure 6—figure supplement 1C-J’’, Figure 7L and Figure 8L in the revised manuscript. 8) The discussion on metabolism and role in aging and lysosome function begs the question on what happens to mTORC1 activity. Do the long-living mutants have lower mTORC1 activity? If so, could this help explain lower tubulation in long-living C. elegans. This may be connected to mTOR modulation of lysosome tubulation and remodelling in mammalian macrophages exposed to LPS (Saric et al. , 2016; Hipolito et al. , 2020). If nothing else, this possibility could be discussed. The TOR signaling pathway regulates longevity in multiple species and inhibition of TOR extends lifespan in model organisms including yeast, C. elegans, fruit flies and mice. The TOR pathway has been shown to link to other longevity pathways such as Insulin/IGF-1 signaling (IIS) and dietary restriction (DR). However, it has not been tested directly whether TOR activity alters in long-lived C. elegans mutants. On the other hand, mTOR is important for lysosomal tubulation in the reformation process (Yu et al. , 2010), and is required for LPS-induced lysosome remodeling in macrophages and dendritic cells (Saric et al. , 2016; Hipolito et al. , 2019). As suggested by the reviewer, we examined whether TOR is involved in forming lysosomal tubules in aged C. elegans adults. We found that knockdown of the C. elegans TORC1 components LET-363/m-15/Raptor or C10H11. 8/mLST8 had no effect on lysosomal tubules in adult hypodermis at day 5, while the length of lysosomal tubules in let-363 RNAi and daf-15 RNAi worms increased at day 1 (Author response image 2A-J). [SEP] Justify:

Output: The text contrasts the claim by discussing the complexities of lifespan and longevity through the lens of the TOR signaling pathway and its effect on various model organisms. It highlights that while the TOR pathway regulates longevity, it has not been directly tested whether TOR activity alters in long-lived C. elegans mutants, questioning the certainty implied in the claim. The text delves into specific research and findings related to mTOR and lysosomal function but does not support the notion of biohacking guaranteeing any specific outcomes related to lifespan.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: Data included the mean ± standard error of the mean (sem) and "T" value. The significance level was set at p < 0. 05. ResultsThe results of the current experimental procedure are presented as mean ± standard error of the mean (sem) for the given number of participants, as shown below. Table 1 presents the anthropometric and physical characteristics of the participants (age, height, body mass, body mass index). Figure 1–3 depicts the primary data of the current study. It was revealed that 8-week training had a significant impact on estrogen, testosterone, and follicle-stimulating hormone (FSH) levels (Fig. 1–3). In addition, there was a 2-fold increase in estrogen levels post-exercise training compared to the basal measurement prior to the initiation of the exercise intervention (Fig. 1). Insert Fig. 1. Furthermore, there was around a 3-fold reduction in testosterone levels after the exercise- regimen (Fig. 2), highlighting the crucial role of chronic exercise regulating testosterone levels in young female participants. In addition, post-exercise training measurements demonstrated a slight reduction (around 15%) in FSH levels (Fig. 2). In contrast, 8-week exercise training had no significant impact on LH and prolactin (Fig. 2–3). Insert Fig. 2. Insert Fig. 3. DiscussionThis study found that high-intensity interval training had a significant effect on estrogen and testosterone hormones in young females. In contrast, no significant changes were detected in the LH, Prolactin, and FSH hormones. However, this could be related to the small sample size of this study. Previous research studies have indicated that exercise has a positive effect on female hormones. Sex hormone levels are considered an objective marker for assessing the level and effectiveness of exposure to physical training and specifying the appropriate physical activity levels and doses, especially in women. In this study, hormonal estrogen levels showed a significant increase. Estrogen plays a crucial role in promoting the development and effectiveness of female reproductive structure and female secondary sex characteristics [8]. Similar results have been reported by Hackney et al. (2020). They assessed seven young women's hormonal responses on a moderate bicycle ergometer training for eight weeks in a fixed relative intensity. The results of their study detected an increase in beta-endorphin, beta lipotropin cortisol, and reproductive hormone levels [9]. Copeland et al. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses the effects of high-intensity interval training on hormone levels in young females, without any mention of urban living or its relationship to stress levels.


Input: Task: corroborate the claim using the given text. Claim: Ocean acidification, caused by increased carbon dioxide, is threatening marine ecosystems globally. [SEP] Text: Pereira et al. 2013 Variables - A global system of harmonized observations is needed to inform scientists and policy-makers DOI: 10. 1126/science. 1229931 Citation: Peer review completion AR: Author's response | RR: Referee report | ED: Editor decision | EF: Editorial file upload AR by on behalf of the Authors (15 Dec 2022) Author's response Author's tracked changes Manuscript ED: Publish subject to technical corrections (26 Dec 2022) by Dear Dr. Dupont and co-authors, Thank you for the resubmission of your manuscript and the response to the referees. I am satisfied with your answer to the comments and with the revised manuscript. Please see below my final comments, which are mainly technical corrections. You may consider those and prepare the final version of your manuscript for publication in Ocean Science. At this stage, you do not need to provide a separate response to the comments. L48-49 „This multi-decadal process, termed “anthropogenic ocean acidification”, causes additional chemical changes, including altering the speciation of dissolved inorganic carbon” While this is all very true, I also think it is trivial and there is no need to cite IPCC here. L71, 72 in situ (no hyphen) L109 delete further (strikethrough) L123 Please define DIC and pCO2 as they are used here for the first time L130-132 These four conditions for the parameters make sense. What about a fifth: It should be relatively easily measurable? L174 … the most mature? L193 TA has not been defined before. Maybe define at line 123 L268 Wittmann (typo) L359 delete: all of (strikethrough) L398 delete: is currently unknow and (strikethrough) L491 Please add the target definition for SDG 14. 3, like also done two lines higher for 14. 3. 1. The reader might get confused by these different targets and sub-targets. L592 on new line. L633 in new line L683 Please add volume number L763 add at end of title: organisms L789 and further: Most 10. 5194/os-19-101-2023, 2023 Short summary Short summary Ocean acidification is a global perturbation of the ocean carbonate chemistry as a consequence of increased carbon dioxide concentration in the atmosphere. [SEP] Justify:

Output: The text corroborates the claim by stating that 'Ocean acidification is a global perturbation of the ocean carbonate chemistry as a consequence of increased carbon dioxide concentration in the atmosphere.' This directly supports the idea that increased carbon dioxide leads to ocean acidification, which impacts marine ecosystems.


Input: Task: contrast the claim using the given text. Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: 9 and lipl-7, encode beta glucuronidase and lipase-like protein, respectively, but how they contribute to lifespan extension induced by the three longevity pathways requires further studies. On the other hand, the IIS and caloric restriction (CR) pathways seem to target different sets of lysosomal genes (hydrolases in IIS and V-ATPase components in CR), while genes upregulated in the mitochondria-defective mutant isp-1 are mostly shared with the IIS pathway. We have discussed this point in the revised manuscript. 12) The end of the Discussion is a bit abrupt. The authors can probably restate the importance of the findings and also it would be of service to the community to highlight specific caveats and shortcomings of the study to avoid excessive extrapolation in future interpretations. We found that the lysosome-defective mutants cup-5 and cpl-1 are slightly short-lived compared with wild type, and both of these mutations significantly reduce the lifespan in long-lived daf-2, eat-2 and isp-1 worms (Figure 9L-Q). This suggests that lysosome function is important for lifespan extension. In the last paragraph of the Discussion, we would like to discuss how lysosome function may contribute to lifespan extension and how regulation of lysosome and autophagy, which are both important for longevity, may be coordinated. In the revised the manuscript, we have revised the text to explain the points more clearly and discussed the limitation of our study as suggested by the reviewer. 13) For quantification and statistical analysis of the data, it is not clear to this reviewer if the authors examined all animals for a specific "read-out" in one day or during independent days. For example, the authors state "At least 10 worms were quantified in each strain at each stage" when describing the method to measure tubule length. Were 10 animals all done in one day or over different days? This comment applies elsewhere and it is important to know. We apologize for not explaining our data more clearly in the original manuscript. For measurement of tubule length, 10 animals were scored in each strain at each day. We have revised the text to clarify this point. 14) For quantitative real-time PCR (qRT-PCR) experiments, it is not clear whether RNA was pooled from multiple worms and if so please state the number. [SEP] Justify:

Output: The text discusses the complexities of lifespan extension through biological mechanisms, indicating that the effects of biohacking are not guaranteed. It specifically notes that 'how they contribute to lifespan extension induced by the three longevity pathways requires further studies,' which contrasts with the claim that biohacking guarantees longevity. Additionally, the mention of 'lysosome function is important for lifespan extension' suggests a nuanced understanding rather than an absolute guarantee.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: (2002) [10] investigated the female hormonal endurance and resistance training responses. They found a significant increase in estradiol levels in response to both training interventions in their study. In addition, the impact of physical activity on hormonal circulation has been confirmed by previous research findings reporting elevated estradiol circulation after resistance exercise and endurance exercise in female participants [11]. Vicissitudes in females' estrogen levels have been reported to be influenced by exercise duration, intensity, menstrual phase, and status [3, 12]. In addition to the increase of estrogen, the current study reported a significant increase in testosterone levels related to the impact of this study's proposed high-intensity interval training. These results were confirmed by the analysis of Gharahdaghi et al. 2021. They reported that resistance exercise could induce a temporary rise in testosterone in young, healthy females. Additionally, the anthropometrical indications of adiposity have been found to be significantly correlated with testosterone concentrations [13]. A study conducted by Kochańska-Dziurowicz et al. (2001) investigated the effect of a proposed acute exercise intervention on a cycle ergometer on testosterone and prolactin levels in 13 young female runners. Their study results addressed a significant elevation in the testosterone concentration, indicated at the end of the exercise and 90 minutes past the completion of the test. In contrast, the testosterone level had returned to the base levels as pre-exercise [14]. On the contrary, literature results have concluded that exercising had no effect on testosterone concentration in trained young women and was not influenced by their menstrual cycle [9, 15]. In addition, it has been revealed that training status contributes to mediating the hormones' response to physical activities. After a six-month resistance training intervention, changes in testosterone levels have only occurred in women [16]. In a study by Schmitz et al. (2007), other results were reported, as they found that physical activity level was inversely related to estrogen in late transition age. The adjusted means of estrogen reported were 24. 6 and 37. 9; a relative difference of 54% in estrogen level was detected when comparing highest to lowest activity (P = 0. 02). Similarly, it was shown that physical activity was inversely related to testosterone levels (a relative difference of 47% was detected when comparing the highest to lowest activity [17]. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses hormonal responses to exercise in women, addressing factors such as testosterone and estrogen levels without mentioning urban living or stress levels. There is no connection between the hormonal effects of physical activity and the assertion that urban living causes increased stress.


Input: Task: corroborate the claim using the given text. Claim: Marine protected areas (MPAs) help conserve biodiversity by restricting human activities in critical habitats. [SEP] Text: This experiment is part of the e. Browse more projects conserving species biodiversity across the tree of life? Rabearisoa, Rachel Meyer, and Camille GaynusBacked by and : 10. 18258/69033Grant: eDNA Innovation$10,005Raised of $10,000 Goal100%Funded on 6/11/24Successfully Funded$10,005pledged100%fundedFundedon 6/11/24? How does this work? assessments are a common tool for evaluating biodiversity richness, but they are costly and time-consuming. Their pertinence can also be limited by several factors, such as the accessibility of sampling areas or the quality of photographs and specimens. This project aims to use digital and molecular tools to 1) catalyze the development of next-generation biodiversity monitoring strategies for a comprehensive inventory and 2) expand environmental awareness in Black communities. Ask the ScientistsDiscussionWhat is the context of this research? In 2017, the of Sciences (CAS) team intensively surveyed the biotic communities on the headland California beach. The study surveyed the unprotected tidepool as well as the (SMCA) created in 2009 to assess how biologically different these areas are. The study found little overlap between eDNA and photographs, with eDNA covering lower trophic, but also that the unprotected tidepool and the SMCA looked identical based on eDNA. This project aims to update the data collected in 2017 and test if the SMCA is now different from the unprotected tidepool in terms of biodiversity richness after 7 years of protection, using the same method of comparing eDNA results to human observation records. What is the significance of this project? The results of this project could demonstrate that eDNA may be useful for finding proxies for diversity in sites that are difficult to monitor with photographs and better inform ecosystem management. Effectively, systematic collection of eDNA can describe differences in spatial and temporal biodiversity variation of the beach, and provides a rich view of the community ecological network, including holobiomes. The two-period data comparison can demonstrate the effectiveness of the SCMA in conserving biodiversity after 7 years of protection. The project will share the experiments and data with the public through interactive web pages of and Black in TV so that it can expand the number of eDNA adopters in California and beyond. What are the goals of the project? [SEP] Justify:

Output: The text supports the claim by discussing a project that assesses biodiversity in a marine protected area (MPA) compared to an unprotected tidepool. It highlights how the project aims to evaluate the effectiveness of the SMCA (State Marine Conservation Area), established in 2009, in conserving biodiversity over seven years of protection. The findings from comparing environmental DNA (eDNA) results and human observations suggest that the SMCA may have played a role in conserving biodiversity, thereby supporting the claim that MPAs help conserve biodiversity by limiting human activities.


Input: Task: contrast the claim using the given text. Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: The authors show that expression of ether lipid biosynthesis genes does not increase with biguanide treatment (Figure 2 —figure supplement 2; Results lines 305 – 313), and FARD-1::RFP levels decrease with phenformin treatment (Figure 2 —figure supplement 2M) and suggest that "post-translational negative feedback of ether lipids on the ether lipid biosynthetic pathway, as has been previously reported" (Results lines 311 – 313)--a citation for these results should be added. These data argue against phenformin and fard-1 overexpression triggering downstream pathways in the same way. Although fard-1 oe increases lifespan in a manner that is not additive with phenformin treatment (Figure 5 A and B), fard-1 overexpression evidently does not trigger the same negative feedback mechanism, as overexpressed FARD-1 levels shown in Figure 2 —figure supplement 2 M appear to be high in vehicle controls, and are lowered with phenformin treatment. If both fard-1 overexpression and phenformin treatment signal similarly to trigger a post-translational negative feedback mechanism (which would presumably be important for lifespan extension), one would expect similar FARD-1 levels in fard-1 oe animals with and without phenformin treatment. It is possible that fard-1 overexpression simply overwhelms – or is insufficient to trigger – negative feedback mechanisms. Data showing overexpressed fard-1 mRNA and FARD-1 protein levels vs. endogenously expressed fard-1 and FARD-1, with and without biguanide treatment, would help clarify these seemingly paradoxical results. Figure 3D (D-H) RNAi of three fatty acid desaturases (D-F) two fatty acid elongases (G and H) …blunt phenformin-mediated lifespan extension in wild type worms. fat-1 RNAi extends lifespan, phen treatment brings this close to wt +phen, and there is no significant difference wt+phen vs. fat-1(RNAi) + phen; it might be technically reasonable to indicate the response is blunted (percent increase) but fat-1 does not appear to be all that impactful on longevity. These data do not impress regarding the importance of fat-1 in phenformin outcome; the discussion should be toned down or eliminated. [SEP] Justify:

Output: The text contrasts the claim by discussing specific biochemical mechanisms and experiments that do not support the idea that biohacking, specifically involving the treatments mentioned, leads to significant increases in lifespan. It states that the research indicates overexpression of fard-1 does not trigger the expected lifespan extension effects when combined with phenformin, which would be necessary for claiming biohacking guarantees longevity.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: The current study illustrated that the increase in estrogen hormone had been linked to a rise in LH and PRL. Despite the significant elevation in estragon levels, no significant changes have been indicated in the study participants' levels of LH and PRL. This finding could be explained by the conclusion of a recent meta-analysis conducted by Ennour-Idrissi et al. , 2015, on the effect of physical activity on sex hormones in women. The meta-analysis results addressed that the impact of physical activity on circulating sex hormones is relatively modest and probably not clinically significant. Also, the levels of sex hormones in the blood may not represent their effects on target tissues. Physical activity may continue to affect sex hormone function by modulating target-tissue sensitivity to these hormones [18]. exercise may induce changes in the levels of reproductive hormones in females, including an increase in estrogen level and a decrease in test level. High-intensity interval training exercise is highly recommended for young women as it leads to increased estrogen levels and reduced testosterone levels, with no effect on trophic hormones (LH and PRL). DeclarationsEthics approval and consent to participate and publication: The study was conducted in accordance with the Declaration of Helsinki, and the protocol was approved by the Board approved the Faculty of study, Mansoura University, Egypt. Written and oral and informed signed consent was obtained from all participants Availability of data and materials: The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request. Competing interests: The authors declare no conflict of interest. Funding: No financial support for the current study. Authors' contributions: contributed to Conceptualization, Formal analysis, Methodology, Supervision, Validation, Visualization, Writing-review & editing. Chrysovalantou E. Xirouchaki contributed to Investigation, data extraction, data analysis and manuscript writing, results discussion. Razek and Alim contributed to Supervision, Writing-original draft, Writing-review & editing. All authors read and approved the fnal manuscript. Acknowledgements: The authors would like to thank all the participants that voluntarily agreed to participate in the current study after signed informed consent. 17. Zanker C, Swaine I. Relation between bone turnover, oestradiol, and energy balance in women distance runners. British journal of sports medicine. 1998;32(2):167 − 71. . [SEP] Justify:

Output: The text does not address the claim regarding urban living and stress levels. Instead, it discusses findings related to sex hormones and the impact of physical activity, which is unrelated to the effects of urban living on stress.


Input: Task: corroborate the claim using the given text. Claim: Marine protected areas (MPAs) help conserve biodiversity by restricting human activities in critical habitats. [SEP] Text: This project aims to 1) empower community science efforts of the program and the nonprofit Black in and 2) inform ecosystem management about species biodiversity richness in the through an innovative biodiversity monitoring practice. Through the analysis of eDNA metabarcoding, we will inform the overlap with human observation and fill the information gaps on biodiversity richness resulting from taxon and visitation bias. With community empowerment as the goal, the project will be paired with interactive web pages and for the public, who are potential eDNA adopters, to explore. wait. . . This budget will help us conduct the surveys and give travel support to the participants. We plan to have 05 scientists who are members of the BIMS on the West Coast, as well as several students from who will collect the samples in Pillar Point. To generate the data with lab, we will buy the materials needed for the sample collections ($125 each for 4 markers, 56 samples). We will extract 56 triplicate sediment samples with the for triplicate library PCRs for each of four metabarcoding markers: MiFish 12S U, CO1, 18S, and 16S, normalize and index libraries and submit for sequencing to 75000 reads per marker per sample on a NextSeq 2000 2x300bp run. Finally, we plan to purchase a digital waterproof camera and its housing to take pictures during the experiment and produce the bioblitz videos for and the interactive web pages. Endorsed byThis is a critical question in is the perfect person to answer it endorse the application of Rabearisoa to lead this project. Ando is an extraordinary graduate student, who our Center is very happy to support in many aspects of her work. This new project will provide insights about the importance of citizen science in documenting the value of eDNA particularly in the context of marine protected areas. We are happy that she will be sharing the results of this work publicly and through the Black in (BIMS) network. Michael BeckProfessor & DirectorUniversity of Cruz, Center for will host bioblitzes over the course of seven days in June 2024. We will make libraries for four metabarcodes from the samples and they will get sequenced at the end of July 2024. Then, we will analyze sequences and upload them to the publicly-available websites. We envision generating science communication material by October 2024 and having a draft manuscript by December 2024. This timeline and the combined team effort will ensure deliverables are met in a timely manner. [SEP] Justify:

Output: The text corroborates the claim by discussing a project focused on citizen science and eDNA monitoring, particularly emphasizing the context of marine protected areas. It suggests that the project aims to document biodiversity and inform ecosystem management, which aligns with the purpose of MPAs in conserving biodiversity by restricting human activities.


Input: Task: contrast the claim using the given text. Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Metformin has been documented to intersect with the bacterial food source to influence longevity PMID: 23540700. This manuscript does not engage that story, but I would encourage authors to add a small statement regarding their take on the interface of the "microbiome" or bacterial influence on biguanide action and possibly ether lipid synthesis. Finally, as the authors point out, identification of the specific lipids necessary for promoting healthy aging is not feasible here; with which I totally agree. The actual mechanism by which ether lipid synthesizing enzymes modulate extended survival for the isp-1, eat-2, and raga-1 backgrounds or +phenformin is not really defined by this work. Still, the highlight of a critical biosynthetic pathway in biguanide outcomes and the implication of SKN-1/NRF2 in the biology is of sufficient importance in the field to merit high-profile publication. Reviewer #2 (Recommendations for the authors): Key points to address: – Address the impact of biguanides on bacterial growth (OP50, HT115) experimentally e. g. bacterial growth, the impact of heat-killed bacteria on key biguanide phenotypes, and their relationship to ether lipids. The impact of biguanide concentration should also be considered in this regard. – Address whether different amounts of biguanide cause the same effect on ether lipids. – Address the direct genetic connections between skn-1 and fard-1 (etc) e. g. by creating a fard-1; skn-1 gof double and examining fat +/- Phenformin. Alternatively, could this be examined using fat measurements from aak-2 and daf-16 +/- fard-1? It would be interesting to see if the mechanism is the same for all of these longevity processes and make the study of even broader relevance. Other points: – Are the error bars in Figure 1 S1A correct? The data is normalised to 1. I am also unclear of the logic here. Metformin makes the worms smaller, but fard-1 and acl-7 RNAi reverse this? Is this the same with the mutants? – Line 283 – 'the' missing? + other punctuation errors scattered about. – The theory that the web-like structures marked by FARD-1::RFP are the ER is intriguing. [SEP] Justify:

Output: The text contrasts the claim by detailing the complexity of the relationship between metformin, bacterial influence, and longevity without supporting the assertion that biohacking can guarantee longevity or double human lifespan. It indicates that while there are biologically significant pathways and mechanisms worth exploring, it does not provide a definitive guarantee for increased lifespan through biohacking methods.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: The strength of weight-bearing bones is similar in amenorrheic and eumenorrheic elite long‐distance runners. Scandinavian journal of medicine & science in sports. 2018;28(5):1559-68. Bjørnerem ønnebø V, Sundsfjord J, Svartberg J, et al. Endogenous sex hormones in relation to age, sex, lifestyle factors, and chronic diseases in a general population: the Tromsø Study. of & Metabolism. 2004;89(12):6039-47. Hirschberg AL. Female hyperandrogenism and elite sport. Endocrine connections. 2020;9(4):R81-R92. Effect of exercise on serum androgens in postmenopausal women: a 12-month randomized clinical trial. . 2004;13(7):1099 − 105. . Gender impacts the post-exercise substrate and endocrine response in trained runners. Journal of the of Sports Nutrition. 2008;5(1):1–10. . Effect of exercise on reproductive hormones in female athletes. of Sport and Exercise Science. 2013;5(1):7–12. . to Intensive, Exercise in Women. Endocrines. 2020;1(2):119 − 24. . Hormonal responses to endurance and resistance exercise in females aged 19–69 years. of A:. 2002;57(4):B158-B65. Mannerkorpi K, Landin-Wilhelmsen K, Larsson A, Cider Å, Arodell O, Bjersing JL. Acute effects of physical exercise on the serum insulin-like growth factor system in women with fibromyalgia. BMC musculoskeletal disorders. 2017;18(1):1–8. . Effects of female reproductive hormones on sports performance. Endocrinology of physical activity and sport: Springer; 2013. p. 281–322. . Testosterone, Oestrogen, and the Growth Hormone/Insulin- Muscle Adaptations. Frontiers in Physiology. 2021;11:1814. Kochańska-Dziurowicz A, Gawel-Szostek V, Gabryś T, Kmita D. Changes in prolactin and testosterone levels induced by acute physical exertion in young female athletes. [SEP] Justify:

Output: The text provided discusses various studies related to hormone levels, exercise, and sports performance without mentioning urban living or its impact on stress levels. Therefore, it is irrelevant to the claim.


Input: Task: corroborate the claim using the given text. Claim: Marine protected areas (MPAs) help conserve biodiversity by restricting human activities in critical habitats. [SEP] Text: This is the very reason for the intergovernmental conference – to bridge the gap between areas and measures to create a comprehensive and coherent system for the conservation and sustainable use of marine biodiversity in areas beyond national jurisdiction. After two substantive sessions of the negotiations, the discussions on area based management tools, including marine protected areas, were well advanced compared to other parts of the negotiations. States had presented developed positions and proposals. However, a number of issues still needed clarification and definition for the negotiations to move forward. However, some issues would need further consideration and work to move negotiations forward from this point. Two of the main issues that would need further discussions were: First – what do we mean by area-based management tools (abmts) and marine protected areas (mpas)? Second – how do we characterize the “global approach” vs the “regional approach”? 1 by abmts and mpas? Looking at existing treaties, there are some definitions of mpa and abmt. on (cbd) art 2 defines a Area as a “geographically defined marine area which is designated and regulated and managed to achieve specific conservation objectives”. The cbd sbssta defined abmt in 2018 as “a geographically defined area other than a Protected Area, which is governed and managed in ways that achieve positive and sustained long-term outcomes for the in situ conservation of biodiversity, with associated ecosystem functions and services and, where applicable, cultural, spiritual, socioeconomic, and other locally relevant values”. In the EU, an mpa is defined as an area with a higher level of protection for marine biodiversity than the surrounding areas. The EU-position in the negotiations has been based on this definition with some additions. For the negotiations the EU and its member states define an mpa as comprehensive management for a specific maritime area, whereas an abmt is decided by a competent organisation for a specific sector or activity but without a specific management objective (a pssa decided by imo would be an example of an abmt). Also, national legislation contains different definitions. The differences in definition and understanding may be a reason for some blockages in the negotiation. To overcome these blockages and move negotiations forward, there is a distinct need to reach a common understanding on what is what when talking about abmts and mpas. 2 vs At the second substantive session of the negotiations, there was already a convergence forming on several points. [SEP] Justify:

Output: The text corroborates the claim by discussing marine protected areas (MPAs) and their role in the conservation and sustainable use of marine biodiversity. It mentions that defined and managed areas, such as MPAs, are intended to achieve specific conservation objectives, which aligns with the claim that MPAs help conserve biodiversity by regulating human activities in crucial habitats.


Input: Task: contrast the claim using the given text. Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Using this approach, we verify through lipidomicMS analysis that biguanides drive somatic fatty acid depletion and increases 16:0 DMA species. Importantly, these effects do not rely on the OP50-1 food source being alive, suggesting that the effects of biguanides on increasing ether lipid biosynthesis and altering somatic lipid stores do not act directly through alterations in bacterial growth or metabolism (Figure 6 —figure supplement 2B-G). We additionally include lifespan analyses that reveal that biguanides still extend lifespan on metabolically killed OP50-1, and that ether lipid deficiency in ads-1 mutant animals completely abrogates both metformin and phenformin-mediated lifespan extension, even when grown on metabolically inactivated and dead bacteria (Figure 6 —figure supplement 3). Combined, these data rigorously advance the conclusion that the effects of biguanides on ether lipid biosynthesis and lifespan extension occurs directly through the nematode, and do not rely upon alterations in bacterial growth or metabolism to exert their pro-longevity effects. We include discussion of these new results in lines 509 to 547. Given that these results contrast with previously published work by others, and the importance to the field, we plan a whole separate manuscript about biguanide effects directly on nematode lifespan versus indirectly through the bacteria. As such, we do not dwell extensively on the subject herein. 3) Please explain in the text why different biguanide concentrations were used in different experiments. We thank the reviewers for the opportunity to clarify the uses of different concentrations of biguanides in our assays. We wish to clarify that our current study is focused on the role of ether lipid machinery in modulation of lifespan and healthy aging – as such, we focused on genetic and biochemical experiments leveraging minimally lifespan extending doses of biguanides (4. 5 mM phenformin and 50 mM metformin) to identify epistatic links and interactions, as utilized by several independent laboratories 4-9. The goal of the 160 mM dosage of metformin used in our prior genetic screens 10 and subsequently highlighted in Figure 1 —figure supplement 1A is to enhance the sensitivity and specificity of our discovery approach to identify effectors of the biological action of biguanides. The 160 mM dose we leveraged causes potent growth inhibition 10. [SEP] Justify:

Output: The text contrasts with the claim by discussing the effects of biguanides on lifespan extension in nematodes and emphasizing that these results do not indicate that biohacking, specifically through biguanides, guarantees longevity or doubles the average human lifespan. It mentions that while biguanides impact lifespan, they do so through interactions within the nematode without a clear implication that this would universally apply to humans or lead to doubling of lifespan.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: Figures AbstractIn order to intercept moving objects, we need to predict the spatiotemporal features of the motion of both the object and our hand. Our errors can result in updates of these predictions to benefit interceptions in the future (adaptation). Recent studies claim that task-relevant variability in baseline performance can help adapt to perturbations, because initial variability helps explore the spatial demands of the task. In this study, we examined whether this relationship is also found in interception (temporal domain) by looking at the link between the variability of hand-movement speed during baseline trials, and the adaptation to a temporal perturbation. 17 subjects performed an interception task on a graphic tablet with a stylus. A target moved from left to right or vice versa, with varying speed across trials. Participants were instructed to intercept this target with a straight forward movement of their hand. Their movements were represented by a cursor that was displayed on a screen above the tablet. To prevent online corrections we blocked the hand from view, and a part of the cursor’s trajectory was occluded. After a baseline phase of 80 trials, a temporal delay of 100 ms was introduced to the cursor representing the hand (adaptation phase: 80 trials). This delay initially caused participants to miss the target, but they quickly accounted for these errors by adapting to most of the delay of the cursor. We found that variability in baseline movement velocity is a good predictor of temporal adaptation (defined as a combination of the rate of change and the asymptotic level of change after a perturbation), with higher variability during baseline being associated with better adaptation. However, cross-correlation results suggest that the increased variability is the result of increased error correction, rather than exploration. Citation: Knelange EB, López-(2020) Increased error-correction leads to both higher levels of variability and adaptation. 15(2): e0227913. : June 26, 2019; Accepted: January 2, 2020; Published: February 4, 2020Copyright: © 2020 Knelange, López-Moliner. This is an open access 10. 17605/OSF. IO/BF7SE. Funding: This work is part of the PACE project, which received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement No 642961. [SEP] Justify:

Output: The text is irrelevant to the claim regarding urban living and stress levels. It discusses a study on hand movement and adaptation in intercepting moving objects without mentioning urban living, stress, or related psychological aspects.


Input: Task: corroborate the claim using the given text. Claim: Marine protected areas (MPAs) help conserve biodiversity by restricting human activities in critical habitats. [SEP] Text: or our and & & -Researchers &Pick & Introductions: & & Geography, Planning & & Sociology, & to a and and or our and & & -Researchers &Pick & Introductions: & & Geography, Planning & & Sociology, & to a and Previous 10. 4337/9781788974912. M. 13 Keywords: ecological economics; ecological economics history; ecological economics terms and definitions; ecological economics methods Full access comprehensive Dictionary brings together an extensive range of definitive terms in ecological economics. Assembling contributions from distinguished scholars, it provides an intellectual map to this evolving subject ranging from the practical to the philosophical. Coastal and ocean regions regulated by governments to preserve unique ecosystem and cultural/historical attributes. MPA restrictions range from near-complete prohibition of human use (for Conservation of Nature (IUCN) Category 1a – Reserve or “No-Take Zone”) to minor limitations (IUCN Categories 5 or 6, allowing sustainable commercial use of seascapes). Scientific research is typically permitted in MPAs. Further reading Agarty 1994; Edgar et al. 2014. See also: Biodiversity conservation, No-take zone, Conservation areas, Cultural services, Ecosystem services. 1994. Advances in marine conservation: the role of marine protected areas. Trends in Ecology & Evolution 9(7): 267–70. Agarty, M. T. 1994. Advances in marine conservation: the role of marine protected areas. Trends in Ecology & Evolution 9(7): 267–70. )| falseSearch 2014. Global conservation outcomes depend on marine protected areas with five key features. Nature 506: 216–20. Edgar, G. J. , Stuart-Smith, R. D. , Willis, T. J. et al. 2014. Global conservation outcomes depend on marine protected areas with five key features. Nature 506: 216–20. )| falseSearch 10. [SEP] Justify:

Output: The text supports the claim by stating that coastal and ocean regions are regulated by governments to preserve unique ecosystems and attributes. It describes the restrictions in MPAs, ranging from near-complete prohibition of human use to minor limitations, which aligns with the notion that these areas are managed to conserve biodiversity by limiting human activities in critical habitats.


Input: Task: contrast the claim using the given text. Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Our prior published work indicates that using this dose to look for gene inactivations that block the growth inhibitory effects of the drug can also identify longevity effectors of metformin10. Thus, we used a similar strategy here to identify fard-1 and acl-7, which were initially identified as gene knockdowns that block the growth inhibitory effects of 160 mM metformin. Thereafter, lower doses of biguanides are used (4. 5 mM phenformin and 50 mM metformin) to elucidate requirements of the ether lipid machinery in biguanide-prompted longevity. We succinctly modify in the text the reasoning for the different biguanide concentrations used in this work (lines 135 to 153). 4) Please address in the text the reviewer's question on the role of oxidative stress and the role of gst-4. We thank the reviewers for allowing us to highlight this important clarification. We have performed reporter imaging experiments in the gst-4 transcriptional reporter strain gst-4p::GFP::NLS (included as Figure 6 —figure supplement 1A-B), suggesting that biguanides do not significantly activate gst-4 expression in either OP50 and HT115 dietary sources, and that phenformin treatment conversely significantly reduced gst-4 expression. We have repeated this experiment numerous times and at multiple timepoints in the lifespan. In fact, the analysis of gst-4 expression indicates that metformin and phenformin decrease gst-4 expression. These data substantiate our claim that the requirement of SKN-1 activity downstream of biguanides to mediate somatic lipid depletion and pro-longevity outcomes is not due to a gst-4 mediated antioxidant role. We additionally include reporter imaging data for expression of dod-24, a metabolic defense stress response factor known to be transcriptionally regulated by SKN-12, revealing that biguanides activate dod-24 expression via a mechanism dependent on both ether lipid machinery and SKN-1 activity (Figure 6F). Concordant with our prior work2, there are multiple “flavors” of skn-1 activation, and the metabolic “flavor” is oppositely regulated to oxidative defenses (thus leading to increased expression of dod-24 and decreased expression of gst-4). Given that these results conflict with the literature and the prevailing notions in the field. [SEP] Justify:

Output: The text contrasts the claim by discussing the results of experiments involving biguanides and their complex mechanisms linked to longevity, without asserting that biohacking, or any method, can guarantee longevity or specifically double the average human lifespan. The findings suggest interactions at a genetic level that affect longevity but do not support the idea that biohacking provides a foolproof means of significantly extending life expectancy.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: We also received funding from grant PSI2017-83493-R of AEI/. There were no commercial relationships. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist. IntroductionThe human race is remarkably skilled in timing tasks like catching or hitting a ball [1, 2]. However, large inter-individual differences can be observed when it comes to these skills. To become successful at ball sports, a person needs to be able to accurately account for continuous changes in both the environment and their own body. To this end, we can use sensory feedback to guide our movement [3]. However, sensory feedback from our movements is processed by our brain with a delay that can reach up to about 150 ms [4–6]. This can lead to unstable movements, because corrections to errors are initiated with a delay. In order to not only rely on sensory feedback and select appropriate motor commands, we are thought to be able to predict the sensory consequences of these motor commands. Studies have shown that our brain maintains an internal forward model that holds the predictions regarding the sensory consequences [7, 8]. However, the outcome of a motor command can change due to systematic disturbances like fatigue in the muscles [9]. Accurate timing of our motor commands in a dynamic world requires continuous evaluation and updating of the predicted consequences of these motor commands [10]. This can be done by evaluating the difference between the actual and the predicted sensory consequences of a motor command (the prediction error [7, 11]). However, prediction errors do not always stem from incorrect motor commands. Noise can come from different stages of the sensorimotor process [12, 13]. Different types of noise associated with neural processes like movement planning [14–18] or execution [19–21] cause variability. In addition, trial-to-trial variability in the outcome of the movement can be caused by inaccurate estimates of the task requirements [22] and disturbances from the outside world [23]. Errors caused by these types of noise do not necessarily require updates of the internal model. Updating the forward model is generally thought to be done by decreasing the prediction error over time (error-based learning) [24, 25]. Dominant theories in the field of motor control suggest that error correction is an optimal process [26, 27]. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses topics related to motor control, error correction in sensory feedback, and human performance, none of which address the connection between urban living and stress levels.


Input: Task: corroborate the claim using the given text. Claim: X-ray crystallography is a biophysical technique used to determine the structures of proteins and other biomolecules. [SEP] Text: 2), analyze the significance of results obtained for each model protein structure, and finally present initial results of modeling an experimental scattering profile with this method. For each example, the problem SAXS profile, the best model profiles, and the corresponding bead models are collected in Fig. 3, A–E. For comparison, Fig. 4 shows three different orthogonal views of a 3D overlay of the corresponding problem structure (in yellow ribbon and side chain representations) and the fitted structure (as a dotted blue surface of the bead model). The results are summarized in Table 1 (without noise) and Table 2 (with noise). Note that the r. m. s. deviation and R factor are not directly comparable between the two tables, because the noise in the problem profile obviously increases their values. As a reference, the corresponding r. m. s. and Rf values between the original problem profile and the same with noise, for each test protein, are indicated in the first column of Table 2, providing an approximate indication of the lowest limit range that each fit could achieve. To be confident about the convergence of the results, and because of the stochastic character of the method, 10 different initial simulations with spheres of radius 6Å were repeated for each test protein. All of these bead models had converging sizes and shapes; actually the majority of the runs at this resolution resulted in practically the same best-fit solution. The resolution was increased by employing this initial solution to constrain the starting configurational space for additional search cycles with decreasing bead radius. Figure 3 Calculated and fitted scattering profiles for the known protein structures of (A) βb2-crystallin (2bb2. pdb), (B) γ-crystallin (4grc. pdb), (C) ribonuclease inhibitor (1bnh. pdb), (D) lysozyme (6lyz. pdb), and (E) two molecules of lysozyme (1rcm. pdb). Solid lines: synthetic profiles calculated from each pdb file with the program DALAI (Pantos et al. , 1996; hydrogen atoms and water molecules have not been taken into account). Points (circles), DALAI_GA simulated profiles. Dotted lines, synthetic profiles with added noise. Dashed lines, corresponding simulated profiles. [SEP] Justify:

Output: The text discusses the analysis and modeling of scattering profiles of known protein structures, which aligns with the use of X-ray crystallography as it is a standard technique to deduce the structures of biomolecules. The mention of calculating and fitting scattering profiles relates directly to the core principles of X-ray crystallography, thus corroborating the claim.


Input: Task: contrast the claim using the given text. Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: we describe these results in the revised text in the Results section in lines 497 to 508 and in the Discussion in lines 659 to 673. Reviewer #1 (Recommendations for the authors): 1. Lipid metabolism and SKN-1 have been implicated in germline disruption longevity pathways (one example of several papers is PMID: 26196144). The longevity data here all appear to have been collected in the background of the fertility inhibitor FuDR. Although the use of FuDR is common in the field and justified, synergistic effects have been documented. The authors should address the question as to whether the key finding of ether lipid requirements for biguanide-mediated longevity is independent of the presence of FuDR. We thank the reviewer for this suggestion. As noted in 1, we have performed lifespan experiments without the use of FUdR (included as Figure 1 —figure supplement 2) for wild type and ether lipid deficient mutants treated with either metformin or phenformin in biological triplicate. These new data reveal that the requirements for the ether lipid machinery in biguanide-mediated lifespan extension are independent of the effects of FUdR, with abrogation of lifespan extension seen in rates comparable to that when using FUdR (Figure 1B-G and Supplementary file 1). We address these important confirmatory results in the text under lines 160 to 165. 2. The authors state that biguanides do not stimulate expression of the skn-1 antioxidant defense effector gst-4 (Discussion, lines 580 – 582), and cite Cabreiro et al. 2013 and Onken and Driscoll, 2010 to support this – in fact, both these papers demonstrate the opposite, showing that biguanide treatment does result in increased gst-4 expression. This calls into question the author's suggestion that biguanides activate ether lipid biosynthesis and skn-1 signaling to trigger metabolic stress defenses rather than canonical oxidative stress pathways. Minimally, this needs to be straightened out in terms of accurate citation and discussion. Better, the argument might be addressed by looking at daf-16 and skn-1 downstream target expression with biguanide treatment or in fard-1(oe) mutants with and without ether lipid biosynthesis gene disruptions. Resistance to oxidative stress could be tested under similar conditions. [SEP] Justify:

Output: The text contrasts the claim by indicating that while there is discussion on lifespan extension and biguanide treatment, it does not provide evidence that biohacking guarantees longevity or doubles the average lifespan. Instead, it focuses on the complexities and dependencies of lifespan experiments, suggesting different outcomes when certain conditions are altered, thereby challenging the notion of a guaranteed doubling of lifespan through biohacking.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: The amount of error correction depends on the reliability of the predicted sensory consequences and the reliability of the received sensory consequences [28]. However, in situations in which error feedback is unavailable or uninformative, the environment needs to be explored in order to find and exploit the most beneficial solution. This type of process is called reinforcement learning [29, 30]. It can also be beneficial in situations where the average end-point error is zero, but the movement is still updated in order to become more efficient [31]. Reinforcement learning, specifically exploration, usually leads to enhanced variability in the explored dimension of the behavior. Furthermore, research suggest that the nervous system could actively regulate this process when needed [32]. For this reason, we hereafter use exploration strategies to refer to the active process of learning through exploration. Some studies have found that reinforcement learning could also accelerate learning in error-based learning tasks [32]. More specifically, a benefit of task-specific baseline variability in adaptation during spatial perturbation paradigms has been found. This means that even if sensory feedback is available to the participant, more variability in the task-specific dimension could facilitate learning. It is thought that the brain has a memory of previously encountered errors [33]. Similarly, it has been proposed that predicted (future) errors might activate learned weights for motor primitives (neural mechanism that coordinate a set of movements rather than independent movements), which could elevate learning [34]. In line with this idea, reinforcement learning could lead to more experience with different movement errors and facilitate correcting future errors [35]. However, the idea that increased variability leads to better adaptation has been questioned by other studies claiming that variability originates from the different types of noise coming from motor control processes, which can have either positive, neutral or negative effects on adaptation [13]. Thus, the role of variability on adaptation is still under debate. The main question remains, can variability caused by exploration strategies directly benefit the updating of the forward model of a motor command, or are the two merely a result of error correction strategies? So far, the main focus of these studies has been the role of spatial and force-field perturbations. However, as large delays are inherent to the sensorimotor system and to contemporary electronic devices, temporal perturbation tasks have given great insights into adaptation in this domain [36–39]. It therefore is valuable to examine if task-specific variability in temporal features of movement can predict adaptation to these delays. [SEP] Justify:

Output: The text does not address the claim about urban living and its impact on stress levels. Instead, it discusses concepts related to reinforcement learning, error correction, and variability in adaptation, which are not pertinent to the assertion that urban living leads to increased stress.


Input: Task: corroborate the claim using the given text. Claim: X-ray crystallography is a biophysical technique used to determine the structures of proteins and other biomolecules. [SEP] Text: This effect can be appreciated in the case of βb2-crystallin (Fig. 4, A and B), in which the model distribution of mass in the link between domains does not exactly fit the crystallographic structure. This is more noticeable in the model obtained from the scattering profile with noise (Fig. 4 B), in which the link is displaced from its original position. Here the effect of the fluctuations induced in the scattering profile is translated into the structure, and the algorithm is able to find a representative structure of the link, which resembles an average of different possible positions of the chain between the two domains. In this same structure the projection of the left domain is split into two adjacent projections in the model. In another example (Fig. 4 E), the left arm of the modeled protein has a definite mass deficiency that is compensated for by some extra beads in other parts of the molecule, as can be observed in this and the other two views of the molecule. The effects of noise are clearly exemplified by the case of lysozyme. It can be observed that in the absence of noise, the method is able to locate the cavity of the active center of the enzyme (Fig. 6 A, left view). The input file with noise results in a model in which the overall globular shape is correctly predicted, but because of a small dispersion of beads, the cavity is less accurately detected. This effect is also present in the models obtained at lower resolution and from experimental SAXS profile (Fig. 6, C and D). Nevertheless, the differences, like dispersion of mass in the hole region and the presence of an isolated sphere, are small enough for the models to have an acceptable overall similarity. Low-resolution protein structure deduced from the x-ray solution scattering profileThe x-ray scattering simulation algorithm provides, in principle, a new procedure for deducing the size and shape of any protein or macromolecular assembly from its solution scattering profile. To our knowledge, this is possible for the first time for any kind of shape, and is applicable to any size, spanning the range from that of smaller proteins to an upper limit dictated only by the lower angle cutoff of the scattering data. The method can operate solely from a scattering profile without any other knowledge about the protein size. The output is a scattering model of the protein, typically consisting of several hundred beads. [SEP] Justify:

Output: The text corroborates the claim by discussing methods related to the structure determination of proteins, specifically mentioning 'The x-ray scattering simulation algorithm' which offers a procedure for deducing the size and shape of proteins from their solution scattering profile. This aligns with the claim that X-ray crystallography is used for determining biomolecular structures.


Input: Task: contrast the claim using the given text. Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: We thank the reviewer for highlighting this textual oversight, and for the opportunity to better expand upon our suggestion that biguanides rely upon SKN-1 induced metabolic stress defense to exert a pro-longevity outcome, independent of its known canonical oxidative stress response functions. We have corrected the discussion of the Onken and Driscoll, 2010 and Cabreiro et al. , 2013 1. 5 to 2-fold increase in gst-4 expression with 50 mM metformin treatment4,5. We have attempted numerous times to reproduce this induction result with both 50 mM metformin and 4. 5 mM phenformin administration, at multiple times across the lifespan. We include as Figure 6 —figure supplement 1A-B data that fails to replicate the subtle increase in gst-4 expression previously reported on either OP50-1 or HT115 food sources, and instead show that phenformin treatment significantly reduces gst-4 expression. We include as Figure 6F data that indicate that phenformin treatment activates expression of the metabolic stress defense factor dod-24, a known transcriptional target of the non-canonical SKN-1 innate immune effector regulon2. The induction of dod-24p::GFP expression is both skn-1 and ether lipid machinery dependent, analogous to the dependencies seen with adult somatic lipid depletion (Figure 6B-E). Thus, we argue that biguanides exert their pro-longevity outcomes via alterations in somatic lipid levels and metabolic stress defense response through an ether lipid and SKN-1 signaling axis independent of the transcription factor’s known role in inducing an oxidative stress response. We have included discussion of these new results in Results (lines 497-508) and (659-673) of the manuscript. The decrease in gst-4 expression seen with phenformin treatment is potentially of great interest, suggesting that phenformin treatment may increase the sensitivity of animals to oxidative stressors. We are focusing on follow ups of this result in manuscripts currently in preparation. Less critical points that should be addressed: 3. The paper would benefit from just a little bit more description of the original genetic screen, although published in Wu 2016. The endpoint of the original screen was for growth/body size changes in high metformin; how did data translate to the longevity endpoint focus here? [SEP] Justify:

Output: The text contrasts the claim by discussing the effects of biguanides like metformin and phenformin on longevity and metabolic stress response without guaranteeing or stating that biohacking will actually double human lifespan. It indicates that the increase in gst-4 expression through metformin treatment was not reproducible and illustrates that phenformin treatment did not increase expression but instead reduced it. This suggests that while there may be potential pro-longevity outcomes associated with these substances, the text does not support the claim that biohacking guarantees a doubling of lifespan.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: Temporal perturbations (delays) require humans to identify a new temporal relationship between the motor command and the sensory consequences. The effect of delays on the spatial prediction error is increased with higher movement speeds (i. e. moving faster increases the gap between hand and delayed feedback), while lower speeds have less effect on the size of the prediction error. Variability in movement speed can therefore help to explore this temporal relationship, and benefit the examination of newly introduced delays. If exploration itself provides a benefit in adaptation, we do not expect the movement speed to be systematically related to previously encountered errors. However, a recent study by [40] found that error correction strategies could explain differences of the learning rate in a balancing task. If error correction rather than exploration is the main benefit for adaptation, higher rates of error correction are to be expected throughout the baseline for people that adapt more. The aim of the study was to examine if higher baseline movement speed variability can predict adaptation in a temporal timing task. As we found a positive relationship, we followed up this analysis by examining if this relationship was the result of exploratory behavior, or if higher variability might be the result of increased error correction. Materials and methods Participants 20 students of the university of Barcelona (20. 3 ±SD 2. 3 years; 15 female) participated in the experiment. All participants gave written consent. In order to be eligible for inclusion, participants’ vision and hearing needed to be normal or corrected to normal, and they needed to be free from movement restrictions or problems. The study was part of a program that has been approved by of Committee (CBUB) (Insitutional review board IRB 00003099) and was conducted in accordance to the Declaration of Helsinki. setup of the experiment is shown in Fig 1A. Participants were seated in front of a graphic tablet (24240), which recorded the movements of a hand-held stylus that the participants used in the experiments. A half-silvered upward facing mirror was located above the graphic tablet. Above the mirror, a projector displayed an image of the task onto a horizontal back-projection screen, at a frame rate of 72 Hz and a resolution of 800 by 600 pixels. The participant could see the reflection of this image in the mirror. The hand and the hand-held stylus were blocked from view by the mirror. A 2. 6-GHz Quad-Core computer recorded the position of the stylus at 125 Hz and controlled the projected image. [SEP] Justify:

Output: The text does not address the claim about urban living and stress levels. It focuses on a study examining the effects of movement speed variability and error correction in a temporal timing task, which is unrelated to the topic of stress associated with urban living.


Input: Task: corroborate the claim using the given text. Claim: X-ray crystallography is a biophysical technique used to determine the structures of proteins and other biomolecules. [SEP] Text: Abola, E. E. ∙ Bernstein, F. C. ∙ Bryant, S. H. . . . Protein data bankAllen, F. H. ∙ Bergerhoff, G. ∙ Sievers, R. Crystallographic Databases-of the of Crystallography, Bonn/Cambridge/Chester, 1987; 107-1322. Andreu, J. M. ∙ Bordas, J. ∙ Díaz, J. F. . . . Low resolution structure of microtubules in solutionJ. Mol. Biol. 1992; 226:169-184CrossrefScopus (140)PubMed3. Bax, B. ∙ Lapatto, R. ∙ Nalini, V. . . . X-ray analysis of beta B2-crystallin and evolution of oligomeric lens proteinsNature. 1990; 347:776-780CrossrefScopus (253)PubMed4. Beavil, A. J. ∙ Young, R. J. ∙ Sutton, B. J. . . . Bent domain structure of recombinant human IgE-Fc in solution by x-ray and neutron scattering in conjunction with an automated curve fitting procedureBiochemistry. 1995; 34:14449-14461CrossrefScopus (74)PubMed5. Boehm, M. K. ∙ Mayans, M. O. ∙ Thornton, J. D. . . . Extended glycoprotein structure of the seven domains in human carcinoembryonic antigen by x-ray and neutron solution scattering and an automated curve fitting procedure: implications for cellular adhesionJ. Mol. Biol. 1996; 259:718-736CrossrefScopus (57)PubMed6. Cantor, C. R. ∙ Schimmel, P. R. Biophysical Chemistry. Part II. Techniques for the Study of and FunctionW. H. Freeman, New York, 1980 811–8197. Chacón, P. , F. Morán, J. F. Dı́az, E. Pantos, and J. M. Andreu. 1998. A genetic algorithm for low resolution protein structure determination. of the 5th on Protein Structure-Function Relationship. Z. Zaidi, editor. [SEP] Justify:

Output: The text corroborates the claim by referencing multiple studies involving X-ray analysis and structural determination of biomolecules like proteins. Although it does not explicitly state that X-ray crystallography is used, the mention of 'x-ray and neutron solution scattering' in conjunction with automated curve fitting procedures implies the application of such techniques in structural biology.