Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: Within the 1915 edition of Therapeutics of Internal Diseases, edited by Harvard medical doctor and the president of the Association of American Physicians, Frederick Forchheimer, it was stated that ‘there are many varieties of lactic acid bacilli tablets on the market for direct ingestion or for the preparation of a lactic acid milk; but none of these have the efficiency or produce the palatability of milk which is common to the true Bulgaricus preparation known as liquid lactobacilline…the signs of autointoxication disappear slowly, and, therefore, for curative and hygienic purposes it is advisable to continue to the use of lactobacilline more or less continuously for several months’ [43]. Chief among the reasons for the administration of lactobacilline and other interventions, it was further stated in the text that ‘patients suffering from neurasthenia, melancholia, hypochondriasis, and allied conditions are much more sensitive to the toxic effects of intestinal putrefaction than are those that have a normal nervous system. There is here illustrated a vicious circle: that is, depressed conditions of the nervous system very readily lead to constipation and autointoxication; and the latter condition, in turn, aggravates and excites the nervous symptoms’[43]. Lactobacilline (or Lacto-bacilline of Metchnikoff) was but one of a long list of Lactobacillus preparations that would be produced commercially for the treatment of autointoxication and its sequelae. The first wave of products focused on Metchnikoff’s Bacillus bulgaricus. Another example was of and their Intesti-Fermin tablets positioned for increasing mental vitality and the treatment of neurasthenia. secured full page advertisements in a wide variety of periodicals, stating that ‘Metchnikoff’s great discoveries now procurable in tablet form’ and that Intesti-Fermin ‘promotes physical and mental health and provides a truly scientific aid to high efficiency in every-day life’ [44]. Metchnikoff distanced himself from the commercial products and brought suit against for using his name in the advertisements [45]. By 1917 the Druggist’s Circular listed some 30 different commercially available Bacillus bulgaricus preparations [46]. However, by the early 1920s L. [SEP] Justify:

Output: The text corroborates the claim by discussing the historical use of lactic acid preparations, specifically lactobacilline, for the maintenance of gut health and the treatment of conditions resulting from intestinal toxicity. It indicates that certain Lactobacillus preparations have been believed to influence gut health and demonstrates a recognition of their potential benefits in both physical and mental health.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: This is relation to narratives between 228-230: "Indeed, our data show that the later the chronotype of participants (measured by the MCTQ mid-sleep phase, mSP [24]), the later their mid-eat phase (mEP) on weekends (Fig. 3E, Tab. S6), with the mSP and mEP being almost antiphasic on average (Fig. 3F, Tab. S10). " This will help readers unfamiliar with circadian biology/chronobiology research understand the contents of this manuscript, particularly Fig 3. We have explained the new chronobiology terms that appear in the 3. 1 Limitations", we have examined the aspect of the reliability of self-reported data and our measures to reduce this uncertainty in more detail. We have also added further details on the measurement of outcomes in the materials and methods section. (3) Selection Criteria: Reevaluate the inclusion criteria and consider discussing the implications on the study's findings of the broad age range, the inclusion of shift work, unmatched cohorts, and inclusion of individuals with normal weight, overweight, and obesity. Provide a subgroup analysis or discuss how BMI might have influenced the results. Even though this is an additional post-hoc analysis, it would directly address one of the major weaknesses of the study design. We have supplemented the analyses and now show in Fig. S2G that neither age nor gender had any influence on weight loss as a result of the intervention. To our knowledge, none of the 100 participants evaluated were shift workers. Even if shift workers were part of the study without our knowledge, we do not consider this to be a problem as long as their shifts allow them to keep to certain eating times. The fact that it turned out that the baseline BMI of the remaining 67 EG and 33 CG participants did not match is discussed in detail in the section "3. 1 Limitations". Our previous analysis in Fig. S2I already showed that there is a negative correlation between baseline BMI and weight loss - an interesting result, as it shows that people with a high BMI particularly benefit from the intervention. In addition, we already showed in Fig. S2J in a subgroup analysis that in all strata the BMI of EG subjects decreased more than that of CG subjects, even if they had the same initial BMI. We do not consider the wide dispersion of the BMIs of the included participants to be a weakness of the study design. [SEP] Justify:

Output: The text contrasts the claim by providing evidence suggesting that factors such as baseline BMI and dietary interventions can influence weight loss. It states, 'the baseline BMI of the remaining 67 EG and 33 CG participants did not match' and highlights that 'there is a negative correlation between baseline BMI and weight loss.' This indicates that not all individuals experience weight gain from certain eating patterns, which directly counters the absoluteness of the claim regarding carbohydrates leading to weight gain.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: 2008;506:708–32. [DOI] [PubMed] 119. Excitatory actions of GABA in the suprachiasmatic nucleus. J Neurosci. 2008;28:5450–9. [DOI] [PubMed] [PMC]120. . Regulation in AVP+ and VIP+ Neurons of the Suprachiasmatic Nucleus. Sci Rep. 2017;7:10226. [DOI] [PubMed] [PMC]121. . Two brain nuclei controlling circadian rhythms are identified by GFAP immunoreactivity in hamsters and rats. Neurosci Lett. 1989;99:55–60. [DOI] [PubMed] 122. . in the via Glutamatergic Signaling. Neuron. 2017;93:1420–35. e5. [DOI] [PubMed] [PMC]123. . System and the as Its Pacemaker. Biology (Basel). 2019;8:13. [DOI] [PubMed] [PMC]124. Costa R, Montagnese S. The role of astrocytes in generating circadian rhythmicity in health and disease. J Neurochem. 2021;157:42–52. [DOI] [PubMed] 125. Chai H, Diaz- Neural Circuit-Specialized Astrocytes: Transcriptomic, Proteomic, Morphological, and Functional Evidence. Neuron. 2017;95:531–49. e9. [DOI] [PubMed] [PMC]126. . The tripartite synapse: roles for gliotransmission in health and disease. Med. 2007;13:54–63. [DOI] [PubMed] 127. Mieda M. The central circadian clock of the suprachiasmatic nucleus as an ensemble of multiple oscillatory neurons. Neurosci Res. 2020;156:24–31. [DOI] [PubMed] 128. Circadian regulation of ATP release in astrocytes. J Neurosci. 2011;31:8342–50. [DOI] [PubMed] [PMC]129. . Circadian rhythm generation and entrainment in astrocytes. J Neurosci. 2005;25:404–8. [SEP] Justify:

Output: The text does not address the claim about the suprachiasmatic nucleus being the master regulator of circadian rhythms directly. Instead, it provides a list of research articles related to various aspects of circadian rhythm research without explicitly confirming or denying the role of the suprachiasmatic nucleus as the central regulator.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: bulgaricus declined in popularity and L. acidophilus was the species of commercial and clinical choice. After publications by scientists Leo F. Rettger and Harry A. Cheplin and colleagues [47], those showing that L. acidophilus can and does live and develop in the intestines of humans and animals - while L. bulgaricus does not - many of these same companies would completely abandon the L. bulgaricus in favor of L. acidophilus. Acidophilus as a mental tonicThe early 1920s witnessed a second wave of enthusiasm for the use of oral ‘bacteriotherapy’ as a means to positively influence mental health. America various producers of acidophilus milk – e. g. Laboratories, Walker-Gordon Laboratories, Cheplin’s - began widespread distribution in tandem with marketing campaigns within medical and popular print media. During the 1920s it was commonplace to see competitive advertisements in medical journals for Lactobacillus acidophilus preparations that were “Accepted” [48]. Although reluctant to officially list such remedies in the absence of scientific support, the on Pharmacy and Chemistry did so at the time because their own nationwide survey of clinicians deemed the Lactobacillus preparations to be of some clinical value [49]. Within medical journals the advertizing was largely restricted to viability of the bacteria and general value. However, within popular press the claims were more direct – for example, Walker-Gordon acidophilus milk campaign in newspapers [50] stated “The results, as thousands of physicians and users testify, are nothing short of amazing. Not only a banishing of mental and physical depression, but a flooding of new vitality throughout the system”. Meanwhile, the competition, Lederle, claimed in the same newspapers that “There can be no question of the efficacy of Lederle acidophilus milk…restoring your energy to its maximum”, going on to urge consumers to choose Lederle over the competition [51]. In support, there were opinion-based newspaper editorials from various scientists claiming value of acidophilus therapy – “Run-Down State” was the headline produced in the syndicated column of one nutritional scientist [52]. In the absence of convincing scientific evidence, this pattern of market-driven assumptions (and consumption) carried on through the early 1930s. [SEP] Justify:

Output: The text discusses the use of Lactobacillus acidophilus, a probiotic, and its impact on human gut health as well as its marketed benefits. It indicates that L. acidophilus can thrive in the intestines and was preferred in bacteriotherapy, showing a move towards its use for digestive health improvement. Additionally, the positive claims about Lactobacillus acidophilus by companies and physicians support the idea that probiotics can indeed support gut health by improving the balance of bacteria, aligning with the claim.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: AbstractObjectiveMany weight loss strategies are based on the restriction of calories or certain foods. Here, we tested a weight loss intervention based solely on increasing the regularity of meals, presuming that this allows the circadian system to optimally prepare the food metabolism for these times. Participants & MethodsIn a two-group, single center randomized-controlled single-blind pilot study (pre-registration DRKS00021419) with participants aged 18-65 years and BMI ≥ 22 kg/m², we used a smartphone application to identify the times at which each participant eats particularly frequently and asked participants of the experimental group to restrict their meals to only these times for six weeks. Control participants received sham treatment. Primary outcome was self-reported body weight/BMI and secondary outcome the well-being of participants. ResultsOf 148 participants entering the pilot study, 121 were randomized and of these 100 (control: 33, experimental: 67) finished the study. Our results show that the more regular the meals of participants of the experimental group became, the more weight/BMI they lost, averaging 2. 62 kg (0. 87 kg/m²); p < 0. 0001 (BMI: p < 0. 0001) compared to an insignificant weight loss of 0. 56 kg (0. 20 kg/m²) in the control group; p = 0. 0918 (BMI: p = 0. 0658). Strikingly, weight loss was not related to changes in self-reported calories, food composition, and other food-related factors. Additionally, physical and mental well-being improved significantly. ConclusionIn summary, increasing the regularity of meals causes participants to lose excess body weight and improves overall well-being. HighlightsIndividual optimal times for meals are determined via an app-based meal diary. Generation of a structure plan for mealtimes are adjusted to individual circadian clocks. Following this plan, participants lost an average body weight of 2. 6 kg over six weeks. Weight loss is achieved without changes in self-reported food quantity or composition. Regular mealtimes contribute to the improvement of the general well-being. 1. IntroductionCircadian clocks induce endogenous 24-hour rhythms in the expression of more than half of all genes across all tissues [1, 2], allowing the body to anticipate daily changes between day and night and to prepare and harmonize physiological processes accordingly. [SEP] Justify:

Output: The text contrasts the claim by presenting evidence that a weight loss intervention focused on meal regularity resulted in participants losing weight without alterations in calorie intake or food composition. This suggests that weight loss can occur regardless of carbohydrate consumption, contradicting the claim that eating carbohydrates always results in weight gain.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: [DOI] [PubMed] [PMC]171. Maywood ES, O' Genetic and molecular analysis of the central and peripheral circadian clockwork of mice. . 2007;72:85–94. [DOI] [PubMed] 172. in VIP-IRES-CRE Mice (JAX 010908). J Biol Rhythms. 2020;35:340–52. [DOI] [PubMed] [PMC]173. Park J, Zhu H, O' Single-and Involved in the Clock. Front Neurosci. 2016;10:481. [DOI] [PubMed] [PMC]174. Suprachiasmatic VIP neurons are required for normal circadian rhythmicity and comprised of molecularly distinct subpopulations. Nat Commun. 2020;11:4410. [DOI] [PubMed] [PMC]175. . Temporally chimeric mice reveal flexibility of circadian period-setting in the suprachiasmatic nucleus. . 2016;113:3657–62. [DOI] [PubMed] [PMC]176. . Role of GABA in the regulation of the central circadian clock of the suprachiasmatic nucleus. J Physiol Sci. 2018;68:333–43. [DOI] [PubMed] [PMC]177. . Seasonal induction of GABAergic excitation in the central mammalian clock. . 2014;111:9627–32. [DOI] [PubMed] [PMC]178. . The effects of GABA and benzodiazepines on neurones in the suprachiasmatic nucleus (SCN) of Syrian hamsters. Brain Res. 1991;552:53–7. [DOI] [PubMed] 179. . GABA networks destabilize genetic oscillations in the circadian pacemaker. Neuron. 2013;78:799–806. [DOI] [PubMed] [PMC]180. Sueviriyapan N, Granados-. Modelling the functional roles of synaptic and extra-synaptic γ-aminobutyric acid receptor dynamics in circadian timekeeping. J R Soc Interface. 2021;18:20210454. [DOI] [PubMed] [PMC]181. Resetting central and peripheral circadian oscillators in transgenic rats. Science. 2000;288:682–5. [SEP] Justify:

Output: The text does not directly address the claim regarding the suprachiasmatic nucleus being the master regulator of circadian rhythms. Instead, it provides a list of studies and related topics without offering specific evidence or conclusions about the role of the suprachiasmatic nucleus in circadian regulation.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: The editors of the Journal of the Association (JAMA) heralded the news of Cohendy’s work by stating that ‘It will henceforth be possible to infect an organism that is free of microorganisms and study the consequences…our attitude toward the microbial population inhabiting our digestive tube will in consequence assume a different significance’ [86]. Sadly, it wouldn’t be until 2004, in a Yakult-funded study, that researchers would give attention to the brain and behavioral aspects of germ-free development and the consequences of introduction of strains of probiotic [87]. It is also noteworthy that during this time researchers identified various strains of lactobacilli, including Metchnikoff’s L. bulgaricus, in garden soil and plant foods [88]. These findings, as discussed in Part II, are of relevance to the modern investigations involving germ-free animals, stress physiology, and cumulative contact with non-pathogenic bacteria via food and incidental contact via time spent in nature (e. g. gardening, farming, nature-based recreation etc. ). Modern medical writers point to the 1958 study of Eiseman, et al. as the first report using fecal microbiota transplantation (fecal enema) with successful outcome [89]. These surgeons obtained feces from healthy donors, suspended it in saline, and transferred it to four patients with enterocolitis as a retention enema. However, it was during the autointoxication era, almost four decades earlier, that physician N. published papers on successful enema-based transfer of bacteria. Specifically, Norman would isolate lactobacilli and non-pathogenic microbes obtained from the stool of healthy infants, mix into a lactose solution, and inject the bacteria into the adult cecum via tube. For Norman, dissatisfied with the results of oral lactobacillus preparations alone, correcting a disordered intestinal microbiota via transfer of non-pathogenic intestinal organisms was central to the treatment of many chronic medical conditions [90, 91]. He theorized that disordered gut microbiota set in motion a systemic ‘protective degeneration’ in that the normal defensive response to the chronic toxin load was the ultimate cause of cellular dysfunction. [SEP] Justify:

Output: The text corroborates the claim by discussing various studies and historical references that highlight the importance of beneficial bacteria, such as lactobacilli, in maintaining gut health. It particularly mentions a 1958 study where fecal microbiota transplantation was successfully used to restore a healthy microbiota in patients suffering from enterocolitis. This indicates the role of specific bacteria in correcting gut microbiota, thus supporting the claim about probiotics and gut health.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: However, this requires exposure to very regular environmental time cues, so-called Zeitgebers, such as food. Thus, on the one hand, the circadian system contributes to the optimization of food metabolism; on the other hand, the intake of food serves as a potent Zeitgeber. Both mouse and human studies have shown the negative consequences of circadian disturbances on metabolism, body weight [3–11], and also mental health [12–14] and demonstrated that restriction of meals to certain time spans of the day can counteract these harmful effects [15–19]. In the recent past, some human studies have shown that restricting food intake to certain times of the day (time-restricted eating, TRE time-restricted feeding, TRF) can indeed lead to weight loss. In most cases, the interventions were successful, and participants lost ∼0. 9 - 3. 5 kg body weight within 12 weeks when they reduced their food intake to 8–10-hour intervals per day [19–22]. Furthermore, they suggest that TRE is more successful when the meal window is earlier in the day rather than later in the day [23]. However, previous human studies merely established rough periods during which participants could still eat irregularly. It has previously been shown that the success of a hypocaloric diet can be increased if the distribution of daily calories consumed is adapted to the individual chronotypes in such a way that morning types consume many calories in the first half of the day and evening types consume many calories in the second half of the day [24]. We expect that the success of previous chrononutrition interventions can be further improved by determining each participant’s eating time profile and creating a personalized meal plan accordingly, even if participants continue to consume their usual amounts and foods. We are testing this in the present pilot study, which is intended to examine in principle whether this assumption and possibly a more in-depth continuation of the study is justified. Therefore, the primary aim is to individually determine and set optimal times for food intake and to correlate the reduction of mealtime variability with alterations in body weight. We include participants of Index (BMI) classifications normal to extremely obese to test whether participants who exceed normal BMIs particularly benefit from the intervention. [SEP] Justify:

Output: The text contrasts the claim by discussing how weight loss can occur through careful management of eating times irrespective of the type of food consumed, including carbohydrates. It mentions that time-restricted feeding can lead to weight loss, suggesting that not all food intake, including carbohydrates, necessarily results in weight gain. Moreover, it highlights the importance of the timing of food intake over strict dietary restrictions, thereby refuting the claim that eating carbohydrates always leads to weight gain.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: Gastrin-releasing peptide promotes suprachiasmatic nuclei cellular rhythmicity in the absence of vasoactive intestinal polypeptide-VPAC2 receptor signaling. J Neurosci. 2005;25:11155–64. [DOI] [PubMed] [PMC]212. Melanopsin (Opn4) requirement for normal light-induced circadian phase shifting. Science. 2002;298:2213–6. [DOI] [PubMed] 213. Role of melanopsin in circadian responses to light. Science. 2002;298:2211–3. [DOI] [PubMed] 214. é C, Weihe E, Schäfer MK, et al. Cyclase-(PACAP)-Glutamate Co-transmission Phase-to by Suprachiasmatic Nucleus. Front Neurosci. 2019;13:1281. [DOI] [PubMed] [PMC]215. Changes in light-induced phase shift of circadian rhythm in mice lacking PACAP. Res Commun. 2003;310:169–75. [DOI] [PubMed] 216. The mood stabilizer valproic acid opposes the effects of dopamine on circadian rhythms. Neuropharmacology. 2016;107:262–70. [DOI] [PubMed] 217. Ashton A, Jagannath A. in Schizophrenia and Signaling. Front Neurosci. 2020;14:636. [DOI] [PubMed] [PMC]218. . Mathematical insights into the role of dopamine signaling in circadian entrainment. Math Biosci. 2023;356:108956. [DOI] [PubMed] 219. üler AD, Steele AD. Dopamine systems and biological rhythms: Let's get a move on. Neurosci. 2022;16:957193. [DOI] [PubMed] [PMC]220. . Delayed circadian rhythm in adults with attention-deficit/hyperactivity disorder and chronic sleep-onset insomnia. Biol Psychiatry. 2010;67:1091–6. [DOI] [PubMed] 221. Retinal dopamine mediates multiple dimensions of light-adapted vision. J Neurosci. 2012;32:9359–68. [SEP] Justify:

Output: The text primarily discusses various biochemical and signaling pathways related to circadian rhythms, particularly focusing on the suprachiasmatic nucleus and its interaction with other signaling molecules. However, it does not directly address whether the suprachiasmatic nucleus is the master regulator of circadian rhythms, making it irrelevant to the claim.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: English 简体中文 6Publishing-Submit a Manuscript F6Publishing-世界华人消化杂志在线投稿 is committed to discovery and dissemination of knowledge About the a All 10. 3748/wjg. v16. i4. 403] of This 4. 0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: Counts in Google of This 2010. doi: 10. 3748/wjg. v16. i4. 403 Probiotics and gut health: A special focus on liver diseases -of Nutrition and Health, University of 21 9of University of Kuopio, PO Box 1627, 70211 Kuopio, FinlandEl-Nezami, Food and Centre, University of Kuopio, PO Box 1627, 70211 Kuopio, Finland; School of Biological Sciences, University of Hong Kong, S5-13 number: $[] Author contributions: Gratz SW, and El-Nezami HS wrote the 403. htm DOI: have been well defined and long used in human and animal health and nutrition. Many of the probiotic strains used today have been isolated from the human gut flora, and it is therefore more a reintroduction of organisms rather than a novel concept. The beneficial effects of probiotics and, especially, the clinical use of probiotics in the management of specific diarrhoeal diseases, including Rotavirus diarrhoea, Traveller’s diarrhoea and others are well accepted[1]. These effects are mainly based on colonisation resistance or the influence of probiotics on microflora balance. When discussing probiotics, it must be remembered that the intestinal microflora, resident in the large intestine, will always outnumber the probiotics that can be administered. Furthermore, probiotic processes will always be confounded by the diversity of the human microbiota and its variability in the face of varied human diets and genetic backgrounds[2]. Within the human gut, we have to separate processes occurring in the distal small intestine from those happening in the colon. [SEP] Justify:

Output: The text corroborates the claim by discussing the role of probiotics in influencing 'microflora balance.' It states that the beneficial effects of probiotics are primarily based on their ability to affect the balance of the intestinal microflora. This supports the assertion that probiotics can improve gut health.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: CG: n=33; EG: n=64-67, missing n-values in the EG are due to the different number of meals for each participant. Detailed statistics in Tables S3. (E) Within group differences of body weight during the study. Body weight was collected at different time points, at the beginning of the study (T0), after the exploration phase (T1), after the intervention phase (T2), and after the follow-up phase (T3). During the follow-up phase, 34 EG participants voluntarily continued the intervention (continuing; black line and open circle) while 33 participants no longer followed the intervention (discontinuing; gray, dashed line and open circle). Only three control subjects continued their intervention in the follow-up phase, which is why a division into continuing and discontinuing was omitted in this group. Data are normalized so that all baseline data at T0 equals 0 to represent change. Differences of all CG and EG participants between T0, T1, and T2 were calculated with a 1-way ANOVA, as were differences between T2 and T3 of CG participants (Bonferroni post-hoc test, **** p ≤ 0. 0001). Differences between T2 and T3 of continuing and discontinuing EG participants were calculated with a paired t-test °° p ≤ 0. 01, °°°° p ≤ 0. 0001. Detailed statistics in Table S4. (F) Between group differences of BMI from T0-T3. Mixed-effect model with Bonferroni post-hoc test comparing CG and EG at different phases during the study, **** p ≤ 0. 0001. Detailed statistics in Table S5. (G) Significant correlation between body weight/BMI and MTVS. The more participants improved their regularity of meals (decreasing MTVS), the more weight/BMI they lost. Linear regression, CG: n=33; EG: n=67, ** p ≤ 0. 01. Detailed statistics in Tab. S6. (H) Significant correlation between body weight/BMI and MTVS of lunch and dinner. The more participants improved their regularity of lunch and dinner (decreasing MTVS), the more weight/BMI they lost. Linear regression, CG: n=33; EG: n=67, ** p ≤ 0. 01. Detailed statistics in Tab. [SEP] Justify:

Output: The text contrasts the claim by presenting findings indicating that participants lost weight or BMI when they improved their meal regularity, regardless of the carbohydrate content. For instance, it specifically states, 'The more participants improved their regularity of meals (decreasing MTVS), the more weight/BMI they lost.' This suggests that weight gain is not solely attributable to carbohydrate intake, as participants could achieve weight loss through other dietary improvements.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: 5-HT1B receptor-mediated presynaptic inhibition of GABA release in the suprachiasmatic nucleus. J Neurophysiol. 2005;93:3157–64. [DOI] [PubMed] 244. Cuesta M, Clesse D, Pévet P, Challet E. New light on the serotonergic paradox in the rat circadian system. J Neurochem. 2009;110:231–43. [DOI] [PubMed] 245. Cohen R, Kronfeld-. The substructure of the suprachiasmatic nucleus: Similarities between nocturnal and diurnal spiny mice. Evol. 2010;75:9–22. [DOI] [PubMed] [PMC]246. . Anticholinergic agents do not block light-induced circadian phase shifts. Brain Res. 1985;348:163–7. [DOI] [PubMed] 247. Modulation of photic resetting in rats by lesions of projections to the suprachiasmatic nuclei expressing p75 neurotrophin receptor. Neurosci. 2004;19:1773–88. [DOI] [PubMed] 248. The cholinergic forebrain arousal system acts directly on the circadian pacemaker. . 2016;113:13498–503. [DOI] [PubMed] [PMC]249. Signals from the brainstem sleep/wake centers regulate behavioral timing via the circadian clock. PLoS One. 2013;8:e70481. [DOI] [PubMed] [PMC]250. . Lack of M4 muscarinic receptors in the striatum, thalamus and intergeniculate leaflet alters the biological rhythm of locomotor activity in mice. Funct. 2020;225:1615–29. [DOI] [PubMed] [PMC]251. Aykan U, Güvel. Neuropharmacologic modulation of the melatonergic system. Explor Neurosci. 2023;2:287–306. 252. Whole-to the of the Suprachiasmatic Nucleus. Front Neurosci. 2018;12:807. [DOI] [PubMed] [PMC]253. -Hansen L. [SEP] Justify:

Output: The text does not provide information that directly supports or contradicts the claim regarding the suprachiasmatic nucleus being the master regulator of circadian rhythms. Instead, it lists various studies and findings related to the suprachiasmatic nucleus and its interactions with other systems but does not explicitly address the claim. Therefore, it is considered irrelevant to the claim.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: The small intestine harbours relatively low numbers of resident intestinal bacteria, but at the same time contains the major part of the gut associated lymphoid tissue (GALT), which samples intestinal microbes[3]. Hence modulation of systemic immune and allergic phenomena might be primarily mediated by the GALT of the small bowel. Supplementing qualitatively and quantitatively optimised microbes to this part of the gut might stimulate Treg cell development and consequent immunomodulation[1]. Within the large intestine, bacterial intervention might cause modulation of the microbial fermentation activity and direct action on the colonic epithelium to alter (suppress) innate immunity. These processes might explain the impact of probiotics on inflammatory and functional bowel disorders. The research field of probiotics is very heavily reviewed, using different clinical and microbiological angles to elucidate the topic. The aim of this review is to summarise the most recent trends in probiotic research, focusing on the clinical use of probiotics and their effects on the healthy and diseased gut and liver. The direct and indirect actions of probiotics on intestinal cells and their consequences on liver (summarised in Figure 1) will be discussed in this review. Open in 1 Potential mechanisms of action by which probiotics can promote GI health and the consequences for the liver. Probiotics and surface-layer proteins competitively exclude microbial pathogens from mucosal surfaces. Tight junction proteins, such as zona occludins-1 and claudin1, remain intact and thereby prevent both uptake of intact macromolecules and translocation of viable organisms (BT) to mesenteric lymph nodes, and ultimately to the liver. Through a cascade of signalling events, probiotics enhance production and secretion of anti-inflammatory cytokines, including interleukin-10 and transforming growth factor-β, by a subset of immune cells, referred to as T regulatory cells. Innate immune responses to probiotics include increased mucin and trefoil factor production by goblet cells and enhanced production of antibacterial defensins by Paneth cells and intestinal epithelia. Probiotics might alter the intestinal microbiota and hence limit intestinal bacteria overgrowth (IBO) and the production of lipopolysaccharides (LPS). and intestinal barrier functionThe intestinal barrier is seen as the first line of defence against pathogens and food allergens entering the intestinal tract, and probiotics have been intensely studied for their involvement in maintaining this barrier. [SEP] Justify:

Output: The text corroborates the claim by detailing how probiotics can modulate the intestinal microbiota, enhance the immune response, and maintain the intestinal barrier, all of which support gut health. It discusses mechanisms like the exclusion of pathogens, production of anti-inflammatory cytokines, and maintenance of intestinal barrier function, which are all related to the beneficial effects of probiotics on gut health.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: S6. (I) Significant correlation between change in BMI, baseline BMI, and improvement in MTVS. Individuals with higher BMI benefit more from similar improvements in MTVS (shades of data points) than individuals with lower BMI in EG participants. Multiple regression, n=67, * p ≤ 0. 05, ** p ≤ 0. 01. Detailed statistics in Tab. S8. 2. 3. Weight changeDuring the exploration phase, when no instructions on eating times were given, CG and EG participants had a statistically non-significant average loss of 0. 17 kg (0. 06 kg/m²) and 0. 21 kg (0. 06 kg/m²), respectively (Figs. 1E, S2B-F, Tabs. S4, S5). However, during the intervention phase, when EG participants took their meals more regularly, they lost an average of about 2. 6 kg (95% CI [-2. 906, -1. 915]) and 0. 81 kg/m² (95% CI [-0. 9729, -0. 6420]) (Figs. 1E, S2B-E, Tabs. S4, S5), which translates to an average weight loss of 0. 40 kg (0. 145 kg/m²) per week during the intervention. The weight loss observed in this group is independent of the age of the participants and their sex (Fig. S2G, Tabs. S6, S2). In contrast, weight and BMI changes of -0. 39 kg (95% CI [-0. 9125, 0. 1307]) and -0. 14 kg/m² (95% CI [-0-3152, 0. 0304]), respectively, were not significant in the CG (Figs. 1E, S2B, C, F, Tabs. S4, S5), resulting in a significant difference in weight loss between groups at the end of the intervention (Figs. 1F, S2C, Tab. S5). The inclusion of the last available weight and BMI data of the drop-outs in an end-point analysis did not lead to any notable change in this result (Fig. S2H, Tab. S5). Four weeks after the intervention ended, all participants were contacted again for a follow-up assessment. [SEP] Justify:

Output: The text contrasts the claim by providing evidence from a study indicating that participants in the intervention group (EG) lost an average of about 2.6 kg during a phase where they followed regular meal times. This suggests that weight loss can occur regardless of the consumption of carbohydrates, contradicting the claim that eating carbohydrates always leads to weight gain.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: Cholecystokinin (CCK)-expressing neurons in the suprachiasmatic nucleus: innervation, light responsiveness and entrainment in CCK-deficient mice. Neurosci. 2010;32:1006–17. [DOI] [PubMed] 254. Cholecystokinin neurons in mouse suprachiasmatic nucleus regulate the robustness of circadian clock. Neuron. 2023;111:2201–17. e4. [DOI] [PubMed] 255. MT1 and MT2 melatonin receptors are expressed in nonoverlapping neuronal populations. J Pineal Res. 2019;67:e12575. [DOI] [PubMed] 256. . The endogenous melatonin (MT) signal facilitates reentrainment of the circadian system to light-induced phase advances by acting upon MT2 receptors. Chronobiol Int. 2012;29:415–29. [DOI] [PubMed] 257. Hunt AE, Al-. Activation of MT2 melatonin receptors in rat suprachiasmatic nucleus phase advances the circadian clock. Physiol. 2001;280:C110–8. [DOI] [PubMed] 258. Drunen RV, Eckel-Mahan K. of the Hypothalamus: to Physiology. Clocks Sleep. 2021;3:189–226. [DOI] [PubMed] [PMC]259. . Melatonin generates an outward potassium current in rat suprachiasmatic nucleus neurones in vitro independent of their circadian rhythm. Neuroscience. 2001;107:99–108. [DOI] [PubMed] 260. . Clock genes in calendar cells as the basis of annual timekeeping in mammals--a unifying hypothesis. J Endocrinol. 2003;179:1–13. [DOI] [PubMed] 261. . A novel human opsin in the inner retina. J Neurosci. 2000;20:600–5. [DOI] [PubMed] [PMC]262. . Melanopsin, ganglion-cell photoreceptors, and mammalian photoentrainment. J Biol Rhythms. 2003;18:227–34. [DOI] [PubMed] 263. . [SEP] Justify:

Output: The text provides information about various studies and findings related to the suprachiasmatic nucleus and its functions, including the roles of cholecystokinin neurons and melatonin receptors. However, it does not directly address or support the claim that the suprachiasmatic nucleus is the master regulator of circadian rhythms. Therefore, it is considered irrelevant to the claim.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: In colonic epithelia, probiotics are suggested to stimulate mucin production, and therefore enhance the self protecting properties of the intestinal epithelium[4]. Furthermore, tight junctional proteins, important for the physical tightness of the epithelial cell layer, are found to be enhanced by probiotics[5,6] and the disruption of tight junctions by pathogens can be counteracted[7]. Besides these effects on the physical barrier function, evidence is mounting that both commensal microflora and specific probiotic supplementations specifically enhance the immunological barrier function of the small intestinal mucosa[8]. For this cross talk between bacteria and the immune system, bacteria derived products including metabolites, cell wall components and DNA, can be sensed by enterocytes and immune competent cells[9]. Commensals, unlike pathogens, are efficiently killed by intestinal macrophages, therefore avoiding an inflammatory response in the mucosa[10]. At the same time, dendritic cells can sample commensals, incorporate them, and transport them to mensenteric lymph nodes. Here, commensal-loaded dendritic cells induce a local immune response with the activation of specific B-cells to produce secretory IgA against these commensals[8,10]. This appears to be a paradox, but this specific and local immune stimulation by commensals and probiotics can actually be considered non-inflammatory in the mucosal environment and the host systemics[8]. Therefore GALT, and specifically the mesenteric lymph nodes, can be considered another layer of intestinal barrier function[3,10]. Probiotics and inflammatory bowel diseases (IBD)The pathogenesis of IBD [ulcerative colitis (UC) and Crohn’s disease] remains unknown, but the intestinal microflora appears to play an important role. Changes in microflora composition have been observed in UC patients, with increased pro-inflammatory bacteria, including Enterobacteriaceae, increased Bacteroides fragilis within the mucosal microflora[11], and decreased protective bacteria, including lactobacilli and bifidobacteria[12]. Probiotic treatment has the potential to decrease the severity of symptoms in IBD via interaction with gut epithelium[13]. [SEP] Justify:

Output: The text corroborates the claim by discussing how probiotics stimulate mucin production and enhance the intestinal epithelial barrier, thereby improving gut health. It mentions that probiotics can positively affect the immune barrier function of the small intestine and contribute to a balanced gut microbiota, which aligns with the claim stating that probiotics support gut health by improving the balance of bacteria.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: 34 of the 67 EG participants reported to have maintained the regularity of their meals and continued to lose body weight significantly, on average another 1. 12 kg (95% CI [-1. 479, -0. 7626]) and 0. 36 kg/m² (95% CI [-0. 4907, -0. 2457]), respectively (Figs. 1E, S2B, D, E, Tab. S4). In contrast, participants who reported to have resumed irregular eating gained a significant average of 0. 48 kg (95% CI [0. 1984, 0. 7616]) and 0. 17 kg/m² (95% CI [0. 07434, 0. 2603]), respectively (Fig. 1E, S2B, D, E, Tab. S4). 2. 4. Relation between weight change and improvement in the regularity of mealsTo examine the extent to which EG participants’ weight loss was effectively related to improvements in meal regularity, we correlated changes in body weight and BMI with individual MTVS changes. Consistent with our hypothesis, a significant relationship exists between weight loss and improvement in regularity in the EG (Fig. 1G, Tab. S6). A breakdown of meals shows that increasing the regularity of lunch and dinner has the greatest effects, with no significant relationship between increasing the regularity of breakfast and weight loss (Fig. 1H, Tab. S6). In contrast, in the CG, there were no or little improvements in regularity and, accordingly, no correlation with weight/BMI changes. Further analyses revealed that all MTVS up to 3, which corresponds to a time window for meals of up to ±45 min, resulted in comparably effective weight loss, whereas the efficiency of weight loss decreases significantly with an MTVS greater than 3 (Tab. 1). Table 1:Association of weekly MTVS with weekly weight loss. The table shows the weekly weight change of all participants during the exploration and the intervention phase while adhering to certain MTVSs in each week. 1-way ANOVA with Bonferroni post-hoc test comparing the mean of each row with the mean of the first row, * p ≤ 0. 05. 2. 5. Relation between weight change and baseline BMIA weight loss intervention which is particularly based on metabolic optimization is likely to be most effective for individuals with exceeded body weight. [SEP] Justify:

Output: The text contrasts the claim by discussing the relationship between meal regularity and weight changes in participants. It demonstrates that individuals who maintained regular eating patterns were able to lose body weight, which directly challenges the claim that eating carbohydrates always leads to weight gain. In fact, the results indicate that meal regularity plays a more significant role in weight management than carbohydrate consumption alone.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: [DOI] [PubMed] [PMC]274. Orexin System: for a Healthy Life. Front Physiol. 2017;8:357. [DOI] [PubMed] [PMC]275. Acute suppressive and long-term phase modulation actions of orexin on the mammalian circadian clock. J Neurosci. 2014;34:3607–21. [DOI] [PubMed] [PMC]276. Flyer-Adams JG, Rivera-. Regulation of Memory by the Pigment-(PDF). J Neurosci. 2020;40:9066–77. [DOI] [PubMed] [PMC]277. Vaze KM, Helfrich-Förster C. for Delaying the Phase of Drosophila's. J Biol Rhythms. 2021;36:442–60. [DOI] [PubMed] [PMC]278. -Förster C, Martínez-Torres D. Pigment-dispersing factor is present in circadian clock neurons of pea aphids and may mediate photoperiodic signalling to insulin-producing cells. Open Biol. 2023;13:230090. [DOI] [PubMed] [PMC]279. . Endothelial and neuronal nitric oxide synthases are present in the suprachiasmatic nuclei of Syrian hamsters and rats. Neurosci. 2000;12:649–61. [DOI] [PubMed] 280. . Signaling in the mammalian circadian clock: the NO/cGMP pathway. Neurochem Int. 2004;45:929–36. [DOI] [PubMed] 281. . Circadian entrainment to light–dark cycles involves extracellular nitric oxide communication within the suprachiasmatic nuclei. Neurosci. 2010;31:876–82. [DOI] [PubMed] 282. . Circadian rhythm and sleep-wake systems share the dynamic extracellular synaptic milieu. Circadian Rhythms. 2018;5:15–36. [DOI] [PubMed] [PMC]283. Vinod C, Jagota A. Daily NO rhythms in peripheral clocks in aging male Wistar rats: protective effects of exogenous melatonin. Biogerontology. [SEP] Justify:

Output: The text does not directly address the claim regarding the suprachiasmatic nucleus (SCN) as the master regulator of circadian rhythms. Instead, it contains references to various studies related to circadian clocks and nitric oxide communication within the SCN, but does not explicitly state or support the claim itself. Therefore, the text is deemed irrelevant to the claim.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: Proposed mechanisms include changes in short chain fatty acids (SCFA) production patterns, reduction in pro-inflammatory cytokine secretion, improving Th1/Th2 ratios, and eliminating pathogens. For example, the production of reuterin has been shown in vitro to reduce growth of pathogens, including Escherichia coli (E. coli), Salmonella enterica, Shigella sonnei, and Vibrio cholera. Adhesion of probiotics to enterocytes and enhancement of barrier function (secretion of B-defensins and mucus, TJ proteins) have also been shown for specific strains in vitro. However, it is unclear whether this strengthening of the intestinal barrier function would also occur in the large intestine, the area most affected by intestinal disease. Some evidence from a mouse model of colitis [interleukin (IL)-10 deficient mice] suggests that probiotic lactobacilli and the VSL#3 mix reduced bacterial translocation (BT) and intestinal permeability in the colon[14,15]. Mechanistic effects can also be observed with non-viable probiotics and culture supernatants in vitro and in animals, which might be a safer therapeutic for patients with impaired intestinal barrier and increased risk of sepsis. Bacteria-free culture supernatant from Lactobacillus plantarum was shown to inhibit inflammatory pathways important for intestinal inflammation, such as nuclear factor (NF)-κB binding activity and proteasome activity, in a young adult mouse colon cell line and in macrophages[16]. This might provide a novel and safe strategy for treatment of IBD, if results can be repeated in vivo. Probiotics and irritable bowel syndrome (IBS)IBS includes a range of symptoms, such as abdominal pain, altered bowel habits, bloating and flatulence in the absence of structural abnormalities in the intestine. As no curative treatment is available for IBS, therapy is palliative and supportive, targeting special symptoms, and is notoriously unsatisfactory. Studies have observed alterations in intestinal microflora in patients and increased symptoms following enteric infections, therefore probiotics might be a useful tool to improve symptoms. A meta analysis of probiotic treatment and IBS[17] included 20 trials with 23 probiotic treatments. This study showed that probiotics were associated with improved global IBS symptoms [risk ratio (RR) = 0. [SEP] Justify:

Output: The text corroborates the claim by discussing the beneficial mechanisms of probiotics, such as changes in short chain fatty acids (SCFA) production, reduction in pro-inflammatory cytokines, and enhancing barrier function. It shows how probiotics can reduce the growth of pathogens and mentions studies suggesting they can improve symptoms of irritable bowel syndrome (IBS), indicating a supportive role for gut health.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: In fact, the higher the baseline BMI of EG participants at T1, the greater the weight loss (Fig. S2I, Tab. S6). Stratifying the subjects by baseline BMI, including the control group, additionally shows that in all strata the BMI of EG subjects decreased more than that of CG subjects, even if they had the same initial BMI (Fig. S2J, Tab. S7). Multiple regression shows that the reduction in MTVS and baseline BMI together predict the weight loss of the participants (Fig. 1I, Tab. S8). These data show that regularity in meal intake can lead to a significant loss of body weight and suggest that this effect is especially pronounced in individuals with a higher BMI. 2. 6. Relation between weight change and self-reported food quantity and compositionBy restricting meals to specific times and shortening the time window in which food is eaten, it is feasible that EG participants ate less or changed food composition during the intervention phase and therefore lost weight. However, on average, the reported food energy ingested by CG and EG participants did not substantially change during the study (Fig. 2A, S2K, L, Tab. S3, 6), apart from a minor average reduction of ∼350 kJ (95% CI [-627. 6, -67. 67]) per day in the EG (Fig. S2K, Tab. S3), and did not differ between CG and the EG. As they are rather small, these differences do not add up to a significant reduction in the total average energy consumed over the course of the study. Accordingly, the determined cumulative average energy intake during the intervention phase did not differ on any day from the estimated energy intake based on an extrapolation of the cumulative food consumption during the exploration phase, neither in the CG nor in the EC group (Fig. 2B). Nevertheless, there were some participants who reported having consumed fewer calories during the intervention phase, while some also reported having ingested more calories. However, consistent with our hypothesis that high regularity of mealtimes optimizes metabolism of similar amounts of food, there is no relationship between reported changes in average daily and cumulative energy intake and change in body weight/BMI of either CG or EG participants (Fig. 2C, D, Tab. S6). [SEP] Justify:

Output: The text contrasts the claim by providing evidence that suggests regularity in meal intake can lead to significant weight loss, particularly in individuals with a higher BMI. It points out that participants assigned to a specific eating group (EG) achieved greater weight loss compared to the control group (CG), despite the average energy intake remaining similar between the two groups. Furthermore, it highlights that there is no relationship between changes in daily energy intake and changes in body weight or BMI. This contradicts the claim that eating carbohydrates is directly linked to weight gain, emphasizing that other factors, such as meal timing and metabolism, can influence weight loss.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: 2016;17:859–71. [DOI] [PubMed] 284. . Is histamine the final neurotransmitter in the entrainment of circadian rhythms in mammals? Sci. 2000;21:293–8. [DOI] [PubMed] 285. Biello SM. Circadian clock resetting in the mouse changes with age. Age (Dordr). 2009;31:293–303. [DOI] [PubMed] [PMC]286. . Neurochemistry in Clinical Practice. In: Bollu PC, editor. Cham: Springer; 2022. 287. Histamine 1 receptor-Gβγ-cAMP/PKA-CFTR pathway mediates the histamine-induced resetting of the suprachiasmatic circadian clock. Mol Brain. 2016;9:49. [DOI] [PubMed] [PMC]288. Boudin H, Pélaprat D, Rostène W, Beaudet A. Cellular distribution of neurotensin receptors in rat brain: immunohistochemical study using an antipeptide antibody against the cloned high affinity receptor. J Comp Neurol. 1996;373:76–89. [DOI] [PubMed] 289. . Widespread expression in adult rat forebrain of mRNA encoding high-affinity neurotensin receptor. J Comp Neurol. 1998;402:475–500. [PubMed] 290. Meyer-. Neurotensin phase-shifts the firing rate rhythm of neurons in the rat suprachiasmatic nuclei in vitro. Neurosci. 2002;16:339–44. [DOI] [PubMed] 291. . Effects of neurotensin on discharge rates of rat suprachiasmatic nucleus neurons in vitro. Neuroscience. 2001;103:663–72. [DOI] [PubMed] 292. Jha PK, Bouâouda H, Kalsbeek A, Challet E. Distinct feedback actions of behavioural arousal to the master circadian clock in nocturnal and diurnal mammals. Rev. 2021;123:48–60. [DOI] [PubMed] 293. . Differential responses of circadian activity onset and offset following GABA-ergic and opioid receptor activation. J Biol Rhythms. 2003;18:297–306. [SEP] Justify:

Output: The text does not directly address or provide evidence related to the claim about the suprachiasmatic nucleus being the master regulator of circadian rhythms. It discusses various studies related to circadian rhythms and neurotransmitters, but does not specifically affirm or reject the role of the suprachiasmatic nucleus in regulating those rhythms.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: 77] and with decreased abdominal pain (RR = 0. 78). Due to the large variety in probiotic strains used, no analysis on strain type was possible. Probiotics used included B. infantis, lactobacilli (L. acidophilus, L. plantarum, L. reuteri, L. rhamosus), Saccharomyces boulardii, Streptococcus faecium, VSL#3 (mix of eight), and other mixes. In a recent systematic review, Brenner et al[18] claimed that 16 randomized controlled human trials met their inclusion criteria, of which 11 had suboptimal study design. They concluded that only one study using a specific strain of B. infantis 35 624 efficiently improved IBS symptoms. Probiotics might offer a treatment possibility for IBS symptoms, but more controlled studies are needed to identify the ideal strain, dose, and duration of treatment. Probiotics after gut surgeryMorbidly obese patients can undergo Roux-en Y gastric bypass surgery (one type of bariatric surgery) for effective and enduring weight loss. This procedure uses restriction in stomach size and intestinal malabsorption as measures for achieving substantial weight loss. Problems that occur postoperationally are alteration of microflora with bacterial overgrowth (BO) in the blind sac of the intestine, intestinal pain, and possibly impaired vitamin B12 status (due to lack of intrinsic factor production from the stomach). This study[19] used probiotic treatment (6 mo, commercial product of unspecified lactobacilli) in 44 post operational patients. BO (measured with hydrogen breath test) improved only after 6 mo, but not earlier. Vitamin B12 status improved, gastrointestinal symptoms remained unchanged, but post operational weight loss was significantly increased in the probiotic group. The authors speculated that increased weight loss might be due to changes in microflora towards extracting fewer calories from the diet, although this was not studied. Probiotics/symbiotics have also been used to prevent postoperative infections in patients undergoing abdominal surgery (biliary cancer, liver transplantation, and pancreaticoduodenectomy). Major infections were pneumonia, urinary tract infection, wound infection, intra-abdominal abscess, and cholangitis. A recent meta analysis[20] found that probiotics reduced overall infections [odds ratio (OR) = 0. [SEP] Justify:

Output: The text corroborates the claim by discussing various studies and findings related to the use of probiotics. It mentions that probiotics may help improve gastrointestinal symptoms and that specific strains, such as B. infantis, were identified as potentially effective in improving symptoms related to Irritable Bowel Syndrome (IBS). Additionally, it highlights the role of probiotics in maintaining gut health post-surgery and mentions improved outcomes in terms of microflora balance and reductions in gastrointestinal symptoms, thereby supporting the idea that probiotics can beneficially influence gut health.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: Likewise, the composition of the ingested foods did not change considerably in either group, and participants reported a normal distribution of the macronutrients of fat, carbohydrate, and protein in both phases of the study (Fig. 2E, S2M, Tab. S3). Also, there was no correlation between weight change and change in reported average daily and cumulative macronutrient intake (Fig. 2F, S2N, Tab. S6). Fig. 2:Changes in body weight/BMI are not related to changes in reported caloric intake and composition of macronutrients. Changes in reported daily caloric intake (A), cumulative caloric intake (B) and food composition (E) and their relationship to weight/BMI changes (C, D, and F). Data in (A) are normalized so that all baseline data of the exploration phase equal 1. To represent the x-fold change, data from the intervention phase are divided by data from the exploration phase of the corresponding participant. (A, E) 2-way repeated-measures ANOVA with Bonferroni post hoc test comparing CG and EG during the exploration or intervention phase and T0-T1 and T1-T2 within groups, * p ≤ 0. 05. Detailed statistics in Tables S3. (B) Mixed-effects model with Bonferroni post hoc test comparing determined and estimated cumulative energy intake. The estimated energy intake is formed as an assumed continuation of the average daily intake during the exploration phase. post hoc test showed no significant differences on any study day. (C, D, and F) Linear regression, CG: n=30; EG: n=67 (some participants were excluded subsequently from this analysis because of several erroneous diary entries about unrealistic amounts of food, e. g. , 30,000 g chicken for lunch). Detailed statistics in Tab. S6. 2. 7. Relation between weight change and other meal timing-related factorsBesides increasing regularity, restricting meals to certain times of the day can also shorten the daily window in which meals are eaten and shift meals to other times of the day. In fact, our intervention caused many EG participants to avoid occasional meals at extremely early or late times, limiting their meals to much shorter intervals of 11 h (95% CI [10. 468, 11. 520]) (Fig. 3A, B, Tab. S3), while those of the CG remained long with 13. [SEP] Justify:

Output: The text contrasts the claim by indicating that there is no correlation between weight change and the change in reported average daily and cumulative macronutrient intake, which includes carbohydrates. It suggests that changes in body weight/BMI are not related to caloric intake or the composition of macronutrients, challenging the assumption that eating carbohydrates necessarily leads to weight gain.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: [DOI] [PubMed] 294. The opioid fentanyl affects light input, electrical activity and Per gene expression in the hamster suprachiasmatic nuclei. Neurosci. 2005;21:2958–66. [DOI] [PubMed] 295. Hamada T, Shibata S. The role of GABAergic neuron on NMDA- and SP-induced phase delays in the suprachiasmatic nucleus neuronal activity rhythm in vitro. Neurosci Lett. 2010;468:344–7. [DOI] [PubMed] 296. . Investigating the role of substance P in photic responses of the circadian system: individual and combined actions with gastrin-releasing peptide. Neuropharmacology. 2010;58:277–85. [DOI] [PubMed] 297. The gut–brain peptide neuromedin U is involved in the mammalian circadian oscillator system. Res Commun. 2004;318:156–61. [DOI] [PubMed] 298. Identification of neuromedin S and its possible role in the mammalian circadian oscillator system. EMBO J. 2005;24:325–35. [DOI] [PubMed] [PMC]299. Expression of the vesicular GABA transporter within neuromedin S+ neurons sustains behavioral circadian rhythms. . 2023;120:e2314857120. [DOI] [PubMed] [PMC]300. Somatostatin regulates central clock function and circadian responses to light. . 2023;120:e2216820120. [DOI] [PubMed] [PMC]301. . Increase in somatostatin immunoreactivity in the suprachiasmatic nucleus of aged Wistar rats. Brain Res. 2002;958:463–7. [DOI] [PubMed] 302. . Aging selectively suppresses vasoactive intestinal peptide messenger RNA expression in the suprachiasmatic nucleus of the Syrian hamster. Res. 2001;87:196–203. [DOI] [PubMed] 303. . of Encoded by the Clock. J Biol Rhythms. 2020;35:353–67. [DOI] [PubMed] [PMC]304. Moore RY. in the Nucleus. J Biol Rhythms. [SEP] Justify:

Output: The text does not directly address the claim regarding the suprachiasmatic nucleus being the master regulator of circadian rhythms. Instead, it lists various studies discussing different aspects of neuronal activity, neuropeptides, and their roles in circadian rhythms without explicitly confirming or denying the claim.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: 26], length of antibiotic treatment need (OR = -4. 01), reduced length of postoperative hospital stays (OR = -2. 7), but did not change overall mortality (OR = 0. 98). Overall the use of probiotics is very promising, although data are very variable (type of surgery, type of infection, and type of probiotic treatment). However, bacteremia might be a potential hazard in these vulnerable patients. The appropriate therapeutic route, length of therapy, time of administration, dosage, and kind of probiotic remain controversial and no uniform preventative strategy can be suggested on based of the current literature. is a longstanding practice of using lactulose in the treatment of hepatic encephalopathy, which suggests involvement of gut microflora in the management of chronic liver disease. Loguercio et al[21] use the phrase “gut liver axis” and suggest that the microflora might affect the liver and be cofactor in aetiology of chronic liver damage. This could happen via modulating chronic damage by ethanol or by contributing to complications such as encephalopathy (production of ammonia, ethanol, acetaldehyde, phenols, endotoxin, and benzodiazepines)[21]. Probiotic actions most relevant to liver disease are modification of intestinal barrier function and prevention of BT. Gram-negative BO, increased permeability, and impaired immunity all contribute to increased BT, and there is a strong correlation between the rate of BT and the severity of cirrhosis. Probiotics might alter gut flora towards protective organisms and increase barrier function[22]. Probiotics and non alcoholic fatty liver disease (NAFLD)NAFLD is the most common form of liver disease in the US; its incidence is rising together with rising problems of obesity and Type II diabetes. NAFLD includes a spectrum of pathologies. Steatosis (fatty liver), is clinically asymptomatic, but might predispose the liver to other insults, such as lipopolysaccharides (LPS) or hepatotoxins, that might lead to cirrhosis. Non-alcoholic steatohepatitis (NASH) is an intermediate state where lobular inflammation occurs. Cirrhosis is the most severe form, responsible for most liver specific morbidity and mortality[23]. Histopathological changes are very similar to alcoholic liver disease, and there might be a common pathway of development. [SEP] Justify:

Output: The text corroborates the claim by suggesting that probiotics might alter gut flora towards protective organisms and increase barrier function. This implies that probiotics can positively influence gut health by potentially improving the balance of bacteria, as indicated by the phrase 'probiotics might alter gut flora towards protective organisms.'


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: 7 h (95% CI [12. 902, 14. 562]). Additionally, compared with before and with the CG, the EG intervention resulted in the first meal of the day being delayed to a later time for many subjects (EG: 09:21 (95% CI [08:58, 09:45]) vs. CG: 08:03 (95% CI [07:32, 08:33])) and the last meal of the day being advanced to an earlier time (EG: 20:17 (95% CI [19:59, 20:35]) vs. CG: 21:31 (95% CI [21:05, 21:57])) (Fig. 3C, D, Tab. S3). However, weight changes of participants do not correlate with these changes in eating characteristics (Fig. 3B-D, Tab. S6). Fig. 3:Influence of other changes in eating times and of personalization of meal schedules on weight loss. (A) 95th percentile of the time period during which food was ingested by 15 example participants during the exploration phase (yellow) and the intervention phase (purple). (B) Change in length of this period and its relation to weight/BMI changes. (C, D) Change in time of first (C) and last (D) caloric intake and their association with weight/BMI changes. (B-D) 2-way repeated-measures ANOVA with Bonferroni post hoc test comparing CG and EG during the exploration or intervention phase and T0-T1 and T1-T2 within groups, *** p ≤ 0. 001, **** p ≤ 0. 0001. Linear regression. EG: n=67, varying n-numbers result from incomplete entries in the diaries. Detailed statistics in Tables S3 and S6. (E) The relation between mid-Sleep phase and mid-Eat phase (brown) on the weekends of the exploration phase. The goodness of fit of this association improves during through EG intervention and affects both workdays and weekend days (purple). Linear regression, n=65, **** p ≤ 0. 0001. Detailed statistics in Table S6. (F) Relation of the mid-Sleep phase (mSP) and mid-Eat phase (mEP) during exploration and intervention phase. [SEP] Justify:

Output: The text contrasts the claim by stating that 'weight changes of participants do not correlate with these changes in eating characteristics,' implying that food intake timing and characteristics do not necessarily lead to weight changes, which includes carbohydrates. This suggests that carbohydrates may not always lead to weight gain, contrary to the claim.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: 2016;31:406–10. [DOI] [PubMed] 305. . Retinal innervation of calbindin-D28K cells in the hamster suprachiasmatic nucleus: ultrastructural characterization. J Biol Rhythms. 2000;15:103–11. [DOI] [PubMed] [PMC]306. . Potential pathways for intercellular communication within the calbindin subnucleus of the hamster suprachiasmatic nucleus. Neuroscience. 2004;123:87–99. [DOI] [PubMed] 307. Ikeda M, Allen CN. Developmental changes in calbindin-D28k and calretinin expression in the mouse suprachiasmatic nucleus. Neurosci. 2003;17:1111–8. [DOI] [PubMed] 308. öhr M, Hauptfleisch S, Lemmer B. Localization of components of the renin–angiotensin system in the suprachiasmatic nucleus of normotensive Sprague–Dawley rats: Part A. Angiotensin I/II, a light and electron microscopic study. Brain Res. 2004;1008:212–23. [DOI] [PubMed] 309. . Angiotensin II regulates the activity of mouse suprachiasmatic nuclei neurons. Neuroscience. 2008;154:839–47. [DOI] [PubMed] 310. Herichová I, Šoltésová D, Szántóová K, Mravec B, Neupauerová D, Veselá A, et al. Effect of angiotensin II on rhythmic per2 expression in the suprachiasmatic nucleus and heart and daily rhythm of activity in Wistar rats. Regul Pept. 2013;186:49–56. [DOI] [PubMed] 311. . Expression of the galanin receptor subtype Gal-R2 mRNA in the rat hypothalamus. J Chem Neuroanat. 1999;16:265–77. [DOI] [PubMed] 312. Mills EG, Izzi-. Functions of galanin, spexin and kisspeptin in metabolism, mood and behaviour. Endocrinol. [SEP] Justify:

Output: The text provided does not directly address the claim regarding the suprachiasmatic nucleus as the master regulator of circadian rhythms. Instead, it lists various studies and findings related to the suprachiasmatic nucleus, but none of the content specifically supports or refutes the claim about its regulatory role in circadian rhythms.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: Data suggest a “multi hit” hypothesis, where initial hits such as obesity and sub-clinical insulin resistance might promote the development of steatosis[23]. This enhances the fatty liver’s vulnerability to subsequent insult (e. g. ethanol and LPS) that increase the production of pro-inflammatory cytokines [e. g. tumor necrosis factor (TNF)-α]. This aggravates insulin resistance and leads to oxidative stress (increased production of reactive oxygen by hepatocytes and liver macrophages) and organelle dysfunctions, which kill hepatocytes and promote accumulation of inflammatory cells in the liver and the development of NASH[24]. Following years of chronic inflammation this might develop into fibrogenic response and cirrhosis. The contribution of microflora in the development of NAFLD is mainly based on increased hepatic oxidative stress by increased production of ethanol and LPS in the intestinal lumen, and subsequent release of inflammatory cytokines in intestinal epithelia and liver macrophages. Both processes then lead to injury of the intestinal epithelium and disrupted intestinal barrier function, which in turn increases hepatic exposure to intestine-derived toxins. This hypothesis is further supported by evidence that intestinal BO exacerbates fatty liver disease in rodents and humans, and that obese patients with NASH have increased prevalence of BO. Furthermore, obese subjects are known to have decreased intestinal motility and are therefore more prone to BO. A recent clinical trial confirms that patients with NASH have increased intestinal permeability and small intestinal BO[25]. From this data, an obvious way to control the development of NAFLD seems to be a manipulation of the gut microflora, mainly by the reduction of BO. This can be achieved by antibiotic treatment, which has been used successfully, but is controversial due to its unspecific impairment of all microflora and its severe side effects[23]. Probiotic therapy, on the other hand, has been suggested to counteract the development of NAFLD on various different levels. Competitive inhibition of pathogens by probiotics might alter their inflammatory effects in intestinal BO, which is associated with NAFLD. Furthermore, improved intestinal epithelium function and decreased BT and endotoxemia following probiotic treatment have been observed in experimental animals and humans[26]. [SEP] Justify:

Output: The text corroborates the claim by discussing the role of probiotics in promoting gut health. It mentions that probiotics can counteract the development of NAFLD (Non-Alcoholic Fatty Liver Disease) by altering inflammatory effects in intestinal conditions and improving intestinal epithelium function. This indicates that probiotics have a beneficial impact on gut health, supporting the claim that they can improve the balance of bacteria.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: Values close to 1 (blue) or -1 (red) indicate high intertwining of the data, values close to 0 (white) indicate independence or orthogonality of the data. The assignment of the coefficients to the independent variables is the same as in (K). 2. 8. Effect of meal schedule personalization on weight lossA key part of our hypothesis involves the personalization of meal schedules. Consistent with the concept of social jet lag (the discrepancy between socially imposed and biological times), our data show that during the exploration phase, eating times on workdays differ from those on work-free days. Because social constraints usually matter less on non-working days, we expect eating times on these days to correspond more closely to individual circadian characteristics, such as the chronotype. The MCTQ questionnaire measures the chronotype based on the mid-sleep phase (mSP), i. e. , the midpoint between sleep onset and waking up [25]. Corresponding to the mSP, we determined the mid-eat phase (mEP), which we define as the midpoint between the first and the last meal of the day. Indeed, our data show that the later the mSP of participants, the later their mEP on weekends (Fig. 3E, Tab. S6), with the mSP and mEP being almost antiphasic on average, i. e. 12 hours apart (Fig. 3F, Tab. S9). The EG intervention maintains most of this relationship. However, the residuals of the regression become smaller, resulting in a model fitting the data better (Fig. 3E, Tab. S6). Interestingly, the closer the intervention brings an observed value to the predicted value, i. e. , the smaller the residual becomes, the more weight the participant loses (Fig. 3G, Tab. S6). This indicates that the personalized adjustment of eating times to the individual chronotype, i. e. , the establishment of a highly accurate phase relation between mEP and mSP, leads to a particularly effective reduction of excess weight. Another part of the hypothesis is that the adaptation of eating times to the times of hunger presumably determined by the circadian system contributes to weight loss. The calculation of individual eating times was based on the frequency of the hours at which meals were eaten on all days of the exploration phase. These days typically included more workdays than non-workdays (Fig. 3H). [SEP] Justify:

Output: The text contrasts the claim by discussing factors related to weight loss that are not directly tied to carbohydrate intake. It mentions the personalization of meal schedules and how aligning eating times with circadian rhythms can lead to effective weight loss, indicating that eating habits and timing play a critical role. This suggests that weight gain is not simply a result of eating carbohydrates but is influenced by various factors, including meal timing and individual circadian characteristics.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: Skip to main content Intended for healthcare professionals Search this journalSearch all journalsEnter search terms. . . Searchsearch Enter search terms. . . Searchsearch Search Access/ProfileAccessView access optionsView profileCreate profile Cart 0 by discipline Select discipline: All disciplines All disciplines Life & & Sciences & HumanitiesSelect subject: All subjects All subjects Cardiology & Medicine & Endocrinology & -legal & Orthopaedics & Medicine & & & & Methods & & & & & Criminology & Economics & & & Management & Marketing & & & & & & & & PlanningBrowse journals Sage publishes a diverse portfolio of fully journals in a variety of disciplines. you can explore our Disciplines Hubs, including: Journal portfolios in each of our subject areas. Links to Books and content from across Sage. for/ Reviewers SocietiesFrequently asked questions In this journal : 3. 5 5-Factor: 5. 7 email alertsYou are adding the following journal to your email alertsNew contentThe NeuroscientistCreate email alert Restricted accessReview 10. 1177/10738584031262149ContentsAbstract1999. Orphanin-FQ/nociceptin (OFQ/N) modulates the activity of suprachiasmatic nucleus neurons. J Neurosci 19:2152–2160. 1997. Functional identification of the mouse circadian clockgene by transgenic BAC rescue. Cell 89:655–667. 2001. A neural circuit for circadian regulation of arousal. 4:732–738. 1995. Nucleoplasmin-targeted aequorin provides evidence for nucleus calcium barrier. Res 216:236–243. 2002. Phototransduction by retinal ganglion cells that set the circadian clock. Science 295:1070–1073. 1989. Nitric oxide mediates glutamate-linked enhancement of cGMP levels in the cerebellum. 86:9030–9033. 1990. Isolation of nitric oxide synthetase, a calmodulin-requiring enzyme. 87:682–685. 1994. Nuclear targeting of aequorin. A new approach for measuring nuclear Ca2+ concentration in intact cells. 16:259–268. 1993. Nuclear Ca2+ concentration measured with specifically targeted recombinant aequorin. EMBO J 12:4813–4819. 1994. [SEP] Justify:

Output: The text does not provide any information directly related to the role of the suprachiasmatic nucleus in circadian rhythms. Instead, it appears to be a fragmented excerpt discussing various research topics and providing citations without addressing the claim. Therefore, it is irrelevant to the claim.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: In a series of feeding studies in mice, Cani et al[27] claimed that high-fat feeding changes the intestinal microflora composition (less bifidobacteria), which led to increased LPS levels in plasma, pro-inflammatory cytokines and increased intestinal permeability. All these effects could be counteracted by prebiotic treatment and increasing bifidobacteria species (summarized in[27]). This would indicate a direct effect of intestinal bacteria on low-grade inflammation, insulin insensitivity, and fat deposition in the liver. Other research suggests a direct decrease in pro-inflammatory cytokines e. g. TNF-αvia downregulation of NF-κB activity by probiotic treatments[14,28-30]. In a study in ob/ob mice, probiotics (VSL#3) and TNF-α antibodies were used to treat NAFLD. Both treatments improved liver function, reduced hepatic fatty acid content, and both interfered with NF-κB signalling and reduced hepatic fatty acid β-oxidation close to levels in lean mice. The authors suggest that this effect might result from improved hepatic insulin resistance[28]. Another study, using the same probiotic in normal mice, measured hepatic natural killer T (NKT)-cell depletion in high-fat fed animals[31]. NKT are unconventional T cells that express both T cell and Killer cell receptors. They regulate hepatic inflammatory process by balancing production of pro- and anti-inflammatory cytokines. Alterations of NKT function might lead to overproduction of TNF-α, causing inflammation in insulin resistance. High-fat diet induced the depletion of NKT from the liver, leading to insulin resistance and steatosis. Probiotics significantly improved all these symptoms and the effect resulted from TNF-α signalling and led to improved insulin signalling[31]. There is some suggestive evidence that probiotics might have efficacy in NAFLD in humans, but more controlled trials are needed[30]. Probiotics and alcoholic liver diseaseIn alcoholic liver disease, bowel liver interactions are well described, and relationships include increased gut permeability, endotoxemia, and TNF-α production[32]. In rats, Lactobacillus GG has been shown to reduce alcohol induced gut leakiness and steatohepatitis[33]. [SEP] Justify:

Output: The text corroborates the claim by providing evidence that probiotics can influence beneficial bacteria in the gut. It discusses various studies, such as the one by Cani et al., indicating that probiotics can counteract negative effects caused by high-fat diets on intestinal microflora and improve liver function and insulin resistance, suggesting a role for probiotics in maintaining gut health and possibly improving bacterial balance.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: Consequently, for some subjects, the EG intervention created a discrepancy between what may have been physiologically optimal eating times, presumably reflected better by data from non-workdays, and the calculated eating times. As the EG participants were instructed to adhere to the calculated eating times even on non-working days, their usual eating times at the weekend were sometimes greatly shifted (Fig. 3I, Tab. S2). However, the magnitude of these shifts does not correlate with weight changes (Fig. S2O, Tab. S6). On the contrary, if the calculated eating times resulted in large shifts of the weekend meals, this also means that previously particularly large "meal jet lags" between working and non-working days were eliminated. Indeed, the more the calculated eating times led to a shift of late weekend breakfasts to earlier times and early weekend dinners to later times, the more the participants lost weight (Fig. 3J, Tab. S6). The independent variables used above for simple regressions may influence each other and therefore their influence on BMI may be confounded. Therefore, a multiple regression with the most important and least multicollinear variables (ΔMTVS, ΔkJ, Δcalorie intake interval, ΔmSp-mEP relation, Δweekend breakfast, Δweekend dinner) was done to study their individual influences on the BMI of EG participants while keeping the other variables constant. According to this analysis, only the change in MTVS and also the resulting elimination of "dinner jet lags" have significant influence on the BMI (Fig. 3K, Tab. S8). The elimination of "breakfast jet lags" and the improvement of the mSP-mEP ratio did not reach significance but showed a strong tendency to influence BMI. In contrast, changes in caloric intake or the time interval during which food is consumed had no effect on the BMI. A concurrent analysis of covariance shows that MTVS is most strongly intertwined with BMI, while other variables play a role to a much lesser extent (Fig. 3L). 2. 9. General well-being outcomesSince stable circadian rhythms are generally associated with many aspects of health, regular entrainment of a variety of peripheral and brain clocks by the Zeitgeber food may enhance overall well-being. [SEP] Justify:

Output: The text contrasts the claim by demonstrating that changes in caloric intake or the timing of food consumption do not necessarily correlate with changes in BMI. Specifically, it states that 'changes in caloric intake or the time interval during which food is consumed had no effect on the BMI,' which implies that not all eating patterns, including those with carbohydrates, lead to weight gain.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: Indem man beide Teile unter der Kontrolle verschiedener, aber überlappender Promotoren exprimiert, kann man ein deutlich spezifischeres Cre-Expressionsmuster erreichen, als es bisher möglich war. Ziel ist es, die funktionelle Anatomie des SCNs zu untersuchen, indem man die sogenannte „Core“-Region des SCN genetisch läsioniert. Es wird sehr interessant sein, die Effekte einer solchen genetischen SCN-Core Läsion auf das zirkadiane System zu untersuchen. wird dazu beitragen, die funktionelle Anatomie dieses komplexen Nukleus besser zu verstehen. Der vierte Teil dieser Arbeit beschäftigt sich mit der Rolle der zirkadianen Uhr als Vermittler zwischen verschiedenen physiologischen Systemen. Es ist bekannt, dass die zirkadiane Uhr und die metabolische Regulation eng miteinander verknüpft sind. Außerdem ist eine kürzere Schlafdauer mit metabolischen Dysfunktionen assoziiert, wie zum Beispiel einer erhöhten Wahrscheinlichkeit von Fettleibigkeit. Eine Möglichkeit ist, dass die metabolischen Effekte von Schlafentzug durch die zirkadiane Uhr vermittelt werden. Daher war die Hypothese dieser Studie, dass in Abwesenheit einer funktionellen zirkadianen Uhr die metabolischen Auswirkungen von Schlafentzug reduziert sind. Um dies zu testen, wurden transgene Mäuse untersucht, die keine funktionelle Uhr besitzen (Per1/2-Doppelmutanten). [SEP] Justify:

Output: The text discusses research related to the suprachiasmatic nucleus (SCN) and its role, but it does not directly address the claim that the SCN is the master regulator of circadian rhythms. Instead, it mentions investigating the functional anatomy of the SCN and its connection to metabolic regulation. Hence, it does not provide relevant support or opposition to the claim.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: The same group also found that the mucosa associated microflora were altered in rats on a high alcohol feed, and this dysbiosis could be counteracted by Lactobacillus GG or oat supplementation[34]. Furthermore, alcoholics have altered microflora with decreased numbers of bifidobacteria and lactobacilli. A recent pilot study[32] compared control subjects with alcoholics in a clinic, either on standard treatment for alcoholic disease (Vitamin B1 & B6 supplements and diazepam, n = 34) or on standard treatment + probiotics (0. 9 × 10e8 CFU B. bifidum and 0. 9 × 10e9 CFU L. plantarum, n = 32) for five consecutive days. No placebo was included in the control group. They found that lactobacilli, bifidobacteria, and enterococci were reduced in alcoholics and the numbers were restored in the probiotic treatment group. E. coli levels were not altered. Liver function parameters [alanine aminotransferase (ALT) and aspartate aminotransferase] were significantly improved by probiotics compared to standard treatment, but remained below levels found in healthy controls. Other liver enzymes (GGT and LDH) were not significantly altered. In the subgroup of alcoholics with well-defined hepatitis, standard treatment only altered total bilirubin, but probiotics improved all the liver parameters mentioned above. The authors concluded that bifidobacteria seemed to play an important role in steatohepatitis of alcoholic and non alcoholic causes, including obesity[35]. In a double blind placebo controlled (sucrose capsule) intervention Lata et al[36] studied the effect of probiotic E. coli Nissle in cirrhotic patients (n = 39, 34 with alcoholic cirrhosis). They found an improvement of intestinal colonization in faeces, and a restoration of “physiological microflora” in faeces (more patients with normal microflora containing lactobacilli and bifidobacteria, less patients with potentially pathogenic bacteria). They also showed trends towards a reduced endotoxin level in blood (P = 0. 07) and a reduced Child-Pugh score (P = 0. 07), which is a measure for severity of overall liver disease. [SEP] Justify:

Output: The text corroborates the claim by providing evidence that probiotics, specifically Lactobacillus GG and oat supplementation, can counteract dysbiosis in alcoholics, which is an imbalance of gut bacteria. It emphasizes that probiotic treatment restored the numbers of beneficial bacteria (lactobacilli and bifidobacteria) that were reduced in alcoholics. Furthermore, it mentions that the probiotic treatment led to improvements in liver function parameters, indicating a broader health benefit linked to gut microflora balance.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: Previously published data show that increased regularity of breakfast in particular, and not so much that of dinner, was identified as a predictor of weight loss [26]. In contrast, in our study, an increase in the regularity of lunch, and somewhat more strongly that of dinner, is related to weight loss. Although the diary entries of some participants show that they changed their energy intake and also the food composition of fat, carbohydrates, and proteins during the study, the observed weight loss is not related to these changes. Related results have already been shown in mice, although here with a restriction to the entire active phase rather than specific eating times. Not surprisingly, mice gain weight and develop diabetes-like states under a high-fat diet [17]. It is surprising, however, that the negative physiological consequences of the high-fat diet can be almost completely prevented if the mice consume the equivalent amounts of high-fat food exclusively during their activity phase and do not receive any food during their sleep phase [17, 27]. There are also similar studies with humans in which the time window of food intake is limited to a certain length. This is, for example, 16:8 intermitted fasting or TRE/TRF, in which meals are taken only during specific time window, yet at unspecified times during that period. The effects of these protocols is mixed and often less pronounced than in our study, as less weight is lost [19–23, 28] or a longer period is required to achieve similar results [29] than in our study - with the caveat that participants with more overweight and older participants participated in these studies than in ours. Besides increased regularity, our intervention has similar effects on eating behavior, such as shortening the hours in which food is eaten. Interestingly, in our study these parameters are not related to the observed weight loss. However, other studies have also explored the effect of restricting individual meals to specific times. In mice, restricting the same amount of high-fat chow to two times per day reduces the development of obesity [30]. And in humans, restricting meals to three fixed, uniform times leads to similar weight loss like we observed in our study - but in combination with calorie reduction and standardized food [31]. The fact that our participants lost weight to a similar extent despite free choice of meals might be due to the individual tailoring of meal schedules. [SEP] Justify:

Output: The text contrasts the claim by highlighting that weight loss can occur regardless of changes to energy intake and food composition, including carbohydrates. It discusses various studies showing that weight loss can be achieved through meal timing and regularity rather than solely by reducing carbohydrate intake.


Input: Task: pass the claim using the given text. Claim: The suprachiasmatic nucleus is the master regulator of circadian rhythms. [SEP] Text: It is likely that the functioning of the clock may depend on the presence of a particular neurotransmitter on a mechanism in which co-localized neurotransmitters interact in a functionally significant manner. With more information available on the role of neurotransmitters in the working of the clock, which is involved in so many functions of the body, better opportunity for neurotransmitter-based manipulation of the clock has also been reported. Problems of shift-work insomnia and ill effects of jet lag are among the clock-related functions for which much attention has been given in recent years. Melatonin has been in use with some success in reducing the above effects. However, search for other chronobiotic agents is continuing and it is likely that there may be some new dimensions given to the problem and its solution in future. A report of a close relationship between circadian clock and cell proliferation makes things even more interesting. Investigations into the role of neurotransmitters in the SCN as well as in the afferent and efferent inputs have come a long way with the advent of newer techniques of positron emission transaxial tomography (PET) scan and polymerase chain reaction (PCR). In both plants and animals, circannual rhythms are widely distributed. Endogenous circannual rhythms form the basis for many seasonal rhythms. A number of neuroendocrine mechanisms have been implicated in the regulation of seasonal changes in the physiology and behaviour of animals. Some of these neuroendocrine pathways are necessary for the regulation of particular overt seasonal responses, though they may not be directly linked to the circadian time-keeping system. Photoperiodic input and circannual function may have profound influence on many of the functions of body. Naturally, neurotransmitters are involved not only in circadian function but also in seasonal processes. It has been postulated that heterogeneity of the clocks which are seen within the SCN may be one of the factors that form the basis of seasonal adaptations [23]. A typical example of the close linkage between seasonal rhythms and affective disorders can be seen in a seasonal form of mood disorder, seasonal affective disorder (SAD). Treatment for SAD based on circadian principles includes not only light therapy but also the use of certain drugs, again based on circadian principles involving neurotransmitters. The SCN has been subdivided into a dorsomedial shell and a ventrolateral core. [SEP] Justify:

Output: The text provides detailed information about various aspects of circadian rhythms, neurotransmitters, and seasonal rhythms but does not explicitly support or oppose the claim that the suprachiasmatic nucleus (SCN) is the master regulator of circadian rhythms. It discusses neurotransmitter interactions and their implications for circadian functions but does not confirm the SCN's role as a master regulator, making the text largely irrelevant to the claim.


Input: Task: corroborate the claim using the given text. Claim: Probiotics can support gut health by improving the balance of bacteria. [SEP] Text: Improved liver function by probiotics has already been published[5], but the mechanism remains unclear. They assume that microflora reduce the toxic load of liver, e. g. reduced endotoxin, which stimulates pro-inflammatory cytokines (TNF-α, IL-1, 6)[22]. Probiotics to cure/alleviate cirrhosis? In cirrhosis there are many conditions that alter microflora and the function of the intestinal epithelium, as recently reviewed in detail[37]. BT is caused by BO, increased permeability, and altered host defence. BT and microflora imbalance are strongly correlated with the severity of cirrhosis[38]. In a rat model of acute liver injury (using either D-galactosamine or endotoxin), probiotic lactobacilli and bifidobacteria attenuated liver injury (ALT and bilirubin), reduced BT, and normalized hepatic TNF-α and glutathione levels compared to liver injury controls[39,40]. Lactobacilli might counteract BT by (1) promoting growth of anaerobes and Gram-positive bacteria while inhibiting gram-negative bacteria, or (2) increasing SCFA while decreasing pH, inducing growth factors and proliferation of microflora, and inhibiting adherence and invasion of pathogens. Patients with liver cirrhosis have imbalanced intestinal microflora with increased aerobes (enterobacter and enterococci) and anaerobes (clostridia), and decreased bifidobacteria counts in stool. In a probiotic intervention trial in cirrhotic patients[38] (mainly caused by hepatitis virus B and C; HBV and HCV) patients received two different probiotic capsules [bifidobacteria + L. acidophilus + Enterococcus or Bacillus subtilis (B. subtilis) + Enterococcus faecium (E. faecium)], two capsules per day for 14 d. In both probiotic groups, bifidobacteria counts increased with treatment, while faecal pH and ammonia levels in faeces and blood decreased. Additionally, B. subtilis + E. faecium decreased clostridia counts and endotoxin levels in the blood of cirrhotic patients. [SEP] Justify:

Output: The text corroborates the claim by detailing how probiotics can improve the balance of intestinal bacteria in patients with liver cirrhosis. It mentions that patients in a probiotic intervention trial saw an increase in bifidobacteria counts and a decrease in harmful bacteria such as clostridia. The text also describes mechanisms by which probiotics promote the growth of beneficial bacteria and inhibit harmful ones, thus supporting the idea that probiotics can enhance gut health.


Input: Task: contrast the claim using the given text. Claim: Eating carbohydrates always leads to weight gain. [SEP] Text: It is true that our data show that scheduling single meals to supposedly circadian optimal eating times of the participants is not essential for successful weight loss. Circadian clocks can adjust flexibly to Zeitgebers and it is apparently more important to choose times for meals when people (have to) eat particularly frequently than the time that is probably genetically determined. That is, if the intervention leads to eating at times that are far from those normally chosen on non-working days, this has no negative impact on weight loss efficiency. Our data suggest that the regularity of eating times seems to be more important than the times themselves. However, our pilot data still show that personalization of meal schedules is nevertheless useful. First, depending on the individual chronotype of the participants, their mealtime windows were earlier or later in the day. And those for whom the intervention optimized this relationship were particularly effective at losing excess weight. Second, weight loss is more successful if the eating time schedule is such that an individual who usually eats dinner at an early time on non-working days, but has dinner later on working days, consistently eats at the later time. This also tends to apply to breakfast if an individual eats breakfast earlier on working days than on non-working days and the meal plan is aligned with the early time of the working days. Since food serves as a Zeitgeber for a large number of tissues, including several brain regions, it can be hypothesized that regular eating not only has a positive effect on body weight, but also on other aspects of well-being. A previous study by Panda et al. [18] has already shown that shortening the eating interval to 10-12 hours per day has a positive effect on the general well-being of the participants. Similarly, in our study, we also found significant improvements in different aspects of subjective well-being over the course of the study, specifically in physical and mental health, sleep quality, and self-efficacy. This shows that adhering to daily structured mealtimes can improve not only metabolic but also other physical and also psychological levels of health. There are several explanatory approaches for why increased meal regularity can lead to weight loss despite equal caloric intake. For example, circadian clocks influence the composition of the microbiome, which regulates metabolic balance and body weight [32–37]. Additionally, circadian clocks help to anticipate mealtimes and provide the necessary digestive components in advance of food intake in advance [38–41]. [SEP] Justify:

Output: The text contrasts the claim by presenting evidence that the timing and regularity of meals, rather than the strict consumption of carbohydrates, play a crucial role in weight management. The text discusses findings that indicate the regularity of eating times is more important for weight loss than the specific times of meals. Additionally, it suggests that weight loss can be successful even with a consistent caloric intake when adjusting meal scheduling to align with individual preferences and circadian rhythms. This implies that not all carbohydrate consumption necessarily leads to weight gain, which directly challenges the absolutism of the claim.