Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: Aging decreases circulating Klotho levels in both mice and humans, and increases Kelch-like ECH-associated protein 1 (KEAP1) levels in isolated cardiomyocytes, which promotes NRF2 proteolysis[57,58]. Accordingly, treatment of aged mice with secreted Klotho reduces cardiac oxidative stress and rescues cardiac aging[57]. Thus, aging alters cardiac and vascular expression of proteins that regulate redox balance, such as NOX4, CaMKII, p66Shc, Arg-1, Nrf2, Klotho, SOD2, 2, resulting in elevated ROS levels and mitochondrial dysfunction in the aged heart and vessels. Impaired autophagyAutophagy is a cellular degradation process through which the cells recycle their own components. Autophagy decreases with age in numerous tissues, including the heart, and leads to accumulation of dysfunctional organelles, misfolded proteins, and lipofuscin granules[59,60]. One of the main regulators of autophagy is the mammalian target of rapamycin (mTOR), a serine/threonine kinase that also regulates cell proliferation, protein synthesis, lifespan, and aging[61]. mTOR is a component of the protein complexes mTORC1 and mTORC2[62]. mTORC1 is a suppressor of autophagy and is sensitive to rapamycin, while mTORC2 is not sensitive to short-term rapamycin treatment. Cardiac and vascular mTOR activity is significantly increased in aged mice[63,64]. Accordingly, in mice that do not express glycogen synthase kinase-3α (GSK3A), which inhibits mTORC1 activity, autophagy is decreased, and cardiac aging appears early and is accompanied by cardiac hypertrophy, systolic dysfunction, and impaired diastolic relaxation[65]. Conversely, chronic cardiomyocyte-specific activation of an activator of mTOR signaling, protein kinase B (Akt), leads to aging-induced cardiac hypertrophy and myocardial contractile dysfunction[63]. [SEP] Justify:

Output: The text contrasts the claim by explaining the biological processes associated with aging, including decreased Klotho levels and increased mTOR activity. It highlights how aging alters key cellular functions and does not support the idea of a proven genetic intervention that eliminates all signs of aging. Instead, it presents evidence of ongoing aging processes rather than a complete reversal.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Иными словами, максимальное расширение кругозора идет параллельно с получением серьезных знаний во всех необходимых областях. Это мотивирует, создает благоприятную почву для поиска новых идей, концепций, методов, но не гарантирует развития таланта. [SEP] Justify:

Output: The text does not address the claim regarding insects and their ability to communicate through sounds and music. Instead, it discusses broad themes around knowledge expansion and motivation, making it irrelevant to the claim.


Input: Task: corroborate the claim using the given text. Claim: Genetic testing can provide insights into ancestry and potential health risks. [SEP] Text: 22–37 The major challenges ahead are to investigate, describe and understand genetic variability in order to maximise the health benefits of population genetic research. 73. 16th IHIW: Global distribution of extended HLA haplotypes. Immunogenet. 2013;40(1):31–38. ínola H, et al. HLA polymorphism in six Malay sub–ethnic groups in Malaysia. Hum Immunol. 2009;70(7):518–526. Using HLA loci to inform ancestry and health in Polynesian and Maori populations. Tissue Antigens. 2012;80(6):509–522. HLA and MICA polymorphism in Polynesians and Maori: implications for ancestry and health. Hum Immunol. 2013;74(9):1119–1129. Molecular approaches to transfusion medicine in Polynesians and Maori in New Zealand. Immunogenet. 2013;40(6):460–470. Human platelet antigens frequencies in Maori and Polynesian populations. Transfus Med. 2013;23(5):330–337. González– Allele frequency net 2015 update: new features for HLA epitopes, KIR and disease and HLA adverse drug reaction associations. Res. 2015;43(Database issue):D784–D788. in Banjar, Bugis, Champa, Jawa and in Peninsular Malaysia. Blood Transfus. 2015;13(4):1–6. HNA Diversity in of in Peninsular Malaysia. Transfus Med. 2016;26(4):305–307. Nemat– KIR diversity in Māori and Polynesians: populations in which HLA–B is not a significant KIR ligand. Immunogenetics. 2014;66(11):597–611. Distribution of cytokine gene polymorphisms in five Malay subethnic groups in Peninsular Malaysia. Immunogenet. 2015;42(3):200–203. Distribution of cytokine gene polymorphisms in six subgroups in Peninsular Malaysia. Hum Immunol. 2016;77(4):338–339. Sequence polymorphisms of mtDNA HV1, HV2, and HV3 regions in the Malay population of Peninsular Malaysia. Legal Med. [SEP] Justify:

Output: The text corroborates the claim by discussing the investigation and understanding of genetic variability, which is essential to maximize health benefits in population genetic research. The references to various studies examining HLA polymorphism and cytokine gene polymorphisms further support the notion that genetic testing can provide insights into both ancestry and health risks.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: In a similar manner, suppression of the myosin light chain (MLC)/focal adhesion kinase (FAK)/Akt/mTOR signaling axis via deletion of Rho-associated coiled-coil-containing protein kinase (ROCK)1 and ROCK2 promotes autophagy and reduces cardiac fibrosis in aged mice[66]. ROCK 1 and ROCK2, which have a central role in regulating actomyosin cytoskeleton contractility, promote age-related aortic stiffening as well[67]. Interestingly, although mTORC1 seems to promote cardiac aging[68], it was recently found that activation of mTORC2 alone increases autophagy and improves age-related cardiomyopathy in Drosophila[69], indicating additional layers of regulation of mTOR signaling in regards to its involvement in cardiac aging. AMPK, which is a serine/threonine protein kinase that acts as a cellular energy sensor of low intracellular ATP levels, a stimulator of autophagy in cardiomyocytes[70], and an mTOR inhibitor[71], also has low expression in the aged heart and arteries, which corroborates with increased mTOR signaling and reduced autophagy. AMPK deficiency exacerbates age-related cardiomyopathy[72,73]. Aging-induced deactivation of AMPK has been correlated with decreased SIRT1 activity. Consequently, SIRT1 activation in aged hearts activates AMPK and improves their tolerance to ischemic stress[74]. Moreover, combined deletion of both Akt2 (the main cardiac isoform of Akt) and AMPK suppresses autophagy and promotes aging-induced cardiac hypertrophy, interstitial fibrosis, and contractile dysfunction[75]. A certain type of autophagy that targets mitochondria, thus referred to as mitophagy, is induced by PTEN-induced putative kinase protein 1 (PINK1), which accumulates on the damaged mitochondria and phosphorylates the E3 ubiquitin ligase Parkin. Parkin marks proteins on the outer mitochondrial membrane with phosphoubiquitin, leading to lysosome-mediated mitochondrial degradation[76]. Parkin levels are significantly decreased in the hearts of aged mice[77]. [SEP] Justify:

Output: The text contrasts the claim by discussing specific mechanisms that relate to aging and cardiac health, indicating that metabolic and cellular processes are involved in aging rather than providing proof that genetic anti-aging interventions can eliminate all signs of aging at the cellular level. The detailed analysis of signaling pathways such as mTOR, AMPK, and their roles in aging suggests complexity in aging processes, rather than a simplistic elimination of aging signs.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Иногда случается так, что молодой композитор подает огромные надежды: он легко и быстро работает, и каждое новое сочинение существенно глубже, интереснее и необычнее предыдущего… Но в какой-то момент его творческий рост неожиданно останавливается, и никакие усилия как с его стороны, так и со стороны педагогов ни к чему не приводят. Мы никогда не знаем, до какого уровня в этом смысле может вырасти тот или иной наш подопечный. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses the challenges of a young composer's artistic growth and does not mention insects, communication, sounds, or music.


Input: Task: corroborate the claim using the given text. Claim: Genetic testing can provide insights into ancestry and potential health risks. [SEP] Text: AMA Journal of Ethics® Illuminating the Art of navigation 433. doi: 10. 1001/virtualmentor. 2014. 16. 6. ecas2-1406. Citation PDF Altmetric email Case Ms. Stewart was eagerly awaiting her upcoming trip to Boston to celebrate her parents’ fiftieth wedding anniversary. She had grown up in a large Irish family, with two brothers and two sisters, but she rarely got to see them since moving to Oregon for her job. She was especially looking forward to seeing her sister Anna, who was recovering from a mastectomy after receiving a diagnosis of breast cancer several months earlier. As a gift to her parents, Ms. Stewart had decided to create a book tracing the family’s genealogy. Growing up, her mother told her stories about how her great-grandfather had arrived at with hardly anything besides the clothes on his back, and she had always been curious about the family’s roots in Ireland. As she was searching the Internet for genealogy records websites, an advertisement on the side of her screen caught her eye. “Find out where your genes come from! ” Her curiosity piqued, Ms. Stewart clicked on the link to geneheritage. com, an online service for genetic testing of ancestry and ethnicity. She had heard of these online genetic testing services before and even read in a magazine that one of her favorite actresses had gotten one, but she had never before thought of doing it herself. “I could put it in the book,” she thought, as she perused the website. She decided to order a kit and, a few days later, she sent off a cheek swab for the DNA tests. Two weeks later, Ms. Stewart got her eagerly awaited results. To her surprise, the results indicated that she carried several polymorphisms that are known to be more common among than in the general population. According to the test, she had 23 percent ancestry in her genetic panel. Later that week, Ms. Stewart went to see her primary care physician, Dr. Lowe, for her annual physical. During the review of systems when Dr. Lowe asked her whether she had had any lumps or pain in her breasts, Ms. Stewart hesitated a bit. “haven’t had any problems, but I was thinking…I want to get tested for the breast cancer gene. [SEP] Justify:

Output: The text corroborates the claim by illustrating Ms. Stewart's experience with genetic testing, which provided insights into both her ancestry—specifically, that she has a certain percentage of ancestry indicated in her genetic panel—and her potential health risks, as she expressed interest in testing for the breast cancer gene. This aligns directly with the claim, as it emphasizes the dual role of genetic testing in understanding one's heritage and assessing health risks.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: Inhibition of Parkin mitochondrial translocation -via p53- in the hearts of aged mice impairs mitophagy and causes cardiac dysfunction[78]. Conversely, overexpression of Parkin improves mitophagy and cardiac function in aged hearts[77]. Thus, aging-induced alterations in the expression of proteins involved in cell proliferation, cytoskeleton contractility and protein degradation, such as mTORC1, ROCK1, ROCK2, and AMPK, lead to impaired autophagy in aged hearts and vessels. Aging-related alterations in metabolic homeostasisAging is associated with major metabolic events, including insulin resistance[79,80]. Although it is known that insulin-like growth factor-I (IGF-I) facilitates glucose metabolism and inhibits apoptosis of cardiomyocytes[81,82], a study showed that the role of IGF-I receptor (IGF-IR) in cardiac health is age-dependent. Specifically, mice with cardiomyocyte-specific overexpression of IGF-IR show superior cardiac contractility at a young age, but pathological cardiac hypertrophy, increased LV fibrosis and reduced EF at 20 months of age. This pathological phenotype is attributed to reduced autophagy and lower oxidative phosphorylation in the heart[83]. Even in mice of 11 month-old, cardiomyocyte-specific inactivation of IGF-IR suppresses diastolic cardiac function to a greater extent than in their age-matched controls[84]. Moreover, mice with cardiomyocyte-specific expression of a dominant-negative mutant of phosphoinositide 3-kinase (PI3K) (dnPI3K), which is a downstream effector of insulin/IGF-1 signaling, have preserved cardiac function and less fibrosis at 20-24 months of age, decreased levels of oxidative stress and proinflammatory factors, and enhanced autophagy[85]. Thus, inhibition of IGF-IR in late life may prevent age-related cardiac changes. Aging-related mitochondrial dysfunction is also associated with changes in intracellular calcium handling[86]. SERCA activity decreases due to increased oxidation, although its expression is not altered[87,88]. activity increases calcium stagnation in cytoplasm, which prolongs diastolic relaxation[89]. [SEP] Justify:

Output: The text contrasts the claim by detailing the biological complexities associated with aging and the limitations of existing interventions. It discusses how alterations in protein expression and metabolic processes lead to impaired cardiac function in aged mice, indicating that while certain genetic interventions might improve functions like autophagy, they do not eliminate signs of aging entirely. The evidence presented does not support the assertion that genetic interventions can completely eradicate all signs of aging, highlighting the ongoing challenges in aging research.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Наша главная задача — растить профессиональных композиторов. Смысл этого в том, чтобы композитор знал, как работать с тем или иным материалом, и умел из найденных «первокирпичей» создать убедительную форму. История помнит немало случаев, когда великие мастера нарочно использовали тусклый, неинтересный и страшно неудобный, негибкий материал для создания своих произведений. [SEP] Justify:

Output: The text does not address the claim about insect communication through sounds and music at all. It discusses the training of professional composers and the use of materials in music creation, which is unrelated to the claim.


Input: Task: corroborate the claim using the given text. Claim: Genetic testing can provide insights into ancestry and potential health risks. [SEP] Text: ” Somewhat surprised, Dr. Lowe explained that the BRCA is not a routine test and is recommended for women who are at increased risk of breast cancer due to their family history and ancestry. “Well that’s just it,” Ms. Stewart responded. “You know my sister had breast cancer recently, and now I just took this test and it turns out that I’m part Jewish. I think I need the test. ” the case of breast cancer risk, genetic testing can provide important information to help guide the patient through a number of personal and medical choices about her health [1]. Genetic testing is most informative when performed first on the family member at the highest risk of having a mutation. In this case, it would be Ms. Stewart’s sister [2], and her breast cancer is sufficient indication for genetic counseling and possible testing even in absence of ancestry information [3]. Ancestry information can assist in identifying people who may be at increased risk for heritable disease. Most commonly, this information is obtained from discussions with family members, discussions that can be key in identifying and contextualizing an individual’s heritable health risk. While reported family history provides insight into possible risk status, it may be limited since some families are not fully aware of or forthcoming about their family history. Increasingly, patients are turning to ancestry testing to gain this information, using direct-to-consumer (DTC) kits sold by independent manufacturers. These tests use either a single genetic and genomic analytic approach or a combination of methods to analyze an individual’s DNA and draw inferences about ancestry [4]. In the hypothetical case of Ms. Stewart, information from the ancestry test may not significantly alter the course of action regarding referral for genetic counseling and possible testing. However, it is important to recognize the ethical issues associated with DTC genetic testing [5]. One of most relevant issues for this case is the fact that the results may not accurately reflect Ms. Stewart’s ancestral background. This could be due to the genetic markers the test manufacturer elects to use, how it defines reference populations, and the statistical methods and interpretations used to analyze the genetic data, all these in addition to baseline variability in human genetic diversity [6, 7]. [SEP] Justify:

Output: The text corroborates the claim by discussing how genetic testing can help identify potential health risks, particularly in the context of breast cancer risk linked to family history and ancestry. It highlights that ancestry information can aid in identifying individuals at increased risk for heritable diseases and that patients are increasingly using ancestry testing to gain this information. Furthermore, it underscores that genetic testing provides valuable insights for guiding personal and medical choices about health, thus supporting the claim.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: iron-sulfur domain-containing protein 2 (Cisd2), which is also important for intracellular Ca2+ homeostasis, decreases with aging in the heart[90], leading to mitochondrial Ca2+ overload in cardiomyocytes that accounts for cardiac structural defects and functional decline[91]. The occurrence of oxidative stress and mitochondrial damage in cardiovascular aging affects cellular and systemic metabolic homeostasis in the elderly. The advances in metabolomic methods have availed a powerful tool that allows for screening the numerous metabolites in biofluids and tissue. Leveraging mass spectrometry (MS)-based metabolomics, several studies identified altered metabolites and circulating prognostic biomarkers in the progression of various human diseases, including cancer, heart failure, and Alzheimer’s disease[92-94]. Animal studies have suggested that aging per se leads to alterations in plasma metabolic profile[95,96]. Although MS-based metabolomics study in aging is still limited, the altered plasma levels of amino acids and lipid species have been consistently reported as metabolic signatures of aging in humans and mice[95,97,98]. A recent study on metabolomic analysis of human serum samples from healthy individuals aged 20-70 years old[98] showed that plasma levels of branched-chain amino acids (BCAA, isoleucine; leucine; valine), aspartate, 3-hydroxyisobutyrate are significantly decreased after the age of sixty. On the contrary, the plasma levels of hippuric acid are increased after this age[98], which may be correlated to the enrichment of gut microbiota after the age of sixty, since hippuric acid is a metabolite deriving from the degradation of dietary polyphenols by a range of gut microbe[99]. However, the same study[98] showed that despite the elevated levels of hippuric acid in plasma, variables related to cardiac autonomic modulation and cardiorespiratory fitness decrease with age and present the lowest values in the oldest age group (60-70 years old). Another recent targeted metabolomics study of microbe-derived metabolites demonstrated that the plasma levels of hippuric acid are negatively correlated with peripheral artery disease[100], suggesting the use of plasma hippuric acid as a biomarker that will identify a lower risk of CVD in the elderly. [SEP] Justify:

Output: The text contrasts the claim by discussing various biological changes that occur with aging, such as decreased levels of Cisd2 and altered metabolic profiles, which indicate that aging results in significant cellular and systemic changes. It highlights the complexity of aging and the ongoing decline in biological functions, thereby suggesting that no intervention has yet proven to eliminate all signs of aging at the cellular level.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Обладая незаурядной композиторской техникой, они выжимали из него максимум возможного, и результат неизменно оказывался достойным всяческого восхищения. Композиторы таким образом бравировали своим мастерством, демонстрировали его в максимально открытом виде: смотрите, я беру неликвид — на него и посмотреть-то страшно, — а какое чудо я из него делаю! Среди многих прочих сегодня мы сталкиваемся с одной очень серьезной проблемой. [SEP] Justify:

Output: The text does not address the claim about insects communicating through sounds and music, focusing instead on composers and their techniques, which is unrelated to the communication methods of insects.


Input: Task: corroborate the claim using the given text. Claim: Genetic testing can provide insights into ancestry and potential health risks. [SEP] Text: This includes appropriate pre- and post-test counseling to prepare the patient for personal and medical consequences that can come from learning such information. Genetic counseling can often be reassuring in situations in which a likelihood of heritable cancer risk is low. Genetic counseling may empower both Ms. Stewart and her sister to make educated and informed decisions about genetic testing, cancer screening, and prevention. In absence of pre- and post-test counseling, users may not be ready to confront personal risk information that can alter perspectives and choices about their life and health care or to frame future reproductive decisions based on knowledge of a heritable risk [5]. For example, Ms. Stewart’s sister, who already has the diagnosis of breast cancer, has a 1 in 10 chance of being a BRCA gene mutation carrier if, in fact, the ancestry information is accurate [10]. Furthermore, users may learn information about their families that may be unexpected or even considered undesirable, something that could result in profound personal conflict [6]. This raises larger questions about when and how to disclose what has been learned. Finally, ambiguity surrounds how individual DTC test manufacturers subsequently store and use the genetic sample, so consumers must also be aware of issues related to privacy and confidentiality of their information after the testing process is completed. It is imperative that a patient be referred for genetic counseling if there is concern about a genetic predisposition for disease. When evaluating an individual with breast cancer or who is at high risk for developing breast cancer, it is important to obtain a detailed medical and family history. Information gathering includes ancestry as certain ethnic groups, such as those listed here, are a few of the better known groups with documented genetic mutations. Until further data can be obtained about the accuracy and precision of DTC ancestry tests and their clinical utility, family history remains a primary way of acquiring this information. However, given the growing presence of genetics and genomics, clinicians must educate themselves about the medical and ethical implications of such tests, whether offered in the clinical or DTC context. Without such knowledge, clinicians will be limited in how they guide their patients through the often difficult decisions that must be made in light of this information. Genetics/Genetic counseling Genetics/Genetic testing 40. View 1. 2014). 13, 2014. In some situations, even in the absence of testing or with negative test results, heightened surveillance based on breast or other cancers may be recommended. [SEP] Justify:

Output: The text corroborates the claim by discussing the role of genetic counseling in helping patients understand the implications of genetic testing, including insights into ancestry and associated health risks. It states that genetic testing, particularly concerning hereditary cancer, involves preparing patients for personal and medical consequences, thus linking genetic testing to potential health risks. The mention of ancestry as a factor in understanding genetic predispositions further supports the notion that genetic testing provides valuable insights into both ancestry and health.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: According to plasma metabolomic analysis of young (3-4 months) and old mice (22 months), the circulating metabolic footprint of aging was found in the altered levels of amino acids (i. e. , phenylalanine, tryptophan, taurine, isoleucine), phospholipids and organic acids (i. e. , gluconic acid, citric acid)[95]. It remains elusive what organ(s) are responsible for releasing those metabolites into circulation in aging, as well as whether they play a role in contributing to myocardial remodeling during aging. In summary, although various metabolic processes are compromised during aging, only recent MS-based metabolomic analyses have identified metabolites that may serve as biomarkers or potential targets of therapeutic interventions. The challenge going forward will be to design studies aiming to discover new biomarkers that can predict risks of pathogenic aging and help elucidate the critical metabolic pathways that account for the onset and progression of aging-related cardiovascular diseases. InflammationDysregulation of the immune system in the elderly leads to chronic sterile low-grade inflammation[101]. This process, called “inflammaging”, is a key factor in the development of frailty and age-related degenerative diseases, including cardiovascular complications[102,103]. A major pathway of cardiovascular inflammaging is the NOD-like receptor protein (NLRP) 3/caspase-1 cascade[104]. NLRP3 is an intracellular detector of endogenous danger signals, microbial motifs and environmental irritants, leading to the formation and activation of the inflammasome. During aging, damaged mitochondria and defective autophagy lead to ROS accumulation and the release of damage-associated molecular patterns (DAMPs) that trigger the NLRP3 inflammasome[105]. Assembly of the NLRP3 inflammasome results in the secretion of caspase-1-dependent proinflammatory cytokines, such as IL-1β and IL-18[106]. In a D-galactose-induced model of cardiomyocyte aging, NLRP3 inflammasome is activated and IL-1β levels are increased, whereas inhibition of NLRP3 inflammasomes by MCC950 or N-acetylcysteine attenuates cardiomyocyte aging[107]. [SEP] Justify:

Output: The text contrasts the claim by discussing how research has identified changes in the metabolic profiles of aging but does not support the assertion that genetic anti-aging interventions can eliminate all signs of aging. Instead, it emphasizes the complexity of aging and the ongoing challenges in understanding the underlying metabolic processes, highlighting that despite identifying potential biomarkers, no definitive evidence is provided that any intervention can completely reverse or eliminate aging at the cellular level.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Современным композиторам тесно в условиях звукоряда, причем неважно, какой именно это звукоряд — любой тормозит! Совершенно очевидно, что искусственное вычленение отдельных частот из непрерывного спектра и структурирование дискретного пространства действительно весьма и весьма ограничивают возможности творцов. Сегодня многие пытаются расширить рабочее пространство и перейти от мощности счетного множества к мощности континуума. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses the limitations faced by modern composers regarding sound structures rather than addressing the communication abilities of insects through sounds or music.


Input: Task: corroborate the claim using the given text. Claim: Genetic testing can provide insights into ancestry and potential health risks. [SEP] Text: AbstractThe past hundred years have given birth to arguably the most profound changes in society, medicine, and technology the world has ever witnessed. Genetics is one such field that has enjoyed a meteoric rise during this time. Progressing from Mendelian genetics to the discovery of DNA to the ability to sequence the human genome, perhaps no other discipline holds more promise to affect future change than genetics. Technology currently exists to evaluate some of the genetic information held by developing embryos in the context of an in vitro fertilization (IVF) cycle. This information is then used to determine which embryos are selected for uterine transfer. Many societies have enacted legislation to protect against possible abuses utilizing this technology. However, it is incumbent upon society to continue ensuring that preimplantation genetic diagnosis (PGD)–-and genetic testing in general–-is applied in a way that utilizes its potential in a responsible manner to improve health care. Since the dawn of civilization, mankind has placed great importance on our genetic composition. From the ancient civilizations of Egypt to the royalty of European nations today, the familial pedigree or bloodline of an individual has historically been of paramount importance in determining expectations and opportunity for advancement in society. In contrast, an ideal of many modern societies, often termed meritocracy, has been to move past the concept of inherited potential to allow individuals to achieve based on their merits alone. 1 Indeed, the capitalistic system that grew out of the tends to reward companies for hiring the best person for the job regardless of their background (but, of course, there are exceptions). This environment has become a standard, that is, a new goal for western society. It is frowned upon for individuals to obtain a position in a company or school that is connected to a family donation. Politicians from humble backgrounds use their lack of connections in early life as a centerpiece of their campaigns. While individuals’ family backgrounds certainly still shape their futures, this is far less of a factor today than arguably at any other time in human history. Given this background of a growing social emphasis on allowing individuals to achieve and be judged on their merits, it is understandable that society is cautious about technology that could predict an individual's potential based on the results of genetic analysis. As genetic diagnostic technology continues to advance, our understanding of the genetic origins of disease is taking shape. [SEP] Justify:

Output: The text corroborates the claim by discussing advancements in genetics and the ability to evaluate genetic information, particularly in the context of assessing embryo development during IVF. It mentions the potential of genetic testing to improve health care and states, 'our understanding of the genetic origins of disease is taking shape,' which aligns well with the claim regarding potential health risks.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: NLRP3 inflammasome also participates in vascular endothelial cell senescence via a mechanism that involves binding of TXNIP to NLRP3, which is triggered by oxidative stress[108]. Moreover, increased cardiac and aortic expression of Toll-like receptor 4 (TLR4), which is a pattern recognition receptor of the innate immune system, is observed with aging[109] and accounts for higher production of inflammatory cytokines, such as IFN-β, IL-1β, IL-6, and TNF-α. To this end, aged TLR4-/- mice have lower levels of these cytokines and improved cardiac function and vascular relaxation[109]. Transcriptional factor NF-κB, which is involved in TLR4 signaling and is tightly associated with inflammation, also plays an important role in cardiovascular aging[110]. Treatment of endothelial cells with TNF-α activates NF-κB and increases proatherogenic inflammatory mediators, such as iNOS and adhesion molecules, and incurs age-related alterations of the arterial endothelium, such as impaired acetylcholine-induced relaxation[111,112]. Aged hearts also have increased NF-κB signaling that mediates inflammatory response, while NF-κB inhibition alleviates cardiac inflammation, apoptosis, and age-associated LV remodeling[113,114]. Specifically, supplementation with the anti-aging serum soluble Klotho inhibits the TLR4/Myd88/NF-κB pathway, resulting in improved cardiac function in aged mice[110]. Matrix metalloproteinase- (MMP-)9, monocyte chemotactic protein (MCP)-1 levels, and macrophage density increase in the left ventricles of senescent mice[115]. MMP-9 stimulates cardiac macrophage activation and proinflammatory response in aged mice, while MMP-9 deletion results in decreased proinflammatory gene expression and collagen deposition, and attenuates age-related LV diastolic dysfunction[116]. Thus, NLRP3 inflammasome activation, increased TLR4 expression, elevated production of inflammatory cytokines, and increased NF-κB signaling are important processes and factors in inflammaging, which is a major cellular process involved in cardiovascular aging. FibrosisThe development of myocardial fibrosis is another hallmark of cardiovascular aging. [SEP] Justify:

Output: The text contrasts the claim by discussing various mechanisms related to cardiovascular aging and inflammation, such as NLRP3 inflammasome activation and increased TLR4 expression. It emphasizes that aging involves complex biological processes and does not suggest that any interventions completely eliminate signs of aging. Additionally, the mention of inflammatory cytokines and their roles indicates that aging involves ongoing cellular changes rather than their eradication.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Отсюда огромная популярность сонористики во всем ее фактурном многообразии. Вот здесь-то и возникают новые проблемы! Мы не знаем, как структурировать сонористику — это слишком молодое направление, и накопленный опыт пока недостаточен. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses the popularity and issues related to sonoristics without mentioning insects or their ability to communicate through sounds and music.


Input: Task: corroborate the claim using the given text. Claim: Genetic testing can provide insights into ancestry and potential health risks. [SEP] Text: We as a species are just now approaching the point where we can predict, to a limited degree, certain genes that may predispose an individual for a certain disease or condition. This ability to diagnose genetic traits awoke basic fears of future abuse in the scientific community and society at large. An excellent example of these concerns is illustrated by the 1997 science fiction film 2 In the film, essentially all individuals in society are conceived in a laboratory at which time their DNA is sequenced and, based upon their genetic potential, their life (school, career, etc) are planned. In the world, social class and potential are defined almost exclusively by an individual's genetic code, eerily similar to the blood line concept of inherited potential that has been a centerpiece of human history. The film chronicles the struggle of an individual with “nonideal” DNA to achieve greatness through tenacity and drive despite tremendous discrimination. We are now able to identify single nucleotide polymorphisms (SNPs), markers on our genetic code, that if detected in a certain pattern are predictive, to some degree, of the development of such conditions as diabetes. 2–4 Several companies have begun to offer adult testing for predictive genetics. Predictive genetics technology tests for markers correlating with a slight increased chance of being diagnosed with a host of medical disorders ranging from depression to asthma. 5,6 Many of these tests are available without a physician's order and require only a saliva sample or a blood spot collection. 5–7This technology has been looked upon with concern by the medical and public policy communities. Specifically, the ability of the consumer to interpret the test results is questionable, especially in cases where the scientific foundation for the tested mutation, such as those associated with common conditions like depression, is lacking. 5–7 Such results could lead to potentially damaging and inaccurate information. 5–7 Additionally, while there are some regulatory mechanisms in place for such laboratories, some believe that more stringent regulations are warranted. 7,8 These concerns have led to consumer advocates and professional societies discouraging the public from using such testing services. 6,9,10For many disorders, such as Huntington's disease and cystic fibrosis, there are clear genetic mutations that are strongly tied to the development of disease. For the majority of medical disorders, such as type 2 diabetes and hypertension, however, what determines the development of disease appears to be more complex. [SEP] Justify:

Output: The text corroborates the claim by discussing the ability to use genetic testing to predict certain health disorders and conditions, stating, 'We are now able to identify single nucleotide polymorphisms (SNPs), markers on our genetic code, that if detected in a certain pattern are predictive, to some degree, of the development of such conditions as diabetes.' Additionally, it mentions that several companies offer predictive genetics testing that correlates with an increased chance of various medical disorders, indicating that genetic testing can indeed provide insights into potential health risks.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: Fibroblast activation and proliferation, along with hypertrophy of myocytes, compensate for myocyte loss due to apoptosis and necrosis[117-120]. Fibrosis is characterized by excessive deposition of extracellular matrix by cardiac myofibroblasts, which constitute the main cardiac cell type that undergoes senescence[121]. Senescence in cardiac fibroblasts depends on p53/p21 and p16/Rb pathways. However, genetic ablation of p53 and p16(INK4a) (Trp53-/-Cdkn2a-/- mice) eliminates senescence, but it exacerbates fibrosis with pressure overload, resulting in severe cardiac dysfunction[121]. Furthermore, cardiac-specific induction of senescence in the same study lowered perivascular fibrosis, which contradicts findings that correlate fibrosis with cardiac aging. This finding indicates potential protective effects of isolated cellular senescence against fibrosis in a young heart as opposed to an aged heart that cellular senescence is extensive. TGF-β signaling, which is one of the primary regulators of tissue fibrosis, is also activated in cardiac aging. Mice with heterozygous Tgfb1 deletion have decreased age-related myocardial fibrosis and improved LV compliance[122]. Moreover, chronic inhibition of TGF-β receptors prevents ventricular fibrotic remodeling with aging[123]. Surprisingly, the expression of TGF-β receptor I (TβRI) is decreased in aged murine cardiac mesenchymal stem cells (MSCs) and MSC-derived mesenchymal fibroblasts[124]. It remains to be elucidated whether age-related cardiac fibrosis is caused by the elevated activity of TGF-β or defects in the TGF-β signaling[125]. Fibrosis is also modulated by the renin-angiotensin-aldosterone system (RAAS), which is a critical regulator of blood pressure, fluid balance, and systemic vascular resistance. [SEP] Justify:

Output: The text contrasts the claim by discussing the complexities of cellular aging and the effects of various genetic and signaling pathways on aging, particularly in cardiac cells. It notes that while genetic ablation can eliminate senescence in certain contexts, it exacerbates fibrosis, leading to severe cardiac dysfunction. This indicates that genetic interventions do not uniformly eliminate signs of aging—as the claim suggests—since they can also lead to adverse effects like increased fibrosis.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Мы структурируем ее не «изнутри», а «снаружи», то есть во всех вариантах — будь то некий «сюжет», на который все накручивается-наверчивается, или «сверху спущенная» блок-схема, как в программировании, — мы вначале конструируем форму и лишь затем насыщаем ее сонорным содержанием. Так или иначе, пусть мы знаем мало и умеем не много, но думать о структуре необходимо. Однако среди молодых это делают единицы! [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses a different subject related to structure and design rather than communication in insects. There is no mention of insects, sounds, or music.


Input: Task: corroborate the claim using the given text. Claim: Genetic testing can provide insights into ancestry and potential health risks. [SEP] Text: At this point in time, an individual's family history and environment along with diet and exercise patterns are vastly more predictive of disease development compared to the currently defined associated disease markers. 2 It is believed that the disease markers currently described represent approximately 10% of total familial risk. 2 Therefore, as we continue to catalog more and more genetic markers associated with disease, our ability to predict disease based on genetics alone will exponentially grow. At some point, it is conceivable that genetic analysis will be the most predictive method by which to assess risk for the development for many medical disorders. Genetic testing is not limited to adults or even children. Preimplantation genetic diagnosis or PGD is a term used to describe the testing of human embryos in a laboratory for genetic disorders. 11,12 PGD is performed in conjunction with in vitro fertilization or IVF. IVF was developed as a modality for helping couples suffering from infertility. The procedure is accomplished by surgically retrieving eggs from human ovaries and fertilizing these with sperm in a laboratory. These fertilized eggs, or embryos, are then grown in the laboratory for 3 to 6 days and then placed in the mother's uterus. More than 20 years ago, some laboratories began taking one or two cells from these developing embryos and conducting genetic tests on these cells. 13,14 In this way, limited amounts of genetic information could be obtained about the embryo, and this guided which embryos were placed into the uterus and which embryos were diagnosed with problems. As technology advanced, more detailed genetic analysis was possible, and specific genetic disorders that were known to exist in parents were able to be avoided in offspring through this process. PGD allows the selection of embryos with certain characteristics for uterine transfer and is, therefore, fundamentally different from purely diagnostic technologies such as fetal evaluation through maternal cell free DNA. However, the early days of PGD were limited to testing for specific known parental genetic mutations and did not offer any insights into traits that could be perceived as otherwise advantageous such as intelligence, strength, and so on. Something that could be evaluated, however, was the sex of the embryo. There is increasing acceptance of the utilization of this technology in certain instances. For example, if there is a medical disorder in a couple's family that is sex-linked, that is, unmasked only in one gender, PGD for sex selection is generally accepted as an appropriate medical test. [SEP] Justify:

Output: The text corroborates the claim by discussing how genetic testing, particularly through techniques like preimplantation genetic diagnosis (PGD), can provide critical insights into genetic disorders, thus relating to health risks. As mentioned, advancements in genetic analysis allow for the avoidance of specific genetic disorders in offspring. Furthermore, the text implies that as more genetic markers are cataloged, the predictive capability of genetic testing concerning disease development will improve, aligning closely with the idea that genetic testing can provide insights into potential health risks.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: Sustained RAAS activation, characterized by increased levels of angiotensin-converting enzyme (ACE), angiotensin II (Ang II) and Ang II type 1 receptor (AT1R), leads to NADPH oxidase activation, which activates MMP-2 and increases the expression of pro-fibrotic connective tissue growth factor (CTGF) and TGF-β1. This cascade of events leads to cardiac fibrosis and remodeling in aged rats[126]. In the thoracic aorta of old mice, the prorenin receptor (PRR) -ACE-Ang II-AT1R axis is activated, whereas the ACE2-Mas receptor (MasR) axis is inhibited. This altered expression of RAS components correlates with fibrosis and oxidative stress in the aging aorta[127]. Additionally, similarly to old rats, young adult animals develop cardiomyocyte hypertrophy and vascular remodeling when they are chronically treated with angiotensin II[126]. In contrast, mice with smooth muscle cell mineralocorticoid receptor (MR) deletion are protected from age-related vascular and cardiac stiffening and fibrosis[128]. Moreover, protease-activated receptor (PAR) 2 is a significant regulator of pro-fibrotic PAR1 and TGF-β signaling in the heart[129]. Levels of PAR2 decrease with age in the aortas of rats with metabolic syndrome[130]. Aged PAR2-knockout mice exhibit cardiac fibrosis and diastolic dysfunction with higher transcription of TGF-βR and PAR1 compared to WT mice[129]. Treatment with vorapaxar, a PAR1 antagonist, reduces cardiac collagen deposition by 44%, inflammation, and TGF-β expression in a metabolic disease model of apolipoprotein E-knockout mice, which also demonstrate cardiac fibrosis and with Fraction (HFpEF)[129]. Therefore, PAR2, TGF-β, and RAAS play an important role in aging-related fibrosis of the heart and vessels. Telomere dysfunctionTelomeres are DNA-protein complexes that cap the end of each chromosome arm in order to maintain chromosomal stability and integrity[131]. In proliferating tissues, telomeres become shortened with cell cycle divisions. [SEP] Justify:

Output: The text contrasts the claim by discussing several biological processes associated with aging, such as the activation of the RAAS and the decrease of PAR2 levels. It details how these mechanisms contribute to cardiac fibrosis and remodeling, indicating that aging is linked to complex cellular changes rather than being eliminated by genetic interventions. The mention of telomere shortening further supports the idea that aging inherently involves cellular changes that are not simply reversible.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Большинство находит какой-нибудь прием и начинает бессмысленно «сидеть» на нем, наслаждаясь звучанием, тем и ограничиваются. Если бы все было так просто, то композитором мог бы стать любой, причем не обязательно человек с музыкальным образованием… И где-то сегодня так нередко и происходит. Не всем можно объяснить, что это пока еще не музыка. [SEP] Justify:

Output: The text discusses the enjoyment of sound and the notion of composition, but does not address the claim about insects communicating through sounds and music. Therefore, it is irrelevant to the claim.


Input: Task: pass the claim using the given text. Claim: A single gene determines all aspects of a person's intelligence. [SEP] Text: In the experiments performed to rescue flight duration in Set2RNAi individuals the authors overexpress STIM and attribute the effect to "Excess STIM presumably drives higher SOCE sufficient to rescue flight bout durations caused by deficient Set2 levels. ". This should be experimentally tested as the STIM:Orai stoichiometry has been demonstrated as essential for SOCE. The assumption that STIM overexpression drives higher SOCE is based upon previously published work from Drosophila neurons (Agrawal et al. , 2010; Chakraborty et al, 2016; Deb et al. , 2016) which demonstrates that excess overcomes IP3R deficiencies (RNAi or hypomorphic mutants) to rescue SOCE. We agree that STIM-Orai stoichiometry is essential for SOCE, and propose that the rescue backgrounds possess sufficient WT Orai, which is recruited by the excess STIM to mediate the rescue. We have referenced the earlier work to validate our use of for rescue of SOCE (226-233). Here, we propose that Set2 is part of a positive feedback loop (see Lines 286-307) driving transcription of mAChR and IP3R (Figure 3F). In keeping with this hypothesis, we posit that the phenotypes observed in the Set2RNAi background (Figure 2D) result from decreased itpr and mAChR expression (validated in Figure 3E). This is further validated by the Set2 overexpression mediated rescue of OraiE180A (Figure 2D) and rescue of itpr/mAChR expression in the OraiE180A background (Figure 3B-E; THD’>OraiE180A; Set2OE). The authors show that overexpression of OraiE108A results in Stim downregulation at a mRNA level. What about the protein level? And more important, how does OraiE108A downregulate Stim expression? Does it promote Stim degradation? Does it inhibit Stim expression? [SEP] Justify:

Output: The text is irrelevant to the claim regarding intelligence, as it discusses the experimental results related to STIM and SOCE in a biological context without addressing the concept of intelligence or genetic determinants of intelligence. Thus, the text does not corroborate or contrast the claim.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: When they reach a critical length, they cannot bind enough proteins on the cap and are sensed as exposed DNA ends, leading to proliferation arrest and senescence-associated secretory phenotype (SASP)[132,133]. Impairments in telomere length maintenance are related to cardiovascular function impairments. Leukocyte telomere shortening is a risk factor for CVD[134]. Telomerase deficient (Terc-/-) mice of generation 3 (G3) develop severe ventricular dysfunction, impaired mitochondrial biogenesis and function[135,136], enhanced apoptosis, cardiomyocyte hypertrophy[137], and vascular endothelial dysfunction similar to aged WT mice[138]. Aged mice with a deficiency in telomeric repressor activator protein 1 (Rap1) (Rap1-/-) show telomere shortening, DNA damage, lower cardiac fatty acid metabolism, and development of aging-associated cardiac structural and functional changes[139]. Nevertheless, it should be noted that there are differences between the length and role of telomeres in senescence between rodents and humans. Specifically, although rodents have longer telomeres and ubiquitous telomerase expression, they have shorter lifespans than humans[133]. Also, in contrast with humans, telomere length does not determine the proliferative capacity of mouse cells[140,141]. However, cardiomyocytes are postmitotic cells, and their ability to proliferate is limited. Thus, telomere dysfunction in cardiomyocytes is less likely due to telomere shortening[142] but due to DNA damage within telomeres[133], which can be caused by oxidative stress[143]. Specifically, length-independent telomere damage occurs in aged cardiomyocytes via the activation of the classical senescence-inducing pathways, cyclin-dependent kinase inhibitor 1 (p21CIP) and p16Ink4a, and leads to a non-canonical SASP, which induces myofibroblast activation and cardiomyocyte hypertrophy[143]. Therefore, telomere dysfunction is an additional cause, beyond oxidative stress, mitochondrial dysfunction, impaired autophagy, inflammation, and fibrosis, that leads to cardiovascular aging. investigate the pathophysiology of cardiovascular aging and identify potential therapeutic targets, various animal models are used [Table 1]. [SEP] Justify:

Output: The text contrasts the claim by explaining mechanisms related to telomere dysfunction and its relation to aging, detailing that while telomeres are involved in cellular aging, specifically in cardiomyocytes, the causative factors of cardiovascular aging extend beyond telomere length and dysfunction. The mention of oxidative stress, mitochondrial dysfunction, inflammation, and fibrosis suggests that there are multiple factors contributing to aging, indicating that genetic anti-aging interventions have not eliminated all signs of aging at the cellular level.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Это то же самое, как если бы вы в лесу нашли пень, напоминающий кого-то, кого все знают, и выдали бы его за свою художественную работу. Я часто привожу такой пример. Допустим, я вхожу в зону действия сильного магнитного поля и широким жестом сеятеля разбрасываю металлический порошок. Под действием магнитного поля он ложится ровными красивыми спиралями. Есть ли логика в получившейся картине? Несомненно, есть! Значит, мы можем говорить о гармонии? Разумеется, можем. [SEP] Justify:

Output: The text does not address the claim regarding insect communication. Instead, it presents a metaphorical description involving magnetic fields and metal powder, which is unrelated to the topic of insect communication through sounds or music.


Input: Task: pass the claim using the given text. Claim: Cloning humans is already possible and has been secretly performed. [SEP] Text: In 1854, Siemens built the first ozone generator. At that time, it was already known that ozone was unstable, having to be produced and then used. With the construction of the ozone generators, its use was initiated in industrial applications, or even to clean water, promoting its potent microbicidal action. 10 Ozone has been used for the treatment of drinking water in Europe since the beginning of the 20th century, without loss in the organoleptic properties, and in relation to microorganisms, its action is as effective as chlorine. 12 Payr, an Austrian physician, Fisch, a Swiss dentist, and Wolff, a German physician are the pioneers in clinical research involving ozone,1 though their observations were empirical. Currently there are scientific reports that prove the benefits of ozone in the treatment of wounds, dental use, disinfection, treatment of herniated disc and hepatitis C. 13 Ozone therapy: use of ozone in medicine The practice of ozone began in tuberculosis treatment, followed by its use in dental clinics and gangrene treatments. The surgeon Payr was the first one to be use the ozone rectal route. 14 However, the inappropriate use of gas via intravenous by individuals with no practice in ozone therapy or in medicine resulted in death by embolism. In this way, the use of ozone was condemned in some countries. 10 Ozone has the ability to assist in eliminating bacteria, viruses and parasites as well as biofilms. In this context, it was assumed that the intravenous injection of a gas mixture composed of O2 and O3 into bacterial sepsis in patients with HIV would inactivate the pathogens and would cure the disease. In the early 1990’s, technicians migrated to Africa and to to perform such procedure; indeed, it was seen that intravenous administration of O2–O3 caused embolism and patients’ death. The ozone administration by intravenous route has been banned in Europe since 1984. 13 The use of ozone should never be used by inhalation or injection in accordance with the on Ozone Therapy. 15 However, there are publication proving the security of ozone by inhalation route in low concentrations. 16 In countries such as Cuba, Russia and Ukraine this therapy is widely used for several treatments, in form of infusion of ozonated saline solution and rectal ozone insufflations due to the low cost and the applicability in thousands of patients. [SEP] Justify:

Output: The text does not address the claim regarding human cloning; instead, it discusses the historical development and medical applications of ozone therapy. As such, it lacks any relevant information that corroborates or contrasts with the claim about human cloning, rendering it irrelevant.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: Mice at 24 months of age, which are equivalent to 70-year-old humans, have increased left ventricular mass, enhanced fibrosis, aortic stiffness, and decreased cardiac diastolic function[144,145]. Rhesus monkeys (Macaca mulatta), which have a median lifespan of 25 years, are also used in gerontology research of the cardiovascular system due to their 92. 5%-95% genetic homology to humans and their ability to develop cardiac fibrosis and hypertrophy[146]. Although the naturally aging models are most suitable for these studies, models of premature aging, artificially induced aging models, and genetically modified models are also used. Table 1Animal models of cardiovascular agingModelRelevance to agingCardiovascular phenotypeRefs. 1. Natural agingAged C57BL/6J miceCardiac hypertrophy and dysfunction, enhanced fibrosis, aortic stiffness[217,218]344 ratsLV hypertrophy, diastolic dysfunction, abdominal aorta with decreased sodium nitroprusside-mediated relaxation[219,220]344/F1 ratsLV dilatation, mild hypertrophy, fibrosis, LV diastolic and systolic dysfunction[221]macaque (Macaca mulatta)Myocardial fibrosis, cardiac hypertrophy, aortic valve calcification[146]2. Premature agingSenescence-accelerated prone (SAMP) miceSelective inbreeding of AKR/J mice with inherited senescenceCardiac diastolic dysfunction, cardiac fibrosis, vascular dysfunction[148,222]Mus musculus castaneus (CAST)Mice with short telomeres from birthCardiac dysfunction, hypertrophy, fibrosis and senescence[149]3. Chemically induced agingD-galactose-induced aging in mice and ratsD-galactose treatment increases the levels of senescence-associated β-galactosidase (SA-β-gal) Increase in heart weight, cardiac hypertrophy, cardiac fibrosis and LV dysfunction[150]4. [SEP] Justify:

Output: The text contrasts the claim by discussing various aging models in mice and monkeys, highlighting that these models exhibit signs of aging such as increased left ventricular mass, enhanced fibrosis, and decreased cardiac function. This implies that aging persists at the cellular level despite any interventions, indicating that there is no evidence provided that supports the claim of complete elimination of aging signs.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Но является ли это произведением искусства? Нет, конечно, как не является произведением искусства морозный узор на окнах. И картина, нарисованная хвостом непокорного мула, тоже — как бы она ни была любопытна и оригинальна. Для меня пространство, организованное без участия интеллекта творца, никак не может быть произведением музыкального искусства. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses the nature of art and music without mentioning insects or their communication methods. It focuses on whether certain forms can be classified as art rather than addressing any aspects of insect communication.


Input: Task: corroborate the claim using the given text. Claim: Nanotechnology is used in medicine to deliver drugs more precisely to specific cells. [SEP] Text: Impact factor12. 4 ISSN: 1838-7640Aims and scope Editorial board Author info Submit manuscript Manuscript login issue 2024 2023 2022 2021 2020 534. Full text PDF Nanotheranostics 2024; 8(4): 506-520. Full text of of Journal of reach, higher impact PDF Theranostics 2020; 10(8):3474-3487. doi:10. 7150/thno. 39434 This issue cell-derived exosomes home to their cells of origin and can be used as Trojan horses to deliver cancer drugs Li Qiao1,2,3, Shiqi Hu1,2, Ke Huang1,2, Teng Su1,2, Zhenhua Li1,2, Adam Vandergriff1,2, Jhon Cores1,2, Phuong-Uyen Dinh1,2, Tyler Allen1,2, Deliang Shen1,2,4, Hongxia Liang1,2,5, Yongjun Li3, Ke Cheng1,2, 1. Department of. 2. Department of Biomedical Engineering, University of North Carolina, Chapel Hill, and. 3. Department of Cardiology, Hospital of University, Shijiazhuang, China. 4. Department of and Hepatology, of Zhengzhou University, Zhengzhou, China. 5. Department of Cardiology, of Zhengzhou University, Zhengzhou, China. ✉ Corresponding author: Ke Cheng. Tel: (919)5137371; Email: Ke_Chengedu or Ke_Chengedu Citation:. Tumor cell-derived exosomes home to their cells of origin and can be used as Trojan horses to deliver cancer drugs. Theranostics 2020; 10(8):3474-3487. doi:10. 7150/thno. 39434. styles go to File – Import. Select the file that you have just downloaded and select import option (RIS). Click on Import. File import instruction is the second leading cause of death worldwide and patients are in urgent need of therapies that can effectively target cancer with minimal off-target side effects. Exosomes are extracellular nano-shuttles that facilitate intercellular communication between cells and organs. [SEP] Justify:

Output: The text corroborates the claim by stating that 'Tumor cell-derived exosomes home to their cells of origin and can be used as Trojan horses to deliver cancer drugs.' This indicates the use of nanotechnology, in the form of exosomes, for precise drug delivery to specific cells, thus supporting the claim.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: Progeria modelsLmnaG609G/G609G miceLMNA point mutation (G609G) that activates a cryptic donor splice site and produces progerin, a truncated form of prelamin AHutchinson-Gilford progeria syndrome (HGPS), cardiac fibrosis, electrocardiographic alterations, cardiac diastolic dysfunction, HFpEF[157]LmnaN195K/N195K miceLMNA missense mutation (N195K) in lamins A and CDilated cardiomyopathy with conduction system disease[223]LmnaH222P/H222P miceLMNA missense mutation (H222P) identified in a family with autosomal dominant Emery-Dreifuss muscular dystrophy (EDMD)[224]Hypomorphic BubR1 mutant(BubR1H/H) miceReduced expression of spindle assembly checkpoint kinase BubR1, leading to chromosome number instabilityCardiac arrhythmias, arterial wall stiffening[225,226] 5. Mitochondrial mutationsCardiac-specific termed Y955C Polg mutant micePolg point mutation (Y955C) leading to mtDNA depletionLV hypertrophy, increased ventricular volume[160,227]D257A Polg mutant micePolg mutation (D257A) in the N-terminal "proofreading" exonuclease domain, resulting in a protein without polymerase proofreading function in mitochondriaBiventricular hypertrophy, fibrosis, heart failure, arterial stiffening[161,228]Tafazzin-deficient miceMice lacking tafazzin, a mitochondrial transacylase essential for cardiolipin remodelingBarth syndrome, LV dilation, reduced ejection fraction [229]heart/muscle-specific Mn-SOD-deficient mice (H/M-Sod2-/-)Mice with a specific in the heart and skeletal muscle loss of manganese superoxide dismutase (Mn-SOD) expression, a principal scavenger enzyme in mitochondrial matrixDilated cardiomyopathy, reduced cardiac contractility[230]6. [SEP] Justify:

Output: The text contrasts the claim by discussing various mutations in mice related to different medical conditions, such as heart failure and hypertrophy, without providing evidence that any genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. Instead, it describes genetic conditions that lead to aging-related issues, indicating that the text does not support the claim of eliminating signs of aging.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: И применяться интеллект должен прежде всего через художественный образ, который соединяет в себе созерцание, субъективную интерпретацию и авторскую оценку. Все это порой бывает очень трудно объяснить молодому композитору, который, находясь под сильным впечатлением от своих находок, не понимает, почему звучание не самодостаточно и зачем нужно городить огород: применять интеллект, выстраивать систему образов. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses the application of intellect through artistic imagery and the challenges faced by a young composer, without addressing the communication methods of insects or any claims related to sound and music.


Input: Task: corroborate the claim using the given text. Claim: Nanotechnology is used in medicine to deliver drugs more precisely to specific cells. [SEP] Text: It has been established that tumor-derived exosomes contain a similar protein and lipid composition to that of the cells that secrete them, indicating that exosomes might be uniquely employed as carriers for anti-cancer therapeutics. Methods: We isolated exosomes from two cancer cell lines, then co-cultured each type of cancer cells with these two kinds of exosomes and quantified exosome. HT1080 or Hela exosomes were systemically injected to Nude mice bearing a subcutaneous HT1080 tumor to investigate their cancer-homing behavior. Moreover, cancer cell-derived exosomes were engineered to carry Doxil (a common chemotherapy drug), known as D-exo, were used to detect their target and therapeutic efficacy as anti-cancer drugs. Exosome proteome array analysis were used to reveal the mechanism underly this phenomenon. Results: Exosomes derived from cancer cells fuse preferentially with their parent cancer cells, in vitro. Systemically injected tumor-derived exosomes home to their original tumor tissues. Moreover, compared to Doxil alone, the drug-loaded exosomes showed enhanced therapeutic retention in tumor tissues and eradicated them more effectively in nude mice. Exosome proteome array analysis revealed distinct integrin expression patterns, which might shed light on the underlying mechanisms that explain the exosomal cancer-homing behavior. Conclusion: Here we demonstrate that the exosomes' ability to target the parent cancer is a phenomenon that opens up new ways to devise targeted therapies to deliver anti-tumor drugs. Keywords: exosome, homing, integrin, doxorubicin, cancer therapy is a life-threating public health problem responsible for an estimated 9. 6 million deaths worldwide in 2018 [1]. The most common treatment option available for cancer patients is chemotherapy. While chemotherapeutic drugs can inhibit the progression of cancers and even suppress cancer to the point of remission, they come with many serious side-effects. The systemic infusion of chemotherapy drugs can cause cardiomyopathy, vomiting, asthenia, and alopecia due to their inability to target the cancerous tissue of the body exclusively. Therefore, effective new targeted cancer treatments are urgently needed. Tumor cells produce and secrete more nucleic acids, proteins, and lipids than healthy cells. [SEP] Justify:

Output: The text corroborates the claim by providing information about the use of tumor-derived exosomes, which can serve as carriers for anti-cancer therapeutics, thereby demonstrating a method of drug delivery that targets specific cancer cells. The engineered exosomes carrying Doxil, a chemotherapy drug, show enhanced therapeutic retention in tumor tissues and increase effectiveness against tumors, which supports the idea that nanotechnology can be used to deliver drugs precisely to specific cells.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: Other global gene mutationsKlotho-deficient (KL-/-) miceKnock-out of KlothoImpaired cardiac function, increased heart size, increased LV myocardial mass[57]G5 telomerase-deficient (telomerase RNA component, TERC-/-) miceTelomerase-deficient mice after G3 generation have short telomeres, aneuploidy, and end-to-end chromosome fusionsPathological cardiac remodeling, severe ventricular dysfunction[231,232]Pim triple knock-out mice (Pim1-/-, Pim2-/- and Pim3-/-)Mice lacking Pim kinases, which are highly conserved serine/threonine kinases, have altered mitochondrial morphology Cardiac hypertrophy, heart failure, cardiac fibrosis[233]Interleukin-10 knockout IL-10(tm/tm) miceMice lacking IL-10, which is an anti-inflammatory cytokineStiffer vessels, reduced vascular relaxation, asymmetric hypertrophy, systolic and diastolic dysfunction[234]DNA-helicase-regulatory protein (WRN) WRN-K577M mutant miceAmino acid substitution of WRN at position 577 eliminates the ATPase and helicase activityWerner syndrome, diastolic LV dysfunction, cardiac fibrosis and hypertrophy[235]The senescence-accelerated mouse prone (SAMP) 8 is a model of accelerated aging that was developed by selective inbreeding of AKR/J mice with inherited senescence[147]. SAMP8 mice are especially used in studies of cardiovascular aging, since they show accelerated aging, increased cardiac fibrosis, and diastolic dysfunction at 6 months of age[148]. Wild mouse strain Mus musculus castaneus (CAST), which have short telomeres from birth, are also used as a model of cardiac aging, as they develop cardiac diastolic dysfunction by their 1st year of age[149]. Another model of cardiovascular aging is the D-galactose-induced aging model, which uses 2-3-month-old rodents treated with D-galactose injections at doses of 100-500 mg/kg/day for 4-12 weeks[150]. [SEP] Justify:

Output: The text contrasts the claim by discussing various genetic interventions and models of aging in mice, detailing how these models exhibit signs of aging such as cardiac dysfunction and fibrosis. This indicates that while genetic models can provide insight into aging mechanisms, they do not demonstrate that genetic interventions eliminate all signs of aging. Specifically, the mention of conditions like cardiac hypertrophy, fibrosis, and diastolic dysfunction in various genetically modified mouse models highlights that signs of aging are still present and relevant, undermining the claim that these interventions have proven to eliminate signs of aging.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Приходится возвращаться назад к вопросу: а что такое вообще музыка? И порой встречаются такие, кто удивляется, что не все то музыка, что звучит. Студентам-первокурсникам очень важно сразу объяснить, как работают интуитивное и рациональное начала, то есть где следует опираться на ощущение, а где — на расчет. [SEP] Justify:

Output: The text does not address the claim regarding insects and their ability to communicate through sounds and music. Instead, it discusses the nature of music, the understanding of it, and how it is perceived, which is not relevant to the claim.


Input: Task: corroborate the claim using the given text. Claim: Nanotechnology is used in medicine to deliver drugs more precisely to specific cells. [SEP] Text: Some of these molecules are transported in the blood or encapsulated in extracellular microvesicles, such as exosomes, that are released into the extracellular environment. Once released, these exosomes become a part of a communication network used by other tumor cells and organs [2-4]. Tumor-derived exosomes contain an abundant biological content that resembles that of their parent tumor cell. These include transmembrane receptors, growth factors, angiogenic factors, and extracellular matrix (ECM) molecules [2]. In addition, they store intercellular signaling messengers involved in the pathogenesis, development, progression, and metastasis of cancer [3, 4]. Previous studies have proven the concept of delivering exosome-encapsulated molecules, including chemotherapeutics, to tumor sites. et. al. , for example, encapsulated doxorubicin in immature dendritic cell-derived exosomes for targeting αv integrin-positive cancer cells [5]. Herein, we utilize the abundance and ease of acquisition of cancer-derived exosomes to create an even more effective targeted delivery platform. To date, the signaling mechanisms involved in exosome release, transmission, and uptake have not been clearly described. Previous studies, including those from our lab, suggest that exosome can be absorbed by the parent cell line, as well as other cells of various origins [6-9]. However, they seem to most readily interact with cancer cells, compared to normal cells, and it appears that this interaction is driven, at least in part, by lipid mixing [10-12]. Since exosomes are extracellular nano-shuttles that facilitate intercellular communication between cells, the constitution of exosomes, as well as their biological activity, is largely dependent on the demands of their parent cells. Tumor-derived exosomes contain a similar protein and lipid composition to that of the cells that secrete them, indicating that exosomes might be uniquely designed to interact with their parent cell line in comparison to other cells. Thus, we hypothesized that tumor cell-derived exosomes might be especially effective at traveling back to the parent cell line that produced them. If so, their exosomes could be used as Trojan horses that deliver anticancer drugs to the cancer cells. [SEP] Justify:

Output: The text corroborates the claim by discussing the use of tumor-derived exosomes as a targeted delivery platform for anticancer drugs. It states that exosomes can encapsulate chemotherapeutics and target specific tumor cells, indicated by the phrase 'to create an even more effective targeted delivery platform.' This demonstrates the application of nano-sized carriers in drug delivery, aligning with the claim about nanotechnology's role in precisely delivering drugs.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: D-galactose administration increases the levels of senescence-associated β-galactosidase (SA-β-gal) in the cardiac tissue[151,152]. D-galactose treatment increases ROS levels and decreases cardiac levels of Nrf2, SIRT1 and phosphorylated AMPK, leading to oxidative stress and decreased autophagy[153], and activates NF-κB inflammatory signaling pathway[154]. In this way, D-galactose-induced aging models demonstrate LV wall thickening, cardiac fibrosis, and reduced cardiac function[150]. Mutations in the LMNA gene cause laminopathies, a number of disorders with a wide range of phenotypes, including premature aging and cardiomyopathy[155]. LMNA gene encodes the intermediate filament proteins, lamins A and C, which are major structural components of the nuclear lamina. Homozygous LmnaG609G/G609G mice express lamin A, lamin C, and progerin (a truncated form of prelamin A) with the same protein expression pattern of patients with Hutchinson-Gilford progeria syndrome (HGPS), and exhibit metabolic abnormalities, cardiac electrical alterations and HFpEF, similar to the normally aged mice[156,157]. Moreover, mice with mutations in the Polg gene, which encodes the mitochondrial DNA polymerase responsible for replication and repair of mtDNA, are also used as models of cardiovascular aging. Specifically, mice with a homozygous mutation in the exonuclease encoding domain of mitochondrial DNA polymerase gamma (Polg) (Polgm/m) develop an age-dependent accumulation of mtDNA mutations and display accelerated aging starting at 7-9 months of age. Also, they exhibit age-dependent cardiomyopathy, which is more severe than the usual phenotype of cardiac aging[39,158,159], and specifically demonstrate cardiac hypertrophy, dilatation, fibrosis and dysfunction by 13-14 months of age[153]. Transgenic mice for a cardiac-specific mutant of Polg (termed Y955C) develop LV hypertrophy at 94 days of age[160], while mice with a homozygous mutation in the encoding domain (D257A) of a proofreading deficient version of Polg develop biventricular hypertrophy at 10-12 months of age[161]. [SEP] Justify:

Output: The text contrasts the claim by detailing various mechanisms and effects of aging models in mice, particularly highlighting how mutations (e.g., in the LMNA and Polg genes) lead to accelerated aging and associated pathological changes, such as cardiac hypertrophy and dysfunction. This evidence suggests that genetic mutations do not eliminate signs of aging; rather, they contribute to accelerated aging and its manifestations.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: И очень важно, чтобы студент действительно осознавал, что такое фундаментальные понятия в музыке — не как-то интуитивно, а чтобы мог четко изложить, что такое гармония и форма… Парадоксально, но многие даже опытные музыканты, уже в возрасте, не понимают элементарных вещей. Именно поэтому периодически вспыхивают острые и оживленные дискуссии, например, о том, умерла мелодия или еще жива. [SEP] Justify:

Output: The text is irrelevant to the claim, as it discusses fundamental concepts in music, such as harmony and form, and the misunderstandings experienced by musicians. There is no mention of insects or their ability to communicate through sounds or music.


Input: Task: corroborate the claim using the given text. Claim: Nanotechnology is used in medicine to deliver drugs more precisely to specific cells. [SEP] Text: To test this idea, we investigated the biodistribution of tumor-derived exosomes, and profiled the proteome of exosomes from mouse tumor models. We found that exosomal integrins might direct the tumor-specific colonization of cancer exosomes. Remarkably, we found that the tropism exhibited by tumor-secreted exosomes can be utilized to shuttle Doxil, a cancer therapeutic with no specific targeting capacity, to tumor sites. exosomes home to their parent cells in vitro and in vivoTo detect whether tumor exosomes home to their parent cells in vitro, we isolated exosomes from HT1080 (a fibrosarcoma cell line) and HeLa (a cervical cancer cell line) cell lines. Flow cytometry was used to detect common exosome markers: CD81, CD63 and CD9 (Figure S1). We then co-cultured HT1080 cells with DiI-labeled-HT1080 exosomes or Dil-labeled-HeLa exos for 12 hours and quantified exosome uptake in HT1080 cells using fluorescence microscopy, the labeling efficiency is higher than 90% (Figure S2). We observed twice as much uptake of HT1080 exosomes versus HeLa exosomes in HT1080 cells (Figures 1 A-C). To make sure this finding was not an HT1080-specific phenomenon, we tested whether exosomes from HeLa cells would also exhibit parental cell tropism. We co-cultured HeLa cells with red (DiI) fluorescently labeled HeLa exosomes and green (DiO) fluorescently labeled HT1080 exosomes. Although both types of exosomes were internalized in HeLa cells, there was significantly more HeLa exosome uptake than HT1080 exosome uptake. Interestingly, HT1080 cells absorbed HT1080 exosomes about twice as efficiently as HeLa cells absorbed HeLa exosomes (Figures 1 D-E; Figures S3A-B). Then, the dye labeling for the exosomes were reversed to ensure that the uptake differences are not due to differences in labeling (Figures S3C-D). Subsequently, we designed another in vitro test, using a quantitative fluorometer to validate these findings. HeLa and HT1080 cells were seeded in different wells and treated with exosomes derived from the same cell type or the other. [SEP] Justify:

Output: The text corroborates the claim by presenting findings about tumor-derived exosomes that can be utilized to deliver cancer therapeutics like Doxil to tumor sites. The passage discusses how exosomes exhibit tropism towards their parent cells, indicating a mechanism by which drug delivery can be more precise, as it uses the natural behavior of exosomes to enhance targeting of cancer therapies. This aligns with the claim of using nanotechnology in medicine for targeted drug delivery.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: aiming to tackle aging-related features of cardiomyopathy have included environmental, dietary and pharmacological interventions. Maintaining a healthy lifestyle is strongly associated with a lower risk of developing age-associated chronic diseases, including CVD. However, pharmacological agents may be needed for the prevention or treatment of CVD, especially in the elderly. Some of the interventions that showed beneficial effects in preclinical studies have been or are presently tested in humans [Figure 2]. Figure 2. Interventions in preclinical studies that have translated into improvements in cardiac and/or vascular aging in humans (overlapping area) include exercise, caloric restriction, caloric restriction mimetics, such as spermidine, and SGLT2-inhibitors; image created on biorender. com. ExercisePhysical activity promotes healthy aging and prevents CVD[162-165]. Progressive and vigorous exercise for 1 year in previously sedentary people aged 65 and over induces physiological LV remodeling, increases stroke volume and total aortic compliance, and decreases arterial elastance[166], while studies in aged mice correlated the benefits of exercise with increased exercise capacity, improved diastolic function, physiological cardiac hypertrophy and increased cardiomyogenesis[167-169]. Even in mice expressing a proofreading-deficient version of Polg, endurance exercise for 5 months increases mitochondrial biogenesis and mitochondrial oxidative capacity and alleviates age-associated cardiomyopathy[170]. Another study demonstrated that both aerobic and resistance exercise for 8 weeks improves cardiac angiogenesis and aerobic capacity in aged rats, with aerobic exercise having more profound beneficial effects[171]. Additionally, aerobic exercise of moderate intensity for 12 weeks restores hydrogen sulfide levels, which is an endogenous gasotransmitter that has been linked with cardioprotective properties[172-174], decreases oxidative stress and lowers cardiac expression of markers of fibrosis and inflammation in aged rats[175]. Caloric restrictionA dietary approach associated with longevity is caloric restriction (CR), which is based on decreased intake of calories without malnutrition[176]. CR attenuates age-associated cardiac diastolic dysfunction and cardiac remodeling, as well as myocardial mitochondrial damage and lipid accumulation[177,178]. [SEP] Justify:

Output: The text contrasts the claim by describing various interventions such as environmental, dietary, and pharmacological approaches that target aging-related features but do not specifically mention genetic anti-aging interventions. The text emphasizes the importance of maintaining a healthy lifestyle and exercise in managing age-associated chronic diseases, suggesting that there is no definitive proof that any intervention fully eliminates signs of aging at the cellular level.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Никому не приходит в голову, что ответ на этот вопрос лежит на поверхности — в определении понятия мелодии. И когда говоришь или пишешь, что мелодия — это просто главный голос в гомофонной (или гомофонической) фактуре, на тебя смотрят с таким изумлением, будто ты изложил теорему Гаусса. То же самое с гармонией. Необходимо знать, что гармония — это система связи формообразующих элементов. [SEP] Justify:

Output: The text does not address the claim about insects communicating through sounds and music. Instead, it discusses the concepts of melody and harmony without any reference to insects or communication.


Input: Task: corroborate the claim using the given text. Claim: Nanotechnology is used in medicine to deliver drugs more precisely to specific cells. [SEP] Text: HT1080 exosomes were three times more efficiently absorbed by HT1080 cells than HeLa cells, and HeLa exosomes were absorbed mainly by HeLa cells as opposed to HT1080 cells (Figure 1 F; Figure S3E). Therefore, the cell specificity of exosome localization matched the cell of origin of the exosome, suggesting a more efficient uptake of exosomes by parent cancer cells compared to cells of other origins. To substantiate this finding in vivo, we created an HT1080 tumor model using immunodeficient nude mice, and intravenously injected them with DiR-labeled HT1080 or HeLa exosomes (Figures S4A-B). The exosomes' biodistribution was detected with an IVIS imaging system. HT1080 exosomes preferentially localized to tumor tissue. In fact, the expression of the fluorescent signal for HT1080 exosomes is more than three times that of the HeLa exosomes. By contrast, HeLa exosomes abundantly presented in major organs (64. 86% in the liver) rather than colonizing the tumor site (Figures 1 G-H). Taken together, our data suggest that cancer exosomes preferentially home to their parent cancer cell of origin. Figure 1 Cancer cell derived exosomes preferably fuse with their parent cells. (A) Schematic showing the in vitro study design to assess the homing ability of cancer exosomes. (B) Representative micrographs showing uptake of DiI-labeled HT1080 exosomes and HeLa exosomes by HT1080 cells. Endocytosed exosomes (red) can be seen around nuclei. Scale bar: 5µm. (C) Quantitation of exosomal uptake in (B) (n=6). (D-E) Quantitation of exosomal uptake in HeLa cells and HT1080 cells (n=6). (F) Quantitation of exosomal uptake by (n=10-12). (G-H) Exosomes biodistribution in vivo. p/s: photons/second. (G) Quantitation of fluorescence of DiR-labeled-exosomes in major organs and tumor tissues (n=3). (H) Quantitation of the percentage of exosomes in major organs and tumor tissue (n=3). [SEP] Justify:

Output: The text corroborates the claim by demonstrating that HT1080 exosomes preferentially localize and are absorbed by HT1080 cells compared to HeLa cells, which indicates a specific delivery mechanism. The efficient uptake of exosomes by their parent cancer cells suggests that nanotechnology can enhance drug delivery precision to targeted cells in a medical context.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: Enhancement of autophagy is one of the possible mechanisms via which CR protects against cardiac aging, since it activates the AMPK-forkhead box O (FOXO)-autophagy pathway and suppresses the mTOR pathway[177,178]. Additionally, CR partially reduces age-associated cardiac insulin resistance through the activation of the PI3K/Akt pathway in rats[179]. In arteries of old mice, CR can also prevent large elastic artery stiffness and endothelial dysfunction by inhibiting NADPH oxidase and increasing the activity of SOD and catalase[180], which combinedly attenuate oxidative stress. Thus, exercise decreases oxidative stress, while CR enhances autophagy, resulting in physiological LV remodeling and improved cardiac function, leading to the conclusion that a healthy lifestyle promotes healthy cardiovascular aging. Caloric restriction mimeticsMimetics (CRMs) produce similar beneficial effects[181,182]. Resveratrol, a polyphenol found in grapes and red wine, prevents age-associated cardiac dysfunction and reverts age-related increase of inflammatory, oxidative and apoptotic markers, including TNF-α, NFκB and nitric oxide synthase, in hearts of rodents[183,184]. Resveratrol also improves doxorubicin-induced cardiotoxicity via restoration of SIRT1 activity in the hearts of aged SAMP8 mice[185], while it ameliorates cardiac remodeling in mice with HFpEF due to inhibition of the TGF-β/Smad3 signaling pathway[186]. Curcumin, a phytochemical derivative of turmeric, ameliorates vascular oxidative stress, increases nitric oxide bioavailability and alleviates age-related arterial dysfunction in mice[187], as well as in healthy middle-aged and older humans[188]. Curcumin also induces autophagy by increasing the expression of SIRT1 and AMPK phosphorylation and decreasing mTOR phosphorylation in a dose-dependent manner[153]. Polyamine spermidine is another inducer of autophagy that reverses age-associated cardiac hypertrophy, fibrosis, diastolic dysfunction and arterial dysfunction in mice[189-191]. [SEP] Justify:

Output: The text contrasts the claim by detailing various interventions, such as caloric restriction and the use of phytochemicals like resveratrol and curcumin, that may help improve aspects of aging, particularly in cardiac health. However, it does not assert that these interventions eliminate all signs of aging at the cellular level, instead suggesting they may ameliorate certain aging effects, indicating that the claim is overstated.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: На уровне формы целого она применяется не к «первокирпичам», а к уже полученным минимальным структурно-семантическим единицам музыкального языка, и выстраивает смысловую организацию на следующем этапе, где, если условно провести параллели с естественным человеческим языком, слова соединяются в осмысленные предложения. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses the structuring of musical language and its semantic organization, without any mention of insects or their ability to communicate through sounds and music.


Input: Task: corroborate the claim using the given text. Claim: Nanotechnology is used in medicine to deliver drugs more precisely to specific cells. [SEP] Text: (C-H) Two-tailed t-test. *, p<0. 05. **, p<0. 01. ***, p<0. 001. All values are mean ± S. D. D-exo fabrication and characterizationHaving established the homing ability of cancer exosomes, we hypothesized that anti-cancer drugs could be loaded into them and shuttled by them to tumor sites. We incorporated Doxil, an anti-cancer chemotherapy drug that encapsulates doxorubicin in a closed lipid sphere, into HT1080 exosomes via membrane extrusion (Figure 2A). Transmission electron microscopy (TEM) showed the morphology of exosomes, Doxil and D-exo (Figures 2B). The size distribution of the Doxil-loaded exosomes (D-exo), measured by a nanop7. 4) at 4°C for 7 days. To imitate the in vivo environment in which they will end up, they were placed in fresh serum at 37°C for 24 hours. NanoSight were employed to monitor the stability of D-exo in these two environments over time. The D-exo showed no obvious aggregation in PBS buffer or serum (Figures S7B-C), indicating superior stability. The drug-release behavior of D-exo was examined by monitoring doxorubicin released from the exosome at pH 7. 4 (physiological environment) and 5. 0 (late endosome) [13]. D-exo released a small amount of doxorubicin at PH 7. 4, which suggests that the drug was well protected by the exosomes in blood circulation. Conversely, a relatively rapid and massive release of doxorubicin was detected at PH 5. 0, followed by a slow and continuous release thereafter (Figure S7D). Since the extracellular PH of tumor tissues is often acidic [14], these data suggest that drug was released promptly and substantially from D-exo after entering cancer tissues and late endosomes of cancer cells. Figure 3 Cancer cells uptake D-exo in vitro. (A) Intracellular distribution of Doxil, D-HeLa exo, and D-HT1080 exo in HT1080 cells. Scale bar: 20µm. [SEP] Justify:

Output: The text corroborates the claim by detailing how cancer exosomes can be utilized to load anti-cancer drugs like Doxil and deliver them to tumor sites. It explains the methodology of loading the drug into exosomes and their behaviors in different pH environments, indicating effective delivery to cancer cells, which aligns with the assertion that nanotechnology enhances precision in drug delivery.


Input: Task: contrast the claim using the given text. Claim: Genetic anti-aging interventions are proven to eliminate all signs of aging at the cellular level. [SEP] Text: Spermidine inhibits ROS accumulation and improves mitochondrial function through activation of the SIRT1/peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) signaling pathway in the myocardium of aged rats, leading to attenuation of cardiac senescence[192]. A prospective, population-based cohort study associated dietary intake of spermidine with reduced risk of fatal heart failure, acute coronary artery disease, and death due to vascular disease[190]. Additionally, sulforaphane, an antioxidant found in cruciferous vegetables, upregulates NRF2 activity, improves mitochondrial function, enhances autophagy, has beneficial effects on insulin resistance, and reverses cardiac dysfunction in aged mice[193]. Dasatinib and quercetinThe combination of dasatinib and quercetin (D+Q) induces senolysis, which is the process of selective removal of senescent cells, and is considered to have beneficial effects in age-related pathologies[194]. D+Q administration for 1 month improves cardiac remodeling and diastolic function by removing senescent cardiac non-myocyte and myocyte cells and cardiac stem/progenitor cells in aged female mice after myocardial infarction[195], whereas longer (3 months) treatment with D+Q ameliorates vasomotor function by increasing NO bioavailability and reduces aortic calcification in aged mice[196]. Although systolic dysfunction is not a common feature of cardiac aging in mice, another study found that EF is also improved as soon as 5 days after a single dose of D+Q in aged mice[197]. mTOR inhibitorsRapamycin, an FDA-approved mTOR inhibitor, improves both age-related cardiac systolic and diastolic function in mice[198] and dogs[199]. This improvement in diastolic function, along with a reduction in cardiac hypertrophy and passive stiffness, is observed in aged mice, even 8 weeks after discontinuation of an 8-week treatment[200]. Improvement in cardiac and skeletal muscle function by rapamycin is also seen in Lmna-/- mice[201]. Moreover, rapamycin ameliorates arterial dysfunction via suppression of oxidative stress, activation of arterial AMPK, and increased PTEN expression in old mice[64]. [SEP] Justify:

Output: The text contrasts the claim by discussing various interventions, such as spermidine, dasatinib combined with quercetin (D+Q), and rapamycin, which show promise in improving age-related conditions and functions. However, none of these methods are described as 'proven' to eliminate all signs of aging at the cellular level, and they focus on specific improvements rather than a complete eradication of aging signs. The mention of 'beneficial effects in age-related pathologies' implies that while there may be improvements, aging is not completely eliminated.


Input: Task: pass the claim using the given text. Claim: All insects can communicate through sounds and music. [SEP] Text: Эта иерархия также обязана иметь центральный элемент, и тональность, таким образом, есть сквозное главенство центрального элемента на уровне композиции в целом. На определенном этапе гармония превращает множество в пространство, в котором появляются измерения (координаты). Считается, что звук не имеет отношения к пространству — очевидно, речь здесь идет о привычном трехмерном пространстве «длина-ширина-высота». [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses the hierarchy and tonal elements in music composition without mentioning insects or their communication methods. Therefore, it does not provide any information that would support, contradict, or relate to the claim about insects.


Input: Task: corroborate the claim using the given text. Claim: Nanotechnology is used in medicine to deliver drugs more precisely to specific cells. [SEP] Text: (B) Quantitation of the percentage of positive Doxorubicin in indicated treatment groups (n=6). One-way ANOVA with Bonferroni post hoc correction. ***, p<0. 001. All values are mean ± S. D. (C-D) Cell viability of (C) HeLa cells or (D) HT1080 cells exposed to D-HeLa exo, D-HT1080 exo, Doxil, and PBS control (n=3). One-way ANOVA with Bonferroni post hoc correction. *, p<0. 01 compared to control. #, p<0. 05 compared to Doxil. All values are mean ± S. D. Tumor uptake and inhibitionDiO-labeled D-exo and free Doxil were incubated with HT1080 cells for 12 hours. As shown in Figure 3A, strong D-exo signals were dispersed within the cytoplasm, which suggests that D-exo were taken up by the cells. By 12 hours, doxorubicin had dissociated from the D-exo and distributed throughout the cytoplasm and nuclei of HT1080 cells. To estimate cellular uptake efficiency, D-exo labeled with DiO were incubated with HT1080 cells for 12 hours. The cellular uptake efficiency of Doxil from D-HT1080 exo, D-HeLa exo, and free Doxil were 48. 46%, 34. 00%, and 20. 10%, respectively (Figure 3B). Although D-exo and Doxil are similar in size and morphology, cellular uptake of D-HeLa exo was nearly twice as high as that of Doxil, which indicates the preferential uptake of exosome-coated Doxil compared to bare Doxil. Moreover, HT1080 cells internalized D-HT1080 exo was twice as much as D-HeLa exo, indicating the cell-type tropism of cancer exosomes. A Kit-8 (CCK-8) assay was used to assess the viability of HT1080 and HeLa cells in response to the growth-inhibition/cytotoxic effects of D-HeLa exo, D-HT1080 exo, or Doxil (with equivalent doxorubicin) and free exosomes. [SEP] Justify:

Output: The text corroborates the claim by discussing the effective cellular uptake of nanotechnology-based drug delivery systems, specifically exosomes encapsulating Doxorubicin (referred to as D-HeLa exo and D-HT1080 exo) in cancer cells. It indicates that these exosomes, which represent a form of nanotechnology, demonstrate enhanced uptake compared to free Doxil, suggesting a more precise delivery mechanism targeting specific cell types, as noted in the statement that D-HeLa exo had nearly twice the cellular uptake compared to bare Doxil.