Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: Exposure to complex chlorinated organic compounds, some of which are probable carcinogens, may occur through contact with slimicides (e. g. , pentachlorophenol), pesticide-treated wood, or compounds formed during the bleaching process. Welders are exposed to hexavalent chromium in stainless steel welding. Perhaps most importantly from a cancer risk perspective, in the past workers (especially maintenance workers) were commonly exposed to asbestos. Table 1Occupational exposures in the pulp and paper industry Production area/job Potential exposures Raw wood preparation (i. e. , debarking, chipping) Wood volatiles, wood dust, spores, fungi, microbes Production of cooking liquor Sulphate: ammonia, hydrogen sulphide, sulphur dioxide, mercaptan, chromate and other contaminants Sulphite: sulphur, sulphur dioxide, calcium carbonate, zinc, sulphuric acid, lead fumes, asbestos, sulphurous acid Pulp production, cooking Sulphate: lime, magnesium, wood volatilesSulphite: pigments, dyes, wood volatilesGround wood: wood volatiles, aniline Pulp bleaching, bleach plant Chlorine compounds, ozone, hydrogen peroxide, boron compounds, caustic acids Wet pulp, paper additives Talc, clays, titanium dioxide, urea and melamine formaldehyde, pigments, dyes Paper rolling, sizing, dying, drying, glazing, coating Urea and melamine formaldehyde, paper dust, coating and pigment dusts plant exposures, asbestos, welding fumes Unknown jobs, power, utility General plant exposures, asbestos Unexposed jobs No significant exposures Important challenges in occupational cancer studies Workers represent a well-defined group of people for epidemiological assessment. The occupational health status of pulp and paper mill workers has been studied for a variety of endpoints, including cancer, pulmonary function, skin diseases, and hearing impairment. For some endpoints, such as cancer and respiratory effects, findings have varied considerably across studies. Exposure assessment has been a significant issue in past studies. Lacking measurement of exposure to specific chemicals, most cohort studies have divided workers into at least three exposure categories: those who work in a paper mill, a sulphate (kraft) pulp mill, or a sulphite pulp mill. For simplicity, workers usually are categorized according to the last job they held, and exposure is defined as duration of employment. [SEP] Justify:

Output: The text contrasts the claim by discussing occupational exposures to various harmful substances, such as asbestos and hexavalent chromium, which are known to pose significant health risks, including cancer. This implies that exposure to industrial hazards cannot be entirely mitigated by biohacking techniques, suggesting that the claim that biohacking can eliminate chronic disease risk is overly simplistic.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: 1-zeo+ (Invitrogen, Groningen, The Netherlands), the p53 (pFC-p53, Stratagene, Offenbach, Germany) or the HIPK2 expression construct. Cells were harvested 20–30 h following transfection and lysed in 100 μl of lysis buffer (20 mpH 7. 4, 150 mM NaCl, 5 mM EDTA, 10% glycerol, 0. 5% Triton X-100, 20 μl/ml protease inhibitor cocktail (Sigma, Taufkirchen, Germany)). The protein concentration was determined by the BCA-Pierce-kit according to the protocol of the manufacturer. analysis, 20–30 μg of protein was separated on 10–20% gradient gels (Bio-) and blotted onto nitrocellulose membranes (Amersham-Pharmacia, Freiburg, Germany) according to standard protocols. The monoclonal anti-p53 antibody DO-7 and the monoclonal anti-p21 (Waf1/Cip1) antibody SX118 were purchased from Phar(Hamburg, Germany), the polyclonal anti-Bax antibody Ab-1 (150-165) from Calbiochem (Schwalbach, Germany), the polyclonal phospho-p53 (Ser 15) (Ab-3), phospho-p53 (Ser 392) (Ab-4) and the monoclonal Mdm2 (Ab-1) antibodies from OncogeneTM (Schwalbach, Germany) research products, the polyclonal phospho-p53 (Ser 20) from New(Frankfurt, Germany), the monoclonal anti-Flag antibody M2 from Stratagene (Offenbach, Germany) and the monoclonal anti-β-actin antibody AC-15 from Sigma (Taufkirchen, Germany). An anti-mouse secondary IgG1 antibody coupled to horseraddish peroxidase (Biotechnology, Heidelberg. Germany) was used at a dilution 1:5000. Antibody reactive bands were detected by using the enhanced chemiluminescence Western detection system (Amersham-Pharmacia, Freiburg, Germany). [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses laboratory procedures involving proteins and antibodies, with no mention of urban living or stress levels.


Input: Task: corroborate the claim using the given text. Claim: Genetic engineering is used in producing insulin for diabetic patients. [SEP] Text: The result showed that differentiated cells secreted C-peptide in a low glucose concentration (5. 5 mmol/L) medium and secreted approximately twice as much in a high glucose concentration (25 mmol/L) medium (Figure 2G). Thus, these differentiated MSCs could respond to changes in glucose concentration by altering their C-peptide production and, presumably, insulin production. Genetic analysis of the differentiated cellsTo determine whether the UCMSCs had been induced to differentiate into pancreatic endocrine cells, gene expression profiles for pancreatic β-cell differentiation markers and hormones were assayed by RT-PCR and real-time RT-PCR. As illustrated in Figure 3, the inductive cells expressed genes of pancreatic β-cell markers PDX1, Pax4, Glut2, Ngn3 and insulin. However, the expression of PDX1, Ngn3, and insulin in differentiated IPCs was significantly greater than that in undifferentiated MSCs (Figure 3). Open in 3 Reverse transcription-polymerase chain reaction and real-time reverse transcription-polymerase chain reaction analysis of the expression of pancreatic β-cell development-related genes and insulin production-related genes. A: RT-PCR of the undifferentiated UCMSCs and those during the phases of differentiation (weeks 3 and 4). At the end of differentiation (week 4), the gene expression of IPCs was similar to that of human islets; B: Real-time RT-PCR analysis of UCMSCs. After three-step induction, the UCMSCs expressed high levels of the specific regulation genes for neogenesis and development of pancreatic β-cells, including PDX1, Ngn3 and of hallmark genes for mature islet cells, including insulin. Compared to those of human islets, the differentiated cells (week 4) expressed more Ngn3 and Pax4 and insulin (P < 0. 05, n = 3). Each gene was tested in triplicate. RT-PCR: Reverse transcription-polymerase chain reaction; UCMSCs: Umbilical cord mesenchymal stem cells. Blood glucose and body weight of rats after surgeryThe blood glucose concentrations and body weight of Px rats and sham rats over the 8 wk of study are shown in Figure 4A and B. [SEP] Justify:

Output: The text corroborates the claim by discussing the expression of insulin in differentiated umbilical cord mesenchymal stem cells (MSCs), which indicates the potential for these cells to be genetically manipulated to produce insulin. The reference to the inducible expression of key pancreatic β-cell markers, including insulin, supports the notion that genetic engineering techniques can be utilized in insulin production for diabetic patients.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: 198670d Jappinen et al. 198762d Henneberger et al. 198960b Band et al. 199753e Henneberger et Lax 199861c Matanoski et al. 199868e Langseth et Andersen 200065d Band et al. 200154d Years of follow-up 18 25 42 25 22 40 42 Type of risk estimate SMR* (n) SIR** (n) SMR (n) SMR (n) SMR (n) (n) SIR (n) All cancers 79* -88 105 -33 120 -36 114* -351 108 -123 82** 117* (464) Oral cavity/ pharynx 103 -7 105 91 -11 Esophagus 147 -11 86 126 -7 Stomach 149 -11 129 -6 72 -1 73 -19 78 94 -17 Colon 48 -5 102 -3 83 -21 71** 130 -23 98 -34 Rectum 121 -16 77 124 -27 Liver 199 -8 116 277* -8 Pancreas 32 -2 305 -5 156* -29 185 -11 74 177* -21 Larynx 202 -3 55 133 -12 Lung 81 -26 90 -9 113 -11 132 -121 95 -35 79** 150** -46 132* -112 Pleura 240 -2 Skin melanoma 172 -5 160 -10 139 -10 Prostate 111 -9 104 -3 67* -19 108 111 -78 Bladder 270 -3 72 -7 110 87 -23 Kidney 148 -4 289 -2 143 -11 143 106 -12 Brain 172* -16 34** 153 -10 Non-Hodgkin's lymphoma 133 -4 69 -6 89 91 -12 Hodgkin's disease 159 -4 40 Multiple myeloma 171 -8 103 -5 Leukemia 67 -3 90 -1 51 -6 60 124 -14 Testis 86 SMR: Standardized mortality ratio SIR: Standardized incidence ratio * Significant at 90% level of significance ** Signficant at 95% level of significance a Cause-specific number of deaths not available; total deaths: 1,539 Langseth and Andersen also found a statistically significant increase in lung cancer incidence among sulphite workers. 64 However, the authors suggest that most of the excess can, in fact, be attributed to smoking. [SEP] Justify:

Output: The text contrasts the claim by indicating that while there is evidence of increased cancer incidence among certain worker populations (e.g., sulphite workers), it attributes most of the excess risk to smoking rather than to the biohacking techniques being discussed. The suggestion that smoking is a primary cause implies that biohacking techniques alone do not fully mitigate risk, thereby refuting the claim that they can entirely eliminate the risk of chronic diseases.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: Fluorometric protein quantification was done by excitation at 485 nm and emission measurement at 510 nm of cellular extracts in a fluorometer (Victor, Wallac, Freiburg, Germany). For reprobing, membranes were treated with stripping buffer (62. 5 mM Tris-HCl pH 6. 7, 2% SDS, 100 mM β-mercaptoethanol) at 50°C for 30 min. Quantitative TaqMan RT--PCR (real time PCR) was carried out by Toplab GmbH (München, Germany) by using an 7700. Sequence specific internal Primers were labelled with FAM/TAMRA. Endogenous reference mRNA was human GAPDH mRNA. AbbreviationsHIPK2: homeodomain-interacting protein kinase 2 MAP: mitogen-activated protein Mdm2: murine double minute clone 2. 1399. CAS PubMed 53. Oncogene. 1999, 18: 7706-7717. 10. 1038/sj. onc. 1202952239. 10. 1002/(SICI)1097-4652(199911)181:2<231::AID-JCP5>3. 0. CO;2-L331. 6034. 10. 1074/jbc. 274. 51. 360312. Nature. 1997, 387: 299-303. 10. 1038/387299a029. 10. 1016/S0378-1119(99)00487-4310. 10. 1038/350426755879. 10. 1074/jbc. 273. 40. 258757377. 10. 1074/jbc. 275. 10. 73731. Proc. Natl. Acad. Sci. USA. 1999, 96: 12350-12355. 10. 1073/pnas. 96. 22. 1235053. Nat. Genet. 1992, 1: 45-49. 1542. 53. J. Virol. 1993, 67: 3111-3117. 1650. CAS PubMed 468. 1132. 7655. 10. 1038/sj. onc. 12030159283. 10. 1074/jbc. 275. 13. 92781758. 53. Proc. [SEP] Justify:

Output: The text is irrelevant to the claim as it provides technical details about a laboratory experiment involving fluorometric protein quantification and does not mention urban living, stress levels, or any related concepts.


Input: Task: corroborate the claim using the given text. Claim: Genetic engineering is used in producing insulin for diabetic patients. [SEP] Text: It indicated the ability of islet generated to synthesize, store and release insulin in response to glucose challenge. In our in vitro studies, RT-PCR and real time RT-PCR were used to examine the expression of β-cell development-related genes before and after induction of differentiation. After 3 wk of differentiation, the IPCs expressed the genes of pancreatic β-cell marker s PDX1, Pax4, Glut2, Ngn3 and insulin. Real-time RT-PCR showed that the expression of PDX1, Ngn3, and insulin was significantly greater in differentiated IPCs than in undifferentiated MSCs. According to a previous study[14], we created the experimental diabetic rat models by removing 90% of the pancreas. We then transplanted the differentiated cells into diabetic rats in order to examine the function of IPCs. The portal vein[22], renal subcapsularspace[23], and tail lateral vein[24] have been previously reported as stem cell transplant locations in the rat. We transplanted the cells into the rat liver through the portal vein as this method is faster and easier to perform. In this study, after transplanting IPCs into diabetic rats, blood glucose levels decreased, suggesting that the transplanted cells secreted functional insulin. Thus, after transplantation, IPC grafts could reduce hyperglycemia in SD rats. At two weeks after transplantation, blood glucose levels decreased to about 18. 7 mmol/L compared to 25. 8 mmol/L in the control SD rats. The body weight of the transplanted diabetic rats increased rapidly, whereas the body weight of the untreated rats increased slowly. In vivo glucose tolerance test results showed that blood glucose levels were decreased in the cell transplantation group. Taken together, our results show that UCMSCs can differentiate into islet-like cells in vitro under certain conditions and function as IPCs both in vivo and in vitro. These results suggest that UCMSCs are a promising stem cell source for β-cell regeneration. However, there are many questions that remain unresolved, such as how to push these cells to become mature β-cells, will the antibodies destroy the insulin-producing cells, and whether tumor formation will happen. Further work is required to address these problems. [SEP] Justify:

Output: The text corroborates the claim by detailing the process of differentiating UCMSCs into islet-like cells and their subsequent ability to secrete functional insulin when transplanted into diabetic rats. This suggests that genetic engineering techniques can contribute to insulin production, aligning with the claim that genetic engineering is involved in insulin production for diabetic patients.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: Estos resultados pueden ayudar a los profesionales de la salud en la práctica diaria para una mejor comprensión del estado de salud de los pacientes y una mejor clasificación de su estado de riesgo. [-] [CA] Els models de risc en l'àmbit de la salut són mètodes estadístics que brinden advertències primerenques sobre el risc d'una persona de patir un episodi advers en el futur. Generalment, utilitzen la informació emmagatzemada. . . [+] [CA] Els models de risc en l'àmbit de la salut són mètodes estadístics que brinden advertències primerenques sobre el risc d'una persona de patir un episodi advers en el futur. Generalment, utilitzen la informació emmagatzemada de forma rutinària en els sistemes d'informació hospitalària per a oferir una probabilitat individual de desenrotllar un resultat negatiu futur en un període determinat. Concretament, en el camp de les malalties cròniques que compartixen factors de risc comú, els models de risc es basen en l'anàlisi d'eixos factors de risc -tensió arterial elevada, glucèmia elevada, lípids sanguinis anormals, sobrecàrrega i obesitat- i les seues mesures biomètriques associades. Estes mesures es recopilen durant la pràctica clínica ben sovint de manera periòdica i, en conseqüència, s'incorporen als models de risc i recolzen la presa de decisions dels metges. [SEP] Justify:

Output: The text contrasts the claim by explaining that risk models in healthcare utilize statistical methods to provide early warnings about an individual's risk of adverse episodes, particularly in chronic diseases. It mentions that these models analyze common risk factors such as high blood pressure and obesity, rather than suggesting that biohacking techniques can completely eliminate risks. This indicates that expectations of biohacking for total risk elimination may be unrealistic.


Input: Task: pass the claim using the given text. Claim: Environmental psychology can predict individual behavior with high accuracy. [SEP] Text: -19 PreprintsProtocolsVideosJournalsTools & a 10. 21203/rs. 2. 11709/v1This work is licensed under a CC BY 4. 0 LicenseStatus:Published21 Oct, 2020Read the published version in →Version 1posted You are reading this latest preprint versionAbstractBackground: Meningiomas, the most common adult brain tumors, recur in up to half of cases[1–3]. This requires timely intervention and therefore accurate risk assessment of recurrence is essential. Our current practice relies heavily on histological grade and extent of surgical excision to predict meningioma recurrence. However, prediction accuracy can be as poor as 50% for low or intermediate grade tumors, which constitute more than 90% of all cases. Moreover, attempts to find molecular markers, particularly for predicting recurrence of intermediate tumors have been impeded by low[4] or heterogenous[5–8] genetic signal. We therefore sought to apply systems-biology approaches to transcriptomic data to better predict meningioma recurrence. Methods: We apply gene co-expression networks to a cohort of 252 adult patients from the publicly-available genetic repository Omnibus. Resultant gene clusters (“modules”) were represented by the first principle component of their expression levels, and their ability to predict recurrence assessed with a logistic regression model. External validation was done using an independent merged cohort of 108 patients using the same modules. We used the bioinformatics database DAVID[9] to examine the gene ontology associations of each module. Results: Using gene co-expression analysis, we were able predict tumor recurrence with high accuracy using a single module which mapped to cell cycle-related functions (AUC of 0. 81 ± 0. 09 in external validation). Further, the module maintained its accuracy with removal of up to 20 of it’s most individually predictive genes, suggesting robustness against noise at the single gene level. Conclusions: With the easy accessibility of gene panels in healthcare diagnostics, our results offer a basis for routine molecular testing in meningioma management. Cancer BiologyOncologyMeningiomabioinformaticstranscriptomicssystems biologyrecurrence predictionFiguresFigure 1Figure 2Figure 3BackgroundMeningiomas constitute approximately 34% of all brain tumors, affect 3% of the adult population[10] with an incidence rate of 8. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses the prediction of meningioma recurrence using gene co-expression networks and systems biology approaches, which is unrelated to environmental psychology or predicting individual behavior.


Input: Task: pass the claim using the given text. Claim: The majority of genetic therapies are still in experimental stages but show promising results. [SEP] Text: , 2011) of histones can have profound consequences on the cell. In most cells, histone availability is tightly regulated at multiple levels, including transcriptionally, post-transcriptionally, and post-translationally (Marzluff et al. , 2008; Bannister and Kouzarides, 2011). For example, in mammalian cultured cells, transcription of canonical histones is highly upregulated during S-phase, when replication occurs, and afterwards throttling of transcription and mRNA turnover bring messages back to very low levels. And in yeast, excess histone proteins are degraded via the ubiquitin-proteasome system (Singh et al. , 2009). For early Drosophila embryos, regulation of histones is particularly challenging. On the one hand, these embryos develop incredibly rapidly: during the first ~90 min after fertilization, nuclei divide near simultaneously every ~8 min, deep within the embryo (cleavage stages); a subset of these nuclei migrates to the surface and divides four more times over the next hour (syncytial blastoderm stages). All these divisions occur near simultaneously and in the absence of cytokinesis. As a result, histone demand goes up exponentially during this period, in a fluctuating manner, as S-phases and mitoses alternate on minute time scales (the entire interphase is dedicated to DNA replication during these cycles). On the other hand, zygotic transcription is minimal during these stages, being upregulated only in late syncytial blastoderm as part of the midblastula transition (MBT). Thus, early embryos cannot control histone expression transcriptionally. Instead, they draw on abundant histone proteins and mRNAs, produced by the mother during oogenesis. Newly fertilized embryos already contain sufficient histone proteins for thousands of nuclei, and they increase histone levels further by translation of the maternal mRNAs. Thus, histone proteins are consistently overabundant. How is chromatin assembly regulated under those conditions? Previous work revealed that for three histones, the canonical histones H2A and H2B as well as H2Av, the single H2A variant in Drosophila, LDs play an important role in regulating histone availability (Li et al. , 2012). [SEP] Justify:

Output: The text is irrelevant to the claim regarding genetic therapies. It discusses the regulation of histones in cellular biology, specifically in Drosophila embryos, without mentioning genetic therapies or their experimental status. Therefore, it does not provide any information that corroborates or contrasts with the claim.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: L'objectiu d'esta tesi és proporcionar una visió nova del risc, associat a un pacient, basada en tecnologies Data-Driven que oferisquen una visió dinàmica de l'evo\-lució dels pacients respecte a la seua condició crònica. Tècnicament, suposa abordar els models de risc incorporant la perspectiva dinàmica i el comportament dels pacients als models de risc gràcies a la informació inclosa en la Història Clínica Electrònica. Els resultats obtinguts al llarg d'esta tesi mostren com les tecnologies de mineria de processos poden aportar una visió dinàmica i interactiva dels models de risc de malalties cròniques. Estos resultats poden ajudar els professionals de la salut en la pràctica diària per a una millor comprensió de l'estat de salut dels pacients i una millor classificació del seu estat de risc. [-] [EN] Risk models in the healthcare domain are statistical methods that provide early warnings about a person's risk for an adverse episode in the future. They usually use the information routinely stored in Hospital. . . [+] [EN] Risk models in the healthcare domain are statistical methods that provide early warnings about a person's risk for an adverse episode in the future. They usually use the information routinely stored in Systems to offer an individual probability for developing a future negative outcome in a given period. Concretely, in the field of chronic diseases that share common risk factors, risk models are based on the analysis of those risk factors -raised blood pressure, raised glucose levels, abnormal blood lipids, and overweight and obesity- and their associated biometric measures. These measures are collected during clinical practice frequently in a periodic manner, and accordingly, they are incorporated into the risk models to support clinicians' decision-making. Data-Driven techniques could be used to create these temporal-aware risk models, considering the patients' history included in Records, and extracting knowledge from raw data. [SEP] Justify:

Output: The text contrasts the claim by discussing the complexity of risk models in healthcare and how they analyze various risk factors associated with chronic diseases. It highlights that while data-driven techniques can improve the understanding and classification of a patient's risk, it does not imply that biohacking techniques can entirely eliminate the risk of chronic diseases. Instead, it suggests that these technologies can aid in risk assessment and management, but do not provide a definitive solution to eliminating risks.


Input: Task: pass the claim using the given text. Claim: Environmental psychology can predict individual behavior with high accuracy. [SEP] Text: 36 and 3. 61 per 100,000 person years in females and males respectively [11]. For over half a century, the prediction of meningioma recurrence has relied solely upon histological features[11] (Organization grading from I to III) and degree of surgical excision [1]. While about 70-80% of fully excised WHO grade I meningiomas do not recur, 20-30% recur over follow-up with half of the recurrences occurring before the tenth year and half after ten years[12]. For WHO grade II lesions completely excised, histology predicts a recurrence of 50% over 5 years [2] and a disease specific survival rate of 69% over 10 years [3]. Given the inherent inaccuracy of histology to predict recurrence, all patients consequently require lifelong monitoring with expensive MRI imaging and clinical follow-up, essentially transforming meningioma into a “chronic disease”. Not only does this represent a significant financial burden but the stress and strain on the psychological well-bring of patients is substantial as they live with the constant uncertainty as to whether the tumor will recur, face future morbidity or require more treatment. It is therefore critical to develop better methods designed to assess the risk of recurrence that take into account the intrinsic biology of the patient’s meningioma. The genetic landscape of meningiomas is the next frontier to our understanding of their biology and its relation to disease recurrence. While some studies have identified chromosomal rearrangements [13], mutations in genes TERT [14], ATK1 [15], SMO [16] and DNA methylation [8] as correlates of tumor recurrence, none of these have successfully translated into routine clinical practice. In addition, studies on transcriptomics have been limited by low signal. However alternative methodology exists to effectively capture additive biological effects and relate them to complex clinical traits [17–19]. Such methods may help extract translatable markers of meningioma recurrence. Gene co-expression networks are an emerging technique used to detect patterns in transcriptomics by incorporating additive signal from relatively low gene expression levels [17, 18, 20]. The technique establishes gene similarity profiles based on shared connectivity and clusters into biologically similar groups called modules. A meta-gene is computed to summarize each module based on its gene expression levels and correlated to a clinical trait. [SEP] Justify:

Output: The text does not address the claim regarding environmental psychology and its predictive capabilities regarding individual behavior. Instead, it discusses meningioma recurrence prediction and related methodologies, which are unrelated to environmental psychology.


Input: Task: corroborate the claim using the given text. Claim: The majority of genetic therapies are still in experimental stages but show promising results. [SEP] Text: Log in or new issue alertsGet alerts Enter your Email address: Subscribe to e2016. | DOI: 10. 1097/01. COT. 0000480383. 29391. 39 —Three new studies with impressive outcomes show the promise of targeted therapies for a variety of patients with relapsed/refractory chronic lymphocytic leukemia (CLL), according to presentations here at the of Meeting. “As we move toward molecular targeted therapies linked to genetic defects, we can begin to talk about a cure for CLL. The hope is to reduce toxicity and to move combinations more upfront where they might be more effective,” said the moderator of a news conference that featured the three studies, Robert Hromas, MD of the University of Florida. Ibrutinib forsmall lymphocytic lymphoma (SLL) primarily affects older patients who often have other chronic diseases or conditions. In this population of patients, chlorambucil has been a standard first-line therapy. Fludarabine-based regimens are unsuitable for frail or older patients, said Alessandra Tedeschi, MD, of Niguarda Cà Granda in Italy, who reported the results of the open-label, multicenter, international -2 trial, which evaluated the use of ibrutinib in previously untreated 269 CLL/SLL patients, age 65 and older (Abstract 495and published simultaneously online in the Journal of Medicine—DOI: 10. 1056/NEJMoa1509388). Ibrutinib is a first-in-class, oral, covalent Bruton's tyrosine kinase inhibitor, which received FDA approval for CLL patients who had one or more prior therapies and for patients with del17p CLL. The results of the trial found that in relapsed/refractory CLL, ibrutinib led to a 78 percent reduction in the risk of disease progression and a 57 percent reduction in the risk of death as compared with ofatumumab. The patients, who had a median age of 73, were randomized to receive either continuous daily doses of ibrutinib or the chemotherapy drug chlorambucil for up to 12 treatment cycles. “By investigator assessment, ibrutinib therapy led to a 91 percent reduction in the risk of progression or death compared with chlorambucil,” Tedeschi said. [SEP] Justify:

Output: The text corroborates the claim by discussing studies that highlight the promising outcomes of targeted therapies, notably ibrutinib for chronic lymphocytic leukemia (CLL). It emphasizes the shift towards molecular targeted therapies linked to genetic defects and suggests the potential for cures, which aligns with the idea that genetic therapies, while still largely in experimental stages, are showing encouraging results.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: Score15 () is a key element of Finland’s national FIN-D2D diabetes prevention program, which has successfully screened over 10% of the Finnish population so far. has been used in Finland to identify high-risk individuals who might benefit from interventions or who would merit further investigation using the oral glucose tolerance test (OGTT). Among those detected by the Finnish study as being at high risk of developing diabetes, 60% of men and 45% of women had already developed abnormal glucose intolerance at baseline. 16 The incidence of diabetes at one-year follow-up was between 18% and 22% among those who had high-risk prediabetes (i. e. both IFG and IGT) at baseline. Of those who completed a lifestyle education program, 17% reduced their body weight by over 5%; as a result, their risk of developing diabetes was 69% lower than that of those with stable weight. 17 However, the generalizability of is limited by the different ethnic make-up of Canada compared to that of Finland. As a result, Canadian diabetes experts adapted to include ethnicity and other key variables (sex, education, macrosomia) to create the Questionnaire (). 18 * This paper describes three main objectives of our study: (1) to develop a risk-scoring prognostic model (similar to score) suitable for Canada’s multi-ethnic population (); (2) to validate the resulting scoring model using a test-set methodology to assess dysglycemia from measured blood tests; and (3) to compare the predictive accuracy of the new model to. * source Between 2007 and 2011, 6475 Canadian adults from seven provinces (and Island) were recruited in a screening study to detect diabetes and prediabetes using the questionnaire. Several large urban sites were deliberately included to ensure a diverse multi-ethnic sample of participants. All participants had their glycemic status confirmed with the oral glucose tolerance test (OGTT, i. e. fasting plasma glucose [FPG] and plasma glucose 2 hours after a 75 g glucose challenge). A subset of participants at three sites also had their glycated hemoglobin (HbA1c ) measured. Most participants were recruited through face-to-face encounters during opportunistic visits at community health centres;19 some were recruited through local mailouts. 20 Most participants were aged 40 to 74 years, although some sites chose to include younger Aboriginal participants and those from other non-White ethnic groups. [SEP] Justify:

Output: The text contrasts the claim by discussing the limitations of diabetes prevention efforts in Finland and Canada. It highlights that while screening and lifestyle interventions can reduce risk, they do not completely eliminate the risk of diabetes, as evidenced by the fact that 60% of high-risk individuals detected in the study already had abnormal glucose intolerance. Furthermore, the text indicates that even among those who engaged in lifestyle education, only 17% significantly reduced their body weight, resulting in a 69% lower risk of developing diabetes compared to those with stable weight, rather than completely eliminating the risk.


Input: Task: pass the claim using the given text. Claim: Environmental psychology can predict individual behavior with high accuracy. [SEP] Text: Highly correlated meta-genes can then be used to predict a phenotype such as recurrence. With the affordability of gene expression profiling, meta-gene based diagnostics of tumor recurrence becomes feasible. With contribution of multiple module genes a meta-gene seeks to holistically represent a biological process. This multi-gene signature provides a robust against fluctuations of individual expression levels. In the current study we hypothesized the existence of meta-genes consisting of gene modules that predict tumor recurrence with high accuracy. By annotating modules correlated with recurrent phenotypes we aim to provide further insight into the underlying biology driving tumor recurrence in addition to the clinical application. MethodsData collection and pre-processing: We identified 17 studies containing meningioma gene expression data in the Omnibus (GEO)[21] with four datasets (GSE43290, GSE1658, GSE74385, and GSE16181) including annotated tumor recurrence (Table 1). Gene expression analysis for these studies was carried out using microarray platforms Genome U133A, Genome U133 Plus 2. 0, HT-12 V4. 0, and SU 912, respectively. Each study was background corrected, log2 transformed and quantile normalized except GSE16181, which had previously been pre-processed. After this step, we filtered to include only genes common to all four studies. Discovery was done using dataset GSE16181 and external validation was done using GSE43290, GSE1658 and GSE74385 datasets merged with ComBat, a well-established Bayesian batch correction tool[22]. Notably, gene expression matrices were globally scaled to a mean of 0 and standard deviation of 1 prior to merging, as previously suggested[23]. Gene module detection and meta-gene computation: Our analysis was based on the well-established Analysis (WGCNA), which has been described in detail elsewhere[18]. We first constructed an adjacency matrix with gene-gene Pearson correlations. Per convention, soft-thresholding was introduced by raising correlations to a common power (a hyperparameter, ß), which was selected as the lowest natural number for which the network approached scale-free topology (r2 ≥ 0. 9). [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses meta-genes and their application in predicting tumor recurrence rather than addressing environmental psychology or predicting individual behavior. There is no mention or exploration of environmental psychology in the provided text.


Input: Task: corroborate the claim using the given text. Claim: The majority of genetic therapies are still in experimental stages but show promising results. [SEP] Text: Further increasing intensity of host preparative lymphodepletion by adding total-body irradiation (TBI) of either 2 or 12 Gy prior to cell transfer in cyclophosphamide and fludarabine lymphodeleted patients was shown to generate response rates up to 52% and 72%, respectively. Of the 25 patients studied in the 12 Gy TBI arm, there were 4 complete responders and at least 2 substantial partial responders (Dudley et al. 2008). The caveat of adoptive cell therapy is its complexity of several critical preparative steps that are both labor intensive and costly which may be the major obstacle to the widespread application of this approach. Up to 4 to 6 weeks of cell culture are required to obtain adequate numbers of reactive lymphocytes for adoptive transfer. Additionally, much akin to the limitation of high dose IL-2, only patients with an excellent functional status are be able to withstand the intensity of adoptive cell therapy which may also involve TBI in addition to IL-2. On the other hand, as the data from the NCI suggest, such potent therapy in highly selected patients does have the potential to induce durable responses and a potential cure. To date, however, only small phase II clinical trials have been completed and no phase III study has been initiated. Meanwhile, further innovations beyond current TIL technology are underway. Current strategies seek to improve the yield of TIL cultures, to use vaccines to stimulate the transferred T cells in vivo, and to employ gene therapy using genetically engineered lymphocytes that express highly reactive T-cell receptors (TCRs) with specific anti-melanoma differentiation antigen activity (gp-100 or MART-1), produce IL-2 or other molecules promoting an effective immune response. The gene therapy approach is of particular interest because the anti-tumor effector T cells could be rapidly expanded for adoptive transfer. Furthermore, it could be of tremendous benefit to patients who do not have autologous reactive TIL available and would otherwise be ineligible for adoptive immunotherapy (Johnson et al. 2009; Yang et al. 2010). The objective response rates in trials employing gene therapy have been reported to be 20% to 45%, and durable tumor regression at all disease sites including the brain has also been observed (Johnson et al. 2009; Morgan et al. 2006; Robbins et al. 2011). Advertisement 3. [SEP] Justify:

Output: The text supports the claim by indicating that gene therapy approaches are being explored and that they are still in experimental phases, as evidenced by references to small phase II clinical trials without completed phase III studies. It also mentions that while these therapies face significant challenges, such as labor-intensive preparative steps and the need for highly selected patients, they have shown promising results with objective response rates of 20% to 45% and the potential for durable responses. This aligns with the claim that genetic therapies are experimental yet show promise.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: Impaired glucose tolerance and impaired fasting glycaemia: the current status on definition and intervention. Diabet Med. 2002;19:708-23. de Group. Relation of impaired fasting and postload glucose with incident type 2 diabetes in a Dutch population: the Hoorn Study. JAMA. 2001;285(16):2109-13. -Parikka P, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Med. 2001;344:1343-50. Knowler WC, Barrett-;. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Med. 2002;346:393-403. . Risk assessment tools for identifying individuals at risk of developing type 2 diabetes. Epidemiol Rev. 2011;33:46-62. . Diabetes risk score: towards earlier detection of type 2 diabetes in general practice. Res Rev. 2000 May-Jun;16(3):164-71. . A new public health tool for risk assessment of abnormal glucose levels. Dis. 2010;7(2):1-9. . Calculator: a simple tool for detecting undiagnosed diabetes and pre-diabetes. Diabetes Care. 2008;31:1040-5. . Tool to assess likelihood of fasting glucose impairment (TAG-IT). Med. 2008;6(6):555-61. ; Health and Survey. Predicting impaired glucose tolerance using common clinical information: data from the third Survey. Diabetes Care. 2003;26(7):2058-62. . The performance of a risk score in predicting undiagnosed hyperglycemia. Diabetes Care. 2002;25:984-8. Detection of undiagnosed diabetes and other hyperglycemia states: the in Communities Study. Diabetes Care. 2003;26(5):1338-43. Lindstrom J, Tuomilehto J. Risk Score: a practical tool to predict type 2 diabetes risk. Diabetes Care. 2003;26(3):725-31. - Cardiometabolic profile of people screened for being at high risk of type 2 diabetes in a national diabetes prevention program (FIN-D2D). Diabetes. 2010;4:231-9. [SEP] Justify:

Output: The text contrasts the claim by discussing various studies and tools related to the prevention and risk assessment of type 2 diabetes, which illustrate that lifestyle changes can reduce the likelihood of developing chronic diseases like diabetes but do not imply that biohacking techniques can entirely eliminate the risk. Instead, it emphasizes managing glucose levels and identifying individuals at risk, suggesting that while interventions can help, they cannot completely negate the risk of chronic diseases.


Input: Task: pass the claim using the given text. Claim: Environmental psychology can predict individual behavior with high accuracy. [SEP] Text: The adjacency matrix was subsequently converted into a biologically-inspired topological overlap map (TOM), wherein pairwise gene similarities are based on comparing their connectivity profiles, a more meaningful measure than direct correlation[24]. Hierarchical clustering with superimposed hybrid adaptive tree cut[25], an unsupervised dendrogram cutting function, was applied to the TOM to identify biologically important gene modules. Finally, representative module “meta-genes” for each sample were calculated using principal component analysis; they are simply the projections of a sample’s modules’ gene expression values on their respective first principal components. Module investigation: We first used a multivariate logistic regression model to identify modules whose meta-gene expression levels differed significantly (p<0. 05) between recurrent and non-recurrent tumors when controlling for histological grade. In order to probe the biological function of relevant modules, we used the well-established and open-source Database for Annotation, Visualization and (DAVID)[9] to analyze their constituent gene lists. Recurrence classifier: A logistic regression classifier was used as our prediction model, with module meta-genes as regressors and recurrence as a binary response. The model was trained with the discovery cohort and tested with both 10-fold cross validation and external validation sets. Computational platform: All analysis was performed using R, an open-source platform for statistical computation and graphics[26]. ResultsWe firstly investigated the differential gene expression profile between recurrent and non-recurrent meningiomas in both cohorts, though no single genes were significantly different (log2 fold change >1 and p<0. 0001) in the validation cohort (Figure 1A). Co-expression networks revealed two gene modules (Figure 1B and C) with significant correlation to recurrence (Mann-Whitney p<0. 05): a “blue” module containing 220 genes and a “turquoise” module consisting of 299 genes. The meta-gene of each module was defined as the first principal component of its expression values[20](Supplementary figure 1). We next investigated whether the meta–genes could be used to predict meningioma recurrence and found good classifier performance with 10-fold cross validation using the “turquoise” module (AUC=0. 87 ±0. 04; Figure 2A). [SEP] Justify:

Output: The text discusses gene expression profiles in relation to meningioma recurrence and the use of logistic regression models for prediction, but it does not address environmental psychology or its ability to predict individual behavior. Thus, it is irrelevant to the claim.


Input: Task: corroborate the claim using the given text. Claim: The majority of genetic therapies are still in experimental stages but show promising results. [SEP] Text: ”The letter to the FDA, which was signed by 34 other scientists, stated that simply on the basis of the three-year data alone these data are “clearly supportive of accelerated approval, however the new four-year data regarding age at loss of ambulation now provide even more compelling data for accelerated approval based on an irreversible morbidity. The hard endpoint of loss of ambulation is not affected by motivational factors. ”As to the low level of dystrophin found in the treated patients, the letter stated that “data from studies on BMD and DMD patients and in mouse and canine dystrophinopathy models support the suggestion that relatively low levels of dystrophin can be functionally significant, even if only expressed in a limited number of fibers. ”After reviewing the evidence, the letter stated, “we conclude that the aggregate data, described in the briefing documents, are providing substantial evidence of efficacy and use in the greater population of boys amenable to exon 51 skipping is appropriate. We suggest that the most scientifically robust way forward and the most ethical choice for the Duchenne community is in the context of an accelerated approval followed by a confirmatory trial. ”Melissa J. Spencer, PhD, a professor of neurology and co-director of the Center for Dystrophy at UCLA who signed the letter to the FDA about the drug, said: “From my point of view, the results are extremely significant. It would be very unlikely to obtain the data they obtained by chance. All the data in the literature suggest that even low levels of dystrophin are likely to be beneficial. How much they need is not clear. More is better obviously. ”Whether or not the FDA advisory committee recommends accelerated approval following its April 25 meeting, she said, “The ongoing phase 3 trial will likely be continued as the confirmatory trial where data on efficacy will be collected and evaluated, and under yet to be determined conditions of the FDA, any DMD patient amenable to exon 51 skipping could be able to get the drug through an academic medical center. ”Even for an older patient who can no longer walk, she said, “The thinking is that maintenance of muscle mass that is remaining can improve a patient's quality of life. ”: -. . [SEP] Justify:

Output: The text corroborates the claim by discussing the ongoing phase 3 trial and the support for accelerated approval, indicating that genetic therapies (in this case, related to Duchenne muscular dystrophy) are in later stages of development and showing efficacy. Statements like 'the evidence... are providing substantial evidence of efficacy' support the notion that genetic therapies are making significant progress, aligning with the claim that while still experimental, they show promising results.


Input: Task: pass the claim using the given text. Claim: Biohacking is universally recognized as a replacement for traditional medical treatment. [SEP] Text: Message second - ectopia of the semen gland A. Y. Nakonechny/ Practical medicine: scientific-practical. journal. - 2003. - No 4. - P. 11-13. Nakonechny A. Y. Genitometric parameters in boys with pathology of the lowering of the testes. Message third - in the case of defective cryptorchidism A. Y. Nakonechny/ Practical medicine: Scientific-practical. Journal. - 2003. - No 5. - P. 8-11. Nevstroyeva V. V. Some barrier-forming structures of the testis V. V. Nevstroyeva, T. V. Bronikhina/ Archive of anat. , histology and embryology. - 1980. - Vol. 79, No 9. - P. 81-91. Neikov G. N. Comparative evaluation of surgical methods for the treatment of cryptorchidism in children G. N. Neykov, V. A. Schwarzkopf/ News of surgery. - 1993. - No5-6. - P. 66-69. Surgical treatment of oblique inguinal hernia M. B. Nemashko/ Clinical surgery. - 1997. - No 7. - P. 96-97. Nesterenko Yu. A. The effect of inguinal hernia repair on the functional state of the testis Yu. A. Nesterenko, V. A. Yarygin/ Surgery. - 1990. - No3. - P. 135-140. Immunological studies in cryptorchidism accompanied by infertility Nikolovsky M. , Tsvetkov D. , Popov A. , Drumcheva M. // Urol. and nephrol. - 1990. - No4. - P. 48-50. Okulov A. B. Surgical aspects of pediatric androgynecology A. B. Okulov/ Mater. of 3rd with international participation “Surgery - 2001". - M, 2001. - P. 421-425. Treatment of cryptorchidism in children Okulov A. B. , Matkovskaya A. N. , Chuvakov G. I. [et al. ]/ Method. recommendation - M. , 1984. - 27 p. [SEP] Justify:

Output: The text provided is a list of scientific articles and studies related to various surgical treatments and medical conditions, primarily focused on children's health issues such as cryptorchidism and hernias. It discusses conventional medical practices without reference to biohacking or any claims regarding its recognition as a replacement for traditional medical treatment. Therefore, the text is irrelevant to the claim and does not provide support for, or contrast with, the assertion made.


Input: Task: pass the claim using the given text. Claim: Environmental psychology can predict individual behavior with high accuracy. [SEP] Text: Importantly, this performance was preserved in the validation cohort (AUC = 0. 81 ± 0. 09; Figure 2B). We also investigated the classifier performance on the subset of grade 2 tumors, since predicting recurrence in these patients is limited by particularly high uncertainty. Our classifier maintained high accuracy with 10-fold cross validation (AUC = 0. 93 ± 0. 05; Figure 2C), though accuracy decreased with external validation (AUC = 0. 75 ± 0. 22; Figure 2D), using the turquoise module. This module was enriched in biological processes related to cell division and metabolism (Figure 3A). Adding the blue module did not contribute to overall model performance. The turquoise meta-gene maintained its predictive accuracy with concurrent removal of up to 20 of the most individually predictive module genes (Figure 3C), and a meta gene built from these genes performed equally to the meta gene of the full module (Figure 3D). To ensure our model is unbiased, we randomly perturbed recurrence labels in the validation cohort, which abolished model performance as expected (2). DiscussionWe have used a simple and robust approach to predicting meningioma recurrence using gene modules, which yields high accuracy with a multi-study validation cohort. Previous analysis of the DNA methylation status of meningiomas has identified classes relevant to disease progression using unsupervised clustering. Grade 2 meningiomas were also observed to be scattered over these methylation classes further indicating diverse biology [8] and underlining the diagnostic problem created by these tumors. In our study, we show that a systems biology approach using meta-genes provides an accurate predictor of tumor recurrence. This principle can be used in marker discovery for other challenging diseases where conventional approaches such as differential gene expression analysis have been unsuccessful. Our results are derived from data obtained under diverse conditions and yet still produce an accurate classier which projects translational value in creating a diagnostic panel. Our study uses publicly available data and is thus limited by sparse annotation and variable follow-up times. The extent of tumor excision in our study was not known. Although this is conventionally held to affect recurrence[27] the relevance has been debated over the past decade[1] and our classifier yields high accuracy purely with gene expression data. While follow-up times are limited for some patients (Table 1) they still represent real life data from the general neurosurgical practice. [SEP] Justify:

Output: The text is irrelevant to the claim because it discusses the accuracy of predictive models in a biological context, specifically regarding tumor recurrence prediction using gene expression data, rather than environmental psychology or predicting individual behavior.


Input: Task: corroborate the claim using the given text. Claim: Personalized medicine uses genetic data to tailor treatments to individual patients. [SEP] Text: Personalized medicine promises to move beyond data regarding the average effectiveness of treatments to identify the best treatment for any individual. In order to provide personalized medicine for depression, we must identify characteristics of individuals that reliably predict differences in benefits and/or adverse effects of alternative depression treatments, including both biological and psychosocial treatments. These personalizing factors might include sociodemographic characteristics, clinical characteristics (such as symptom patterns or comorbidities), and biological markers (such as neuroimaging or genetic variation). This review examines evidence that specific patient characteristics can guide selection of initial treatment for adult outpatients with unipolar depression. We begin by presenting a conceptual model for personalized treatment in order to clarify the type of evidence relevant to treatment selection. We then consider the following three specific clinical decisions: the choice between psychotherapy and antidepressant medication, selection of a specific antidepressant medication, and selection of a specific psychotherapy. For each of these three decisions, our review first clarifies the types of evidence that can and cannot inform treatment selection. We then review potentially informative evidence regarding specific factors hypothesized to inform initial treatment choice. Since fewer data exist to guide subsequent treatment choices, we do not consider second-line therapies or therapies for treatment-resistant depression. for Personalized Treatment: Is Relevant? We hope to identify measurable characteristics of individual patients that can guide selection of treatment. Our question concerns differential efficacy (Do patients with show better response to than to Treatment B? ). This is often expressed as a moderator effect (X moderate the difference in response rates between). It is essential to distinguish moderators or predictors of differential efficacy from more general predictors of depression outcome (13). Previous research has often conflated these two concepts. Two study designs could produce the evidence needed to personalize treatment selection. First, we might compare alternative treatments in an unselected group of patients and examine whether a specific patient characteristic moderates the relationship between treatment type and outcome (14–16). One example would be a randomized trial comparing cognitive therapy and interpersonal psychotherapy in which we examine whether co-occurring personality disorder moderates (or interacts with) the effect of treatment type (17). Second, we might select a group of patients with a specific characteristic and then compare outcomes in patients receiving alternative treatments. One example would be a study limited to patients with depression and co-occurring personality disorder in which we compare cognitive therapy and interpersonal therapy (18). [SEP] Justify:

Output: The text corroborates the claim by discussing how personalized medicine aims to identify specific characteristics, including genetic variation, that can inform treatment choices for individual patients. It emphasizes the need for personalizing factors, such as biological markers and clinical characteristics, to guide treatment selection, which aligns with the concept of using genetic data for tailored medical treatments.


Input: Task: contrast the claim using the given text. Claim: Biohacking is universally recognized as a replacement for traditional medical treatment. [SEP] Text: То есть, по мнению автора, биохакинг — именно гаражная наука, которая движима энтузиазмом исследователей, находящихся вне и внутри академии. Главными качествами которых являются любопытство и тяга возиться с экспериментальным оборудованием. В комментариях к публикации сразу же возникла дискуссия: считать ли человека, пытающегося в домашних условиях изготовить «искусственное мясо» биохакером. [SEP] Justify:

Output: The text contrasts the claim by discussing the nature of biohacking as a type of 'garage science' led by enthusiasts rather than being recognized as a formal substitute for traditional medical treatment. It highlights the experimental and amateur aspects of biohacking without mentioning its acceptance as a legitimate replacement for established medical practices.


Input: Task: pass the claim using the given text. Claim: Environmental psychology can predict individual behavior with high accuracy. [SEP] Text: Though our results are largely exploratory at present, further optimization of a predictive gene module using prospectively gathered cohorts with greater follow up times may ultimately translate into a novel approach to care of patients with meningioma at the bedside. ConclusionsWe apply gene co-expression networks to a cohort of 252 adult meningiomas and derive a cluster of genes which is able to predict meningioma recurrence with high accuracy. With the wide accessibility of custom-made mini-arrays, our findings support, and should encourage, the shift to include this or a similar classifier in routine clinical care. 35. The role of radiotherapy following gross-total resection of atypical meningiomas. J Neurosurg. 2012;117:679–86. -Hanjani S, Martuza RL, et al. Long-term recurrence rates of atypical meningiomas after gross total resection with or without postoperative adjuvant radiation. Neurosurgery. 2009;64:56–60. 1 as a Factor for Meningioma Proliferation. Cell Rep. 2018;22:3672–83. Clark VE, Erson-Özduman K, et al. Genomic analysis of non-NF2 meningiomas reveals mutations in TRAF7, KLF4, AKT1, and SMO. Science (80- ). 2013;339:1077–80. Å Integrated genomic analyses of de novo pathways underlying atypical meningiomas. Nat Commun. 2017;8. Recurrent somatic mutations in POLR2A define a distinct subset of meningiomas. Nat Genet. 2016;48:1253–9. DNA methylation-based classification and grading system for meningioma: a multicentre, retrospective analysis. Lancet Oncol. 2017;18:682–94. . Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources. Nat Protoc. 2009;4:44–57. Vernooij M, Ikram M. Incidental findings on brain MRI in the general population. N Med. 2007;:1821–8. Meningiomas: knowledge base, treatment outcomes, and uncertainties. A RANO review. J Neurosurg. 2015;122:4–23. [SEP] Justify:

Output: The text is irrelevant to the claim because it discusses gene co-expression networks related to meningioma recurrence, without addressing environmental psychology or individual behavior prediction at all.


Input: Task: corroborate the claim using the given text. Claim: Personalized medicine uses genetic data to tailor treatments to individual patients. [SEP] Text: If replicated, this finding could inform medication choice for this subgroup of patients. The Genome-Drugs for Depression project (62) used genome-wide association analyses in patients treated with nortriptyline or escitalopram to identify moderator effects (at a suggestive level of statistical significance) for two novel genetic variations. If replicated, these findings could inform the choice between these two medications. of again begin by pointing out that most previous studies cannot, by design, guide treatment selection. Included in this group are cohort studies of patients treated with a single medication or group of medications that examine genetic predictors of specific adverse effects, such as insomnia (63), sexual dysfunction (64, 65), and development of suicidal ideation (66). These cohort studies cannot distinguish general predictors of experiencing adverse effects from moderators or differential predictors of more adverse effects with one treatment than with another. For example, the serotonin receptor variation previously associated with insomnia during fluoxetine treatment may instead be associated with a general tendency to experience adverse effects with a range of medications (67, 68). In the same way, finding that a particular genetic variation is associated with suicidal ideation during treatment with citalopram (66, 69) could simply imply that this variation is associated with either suicidal ideation in general or suicidal ideation during treatment with any antidepressant. Neither of these latter interpretations would argue for or against the use of citalopram in this subgroup of patients. Of studies examining adverse events, only one has included patients treated with alternative drugs (70), finding that variation in a gene coding for the HTR2A serotonin receptor was associated with adverse effects with paroxetine but not with mirtazapine. Because no test for interaction or moderation was reported, this finding does not definitively address our question regarding personalized treatment: Does variation in HTR2A identify a group of patients who experience significantly fewer adverse effects during mirtazapine treatment than during paroxetine treatment? The finding of a significant relationship in patients treated with one drug and not in those treated with the other can sometimes reflect low statistical power rather than a true interaction or moderator effect. Selection of a Specific PsychotherapyWhile research on differential response to medications has focused on biomarkers and genetic variation, the limited research on differential response to psychotherapies has focused more on clinical characteristics (Table 3). [SEP] Justify:

Output: The text corroborates the claim by discussing how genetic variations may influence medication selection and treatment outcomes for individual patients. Specifically, it mentions the Genome-Drugs for Depression project, which aimed to identify genetic predictors that could guide medication choice for patients treated with nortriptyline or escitalopram. This aligns with the concept of personalized medicine, as it emphasizes using genetic data to tailor treatments to specific subgroups of patients, thereby supporting the claim that personalized medicine utilizes genetic information for individualized treatment plans.


Input: Task: contrast the claim using the given text. Claim: Biohacking is universally recognized as a replacement for traditional medical treatment. [SEP] Text: В данном случае один из основных вопросов был сформулирован следующим образом: «Как система здравоохранения должна реагировать на движение биохакинга? ». При этом биохакинг был определен как «технология, которая позволяет активным людям поддерживать уровень здоровья и продлевать жизнь». В этом контексте биохакинг все меньше становится похож на движимое любопытством «гаражное» исследование, оказываясь формой медицинской заботы о себе. [SEP] Justify:

Output: The text contrasts the claim by discussing how biohacking is defined as a technology for self-care rather than a replacement for medical treatment. It emphasizes the evolving perception of biohacking from a mere curiosity to a form of healthcare, suggesting that it complements rather than replaces traditional medical approaches.


Input: Task: pass the claim using the given text. Claim: Environmental psychology can predict individual behavior with high accuracy. [SEP] Text: Jääskeläinen J. Seemingly complete removal of histologically benign intracranial meningioma: Late recurrence rate and factors predicting recurrence in 657 patients. A multivariate analysis. Surg Neurol. 1986;26:461–9. -Gimbel H, König J, Zang KD, et al. Predictive value of progression-associated chromosomal aberrations for the prognosis of meningiomas: a retrospective study of 198 cases. J Neurosurg. 2001;95:601–7. . High incidence of activating TERT promoter mutations in meningiomas undergoing malignant progression. Brain Pathol. 2014;24:184–9. Yesilöz Ü, Frequent AKT1E17Kmutations in skull base meningiomas are associated with mTOR and ERK1/2 activation and reduced time to tumor recurrence. Neuro Oncol. 2017;19:1088–96. . SMO mutation status defines a distinct and frequent Molecular subgroup in olfactory groove meningiomas. Neuro Oncol. 2017;19:345–51. Integrating genetic and network analysis to characterize genes related to mouse weight. PLoS Genet. 2006;2:1182–92. . , Zhu S, Felciano RM, et al. Analysis of oncogenic signaling networks in glioblastoma identifies ASPM as a molecular target. Acad Sci. 2006;103:17402–7. -Ramahi I, et al. Integrated genomics and proteomics define huntingtin CAG length-dependent networks in mice. Nat Neurosci. 2016;19:623–33. Langfelder P, Horvath S. WGCNA: package for weighted correlation network analysis. BMC Bioinformatics. 2008;9. : archive for functional genomics data sets — update. Res. 2013;41 June:991–5. Effects in Analysis of Data : of Adjustment Methods. PLoS One. 2011;6. . Robust meta-analysis of gene expression using the elastic net. Res. 2015;43:1–11. Zhang B, Horvath S. A for Co-expression Network Analysis. Biol. 2005;4. Package ‘ dynamicTreeCut. ’ 2016;:1–14. [SEP] Justify:

Output: The text does not address environmental psychology or its ability to predict individual behavior, containing instead a collection of studies and data related to neurosurgery and genetic mutations in meningiomas. Thus, it is irrelevant to the claim about environmental psychology.


Input: Task: corroborate the claim using the given text. Claim: Personalized medicine uses genetic data to tailor treatments to individual patients. [SEP] Text: Research designs that consider only a single episode of treatment per person cannot examine whether any particular response pattern (e. g. , gastrointestinal side effects with a specific SSRI, responding favorably to interpersonal psychotherapy) is stable within individuals across episodes of treatment. Third, accurately predicting response to specific treatments may require combinations of several weak predictors rather than a single powerful one (73). For example, response to a specific antidepressant drug might be simultaneously moderated by a large number of variants of small effect. A recent genome-wide association study suggests that this may be the case (54). Developing rules for treatment selection based on multiple predictors will require useful theory regarding treatment mechanisms, large sample sizes, and healthy skepticism regarding predictors identified only after multiple comparisons. Given the large sample sizes needed to detect moderators of treatment effectiveness, randomized trials to inform personalized treatment may need to adopt broader recruitment strategies and more efficient methods for outcome assessment. Large, pragmatic trials have been proposed as a more efficient strategy for comparative effectiveness research (74). These methods could be extended to address questions of differential treatment effectiveness. Recruitment for randomized trials to identify moderators of treatment response might incorporate information regarding response to past treatments. Traditional clinical trials typically consider past treatment only for safety reasons, excluding patients with histories of adverse reactions to a study treatment. Future trials might consider past treatment response in order to select particularly informative samples of participants. For example, a study to identify genetic predictors of favorable response to drug A over drug B might preferentially include patients with past exposures to drug A and/or drug B. Information regarding past response could be combined with new data to more accurately distinguish true treatment effects from other sources of variation in outcome. Another alternative approach would use observational data from large, population-based samples of patients treated under naturalistic conditions. This approach has led to significant advances in personalizing treatment for other chronic health conditions (75, 76). Observational studies permit examination of thousands of patients rather than the hundreds typically enrolled in clinical trials. Most important, longitudinal data would permit study of multiple treatment episodes per patient, including exposures to similar and dissimilar treatments. These data could serve in two ways. First, only such longitudinal data could evaluate the stability of potential treatment response phenotypes prior to expending resources searching for a corresponding genotype. Second, observational studies could identify potential moderators or differential predictors for definitive evaluation in subsequent randomized trials. [SEP] Justify:

Output: The text corroborates the claim by discussing the importance of genetic predictors in personalizing treatment. It mentions that 'a study to identify genetic predictors of favorable response to drug A over drug B might preferentially include patients with past exposures to drug A and/or drug B,' indicating that genetic data is being utilized to tailor treatments based on individual patient responses. The text also highlights advances in personalizing treatment for chronic health conditions, aligning with the notion of personalized medicine.


Input: Task: contrast the claim using the given text. Claim: Biohacking is universally recognized as a replacement for traditional medical treatment. [SEP] Text: В этом контексте биохакинг все меньше становится похож на движимое любопытством «гаражное» исследование, оказываясь формой медицинской заботы о себе. Другая дискуссия проходила оффлайн в 2019 году в Аналитическом центре при Правительстве России [1]. В данном случае один из основных вопросов был сформулирован следующим образом: «Как система здравоохранения должна реагировать на движение биохакинга? ». [SEP] Justify:

Output: The text contrasts the claim by suggesting that biohacking is becoming less like a 'garage' research movement and is being viewed as a form of self-care within the medical domain. It raises the question of how the healthcare system should respond to the biohacking movement, indicating that it is not universally recognized as a replacement for traditional medical treatment.


Input: Task: pass the claim using the given text. Claim: Every ancient civilization relied on the same staple crops. [SEP] Text: Health & 17, 2020 Improving the iron delivery from staple food crops and food products of Agriculture and Cornell University, has pioneered several techniques to assess how much iron (Fe) is bioavailable from foods, meals and the overall diet. Such techniques are essential to identify and optimise dietary sources of Fe and alleviate iron deficiency, one of the leading global nutritional deficiencies. Staple food crops are a focus of this research, particularly beans as they are relatively high in Fe and a major staple in regions where Fe deficiency is prevalent. Measurement of Fe delivery from foods is challenging as greater Fe content does not always equate to more absorbable iron; hence the need for efficient tools to assess the nutritional quality of this essential micronutrient. A balanced diet must include adequate sources of all macro- and micronutrients. However, deficiencies in micronutrients, such as vitamins and minerals are common. Perhaps the most common nutritional deficiency worldwide is iron deficiency. Iron has many roles in human health, but it is arguably best known for its role in the molecule haemoglobin, a protein in red blood cells which transports oxygen around the body. The consequences of mild iron deficiency can be fatigue and lethargy, whereas more severe deficiencies can lead to health issues such as heart problems, increased risk of infections, pregnancy complications, and in children, cognitive deficiencies and poor neurological development. FuzullHanum/Shutterstock. com There are many good dietary sources of iron, including animal and plant sources. Animal sources of iron, such as red meat, are more easily absorbed by the body compared to plant-based sources, such as maize, wheat, beans, chickpeas, peas and lentils. However, it is often difficult and expensive to assess iron bioavailability from foods. The term ‘bioavailable’ refers to the iron that is accessible to the body for absorption, compared to iron which may be bound to other components of food thus rendering it unavailable to the body. Early work carried out by Glahn of the US Department of Agriculture produced methods that could be used for assessing bioavailable iron from foods. Glahn’s method provided a way by which food companies, crop breeders and nutrition professionals can measure iron bioavailability and therefore identify and develop food products and processing practices that can deliver more bioavailable Fe in the food supply. Yellow beans have unique qualities and nutritional traits that help improve the delivery of iron from a plant-based diet. [SEP] Justify:

Output: The text discusses research on iron bioavailability from staple food crops and does not address the claim about ancient civilizations using the same staple crops. It talks about nutritional deficiencies and dietary sources of iron without making any claims about the uniformity of staple crops across civilizations.


Input: Task: corroborate the claim using the given text. Claim: Personalized medicine uses genetic data to tailor treatments to individual patients. [SEP] Text: : Influence of the tyrosine hydroxylase Val81MET polymorphism and catechol-O-methyltransferase Val158MET polymorphism on the antidepressant effect of milnacipran. 2008; 23:121–128CrossrefPubMed51. : Association study of two serotonin 1A receptor gene polymorphisms and fluoxetine treatment response in Chinese major depressive disorders. 2006; 16:498–503CrossrefPubMed52. : Age-dependent antidepressant pharmacogenomics: polymorphisms of the serotonin transporter and G protein beta3 subunit as predictors of response to fluoxetine and nortriptyline. Neuropsychopharmacol 2003; 6:339–346CrossrefPubMed53. : Sequence analysis of the serotonin transporter and associations with antidepressant response. 2005; 58:374–381CrossrefPubMed54. -Myhsok B: A genomewide association study points to multiple loci that predict antidepressant drug treatment outcome in depression. Psychiatry 2009; 66:966–975CrossrefPubMed55. : The serotonin transporter polymorphism, 5is associated with a faster response time to sertraline in an elderly population with major depressive disorder. Psychopharmacology (Berl) 2004; 174:525–529CrossrefPubMed56. : The catechol-O-methyltransferase Val108/158Met polymorphism affects short-term treatment response to mirtazapine, but not to paroxetine in major depression. 2005; 5:49–53CrossrefPubMed57. : 941G polymorphism and short-term treatment response to mirtazapine and paroxetine in major depression. 2007; 144:325–331Crossref58. : A monoamine oxidase B gene variant and short-term antidepressant treatment response. 2007; 31:1370–1377CrossrefPubMed59. : The alpha 2A-adrenergic receptor gene polymorphism modifies antidepressant responses to milnacipran. J 2008; 28:518–524CrossrefPubMed60. : Monoamine transporter gene polymorphisms and antidepressant response in Koreans with late-life depression. JAMA 2006; 296:1609–1618CrossrefPubMed61. : The G196A polymorphism of the brain-derived neurotrophic factor gene and the antidepressant effect of milnacipran and fluvoxamine. [SEP] Justify:

Output: The text supports the claim by detailing the influence of specific genetic polymorphisms on antidepressant responses, indicating that genetic data is being utilized to personalize treatment strategies for individual patients with depression. For example, mentions of polymorphisms such as 'tyrosine hydroxylase Val81MET' and 'catechol-O-methyltransferase Val158MET' highlight how these genetic factors can predict treatment outcomes, demonstrating the application of personalized medicine in psychiatric care.


Input: Task: contrast the claim using the given text. Claim: Biohacking is universally recognized as a replacement for traditional medical treatment. [SEP] Text: При этом биохакинг был определен как «технология, которая позволяет активным людям поддерживать уровень здоровья и продлевать жизнь». В этом контексте биохакинг все меньше становится похож на движимое любопытством «гаражное» исследование, оказываясь формой медицинской заботы о себе. 3 Кажется, что мы имеем дело с двумя очень слабо связанными значениями термина «биохакинг». [SEP] Justify:

Output: The text contrasts the claim by stating that biohacking is defined as a technology for maintaining health and prolonging life, but it also indicates that there are weak connections between the meanings of 'biohacking,' suggesting that it is not universally recognized as a replacement for traditional medical treatment.


Input: Task: pass the claim using the given text. Claim: Every ancient civilization relied on the same staple crops. [SEP] Text: A bioassay to assess iron bioavailability developed a model known as the Caco-2 cell bioassay for iron bioavailability. The Caco-2 cell line is a human intestinal cell line widely used for studies of nutrient uptake. coupled simulated stomach and intestinal digestion with Caco-2 cell cultures to produce a model of the upper human intestinal tract. These experimental conditions enabled to accurately assess the most critical step that determines iron bioavailability, uptake by the intestinal epithelial cell. Iron uptake is assessed via measurement of the iron storage protein, ferritin, which has been shown to form in direct proportion to Fe uptake. Caco-2 cells provide breeders a cost-effective tool for evaluating the iron bioavailability of pulse crops. Measurement of intestinal cell ferritin enables high throughput of the model system, makes it extremely cost efficient, and negates challenges and flaws of other methods that have been used to assess iron bioavailability. Since the model’s inception in 1998, it has been thoroughly validated via direct comparison to numerous animal and human studies, predicting the correct effect on Fe bioavailability observed in the corresponding in vivo trial. This thorough validation of the model now means that it can be applied with confidence in applications such as plant breeding for improved Fe bioavailability from staple food crops, or for food science applications to optimise Fe nutrition in food products. It is important to note that the Caco-2 cell bioassay predicts the amount of Fe that can be delivered from a food. This distinction is a key feature of the bioassay as the chemical nature of Fe and its interaction with food components means that Fe concentration in a food or meal does not always correlate with Fe absorption. The bioassay is therefore a practical and data-driven approach to Fe nutrition. A Focus on the past 20 years there have been numerous applications of the Caco-2 cell bioassay. Perhaps the most notable applications have been the ongoing studies of Fe delivery from the common bean. Dr Glahn’s research was the first to demonstrate that the colour of the seed coat can have profound effects on Fe delivery from beans. Studies have shown that beans in market classes such as red, red-mottled, dark red, purple, cranberry and black generally have low Fe bioavailability; whereas most white and some yellow bean varieties have higher Fe bioavailability. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses a bioassay model for assessing iron bioavailability in crops, particularly focusing on modern applications and nutritional studies of beans. It does not address or provide information about staple crops used by ancient civilizations or whether they relied on the same types.


Input: Task: corroborate the claim using the given text. Claim: Personalized medicine uses genetic data to tailor treatments to individual patients. [SEP] Text: J Psychopharmacol 2007; 21:650–656CrossrefPubMed62. -: Genome-wide pharmacogenetics of antidepressant response in the project. Psychiatry 2010; 167:555–564CrossrefPubMed63. -: Serotonin transporter polymorphisms and adverse effects with fluoxetine treatment. 2003; 54:879–883CrossrefPubMed64. : Serotonin 2A-1438 G/A and G-protein beta3 subunit C825T polymorphisms in patients with depression and SSRI-associated sexual side-effects. Neuropsychopharmacology 2006; 31:2281–2288CrossrefPubMed65. : Genetic and clinical predictors of sexual dysfunction in citalopram-treated depressed patients. Neuropsychopharmacology 2009; 34:1819–1828CrossrefPubMed66. : Association between treatment-emergent suicidal ideation with citalopram and polymorphisms near cyclic adenosine monophosphate response element binding protein in the STAR*D study. Psychiatry 2007; 64:689–697CrossrefPubMed67. van Os J, Prins M: Serotonin transporter polymorphisms and the occurrence of adverse events during treatment with selective serotonin reuptake inhibitors. Psychopharmacol 2007; 22:137–143CrossrefPubMed68. : Association between a functional serotonin transporter polymorphism and citalopram treatment in adult outpatients with major depression. Psychiatry 2007; 64:783–792CrossrefPubMed69. -Mahon F: Genetic markers of suicidal ideation emerging during citalopram treatment of major depression. Psychiatry 2007; 164:1460–1461CrossrefPubMed70. : Pharmacogenetics of antidepressant medication intolerance. Psychiatry 2003; 160:1830–1835CrossrefPubMed71. : The role of avoidance and obsessiveness in matching patients to cognitive and interpersonal psychotherapy: empirical findings from the treatment for depression collaborative research program. J Psychol 1996; 64:951–958CrossrefPubMed72. : Attachment as moderator of treatment outcome in major depression: a randomized control trial of interpersonal psychotherapy versus cognitive behavior therapy. J Psychol 2006; 74:1041–1054CrossrefPubMed73. Goldstein DB: Common genetic variation and human traits. [SEP] Justify:

Output: The text provides multiple references and studies regarding genetic polymorphisms, specifically mentioning how genetic factors are related to antidepressant responses. This supports the claim by indicating that genetic data is used to understand how different patients may respond to treatments, which is a key aspect of personalized medicine.


Input: Task: contrast the claim using the given text. Claim: Biohacking is universally recognized as a replacement for traditional medical treatment. [SEP] Text: Разумеется, эти практики серьезно отличаются друг от друга, как и их риски в сферах здравоохранения и биобезопасности. Кажется, что мы имеем дело с двумя очень слабо связанными значениями термина «биохакинг». Наиболее явным вариантом его практик в первом смысле является расположенная вне академических институций лаборатория, часть оборудования которой изготовлена самостоятельно работающими в ней энтузиастами. [SEP] Justify:

Output: The text contrasts the claim by emphasizing that biohacking and traditional medical treatment are significantly different and that their associated risks in healthcare and biosafety are also distinct. It indicates that the practices and meanings attributed to biohacking vary greatly, suggesting that it is not universally recognized as a valid replacement for conventional medicine.


Input: Task: pass the claim using the given text. Claim: Every ancient civilization relied on the same staple crops. [SEP] Text: Seed coat colour is due to the presence or absence of compounds known as polyphenols. Storage cells in a bean seed (Phaseolus vulgaris), imaged with scanning electron microscopy. Further studies by the Glahn research team identified compounds in a class of polyphenols known as flavonols, specifically designating the flavonols quercetin and myricetin as inhibitors of Fe uptake. Additional inhibitors of Fe uptake were identified in the polyphenol class of cyanidins; however, most importantly this research identified polyphenolic compounds in the flavonol class that promote Fe uptake. Specifically, the compounds known as kaempferol, kaempferol 3-glucoside, catechin and epicatechin have been shown to promote Fe uptake. Moreover, certain varieties in the yellow bean market class have been identified that are high in these compounds and have little or no inhibitory polyphenols and thus exhibit high Fe bioavailability. Recently, the slow-darkening trait observed in some varieties of pinto beans also results in high levels of these Fe uptake promoting polyphenols, and low levels of the inhibitory compounds thus delivering more Fe for absorption. Additional studies of beans by the Glahn lab have looked at the components of the bean seed in regards to Fe concentration and bioavailability. These studies found that within the cotyledon, i. e. the centre white part of the bean, the individual cotyledon cell walls do not break down due to cooking, chewing or gastrointestinal digestion. Given that 70-95% of the Fe in a bean is located in the cotyledon, within the cotyledon cells, this observation represents a new factor affecting Fe delivery from beans. This same factor applies to other legumes. Identifying this factor is significant as it identifies an obstacle that can be overcome to unlock additional Fe nutrition from beans and other legumes. A microscopic image of cooked Trypan blue stained cotyledon cells from white (navy) bean seeds following in vitro gastric and intestinal digestion (magnification 80Å~). This image illustrates how the low pH and enzymes of the gastrointestinal tract have little effect on the intact cell wall structure. Glahn et al. , FoodFunct. 2016. doi:10. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses polyphenolic compounds in bean seeds and their effects on iron uptake in nutrition. It does not address the topic of staple crops in ancient civilizations or make any comparison across different civilizations regarding their agricultural practices.


Input: Task: corroborate the claim using the given text. Claim: Personalized medicine uses genetic data to tailor treatments to individual patients. [SEP] Text: Sequencing cancer genomes to tailor treatments to individual patientsScreening for hundreds of mutations in tumours is the most promising route to customised drug treatments for cancer. Genomics 02 December 2014 link to page Download PDF Genome sequencing could provide a route to customised drug treatments for cancerJames King-Holmes LibraryIn 2010, an elderly woman with metastatic bladder cancer who was participating in a clinical trial at Center (MSKCC) in had an extraordinary response to everolimus, a drug that inhibits the mTOR (mammalian target of rapamycin) signalling pathway. The mTOR pathway integrates intracellular and extracellular signals and acts as a central regulator of cell metabolism, growth, proliferation and survival. The woman was the only patient who had complete resolution of metastatic disease out of 37 participants in the trial, and researchers started to look at one gene at a time to try to find out why she responded to treatment. When they found nothing abnormal in the genes they looked at, the team turned to whole-genome sequencing of the tumour to investigate the genetic basis of her remission. They discovered that of the 17,000 mutations located in the genome, one led to a loss-of-function mutation in the tuberous sclerosis complex 1 (TSC1) gene, which correlates with everolimus sensitivity, and was key to her responding to treatment[1]. “The reason we could solve that mystery was because we were able to look at every single gene,” says Solit, a medical oncologist involved in the trial. Although whole-genome sequencing is currently too expensive to do in every cancer patient, it is the best way to characterise and identify DNA or RNA sequences so as to discover the acquired alterations that are driving cancer growth. Profiling tumour DNA helps to prioritise anti-cancer treatment by identifying specific therapies to which the patient’s cancer may be sensitive or resistant. Some molecular profiling tests are relatively simple, pointing the proverbial narrow laser beam at selected areas in the genes of interest. But many researchers are now opting to significantly increase the scope of that beam. [SEP] Justify:

Output: The text corroborates the claim by detailing how whole-genome sequencing and molecular profiling of tumor DNA are methods used in personalized medicine to identify specific therapies for cancer patients. It discusses an example of a patient whose response to treatment was linked to a genetic mutation discovered through sequencing, exemplifying how genetic data can inform individualized treatment plans.


Input: Task: contrast the claim using the given text. Claim: Biohacking is universally recognized as a replacement for traditional medical treatment. [SEP] Text: Во втором смысле мы будем иметь дело с тяготеющими к трансгуманизму практиками приема лекарственных средств без назначения врача, и изменениями в образе жизни, мотивированными собственным истолкованием результатов биологических исследований. Разумеется, эти практики серьезно отличаются друг от друга, как и их риски в сферах здравоохранения и биобезопасности. Кажется, что мы имеем дело с двумя очень слабо связанными значениями термина «биохакинг». [SEP] Justify:

Output: The text contrasts the claim by discussing practices associated with biohacking that differ significantly from traditional medical treatment. It emphasizes that biohacking involves self-directed practices motivated by individual interpretations of biological research and differs greatly in terms of risk and intent compared to conventional healthcare.


Input: Task: pass the claim using the given text. Claim: Every ancient civilization relied on the same staple crops. [SEP] Text: 1039/c6fo00490c Finally, the Caco-2 cell bioassay has found that the fast-cooking trait, highly desirable to many bean consumers, has been linked to improved Fe delivery. Fast cooking is believed to be associated with the same polyphenolic compounds that promote Fe uptake, as well as genes that may control thickness of cotyledon cell walls. In summary, the above observations are all good news for bean growers, food producers and consumers who seek improved Fe nutrition from this staple food crop. This research gives new targets for bean breeders, and ultimately provides enhanced nutritional quality for consumers and value-added traits for producers. Other applications of the Caco-2 for Maize: The Caco-2 cell has identified the germ fraction (ie. embryo) of the maize kernel as the major component that inhibits Fe uptake from maize. Thus, degermed maize flour may represent an opportunity to provide improved Fe nutrition. In addition, these studies suggested that identifying and/or developing maize varieties with higher Fe density in the endosperm of the kernel should also provide more bioavailable Fe. Lentils: Red lentils are commonly dehulled post-harvest. The Caco-2 cell bioassay has identified the dehulling process as improving Fe delivery from lentils. Yellow bean breeding lines with fast cooking times and improved iron bioavailability being tested at the Farm, Michigan. Peas: Overall, peas have been identified as an excellent legume to deliver more bioavailable Fe. for Infants: As infants are particularly prone to Fe deficiency, complementary foods represent an excellent application of the Caco-2 cell bioassay to identify specific foods and food combinations to improve Fe nutrition for this vulnerable age group. Food Products: Major food companies routinely make use of the Caco-2 cell bioassay to identify optimal formulations to deliver bioavailable Fe while balancing sensory and other quality concerns. Poultry model for iron bioavailability Human studies of Fe bioavailability are expensive and time-consuming; thus, there is a critical need for the combination of the Caco-2 cell bioassay and an animal model to refine objectives for definitive human studies, and if possible reduce the number of human trials. Thus, to complement the bioassay, and his research team also developed a poultry model for iron bioavailability studies. [SEP] Justify:

Output: The text is irrelevant to the claim about staple crops in ancient civilizations. It discusses the role of the Caco-2 cell bioassay in assessing iron bioavailability in various food crops like beans, maize, lentils, and peas, which does not address the claim regarding ancient civilizations or their reliance on staple crops.


Input: Task: corroborate the claim using the given text. Claim: Personalized medicine uses genetic data to tailor treatments to individual patients. [SEP] Text: “Our approach is to put the flood light on that cancer gene — the entire coding sequence of the gene — to identify additional areas with potential vulnerability to targeted drugs,” says Vincent Miller, a medical oncologist and chief medical officer at (Cambridge, Massachussetts), which manufactures two comprehensive genomic-profiling assays. Gene alterationsMost human tumours are caused by acquired alterations within the cancer genome, leading to oncogene activation or tumour suppressor gene inactivation. Oncogenes are derived from normal genes (proto-oncogenes) involved in the regulation of cell growth. Alterations to the nucleotide sequence, or the amount of protein the proto-oncogene produces, can lead to changes that drive the unchecked growth typical of cancer. Oncogenes can be activated or tumour suppressor genes inactivated in four main ways: single nucleotide polymorphisms, referred to as point mutations, which result from a base substitution at one nucleotide; small duplications of consecutive nucleotides, insertions or deletions involving one or a few nucleotides, or more complex mutations involving a combination of deletions and insertions of one or a few nucleotides; exon or gene copy number changes; and structural variants such as translocations or inversions that often result in fusion genes (see figure). Medicine debuted its FoundationOne assay for malignant solid tumours in 2012, it tested the DNA sequence of 136 genes. Just two years later, the product now tests for alterations in 315 cancer genes, which includes sequencing parts of certain genes, referred to as introns, that aren’t normally coded. The assay — which costs US$5,800 and may not be completely covered by health insurance — reveals all classes of genomic alterations, including base substitutions, insertions, deletions, copy number alterations and selected fusions. The company reported that more than 9,000 patients were tested with FoundationOne in 2013. In 2014, the projected number is around 25,000. “This is a very brisk ramp for what’s basically a new approach with a steep learning curve,” says Miller. A second assay, FoundationOne Heme, which costs US$7,200 and primarily targets blood cancer and sarcomas, was co-developed with researchers at MSKCC. [SEP] Justify:

Output: The text corroborates the claim by discussing genomic-profiling assays that utilize genetic data to identify vulnerabilities in cancer genes, which are essential for tailoring treatments to individual patients. It explains how alterations in the cancer genome lead to personalized approaches, such as the FoundationOne assay, which tests for specific gene alterations to inform targeted drug treatments.


Input: Task: contrast the claim using the given text. Claim: Biohacking is universally recognized as a replacement for traditional medical treatment. [SEP] Text: Разумеется, эти практики серьезно отличаются друг от друга, как и их риски в сферах здравоохранения и биобезопасности. 4 Однако с точки зрения их ролей в системе отношений между институциональной наукой и обществом, эти практики имеют больше сходств, чем различий. В данной статье мы представим генерализованное понимание роли биохакинга в существующей системе социального распределения знания. [SEP] Justify:

Output: The text contrasts the claim by discussing the differences and similarities between biohacking and traditional medical practices, suggesting that they play distinct roles in healthcare and safety. This indicates a lack of universal recognition of biohacking as a replacement for traditional treatment.


Input: Task: pass the claim using the given text. Claim: Every ancient civilization relied on the same staple crops. [SEP] Text: In combination with the bioassay, the poultry model has been validated in direct parallel comparison to human trials. In studies of crops such as beans and pearl millet, the bioassay and the poultry model correctly predicted the human efficacy studies. As a result, the combination of these research tools now represent a popular approach to studies of Fe nutrition. Lentil crop. Dr Glahn’s research has identified that the dehulling process improves Fe delivery in lentils. What can people do at home to minimise their risk of iron deficiency and to maximise the bioavailability of iron in their diet? <> Humans require a diversity of foods for optimal Fe nutrition, which also promotes other beneficial nutritional outcomes. Therefore, consumption of diverse diet of nutrient dense foods containing a variety of “protein foods“, such as legumes (beans and peas), lean meat (poultry and beef), seafood, eggs, and nuts. In addition, a variety of vegetables and whole fruits are highly recommended. Whole grains should make up at least half of all grain intake. Recommended amounts of dairy products should also be followed. Adherence to these dietary guidelines generates a healthy intestinal tract that facilitates Fe absorption and overall health. Improving the iron delivery from staple food crops and food products was last modified: November 8th, 2023 Keywords: Beansbioavailable ironCaco-2 cell bioassayFeflavonolsironiron bioavailabilityiron deliverymicronutrientsof Agriculture and this 193. Advance online publication. & Glahn RP. (2020). Polyphenolic profiles of yellow bean seed coats and their relationship with iron bioavailability. J Chem, 68(3), 769–778. & Tako E. (2019). An in vivo (Gallus gallus) feeding trial demonstrating the enhanced iron bioavailability properties of the fast cooking Manteca yellow bean (Phaseolus vulgaris L. ). Nutrients, 11(8), 1768. & Glahn RP. (2018). The fast cooking and enhanced iron bioavailability properties of the Manteca yellow bean (Phaseolus vulgaris L. ). Nutrients, 10(11), 1609. . (2014). Iron bioavailability in low phytate pea. Crop Science. 55(1):320-330. & Wiesinger JA. (2016). [SEP] Justify:

Output: The text does not address the claim regarding ancient civilizations relying on the same staple crops. Instead, it discusses modern research on iron bioavailability in various crops like beans and lentils, dietary recommendations, and the importance of a diverse diet for nutrition. This content is unrelated to the claim, making it irrelevant.