Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: 21% (IC95% 3. 07–8. 22%) 99. 81% (IC95%. 99. 31–99. 98%) 77. 25% (IC95%. 76. 79–77. 69%) 89. 47% (IC95%. 66. 38–97. 34%) 0. 930 (IC95%. 0. 9158 to 0. 945) -0. 01 (IC95%. -0. 14 to 0. 11) 12. 23 (IC95%. 10. 64 to 13. 83) p = 6. 981 XGBoost 92. 33% (IC95% 88. 89–94. 98%) 95. 62% (IC95% 94. 20–96. 78%) 97. 57% (IC95% 96. 50–98. 32%) 86. 74% (IC95%. 83. 12–89. 69%) 0. 982 (IC95%. 0. 9755 to 0. 9891) 0. 01 (IC95%. -0. 23 to 0. 25) 1. 2 (IC95%. 1. 07 to 1. 34) *Sensitivity (Sens) is the ability of the model to correctly rule out patients with the outcome of interest. ^Specificity (Spec) is the ability of the model to correctly detect patients without the outcome of interest. ̈Negative predictive value (NPV) is the probability that a patient will not have the outcome of interest if the model classifies it as such. +Positive predictive value (PPV) is the probability that a patient will have the outcome of interest if the model classifies it as such. (Area under the ROC curve) is a numerical measure that evaluates the model's ability to differentiate between patients with and without the outcome of interest. 95% CI calculated by DeLong DeLong's Test: Test to define differences between areas under the curve Sample size calculation. A formal sample size calculation was not made because there was a fixed cohort of users. Imputation of missing data A data imputation process was performed to variables with less than 20% data losses using the K (KNN) algorithm, an imputation technique that uses information from existing data to estimate missing values. The algorithm selects a number k of observations closest to the observation with the missing value (neighbors) in the complete dataset. Then use the mean of those k neighbors to estimate the missing value. [SEP] Justify:

Output: The text contrasts the claim by discussing various statistical measures and diagnostic outcomes related to a biohacking study, but does not suggest that biohacking techniques can completely eliminate the risk of chronic diseases. Instead, it focuses on sensitivity, specificity, predictive values, and model performance in assessing outcomes, which implies partial effectiveness rather than total elimination of risks.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: (D): [] transformed cells corresponding result has been observed for the BY yeast background (lower panels). While the general trend for both strains is similar, in this case, accordingly to the higher robustness observed for this genetic background (compare the behaviors of the GRF18U and BY cells in Figure 3 and 4 ) a lower accumulation of ROS has been detected. Taken together these data allow a more deeper analysis of the data shown in Figure 3 where increasing H2O2 concentration lead to longer delays of growth. These longer delays are clearly due to decreasing fractions of viable cells at the time of inolucum. The same cells analysed by flow cytometry can also be analysed with a fluorescence microscope for ROS accumulation. In the wild type strain, cells with a strong and granular rhodamine staining are quite frequent and well represented, while in the producing strain almost no signal for ROS is detectable (data not shown). All the described data demonstrate that the endogenous production of the antioxidant L-AA protects cells from oxidative damage, scavenging the intracellular production of ROS and/or increasing cell viability. DiscussionWe report for the first time the biosynthesis of vitamin C by recombinant S. cerevisiae cells starting from D-glucose. Accumulation of ascorbic acid was proven to be successful in two different strains (Figure 2). Furthermore, we proved that the intracellular accumulation of L-AA leads to an improved robustness of the recombinant yeasts during growth under different stress conditions. The recombinant yeasts that are functionally transformed to produce L-ascorbic acid generate lower levels of ROS (Fig. 5) and exhibit improved growth and a higher viability under conditions of organic (Fig. 4b) and inorganic (Fig. 4a) acid stresses as well as oxidative stress (Fig. 3c and d). These are physiological conditions often encountered during industrial large scale fermentations. For each yeast background, the degree of robustness seems to be directly related to the amount of intracellularly produced vitamin C (Fig. 2, 3 and 4). In accordance with our data it has been shown before that the addition of ascorbic acid to the growth medium has beneficial effects for heterologous protein production in yeasts [22]. [SEP] Justify:

Output: The text discusses the biosynthesis of vitamin C by recombinant yeast cells and their robustness under various stress conditions, mentioning factors such as ROS accumulation and cell viability. However, it does not address the claim regarding urban living and stress levels, making the relevance of the text to the claim entirely unrelated.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: So far, most of the current crop of potential approaches have only been tested in cells grown in laboratory dishes or in animal models. But all this activity reflects the field’s renewed optimism that somehow, correcting the genetic defect that causes cystic fibrosis will soon be possible. Prototype diseaseCystic fibrosis is caused by mutations in the gene that encodes the cystic fibrosis transmembrane conductance regulator (CFTR). This protein sits in the cell membrane and helps regulate the flux of water and negatively charged chloride ions into and out of cells. CFTR’s broad function means that the disease affects a variety of organs, including the lung, pancreas, liver, intestine and testes. Without functional CFTR protein, the body has trouble making sweat, digestive fluids and mucus normally. However, most people with the disease die from lung complications: the mucus that clogs the airways of cystic fibrosis patients makes their lungs vulnerable to infection and scarring, and even in developed countries half of patients die before the age of 40 years. Cystic fibrosis was really at that moment the prototype disease to be used for gene therapyThe CFTR gene was identified in 1989, touching off a wave of enthusiasm for developing a gene therapy cure for the disorder. “Cystic fibrosis was really at that moment the prototype disease to be used for gene therapy,” says Marianne Carlon, a gene therapy researcher at in Leuven, Belgium. “Theoretically, cystic fibrosis is easy,” says Carlon. It’s a recessive, single-gene disorder, meaning that two mutated copies of CFTR are necessary to produce the disease — and, by extension, delivering a single functional copy of that gene to airway cells ought to alleviate it. And in the lung, gene therapy can be delivered by inhalation rather than more invasive methods. Source: Marianne CarlonMarianne Carlon, a gene therapy researcher at in Leuven, Belgium, says liposomes are not very efficient at getting their genetic cargo into the host nucleusCystic fibrosis was also a compelling target because it is one of the most common lethal inherited diseases, with more than 90,000 sufferers worldwide, so gene therapy could help many people. Between 1993 and 2015, scientists conducted more than two dozen clinical trials involving about 450 patients[2]. [SEP] Justify:

Output: The text corroborates the claim by discussing the research efforts in gene therapy specifically targeting cystic fibrosis, indicating it as a 'prototype disease to be used for gene therapy' due to its genetic basis and the potential to correct the defect causing the disease. It further mentions ongoing clinical trials and the optimistic outlook of researchers, aligning with the claim regarding research into gene therapy for treating diseases such as cystic fibrosis.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: · Supplement 1 · Spring 2014 Monitoring chronic diseases in Canada: the K. C. Roberts, MSc; T-L. Bennett, MSc; E. R. Driscoll, MSc; G. ; L. This 0. 8 Mb - 34 pages) Submit a manuscript the Editors Methods: Available national and international health indicators, frameworks and national health databases were reviewed to identify potential indicators. To make sure that a comprehensive and balanced set of indicators relevant to chronic disease prevention was included, a conceptual model with "core domains" for grouping eligible indicators was developed. Specific selection criteria were applied to identify key measures. Extensive consultations with a broad range of government partners, nongovernmental organizations and public health practitioners were conducted to reach consensus and refine and validate the Framework. Results: contains 41 indicators organized in a model comprised of 6 core domains: social and environmental determinants, early life/childhood risk and protective factors, behavioural risk and protective factors, risk conditions, disease prevention practices, and health outcomes/status. Also planned is an annual release of updated data on the proposed set of indicators, including national estimates, breakdowns by demographic and socioeconomic variables, and time trends. Conclusions: Understanding the evidence related to chronic diseases and their determinants is key to interpreting trends and crucial to the development of public health interventions. and its related products have the potential of becoming an indispensable tool for evidence-informed decision making in Canada. diseases such as diabetes, cancer, arthritis, mental illness, and cardiovascular and chronic respiratory diseases are major contributors to reduced quality of life, loss of productivity, and increased hospitalization and health care costs as well as premature death in Canada. Footnote 1 Out of every 5 Canadians aged 20 years or older, 3 have a chronic disease and 4 are at risk of developing a chronic condition. Footnote 2 The importance of identifying and addressing the risk factors and determinants of chronic disease has long been recognized as central to the prevention of chronic disease. Footnote 3 Understanding the evidence surrounding chronic diseases and their determinants is key to interpreting trends and crucial to developing public health interventions that can effectively reduce rates of chronic disease and improve the population's health and quality of life. Since its inception in 2005, the Agency of Canada (the Agency) has collaborated with provincial and territorial ministries of health to develop and implement several pan-Canadian chronic disease strategies, policies and programs aimed at reducing and preventing chronic diseases. [SEP] Justify:

Output: The text contrasts the claim by discussing chronic diseases and emphasizing the importance of understanding their determinants and addressing risk factors as crucial to prevention. It notes that chronic diseases are significant contributors to healthcare challenges, and while strategies are being developed to combat them, it does not support the assertion that biohacking techniques can 'entirely eliminate' the risk.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: Furthermore, the respective yeast strains are a major step for the development of a cell factory for the production of vitamin C itself, one of the most important specialty chemicals manufactured in the world. This aim has been long sought for, but never reached up to now [23]–[25]. In this respect, it is noteworthy that we have previously shown that (i) yeast cells do have one or more transporters which allow the accumulation of intracellularly produced ascorbic acid in the culture medium (i. e. , thus greatly facilitating the purification procedures) and (ii) that S. cerevisiae cells are quite tolerant to high concentrations of ascorbic acid (at least 40–50 g/L) [16]. Consequently, the industrial production of ascorbic acid by a one-step fermentation from D-glucose appears closer then ever. One final general consideration can be made considering the role of ROS. It is well known that the production of ROS is common for many types of cancer cells and that vitamin C has a positive effect in reducing the incidence of stomach, lung and colorectal cancer [26], [27]. On the other hand vitamin C can under certain circumstances even increase the generation of ROS and could have detrimental effects at least under certain circumstances [28]–[30]. Hopefully, S. cerevisiae cells endogenously producing vitamin C could represent a well suited cellular model to study the genesis/protection of ROS and genotoxicity in higher eukaryotic organisms. Materials and strains, transformation, media and cultivation The S. cerevisiae parental strains used in this study were GRF18U [31] (MATα; ura3; leu2-3,112; his3-11,15; cir+), and BY4742 (MATa; ura3Δ0; his3Δ1; leu2Δ0; lys2Δ0; cir+), EuroNo. Y10000- Yeast transformations were performed according to the LiAc/PEG/ss-DNA protocol [32] and both strains were transformed with one or more of the constructs described below, in parallel with the corresponding empty plasmid(s). The presence of the heterologous genes was confirmed by PCR analysis. For each set of transformation at least three independent clones were initially tested, showing no meaningful differences among them. [SEP] Justify:

Output: The text does not address the claim regarding urban living and stress levels. Instead, it focuses on the development of yeast strains for the production of vitamin C and the implications of reactive oxygen species (ROS) in cancer. Therefore, it is irrelevant to the claim about urban living and stress.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: These drugs have raised the bar for gene therapy because they target the underlying molecular defect, rather than merely treating cystic fibrosis symptoms as past treatments have done. But the drugs only help patients with a few of the nearly 2,000 known CFTR mutations. “That leaves out a lot of people,” says Parsons. The most impressive CFTR corrector so far, ivacaftor, is most effective in those with so-called class III mutations, who total around 4% of cystic fibrosis patients. A second formulation — a combination of ivacaftor and another molecule, lumacaftor — targets the most common mutation, known as Phe508del, which accounts for about 70% of CFTR mutations in Caucasians. But its effectiveness is much more modest. This leaves a big opening for gene therapy, since the majority of approaches to that treatment would help regardless of the mutation a patient carries. The UK consortium’s trial, published in 2015, was open to patients with any CFTR mutation, for example (although the majority carried Phe508del, as expected given its prevalence)[1]. The team chose a liposome vector because, unlike viruses, liposomes do not trigger an immune reaction and so can be administered over and over again. But the approach has its disadvantages. “Liposomes are nice for a proof of concept,” says Carlon, who was not involved in the work. However, they “really are not very efficient at getting their genetic cargo into the host nucleus”. Using liposomes to deliver gene therapy in cystic fibrosis Editorial adviser: Patients with cystic fibrosis lack functional CFTR protein, which is needed to make thin, watery mucus that keeps the lungs healthy. Normal CFTR gene can be delivered via inhalation of nebulised liposomes mixed with plasmid DNA encoding the protein. The liposomes enhance transport of the CFTR gene into host airway cells via endocytosis or direct fusion with the cell membrane. The plasmid then passes into the cell nucleus where the normal CFTR is transcribed, enabling the cell to make CFTR proteins. The UK consortium researchers suspect that this lack of efficiency accounts for the modest clinical results seen in the trial. They say the effectiveness may be improved by delivering a larger dose to the lungs with each gene therapy treatment. [SEP] Justify:

Output: The text corroborates the claim by discussing the potential of gene therapy specifically for cystic fibrosis, detailing how normal CFTR genes can be delivered via inhalation of nebulised liposomes. It highlights that the approach aims to address the underlying problem of the disease, aligning with the research aspect mentioned in the claim. Moreover, it indicates that gene therapy could benefit patients regardless of their specific CFTR mutations, underscoring the ongoing research and application of gene therapy for treating cystic fibrosis.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: The many chronic disease risk and protective factors that accumulate over the life course have been central to these strategies, most notably the 2005 Integrated Pan-Living Strategy,Footnote 4 endorsed by Canada's federal, provincial and territorial Ministers of Health and Health Promotion/Healthy Living. Given the need for an evidence base to inform policy and programmatic decision making and the move towards an integrated approach to chronic disease prevention, the Agency identified a requirement for a comprehensive approach to surveillance and reporting on chronic diseases and their associated determinants. An in-depth environmental scan revealed the absence of an appropriate national indicator framework (or set of indicators) to meet the Agency's needs. Some frameworks, such as the joint for Health Information–5 emphasize areas beyond the scope of chronic disease surveillance (e. g. a portion of the Framework is devoted to "health system performance" and "community and health system characteristics," which encompass areas broader than chronic disease surveillance). Others took a more narrow or detailed focus on a specific condition or stage of life. Footnote 6Footnote 7Footnote 8 As a result, the Agency undertook the development of a new indicator framework that focuses on integrated chronic disease surveillance. This report describes the approach taken to develop the (the Framework). This approach began with identifying the guiding principles for the Framework and developing a conceptual model upon which to group indicators to make sure the scope of the final Framework met Agency needs. The approach concluded with broad consultations with content/science experts and policy/program decision makers who are the Framework's key intended audience. This report also presents current and potential applications of the Framework that guide effective public health action to prevent chronic disease in Canada. Identifying the Framework's audience The rationale for developing the Framework was the need to provide timely and easily accessible information about trends in chronic disease that decision makers could use to identify key areas on which to focus preventative measures and develop health policies and strategies, and increase public and stakeholder understanding of the health of the population and the factors that affect it. Public health policy analysts and practitioners involved in chronic disease prevention at the federal, provincial and territorial levels were identified as the primary users of the data generated from the Framework. Understanding the information needs of these groups was therefore critical to the development of the Framework and the selection of relevant indicators. These indicators may also be used by other programs and jurisdictions for, among other reasons, comparison. [SEP] Justify:

Output: The text contrasts with the claim by discussing the complexities of chronic disease prevention and the need for an integrated approach, noting that while there are numerous factors influencing chronic diseases, no biohacking technique is mentioned as capable of entirely eliminating the risk. It emphasizes the requirement for a comprehensive framework and the varied determinants of chronic diseases, indicating that prevention is multifaceted and not wholly resolvable through biohacking techniques alone.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: The resulting S. cerevisiae strains constructed in this study are listed in Table 2, with their respective genotypes. In GRF18U the plasmid integration is locus specific (the auxotrophies were generated by multiple point mutations of the target genes), while integration is randomly directed in cells of the BY background. Download: PPTPowerPoint slidePNGlarger imageTIFForiginal imageTable 2. List of yeast strains constructed and used in this study cultures were grown in minimal synthetic medium (0. 67% w/v YNB Biolife without amino acids) with 2% w/v of D-glucose as carbon source. When required, supplements such as leucine, uracil, lysine and histidine were added to a final concentration of 50 mg/l, while the antibiotic nourseotricine sulphate (clo) was added to a final concentration of 100 mg/l. In the case of growth under oxidative or acidic stress, the desired stress condition was imposed by adding different concentrations of H2O2 (specifically 2, 2. 5, 3 and 3. 5 mM) or of lactic acid (45 g/l) directly to the medium or by lowering the medium pH to 2. 2 with HCl 6N. In the case of lactic acid addition, the pH value was adjusted to 3 with NaOH 4N. Yeast cells were inoculated at an initial optical density of 0. 1 (always 660 nm where not differently specified) and then optical density was measured at specific intervals of time over at least 55 hours from the inoculum. Each experiment was repeated at least three times. All strains were grown in shake flasks at 30°C and 160 rpm and the ratio of flask volume/medium was of 5/1. Gene amplification and expression plasmid construction All genes for the reconstruction of the L-AA pathway in yeast were PCR amplified on a 9700 (PE Appl. Biosystems, Inc. ) using Pwo DNA Polymerase (Roche Diagnostics) and following the manufacturer's instructions. Template DNA for and AtMIP was a cDNA library from A. thaliana (ATCC 77500) [33]; template DNA for ScALO1 consisted of 50 ng of genomic DNA from S. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses a scientific study involving yeast strains and their growth conditions, with no mention of urban living or stress levels. Therefore, it does not provide any evidence or argument related to the claim about urban living and stress.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: Several other groups around the world are working on other non-viral approaches to gene therapy, such as DNA nanop2017. The outcome of that trial will determine the fate of the group’s liposome work: if the greater efficiency of the lentiviral vector pans out, the consortium will focus its efforts there, but this isn’t yet certain. Parsons says the consortium’s viral-vector results so far look “very promising”. For the past decade, he has been working on a different lentiviral vector for cystic fibrosis gene therapy, based on the human immunodeficiency virus (HIV). Parsons’s protocol involves treating the airways just prior to gene therapy with lysophosphatidylcholine (LPC), a molecule that causes the tight junctions between airway cells to open briefly[6]. This opening enables the gene therapy vector to reach the underside of airway cells, where this particular vector happens to be able to enter more easily. It also allows access to the stem cells that renew the airway lining, which are typically located beneath the surface of the airway. “If you can target stem cells it changes the game,” says Parsons. Delivering a healthy copy of CFTR to airway stem cells could permit one-time gene therapy leading to permanent correction of the defect. LPC is a molecule normally found in the lungs. However, opening the tight junctions between airway cells, even briefly, could be risky — especially in the already compromised and often bacteria-infected lungs of cystic fibrosis patients. Parsons says the procedure doesn’t cause harm in animal studies, and has a five-year plan to begin human trials. Adeno-associated viral vectorsOther researchers are taking a new look at adeno-associated virus (AAV), a vector that was used in some early cystic fibrosis gene therapy trials but did not show effectiveness. More recently, “AAV gene therapy has been shown to be successful in other disease areas,” says Carlon, who is working on one AAV project at Catholic University. “I think that really fuelled reinvestigating this vector system for cystic fibrosis,” she adds. [SEP] Justify:

Output: The text corroborates the claim by discussing ongoing research into gene therapy specifically for cystic fibrosis, mentioning various approaches such as the use of lentiviral vectors and new strategies involving adeno-associated viral vectors. It highlights that researchers like Parsons are actively working on gene therapy protocols aimed at treating cystic fibrosis and that human trials are planned, aligning well with the claim that gene therapy is being researched for treating diseases.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: Guiding principles The Framework's 4 guiding principles prioritize prevention of chronic diseases and emphasize the need to better address common risk factors that lead to chronic diseases and disease burdens across populations. These principles are intended to both guide the selection of and reporting on indicators. Life course approach Health care practitioners are identifying chronic diseases and risk factors among younger and younger Canadian populations, which makes the selection of indicators that capture this emerging trend very important. Footnote 9Footnote 10Footnote 11 As a result, the Framework incorporates indicators for the various stages of life, from before birth and through early childhood and adolescence to the end of life (see Figure 1). Footnote 12Footnote 13 1 Life-course Diagram [1, Text Equivalent] incorporates indicators from multiple levels of the life-course, beginning before birth and early childhood and continuing to later adult life through until death. Factors such as socioeconomic factors and environmental factors are relevant across the entire life course. Prenatal, early life and childhood factors can only exert an influence during these stages of life, even if the impacts are long lasting. Behavioural risk factors, risk conditions, disease and the burden of illness all become more relevant as the life course progresses. Connections are made among the pathways that operate across an individual’s life course to influence the development of chronic disease and the different stages of disease prevention with primary focus on primordial prevention/health promotion and primary prevention. Disease prevention With a renewed focus on prevention, the Agency needed to move beyond reporting on single diseases towards a more comprehensive approach that takes into account the broader determinants of health as well as the risk factors and biological markers that contribute to the development of a variety of chronic diseases. Health equity approach The burden of chronic disease is not distributed evenly across the population and certain groups of Canadians face higher rates of chronic disease and poorer health. In general, people in less advantageous socioeconomic circumstances (e. g. lower income, poor working conditions, poor social support, etc. ) are less healthy than those at a higher socioeconomic status. Understanding the differences in health between population groups is critical to developing programs and policies that reduce these differences. In order to identify disparity gradients with the population, the Framework selects and prioritizes those indicators that could be stratified as per the Organization's recommendations for developing a "national health equity surveillance system. [SEP] Justify:

Output: The text contrasts the claim by discussing the importance of a comprehensive approach to disease prevention that acknowledges the influence of various risk factors and the broader determinants of health. It emphasizes that chronic diseases are influenced by socioeconomic factors, environmental factors, and behavioral risk factors throughout an individual's life course. This suggests that biohacking techniques alone cannot entirely eliminate the risk of chronic diseases without addressing these underlying factors.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: cerevisiae GRF18U, extracted with a standard method (according to [34], slightly modified) RnFGT was PCR amplified from a kidney cDNA library (Origene, CR-1003). The following primer pairs were used: for ALO1: ALO1for and ALO1rev for LGDH,: and for ME: and for MIP: and for and. The PCR fragments were sub-cloned into the pSTBlue-1 vector using the Cloning kit (Novagen) and checked by sequence analysis. The obtained sequences were the same as those reported in Genebank except for MIP in which two silent point substitutions (A271T and T685G) were detected. Finally, the coding sequences were EcoRI cut and sub-cloned into S. cerevisiae expression vectors of the YX series (R&D Systems, Inc. ) or derivates (pYX012bT and pYX062, generated for this study, see below) and into the centromeric expression vectors pZ3, pZ3bT [35] and pZ5 (this study, see below). In detail, ALO1 was sub-cloned into pYX042 (integrative, LEU2 auxotrophic marker, ScTPI promoter); LGDH was sub-cloned into pYX022 (integrative, HIS3 auxotrophic marker, ScTPI promoter), and ME and MIP into pYX062 (integrative, LYS2 auxotrophic marker, PCR amplified with oligonucleotides LYS2for and LYS2rev from S. cerevisiae genome and substituted to the URA3 auxotrophic marker in the plasmid pYX012 DraIII/NotI cut and blunt ended, ScTPI promoter) and pYX012 (integrative, URA3 auxotrophic marker, ScTPI promoter) respectively. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses scientific methodologies related to molecular biology and genetic engineering without any mention of urban living or stress levels.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: AAV gene therapy has been shown to be successful in other disease areas — I think that really fuelled reinvestigating this vector system for cystic fibrosisEarly work with AAV used a form of the virus called AAV2, which isn’t very efficient at getting into airway cells. team is working with an improved form called AAV5. They also added a stronger promoter, a region of DNA that enables a gene to be turned on. Animal studies suggest that the vector can produce long-lasting gene expression — at least 15 months in the mouse[7]. And the researchers say they do not see a fall off in gene expression caused by an immune response to the vector, even after three doses of the therapy[8]. Next, the team plans to test whether the AAV therapy can improve lung function in a pig or ferret model of cystic fibrosis. Additional strategies for correcting the CFTR gene make use of the latest molecular techniques. Researchers at University in Baltimore, Maryland, have packaged a truncated version of CFTR in an AAV vector that works by transcomplementation[9]. In this process, small fragments of healthy CFTR protein encoded by the genetic material in the vector interact with the host cell’s mutant CFTR and improve its function. In essence, this strategy gives cells the ability to make their own CFTR corrector drugs. And, as with CFTR correctors, each transcomplementation-based gene therapy product will only target one or a subset of CFTR mutations. “It’s working very well on Phe508del,” reports Liudmila Cebotaru, who is leading the project at University. But some mutations may not be able to be rescued by this strategy. Source: Liudmila CebotaruLiudmila Cebotaru, a researcher at University, has packaged a truncated version of CFTR in an adeno-associated virus vector that works by transcomplementationOther approaches using gene-editing technologies, such as and zinc-finger nucleases, are also mutation-specific[10]. But gene editing, which fixes a patient’s own DNA, has some advantages over gene addition, the usual strategy for gene therapy that simply adds a healthy copy of a gene to a patient’s genome. [SEP] Justify:

Output: The text corroborates the claim by discussing AAV gene therapy and its application to cystic fibrosis. It describes how researchers are developing improved AAV vectors to enhance gene therapy for cystic fibrosis, highlighting ongoing research efforts aimed at correcting the CFTR gene, which is directly relevant to treating cystic fibrosis. Additionally, the mention of other gene-editing technologies underscores the wider context of gene therapy research for similar diseases.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: "Footnote 14 burden of chronic diseases is not simply a sum of the impacts of each individual chronic disease, but often involves a complex interaction between several diseases, which presents additional challenges to Canadians. This concept of multimorbidityFootnote 15 is a critical public health issue and an independent predictor of adverse health outcomes, including decreased quality of life and increased health care costs, disability and premature mortality. As a result, the Agency incorporated the identification of relevant multimorbidity indicators as a key component of the Framework. Structuring the is no shortage of national or international health data, gathered using active (e. g. surveys) or passive (e. g. secondary use of administrative data) means, that can potentially be used to report on a wide range of areas that relate to the health of Canadians. Thus, the challenge in developing this Framework lay in identifying those measures that are the most important and relevant at providing an accurate picture of chronic disease in Canada and in ensuring alignment with other related frameworks. To make sure that the Framework contains a comprehensive and balanced set of indicators that are relevant and key to chronic disease prevention, the Agency identified specific a priori indicator selection criteria (Table 1), developed a conceptual model with core domains into which indicators would be grouped (Table 2) and defined a prioritization process at the outset. TABLE 1 Indicator selection criteria indicator is clearly relevant to chronic disease prevention and control and/or is a plausible proxy for the underlying (i. e. gold standard) measure. soundness: The scientific evidence supporting a link between the performance of an indicator and chronic diseases is strong. Validity: The indicator appears reasonable as a measure of what it is intended to measure (face validity), and the components of the indicator make sense (construct validity). Reliability: The same results can be obtained if measurements are repeated under identical conditions. Meaningful and useful The information must be easy to understand, relevant for government plans and priorities and useful for public health action (e. g. targets population groups that are likely more affected). Amenable to change Provides information that can lead to action for change: inform and influence policy or funding, alter behaviour of health services providers, or increase general understanding in the community (e. g. improve behaviours, outcomes and health services utilization). good quality data are already available, or data collection can be put in place at a relatively low cost. can be regularly collected and compared over time. [SEP] Justify:

Output: The text contrasts the claim by explaining the complex nature of chronic diseases and multimorbidity, highlighting that simply addressing individual chronic diseases is not sufficient to eliminate risk. It discusses the interactions between diseases as predictors for adverse health outcomes, emphasizing that chronic disease prevention requires a comprehensive approach and cannot be eliminated by biohacking techniques alone.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: ME EcoRI cut and blunt ended was also sub-cloned into pZ3bT (centromeric, G418R dominant marker, ZbTPI promoter) XbaI cut, blunt ended: the expression cassette bT promoter-AtME-polyA terminator was then PCR amplified with oligonucleotides btand polywhich has a recognition sequence for KpnI at the 5′ site; the cassette was then subcloned into pSTBlue-1 vector, and, after sequencing, KpnI excised and sub-cloned into pYX012-MIP KpnI cut, resulting in the pYX012 bTME-MIP expression vector. This construct allowed the integration of two heterologous genes into the yeast genome at the same time by the use of single marker of selection. cut was sub-cloned into pZ5. This is a centromeric vector derived from pBR1 (pYX022 in which the ARS-CEN fragment from Ycplac33 has been inserted [35]). pBR1 was cut KpnI and blunt ended, and the nourseotricine cassette (NatR) PvuII/SacI cut and blunt ended from pAG25 [36], has been inserted. All the restriction and modification enzymes used were from Biolabs (Hitchin, Herts, UK) or from (Mannheim, Germany). Standard procedures [37] were employed for all cloning purposes. All plasmids generated and utilized for the present study are described in Table 1. Determination of L-ascorbic acid For intracellular L-ascorbic acid determinations yeast cells were inoculated at an initial optical density of 0. 05 in minimal medium and grown for about 18 hours in order to reach a mid-exponential phase of growth. Cells were then harvested by centrifugation at 4000 rpm for 5 min at 4°C, washed once with ice-cold distilled water and then resuspended in about three times volume of ice-cold 10% (w/v) trichloroacetic acid, vortexed vigorously, and kept in ice for 20 minutes. The supernatant was then cleared from cell debris by centrifugation. Ascorbic acid was determined spectrophotometrically following a method adapted from that of Sullivan et Clarke [16], [19]. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses genetic cloning methods and laboratory procedures without mentioning urban living or stress levels. There is no relationship between the concepts presented in the text and the claim regarding the effect of urban living on stress.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: “You’ll get the subtleties of the gene back as well,” such as when and in what amount and in what form the gene is expressed, says Patrick Harrison, who is working on this approach at Cork in Ireland. Harrison’s current work targets three CFTR mutations that can all be ameliorated by cutting a few DNA base pairs out of the mutated gene. The counterintuitive strategy is a good test case for gene editing because it only requires a single step, cutting the DNA, rather than also inserting a corrected sequence. “It will be more efficient and it will be simpler,” Harrison says. “It will also work in cells that aren’t dividing very quickly, which is often the case in lung tissue. ”The only gene-editing strategy for cystic fibrosis that has been tested in humans so far is QR-010, a molecule developed by the Dutch biotechnology company ProQR to correct the Phe508del mutation, which has just entered phase I clinical trials. The company’s approach is unique in that its gene therapy aims to edit not the mutant DNA itself but the messenger RNA that the cell produces as a template for building a protein[3]. On account of its complexity, gene editing will be difficult to take from research tool to clinic, but that doesn’t mean it and any other avenues shouldn’t be investigated. “I think it’s very good for the field that there are lots of different approaches,” says Alton. “It doesn’t matter which of us gets there, it’s just important for the patients that one of us gets there. ”Drug treatments for cystic fibrosis Drug classMechanismExamplesBronchodilatorsWiden the airways to help other medications reach the lungs. Salbutamol, salmeterol. Mucus thinnersMake mucus less sticky so it is easier to remove from lungs through chest physical therapy or coughing. Hypertonic saline, dornase alpha, mannitol. Pancreatic enzymesHelp the body to digest food and absorb nutrients (replacing enzymes normally produced by the body that cannot always reach the digestive system because they are blocked by thick, sticky mucus). Pancreatin. [SEP] Justify:

Output: The text corroborates the claim by discussing ongoing research in gene therapy specifically targeting cystic fibrosis. It mentions Patrick Harrison's work on CFTR mutations and highlights the QR-010 molecule, a gene therapy approach developed to correct the Phe508del mutation in cystic fibrosis, which has entered phase I clinical trials. This explicitly supports the idea that gene therapy is being researched for treating diseases like cystic fibrosis.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: 9% CCHS (2012) rate due to a major chronic disease (cardiovascular diseases, all cancers, chronic respiratory disease), total population 458. 0 per 100 000 CVS (2009) Mortality rate due to cardiovascular diseases, total population 203. 7 per 100 000 CVS (2009) Mortality rate due to cancer, total population 210. 9 per 100 000 CVS (2009) Mortality rate due to chronic respiratory diseases, total population 43. 5 per 100 000 CVS (2009) Mortality rate due to suicide, total population 11. 5 per 100 000 CVS (2009) All-cause mortality rate ratios among people with and without diabetes, population aged 20+ years 2. 0 rate ratio755. 4 per 100 000 CVS (2009) Potential years of life lost due to chronic respiratory diseases 118. 1 per 100 000 CVS (2009) Potential years of life lost due to suicide 362. 1 per 100 000 CVS (2009) Probability of dying (%) between ages 30 and 69 years from major chronic diseases (cardiovascular disease, cancer, chronic respiratory disease, diabetes) 11. 4% CVS (2009) Probability of dying (%) between ages 30 and 69 years from cardiovascular disease 3. 5% CVS (2009) Probability of dying (%) between ages 30 and 69 years from cancer 7. 1% CVS (2009) Probability of dying (%) between ages 30 and 69 years from chronic respiratory diseases 0. 7% CVS (2009) Probability of dying (%) between ages 30 and 69 years from diabetes 0. 5% CVS (2009) Abbreviations: and Survey; HDL-C, high-density lipoprotein cholesterol; SLID, Survey of Labour and Income Dynamics; TC, total cholesterol. 1. Education is intricately linked with the health of the population and is an important determinant of health. Endnote 1 Education contributes to health and prosperity by: equipping people with knowledge and skills for problem solving, helping provide a sense of control and mastery over life circumstances, increasing opportunities for job and income security and job satisfaction, and improving people's ability to access and understand information to keep them healthy. of adult population with less than a high (secondary) school education, population aged 20 years and older. of adults who report that their highest level of completed education is less than high (secondary) school expressed as a proportion of the total population. Data source. [SEP] Justify:

Output: The text provides statistical data regarding mortality rates from various chronic diseases, such as cardiovascular diseases, cancers, and respiratory diseases. These figures imply that chronic diseases remain a significant risk, suggesting that biohacking techniques are unlikely to completely eliminate this risk as claimed. Instead, it highlights that education and understanding of health determinants play a critical role in mitigating such risks, contrasting with the claim that biohacking can fully eliminate them.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: We previously confirmed the identity of ascorbic acid by HPLC using yeast cells functionally transformed to produce ascorbic acid from L-galactose [16]. Flow cytometric analyses Reactive oxygen species (ROS) were detected by Dihydrorhodamine 123 as described in [20]. Cells were incubated with Dihydrorhodamine 123 (DHR 123, Co. , St. ) for 2 h, washed twice with PBS buffer and subsequently resuspended in propidium iodide solution 0. 46 mM for the identification of dead or severely compromised cells. Samples were then analyzed using a Quanta™ SC flow cytometer () equipped with a diode laser (excitation wavelength 488 nm, laser power 22 mW). The fluorescence emission was measured through a 525–550 nm band pass filter (FL1 parameter) for DHR signal and through a 670 nm long pass filter (FL3 parameter) for PI signal. The sample flow rate during analysis did not exceed 600–700 cells/s. A total of 20,000 cells was measured for each sample. Data analysis was performed afterwards with WinMDI 2. 8 software, build#13 01-19-2000 (Purdue University, [ Fluorescence microscopy Samples of the same yeast cultures treated and FACS analyzed for ROS content were also directly analysed using a 90i fluorescence microscope (excitation, 488 nm) using standard FITC filters. Images were taken using the software Metamorph 2. 2. 1. (2003) Oxidative stress in submerged cultures of fungi. Biotechnol 23: 267–302. View 2. (2004) Stress in recombinant protein producing yeasts. J Biotechnol 113: 121–135. View 3. (2007) Mechanisms of cell death in oxidative stress. Signal 9: 49–89. View 4. (2005) Complex cellular responses to reactive oxygen species. Biol 15: 319–326. View 5. Apel K, (2004) Reactive oxygen species: metabolism, oxidative stress, and signal transduction. 55: 373–399. View 6. (1991) Vitamin C: newer insights into its biochemical functions. 49: 65–70. View 7. (1990) Cellular functions of ascorbic acid. Biol 68: 1166–1173. View 8. [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses methodologies and findings related to ascorbic acid and reactive oxygen species, without mentioning urban living or stress levels at all. Therefore, it does not provide any support or contradiction to the claim.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: Murine models of human genetic diseases have been created using gene-targeted embryonic stem cells for over a decade, however, for many diseases, such as cystic fibrosis (CF), mice have failed to replicate crucial aspects of the human phenotype. In two recent back-to-back publications by Sun et al. 1 and Rogers et al. ,2 pig and ferret models for CF have been created for the first time. The embryonic stem cell-based cloning strategies developed for mice had never worked for other species, but 10 years ago somatic cell nuclear transfer came to the rescue and paved the way for the creation of Dolly the sheep. Nuclei isolated from somatic cells (fetal fibroblasts) were transferred into enucleated donor oocytes, which were subsequently implanted into pseudopregnant sheep, thereby opening the possibility of manipulating the genome of the somatic cells before transfer. Gene targeting of somatic cells suitable for somatic cell nuclear transfer has been challenging, however, and only a few gene-targeted non-rodent models have been generated to date. These include pigs for organ transplantation, and sheep for the production of secreted protein. The two recent papers by Sun et al. 1 and Rogers et al. 2 employ somatic cell nuclear transfer of gene-targeted fetal fibroblasts to generate pig and ferret models of genetic disease. The authors have targeted the CF gene, but the technology used will be widely applicable for other genetic diseases as well. During the course of their research the authors, many based at the University of Iowa, had to overcome several important hurdles. The first was that classical homologous recombination used to ‘knockout’ specific genes is extremely inefficient in somatic cells, compared with murine embryonic stem cells. Most gene-targeting strategies to date have employed promoter-trap strategies, which involve the insertion of a targeting construct carrying a promoterless selectable marker gene (such as antibiotic resistance) close to the promoter of a transcribed gene (‘promoter-trap’). This leads to expression of the selectable marker and enrichment of those cells in which recombination events have occurred when exposed to the relevant antibiotic. Promoter-traps require the target gene to be expressed but, unfortunately, the CF gene (CFTR) is not expressed in fetal fibroblasts so alternative strategies had to be sought. [SEP] Justify:

Output: The text corroborates the claim by discussing the development of gene-targeted models for cystic fibrosis (CF) and emphasizing the use of somatic cell nuclear transfer to create pig and ferret models of genetic disease. The mention of targeted research on the CF gene indicates that gene therapy approaches are indeed being applied to treat this disease. Furthermore, the text notes that the techniques developed for these models can be widely applicable for other genetic diseases, supporting the broader claim regarding the research into gene therapy for diseases like cystic fibrosis.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: Chronic exposure to second-hand smoke at a young age has also been linked to heart diseases and neurological disorders (sudden infant death, sleep difficulties) and certain cancers in adults (lung and breast cancer). Endnote 15Endnote 16 Passive smoking poses a greater risk to children than to adults in the same setting due to children's higher breathing rates per body weight and higher lung surface area relative to that of adults. Endnote 17 In addition, younger children do not always have a choice of environment and cannot remove themselves from exposure in the way an adult could. Growing up in a smoke-free home is essential for children's optimal growth and development. of households with children aged less than 12 years regularly exposed to environmental tobacco smoke at home. of households with children aged less than 12 years living in the household with at least one person (including family members or visitors) smoking inside their home regularly (every day or almost every day). Data source. households with children aged less than 12 years living in the household. Methods of calculation Numerator: Number of households reporting having children aged less than 12 years living in the household and with at least one person smoking inside their home regularly. Denominator: Number of households reporting having children aged less than 12 years living in the household. Additional notes A low rate can be interpreted as a positive result. C. 7. There is strong evidence that smoking tobacco is related to more than 24 chronic diseases and conditions such as respiratory disease, cardiovascular disease and cancer. Smoking tobacco: has negative effects on nearly every organ of the body reduces overall health is the leading cause of preventable death has negative health impacts on people of all ages: unborn babies, infants, children, adolescents, adults and seniors. Endnote 18 Lung cancer is the leading cause of death due to cancer in Canada. Smoking tobacco is the single most important preventable cause of lung cancer, accounting for 85% of all new cases of lung cancer in Canada. Endnote 18 Measure(s) Percentage of population who report being current smokers (daily and occasional), population aged 15 years and older. Percentage of population who report being current daily smokers, population aged 15 years and older. of people aged 15 years and older who report that at the present time they smoke cigarettes "daily and occasionally" or just "daily. " Data source. aged 15 years and older. [SEP] Justify:

Output: The text contrasts the claim by discussing the harmful effects of smoking tobacco, which is linked to over 24 chronic diseases, emphasizing that smoking is a leading cause of preventable death and negatively affects health at all ages. This indicates that there are significant risk factors for chronic diseases that biohacking techniques may not eliminate.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: (1986) New concepts in the biology and biochemistry of ascorbic acid. N Med 314: 892–902. View 9. (1998) D-Erythroascorbic acid is an important antioxidant molecule in Saccharomyces cerevisiae. 30: 895–903. View 10. (2000) The biosynthesis of erythroascorbate in Saccharomyces cerevisiae and its role as an antioxidant. 28: 183–192. View 11. (2001) Deficiency of D-erythroascorbic acid attenuates hyphal growth and virulence of Candida albicans. 69: 3939–3946. View 12. (1998) The biosynthetic pathway of vitamin C in higher plants. Nature 393: 365–369. View 13. (1997) Ascorbate metabolism and its regulation in animals. 23: 793–803. View 14. Klis FM (1994) Review: cell wall assembly in yeast. Yeast 10: 851–869. View 15. (2000) Biosynthesis of L-ascorbic acid (vitamin C) by Saccharomyces cerevisiae. 186: 245–250. View 16. (2004) Production of L-ascorbic acid by metabolically engineered Saccharomyces cerevisiae and Zygosaccharomyces bailii. Microbiol 70: 6086–6091. View 17. (2007) Arabidopsis VTC2 Encodes a GDP-L-Galactose Phosphorylase, the Enzyme in the Smirnoff-to in Plants. J 282: 18879–18885. View 18. (1998) GDP-L-fucose pyrophosphorylase. Purification, cDNA cloning, and properties of the enzyme. J 273: 30165–30174. View 19. (1955) A highly specific procedure for ascorbic acid. . 38: 514–518. View 20. (1999) Oxygen stress: a regulator of apoptosis in yeast. J 145: 757–767. View 21. (1987) Discrimination of viable and non-viable cells using propidium iodide in two color immunofluorescence. Cytometry 8: 413–420. View 22. [SEP] Justify:

Output: The text provided lists various scientific articles related to ascorbic acid and its biosynthesis, but it does not address or provide any information regarding the relationship between urban living and stress levels. Therefore, it is irrelevant to the claim.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: The selection of adeno-associated virus to deliver the targeting vector was an inspired decision. Various adeno-associated virus serotypes efficiently transduce fetal fibroblasts and deliver single-stranded DNA to the nucleus, avoiding the need for large quantities of DNA to be delivered by other means and reducing the risk of random, non-homologous recombination. The targeting frequency was approximately 0. 01% in pig and 0. 5–2% in ferret fibroblasts. The second hurdle was that fetal fibroblasts have a short life span and undergo rapid senescence when in culture, which proved a particular problem in the ferret. This was overcome by performing an additional round of nuclear transfer (‘rejuvenation’). Following the initial PCR screening, positive but senescing clones were transferred into recipient oocytes and re-implanted into pseudopregnant ferrets. Three-week-old fetuses were subsequently harvested to collect fetal fibroblasts for additional analysis by southern blotting. Porcine fetal fibroblasts were less prone to senescence, and the additional ‘rejuvenation’ step was not required. The gene-targeted fetal fibroblasts were transferred into oocytes, which were re-implanted into pseudopregnant females and a total of 13 healthy heterozygote pigs and 8 healthy heterozygote ferrets were born (see also Table 1). All heterozygote animals were males, because the fetal fibroblasts were derived from male animals, allowing for rapid expansion of animal numbers and generation of heterozygote females, which is currently ongoing. The selection of pigs and ferrets as potential models for CF was an obvious choice as lung architecture, CFTR expression and the pharmacological properties of CFTR are similar in both species to humans. The authors opted to generate heterozygote pigs and ferrets by disrupting exon 10 of the CFTR gene (null mutation), a strategy that was moderately successful in knocking out murine CFTR. In addition, pig heterozygotes were produced with a phenylalanine deletion (ΔF508), which is the most common mutation in humans. [SEP] Justify:

Output: The text corroborates the claim by discussing how gene therapy techniques are being applied to cystic fibrosis (CF). It describes the selection of models (pigs and ferrets) that have similar lung architecture and CFTR expression to humans, implying an ongoing research effort to utilize gene therapy to address CF. The specific mention of disrupting the CFTR gene aligns directly with the context of researching gene therapy for treating cystic fibrosis.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: (Physical Activity), Strong evidence supports a dose-response between physical activity and health: the most physically active people have the lowest risk of poor health. Endnote 19 Increments on physical activity have been significantly associated with reduced all-cause mortality risk and found to be an important factor in the prevention and control of chronic diseases such as cardiovascular diseases,Endnote 26 stroke,Endnote 27 cancerEndnote 28 and type 2 diabetes. Endnote 29Endnote 30Endnote 31 of population who are physically "active" or "moderately active" during their leisure time, population aged 20 years and older. of people aged 20 years and older who are classified as "active" or "moderately active" according to the (LTPA) Index. Data source. aged 20 years and older. Methods of calculation Numerator: Number of people aged 20 years and older who are physically "active" or "moderately active" during leisure time. Denominator: total population aged 20 years and older. Additional notes LTPA Index is a composite measure that categorizes individuals as "active," "moderately active" or "inactive" based on responses to questions on total daily energy expended during leisure time activities in the previous 3 months. It is a proxy measure of total physical activity. A high rate for this indicator can be interpreted as a positive result. 10. (Screen Time) suggests that sedentary behaviour has direct physiological effects on metabolism and vascular health. Endnote 30Endnote 31 A dose-response relationship between the time spent in sedentary behaviours and increase in all-cause and cardiovascular disease mortality has also beenfound. Endnote 32 Television viewing and computer use are the most widely studied sedentary behaviours and data on these activities are readily available in a number of surveys. Recent studies have found that screen time (time spent viewing television, using computers or playing video games) is positively associated with inactive leisure time, a poor diet and obesity. Endnote 33 Excessive screen time increases the risk of obesity and weight gain regardless of physical activity levels and increases the risk of cardiovascular events and mortality. Endnote 34Endnote 35 of population who report spending more than 14 hours per week watching television and/or using computers during leisure time, population aged 12 years and older. of people aged 12 years and older who report spending more than 14 hours per week watching television and/or using computers during leisure time. Data source. aged 12 years and older. [SEP] Justify:

Output: The text contrasts the claim by indicating that while physical activity is important for reducing the risk of chronic diseases, it does not suggest that biohacking techniques can completely eliminate such risks. The evidence presented focuses on the relationship between physical activity and health outcomes, emphasizing that higher physical activity levels correlate with lower risks of chronic illness, rather than supporting the idea that any technique can completely remove those risks.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: (2006) Improvement of cell viability and hirudin production by ascorbic acid in Pichia pastoris fermentation. Biotechnol 72: 837–844. View 23. Hancock RD, (2002) Biotechnological approaches for L-ascorbic acid production. 20: 299–305. View 24. Bremus C, Herrmann U, Bringer-Meyer S, (2006) The use of microorganisms in L-ascorbic acid production. J Biotechnol 124: 196–205. View 25. (2006) Biotechnological production of vitamins. and Biotechnology 44: 381–396. View 26. (2006) Free radicals, metals and antioxidants in oxidative stress-induced cancer. Interact 160: 1–40. View 27. (1991) Dietary antioxidants and the risk of lung cancer. Epidemiol 134: 471–479. View 28. Naidu KA (2003) in human health and disease is still a mystery? An overview. 2: 7. View 29. O'(2003) Complexities of chromium carcinogenesis: role of cellular response, repair and recovery mechanisms. 533: 3–36. View 30. (2002) Role of ascorbic acid in stratum corneum lipid models exposed to UV irradiation. 19: 982–990. View 31. van Dijken JP, et al. (1999) NADH reoxidation does not control glycolytic flux during exposure of respiring Saccharomyces cerevisiae cultures to glucose excess. 171: 133–140. View 32. (2002) Transformation of yeast by lithium acetate/single-stranded carrier DNA/polyethylene glycol method. 350: 87–96. View 33. (1992) Complementation of Saccharomyces cerevisiae auxotrophic mutants by Arabidopsis thaliana cDNAs. 2: 417–422. View 34. Hoffman CS, (1987) A ten-minute DNA preparation from yeast efficiently releases autonomous plasmids for transformation of Escherichia coli. Gene 57: 267–272. View 35. (2004) The yeast Zygosaccharomyces bailii: a new host for heterologous protein production, secretion and for metabolic engineering applications. 4: 493–504. View 36. [SEP] Justify:

Output: The text provided is irrelevant to the claim as it discusses various scientific studies and biotechnological approaches, none of which mention urban living or stress levels. It focuses on topics related to biochemistry and production processes rather than addressing any relationship between living conditions and stress.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: Table 1 Cloning of CFTR-targeted pigs and ferrets by SCNTFull size tableAlthough CF is a multiorgan disorder involving the intestine and pancreas, most morbidity and mortality is caused by progressive pulmonary infections and inflammation ultimately leading to respiratory failure. To aid understanding of pathophysiology, and help with the development of new treatments, a good animal model should recapitulate CF lung disease as closely as possible. The CF knockout mouse model failed at this hurdle, developing the characteristic CF ion transport abnormalities (the CF gene encodes a chloride channel) only in the nasal epithelium. Although animals show extensive CF intestinal pathology, they do not develop CF lung disease. The exact reason for this is unknown but it has been suggested that expression of alternative chloride channels in the murine lung,3 as well as the short life expectancy of mice (approximately 2 years), may explain the findings. Pigs have a life expectancy of 10–15 years and so may help to disentangle these factors. Interestingly, Liu et al. 4 have recently shown that the porcine ΔF508 mutation has a much milder phenotype (processing defect) when assessed in vitro, which could potentially affect the phenotype in ΔF508 pigs. These findings further highlight the importance of species-specific differences and underline that success cannot be taken for granted. Chris Rogers, of the University of Iowa, reported at the American Society for Gene Therapy meeting in Boston this year that the first 20 CF piglets had been born. All had abnormal ion transport in the nose and showed blockage of the distal small intestine (meconium ileus) and severe pancreatic pathology perinatally. Unsurprisingly at this early stage, there was no evidence of lung disease but the gut and pancreatic pathologies were much more pronounced in the pigs than is seen in humans, and the reasons for this are currently unclear. The next challenges will be to overcome the perinatal intestinal disease and to assess the ion transport properties of the porcine lung, as an early indicator of potential CF lung disease. The first CF ferrets are eagerly awaited. We have no doubt that CF pigs and ferrets will significantly catalyze CF research if the animals recapitulate human lung disease. However, it is important to note that husbandry and breeding will not be straightforward. [SEP] Justify:

Output: The text corroborates the claim by discussing ongoing research into animal models, such as CF pigs and ferrets, specifically aimed at understanding cystic fibrosis (CF) to aid in developing new treatments. It mentions that gene therapy research is catalyzed by animal models that closely mimic human CF lung disease, indicating that such research is relevant for treating conditions like cystic fibrosis.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: The consumption of SSBs, particularly soda and fruit drinks, which provide little nutritional value and have little impact on satiety, has been associated with excess energy intake. Large cohort and experimental studies show a strong positive association between greater intakes of SSBs and weight gain and obesity in both children and adults. Endnote 48 of population who report drinking SSBs daily, population aged 5 to 19 years. of children and youth who report consuming SSBs every day. Data source. aged 5 to 19 years. Methods of calculation Numerator: Number of people aged 5 to 19 years who report consuming SSBs at least once a day every day. Denominator: Total population, aged 5 to 19 years. Additional notes Children were classified as drinking SSBs (i. e. regular soft drinks, sport drinks or fruit drinks) every day if their average daily consumption was equal or greater than 1 SSB per day. Canada's Food GuideEndnote 47 recommends limiting beverages high in calories, such as fruit-flavoured drinks, soft drinks, sports and energy drinks and sweetened hot or cold drinks. A low rate for this indicator can be interpreted as a positive result. 13. to the Organization, unsafe alcohol use is the third most harmful risk factor for chronic diseases in developed countries. Endnote 49 Long-term excess alcohol consumption is associated with increased risk of chronic diseases such as chronic liver disease, certain cancers, cardiovascular diseases (hypertensive heart disease, ischemic heart disease, stroke) and premature death. Endnote 50 National Low-were developed to help Canadians moderate their alcohol consumption and reduce immediate and long-term alcohol-related harm. Endnote 51 of population who exceed low-risk alcohol drinking guidelines for chronic drinking, population aged 15 years and older. of people aged 15 years and older who report drinking alcohol over the Canadian guidelines on low-risk drinking aimed at reducing long-term health risks. Data source (), Health Canada. aged 15 years and older. Methods of calculation Numerator: Number of people aged 15 years and older who report drinking alcohol over the Canadian guidelines on low-risk drinking. Denominator: Total Population, aged 15 years and older. Additional notes The latest Canadian guidelines for low-risk drinking for long-term health risks recommend no more than 10 standard drinks* per week for women and no more than 15 standard drinks per week for men. Endnote 49 *A standard drink is equivalent to 13. 6 g of alcohol. [SEP] Justify:

Output: The text contrasts the claim by discussing factors such as the consumption of sugar-sweetened beverages (SSBs) and alcohol, which are associated with an increased risk of chronic diseases. It emphasizes that excess intake of SSBs leads to weight gain and obesity, while long-term alcohol consumption is linked to chronic liver disease, cancers, and cardiovascular diseases. These points highlight the complexity of managing chronic disease risk and suggest that biohacking techniques alone cannot eliminate these risks.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: (1999) Three new dominant drug resistance cassettes for gene disruption in Saccharomyces cerevisiae. Yeast 15: 1541–1553. View 37. (1989) Molecular Cloning: A Laboratory Manual. New York: Press. [SEP] Justify:

Output: The text does not address the claim regarding urban living and stress levels. It appears to reference scientific publications related to yeast genetics, which is unrelated to the topic of urban living and stress.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: Log in or new issue alertsGet alerts Enter your Email address: Subscribe to e2019. | DOI: 10. 1097/01. COT. 0000553522. 97449. 60 gene therapy; sickle cell anemia: gene therapy; sickle cell anemiaA recently developed gene therapy reversed disease symptoms in two sickle cell anemia (SCA) patients, opening the door for a potentially new approach for this patient population, especially those in resource-challenged areas. “One year after treatment of our first patient and 6 months after treatment of our second patient, both have seen a remarkable improvement in the quality of life due to remarkable reduction in disease symptoms. This includes near elimination of chronic pain and sickling events and improved anemia,” said study author Punam Malik, MD, Director of Cincinnati Children's Cell Center. “Although it's still early post-treatment, these preliminary results are quite promising. If sustained this therapy will provide a transportable, safe, and feasible gene therapy for all SCA patients. ” While sickle cell disease (SCD) is rare in the U. S. , there is a huge global burden, noted Malik. “There are 2,000 children with sickle cell disease born per year in the U. S. while 300,000 babies are born with the disease every year in Africa alone,” she emphasized. “And so, we need more curative therapies because there just aren't enough. Punam Malik, MD: Punam Malik, MD“These children cannot afford hydroxyurea, the approved drug for SCD, or the necessary monitoring for the treatment,” she explained, adding that they also do not have the option of a myeloablative transplant from a matched sibling. Even if this approach was available, only 15 percent have a match, leaving 85 percent of patients without a curative option, Malik noted. Recognizing this unmet need, Malik and her team sought to develop a new treatment approach to fill the void for these patients. “Based upon our preclinical data, we embarked upon a Conditioning (RIC) Phase I/II on in Patients with SCA with a modified γ-Globin LV (NCT02186418), hypothesizing this approach will be safe, feasible, and efficacious,” according to study authors. [SEP] Justify:

Output: The text corroborates the claim by detailing a recent development in gene therapy that has successfully reversed disease symptoms in two patients with sickle cell anemia. The approach is portrayed as a promising new treatment option, especially in resource-challenged areas, which aligns with the idea that gene therapy is being researched for diseases including sickle cell anemia.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: A low rate for this indicator can be interpreted as a positive result. 14. to chronic stress, a state of prolonged tension from internal or external stressors, triggers predictable biochemical and physiological changes in the body that are detrimental to the nervous and immune system. Endnote 52 Epidemiological evidence shows that chronic stress is associated with the development of many common chronic diseases. Endnote 53Endnote 54 Chronic stress has been shown to increase heart rate and blood pressure that eventually lead to serious consequences such as cardiovascular diseases (myocardial infarction, heart failure, stroke)Endnote 55Endnote 56 and mental illness. In addition, increased exposure to stress can contribute to poorer coping skills and poorer health behaviours such as smoking, excess alcohol consumption and unhealthy eating habits that are detrimental to health and contribute to chronic diseases. of population who report life to be "quite a bit" or "extremely" stressful most days in the previous 12 months, population aged 12 years and older. of people aged 12 years and older who report that in the last year most days were "quite a bit stressful" or "extremely stressful" (versus "not at all stressful," "not very stressful" or "a bit stressful"). Data source. aged 12 years and older. Methods of calculation Numerator: Number of people, aged 12 years and older who report life to be "quite a bit" or "extremely" stressful most days in the last 12 months. Denominator: Total population, aged 12 years and older. Additional notes Self-perceived life stress is used as a proxy for chronic stress and measures the perception that life feels quite a bit or extremely stressful most days in the last year. A low rate for this indicator can be interpreted as a positive result. D. 15. Obesity is defined as excessive accumulation of body fat that presents a risk for health. Endnote 57 Obesity is a risk factor for a number of chronic conditions such as cardiovascular diseases, certain types of cancer, type 2 diabetes, osteoarthritis, mental health conditions and other negative health outcomes. Endnote 58Endnote 59Endnote 60 Among children, excess body fat has also been found to correlate with negative health outcomes, both in the short and longer term. Endnote 61Endnote 62 Obesity is one of the main health challenges in Canada. (WHO) considers obesity to be the fifth leading risk factor for global deaths. The fundamental cause of obesity and overweight is an imbalance between energy consumed and energy expended. [SEP] Justify:

Output: The text contrasts the claim by discussing how chronic stress and obesity are significant risk factors for various chronic diseases, indicating that simply biohacking may not be effective in fully eliminating these risks. It emphasizes that chronic stress can lead to biochemical changes in the body, resulting in serious health consequences, and that obesity is inherently linked to numerous chronic conditions.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: HIPK2 overexpression leads to stabilization of p53 protein and increased p53 transcriptional activity by decreasing Mdm2 protein levels 53. Instead, HIPK2 leads to a downregulation of p53-induced Mdm2 protein and this may lead to stabilization of p53. Overexpression of HIPK2 does not lead to a change of Mdm2 mRNA expression. The data suggest that HIPK2 plays a critical role in p53 mediated cellular responses by removing the p53 inhibitor protein Mdm2 via modification of the protein itself or its intracellular movement. BackgroundThe tumor suppressor protein p53 contributes to the control of cell cycle checkpoints and apoptosis and is frequently lost or mutated in multiple types of human cancers [1]. DNA damaging agents induce p53 accumulation and induction of p53-mediated transcription [2, 3]. Several proteins are known to play a crucial role in the stabilization and activation of p53 [4, 5]. The association with murine double minute clone 2 (Mdm2) leads to a susceptibility of p53 for proteolysis [6, 7] and thus, p53 protein levels are regulated post-transcriptionally [8]. Homeodomain-interacting protein kinase 2 (HIPK2) has been recently described as a member of a family of nuclear kinases that act as co-repressors for homeodomain transcription factors [9] and it is a potential interaction partner for interferon type I induced Mx GTPases with antiviral activity against several RNA viruses [10]. HIPK2 is regulated by the ubiquitin-like protein SUMO-1 and the covalent SUMO-1 modification correlates with its localization to nuclear speckles or nuclear dots [11]. Here we address the question whether HIPK2 modifies transcription regulated by transcription factors other than homeoproteins. We found that HIPK2 activates transcription mediated by p53 specific promoter elements. HIPK2 also enhances expression levels of p53 protein. Both effects on p53 are not observed with a kinase defective mutant and large amino and carboxy-terminal deletion mutants of HIPK2. The DNA damaging anti-cancer drug doxorubicin enhances HIPK2-induced expression or stability of p53. HIPK2 overexpression downregulates Mdm2 protein levels. [SEP] Justify:

Output: The text is irrelevant to the claim regarding urban living and stress levels. It discusses the biological mechanisms of HIPK2 and its effects on the p53 protein without addressing any relationships to urban living or stress.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: “Moreover, RIC will have significantly less toxicity [and] costs, and be implementable in many transplant centers, including those in some of the resource-poor countries, where supportive therapies for myeloablative transplants are unavailable, and where majority of SCA patients exist. ” Abstract 1021 Malik and her colleagues developed the gene therapy utilizing a modified gamma globin lentivirus vector to transfer a healthy fetal hemoglobin gene into a patient's hematopoietic stem cells (HSC). While the fetal hemoglobin gene normally switches off shortly after birth, researchers have observed some adults never stop producing fetal hemoglobin; when sufficient quantities are present, red blood cell sickling is prevented. “The lentivirus vector we developed carries the fetal hemoglobin gene,” Malik explained. “This gene therapy approach places a fetal hemoglobin gene in the bone marrow cells that cannot switch off. ” Researchers collected CD34+ HSC via bone marrow harvest and/or plerixafor mobilized peripheral blood stem collection, selected for CD34+ cells and transduced, according to Malik. “Following delivery of the vector into the patient's stem cells, the patient receives reduced intensity chemotherapy before the infusion of the genetically corrected cells,” she explained. A single dose of IV melphalan was administered 36 hours prior to infusion of γ-globin modified-HSC. Following infusion, the investigators monitored patients for adverse events, engraftment, vector copy number, modified fetal hemoglobin expression, and clinical features of SCA. To date, researchers have treated two patients with this new approach and initial findings are promising. The patients (35 and 25 years old) both had severe disease. Patient 1 received 1x106 CD34+ cells/kgbw compared to 6. 9x106 CD34+ cells/kgbw for patient 2. “Patients recovered their blood counts within a week to 10 days and recovered from the chemotherapy effects by 2 weeks,” Malik noted. Since receiving this treatment, both patients have seen improvements in their disease symptoms. “Twenty percent of the circulating hemoglobin in patient 1 is coming from the vector, and this has resulted in a tremendous improvement in their sickle cell disease symptoms,” Malik reported. [SEP] Justify:

Output: The text corroborates the claim by describing a specific gene therapy developed by Malik and her colleagues that utilizes a modified gamma globin lentivirus vector to treat sickle cell anemia (SCA). It details how this gene therapy works by transferring a healthy fetal hemoglobin gene into a patient's hematopoietic stem cells, which aligns with the notion that gene therapy is being explored for treating diseases such as sickle cell anemia. Additionally, the text reports on initial findings demonstrating promising results from this approach, thereby supporting the research aspect mentioned in 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: Endnote 98 Annual influenza immunization can prevent the onset of influenza, help control an acute episode of influenza if it occurs, and generally help with the control and management of chronic disease complications. Endnote 99 To reduce morbidity and mortality associated with influenza, the on Immunizations (NACI) recommends that immunization programs focus on those at high risk of influenza-related complications, among other priority groups. According to NACI's 2011/12 recommendations, chronic diseases associated with higher risk of influenza-related complications include cardiac or pulmonary disorders, diabetes and other metabolic diseases, cancer and immune-compromising conditions (due to underlying disease and/or therapy, etc. ). Endnote 100 of population aged 12 years and older and living with a chronic health condition* who report having a seasonal flu shot in the previous 12 months. of people aged 12 years and older and living with a chronic disease who report having had an influenza immunization (flu shot) in the previous 12 months. Data source. aged 12 years and older living with a chronic disease. Methods of calculation Numerator: Number of people aged 12 years and older living with a chronic disease* who report having had a flu shot in the previous 12 months. Denominator: Total population aged 12 years and older living with a chronic disease. * Additional notes *The chronic diseases included are cardiovascular diseases (heart disease, stroke), chronic respiratory diseases (asthma, chronic obstructive pulmonary disease [COPD]), diabetes and cancer (all types). A high rate for this indicator can be interpreted as a positive result. F. Health Outcomes/Status 25. (Self-Rated Health) Rationale Self-rated health measures an individual's perception of his or her overall health. Research shows that a person's appraisal of their general health is a powerful predictor of morbidity and mortality, even after controlling for a variety of sociodemographic, psychosocial and physical health status indicators. Endnote 101 Poor self-perceived health is associated with the presence of chronic diseases, level of disability, pain and health risk behaviours, such as lower levels of physical activity and smoking, among others. Endnote 102Endnote 103 of population who rate their health as "very good" or "excellent," population aged 12 years and older. of people aged 12 years and older who rate their health as "excellent" or "very good," expressed as a proportion of the total population aged 12 years and older. [SEP] Justify:

Output: The text contrasts the claim because it discusses the role of influenza immunization in managing complications of chronic diseases, indicating that while certain interventions can help control some health issues, they do not eliminate the risk of chronic diseases overall. It highlights that individuals with chronic diseases are at higher risk for influenza-related complications, further confirming that chronic diseases cannot be entirely eliminated through biohacking techniques alone.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: Therefore, the observed effects of HIPK2 on p53 seem to be mediated by Mdm2. We conclude that an important function of HIPK2 is the stabilization and activation of p53 by inducing degradation of Mdm2. ResultsHIPK2 activates p53-mediated transcriptionSince HIPK2 has been described as a nuclear protein that interacts with homeodomain containing transcription factors [9, 11], we looked for an influence of HIPK2 on transcription mediated by several transcription factors such as p53, NFκB and Elk1. The tumorsuppressor p53 is a transcription factor that binds to DNA and is involved in the cell cycle and apoptosis. To test a possible transcriptional transactivation activity of HIPK2, expression vectors encoding wildtype or the mutated HIPK2 proteins (AC, AN and K221A) were transfected into 293 (Fig. 1A) and HeLa (Fig. 1B) cells together with p53-luc, a luciferase reporter gene under the control of the p53-specific enhancer element ()15. The p53-specific enhancer element is derived from the sequence comparison of promoters of p53-inducible genes [12, 13]. HeLa cells have been found to contain endogenous transcriptionally active p53 protein by the intrinsic ability to transactivate p53-responsive promoter elements [14]. In line with this, endogenous p53 of the HeLa cells used in our experiments had transcriptional activity and wildtype sequence (data not shown). Activation of the luciferase activity by cotransfection of 50 ng of the reporter plasmid encoding p53 (pFC-p53) was 250 fold for 293 and 160 fold for HeLa cells, respectively (data not shown). The luciferase value of vector and p53-luc transfected cells were standardized for a value of 1 in each assay, to control for activation of the p53 specific enhancer element by endogenous p53. The intrinsic activity of endogenous p53 was approximately 20 fold above the blank controls (data not shown). Wildtype HIPK2 induced a 40 fold increase of p53-mediated transcription in 293 cells compared to the increase in vector transfected control cells (Fig. 1A). [SEP] Justify:

Output: The text is irrelevant to the claim as it discusses the role of HIPK2 in regulating p53-mediated transcription, without any mention of urban living or stress levels. There's no connection or data provided that would support or contest the idea proposed in the claim.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: “The second patient is not producing as much as the first patient, at last analysis it was about 12 percent fetal hemoglobin, but that is sufficient to be completely be free of symptoms of sickle cell disease. ” In the 2 years prior to transplant, both patients were admitted more than 5-6 times per year for pain crises, according to the researchers. Additionally, they required opiates to manage chronic pain. One year following therapy, the first patient no longer requires daily oral opioids and has had one acute sickle cell event. Patient 2 no longer uses oral opioids and has had no vaso-occlusive events, investigators reported. Building on the initial success of the therapy, Malik and her team plan to continue to explore the potential of this approach. “In this phase I/II trial, we are approved for 10 patients, so our goal this year is to recruit more,” Malik noted. And while the team is in the rapidly recruiting phase right now, they are already looking at how they can expand the impact of this therapy. “The first two patients were patients that we learned a lot from and I think it will only get better,” Malik told Oncology Times. “From the lessons learned we will only continue to improve our methodology. “And it is our hope to lower the age to children because this gene therapy has implications for all sickle cell disease patients. ” If further study solidifies the benefit of this approach, it has a variety of practice implications. “This therapy has the potential to be a curative option available to children as soon as they are diagnosed with sickle cell disease,” noted Malik. “We could treat these patients before they ever develop symptoms of the disease. ” Many adults with sickle cell disease have chronic organ damage, making it difficult for them to withstand myeloablative transplant. “Our approach with reduced intensity transplant offers similar benefit with less toxicity,” Malik explained. And while there are other curative gene therapy options being developed in the field, she noted the value of having multiple choices. “Patients can choose whether they want a mild intensity regimen with fewer side effects that provides symptom relief, or they want to go for complete replacement of their sickle bone marrow with normal bone marrow from a sibling or genetically corrected cells. [SEP] Justify:

Output: The text corroborates the claim by providing evidence of ongoing research into gene therapy for sickle cell disease. It details the outcomes of patients treated with gene therapy, indicating that this approach could be curative and beneficial for children diagnosed with the disease. The mention of expanding the therapy and its implications for all sickle cell disease patients aligns directly with the claim that gene therapy is being researched to treat specific diseases.


Input: Task: contrast the claim using the given text. Claim: Most biohacking techniques can entirely eliminate the risk of chronic diseases. [SEP] Text: Denominator: Total population over a given time period. Additional notes *The chronic diseases included are diabetes, cardiovascular diseases (heart disease, and stroke), chronic respiratory diseases (asthma, chronic obstructive pulmonary disease [COPD]), arthritis, mental illness (all mental disorders, mood disorders and/or anxiety) and cancer (all cancers, prostate, breast, colorectal and lung cancer). In addition, the prevalence of individuals with at least 1 major chronic disease (cancer, diabetes, cardiovascular disease, chronic obstructive pulmonary disease) is measured. Estimates are calculated using both self-report data (CCHS) and administrative data (CCDSS). The prevalence of "use of service for diagnosed mental illness" is used as a proxy for mental illness prevalence. Prevalence of cancer is measured as "person-based 5-year cancer prevalence," that is, the number of individuals living with or beyond cancer that were diagnosed in the 5 years before the specified date, also known as index date. All rates presented are crude except for trends where rates are age-standardized to the 1991 Canadian population. A low rate for this indicator can be interpreted as a positive result. 30. Morbidity (Incidence Rate) is a measure of the number of new cases of a disease that develop in a population over a specific time period. As a result, incidence is much more sensitive to changes over time (trends) than is prevalence. Endnote 116 Incidence rate is influenced by 2 main groups of factors: the underlying rate of disease incidence occurrence, which reflects the prevalence of risk factors and hence the success of primary prevention efforts, and/or the rate of disease detection and diagnosis of a specific chronic disease, which can be influenced by the intensity and effectiveness of disease screening or preventive programs. Measure(s) Incidence rate of chronic disease(s). * of newly diagnosed cases of a disease* per 100 000 population. Data source of The lower age limit of the population varies by specific disease: Population of children and youth aged 19 years and younger for diabetes and asthma. Population aged 20 years and older for diabetes and asthma. Population aged 35 years and older for COPD. Total population 0 years and older by sex for cancer. Methods of calculation Numerator: Number of new cases of a specific chronic disease diagnosed in the population in a particular year. Denominator: Total population at risk for the specific chronic disease in a particular year. [SEP] Justify:

Output: The text contrasts the claim by detailing how chronic diseases are measured and what factors influence their incidence rates, suggesting that while some biohacking techniques might help reduce risks, they cannot entirely eliminate them. The mention of primary prevention efforts and the multitude of chronic diseases emphasizes the complexity and multifactorial nature of chronic disease risk, which contradicts the assertion that biohacking can completely remove the risk.


Input: Task: pass the claim using the given text. Claim: Urban living always leads to increased stress levels. [SEP] Text: No such strong increase was observed with the kinase defective HIPK2 mutant K221A, a carboxy-terminal HIPK2 deletion mutant AC or an amino-terminal deletion mutant AN (Fig. 1A and 1B). But luciferase activity induced by the HIPK2 mutants was above the vector controls. Protein expression of recombinant HIPK2 in HeLa cells was shown in Western analysis after transient transfection of a Flag-tagged wildtype HIPK2 expression construct as described [26] (Fig. 1D). Expression of overexpressed and endogenous HIPK2 protein in HeLa cells was not detected by using a polyclonal anti-HIPK2 antiserum [26] (data not shown). Figure 1Activation of p53-mediated transcription by HIPK2 overexpression. 293 (A), HeLa (B) and Saos2 (C) cells were cotransfected with a p53-luciferase reporter construct and the indicated HIPK2 constructs or vector. Results represent the mean of three independent experiments. Bars, SD. (D) Western analysis of transient overexpression of Flag-tagged wildtype HIPK2 in HeLa cells (right lane) compared to vector-transfected control cells (left lane) with an anti-Flag antibody. Full size image To test whether HIPK2 activates transcription mediated by p53 responsive elements via p53, we transiently transfected human Saos2 cells, which lack p53 expression [15], with different HIPK2 expression constructs (Fig. 1C). Expression of wildtype HIPK2 did not lead to a significant increase in luciferase activity compared to its mutants, K221A and AC, and the vector control. However, transfection of 50 ng of pFC-p53 into Saos2 cells resulted in a 200 fold increase in luciferase activity and this increase was not further enhanced in the presence of HIPK2 (data not shown). Taken together, HIPK2 activates transcription mediated by p53 specific promoter elements and p53 is required for this effect. The enhancement of transcription is diminished by different mutations of HIPK2. [SEP] Justify:

Output: The text is irrelevant (pass) to the claim regarding urban living and stress levels. The provided text focuses on scientific details about HIPK2 mutations and their effect on transcription and does not mention urban living, stress, or any related topic.


Input: Task: corroborate the claim using the given text. Claim: Gene therapy is being researched to treat diseases like cystic fibrosis and sickle cell anemia. [SEP] Text: Skip to Our site uses cookies to improve your experience. You can find out more about our use of cookies in About Cookies, including instructions on how to turn off cookies if you wish to do so. By continuing to browse this site you agree to us using cookies as described in About Cookies. I accept evidence. Informed decisions. Better health. search Open menu language : language : Review language Select your preferred language for and other content. Sections without translation will be in English. Español فارسی Français हिन्दी Indonesia 日本語 한국어 ês Русский Română தமிழ் ภาษาไทย 繁體中文 简体中文 Website language Select your preferred language for the website. English Español (CDSR) for trials What's new (search and ) is created Search help quick guides Search FApublications in the of Editorial policies Information for authors translations What's new Data reuse options Permissions and reprints Media information Contact us Terms and conditions Known issues content content and plain language summary only and plain language summary only Cite this 0 language summary Authors' conclusions Discussion 10. 1002/14651858. CD007652. pub7 Collapse all Expand all Abstract available in English Español فارسی Français 한국어 ภาษาไทย 简体中文 cell disease encompasses a group of genetic disorders characterized by the presence of at least one hemoglobin S (Hb S) allele, and a second abnormal allele that could allow abnormal haemoglobin polymerisation leading to a symptomatic disorder. Autosomal recessive disorders (such as sickle cell disease) are good candidates for gene therapy because a normal phenotype can be restored in diseased cells with only a single normal copy of the mutant gene. This is an update of a previously published Cochrane Review. [SEP] Justify:

Output: The text corroborates the claim by discussing how sickle cell disease—which is directly mentioned—encompasses genetic disorders that can benefit from gene therapy. It indicates that autosomal recessive disorders, such as sickle cell disease, are suitable candidates because a normal phenotype can be restored in diseased cells with the introduction of a normal gene.