Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: The claims that nucleosomes, myosin complex, and mitochondrial proteins are enriched for LLPs are well supported by GO enrichment analysis and well described within the known body of evidence that these proteins are generally long-lived in other tissues. Weaknesses: Comment 1: One small potential weakness is the lack of a mechanistic explanation of if/why turnover may be accelerating at the 6-10 month interval compared to 1-6. Response 1: At the 6-month time point, we detected more long lived proteins than the 10 month time point in both the ovary and the oocyte. We anticipated this because proteins are degraded over time, and substantially more time has elapsed at the later time point. Moreover, at the 6–10-month time point, age-related tissue dysfunction is already evident in the ovary. For example, in 6-9 month old mice, there is already a deterioration of chromosome cohesion in the egg which results in increased interkinetochore distances (Chiang et al. , 2010), and by 10 months, there are multinucleated giant cells present in the ovarian stroma which is consistent with chronic inflammation (Briley et al. , 2016). Thus, the observed changes in protein dynamics may be another early feature of aging progression in the ovary. Comment 2: A mild weakness is the open-ended explanation of OSE label retention. This is a very interesting finding, and the claims in the paper are nuanced and perfectly reflect the current understanding of OSE repair. However, if the sections are available and one could look at the spatial distribution of OSE signal across the ovarian surface it would interesting to note if label retention varied by regions such as the CLs or hilum where more/less OSE division may be expected. Response 2: We agree that the enrichment of long-lived molecules in the OSE is interesting. To make interpretable conclusions about the dynamics of long-lived molecules in the OSE, we would need to generate a series of samples at precise stages of the estrous cycle or ideally across a timecourse of ovulation to capture follicular rupture and repair. These samples do not currently exist and are beyond the scope of this study. However, this idea is an important future direction and it has been added to the discussion (lines 221-223). Furthermore, from a practical standpoint, MIMS imaging is resource and time intensive.

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: (E) Liver lysates from healthy mice were analyzed for P-JNK, P-p65, P-ERK, P-STAT3, and β-actin by Western blotting. Figure 5—figure supplement 1—source data 1 Analyses of gut microbiota composition and inflammatory responses in healthy WT andNlrp12-/-mouse livers. Download elife-40396-fig5-figsupp1-data1-v2. zip Figure 6 with 1 supplement Download asset Open asset NLRP12 downregulates JNK activation in hepatocytes. (A) Primary hepatocytes from healthy WT and Nlrp12-/- mouse livers were isolated and cultured. Hepatocytes were stimulated with LPS for the indicated time and analyzed for the activation of JNK, p38, ERK, and p65 by Western blotting. (B) Primary hepatocytes from healthy WT and Nlrp12-/- mouse livers were stimulated with LPS in the presence of absence of JNK inhibitor. The expression of inflammatory and proliferative molecules was measured by real-time qPCR. Data represent means ± SD (n = 3 replicates). Statistical difference was determined by two-tailed unpaired t-test. (C) HepG2 cells stably expressing either GFP or NLRP12 were stimulated with LPS and analyzed for the activation of JNK, p38, ERK, and p65 by Western blotting. (D) Primary hepatocytes isolated from untreated WT and Nlrp12-/- mouse livers were stimulated with LPS for the indicated time periods and analyzed for cMyc, P-cJun, Cyclin d1, and P-JNK by Western blotting. (E–F) Primary hepatocytes grown on coverslip were treated with or without LPS for 1 hr and immunostained for P-cJun (green) and cMyc (green). Cellular morphology was visible with filamentous actin (F-actin) staining (red). DAPI (blue) was used for nuclear staining. (F) P-cJun and cMyc fluorescence intensities were measured by software. Data represent means ± SD (n = 20) and is representative of three independent experiments. Statistical difference was determined by two-tailed unpaired t-test.

Output: pass


Input: Claim: Some studies suggest that quantum coherence may play a role in how birds navigate using Earth's magnetic field. [SEP] Text: model for photoreceptor-based magnetoreception in birds, Biophys. J. 78, 2000. 10. birds use head scans to detect the direction of the earth's magnetic field, Curr. Biol. 14, 2004. 11. Henrik Mouritsen, Ulrike Janssen-and neuronal-activity markers colocalize in the retina of migratory birds during magnetic orientation, Proc. Nat'l Acad. Sci. USA 101, no. 39, 2004. 12. . Timmel, P. J. Hore, Henrik Mouritsen, Chemical magnetoreception: bird cryptochrome 1a is excited by blue light and forms long-lived radical-pairs, 2, pp. e1106, 2007. 13. F. Cintolesi, T. Ritz, C. recombination of an immobilized photoinduced radical pair in a 50μT magnetic field: a model avian photomagnetoreceptor, Chem. Phys. 294, 2003. 14. D. Varshalovich, A. Moskalev, V. Hersonskij, of Angular Momentum, World Scientific, Singapore, 1988.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: In humans, oocytes initiate meiosis during fetal development, and by birth, all oocytes are arrested at prophase of meiosis I (17, 18). This cell cycle arrest is maintained until ovulation, which occurs any time between puberty and menopause, and thus can span decades. The oocytes are particularly sensitive to protein metabolism alterations because they contribute the bulk cytoplasm to the embryo following fertilization. Thus, maternal proteins produced during oogenesis are essential to generate high-quality gametes (9). The ovarian microenvironment is a critical determinant of gamete quality and has been shown to become fibro-inflamed and stiff with age (19-21). Although a small number of oocyte-specific proteins have been identified as long-lived, including cohesins and several centromere-specific histones, there has not been a discovery-based approach to define the long-lived proteome of the ovary and oocyte. Thus, the potential contribution of LLPs to the age-related deterioration of the reproductive system in mammals remains to be elucidated. In this study we used multi-generational whole animal metabolic stable isotope labeling and leading mass spectrometry (MS)-based quantitative proteomic approaches to visualize and identify ovarian and oocyte long lived macromolecules in vivo during milestones relevant to the reproductive system. Exceptional longevity of ovarian structures and molecules in mammalsThe mammalian ovary is a structurally complex, heterogenous, and dynamic organ with follicles at different stages of development, remnants of ovulation (corpora lutea), and a heterogeneous stroma (22) (Fig. 1A). Very little is known about the long-term homeostasis and relative turnover of the ovarian tissue components during aging. To address this, we visualized the lifespan of ovarian macromolecules in mammals using a combination of stable isotope labelling and multi-isotope imaging mass spectrometry (MIMS) (fig. S1A). First, using a two-generational metabolic labelling of animals with 15N, we generated a cohort of fully 15N-labelled female pups, which were kept on 15N-chow until one month of age. This was then followed by an 14N-chow chase for 6 months. Since at this age mice begin to manifest reproductive aging phenotypes, including follicle loss (fig.

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: (G–H) Nlrp12-/- primary hepatocytes were transiently transfected with either GFP or Nlrp12 constructs followed by stimulation with LPS. The levels of P-JNK, cMyc, P-cJun, and P-p65 were measured by Western blotting (G) and the expression KC (Cxcl1), MIP2 (Cxcl2), and MCP1 (Ccl2) was analyzed by real-time qPCR (H). Data represent means ± SD (n = 3 replicates) and is representative of three independent experiment. Statistical difference was determined by two-tailed unpaired t-test. Figure 6—source data 1 NLRP12 negatively regulates JNK activation and production of inflammatory molecules in hepatocytes. Download elife-40396-fig6-data1-v2. zip Figure 6—figure supplement 1 Download asset Open asset NLRP12 downregulates multiple JNK activating pathways in hepatocytes. (A) For checking the purity of primary hepatocytes, hepatocytes isolated from healthy WT and Nlrp12-/- mouse livers were immunostained with antibody for hepatocyte-specific marker Albumin and counterstained with DAPI. (B) Primary hepatocytes from WT and Nlrp12-/- healthy mouse livers were cultured and stimulated with LPS (1 μg/mL), PGN (10 μg/mL), TNFα (20 ng/mL), and IL-6 (20 ng/mL) for 4 hr. The expression of indicated genes was analyzed by real-time qPCR. Data represent means ± SD (n = 3) and representative of three independent experiments. *p<0. 05. **p<0. 01, ***p<0. 001. Statistical difference was determined by two-tailed unpaired t-test. (C) HepG2 cells stably expressing either GFP or NLRP12 were stimulated with LPS (1 μg/mL), PGN (10 μg/mL), TNFα (20 ng/mL), and IL-6 (20 ng/mL) for 4 hr, and the expression of indicated genes was analyzed by real-time qPCR. Data represent means ± SD (n = 3) and representative of three independent experiments. *p<0. 05. **p<0. 01, ***p<0.

Output: pass


Input: Claim: Quantum biology is a relatively new field that merges principles of quantum mechanics and biology. [SEP] Text: of this paper, YinYang bipolar quantum agent (BQA), bipolar quantum geometry (BQG) and 2-dimensional generic bipolar quantum superposition are introduced with a geometrical and logical exposition of Dirac 3-polarizer experiment. While the exposition qualifies BQG as a geometry of light, it is shown in this paper that the logical exposition can be extended to an analytical paradigm of quantum mechanics and quantum biology. It is shown that BQG as the geometry of light is also the geometry of Nature with a logical unification of matter and antimatter atoms into a bipolar quantum cellular automaton (BQCA) through multidimensional YinYang bipolar quantum superposition using bipolar quantum linear algebra (BQLA). With the BQCA interpretation of quantum mechanics, it is shown matter and antimatter self-organization and spacetime emergence is logically possible within BQG. A scalable BQCA model for biological repression-activation and/or degeneration-regeneration is introduced. Bipolar cellular division and bipolar fractality are proposed. Background independent normal and abnormal bipolar fractal branching is proposed. A discussion on quantum gravity and mathematical abstraction is presented. A few challenges and predictions are posted. It is contended that and BQCA constitute an analytical paradigm of quantum mechanics and quantum biology that may contribute to equilibrium-based analysis of quantum decoherence and collapse as associated with quantum measurement. Key words bipolar quantum linear algebra, multidimensional bipolar quantum superposition, bipolar quantum cellular automaton, background independence, equilibrium-based bipolar fractality, analytical quantum biology, quantum gravity, five challenges for a theory of everything, falsifiability [1] bipolar quantum agent (BQA), bipolar quantum geometry (BQG) and bipolar quantum superposition (BQS) are introduced based on bipolar dynamic logic (BDL) and bipolar quantum linear algebra (BQLA) [2-5]. and BQS have led to a logical exposition of Dirac 3-polarizer experiment [6]. The logical exposition suggests that BQG can serve as a geometry of light. The exposition, however, could be deemed isolated and accidental unless the result can be mathematically and physically generalized. This paper presents such a generalization. We show that BQG can be further extended to an analytical paradigm of quantum mechanics and quantum biology.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Myosin and actin were also identified as LLPs with relatively high fractional abundance indicating exceptional longevity beyond 6-months. These proteins play numerous roles in oocyte maturation, fertilization, and egg activation, including nuclear positioning, spindle rotation and anchoring, chromosome segregation, cytokinesis, cortical granule exocytosis, and cytoplasmic flow (19, 38-42). Defects in many of these processes have been reported with advanced reproductive age, but whether long-lived pools of actin and myosins contribute to this etiology remains to be elucidated (43). Interestingly, F-actin stabilization restricts chromosome segregation errors due to cohesion loss which increase with age, so long lived pools of actin may confer a beneficial effect and protect against aneuploidy (42). Mitochondrial proteins were the predominant LLPs in isolated oocytes across the reproductive lifespan, and it is plausible that 15N cytoplasmic hotspots in oocytes that were observed in MIMS may correspond to mitochondria. Various aspects of mitochondrial dysfunction have been long-implicated in the age-dependent decline in gamete quality, with an age-dependent decrease in the number of mitochondria, an increase in abnormal morphology, and altered subcellular distribution (44). Moreover, mtDNA copy number decreases with age, whereas mtDNA mutations increase (45, 46). Finally, the functional capacity of mitochondria decreases with age with decreased membrane potential, increased reactive oxygen species, increased oxidative stress, and decrease energy output (47). Although it is possible that oocyte long lived mitochondrial proteins deteriorate with age and contribute to mitochondrial dysfunction, a different model is emerging for these proteins. Mitochondrial proteins are exceptionally long lived in tissues containing long-lived terminally differentiated cells and have now been documented in the brain (neurons), heart (cardiac myocytes), and the ovary (oocytes) (13). These mitochondrial LLPs are primarily localized to the cristae invaginations, which are throughout to serve as long-term stable ultrastructure within mitochondria. This strategic enrichment is hypothesized to serve as a lifelong structural pillar of mitochondria to support and maintain these organelles over long time frames (16). Although mitochondrial LLPs persist for at least 6 months in oocyte, the majority were undetectable by 10 months.

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: 001. Statistical difference was determined by two-tailed unpaired t-test. (D) Nlrp12-/- primary hepatocytes were stimulated with LPS in the presences or absence of JNK inhibitor. The levels of cMyc, P-cJun, and P-JNK were measured by Western blotting. (E) NLRP12 was knocked down in HepG2 cells usingCas9 technology. Cells were then stimulated with LPS (1 ug/ml) and the activation of JNK was measured by Western blotting. Figure 6—figure supplement 1—source data 1 NLRP12 downregulates inflammatory responses in hepatocytes in responses to multiple stimuli. Download elife-40396-fig6-figsupp1-data1-v2. zip Figure 7 with 1 supplement Download asset Open asset NLRP12 regulates hepatocyte proliferation via JNK activation. (A–B) Primary hepatocytes from WT and Nlrp12-/- mouse livers were treated with LPS in the presence or absence of a JNK inhibitor. The proliferation of hepatocytes was monitored in real-time by IncuCyte live cell image analyzer. (A) Representative images of hepatocytes captured by IncuCyte are shown. (B) The changes in cell confluence were used as a surrogate marker of cell proliferation. Data represent means ± SD (n = 5 replicates) and is representative of three independent experiments. Statistical difference was determined by two-tailed unpaired t-test. (C) WT and Nlrp12-/- hepatocytes were treated with LPS for 24 hr followed by 1 hr incubation with BrdU. Cells were then immunostained with anti-BrdU antibody and BrdU incorporation (S phase) was analyzed by flow cytometry. (D) Percentage of S phase cells as analyzed by flow cytometry was quantitatively analyzed. Data represent means ± SD (n = 3 replicates) and is representative of two independent experiments. Statistical difference was determined by two-tailed unpaired t-test. (E–F) Hepatocytes stained with anti-BrdU (green) were observed and counted under the 20X microscopic objective. DAPI (blue) was used for nucleus staining. Data represent means ± SD (n = 30 replicates) and is representative of two independent experiments.

Output: pass


Input: Claim: Quantum biology is a relatively new field that merges principles of quantum mechanics and biology. [SEP] Text: Multidimensional equilibrium of bipolar quantum agents ∀(x, y), (u, v) ∈ B∞ = [−∞, 0] × [0, +∞], we have Bipolar Addition: (x, y) + (u, v) ≡ (x + u, y + v). (2a) Bipolar Multiplication: (x, y) × (u, v) ≡ (xv + yu, xu + yv); (2b) Algebra: E(t+1) = M(t)´ E(t). (2c) Power Law: E(t+n) = Mn(t) ´ E(t). (2d) In Eq. (2c) M(t) is a bipolar quantum logic gate matrix [18] that characterizes the nucleus bipolar regulation center of the electron-positron pairs of a matter or antimatter atom; E(t) is the bipolar energy vector of the pairs of an atom. The unification is realized in the background independent BQG (cf. Part I). Figure 2 shows an equilibrium-based unification of matter and antimatter atoms as a bipolar quantum cellular automaton (BQCA) – a multidimensional bipolar dynamic equilibrium emerged from bipolar interaction and bipolar quantum superposition. The matter-antimatter BQCA unification can be deemed a result of self-organization of multiple BQAs through bipolar quantum superposition in BQG. It is shown that the BQCA also leads to the unification of wave-p2. (a) Matter atom as bipolar quantum agent; (b) Antimatter atom as bipolar quantum agent; (c) Bipolar equilibrium-based unification of matter and antimatter into a bipolar cellular automaton (adapted from [2,16]) Toward an analytical paradigm of quantum mechanics and quantum biology In this section we show that the BQCA model for matter-antimatter unification presented in last section can be scaled to physical and biological system models with conservational, regenerating, degenerating or repression and activation properties. These properties make it possible to describe different biological systems as BQAs at the molecular, cell and organism levels.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Thus, it is tempting to speculate that a stable pool of mitochondrial LLPs provides structural support for the maintenance of mitochondrial structure and function early during the reproductive lifespan. However, turnover of mitochondrial LLPs later in the reproductive lifespan may serve as a biological timer of aging. Because mitochondria are maternally inherited, these mitochondrial LLPs formed during fetal development of the mother are likely transferred to the embryo and impact subsequent generations (48). AcknowledgementsFundingThis research was supported by 21HD098498 to JNS and 21AG072343 to JNS. EKBW was supported by the 32 NS106812 and 99NS126639. Author contributionsConceptualization: Methodology: : Visualization: Funding acquisition: Project administration: Supervision: Writing – original draft: Writing – review & editing: all authors. Competing interestsThe authors declare no competing interests. Data and materials availabilityAll data generated or analyzed during this study are included in the manuscript and supporting files. RAW MS data has also been deposited at MassIVE under the accession number MSV000092217Supplementary MaterialsMaterials and MethodsFigs. S1 to S3Tables S1 and S2Table S1. Summary of proteins identified in 6- and 10-month chase ovaries. Table S2. Summary of proteins identified in 6 and 10-month chase oocytes. Fig. S1:Multi-generational whole animal pulse-chase labeling design along the reproductive aging continuum. (A) Wild-type female FVB mice (n=3) were fed a 15N-diet for 13 weeks and were maintained on a 15N-labeled diet through breeding, pregnancy, and weaning to produce 15N-labeled pups. Labeled pups were sacrificed after switching over to a 14N-diet for a chase period of 6- or 10-months. Ovaries and oocytes were designated for NanoSIMS, or liquid-chromatography/mass spectrometry. Female FVB mice experience age-associated changes in ovarian reserve, ovarian microenvironment, and gamete quality. (B) Representative images of each follicle class from mice of 6 weeks old and 6 months old. (C) Average follicle number per area of ovarian section from mice of the following ages: 6 weeks, 6 months, and 10 months (N= 3 mice per age cohort).

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: Statistical difference was determined by two-tailed unpaired t-test. (G) The proposed mechanism of NLRP12-mediated regulation of HCC. Figure 7—source data 1 Assesment of the role of Nlrp12 in hepatocyte proliferation. Download elife-40396-fig7-data1-v2. zip Figure 7—figure supplement 1 Download asset Open asset JNK-dependent hepatocyte proliferation is regulated by NLRP12. (A) Primary hepatocytes from WT and Nlrp12-/- mouse livers were treated with LPS in the presence or absence of JNK inhibitor. The cellular proliferation was monitored in real time with the continuous presence of indicated treatments until the end of each experiment by IncuCyte live cell image analyzer. Representative images of hepatocytes captured by IncuCyte. (B) The hepatocytes from healthy WT and Nlrp12-/- mice were cultured and treated with LPS for 24 hr in the presence or absence of JNK inhibitor. Hepatocytes were immunostained for Ki67 (green) and F-actin (red), and counterstained with DAPI (blue). (C) Percentage of Ki67-positive cells per field under 20X objective. 10 independent fields were counted from each experiment and representative of three independent experiments. Data represent means ± SD (n = 10). *p<0. 05. **p<0. 01, ***p<0. 001. Statistical difference was determined by two-tailed unpaired t-test. Figure 7—figure supplement 1—source data 1 Analysis of Ki67-positive cells in LPS-stimulated hepatocytes. Download elife-40396-fig7-figsupp1-data1-v2. zip Author response image 1 Download asset Open asset Analysis of gene alterations of different innate immune genes using cBioportal. Author response image 2 Download asset Open asset Gross anatomy of DEN and DEN plus CCL4-treated mice. resources table Reagent type or resourceDesignationSource or referenceIdentifiersAdditional informationGenetic reagent (M. musculus)C57BL/6:MGI:3028467 JAX:000664Genetic reagent (M.

Output: pass


Input: Claim: Quantum biology is a relatively new field that merges principles of quantum mechanics and biology. [SEP] Text: Scalable fractality of BQCA Without a formal geometrical and logical basis for quantum mechanics, after seven decades since its inception, quantum biology [20] is still a research area in its infancy. Although the Yin and Yang of Nature have been recognized as fundamental and ubiquitous bipolar coexistence in biology [21] and genomics [22], no formal geometrical and logical model had been available for reasoning on the Yin and Yang for thousands of years until recently. It is a living proof to Einstein’s assertion [23] that “the axiomatic basis of theoretical physics cannot be extracted from experience but must be freely invented. ” The above dilemma can be best illustrated with two mysteries. One is in the process of photosynthesis where “P3. Equilibrium-based bipolar scalability and fractality of BQCA: (a) Bipolar scalability and fractality; (b) BQG as a background independent bipolar fractal geometry With complete background independence, BQG makes bipolar quantum cellular automaton-based fractal emergence, branching, regulation, and communication possible through bipolar quantum superposition and entanglement. In BQG, spacetime can emerge and disappear following the arrivals and departures of BQAs or fractals. A BQA as a dynamic equilibrium is to the Yin and the Yang of bipolar relativity as gravity is to space and time of general relativity but with fundamentally different syntax, semantics, and basic postulates. While space and time are not direct opposites and cannot form a bipolar dynamic equilibrium, bipolar interaction and complementarity is posited to cause the emergence of BQAs as well as spacetime through bipolar quantum superposition and entanglement in a bipolar dynamic equilibrium process [1,2]. Since the Yin and the Yang are two reciprocal and interdependent opposites of a dynamic equilibrium that are completely background independent and ubiquitous, BQG is fundamentally different from Euclidian, Hilbert, and spacetime geometries. The new geometry is quadrant-irrelevant and shape-free because bipolar identity, interaction, superposition, separation, and entanglement can be accounted for in the geometry without quadrants. With the shape-free and quadrant-irrelevant properties, BQG can support bipolar fractality anywhere in any amount of bipolar energy or information for investigating into the quantum nature of shaped fractals in micro and meso scales.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: In humans, oocytes initiate meiosis during fetal development, and by birth, all oocytes are arrested at prophase of meiosis I (17, 18). This cell cycle arrest is maintained until ovulation, which occurs any time between puberty and menopause, and thus can span decades. The oocytes are particularly sensitive to protein metabolism alterations because they contribute the bulk cytoplasm to the embryo following fertilization. Thus, maternal proteins produced during oogenesis are essential to generate high-quality gametes (9). The ovarian microenvironment is a critical determinant of gamete quality and has been shown to become fibro-inflamed and stiff with age (19-21). Although a small number of oocyte-specific proteins have been identified as long-lived, including cohesins and several centromere-specific histones, there has not been a discovery-based approach to define the long-lived proteome of the ovary and oocyte. Thus, the potential contribution of LLPs to the age-related deterioration of the reproductive system in mammals remains to be elucidated. In this study we used multi-generational whole animal metabolic stable isotope labeling and leading mass spectrometry (MS)-based quantitative proteomic approaches to visualize and identify ovarian and oocyte long lived macromolecules in vivo during milestones relevant to the reproductive system. Exceptional longevity of ovarian structures and molecules in mammalsThe mammalian ovary is a structurally complex, heterogenous, and dynamic organ with follicles at different stages of development, remnants of ovulation (corpora lutea), and a heterogeneous stroma (22) (Fig. 1A). Very little is known about the long-term homeostasis and relative turnover of the ovarian tissue components during aging. To address this, we visualized the lifespan of ovarian macromolecules in mammals using a combination of stable isotope labelling and multi-isotope imaging mass spectrometry (MIMS) (fig. S1A). First, using a two-generational metabolic labelling of animals with 15N, we generated a cohort of fully 15N-labelled pups. After birth, labelled females were kept with the labelled dam until weaning, at which time their food source was switched to the 14N-chow chase.

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: musculus)Nlrp12-/- C57BL/6JPMID:12563287RRID: MGI:2676630Cell line (Homo Sapiens)HepG2:CVCL_0027Recombinant DNA reagentpcDNA4/TOInvitrogenCat#V1020-20Recombinant DNA reagentpcDNA4/TO-Nlrp12This paperFull length Nlrp12 (mouse) cDNA was cloned into pcDNA4/reagentpcDNA4/TO-NLRP12This paperFull length NLRP12 (human) cDNA was cloned into pcDNA4/reagentNLRP12 sg/Cas9 All-in-(Human)ABM IncCat # K1434706Recombinant DNA reagentScrambled sg/Cas9 All-in-one # K010AntibodyRabbit polyclonal anti-NLRP12:SCR_001456 Cat # OAAB04256WB: 1:500AntibodyRabbit monoclonal anti-p44/42 (Erk1/2):AB_390779 Cat # 4695,WB: 1:2000AntibodyRabbit monoclonal anti-Phospho- SAPK/:AB_823588 Cat # 4668WB: 1:1000AntibodyRabbit monoclonal anti-p38 :AB_10999090 Cat # 8690WB: 1:1000AntibodyRabbit monoclonal anti-Phospho-:AB_2315049 Cat # 4060WB: 1:1000AntibodyRabbit monoclonal anti-c:AB_1903938 Cat # 5605WB: 1:1000, IF:1:100AntibodyMouse monoclonal anti b-actinSigmaRRID:AB_476697.

Output: pass


Input: Claim: Quantum biology is a relatively new field that merges principles of quantum mechanics and biology. [SEP] Text: Part I) and BDL has been proven a bipolar dynamic generalization of Boolean logic (BL). It has been show that the two together leads to an analytical paradigm of quantum mechanics and quantum biology. Furthermore, BDL does satisfy the simplicity criterion set forth by Einstein and has passed a major falsifiability test with a logical exposition ofthe longstanding puzzle of Dirac 3-polarizer experiment. While background independent geometry has been advocated by the quest for quantum gravity [8], no formal logical system has been reported for completely background independent geometrical reasoning with logically definable causality besides BDL [2]. A distinguishing factor lies in YinYang bipolar complementarity. No matter time is real or unreal, fundamentally different from the Yin and the Yang of Nature, space and time are not bipolar interactive and cannot form bipolar dynamic equilibrium, symmetry or quantum superposition for quantum gravity. This could be the reason why other approaches to quantum gravity so far stopped short in finding a unique logical foundation as a general theoretical basis for physics. It is contended that the equilibrium-based approach has opened an Eastern road toward quantum gravity [2,16] and will lead to a quantum reincarnation of philosophy [17]. Remarkably, a cellular automaton interpretation of quantum mechanics is proposed and strongly advocated by Gerardus ‘t Hooft [28]. ‘t Hooft points out that “Einstein may still have been right, when he objected against the conclusions drawn by Bohr and Heisenberg. It may well be that, at its most basic level, there is no randomness in nature, no fundamentally statistical aspect to the laws of evolution. Everything, up to the most minute detail, is controlled by invariable laws. Every significant event in our universe takes place for a reason, it was caused by the action of physical law, not just by chance. ” ‘t Hooft stated: “We set up a systematic study of the Interpretation of quantum mechanics. We hope to inspire more physicists to do so, to consider seriously the possibility that quantum mechanics as we know it is not a fundamental, mysterious, impenetrable feature of our physical world, but rather an instrument to statistically describe a world where the physical laws, at their most basic roots, are not quantum mechanical at all.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: S3G) for mitochondrial proteins across the two timepoints. Our results indicate that while there are no significant differences in total mitochondrial protein abundance at 6- and 10-months post-chase, the pool of long lived mitochondrial proteins decreased significantly, with the majority of proteins being turned over at the later timepoint. Hierarchical clustering of the LLPs identified at the 6-month timepoint revealed mitochondrial proteins and myosins as the two protein groups with the highest fractional abundance in the oocyte (Fig. 3C). In particular, mitochondria exhibited a wide range of FA values ranging from 1. 10% to 98. 9%, with an average of 55. 9 ± 35. 1 of 15N-remaing at 6-months (table S2). FA values for myosins was markedly higher than both actin and tubulin with an average FA value of 80. 97 ± 19. 8 % for myosins, 31. 4 ± 15. 6% for actins, and only 8. 3 ± 1. 4% for tubulins. This indicates that while all three cytoskeletal components are long-lived, nearly 81% of the myosin protein pool persists throughout the 6-month timepoint, whereas only 31% of actin protein pool and 8. 3% of tubulin protein pool persists throughout the same length of time. Histones were also identified as LLPs in oocytes with average FA values of 7. 7 ± 9. 8. Mitochondrial proteins, histones, myosins, and tubulins have been previously identified as LLPs in brain and heart tissues, which are known to contain long-lived terminally differentiated cells (i. e. neurons in the brain and cardiac myocytes in the heart) (13). Importantly, however, this is the first time that a subset of the same proteins has been identified as long lived in the germ cell (Fig. 3D). Interestingly, the fractional abundance of mitochondrial LLPs in the brain (10. 2 ± 6. 6%)(13) and myosins in the heart (4. 6 ± 8. 1%)(13) is much lower in than the same LLPs quantified in the oocyte (55. 9 ± 35. 1)(Fig. 3D).

Output: pass


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: Cat # A2228WB: 1:10000AntibodyRabbit polyclonal anti-SAPK/:AB_2250373 Cat # 9252WB: 1:5000AntibodyRabbit monoclonal anti-Phospho-p44/42 (ERK1/2):AB_2315112 Cat # 4370WB: 1:2000AntibodyRabbit monoclonal anti-Phospho-c:AB_2129575 Cat # 3270WB: 1:1000, IF:1:100AntibodyRabbit monoclonal anti-Phospho-p38 :AB_331762 Cat # 9215WB: 1:1000AntibodyRabbit monoclonal anti-Phospho-STAT3:AB_2491009 Cat # 9145WB: 1:1000AntibodyRabbit monoclonal Phospho-NF-kB p65:AB_331284 Cat # 3033WB: 1:2000AntibodyRabbit monoclonal anti-Cyclin d1:AB_2259616 Cat # 2978WB: 1:1000AntibodyRabbit polyclonal anti-:AB_329827. Cat # 9272WB: 1:1000AntibodyRabbit monoclonal anti-Ki67abcamRRID:AB_302459 Cat # ab16667IF:1:100AntibodyRat monoclonal anti-F4/80 (Clone CI:A3-1):AB_323806 Cat # MCA497GAIF:1:100AntibodyMouse monoclonal anti-FlagM2SigmaRRID:AB_262044 Cat # F1804WB: 1:10000AntibodyMouse monoclonal anti-α-BrdUCell signalingRRID:AB_10548898 Cat # 5292IF: 1:200AntibodyRat monoclonal anti-CD16/CD32 (clone 2. 4G2):AB_394656 clone 2. 4G21 μg/ 106 cellsAntibodyMouse monoclonal anti-CD45. 2 :AB_492873 Cat # NC01234371:100AntibodyRat monoclonal PerCP-Cyanine5.

Output: pass


Input: Claim: Quantum biology is a relatively new field that merges principles of quantum mechanics and biology. [SEP] Text: ” However, ‘t Hooft conceded: “Sure, we do not know how to formulate the most basic laws at present, but we are collecting indications that a classical world underlying quantum mechanics does exist. ” Now, BDL and BQLA have led to a bipolar quantum cellular automaton (BQCA) interpretation of quantum mechanics. Not only has BQCA logically unified matter and antimatter atoms [16], it also has led to a cellular model for quantum biology with scalable bipolar quantum fractality. BQCA is expected to serve as a mathematical basis for swarm quantum intelligence as well. Some questions remain, however, including: whether the world modeled with BQCA can be regarded as a classical world underlying quantum mechanics sought by ‘t Hooft [28]; whether BQCA will lead to swarm quantum intelligence for solving some mysteries in quantum biology such as the ability of birds to navigate using Earth’s magnetic field or the puzzle of the inner workings in photosynthesis [24]; whether the BQCA model constitutes a fundamental departure from quantum decoherence and collapse theories associated with quantum measurement. While all three questions are gigantic research topics. The third one is a most critical one for quantum computing. The BQCA interpretation of quantum mechanics provides an equilibrium-based analytical basis for quantum measurement, decoherence and collapse. Without bipolarity, there seems to be no way to call upon anything external factor to disrupt the autonomous evolution of a quantum entanglement in the existing decoherence and collapse theories in quantum mechanics [cf. 29]. With bipolarity, however, all quantum and gravitational action-reaction or negative-positive energies can be blended together into an energy/information conservational or non-conservational bipolar quantum gate matrix for generalized-CPT (G-CPT) [15] symmetry analysis which may leads to a solution to the collapse problem. Notably, limitations of fractal geometry have been identified. In particular, experimental result shows that the many orders of magnitude of the fractal power law described in the seminal book by Mandelbrot [7] are not supported in an unequivocal way by data collected [10]. While this limitation is observed in macro scales, bipolar quantum geometry provides a platform for investigating into the quantum nature of fractals.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: In contrast, histones were less long-lived in the oocyte compared to the brain, and there was no significant difference observed for tubulins (Fig. 3D). Thus, although the identity of long-lived proteins may be conserved across tissues with long-lived cells, differences in fractional abundance may reflect tissue specific functions and requirements. DiscussionIn this study, multi-generational whole animal metabolic stable isotope labeling, paired with multi modal MS-based quantitative approaches enabled visualization and identification of ovarian and oocyte long lived macromolecules in vivo. Our findings provide a novel framework for how long-lived structures may regulate gamete quality. Long-lived macromolecules localized throughout the ovary including the follicular compartment with prominent signals in the granulosa cells of primordial and primary follicles relative to later stage growing follicles. These findings are consistent with the knowledge that the squamous pre-granulosa cells surrounding the oocyte within primordial follicles form early in development which coincided with the 15N-labelling pulse period. These squamous granulosa cells are generally thought to lack the ability to undergo mitotic division until follicles are activated to grow, so it is not surprising that we observed long lived macromolecules persisting within them (32). In contrast, granulosa cells in growing follicles are generated by cell divisions that take place during follicle activation and growth which coincided with the 14N-chase period. Thus, long-lived structures (i. e. enriched with 15N) were diluted through cell divisions during follicle growth. Moreover, during follicle growth, granulosa cells proliferate and differentiate adding new pools of synthesized proteins and molecules. Our results demonstrate that macromolecules formed early in development can persist in squamous granulosa cells for months. Thus, it is possible that these long-lived molecules will accumulate more damage in primordial follicles that remain quiescent for longer periods relative to those that activate earlier. Whether such damage occurs and how it translates into decreased follicle survival or gamete quality will require further investigation. Within the extrafollicular ovarian environment, the OSE exhibited a striking enrichment of long-lived molecules. The OSE is highly dynamic due to repeated post-ovulation wound healing and repair, and its regenerative capacity occurs through a somatic stem/progenitor cell-mediated process (33).

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: 5 Anti-Human/Mouse CD11b (M1/70):AB_2621885 Cat# 65–01121:100AntibodyRat monoclonal APC Anti-Mouse F4/80 Antigen (BM8. 1):AB_2621602 Cat # 20–48011:100AntibodyRat monoclonal Ready Anti-Mouse Ly-6G (Gr-1) (RB6-8C5):AB_2621463 Cat # 40–59311:100AntibodyMonoclonal Anti-CD11c conjugated with :AB_2621747 Cat # 50–01141:100AntibodyMonoclonal PE/Cy7 anti-mouse TCR β chainBiolegendRRID:AB_893627 Cat # 1092211:100Chemical compoundZeocinInvivogenCat # ant-zn-1(100 μg/ml)Chemical compoundLipofectamine 3000Thermo FisherCat # L3000015Chemical compoundMycoplasma KitSigmaCat#11663925910Chemical compoundcoli-derived LPSInvivogenCat # tlrl-smlpsChemical compoundPGNInvivogenCat # tlrl-pgnsaRecombinant proteinIL-6PeprotechCat # 200–06Recombinant proteinTNFαPeprotechCat # 315-01ACommercial kit-FluoresceinRocheCat # 11684795910Commercial kitMulti-target ELISA kitTechnologyCat # 7276Commercial kitPathsan Phospho-p44/42 kitTechnologyCat # 7177CSoftware, algorithmsoftwareBD BioscienceSoftware, algorithmFlowjo v10:SCR_008520Software, algorithmGraphPad Prismgraphpad. comRRID:SCR_002798Software, algorithmQIIME 1. 8. 0Qiime. orgRRID:SCR_008249 PMC3156573 Additional files Supplementary file 1 List of primers of mouse and human genes. All primers used in this study to measure the expression of mouse genes (1) and of human genes (2) by real-time qPCR analysis. Download elife-40396-supp1-v2.

Output: pass


Input: Claim: Research in quantum biology may help scientists understand previously unexplained biological phenomena. [SEP] Text: New traffic light system to guide cell development Anticancer drugs which work by targeting microtubules to slow cell growth and replication, can be used as tools to study these processes in a research setting. Previously, drugs like nocodazole were used to stop microtubules from expanding (polymerising). However, because of the widespread importance of microtubules in many cell functions, from protein transport to cell division, impacting microtubules has many side effects for the cell. The same principles from experiments by Zenker and others have the potential to be used across the medical field. Zenker applied a group of reversibly light-switchable drugs called photostatins (PSTs). The PSTs are not active in the dark, but when they are lit up in UV light they can cause a chemical reaction, blocking the expansion of microtubules within the cell. PSTs provide the chance to manipulate microtubule filament formation with high precision in real-time within a cell. This is because their effects on blocking microtubule polymerisation can be reversed by washing off the PSTs or by applying green light. This huge discovery allowed Zenker and colleagues to inhibit microtubule polymerisation in a much more controlled, targeted manner than current anticancer drugs by using directed light. Zenker and colleagues were the first to apply this methodology using PSTs to manipulate the microtubule cytoskeleton in a living, three-dimensional subject – ie, the mouse embryo – as outlined in their 2017 and 2021 publications. pinkeyes/Shutterstock. com The future for photostatins PSTs are a powerful tool for research that enable real-time manipulation of microtubules – the motorways of cells – both in time and space. Use of PSTs in research could minimise the side effects on microtubule function in embryonic, pluripotent and pluripotent-like cells, compared to the drugs that were previously used. Using PSTs and a 3D live embryo mouse model allows Zenker and colleagues to study cell development during early-stage embryo development. This work can improve our understanding on how the microtubule networks form and function in a cell. The same principles from experiments by Zenker and others have the potential to be used across the medical field. The possibilities range from regenerative medicines to cancer treatments, in addition to studying healthy cells.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Interestingly, long-lived proteins are retained in other cells undergoing repeated asymmetric divisions and are speculated to contribute to the reproductive aging process (34). Consistent with this possibility, the architecture and wound healing ability of the OSE is altered with advanced reproductive age (35). Furthermore, nuclear enrichment of the 15N signal was highest in cells of the OSE. It is plausible that the older template DNA is segregated into the daughter cell destined to become the stem cell to ensure genetic stability of the OSE. Better understanding of the dynamics of long lived molecules in the OSE will require generation of specific samples at precise stages of the estrous cycle and across a time course of ovulation to capture follicular rupture and repair. Through LC-MS/MS analysis, we identified specific long-lived proteins in the mammalian ovary across the reproductive lifespan. LLPs tend to be part of large protein complexes and include histones, nuclear pore complex proteins, lamins, myelin proteins, and mitochondrial proteins (16). In the ovary, the major categories of LLPs included histones, cytoskeletal proteins, and mitochondrial proteins. ZP3 was an oocyte-derived protein identified to be long-lived for at least 6 months. ZP3 is a protein that comprises the zona pellucida (ZP) or glycoprotein matrix of the oocyte, and it is expressed in oocytes of actively growing follicles beginning at the primary stage when the ZP begins to form (36). However, during the pulse period, there would have been very few growing follicles in the ovary because of the immature age of the mice, and most importantly, none of these follicles would have persisted 6 months since folliculogenesis only takes approximately 21 days (37). These findings suggest that ZP3 may be expressed earlier in oocyte development than previously anticipated. Because LLPs can be at the core of scaffold complexes, a primitive zona may exist at the primordial follicle stage upon which the bona fide ZP is established in growing follicles (38, 39). Consistent with this, expression of ZP proteins has been observed in human primordial follicles (39). Interestingly, there are documented age-related defects in the structure and function of the ZP which occur with time-dependent scaffold deterioration. An alternate explanation for our observation is that ZPs from atretic follicles persist and become incorporated into the ovarian matrix.

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: Figures AbstractRecent findings on stress induced structural plasticity in rodents have identified important differences between the hippocampus and amygdala. The same chronic immobilization stress (CIS, 2h/day) causes growth of dendrites and spines in the basolateral amygdala (BLA), but dendritic atrophy in hippocampal area CA3. CIS induced morphological changes also differ in their temporal longevity- BLA hypertrophy, unlike CA3 atrophy, persists even after 21 days of stress-free recovery. Furthermore, a single session of acute immobilization stress (AIS, 2h) leads to a significant increase in spine density 10 days, but not 1 day, later in the BLA. However, little is known about the molecular correlates of the differential effects of chronic and acute stress. Because BDNF is known to be a key regulator of dendritic architecture and spines, we investigated if the levels of BDNF expression reflect the divergent effects of stress on the hippocampus and amygdala. CIS reduces BDNF in area CA3, while it increases it in the BLA of male Wistar rats. CIS-induced increase in BDNF expression lasts for at least 21 days after the end of CIS in the BLA. But CIS-induced decrease in area CA3 BDNF levels, reverses to normal levels within the same period. Finally, BDNF is up regulated in the BLA 1 day after AIS and this increase persists even 10 days later. In contrast, AIS fails to elicit any significant change in area CA3 at either time points. Together, these findings demonstrate that both acute and chronic stress trigger opposite effects on BDNF levels in the BLA versus area CA3, and these divergent changes also follow distinct temporal profiles. These results point to a role for BDNF in stress-induced structural plasticity across both hippocampus and amygdala, two brain areas that have also been implicated in the cognitive and affective symptoms of stress-related psychiatric disorders. Citation: Lakshminarasimhan H, (2012) to on the Levels of in the Hippocampus and Amygdala. 7(1): e30481. Kenji Hashimoto, Center for Health, JapanReceived: September 22, 2011; Accepted: December 16, 2011; Published: January 17, 2012Copyright: © 2012 Lakshminarasimhan, Chattarji. This is an open-access 1.

Output: pass


Input: Claim: Machine learning algorithms can analyze satellite imagery to track deforestation and land use changes. [SEP] Text: environments play a crucial role in maintaining the stability of river ecosystems as well as biodiversity. Furthermore, the appropriate management of small rivers has a significant impact not only on stable water supplies but also on water resource management. Wide monitoring of the riverside environment including land covers and their changes is an important issue in water resource management. This study aims to develop a high-resolution (10 m) model for classifying riverside land cover by integrating Sentinel-1 synthetic aperture radar (SAR) data and terrestrial characteristics using machine learning algorithms. We constructed a total of 3,284 landcover reference point datasets near the four major rivers of with five classes: water, barren, grass, forest, and built-up. Forest and classification models were developed using eight input variables derived from SAR signal and digital terrain data. The models showed an overall cross-validation accuracy exceeding 80% while maintaining consistent spatial distributions, except for the barren class. The false alarms on barren would be corrected through additional sampling processes and incorporating optical characteristics in further study. The high-resolution riverside land cover maps are expected to contribute to the establishment of a comprehensive management system for water resources such as riverside land cover change detection, river ecosystem monitoring, and flood hazard management. Furthermore, the utilization of the next generation medium satellite 5 (C-band SAR) would improve the performance of riverside land cover classification algorithm in the future. Keywords: Riverside, Land cover, Classification, Remote sensing, Synthetic aperture radar 1.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Skip to main content Get published My account Search all SpringerOpen 0. 40 in 1832, 0. 56 in 1928, and 0. 69 in 2019. Over time, life expectancy gradually approaches the human lifespan record (both in absolute and relative terms); as a result, the distribution is increasingly squeezed within a shorter age range, thus reducing its variability. These general trends are not exclusive to Swedish women. They have been observed in the majority of countries with available data, for both women and men. Fig. 1(Source: Authors’ elaboration based on the HMD data)Age-at-death distributions for Swedish females in 1832 (dashed), 1928 (dotted), and 2019 (solid). Black and grey vertical lines refer to life expectancy and record lifespan up until that year, respectivelyFull size imageIn this setting, it is not surprising that lifespan inequality tends to decrease as life expectancy approaches the maximal lifespan. Given the mechanically driven appearance of such relationship, in this paper we ask: could it have been otherwise? Put differently, could lifespan inequality have behaved differently when life expectancy gradually approaches the maximal lifespan, or is the strong relationship between both variables an artifact of the way in which inequality is measured? This is a question with important theoretical and practical implications. From a theoretical perspective, studying the relationship between average longevity and lifespan variability is fundamental for a proper understanding of the dynamics in human mortality, and is crucial for forecasting future patterns of population health (see related work by Bohk-Ewald et al. , 2017; Nigri et al. , 2021a, 2021b; Rabbi & Mazzuco, 2021). From a practical and policy-making perspective, it is very important to know whether and to what extent the normatively desirable goals of increasing longevity and reducing lifespan variability can be achieved simultaneously or if one can only be attained to the detriment of the other (Benach et al. , 2011, 2013; Smits & Monden, 2009; Vaupel et al. , 2011). The fact that longevity and lifespan variability are so strongly connected raises several issues. First, it might be argued that it is not immediately clear that studying lifespan inequality can provide new insights beyond what we already know from studying life expectancy alone. Second, the comparison of lifespan inequalities for distributions with very different life expectancy levels is compromised.

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: Chronic stress regulates BDNF expression in CA3 and BLA in contrasting manner. Data are presented as mean ± SEM. A Experimental design of chronic stress (CIS+1d) followed by micro dissection of area CA3 from transverse hippocampal sections or BLA from coronal sections. B BDNF expression in area CA3 is decreased after chronic stress (Control, n = 5; CIS+1d, n = 5), C Chronic stress up regulates BDNF expression in BLA (Control, n = 6; CIS+1d, n = 8). Chronic stress induced changes in BDNF expression profile is normalized to respective control level. D Serum corticosterone levels are up regulated after chronic stress in comparison to controls (Control, n = 5; CIS+1d, n = 6). Significant differences *, p<0. 05; Unpaired, two-tailed, Student's t-test was used to compare stress and control groups. Download: PPTPowerPoint slidePNGlarger imageTIFForiginal imageFigure 2. Contrasting profiles of BDNF in CA3 and BLA in response to recovery from chronic stress. Data are presented as mean ± SEM A Experimental design of 21 days of recovery from chronic stress paradigm (CIS+21d). B BDNF expression in area CA3 comes back to control levels post recovery from chronic stress (Control, n = 6; CIS+21d, n = 6), C Chronic stress induced up regulation in BDNF expression in BLA persists even after twenty one days of recovery (Control, n = 4; CIS+21d, n = 6). BDNF expression profile is normalized to respective control level. D The up regulation of serum corticosterone levels persists even after recovery from chronic stress (Control, n = 7; CIS+21d, n = 6). Significant differences *, p<0. 05; Unpaired, two-tailed, Student's t-test was used to compare stress and control groups. Download: PPTPowerPoint slidePNGlarger imageTIFForiginal imageFigure 3. Acute stress modulates BDNF profile differentially in CA3 and BLA. Data are presented as mean ± SEM. A Experimental design of acute stress (AIS+1d) and recovery for 10 days from acute stress (AIS+10d).

Output: pass


Input: Claim: Machine learning algorithms can analyze satellite imagery to track deforestation and land use changes. [SEP] Text: 우리나라 주요 하천 수변환경의 변화를 정량적으로 분석할 수 있으며, 수변환경의 체계적인 관리 계획 및 토지이용 계획 수립 등과 같은 의사결정에 참고 자료로 활용할 수 있을 것이다. 따라서 본 연구에서는 Sentinel-1 SAR 인공위성 영상과 지표면 특성을 고려하기 위한 지형 자료를 융합·활용하여 한반도 지역의 주요 하천에서의 10 m 급 수변피복 탐지 알고리즘 개발 및 하천수변피복의 분포에 대해서 분석을 수행하였다. 2.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Alongside these issues, there is the unresolved debate of whether inequality should be measured in absolute or relative terms, a decision that depends on normative values and which might lead to inconsistent and conflicting conclusions (Asada, 2010; Clarke et al. , 2002; Erreygers & van Ourti, 2011; Houweling et al. , 2007; Mackenbach, 2015). Therefore, we propose a new approach to lifespan inequality measurement that, unlike existing measures, explicitly takes into consideration the shrinking room for variability that ensues when both life expectancy and maximal lifespan get closer over time. The idea is quite simple: we propose a new normalization procedure that compares observed inequality with respect to the maximal inequality one could possibly observe in a hypothetical distribution having the same mean. In this way, we obtain a normalized index of inequality, measuring how far we are from the inequality-maximizing scenario. As shown below, this approach assumes that individuals’ length of life cannot exceed the maximal lifespan \(\omega\). Given the uncertainty surrounding that value, we develop simple methods to investigate the robustness of any statement one might want to make with regard to alternative values of \(\omega\). The role of a maximal lifespan (or to quote Myers and Manton (1984): the “biological limits on normal life span of human species”) in determining changes in length-of-life variation has long been acknowledged by researchers. Although the upper boundary is sometimes with respect to life expectancy at the population level (Fries, 1980), individual-level maximal lifespan is implied. Because of such a limit, both morbidity and mortality tend to be pushed into a smaller age range (Cheung et al. , 2005; Fries, 1980; Wilmoth & Horiuchi, 1999). The observed decreasing trends of lifespan variability together with increasing life expectancy in the past decades generally agree with this theoretical prediction. Unlike prior research (which implicitly assumed that the observed relationship between both variables could be driven by the existence of such upper bound), we explicitly incorporate the maximal lifespan \(\omega\) as a key ingredient that could be taken into consideration when measuring lifespan inequality. With our approach, we may see patterns that may have been hidden in common inequality measures. First, the steady decline in lifespan inequality as measured by conventional measures may no longer hold, particularly for countries with high levels of longevity.

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: B BDNF expression in area CA3 in response to acute stress. Acute stress does not change the BDNF levels in CA3 (Control, n = 9; AIS+1d, n = 9; AIS+10d, n = 6, F(2,21) = 2. 11, p>0. 05). C Acute stress up regulates BDNF expression in BLA and this up regulation persists even after recovery (Control, n = 6; AIS+1d, n = 5; AIS+10d, n = 6, F(2,14) = 4. 82, p<0. 05). BDNF expression profile was normalized to respective control levels and evaluated by Fisher's post-hoc. D Effect of acute stress and recovery from acute stress on serum corticosterone levels (Control, n = 11; AIS+1d, n = 5; AIS+10d, n = 6, Kruskal-χ2(2) = 10. 01, p<0. 05, Mann-Whitney post-hoc, p<0. 05). Significant differences *, p<0. 05. Body weights The net change in weights of rats between the beginning and end points of the experiments was divided by the starting weight and multiplied by 100 to calculate percentage gain in body weights. Corticosterone measurements Rats were weighed and sacrificed by rapid decapitation under deep anesthesia (halothane) and trunk blood was collected within 3 minutes for each animal; all samples were collected between 10 AM and 1 PM. Samples were centrifuged at 16000 rcf for 5 min at 4°C, and serum was stored at −80°C. Serum corticosterone level was determined by using Correlate - EIA kit according to the manufacturer's instructions (Assay designs). Absorbance at 405 nm was determined by microplate reader (Biorad). Corticosterone concentration (ng/ml) was determined using the standard curve. Anesthesia, decapitation and blood collection was conducted rapidly (within 3′) in an adjacent room in order to minimize stress effects and keep the time to blood collection standardized. Tissue collection and BDNF measurements Basolateral amygdala (BLA) was micro dissected from 400 µm thick coronal sections obtained from McChopper.

Output: pass


Input: Claim: Machine learning algorithms can analyze satellite imagery to track deforestation and land use changes. [SEP] Text: 보다 견고한 수변피복 탐지 모델 개발을 위하여 참조 자료 구축 시, 2019년 1년간 피복의 변화가 없고, 중심격자 주위 3×3 격자 내 동일한 피복을 가지는 픽셀을 대상으로 선정하였다. 2. 3 인공지능 기반 수변피복 탐지 알고리즘 본 연구에서는 수변피복 탐지 모델로 활용하기 위한 인공지능 알고리즘으로 (RF) 및 (LGBM)을 이용하였다.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Unexpected increase in longevity Death from aging is technically death from age-related diseases, which are manifestations of advanced aging [1]. But, historically, most people died young and, of course, not from age-related diseases but, rather, from starvation and epidemics (cholera, smallpox, tuberculosis and many currently rare infections) as well as from physical violence. Just three centuries ago, life expectancy was less than 16 years and 75% of people born in London in 1662 died before they reached the age of 26 (Graunt's life table). The progress of civilization eliminated many causes of death that killed young people in the past. This dramatically increased the average lifespan. In addition, modern medicine extended lifespan of old people by treating age-related diseases. But maximal lifespan seemed to be not affected. It was assumed that human life span is close to its upper limits. However, surprising demographists and gerontologists, it was shown that life expectancy continues to increase at an astonishing pace [2,3]. In the countries with the highest life expectancies, the long term increase in life expectancy proceeds at a pace of 2. 5 years per 10 years, or six hours per day [4]. A century ago, the chance to become centenarian (a person older than 100 years) was a hundred times lower. Furthermore, as calculated, most babies born since 2000 in countries with long life expectancies will celebrate their 100th birthdays [5]. Most astonishingly, people are reaching very old age in better health. But then they deteriorate fast, seemingly indicating that the rate of aging was not changed but just aging was postponed [3]. "Taken together, these findings are so perplexing that they can be dubbed the ‘longevity riddle': why do the evolutionary forces that shaped human aging provide a license to alter the level of health but not the rate of debilitation? " [3]. So why can aging be delayed but not slowed? Or can aging be slowed? In order to solve the longevity riddle, we should turn gerontology on its head. It has been always assumed that aging is caused by damage. As recently argued, aging is not driven by damage, but, in contrast, leads to damage (organ damage) [6-8]. And aging is driven in part by mTOR (mammalian target of rapamycin).

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: Area CA3 was dissected from 400 µm thick transverse hippocampal sections obtained using the chopper (Figure 1A). Tissue was lysed in the presence of protease inhibitor cocktail (Roche). BDNF was estimated using BDNF Emax immunoassay kit (Promega) according to manufacturer's protocol. Protein levels were estimated using BCA kit (Pierce). Levels of BDNF were normalized to protein levels. Data analysis Percentage changes in body weight gain were compared between control and experimental groups using unpaired Student's t test assuming unequal variances. Corticosterone measurements and BDNF data were analyzed using unpaired Student's t test assuming unequal variances in the case of CIS and CIS+21d. In case of corticosterone measurements for AIS and AIS+10d, Kruskal–Wallis test followed by Mann–Whitney post-hoc test with Bonferroni's adjustment was used because the data distributions called for a non-parametric analysis. For the analysis of the data, ANOVA followed by post-hoc Fisher's least significant difference (LSD) test was used for pairwise comparison in the case of AIS and AIS+10d. P-values less than 0. 05 were considered significant. stress elicits opposite effects on BDNF levels in the BLA and area CA3 As described above, chronic immobilization stress (CIS; 2 h/day for 10 days) leads to contrasting patterns of dendritic remodeling in the BLA versus hippocampal area CA3. Specifically, 1 day after the termination of stress, the same CIS that caused dendritic atrophy in the CA3 pyramidal neurons, elicited dendritic growth and spinogenesis in the BLA principal neurons. As BDNF promotes dendritic and spine growth [18], we reasoned that the levels of BDNF expression may reflect the divergent effects of chronic stress on neuronal morphology in the BLA versus area CA3. To test this prediction, we conducted ELISA analysis on tissue micro-dissected from these two brain regions in control and CIS treated rats (Figure 1A). There was significantly lower levels of BDNF protein in the area CA3 1 day after chronic stress (Control, 1. 00±0. 11; n = 5; CIS+1d, 0. 43±0.

Output: pass


Input: Claim: Machine learning algorithms can analyze satellite imagery to track deforestation and land use changes. [SEP] Text: 더 나아가 추후에 차세대 수자원위성을 활용한다면 본 하천 수변피복탐지, 분석 알고리즘의 고도화를 통하여 유량 관리 및 수재해 관리, 미계측 지역에 대한 확장 분석, 수재해에 취약 국가에 대한 공적개발 원조를 통한 국제협력 도모 등 다양한 활용이 가능할 것이다. of behalf of all authors, the corresponding author states that there is no conflict of interest. This research was supported by of System for Satellite from K-water. data that support the findings of this study are openly available in at Fig. 1. Study area and spatial distribution of reference data (five classes). Fig. 2. Comparison of validation results for land cover classification on riversides based on RF and LGBM by different schemes. VV, Vertical-Vertical; VH, Vertical-Horizontal; IA, incidence angle; CR, Cross Ratio; RF, Random Forest;. Fig. 3. Comparison of land cover classification results in Spring (April 3, 2019; above) and Autumn (September 30, 2019; below) using RF and LGBM within the same area (Geum River). RF, Random Forest;. Table 1.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: TOR-driven quasi-programmed aging and age-related diseases The mTOR intracellular signaling pathway is activated by numerous signals including glucose, amino acids, fat acids and other nutrients, insulin and some other hormones, growth factors and cytokines [9-11]. In response, it increases cellular functions and cellular mass growth [12]. When the cell cycle is blocked, mTOR drives cellular senescence [13]. Cellular aging can be defined as over-activation of signaling pathways (such as mTOR) with secondary signal resistance [14]. In turn this slowly leads to diseases of aging (hypertension, atherosclerosis, macular degeneration, insulin resistance, obesity, neurodegeneration, cancer, osteoporosis, organ hypertrophy). For example, TOR-dependent activation of osteoclasts causes bone resorption (osteoporosis) [15]. But these aging processes are relatively silent (subclinical, no obvious deterioration) until aging culminates in "catastrophes" - organ damage. For example, osteoporosis can lead to broken hip and atherosclerosis can lead to infarction. Then deterioration can be quick, leading to death in a mater of hours or years or decades, depending on the level of medical care. Morbid phase When diseases become clinical then deterioration may be fast. For example, high blood pressure, thrombosis and atherosclerosis can culminate in stroke. This will initiate a chain of deteriorations (immobility - pneumonia, etc. ) that are TOR-independent. The duration of this morbid (deterioration) phase is almost solely determined by the level of medical care. Furthermore, age-related blindness and Alzheimer's disease are rarely lethal anymore. Medicine may dramatically prolong the morbidity phase, delaying death. Thus, the speed of deterioration is almost independent from the aging process and cannot serve as a marker of aging or the rate of aging. The rate of aging is actually determined by the age of the onset of age-related diseases. Slowing down the aging process (by calorie restriction, rapamycin or genetic manipulation) delays diseases. "Thought experiment": how would rapamycin affect longevity in 1667 versus 1967 Rapamycin is an anti-aging drug, which is currently used to prevent donor organ rejections [16]. Rapamycin delays cancer in animals and humans (see for review [17]).

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: 07; data normalized to control animals; n = 5, P<0. 05; Figure 1B). In striking contrast, the same chronic stress led to significantly higher levels of BDNF protein in the BLA 1 day later (Control, 1. 00±0. 01; n = 6; CIS+1d, 1. 44±0. 15; data normalized to control animals; n = 8; P<0. 05; Figure 1C). Thus, these data indicate that similar to its differential effects on dendritic arborization, CIS also modulates BDNF levels in the area CA3 and BLA in contrasting fashion. We also confirmed the efficacy of our CIS paradigm by assessing two widely used indicators of stress. First, we measured, 1 day after the end of the 10 day CIS protocol, the blood serum levels of corticosterone, a common indicator of HPA axis activation. There was a significant increase in the levels of corticosterone in CIS animals relative to control animals (Control, 83. 8±42. 2 ng/ml of serum; n = 5; CIS+1d, 338. 2±94. 8 ng/ml of serum; n = 6; P<0. 05; Figure 1D). Second, we compared changes in body weight (Table 1) and found a significant reduction in the percentage weight gained 1 day after CIS (Control, 30. 26±1. 37%; n = 12; CIS+1d, 14. 4±1. 94%; n = 12; P<0. 05). Download: PPTPowerPoint slidePNGlarger imageTIFForiginal imageTable 1. Summary of body weight measures. Recovery after chronic stress fails to reverse elevated levels of BDNF in the BLA, but not in area CA3 Earlier studies have reported that the impact of chronic stress also differs between the hippocampus and amygdala in terms of its temporal persistence. For instance, dendritic hypertrophy in the BLA persists even after 21 days of stress-free recovery following 10 days of CIS. On the other hand, CIS-induced hippocampal CA3 atrophy is reversible within the same 21-day period of recovery.

Output: pass


Input: Claim: AI can optimize renewable energy grids by forecasting energy demand and supply. [SEP] Text: IntroductionIndia's progress and future prosperity depend on access to affordable, clean, and reliable energy. However, India faces several challenges such as unreliable electricity supply, dependence on solid biomass for cooking, financially struggling electricity distribution companies, and poor air quality. Despite these challenges, India has made remarkable progress in its energy development, including expanding renewable energy sources, promoting energy-efficient LED lighting, and bringing electricity connections to millions of citizens. As the world's third-largest energy-consuming country, India's energy demands and infrastructure are expected to grow significantly, driven by population growth, urbanization, changing infrastructure, and increased competition. Accurate demand forecasting is essential to meet the electricity demands of the residential, industrial, and agricultural sectors while integrating renewable energy. To address these challenges, (SG) technology offers a solution through Management (DSM) in long term perspective and (DR) programs to address short term demand deviations from the forecast. SG is a modern electric infrastructure that integrates information and electrical infrastructure [1]. This technology uses advanced sensors, communication networks, and control systems to collect real-time data on energy demand and supply. With this data, utilities can implement DR programs that incentivize customers to reduce energy usage during peak demand periods. Management (DRM) is an application of SG that provides various incentives to consumers to shift from peak load consumption to off-peak load consumption [2, 3]. To change electricity consumption behavior, (SM) can be used to implement prescribed tariff rates. SMs are a vital part of SG, and their data is analyzed to forecast load (demand) accurately and manage energy consumption. In the residential sector, SMs play a crucial role for consumers as they keep a record of their consumption and communicate the data to the head end system. (LF), load analysis, and load management are principal applications of SM data. In load management, customers are categorized based on their electricity consumption behavior (load profiling), so that DSM and DR measures could be implemented accordingly. However, obtaining real-time SM data for research could be challenging due to data privacy and security constraints [4]. To overcome this, several open-source datasets, including. Commission for (CER), resident load 2012&14, ISO England, are available for experimental analysis. Accurate demand forecasting is critical for utilities to plan and book energy supply and avoid blackouts or brownouts.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: It also delays other age-related diseases in animal models of accelerated diseases. For example, rapamycin and its analogs delay atherosclerosis [18-23]. mTOR is involved in age-related diseases exactly because it is involved in aging. In fact, rapamycin prolongs life span in mice and flies [24-27]. It is expected that, in adult humans, rapamycin (at correct doses and schedules) will prolong healthy and maximal lifespan [16]. But consider rapamycin administered for life, starting from childhood. Then its effect on longevity will depend on the level of civilization and will be opposite in the 17th and 20th centuries. Scenario 1. Assume that in 1667, 3 out of 4 newborns were randomly prescribed rapamycin for life. Rapamycin would slow down developmental growth (a disadvantage for survival, especially for orphans). Malnutrition and stresses would be less tolerated, because the nutrient sensing pathway is deactivated by rapamycin. Reduced muscle mass and fat stores would increase chances of death from violence and famine. In infants with natural immunotolerance, rapamycin would further decrease immunity against infections, which were numerous, incurable and non-preventable in 17th century. So, if 3 out of 4 people must die before the age of 26 (1667 in London), they would be those who were treated with rapamycin. The control group would survive and develop diseases of aging at normal (early) age. Scenario 2. In 20th century London, sanitation, vaccination and other measures have greatly reduced epidemics. The discovery of antibiotics has further prevented death from infections. Famine and violent death are not common either. Those who were treated with rapamycin for life will survive into adulthood and then will age slowly. In the rapamycin-treated group, diseases will be delayed. Furthermore, even its ability to cause immunologic tolerance (‘rejuvenate' immunity) will be beneficial in the elderly by decreasing hyper-immunity and autoimmunity. (Note: rapamycin improves immunity in old animals [28]). So, now, the rapamycin treated group becomes centenarians in good heath.

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: Since the data presented so far indicates that the CIS-induced increase and decrease in BDNF levels parallels BLA hypertrophy and CA3 atrophy respectively, we tested if the temporal profile of BDNF levels during post-stress recovery also differ in the two regions. Twenty one days after the end of CIS, we found no difference in BDNF levels in area CA3 between control and CIS animals (Control, 1. 00±0. 15; n = 6; CIS+21d, 1. 00±0. 2; data normalized to control animals; n = 6; P>0. 05; Figure 2B). In the BLA, by contrast, BDNF levels remained significantly elevated even after the same post-CIS recovery period (Control, 1. 00±0. 02; n = 4; CIS+21d, 2. 3±0. 49; data normalized to control animals; n = 6; P<0. 05; Figure 2C). Thus, unlike CA3 area, CIS-induced up-regulation of BDNF protein levels in the BLA persists up to 21 days after the end of stress. We also monitored the impact of CIS on blood serum levels of corticosterone and relative gain in body weight after the same recovery period. Corticosterone levels remained elevated even 21 days after CIS (Control, 43. 0±11. 7 ng/ml of serum; n = 7; CIS+21d, 146. 3±34. 9 ng/ml of serum; n = 6; P<0. 05; Figure 2D). In contrast, there was no difference in the percentage gain in body weight between stressed and unstressed animals after the recovery period (Control, 73. 41±4. 1%; n = 4; CIS+21d, 70. 0±3. 5% n = 6 P>0. 05) (Table 1). Acute stress also differs in its impact on BDNF expression over time in the BLA and area CA3 The results described so far show that BDNF levels in area CA3 and BLA, following exposure to CIS, are strikingly different both in terms of the direction and time course of change.

Output: pass


Input: Claim: AI can optimize renewable energy grids by forecasting energy demand and supply. [SEP] Text: The integration of renewable energy sources, such as wind and solar power, further increases the complexity of demand forecasting as these sources are intermittent and less predictable than traditional fossil fuel sources. SG technology, using advanced analytics, weather forecast models and machine learning algorithms, can help utilities forecast energy demand more accurately, optimize energy supply and distribution, and create a reliable, efficient, greener and cost-effective energy system. Classification and Utility ChargesElectricity consumers can be classified into four sectors based on their usage: Residential, Industrial, Commercial, and Agricultural. Each sector's electricity demand is influenced by various factors. For example, residential electricity consumption depends on the time of day, type of day (working days), seasons, temperature, type of equipment; while industrial electricity consumption depends on the appliances used in the industry like shiftable, non-shiftable appliances [1, 5]. Similarly, commercial electricity consumption depends on the night ratio and the peak ratio, while agricultural electricity consumption depends on factors such as irrigation, crop type, season soil and land–water level. One common factor affecting energy demand in all sectors is weather information. Overestimation of the budget due to excess electricity generation can lead to financial crises, while under-generation of electricity can result in supply shortages. The utility requires short-term, medium-term, and long-term forecasts to plan and distribute energy to consumers, provide much in time information to power plants for energy planning, and make financial decisions for energy purchases. Utility charges for electricity consumption are based on the rate of usage with different slab and Time of Day (TOD), known as a tariff. Consumption rate varies with respect to different types of users. The government provides some subsidies to the domestic (rural, urban) users, lifeline consumers and those agriculture (irrigation) consumers who use the electricity at the limited range define by the utility. There exist different types of tariff plans: normal, prepaid, normal-TOD, and prepaid-TOD, which are applicable to different consumers, depending on their sector and usage. In TOD based system the price of electricity varies according to the time of electricity usage. Additional variation in tariff rates occurs due to the season like summer, winter and monsoon. The difference between the normal scheme and prepaid scheme is a mode of the payment after usage of the electricity or before usage of electricity respectively.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: But because deterioration is mTOR-independent, this group will deteriorate at the same rate (but later in life) as the control group, assuming that the medical treatment is equal in both groups (in reality, younger patients are treated more intensively. ) The revealed-slow-aging hypothesis Thus, while slow aging was a disadvantage in 1667, it became an advantage in 1967. In the past, mostly fast-aging individuals could survive into chronologically old age (Figure 2A). Now, slow-aging individuals can survive into chronologically old age (Figure 2B). Therefore, demographists observe an increasing number of individuals who are healthy at advanced chronological ages with delayed onset of diseases, who then deteriorate at the same rate as younger patients (Figure 1A vs 1B). Figure 1. Fast and slow aging. In slow aging, the onset of deterioration is postponed but the rate of deterioration is not changed. Importantly, current increase in healthy lifespan (increased longevity with late onset of age-related diseases) is not caused by natural selection. It happens in the same generation. Slow aging was not selected but was simply revealed (Figure 2 B). Until recently, most slow-aging individuals died prematurely. They (we) did not necessarily die young but nevertheless died not from aging. For example, at the same chronological age when fast-aging individuals died from heart attack, healthy slow-aging individuals died from malnutrition and infections, for instance. Elimination of premature death greatly enriched chronologically old population with slow-aging (biologically young) individuals (Figure 2). To be possibly correct, the hypothesis requires a high proportion of slow-aging individuals at birth (Figure 2). Otherwise, there would be too few slow-aging individuals to make a difference later (Figure 2 A vs B). Why was not slow aging selected out? Slow aging must be beneficial for women, by increasing their reproductive period. In fact, female's fertility is decreasing early in life (starting from late twenties, long before menopause). This reproductive aging is one of the earliest manifestations of aging in females. So slow aging benefits females. Also, as I will discuss elsewhere, women do not need to be as robust as men, so can afford to age slower (see forthcoming 2. Preferential survival fast- versus slow-aging individuals.

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: In contrast to the robust effects seen when the 2 h immobilization stress is repeated for 10 consecutive days, only a single episode of the same stress (acute immobilization stress or AIS) is known to trigger a different temporal pattern of changes in the BLA. fails to affect spine density or dendritic arborization, when measured 1 day later. However, the same AIS leads to a gradual increase in spine density 10 days later in the BLA. Therefore, next we examined if AIS modulates BDNF levels in the hippocampus and amygdala over time. We found only a modest reduction in BDNF in area CA3 that was not statistically significant either 1 or 10 days after AIS (Control, 1. 00±0. 11; n = 9; AIS+1d, 0. 73±0. 05; data normalized to control animals; n = 9; AIS+10d, 1. 02±0. 19; data normalized to control animals; n = 6; P>0. 05; Figure 3B). However, the same AIS caused a significant increase in BDNF levels in the BLA 1 day later (Control, 1. 00±0. 06; n = 6; AIS+1d, 2. 31±0. 24; data normalized to control animals; n = 5; P<0. 05; Figure 3C). Moreover, this AIS-induced elevation in BDNF levels persisted in the BLA even after 10 days (CTR, 1. 00±0. 06; n = 6; AIS+10d, 1. 98±0. 46; data normalized to control animals; n = 6; P<0. 05; Figure 3C). These findings demonstrate that even a shorter duration of stress triggers changes in BDNF in the BLA and CA3 area that differ considerably in their direction and temporal features. Since the AIS paradigm is expected to be less severe compared to CIS, we also monitored its impact on serum levels of corticosterone and body weight gain at the same time points after AIS when BDNF protein levels were measured. Relative to controls, AIS caused a significant increase in corticosterone levels 1 day later (Control, 83. 8±26. 0 ng/ml of serum; n = 11, AIS+1d, 594. 7±221.

Output: pass


Input: Claim: AI can optimize renewable energy grids by forecasting energy demand and supply. [SEP] Text: The implementation of various ML and DL algorithms on load forecasting is provided in Section "to Load Forecasting". Section "Management (DSM)" provides introduction of demand response management. Sector-wise DR programs are described in Section "Programs". Section "Challenges and Guidance" discusses challenges in SG. Section "Conclusion" summarises the conclusion and future scope of work in SG. Load ForecastingForecasting is a component of data science to predict future parameters based on a set of historical data and trends. Load management is used to schedule the load according to various parameters in the different sectors. Load or demand forecasting is a feature of DSM and it is categorized according to time horizon [8] i. e. Very Short-Term LF (VSTLF), Short-Term LF (STLF), Medium-Term LF (MTLF) and Long-Term LF (LTLF). The time horizon-based classification of load forecasting is presented in Table 1. Table 1 Classification of Time horizon-based load forecastingFull size tableTime-series based load forecasting depends on its previous stored load history (historical data). Statistical and (AI) based intelligent techniques are generally used for load forecasting. To predict the time-series based load forecasting, external features are also considered as an input along with time series data. The statistical approaches are categorized as regression analysis and time series analysis. In regression analysis electricity consumption depends on independent variables like weather data. Average (ARIMA) and Seasonal-ARIMA (), techniques are used for predicting the future value of the electricity consumption from the historical data. These techniques are also known as Time series techniques. An AI based intelligent approach uses ML and DL algorithms [8] for example (NN), fuzzy regression, support vector regression, decision tress, etc. Most of the ML and DL algorithms help to improve accuracy of load forecasting, efficiency of load scheduling and effectiveness of load monitoring in the SG environment. A typical load forecasting technique is depicted in Fig. 1, where historical load and weather history is input to the modeling process block feeding to the extrapolating process block. Another input to the second block is weather forecast and thus the trained model forecasts the future load. Fig. 1TechniqueFull size imageWorkflow of TechniquesThis section explains detailed architecture of load forecasting workflow. It will help the readers to understand how a forecasting technique can be applied and implemented on a dataset. The workflow involves mainly four steps, i.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: (A) In the past, slow-aging individuals (open circles) died prematurely and fast-aging individuals (closed circles) survived into old age. (B) Now, slow-aging individuals (open circles) survived into old age as healthy (biologically young) and outlive faster aging individuals (closed circles). Figure 3. Traditional medicine increases survival (extends deterioration phase) without affecting the onset of deterioration. The prospect of longevity Today, most slow-aging individuals, with less active mTOR, do not die early in life from malnutrition and infections and can reach chronologically old age. Exactly because they are slow-aging (young biologically), they are able to reach old age in good health. This may explain the current increase in longevity. But this trend is probably close to saturation and will be saturated by 2050 (a century after invention of antibiotics) in the countries with the highest longevity. The reason is that the rate of aging was not affected by elimination of death from famine and infections. Yet, aging could be slowed by rapamycin, a drug currently approved to prevent organ rejection. (Note: rapamycin, as an anti-aging drug, perhaps should not be administrated until after growth is completed). Based on data with calorie restriction and rapamycin in mice, lifespan might be increased on 30 percent. Then we will observe 140-150 years old individuals and average lifespan will exceed 100. Solution of heath care crisis and further prospect on longevity Currently, by treating each disease individually and focusing on advanced diseases, traditional medical interventions lengthen the morbidity phase (Figure 3). So, traditional medicine increases number of old people in bad health. However, extension of lifespan by lengthening only the morbidity phase will make the cost of medical care unsustainable for society. Anti-aging medicine can solve this crisis by delaying the morbidity (deterioration) phase (Figure 4). There is incorrect perception that anti-aging drugs would increase a number of people suffering with age-related diseases. In contrast, such old people will be healthy because they will be only chronologically old but biologically young. They will be healthier for longer (until they reach biological age of deterioration). Biological age is by itself determined by the sum of all diseases of aging [1]. In other words, diseases of aging are manifestations of biological aging. It is impossible to dissociate biological aging and diseases of aging. Healthy aging is healthy non-aging (or slow aging).

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: 2 ng/ml of serum n = 5 P<0. 05; Figure 3D). 10 days after AIS, corticosterone levels continued to remain high, although the difference was no longer statistically significant (Control, 83. 8±26. 0 ng/ml of serum; n = 11; AIS+10d, 232. 9±78. 9 ng/ml of serum; n = 6; P>0. 05). Further, unlike did not cause any significant change in the percentage of body weight gain 1 day later (Control, 1. 31±0. 31%; n = 6; AIS+1d, 0. 93±0. 41%; n = 5; P>0. 05) (Table 1). This absence of any effect on body weight was also seen after 10 days (Control, 30. 26±1. 37%; n = 12; AIS + 10d, 17. 37±5. 39%; n = 6; P>0. 05) (Table 1). Taken together, it is only 1 day after CIS that we observed a significant effect of stress on body weight gain. DiscussionThis study explored two key facets of stress-induced modulation of BDNF expression in the hippocampus and amygdala – one in terms of region-specific differences, and the other in the temporal domain. Because BDNF regulates dendritic architecture and spines, both major targets of stress-induced structural plasticity, we hypothesized that the levels of BDNF expression would reflect the divergent effects of stress on the hippocampus and amygdala. To test this hypothesis, we used two very different paradigms of immobilization stress – an acute paradigm involving a single 2 h session (AIS) and a chronic version wherein the same 2-hour stress was repeated for 10 consecutive days (CIS). First, we tested whether chronic stress elicits changes in BDNF protein levels that parallel the contrasting patterns of dendritic remodeling observed previously in the amygdala and hippocampus. We report that the same CIS has strikingly opposite effects on BDNF expression one day after the end of CIS – it reduces BDNF in area CA3, while it increases BDNF in the BLA. This contrasting modulation was accompanied by a significant up-regulation in circulating corticosterone levels.

Output: pass


Input: Claim: AI can optimize renewable energy grids by forecasting energy demand and supply. [SEP] Text: e. , Collection and Pre-processing of data, from exogenous and endogenous data, Training a model with different load forecasting techniques and Error Analysis. The architecture is depicted in Fig. 2, representing the flow of load forecasting steps. Fig. 2Workflow of TechniqueFull size imageThe initial stage of load forecasting is to acquire application-based data. The collected data may be univariate or multivariate. For univariate load forecasting we need only the historical load data at the different granularity of time. The model contains the time series features or endogenous features. The time series features contain a) date and time features; b) window size; c) lag values. The date and time features contain minutes, hours, day and month etc. , window size contains the average, min, max of the load or previous day, previous 2-day load at the same hour etc. , lag value is previous same hour load, previous same weekday load etc. If there is any dependency of climate in the electricity consumption then we need multivariate load forecasting. For example, today’s consumption depends on the previous day’s same hour load, temperature and humidity then we need to extract exogenous data. Two variable humidity and temperature except the load is also dependent on the time, it is known as multivariate load forecasting. The second step is feature selection and extraction: After identifying the application the next step is feature selection. Feature selection is vital step for load forecasting as it affects the model accuracy according to the application. The feature selection can be done using EMD [13], Mutual Information, [14]. Mutual information with transudative model given in [15]. To select the candidate input, four feature selection techniques defined in [16, 17] named as (AC) to select the lag values, between two features (lag variable and target variable), RelieF select features according to ranked order and Correlation based (CFS) for good feature-subset selection. Among them, RelieF is an instance-based approach. KS-test based feature selection (KSBFS) used for classes, η2 based feature selection (EBFS) for qualitative variables [18]. The third step is, Train the model with Load forecasting: Various load forecasting techniques explained in Section "to Load Forecasting". The load forecasting techniques can be selected according to time horizon requirement.

Output: corroborate


Input: Claim: Biohacking guarantees longevity by doubling the average human lifespan. [SEP] Text: Deceleration of aging, manifested as "healthy aging", increases the ratio of healthy to unhealthy people (Figure 4). Furthermore, the ability to work is determined by biological age. Slow aging may delay retirement until later in life (as also suggested by Vaupel [3]) and in turn may provide the means for society to support further development of increasingly powerful (and expensive) conventional medicine. Then lifespan can be extended by both anti-aging medical intervention (to delay morbidity) and specialized medical intervention (to prolong morbidity stage). Figure 4. Anti-aging drugs will delay the onset of deterioration without affecting deterioration. In conclusion, the progress of medicine 60-100 years ago (in prevention and treatment of non-age-related diseases) allowed slow-aging individuals to survive long enough to die from late onset age-related diseases (in other words to die from postponed aging). Civilization increased a proportion of slow-aging persons among the elderly, without actually slowing the aging process. Rapamycin will be used to slow down aging itself, further extending healthy lifespan. The extent of lifespan extension will depend on the future discoveries. And future discoveries are predictably unpredictable [31]. 1. Blagosklonny MV Validation of anti-aging drugs by treating age-related diseases. Aging. 2009; 1:281-288. [PubMed] 2. and Horiuchi S. Increase of maximum life-span in Sweden, 1861-1999. Science. 2000; 289:2366-2368. [PubMed] 3. Vaupel JW Biodemography of human ageing. Nature. 2010; 464:536-542. [PubMed] 4. W. Demography. Broken limits to life expectancy. Science. 2002; 296:1029-1031. [PubMed] 5. and Vaupel JW. Ageing populations: the challenges ahead. Lancet. 2009; 374:1196-1208. [PubMed] 6. Blagosklonny MV Aging and immortality: quasi-programmed senescence and its pharmacologic inhibition. Cell Cycle. 2006; 5:2087-2102. [PubMed] 7. Blagosklonny MV Aging: ROS or TOR. Cell Cycle. 2008; 7:3344-3354. [PubMed] 8. -driven aging: speeding car without brakes. Cell Cycle.

Output: contrast


Input: Claim: Urban living always leads to increased stress levels. [SEP] Text: Second, in light of earlier reports on the unique temporal features of structural plasticity elicited in the amygdala by both chronic and acute stress, we tested whether changes in BDNF levels also exhibit distinct patterns across time in the two areas. We find that not only does CIS elevate BDNF levels in the BLA, but this increase lasts for at least 21 days after the end of CIS, which is consistent with earlier findings on CIS-induced dendritic hypertrophy in the BLA persisting for the same duration after stress. In area CA3, however, CIS-induced decrease in BDNF levels reverses to normal levels within the same post-stress period of 21 days. This in turn is consistent with the previously reported reversal of CA3 dendritic atrophy over the same time frame. However, levels of corticosterone remain elevated even after 21 days of recovery from stress. Finally, even acute immobilization stress (AIS) modulates BDNF expression differentially in the two brain areas. Exposure to AIS caused a trend in lower BDNF levels in the CA3 area one day later, but neither was this decrease statistically significant nor did it last for 10 days post-stress. In contrast, the same AIS caused a more robust increase in BDNF levels in the BLA that remained significantly above control levels even 10 days after AIS. Interestingly, according to an earlier study, AIS led to a delayed increase in BLA spine-density that was manifested 10 days, but not 1 day after AIS. However, we find the highest levels of BDNF in the BLA 1 day after AIS. Ten days after AIS, the BLA continues to express significantly higher levels of BDNF, albeit at levels that are lower than the 1-day time point. Thus, AIS appears to trigger a rise in BDNF relatively soon after stress that precedes the gradual build-up in spine-density in the BLA. Future studies will be necessary to examine if this initial peak in BDNF levels serves as an early signal for plasticity mechanisms that eventually culminates in delayed BLA spinogenesis 10 days later. The contrasting effects of stress on BDNF shed new light on earlier findings on the differential patterns of cellular changes elicited by chronic and acute stress in the amygdala versus hippocampus.

Output: pass