Watrous (STOC 2006) proved that plugging classical bit commitment scheme that is secure against quantum attack into the GMW-type construction of zero-knowledge gives a classical zero-knowledge proof that is secure against quantum attack. In this paper, we showed that plugging quantum bit commitment scheme (allowing quantum computation and communication) into the GMW-type construction also gives a quantum zero-knowledge proof, as one expects. However, since the binding condition of quantum bit commitment scheme is inherently different from its classical counterpart, compared with Watrous ’ security proof, here we encounter new difficulty in soundness analysis. To overcome the difficulty, we take a geometric approach, managing to reduce quantum soundness analysis to classical soundness analysis. We also propose a formalization of non-interactive quantum bit commitment scheme, which may come in handy in other places. Moreover, inspired by our formalization, we generalize Naor’s construction of bit commitment scheme to the quantum setting, achieving non-interactive commit stage. We hope quantum bit commitment scheme can find more applications in quantum cryptog-raphy. 1
A probabilistically Checkable Proof (PCP) allows a randomized verifier, with oracle access to a purported proof, to probabilistically verify an input statement of the form “x ∈ L” by querying only few bits of the proof. A PCP of proximity (PCPP) has the additional feature of allowing the verifier to query only few bits of the input x, where if the input is accepted then the verifier is guaranteed that (with high probability) the input is close to some x′ ∈ L.
Jan 1, 2014·25th IET Irish Signals & Systems Conference 2014 and 2014 China-Ireland International Conference on Information and Communities Technologies (ISSC 2014/CIICT 2014)
The advent of the IoT with an estimated 50 billion internet enabled devices by the year 2020 raises questions about the suitability and scalability of existing mechanisms to provide privacy, data integrity and end-entity authentication between communicating peers. In this paper we present a new protocol that combines zero-knowledge proofs and key exchange mechanisms to provide secure and authenticated communication in static M2M networks, therefore addressing all the above problems. The protocol is suitable for devices with limited computational resources and can be deployed in wireless sensor networks. While the protocol requires an a-priori knowledge about the network setup and structure, it guarantees perfect forward secrecy.
Are there differences between the sale of an unopened Super Mario Bros. computer game and of the digital collage of 5,000 images? Viewed from the perspective of the doctrine of exhaustion, we can easily conclude that the two transfers have significant differences. The auction of the tangible data carrier of the Super Mario’s 1986 edition (for $660,000) 1 fits well into the doctrine. The auction of the NFT (non-fungible token) representing Beeple’s “Everdays: the First 5000 Days” (for an equivalent of an astounding $69.3 million) 2 seems to be hype with a snowball effect rather than a modern encapsulation of digital exhaustion. Some commentators, 3 including the present author in collaboration with Alexandra Giannapoulou, João Pedro Quintais, and Balázs Bodó, 4 have thoroughly introduced the incompatibility of the NFT mania with the existing copyright status quo, and so – in connection with the present book’s topic – the sale of tokenized information, which is capable of representing information related to digital artworks, is practically excluded from the scope of the exhaustion of the right of distribution. At the same time, NFTs de facto offer a “code-based digital ecosystem that has practical consequences for the copyright-relevant fields of creativeness.” 5 The sale and resale of NFTs is possible; an exchange of information and title to “own” and “trade” information related to copyrightable subject matter is technologically guaranteed. In line with that, a quasi-exhaustion regime has also emerged. As such, the NFT mania can practically evidence the need for and modern technology’s capability of offering digital marketplaces for artworks as well.
Zero knowledge proof system which has received extensive attention since it was proposed is an important branch of cryptography and computational complexity theory. Thereinto, noninteractive zero knowledge proof system contains only one message sent by the prover to the verifier. It is widely used in the construction of various types of cryptographic protocols and cryptographic algorithms because of its good privacy, authentication, and lower interactive complexity. This paper reviews and analyzes the basic principles of noninteractive zero knowledge proof system, and summarizes the research progress achieved by noninteractive zero knowledge proof system on the following aspects: the definition and related models of noninteractive zero knowledge proof system, noninteractive zero knowledge proof system of NP problems, noninteractive statistical and perfect zero knowledge, the connection between noninteractive zero knowledge proof system, interactive zero knowledge proof system, and zap, and the specific applications of noninteractive zero knowledge proof system. This paper also points out the future research directions.
Fabrice Benhamouda, Stephan Krenn, Vadim Lyubashevsky, Krzysztof Pietrzak
Abstract. We design an efficient commitment scheme, and companion zero-knowledge proofs of knowledge, based on the learning with errors over rings (RLWE) problem. In particular, for rings in which almost all elements have inverses, we construct a perfectly binding commitment scheme whose hiding property relies on the RLWE assumption. Our scheme maps elements from the ring (or equivalently, n elements from Fq) to a small constant number of ring elements. We then construct Σ-protocols for proving, in a zero-knowledge manner, knowledge of the message contained in a commitment. We are able to further extend our basic protocol to allow us to prove additive and multiplicative relations among committed values. Our protocols have a communication complexity of O(Mn log q) and achieve a negligible knowledge error in one run. Here M is the constant from a rejection sampling technique that we employ, and can be set close to 1 by adjusting other parameters. Previously known Σ-protocols for LWE-related languages either relied on “smudging ” out the error (which necessitates working over large fields, resulting in poor efficiency) or only achieved a noticeable or even constant knowledge error (thus requiring many repetitions of the protocol).
We present a construction for non-interactive zero-knowledge proofs of knowledge in the random oracle model from general sigma-protocols. Our construction is secure against quantum adversaries. Prior constructions (by Fiat-Shamir and by Fischlin) are only known to be secure against classical adversaries, and Ambainis, Rosmanis, Unruh (FOCS 2014) gave evidence that those constructions might not be secure against quantum adversaries in general. To prove security of our constructions, we additionally develop new techniques for adaptively programming the quantum random oracle.
Eli Ben‐Sasson, Alessandro Chiesa, Christina Garman, Matthew Green · 7 authors
Bit coin is the first digital currency to see widespread adoption. While payments are conducted between pseudonyms, Bit coin cannot offer strong privacy guarantees: payment transactions are recorded in a public decentralized ledger, from which much information can be deduced. Zero coin (Miers et al., IEEE S&P 2013) tackles some of these privacy issues by unlinking transactions from the payment's origin. Yet, it still reveals payments' destinations and amounts, and is limited in functionality. In this paper, we construct a full-fledged ledger-based digital currency with strong privacy guarantees. Our results leverage recent advances in zero-knowledge Succinct Non-interactive Arguments of Knowledge (zk-SNARKs). First, we formulate and construct decentralized anonymous payment schemes (DAP schemes). A DAP scheme enables users to directly pay each other privately: the corresponding transaction hides the payment's origin, destination, and transferred amount. We provide formal definitions and proofs of the construction's security. Second, we build Zero cash, a practical instantiation of our DAP scheme construction. In Zero cash, transactions are less than 1 kB and take under 6 ms to verify - orders of magnitude more efficient than the less-anonymous Zero coin and competitive with plain Bit coin.
One of important issues of information security in the interaction of users is the use of methods and tools, allowing one party to make sure of the authenticity of another party. The proof of knowledge protocols which have the additional property of zero-knowledge are applied to solve this problem. The protocols based on asymmetric encryption have received wide acceptance, such as the Fiat-Shamir, Schnorr, Okamoto, Guillou-Quisquater, Brickell-McCurley, Feige-Fiat-Shamir protocols. Cryptographic strength of these protocols is defined by discrete logarithms in a finite prime field, as well as an increase in the number of accreditation cycles. As a result of the development of methods and tools of cryptanalysis and rapid development of technologies and power of computing systems, there is a need to increase the sizes of system-wide parameters of the protocol, leading to increased resource intensity and performance complexity of basic operations in the fields.Cryptographic zero-knowledge protocols on elliptic curves are proposed in the paper. The strength of cryptosystems on elliptic curves is based on the difficulty of solving the discrete logarithm problem in the group of elliptic curve points, and is more difficult than the discrete logarithm problem in the finite field. The completeness and soundness of protocols were determined, computation examples were given. The tools of the Strength Protocol Animator package were applied to verify the protocols for resistance to enemy attacks. Consequently, the use of cryptographic protocols on elliptic curves will significantly reduce the sizes of protocol parameters and increase the cryptographic strength
Mathematics has been considered as very important subject since ancient times. We find very elaborate proof of this in Vedas, which were compiled around 6000 BC. The concept of division, addition etc. was used even that time. Concepts of zero and infinite were also there. We also find roots of Beez Ganit in Vedas. When Indian Beez Ganit reached Arab, they called it Algebra. Algebra was name of the Arabic book that described Indian concepts. This knowledge reached Europe from there. This fact was well known to intellectuals of India, which is why they gave special importance to the development of Mathematics, right from the beginning. When this knowledge was negligible in Arab and Europe, India had acquired great achievements. This paper discusses development of mathematics in India from ancient time. Key words: Mathematics, India, Mathematicians, History
Simone Fatichi, Sebastian Leuzinger, Christian Körner
Knowledge of future terrestrial carbon (C) pools and fluxes is based on simulations by Dynamic Global Vegetation Models (DGVMs; Cox et al., 2000; Sitch et al., 2008). For simplicity we used the DGVMs acronym to include all of the models able to simulate C and vegetation dynamics at large spatial scales, which are sometimes referred to as Terrestrial Biosphere Models, Terrestrial Ecosystem Models, vegetation components of Earth System Models, and Land Ecosystem Models. DGVMs are now typically coupled to climate models to account for biophysical and biogeochemical feedback caused by vegetation (Bonan, 2008; Chapin et al., 2008; Anderson et al., 2011). The ultimate aim is to simulate climate–vegetation dynamics that explicitly account for mutual interactions and thus provide us with a better spatiotemporal description of water fluxes together with the most realistic scenarios for the future climate and C cycle (Friedlingstein et al., 2006; Thornton et al., 2007; Bonan et al., 2011). Current DGVMs are simulating long-term tree and forest stand growth as a consequence of the amount of assimilated C, triggering an inevitable positive feedback between C assimilation and growth. The key factors affecting stomatal aperture and C assimilation are atmospheric CO2 concentration, water availability, light, vapor pressure deficit and temperature (Sellers et al., 1997; Lawson et al., 2011). However, direct control of C sinks (defined as growth in the sense of C investment on plant tissue expansion) via environmental factors has been shown to be more important than indirect control via photosynthesis (the C source, see Fig. 1). For example, water- or temperature-limited plants tend to reduce growth but increase C storage (Körner, 2003; Sala & Hoch, 2009; Woodruff & Meinzer, 2011; Sala et al., 2012), which suggests that environmental controls act first on sink activity rather than source activity (Körner, 2013). Nevertheless, in all existing DGVMs, plant growth is driven by photosynthesis directly without considering water and thermal limitations via metabolic, cambial and meristematic activity (blue arrows in Fig. 1; Bonan et al., 2003; Sitch et al., 2003; Krinner et al., 2005). The entire photosynthesized net C (the source) is then partitioned among different C pools, mostly based on allometric rules derived from observations (Poorter et al., 2012) or using simplified functional allocation schemes (Friedlingstein et al., 1998; Franklin et al., 2012). Allocation to carbohydrate reserves, root exudates and export to symbionts are mostly missing. This opens up a huge discrepancy between the way plant growth is modeled today (blue arrows in Fig. 1) and the way it is understood based on experimental evidence (red arrows in Fig. 1). In this article, we suggest a revised hierarchy of plant growth control by removing the causal link from C assimilation to plant growth and by providing a description of the mechanistic connections among processes. Available soil water, temperature, nutrients, light, and CO2 are indisputably the key drivers of plant growth (Boisvenue & Running, 2006; McMurtrie et al., 2008; Ågren et al., 2012; Fig. 1). The former three (water, temperature, and nutrients) are fundamentally different from the latter two (light and CO2) because they can affect both sink and source activities, while light and CO2 only affect the source activity (C assimilation, Fig. 1). In this section, we compare the hierarchy of such limitations based on experimental evidence, which will lead into the discussion of strategies for modeling plant growth. When water limitations occur, there is evidence that cambial and leaf growth are inhibited at much lower levels of water stress (higher water potentials) than photosynthesis (Fig. 2; Boyer, 1970; Hsiao, 1973; Hsiao et al., 1976; Muller et al., 2011; Tardieu et al., 2011). Because organ expansion is affected earlier and more intensively than photosynthesis, plants experiencing soil water deficit often accumulate nonstructural carbohydrates (NSC) and reduce growth (Würth et al., 2005; Woodruff & Meinzer, 2011). Drought stressed or more apical parts of trees show lower xylem- or leaf-water potential than well-watered or more basal parts. This decrease in xylem- or leaf-water potential implies a reduction in cell turgor and in the capacity to transport sugars (Woodruff et al., 2004; Sala et al., 2011; Woodruff & Meinzer, 2011). Specifically, lower cell turgor has the potential to limit cell wall expansion, cell wall synthesis and protein synthesis (Lockhart, 1965; Hsiao, 1973; Sala et al., 2011). This means that C assimilation continues while sink activity (tissue growth) is inhibited, which most likely explains the accumulation of NSC in stressed plants (Körner, 2003). For example, Sala & Hoch (2009) showed that in Pinus ponderosa, mobile C compounds increase with increasing tree height. The possibility of plants actively prioritizing storage over growth allows additional interpretations of the role of accumulating NSC, for example, to maintain the integrity of the hydraulic system (Sala et al., 2012) or for signaling purposes (Rolland et al., 2006). However, recent evidence seems to support that when hydraulic transport is not affected, NSC is significantly depleted as a consequence of C demand (Hartmann et al., 2013; Sevanto et al., 2013). Exacerbation of these mechanisms (low turgor and incapability to transport sugars) also seems to play an important role in tree mortality and therefore long-term forest dynamics (McDowell, 2011; McDowell et al., 2011). Inhibition of sink activity via low water potentials and the resulting accumulation of photo-assimilates in leaves can also lead to direct feedback, that is downregulating photosynthesis (Paul & Foyer, 2001; Nikinmaa et al., 2013), which demonstrates a direct control of photosynthesis via growth (red horizontal arrow in Fig. 1). Similarly to water stressed plants, temperature-limited plants such as trees at the treeline and winter crops are typically limited by sink activity (tissue expansion) earlier than by source activity (C assimilation; Fig. 1; Körner, 2012). Consequently, cold-limited plants show an increase rather than a decrease in NSC with colder temperatures (Körner, 2008; Fajardo et al., 2012; Hoch & Körner, 2012). Temperature influences several metabolic processes (e.g. cell doubling time), determining the potential growth rate of organs in the absence of other growth limiting factors (Pantin et al., 2012). Most temperature-controlled processes of plant growth have been summarized by Boltzmann–Arrhenius type equations, which describe a decrease in growth rates at sub-optimal and supra-optimal temperatures (Parent et al., 2010). Furthermore, a 5–6°C threshold has often been identified to limit growth in cold adapted species, irrespective of photosynthetic activity which typically ceases only at freezing point (Körner, 2008). Nutrient limitation is well known to exert a negative feedback on photosynthesis via the amount of fundamental enzymes needed for C assimilation that can be produced. The amount of synthesized Rubisco, for example, is strongly controlled by nitrogen availability (Kattge et al., 2009). However, nutrients also act as direct plant growth control due to the relatively constant stoichiometry of plant tissue composition (Sterner et al., 2002; Leuzinger & Hättenschwiler, 2013). This has emerged clearly from FACE experiments where progressive nitrogen limitation (Luo et al., 2004) has been demonstrated to limit plant growth (Norby et al., 2010). While plants have the capacity to recruit additional nutrients by expanding their root system and via mycorrhizal symbioses, nutrient limitations are likely to progressively emerge at the landscape scale. Importantly, no study has been able to clearly quantify nutrient limitation acting on sink (tissue growth) vs source activity (C assimilation). Light as well as atmospheric CO2 clearly limit photosynthesis (the source), and unlike the previous factors discussed, they do not affect the C sinks directly. Therefore, the question here is whether (and if yes, when) the effect of CO2 and light is limiting sink activity (growth) via source activity (blue arrows from source to sink activity via the tree in Fig. 1). In other words, is plant growth C limited and under what conditions? Arguments in favor of C limitation of plant growth are either based on young seedlings and saplings in the forest understory or on individual leaves in dense canopies that are almost always operating below light saturation (Turner, 2001; Lloyd & Farquhar, 2008). Accordingly, CO2 was found to have a stimulatory effect on growth of plants in the understory (Würth et al., 1998; Hättenschwiler & Körner, 2000). Lloyd & Farquhar (2008) inferred that growth of tropical forests is C limited using the relationship between growth and photosynthesis: Np = Gp[1 − φ] where Np is net primary production (new growth), Gp is the average rate of photosynthesis, and φ is the proportion of assimilated C lost via total respiration plus volatile organic C emissions and root C exudation. They argue that higher Gp as a consequence of increasing CO2 concentration or incoming light necessarily leads to enhanced growth. However, we propose that this equation should generally read Np = Gp(Np)[1 − φ(Gp(Np))], thus not be interpreted as a direct causal link between photosynthesis and growth, because φ is a function of Gp, and Np can feedback on photosynthesis, that is, Gp = f(Np). Rewritten in these terms the equation is highly nonlinear and an increase in Gp does not imply a proportional increase in growth. Leaf level light responses of seedling and single leaves are difficult to extrapolate to the forest level, because this would imply that a forest stand behaves like a single leaf or shadowed tree. Light and consequently CO2 limitations of individual leaves, saplings or trees are not a demonstration that the entire forest community operates below its CO2 uptake capacity and even less that C acquisition is limiting forest growth (Körner, 2009; Clark et al., 2013). The Leaf Area Index (LAI) in several ecosystems (e.g. tropical forest, alpine grassland) may be higher than needed to sustain maximal productivity (Amiro et al., 2010; Gough et al., 2013; S. Fatichi, M. J. Zeeman, J. Fuhrer & P. Burlando, unpublished). Many studies suggest that partial (moderate) defoliation hardly affects tree growth or forest productivity (Ericsson et al., 1985; Hoogesteger & Karlsson, 1992; Reich et al., 1993; Kaitaniemi et al., 1999; Volin et al., 2002). A larger than necessary LAI typically has evolutionary rather than physiological reasons: to shade competing neighbors and thus limit their performance; as insurance against herbivory and storm damage; and as an additional option to store nutrients (especially in evergreen trees). Therefore, while light and CO2 may limit growth at the leaf or plant level, they unlikely do so at the landscape (whole forest) level and in the longer term (Leuzinger & Hättenschwiler, 2013). Short-term benefits of extra light (Graham et al., 2003) or elevated CO2 (Norby & Zak, 2011) can only be sustained to the extent a higher growth rate is supported by higher nutrient availability. Current atmospheric CO2 concentration (close to 400 ppm) additionally represents a rather exceptional forcing in the evolutionary context, with the current species having evolved in CO2 concentrations between 180 and 290 ppm (Siegenthaler et al., 2005; Lüthi et al., 2008). This suggests that C availability is at least less limiting nowadays (Körner, 2006). Accordingly, CO2 enrichment experiments with closed forest canopies did not show a sustained stimulation of growth by elevated CO2, except under high nutrient availability (Finzi et al., 2007; Norby et al., 2010; Bader et al., 2013; Sigurdsson et al., 2013). The differential sensitivity of C source and sink activities to water, temperature, and nutrient controls could lead to an imbalance between C supplied by photosynthesis and C used for tissue growth and respiratory costs. A mismatch between these two quantities would be sub-optimal and create a long-term surplus of assimilated C. In normal conditions, this situation is avoided through at least three mechanisms. First, in the short term, acclimation of photosynthesis occurs through negative feedback given by accumulation of starch or higher concentration of sucrose at the leaf level (Paul & Foyer, 2001). However, such a strategy would not be very effective to counteract mid/long-term source–sink imbalance. Second, therefore, in the mid-term, plants use sophisticated mechanisms of C storage at the leaf and whole plant level through accumulation and depletion of NSC (Kozlowski, 1992; Hoch et al., 2003; Gough et al., 2009; Richardson et al., 2013). Fluctuations of NSC are expected to buffer the difference between C supply and demand for timescales from hours to a few years. NSC dynamics are likely to be actively controlled by plants rather than a pure passive deposit of C (Sala et al., 2012). Third, in the long-term, evolutionary processes likely fine-tuned the photosynthesis apparatus (C source) to match long-term investment capacity (C sinks), which is the first to be controlled by environmental limitations. This of source–sink can be summarized as controls (Körner, and the between sinks and which is likely for the hierarchy of controls in the enrichment experiments as well as of water or temperature limitations have the possibility to the between C and For an increase of NSC is typically found in CO2 enrichment Furthermore, atmospheric CO2 almost always enhanced photosynthesis with or no et al., 2005; Bader et al., 2010). However, this typically does not into enhanced growth, in the term and for forests (Leuzinger et al., 2011; Norby & Zak, 2011; Bader et al., 2013). Because the C has to be this imbalance has several the of the & 2013). the extra C is and et al., 2006). Therefore, the of the extra C in CO2 experiments is to root exudates and export to et al., 2012). C assimilation respiration because of the larger and and thus transport respiration & 2000). if root is as a et al., a larger concentration in would more exudates due to the concentration the nutrient limitation through under elevated CO2 et al., 1993; Hättenschwiler & Körner, The use of experiments (e.g. with elevated CO2) is to the C source–sink and therefore the drivers of plant growth, under different environmental there is evidence that tissue growth is mostly under direct control of environmental rather than via the of assimilated C (Fig. and arrows in Fig. which for a of the hierarchy of plant growth control in This implies a from the current C source driven to where C sinks are the Because processes shown in Fig. are strongly and by it is to with either in the short For example, production will decrease with whether the is on growth or whether temperature assimilation and thus growth. However, the processes are fundamentally argue that if these processes and the are not it is unlikely DGVMs will simulate future C storage except under when photosynthesis may as shown in a in Fig. Furthermore, forest and composition are likely to feedback on C assimilation, they will also in long-term C the role of temperature and plant water in growth, of the existing DGVMs we are of include such a even in a simplified or et al., et al., 1997; et al., 2001; Bonan et al., 2003; Sitch et al., 2003; Krinner et al., 2005; et al., 2007; et al., 2009; Clark et al., 2011; et al., 2013; et al., 2013). the of the potential role of nutrients in limiting C from ecosystems et al., nitrogen and more have been in DGVMs et al., 2006; & 2008; & 2010; et al., 2012). However, all these models thermal and water limitations only in to C assimilation but not in to cambial or meristematic The of DGVMs also the that C processes such as photosynthesis (e.g. leaf are while processes of plant growth such as the rate of cell cell expansion, transport or cambial growth (C sink are much to quantify at high (Körner, 2013), even and to a source of et al., 2006; et al., 2013; & 2013). The of C fluxes and the between C and water through stomatal mostly to the of models and of and photosynthesis fluxes (Sellers et al., rather than plant growth. models that et al., to up the of DGVMs, and while they C assimilation, they in plant growth control that is based on observations in controlled but supported by observations in a the key of DGVMs and are almost to of the photosynthesis as for by et Fig. see also Bonan et al., 2012). short few from such DGVMs are typically by C fluxes derived from et al., 2006; et al., However, such only C and not plant growth that is they at show a over a given DGVMs are used to future from C pools and in models may lead us to a because of the Fig. that in models allocation can be controlled to extent by nutrients and environmental For water and light availability can control the differential C allocation to and (Friedlingstein et al., 1998; Krinner et al., 2005). However, this is rather different from having environmental directly control growth because the assimilated C is necessarily to C export to symbionts are mostly and mobile C are only in a of models in a simplified et al., 2005; et al., 2008; & 2010; et al., 2012; et al., 2012; et al., 2013). Therefore, C assimilation is typically to growth, which evidence that between assimilation and growth et al., 2006; Gough et al., 2009; Richardson et al., 2013). This also implies that if more C is assimilated in a under of elevated atmospheric CO2) the vegetation will more with positive feedback to C assimilation through which us with the for the way is to to the existing of DGVMs by direct growth control based on environmental drivers (Leuzinger et al., 2013; see also Fig. we tissue is controlled by environmental the amount of C to be to growth at a given should be of the amount of assimilated C. growth is by the limiting the of all other factors water, and nutrient are this with the that is the C source However, we argue that this is and only under such as in a a modeling the of or of species or plant functional type growth responses to environmental controls (water, temperature, This does not to the current of the could be but no longer the amount of C used for growth. The needed for such will a large of experimental A more to DGVMs on a more realistic of C models that simulate C and water fluxes the nutrient allocation to and from nonstructural C storage and to and root (Fig. This in its was in studies and more have been in models that et al., 2005; et al., 2010; et al., 2012) simulate transport et al., 2002; et al., as well as fluxes and cell growth activities & 2010; et al., 2010). This in the most components where C and water fluxes and are the plant between and in the (Fig. modeling of C assimilation and 1) is in most DGVMs et al., 2011). However, in the water and assimilated C are by leaf water and C and are to buffer the of C assimilation, an almost constant of sucrose to the at the & growth and can be explicitly modeled as a function of cell wall and protein and cell the that nutrients and C are is driven by cell turgor a threshold (Lockhart, which for water limitation to growth. cell typically a Boltzmann–Arrhenius function of temperature (Parent et al., with a temperature most for growth, which represents the thermal limitation to growth. When these two controls are plant growth can be A given by the of water potential and pressure that in also on sucrose concentration, is turgor In to for and et al., can be used for and transport and This will create a coupled system where and in and in and tissue (e.g. are The C is modeled as the of carbohydrates in the and by the of storage This C is then for growth, and for root and export to growth control by nutrients can also be in such a because nutrient through root uptake or can be explicitly and are up both via and actively through the of concentration et al., 2003; & 2012). C can be modeled as a et al., while modeling with is more and from understood which a in providing see While the mechanistic of for example, the leaf water and C or transport is relatively and can be into a of for the of C storage and sink as well as with to storage is a function of plant environmental and For at and C is from storage at the of the to support cambial activity and growth. also C their for example, leaves storage the is not and likely to with plant and plant stress (e.g. such of C allocation are not understood and the of Fig. will a spatial of C allocation with the more parts less C. a of the C sink is and the key for such a that a of the in Fig. is not given the limited we argue that current is for modeling most of the also that such components may to be in DGVMs and would a large of However, its can the for of environmental control of growth and of mechanistic C allocation schemes that could be into A where plant transport and tissue expansion are using well and among as was for photosynthesis is likely to way of modeling plant growth. a can also the of on plant C storage and sink which is fundamental for increasing and long-term scenarios for the C The of photosynthetic and the of mechanistic models of C assimilation that simulate observations have the of DGVMs, which have few over the identified 2006; et al., the of models mostly However, current physiological of tissue growth and expansion is in to it is in Current scenarios the between climate and vegetation are likely affected by a of plant growth and are therefore argue that direct environmental controls water and nutrient on tissue expansion and meristematic activity are fundamental than on the of C because they mostly limiting to plant growth photosynthesis Because C can only be to the extent other nutrients as well as water availability and temperature these drivers of growth will be over C assimilation This in of plant growth drivers has for the of terrestrial C fluxes and storage in the The of the in DGVMs will be but fundamental for future of the C In to this we two of different to growth in current DGVMs to growth limiting to mechanistic of plant transport and tissue expansion as was for photosynthesis While additional may be to of the we argue that there is evidence to the of the of current DGVMs, from to a plant growth. The three and the for on an earlier of this with are also
Masayuki Abe, Jan Camenisch, Maria Dubovitskaya, Ryo Nishimaki
In this paper, we provide the first scheme that realises an attribute-based access control system for static resources that offers maximal privacy and is secure in the universal composability framework (UC). More precisely, we offer a protocol for adaptive oblivious transfer, where the sender can enforce an attribute-based access control policy for each record and nevertheless learns neither which record a user retrieves nor which attributes a user has. As additional results we provide a new structure-preserving signature scheme from the SXDH assumption and a new universally composable adaptive oblivious transfer protocol that is secure under two DDH-like assumptions and is the most efficient one secure under ``non $q$-type'' assumptions. We believe the new signature scheme to be of independent interest as a building block that is compatible with Groth-Sahai non-interactive zero-knowledge proofs.
We present BLACRONYM, a suite of new communication- and computation-efficient protocols for anonymous blacklisting without trusted third parties. Our protocols improve on Tsang et al.'s Blacklistable Anonymous Credentials (BLAC) system and its variants by incorporating novel batch zero-knowledge proof and verification techniques. BLACRONYM provides comparable functionality and security guarantees to those of BLAC and its derivatives, but it is substantially faster and consumes much less bandwidth. At the heart of BLACRONYM is the first batch zero-knowledge protocol in the literature for proofs of partial knowledge over non-monotone access structures; we suspect that our new techniques will find applications in speeding up other cryptographic constructions that require proofs of similar statements.
Antonis Papadimitriou, Mingchen Zhao, Andreas Haeberlen
In this paper, we discuss the problem of detecting general faults in distributed systems that handle confidential information. Detecting non-crash faults is difficult in this setting because, to check the behavior of a given node, we need to know its expected behavior -- but that can depend on the confidential information. Classical zero-knowledge proofs are difficult to apply because they are designed to verify functions with a fixed number of inputs, but in many distributed systems, both the size and the number of a node's "inputs" (the messages it has received from other nodes) are not known.
Hormones, growth factors, and cytokines coordinate metabolism between tissues and within tissues. The transforming growth factor superfamily signaling pathway encompasses members of the TGFβ, activin, bone morphogenetic protein, Nodal, and growth and differentiation factor subfamilies, in addition to numerous other ligands, receptors, coreceptors, downstream signaling effectors, and regulating molecules. The elaborate multifunctional effects of this superfamily are highly cell-type and context-dependent (1, 2). Many of these ligands are involved in organ specification, patterning, proliferation, and differentiation, including important roles in the pancreas (3, 4). Studies of transgenic and knockout mice highlight the importance of this signaling pathway in islet development (5), and more recent work has also implicated the TGFβ superfamily in adult β-cell function and maturity (6, 7). In this issue of Endocrinology, Boerner and colleagues (8) report a novel role for Nodal, a secreted TGFβ superfamily member known for its roles in early embryogenesis and its mitogenic signaling through Smad2/3 and Smad4. Detailed studies on the role of Nodal in adult β-cells had not been reported. Boerner et al (8) identified Nodel in adult islets and used complementary techniques, including flow cytometry, to demonstrate that Nodal stimulates human pancreatic β-cell proliferation. This contrasts with studies employing pancreatic cell lines wherein Nodal was reported to induce apoptosis and inhibit proliferation (9, 10) and highlights the need to perform proliferation studies in nontransformed cells. This novel role of Nodal adds to the numerous roles that this family appears to have on adult pancreatic cells. Here, we will review developments in the field of TGFβ signaling in islets and emphasize that delineating clear roles of this signaling pathway has been quite challenging. Genetically engineered mouse models have provided insight, as well as confusion, on the roles of TGFβ family members (Table 1). Life-long global knockouts can provide information on gene function in the whole organism over its entire lifetime. Distinguishing effects of TGFβ family members on adult β-cell physiology from effects on development is not possible without conditional loss-of-function or gain-of-function models, but these are relatively few in number (11–13). Despite these caveats, a picture of multiple effects of TGFβ signaling on adult β-cell homeostasis has begun to emerge. A recurring phenotype manifested in adult mice carrying mutations in various TGFβ superfamily genes includes decreased β-cell mass, impaired glucose tolerance, and in some cases diabetes. Table 1 provides a glimpse of the plethora of effects of this superfamily, and its downstream signaling molecules, on pancreatic islets. Deletion of the negative downstream effector of TGFβ signaling Smad7 (14) in Pdx1-expressing cells decreased hormone-positive cells in late development (5). On the other hand, conditional overexpression of Smad7 in adult Pdx1-expressing cells altered the β-cell gene signature and reduced pancreatic insulin production and release, leading to diabetes (11). Furthermore, Smad7 appears to be crucial for beta-cell proliferation after partial pancreatectomy (50). Thus, the same TGFβ effector can have opposing roles depending on the temporal context. Moreover, the TGFβ signaling effectors can have opposing roles, given that Smad3 appears to be a negative regulator of insulin secretion and glucose tolerance (13). Taken together, many lines of evidence clearly suggest a role of this signaling pathway in regulating β-cell mass and function. More inducible knockout mouse studies are needed to clarify the specific cell targets and mechanisms of actions of this family on pancreatic cells. Pancreatic Actions of the TGFβ Superfamily Abbreviations: ALK, activin receptor-like kinase, ActR, activin receptor; BMP, bone morphogenetic protein; GDF, growth and differentiation factor. Pancreatic Actions of the TGFβ Superfamily Abbreviations: ALK, activin receptor-like kinase, ActR, activin receptor; BMP, bone morphogenetic protein; GDF, growth and differentiation factor. The effects of the TGFβ superfamily ligands on adult pancreatic β-cells can be directly tested in vitro, bypassing the complexities of the in vivo environment. For example, acute activin A treatment increased glucose-stimulated insulin secretion from human (15) and rat (16) islets, whereas prolonged treatment decreased glucose-stimulated insulin secretion from mouse islets, an effect reversed by the endogenous antagonist follistatin (17). β-Cell proliferation was increased by activin A treatment in adult rat islets (18) and a mouse β-cell line (17). Interestingly, there appears to be a species difference in the islet expression and action of activin A, follistatin, and TGFβ1 (19). Although TGFβ1 acutely stimulates glucose-stimulated insulin release from rat islets (19), prolonged treatment of human islet cells with TGFβ1 had a negative impact on the expression of genes important for β-cell function, likely via the Smad3 pathway (13). Interestingly, Boerner et al (8) did not report evidence of β-cell dedifferentiation, although β-cell function remains to be rigorously investigated in this model. The range of (and sometimes opposing) effects of the same factors observed on pancreatic cells illustrates the complexity and context-dependence of this signaling pathway. Although studies using animals with genetic manipulations are crucial, results from human islets are vital to uncover any species differences and for future clinical translation. One of the most important contributions of the Boerner study was the use of islets from human donors (8). Studies with human islets, or at least >1-year-old mice (which are equally refractory to β-cell proliferation), are crucial for clinical translation of the limited basic knowledge around primary β-cell proliferation mechanisms (20). The ultimate goal of this research is to provide the basis for a diabetes cure. Diabetes results from the immune-mediated destruction (type 1 diabetes) or functional failure (type 2 diabetes) of pancreatic insulin-producing β-cells (21). There are theoretically numerous approaches to treating or reversing diabetes using cell-based therapy, including in vivo regeneration via induction of replication of remaining β-cells, transdifferentiation of other adult cell types (in vivo and in vitro) and differentiation of embryonic (or induced) pluripotent stem cells into functional β-cells (22). Significant preclinical obstacles remain for each of these approaches. At this point, islet transplantation from cadaveric donors remains the only viable alternative to insulin therapy for treating type 1 diabetes (23). Nevertheless, the lack of islet donor tissue prevents widespread patient access to this therapy. Hence, the expansion of primary human islets is of great interest to the diabetes research community. Various studies have shown efficient induction of young rodent β-cell proliferation, yet the same approaches have either not been tested or failed to produce significant results on adult human β-cells (20, 24). Failure to induce proliferation in human islets could be in part a species difference and the fact that the human islet donor age is generally much higher in relative comparison with the young adolescent mice being used for studies (25). As has been elegantly shown, β-cell proliferation in mice and humans ceases to nearly zero after 1 and 30 years of age, respectively (26, 27). Hence, any study showing that a ligand can overcome this resistance of adult human β-cells to reenter the cell cycle, and stimulate proliferation even modestly, is an important contribution to the field. Boerner et al (8) found an ∼1.5-fold increase in human β-cell proliferation with Nodal treatment without affecting viability. Because it is estimated that only 1% of type 1 diabetes patients can be treated with the current scarce availability of donor islets (28) and the fact that a single patient requires at least 103 islet equivalents (from ∼2 pancreas donors) per kilogram of body weight (29), the expansion of islets from a single human donor pancreas would require at least an ∼200-fold increase for a widespread application of human islet transplantation. Therefore, more extensive research in human β-cell expansion is needed. Boerner et al (8) echoed statements by many in the field when they proposed in their paper that the ultimate therapeutic approach may require simultaneously harnessing multiple local signaling pathways. Indeed, genomic advances have revealed that islets produce hundreds of soluble ligands and express hundreds of receptors for ligands produced locally and in other tissues (30). It is clear that using high-throughput approaches will be required to make breakthroughs in this area. Pancreatic β-cell proliferation is exceedingly hard to measure in samples from humans and older adult rodents, given the rarity of events and the potential for false-positives with semiautomated counting. This means that there must be exceptional rigor. Bulk measurements of DNA synthesis are clearly unacceptable in heterogeneous human islet cell cultures where β-cells usually make up a minority of endocrine cells, to mention nothing of the fibroblast-like cells that dominate these cultures after a few days. Imaging must be of sufficient X, Y, and Z resolution such that highly proliferative fibroblasts, which overlay virtually all human islet cultures, are not mistaken for proliferating β-cells. In this regard, the use of flow cytometry by Boerner et al (8) to detect human β-cell proliferation is an important technical proof-of-concept. Clearly, the bar for measuring β-cell proliferation needs to continue to get higher to prevent costly false-positives in the field. Even considering the technical limitations, only a handful of studies have shown significant in vitro stimulation of human β-cell proliferation. These include cocktails of 1) hepatocyte growth factor, fibroblast growth factor 4, nicotinamide and fibrin gel (∼2-fold) (31), the L-type calcium channel agonist Bay K8644 (∼1.5-fold) (32), a diarylamide compound WS6 (∼5-fold) (33), and glycogen synthase kinase-3 inhibitors (∼2-fold) (34). It remains unclear whether any ligand alone will be able to safely increase human β-cell proliferation to therapeutic levels in vivo. It is not clear at this point whether TGFβ superfamily ligands are useful therapeutic targets for manipulating β-cell mass or function in vivo, because they may have off-target systemic effects. Most of the TGFβ family ligands share the same receptors, downstream effectors and antagonists (1) and are expressed ubiquitously in various tissues, including pancreatic islets (8, 12, 17, 19, 30, 35). Thus, the local concentration and length of exposure of the ligands as well as the combination of receptors, effectors and antagonists locally expressed will ultimately provide the final concerted effect on the β-cell, both in vivo and in vitro. Nodal and other TGFβ family members may be more promising factors for in vitro differentiation, expansion, and maturation of pancreatic β-cells. However, for human in vitro β-cell expansion to become clinically relevant, much more potent mitogens and/or combinations of factors working synergistically to retain β-cell maturity, viability, and function need to be evaluated. It will take the collaborative efforts between disciplines from basic β-cell biologists to physicians and engineers (36) to accomplish such an endeavor. Disclosure Summary: The authors have nothing to disclose.