Activation Methods of Carbonaceous Materials Obtained from Agricultural Waste

Activated carbons belong to the most widely used adsorbent materials. The utility of these materials mainly depends on their chemical surface and porous structure. The method of activation and the nature of the used precursor greatly influence the pore structure and surface functional groups of the activated carbon. Therefore, the main objective of current investigations is to develop or modify the activation method in an optimal manner using appropriate precursors. This review compiles the results of various studies on the synthesis of activated carbons from agricultural waste. Various activation methods, such as physical, chemical, physicochemical, and microwave activation, are discussed. The effects of carbonization and activation parameters, such as temperature, activating agent, and residence time, toward the properties of the activated carbon are reviewed.     

Computational modeling of chemical reactions and interstitial growth and remodeling involving charged solutes and solid-bound molecules

Mechanobiological processes are rooted in mechanics and chemistry, and such processes may be modeled in a framework that couples their governing equations starting from fundamental principles. In many biological applications, the reactants and products of chemical reactions may be electrically charged, and these charge effects may produce driving forces and constraints that significantly influence outcomes. In this study, a novel formulation and computational implementation are presented for modeling chemical reactions in biological tissues that involve charged solutes and solid-bound molecules within a deformable porous hydrated solid matrix, coupling mechanics with chemistry while accounting for electric charges. The deposition or removal of solid-bound molecules contributes to the growth and remodeling of the solid matrix; in particular, volumetric growth may be driven by Donnan osmotic swelling, resulting from charged molecular species fixed to the solid matrix. This formulation incorporates the state of strain as a state variable in the production rate of chemical reactions, explicitly tying chemistry with mechanics for the purpose of modeling mechanobiology. To achieve these objectives, this treatment identifies the specific theoretical and computational challenges faced in modeling complex systems of interacting neutral and charged constituents while accommodating any number of simultaneous reactions where reactants and products may be modeled explicitly or implicitly. Several finite element verification problems are shown to agree with closed-form analytical solutions. An illustrative tissue engineering analysis demonstrates tissue growth and swelling resulting from the deposition of chondroitin sulfate, a charged solid-bound molecular species. This implementation is released in the open-source program FEBio (www.febio.org). The availability of this framework may be particularly beneficial to optimizing tissue engineering culture systems by examining the influence of nutrient availability on the evolution of inhomogeneous tissue composition and mechanical properties, the evolution of construct dimensions with growth, the influence of solute and solid matrix electric charge on the transport of cytokines, the influence of binding kinetics on transport, the influence of loading on binding kinetics, and the differential growth response to dynamically loaded versus free-swelling culture conditions.     

Modeling of DNAPL-Dissolution,Rate-Limited Sorption and Biodegradation Reactions in Groundwater Systems

This article presents an approach for modeling the dissolution process of single component dense non-aqueous phase liquids (DNAPL), such as tetrachloroethene and trichloroethene, in a biologically reactive porous medium. In the proposed approach, the overall transport processes are conceptualized as three distinct reactions. Firstly, the dissolution (or dissolving) process of a residual DNAPL source zone is conceptualized as a mass-transfer limited reaction. Secondly, the contaminants dissolved from the DNAPL source are allowed to partition between sediment and water phases through a rate-limited sorption reaction. Finally, the contaminants in the solid and liquid phases are allowed to degrade by a set of kinetic-limited biological reactions. Although all of these three reaction processes have been researched in the past, little progress has been made towards understanding the combined effects of these processes. This work provides a rigorous mathematical model for describing the coupled effects of these three fundamental reactive transport mechanisms. The model equations are then solved using the general-purpose reactive transport code RT3D (Clement, 1997).     

Modeling of DNAPL-Dissolution, Rate-Limited Sorption and Biodegradation Reactions in Groundwater Systems

This article presents an approach for modeling the dissolution process of single component dense non-aqueous phase liquids (DNAPL), such as tetrachloroethene and trichloroethene, in a biologically reactive porous medium. In the proposed approach, the overall transport processes are conceptualized as three distinct reactions. Firstly, the dissolution (or dissolving) process of a residual DNAPL source zone is conceptualized as a mass-transfer limited reaction. Secondly, the contaminants dissolved from the DNAPL source are allowed to partition between sediment and water phases through a rate-limited sorption reaction. Finally, the contaminants in the solid and liquid phases are allowed to degrade by a set of kinetic-limited biological reactions. Although all of these three reaction processes have been researched in the past, little progress has been made towards understanding the combined effects of these processes. This work provides a rigorous mathematical model for describing the coupled effects of these three fundamental reactive transport mechanisms. The model equations are then solved using the general-purpose reactive transport code RT3D (Clement, 1997).     

High local protein concentrations at promoters: strategies in prokaryotic and eukaryotic cells

The speed of chemical reactions is proportional to the concentration of molecules involved. Since proteins catalyze most of the essential reactions inside a living cell, their concentration should be as high as possible. An economical way to achieve this is through the establishment of small cell compartments. We propose that within these compartments, two types of local concentration effects are at work. (1) With local concentration type I reactions, multimeric proteins bound to a specific DNA sequence have an increased local concentration for a second DNA site sufficiently close-by, or for proteins bound to such a site. (2) For type II effects, DNA can be used as a scaffold to build unique nucleoprotein complexes that would otherwise not exist free in solution. These complexes are proficient in establishing longer-range interactions with similarly unique complexes located far away on the genome. We discuss the consequences of these local concentration effects in the light of the markedly different sizes of prokaryotic and eukaryotic cells and of their genomes.     

A unified model for signal transduction reactions in cellular membranes.

An analytical solution is obtained for the steady-state reaction rate of an intracellular enzyme, recruited to the plasma membrane by active receptors, acting upon a membrane-associated substrate. Influenced by physical and chemical effects, such interactions are encountered in numerous signal-transduction pathways. The generalized modeling framework is the first to combine reaction and diffusion limitations in enzyme action, the finite mean lifetime of receptor-enzyme complexes, reactions in the bulk membrane, and constitutive and receptor-mediated substrate insertion. The theory is compared with other analytical and numerical approaches, and it is used to model two different signaling pathway types. For two-state mechanisms, such as activation of the Ras GTPase, the diffusion-limited activation rate constant increases with enhanced substrate inactivation, dissociation of receptor-enzyme complexes, or crowding of neighboring complexes. The latter effect is only significant when nearly all of the substrate is in the activated state. For regulated supply and turnover pathways, such as phospholipase C-mediated lipid hydrolysis, an additional influence is receptor-mediated substrate delivery. When substrate consumption is rapid, this process significantly enhances the effective enzymatic rate constant, regardless of whether enzyme action is diffusion limited. Under these conditions, however, enhanced substrate delivery can result in a decrease in the average substrate concentration.     

Building the cellular puzzle: control in multi-level reaction networks

Quantitative conceptual tools dealing with control and regulation of cellular processes have been mostly developed for and applied to the pathways of intermediary metabolism. Yet, cellular processes are organized in different levels, metabolism forming the lowest level in a cascade of processes. Well-known examples are the DNA-mRNA-enzyme-metabolism cascade and the signal transduction cascades consisting of covalent modification cycles. The reaction network that constitutes each level can be viewed as a "module" in which reactions are linked by mass transfer. Although in principle all of these cellular modules are ultimately linked by mass transfer, in practice they can often be regarded as "isolated" from each other in terms of mass transfer. Here modules can interact with each other only by means of regulatory or catalytic effects-a chemical species in one module may affect the rate of a reaction in another module by binding to an enzyme or transport system or by acting as a catalyst. This paper seeks to answer two questions about the control and regulation of such multi-level reaction networks: (i) How can the control properties of the system as a whole be expressed in terms of the control properties of individual modules and the effects between modules? (ii) How do the control properties of a module in its isolated state change when it is embedded in the whole system through its connections with the other modules? In order to answer these questions a quantitative theoretical framework is developed and applied to systems containing two, three or four fully interacting modules; it is shown how it can be extended in principle to n modules. This newly developed theory therefore makes it possible to quantitatively dissect intermodular, internal and external regulation in multi-level systems.     

The chemical and biological versatility of riboflavin

Since their discovery and chemical characterization in the 1930s, flavins have been recognized as being capable of both one- and two-electron transfer processes, and as playing a pivotal role in coupling the two-electron oxidation of most organic substrates to the one-electron transfers of the respiratory chain. In addition, they are now known as versatile compounds that can function as electrophiles and nucleophiles, with covalent intermediates of flavin and substrate frequently being involved in catalysis. Flavins are thought to contribute to oxidative stress through their ability to produce superoxide, but at the same time flavins are frequently involved in the reduction of hydroperoxides, products of oxygen-derived radical reactions. Flavoproteins play an important role in soil detoxification processes via the hydroxylation of many aromatic compounds, and a simple flavoprotein in liver microsomes catalyses many reactions similar to those carried out by cytochrome P450 enzymes. Flavins are involved in the production of light in bioluminescent bacteria, and are intimately connected with light-initiated reactions such as plant phototropism and nucleic acid repair processes. Recent reports also link them to programmed cell death. The chemical versatility of flavoproteins is clearly controlled by specific interactions with the proteins with which they are bound. One of the main thrusts of current research is to try to define the nature of these interactions, and to understand in chemical terms the various steps involved in catalysis by flavoprotein enzymes.     

Insect predators affect plant resistance via density- and trait-mediated indirect interactions

Predators can affect herbivores both through direct consumption (density-mediated interactions) and by changing behavioural, physiological or morphological attributes of the prey (trait-mediated interactions). These effects on the herbivore can in turn affect the plant through density- and trait-mediated indirect interactions (DMIIs and TMIIs). While the effects of DMIIs and TMIIs imposed by predators has been shown to influence plant density and plant communities, we know little about the effects on plant quality. In addition, the DMII and TMII components of the predator may influence each other so that the total effect of the predator on the plant is not simply the sum of the DMII and TMII. We examined DMIIs and TMIIs between a stinkbug predator and a caterpillar, and show how these interactions affect plant quality, as measured by damage, resistance to herbivores, and a defence chemical, peroxidase. We used novel methods to estimate the independent and non-additive contribution of DMIIs and TMIIs to the plant phenotype. Both predator-induced DMIIs and TMIIs caused decreases in the amount of caterpillar herbivory on plants; a strong non-additive effect between the two resulted from redundancy in their effects. TMIIs initiated by the predator were primarily responsible for a decrease in induced plant resistance. However, DMIIs predominated for reducing the production of peroxidase. These data demonstrate how DMIIs and TMIIs initiated by predators cascade through tri-trophic interactions to affect plant damage and induced resistance.     

Modifications of nucleosides by endogenous mutagens-DNA adducts arising from cellular processes

DNA damage plays a significant role in mutagenesis, carcinogenesis and ageing. Chemical transformations leading to DNA damage include reactions of the base units with agents of endogenous and exogenous origin. The vast majority of damage arising from cellular processes such as metabolism and lipid peroxidation are identical or very similar to those induced by exposure to environmental agents. A detailed knowledge of the types and prevalence of endogenous DNA damage provides insight into the chemical nature of species involved in these modifications and may be of help in understanding their influence on the induction of cancer or other diseases. This knowledge may also be essential to the development of rational chemopreventive strategies directed against the initiation of oxidative stress- and lipid peroxidation-associated pathology.The present work reviews findings regarding the interaction between DNA bases and various reactive species arising from lipid peroxidation and other cellular processes, drawing attention to the mechanism responsible for the formation of the resulted modifications. The biological consequences of these interactions are also briefly discussed.     

Chemical properties of catechols and their molecular modes of toxic action in cells, from microorganisms to mammals

Catechols can undergo a variety of chemical reactions. In this review, we particularly focus on complex formations and the redox chemistry of catechols, which play an inportant role in the toxicity of catechols. In the presence of heavy metals, such as iron or copper, stable complexes can be formed. In the presence of oxidizing agents, catechols can be oxidized to semiquinone radicals and in a next step to o‐benzoquinones. Heavy metals may catalyse redox reactions in which catechols are involved. Further chemical properties like the acidity constant and the lipophilicity of different catechols are shortly described as well. As a consequence of the chemical properties and the chemical reactions of catechols, many different reactions can occur with biomolecules such as DNA, proteins and membranes, ultimately leading to non‐repairable damage. Reactions with nucleic acids such as adduct formation and strand breaks are discussed among others. Interactions with proteins causing protein and enzyme inactivation are described. The membrane–catechol interactions discussed here are lipid peroxidation and uncoupling. The deleterious effect of the interactions between catechols and the different biomolecules is discussed in the context of the observed toxicities, caused by catechols.     

The chemical defense ecology of marine unicellular plankton: constraints, mechanisms, and impacts

The activities of unicellular microbes dominate the ecology of the marine environment, but the chemical signals that determine behavioral interactions are poorly known. In particular, chemical signals between microbial predators and prey contribute to food selection or avoidance and to defense, factors that probably affect trophic structure and such large-scale features as algal blooms. Using defense as an example, I consider physical constraints on the transmission of chemical information, and strategies and mechanisms that microbes might use to send chemical signals. Chemical signals in a low Re, viscosity-dominated physical environment are transferred by molecular diffusion and laminar advection, and may be perceived at nanomolar levels or lower. Events that occur on small temporal and physical scales in the "near-field" of prey are likely to play a role in cell-cell interactions. On the basis of cost-benefit optimization and the need for rapid activation, I suggest that microbial defense system strategies might be highly dynamic. These strategies include compartmented and activated reactions, utilizing both pulsed release of dissolved signals and contact-activated signals at the cell surface. Bioluminescence and extrusome discharge are two visible manifestations of rapidly activated microbial defenses that may serve as models for other chemical reactions as yet undetected due to the technical problems of measuring transient chemical gradients around single cells. As an example, I detail an algal dimethylsulfoniopropionate (DMSP) cleavage reaction that appears to deter protozoan feeding and explore it as a possible model for a rapidly activated, short-range chemical defense system. Although the exploration of chemical interactions among planktonic microbes is in its infancy, ecological models from macroorganisms provide useful hints of the complexity likely to be found.     

Solvent structure and enzyme activity

Enzymes are fluctuating particles in thermal equilibrium with their solvent environment. A variety of models of enzyme action have postulated selective excitation of enzyme vibrational modes or triggering of correlated motion of catalytic groups through collisions with solvent particles as the basis of catalytic activity. Solvent composition and structure are expected to influence such interactions. Solutes such as p-dioxane, t-butanol, and tetraalkylammonium chlorides are known to be strong perturbants of the structure of water. However, when the kinetic parameters of two enzymes, carboxypeptidase A and alpha-chymotrypsin, were examined carefully in aqueous mixtures containing these solutes, no significant influence of solvent structure or mass composition on the catalytic rate constant was found. The results indicate, furthermore, that, within the low viscosity limit, fluctuations in enzyme structure that are responsible for activated processes in the catalytically rate limiting step appear not to be significantly influenced by dynamic processes in the bulk solvent.     

A discussion of the chemistry of oxidative and nitrosative stress in cytotoxicity

Nitric oxide (NO) has been shown to be a key bioregulatory agent in a wide variety of biological processes, yet cytotoxic properties have been reported as well. This dichotomy has raised the question of how this potentially toxic species can be involved in so many fundamental physiological processes. We have investigated the effects of NO on a variety of toxic agents and correlated how its chemistry might pertain to the observed biology. The results generate a scheme termed the chemical biology of NO in which the pertinent reactions can be categorized into direct and indirect effects. The former involves the direct reaction of NO with its biological targets generally at low fluxes of NO. Indirect effects are reactions mediated by reactive nitrogen oxide species, such as those generated from the NO/O2 and NO/O2- reactions, which can lead to cellular damage via nitrosation or oxidation of biological components. This report discusses several examples of cytotoxicity involved with these stresses.     

Microbially influenced corrosion as a model system for the study of metal microbe interactions: a unifying electron transfer hypothesis

The general term biomineralisation refers to biologically induced mineralisation in which an organism modifies its local microenvironment creating conditions such that there is chemical precipitation of mineral phases extracellularly. Most usually this results from an oxidation or reduction carried out by some microbial species, with the formation of a recognised biomineralised product. These reactions play a major role in microbial physiology and ecology, and are of central importance to such engineering consequences as microbial mining and microbially influenced corrosion. This paper will examine metal microbe interactions, both in naturally occurring microbial ecosystems and in two particular cases of biocorrosion, with the objective of putting forward a unifying hypothesis relevant to the understanding of each of these apparently disparate processes.     

Signaling and stress: The redox landscape in NOS2 biology

Nitric oxide (NO) has a highly diverse range of biological functions from physiological signaling and maintenance of homeostasis to serving as an effector molecule in the immune system. However, deleterious as well as beneficial roles of NO have been reported. Many of the dichotomous effects of NO and derivative reactive nitrogen species (RNS) can be explained by invoking precise interactions with different targets as a result of concentration and temporal constraints. Endogenous concentrations of NO span five orders of magnitude, with levels near the high picomolar range typically occurring in short bursts as compared to sustained production of low micromolar levels of NO during immune response. This article provides an overview of the redox landscape as it relates to increasing NO concentrations, which incrementally govern physiological signaling, nitrosative signaling and nitrosative stress-related signaling. Physiological signaling by NO primarily occurs upon interaction with the heme protein soluble guanylyl cyclase. As NO concentrations rise, interactions with nonheme iron complexes as well as indirect modification of thiols can stimulate additional signaling processes. At the highest levels of NO, production of a broader range of RNS, which subsequently interact with more diverse targets, can lead to chemical stress. However, even under such conditions, there is evidence that stress-related signaling mechanisms are triggered to protect cells or even resolve the stress. This review therefore also addresses the fundamental reactions and kinetics that initiate signaling through NO-dependent pathways, including processes that lead to interconversion of RNS and interactions with molecular targets.     

Environmental constraints upon locomotion and predator-prey interactions in aquatic organisms: an introduction

Environmental constraints in aquatic habitats have become topics of concern to both the scientific community and the public at large. In particular, coastal and freshwater habitats are subject to dramatic variability in various environmental factors, as a result of both natural and anthropogenic processes. The protection and sustainable management of all aquatic habitats requires greater understanding of how environmental constraints influence aquatic organisms. Locomotion and predator-prey interactions are intimately linked and fundamental to the survival of mobile aquatic organisms. This paper summarizes the main points from the review and research articles which comprise the theme issue 'Environmental constraints upon locomotion and predator-prey interactions in aquatic organisms'. The articles explore how natural and anthropogenic factors can constrain these two fundamental activities in a diverse range of organisms from phytoplankton to marine mammals. Some major environmental constraints derive from the intrinsic properties of the fluid and are mechanical in nature, such as viscosity and flow regime. Other constraints derive from direct effects of factors, such as temperature, oxygen content of the water or turbidity, upon the mechanisms underlying the performance of locomotion and predator-prey interactions. The effect of these factors on performance at the tissue and organ level is reflected in constraints upon performance of the whole organism. All these constraints can influence behaviour. Ultimately, they can have an impact on ecological performance. One issue that requires particular attention is how factors such as temperature and oxygen can exert different constraints on the physiology and behaviour of different taxa and the ecological implications of this. Given the multiplicity of constraints, the complexity of their interactions, and the variety of biological levels at which they can act, there is a clear need for integration between the fields of physiology, biomechanics, behaviour, ecology, biological modelling and evolution in both laboratory and field studies. For studies on animals in their natural environment, further technological advances are required to allow investigation of how the prevailing physico-chemical conditions influence basic physiological processes and behaviour.     

A network model of early events in epidermal growth factor receptor signaling that accounts for combinatorial complexity

We consider a model of early events in signaling by the epidermal growth factor (EGF) receptor (EGFR). The model includes EGF, EGFR, the adapter proteins Grb2 and Shc, and the guanine nucleotide exchange factor Sos, which is activated through EGF-induced formation of EGFR-Grb2-Sos and EGFR-Shc-Grb2-Sos assemblies at the plasma membrane. The protein interactions involved in signaling can potentially generate a diversity of protein complexes and phosphoforms; however, this diversity has been largely ignored in models of EGFR signaling. Here, we develop a model that accounts more fully for potential molecular diversity by specifying rules for protein interactions and then using these rules to generate a reaction network that includes all chemical species and reactions implied by the protein interactions. We obtain a model that predicts the dynamics of 356 molecular species, which are connected through 3749 unidirectional reactions. This network model is compared with a previously developed model that includes only 18 chemical species but incorporates the same scope of protein interactions. The predictions of this model are reproduced by the network model, which also yields new predictions. For example, the network model predicts distinct temporal patterns of autophosphorylation for different tyrosine residues of EGFR. A comparison of the two models suggests experiments that could lead to mechanistic insights about competition among adapter proteins for EGFR binding sites and the role of EGFR monomers in signal transduction.     

How do biomolecular systems speed up and regulate rates?

The viability of a biological system depends upon careful regulation of the rates of various processes. These rates have limits imposed by intrinsic chemical or physical steps (e.g., diffusion). These limits can be expanded by interactions and dynamics of the biomolecules. For example, (a) a chemical reaction is catalyzed when its transition state is preferentially bound to an enzyme; (b) the folding of a protein molecule is speeded up by specific interactions within the transition-state ensemble and may be assisted by molecular chaperones; (c) the rate of specific binding of a protein molecule to a cellular target can be enhanced by mechanisms such as long-range electrostatic interactions, nonspecific binding and folding upon binding; (d) directional movement of motor proteins is generated by capturing favorable Brownian motion through intermolecular binding energy; and (e) conduction and selectivity of ions through membrane channels are controlled by interactions and the dynamics of channel proteins. Simple physical models are presented here to illustrate these processes and provide a unifying framework for understanding speed attainment and regulation in biomolecular systems.     

Microbially Influenced Corrosion as a Model System for the Study of Metal Microbe Interactions: A Unifying Electron Transfer Hypothesis

The general term biomineralisation refers to biologically induced mineralisation in which an organism modifies its local microenvironment creating conditions such that there is chemical precipitation of mineral phases extracellularly. Most usually this results from an oxidation or reduction carried out by some microbial species, with the formation of a recognised biomineralised product. These reactions play a major role in microbial physiology and ecology, and are of central importance to such engineering consequences as microbial mining and microbially influenced corrosion. This paper will examine metal microbe interactions, both in naturally occurring microbial ecosystems and in two particular cases of biocorrosion, with the objective of putting forward a unifying hypothesis relevant to the understanding of each of these apparently disparate processes.