bluuebunny/crossref_metadata_2025_split huggingface dataset:
PolyHIPEs — Porous Polymers from High Internal Phase Emulsions
Authors: Silverstein Michael S. , Cameron Neil R. 
Published: September 2010

Abstract
A large variety of porous polymers, generally known as polyHIPEs, have been synthesized using high internal phase emulsions (HIPEs) as templates for the porous structure. HIPEs are formed by mixing two immiscible liquids in the presence of an emulsifier, usually a surfactant, such that the internal phase content is more than 74 %. PolyHIPE are synthesized through the polymerization of monomers in the external phase. The internal phase can be evacuated through holes that develop in the polymer walls, yielding a porous polymer. Hydrophobic polymers can be synthesized within water‐in‐oil emulsions and hydrophilic polymers can be synthesized within oil‐in‐water emulsions. The types of materials synthesized include copolymers, interpenetrating polymer networks, biodegradable materials, organic‐inorganic hybrids that can be pyrolyzed to porous inorganics, nanocomposites, and hydrophobic‐hydrophilic bicontinuous polymers. The large number of methods available to functionalize polyHIPEs have enhanced their utility for such applications as chemical synthesis, chromatography, ion exchange, separation, sensing, tissue engineering, and controlled drug delivery, to name but a few. This article describes HIPE formation and stability, polyHIPE synthesis and functionalization, polyHIPE morphology, polyHIPE properties, a variety of different polyHIPE‐based materials, and polyHIPE applications.
Chemical Synapses
Authors: Thiele Sherri , Nash Joanne 
Published: September 2010

Abstract

Chemical synapses are among the most elaborate junctions existing between two cells, enabling communication between neurons through chemical neurotransmission within milliseconds. This fast rate of transmission is achieved through three subsynaptic compartments; the presynaptic bouton, the synaptic cleft and the postsynaptic junction. The presynaptic bouton packages neurotransmitters into synaptic vesicles then releases them into the synaptic cleft. Release of synaptic vesicles occurs through several distinct stages, coordinated by a group of specialised proteins. The postsynaptic density (PSD) has evolved into a complex neurotransmitter reception apparatus, which enables the postsynaptic terminal to modulate the downstream response to neurotransmitters. Following activation of receptors on the postsynaptic membrane, neurotransmitters are taken back up into the presynaptic bouton and repackaged into synaptic vesicles (SVs). The synaptic cleft contains proteins that ensure that active zone and PSD remain in proximity. These proteins are also required during synaptogenesis to ensure that the synapse forms properly.

Key Concepts:

There are three major structural components that define the synapse: the presynaptic bouton (also known as presynaptic terminal), postsynaptic junction (also known as postsynaptic terminal) and the synaptic cleft.

The presynaptic bouton is responsible for packaging neurotransmitters into synaptic vesicles, then releasing their contents into the synaptic cleft in response to calcium influx.

Synaptic vesicles are released at a specialised site within the presynaptic bouton known as the active zone.

Synaptic vesicles are released by a process known as exocytosis through several distinct steps involving specialised proteins that form a highly interactive and dynamic protein complex at the site of synaptic vesicle release.

Interpretation of the presynaptic message takes place at the postsynaptic membrane through transmembrane proteins called receptors.

The postsynaptic density is situated adjacent to the postsynaptic membrane within the postsynaptic terminal, juxtaposed to the presynaptic active zone.

The postsynaptic density is composed of receptors, scaffolding and adhesion proteins, kinases and phosphatases, as well as cytoskeletal elements, which are linked together to form macromolecular complexes.

The postsynaptic density of excitatory synapses is thicker (more pronounced) than the postsynaptic density of inhibitory synapses.

The synaptic cleft is a narrow space, approximately 20–30 nm wide situated between the presynaptic and the postsynaptic plasma membranes.

The synaptic cleft is composed of proteinaceous and carbohydrate‐rich cell adhesion molecules.
Immune Defence: Microbial Interference
Authors: Merino S , Tomás JM 
Published: September 2010

Abstract

The immune system controls the host–microbe interactions, the outcome of which can range from symbiotic coexistence with commensally microbiota, to mild asymptomatic infections, to highly virulent infectious diseases. This control is achieved by two defence mechanisms: the innate immune defence, which consists in a nonspecific mechanism, and the adaptive immunity defence, acquired over time following infections or vaccination. Despite the sophisticated immune system, extracellular and intracellular pathogens have developed numerous, and often ingenious strategies, to evade, interfere or eradicate the effectiveness of host immune defences. Although the strategies used by viral and bacterial pathogens are numerous, there are several general mechanisms shared between these microbial pathogens. The success of each pathogen depends on the coordinated activities of its virulence factors to overcome host barriers to colonisation and its ability to mount an effective anti‐immune response within the infected host, which can ultimately result in acute disease or chronic infection.

Key Concepts:

Immunoglobulin proteases cleave antibodies rendering them nonfunctional and leading to deficiencies in the immune system.

Complement regulators prevent complement activation and cell destruction.

Interference with major histocompatibility complexes overcomes T‐cell recognition.

Microbial interference with cytokines modulates intracellular signalling critical to the regulation, proliferation and differentiation of lymphocytes, which drive inflammation.

Intracellular resistance allows microorganisms to circumvent humoral defence mechanisms and spread within the host.

Immunosuppresion reduces T or B lymphocytes’ defence.
Complement: Classical and Lectin Pathways
Authors: Arlaud Gérard J , Thielens Nicole M 
Published: September 2010

Abstract

The classical and
lectin
pathways of complement are major recognition systems of innate immunity that are found in mammals and other animal species. By means of several multimolecular proteases –
C1
, the
mannan‐binding lectin
(MBL)–
MBL‐associated serine protease 2
(MBL–MASP‐2) and the
ficolin–
MASP‐2 complexes – each comprising a recognition protein and a protease component, they detect pathogens and other targets and thereby trigger proteolytic reactions. Both pathways converge to the formation of
C3 convertase
, a complex protease that cleaves
C3
, the central component of the complement system. Proteolytic cleavage of
C3
generates a series of fragments and elicits various effector mechanisms, including inflammation and phagocytosis. These mechanisms contribute to the elimination of pathogenic microorganisms and altered host cells from blood and tissues and modulate the adaptive immune response.

Key Concepts:

C1q, MBL and ficolins are pattern‐recognition molecules able to sense conserved motifs on pathogens and altered self‐cells.

C1q is a major sensor of apoptotic cells and regulator of immune tolerance.

Proteolytic cleavage of C3 is pivotal for amplification of the complement response and labelling of the target particles.

Target recognition, proteolysis and complex formation generate conformational changes that underlie complement functioning.

Complement activation and activity are tightly regulated to avoid noxious side effects on normal host cells and tissues.
Amino Acid Biosynthesis
Authors: Deferrari Giacomo , Mannucci Irene , Garibotto Giacomo 
Published: September 2010

AbstractAmino acids are classically considered as the building blocks for the synthesis of proteins. Besides this, some of them play a major role in other functions, such as regulation of protein turnover and signal transduction, transport of nitrogen and carbon across the organs, or neurotransmission. The unique characteristics of amino acids are the presence of a free amino group in the α‐carbon and a free carboxyl group. The amino acids differ from each other with respect to their side‐chains. The amino acids are classified into subgroups according to their similarity in carbon skeleton, substituent groups or a common metabolic pathway. The biosynthesis of amino acids involves several biochemical pathways in which amino acids are assembled from other precursors. The biosynthesis of amino acids is distinct from that involving lipids or carbohydrates because it includes the use of nitrogen.Key Concepts:Amino acids are classically considered as the building blocks from which proteins are synthesised. Besides this, some of them play a major role in the regulation of protein turnover and signal transduction, transport of nitrogen and carbon across the organs, and neurotransmission.The biosynthesis of amino acids involves several biochemical pathways in which amino acids are assembled from other precursors. The biosynthesis of amino acids is distinct from that involving lipids or carbohydrates because it includes the use of nitrogen.The fixation of nitrogen is a process that converts atmospheric nitrogen to a form that can be used biologically.The pathways for the synthesis of essential amino acids are present only in microorganisms and plants.Nine of 12 nonessential amino acids are synthesised from amphibolic intermediates, whereas three amino acids (tyrosine, cysteine and hydroxylysine) derive from essential amino acids. Amino acid transaminases, glutamate dehydrogenase and glutamine synthetase play a central role in the synthesis of nonessential amino acids.The major pathway by which ammonia is incorporated into amino acids is through the reductive amination of α‐ketoglutarate to glutamate. Ammonia is highly toxic for animals. Glutamine is a nontoxic carrier of ammonia.In the human adult as much as 200–250 g of proteins are degraded daily, and their constituent amino acids are in large part reutilised in protein synthesis.Amino acid deficiency states can result if any of the essential amino acid is present in inadequate amounts or omitted from the diet.Alanine, glutamate and glutamine are crucial links between energy and protein metabolism. Moreover, glutamine and alanine biosynthesis in the peripheral tissues (muscle) provides a means for the transport of carbon to the liver for gluconeogenesis and nitrogen for ureagenesis.There are several nonprotein functions of amino acids, such as the biosynthesis of purines and pyrimidines, which involve more nonessential than essential amino acids.
Major Histocompatibility Complex (
MHC
): Mouse
Authors: Stuart Patrick M 
Published: September 2010

Abstract

The major histocompatibility complex (MHC) of the mouse, which is called the
H2
complex, is located on chromosome 17. It contains genes critical to the functioning of the immune system, the products of which are intimately involved in the initiation of immune responses. The proteins made by these genes display a significant amount of polymorphism, or sequence variability. Few genes possess this degree of polymorphism, but it is critical to the immune response and to the survival of a species. The chief characteristic of MHC molecules is their ability to bind small peptides. These bound peptides along with specific areas of the MHC molecule are the structures that interact with the T‐cell receptor (TCR) leading to activation of a T‐cell immune response, which in turn can active other cells of immune system. Thus they determine which TCR's are functional which in turn indicates which peptides a T cell will respond to.

Key Concepts:

The historical background and the genetics of MHC development are described.

The expression and function of MHC class I genes is described.

The function of CD8+ T cells requires expression of MHC class I genes.

Peptide loading is required for MHC class I expression.

MHC class I polymorphism is important for species resistance to infectious disease.

The expression and function of MHC class II genes is described.

MHC class II expression is required for generation and function of CD4 T cells.

Nonclassical class I molecules are important in generating responses to commonly expressed molecules expressed by pathogenic organisms.

The function of other genes found within the H2 complex is described.
Inflammation: Chronic
Authors: Kumar Rakesh K , Wakefield Denis 
Published: September 2010

Abstract

Chronic inflammation may result from failure to eliminate an irritant that causes acute inflammation, from an autoimmune response to a self‐antigen, or may be caused by an innately chronic irritant of low intensity that persists. It is a biologically distinct pattern of response that is characterised by simultaneous inflammation and repair. Recruitment and activation of macrophages is typical of chronic inflammation, and is often accompanied by recruitment of cell types participating in an immunological response, notably T lymphocytes. Significant destruction of tissue may occur. Repair, which involves induction of granulation tissue, may lead to subsequent scarring. The chronic inflammatory response is regulated by the coordinated action of various cytokines and growth factors. Many common and clinically important disease states result from chronic inflammation, and this process also contributes to other diseases which are not primarily identified as inflammatory.

Key Concepts:

Chronic inflammation is a key process underlying many common and important diseases, as well as other disease states which are not obviously inflammatory.

Compared to acute inflammation, chronic inflammation is a biologically distinct pattern of response, characterised by simultaneous inflammation and repair.

Macrophages and their derivatives are key participants in a chronic inflammatory response.

The immune response contributes to the pathogenesis of many chronic inflammatory diseases.

Chronic inflammation is regulated by a complex interaction between cytokines that promote inflammatory cell recruitment/activation and growth factors that promote healing.
Bacterial Capsules and Evasion of Immune Responses
Authors: Merino S , Tomás JM 
Published: September 2010

Abstract

The bacterial surface contains various structures that are capable of activating the host defences and consequently inducing host immune responses. Bacterial capsules are one of the most external structures on the bacterial surface, which may completely surround all the antigenic molecules or may be coexpressed with other bacterial antigens. They are involved in a wide range of biological processes, such as prevention of desiccation, adherence and resistance to nonspecific and specific host immunity.
Gram‐negative and Gram‐positive capsular polysaccharides contribute to the bacterial resistance of host immune responses by different mechanisms. Usually, capsular polysaccharides that mask the underlying cell surface structures activate weakly or not at all the immune system, whereas bacterial capsules coexpressed with other bacterial antigens activate the immune system but mask opsonines and prevent complement attack complex formation, as well as phagocytosis.

Key Concepts:

Bacterial capsules completely surround bacterial cell and enhance the ability of bacteria to cause disease.

Polysaccharides are polymeric carbohydrate structures, formed of one or more sugar residues repeating units joined together by glycosidic bonds.

Antigenic variation modifies microorganism's surface structures and allows them to overcome the immune response.
Bacterial
DNA
Polymerase I
Authors: Allen William J , Li Ying , Waksman Gabriel 
Published: September 2010

Abstract

Bacterial
deoxyribonucleic acid (DNA) polymerase I
is a family of enzymes involved in bacterial DNA synthesis and lesion repair. These enzymes have a multidomain structure, consisting of a single polypeptide chain that encompasses a distinct polymerase domain, a proofreading 3′–5′
exonuclease
and/or a 5′–3′
exonuclease
activity. Members of the
polymerase I
family have been investigated extensively, both because of their vital role in replicating and maintaining bacterial chromosomes, and because of their importance as tools in molecular biology, in particular for the polymerase chain reaction (PCR) and DNA sequencing. Studies on the

Escherichia coli

DNA polymerase I
in particular have yielded significant insights into the mechanism of DNA polymerisation which is shared by almost all other nucleotide polymerases.

Key Concepts:

Bacterial DNA polymerase I enzymes are multidomain proteins with separate polymerisation, proofreading and 5′–3′ exonuclease functions.

They perform a vital function in bacteria by carrying out DNA repair and some aspects of chromosomal replication.

Polymerases incorporate one nucleotide at a time to the 3′ end of the primer DNA strand in a template‐directed manner.

Members of the DNA polymerase I family are able to replicate DNA with far greater accuracy than base pairing alone can account for.

The polymerisation reaction is a multistep process during which the enzyme switches between substrate binding and nucleotide incorporation conformations.

The 5′–3′ exonuclease allows the polymerase to degrade RNA primers and to assist with DNA repair.

Thermostable family I DNA polymerases are used extensively in polymerase chain reaction to amplify DNA and for DNA sequencing.
Eukaryotic Replication Origins and Initiation of
DNA
Replication
Authors: DePamphilis Melvin L , Aladjem Mirit I 
Published: September 2010

Abstract

Eukaryotic
deoxyribonucleic acid
(DNA) replication begins at specific genomic sites called replication origins that serve as assembly sites for prereplication complexes (preRCs). PreRCs include proteins that recognise origin sequences,
helicases
that separate the two strands of DNA and accessory proteins that facilitate
helicase
binding and interaction with cell cycle regulatory pathways. Assembly of preRCs is required for initiation of DNA replication which occurs after those complexes recruit additional proteins including
DNA polymerases
. The sequence requirements for replication origins vary but they all include several distinct DNA elements that act synergistically to facilitate preRC assembly. The number of potential replication origins is higher than the number of actual replication initiation sites. Epigenetic processes and metabolic conditions dynamically select the location of replication initiation events of each cell cycle to insure complete and accurate replication of the entire genome in coordination with gene expression and chromatin condensation.

Key Concepts:

Replication initiates at distinct chromosomal locations that recruit prereplication (preRC) complexes.

PreRCs are recruited sequentially, each step subject to strict regulation to prevent rereplication.

Cyclin‐dependent kinases (CDK) levels change during the cell cycle. Low CDK activity is required for preRC assembly as cells exit mitosis. High CDK activity is required for activation of existing preRCs and initiation of DNA synthesis, while simultaneously suppressing assembly of new preRCs.

Replication origin sequences vary among metazoans, but the functions of proteins that bind replication origins are conserved.

Eukaryotic origins exhibit a modular structure. Modularity is detectable in single‐cell eukaryotes such as yeast and is more pronounced in metazoans, in which replication origins often cluster.

Not all potential replication origins are activated in each cell cycle. Utilisation of replication origins is regulated dynamically to facilitate coordination with other metabolic processes occurring on chromatin.

Either hyperactivation or suppression of replication origins can damage DNA and cause chromosomal rearrangements, suggesting that spacing replication initiation events at defined intervals facilitates genomic stability.
Blastoderm Formation and Cellularisation inDrosophila melanogaster
Authors: Kotadia Shaila , Crest Justin , Tram Uyen , Riggs Blake , Sullivan William 
Published: September 2010

AbstractImmediately following fertilisation inDrosophilaand many other arthropods, the embryo undergoes a series of rapid syncytial nuclear divisions. These divisions are driven by maternally supplied components and occur in the absence of zygotic transcription. Unlike typical cell divisions, these divisions alternate between S and M phases, resulting in cell cycles that last only from 10 to 25 min. After four rounds of division, the nuclei undergo axial expansion, a process that relies on microfilaments. Subsequently migration of the nuclei to the cortex relies on microtubules. Once at the cortex, the nuclear divisions occur on a single plane and rely on partial cleavage furrows to maintain an even distribution. The cortical nuclear divisions continue until the mid‐blastula transition (MBT), at which time cellularisation results in the formation of a multicellular embryo.Key Concepts:Fertilisation triggers a series of events that induces the first mitotic cycle, a gonomeric division between the male and female pronucleus.After fertilisation, the embryo undergoes 13 synchronous divisions within a syncytium.Divisions 10–13 occur at the cortex of the embryo and require reorganisation of actin and membrane into metaphase furrows.At cycle 14, the cell cycle pauses and cellularisation occurs forming individual somatic cells.Cellularisation, a key feature of the mid‐blastula transition, marks the time at which zygotic transcription occurs and maternal products are degraded.
Autoimmune Disease: Pathogenesis
Authors: Bellone Matteo 
Published: September 2010

AbstractAutoimmune diseases are a vast array of organ‐specific as well as systemic diseases, whose pathogenesis stems from the activation of B‐ and T lymphocytes reacting against antigens of the body's own tissues (defined as ‘self’). T‐ and B lymphocytes are the main components of the adaptive arm of the immune system, and their major task is to rapidly and efficiently remove pathogens (e.g. viruses or bacteria) in the absence of relevant tissue damage and self‐recognition. In physiologic conditions, the ability of the immune system to avoid responsiveness to self‐antigens is obtained by the cooperative efforts of central and peripheral tolerance mechanisms. Alteration of either one of the two mechanisms favours the induction of autoimmune diseases that may either cause complete and irreversible loss of function of the targeted tissue or its hyperfunction.Key Concepts:Autoimmune diseases are the result of specific immune responses directed against structures of the self.Autoimmune diseases are the consequence of an altered function of the immune system.Autoimmune disease may involve a single tissue or multiple organs.Consequences of an autoimmune reaction may either be the loss of function or the hyperfunction of the target tissue.An autoimmune response may be primarily T‐ or B‐cell‐mediated, or both.
Evolution: History
Authors: Bowler Peter J 
Published: September 2010

AbstractThe modern theory of evolution was founded by Charles Darwin, but an overview of the history of evolutionism shows that ideas of the transformation of species predated the publication of hisOrigin of Speciesin 1859. Various theories of progressive and purposeful change in the organic world had begun to circulate even before Darwin's more radical theory was injected into the debate. Natural selection was regarded as a materialistic idea, and through the late nineteenth century naturalists searched for alternatives that would allow them to believe that the history of life had an ultimate purpose. A complex series of developments in the early twentieth century was needed to create the genetical theory of natural selection accepted by most biologists today.