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Biology, Volume 4, Issue 3 (September 2015) , Pages 460-606

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Open AccessArticle cAMP-Inhibits Cytoplasmic Phospholipase A2 and Protects Neurons against Amyloid-β-Induced Synapse Damage
Biology 2015, 4(3), 591-606; https://doi.org/10.3390/biology4030591
Received: 13 July 2015 / Revised: 26 August 2015 / Accepted: 7 September 2015 / Published: 16 September 2015
Cited by 5 | Viewed by 1984 | PDF Full-text (1145 KB) | HTML Full-text | XML Full-text
Abstract
A key event in Alzheimer’s disease (AD) is the production of amyloid-β (Aβ) peptides and the loss of synapses. In cultured neurons Aβ triggered synapse damage as measured by the loss of synaptic proteins. α-synuclein (αSN), aggregates of which accumulate in Parkinson’s disease, [...] Read more.
A key event in Alzheimer’s disease (AD) is the production of amyloid-β (Aβ) peptides and the loss of synapses. In cultured neurons Aβ triggered synapse damage as measured by the loss of synaptic proteins. α-synuclein (αSN), aggregates of which accumulate in Parkinson’s disease, also caused synapse damage. Synapse damage was associated with activation of cytoplasmic phospholipase A2 (cPLA2), an enzyme that regulates synapse function and structure, and the production of prostaglandin (PG) E2. In synaptosomes PGE2 increased concentrations of cyclic adenosine monophosphate (cAMP) which suppressed the activation of cPLA2 demonstrating an inhibitory feedback system. Thus, Aβ/αSN-induced activated cPLA2 produces PGE2 which increases cAMP which in turn suppresses cPLA2 and, hence, its own production. Neurons pre-treated with pentoxifylline and caffeine (broad spectrum phosphodiesterase (PDE) inhibitors) or the PDE4 specific inhibitor rolipram significantly increased the Aβ/αSN-induced increase in cAMP and consequently protected neurons against synapse damage. The addition of cAMP analogues also inhibited cPLA2 and protected neurons against synapse damage. These results suggest that drugs that inhibit Aβ-induced activation of cPLA2 and cross the blood–brain barrier may reduce synapse damage in AD. Full article
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Open AccessHypothesis Homeostasis as the Mechanism of Evolution
Biology 2015, 4(3), 573-590; https://doi.org/10.3390/biology4030573
Received: 2 July 2015 / Revised: 11 August 2015 / Accepted: 8 September 2015 / Published: 15 September 2015
Cited by 11 | Viewed by 4599 | PDF Full-text (788 KB) | HTML Full-text | XML Full-text
Abstract
Homeostasis is conventionally thought of merely as a synchronic (same time) servo-mechanism that maintains the status quo for organismal physiology. However, when seen from the perspective of developmental physiology, homeostasis is a robust, dynamic, intergenerational, diachronic (across-time) mechanism for the maintenance, perpetuation and [...] Read more.
Homeostasis is conventionally thought of merely as a synchronic (same time) servo-mechanism that maintains the status quo for organismal physiology. However, when seen from the perspective of developmental physiology, homeostasis is a robust, dynamic, intergenerational, diachronic (across-time) mechanism for the maintenance, perpetuation and modification of physiologic structure and function. The integral relationships generated by cell-cell signaling for the mechanisms of embryogenesis, physiology and repair provide the needed insight to the scale-free universality of the homeostatic principle, offering a novel opportunity for a Systems approach to Biology. Starting with the inception of life itself, with the advent of reproduction during meiosis and mitosis, moving forward both ontogenetically and phylogenetically through the evolutionary steps involved in adaptation to an ever-changing environment, Biology and Evolution Theory need no longer default to teleology. Full article
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Open AccessArticle The Impact of Photobleaching on Microarray Analysis
Biology 2015, 4(3), 556-572; https://doi.org/10.3390/biology4030556
Received: 29 June 2015 / Revised: 20 August 2015 / Accepted: 8 September 2015 / Published: 11 September 2015
Cited by 2 | Viewed by 1989 | PDF Full-text (1017 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
DNA-Microarrays have become a potent technology for high-throughput analysis of genetic regulation. However, the wide dynamic range of signal intensities of fluorophore-based microarrays exceeds the dynamic range of a single array scan by far, thus limiting the key benefit of microarray technology: parallelization. [...] Read more.
DNA-Microarrays have become a potent technology for high-throughput analysis of genetic regulation. However, the wide dynamic range of signal intensities of fluorophore-based microarrays exceeds the dynamic range of a single array scan by far, thus limiting the key benefit of microarray technology: parallelization. The implementation of multi-scan techniques represents a promising approach to overcome these limitations. These techniques are, in turn, limited by the fluorophores’ susceptibility to photobleaching when exposed to the scanner’s laser light. In this paper the photobleaching characteristics of cyanine-3 and cyanine-5 as part of solid state DNA microarrays are studied. The effects of initial fluorophore intensity as well as laser scanner dependent variables such as the photomultiplier tube’s voltage on bleaching and imaging are investigated. The resulting data is used to develop a model capable of simulating the expected degree of signal intensity reduction caused by photobleaching for each fluorophore individually, allowing for the removal of photobleaching-induced, systematic bias in multi-scan procedures. Single-scan applications also benefit as they rely on pre-scans to determine the optimal scanner settings. These findings constitute a step towards standardization of microarray experiments and analysis and may help to increase the lab-to-lab comparability of microarray experiment results. Full article
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Open AccessReview Multi-Facial, Non-Peptidic α-Helix Mimetics
Biology 2015, 4(3), 540-555; https://doi.org/10.3390/biology4030540
Received: 21 July 2015 / Revised: 11 August 2015 / Accepted: 14 August 2015 / Published: 31 August 2015
Cited by 5 | Viewed by 1876 | PDF Full-text (924 KB) | HTML Full-text | XML Full-text
Abstract
α-Helices often recognize their target proteins at protein–protein interfaces through more than one recognition face. This review describes the state-of-the-art in the design of non-peptidic α-helix mimetics that reproduce functionality from multiple faces of an α-helix. Full article
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Open AccessReview The Mucosal Immune System of Teleost Fish
Biology 2015, 4(3), 525-539; https://doi.org/10.3390/biology4030525
Received: 2 June 2015 / Revised: 5 August 2015 / Accepted: 5 August 2015 / Published: 12 August 2015
Cited by 42 | Viewed by 3905 | PDF Full-text (181 KB) | HTML Full-text | XML Full-text
Abstract
Teleost fish possess an adaptive immune system associated with each of their mucosal body surfaces. Evidence obtained from mucosal vaccination and mucosal infection studies reveal that adaptive immune responses take place at the different mucosal surfaces of teleost. The main mucosa-associated lymphoid tissues [...] Read more.
Teleost fish possess an adaptive immune system associated with each of their mucosal body surfaces. Evidence obtained from mucosal vaccination and mucosal infection studies reveal that adaptive immune responses take place at the different mucosal surfaces of teleost. The main mucosa-associated lymphoid tissues (MALT) of teleosts are the gut-associated lymphoid tissue (GALT), skin-associated lymphoid tissue (SALT), the gill-associated lymphoid tissue (GIALT) and the recently discovered nasopharynx-associated lymphoid tissue (NALT). Teleost MALT includes diffuse B cells and T cells with specific phenotypes different from their systemic counterparts that have co-evolved to defend the microbe-rich mucosal environment. Both B and T cells respond to mucosal infection or vaccination. Specific antibody responses can be measured in the gills, gut and skin mucosal secretions of teleost fish following mucosal infection or vaccination. Rainbow trout studies have shown that IgT antibodies and IgT+ B cells are the predominant B cell subset in all MALT and respond in a compartmentalized manner to mucosal infection. Our current knowledge on adaptive immunity in teleosts is limited compared to the mammalian literature. New research tools and in vivo models are currently being developed in order to help reveal the great intricacy of teleost mucosal adaptive immunity and help improve mucosal vaccination protocols for use in aquaculture. Full article
(This article belongs to the Special Issue Current Understanding of Fish Immune Systems)
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Open AccessReview Antibody Affinity Maturation in Fishes—Our Current Understanding
Biology 2015, 4(3), 512-524; https://doi.org/10.3390/biology4030512
Received: 22 May 2015 / Revised: 13 July 2015 / Accepted: 23 July 2015 / Published: 31 July 2015
Cited by 5 | Viewed by 2115 | PDF Full-text (378 KB) | HTML Full-text | XML Full-text
Abstract
It has long been believed that fish lack antibody affinity maturation, in part because they were thought to lack germinal centers. Recent research done on sharks and bony fishes indicates that these early vertebrates are able to affinity mature their antibodies. This article [...] Read more.
It has long been believed that fish lack antibody affinity maturation, in part because they were thought to lack germinal centers. Recent research done on sharks and bony fishes indicates that these early vertebrates are able to affinity mature their antibodies. This article reviews the functionality of the fish homologue of the immunoglobulin (Ig) mutator enzyme activation-induced cytidine deaminase (AID). We also consider the protein and molecular evidence for Ig somatic hypermutation and antibody affinity maturation. In the context of recent evidence for a putative proto-germinal center in fishes we propose some possible reasons that observed affinity maturation in fishes often seems lacking and propose future work that might shed further light on this process in fishes. Full article
(This article belongs to the Special Issue Current Understanding of Fish Immune Systems)
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Open AccessReview The Regulation of Reverse Cholesterol Transport and Cellular Cholesterol Homeostasis by MicroRNAs
Biology 2015, 4(3), 494-511; https://doi.org/10.3390/biology4030494
Received: 5 June 2015 / Revised: 22 July 2015 / Accepted: 23 July 2015 / Published: 28 July 2015
Cited by 9 | Viewed by 3449 | PDF Full-text (388 KB) | HTML Full-text | XML Full-text
Abstract
MicroRNAs (miRNAs) are small, non-coding RNAs that have the ability to post-transcriptionally regulate gene expression. Hundreds of miRNAs have been identified in humans and they are involved in the regulation of almost every process, including cholesterol transport, metabolism, and maintenance of cholesterol homeostasis. [...] Read more.
MicroRNAs (miRNAs) are small, non-coding RNAs that have the ability to post-transcriptionally regulate gene expression. Hundreds of miRNAs have been identified in humans and they are involved in the regulation of almost every process, including cholesterol transport, metabolism, and maintenance of cholesterol homeostasis. Because of their small size and their ability to very specifically regulate gene expression, miRNAs are attractive targets for the regulation of dyslipidemias and other lipid-related disorders. However, the complex interactions between miRNAs, transcription factors, and gene expression raise great potential for side effects as a result of miRNA overexpression or inhibition. Many dietary components can also target specific miRNAs, altering the expression of downstream genes. Therefore, much more research is necessary to fully understand the role(s) of each miRNA in the body and how they may be impacted by diet and health. The present review aims to summarize the known roles of miRNAs in the regulation of reverse cholesterol transport and the maintenance of cholesterol homeostasis, as well as the potential clinical consequences of their manipulation. Full article
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Open AccessReview Sensors of Infection: Viral Nucleic Acid PRRs in Fish
Biology 2015, 4(3), 460-493; https://doi.org/10.3390/biology4030460
Received: 22 May 2015 / Revised: 19 June 2015 / Accepted: 19 June 2015 / Published: 8 July 2015
Cited by 13 | Viewed by 2923 | PDF Full-text (603 KB) | HTML Full-text | XML Full-text
Abstract
Viruses produce nucleic acids during their replication, either during genomic replication or transcription. These nucleic acids are present in the cytoplasm or endosome of an infected cell, or in the extracellular space to be sensed by neighboring cells during lytic infections. Cells have [...] Read more.
Viruses produce nucleic acids during their replication, either during genomic replication or transcription. These nucleic acids are present in the cytoplasm or endosome of an infected cell, or in the extracellular space to be sensed by neighboring cells during lytic infections. Cells have mechanisms of sensing virus-generated nucleic acids; these nucleic acids act as flags to the cell, indicating an infection requiring defense mechanisms. The viral nucleic acids are called pathogen-associated molecular patterns (PAMPs) and the sensors that bind them are called pattern recognition receptors (PRRs). This review article focuses on the most recent findings regarding nucleic acids PRRs in fish, including: Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), cytoplasmic DNA sensors (CDSs) and class A scavenger receptors (SR-As). It also discusses what is currently known of the downstream signaling molecules for each PRR family and the resulting antiviral response, either type I interferons (IFNs) or pro-inflammatory cytokine production. The review highlights what is known but also defines what still requires elucidation in this economically important animal. Understanding innate immune systems to virus infections will aid in the development of better antiviral therapies and vaccines for the future. Full article
(This article belongs to the Special Issue Current Understanding of Fish Immune Systems)
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