Island extinctions: processes, patterns, and potential for ecosystem restoration

Extinctions have altered island ecosystems throughout the late Quaternary. Here, we review the main historic drivers of extinctions on islands, patterns in extinction chronologies between islands, and the potential for restoring ecosystems through reintroducing extirpated species. While some extinctions have been caused by climatic and environmental change, most have been caused by anthropogenic impacts. We propose a general model to describe patterns in these anthropogenic island extinctions. Hunting, habitat loss and the introduction of invasive predators accompanied prehistoric settlement and caused declines of endemic island species. Later settlement by European colonists brought further land development, a different suite of predators and new drivers, leading to more extinctions. Extinctions alter ecological networks, causing ripple effects for islands through the loss of ecosystem processes, functions and interactions between species. Reintroduction of extirpated species can help restore ecosystem function and processes, and can be guided by palaeoecology. However, reintroduction projects must also consider the cultural, social and economic needs of humans now inhabiting the islands and ensure resilience against future environmental and climate change

Susceptibility of Anopheles stephensi to Plasmodium gallinaceum: A Trait of the Mosquito, the Parasite, and the Environment

Vector susceptibility to Plasmodium infection is treated primarily as a vector trait, although it is a composite trait expressing the joint occurrence of the parasite and the vector with genetic contributions of both. A comprehensive approach to assess the specific contribution of genetic and environmental variation on "vector susceptibility" is lacking. Here we developed and implemented a simple scheme to assess the specific contributions of the vector, the parasite, and the environment to "vector susceptibility." To the best of our knowledge this is the first study that employs such an approach.We conducted selection experiments on the vector (while holding the parasite "constant") and on the parasite (while holding the vector "constant") to estimate the genetic contributions of the mosquito and the parasite to the susceptibility of Anopheles stephensi to Plasmodium gallinaceum. We separately estimated the realized heritability of (i) susceptibility to parasite infection by the mosquito vector and (ii) parasite compatibility (transmissibility) with the vector while controlling the other. The heritabilities of vector and the parasite were higher for the prevalence, i.e., fraction of infected mosquitoes, than the corresponding heritabilities of parasite load, i.e., the number of oocysts per mosquito.The vector's genetics (heritability) comprised 67% of "vector susceptibility" measured by the prevalence of mosquitoes infected with P. gallinaceum oocysts, whereas the specific contribution of parasite genetics (heritability) to this trait was only 5%. Our parasite source might possess minimal genetic diversity, which could explain its low heritability (and the high value of the vector). Notably, the environment contributed 28%. These estimates are relevant only to the particular system under study, but this experimental design could be useful for other parasite-host systems. The prospects and limitations of the genetic manipulation of vector populations to render the vector resistant to the parasite are better considered on the basis of this framework

Induction of Glucose Metabolism in Stimulated T Lymphocytes Is Regulated by Mitogen-Activated Protein Kinase Signaling

T lymphocytes play a critical role in cell-mediated immune responses. During activation, extracellular and intracellular signals alter T cell metabolism in order to meet the energetic and biosynthetic needs of a proliferating, active cell, but control of these phenomena is not well defined. Previous studies have demonstrated that signaling from the costimulatory receptor CD28 enhances glucose utilization via the phosphatidylinositol-3-kinase (PI3K) pathway. However, since CD28 ligation alone does not induce glucose metabolism in resting T cells, contributions from T cell receptor-initiated signaling pathways must also be important. We therefore investigated the role of mitogen-activated protein kinase (MAPK) signaling in the regulation of mouse T cell glucose metabolism. T cell stimulation strongly induces glucose uptake and glycolysis, both of which are severely impaired by inhibition of extracellular signal-regulated kinase (ERK), whereas p38 inhibition had a much smaller effect. Activation also induced hexokinase activity and expression in T cells, and both were similarly dependent on ERK signaling. Thus, the ERK signaling pathway cooperates with PI3K to induce glucose utilization in activated T cells, with hexokinase serving as a potential point for coordinated regulation

Rab proteins and Rab-associated proteins: major actors in the mechanism of protein-trafficking disorders

Ras-associated binding (Rab) proteins and Rab-associated proteins are key regulators of vesicle transport, which is essential for the delivery of proteins to specific intracellular locations. More than 60 human Rab proteins have been identified, and their function has been shown to depend on their interaction with different Rab-associated proteins regulating Rab activation, post-translational modification and intracellular localization. The number of known inherited disorders of vesicle trafficking due to Rab cycle defects has increased substantially during the past decade. This review describes the important role played by Rab proteins in a number of rare monogenic diseases as well as common multifactorial human ones. Although the clinical phenotype in these monogenic inherited diseases is highly variable and dependent on the type of tissue in which the defective Rab or its associated protein is expressed, frequent features are hypopigmentation (Griscelli syndrome), eye defects (Choroideremia, Warburg Micro syndrome and Martsolf syndrome), disturbed immune function (Griscelli syndrome and Charcot–Marie–Tooth disease) and neurological dysfunction (X-linked non-specific mental retardation, Charcot–Marie–Tooth disease, Warburg Micro syndrome and Martsolf syndrome). There is also evidence that alterations in Rab function play an important role in the progression of multifactorial human diseases, such as infectious diseases and type 2 diabetes. Rab proteins must not only be bound to GTP, but they need also to be ‘prenylated’—i.e. bound to the cell membranes by isoprenes, which are intermediaries in the synthesis of cholesterol (e.g. geranyl geranyl or farnesyl compounds). This means that isoprenylation can be influenced by drugs such as statins, which inhibit isoprenylation, or biphosphonates, which inhibit that farnesyl pyrophosphate synthase necessary for Rab GTPase activity. Conclusion: Although protein-trafficking disorders are clinically heterogeneous and represented in almost every subspeciality of pediatrics, the identification of common pathogenic mechanisms may provide a better diagnosis and management of patients with still unknown Rab cycle defects and stimulate the development of therapeutic agents

Low linkage disequilibrium in wild Anopheles gambiae s.l. populations

<p>Abstract</p> <p>Background</p> <p>In the malaria vector <it>Anopheles gambiae</it>, understanding diversity in natural populations and genetic components of important phenotypes such as resistance to malaria infection is crucial for developing new malaria transmission blocking strategies. The design and interpretation of many studies here depends critically on Linkage disequilibrium (LD). For example in association studies, LD determines the density of Single Nucleotide Polymorphisms (SNPs) to be genotyped to represent the majority of the genomic information. Here, we aim to determine LD in wild <it>An. gambiae s.l</it>. populations in 4 genes potentially involved in mosquito immune responses against pathogens (<it>Gambicin</it>, <it>NOS</it>, <it>REL2 </it>and <it>FBN9</it>) using previously published and newly generated sequences.</p> <p>Results</p> <p>The level of LD between SNP pairs in cloned sequences of each gene was determined for 7 species (or incipient species) of the <it>An. gambiae </it>complex. In all tested genes and species, LD between SNPs was low: even at short distances (< 200 bp), most SNP pairs gave an r²< 0.3. Mean r²ranged from 0.073 to 0.766. In most genes and species LD decayed very rapidly with increasing inter-marker distance.</p> <p>Conclusions</p> <p>These results are of great interest for the development of large scale polymorphism studies, as LD generally falls below any useful limit. It indicates that very fine scale SNP detection will be required to give an overall view of genome-wide polymorphism. Perhaps a more feasible approach to genome wide association studies is to use targeted approaches using candidate gene selection to detect association to phenotypes of interest.</p

Rab27a and Rab27b control different steps of the exosome secretion pathway

Exosomes are secreted membrane vesicles that share structural and biochemical characteristics with intraluminal vesicles of multivesicular endosomes (MVEs). Exosomes could be involved in intercellular communication and in the pathogenesis of infectious and degenerative diseases. The molecular mechanisms of exosome biogenesis and secretion are, however, poorly understood. Using an RNA interference (RNAi) screen, we identified five Rab GTPases that promote exosome secretion in HeLa cells. Among these, Rab27a and Rab27b were found to function in MVE docking at the plasma membrane. The size of MVEs was strongly increased by Rab27a silencing, whereas MVEs were redistributed towards the perinuclear region upon Rab27b silencing. Thus, the two Rab27 isoforms have different roles in the exosomal pathway. In addition, silencing two known Rab27 effectors, Slp4 (also known as SYTL4, synaptotagmin-like 4) and Slac2b (also known as EXPH5, exophilin 5), inhibited exosome secretion and phenocopied silencing of Rab27a and Rab27b, respectively. Our results therefore strengthen the link between MVEs and exosomes, and introduce ways of manipulating exosome secretion in vivo

Development of a healthy biscuit: an alternative approach to biscuit manufacture

OBJECTIVE: Obesity (BMI >30) and related health problems, including coronary heart disease (CHD), is without question a public health concern. The purpose of this study was to modify a traditional biscuit by the addition of vitamin B(6), vitamin B(12), Folic Acid, Vitamin C and Prebiotic fibre, while reducing salt and sugar. DESIGN: Development and commercial manufacture of the functional biscuit was carried out in collaboration with a well known and respected biscuit manufacturer of International reputation. The raw materials traditionally referred to as essential in biscuit manufacture, i.e. sugar and fat, were targeted for removal or reduction. In addition, salt was completely removed from the recipe. PARTICIPANTS: University students of both sexes (n = 25) agreed to act as subjects for the study. Ethical approval for the study was granted by the University ethics committee. The test was conducted as a single blind crossover design, and the modified and traditional biscuits were presented to the subjects under the same experimental conditions in a random fashion. RESULTS: No difference was observed between the original and the modified product for taste and consistency (P > 0.05). The modified biscuit was acceptable to the consumer in terms of eating quality, flavour and colour. Commercial acceptability was therefore established. CONCLUSION: This study has confirmed that traditional high-fat and high-sugar biscuits which are not associated with healthy diets by most consumers can be modified to produce a healthy alternative that can be manufactured under strict commercial conditions

Differential Regulation and Recovery of Intracellular Ca2+ in Cerebral and Small Mesenteric Arterial Smooth Muscle Cells of Simulated Microgravity Rat

BACKGROUND: The differential adaptations of cerebrovasculature and small mesenteric arteries could be one of critical factors in postspaceflight orthostatic intolerance, but the cellular mechanisms remain unknown. We hypothesize that there is a differential regulation of intracellular Ca(2+) determined by the alterations in the functions of plasma membrane Ca(L) channels and ryanodine-sensitive Ca(2+) releases from sarcoplasmic reticulum (SR) in cerebral and small mesenteric vascular smooth muscle cells (VSMCs) of simulated microgravity rats, respectively. METHODOLOGY/PRINCIPAL FINDINGS: Sprague-Dawley rats were subjected to 28-day hindlimb unweighting to simulate microgravity. In addition, tail-suspended rats were submitted to a recovery period of 3 or 7 days after removal of suspension. The function of Ca(L) channels was evaluated by patch clamp and Western blotting. The function of ryanodine-sensitive Ca(2+) releases in response to caffeine were assessed by a laser confocal microscope. Our results indicated that simulated microgravity increased the functions of Ca(L) channels and ryanodine-sensitive Ca(2+) releases in cerebral VSMCs, whereas, simulated microgravity decreased the functions of Ca(L) channels and ryanodine-sensitive Ca(2+) releases in small mesenteric VSMCs. In addition, 3- or 7-day recovery after removal of suspension could restore the functions of Ca(L) channels and ryanodine-sensitive Ca(2+) releases to their control levels in cerebral and small mesenteric VSMCs, respectively. CONCLUSIONS: The differential regulation of Ca(L) channels and ryanodine-sensitive Ca(2+) releases in cerebral and small mesenteric VSMCs may be responsible for the differential regulation of intracellular Ca(2+), which leads to the altered autoregulation of cerebral vasculature and the inability to adequately elevate peripheral vascular resistance in postspaceflight orthostatic intolerance

The Volunteer Satisfaction Index: A Validation Study in the Chinese Cultural Context

Using a Hong Kong-sourced sample of 261 participants, this study set out to validate the Volunteer Satisfaction Index (VSI) in the Chinese cultural context and to evaluate its psychometric properties. The VSI was originally developed by Galindo-Kuhn and Guzley (2001) to measure the outcomes of volunteer experiences. In this study, exploratory factor analysis (EFA) yielded a different factor structure from that proposed by the scale developer. The three factors found were personal gain, relationship within organization and relationship with peers. Cronbach’s alpha values were high for all three subscales. Results from correlation and regression analysis also confirmed the construct and criterion-related validity of the scale. Thus, the reliability and validity of the scale were confirmed. Implications for the assessment of volunteer satisfaction and further directions for cross-cultural studies on related topics are discussed