bluuebunny/crossref_metadata_2025 huggingface dataset:
Allometry and Metabolic Scaling in Ecology
Authors: Anderson‐Teixeira Kristina J , Savage Van M , Allen Andrew P , Gillooly James F
Published: December 2009

Body size affects the structure and function of all levels of biological organization. In ecological systems, body size strongly influences individuals (e.g. rates of individual growth, reproduction and mortality), populations (e.g. population growth rate, abundance and space use), communities (e.g. community abundance, food‐web structure and interspecific interactions) and ecosystems (e.g. flux, storage and turnover of materials and energy). This is because individual metabolic rate – the rate at which an organism takes up and utilizes energy and materials – is largely controlled by body size. Here we review how body‐size allometries at the individual level affect the structure and function of populations, communities and ecosystems. We use these results to identify and highlight exciting new applications of allometric theory in ecology.

Key concepts:

Body size sets an organism's metabolic rate and thereby controls its rates of growth, reproduction and mortality.

Body size is a key predictor of population growth rate, density and carrying capacity through its effects on individual‐level rates of birth, death and resource use.

Body size influences community structure through its effects on individual‐level resource demands, individual life histories and interspecific interactions.

Body size affects predator–prey dynamics and food‐web interactions partially through its effects on metabolic rate.

The contribution of biota to the cycling of energy and materials in ecosystems is affected by species’ size distributions, and by the flux, storage and turnover of energy and elements in individuals which, in turn, is controlled by metabolic rate.

Allometric models provide a baseline for understanding the structure and function of complex ecological systems, and a means to quantitatively link different levels of biological organization.
Cell Death inC. elegans
Authors: Sendoel Ataman , Hengartner Michael O
Published: December 2009

Programmed cell death plays a central role in the development of most multicellular animals. During the development ofCaenorhabditis elegans, a total of 1090 cells are generated, 131 of which are destined to die. Genetic studies focusing on the control of the fate of these 131 cells revealed an evolutionary conserved set of genes essential for all programmed cell deaths inC. elegans. In a cell undergoing apoptosis, the BH3‐only domain proteinEGL‐1binds to theCED‐9–CED‐4complex on the outer mitochondrial membrane resulting in the release ofCED‐4, which in turn activates the effector caspaseCED‐3. These at the time pioneering findings establishedC. elegansas a prime model system to study apoptosis, a system that still today provides a stage for new inspiring science, such as studies onC. elegansapoptotic cell clearance and on deoxyribonucleic acid (DNA) damage‐induced apoptosis.

Key concepts:

Caenorhabditis elegansas a model organism has been introduced by Sidney Brenner in the 1960s.

The completeC. eleganscell lineage was described in 1983 by John Sulston.

The cell lineage inC. elegansis invariant: during the development of an animal, a total of 1090 cells are generated, 131 of which are destined to die.

The basis for analysing programmed cell death inC. eleganswas delineation of the complete cell lineage.

There are three waves of programmed cell death inC. elegans: a first wave can be observed in embryos, the second smaller wave during the second larval stage, whereas the third wave occurs in the adult germline.

Germline apoptosis is a stochastic process in which half of the germ cells undergo apoptotic cell death.

CED‐4 and CED‐3 are killer proteins essential for all programmed cell deaths inC. elegans.

CED‐9 is homologous to Bcl‐2 and protects from cell death.

In a cell undergoing apoptosis, the BH3‐only domain protein EGL‐1 inhibits CED‐9 from inhibiting CED‐4.

The central cell death pathway is conserved through evolution; homologues of EGL‐1, CED‐9, CED‐4 and CED‐3 are present in mammals, where they control the mitochondrial pathway for apoptosis.

Apoptotic cell clearance is controlled via two partially redundant intracellular signalling cascades that converge at the Rac1 homologue CED‐10.

DNA damage‐induced germline apoptosis is triggered by a genomic integrity checkpoint and activates a pathway including the p53 homologue CEP‐1.
Structures, Domains and Functions in Cell Death (
DD
,
DED
,
CARD
,
PYD
)
Authors: Wu Hao , Lo Yu‐Chih
Published: December 2009

The death domain (DD), death effector domain (DED), caspase‐recruitment domain (CARD) and pyrin domain (PYD) are subfamilies of the DD superfamily. By mediating homotypic interactions, these proteins play important roles in the assembly and activation of apoptotic signalling complexes. They are responsible for caspase recruitment and for formation of oligomeric platforms for signalling. DD superfamily proteins have a common six‐helical bundle fold and show different surface features for each of the subfamilies. Most interestingly, the homotypic interactions within each subfamily are mostly mediated by asymmetric contacts, in which different surfaces of the interaction partners are adjacent to each other. The DD superfamily proteins appear to use three common types of asymmetric interactions to assemble into large oligomeric complexes.

Key concepts

Death domains (DDs), death effector domains (DEDs), caspase‐recruitment domains (CARDs) and pyrin domains (PYDs) are protein:protein interaction modules for formation of caspase‐activating complexes.

DDs, DEDs, CARDs and PYDs share a common six‐helical bundle fold.

Interactions within these domains are mostly asymmetric and conserved.
Evolution of Caspase‐1 Inhibitors
Authors: da Cunha Julia Pinheiro Chagas , Galante Pedro Alexandre F , de Souza Sandro José
Published: December 2009

CARD only protein 1 (
COP1
), inhibitory caspase recruitment domain (INCA) and ICEBERG are caspase recruitment domain (CARD)‐only proteins that inhibit the activation of cysteine‐dependent
ASPartyl‐specific proteASE
(caspase)‐1 or CASP‐1. Although CASP‐1 is widespread in vertebrates, CASP‐1 inhibitors are exclusively found in primates. The most ancient CASP‐1 inhibitor was found in the genome of a tree shrew, an ancestor of primates. The inhibitors are mapped in tandem at human chromosome 11 and their origin is directly and indirectly related to CASP‐1 gene duplications. Different stop codons arose in the duplicated copies just upstream of the catalytic domain of CASP‐1 generating CARD‐only proteins. In this review we discuss the most recent findings regarding the evolution of both caspases and their inhibitors.

Key concepts

COP, INCA and ICEBERG are CASP‐1 inhibitors.

COP, INCA and ICEBERG arose directly or indirectly from CASP‐1 duplications.

Procaspase‐1 contains a CARD and peptidase C14 domain, but the inhibitors contain only the CARD domain.

Stop codons upstream of the peptidase C14 domain where important for the generation of CASP‐1 inhibitors.
Evolution of Traits Deduced from Genome Comparisons
Authors: Tung Jenny , Wray Gregory A
Published: December 2009

One of the major aims in evolutionary enomics is to leverage comparative genomic data sets to understand the evolution of adaptively important traits. These comparisons may occur at multiple scales, but can be roughly classed into those that focus on differences between closely related species and those that aim to explain broad patterns across diverse groups of organisms. Perhaps the most significant contributions of genome comparisons thus far have been in highlighting broad evolutionary trends, such as identifying gene sets or pathways that have been adaptively important in the evolution of specific lineages, including our own. In contrast, the establishment of concrete links between genetic variation and specific traits remains rare, despite a handful of exciting early successes. We anticipate that the addition of more genome sequences will rapidly advance the field. In particular, we look forward to increasing integration between comparative genomic analyses and ecological and phenotypic data sets.

Key concepts:

Comparisons between closely related species allow investigators to search for the genetic basis of recently evolved differences that distinguish those species.

Comparisons across organisms that share a distant common ancestor allow investigators to search for the genetic basis of major shared differences that define these groups of related organisms.

Genome comparisons often identify broad trends in trait evolution instead of specific genetic differences that influence a specific trait.

Identification of specific genes that influence a specific trait requires not only genome‐scale comparisons but also statistical filtering and experimental validation.

Identification of regions of the genome that evolved under positive selection or that are functionally important is a useful method for narrowing down genome‐wide differences to those that are most likely to have phenotypic effects.
Evolution and Organization of Monotreme Sex Chromosomes
Authors: Grützner Frank
Published: December 2009

Monotremes have an unusually complex sex chromosome system which shares extensive homology to bird sex chromosomes and no homology to sex chromosomes in other mammals. This has entirely changed the way we think about the evolution of sex chromosomes in mammals as it suggests that birds and early mammals shared the sex chromosomes which evolved in the reptilian common ancestor. The sex chromosomes of marsupial and eutherian mammals have evolved much later, after the divergence of monotremes. With 10 sex chromosomes in platypus and 9 sex chromosomes in echidna, monotremes feature the most complex sex chromosomes system described in any mammal. This remarkably complex sex chromosome system raises fundamental questions about its evolution, meiotic organization and dosage compensation and about sex determination in monotremes.

Key concepts

Monotremes
are the only egg‐laying mammals. Because they diverged earlier than any other living mammal they provide unique insights into mammalian evolution.

Sex chromosomes
can be found in various plant and animal species and play an important role in determining sex. In contrast to autosomes most sex chromosomes show cytologically detectable differences in the heterogametic sex (e.g. X‐ and Y‐chromosome in male mammals and Z‐ and W‐chromosome in female birds).

Most sex chromosome systems comprise one or two chromosomes (XX/XY, X0/XX, ZZ/ZW) but translocations between autosomes and sex chromosomes can occasionally lead to
multiple sex chromosomes
.

Sex chromosomes evolved
from autosomes by suppression of recombination and accumulation of sexual antagonistic genes (genes that are beneficial for one of the two sexes), which leads to differentiation of the two sex chromosomes.

At
meiosis
homologous chromosomes pair, recombine and segregate into haploid gametes (sperms and eggs).

Sex chromosome pairing at meiosis is incomplete and leads to
meiotic sex chromosome inactivation
of both X‐ and Y‐chromosome which become visible as so‐called sex body during male meiosis.

The massive gene loss on Y‐ and W‐chromosome leads to a dosage imbalance between homogametic (ZZ or XX) and heterogametic (XY or ZW) sex.
Dosage compensation mechanisms
lead to silencing or upregulation of genes on X‐ or Z‐chromosome to balance gene dosage between sexes.

In most mammals, dosage compensation is achieved by
X‐chromosome inactivation
of one of the X‐chromosomes in XX females.

Sex determination
is a developmental process where two very different organs (i.e. testis and ovary) develop from undifferentiated germ cells during a critical window at early embryo development.
OPA
1 and Its Clinical Implications
Authors: Trevisson Eva , Salviati Leonardo , Scorrano Luca
Published: December 2009

Autosomal dominant optic atrophy (ADOA) or Kjer disease (MIM #
165500
) is a primary inherited nonsyndromic optic neuropathy that results in loss of retinal ganglion cells, leading to the clinical appearance of optic atrophy. It is caused by mutations in
optic atrophy 1
(
OPA1
), a dynamin‐related protein of the inner mitochondrial membrane. Recent evidence supports a role for
OPA1
in the regulation of the process of cristae remodelling during apoptosis, by which the complete release of mitochondrial stores of cytochrome
c
is achieved, supporting a role for apoptosis in the pathogenesis of ADOA. Here we review the basic clinical features of ADOA, the biology of
OPA1
and its role in the regulation of mitochondrial shape changes during apoptosis.

Key concepts

Mitochondrial shape changes during apoptosis.

Cristae are the main store of cytochrome
c
.

The complete release of cytochrome
c
is accompanied by the remodelling of the cristae.

The dynamin‐related protein OPA1 regulates the shape of the cristae.

Dis‐oligomerization of OPA1 is a key event in the release of cytochrome
c
during apoptosis.
Stem Cell Niches in
Drosophila
Authors: Yamashita Yukiko M
Published: December 2009

Adult stem cells supply a continual source of highly differentiated cells throughout the life of an organism. They are able to maintain an undifferentiated state and possess unlimited proliferation capacity. Many stem cells reside in a special microenvironment known as a niche that specifies stem cell identity and protects them from differentiation by providing essential molecular signals. Because of its essential requirement to maintain stem cells, the stem cell niche also limits the number of stem cells, safeguarding against cancer.

Drosophila melanogaster

has served as an ideal model system to study stem cells and their niches, thanks to the well‐understood signalling pathways, elegant genetics and relatively simple anatomy. Studies in

Drosophila

have provided a fundamental framework for understanding mammalian stem cells and their niches. Here, I give an overview of how stem cells are regulated by their niches in

Drosophila

.

Key concepts

Adult stem cells: Cells found in adult tissues that are capable of proliferation over a prolonged time period (throughout the life of the organism) and of further differentiation to produce various types of differentiated cells in the tissue.

Self‐renewal: The phenomenon by which stem cells produce stem cells on cell division. Stem cell characteristics, including undifferentiated state, proliferative potential and developmental potential to differentiate, are maintained.

Niche: A microenvironment in which stem cell characteristics (such as stem cell identity and proliferation potential) are maintained.

Asymmetric stem cell division: A form of stem cell division in which one stem cell and one differentiated cell are created, thereby maintaining stem cell number.
Cytoskeleton in Axon Growth
Authors: Stiess Michael , Bradke Frank
Published: December 2009

During development, neurons extend two different types of processes, typically several short dendrites and one long axon. The axon forms synapses with dendrites of other neurons to integrate into a neuronal network. Axons can extend to enormous lengths. Their growth is guided and exactly controlled to guarantee the correct neuronal connections. Microtubules and actin filaments, the two major cytoskeletal elements, are the key players in these processes. They form the backbone for axon extension, provide the construction material for axon elongation, and are the site of convergence of extracellular and intrinsic signals. Correct path finding of the axon is ensured by a specialized and highly dynamic structure at the tip of the growing axon, the growth cone. Its dynamic cytoskeleton is the machinery that establishes, controls and directs axon growth. Overall, the cytoskeleton determines the distinction of axons and dendrites and aberrant changes in the cytoskeleton are a major cause of regenerative failure after spinal cord injury.

Key concepts:

The growth cone is the highly motile tip of a growing axon, where the axon becomes elongated.

Growth cone motility is regulated by cytoskeletal dynamics.

Actin filaments determine growth cone shape and are involved in path finding.

Microtubules give structure to the axon shaft and are essential for axon elongation.

Guidance cues act on the cytoskeleton in the growth cone.

A dynamic interaction between actin filaments and microtubules is necessary to steer axon growth.

The cytoskeleton regulates neuronal polarity.

Injury induced pathological changes of the cytoskeleton are a major cause for lack of regeneration after spinal cord injury.
Theory of Cooperation
Authors: Gardner Andy , Griffin Ashleigh S , West Stuart A
Published: December 2009

Cooperation is defined as any adaptation that has evolved, at least in part, to increase the reproductive success of the actor's social partners. Inclusive fitness theory reveals that cooperation can be favoured by natural selection owing to either direct fitness benefits (mutually beneficial cooperation) or indirect fitness benefits (altruistic cooperation). Direct fitness benefits can arise as a simple byproduct of cooperation, or else owing to the existence of enforcement mechanisms, which may be fixed or conditioned according to the individual's cooperative behaviour. Indirect fitness benefits can arise when cooperation occurs between genetically similar individuals, as a consequence of limited dispersal, kin discrimination or greenbeard mechanisms. These theoretical mechanisms are illustrated with empirical examples, from laboratory experiments to field studies.

Key concepts:

The function of Darwinian adaptation is to maximize the organism's inclusive fitness.

Inclusive fitness describes how well an organism transmits copies of its genes to future generations.

Direct fitness is the part of inclusive fitness that comes from the organism's own reproductive success.

Indirect fitness is the part of inclusive fitness that comes from the reproductive success of the organism's genetic relatives.

Cooperation is any adaptation whose function is, at least in part, to increase the reproductive success of a social partner.

Cooperation is mutually beneficial if the actor also benefits and altruistic if the actor suffers a net loss of reproductive success.

Mutually beneficial cooperation is favoured by direct fitness benefits.

Direct fitness benefits can arise as a byproduct or owing to enforcement mechanisms.

Altruistic cooperation is favoured by indirect fitness benefits.

Indirect fitness benefits can arise as a consequence of limited dispersal, kin discrimination or greenbeard mechanisms.
From Reactive Oxygen and Nitrogen Species to Therapy
Authors: McKercher Scott R , Nakamura Tomohiro , Lipton Stuart A
Published: December 2009

Excessive free radicals, including reactive oxygen species (ROS) and nitric oxide (NO), contribute to pathological production of misfolded proteins, synaptic damage and apoptosis. Misfolded protein aggregates occur in several chronic neurodegenerative disorders, including Parkinson and Alzheimer diseases. In rare cases, the cause is a genetic mutation; the majority is sporadic and may be a response to environmental factors that generate free radicals. Overactivity of the
N
‐methyl‐
d
‐aspartate (NMDA)‐subtype of glutamate receptor can generate ROS and NO species that mediate protein misfolding, synaptic damage and apoptosis, and thus, neurodegenerative disease. We review current evidence that excessive ROS and NO contribute to protein misfolding by
S
‐nitrosylation of the
E3 ubiquitin ligase
parkin and
protein‐disulfide isomerase
. We also discuss NMDA receptor antagonists memantine and NitroMemantine, drugs that block excessive glutamate excitation, thereby limiting production of ROS and NO, and therapeutic electrophiles, drugs that protect cells from oxidative stress by activating the Nrf2 transcriptional pathway.

Key Concepts:

S
‐nitrosylation or transfer of the NO group to critical cysteine thiol can regulate protein function.

Under pathological circumstances, aberrant
S
‐nitrosylation reactions can contribute to protein misfolding, neuronal injury and neurodegeneration.
The Molecular Genetics of Type 2 Diabetes: Past, Present and Future
Authors: Tan Jonathan T , Chia Kee Seng , Ku Chee Seng
Published: December 2009

Type 2 diabetes is a metabolic disorder which is characterized by elevated blood glucose levels. This common disease affects more than 170 million individuals worldwide. It is a complex disease caused by a combination of multiple genetic factors and environmental exposures. Early attempts to decipher the genetics of type 2 diabetes achieved limited success with only a handful of loci identified showing convincing association. However, with the advent of genome‐wide association studies, much progress has been made in recent years in understanding the genetics of type 2 diabetes. Over a dozen novel susceptibility loci showing consistent and robust associations across different populations have been identified, with the risk associated with the majority of these loci exerting their effect through pancreatic β‐cell dysfunction, leading to impairment in insulin secretion, in the patho‐physiology of diabetes.

Key concepts

Type 2 diabetes is characterized by hyperglycaemia (elevated blood glucose level) as a consequence of the body's inability to maintain blood glucose homeostasis.

This common disease affects more than 170 million individuals worldwide, and this has been projected to increase to over 360 million by 2030.

It is a polygenic disease with many genetic variants, each contributing a modest effect with additional gene–gene and gene–environment interactions adding further complexity.

As with many other complex diseases, the molecular pathways or mechanisms underlying the development of type 2 diabetes have remained poorly understood.

Genetic studies of diseases have traditionally relied on two methods to discover the responsible genes: whole genome linkage mapping and candidate gene association studies.

Genetic studies of the past were largely unsuccessful with only a handful of loci showing convincing association with type 2 diabetes.

Genome‐wide association study is a comprehensive and unbiased approach of interrogating a large number of genetic markers across the genome to identify statistical association between genetic variants and phenotypes.

In contrast to linkage studies, it is usually carried out in unrelated individuals, and unlike candidate gene studies, it does not require any prior supposition of the biological function of genes or pathogenesis of the disease.

The findings from genome‐wide association studies have made some advances in our understanding and knowledge of the genetic basis of this common disease, and it has also implicated the importance of β‐cell dysfunction and impairment in insulin secretion in the patho‐physiology of type 2 diabetes.

Cumulatively, all the type 2 diabetes susceptibility SNPs that have been identified account for only a small proportion of the heritability (approximately 10%); with the majority of the genetic predisposition remaining unexplained, indicating that much still remains to be discovered and understood of the genetic basis of this complex disease.
Comparison of nanoclay and carbon nanofiber particles on rheology of molten polystyrene nanocomposites under supercritical carbon dioxide
Authors: Guo Zhihua , Yeh Shu‐Kai , Wingert Maxwell J. , Ellis Jeffrey L. , Tomasko David L. , Lee L. James
Published: December 2009

The effects of nanoparticles and high‐pressure carbon dioxide (CO2) on shear viscosity of polystyrene (PS) were studied. Master curves of PS, PS + 5 wt % carbon nanofibers (CNFs), and PS + 5 wt % nanoclay (Southern Clay 20A) without CO2 were created based on parallel‐plate measurements. The results showed that addition of nanoparticles increased the viscosity of the neat polymer. Steady‐state shear viscosity of PS in the presence of CO2 and nanoparticles was measured by a modified Couette rheometer. The effect of supercritical CO2 on these systems was characterized by shift factors. It was found that under the same temperature and CO2 pressure, CO2 reduced the viscosity less for both PS‐20A and PS‐CNFs than neat PS. Between the two types of nanoparticles, CNFs showed a larger viscosity reduction than 20A, indicating a higher CO2 affinity for CNFs than 20A. However, the advantage of CNFs over 20A for larger viscosity reduction decreased with higher temperature. A gravimetric method (magnetic suspension balance) was used to measure the excess adsorption of CO2 onto CNFs and nanoclay, thus, CO2 showed a higher affinity for CNFs. © 2009 Wiley Periodicals, Inc. J Appl Polym Sci, 2010
Metabolic stability and determination of cytochrome P450 isoenzymes' contribution to the metabolism of medetomidine in dog liver microsomes
Authors: Duhamel Marie‐Claude , Troncy Éric , Beaudry Francis
Published: December 2009

Medetomidine is a potent and selectiveα2‐adrenergic agonist. The activation ofα2‐adrenergic receptor mediates a variety of effects including sedation, analgesia, relief of anxiety, vasoconstriction and bradycardia. However, our main interest is the sedative effects of medetomidine when used as a premedicant prior surgery in companion animals, especially in dogs. Recently, data suggested that following intravenous infusion at six dosing regiments non‐linear pharmacokinetics was observed. Major causes of non‐linear pharmacokinetics are the elimination of the drug not following a simple first‐order kinetics and/or the elimination half‐life changing due to saturation of an enzyme system. The goal of this study was to establish the metabolic stability and determine the metabolic pathway of medetomidine in dog liver microsomes. Consequently, Michaelis–Menten parameters (Vmax,Km),T1/2andCLiwere determined. The incubations were performed in a microcentrifuge tube and containing various concentrations of medetomidine (10–5000 nm), 1 mg/mL of microsomal proteins suspended in 0.1 mphosphate buffer, pH 7.4. Microsomal suspensions were preincubated with NADPH (1 mm) for 5 min at 37°C prior to fortification with medetomidine. Samples were taken at various time points for kinetic information and the initial velocity (vi) was determined after 10 min incubation. The reaction was stopped by the addition of an internal standard solution (100 ng/mL of dextrometorphan in acetone). Medetomidine concentrations were determined using a selective and sensitive HPLC‐ESI/MS/MS method. Using non‐linear regression, we determined aKmvalue of 577 nm, indicating relatively low threshold enzyme saturation consistent with previousin vivoobservation. The metabolic stability was determined at a concentration of 100 nm(≪Km) and the observedT1/2was 90 min with aCLiof 0.008 mL/min indicating moderately low clearance in dog liver microsomes, also consistent with previousin vivodata. Moreover, results suggest that principally medetomidine is metabolized by the CYP3A with a small contribution from CYP2D and CYP2E. The participation of CYP3A is an important discovery since medetomidine is used as a premedicant in combination with fentanyl, ketamine and/or midazolam. These findings combined with a lowKmvalue may indicate that medetomidine can competitively inhibit the metabolism of these drugs and consequently significantly impair metabolic clearance. Copyright © 2009 John Wiley & Sons, Ltd.
Amino Acid Based Low‐Molecular‐Weight Ionogels as Efficient Dye‐Adsorbing Agents and Templates for the Synthesis of TiO2 Nanoparticles
Authors: Dutta Sounak , Das Dibyendu , Dasgupta Antara , Das Prasanta Kumar
Published: December 2009

The gelation of ionic liquids is attracting significant attention because of its large spectrum of applications across different disciplines. These ‘green solvents’ have been the solution to a number of common problems due to their eco‐friendly features. To expand their applications, the gelation of ionic liquids has been achieved by using amino acid‐based low‐molecular‐weight compounds. Variation of individual segments in the molecular skeleton of the gelators, which comprise the amino acid and the protecting groups at the N and C termini, led to an understanding of the structure–property correlation of the ionogelation process. An aromatic ring containing amino acid‐based molecules protected with a phenyl or cyclohexyl group at the N terminus were efficient in the gelation of ionic liquids. In the case of aliphatic amino acids, gelation was more prominent with a phenyl group as the N‐terminal protecting agent. The probable factors responsible for this supramolecular association of the gelators in ionic liquids have been studied with the help of field‐emission SEM, 1H NMR, FTIR, and luminescence studies. It is the hydrophilic–lipophilic balance that needs to be optimized for a molecule to induce gelation of the green solvents. Interestingly, to maximize the benefits from using these green solvents, these ionogels have been employed as templates for the synthesis of uniform‐sized TiO2 nanoparticles (25–30 nm). Furthermore, as a complement to their applications, ionogels serve as efficient adsorbents of both cationic and anionic dyes and were distinctly better relative to their organogel counterparts.
PDF receptor expression reveals direct interactions between circadian oscillators in drosophila
Authors: Im Seol Hee , Taghert Paul H.
Published: December 2009

Daily rhythms of behavior are controlled by a circuit of circadian pacemaking neurons. In Drosophila, 150 pacemakers participate in this network, and recent observations suggest that the network is divisible into M and E oscillators, which normally interact and synchronize. Sixteen oscillator neurons (the small and large lateral neurons [LNvs]) express a neuropeptide called pigment‐dispersing factor (PDF) whose signaling is often equated with M oscillator output. Given the significance of PDF signaling to numerous aspects of behavioral and molecular rhythms, determining precisely where and how signaling via the PDF receptor (PDFR) occurs is now a central question in the field. Here we show that GAL4‐mediated rescue of pdfr phenotypes using a UAS‐PDFR transgene is insufficient to provide complete behavioral rescue. In contrast, we describe a ∼70‐kB PDF receptor (pdfr) transgene that does rescue the entire pdfr circadian behavioral phenotype. The transgene is widely but heterogeneously expressed among pacemakers, and also among a limited number of non‐pacemakers. Our results support an important hypothesis: the small LNv cells directly target a subset of the other crucial pacemaker neurons cells. Furthermore, expression of the transgene confirms an autocrine feedback signaling by PDF back to PDF‐expressing cells. Finally, the results present an unexpected PDF receptor site: the large LNv cells appear to target a population of non‐neuronal cells that resides at the base of the eye. J. Comp. Neurol. 518:1925–1945, 2010. © 2009 Wiley‐Liss, Inc.
Trans‐free fats through interesterification of canola oil/palm olein or fully hydrogenated soybean oil blends
Authors: Farmani Jamshid , Safari Mohammad , Hamedi Manouchehr
Published: December 2009

Binary blends of canola oil (CO) and palm olein (POo) or fully hydrogenated soybean oil (FHSBO) were interesterified using commercial lipase, Lypozyme TL IM, or sodium methoxide. Free fatty acids (FFA) and soap content increased and peroxide value (PV) decreased after enzymatic or chemical interesterification. No difference was observed between the PV of enzymatically and chemically interesterified blends. Enzymatically interesterified fats contained higher FFA and lower soap content than chemically prepared fats. Slip melting point (SMP) and solid‐fat content (SFC) of CO and POo blends increased, whereas those of CO and FHSBO blends decreased after chemical or enzymatic interesterification. Enzymatically interesterified CO and POo blends had lower SMP and SFC (at some temperatures) than chemically interesterified blends. The status was reverse when comparing chemically and enzymatically interesterified CO and FHSBO blends. The induction period for oxidation at 120°C of blends decreased after interesterification. However, chemically interesterified blends were more oxidatively stable than enzymatically interesterified blends. Interesterified blends of CO and POo or FHSBO displayed characteristics suited to application as trans‐free soft tub, stick, roll‐in and baker's margarine, cake shortening and vanaspati fat.
Variability of the essential oil composition in the sage collection of the Genebank Gatersleben: a new viridiflorol chemotype
Authors: Lamien‐Meda Aline , Schmiderer Corinna , Lohwasser Ulrike , Börner Andreas , Franz Chlodwig , Novak Johannes
Published: December 2009

The variation in quantity and quality of the essential oils of garden sage (Salvia officinalis L.) collection, cultivated at the Leibniz Institute of Plant Genetics and Crop Plant Research in Gatersleben, Germany, was studied. The aerial parts of 10 individual plants per accession (19 accessions) were collected at the beginning of the flowering period in two consecutive years from the same experimental field, and essential oil (EO) content and composition were analysed. The EO quantity was in the ranges 0.3–2.2% w/w in the first year and 0.9–2.5% w/w in the second year. The highest EO content was observed in a Croatian accession. The mean EO quantities in the second year were 1–1.6‐fold higher than in the first year, and the correlation between the two years' EO content was 0.77. The essential oil composition was not variable from 2007 to 2008 and was comparable to results already published, with the exception of two accessions from Romania with viridiflorol as dominant compound and low amounts of α‐ and β‐thujone, representing a new Salvia officinalis chemotype which would be ideal and safer for drinks and meals. Copyright © 2009 John Wiley & Sons, Ltd.
Three Terpenoids and a Tocopherol‐Related Compound from Ricinus communis
Authors: Tan Qin‐Gang , Cai Xiang‐Hai , Du Zhi‐Zhi , Luo Xiao‐Dong
Published: December 2009

Four new compounds named (3E,7Z,11E)‐19‐hydroxycasba‐3,7,11‐trien‐5‐one (1), 6α‐hydroxy‐10β‐methoxy‐7α,8α‐epoxy‐5‐oxocasbane‐20,10‐olide (2), 15α‐hydroxylup‐20(29)‐en‐3‐one (3), and (2R,4aR, 8aR)‐3,4,4a,8a‐tetrahydro‐4a‐hydroxy‐2,6,7,8a‐tetramethyl‐2‐(4,8,12‐trimethyltridecyl)‐2H‐chromene‐5,8‐dione (4) were isolated from the MeOH extracts of the aerial parts of Ricinus communis L. by chromatographic methods. Their structures were elucidated by extensive spectroscopic experiments.
Analytical model for fully three‐dimensional radial dispersion in a finite‐thickness aquifer
Authors: Chen Jui‐Sheng
Published: December 2009

Analytical solutions for contaminant transport in a non‐uniform flow filed are very difficult and relatively rare in subsurface hydrology. The difficulty is because of the fact that velocity vector in the non‐uniform flow field is space‐dependent rather than constant. In this study, an analytical model is presented for describing the three‐dimensional contaminant transport from an area source in a radial flow field which is a simplest case of the non‐uniform flow. The development of the analytical model is achieved by coupling the power series technique, the Laplace transform and the two finite Fourier cosine transform. The developed analytical model is examined by comparing with the Laplace transform finite difference (LTFD) solution. Excellent agreements between the developed analytical model and the numerical model certificate the accuracy of the developed model. The developed model can evaluate solution for Peclet number up to 100. Moreover, the mathematical behaviours of the developed solution are also studied. More specifically, a hypothetical convergent flow tracer test is considered as an illustrative example to demonstrate the three‐dimensional concentration distribution in a radial flow field. The developed model can serve as benchmark to check the more comprehensive three‐dimensional numerical solutions describing non‐uniform flow contaminant transport. Copyright © 2009 John Wiley & Sons, Ltd.
miR‐212 is downregulated and suppresses methyl‐CpG‐binding protein MeCP2 in human gastric cancer
Authors: Wada Rie , Akiyama Yoshimitsu , Hashimoto Yutaka , Fukamachi Hiroshi , Yuasa Yasuhito
Published: December 2009

To clarify the role of micro (mi) RNAs in gastric carcinogenesis, we studied the expression and function of miRNAs in gastric carcinoma (GC) cells. Initially, we performed microarray analysis using total RNA from 3 human GC cell lines and noncancerous gastric tissue. Among the downregulated miRNAs in GC cells, miR‐212 expression was decreased in all 8 GC cell lines examined and a significant decrease of miR‐212 expression in human primary GC tissues was also observed in 6 of 11 cases. Transfection of the precursor miR‐212 molecule induced decreased growth of 3 GC cell lines. Using 3 different databases, methyl‐CpG‐binding protein MeCP2 was postulated to be a target of miR‐212. As seen on reporter assaying, miR‐212 repressed the construct with the MECP2 3′‐UTR. Ectopic expression of miR‐212 repressed expression of the MeCP2 protein but not the MECP2 mRNA level. These data suggest that downregulation of miR‐212 may be related to gastric carcinogenesis through its target genes, such as MECP2.
TGF‐β inactivation and TGF‐α overexpression cooperate in an in vivo mouse model to induce hepatocellular carcinoma that recapitulates molecular features of human liver cancer
Authors: Baek Ji Yeon , Morris Shelli M. , Campbell Jean , Fausto Nelson , Yeh Matthew M. , Grady William M.
Published: December 2009

Hepatocellular carcinoma (HCC) results from the cumulative effects of deregulated tumor suppressor genes and oncogenes. The tumor suppressor and oncogenes commonly affected include growth factors, receptors and their downstream signaling pathway components. The overexpression of transforming growth factor alpha (TGF‐α) and the inhibition of TGF‐β signaling are especially common in human liver cancer. Thus, we assessed whether TGF‐α overexpression and TGF‐β signaling inactivation cooperate in hepatocarcinogenesis using an in vivo mouse model, MT1/TGFa;AlbCre/Tgfbr2flx/flx mice (“TGFa;Tgfbr2hepko”), which overexpresses TGF‐α and lacks a TGF‐β receptor in the liver. TGF‐β signaling inactivation did not alter the frequency or number of cancers in mice with overexpression of TGF‐α. However, the tumors in the TGFa;Tgfbr2hepko mice displayed increased proliferation and increased cdk2, cyclin E and cyclin A expression as well as decreased Cdkn1a/p21 expression compared to normal liver and compared to the cancers arising in the TGF‐α overexpressing mice with intact TGF‐β receptors. Increased phosphorylated ERK1/2 expression was also present in the tumors from the TGFa;Tgfbr2hepko mice and correlated with downregulated Raf kinase inhibitor protein expression, which is a common molecular event in human HCC. Thus, TGF‐β signaling inactivation appears to cooperate with TGF‐α in vivo to promote the formation of liver cancer that recapitulates molecular features of human HCC.
Cracking down on youth tobacco may influence drug use
Authors: Jason Leonard A. , Pokorny Steven B. , Adams Monica , Nihls Annie , Kim Hyo Yeon , Hunt Yvonne
Published: December 2009

This study evaluated the influence of tobacco possession–use–purchase (PUP) law enforcement and illicit drug use and offers. Twenty‐four towns were randomly assigned into two conditions. Both conditions focused on reducing minors' access to commercial sources of tobacco. The communities assigned to the experimental condition also increased their PUP law enforcement, whereas among communities in the control condition, PUP law enforcement remained at low levels. A hierarchical linear modeling analytical approach was selected due to the multilevel data and nested design. The likelihood of a child currently using drugs, ever having used drugs, or illicit drug offers was lower in the experimental versus control conditions. These outcomes suggest that police efforts to reduce specific substance use behaviors (i.e., underage tobacco use) may have a positive spillover effect and help reduce teen drug use and illicit drug offers. © 2009 Wiley Periodicals, Inc.
20,23‐dihydroxyvitamin D3, novel P450scc product, stimulates differentiation and inhibits proliferation and NF‐κB activity in human keratinocytes
Authors: Janjetovic Zorica , Tuckey Robert C. , Nguyen Minh N. , Thorpe Edwin M. , Slominski Andrzej T.
Published: December 2009

We have examined effects of the 20,23‐dihydroxyvitamin D3 (20,23(OH)2D3), on differentiation and proliferation of human keratinocytes and the anti‐inflammatory potential of 20,23(OH)2D3 from its action on nuclear factor‐κB (NF‐κB). 20,23(OH)2D3 inhibited growth of keratinocytes with a potency comparable to that for 1,25‐dihydroxyvitamin D3 (1,25(OH)2D3). Cell cycle analysis showed that this inhibition was associated with G1/G0 and G2/M arrests. 20,23(OH)2D3 stimulated production of involucrin mRNA and inhibited production of cytokeratin 14 mRNA in a manner similar to that seen for 1,25(OH)2D3. Flow cytometry showed that these effects were accompanied by increased involucrin protein expression, and an increase in the cell size and granularity. Silencing of the vitamin D receptor (VDR) by corresponding siRNA abolished the stimulatory effect on involucrin gene expression demonstrating an involvement of VDR in 20,23(OH)2D3 action. This mode of action was further substantiated by stimulation of CYP24 gene expression and stimulation of the CYP24 promoter‐driven reporter gene activity. 20,23(OH)2D3 displayed several fold lower potency for induction of CYP24 gene expression than 1,25(OH)2D3. Finally, 20,23(OH)2D3 inhibited the transcriptional activity of NF‐κB in keratinocytes as demonstrated by EMSA, NF‐κB‐driven reporter gene activity assays and measurements of translocation of p65 from the cytoplasm to the nucleus. These inhibitory effects were connected with stimulation of the expression of IκBα with subsequent sequestration of NF‐κB in the cytoplasm and consequent attenuation of transcriptional activity. In summary, we have characterized 20,23(OH)2D3 as a novel secosteroidal regulator of keratinocytes proliferation and differentiation and a modifier of their immune activity. J. Cell. Physiol. 223: 36–48, 2010. © 2009 Wiley‐Liss, Inc.
Genomic organization of microRNAs
Authors: Olena Abigail F. , Patton James G.
Published: December 2009

microRNAs (miRNAs) are small (∼22 nt) noncoding RNAs that have been shown to regulate gene expression post‐transcriptionally. They function by pairing with the 3′ UTR of target mRNAs and repressing translation or by targeting the mRNA for degradation. miRNAs are involved in diverse aspects of development, maintenance, and disease, and are largely evolutionarily conserved in metazoans. Searching the genomes of organisms from viruses to worms to humans has revealed potentially thousands of miRNA genes. Understanding the patterns of genomic organization between species cannot only help to refine tools to identify new miRNAs, but also provide insight into miRNA biogenesis and function. J. Cell. Physiol. 222: 540–545, 2010. © 2009 Wiley‐Liss, Inc.
Upregulation of MMP‐9 production by TNFα in keratinocytes and its attenuation by vitamin D
Authors: Bahar‐Shany K. , Ravid A. , Koren R.
Published: December 2009

MMP‐9, a member of the matrix metalloproteinase family that degrades collagen IV and processes chemokines and cytokines, participates in epidermal remodeling in response to stress and injury. Limited activity of MMP‐9 is essential while excessive activity is deleterious to the healing process. Tumor necrosis factor (TNFα), a key mediator of cutaneous inflammation, is a powerful inducer of MMP‐9. Calcitriol, the hormonally active vitamin D metabolite, and its analogs are known to attenuate epidermal inflammation. We aimed to examine the modulation of MMP‐9 by calcitriol in TNFα‐treated keratinocytes. The immortalized HaCaT keratinocytes were treated with TNFα in the absence of exogenous growth factors or active ingredients. MMP‐9 production was quantified by gelatin zymography and real‐time RT‐PCR. Activation of signaling cascades was assessed by western blot analysis and DNA‐binding activity of transcription factors was determined by EMSA. Exposure to TNFα markedly increased the protein and mRNA levels of MMP‐9, while pretreatment with calcitriol dose dependently reduced this effect. Employing specific inhibitors we established that the induction of MMP‐9 by TNFα was dependent on the activity of the epidermal growth factor receptor, c‐Jun‐N‐terminal kinase (JNK), NFκB and extracellular signal‐regulated kinase‐1/2. The effect of calcitriol was associated with inhibition of JNK activation and reduction of DNA‐binding activities of the transcription factors activator protein‐1 (AP‐1) and NFκB following treatment with TNFα. By down‐regulating MMP‐9 levels active vitamin D derivatives may attenuate deleterious effects due to excessive TNFα‐induced proteolytic activity associated with cutaneous inflammation. J. Cell. Physiol. 222: 729–737, 2010. © 2009 Wiley‐Liss, Inc.
Kinetic properties of ASC protein aggregation in epithelial cells
Authors: Cheng Jun , Waite Andrea L. , Tkaczyk Eric R. , Ke Kevin , Richards Neil , Hunt Alan J. , Gumucio Deborah L.
Published: December 2009

Apoptosis‐associated speck‐like protein with CARD domain (ASC), an adaptor protein composed of caspase recruitment and pyrin domains, can efficiently self‐associate to form a large spherical structure, called a speck. Although ASC aggregation is generally involved with both inflammatory processes and apoptosis, the detailed dynamics of speck formation have not been characterized. In this report, speck formation in HeLa cells transfected with ASC is examined by time‐lapse live‐imaging by confocal laser scanning microscopy. The results show that ASC aggregation is a very rapid and tightly regulated process. Prior to speck formation, soluble ASC aggregation is a low probability event, and the affinity of ASC subunits for one another is very low. Following a speck nucleation event, the affinity for further addition of ASC subunits increases dramatically, and aggregation is a highly energetically favorable reaction (Gibbs free energy ∼ −40 kJ/mol). This leads to a rapid depletion of soluble ASC, making it highly unlikely that a second speck will form inside the same cell and assuring that speck formation is “all or none,” with a well‐defined end point. Comparison with kinetic models of the aggregation process indicates diffusion, instead of active transport, is the dominant process for speck growth. Though speck formation and aggresome formation share some properties, we show that the two processes are distinct. J. Cell. Physiol. 222: 738–747, 2010. © 2009 Wiley‐Liss, Inc.
Nucleophilic debenzoylation of p‐nitrophenyl benzoate in cationic micellar media
Authors: Sar Santosh K. , Rathod Nutan , Pandey Piyush Kant
Published: December 2009

Pseudo‐first‐order rate constants for the nucleophilic debenzoylation reaction of p‐nitrophenyl benzoate with various hydroxamate ions [RC = ONHO−] were investigated in aqueous cationic micellar media at pH 7.8 and 27°C. The kinetic rate data of the reaction revealed that the nucleophilic reactivity sequence of these hydroxamate ions is generally benzohydroxamic acid > salicylhydroxamic acid > acetohydroxamic acid. The kobs value increases upon addition of cationic surfactants to the reaction medium involving interfacial ion exchange between bulk aqueous media and micellar pseudophase. The effect of surfactant head and tail group is discussed. © 2009 Wiley Periodicals, Inc. Int J Chem Kinet 42: 106–112, 2010