bluuebunny/crossref_metadata_2025 huggingface dataset:
A biogeographical study of the threatened ant Dinoponera lucida Emery (Hymenoptera: Formicidae: Ponerinae) using a cytogenetic approach
Authors: MARIANO CLÉA DOS SANTOS FERREIRA , POMPOLO SILVIA DAS GRAÇAS , BARROS LUÍSA ANTÔNIA CAMPOS , MARIANO‐NETO EDUARDO , CAMPIOLO SOFIA , DELABIE JACQUES HUBERT CHARLES
Published: July 2008

Abstract. 

Ants of the genus Dinoponera belong to a convergent group, in which there is no morphologically specialized caste of reproducing females and reproduction is by fertilized workers known as gamergates. Dinoponera lucida Emery, which is native to Brazilian Atlantic rain forest, is included on the official list of Brazilian fauna species threatened with extinction, due to habitat fragmentation, loss of their natural habitat and to peculiarities in their biology.

Karyotype variation was studied among D. lucida populations in the states of Bahia and Espirito Santo, Brazil. The cytogenetic study was carried out on brain ganglia and/or on male and/or female gonads. Banding techniques, such as sequential staining with DA/CMA3/DAPI fluorochromes and FISH, were also applied.

The diploid chromosome numbers ranged from 106 to 120. Variations in the karyotype were detected in the populations from Bahia, while in Espirito Santo the karyotypes were the same everywhere. Most of the chromosomes were small in size and acrocentric, except for a differentiated pair (AMt). This pair exhibited polymorphism in the different populations.

The karyotype variation detected in D. lucida suggested that the original population has previously been divided into two allopatric populations distributed in two different refugial areas of Atlantic rain forest in the early Quaternary. They probably developed in parallel and differentiated in karyotype composition. When the Atlantic rain forest regained its continuous distribution along with the Brazilian coast, the two groups came to occupy the continuous area of occurrence of the species that is seen today.
Parasitism of the beech leaf‐miner weevil in a woodland: patch size, edge effects and parasitoid species identity
Authors: WOODCOCK B. A. , VANBERGEN A. J.
Published: July 2008

Abstract.

Deciduous woodlands are a key habitat for the diversity of invertebrates within the primarily agricultural landscape of lowland Scotland. Little is known, however, of the contribution that within‐site heterogeneity plays in maintaining invertebrate diversity within these habitats. We consider how habitat heterogeneity affects the beech leaf‐mining weevil,Rhynchaenus fagiL. (Curculionidae, Coleoptera), and its associated polyphagous parasitoids.

This was carried out by investigating host density and parasitism rates of the weevil as it fed on 88 beech treesFagus sylvaticaL. (Fagaceae) occurring in patches within a birch woodland. We aimed to assess how patch site, isolation and patch quality influenced parasitism rates and parasitoid diversity.

Herbivore leaf‐mine abundance was greatest where beech trees were located on the edge. Parasitism rates were also affected by the location of the host insect at the woodland edge and interior. Depending on parasitoid species identity, parasitism rates showed independent, direct, and inverse responses to the density of leaf mines. Parasitism rates showed direct and inverse responses to the patch sizes of beech trees, while overall parasitoid diversity was negatively correlated with patch size.

Heterogeneity in the location of the beech trees within this birch woodland plays a key role in determining local patterns of parasitism rates and parasitoid diversity. It is suggested that within‐site variation in the area of high quality resource patches, represented by the beech trees, was key to structuring these parasitoid communities. Niche separation was promoted by individual species’ capacity to locate host insects in this spatially complex habitat.
Cancer stem cells and human malignant melanoma
Authors: Schatton Tobias , Frank Markus H
Published: July 2008

Cancer stem cells (CSC) have been identified in hematological malignancies and several solid cancers. Similar to physiological stem cells, CSC are capable of self‐renewal and differentiation and have the potential for indefinite proliferation, a function through which they may cause tumor growth. Although conventional anti‐cancer treatments might eradicate most malignant cells in a tumor, they are potentially ineffective against chemoresistant CSC, which may ultimately be responsible for recurrence and progression. Human malignant melanoma is a highly aggressive and drug‐resistant cancer. Detection of tumor heterogeneity, undifferentiated molecular signatures, and increased tumorigenicity of melanoma subsets with embryonic‐like differentiation plasticity strongly suggest the presence and involvement of malignant melanoma stem cells (MMSC) in the initiation and propagation of this malignancy. Here, we review these findings in the context of functional properties ascribed to melanocyte stem cells and CSC in other cancers. We discuss the association of deregulated signaling pathways, genomic instability, and vasculogenic mimicry phenomena observed in melanoma subpopulations in light of the CSC concept. We propose that a subset of MMSC may be responsible for melanoma therapy‐resistance, tumor invasiveness, and neoplastic progression and that targeted abrogation of a MMSC compartment could therefore ultimately lead to stable remissions and perhaps cures of metastatic melanoma.
How to make a melanoma: what do we know of the primary clonal events?
Authors: Bennett Dorothy C.
Published: July 2008

Rapid advances have been made in our knowledge of the commonest genetic and epigenetic alterations found in human sporadic melanomas. Valuable recent contributions came from analyses of gene copy number by comparative genome hybridization, and from large‐scale gene expression profiling. All of the commonest affected genes encode regulatory components. Loci with established importance in melanoma, like CDKN2A, BRAF and PTEN, have been joined by some less familiar genes including transcription factor sequences TBX2 and STK11 (LKB). This knowledge is reviewed in relation to the cellular signaling pathways affected by these molecules, their biological outcomes, and the implications as to what changes are required overall to generate a melanoma. The data support a model in which genesis of melanoma requires changes that (1) initiate clonal expansion, (2) overcome cell senescence, and (3) reduce apoptosis.
Meeting Report: Fourth International Congress of the Society for Melanoma Research
Authors: Fisher David E. , Medrano Estela E. , McMahon Martin , Soengas Marisol S. , Schuchter Lynn , Wolchok Jedd D. , Merlino Glenn
Published: July 2008

The 4th international melanoma congress of the Society for Melanoma Research (SMR), organized by Marianne Berwick (University of New Mexico), Paul Chapman (Memorial Sloan‐Kettering Cancer Center), Rene Gonzalez (University of Colorado) and Ze’ev Ronai (Burnham Institute), was held at the Marriott Hotel in downtown New York on November 2007. The congress was attended by a record high number of attendees (over 500 delegates) who joined to discuss recent advances in melanoma biology and therapy. About 40% of the participants arrived from 39 countries, a testament to the high impact of this annual gathering on the international melanoma community. Over 120 of the participants were students or postdoctoral fellows, representing a most impressive fraction of young scientists engaged in melanoma research. The meeting consisted of more than 50 plenary and minisymposia presentations, stimulating the exchange of unpublished data and novel ideas, and helping to forge new collaborations that are anticipated to facilitate significant advances in basic, translational and clinical melanoma research. Another major focus of this meeting was over 160 posters, which were heavily attended and provided an effective forum for extensive informal discussions. This report will highlight the major scientific themes and advances of this most successful meeting, and provide a useful perspective on the current state of melanoma research, as well as where the field should be heading.
Nonalcoholic steatohepatitis and hepatocellular carcinoma in galectin‐3 knockout mice
Authors: Nakanishi Yuko , Tsuneyama Koichi , Nomoto Kazuhiro , Fujimoto Makoto , Salunga Thucydides L. , Nakajima Takahiko , Miwa Shigeharu , Murai Yoshihiro , Hayashi Shinichi , Kato Ichiro , Hiraga Koichi , Hsu Daniel K. , Liu Fu‐Tong , Takano Yasuo
Published: July 2008

Aim: Nonalcoholic fatty liver disease (NAFLD) represents a growing health concern due to its rapidly increasing prevalence worldwide. Nonalcoholic steatohepatitis (NASH) is a progressing form of NAFLD, and recently many studies have reported that it could eventually develop into hepatocellular carcinoma (HCC). We previously reported that 6‐month‐old male galectin‐3 knockout (gal3−/−) mice developed clinicopathological features similar to those of NAFLD in humans. Our aim was to investigate the changes in liver histology in gal3−/−mice by long‐term observation.

Methods: We initially investigated three 15‐month‐old gal3−/−mice, of which two developed multiple liver nodules with dysplastic changes. Then, we histopathologically examined the liver specimens of the 15‐, 20‐ and 25‐month‐old gal3−/−mice and attempted to evaluate the liver morphology by contrast enhanced computed tomography (CT) before sacrifice.

Results: At the age of 15 months or later, gal3−/−mice developed liver nodules with varying degrees of architectural and nuclear atypia based on mild to moderate delicate zone 3 fibrosis. In addition, we successfully confirmed the presence of some of the liver nodules by CT. We report herein that gal3−/−mice develop dysplastic liver nodules and HCC.

Conclusions: We believe that it would be interesting to use this murine model to investigate liver carcinogenesis based on a natural history of NAFLD. Furthermore, CT scanning might be a useful tool for longitudinal evaluation of morphological changesin vivo.
Gene expression profiling of non‐alcoholic steatohepatitis using gene set enrichment analysis
Authors: Yoneda Masato , Endo Hiroki , Mawatari Hironori , Nozaki Yuichi , Fujita Koji , Akiyama Tomoyuki , Higurashi Takuma , Uchiyama Takashi , Yoneda Kyoko , Takahashi Hirokazu , Kirikoshi Hiroyuki , Inamori Masahiko , Abe Yasunobu , Kubota Kensuke , Saito Satoru , Kobayashi Noritoshi , Yamaguchi Naotaka , Maeyama Shiro , Yamamoto Shogo , Tsutsumi Shuichi , Aburatani Hiroyuki , Wada Koichiro , Hotta Kikuko , Nakajima Atsushi
Published: July 2008

Aim:  Non‐alcoholic steatohepatitis (NASH) is a subset of non‐alcoholic fatty liver disease (NAFLD) and sometimes progresses to cirrhosis and liver failure. In this study we analyzed the expression profile of genes and biological pathways involved in NASH in comparison with non‐NASH by gene set enrichment analysis (GSEA) employing a DNA microarray technique.

Methods:  mRNA from liver biopsy specimens was collected from a group of NASH patients and a group of non‐NASH patients. We analyzed the relative abundance of mRNA using high‐density oligonucleotide microarrays containing probes for 54 675 known genes, and investigated the pathogenetic mechanisms of NASH by means of a powerful technique for analyzing molecular profiling data, GSEA.

Results:  The results showed that the level of expression of 27 gene sets was significantly higher and the level of expression of 25 gene sets was significantly lower in the NASH samples than in the non‐NASH samples. Based on these results we created an online, publicly available, searchable database containing the data for the gene expression profiles of the NASH patients (http://www2.genome.rcast.u‐tokyo.ac.jp/___/NASH/NASH_GSEA2/).

Conclusion:  Our data revealed differences in expression of many gene sets that are involved in the pathogenesis of NASH.
Growth hormone excess and the development of growth hormone receptor antagonists
Authors: Higham C. E. , Trainer P. J.
Published: July 2008

In 1990, a single amino acid substitution in the growth hormone (GH) gene at position 119 was found to transform the consequent protein from an agonist to an antagonist at the growth hormone receptor (GHR). Further amino acid substitutions plus prolongation of the half‐life of the protein by pegylation resulted in the first clinically effective GHR antagonist, pegvisomant. Following extensive clinical trials, this medication has emerged as the most efficacious therapy for treatment‐resistant acromegaly. Subsequent advances in our understanding of GH–GHR interactions and downstream GH signalling pathways suggest that pegvisomant binds to preformed GHR dimers and prevents rotational changes within the receptor–GH complex necessary for intracellular signalling to occur. This article reviews the discovery of pegvisomant, from initial experimental data to successful licensing of the drug for treatment‐resistant acromegaly, and discusses its other potential therapeutic uses in diseases with abnormalities in the GH–IGF‐I axis.
AKAP150‐anchored PKA activity is important for LTD during its induction phase
Authors: Lu Yuan , Zhang Mingxu , Lim Indra A. , Hall Duane D. , Allen Margaret , Medvedeva Yuliya , McKnight G. Stanley , Usachev Yuriy M. , Hell Johannes W.
Published: July 2008

Protein kinase A (PKA) is thought to tonically maintain an enhanced level of postsynaptic AMPA receptor responses. Injection of PKA inhibitory peptides leads to a run‐down of AMPA receptor responses and prevents long‐term depression (LTD). This run‐down of AMPA receptor activity was proposed to occlude a further reduction that would otherwise constitute LTD. PKA is recruited to postsynaptic sites by the A kinase anchor protein AKAP150. We found that LTD was strongly impaired in acute hippocampal slices from 2‐week‐old mice in which the PKA binding site on AKAP150 had been genetically deleted (D36 mice). However, basal postsynaptic AMPA and NMDA receptor activity was indistinguishable between D36 and WT mice. During extracellular recordings of field EPSPs and during intracellular recording of EPSCs from hippocampal slices from WT mice, H‐89 and KT5720, two structurally different PKA inhibitors, inhibited LTD by more than 70% without affecting basal synaptic transmission or basal phosphorylation of serine 845 on GluR1. Collectively our data indicate that AKAP150‐anchored PKA activity is required to induce LTD and not merely to maintain a tonically heightened activity level of AMPA receptors as proposed earlier.
Modifications of the interactions in the motor networks when a movement becomes automatic
Authors: Wu Tao , Chan Piu , Hallett Mark
Published: July 2008

A crucial feature of the motor system is the ability to control some movements automatically. We have previously shown that all parts of the motor networks reduce their activity with automaticity, and, while this change may indicate increased efficiency in terms of neural processing, it is not clear how motor skill can be maintained after a reduction of neural activity. In the current study, we used functional MRI (fMRI) to investigate influences on the effective connectivity of the brain motor networks when movements become automatic. Subjects practiced a sequential movement until they could execute it automatically, and task‐related brain fMRI activation was measured before and after they achieved automaticity. Using the psychophysiological interaction (PPI) method, we found that the cerebellum, cingulate motor area, supplementary motor area, and putamen had significantly greater connectivity, whereas the precuneus had less connectivity in the motor networks at the automatic stage. Our findings demonstrate that the importance of the attention networks decrease when movements become automatic. Moreover, the process of automaticity is accompanied by a strengthened interaction of central motor networks even though the magnitude of the activation is decreased. We speculate that this increase in connectivity reflects more efficient neural coding of movement at the automatic stage.
Graded sympatholytic effect of exogenous ATP on postjunctional α‐adrenergic vasoconstriction in the human forearm: implications for vascular control in contracting muscle
Authors: Kirby Brett S. , Voyles Wyatt F. , Carlson Rick E. , Dinenno Frank A.
Published: July 2008

Recent evidence suggests that adenosine triphosphate (ATP) can inhibit vasoconstrictor responses to endogenous noradrenaline release via tyramine in the skeletal muscle circulation, similar to what is observed in contracting muscle. Whether this involves direct modulation of postjunctional α‐adrenoceptor responsiveness, or is selective for α1‐ or α2‐receptors remains unclear. Therefore, in Protocol 1, we tested the hypothesis that exogenous ATP can blunt direct postjunctional α‐adrenergic vasoconstriction in humans. We measured forearm blood flow (FBF; Doppler ultrasound) and calculated the vascular conductance (FVC) responses to local intra‐arterial infusions of phenylephrine (α1‐agonist) and dexmedetomidine (α2‐agonist) during moderate rhythmic handgrip exercise (15% maximum voluntary contraction), during a control non‐exercise vasodilator condition (adenosine), and during ATP infusion in eight young adults. Forearm hyperaemia was matched across all conditions. Forearm vasoconstrictor responses to direct α1‐receptor stimulation were blunted during exercise versus adenosine (ΔFVC =−11 ± 3%versus−39 ± 5%; P< 0.05), and were abolished during ATP infusion (−3 ± 2%). Similarly, vasoconstrictor responses to α2‐receptor stimulation were blunted during exercise versus adenosine (−13 ± 4%versus−40 ± 8%; P< 0.05), and were abolished during ATP infusion (−4 ± 4%). In Prototol 2 (n= 10), we tested the hypothesis that graded increases in ATP would reduce α1‐mediated vasoconstriction in a dose‐dependent manner compared with vasodilatation evoked via adenosine. Forearm vasoconstrictor responses during low dose adenosine (−38 ± 3%) and ATP (−33 ± 2%) were not significantly different from rest (−40 ± 3%; P> 0.05). In contrast, vasoconstrictor responses during moderate (−22 ± 6%) and high dose ATP (−8 ± 5%) were significantly blunted compared with rest, whereas the responses during adenosine became progressively greater (moderate =−48 ± 4%, P= 0.10; high =−53 ± 6%, P< 0.05). We conclude that exogenous ATP is capable of blunting direct postjunctional α‐adrenergic vasoconstriction, that this involves both α1‐ and α2‐receptor subtypes, and that this is graded with ATP concentrations. Collectively, these data are consistent with the conceptual framework regarding how muscle blood flow and vascular tone are regulated in contracting muscles of humans.
Functional circuitry of visual adaptation in the retina
Authors: Demb Jonathan B.
Published: July 2008

The visual system continually adjusts its sensitivity, or ‘adapts’, to the conditions of the immediate environment. Adaptation increases responses when input signals are weak, to improve the signal‐to‐noise ratio, and decreases responses when input signals are strong, to prevent response saturation. Retinal ganglion cells adapt primarily to two properties of light input: the mean intensity and the variance of intensity over time (contrast). This review focuses on cellular mechanisms for contrast adaptation in mammalian retina. High contrast over the ganglion cell's receptive field centre reduces the gain of spiking responses. The mechanism for gain control arises partly in presynaptic bipolar cell inputs and partly in the process of spike generation. Following strong contrast stimulation, ganglion cells exhibit a prolonged after‐hyperpolarization, driven primarily by suppression of glutamate release from presynaptic bipolar cells. Ganglion cells also adapt to high contrast over their peripheral receptive field. Long‐range adaptive signals are carried by amacrine cells that inhibit the ganglion cell directly, causing hyperpolarization, and inhibit presynaptic bipolar terminals, reducing gain of their synaptic output. Thus, contrast adaptation in ganglion cells involves multiple synaptic and intrinsic mechanisms for gain control and hyperpolarization. Several forms of adaptation in ganglion cells originate in presynaptic bipolar cells.
Synaptic physiology of direction selectivity in the retina
Authors: Zhou Z. Jimmy , Lee Seunghoon
Published: July 2008

Detection of the direction of image movement is accomplished first in the retina by an elegant neuronal circuit, which integrates multiple levels of spatially asymmetric synaptic interactions among subsets of bipolar, amacrine and ganglion cells. Central to these interactions is the asymmetric GABAergic inhibition exerted by the starburst amacrine cell (SAC), a cholinergic and GABAergic interneuron with a radially symmetric dendritic tree. SACs make reciprocal GABAergic synapses on each other to create a direct inhibitory receptive field surround, which suppresses the response of each SAC to centripetal image movement. Each radially projecting branch of a SAC responds to image movement with a centrifugal bias and, through directionally asymmetric synaptic connections with the dendrites of direction‐selective ganglion cells (DSGCs), exerts a spatially offset inhibition that vetoes the response of DSGCs to image movement in a specific (null) direction. Recent physiological studies have greatly advanced our understanding of the mechanism of direction selectivity and also revealed a new level of complexity that remains to be understood.
One-Third of Reef-Building Corals Face Elevated Extinction Risk from Climate Change and Local Impacts
Authors: Carpenter Kent E. , Abrar Muhammad , Aeby Greta , Aronson Richard B. , Banks Stuart , Bruckner Andrew , Chiriboga Angel , Cortés Jorge , Delbeek J. Charles , DeVantier Lyndon , Edgar Graham J. , Edwards Alasdair J. , Fenner Douglas , Guzmán Héctor M. , Hoeksema Bert W. , Hodgson Gregor , Johan Ofri , Licuanan Wilfredo Y. , Livingstone Suzanne R. , Lovell Edward R. , Moore Jennifer A. , Obura David O. , Ochavillo Domingo , Polidoro Beth A. , Precht William F. , Quibilan Miledel C. , Reboton Clarissa , Richards Zoe T. , Rogers Alex D. , Sanciangco Jonnell , Sheppard Anne , Sheppard Charles , Smith Jennifer , Stuart Simon , Turak Emre , Veron John E. N. , Wallace Carden , Weil Ernesto , Wood Elizabeth
Published: July 2008

The conservation status of 845 zooxanthellate reef-building coral species was assessed by using International Union for Conservation of Nature Red List Criteria. Of the 704 species that could be assigned conservation status, 32.8% are in categories with elevated risk of extinction. Declines in abundance are associated with bleaching and diseases driven by elevated sea surface temperatures, with extinction risk further exacerbated by local-scale anthropogenic disturbances. The proportion of corals threatened with extinction has increased dramatically in recent decades and exceeds that of most terrestrial groups. The Caribbean has the largest proportion of corals in high extinction risk categories, whereas the Coral Triangle (western Pacific) has the highest proportion of species in all categories of elevated extinction risk. Our results emphasize the widespread plight of coral reefs and the urgent need to enact conservation measures.
Bacterial, Fungal, Parasitic, and Viral Myositis
Authors: Crum-Cianflone Nancy F.
Published: July 2008

Infectious myositis may be caused by a broad range of bacterial, fungal, parasitic, and viral agents. Infectious myositis is overall uncommon given the relative resistance of the musculature to infection. For example, inciting events, including trauma, surgery, or the presence of foreign bodies or devitalized tissue, are often present in cases of bacterial myositis. Bacterial causes are categorized by clinical presentation, anatomic location, and causative organisms into the categories of pyomyositis, psoas abscess, Staphylococcus aureus myositis, group A streptococcal necrotizing myositis, group B streptococcal myositis, clostridial gas gangrene, and nonclostridial myositis. Fungal myositis is rare and usually occurs among immunocompromised hosts. Parasitic myositis is most commonly a result of trichinosis or cystericercosis, but other protozoa or helminths may be involved. A parasitic cause of myositis is suggested by the travel history and presence of eosinophilia. Viruses may cause diffuse muscle involvement with clinical manifestations, such as benign acute myositis (most commonly due to influenza virus), pleurodynia (coxsackievirus B), acute rhabdomyolysis, or an immune-mediated polymyositis. The diagnosis of myositis is suggested by the clinical picture and radiologic imaging, and the etiologic agent is confirmed by microbiologic or serologic testing. Therapy is based on the clinical presentation and the underlying pathogen.
Pertussis Vaccination for Health Care Workers
Authors: Sandora Thomas J. , Gidengil Courtney A. , Lee Grace M.
Published: July 2008

Pertussis, an acute respiratory infection caused by Bordetella pertussis, classically manifests as a protracted cough illness. The incidence of pertussis in the United States has been increasing in recent years. Immunity wanes after childhood vaccination, leaving adolescents and adults susceptible to infection. The transmission of pertussis in health care settings has important medical and economic consequences. Acellular pertussis booster vaccines are now available for use and have been recommended for all adolescents and adults. These vaccines are safe, immunogenic, and effective. Health care workers are a priority group for vaccination because of their increased risk of acquiring infection and the potential to transmit pertussis to high-risk patients. Health care worker vaccination programs are likely to be cost-effective, but further research is needed to determine the acceptability of pertussis vaccines among health care workers, the duration of immunity after booster doses, and the impact of vaccination on the management of pertussis exposures in health care settings.
Polymyxins Revisited
Authors: Landman David , Georgescu Claudiu , Martin Don Antonio , Quale John
Published: July 2008

The global emergence of multidrug-resistant gram-negative bacilli has spurred a renewed interest in polymyxins. Once discarded due to concerns regarding nephrotoxicity and neurotoxicity, polymyxins now hold an important role in the antibiotic armamentarium. However, more reliable information is needed to determine the optimal dosing of these agents. Also, unanswered questions regarding in vitro testing remain, including questions regarding the reliability of automated systems and the establishment of appropriate breakpoints for defining susceptibility. Most contemporary clinical studies examining the use of these agents have involved patients with infections due to multidrug-resistant Pseudomonas aeruginosa and Acinetobacter baumannii strains. It has been reassuring that polymyxin therapy for resistant bacteria has resulted in clinical responses and toxicity rates similar to those for carbapenem therapy for susceptible isolates. While most surveillance studies demonstrated high rates of susceptibility, several reports noted the emergence of polymyxin-resistant nosocomial pathogens. Polymyxins have assumed an important antibiotic niche for therapy for hospital-acquired infections; further studies defining the optimal use of these agents will likely extend the duration of their clinical usefulness.
Increasing Importance of
Balamuthia mandrillaris
Authors: Matin Abdul , Siddiqui Ruqaiyyah , Jayasekera Samantha , Khan Naveed Ahmed
Published: July 2008

Balamuthia mandrillaris
is an emerging protozoan parasite, an agent of granulomatous amoebic encephalitis involving the central nervous system, with a case fatality rate of >98%. This review presents our current understanding of
Balamuthia
infections, their pathogenesis and pathophysiology, and molecular mechanisms associated with the disease, as well as virulence traits of
Balamuthia
that may be potential targets for therapeutic interventions and/or for the development of preventative measures.
Acinetobacter baumannii
: Emergence of a Successful Pathogen
Authors: Peleg Anton Y. , Seifert Harald , Paterson David L.
Published: July 2008

Acinetobacter baumannii
has emerged as a highly troublesome pathogen for many institutions globally. As a consequence of its immense ability to acquire or upregulate antibiotic drug resistance determinants, it has justifiably been propelled to the forefront of scientific attention. Apart from its predilection for the seriously ill within intensive care units,
A. baumannii
has more recently caused a range of infectious syndromes in military personnel injured in the Iraq and Afghanistan conflicts. This review details the significant advances that have been made in our understanding of this remarkable organism over the last 10 years, including current taxonomy and species identification, issues with susceptibility testing, mechanisms of antibiotic resistance, global epidemiology, clinical impact of infection, host-pathogen interactions, and infection control and therapeutic considerations.
DIGITAL WATERMARKING IN THE SINGULAR VECTOR DOMAIN
Authors: AGARWAL RASHMI , SANTHANAM M. S.
Published: July 2008

Many current watermarking algorithms insert data in the spatial or transform domains like the discrete cosine, the discrete Fourier, and the discrete wavelet transforms. In this paper, we present a data-hiding algorithm that exploits the singular value decomposition (SVD) representation of the data. We compute the SVD of the host image and the watermark and embed the watermark in the singular vectors of the host image. The proposed method leads to an imperceptible scheme for digital images, both in grey scale and color and is quite robust against attacks like noise and JPEG compression.
VISUAL SPEECH RECOGNITION USING DYNAMIC FEATURES AND SUPPORT VECTOR MACHINES
Authors: YAU WAI CHEE , KUMAR DINESH KANT , ARJUNAN SRIDHAR POOSAPADI
Published: July 2008

This paper presents a vision based technique to identify the unspoken phones using a small camera that is located on the headset of the speaker. The system is based on temporal integration of the video data to generate motion history image (MHI). The paper proposes the use of global features to classify the MHI and compares the use of image moments with Discrete Cosine Transform (DCT). A comparison between Zernike moments (ZM) with DCT indicates that while the accuracy of classification for both techniques is very comparable (96% for ZM and 94% for DCT) when there is no relative motion between the camera and the mouth, ZM is resilient to rotation of the camera and continues to gives good results despite rotation but DCT is sensitive to rotation.

Based on the accuracy of the system and its resilience to movement artefacts such as rotation, the authors propose the use of such a system for human computer interface. Such a system could be invaluable when it is important to communicate without making a sound, such as giving passwords when in an open office or in public spaces.
GRAPH-BASED ORDERING SCHEME FOR COLOR IMAGE FILTERING
Authors: LEZORAY O. , MEURIE C. , ELMOATAZ A.
Published: July 2008

This paper presents a graph-based ordering scheme of color vectors. A complete graph is defined over a filter window and its structure is analyzed to construct an ordering of color vectors. This graph-based ordering is constructed by finding a Hamiltonian path across the color vectors of a filter window by a two-step algorithm. The first step extracts, by decimating a minimum spanning tree, the extreme values of the color set. These extreme values are considered as the infimum and the supremum of the set of color vectors. The second step builds an ordering by constructing a Hamiltonian path among the vectors of color vectors, starting from the infimum and ending at the supremum. The properties of the proposed graph-based ordering of vectors are detailed. Several experiments are conducted to assess its filtering abilities for morphological and median filtering.
Host Restriction Factors Blocking Retroviral Replication
Authors: Wolf Daniel , Goff Stephen P.
Published: July 2008

Retroviruses are highly successful intracellular parasites, and as such they are found in nearly all branches of life. Some are relatively benign, but many are highly pathogenic and can cause either acute or chronic diseases. Therefore, there is tremendous selective pressure on the host to prevent retroviral replication, and for this reason cells have evolved a variety of restriction factors that act to inhibit or block the viruses. This review is a survey of the best-characterized restriction factors capable of inhibiting retroviral replication and aims to highlight the diversity of strategies used for this task.
Colitis immunoregulation by CD8+T cell requires T cell cytotoxicity and B cell peptide antigen presentation
Authors: McPherson Michael , Wei Bo , Turovskaya Olga , Fujiwara Daisuke , Brewer Sarah , Braun Jonathan
Published: July 2008

Deficient immunoregulation by CD4+T cells is an important susceptibility trait for inflammatory bowel disease, but the role of other regulatory cell types is less understood. This study addresses the role and mechanistic interaction of B cells and CD8+T cells in controlling immune-mediated colitis. The genetic requirements for B cells and CD8+T cells to confer protective immunoregulation were assessed by cotransfer with colitogenic Gαi2−/−T cells into immune-deficient mice. Disease activity in Gαi2−/−T cell recipients was evaluated by CD4+T intestinal lymphocyte abundance, cytokine production levels, and large intestine histology. B cells deficient in B7.1/B7.2, CD40, major histocompatibility complex (MHC) II (Abb), or native B cell antigen receptor (MD4) were competent for colitis protection. However, transporter-1-deficient B cells failed to protect, indicating a requirement for peptide MHC I presentation to CD8+T cells. CD8+T cells deficient in native T cell receptor repertoire (OT-1) or cytolysis (perforin−/−) also were nonprotective. These finding reveal an integrated role for antigen-specific perforin-dependent CD8+T cell cytotoxicity in colitis immunoregulatory and its efficient induction by a subset of mesenteric B lymphocytes.
Cardiovascular effects of prorenin blockade in genetically spontaneously hypertensive rats on normal and high-salt diet
Authors: Susic Dinko , Zhou Xiaoyan , Frohlich Edward D. , Lippton Howard , Knight Martha
Published: July 2008

Recent reports have demonstrated a potential role of tissue prorenin in the pathogenesis of cardiovascular and renal damage. This study was designed to examine the role of prorenin in the pathogenesis of target organ damage in spontaneously hypertensive rats (SHRs), the best naturally occurring experimental model of essential hypertension. To this end, we studied 20-wk-old male SHRs receiving a normal diet and 8-wk-old male SHRs given food with 8% NaCl. One-half the rats in each group were given prorenin inhibitor (PRAM-1, 0.1 mg·kg−1·day−1) via osmotic minipumps; the other half served as controls. Arterial pressure, left ventricular function, cardiovascular mass indexes, cardiac fibrosis, and renal function were examined at the end of the experiment. Arterial pressure was unaffected by PRAM-1 in rats on either regular or salt-excess diets. In those rats receiving a normal diet, the blockade of prorenin activation consistently reduced left ventricular mass but affected no other variable. Salt-loaded rats given PRAM-1 for 8 wk demonstrated ( 1) reduced serum creatinine level, ( 2) decreased left ventricular mass, ( 3) improved left ventricular function, and ( 4) reduced left ventricular fibrosis. These data demonstrated that the blockade of nonproteolytic activation of prorenin exerted significant cardiovascular and renal benefit in SHRs with cardiovascular damage produced by salt excess and suggested that the activation of cardiovascular or renal prorenin may be a major mechanism that mediates cardiac and renal damage in this form of accelerated hypertension.
The impact of endurance exercise training on left ventricular systolic mechanics
Authors: Baggish Aaron L. , Yared Kibar , Wang Francis , Weiner Rory B. , Hutter Adolph M. , Picard Michael H. , Wood Malissa J.
Published: July 2008

Although exercise training-induced changes in left ventricular (LV) structure are well characterized, adaptive functional changes are incompletely understood. Detailed echocardiographic assessment of LV systolic function was performed on 20 competitive rowers (10 males and 10 females) before and after endurance exercise training (EET; 90 days, 10.7 ± 1.1 h/wk). Structural changes included LV dilation (end-diastolic volume = 128 ± 25 vs. 144 ± 28 ml, P < 0.001), right ventricular (RV) dilation (end-diastolic area = 2,850 ± 550 vs. 3,260 ± 530 mm2, P < 0.001), and LV hypertrophy (mass = 227 ± 51 vs. 256 ± 56 g, P < 0.001). Although LV ejection fraction was unchanged (62 ± 3% vs. 60 ± 3%, P = not significant), all direct measures of LV systolic function were altered. Peak systolic tissue velocities increased significantly (basal lateral S′Δ = 0.9 ± 0.6 cm/s, P = 0.004; and basal septal S′Δ = 0.8 ± 0.4 cm/s, P = 0.008). Radial strain increased similarly in all segments, whereas longitudinal strain increased with a base-to-apex gradient. In contrast, circumferential strain (CS) increased in the LV free wall but decreased in regions adjacent to the RV. Reductions in septal CS correlated strongly with changes in RV structure (ΔRV end-diastolic area vs. ΔLV septal CS; r2 = 0.898, P < 0.001) and function (Δpeak RV systolic velocity vs. ΔLV septal CS, r2 = 0.697, P < 0.001). EET leads to significant changes in LV systolic function with regional heterogeneity that may be secondary to concomitant RV adaptation. These changes are not detected by conventional measurements such as ejection fraction.
Reactive oxygen species mediate RhoA/Rho kinase-induced Ca2+ sensitization in pulmonary vascular smooth muscle following chronic hypoxia
Authors: Jernigan Nikki L. , Walker Benjimen R. , Resta Thomas C.
Published: July 2008

Recent evidence supports a prominent role for Rho kinase (ROK)-mediated pulmonary vasoconstriction in the development and maintenance of chronic hypoxia (CH)-induced pulmonary hypertension. Endothelin (ET)-1 contributes to the pulmonary hypertensive response to CH, and recent studies by our laboratory and others indicate that pulmonary vascular reactivity following CH is largely independent of changes in vascular smooth muscle (VSM) intracellular free calcium concentration ([Ca2+]i). In addition, CH increases generation of reactive oxygen species (ROS) in pulmonary arteries, which may underlie the shift toward ROK-dependent Ca2+ sensitization. Therefore, we hypothesized that ROS-dependent RhoA/ROK signaling mediates ET-1-induced Ca2+ sensitization in pulmonary VSM following CH. To test this hypothesis, we determined the effect of pharmacological inhibitors of ROK, myosin light chain kinase (MLCK), tyrosine kinase (TK), and PKC on ET-1-induced vasoconstriction in endothelium-denuded, Ca2+-permeabilized small pulmonary arteries from control and CH (4 wk at 0.5 atm) rats. Further experiments examined ET-1-mediated, ROK-dependent phosphorylation of the regulatory subunit of myosin light chain phosphatase (MLCP), MYPT1. Finally, we measured ET-1-induced ROS generation in dihydroethidium-loaded small pulmonary arteries and investigated the role of ROS in mediating ET-1-induced, RhoA/ROK-dependent Ca2+ sensitization using the superoxide anion scavenger, tiron. We found that CH increases ET-1-induced Ca2+ sensitization that is sensitive to inhibition of ROK and MLCK, but not PKC or TK, and correlates with ROK-dependent MYPT1Thr696 phosphorylation. Furthermore, tiron inhibited basal and ET-1-stimulated ROS generation, RhoA activation, and VSM Ca2+ sensitization following CH. We conclude that CH augments ET-1-induced Ca2+ sensitization through ROS-dependent activation of RhoA/ROK signaling in pulmonary VSM.
Nicotine administration and withdrawal affect survival in systemic inflammation models
Authors: Steiner Alexandre A. , Oliveira Daniela L. , Roberts Jennifer L. , Petersen Scott R. , Romanovsky Andrej A.
Published: July 2008

How different regimens of nicotine administration and withdrawal affect systemic inflammation is largely unknown. We studied the effects of chronic and acute nicotine administration and of nicotine withdrawal on the outcome of aseptic and septic systemic inflammation. Male C57BL/6 mice were implanted with subcutaneous osmotic pumps (to deliver nicotine) and intrabrain telemetry probes (to measure temperature). Aseptic inflammation was induced by lipopolysaccharide (40 mg/kg ip); sepsis was induced by cecal ligation and puncture. The chronic nicotine administration group received nicotine (28 mg·kg−1·day−1) for 2 wk before the induction of inflammation and continued receiving nicotine until the end of the experiment; the acute nicotine administration group received saline for 2 wk and nicotine thereafter; the nicotine withdrawal group received nicotine for 2 wk and saline thereafter; and the no-nicotine group was infused with saline throughout the experiment. Compared with no nicotine, the chronic nicotine administration did not affect survival in either model of inflammation, possibly due to the development of nicotine tolerance. The acute nicotine administration increased the survival rate in aseptic inflammation from 11 to 33% (possibly by suppressing inflammation) but worsened the outcome of sepsis (possibly because the suppression of inflammation promoted microbial proliferation). Oppositely to acute nicotine, nicotine withdrawal increased the survival rate in sepsis from 18 to 40%. The effects on survival were not due to changes in body temperature. We conclude that acute nicotine administration and nicotine withdrawal affect survival in systemic inflammation and that these effects strongly depend on whether inflammation is aseptic or septic.
Physiology and Pathophysiology of Potassium Channels in Gastrointestinal Epithelia
Authors: Heitzmann Dirk , Warth Richard
Published: July 2008

Epithelial cells of the gastrointestinal tract are an important barrier between the “milieu interne” and the luminal content of the gut. They perform transport of nutrients, salts, and water, which is essential for the maintenance of body homeostasis. In these epithelia, a variety of K+channels are expressed, allowing adaptation to different needs. This review provides an overview of the current literature that has led to a better understanding of the multifaceted function of gastrointestinal K+channels, thereby shedding light on pathophysiological implications of impaired channel function. For instance, in gastric mucosa, K+channel function is a prerequisite for acid secretion of parietal cells. In epithelial cells of small intestine, K+channels provide the driving force for electrogenic transport processes across the plasma membrane, and they are involved in cell volume regulation. Fine tuning of salt and water transport and of K+homeostasis occurs in colonic epithelia cells, where K+channels are involved in secretory and reabsorptive processes. Furthermore, there is growing evidence for changes in epithelial K+channel expression during cell proliferation, differentiation, apoptosis, and, under pathological conditions, carcinogenesis. In the future, integrative approaches using functional and postgenomic/proteomic techniques will help us to gain comprehensive insights into the role of K+channels of the gastrointestinal tract.
LDL Receptor-Related Protein 1: Unique Tissue-Specific Functions Revealed by Selective Gene Knockout Studies
Authors: Lillis Anna P. , Van Duyn Lauren B. , Murphy-Ullrich Joanne E. , Strickland Dudley K.
Published: July 2008

The LDL receptor-related protein (originally called LRP, but now referred to as LRP1) is a large endocytic receptor that is widely expressed in several tissues. LRP1 is a member of the LDL receptor family that plays diverse roles in various biological processes including lipoprotein metabolism, degradation of proteases, activation of lysosomal enzymes, and cellular entry of bacterial toxins and viruses. Deletion of the LRP1 gene leads to lethality in mice, revealing a critical, but as of yet, undefined role in development. Tissue-specific gene deletion studies reveal an important contribution of LRP1 in the vasculature, central nervous system, macrophages, and adipocytes. Three important properties of LRP1 dictate its diverse role in physiology: 1) its ability to recognize more than 30 distinct ligands, 2) its ability to bind a large number of cytoplasmic adaptor proteins via determinants located on its cytoplasmic domain in a phosphorylation-specific manner, and 3) its ability to associate with and modulate the activity of other transmembrane receptors such as integrins and receptor tyrosine kinases.
Translational Research to Generate Evidence for Rational and Efficient Introduction of New Vaccines in Developing Countries: The Experience of the International Vaccine Institute
Authors: Clemens John
Published: July 2008

Introduction of new vaccines into affluent countries has occurred at a breathtaking pace in recent years. By comparison, few new-generation vaccines have been introduced into public health programs for the poor in developing countries, and, for those that have, introduction has been painfully slow. Limited financial resources have retarded the introduction. However, the slow pace also stems from a dearth of evidence needed for rational policy decisions. Inadequate support to conduct phase 1 studies of vaccine candidates targeted against diseases of developing countries is a well-known obstacle. Additionally, other types of translational research are needed to generate the necessary evidence for policy. Many vaccines have been shown to perform less well in impoverished populations in the developing world than in persons residing in more affluent countries. Consequently, phase 2 and phase 3 trials are a second essential type of translational research needed for the introduction of vaccines in developing countries. Moreover, even for vaccines that achieve licensure via clinical trials in developing countries, doubts may remain about whether the burden of disease warrants vaccine introduction, whether the administration of the vaccine in public health programs will be cost-effective, whether vaccine introduction will be programmatically feasible and acceptable, and whether the introduction of the vaccine will be financially sustainable. To address these residual doubts, a third type of translational research is needed. Since its inception in 1987, the International Vaccine Institute, an international, non-profit research and development organization located in Seoul, Korea, has conducted translational research on new vaccine introduction for a variety of diseases in 22 countries in Asia, Africa and Latin America. In this paper, we describe translational research projects undertaken by the International Vaccine Institute and lessons learned about strategies to increase the impact of translational research on vaccine policy for the developing world.