bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anthropo‐entomophagy: Cultures, evolution and sustainability
Authors: RAMOS‐ELORDUY Julieta 
Published: September 2009

AbstractEnvironmental cycles and human factors have altered ecosystems throughout the world. Natural resources have acquired high value because they are important to life and the survival of human beings. Among these resources are edible insects. They have many important features and, to date, up to 2086 species are consumed by 3071 ethnic groups. Rural people, who primarily search, gather, fix, commercialize and store this important natural resource, do not exterminate them. This is because rural people exploit only the central part of the insects' population curves. Nonetheless, some species are overexploited. Anthropo‐entomophagy (eating of insects by humans) constitutes a major source of nutrition and these foods are eaten in 130 countries, with the African and American continents being the most entomophagous until now. It exists in protocultures (care is given to the edible insect species) and formal cultures, such as in Mexico, which date back to prehisphanic times. According to anthropologists the “saving gene theory” is based on insect ingestion, which, since the Paleolithic era, has given human beings reproductive success. The evolution of anthropo‐entomophagy has been achieved in many ways, from the point of view of collection, fixing, marketing and consumption, and for the insects' organoleptical qualities. The sustainability of these species is fundamental; therefore, it is necessary to take certain measures for species conservation. In Mexico, more than 100 species of edible insects have been tested for their sustainability over 500 years, from the Spanish conquest to the present.
Alterations in Two-Component Regulatory Systems of
phoPQ
and
pmrAB
Are Associated with Polymyxin B Resistance in Clinical Isolates of
Pseudomonas aeruginosa
Authors: Barrow Kaddy , Kwon Dong H. 
Published: September 2009

ABSTRACT

Polymyxins are often the only option to treat acquired multidrug-resistant
Pseudomonas aeruginosa
. Polymyxin susceptibility in
P. aeruginosa
PAO1 is associated with the lipopolysaccharide structure that is determined by
arnBCADTEF
and modulated by
phoPQ
and
pmrAB
. We examined five clonally unrelated clinical isolates of polymyxin B-resistant
P. aeruginosa
to investigate the molecular basis of polymyxin resistance. All isolates grew with 4 μg/ml polymyxin B (MIC, 8 μg/ml), whereas
P. aeruginosa
PAO1 grew with 0.25 μg/ml polymyxin B (MIC, 0.5 μg/ml). The resistant isolates were converted to susceptible ones (the MICs fell from 8 to 0.5 μg/ml) following the introduction of
phoPQ
(four isolates) and
pmrAB
(one isolate), which had been cloned from strain PAO1. DNA sequence analysis revealed that a single-nucleotide substitution in three isolates replaced a single amino acid of PhoQ, the deletion of 17 nucleotides in one isolate truncated the protein of PhoQ, and two nucleotide substitutions in one isolate replaced two amino acids of PmrB. The involvement of these amino acid substitutions or the truncated protein of PhoQ and PmrB in polymyxin B resistance was confirmed using strain PAO1 lacking
phoPQ
or
pmrAB
that was transformed by
phoPQ
or
pmrAB
containing the amino acid substitutions or the truncated protein. The resistant clinical isolates were sensitized by the inactivation of
arnBCADTEF
(the MICs fell from 8 to 0.5 μg/ml). These results suggest that polymyxin B resistance among clinical isolates of
P. aeruginosa
is associated with alterations in two-component regulatory systems of
phoPQ
or
pmrAB
.
Therapeutic Drug Monitoring of Posaconazole: a Monocentric Study with 54 Adults
Authors: Lebeaux David , Lanternier Fanny , Elie Caroline , Suarez Felipe , Buzyn Agnès , Viard Jean-Paul , Bougnoux Marie-Elisabeth , Lecuit Marc , Jullien Vincent , Lortholary Olivier 
Published: September 2009

ABSTRACT

Posaconazole is a potent broad-spectrum triazole antifungal. Little is known about the prevalence and risk factors for low plasma posaconazole concentrations (PPCs). We retrospectively reviewed all adult patients whose PPCs were measured after at least 5 days of treatment between April 2006 and July 2008 at the Hôpital Necker Enfants Malades. A low PPC was defined as a concentration lower than 500 ng/ml. Fifty-four patients were included: 36 receiving prophylactic (200 mg three times a day) and 18 receiving curative (400 mg twice a day) posaconazole therapy. The prevalence of low PPCs was 44% (16/36) in the prophylaxis group and 22% (4/18) in the curative-treatment group. In the prophylaxis group, low PPCs tended to be more frequent in cases of digestive disease (62.5% versus 30%;
P
= 0.051) and were significantly more frequent among patients with diarrhea (71.4% versus 27%;
P
= 0.009) or mucositis (100% versus 33%;
P
= 0.004). In the curative-treatment group, low PPCs were significantly more frequent in cases of diarrhea (75% versus 7%;
P
= 0.018). In the prophylaxis group, the only two patients who subsequently developed invasive fungal infections exhibited low PPCs. The only adverse event was hepatotoxicity for 2/54 patients (3.7%), which was not related to high plasma drug concentrations. In conclusion, low PPC is common, significantly more frequent in cases of diarrhea or mucositis, and potentially associated with subsequent invasive fungal infection. Therapeutic drug monitoring of posaconazole is therefore mandatory for immunosuppressed adults, at least for those with gastrointestinal disorders.
Unbound Cephalothin Pharmacokinetics in Adult Burn Patients Are Related to the Elapsed Time after Injury
Authors: Dalley Andrew J. , Deans Renae , Lipman Jeffrey , Venkatesh Bala , Rudd Michael , Roberts Michael S. , Cross Sheree E. 
Published: September 2009

ABSTRACT
Cephalothin (cefalotin) pharmacokinetics were evaluated for nine severely burned patients (42% ± 9% mean burn areas) and five healthy volunteers by using non-plasma-protein-bound concentration-time profiles. Burn patients gave increased mean residence times (36%) and reduced total clearances (25%). Mean residence times and distribution volumes increased between 1 and 4 days posttrauma, suggesting that burn patient pharmacokinetics change during the initial fluid resuscitation phase of treatment.
A Naturally Occurring Rgg Variant in Serotype M3
Streptococcus pyogenes
Does Not Activate
speB
Expression Due to Altered Specificity of DNA Binding
Authors: Kappeler Kyle V. , Anbalagan Srivishnupriya , Dmitriev Alexander V. , McDowell Emily J. , Neely Melody N. , Chaussee Michael S. 
Published: September 2009

ABSTRACT

The transcriptional regulator Rgg of
Streptococcus pyogenes
is essential for expression of the secreted cysteine protease SpeB. Although all isolates of
S. pyogenes
possess the
speB
gene, not all of them produce the protein in vitro. In a murine model of infection, the absence of SpeB production is associated with invasive disease. We speculated that naturally occurring mutations in
rgg
, which would also abrogate SpeB production, may be present in invasive isolates of
S. pyogenes
. Examination of the inferred Rgg sequences available in public databases revealed that the
rgg
gene in strain MGAS315 (a serotype M3 strain associated with invasive disease) encodes a proline at amino acid position 103 (Rgg
103P
); in contrast, all other strains encode a serine at this position (Rgg
103S
). A caseinolytic assay and Western blotting indicated that strain MGAS315 does not produce SpeB in vitro. Gene-swapping experiments showed that the
rgg
gene of MGAS315 is solely responsible for the lack of SpeB expression. In contrast to Rgg
103S
, Rgg
103P
does not bind to the
speB
promoter in gel shift assays, which correlates with a lack of
speB
expression. Despite its inability to activate
speB
expression, Rgg
103P
retains the ability to bind to DNA upstream of
norA
and to influence its expression. Overall, this study illustrates how variation at the
rgg
locus may contribute to the phenotypic diversity of
S. pyogenes
.
Distinctive Profiles of Infection and Pathology in Hamsters Infected with
Clostridium difficile
Strains 630 and B1
Authors: Goulding David , Thompson Harold , Emerson Jenny , Fairweather Neil F. , Dougan Gordon , Douce Gill R. 
Published: September 2009

ABSTRACT

Currently, the Golden Syrian hamster is widely considered an important model of
Clostridium difficile
disease, as oral infection of this animal pretreated with antibiotics reproduces many of the symptoms observed in humans. Two
C. difficile
strains, B1 and 630, showed significant differences in the progression and severity of disease in this model. B1-infected hamsters exhibited more severe pathology and a shorter time to death than hamsters infected with 630. Histological changes in the gut did not correlate with absolute numbers of
C. difficile
bacteria, but there were clear differences in the distribution of bacteria within gut tissues. Light, scanning, and transmission electron microscopy revealed high numbers of B1 bacteria at the mucosal surface of the tissue, whereas 630 bacteria were more frequently associated with the crypt regions. Both B1 and 630 bacteria were frequently observed within polymorphonuclear leukocytes, although, interestingly, a space frequently separated B1 bacteria from the phagosome wall, a phenomenon not observed with 630. However, pilus-like structures were detected on 630 located in the crypts of the gut tissue. Furthermore, B1 bacteria, but not 630 bacteria, were found within nonphagocytic cells, including enterocytes and muscle cells.
Bcl-2 Regulates the Onset of Shiga Toxin 1-Induced Apoptosis in THP-1 Cells
Authors: Lee Moo-Seung , Cherla Rama P. , Leyva-Illades Dinorah , Tesh Vernon L. 
Published: September 2009

ABSTRACT

Shiga toxins (Stxs), which are proteins expressed by the enteric pathogens
Shigella dysenteriae
serotype 1 and some serotypes of
Escherichia coli
, are potent protein synthesis inhibitors. Stx-producing organisms cause bloody diarrhea with the potential to progress to acute renal failure and central nervous system complications. Studies using animal models of these diseases have shown that Stxs are major virulence factors, and purified toxins have been shown to be capable of killing many types of cells in vitro. We showed that Stx type 1 (Stx1) rapidly induced apoptosis in undifferentiated, monocytic THP-1 cells through a mechanism involving the endoplasmic reticulum (ER) stress response. Rapid apoptosis correlated with increased expression of C/EBP homologous protein (CHOP), TRAIL, and DR5, while expression of the antiapoptotic factor Bcl-2 was downregulated. Stx1 treatment of differentiated, macrophage-like THP-1 cells was associated with cytokine production and delayed apoptosis. The mechanisms contributing to cell maturation-dependent differences in responses to Stx1 are unknown. We show here that in macrophage-like cells, Stx1 activated the proximal ER stress sensors RNA-dependent protein kinase-like ER kinase and inositol-requiring ER signal kinase 1α but did not activate activating transcription factor 6. Proapoptotic signaling pathways mediated by CHOP and by Bax and Bak were activated by Stx1. However, the toxin also activated prosurvival signaling through increased expression, mitochondrial translocation, and alternative phosphorylation of Bcl-2.
Role for theBurkholderia pseudomalleiCapsular Polysaccharide Encoded by thewcbOperon in Acute Disseminated Melioidosis
Authors: Warawa Jonathan M. , Long Dan , Rosenke Rebecca , Gardner Don , Gherardini Frank C. 
Published: September 2009

ABSTRACTThe capsular polysaccharide ofBurkholderia pseudomalleiis an essential virulence determinant that is required for protection from host serum cidal activity and opsonophagocytosis. In this study, the immune response directed against aB. pseudomalleicapsule mutant (JW270) was investigated in an acute respiratory murine model. JW270 was significantly attenuated in this model (∼2 logs) to levels resembling those of avirulentBurkholderia thailandensis. At lethal doses, JW270 colonized the lung, liver, and spleen at levels similar to the wild-type strain levels and was found to trigger reduced pathology in the liver and spleen. Several cytokine responses were altered in these tissues, and importantly, the levels of gamma interferon were reduced in the livers and spleens of JW270-infected mice but not in the lungs. These results suggest that the capsular polysaccharide ofB. pseudomalleiis a critical virulence determinant in respiratory tract infections and that it is an important antigen for generating the Th1 immune response commonly observed in systemic melioidosis. Furthermore, the data suggest that host recognition ofB. pseudomalleicapsular polysaccharide in the lungs may not be as important to the disease outcome as the innate immune response in the peripheral organs.
Evaluation of a New Test, GenoType HelicoDR, for Molecular Detection of Antibiotic Resistance inHelicobacter pylori
Authors: Cambau Emmanuelle , Allerheiligen Vera , Coulon Céline , Corbel Céline , Lascols Christine , Deforges Lionel , Soussy Claude-James , Delchier Jean-Charles , Megraud Francis 
Published: September 2009

ABSTRACTThe eradication rate ofHelicobacter pyloriby standard therapy is decreasing due to antibiotic resistance, mainly to clarithromycin. Our aim was to provide a new molecular test to guide the treatment of new and relapsed cases. We first studied 126H. pyloristrains for phenotypic (MIC) and genotypic resistance to clarithromycin (rrlmutation) and levofloxacin (gyrAmutation) and then developed a DNA strip genotyping test on the basis of the correlation results and literature data. Clinical strains (n= 92) and gastric biopsy specimens containingH. pylori(n= 105) were tested blindly with the new molecular test GenoType HelicoDR. The presence of mutations or the absence of hybridization with wild-type sequences was predictive, inrrlfor clarithromycin resistance in 91 cases (mostly the A2147G mutation) and ingyrAfor levofloxacin resistance in 58 cases (mutations at codon 87 or 91). Genotyping revealed a mix of genotypes in 33% of the cases, reflecting a coinfection or selection for resistant mutants. The sensitivity and specificity of detecting resistance were 94% and 99% for clarithromycin and 87% and 98.5% for levofloxacin, respectively. The concordance scores were 0.96 for clarithromycin and 0.94 for levofloxacin. With global resistance rates of 46% for clarithromycin and 25% for levofloxacin, which were observed for consecutive positive biopsy specimens from 2007 and 2008, the positive and negative predictive values for detecting resistance were 99% and 94% for clarithromycin and 96% and 96% for fluoroquinolone. GenoType HelicoDR is efficient at detecting mutations predictive of antibiotic resistance inH. pyloriwhen applied to strains or directly to gastric biopsy specimens.
Transgenic Expression of the 3D Polymerase Inhibits Theiler's Virus Infection and Demyelination
Authors: Kerkvliet Jason , Zoecklein Laurie , Papke Louisa , Denic Aleksandar , Bieber Allan J. , Pease Larry R. , David Chella S. , Rodriguez Moses 
Published: September 2009

ABSTRACTThe RNA-dependent RNA polymerase 3Dpolis required for the elongation of positive- and negative-stranded picornavirus RNA. During the course of investigating the effect of the transgenic expression of viral genes on the host immune response, we evaluated the viral load present in the host after infection. To our surprise, we found that 3D transgenic expression in genetically susceptible FVB mice led to substantially lower viral loads after infection with Theiler's murine encephalomyelitis virus (TMEV). As a result, spinal cord damage caused by chronic viral infection in the central nervous system was reduced in FVB mice that expressed 3D. This led to the preservation of large-diameter axons and motor function in these mice. The 3D transgene also lowered early viral loads when expressed in FVB-Dbmice resistant to persistent TMEV infection. The protective effect of 3D transgenic expression was not altered in FVB-Rag−/−.3D mice that are deficient in T and B cells, thus ruling out a mechanism by which the overexpression of 3D enhanced the adaptive immune clearance of the virus. Understanding how endogenously overexpressed 3D polymerase inhibits viral replication may lead to new strategies for targeting therapies to all picornaviruses.
Evolutionary Dynamics of GII.4 Noroviruses over a 34-Year Period
Authors: Bok Karin , Abente Eugenio J. , Realpe-Quintero Mauricio , Mitra Tanaji , Sosnovtsev Stanislav V. , Kapikian Albert Z. , Green Kim Y. 
Published: September 2009

ABSTRACT

Noroviruses are a major cause of epidemic gastroenteritis in children and adults, and GII.4 has been the predominant genotype since its first documented occurrence in 1987. This study examined the evolutionary dynamics of GII.4 noroviruses over more than three decades to investigate possible mechanisms by which these viruses have emerged to become predominant. Stool samples (
n
= 5,424) from children hospitalized at the Children's Hospital in Washington, DC, between 1974 and 1991 were screened for the presence of noroviruses by a custom multiplex real-time reverse transcription-PCR. The complete genome sequences of five GII.4 noroviruses (three of which predate 1987 by more than a decade) in this archival collection were determined and compared to the sequences of contemporary strains. Evolutionary analysis determined that the GII.4 VP1 capsid gene evolved at a rate of 4.3 × 10
−3
nucleotide substitutions/site/year. Only six sites in the VP1 capsid protein were found to evolve under positive selection, most of them located in the shell domain. No unique mutations were observed in or around the two histoblood group antigen (HBGA) binding sites in the P region, indicating that this site has been conserved since the 1970s. The VP1 proteins from the 1974 to 1977 noroviruses contained a unique sequence of four consecutive amino acids in the P2 region, which formed an exposed protrusion on the modeled capsid structure. This protrusion and other observed sequence variations did not affect the HBGA binding profiles of recombinant virus-like particles derived from representative 1974 and 1977 noroviruses compared with more recent noroviruses. Our analysis of archival GII.4 norovirus strains suggests that this genotype has been circulating for more than three decades and provides new ancestral strain sequences for the analysis of GII.4 evolution.
Mouse Hepatitis Virus Stem-Loop 2 Adopts a uYNMG(U)a-Like Tetraloop Structure That Is Highly Functionally Tolerant of Base Substitutions
Authors: Liu Pinghua , Li Lichun , Keane Sarah C. , Yang Dong , Leibowitz Julian L. , Giedroc David P. 
Published: September 2009

ABSTRACT

Stem-loop 2 (SL2) of the 5′-untranslated region of the mouse hepatitis virus (MHV) contains a highly conserved pentaloop (C47-U48-U49-G50-U51) stacked on a 5-bp stem. Solution nuclear magnetic resonance experiments are consistent with a 5′-uYNMG(U)a or uCUYG(U)a tetraloop conformation characterized by an
anti
-C47-
syn
-G50 base-pairing interaction, with U51 flipped out into solution and G50 stacked on A52. Previous studies showed that U48C and U48A substitutions in MHV SL2 were lethal, while a U48G substitution was viable. Here, we characterize viruses harboring all remaining single-nucleotide substitutions in the pentaloop of MHV SL2 and also investigate the degree to which the sequence context of key pentaloop point mutations influences the MHV replication phenotype. U49 or U51 substitution mutants all are viable; C47 substitution mutants also are viable but produce slightly smaller plaques than wild-type virus. In contrast, G50A and G50C viruses are severely crippled and form much smaller plaques. Virus could not be recovered from G50U-containing mutants; rather, only true wild-type revertants or a virus, G50U/C47A, containing a second site mutation were recovered. These functional data suggest that the Watson-Crick edges of C47 and G50 (or A47 and U50 in the G50U/C47A mutant) are in close enough proximity to a hydrogen bond with U51 flipped out of the hairpin. Remarkably, increasing the helical stem stability rescues the previously lethal mutants U48C and G50U. These studies suggest that SL2 functions as an important, but rather plastic, structural element in stimulating subgenomic RNA synthesis in coronaviruses.
Identification and Characterization of Broadly Neutralizing Human Monoclonal Antibodies Directed against the E2 Envelope Glycoprotein of Hepatitis C Virus
Authors: Broering Teresa J. , Garrity Kerry A. , Boatright Naomi K. , Sloan Susan E. , Sandor Frantisek , Thomas William D. , Szabo Gyongyi , Finberg Robert W. , Ambrosino Donna M. , Babcock Gregory J. 
Published: September 2009

ABSTRACT
Nearly all livers transplanted into hepatitis C virus (HCV)-positive patients become infected with HCV, and 10 to 25% of reinfected livers develop cirrhosis within 5 years. Neutralizing monoclonal antibody could be an effective therapy for the prevention of infection in a transplant setting. To pursue this treatment modality, we developed human monoclonal antibodies (HuMAbs) directed against the HCV E2 envelope glycoprotein and assessed the capacity of these HuMAbs to neutralize a broad panel of HCV genotypes. HuMAb antibodies were generated by immunizing transgenic mice containing human antibody genes (HuMAb mice; Medarex Inc.) with soluble E2 envelope glycoprotein derived from a genotype 1a virus (H77). Two HuMAbs, HCV1 and 95-2, were selected for further study based on initial cross-reactivity with soluble E2 glycoproteins derived from genotypes 1a and 1b, as well as neutralization of lentivirus pseudotyped with HCV 1a and 1b envelope glycoproteins. Additionally, HuMAbs HCV1 and 95-2 potently neutralized pseudoviruses from all genotypes tested (1a, 1b, 2b, 3a, and 4a). Epitope mapping with mammalian and bacterially expressed proteins, as well as synthetic peptides, revealed that HuMAbs HCV1 and 95-2 recognize a highly conserved linear epitope spanning amino acids 412 to 423 of the E2 glycoprotein. The capacity to recognize and neutralize a broad range of genotypes, the highly conserved E2 epitope, and the fully human nature of the antibodies make HuMAbs HCV1 and 95-2 excellent candidates for treatment of HCV-positive individuals undergoing liver transplantation.
Identification of Proteins fromPrunus persicaThat Interact with Peach Latent Mosaic Viroid
Authors: Dubé Audrey , Bisaillon Martin , Perreault Jean-Pierre 
Published: September 2009

ABSTRACTPeach latent mosaic viroid (PLMVd) is a small, single-stranded, circular RNA pathogen that infectsPrunus persicatrees. As with all other known viroids, the PLMVd genome does not encode any proteins. Consequently, it must interact with host cellular factors in order to ensure its life cycle. With the objective of identifying cellular proteins that interact with PLMVd, Northwestern hybridizations were performed using partially purified peach leaf extracts. Mass spectrometric analysis of the detected RNA-protein complexes led to the identification of six putative RNA-binding proteins. One of these was found to be elongation factor 1-alpha (eEF1A), and because of its known involvement in the replication and translation of various RNA viruses, further characterizations were performed. Initially, the existence of this interaction received support from an experiment that immunoprecipitated the eEF1A from a crude extract of infected peach leaves, coupled with reverse transcription-PCR detection of the PLMVd. Subsequently, eEF1A interaction with PLMVd strands of both polarities was confirmed in vitro by electrophoresis mobility shift assays, fluorescence spectroscopy, and the prediction of an altered PLMVd RNase mapping profile in the presence of the protein. The potential contribution of eEF1A to the molecular biology of PLMVd, including for viroid replication, is discussed.