bluuebunny/crossref_metadata_2025_split huggingface dataset:
Permanent Genetic Resources added to Molecular Ecology Resources Database 1 June 2011–31 July 2011
Authors:   Molecular Ecology Resources Primer Development Consortium, BARKER F. KEITH , BELL JAMES J. , BOGDANOWICZ STEVEN M. , BONATTO S. L. , CEZILLY FRANK , COLLINS SARAH M. , DUBREUIL CHRISTINE , DUFORT MATTHEW J. , ERAUD CYRIL , FUSEYA REIKO , HEAP E. A. , JACOBSEN N. , MADDERS M. , McEWING R. , MICHEL ANDREW P. , MOUGEOT F. , OGDEN R. S. , ORANTES LUCIA C. , OTHMAN A. S. , PARENT ÉRIC , PULIDO‐SANTACRUZ P. , RIOUX‐PARÉ RACHEL , ROBERTS M. F. , ROSAZLINA R. , SAKAMOTO TAKASHI , De‐LEÓN PELAYO SALINAS , SÉVIGNY JEAN‐MARIE , ST‐ONGE PHILIPPE , TERRAUBE J. , TINGAY R. E. , TREMBLAY RÉJEAN , WATANABE SEIICHI , WATTIER RÉMI A. 
Published: September 2011

AbstractThis article documents the addition of 112 microsatellite marker loci and 24 pairs of single nucleotide polymorphism (SNP) sequencing primers to the Molecular Ecology Resources Database. Loci were developed for the following species: Agelaius phoeniceus, Austrolittorina cincta, Circus cyaneus, Circus macrourus, Circus pygargus, Cryptocoryne × purpurea Ridl. nothovar. purpurea, Mya arenaria, Patagioenas squamosa, Prochilodus mariae, Scylla serrata and Scytalopus speluncae. These loci were cross‐tested on the following species: Cryptocoryne × purpurea nothovar. purpurea, Cryptocoryne affinis, Cryptocoryne ciliata, Cryptocoryne cordata var. cordata, Cryptocoryne elliptica, Cryptocoryne griffithii, Cryptocoryne minima, Cryptocoryne nurii and Cryptocoryne schulzei. This article also documents the addition of 24 sequencing primer pairs and 24 allele‐specific primers or probes for Aphis glycines.
From Hypertension to Stroke: Mechanisms and Potential Prevention Strategies
Authors: Yu Jian‐Guang , Zhou Rui‐Rui , Cai Guo‐Jun 
Published: September 2011

SUMMARYStroke is a major cause of disability and death worldwide. Prevention aimed at risk factors of stroke is the most effective strategy to curb the stroke pandemic. Hypertension is one of the most important risk factors for stroke. Despite the substantial evidence of the benefits of lowering blood pressure, conventional treatment does not normalize the burden of major cardiovascular events in patients with hypertension. Fully understanding the factors involved in the hypertension‐induced stroke helps to develop new strategies for stroke prevention. Antihypertensive therapies selected should have positive blood pressure‐independent effects on stroke risk. This review summarizes the factors involved in the hypertension‐induced stroke, such as oxidative stress, inflammation, and arterial baroreflex dysfunction, and potential strategies for its prevention, therefore, provides clues for clinicians.
Tumor markers are elevated in patients with rheumatoid arthritis and do not indicate presence of cancer
Authors: BERGAMASCHI Samuel , MORATO Edelton , BAZZO Maria , NEVES Fabricio , FIALHO Sonia , CASTRO Glaucio , ZIMMERMANN Adriana , PEREIRA Ivanio 
Published: September 2011

AbstractAim:  To investigate serum levels of tumor markers in patients with rheumatoid arthritis (RA) and their association with disease activity or the presence of cancer.Method:  We performed an observational cohort study including 100 patients with RA and control subjects. Serum levels of tumor markers carcinoembryonic antigen (CEA), cancer antigen (CA) 125, CA 19–9 and CA 15–3 were evaluated along with clinical and laboratorial RA data. Association tests between tumor markers levels and RA disease activity parameters were performed. Patients with abnormal tests were submitted to further investigation, including chest X‐ray, colonoscopy, abdominal ultrasonography, upper gastrointestinal endoscopy and mammography, depending on the type of tumor marker that was elevated.Results:  Patients with RA had high levels of CEA and CA 19–9 more frequently than controls (P < 0.05). No correlation was found between tumor markers and RA disease activity assessed by the Disease Activity Score 28. Two neoplasms were found, but only one was related to high tumor marker (an ovarian carcinoma with high CA 125 levels).Conclusion:  High tumor markers were frequently found in RA patients, even with controlled disease and were not related to actual cancer. Therefore, small increases of these markers in RA cases probably do not warrant a search for an occult neoplasm.
Response to gemcitabine–platinum chemotherapy by single nucleotide polymorphisms of RRM1 and ERCC1 genes in patients with non‐small‐cell lung cancer
Authors: Oh In‐Jae , Ban Hee‐Jung , Kim Kyu‐Sik , Song Sang‐Yun , Na Kook‐Joo , Kim Yun‐Hyeon , Ahn Sung‐Ja , Choi Song , Cho Hyun‐Ju , Kim Young‐Chul 
Published: September 2011

AbstractBackground:  RRM1, the regulatory subunit of ribonucleotide reductase, is involved in carcinogenesis and the response to gemcitabine. Two single nucleotide polymorphisms (SNP) in the RRM1 gene (RR37 and RR524) impact promoter activity and are associated with prognosis. The excision repair cross‐complementation group 1 protein (ERCC1) is associated with platinum resistance. A SNP of the ERCC1 gene (T19007C) has been reported as a prognostic marker in platinum‐treated non‐small‐cell lung cancer (NSCLC).Materials and methods:  Patients with stage IIIB or IV NSCLC were treated with gemcitabine and platinum (GP) as first‐line chemotherapy. Adenocarcinoma was the most frequent histological type, followed by squamous cell carcinoma and then other types. SNP were analyzed with real time‐polymerase chain reaction using genomic DNA extracted from peripheral blood.Results:  Based on responses to GP patients were classified as responders or non‐responders. The response rate was significantly higher in patients with the RR AC‐CT genotype (35/64, 54.7%) compared to those with the RR CC‐TT genotype (56/147, 38.1%, P= 0.025). No significant difference in response rate was observed according to ERCC1 genotype. In 128 patients with non‐squamous cell lung cancer, RR AC‐CT + ERCC1 CC (63.2%) and RR AC‐CT + ERCC1 CT/TT (61.9%) showed higher response rates compared to RR CC‐TT + ERCC1 CC (36.5%), and RR CC‐TT + ERCC1 CT/TT (22.2%; P= 0.004). Progression‐free and overall survival times were not different between genotypes.Conclusions:  We observed significantly different responses to the GP regimen according to SNP of the RRM1 and ERCC1 genes.
Reading development in a tracked school system: A longitudinal study over 3 years using propensity score matching
Authors: Retelsdorf Jan , Becker Michael , Köller Olaf , Möller Jens 
Published: September 2011

Background. Assigning students to different school tracks on the basis of their achievement levels is a widely used strategy that aims at giving students the best possible learning opportunity. There is, however, a growing body of literature that questions such positive effects of tracking.Aims. This study compared the developmental trajectories of reading comprehension and decoding speed between students at academic track schools that typically prepare students for university entrance and students at non‐academic track schools that usually prepare students for vocational education.Sample. In a longitudinal design with three occasions of data collection, the authors drew on a sample of N= 1,508 5th graders (age at T1 about 11 years, age at T3 about 14 years) from 60 schools in Germany. The academic track sample comprised n= 568 students; the non‐academic track sample comprised n= 940 students.Method. Achievement measures were obtained by standardized tests of reading comprehension and decoding speed. Students at the different tracks were closely matched using propensity scores. To compare students’ growth trajectories between the different school tracks, we applied multi‐group latent growth curve models.Results. Comparable results were recorded for the complete (unmatched) sample and for the matched pairs. In all cases, students at the different tracks displayed a similar growth in reading comprehension, whereas larger growth rates for students at academic track schools were recorded for decoding speed.Conclusions. Our findings contribute to an increasing body of literature suggesting that tracking might have undesired side effects.
Absolute Bioavailability of
cis
-Mirincamycin and
trans
-Mirincamycin in Healthy Rhesus Monkeys and
Ex Vivo
Antimalarial Activity against Plasmodium falciparum
Authors: Khemawoot Phisit , Saunders David , Rasameesoraj Maneerat , Melendez Victor , Imerbsin Rawiwan , Ohrt Colin , Fracisco Susan , Teja-isavadharm Paktiya 
Published: September 2011

ABSTRACT

The pharmacokinetics, oral bioavailability, and
ex vivo
antimalarial activity of mirincamycin isomers in a healthy rhesus monkey model were assessed to support lead optimization of novel nonhemolytic drugs for radical cure and causal prophylaxis of malaria. Fourteen male rhesus monkeys were randomized to four groups, which included
cis
and
trans
isomers by the oral and intravenous routes, with vehicle-only controls for each dosing route. Concentration-time data were collected for 7 days and were analyzed by noncompartmental analysis.
cis
-Mirincamycin had an absolute oral bioavailability of 13.6%, which was slightly higher than that of
trans
-mirincamycin (11.7%), but this difference was not statistically significant. There was a statistically significant difference between the area under the concentration-time curve from zero to 48 h (AUC
0–48
) of
cis
-mirincamycin and that of
trans
-mirincamycin after oral dosing. When cultured
in vitro
with the W2 clone of
Plasmodium falciparum
, the 50% inhibitory concentrations for
cis
-mirincamycin,
trans
-mirincamycin, and dihydroartemisinin were 11,300, 12,300, and 2.30 nM, respectively. However, when dosed primate plasma was cultured
ex vivo
against the W2 clone, both isomers had much greater relative potencies than their
in vitro
activities relative to results for dihydroartemisinin, an increase of approximately 100-fold for the
cis
isomer and 150-fold for the
trans
isomer. Further, oral
ex vivo
activity was significantly higher than intravenous activity for both isomers, particularly during the first 90 min following dosing, suggesting the first-pass formation of one or more metabolites with blood-stage antimalarial activity. Identification of the metabolic pathways and metabolites may help to further delineate the properties of this class of drugs with previously demonstrated liver-stage antimalarial activity.
An Escherichia coli O157-Specific Engineered Pyocin Prevents and Ameliorates Infection by E. coli O157:H7 in an Animal Model of Diarrheal Disease
Authors: Ritchie Jennifer M. , Greenwich Jennifer L. , Davis Brigid M. , Bronson Roderick T. , Gebhart Dana , Williams Steven R. , Martin David , Scholl Dean , Waldor Matthew K. 
Published: September 2011

ABSTRACT

AvR2-V10.3 is an engineered R-type pyocin that specifically kills
Escherichia coli
O157, an enteric pathogen that is a major cause of food-borne diarrheal disease. New therapeutics to counteract
E. coli
O157 are needed, as currently available antibiotics can exacerbate the consequences of infection. We show here that orogastric administration of AvR2-V10.3 can prevent or ameliorate
E. coli
O157:H7-induced diarrhea and intestinal inflammation in an infant rabbit model of infection when the compound is administered either in a postexposure prophylactic regimen or after the onset of symptoms. Notably, administration of AvR2-V10.3 also reduces bacterial carriage and fecal shedding of this pathogen. Our findings support the further development of pathogen-specific R-type pyocins as a way to treat enteric infections.
Digallate Dimers of (−)-Epigallocatechin Gallate Inactivate Herpes Simplex Virus
Authors: Isaacs Charles E. , Xu Weimin , Merz George , Hillier Sharon , Rohan Lisa , Wen Guang Y. 
Published: September 2011

ABSTRACT

Topical microbicides are potentially an alternative method to vaccines for reducing the spread of herpes simplex virus (HSV). We have previously shown (S. Liu et al., Biochim. Biophys. Acta 1723:270–281, 2005) that the catechin (−)-epigallocatechin gallate (EGCG) inactivates HSV at neutral pH; however, to function in the female genital tract EGCG must also be effective at acidic pH. EGCG inactivated HSV-1 and HSV-2 at pH 8.0 by 3 log
10
to 4 log
10
but was ineffective at pH 5.7. The EGCG digallate dimers theasinensin A, P2, and theaflavin-3,3′-digallate (TF-3) inactivated both viruses by 3 log
10
to 4 log
10
at pH 5.7 and as much as 5 log
10
at pH 8.0. TF-3 inactivated HSV-1 and HSV-2 by 4 to 5 log
10
in the pH range of 4.0 to 5.7. Dimers with one gallate moiety had antiviral activity intermediate between the activities of EGCG and digallate dimers. Confocal and electron microscopy showed that theasinensin A did not damage Vero cells. All EGCG dimers inactivated enveloped viruses with class I, class II, and class III (HSV-1, HSV-2) fusion proteins more effectively than did monomeric EGCG. EGCG had no activity against the nonenveloped viruses tested, but TF-3 reduced the titer of 4 of 5 nonenveloped viruses by ≅2 to 3.5 log
10
. Results also showed that HSV-1 glycoprotein B (gB) was aggregated more rapidly by theasinensin A than EGCG, which, when taken together with the nonenveloped virus data, suggests that dimers may inhibit the function of viral proteins required for infectivity. Digallate dimers of EGCG appear to have excellent potential as microbicidal agents against HSV at acidic and neutral pHs.
The Type III System-Secreted Effector EspZ Localizes to Host Mitochondria and Interacts with the Translocase of Inner Mitochondrial Membrane 17b
Authors: Shames Stephanie R. , Croxen Matthew A. , Deng Wanyin , Finlay B. Brett 
Published: September 2011

ABSTRACT

Enteropathogenic and enterohemorrhagic
Escherichia coli
(EPEC and EHEC, respectively) are attaching and effacing (A/E) bacterial pathogens that cause severe diarrheal disease worldwide. To cause disease, A/E pathogens require a type III secretion system, which facilitates transport of bacterial effector proteins directly into infected host cells. One of these effector proteins translocated by the type III secretion system, EspZ, is essential for A/E pathogen infection and functions to prevent rapid death of EPEC-infected cells. We further investigated the mechanism of EspZ-mediated protection of infected host cells and found that a severe decrease in host mitochondrial membrane potential (Δψ
m
) occurs concurrently with host cell lysis during infection with EPEC lacking EspZ (Δ
espZ
). It was also demonstrated that EspZ localizes to host cell mitochondria and interacts with the translocase of inner mitochondrial membrane 17b (TIM17b). In addition, host cell cytotoxicity was exacerbated in the absence of TIM17b during wild-type (WT) EPEC infection. The findings of this study together provide the first evidence that EspZ localizes to host mitochondria and that TIM17b contributes to protection against rapid cell death during EPEC infection.
The Iron-Repressed, AraC-Like Regulator MpeR Activates Expression of
fetA
in Neisseria gonorrhoeae
Authors: Hollander Aimee , Mercante Alexandra Dubon , Shafer William M. , Cornelissen Cynthia Nau 
Published: September 2011

ABSTRACT

Neisseria gonorrhoeae
is an obligate human pathogen that causes the common sexually transmitted infection gonorrhea. Gonococcal infections cause significant morbidity, particularly among women, as the organism ascends to the upper reproductive tract, resulting in pelvic inflammatory disease, ectopic pregnancy, and infertility. In the last few years, antibiotic resistance rates have risen dramatically, leading to severe restriction of treatment options for gonococcal disease. Gonococcal infections do not elicit protective immunity, nor is there an effective vaccine to prevent the disease. Thus, further understanding of the expression, function, and regulation of surface antigens could lead to better treatment and prevention modalities in the future. In the current study, we determined that an iron-repressed regulator, MpeR, interacted specifically with the DNA sequence upstream of
fetA
and activated FetA expression. Interestingly, MpeR was previously shown to regulate the expression of gonococcal antimicrobial efflux systems. We confirmed that the outer membrane transporter FetA allows gonococcal strain FA1090 to utilize the xenosiderophore ferric enterobactin as an iron source. However, we further demonstrated that FetA has an extended range of substrates that encompasses other catecholate xenosiderophores, including ferric salmochelin and the dimers and trimers of dihydroxybenzoylserine. We demonstrated that
fetA
is part of an iron-repressed, MpeR-activated operon which putatively encodes other iron transport proteins. This is the first study to describe a regulatory linkage between antimicrobial efflux and iron transport in
N. gonorrhoeae
. The regulatory nidus that links these systems, MpeR, is expressed exclusively by pathogenic neisseriae and is therefore expected to be an important virulence factor.
Perceived barriers and facilitators to physical activity for children with disability: a systematic review
Authors: Shields Nora , Synnot Anneliese Jane , Barr Megan 
Published: September 2011

AimThe aim of this systematic review was to investigate the perceived barriers and facilitators to physical activity among children with disability.Methods10 electronic databases were searched from the earliest time available to September 2010 to identify relevant articles. Articles were included if they examined the barriers or facilitators to physical activity for children with disability and were written in English. Articles were excluded if they included children with an acute, transient or chronic medical condition, examined sedentary leisure activities, or societal participation in general. Two reviewers independently assessed the search yields, extracted the data and assessed trial quality. Data were analysed descriptively.Results14 articles met the inclusion criteria. Barriers included lack of knowledge and skills, the child's preferences, fear, parental behaviour, negative attitudes to disability, inadequate facilities, lack of transport, programmes and staff capacity, and cost. Facilitators included the child's desire to be active, practising skills, involvement of peers, family support, accessible facilities, proximity of location, better opportunities, skilled staff and information.ConclusionPersonal, social, environmental, and policy and programme-related barriers and facilitators influence the amount of activity children with disability undertake. The barriers to physical activity have been studied more comprehensively than the facilitators.
Is It Downhill from Here? Eliminating Leukemic Stem Cells and Curing Chronic Myeloid Leukemia
Authors: Smith Catherine C. , Shah Neil P. 
Published: September 2011

Abstract
Patients with chronic phase chronic myeloid leukemia who respond to imatinib have a rapid initial decrease in BCR-ABL transcript levels (α), followed by a slow decline (β). The rate of β decrease is consistent with declining leukemic stem cells and may predict which patients may safely discontinue therapy. Clin Cancer Res; 17(21); 6605–7. ©2011 AACR.
Effect of Hypoxia-Inducible Factor-1α Gene Therapy on Walking Performance in Patients With Intermittent Claudication
Authors: Creager Mark A. , Olin Jeffrey W. , Belch Jill J.F. , Moneta Gregory L. , Henry Timothy D. , Rajagopalan Sanjay , Annex Brian H. , Hiatt William R. 
Published: September 2011

Background—
Hypoxia-inducible factor-1α (HIF-1α) is a transcriptional regulatory factor that orchestrates cellular responses to hypoxia. It increases collateral vessel growth and blood flow in models of hind-limb ischemia. This study tested whether intramuscular administration of Ad2/HIF-1α/VP16, an engineered recombinant type 2 adenovirus vector encoding constitutively active HIF-1α, improves walking time in patients with peripheral artery disease and intermittent claudication.

Methods and Results—

Two hundred eighty-nine patients with claudication were randomized in a double-blind manner to 1 of 3 doses of Ad2/HIF-1α/VP16 (2×10
9
, 2×10
10
, or 2×10
11
viral particles) or placebo, administered by 20 intramuscular injections to each leg. Graded treadmill tests were performed at baseline and then 3, 6, and 12 months after treatment. The primary end point was the change in peak walking time from baseline to 6 months. The secondary end point was change in claudication onset time, and tertiary end points included changes in ankle-brachial index and quality-of-life assessments. Median peak walking time increased by 0.82 minutes (interquartile range, −0.05–1.93 minutes) in the placebo group and by 0.82 minutes (interquartile range, −0.07–2.12 minutes), 0.28 minutes (interquartile range, −0.37–1.70 minutes), and 0.78 minutes (interquartile range, −0.02–2.10 minutes) in the HIF-1α 2×10
9
, 2×10
10
, and 2×10
11
viral particle groups, respectively (
P
=NS between placebo and each HIF-1α treatment group). There were no significant differences in claudication onset time, ankle-brachial index, or quality-of-life measurements between the placebo and each HIF-1α group.

Conclusions—
Gene therapy with intramuscular administration of Ad2/HIF-1α/VP16 is not an effective treatment for patients with intermittent claudication.

Clinical Trial Registration—

URL:
http://www.clinicaltrials.gov
. Unique identifier: NCT00117650.
Disruption of Na
+
,HCO
3
−
Cotransporter NBCn1 (slc4a7) Inhibits NO-Mediated Vasorelaxation, Smooth Muscle Ca
2+
Sensitivity, and Hypertension Development in Mice
Authors: Boedtkjer Ebbe , Praetorius Jeppe , Matchkov Vladimir V. , Stankevicius Edgaras , Mogensen Susie , Füchtbauer Annette C. , Simonsen Ulf , Füchtbauer Ernst-Martin , Aalkjaer Christian 
Published: September 2011

Background—

Disturbances in pH affect artery function, but the mechanistic background remains controversial. We investigated whether Na
+
,HCO
3
−
cotransporter NBCn1, by regulating intracellular pH (pH
i
), influences artery function and blood pressure regulation.

Methods and Results—

Knockout of NBCn1 in mice eliminated Na
+
,HCO
3
−
cotransport and caused a lower steady-state pH
i
in mesenteric artery smooth muscle and endothelial cells in situ evaluated by fluorescence microscopy. Using myography, arteries from NBCn1 knockout mice showed reduced acetylcholine-induced NO-mediated relaxations and lower rho-kinase-dependent norepinephrine-stimulated smooth muscle Ca
2+
sensitivity. Acetylcholine-stimulated NO levels (electrode measurements) and N-nitro-l-arginine methyl ester–sensitive l-arginine conversion (radioisotope measurements) were reduced in arteries from NBCn1 knockout mice, whereas relaxation to NO-donor S-nitroso-N-acetylpenicillamine, acetylcholine-induced endothelial Ca
2+
responses (fluorescence microscopy), and total and Ser-1177 phosphorylated endothelial NO-synthase expression (Western blot analyses) were unaffected. Reduced NO-mediated relaxations in arteries from NBCn1 knockout mice were not rescued by superoxide scavenging. Phosphorylation of myosin phosphatase targeting subunit at Thr-850 was reduced in arteries from NBCn1 knockout mice. Evaluated by an in vitro assay, rho-kinase activity was reduced at low pH. Without CO
2
/HCO
3
−
, no differences in pH
i
, contraction or relaxation were observed between arteries from NBCn1 knockout and wild-type mice. Based on radiotelemetry and tail-cuff measurements, NBCn1 knockout mice were mildly hypertensive at rest, displayed attenuated blood pressure responses to NO-synthase and rho-kinase inhibition and were resistant to developing hypertension during angiotensin-II infusion.

Conclusions—
Intracellular acidification of smooth muscle and endothelial cells after knockout of NBCn1 inhibits NO-mediated and rho-kinase–dependent signaling in isolated arteries and perturbs blood pressure regulation.