bluuebunny/crossref_metadata_2025_split huggingface dataset:
Survival of horses following strangulating large colon volvulus
Authors: SUTHERS J. M. , PINCHBECK G. L. , PROUDMAN C. J. , ARCHER D. C. 
Published: September 2012

SummaryReasons for performing study: The pattern of long‐term survival and specific factors associated with long‐term survival have not previously been evaluated in horses with a strangulating large colon volvulus (LCV).Objectives: To provide data on the long‐term survival of horses with LCV and to identify pre‐, intra‐ and post operative variables associated with survival.Methods: Clinical data and long‐term follow‐up information were obtained from 116 horses with a strangulating LCV (≥360°) undergoing general anaesthesia. Two multivariable Cox proportional hazards models for post operative survival time were developed: Model 1 included all horses and evaluated preoperative variables and Model 2 included horses that survived anaesthesia and evaluated pre‐, intra‐ and post operative variables.Results: The study population comprised 116 horses. Eighty‐nine (76.7%) survived general anaesthesia. Of these, the percentage that survived until discharge, to one year and to 2 years was 70.7%, 48.3% and 33.7%, respectively. Median survival time for horses that survived general anaesthesia was 365 days. In Model 1 increased preoperative packed cell volume (PCV) was significantly associated with reduced post operative survival (hazard ratio [HR] 1.08, 95% confidence interval [CI] 1.05–1.11). However, this effect changed over time. In Model 2 abnormal serosal colour intraoperatively (HR 3.61, 95% CI 1.55–8.44), increased heart rate at 48 h post surgery (HR 1.04, 95% CI 1.02–1.06), and colic during post operative hospitalisation (HR 2.63, 95% CI 1.00–6.95), were all significantly associated with reduced post operative survival.Conclusions: Survival time in horses with a LCV was associated with preoperative PCV, serosal colour, heart rate at 48 h post operatively and colic during post operative hospitalisation.Potential relevance: This study provides evidence‐based information on the long‐term survival of horses with LCV and identifies parameters that may assist decision‐making by clinicians and owners.
Fine‐scale spatiotemporal patterns of genetic variation reflect budding dispersal coupled with strong natal philopatry in a cooperatively breeding mammal
Authors: Nichols Hazel J. , Jordan Neil R. , Jamie Gabriel A. , Cant Michael A. , Hoffman Joseph I. 
Published: September 2012

AbstractThe relatedness structure of animal populations is thought to be a critically important factor underlying the evolution of mating systems and social behaviours. While previous work has shown that population structure is shaped by many biological processes, few studies have investigated how these factors vary over time. Consequently, we explored the fine‐scale spatiotemporal genetic structure of an intensively studied population of cooperatively breeding banded mongooses (Mungos mungo) over a 10‐year period. Overall population structure was strong (average FST = 0.129) but groups with spatially overlapping territories were not more genetically similar to one another than noncontiguous groups. Instead, genetic differentiation was associated with historical group‐fission (budding) events, with new groups diverging from their parent groups over time. Within groups, relatedness was high within but not between the sexes, although the latter increased over time since group formation due to group founders being replaced by philopatric young. This trend was not mirrored by a decrease in average offspring heterozygosity over time, suggesting that close inbreeding may often be avoided, even when immigration into established groups is virtually absent and opportunities for extra‐group matings are rare. Fine‐scale spatiotemporal population structure could have important implications in social species, where relatedness between interacting individuals is a vital component in the evolution of patterns of inbreeding avoidance, reproductive skew and kin‐selected helping and harming.
Mutations in the essential FAS II β‐hydroxyacyl ACP dehydratase complex confer resistance to thiacetazone in Mycobacterium tuberculosis and Mycobacterium kansasii
Authors: Belardinelli Juan M. , Morbidoni Héctor R. 
Published: September 2012

SummaryIt has recently been shown that the anti‐mycobacterial pro‐drug thiacetazone (TAC) inhibits the conversion of double bonds of mycolic acid precursors into cyclopropyl rings in Mycobacterium bovis var BCG, M. marimum and M. chelonae by affecting the cyclopropyl mycolic acid synthases (CMASs) as judged by the build‐up of unsaturated mycolate precursors. In our hands, TAC inhibits mycolic acid biosynthesis in Mycobacterium tuberculosis and M. kansasii with almost negligible accumulation of those precursors. Our observations that ‘de novo’ biosynthesis of all the mycolic acid families decreased upon TAC treatment prompted us to analyse the role of each one of the Type II Fatty Acid Synthase (FASII) enzymes. Overexpression of the hadABC operon, encoding the essential FASII dehydratase complex, but not of any of the remaining FASII genes acting on the elongation of fatty acyl chains leading to the synthesis of meromycolic acids, resulted in high level of resistance to TAC in M. tuberculosis. Spontaneous M. tuberculosis and M. kansasii TAC‐resistant mutants isolated during this work revealed mutations in the hadABC genes strongly supporting our proposal that these enzymes are new players in the resistance to this anti‐mycobacterial compound.
Unravelling mitochondrial retrograde regulation in the abiotic stress induction of rice ALTERNATIVE OXIDASE 1 genes
Authors: LI CHUN‐RONG , LIANG DAN‐DAN , LI JUAN , DUAN YONG‐BO , LI HAO , YANG YA‐CHUN , QIN RUI‐YING , LI LI , WEI PENG‐CHENG , YANG JIAN‐BO 
Published: September 2012

ABSTRACTMitochondrial retrograde regulation (MRR) is the transduction of mitochondrial signals to mediate nuclear gene expression. It is not clear whether MRR is a common regulation mechanism in plant abiotic stress response. In this study, we analysed the early abiotic stress response of the rice OsAOX1 genes, and the induction of OsAOX1a and OsAOX1b (OsAOX1a/b) was selected as a working model for the stress‐induced MRR studies. We found that the induction mediated by the superoxide ion (O2·‐)‐generating chemical methyl viologen was stronger than that of hydrogen peroxide (H2O2). The addition of reactive oxygen species (ROS) scavengers demonstrated that the stress induction was reduced by eliminating O2·‐. Furthermore, the stress induction did not rely on chloroplast‐ or cytosol‐derived O2·‐. Next, we generated transgenic plants overexpressing the superoxide dismutase (SOD) gene at different subcellular locations. The results suggest that only the mitochondrial SOD, OsMSD, attenuated the stress induction of OsAOX1a/b specifically. Therefore, our findings demonstrate that abiotic stress initiates the MRR on OsAOX1a/b and that mitochondrial O2·– is involved in the process.
Hemodialysis Adequacy and the Hospitalized End‐Stage Renal Disease Patient—Raising Awareness
Authors: Kanagasundaram Nigel Suren 
Published: September 2012

AbstractAssessment of hemodialysis adequacy may require different approaches for the stable, outpatient with end‐stage renal disease (ESRD) and for the sick, inpatient with acute kidney injury (AKI). Variability of urea distribution volume, urea generation, and treatment schedule, for instance, complicates dialysis dosing in the latter group although progress has been made in our understanding of their needs. There is a third population, however, for whom hemodialysis dosing requirements remain unclear—the hospitalized ESRD patient. This commentary discusses the key urea kinetic differences between stable ESRD and AKI to give the context to where, on the intervening spectrum, the hospitalized ESRD patient might lie. The limited literature examining hemodialysis dosing in this population is discussed along with those outstanding questions that might form the basis of a future research agenda.
Comparison of Immune Responses to the O-Specific Polysaccharide and Lipopolysaccharide of Vibrio cholerae O1 in Bangladeshi Adult Patients with Cholera
Authors: Johnson Russell A. , Uddin Taher , Aktar Amena , Mohasin M. , Alam Mohammad Murshid , Chowdhury Fahima , Harris Jason B. , LaRocque Regina C. , Kelly Bufano Meagan , Yu Yanan , Wu-Freeman Ying , Leung Daniel T. , Sarracino David , Krastins Bryan , Charles Richelle C. , Xu Peng , Kováč Pavol , Calderwood Stephen B. , Qadri Firdausi , Ryan Edward T. 
Published: September 2012

ABSTRACTImmunity againstVibrio choleraeO1 is serogroup specific, and serogrouping is defined by the O-specific polysaccharide (OSP) part of lipopolysaccharide (LPS). Despite this, human immune responses toV. choleraeOSP have not previously been characterized. We assessed immune responses againstV. choleraeOSP in adults with cholera caused byV. choleraeO1 El Tor serotype Inaba or Ogawa in Dhaka, Bangladesh, using O1 OSP-core–bovine serum albumin (OSPc:BSA) conjugates; responses targeted OSP in these conjugates. Responses of Inaba-infected patients to Inaba OSP and LPS increased significantly in IgG, IgM, and IgA isotypes from the acute to convalescent phases of illness, and the responses correlated well between OSP and LPS (R= 0.86, 0.73, and 0.91, respectively;P< 0.01). Plasma IgG, IgM, and IgA responses to Ogawa OSP and LPS in Ogawa-infected patients also correlated well with each other (R= 0.60, 0.60, and 0.92, respectively;P< 0.01). Plasma IgM responses to Inaba OSP and Ogawa OSP correlated with the respective serogroup-specific vibriocidal antibodies (R= 0.80 and 0.66, respectively;P< 0.001). Addition of either OSPc:BSA or LPS, but not BSA, to vibriocidal assays inhibited vibriocidal responses in a comparable and concentration-dependent manner. Mucosal IgA immune responses to OSP and LPS were also similar. Our study is the first to characterize anti-OSP immune responses in patients with cholera and suggests that responses targetingV. choleraeLPS, including vibriocidal responses that correlate with protection against cholera, predominantly target OSP. Induction of anti-OSP responses may be associated with protection against cholera, and our results may support the development of a vaccine targetingV. choleraeOSP.
Evidence Supporting a Zoonotic Origin of Human Coronavirus Strain NL63
Authors: Huynh Jeremy , Li Shimena , Yount Boyd , Smith Alexander , Sturges Leslie , Olsen John C. , Nagel Juliet , Johnson Joshua B. , Agnihothram Sudhakar , Gates J. Edward , Frieman Matthew B. , Baric Ralph S. , Donaldson Eric F. 
Published: September 2012

ABSTRACT

The relationship between bats and coronaviruses (CoVs) has received considerable attention since the severe acute respiratory syndrome (SARS)-like CoV was identified in the Chinese horseshoe bat (Rhinolophidae) in 2005. Since then, several bats throughout the world have been shown to shed CoV sequences, and presumably CoVs, in the feces; however, no bat CoVs have been isolated from nature. Moreover, there are very few bat cell lines or reagents available for investigating CoV replication in bat cells or for isolating bat CoVs adapted to specific bat species. Here, we show by molecular clock analysis that alphacoronavirus (α-CoV) sequences derived from the North American tricolored bat (
Perimyotis subflavus
) are predicted to share common ancestry with human CoV (HCoV)-NL63, with the most recent common ancestor between these viruses occurring approximately 563 to 822 years ago. Further, we developed immortalized bat cell lines from the lungs of this bat species to determine if these cells were capable of supporting infection with HCoVs. While SARS-CoV, mouse-adapted SARS-CoV (MA15), and chimeric SARS-CoVs bearing the spike genes of early human strains replicated inefficiently, HCoV-NL63 replicated for multiple passages in the immortalized lung cells from this bat species. These observations support the hypothesis that human CoVs are capable of establishing zoonotic-reverse zoonotic transmission cycles that may allow some CoVs to readily circulate and exchange genetic material between strains found in bats and other mammals, including humans.
Hepatitis C Virus Infection Suppresses GLUT2 Gene Expression via Downregulation of Hepatocyte Nuclear Factor 1α
Authors: Matsui Chieko , Shoji Ikuo , Kaneda Shusaku , Sianipar Imelda Rosalyn , Deng Lin , Hotta Hak 
Published: September 2012

ABSTRACT
Hepatitis C virus (HCV) infection causes not only intrahepatic diseases but also extrahepatic manifestations, including type 2 diabetes. We previously reported that HCV replication suppresses cellular glucose uptake by downregulation of cell surface expression of glucose transporter 2 (GLUT2) (D. Kasai et al., J. Hepatol. 50:883–894, 2009). GLUT2 mRNA levels were decreased in both HCV RNA replicon cells and HCV J6/JFH1-infected cells. To elucidate molecular mechanisms of HCV-induced suppression of GLUT2 gene expression, we analyzed transcriptional regulation of the GLUT2 promoter using a series of GLUT2 promoter-luciferase reporter plasmids. HCV-induced suppression of GLUT2 promoter activity was abrogated when the hepatocyte nuclear factor 1α (HNF-1α)-binding motif was deleted from the GLUT2 promoter. HNF-1α mRNA levels were significantly reduced in HCV J6/JFH1-infected cells. Furthermore, HCV infection remarkably decreased HNF-1α protein levels. We assessed the effects of proteasome inhibitor or lysosomal protease inhibitors on the HCV-induced reduction of HNF-1α protein levels. Treatment of HCV-infected cells with a lysosomal protease inhibitor, but not with a proteasome inhibitor, restored HNF-1α protein levels, suggesting that HCV infection promotes lysosomal degradation of HNF-1α protein. Overexpression of NS5A protein enhanced lysosomal degradation of HNF-1α protein and suppressed GLUT2 promoter activity. Immunoprecipitation analyses revealed that the region from amino acids 1 to 126 of the NS5A domain I physically interacts with HNF-1α protein. Taken together, our results suggest that HCV infection suppresses GLUT2 gene expression via downregulation of HNF-1α expression at transcriptional and posttranslational levels. HCV-induced downregulation of HNF-1α expression may play a crucial role in glucose metabolic disorders caused by HCV.
Complete Genome Sequence of the Enterobacter cancerogenus Bacteriophage Enc34
Authors: Kazaks Andris , Dislers Andris , Lipowsky Gerd , Nikolajeva Vizma , Tars Kaspars 
Published: September 2012

ABSTRACT

Enterobacter cancerogenus
is widely distributed in nature and is generally recovered from environmental or vegetal sources. In some cases, it has also been associated with human infections. In this study, the complete genomic sequence of virulent
E. cancerogenus
bacteriophage Enc34 was determined. The Enc34 genome is 60,364 bp in length and contains 80 open reading frames. To our knowledge, this is the first report of a bacteriophage infecting
E. cancerogenus
.
Overexpression of the Ubiquitin-Specific Protease 7 Resulting from Transfection or Mutations in the ICP0 Binding Site Accelerates Rather than Depresses Herpes Simplex Virus 1 Gene Expression
Authors: Kalamvoki Maria , Gu Haidong , Roizman Bernard 
Published: September 2012

ABSTRACT
Earlier studies reported that ICP0, a key regulatory protein encoded by herpes simplex virus 1 (HSV-1), binds ubiquitin-specific protease 7 (USP7). The fundamental conclusion of these studies is that depletion of USP7 destabilized ICP0, that ICP0 mediated the degradation of USP7, and that amino acid substitutions in ICP0 that abolished binding to USP7 significantly impaired the ability of HSV-1 to replicate. We show here that, indeed, depletion of USP7 leads to reduction of ICP0 and that USP7 is degraded in an ICP0-dependent manner. However, overexpression of USP7 or substitution in ICP0 of a single amino acid to abolish binding to USP7 accelerated the accumulation of viral mRNAs and proteins at early times after infection and had no deleterious effect on virus yields. A clue as to why USP7 is degraded emerged from the observation that, notwithstanding the accelerated expression of viral genes, the plaques formed by the mutant virus were very small, implying a defect in virus transmission from cell to cell.
Complete Genome Sequence of Canine Papillomavirus Type 10
Authors: Luff Jennifer , Moore Peter , Zhou Dan , Wang Jingang , Usuda Yukari , Affolter Verena , Schlegel Richard , Yuan Hang 
Published: September 2012

ABSTRACT

Papillomaviruses are epitheliotropic, nonenveloped, circular, double-stranded DNA viruses within the family
Papillomaviridae
that are associated with benign and malignant tumors in humans and animals. We report the complete genome sequence of canine papillomavirus type 10 identified from a pigmented plaque located on the head of a mixed-breed bloodhound.
Double-barrel extracranial–intracranial bypass surgery followed by endovascular carotid artery occlusion in a patient with an extracranial giant internal carotid artery aneurysm due to Ehlers–Danlos syndrome
Authors: Perrin Jason Michael , Turowski Bernd , Steiger Hans-Jakob , Hänggi Daniel 
Published: September 2012

ObjectiveIn this case report we describe a successful interdisciplinary approach (including flow redirection and endovascular occlusion) applied to a patient with a continuously growing extracranial giant aneurysm of the right internal carotid artery (ICA) due to known Ehlers–Danlos syndrome.Case presentationA 42-year-old man with a continuously growing extracranial giant aneurysm of the right ICA sought treatment after failed surgery of a similar lesion of the left ICA. A multidisciplinary consultation was held at the end of 2008.Treatment strategyThe treatment strategy consisted of flow redirection in order to secure sufficient cerebral perfusion prior to surgical trapping of the carotid aneurysm. Flow redirection was achieved by placement of a double-barrel extracranial–intracranial bypass. Subsequent surgical trapping failed due to the extreme size of the aneurysm, making certain identification of surrounding structures impossible. The aneurysm was then successfully occluded by neuroradiological intervention. In a further procedure, a large intra-aneurysmal hematoma was surgically removed to reduce the remaining bulging aneurysm sac.ConclusionsThis case report describes a successful interdisciplinary approach for the treatment of a rare giant extracranial ICA aneurysm in a patient with Ehlers–Danlos syndrome. Treatment options for this type are few and carry high risks. Flow redirection via extracranial–intracranial bypass followed by endovascular occlusion appears to be a good treatment approach.
Targeting the PI3K Pathway in the Brain—Efficacy of a PI3K Inhibitor Optimized to Cross the Blood–Brain Barrier
Authors: Salphati Laurent , Heffron Timothy P. , Alicke Bruno , Nishimura Merry , Barck Kai , Carano Richard A. , Cheong Jonathan , Edgar Kyle A. , Greve Joan , Kharbanda Samir , Koeppen Hartmut , Lau Shari , Lee Leslie B. , Pang Jodie , Plise Emile G. , Pokorny Jenny L. , Reslan Hani Bou , Sarkaria Jann N. , Wallin Jeffrey J. , Zhang Xiaolin , Gould Stephen E. , Olivero Alan G. , Phillips Heidi S. 
Published: September 2012

Abstract
Purpose: Glioblastoma (GBM), the most common primary brain tumor in adults, presents a high frequency of alteration in the PI3K pathway. Our objectives were to identify a dual PI3K/mTOR inhibitor optimized to cross the blood–brain barrier (BBB) and characterize its brain penetration, pathway modulation in the brain and efficacy in orthotopic xenograft models of GBM.
Experimental Design: Physicochemical properties of PI3K inhibitors were optimized using in silico tools, leading to the identification of GNE-317. This compound was tested in cells overexpressing P-glycoprotein (P-gp) or breast cancer resistance protein (BCRP). Following administration to mice, GNE-317 plasma and brain concentrations were determined, and phosphorylated biomarkers (pAkt, p4EBP1, and pS6) were measured to assess PI3K pathway suppression in the brain. GNE-317 efficacy was evaluated in the U87, GS2, and GBM10 orthotopic models of GBM.
Results: GNE-317 was identified as having physicochemical properties predictive of low efflux by P-gp and BCRP. Studies in transfected MDCK cells showed that GNE-317 was not a substrate of either transporter. GNE-317 markedly inhibited the PI3K pathway in mouse brain, causing 40% to 90% suppression of the pAkt and pS6 signals up to 6-hour postdose. GNE-317 was efficacious in the U87, GS2, and GBM10 orthotopic models, achieving tumor growth inhibition of 90% and 50%, and survival benefit, respectively.
Conclusions: These results indicated that specific optimization of PI3K inhibitors to cross the BBB led to potent suppression of the PI3K pathway in healthy brain. The efficacy of GNE-317 in 3 intracranial models of GBM suggested that this compound could be effective in the treatment of GBM. Clin Cancer Res; 18(22); 6239–48. ©2012 AACR.
Freezing of Raindrops in Deep Convective Updrafts: A Microphysical and Polarimetric Model
Authors: Kumjian Matthew R. , Ganson Scott M. , Ryzhkov Alexander V. 
Published: September 2012

Abstract
Polarimetric radar observations of convective storms routinely reveal positive differential reflectivity ZDR extending above the 0°C level, indicative of the presence of supercooled liquid particles lofted by the storm’s updraft. The summit of such “ZDR columns” is marked by a zone of enhanced linear depolarization ratio LDR or decreased copolar cross-correlation coefficient ρhv and a sharp decrease in ZDR that together mark a particle freezing zone. To better understand the relation between changes in the storm updraft and the observed polarimetric variables, it is necessary to first understand the physics governing this freezing process and the impact of freezing on the polarimetric variables.
A simplified, one-dimensional explicit bin microphysics model of stochastic drop nucleation by an immersed foreign particle and subsequent deterministic freezing is developed and coupled with an electromagnetic scattering model to explore the impact of the freezing process on the polarimetric radar variables. As expected, the height of the ZDR column is closely related to the updraft strength and initial drop size distribution. Additionally, the treatment of the stochastic nucleation process can also affect the depth of the freezing zone, underscoring the need to accurately depict this process in parameterizations. Representation of stochastic nucleation and deterministic freezing for each drop size bin yields better agreement between observations and the modeled vertical profiles of the surface reflectivity factor ZH and ZDR than bulk microphysics schemes. Further improvements in the representation of the LDR cap, the observed ZDR gradient in the freezing zone, and the magnitude of the ρhv minimum may require inclusion of accretion, which was not included in this model.
Atrial septal defect closure and de novo migraine: Exclusive ticlopidine efficacy
Authors: Benemei Silvia , Rossi Eleonora , Marcucci Rossella , Giusti Betti , Geppetti Pierangelo 
Published: September 2012

Background: De novo onset or aggravation of migraine has been observed after atrial septal defect closure (ASDC), whereas antiplatelet drugs, such as clopidogrel, used to prevent post-ASDC thromboembolic events, have been associated with migraine amelioration. Case: We report the case of a woman who, after ASDC, experienced de novo severe migraine with aura. Whereas use of acetylsalicylic acid or clopidogrel had no effect, ticlopidine use was associated with migraine amelioration. Migraine relapsed after two ticlopidine dechallenges, and disappeared after drug rechallenges. Conclusion: A ticlopidine trial could be proposed to patients with migraine which occurs or worsens immediately after ASDC and does not improve with clopidogrel.