bluuebunny/crossref_metadata_2025_split huggingface dataset:
Draft Genome Sequence of the Pathogenic Oomycete Pythium insidiosum Strain Pi-S, Isolated from a Patient with Pythiosis
Authors: Rujirawat Thidarat , Patumcharoenpol Preecha , Lohnoo Tassanee , Yingyong Wanta , Lerksuthirat Tassanee , Tangphatsornruang Sithichoke , Suriyaphol Prapat , Grenville-Briggs Laura J. , Garg Gagan , Kittichotirat Weerayuth , Krajaejun Theerapong 
Published: June 2015

ABSTRACT

Pythium insidiosum
is an oomycete that causes a life-threatening infectious disease called pythiosis in humans and animals living in tropical and subtropical countries. Here, we report the first draft genome sequence of
P. insidiosum
. The genome of
P. insidiosum
is 53.2 Mb and contains 14,962 open reading frames.
Draft Genome Sequence of the First Human Isolate of the Ruminant Pathogen Mycoplasma capricolum subsp.
capricolum
Authors: Seersholm Frederik Valeur , Fischer Anne , Heller Martin , Jores Joerg , Sachse Konrad , Mourier Tobias , Hansen Anders Johannes 
Published: June 2015

ABSTRACT

Mycoplasma capricolum
subsp.
capricolum
is a well-known pathogen of small ruminants. A recent human case of septicemia involving this agent raised the question of its potential pathogenicity to humans. We present the first draft genome sequence of a human
Mycoplasma capricolum
subsp.
capricolum
isolate.
Genome Sequences of Mycobacteriophages AlanGrant, Baee, Corofin, OrangeOswald, and Vincenzo, New Members of Cluster B
Authors: Pope Welkin H. , Carbonara Maria E. , Cioffi Hanna M. , Cruz Tyler , Dang Brian Q. , Doyle Alexander N. , Fan Olivia H. , Gallagher Molly , Gentile Gabrielle M. , German Brian A. , Farrell Margaret E. , Gerwig Madeline , Hunter Kelsey L. , Lefever Virginia E. , Marfisi Nicole A. , McDonnell Jill E. , Monga Jappmann K. , Quiroz Kevin G. , Pong Alexandra C. , Rimple Patrick A. , Situ Michelle , Sohnen Peri C. , Stockinger Annmarie N. , Thompson Paige K. , Torchio Nicole M. , Toner Chelsea L. , Ulbrich Megan C. , Vohra Neelam I. , Zakir Aala , Adkins Nancy L. , Brown Bryony R. , Churilla Bryce M. , Kramer Zachary J. , Lapin Jonathan S. , Montgomery Matthew T. , Prout Ashley K. , Grubb Sarah R. , Warner Marcie H. , Bowman Charles A. , Russell Daniel A. , Hatfull Graham F. 
Published: June 2015

ABSTRACT

AlanGrant, Baee, Corofin, OrangeOswald, and Vincenzo are newly isolated phages of
Mycobacterium smegmatis
mc
2
155 discovered in Pittsburgh, Pennsylvania, USA. All five phages share nucleotide similarity with cluster B mycobacteriophages but span considerable diversity with Corofin and OrangeOswald in subcluster B3, AlanGrant and Vincenzo in subcluster B4, and Baee in subcluster B5.
Genome Sequences of Cluster G Mycobacteriophages Cambiare, FlagStaff, and MOOREtheMARYer
Authors: Pope Welkin H. , Augustine David A. , Carroll Daniel C. , Duncan Julia C. , Harwi Kyle M. , Howry Rachel , Jagessar Bhavita , Lum Brandon A. , Meinert Justin W. , Migliozzi Jeffrey S. , Milliken Katherine A. , Mitchell Chandler J. , Nalatwad Akanksha S. , Orlandini Kaila C. , Rhein Michael J. , Saravanan Vishmayaa , Seese Brett A. , Schiebel Johnathon G. , Thomas Kayla B. , Adkins Nancy L. , Cohen Karen L. , Iyengar Varun B. , Kim Hannah , Kramer Zachary J. , Montgomery Matthew T. , Schafer Claire E. , Wilkes Kellyn E. , Grubb Sarah R. , Warner Marcie H. , Bowman Charles A. , Russell Daniel A. , Hatfull Graham F. 
Published: June 2015

ABSTRACT

Mycobacteriophages Cambiare, FlagStaff, and MOOREtheMARYer are newly isolated phages of
Mycobacterium smegmatis
mc
2
155 recovered from soil samples in Pittsburgh, PA. All three genomes are closely related to cluster G mycobacteriophages but differ sufficiently in nucleotide sequence and gene content to warrant division of cluster G into several subclusters.
Genome Sequence of a Newly Isolated Mycobacteriophage, ShedlockHolmes
Authors: Pope Welkin H. , Carter Jordan T. , Dasher Kegan L. , Haynberg Mikaela C. , Reddi Anoop , Shedlock Kathleen A. , Lapin Jonathan S. , Prout Ashley K. , Grubb Sarah R. , Warner Marcie H. , Bowman Charles A. , Russell Daniel A. , Hatfull Graham F. 
Published: June 2015

ABSTRACT

Mycobacteriophage ShedlockHolmes is a newly isolated phage infecting
Mycobacterium smegmatis
mc
2
155. It has a 61,081-bp genome containing 99 predicted protein-coding genes and one tRNA gene. ShedlockHolmes is closely related to mycobacteriophages Pixie, Keshu, and MacnCheese and is a new member of subcluster K3.
Draft Genome Sequence of Bacillus coagulans NL01, a Wonderful
l
-Lactic Acid Producer
Authors: Zheng Zhaojuan , Jiang Ting , Lin Xi , Zhou Jie , Ouyang Jia 
Published: June 2015

ABSTRACT

Here, we report the draft genome sequence of
Bacillus coagulans
NL01, which could produce high optically pure
l
-lactic acid using xylose as a sole carbon source. The draft genome is 3,505,081 bp, with 144 contigs. About 3,903 protein-coding genes and 92 rRNAs are predicted from this assembly.
Genome Sequence of the Alkaline-Tolerant
Cellulomonas
sp. Strain FA1
Authors: Cohen Michael F. , Hu Ping , Nguyen My Vu , Kamennaya Nina , Brown Natasha , Woyke Tanja , Kyrpides Nikos , Holman Hoi-Ying , Torok Tamas 
Published: June 2015

ABSTRACT

We present the genome of the cellulose-degrading
Cellulomonas
sp. strain FA1 isolated from an actively serpentinizing highly alkaline spring. Knowledge of this genome will enable studies into the molecular basis of plant material degradation in alkaline environments and inform the development of lignocellulose bioprocessing procedures for biofuel production.
Genome Sequence of a Klebsiella pneumoniae Sequence Type 258 Isolate with Prophage-Encoded K. pneumoniae Carbapenemase
Authors: Chen Liang , Chavda Kalyan D. , DeLeo Frank R. , Bryant Kendall A. , Jacobs Michael R. , Bonomo Robert A. , Kreiswirth Barry N. 
Published: June 2015

ABSTRACT

We present the draft genome sequence of a
Klebsiella pneumoniae
carbapenemase (KPC)-producing sequence type 258 (ST258)
K. pneumoniae
strain, ST258_FL. Uniquely, strain ST258_FL harbors two copies of the
bla
KPC
gene on the chromosome, one of which is integrated into a prophage.
Genome Sequence of Rhizobacterium Serratia marcescens Strain 90-166, Which Triggers Induced Systemic Resistance and Plant Growth Promotion
Authors: Jeong Haeyoung , Kloepper Joseph W. , Ryu Choong-Min 
Published: June 2015

ABSTRACT

The rhizobacterium
Serratia marcescens
strain 90-166 elicits induced systemic resistance against plant pathogens and herbivores and promotes plant growth under greenhouse and field conditions. Strain 90-166 secretes volatile compounds, siderophores, salicylic acid, and quorum-sensing autoinducers as bacterial determinants toward plant health. Herein, we present its draft genome sequence.
Draft Genome Sequence of
Shewanella
sp. ECSMB14102, a Mussel Recruitment-Promoting Bacterium Isolated from the East China Sea
Authors: Yang Jin-Long , Guo Xing-Pan , Chen Yu-Ru , Gao Wei , Ding De-Wen 
Published: June 2015

ABSTRACT

Shewanella
sp. ECSMB14102, which promotes recruitment of the mussel
Mytilus coruscus
, was isolated from natural biofilms formed on glass slides submerged in the East China Sea. Here, we present the draft genome sequence, which comprises 4.41 Mb with a G+C content of 52.2%. The genomic information in this strain will contribute to deepening our understanding of bacteria-animal interaction.
Genome Sequences of Pseudomonas amygdali pv. tabaci Strain ATCC 11528 and pv. lachrymans Strain 98A-744
Authors: Jeong Haeyoung , Kloepper Joseph W. , Ryu Choong-Min 
Published: June 2015

ABSTRACT

Certain pathovars of
Pseudomonas amygdali
, which is newly reclassified from
Pseudomonas syringae
by DNA-DNA hybridization and ribotyping, cause many serious diseases of major crop plants. Herein, we present draft genome sequences of
P. amygdali
pv. tabaci strain ATCC 11528 and
P. amygdali
pv. lachrymans strain 98A-744.
Systematic review of rehabilitation programmes initiated within 90 days of a transient ischaemic attack or ‘minor’ stroke: a protocol
Authors: Heron Neil , Kee Frank , Donnelly Michael , Cupples Margaret E 
Published: June 2015

IntroductionTransient ischaemic attacks (TIAs) and strokes are highly prevalent conditions. Stroke killed 5.7 million people worldwide in 2005 and is estimated to cause 6.5 million deaths globally in 2015. Stroke survivors are often left with considerable disability. Many strokes are preceded by a TIA/‘minor’ stroke in the previous 90 days and therefore the immediate period after a TIA/minor’ stroke is a crucial time to intervene to tackle known vascular risk factors. Although rehabilitation following a TIA/minor stroke is widely recommended, there is a paucity of research that offers an evidence base on which the development or optimisation of interventions can be based, particularly for home-based approaches and non-pharmacological interventions in the acute period following the initial TIA/‘minor’ stroke. This systematic review will investigate the effect of rehabilitation programmes initiated within 90 days of the diagnosis of a TIA or ‘minor’ stroke aimed at reducing the subsequent risk of stroke.Methods/designThis systematic review will be reported in line with the Preferred Reporting Items for Systematic Reviews and Meta-analyses(PRISMA) guidance. Randomised and quasi-randomised controlled trials of rehabilitation programmes initiated within 90 days of a TIA or ‘minor’ stroke will be included. Articles will be identified through a comprehensive search of the following databases, guided by a medical librarian: the Cochrane Library, Web of Science, MEDLINE, Embase, CINAHL and PsycINFO. Two review authors will independently screen articles retrieved from the search for eligibility and extract relevant data on methodological issues. A narrative synthesis will be completed when there is insufficient data to permit a formal meta-analysis.DiscussionThis review will be of value to clinicians and healthcare professionals working in TIA and stroke services as well as to general practitioners/family physicians who care for these patients in the community and to researchers involved in designing and evaluating rehabilitation interventions.Trial registration numberCRD42015016450.
Infundibular dilations of the posterior communicating arteries: pathogenesis, anatomical variants, aneurysm formation, and subarachnoid hemorrhage
Authors: Chen Ching-Jen , Moosa Shayan , Ding Dale , Raper Daniel M , Burke Rebecca M , Lee Cheng-Chia , Chivukula Srinivas , Wang Tony R , Starke Robert M , Crowley R Webster , Liu Kenneth C 
Published: June 2015

BackgroundCerebrovascular infundibular dilations (IDs) are triangular-shaped widenings less than 3 mm in diameter, which are most commonly found at the posterior communicating artery (PCoA). The aims of this systematic review are to elucidate the natural histories of IDs, determine their risk of progression to significant pathology, and discuss potential management options.MethodsA comprehensive literature search of PubMed was used to find all case reports and series relating to cerebral IDs. IDs were classified into three types: type I IDs do not exhibit morphological change over a long follow-up period, type II IDs evolve into saccular aneurysms, while type III IDs are those that result in subarachnoid hemorrhage without prior aneurysmal progression. Data were extracted from studies that demonstrated type II or III IDs.ResultsWe reviewed 16 cases of type II and seven cases of type III IDs. For type II IDs, 81.3% of patients were female with a median age at diagnosis of 38. All type II IDs were located at the PCoA without a clear predilection for sidedness. Median time to aneurysm progression was 7.5 years. For type III IDs there was no clear gender preponderance and the median age at diagnosis was 51. The PCoA was involved in 85.7% of cases, with 57.1% of IDs occurring on the left. Most patients were treated with clipping. Risk factors for aneurysm formation appear to be female gender, young age, left-sided localization, coexisting aneurysms, and hypertension.ConclusionsIDs can rarely progress to aneurysms or rupture. Young patients with type II or III IDs with coexisting aneurysms or hypertension may benefit from long-term imaging surveillance.
Identification and Functional Validation of Reciprocal microRNA–mRNA Pairings in African American Prostate Cancer Disparities
Authors: Wang Bi-Dar , Ceniccola Kristin , Yang Qi , Andrawis Ramez , Patel Vyomesh , Ji Youngmi , Rhim Johng , Olender Jacqueline , Popratiloff Anastas , Latham Patricia , Lai Yinglei , Patierno Steven R. , Lee Norman H. 
Published: June 2015

Abstract
Purpose: African Americans (AA) exhibit higher rates of prostate cancer incidence and mortality compared with European American (EA) men. In addition to socioeconomic influences, biologic factors are believed to play a critical role in prostate cancer disparities. We investigated whether population-specific and -enriched miRNA–mRNA interactions might contribute to prostate cancer disparities.
Experimental Design: Integrative genomics was used, combining miRNA and mRNA profiling, miRNA target prediction, pathway analysis, and functional validation, to map miRNA–mRNA interactions associated with prostate cancer disparities.
Results: We identified 22 AA-specific and 18 EA-specific miRNAs in prostate cancer versus patient-matched normal prostate, and 10 “AA-enriched/-depleted” miRNAs in AA prostate cancer versus EA prostate cancer comparisons. Many of these population-specific/-enriched miRNAs could be paired with target mRNAs that exhibited an inverse pattern of differential expression. Pathway analysis revealed EGFR (or ERBB) signaling as a critical pathway significantly regulated by AA-specific/-enriched mRNAs and miRNA–mRNA pairings. Novel miRNA–mRNA pairings were validated by qRT-PCR, Western blot, and/or IHC analyses in prostate cancer specimens. Loss/gain of function assays performed in population-specific prostate cancer cell lines confirmed miR-133a/MCL1, miR-513c/STAT1, miR-96/FOXO3A, miR-145/ITPR2, and miR-34a/PPP2R2A as critical miRNA–mRNA pairings driving oncogenesis. Manipulating the balance of these pairings resulted in decreased proliferation and invasion, and enhanced sensitization to docetaxel-induced cytotoxicity in AA prostate cancer cells.
Conclusions: Our data suggest that AA-specific/-enriched miRNA–mRNA pairings may play a critical role in the activation of oncogenic pathways in AA prostate cancer. Our findings also suggest that miR-133a/MCL1, miR-513c/STAT1, and miR-96/FOXO3A may have clinical significance in the development of novel strategies for treating aggressive prostate cancer. Clin Cancer Res; 21(21); 4970–84. ©2015 AACR.
Treatment with Ibrutinib Inhibits BTK- and VLA-4–Dependent Adhesion of Chronic Lymphocytic Leukemia Cells In Vivo
Authors: Herman Sarah E.M. , Mustafa Rashida Z. , Jones Jade , Wong Deanna H. , Farooqui Mohammed , Wiestner Adrian 
Published: June 2015

Abstract
Purpose: Ibrutinib leads to a transient lymphocytosis in patients with chronic lymphocytic leukemia (CLL) that develops within hours of starting drug and is due to the efflux of cells from lymphoid tissues into the blood. We therefore sought to investigate the in vivo effect of ibrutinib on migration and adhesion of CLL cells.
Experimental Design: Patients received single-agent ibrutinib (420 mg daily) on an investigator-initiated phase II trial. Serial blood samples were collected pretreatment and during treatment for ex vivo functional assays.
Results: Adhesion of CLL cells to fibronectin was rapidly (within hours) and almost completely inhibited (median reduction 98% on day 28, P &lt; 0.001), while the effect on migration to chemokines was more moderate (median reduction 64%, P = 0.008) and less uniform. Although cell surface expression of key adhesion molecules such as CD49d, CD29, and CD44 were modestly reduced, this was only apparent after weeks of treatment. Stimulation of CLL cells from patients on ibrutinib with PMA, which activates PKC independent of BTK, restored the ability of the cells to adhere to fibronectin in a VLA-4–dependent manner. Finally, the addition of ibrutinib to CLL cells adhered to fibronectin in vitro caused the detachment of 17% of the cells, on average; consisten t with in vivo observations of an increasing lymphocytosis within 4 hours of starting ibrutinib.
Conclusions: Inhibition of BTK and VLA-4–dependent adhesion of CLL cells to stroma and stromal components provides a mechanistic explanation for the treatment-induced lymphocytosis and may reduce CD49d-dependent prosurvival signals in the tissue microenvironment. Clin Cancer Res; 21(20); 4642–51. ©2015 AACR.
Novel Anti-TM4SF1 Antibody–Drug Conjugates with Activity against Tumor Cells and Tumor Vasculature
Authors: Visintin Alberto , Knowlton Kelly , Tyminski Edyta , Lin Chi-Iou , Zheng Xiang , Marquette Kimberly , Jain Sadhana , Tchistiakova Lioudmila , Li Dan , O'Donnell Christopher J. , Maderna Andreas , Cao Xianjun , Dunn Robert , Snyder William B. , Abraham Anson K. , Leal Mauricio , Shetty Shoba , Barry Anthony , Zawel Leigh , Coyle Anthony J. , Dvorak Harold F. , Jaminet Shou-Ching 
Published: June 2015

Abstract
Antibody–drug conjugates (ADC) represent a promising therapeutic modality for managing cancer. Here, we report a novel humanized ADC that targets the tetraspanin-like protein TM4SF1. TM4SF1 is highly expressed on the plasma membranes of many human cancer cells and also on the endothelial cells lining tumor blood vessels. TM4SF1 is internalized upon interaction with antibodies. We hypothesized that an ADC against TM4SF1 would inhibit cancer growth directly by killing cancer cells and indirectly by attacking the tumor vasculature. We generated a humanized anti-human TM4SF1 monoclonal antibody, v1.10, and armed it with an auristatin cytotoxic agent LP2 (chemical name mc-3377). v1.10-LP2 selectively killed cultured human tumor cell lines and human endothelial cells that express TM4SF1. Acting as a single agent, v1.10-LP2 induced complete regression of several TM4SF1-expressing tumor xenografts in nude mice, including non–small cell lung cancer and pancreas, prostate, and colon cancers. As v1.10 did not react with mouse TM4SF1, it could not target the mouse tumor vasculature. Therefore, we generated a surrogate anti-mouse TM4SF1 antibody, 2A7A, and conjugated it to LP2. At 3 mpk, 2A7A-LP2 regressed several tumor xenografts without noticeable toxicity. Combination therapy with v1.10-LP2 and 2A7A-LP2 together was more effective than either ADC alone. These data provide proof-of-concept that TM4SF1-targeting ADCs have potential as anticancer agents with dual action against tumor cells and the tumor vasculature. Such agents could offer exceptional therapeutic value and warrant further investigation. Mol Cancer Ther; 14(8); 1868–76. ©2015 AACR.
Regulatory B Cell–Specific Interleukin-10 Is Dispensable for Atherosclerosis Development in Mice
Authors: Sage Andrew P. , Nus Meritxell , Baker Lauren L. , Finigan Alison J. , Masters Leanne M. , Mallat Ziad 
Published: June 2015

Objective—
To determine the role of regulatory B cell–derived interleukin (IL)-10 in atherosclerosis.

Approach and Results—

We created chimeric
Ldlr

−/−

mice with a B cell–specific deficiency in IL-10, and confirmed that purified B cells stimulated with lipopolysaccharide failed to produce IL-10 compared with control
Ldlr

−/−

chimeras. Mice lacking B-cell IL-10 demonstrated enhanced splenic B-cell numbers but no major differences in B-cell subsets, T cell or monocyte distribution, and unchanged body weights or serum cholesterol levels compared with control mice. After 8 weeks on high-fat diet, there were no differences in aortic root or aortic arch atherosclerosis. In addition to plaque size, plaque composition (macrophages, T cells, smooth muscle cells, and collagen) was similar between groups.

Conclusions—
In contrast to its prominent regulatory role in many immune-mediated diseases and its proposed modulatory role in atherosclerosis, B cell–derived IL-10 does not alter atherosclerosis in mice.
DNA Methylation Dynamics in Human Carotid Plaques After Cerebrovascular Events
Authors: Zaina Silvio , Gonçalves Isabel , Carmona F. Javier , Gomez Antonio , Heyn Holger , Mollet Inês G. , Moran Sebastian , Varol Nuray , Esteller Manel 
Published: June 2015

Objective—
To understand whether cerebrovascular events, a major complication of atherosclerosis, are associated with any specific DNA methylation changes in the carotid plaque.

Approach and Results—

We profiled the DNA methylomes of human symptomatic carotid plaques obtained from patients who had cerebrovascular events (n=19) and asymptomatic counterparts (n=19) with a high-density microarray (≈485 000 CpG sites, Illumina), and crossed DNA methylation data with RNAseq-based expression data from an independent symptomatic carotid plaque set (n=8). Few (30) CpGs showed a significant (
P
<0.05; absolute Delta-Beta,
>
0.20) differential methylation between the 2 groups. Within symptomatic carotid plaques, DNA methylation correlated significantly with postcerebrovascular event time (range, 3–45 days;
r
-value range, −0.926 to 0.857;
P
<0.05) for ≈45 000 CpGs, the vast majority of which became hypomethylated with increasing postcerebrovascular event time. Hypomethylation was not due to erasure of the gene-body and CG-poor region hypermethylation that accompany the progression of stable lesions, but rather targeted promoters and CpG islands. Noticeably, promoter hypomethylation and increased expression of genes involved in the inhibition of the inflammatory response, defense against oxidative stress, and active DNA demethylation were observed with increasing postcerebrovascular event time. Concomitantly, histological changes consistent with phagocyte-driven plaque healing were observed.

Conclusions—
Weak changes in the DNA methylome distinguish symptomatic from asymptomatic plaques, but a widespread demethylation resulting in permissive transcriptional marks at atheroprotective gene promoters is established in plaques after a cerebrovascular event, thus mirroring previous observations that ruptured plaques tend to revert to a stable structure. The identified loci are candidate targets to accelerate the pace of carotid plaque stabilization.
Exercise Promotes Collateral Artery Growth Mediated by Monocytic Nitric Oxide
Authors: Schirmer Stephan H. , Millenaar Dominic N. , Werner Christian , Schuh Lisa , Degen Achim , Bettink Stephanie I. , Lipp Peter , van Rooijen Nico , Meyer Tim , Böhm Michael , Laufs Ulrich 
Published: June 2015

Objective—
Collateral artery growth (arteriogenesis) is an important adaptive response to hampered arterial perfusion. It is unknown whether preventive physical exercise before limb ischemia can improve arteriogenesis and modulate mononuclear cell function. This study aimed at investigating the effects of endurance exercise before arterial occlusion on MNC function and collateral artery growth.

Approach and Results—
After 3 weeks of voluntary treadmill exercise, ligation of the right femoral artery was performed in mice. Hindlimb perfusion immediately after surgery did not differ from sedentary mice. However, previous exercise improved perfusion restoration ≤7 days after femoral artery ligation, also when exercise was stopped at ligation. This was accompanied by an accumulation of peri-collateral macrophages and increased expression of endothelial nitric oxide synthase and inducible nitric oxide synthase (iNOS) in hindlimb collateral and in MNC of blood and spleen. Systemic monocyte and macrophage depletion by liposomal clodronate but not splenectomy attenuated exercise-induced perfusion restoration, collateral artery growth, peri-collateral macrophage accumulation, and upregulation of iNOS. iNOS-deficient mice did not show exercise-induced perfusion restoration. Transplantation of bone marrow–derived MNC from iNOS-deficient mice into wild-type animals inhibited exercise-induced collateral artery growth. In contrast to sedentary controls, thrice weekly aerobic exercise training for 6 months in humans increased peripheral blood MNC iNOS expression.

Conclusions—
Circulating mononuclear cell–derived inducible nitric oxide is an important mediator of exercise-induced collateral artery growth.