bluuebunny/crossref_metadata_2025_split huggingface dataset:
Meningothelial Hamartoma Associated with Nevus Sebaceus
Authors: Crittenden Sunita C. , Sonnier George B. 
Published: December 2013

AbstractMeningothelial hamartoma is a rare lesion of ectopic meningothelial elements that usually presents on the scalp at birth or in early childhood. The characteristic spindle cells infiltrate through collagen and stain positively for epithelial membrane antigen and vimentin but are negative for CD31 and CD34. This distinguishes meningothelial hamartoma from vascular tumors. Nevus sebaceus is a fairly common lesion that has been associated with several different benign tumors, including trichoblastoma and syringocystadenoma papilliferum. We describe the case of a 17‐month‐old girl who presented with a meningothelial hamartoma in association with a nevus sebaceus. To the best of our knowledge, this is the second case reported.
Bilateral Exchange Rates and Jobs
Authors: Bekkers Eddy , Francois Joseph 
Published: December 2013

AbstractWe study the labor market effects of realignment in fixed bilateral exchange rates, such as China's peg to the US dollar. We employ the open economy model by de Melo and Robinson to identify the core parameters of the real, trade side of the economy driving the unemployment effects of bilateral exchange rate realignment. A small open economy version of the model is explored analytically and a large multicountry version numerically. Analytics in the small open economy model show that unemployment effects of adjusting of a bilateral peg hinge on the fraction exported to and imported from the trading partner. A larger fraction exported to and a smaller fraction imported from the trading partner make it more likely that revaluation of a trading partner's currency has beneficial effects. Numerics in the large economy model show that Chinese revaluation can generate both positive and negative unemployment effects depending upon underlying parameter values. Adverse unemployment effects can go along with an improving trade balance.
Effect of crop residue biochar on soil acidity amelioration in strongly acidic tea garden soils
Authors: Wang L. , Butterly C. R. , Wang Y. , Herath H. M. S. K. , Xi Y. G. , Xiao X. J. 
Published: December 2013

AbstractStrongly acidic soil (e.g. pH < 5.0) is detrimental to tea productivity and quality. Wheat, rice and peanut biochar produced at low temperature (max 300 °C) and differing in alkalinity content were incorporated into Xuan‐cheng (Ultisol; initial pHsoil/water = 1/2.5 4.12) and Ying‐tan soil (Ultisol; initial pH soil/water = 1/2.5 4.75) at 10 and 20 g/kg (w/w) to quantify their liming effect and evaluate their effectiveness for acidity amelioration of tea garden soils. After a 65‐day incubation at 25 °C, biochar application significantly (P < 0.05) increased soil pH and exchangeable cations and reduced Al saturation of both tea soils. Association of H+ ions with biochar and decarboxylation processes was likely to be the main factor neutralizing soil acidity. Further, biochar application reduced acidity production from the N cycle. Significant (P < 0.05) increases in exchangeable cations and reductions in exchangeable acidity and Al saturation were observed as the rate of biochar increased, but there were no further effects on soil pH. The lack of change in soil pH at the higher biochar rate may be due to the displacement of exchangeable acidity and the high buffering capacity of biochar, thereby retarding a further liming effect. Hence, a significant linear correlation between reduced exchangeable acidity and alkalinity balance was found in biochar‐amended soils (P < 0.05). Low‐temperature biochar of crop residues is suggested as a potential amendment to ameliorate acidic tea garden soils.
Draft Genome Sequence of “
Candidatus
Halobonum tyrrellensis” Strain G22, Isolated from the Hypersaline Waters of Lake Tyrrell, Australia
Authors: Ugalde Juan A. , Narasingarao Priya , Kuo Sidney , Podell Sheila , Allen Eric E. 
Published: December 2013

ABSTRACT

We report the draft 3.675-Mbp genome sequence of “
Candidatus
Halobonum tyrrellensis” strain G22, a novel halophilic archaeon isolated from the surface hypersaline waters of Lake Tyrrell, Australia. The availability of the first genome from the “
Candidatus
Halobonum” genus provides a new genomic resource for the comparative genomic analysis of halophilic
Archaea
.
Complete Genome Sequence of Porcine Encephalomyocarditis Virus Strain BD2
Authors: Yuan Wanzhe , Zhang Xiuyuan , Sun Jiguo 
Published: December 2013

ABSTRACT
Encephalomyocarditis virus (EMCV) causes acute myocarditis in young pigs or reproductive failure in sows, and it is divided into two main groups. Here, we report the complete genome sequence of EMCV strain BD2, which belongs to group I.
High-Quality Draft Genome Sequences of Xanthomonas axonopodis pv. glycines Strains CFBP 2526 and CFBP 7119
Authors: Darrasse A. , Bolot S. , Serres-Giardi L. , Charbit E. , Boureau T. , Fisher-Le Saux M. , Briand M. , Arlat M. , Gagnevin L. , Koebnik R. , Noël L. D. , Carrère S. , Jacques M. A. 
Published: December 2013

ABSTRACT

We report here the high-quality draft genome sequences of two strains of
Xanthomonas axonopodis
pv. glycines, the causal agent of bacterial pustule on soybeans. Comparison of these genomes with those of phylogenetically closely related pathovars of
Xanthomonas
spp. will help to understand the mechanisms involved in host specificity and adaptation to host plants.
Draft Genome Sequence of Staphylococcus simulans UMC-CNS-990, Isolated from a Case of Chronic Bovine Mastitis
Authors: Calcutt Michael J. , Foecking Mark F. , Hsieh Hsin-Yeh , Perry Jeanette , Stewart George C. , Middleton John R. 
Published: December 2013

ABSTRACT

Coagulase-negative staphylococci are frequently isolated from cases of subclinical bovine mastitis. Reported here is a draft genome sequence of
Staphylococcus simulans
UMC-CNS-990, an isolate recovered from a chronic intramammary infection of a Holstein cow. Unexpectedly, a cluster of genes encoding gas vesicle proteins was found within the 2,755-kb genome.
Draft Genome Sequence of Fusobacterium nucleatum subsp.
vincentii
ChDC F8, Isolated from a Human Subgingival Plaque in the Republic of Korea
Authors: Park Soon-Nang , Cho Eugene , Kim Hwa-Sook , Kim Dae-Soo , Jung Jaeeun , Baek Jeong-Hun , Kyong Lim Yun , Jo Eojin , Chang Young-Hyo , Hwan Shin Jeong , Kim Jihun , Choi Sang-Haeng , Kang Jihee , Choi YongUn , Park Hong-Seog , Kim Hongik , Kook Joong-Ki 
Published: December 2013

ABSTRACT

Fusobacterium nucleatum
is a Gram-negative, nonmotile, obligately anaerobic rod bacterium which might play an important role in the initiation and progression of periodontal diseases.
F. nucleatum
subsp.
vincentii
ChDC F8 (KCOM 1231) was isolated from a human gingivitis lesion. Here, we report the draft genome sequence of the strain.
Full
-
Genome Sequence of Hibiscus Chlorotic Ringspot Virus from Israel
Authors: Luria Neta , Reingold Victoria , Lachman Oded , Dombrovsky Aviv 
Published: December 2013

ABSTRACT

Hibiscus rosa-sinensis
is one of the most prevalent ornamental plants grown in private and public gardens. Hibiscus chlorotic ringspot virus (HCRSV) is a member of the
Carmovirus
genus, with a positive single-strand RNA that putatively encodes seven proteins. The complete genome of the first Israeli isolate of HCRSV, HCRSV-IL, comprises 3,908 nucleotides and shows 93% nucleotide sequence identity to the Singapore isolate and 87% identity to the Taiwanese isolate.
The CXCL7/CXCR1/2 Axis Is a Key Driver in the Growth of Clear Cell Renal Cell Carcinoma
Authors: Grépin Renaud , Guyot Mélanie , Giuliano Sandy , Boncompagni Marina , Ambrosetti Damien , Chamorey Emmanuel , Scoazec Jean-Yves , Negrier Sylvie , Simonnet Hélène , Pagès Gilles 
Published: December 2013

AbstractMutations in the von Hippel–Lindau gene upregulate expression of the central angiogenic factor VEGF, which drives abnormal angiogenesis in clear cell renal cell carcinomas (ccRCC). However, the overexpression of VEGF in these tumors was not found to correlate with overall survival. Here, we show that the proangiogenic, proinflammatory cytokine CXCL7 is an independent prognostic factor for overall survival in this setting. CXCL7 antibodies strongly reduced the growth of ccRCC tumors in nude mice. Conversely, conditional overexpression of CXCL7 accelerated ccRCC development. CXCL7 promoted cell proliferation in vivo and in vitro, in which expression of CXCL7 was induced by the central proinflammatory cytokine interleukin (IL)-1β. ccRCC cells normally secrete low amounts of CXCL7; it was more highly expressed in tumors due to high levels of IL-1β there. We found that a pharmacological inhibitor of the CXCL7 receptors CXCR1 and CXCR2 (SB225002) was sufficient to inhibit endothelial cell proliferation and ccRCC growth. Because CXCR1 and CXCR2 are present on both endothelial and ccRCC cells, their inhibition affected both the tumor vasculature and the proliferation of tumor cells. Our results highlight the CXCL7/CXCR1/CXCR2 axis as a pertinent target for the treatment of ccRCC. Cancer Res; 74(3); 873–83. ©2013 AACR.
Histone Chaperone CHAF1A Inhibits Differentiation and Promotes Aggressive Neuroblastoma
Authors: Barbieri Eveline , De Preter Katleen , Capasso Mario , Chen Zaowen , Hsu Danielle M. , Tonini Gian Paolo , Lefever Steve , Hicks John , Versteeg Rogier , Pession Andrea , Speleman Frank , Kim Eugene S. , Shohet Jason M. 
Published: December 2013

AbstractNeuroblastoma arises from the embryonal neural crest secondary to a block in differentiation. Long-term patient survival correlates inversely with the extent of differentiation, and treatment with retinoic acid or other prodifferentiation agents improves survival modestly. In this study, we show the histone chaperone and epigenetic regulator CHAF1A functions in maintaining the highly dedifferentiated state of this aggressive malignancy. CHAF1A is a subunit of the chromatin modifier chromatin assembly factor 1 and it regulates H3K9 trimethylation of key target genes regulating proliferation, survival, and differentiation. Elevated CHAF1A expression strongly correlated with poor prognosis. Conversely, CHAF1A loss-of-function was sufficient to drive neuronal differentiation in vitro and in vivo. Transcriptome analysis of cells lacking CHAF1A revealed repression of oncogenic signaling pathways and a normalization of glycolytic metabolism. Our findings demonstrate that CHAF1A restricts neural crest differentiation and contributes to the pathogenesis of high-risk neuroblastoma. Cancer Res; 74(3); 765–74. ©2013 AACR.
Targeting Akt3 Signaling in Triple-Negative Breast Cancer
Authors: Chin Y. Rebecca , Yoshida Taku , Marusyk Andriy , Beck Andrew H. , Polyak Kornelia , Toker Alex 
Published: December 2013

Abstract
Triple-negative breast cancer (TNBC) is currently the only major breast tumor subtype without effective targeted therapy and, as a consequence, in general has a poor outcome. To identify new therapeutic targets in TNBC, we performed a short hairpin RNA (shRNA) screen for protein kinases commonly amplified and overexpressed in breast cancer. Using this approach, we identified AKT3 as a gene preferentially required for the growth of TNBCs. Downregulation of Akt3 significantly inhibits the growth of TNBC lines in three-dimensional (3D) spheroid cultures and in mouse xenograft models, whereas loss of Akt1 or Akt2 have more modest effects. Akt3 silencing markedly upregulates the p27 cell-cycle inhibitor and this is critical for the ability of Akt3 to inhibit spheroid growth. In contrast with Akt1, Akt3 silencing results in only a minor enhancement of migration and does not promote invasion. Depletion of Akt3 in TNBC sensitizes cells to the pan-Akt inhibitor GSK690693. These results imply that Akt3 has a specific function in TNBCs; thus, its therapeutic targeting may provide a new treatment option for this tumor subtype. Cancer Res; 74(3); 964–73. ©2013 AACR.
Inhibition of Insulin-like Growth Factor–Binding Protein-3 Signaling through Sphingosine Kinase-1 Sensitizes Triple-Negative Breast Cancer Cells to EGF Receptor Blockade
Authors: Martin Janet L. , de Silva Hasanthi C. , Lin Mike Z. , Scott Carolyn D. , Baxter Robert C. 
Published: December 2013

Abstract
The type I EGF receptor (EGFR or ErbB1) and insulin-like growth factor–binding protein-3 (IGFBP-3) are highly expressed in triple-negative breast cancer (TNBC), a particularly aggressive disease that cannot be treated with conventional therapies targeting the estrogen or progesterone receptors (ER and PR), or HER2. We have shown previously in normal breast epithelial cells that IGFBP-3 potentiates growth-stimulatory signaling transduced by EGFR, and this is mediated by the sphingosine kinase-1 (SphK1)/sphingosine 1-phosphate (S1P) system. In this study, we investigated whether cotargeting the EGFR and SphK1/S1P pathways in TNBC cells results in greater growth inhibition compared with blocking either alone, and might therefore have novel therapeutic potential in TNBC. In four TNBC cell lines, exogenous IGFBP-3 enhanced ligand-stimulated EGFR activation, associated with increased SphK1 localization to the plasma membrane. The effect of exogenous IGFBP-3 on EGFR activation was blocked by pharmacologic inhibition or siRNA-mediated silencing of SphK1, and silencing of endogenous IGFBP-3 also suppressed EGF-stimulated EGFR activation. Real-time analysis of cell proliferation revealed a combined effect of EGFR inhibition by gefitinib and SphK1 inhibition using SKi-II. Growth of MDA-MB-468 xenograft tumors in mice was significantly inhibited by SKi-II and gefitinib when used in combination, but not as single agents. We conclude that IGFBP-3 promotes growth of TNBC cells by increasing EGFR signaling, that this is mediated by SphK1, and that combined inhibition of EGFR and SphK1 has potential as an anticancer therapy in TNBC in which EGFR and IGFBP-3 expression is high. Mol Cancer Ther; 13(2); 316–28. ©2013 AACR.
PP6C Hotspot Mutations in Melanoma Display Sensitivity to Aurora Kinase Inhibition
Authors: Gold Heidi L. , Wengrod Jordan , de Miera Eleazar Vega-Saenz , Wang Ding , Fleming Nathaniel , Sikkema Lisa , Kirchhoff Tomas , Hochman Tsivia , Goldberg Judith D. , Osman Iman , Gardner Lawrence B. 
Published: December 2013

Abstract
Recent whole genome melanoma sequencing studies have identified recurrent mutations in the gene encoding the catalytic subunit of serine/threonine phosphatase 6 (PPP6C/PP6C). However, the biochemical, functional, and clinical ramifications of these mutations are unknown. Sequencing PP6C from patients with melanoma (233 primary and 77 metastatic specimens) with extended prospective clinical outcome revealed a large number of hotspot mutations in patients with both primary and metastatic melanoma. Despite minimal association between stage and presence of PP6C mutations in patients with primary melanoma, a subpopulation of cells within each tumor did contain PP6C mutations, suggesting PP6C mutation is an early, but non–tumor-initiating event in melanoma. Among patients with primary melanoma with PP6C mutations, patients with stop mutations had significantly shorter recurrence-free survival compared with patients without stop mutations. In addition, PP6C mutations were independent of commonly observed BRAF and NRAS mutations. Biochemically, PP6C mutations could be classified as those that interact with PP6C regulatory subunits and those that do not. Mutations that did not bind to PP6C regulatory subunits were associated with increased phosphorylation of Aurora kinase, a PP6C substrate, and mitotic defects. However, both classes of PP6C mutations led to increased sensitivity to Aurora kinase inhibition. Together, these data support for the first time that PP6C mutations are molecularly, biochemically, and clinically heterogeneous.
Implications: PP6C mutations have distinct functional and clinical consequences in melanoma, and confer sensitivity to Aurora A kinase inhibitors. Mol Cancer Res; 12(3); 433–9. ©2013 AACR.
Evaluation of Links Between High-Density Lipoprotein Genetics, Functionality, and Aortic Valve Stenosis Risk in Humans
Authors: Arsenault Benoit J. , Dubé Marie-Pierre , Brodeur Mathieu R. , de Oliveira Moraes Adriana Benjamin , Lavoie Véronique , Kernaleguen Anne-Elen , Guauque-Olarte Sandra , Mathieu Patrick , Pibarot Philippe , Messika-Zeitoun David , Bossé Yohan , Rhainds David , Rhéaume Éric , Tardif Jean-Claude 
Published: December 2013

Objective—
Studies have shown that high-density lipoprotein (HDL)–raising compounds induce regression of aortic valve stenosis (AVS) in animal models. However, whether patients with AVS have an impaired HDL metabolism is unknown.

Approach and Results—

A total of 1435 single nucleotide polymorphisms in genes associated with HDL cholesterol levels (in or around
GALNT2, LPL, ABCA1, APOA5, SCARB1, LIPC, CETP, LCAT, LIPG, APOC4
, and
PLTP
) were genotyped in 382 patients with echocardiography-confirmed AVS (aortic jet velocity ≥2.5 m/s) and 401 controls. After control for multiple testing, none of the genetic variants showed a positive association with case/control status (adjusted
P
≥0.05 for all single nucleotide polymorphisms tested). In a subsample of this cohort, HDL cholesterol levels, apolipoprotein AI levels, lecithin-cholesterol acyltransferase activity, pre–β-HDL, HDL size, and 4 parameters of cholesterol efflux capacity were measured in apolipoprotein B–depleted serum samples from 86 patients with and 86 patients without AVS. Cholesterol efflux capacity was measured using J774 macrophages with and without stimulation of ATP-binding cassette A-1 expression by cAMP, and HepG2 hepatocytes for scavenger receptor class B type 1–mediated efflux. None of these parameters were different between cases and controls. However, compared with patients without coronary artery disease, sera from patients with coronary artery disease had lower HDL cholesterol levels, scavenger receptor class B type 1–mediated efflux, and HDL size (
P
≤0.003), independently of the presence or absence of AVS.

Conclusions—
Results of the present study suggest that, based on HDL genetics and HDL functionality, HDL metabolism does not seem to predict the risk of AVS. Because of our limited sample size, additional studies are needed to confirm these findings.
Macrophage Migration Inhibitory Factor Deficiency Augments Doxorubicin‐Induced Cardiomyopathy
Authors: Xu Xihui , Bucala Richard , Ren Jun 
Published: December 2013

Background

Recent evidence has depicted a role of macrophage migration inhibitory factor (
MIF
) in cardiac homeostasis under pathological conditions. This study was designed to evaluate the role of
MIF
in doxorubicin‐induced cardiomyopathy and the underlying mechanism involved with a focus on autophagy.

Methods and Results

Wild‐type (WT) and
MIF
knockout (
MIF
−/−
) mice were given saline or doxorubicin (20 mg/kg cumulative, i.p.). A cohort of
WT
and
MIF
−/−
mice was given rapamycin (6 mg/kg, i.p.) with or without bafilomycin A1 (BafA1, 3 μmol/kg per day, i.p.) for 1 week prior to doxorubicin challenge. To consolidate a role for
MIF
in the maintenance of cardiac homeostasis following doxorubicin challenge, recombinant mouse
MIF
(
rmMIF
) was given to
MIF
−/−
mice challenged with or without doxorubicin. Echocardiographic, cardiomyocyte function, and intracellular Ca
2+
handling were evaluated. Autophagy and apoptosis were examined. Mitochondrial morphology and function were examined using transmission electron microscopy,
JC
‐1 staining, Mito
SOX
Red fluorescence, and mitochondrial respiration complex assay.
DHE
staining was used to evaluate
reactive oxygen species (ROS
) generation.
MIF
knockout exacerbated doxorubicin‐induced mortality and cardiomyopathy (compromised fractional shortening, cardiomyocyte and mitochondrial function, apoptosis, and
ROS
generation). These detrimental effects of doxorubicin were accompanied by defective autophagolysosome formation, the effect of which was exacerbated by
MIF
knockout. Rapamycin pretreatment rescued doxorubicin‐induced cardiomyopathy in
WT
and
MIF
−/−
mice. Blocking autophagolysosome formation using BafA1 negated the cardioprotective effect of rapamycin and
rmMIF
.

Conclusions

Our data suggest that
MIF
serves as an indispensable cardioprotective factor against doxorubicin‐induced cardiomyopathy with an underlying mechanism through facilitating autophagolysosome formation.
Rad GTPase Deletion Increases L‐type Calcium Channel Current Leading to Increased Cardiac Contraction
Authors: Manning Janet R. , Yin Guo , Kaminski Catherine N. , Magyar Janos , Feng Han‐Zhong , Penn John , Sievert Gail , Thompson Katherine , Jin J.‐P. , Andres Douglas A. , Satin Jonathan 
Published: December 2013

Background

The small
GTP
ase Rad is a negative regulator of voltage‐dependent L‐type calcium channel current (

I
C

aL
); however, the effects of Rad ablation on cardiomyocyte function are unknown. The objective of this study is to test the hypothesis that Rad‐depletion causes positive inotropic effects without inducing cardiac hypertrophy.

Methods and Results

Ventricular myocytes from adult Rad
−/−
mice were isolated and evaluated by patch‐clamp recordings for I
Ca,L
and action potentials, Ca
2+
transients, and sarcomere shortening. Maximum I
CaL
is elevated in Rad
−/−
(maximal conductance 0.35±0.04 picoSiemens/picoFarad (
pS
/
pF
) wild‐type; 0.61±0.14
pS
/
pF
Rad
−/−
), decay kinetics are faster, and I
Ca,L
activates at lower voltages (activation midpoint −7.2±0.6 wild‐type; −11.7±0.9 Rad
−/−
) mimicking effects of β‐adrenergic receptor stimulation. Diastolic and twitch calcium are elevated in Rad
−/−
(
F
340/380
: 1.03 diastolic and 0.35 twitch for wild‐type; 1.47 diastolic and 0.736 twitch for Rad
−/−
) and sarcomere shortening is enhanced (4.31% wild‐type; 14.13% Rad
−/−
) at lower pacing frequencies. Consequentially, frequency‐dependence of Ca
2+
transients is less in Rad
−/−
, and the frequency dependence of relaxation is also blunted. In isolated working hearts, similar results were obtained; chiefly, +
dP
/dt was elevated at baseline and developed pressure was relatively nonresponsive to acute β‐adrenergic receptor stimulation. In single cells, at subphysiological frequencies, nonstimulated calmodulin‐dependent protein kinase–sensitive calcium release is observed. Remarkably, Rad
−/−
hearts did not show hypertrophic growth despite elevated levels of diastolic calcium.

Conclusions

This study demonstrates that the depletion of Rad
GTP
ase is equivalent to sympathomimetic β‐adrenergic receptor, without stimulating cardiac hypertrophy. Thus, targeting Rad
GTP
ase is a novel potential therapeutic target for Ca
2+
‐homeostasis–driven positive inotropic support of the heart.