bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hilgardite polytype distribution in Sussex, New Brunswick evaporite deposits
Authors: Grice J. D. , Rowe R. 
Published: May 2014

AbstractHilgardite, Ca2B5O9Cl·H2O, has a zeolite-type framework structure consisting of cross-linked (010) layers of borate sheets having the fundamental building block (FBB) = 2Δ3☐:<Δ2☐>-<Δ2☐>. These layers are polar and the orientation, plus the number of layers in a sequence, determine the polytype. To date three hilgardite polytypes have been described: hilgardite-1A, -3A and -4M. A reliable means of polytype identification by micro X-ray powder diffraction (mXRPD) is outlined. Two polytypes are identified in the Sussex New Brunswick potash deposits: hilgardite-1A and -3A. Both cells are refined with XRPD data: hilgardite-1A, a 6.456(1), b 6.558(1), c 6.295(1) Å, α 61.62(1), β 118.76(1), γ 108.82(2)°, V 205.23(4) Å3 and hilgardite-3A, a 17.484(6), b 6.487(3), c 6.321(3) Å, α 60.78(3), β 79.58(3), γ 84.16(3)°, V 615.3(3) Å3. Hilgardite polytype assemblages are determined for 24 Millstream deposit core samples and 43 Penobsquis deposit core samples. The Millstream deposit occurs as an isolated, inner basin during evaporite formation. Borate formation from this marine environment was during the last stages of evaporation. Simple Mg-Ca borates precipitated from this highly saline brine. It underwent subsequent minor folding and all hilgardite samples are the hilgardite-1A polytype. The Penobsquis deposit occurs as an open fore-basin. This larger, less saline basin also precipitated borate minerals during the final stages of evaporation. The borate assemblage here is much more complex with borate minerals that have essential Ca, K, Fe, Mg and Sr. This deposit was subjected to major folding and recrystallization. Both hilgardite-1A and -3A occur here. Polytype-3A is concentrated in areas of maximum folding and it is proposed that pressure is the main control of hilgardite polytypes. Strontium substitution has no effect on polytype formation.
Leukocytes require ADAM10 but not ADAM17 for their migration and inflammatory recruitment into the alveolar space
Authors: Pruessmeyer Jessica , Hess Franz Martin , Alert Henriette , Groth Esther , Pasqualon Tobias , Schwarz Nicole , Nyamoya Stella , Kollert Jos , van der Vorst Emiel , Donners Marjo , Martin Christian , Uhlig Stefan , Saftig Paul , Dreymueller Daniela , Ludwig Andreas 
Published: May 2014

Key PointsADAM10 but not ADAM17 on leukocytes is essential for chemokine-induced signaling, adhesion, cytoskeletal rearrangement, and migration. Leukocyte-expressed ADAM10 promotes leukocyte recruitment and edema formation in a murine model of acute pulmonary inflammation.
Phase 2 randomized study of bortezomib-melphalan-prednisone with or without siltuximab (anti–IL-6) in multiple myeloma
Authors: San-Miguel Jesús , Bladé Joan , Shpilberg Ofer , Grosicki Sebastian , Maloisel Frédéric , Min Chang-Ki , Polo Zarzuela Marta , Robak Tadeusz , Prasad Sripada V. S. S. , Tee Goh Yeow , Laubach Jacob , Spencer Andrew , Mateos María-Victoria , Palumbo Antonio , Puchalski Tom , Reddy Manjula , Uhlar Clarissa , Qin Xiang , van de Velde Helgi , Xie Hong , Orlowski Robert Z. 
Published: May 2014

Key Points
Adding siltuximab to VMP did not improve CR, progression-free survival, or overall survival but improved very good partial response in MM. This suggests that the association of less than CR with long-term outcomes and the role of IL-6 in MM should be reassessed.
How I treat sinusoidal obstruction syndrome
Authors: Chao Nelson 
Published: May 2014

AbstractSinusoidal obstruction syndrome (SOS), previously called veno-occlusive disease (VOD) can be a difficult problem after hematopoietic cell transplantation (HCT). The overall incidence has changed since the early days of allogeneic HCT. Prophylaxis and treatment remain important components of supportive care. As the indication and the comorbidities for HCT continue to change, especially with older and more infirm patients, SOS remains an important area for clinicians. I discuss how SOS could be addressed, from prophylaxis to diagnosis and potential therapy.
Obstructive sleep apnoea treatment and fasting lipids: a comparative effectiveness study
Authors: Keenan Brendan T. , Maislin Greg , Sunwoo Bernie Y. , Arnardottir Erna Sif , Jackson Nicholas , Olafsson Isleifur , Juliusson Sigurdur , Schwab Richard J. , Gislason Thorarinn , Benediktsdottir Bryndis , Pack Allan I. 
Published: May 2014

Obstructive sleep apnoea (OSA) is associated with cardiovascular disease. Dyslipidaemia has been implicated as a mechanism linking OSA with atherosclerosis, but no consistent associations with lipids exist for OSA or positive airway pressure treatment. We assessed the relationships between fasting lipid levels and obesity and OSA severity, and explored the impact of positive airway pressure treatment on 2-year fasting lipid level changes.Analyses included moderate-to-severe OSA patients from the Icelandic Sleep Apnoea Cohort. Fasting morning lipids were analysed in 613 untreated participants not on lipid-lowering medications at baseline. Patients were then initiated on positive airway pressure and followed for 2 years. Sub-classification using propensity score quintiles, which aimed to replicate covariate balance associated with randomised trials and, therefore, minimise selection bias and allow causal inference, was used to design the treatment group comparisons. 199 positive airway pressure adherent patients and 118 non-users were identified.At baseline, obesity was positively correlated with triglycerides and negatively correlated with total cholesterol, and low-density and high-density lipoprotein cholesterol. A small correlation was observed between the apnoea/hypopnoea index and high-density lipoprotein cholesterol. No effect of positive airway pressure adherence on 2-year fasting lipid changes was observed.Results do not support the concept of changes in fasting lipids as a primary mechanism for the increased risk of atherosclerotic cardiovascular disease in OSA.
Lung transplantation in telomerase mutation carriers with pulmonary fibrosis
Authors: Silhan Leann L. , Shah Pali D. , Chambers Daniel C. , Snyder Laurie D. , Riise Gerdt C. , Wagner Christa L. , Hellström-Lindberg Eva , Orens Jonathan B. , Mewton Juliette F. , Danoff Sonye K. , Arcasoy Murat O. , Armanios Mary 
Published: May 2014

Lung transplantation is the only intervention that prolongs survival in idiopathic pulmonary fibrosis (IPF). Telomerase mutations are the most common identifiable genetic cause of IPF, and at times, the telomere defect manifests in extrapulmonary disease such as bone marrow failure. The relevance of this genetic diagnosis for lung transplant management has not been examined.We gathered an international series of telomerase mutation carriers who underwent lung transplant in the USA, Australia and Sweden.The median age at transplant was 52 years. Seven recipients are alive with a median follow-up of 1.9 years (range 6 months to 9 years); one died at 10 months. The most common complications were haematological, with recipients requiring platelet transfusion support (88%) and adjustment of immunosuppressives (100%). Four recipients (50%) required dialysis for tubular injury and calcineurin inhibitor toxicity. These complications occurred at significantly higher rates relative to historic series (p<0.0001).Our observations support the feasibility of lung transplantation in telomerase mutation carriers; however, severe post-transplant complications reflecting the syndromic nature of their disease appear to occur at higher rates. While these findings need to be expanded to other cohorts, caution should be exercised when approaching the transplant evaluation and management of this subset of pulmonary fibrosis patients.
Club cell 10-kDa protein attenuates airway mucus hypersecretion and inflammation
Authors: Tokita Erika , Tanabe Tsuyoshi , Asano Kazuhito , Suzaki Harumi , Rubin Bruce K. 
Published: May 2014

Bacterial lipopolysaccharide (LPS) and interleukin (IL)-13 increase mucus secretion and inflammatory cytokine production in normal human bronchial epithelial (NHBE) cells. We evaluated the effect of club cell 10-kDa protein (CC10), an anti-inflammatory protein produced by epithelial cells, on mucus secretion, cell morphology and inflammatory cytokine production.NHBE cells were cultured at an air–liquid interface with CC10 or vehicle and exposed to LPS on day 14. Mucin MUC5AC, IL-8 and granulocyte-macrophage colony-stimulating factor were measured in cell supernatants. MUC5AC and IL-8 mRNA expression were measured by real-time PCR. Western blotting was used to evaluate nuclear factor (NF)-κB and extracellular signal-regulated kinase (ERK) activation. Cells were evaluated histologically. Additionally, NHBE cells were exposed to IL-13 and CC10 for 14 days, and secretion of the mucins MUC5AC and MUC5B was measured.MUC5AC secretion stimulated either by LPS or by IL-13 was attenuated by CC10 at 20 ng·mL−1(p<0.05). CC10 at 20 ng·mL−1also attenuated IL-8 secretion (p<0.05). MUC5AC and IL-8 mRNA expression were also decreased by CC10 (p<0.05). CC10 attenuated phosphorylation of NF-κB (p<0.05) and ERK1/2 (p<0.05).CC10 attenuates LPS-induced mucus secretion in airway cells, in part due to inhibition of NF-κB and ERK phosphorylation.
Prognostic value of exercise pulmonary haemodynamics in pulmonary arterial hypertension
Authors: Chaouat Ari , Sitbon Olivier , Mercy Magalie , Ponçot-Mongars Raphaëlle , Provencher Steeve , Guillaumot Anne , Gomez Emmanuel , Selton-Suty Christine , Malvestio Pascale , Regent Denis , Paris Christophe , Hervé Philippe , Chabot François 
Published: May 2014

The aim of the study was to investigate the prognostic value of right heart catheterisation variables measured during exercise.55 incident patients with idiopathic, familial or anorexigen-associated pulmonary arterial hypertension (PAH) underwent right heart catheterisation at rest and during exercise and 6-min walk testing before PAH treatment initiation. Patients were treated according to recommendations within the next 2 weeks. Right heart catheterisation was repeated 3–5 months into the PAH treatment in 20 patients.Exercise cardiac index decreased gradually as New York Heart Association (NYHA) functional class increased whereas cardiac index at rest was not significantly different across NYHA groups. Baseline 6-min walk distance correlated significantly with exercise and change in cardiac index from rest to exercise (r=0.414 and r=0.481, respectively; p<0.01). Change in 6-min walk distance from baseline to 3–5 months under PAH treatment was highly correlated with change in exercise cardiac index (r=0.746, p<0.001). The most significant baseline covariates associated with survival were change in systolic pulmonary artery pressure from rest to exercise and exercise cardiac index (hazard ratio 0.56 (95% CI 0.37–0.86) and 0.14 (95% CI 0.05–0.43), respectively).Change in pulmonary haemodynamics during exercise is an important tool for assessing disease severity and may help devise optimal treat-to-target strategies.
Intermittent hypoxia-induced protein phosphatase 2A activation reduces PC12 cell proliferation and differentiation
Authors: Chen Tsung-I , Chiu Hung-Wen , Pan Yi-Chung , Hsu Shih-Ting , Lin Jian-Hong , Yang Kun-Ta 
Published: May 2014

Abstract

Background
Intermittent hypoxia (IH) plays a critical role in sleep breathing disorder-associated hippocampus impairments, including neurocognitive deficits, irreversible memory and learning impairments. IH-induced neuronal injury in the hippocampus may result from reduced precursor cell proliferation and the relative numbers of postmitotic differentiated neurons. However, the mechanisms underlying IH-induced reactive oxygen species (ROS) generation effects on cell proliferation and neuronal differentiation remain largely unknown.

Results
ROS generation significantly increased after 1–4 days of IH without increased pheochromocytoma-12 (PC12) cell death, which resulted in increased protein phosphatase 2A (PP2A) mRNA and protein levels. After 3–4 days of IH, extracellular signal-regulated kinases 1/2 (ERK1/2) protein phosphorylation decreased, which could be reversed by superoxide dismutase (SOD), 1,10-phenanthroline (Phe), the PP2A phosphorylation inhibitors, okadaic acid (OKA) and cantharidin, and the ERK phosphorylation activator nicotine (p < 0.05). In particular, the significantly reduced cell proliferation and increased proportions of cells in the G0/G1 phase after 1–4 days of IH (p < 0.05), which resulted in decreased numbers of PC12 cells, could be reversed by treatment with SOD, Phe, PP2A inhibitors and an ERK activator. In addition, the numbers of nerve growth factor (NGF)-induced PC12 cells with neurite outgrowths after 3–4 days of IH were less than those after 4 days of RA, which was also reversed by SOD, Phe, PP2A inhibitors and an ERK activator.

Conclusions
Our results suggest that IH-induced ROS generation increases PP2A activation and subsequently downregulates ERK1/2 activation, which results in inhibition of PC12 cell proliferation through G0/G1 phase arrest and NGF-induced neuronal differentiation.
Transcriptomic analysis of differential host gene expression upon uptake of symbionts: a case study with Symbiodinium and the major bioeroding sponge Cliona varians
Authors: Riesgo Ana , Peterson Kristin , Richardson Crystal , Heist Tyler , Strehlow Brian , McCauley Mark , Cotman Carlos , Hill Malcolm , Hill April 
Published: May 2014

Abstract

Background
We have a limited understanding of genomic interactions that occur among partners for many symbioses. One of the most important symbioses in tropical reef habitats involves Symbiodinium. Most work examining Symbiodinium-host interactions involves cnidarian partners. To fully and broadly understand the conditions that permit Symbiodinium to procure intracellular residency, we must explore hosts from different taxa to help uncover universal cellular and genetic strategies for invading and persisting in host cells. Here, we present data from gene expression analyses involving the bioeroding sponge Cliona varians that harbors Clade G Symbiodinium.

Results
Patterns of differential gene expression from distinct symbiont states (“normal”, “reinfected”, and “aposymbiotic”) of the sponge host are presented based on two comparative approaches (transcriptome sequencing and suppressive subtractive hybridization (SSH)). Transcriptomic profiles were different when reinfected tissue was compared to normal and aposymbiotic tissue. We characterized a set of 40 genes drawn from a pool of differentially expressed genes in “reinfected” tissue compared to “aposymbiotic” tissue via SSH. As proof of concept, we determined whether some of the differentially expressed genes identified above could be monitored in sponges grown under ecologically realistic field conditions. We allowed aposymbiotic sponge tissue to become re-populated by natural pools of Symbiodinium in shallow water flats in the Florida Keys, and we analyzed gene expression profiles for two genes found to be increased in expression in “reinfected” tissue in both the transcriptome and via SSH. These experiments highlighted the experimental tractability of C. varians to explore with precision the genetic events that occur upon establishment of the symbiosis. We briefly discuss lab- and field-based experimental approaches that promise to offer insights into the co-opted genetic networks that may modulate uptake and regulation of Symbiondinium populations in hospite.

Conclusions
This work provides a sponge transcriptome, and a database of putative genes and genetic pathways that may be involved in Symbiodinium interactions. The relative patterns of gene expression observed in these experiments will need to be evaluated on a gene-by-gene basis in controlled and natural re-infection experiments. We argue that sponges offer particularly useful characteristics for discerning essential dimensions of the Symbiodinium niche.
The general solutions of an auxiliary ordinary differential equation using complex method and its applications
Authors: Yuan Wenjun , Huang Zifeng , Fu Maozhun , Lai Jinchun 
Published: May 2014

AbstractIn this paper, we employ the complex method to obtain all meromorphic solutions of an auxiliary ordinary differential equation at first, and then find all meromorphic general solutions of in combination the Newell-Whitehead equation, the NLS equation, and the Fisher equation with degree three. Our result shows that all rational and simply periodic exact solutions of the combined the Newell-Whitehead equation, NLS equation, and Fisher equation with degree three are solitary wave solutions, and the method is simpler than other methods.MSC:30D35, 34A05.
Functional properties of the HIV-1 long terminal repeat containing single-nucleotide polymorphisms in Sp site III and CCAAT/enhancer binding protein site I
Authors: Shah Sonia , Alexaki Aikaterini , Pirrone Vanessa , Dahiya Satinder , Nonnemacher Michael R , Wigdahl Brian 
Published: May 2014

AbstractBackgroundHIV-1 gene expression is driven by the long terminal repeat (LTR), which contains many binding sites shown to interact with an array of host and viral factors. Selective pressures within the host as well as the low fidelity of reverse transcriptase lead to changes in the relative prevalence of genetic variants within the HIV-1 genome, including the LTR, resulting in viral quasispecies that can be differentially regulated and can potentially establish niches within specific cell types and tissues.MethodsUtilizing flow cytometry and electromobility shift assays, specific single-nucleotide sequence polymorphisms (SNPs) were shown to alter both the phenotype of LTR-driven transcription and reactivation. Additional studies also demonstrated differential loading of transcription factors to probes derived from the double-variant LTR as compared to probes from the wild type.ResultsThis study has identified specific SNPs within CCAAT/enhancer binding protein (C/EBP) site I and Sp site III (3 T, C-to-T change at position 3, and 5 T, C-to-T change at position 5 of the binding site, respectively) that alter LTR-driven gene transcription and may alter the course of viral latency and reactivation. The HIV-1 LAI LTRs containing the SNPs of interest were coupled to a plasmid encoding green fluorescent protein (GFP), and polyclonal HIV-1 LTR-GFP stable cell lines utilizing bone marrow progenitor, T, and monocytic cell lines were constructed and utilized to explore the LTR phenotype associated with these genotypic changes.ConclusionsAlthough the 3 T and 5 T SNPs have been shown to be low-affinity binding sites, the fact that they can still result in effective HIV-1 LTR-driven gene expression, particularly within the TF-1 cell line, has suggested that the low binding site affinities associated with the 3 T C/EBP site I and 5 T Sp site III are potentially compensated for by the interaction of nuclear factor-κB with its corresponding binding sites under selected physiological and cellular conditions. Additionally, tumor necrosis factor-α and Tat can enhance basal transcription of each SNP-specific HIV-1 LTR; however, differential regulation of the LTR is both SNP- and cell type-specific.
Elevated plasma thrombomodulin and angiopoietin-2 predict the development of acute kidney injury in patients with acute myocardial infarction
Authors: Liu Kuan-Liang , Lee Kuang-Tso , Chang Chih-Hsiang , Chen Yung-Chang , Lin Shu-Min , Chu Pao-Hsien 
Published: May 2014

Abstract
Introduction
Acute kidney injury (AKI) following acute myocardial infarction (AMI) is associated with unfavorable prognosis. Endothelial activation and injury were found to play a critical role in the development of both AKI and AMI. This pilot study aimed to determine whether the plasma markers of endothelial injury and activation could serve as independent predictors for AKI in patients with AMI.

Methods
This prospective study was conducted from March 2010 to July 2012 and enrolled consecutive 132 patients with AMI receiving percutaneous coronary intervention (PCI). Plasma levels of thrombomodulin (TM), von Willebrand factor (vWF), angiopoietin (Ang)-1, Ang-2, Tie-2, and vascular endothelial growth factor (VEGF) were measured on day 1 of AMI. AKI was defined as elevation of serum creatinine of more than 0.3 mg/dL within 48 hours.

Results
In total, 13 out of 132 (9.8%) patients with AMI developed AKI within 48 hours. Compared with patients without AKI, patients with AKI had increased plasma levels of Ang-2 (6338.28 ± 5862.77 versus 2412.03 ± 1256.58 pg/mL, P = 0.033) and sTM (7.6 ± 2.26 versus 5.34 ± 2.0 ng/mL, P < 0.001), and lower estimated glomerular filtration rate (eGFR) (46.5 ± 20.2 versus 92.5 ± 25.5 mL/min/1.73 m2, P < 0.001). Furthermore, the areas under the receiver operating curves demonstrated that plasma thrombomodulin (TM) and Ang-2 levels on day 1 of AMI had modest discriminative powers for predicting AKI development following AMI (0.796, P <0.001; 0.833, P <0.001; respectively).

Conclusions
Endothelial activation, quantified by plasma levels of TM and Ang-2 may play an important role in development of AKI in patients with AMI.
4sUDRB-seq: measuring genomewide transcriptional elongation rates and initiation frequencies within cells
Authors: Fuchs Gilad , Voichek Yoav , Benjamin Sima , Gilad Shlomit , Amit Ido , Oren Moshe 
Published: May 2014

AbstractAlthough transcriptional elongation by RNA polymerase II is coupled with many RNA-related processes, genomewide elongation rates remain unknown. We describe a method, called 4sUDRB-seq, based on reversible inhibition of transcription elongation coupled with tagging newly transcribed RNA with 4-thiouridine and high throughput sequencing to measure simultaneously with high confidence genome-wide transcription elongation rates in cells. We find that most genes are transcribed at about 3.5 Kb/min, with elongation rates varying between 2 Kb/min and 6 Kb/min. 4sUDRB-seq can facilitate genomewide exploration of the involvement of specific elongation factors in transcription and the contribution of deregulated transcription elongation to various pathologies.