bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dynamical confirmation of a stellar mass black hole in the transient X-ray dipping binary MAXI J1305-704
Authors: Mata Sánchez D , Rau A , Álvarez Hernández A , van Grunsven T F J , Torres M A P , Jonker P G 
Published: June 2021

ABSTRACT
MAXI J1305-704 has been proposed as a high-inclination candidate black hole X-ray binary in view of its X-ray properties and dipping behaviour during outburst. We present photometric and spectroscopic observations of the source in quiescence that allow us to reveal the ellipsoidal modulation of the companion star and absorption features consistent with those of an early K-type star ($T_{\rm eff}=4610^{+130}_{-160}\, {\rm K}$). The central wavelengths of the absorption lines vary periodically at $P_{\rm orb}=0.394\pm 0.004\, {\rm d}$ with an amplitude of $K_2=554\pm 8\, {\rm km \, s^{-1}}$. They imply a mass function for the compact object of $f(M_1)=6.9\pm 0.3\, {\rm M}_\odot$, confirming its black hole nature. The simultaneous absence of X-ray eclipses and the presence of dips set a conservative range of allowed inclinations $60\, {\rm deg}\lt i\lt 82\, {\rm deg}$, while modelling of optical light curves further constrain it to $i=72^{+5}_{-8}\, {\rm deg}$. The above parameters together set a black hole mass of $M_1= 8.9_{-1.0}^{+1.6}\, {\rm M}_{\odot }$ and a companion mass of $M_2= 0.43\pm 0.16\, {\rm M}_{\odot }$, much lower than that of a dwarf star of the observed spectral type, implying it is evolved. Estimates of the distance to the system ($d=7.5^{+1.8}_{-1.4}\, {\rm kpc}$) and space velocity ($v_{\rm space}=270\pm 60 \, {\rm km\, s^{-1}}$) place it in the Galactic thick disc and favour a significant natal kick during the formation of the BH if the supernova occurred in the Galactic Plane.
Study of rotational splittings in δ Scuti stars using pattern finding techniques
Authors: Ramón-Ballesta A , García Hernández A , Suárez J C , Rodón J R , Pascual-Granado J , Garrido R 
Published: June 2021

ABSTRACT
Detecting and understanding rotation in stellar interiors is nowadays one of the unsolved problems in stellar physics. Asteroseismology has been able to provide insights on rotation for the Sun, solar-like stars, and compact objects like white dwarfs. However, this is still very difficult for intermediate-mass stars. These stars are moderate-to-rapid rotators. Rotation splits and shifts the oscillation modes, which makes the oscillation spectrum more complex and harder to interpret. Here we study the oscillation patterns of a sample of benchmark δ Sct stars belonging to eclipsing binary systems with the objective of finding the frequency spacing related to the rotational splitting (δr). For this task, we combine three techniques: the Fourier transform, the autocorrelation function, and the histogram of frequency differences. The last two showed a similar behaviour. For most of the stars, it was necessary to determine the large separation (Δν) prior to spot δr. This is the first time we may clearly state that one of the periodicities present in the p modes oscillation spectra of δ Sct stars corresponds to the rotational splitting. This is true independent of the stellar rotation rate. These promising results pave the way to finding a robust methodology to determine rotational splittings from the oscillation spectra of δ Sct stars and, thus, understanding the rotational profile of intermediate-mass pulsating stars.
Association of T2285C polymorphism in PARP1 gene coding region with its expression, activity and NSCLC risk along with prognosis
Authors: Wang Yan , Xia Xiao Bing , Tang Hui Zhuo , Cai Jing Ran , Shi Xiang Kui , Ji Huai Xue , Yan Xiao Nan , Xu Tie 
Published: June 2021

Abstract
Poly (ADP-ribose) polymerase-1 (PARP1), a DNA repair gene, is the crucial player in the maintenance of genome integrity. T2285C polymorphism in coding region of PARP1 has been reported to be associated with susceptibility to tumours. We explored the relationship and mechanism of T2285C polymorphism of PARP1 to its expression and activity along with risk and prognosis in non-small cell lung cancer (NSCLC). mRNA expression was measured using quantitative RT–PCR assay or collected from TCGA dataset. Protein expression was examined with immunoblotting assay. Genotypes were determined by PCR-RFLP and sequencing approaches. PARP1 activity was determined with enzyme activity assay. Regulation of SIRT7 to PARP1 was determined by overexpression and small interference experiment. Association of PARP1 T2285C polymorphism with NSCLC risk was evaluated via multiple logistic regression analysis. Comparison of treatment response and progression-free survival (PFS) of NSCLC patients among different genotypes or regimens was made by chi-square test. Results indicated that mRNA and protein expression of PARP1 dramatically increased in NSCLC tissues in comparison with paired para-carcinoma tissues (P &lt; 0.05). TC/CC mutant genotypes were associated with markedly enhanced PARP1 mRNA level compared with TT genotype (P = 0.011). No significant difference was discovered in PARP1 protein expression among TT, TC or CC genotypes (P &gt; 0.05). Subjects with variant allele C had higher risk of NSCLC in comparison with allele T carriers [odds ratio = 1.560; P = 0.000]. NSCLC patients carrying mutational TC or CC genotypes were correlated with unfavourable response to platinum-based chemotherapy (TT vs. TC vs. CC, P = 0.010), and shorter PFS compared with TT genotype (TT vs. TC vs. CC, P = 0.009). T2285C mutation of PARP1 resulted in the enhancement of its mRNA, but the decrease of enzyme activity in tumour cell. Overexpression of SIRT7 attenuated PARP1 expression and activity. These findings suggest the variant allele C of T2285C polymorphism of PARP1 linked to an increase of NSCLC risk, and unfavourable efficacy and prognosis of NSCLC patients with platinum-based chemotherapy, which might be associated with enhancement of its mRNA expression and the diminishment of activity. Identification of PARP1 T2285C polymorphism and mRNA expression may be the promising way for the individualised treatment of NSCLC.
Osteobiologics
Authors: Golubovsky Joshua L , Ejikeme Tiffany , Winkelman Robert , Steinmetz Michael P 
Published: June 2021

Abstract

BACKGROUND
Osteobiologics are engineered materials that facilitate bone healing and have been increasingly used in spine surgery. Autologous iliac crest bone grafts have been used historically, but morbidity associated with graft harvesting has led surgeons to seek alternative solutions. Allograft bone, biomaterial scaffolds, growth factors, and stem cells have been explored as bone graft substitutes and supplements.

OBJECTIVE
To review current and emerging osteobiologic technologies.

METHODS
A literature review of English-language studies was performed in PubMed. Search terms included combinations of “spine,” “fusion,” “osteobiologics,” “autologous,” “allogen(e)ic,” “graft,” “scaffold,” “bone morphogenic protein,” and “stem cells.”

RESULTS
Evidence supports allograft bone as an autologous bone supplement or replacement in scenarios where minimal autologous bone is available. There are promising data on ceramics and P-15; however, comparative human trials remain scarce. Growth factors, including recombinant human bone morphogenic proteins (rhBMPs) 2 and 7, have been explored in humans after successful animal trials. Evidence continues to support the use of rhBMP-2 in lumbar fusion in patient populations with poor bone quality or revision surgery, while there is limited evidence for rhBMP-7. Stem cells have been incredibly promising in promoting fusion in animal models, but human trials to this point have only involved products with questionable stem cell content, thereby limiting possible conclusions.

CONCLUSION
Engineered stem cells that overexpress osteoinductive factors are likely the future of spine fusion, but issues with applying viral vector-transduced stem cells in humans have limited progress.
Genomic Basis of Transcriptome Dynamics in Rice under Field Conditions
Authors: Kashima Makoto , Sakamoto Ryota L , Saito Hiroki , Ohkubo Satoshi , Tezuka Ayumi , Deguchi Ayumi , Hashida Yoichi , Kurita Yuko , Iwayama Koji , Adachi Shunsuke , Nagano Atsushi J 
Published: June 2021

Abstract
How genetic variations affect gene expression dynamics of field-grown plants remains unclear. Expression quantitative trait loci (eQTL) analysis is frequently used to find genomic regions underlying gene expression polymorphisms. This approach requires transcriptome data for the complete set of the QTL mapping population under the given conditions. Therefore, only a limited range of environmental conditions is covered by a conventional eQTL analysis. We sampled sparse time series of field-grown rice from chromosome segment substitution lines (CSSLs) and conducted RNA sequencing (RNA-Seq). Then, by using statistical analysis integrating meteorological data and the RNA-Seq data, we identified 1,675 eQTLs leading to polymorphisms in expression dynamics under field conditions. A genomic region on chromosome 11 influences the expression of several defense-related genes in a time-of-day- and scaled-age-dependent manner. This includes the eQTLs that possibly influence the time-of-day- and scaled-age-dependent differences in the innate immunity between Koshihikari and Takanari. Based on the eQTL and meteorological data, we successfully predicted gene expression under environments different from training environments and in rice cultivars with more complex genotypes than the CSSLs. Our novel approach of eQTL identification facilitated the understanding of the genetic architecture of expression dynamics under field conditions, which is difficult to assess by conventional eQTL studies. The prediction of expression based on eQTLs and environmental information could contribute to the understanding of plant traits under diverse field conditions.
Skewed Allegiances: Recalibrating Humanitarian Accountability towards Gender
Authors: Lokot Michelle 
Published: June 2021

Abstract
Humanitarian actors often face competing accountabilities that may skew “upwards” in favour of donors. With increasing requirements on humanitarian actors to demonstrate efficiency and impact, accountability has often become depoliticised, reduced to technical frameworks and bureaucratic processes. Within humanitarian work focused on promoting gender equality, the problems in how accountability is framed have particular ramifications, affecting how gender issues are positioned, how gender-related data are presented and the assumptions underlying interventions that seek to address gender inequality. This article is based on ethnographic research in Jordan, specifically interviews with humanitarian practitioners and Syrian refugees. It explores how accountability for gender issues is positioned within the humanitarian sector. The article challenges the fixation on collecting quantitative data on gender-based violence and suggests that humanitarian assumptions about refugee populations may lead to stereotypical and homogenous representations about refugees that fail to recognise complexity. It provides examples of gaps in humanitarian assistance experienced by Syrian refugees in Jordan. The article also suggests that accountability for social transformation and change may be shifting from humanitarian actors towards refugees themselves. The article recommends that approaches to humanitarian accountability should prioritise listening, and being honest about failures and gaps in knowledge.
N‐acetylcysteine attenuates ventilator‐induced diaphragm dysfunction in rats
Authors: Agten Anouk , Maes Karen , Smuder Ashley , Powers Scott K , Decramer Marc , Gayan‐Ramirez Ghislaine 
Published: June 2021

Controlled mechanical ventilation (CMV) results in diaphragmatic dysfunction and oxidative stress. We examined whether an anti‐oxidant, N‐acetylcysteine (NAC), would restore the redox‐balance in the diaphragm and prevent the deleterious effects of CMV.Anesthetized rats were submitted for 24h to either spontaneous breathing while receiving 150mg/kg NAC (SBNAC) or saline (SBSAL) or to CMV while receiving 150mg/kg NAC (MVNAC) or saline (MVSAL).After 24 hours, diaphragm forces were significantly lower in MVSAL compared to all groups (−21%, p<0.01). Administration of NAC completely abolished this decrease. Protein oxidation was significantly increased in MVSAL (+43%, p<0.0001) and was restored in MVNAC. Diaphragm caspase‐3 and calpain activity were significantly increased in MVSAL compared to all groups (p<0.0001). These data show that the administration of NAC was able to preserve the diaphragm from the deleterious effects of CMV.Supported by AstraZeneca Farmaceuticals and FWO Vlaanderen
Selectivity of PKC isoforms in the regulation of Na+‐K+‐2Cl− cotransporter (NKCC1) in secretory epithelia
Authors: TANG JUN , Bouyer Patrice , Mykoniatis Andreas , Buschmann Mary , Matlin Karl S. , Matthews Jeffrey B. 
Published: June 2021

NKCC1 drives basolateral Cl− entry in secretory epithelia. Activation of PKC by phorbol 12‐myristate 13‐acetate (PMA) reduces colonic epithelial Cl− secretory response to cAMP and surface NKCC1. The study was to define selectivity of PKCs in regulating epithelial NKCC1.T84 monolayers uninfected or infected with adenoviruses expressing human PKC (α, δ, ε)‐specific shRNAs or non‐target LacZ‐shRNA were treated with PMA or vehicle, followed by measurement of Cl− secretion (short‐circuit current, Isc). NKCC1 signal in the cells was assessed by immunofluorescence. NKCC1 surface expression was examined by basolateral surface biotinylation assay.We found proteins of PKC (α, δ, ε) in shPKCs cells were decreased by ~85% after 72h infection. PMA reduced forskolin (FSK)‐stimulated Cl− secretion much less in shPKCδ or shPKCε cells than shLacZ or uninfected cells. There was no significant difference in PMA‐reduced Cl− secretion between shPKCα and shLacZ. In shLacZ and shPKCα cells, PMA induced a redistribution of NKCC1 signal to intracellular vesicles; the effect was not observed in shPKCδ or shPKCε cells. PMA caused a dramatic decrease in basolateral biotinylated NKCC1 in shLacZ or shPKCα, but not in shPKCδ or shPKCε cells.In conclusion, depletion of PKC δ or ε, but not PKCα, prevents PMA inhibition of T84 Cl− secretion via a mechanism involving stabilization of the basolateral membrane NKCC1.Received NIH grant DK48010.
FK506 binding protein (FKBP12) may contribute to 4‐chloro‐m‐cresol induced adenosine in human B cells
Authors: Bina Saiid , Capacchione John , Bayarsaikhan Munkhuu , Muldoon Sheila , Bunger Rolf 
Published: June 2021

IntroductionRyanodine receptor (RyR1) agonist 4‐chloro‐m‐cresol (4CmC) stimulates normoxic adenosine (ADO) production in B cells, especially from malignant hyperthermia susceptible individuals. In an attempt to identify a pathway for this action of 4CmC, FK506, an immunosuppressant drug that disrupts the interaction of FK506‐binding protein (FKBP12) with RyR1, and Xestospongin C (XeC), a specific inhibitor of IP3R were tested. FKBP12 forms a complex with the RyR and IP3R to regulate their physiological release of intracellular Ca2+.MethodsB cells were suspended in HBSS + ADO deaminase inhibitor (EHNA) followed by addition of FK506 or XeC and incubated at 37°C for 10 min. In a 2nd experiment; 10min after addition of FK506 or XeC, 4CmC (2mM) was applied and incubation continued for 30 min. After cellular reactions termination, supernatant [ADO] was assayed using HPLC.Results(means ± SEM for 106 cells): ADO basal level was 0.422 ± 0.097μM (n=7). FK506 (2, 20, 200μM) increased ADO levels by 59 ± 4, 207 ± 21, and 240 ± 24% respectively. FK506 (2, 20, 200μM) increased the sensitivity of B cells to 4CmC by 4±5, 13±4, and 49±10%. XeC did not alter basal or 4CmC‐induced ADO in B cells.ConclusionFK506 likely displaces FKBP12 from the RyR1 receptor in B cells resulting in leaky Ca2+ channels and to cytosolic Ca2+ accumulation. This stimulates Ca2+ pumping, generating ADP and AMP leading to formation of ADO in the presence of EHNA.
Vitamin D regulates MUC17 expression in Caco‐2 cells.
Authors: Tabikh Sara Q , Tang Eva YK , Resta Silvia 
Published: June 2021

Mucins are components of the gastrointestinal barrier and their downregulation contributes to chronic gut inflammation. Calcium plays an important role in stabilizing negatively charged mucins expressed by intestinal cells. Vitamin D regulates intestinal calcium absorption, through the nuclear vitamin D receptor (VDR). MUC17 gene regulator contains a VDR responsive element. We hypothesized that lack of VDR expression would disrupt mucin expression in intestinal epithelial cells. Caco‐2 cells treated with siVDR or untreated control were tested for MUC17 mRNA expression by PCR and by immuno‐histochemistry. Treatment with low calcium concentration by calcium switch and vitamin D3 was also studied. siVDR Caco‐2 cells had lower levels of MUC17 vs controls (p<0.01). MUC17 mRNA expression was decreased by 2.5 in siVDR cells. In cell exposed to low calcium no MUC17 was detectable. Restoration of calcium levels in the siVDR Caco‐2 evoked a rapid short‐lived recovery of MUC17 mRNA expression, albeit the mucin expression remained unchanged. Vitamin D3 treatment had no effect on siVDR Caco‐2. However, untreated controls, expressing normal levels of VDR showed an increased MUC17 mRNA and protein expression. Our data support the hypothesis that vitamin D has a protective effect on the gut epithelial barrier by promoting mucin expression and homeostasis.NIH‐DK062096 (SR).
Effects of Aminoguanidine (AG) in a Rat Pancreatic Tumor Cell line
Authors: Chowdhury Parimal 
Published: June 2021

Aminoguanidine is a compound that reportedly exerts both pro‐ and antioxidant effects. In animal models and in humans it was shown as an antioxidant against lipid peroxidation. The current study evaluated the direct effect of AG on rat pancreatic tumor cell.MethodsAR42J cells were grown in F‐12 nutrient medium at 370C and 5% CO2. At log phase, they were separated, sub cultured for 3 days at specified dose and time with hydrogen peroxide and aminoguanidine. The cellular extracts were subjected to Western blotting employing antibodies to ERK ½ and analyzed further by immunohistochemistry. Cell proliferation lipid peroxidation assay was also conducted. Cell functional assay was conducted with CCK‐8 (10–10 M) incubated for 30 min at 370C and was assessed by the amount of amylase released in the media.ResultsIncubation of AR42J cells with aminoguanidine induced 3–5 fold activation of phospho ERK‐1/2. This was confirmed by immunohistochemistry with FITC conjugated antibody to ERK1/2. CCK‐stimulated amylase release was enhanced in the presence of aminoguanidine.ConclusionThese data suggest that ERK‐1/2, a proliferative signal of MAPK pathway, is induced and enhanced in AR42J cells by aminoguanidine. This is coupled with enhanced cell function and proliferation suggesting that aminoguanidine acts as a pro‐oxidant in this cell line.
Expression of PDE5 and its stimulation by cGMP‐dependent protein kinase (PKG) determine the magnitude of smooth muscle relaxation in different regions of the stomach
Authors: Al‐Shboul Othman , Mahavadi Sunila , Grider John R , Murthy Karnam S. 
Published: June 2021

The contractile phenotypes of proximal and distal gastric smooth muscle are distinct with proximal smooth muscle exhibiting tonic characteristics and distal smooth muscle phasic characteristics. In smooth muscle, the main cGMP hydrolyzing enzyme phosphodiesterase 5 (PDE5) plays an important role in determining the strength and duration of cGMP signaling, and thus muscle relaxation. The activity of PDE5 is stimulated by phosphorylation via PKG.AimTo determine the expression and regulation of PDE5 activity in proximal versus distal regions of the stomach.MethodsExpression of PDE5 and PKG‐mediated phosphorylation of PDE5 at Ser 92 were measured by western blot. PDE5 activity was measured using [3H]cGMP and cGMP‐mediated relaxation was measured by scanning micrometry.ResultsMuscle cells from proximal stomach contained 2 times more PDE5 than muscle cells from distal stomach. Activation of PKG by the NO‐donor caused an increase in PDE5 phosphorylation and activity, but the responses were higher in muscle cells from proximal stomach. In contrast, muscle relaxation was greater in muscle cells from distal stomach consistent with the lower amounts of PDE5 in muscle cells from this region.Conclusion. Higher expression of PDE5 and greater PKG‐mediated augmentation of PDE5 activity in muscle cells from proximal stomach correlate with the tonic phenotype of muscle in proximal stomach relative to distal stomach.
Effect of ezetimibe on the response of incretin secretion to intestine lipid ingestion
Authors: Yang Li , Li Xiaoming , Ji Yong , Wang David Q.‐H. , Howles Philip N. , Hui David Y. , Tso Patrick 
Published: June 2021

BackgroundEzetimibe (EZ) is a potent inhibitor of cholesterol absorption by enterocytes. Although EZ minimally affects fat absorption, it is unknown if EZ affects the secretion of incretins glucose‐dependent insulinotropic polypeptide (GIP) and glucagon‐like peptide‐1 (GLP‐1) during triglyceride (TG) absorption.AimWe determined if EZ influences the lymphatic secretion of incretins stimulated by the ingestion of Ensure.MethodsIn SD rats, the mesenteric lymph duct was cannulated and a duodenal infusion tube was installed. EZ (0.67 mg/kg) or saline was infused duodenally 2 h prior to the feeding of a 3 ml bolus dose of Ensure (4.43 kcal). To determine glucose, TG, cholesterol, GIP, and GLP‐1 concentrations, lymph samples were collected 2 h before and 2 h after infusion of Ensure.ResultsEZ did not affect lymph flow, glucose or TG output stimulated by Ensure compared with the control rats. As expected, EZ did significantly reduce lymphatic cholesterol output. Interestingly, EZ significantly reduced the stimulation of lymphatic secretion of GIP and GLP‐1 induced by Ensure.ConclusionsReduced secretion of GIP and GLP‐1 by the enteroendocrine cells is associated with decreased cholesterol secretion in EZ‐treated rats. Moreover, this response of intestinal incretin secretion is independent from the uptake of dietary TG. The mechanism involved remains to be elucidated. This work was supported by NIH.
Growth factors EGF and HGF suppress hepcidin by direct interference with bone morphogenetic protein signaling
Authors: Goodnough Julia B , Ganz Tomas 
Published: June 2021

The iron‐regulatory hormone hepcidin is a 25‐amino‐acid peptide synthesized in the liver. Hepcidin inhibits iron export into plasma and is in turn regulated by iron through a BMP6‐activated pathway. Erythropoietic activity and certain liver diseases decrease hepcidin synthesis through unknown mechanisms.We found that hepatocyte growth factor (HGF) was a potent suppressor of hepcidin in hepatocytes and in hepatic cell lines. At physiologic concentrations, HGF dose‐dependently suppressed hepcidin mRNA and hepcidin promoter‐luciferase. HGF also opposed hepcidin induction by BMP6 in both systems. HGF was likely acting directly on BMP signaling because HGF prevented the induction of an unrelated BMP‐sensitive reporter by BMP6, as well as ‐2, ‐4, and ‐9. In primary mouse hepatocytes, BMP‐driven Smad1/5/8 nuclear translocation was suppressed by HGF. The hepatocytes displayed increased activation of the MAP kinase Erk and related phosphorylation of a regulatory motif in R‐Smads known to result in nuclear exclusion. Thus, decreased nuclear concentration of activated Smad1/5/8 is a likely mechanism of the HGF suppression of hepcidin response to BMP. EGF also suppressed the induction of hepcidin mRNA and the hepcidin‐luciferase reporter by BMPs, likely by a similar mechanism. EGF, HGF or other growth factors using MAPKs could mediate the suppression of hepcidin in chronic liver diseases.This research is supported by National Institutes of Health grant #1F30DK082151.