bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of population susceptibility to upcoming seasonal influenza epidemic strain using interepidemic emerging influenza virus strains
Authors: Chen Lin-Lei , Wu Wai-Lan , Chan Wan-Mui , Fong Carol H. Y. , Ng Anthony C. K. , Ip Jonathan D. , Lu Lu , Dissanayake Thrimendra K. , Ding Xixia , Cai Jian-Piao , Zhang Anna J. X. , Tam Sidney , Hung Ivan F. N. , Chan Kwok-Hung , Yuen Kwok-Yung , To Kelvin K. W. 
Published: September 2019

Abstract
Seasonal influenza virus epidemics have a major impact on healthcare systems. Data on population susceptibility to emerging influenza virus strains during the interepidemic period can guide planning for resource allocation of an upcoming influenza season. This study sought to assess the population susceptibility to representative emerging influenza virus strains collected during the interepidemic period. The microneutralisation antibody titers (MN titers) of a human serum panel against representative emerging influenza strains collected during the interepidemic period before the 2018/2019 winter influenza season (H1N1-inter and H3N2-inter) were compared with those against influenza strains representative of previous epidemics (H1N1-pre and H3N2-pre). A multifaceted approach, incorporating both genetic and antigenic data, was used in selecting these representative influenza virus strains for the MN assay. A significantly higher proportion of individuals had a ⩾four-fold reduction in MN titers between H1N1-inter and H1N1-pre than that between H3N2-inter and H3N2-pre (28.5% (127/445) vs. 4.9% (22/445), P < 0.001). The geometric mean titer (GMT) of H1N1-inter was significantly lower than that of H1N1-pre (381 (95% CI 339–428) vs. 713 (95% CI 641–792), P < 0.001), while there was no significant difference in the GMT between H3N2-inter and H3N2-pre. Since A(H1N1) predominated the 2018–2019 winter influenza epidemic, our results corroborated the epidemic subtype.
Suicidal ideation in patients with cancer: A systematic review of prevalence, risk factors, intervention and assessment
Authors: Kolva Elissa , Hoffecker Lilian , Cox-Martin Emily 
Published: September 2019

AbstractObjectivesSuicidal ideation (SI) underlies risk of death by suicide. It is well established that patients with cancer are at increased risk of death by suicide. Therefore, understanding SI in patients with cancer is critically important. The goal of this systematic review was to investigate the prevalence, risk factors, intervention, and assessment of SI in patients with cancer.MethodsThis systematic review was registered with the PROSPERO database (CRD42018115405) and was guided by the PRISMA statement. We searched Medline, PsycInfo, Embase, CINAHL, the Cochrane Database of Systematic Reviews, and Cochrane Central. Two reviewers independently screened abstracts and assessed for quality assurance using a revised Newcastle-Ottawa Scale.ResultsWe identified 439 studies to screen for eligibility. Eligible studies included adults with cancer diagnoses and listed SI as an outcome. Ultimately, 44 studies were included in the analyses. Prevalence of SI ranged greatly from 0.7% to 46.3%. Single items drawn from validated measures were the most frequent method of assessing SI (n = 20, 45.5%); additional methods included validated measures and psychological interviews. Commonly identified risk factors for SI included age, sex, and disease/treatment-related characteristics, as well as psychological constructs including depression, anxiety, hopelessness, existential distress, and social support.Significance of ResultsAssessment of SI in patients with cancer is the concern of researchers worldwide. Prevalence of SI varied with study population and was likely influenced by the method of assessment. Psychological distress consistently predicted SI. Increasing awareness of demographic, clinical, and psychological associations is critical for risk assessment and intervention development.
Effects of a multidisciplinary quality of life intervention on sleep quality in patients with advanced cancer receiving radiation therapy
Authors: Gentry Melanie T. , Atherton Pamela J. , Lapid Maria , Rosen Preetha Sharone , Kung Simon , Richardson Jarrett , Niazi Shehzad K. , Bobo William V. , Clark Matthew M. , Rummans Teresa A. 
Published: September 2019

AbstractObjectivesSleep disturbances are prevalent in cancer patients, especially those with advanced disease. There are few published intervention studies that address sleep issues in advanced cancer patients during the course of treatment. This study assesses the impact of a multidisciplinary quality of life (QOL) intervention on subjective sleep difficulties in patients with advanced cancer.MethodThis randomized trial investigated the comparative effects of a multidisciplinary QOL intervention (n = 54) vs. standard care (n = 63) on sleep quality in patients with advanced cancer receiving radiation therapy as a secondary endpoint. The intervention group attended six intervention sessions, while the standard care group received informational material only. Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI) and Epworth Sleepiness Scale (ESS), administered at baseline and weeks 4 (post-intervention), 27, and 52.ResultsThe intervention group had a statistically significant improvement in the PSQI total score and two components of sleep quality and daytime dysfunction than the control group at week 4. At week 27, although both groups showed improvements in sleep measures from baseline, there were no statistically significant differences between groups in any of the PSQI total and component scores, or ESS. At week 52, the intervention group used less sleep medication than control patients compared to baseline (p = 0.04) and had a lower ESS score (7.6 vs. 9.3, p = 0.03).Significance of resultsA multidisciplinary intervention to improve QOL can also improve sleep quality of advanced cancer patients undergoing radiation therapy. Those patients who completed the intervention also reported the use of less sleep medication.
Distribution of herbicide-resistant waterhemp (Amaranthus tuberculatus) across row crop production systems in Texas
Authors: Singh Vijay , Garetson Russ , McGinty Josh , Dotray Peter , Morgan Gaylon , Nolte Scott , Bagavathiannan Muthukumar 
Published: September 2019

AbstractWe conducted a survey in the major row-crop production regions of Texas to determine the response of waterhemp to glyphosate (5-enolpyruvylshikimate-3-phosphate synthase [EPSPS] inhibitor), atrazine (photosystem II [PSII] inhibitor), pyrithiobac (acetolactate synthase [ALS] inhibitor), tembotrione (hydroxyphenylpyruvate dioxygenase [HPPD] inhibitor), fomesafen (protoporphyrinogen oxidase [PPO] inhibitor), and dicamba (synthetic auxin). We evaluated 127 accessions for these herbicides. Resistance was confirmed on the basis of plant survival within an accession, and the injury ratings of surviving plants were used to categorize each accession as resistant (<50% injury) or less sensitive (50% to 89% injury). For glyphosate, approximately 27% of all tested accessions were resistant and 20% were less sensitive. The Gulf Coast region had the most glyphosate-resistant accessions (46% of the accessions from this region), followed by the Blacklands region (9%). A dose-response assay of the most resistant waterhemp accession (TX-25) exhibited 17-fold resistance to glyphosate when compared with a susceptible standard. Waterhemp resistance to atrazine also was common in the Gulf Coast region. The accession with the greatest atrazine resistance (TX-31) exhibited 47- and 68-fold resistance to this herbicide when applied POST and PRE, respectively. Widespread resistance to pyrithiobac was observed in waterhemp accessions throughout the Blacklands and Gulf Coast regions. The most resistant accession identified in this study was 61-fold resistant compared with a susceptible standard. No high-level resistance was detected for tembotrione, dicamba, or fomesafen, but high variability in sensitivity to tembotrione and dicamba was observed. One waterhemp accession exhibited reduced sensitivity to fomesafen; the rest were sensitive. Overall, at least two accessions exhibited resistance or reduced sensitivity to herbicides with five different sites of action. The study illustrates the prevalence of multiple herbicide resistance in waterhemp accessions in Texas and emphasizes the need to implement diversified management tactics.
Sugarcane response and fall panicum (Panicum dichotomiflorum) control with topramezone and triazine herbicides
Authors: Negrisoli Raphael M. , Odero D. Calvin , MacDonald Gregory E. , Sellers Brent A. , Laughinghouse H. Dail 
Published: September 2019

AbstractField studies were conducted on organic soils in Belle Glade, FL, in 2016 to 2017 to evaluate sugarcane tolerance and fall panicum control with topramezone applied alone or in combination with triazine herbicides (atrazine, metribuzin, ametryn). Treatments included topramezone (25 and 50 g ai ha−1) applied alone or in combination with atrazine (2,240 g ai ha−1), metribuzin (2,240 g ai ha−1), and ametryn (440 g ha−1) on four plant cane varieties to evaluate tolerance, and on second ratoon fields to determine efficacy on fall panicum control. Topramezone applied alone had no effect on sugarcane chlorophyll fluorescence (i.e., the ratio of variable fluorescence to maximum fluorescence), total chlorophyll, and carotenoid 7 to 28 d after treatment (DAT), suggesting sugarcane tolerance. Significant reduction of these parameters occured 7 to 14 DAT when topramezone (50 g ai ha−1) was applied with ametryn or metribuzin; however, reductions were not detected thereafter, indicating recovery. Sugarcane yield was not affected by topramezone applied alone or in combination with the triazine herbicides. Topramezone (50 g ai ha−1) plus metribuzin resulted in acceptable control of fall panicum (84%) with limited to no regrowth of meristematic tissue at sugarcane canopy closure, equivalent to 56 to 70 DAT. These results indicate that when sequential applications of topramezone, applied alone or in combination with these triazine herbicides, are required for efficacious weed control, topramezone applications alone can be made after 7 d, whereas the combinations can be made after 14 or 21 d, depending on sugarcane sensitivity.
Autologous haematopoietic stem cell transplantation and other cellular therapy in multiple sclerosis and immune-mediated neurological diseases: updated guidelines and recommendations from the EBMT Autoimmune Diseases Working Party (ADWP) and the Joint Accreditation Committee of EBMT and ISCT (JACIE)
Authors:   for the European Society for Blood and Marrow Transplantation (EBMT) Autoimmune Diseases Working Party (ADWP) and the Joint Accreditation Committee of the International Society for Cellular Therapy (ISCT) and EBMT (JACIE), Sharrack Basil , Saccardi Riccardo , Alexander Tobias , Badoglio Manuela , Burman Joachim , Farge Dominique , Greco Raffaella , Jessop Helen , Kazmi Majid , Kirgizov Kirill , Labopin Myriam , Mancardi Gianluigi , Martin Roland , Moore John , Muraro Paolo A. , Rovira Montserrat , Sormani Maria Pia , Snowden John A. 
Published: September 2019

Abstract
These updated EBMT guidelines review the clinical evidence, registry activity and mechanisms of action of haematopoietic stem cell transplantation (HSCT) in multiple sclerosis (MS) and other immune-mediated neurological diseases and provide recommendations for patient selection, transplant technique, follow-up and future development. The major focus is on autologous HSCT (aHSCT), used in MS for over two decades and currently the fastest growing indication for this treatment in Europe, with increasing evidence to support its use in highly active relapsing remitting MS failing to respond to disease modifying therapies. aHSCT may have a potential role in the treatment of the progressive forms of MS with a significant inflammatory component and other immune-mediated neurological diseases, including chronic inflammatory demyelinating polyneuropathy, neuromyelitis optica, myasthenia gravis and stiff person syndrome. Allogeneic HSCT should only be considered where potential risks are justified. Compared with other immunomodulatory treatments, HSCT is associated with greater short-term risks and requires close interspeciality collaboration between transplant physicians and neurologists with a special interest in these neurological conditions before, during and after treatment in accredited HSCT centres. Other experimental cell therapies are developmental for these diseases and patients should only be treated on clinical trials.
Retinoid X receptor gamma (RXRG) is an independent prognostic biomarker in ER-positive invasive breast cancer
Authors: Joseph Chitra , Al-Izzi Sara , Alsaleem Mansour , Kurozumi Sasagu , Toss Michael S , Arshad Maariya , Goh Fang Qin , Alshankyty Ibraheem M. , Aleskandarany Mohammed A. , Ali Simak , Ellis Ian O. , Mongan Nigel P. , Green Andrew R. , Rakha Emad A. 
Published: September 2019

AbstractBackgroundRetinoid X Receptor Gamma (RXRG) is a member of the nuclear receptor superfamily and plays a role in tumour suppression. This study aims to explore the prognostic significance of RXRG in breast cancer.MethodsPrimary breast cancer tissue microarrays (n = 923) were immuno-stained for RXRG protein and correlated with clinicopathological features, and patient outcome.ResultsNuclear RXRG expression was significantly associated with smaller tumour size (p = 0.036), lower grade(p < 0.001), lobular histology (p = 0.016), lower Nottingham Prognostic Index (p = 0.04) and longer breast cancer-specific survival (p < 0.001), and longer time to distant metastasis (p = 0.002). RXRG expression showed positive association with oestrogen receptor (ER)-related biomarkers: GATA3, FOXA1, STAT3 and MED7 (allp < 0.001) and a negative correlation with the Ki67 proliferation marker. Multivariate analysis demonstrated RXRG protein as an independent predictor of longer breast cancer-specific survival and distant metastasis-free survival. In the external validation cohorts,RXRGexpression was associated with improved patients’ outcome (p = 0.025). In ER-positive tumours, high expression of RXRG was associated with better patient outcome regardless of adjuvant systemic therapy. ER signalling pathway was the top predicted master regulator of RXRG protein expression (p = 0.005).ConclusionThis study provides evidence for the prognostic value of RXRG in breast cancer particularly the ER-positive tumours.
T-cell receptor signal strength and epigenetic control of Bim predict memory CD8+ T-cell fate
Authors: Li Kun-Po , Ladle Brian H. , Kurtulus Sema , Sholl Allyson , Shanmuganad Sharmila , Hildeman David A. 
Published: September 2019

AbstractMost effector CD8+T cells die, while some persist and become either “effector” (TEM) or “central” (TCM) memory T cells. Paradoxically, effector CD8+T cells with greater memory potential have higher levels of the pro-apoptotic molecule Bim. Here, we report, using a novel Bim-mCherry knock-in mouse, that cells with high levels of Bim preferentially develop into TCMcells. Bim levels remained stable and were regulated by DNA methylation at the Bim promoter. Notably, high levels of Bcl-2 were required for Bimhicells to survive. Using Nur77-GFP mice as an indicator of TCR signal strength, Nur77 levels correlated with Bim expression and Nur77hicells also selectively developed into TCMcells. Altogether, these data show that Bim levels and TCR signal strength are predictive of TEM- vs. TCM-cell fate. Further, given the many other biologic functions of Bim, these mice will have broad utility beyond CD8+T-cell fate.
Correction: In vitro expansion impaired the stemness of early passage mesenchymal stem cells for treatment of cartilage defects
Authors: Jiang Tongmeng , Xu Guojie , Wang Qiuyan , Yang Lihui , Zheng Li , Zhao Jinmin , Zhang Xingdong 
Published: September 2019

Following the publication of this article, the authors noticed that Fig. 5c in the original manuscript is incorrect due to an error in image handling during the creation of the figure. Specifically, the image for the group P3 BMSCs of time point 21d and the image in the group BMMNCs of time point 14d were incorrect. These linked to the group for BMMNCs of time point 21d, which was also, as a result, incorrect.An amendment to this paper has been published and can be accessed via a link at the top of the paper.
The stem cell-associated transcription co-factor, ZNF521, interacts with GLI1 and GLI2 and enhances the activity of the Sonic hedgehog pathway
Authors: Scicchitano Stefania , Giordano Marco , Lucchino Valeria , Montalcini Ylenia , Chiarella Emanuela , Aloisio Annamaria , Codispoti Bruna , Zoppoli Pietro , Melocchi Valentina , Bianchi Fabrizio , De Smaele Enrico , Mesuraca Maria , Morrone Giovanni , Bond Heather M. 
Published: September 2019

AbstractZNF521 is a transcription co-factor with recognized regulatory functions in haematopoietic, osteo-adipogenic and neural progenitor cells. Among its diverse activities, ZNF521 has been implicated in the regulation of medulloblastoma (MB) cells, where the Hedgehog (HH) pathway, has a key role in the development of normal cerebellum and of a substantial fraction of MBs. Here a functional cross-talk is shown for ZNF521 with the HH pathway, where it interacts with GLI1 and GLI2, the major HH transcriptional effectors and enhances the activity of HH signalling. In particular, ZNF521 cooperates with GLI1 and GLI2 in the transcriptional activation of GLI (glioma-associated transcription factor)-responsive promoters. This synergism is dependent on the presence of the N-terminal, NuRD-binding motif in ZNF521, and is sensitive to HDAC (histone deacetylase) and GLI inhibitors. Taken together, these results highlight the role of ZNF521, and its interaction with the NuRD complex, in determining the HH response at the level of transcription. This may be of particular relevance in HH-driven diseases, especially regarding the MBs belonging to the SHH (sonic HH) subgroup where a high expression of ZNF521 is correlated with that of HH pathway components.
microRNA-17 functions as an oncogene by downregulating Smad3 expression in hepatocellular carcinoma
Authors: Lu Zhufeng , Li Xiuhua , Xu Yongfeng , Chen Miaomiao , Chen Wei , Chen Tao , Tang Qinghe , He Zhiying 
Published: September 2019

AbstractThe sekelsky mothers against dpp3 (Smad3) functions as a transcriptional modulator activated by transforming growth factor-β (TGF-β). Accumulated evidences indicated that Smad3 played the important roles in carcinogenesis and progression of hepatocellular carcinoma (HCC). Up to now, the regulatory mechanism of Smad3 in HCC still remains unclear. It has been known that some particular microRNAs (miRNAs) involve in carcinogenesis through the regulation of gene expressions with targeting mRNAs. In our study, the unknown candidates of miRNAs that target Smad3 mRNA were searched by using a newly established in vivo approach, the miRNA in vivo precipitation (miRIP). Using a loss-of-function assay, we demonstrated that miR-17 directly targeted Smad3 in HCC cells and inhibition on miR-17 increased Smad3 expression. Furthermore, we found that downregulation on Smad3 expression was consistent with high level of miR-17 in HCC tissues of patients when compared with around normal liver tissues. The manipulated miR-17 silence in HCC cells suppressed their growth of both in vitro and in vivo. Such suppression on cell growth could be recovered through downregulating Smad3. In addition, miR-17 affected cell proliferation through arresting cell cycle in G1 phase. The negative correlation between levels of miR-17 and protein levels of Smad3 was supported by the results of analysis with HCC tissue chip. In summary, for the first time, we confirmed that miR-17 directly targeted Smad3 mRNA and downregulated Smad3 protein expression in HCC. Our results indicated that the increased expression of miR-17 promoted carcinogenesis of HCC through down-regulations of Smad3, suggesting miR-17 might serve as the potential diagnostic and therapeutic targets for clinical HCC.
Functional variants in ADH1B and ALDH2 are non-additively associated with all-cause mortality in Japanese population
Authors: Sakaue Saori , Akiyama Masato , Hirata Makoto , Matsuda Koichi , Murakami Yoshinori , Kubo Michiaki , Kamatani Yoichiro , Okada Yukinori 
Published: September 2019

Abstract
The functional variants involved in alcohol metabolism, the A allele of rs1229984:A > G in ADH1B and the A allele of rs671:G > A in ALDH2, are specifically prevalent among East Asian population. They are shown to be under recent positive selection, but the reasons for the selection are unknown. To test whether these positively selected variants have beneficial effects on survival in modern population, we performed the survival analyses using the large-scale Japanese cohort (n = 135,974) with genotype and follow-up survival data. The rs671-A allele was significantly associated with the better survival in the additive model (HR for mortality = 0.960, P = 1.7 × 10−5), and the rs1229984-A had both additive and non-additive effects (HR = 0.962, P = 0.0016 and HR = 0.958, P = 0.0066, respectively), which was consistent with the positive selection. The favorable effects of these alleles on survival were independent of the habit of alcohol consumption itself. The heterogenous combinatory effect between rs1229984 and rs671 genotype was also observed (HRs for AA genotype at rs671 were 1.03, 0.80, and 0.90 for GG, GA, and AA genotype at rs1229984, respectively), supposedly reflecting the synergistic effects on survival.
Severe neurodevelopmental disease caused by a homozygous TLK2 variant
Authors: Töpf Ana , Oktay Yavuz , Balaraju Sunitha , Yilmaz Elmasnur , Sonmezler Ece , Yis Uluc , Laurie Steven , Thompson Rachel , Roos Andreas , MacArthur Daniel G. , Yaramis Ahmet , Güngör Serdal , Lochmüller Hanns , Hiz Semra , Horvath Rita 
Published: September 2019

AbstractA distinct neurodevelopmental phenotype characterised mainly by mild motor and language delay and facial dysmorphism, caused by heterozygous de novo or dominant variants in the TLK2 gene has recently been described. All cases reported carried either truncating variants located throughout the gene, or missense changes principally located at the C-terminal end of the protein mostly resulting in haploinsufficiency of TLK2. Through whole exome sequencing, we identified a homozygous missense variant in TLK2 in a patient showing more severe symptoms than those previously described, including cerebellar vermis hypoplasia and West syndrome. Both parents are heterozygous for the variant and clinically unaffected highlighting that recessive variants in TLK2 can also be disease causing and may act through a different pathomechanism.