bluuebunny/crossref_metadata_2025_split huggingface dataset:
Childbirth outcomes and ethnic disparities in Suriname: a nationwide registry-based study in a middle-income country
Authors: Verschueren Kim J. C. , Prüst Zita D. , Paidin Raëz R. , Kodan Lachmi R. , Bloemenkamp Kitty W. M. , Rijken Marcus J. , Browne Joyce L. 
Published: May 2020

Abstract
Background
Our study aims to evaluate the current perinatal registry, analyze national childbirth outcomes and study ethnic disparities in middle-income country Suriname, South America.

Methods
A nationwide birth registry study was conducted in Suriname. Data were collected for 2016 and 2017 from the childbirth books of all five hospital maternity wards, covering 86% of all births in the country. Multinomial regression analyses were used to assess ethnic disparities in outcomes of maternal deaths, stillbirths, teenage pregnancy, cesarean delivery, low birth weight and preterm birth with Hindustani women as reference group.

Results
18.290 women gave birth to 18.118 (98%) live born children in the five hospitals. Hospital-based maternal mortality ratio was 112 per 100.000 live births. Hospital-based late stillbirth rate was 16 per 1000 births. Stillbirth rate was highest among Maroon (African-descendent) women (25 per 1000 births, aOR 2.0 (95%CI 1.3–2.8) and lowest among Javanese women (6 stillbirths per 1000 births, aOR 0.5, 95%CI 0.2–1.2). Preterm birth and low birthweight occurred in 14 and 15% of all births. Teenage pregnancy accounted for 14% of all births and was higher in Maroon women (18%) compared to Hindustani women (10%, aOR 2.1, 95%CI 1.8–2.4). The national cesarean section rate was 24% and was lower in Maroon (17%) than in Hindustani (32%) women (aOR 0.5 (95%CI 0.5–0.6)). Cesarean section rates varied between the hospitals from 17 to 36%.

Conclusion
This is the first nationwide comprehensive overview of maternal and perinatal health in a middle income country. Disaggregated perinatal health data in Suriname shows substantial inequities in outcomes by ethnicity which need to be targetted by health professionals, researchers and policy makers.
RNA-seq and network analysis reveal unique glial gene expression signatures during prion infection
Authors: Carroll James A. , Race Brent , Williams Katie , Striebel James , Chesebro Bruce 
Published: May 2020

AbstractBackgroundPrion diseases and prion-like disorders, including Alzheimer’s disease and Parkinson’s disease, are characterized by gliosis and accumulation of misfolded aggregated host proteins. Ablating microglia in prion-infected brain by treatment with the colony-stimulating factor-1 receptor (CSF-1R) inhibitor, PLX5622, increased accumulation of misfolded prion protein and decreased survival time.MethodsTo better understand the role of glia during neurodegeneration, we used RNA-seq technology, network analysis, and hierarchical cluster analysis to compare gene expression in brains of prion-infected versus mock-inoculated mice. Comparisons were also made between PLX5622-treated prion-infected mice and untreated prion-infected mice to assess mechanisms involved in disease acceleration in the absence of microglia.ResultsRNA-seq and network analysis suggested that microglia responded to prion infection through activation of integrin CD11c/18 and did not adopt the expression signature associated with other neurodegenerative disease models. Instead, microglia acquired an alternative molecular signature late in the disease process. Furthermore, astrocytes expressed a signature pattern of genes which appeared to be specific for prion diseases. Comparisons were also made with prion-infected mice treated with PLX5622 to assess the impact of microglia ablation on astrocyte gene expression during prion infection. In the presence of microglia, a unique mix of transcripts associated with A1- and A2-reactive astrocytes was increased in brains of prion-infected mice. After ablation of microglia, this reactive astrocyte expression pattern was enhanced. Thus, after prion infection, microglia appeared to decrease the overall A1/A2-astrocyte responses which might contribute to increased survival after infection.ConclusionsRNA-seq analysis indicated dysregulation of over 300 biological processes within the CNS during prion disease. Distinctive microglia- and astrocyte-associated expression signatures were identified during prion infection. Furthermore, astrogliosis and the unique astrocyte-associated expression signature were independent of microglial influences. Astrogliosis and the unique astrocyte-associated gene expression pattern were increased when microglia were ablated. Our findings emphasize the potential existence of alternative pathways for activating the A1/A2 paradigm in astrocytes during neurodegenerative disease.
Correction to: Long non-coding RNA PXN-AS1 suppresses pancreatic cancer progression by acting as a competing endogenous RNA of miR-3064 to upregulate PIP4K2B expression
Authors: Yan Jiayan , Jia Yunxi , Chen Han , Chen Wei , Zhou Xiaoying 
Published: May 2020

In the original publication of this manuscript [1], there are errors in Fig. 3. The authors declare that the identified errors do not change the results or conclusions of this paper.
SH3BGRL confers innate drug resistance in breast cancer by stabilizing HER2 activation on cell membrane
Authors: Li Hui , Zhang Mingming , Wei Yanli , Haider Farhan , Lin Yitong , Guan Wen , Liu Yanbin , Zhang Shaoyang , Yuan Ronghua , Yang Xia , Yang Shulan , Wang Haihe 
Published: May 2020

Abstract
Background
HER2-positive breast cancer is usually associated to the more aggressive progression and the worse prognosis, but the mechanism underlying the innate resistance to HER2-targeted therapy remains elusive. The scaffold protein SH3-domain-binding glutamic acid-rich protein-like protein (SH3BGRL) is indicated as a tumor suppressor in some cancers, but it is highly expressed in breast cancers. Here we characterized the tumorigenic function of SH3BGRL in HER2-expressing breast cancer cells and the subsequent effect in HER2-targeted therapies.

Methods
The interaction of SH3BGRL to HER2 were characterized with various truncated SH3BGRL mutants by immunoprecipitation and molecule docking simulation. The physiological roles of SH3BGRL interacting with HER2 in tumor progression and therapy implication were characterized by gain and loss of function approaches in vitro and in vivo. Immunohistochemistry was used for detections of SH3BGRL and p-HER2 (Y1196) expressions in xenografted tumors and human breast cancer tissues. Clinical relevance of SH3BGRL expression with HER2 was validated with both breast patient sample and the public data analyses.

Results
Our results demonstrated that SH3BGRL directly binds with HER2 on cell membrane via its motifs α1, α2 helixes and β3 sheet, which postpones HER2 internalization upon EGF stimulation. Consequently, the association between SH3BGRL and HER2 contributed to the prolonged HER2 phosphorylation at specific tyrosine sites, especially at Y1196, and their downstream signaling activation. The relevance between SH3BGRL expression and p-HER2 (Y1196) phosphorylation was validated in both xenografted tumors and the breast cancer patient tissues. Mechanistically, SH3BGRL promoted breast tumor cell proliferation and survival, while reduced the cell sensitivity to anti-tumor drugs, especially to the HER2-targeted drugs. In contrast, Silencing SH3BGRL or inhibiting its downstream signals efficiently induced apoptosis of breast tumor cells with HER2 and SH3BGRL doubly positive expression. Database analysis also highlighted that SH3BGRL is a poor prognostic marker, especially for HER2-positive breast cancers.

Conclusions
Our results disclose SH3BGRL as a novel posttranslational modulator of HER2 hyperactivation, which can lead to the intrinsic resistance to HER2-targeted therapy. SH3BGRL would be a pivotal therapy target and a diagnostic marker to HER2-positve patients. Thus, targeting SH3BGRL or the downstream signaling could relieve the innate resistance to some HER2-tageted therapies for both HER2 and SH3BGRL-postive breast cancers.
SNCG promotes the progression and metastasis of high-grade serous ovarian cancer via targeting the PI3K/AKT signaling pathway
Authors: Zhang Jing , Liu Xiao-han , Li Cong , Wu Xiao-xing , Chen Yan-lin , Li Wen-wen , Li Xian , Gong Fan , Tang Qin , Jiang Dan 
Published: May 2020

Abstract
Background
The poor prognosis of patients with ovarian cancer is mainly due to cancer progression. γ-Synuclein (SNCG) has reported as a critical player in cancer metastasis. However, its biological roles and mechanism are yet incompletely understood in ovarian cancer, especially in high-grade serous ovarian cancer (HGSOC).

Methods
This is a retrospective study of 312 patients with ovarian cancer at a single center between 2006 and 2016. Ovarian cancer tissues were stained by immunohistochemistry to analyze the relationship between SNCG expression and clinicopathologic factors. The clinical outcomes versus SNCG expression level were evaluated by Kaplan–Meier method and multiple Cox regression analysis. Next, systematical functional experiments were given to examine the proliferation and metastatic abilities of SNCG both in vitro and in vivo using loss- and gain- of function approaches. Furthermore, the mechanisms of SNCG overexpression were examined by human phospho-kinase array kit and western blot analysis.

Results
Clinically, the expression of SNCG was significantly upregulated in ovarian cancer compared with the borderline and benign tumor, normal ovary, and fallopian tube. Notably, the high level of SNCG correlated with high-risk clinicopathologic features and showed poor survival for patients with HGSOC, indicating an independent prognostic factor for these patients. Functionally, we observed that overexpression of SNCG promoted cell proliferation, tumor formation, migration, and invasion both in vitro and in vivo. Mechanistically, we identified that SNCG promoted cancer cell metastasis through activating the PI3K/AKT signaling pathway.

Conclusions
Our results reveal SNCG up-regulation contributes to the poor clinical outcome of patients with HGSOC and highlight the metastasis-promoting function of SNCG via activating the PI3K/Akt signaling pathway in HGSOC.
Phenotypic heterogeneity by site of infection in surgical sepsis: a prospective longitudinal study
Authors: Stortz Julie A. , Cox Michael C. , Hawkins Russell B. , Ghita Gabriela L. , Brumback Babette A. , Mohr Alicia M. , Moldawer Lyle L. , Efron Philip A. , Brakenridge Scott C. , Moore Frederick A. 
Published: May 2020

Abstract
Background
The role of site of infection in sepsis has been poorly characterized. Additionally, sepsis epidemiology has evolved. Early mortality has decreased, but many survivors now progress into chronic critical illness (CCI). This study sought to determine if there were significant differences in the host response and current epidemiology of surgical sepsis categorized by site of infection.

Study design
This is a longitudinal study of surgical sepsis patients characterized by baseline predisposition, insult characteristics, serial biomarkers, hospital outcomes, and long-term outcomes. Patients were categorized into five anatomic sites of infection.

Results
The 316 study patients were predominantly Caucasian; half were male, with a mean age of 62 years, high comorbidity burden, and low 30-day mortality (10%). The primary sites were abdominal (44%), pulmonary (19%), skin/soft tissue (S/ST, 17%), genitourinary (GU, 12%), and vascular (7%). Most abdominal infections were present on admission and required source control. Comparatively, they had more prolonged proinflammation, immunosuppression, and persistent organ dysfunction. Their long-term outcome was poor with 37% CCI (defined as > 14 in ICU with organ dysfunction), 49% poor discharge dispositions, and 30% 1-year mortality. Most pulmonary infections were hospital-acquired pneumonia. They had similar protracted proinflammation and organ dysfunction, but immunosuppression normalized. Long-term outcomes are similarly poor (54% CCI, 47% poor disposition, 32% 1-year mortality). S/ST and GU infections occurred in younger patients with fewer comorbidities, less perturbed immune responses, and faster resolution of organ dysfunction. Comparatively, S/ST had better long-term outcomes (23% CCI, 39% poor disposition, 13% 1-year mortality) and GU had the best (10% CCI, 20% poor disposition, 10% 1-year mortality). Vascular sepsis patients were older males, with more comorbidities. Proinflammation was blunted with baseline immunosuppression and organ dysfunction that persisted. They had the worst long-term outcomes (38% CCI, 67% poor disposition, 57% 1-year mortality).

Conclusion
There are notable differences in baseline predisposition, host responses, and clinical outcomes by site of infection in surgical sepsis. While previous studies have focused on differences in hospital mortality, this study provides unique insights into the host response and long-term outcomes associated with different sites of infection.
Bone marrow mesenchymal stem cells improve bone erosion in collagen-induced arthritis by inhibiting osteoclasia-related factors and differentiating into chondrocytes
Authors: Gao Jinfang , Zhang Gailian , Xu Ke , Ma Dan , Ren Limin , Fan Jingjing , Hou Jianwen , Han Jian , Zhang Liyun 
Published: May 2020

Abstract
Background
Rheumatoid arthritis (RA) is characterized by joint inflammation and damage to the cartilage and bone in collagen-induced arthritis (CIA). Mesenchymal stem cells (MSCs) can improve articular symptoms and reduce bone erosion in CIA rats; however, the underlying mechanism remains unknown. This study aimed to investigate the mechanism underlying MSC-induced improvement of bone destruction in CIA.

Methods
Wistar rats were divided into a normal group, CIA control group, MTX intervention group, and BMSC intervention group, each comprising 8 rats. Serum RANKL, OPG, and CXCL10 levels of all groups were determined via flow cytometry after 42 days of interventions. RANKL, OPG, TRAF6, CXCL10, and CXCR3 were detected on the synovial membrane via immunohistochemistry, and their relative mRNA levels were determined via RT-PCR analysis. BMSCs were labeled with GFP and administered to CIA rats via the tail vein. At different time points, the distribution of implanted GFP-MSCs in synovial tissues was observed using a fluorescence microscope, and the potential of GFP-MSCs to differentiate into chondrocytes was assessed via immunofluorescence analysis.

Results
BMSC transplantation improved joint inflammation and inhibited bone destruction in CIA rats. BMSCs inhibited the expression of serum CXCL10 and CXCL10 and CXCR3 expression at the synovial membrane. Moreover, protein and mRNA expression analyses revealed that BMSCs potentially regulated RANKL/OPG expression levels in the serum and synovial tissue. Upon implantation into CIA rats, GFP-MSCs were traced in the joints. GFP-positive cells were observed in the cartilage tissue from day 11 and until 42 days after transplantation. Anti-type II collagen/GFP double-positive cells were observed in the articular cartilage (especially damaged cartilage) upon immunofluorescence staining of anti-type II collagen.

Conclusions
BMSCs improve bone destruction in CIA by inhibiting the CXCL10/CXCR3 chemotactic axis, regulating the RANKL/OPG ratio, and directly differentiating into chondrocytes.
Distinct transcriptome signatures of Helicobacter suis and Helicobacter heilmannii strains upon adherence to human gastric epithelial cells
Authors: Berlamont Helena , De Witte Chloë , Bauwens Eva , Min Jou Hannah , Ducatelle Richard , De Meester Ellen , Gansemans Yannick , Deforce Dieter , Van Nieuwerburgh Filip , Haesebrouck Freddy , Smet Annemieke 
Published: May 2020

AbstractThe porcineHelicobacter suisand canine-felineH. heilmanniiare gastricHelicobacterspecies with zoonotic potential. However, little is known about the pathogenesis of human infections with theseHelicobacterspecies. To gain more insight into the interactions of both zoonoticHelicobacterspecies with human gastric epithelial cells, we investigated bacterial genes that are differentially expressed in aH. suisandH. heilmanniistrain after adhesion to the human gastric epithelial cell line MKN7. In vitroHelicobacter-MKN7 binding assays were performed to obtain bacterial RNA for sequencing analysis.H. suisandH. heilmanniibacteria attached to the gastric epithelial cells (i.e. cases) as well as unbound bacteria (i.e. controls) were isolated, after which prokaryotic RNA was purified and sequenced. Differentially expressed genes were identified using the DESeq2 package and SARTools pipeline in R. A list of 134 (83 up-regulated and 51 down-regulated) and 143 (60 up-regulated and 83 down-regulated) differentially expressed genes (padj ≤ 0.01; fold change ≥ 2) were identified for the adherentH. suisandH. heilmanniistrains, respectively. According to BLASTp analyses, only 2 genes were commonly up-regulated and 4 genes commonly down-regulated in both pathogens. Differentially expressed genes of theH. suisandH. heilmanniistrains belonged to multiple functional classes, indicating that adhesion of both strains to human gastric epithelial cells evokes pleiotropic adaptive responses. Our results suggest that distinct pathways are involved in human gastric colonization ofH. suisandH. heilmannii. Further research is needed to elucidate the clinical significance of these findings.
Achieve data privacy and clustering accuracy simultaneously through quantized data recovery
Authors: Wang Ren , Wang Meng , Xiong Jinjun 
Published: May 2020

AbstractThis paper develops a data collection and processing framework that achieves individual users’ data privacy and the operator’s information accuracy simultaneously. Data privacy is enhanced by adding noise and applying quantization to the data before transmission, and the privacy of an individual user is measured by information-theoretic analysis. This paper develops a data recovery and clustering method for the operator to extract features from the privacy-preserving, partially corrupted, and partially observed measurements of a large number of users. To prevent cyber intruders from accessing the data of many users, it also develops a decentralized algorithm such that multiple data owners can collaboratively recover and cluster the data without sharing the raw measurements directly. The recovery accuracy is characterized analytically and showed to be close to the fundamental limit of any recovery method. The proposed algorithm is proved to converge to a critical point from any initial point. The method is evaluated on recorded Irish smart meter data and UMass smart microgrid data.
On strongly starlike and strongly convex functions with bounded radius and bounded boundary rotation
Authors: Hussain Sabir , Ahmad Khalil 
Published: May 2020

AbstractIn this paper, we introduce and investigate new classes of normalized analytic functions in an open unit disk with bounded radius and bounded boundary rotation by using the subordination. We discuss inclusion results, co-efficient bounds, growth and distortion theorems of the classes. Moreover, we compute the radii of strong starlikeness, convexity and starlikeness of the classes. It is interesting to mention that most of our findings are best possible as compared to the existing results in the literature.
Global exponential asymptotic stability of RNNs with mixed asynchronous time-varying delays
Authors: Jia Songfang , Chen Yanheng 
Published: May 2020

AbstractThe present article addresses the exponential stability of recurrent neural networks (RNNs) with distributive and discrete asynchronous time-varying delays. Some novel algebraic conditions are obtained to ensure that for the model there exists a unique balance point, and it is global exponential asymptotically stable. Meanwhile, it also reveals the difference about the equilibrium point between systems with and without distributed asynchronous delay. One numerical example and its Matlab software simulations are given to illustrate the correctness of the present results.
The extents of metabolic syndrome among Antiretroviral Therapy exposed and ART naïve adult HIV patients in the Gedeo-zone, Southern-Ethiopia: a comparative cross-sectional study
Authors: Bune Girma Tenkolu , Yalew Alemayehu Worku , Kumie Abera 
Published: May 2020

AbstractBackgroundHIV infection and Antiretroviral Therapy (ART) has been associated with metabolic syndrome (MS). The prevalence of MS varies substantially between populations and is not yet well-known in sub-Saharan Africa (SSA), including Ethiopia. The current study aims to estimate and evaluate the magnitude of MS among ART exposed and ART naïve HIV-infected patients.MethodsA comparative cross-sectional design was employed among the randomly chosen PLHIVs from two hospitals and two health centers, found in the Gedeo zone, southern-Ethiopia. Data collection was run beginning from December 29th, 2017 up to January 22nd − 2019, using the WHO steep tool; eventually, the completed data entered into Epidata (V-3.1) and exported to SPSS (V− 22) for analysis. The revised international diabetes federation criterion was used to define MS and its components. The mean, standard deviations and proportions were used as a descriptive summary. Categorical data and the proportion of MS in the two groups were compared using binary logistic regression, and results were reported statistically significant withp-value is less than 5%.ResultsA total of 633 (n = 422 on ART andn = 211 ART-naive) PLHIVS was involved, with an overall response rate of 96.2%. The cumulative proportion of MS was 42.5%(95% CI: 39.2–45.7), with 43.4%(95% CI: 39.1–47.4) among ART exposed and 40.8% (95% CI: 35.5–46.0) among ART naïve patients (P > 0.005). However, the difference was not statistically significant and signified that ART has no association with an increased proportion of MS.ConclusionOverall this study demonstrated the presence of an elevated degree of overall MS among PLHIVs. Besides, although the difference was not statistically significant, a relatively higher proportion of MS was realized in the ART exposed than ART naïve groups. Implicated that at the time of the entire test and treatment approaches employed in this target group, routine screening of MS incorporated through HIV care and management system will be a vibrant action.