bluuebunny/crossref_metadata_2025_split huggingface dataset:
A tentacle for every occasion: comparing the hunting tentacles and sweeper tentacles, used for territorial competition, in the coral Galaxea fascicularis
Authors: Yosef Oshra , Popovits Yotam , Malik Assaf , Ofek-Lalzer Maya , Mass Tali , Sher Daniel 
Published: August 2020

Abstract
Background
Coral reefs are among the most diverse, complex and densely populated marine ecosystems. To survive, morphologically simple and sessile cnidarians have developed mechanisms to catch prey, deter predators and compete with adjacent corals for space, yet the mechanisms underlying these functions are largely unknown. Here, we characterize the histology, toxic activity and gene expression patterns in two different types of tentacles from the scleractinian coral Galaxea fascilcularis – catch tentacles (CTs), used to catch prey and deter predators, and sweeper tentacles (STs), specialized tentacles used for territorial aggression.

Results
STs exhibit more mucocytes and higher expression of mucin genes than CTs, and lack the ectodermal cilia used to deliver food to the mouth and remove debris. STs and CTs also express different sensory rhodopsin-like g-protein coupled receptors, suggesting they may employ different sensory pathways. Each tentacle type has a different complement of stinging cells (nematocytes), and the expression in the two tentacles of genes encoding structural nematocyte proteins suggests the stinging cells develop within the tentacles. CTs have higher neurotoxicity to blowfly larvae and hemolytic activity compared to the STs, consistent with a role in prey capture. In contrast, STs have higher phospholipase A2 activity, which we speculate may have a role in inducing tissue damage during territorial aggression. The expression of genes encoding cytolytic toxins (actinoporins) and phospholipases also differs between the tentacle types.

Conclusions
These results show that the same organism utilizes two distinct tentacle types, each equipped with a different venom apparatus and toxin composition, for prey capture and defense and for territorial aggression.
SOX10-regulated promoter use defines isoform-specific gene expression in Schwann cells
Authors: Fogarty Elizabeth A. , Kitzman Jacob O. , Antonellis Anthony 
Published: August 2020

Abstract
Background
Multicellular organisms adopt various strategies to tailor gene expression to cellular contexts including the employment of multiple promoters (and the associated transcription start sites (TSSs)) at a single locus that encodes distinct gene isoforms. Schwann cells—the myelinating cells of the peripheral nervous system (PNS)—exhibit a specialized gene expression profile directed by the transcription factor SOX10, which is essential for PNS myelination. SOX10 regulates promoter elements associated with unique TSSs and gene isoforms at several target loci, implicating SOX10-mediated, isoform-specific gene expression in Schwann cell function. Here, we report on genome-wide efforts to identify SOX10-regulated promoters and TSSs in Schwann cells to prioritize genes and isoforms for further study.

Results
We performed global TSS analyses and mined previously reported ChIP-seq datasets to assess the activity of SOX10-bound promoters in three models: (i) an adult mammalian nerve; (ii) differentiating primary Schwann cells, and (iii) cultured Schwann cells with ablated SOX10 function. We explored specific characteristics of SOX10-dependent TSSs, which provides confidence in defining them as SOX10 targets. Finally, we performed functional studies to validate our findings at four previously unreported SOX10 target loci: ARPC1A, CHN2, DDR1, and GAS7. These findings suggest roles for the associated SOX10-regulated gene products in PNS myelination.

Conclusions
In sum, we provide comprehensive computational and functional assessments of SOX10-regulated TSS use in Schwann cells. The data presented in this study will stimulate functional studies on the specific mRNA and protein isoforms that SOX10 regulates, which will improve our understanding of myelination in the peripheral nerve.
CD16 expression on neutrophils predicts treatment efficacy of capecitabine in colorectal cancer patients
Authors: Lu Yu , Huang Yizhou , Huang Lei , Xu Yanjie , Wang Zien , Li Han , Zhang Ting , Zhong Ming , Gao Wei-qiang , Zhang Yan 
Published: August 2020

Abstract
Background
Early detection of capecitabine-resistance could largely increase overall survival of colorectal cancer (CRC) patients. Previous studies suggested examination of immune cells in peripheral blood would help to predict efficacy of chemotherapy.

Methods
We examined the immunological characteristics of peripheral blood in CRC patients with capecitabine treatment. We analyzed the relationships between the abnormal immune cell population in capecitabine-resistance patients and major clinical features. Furthermore, RNA sequencing, analyses of cell surface marker expression and the correlations with other major immune cell populations were performed using this population to explore the possible function of these cells.

Results
The expression level of CD16 on neutrophils was down-regulated in capecitabine-resistant CRC patients. Patients with CD16low/−neutrophils after capecitabine therapy had adverse clinical features. What’s important, the change of CD16 expression level on neutrophils appeared much earlier than CT scan. RNA sequencing revealed that CD16low/−neutrophils in capecitabine-resistant patients had lower expression level of neutrophil-related genes, compared to CD16+neutrophils in capecitabine-sensitive patients, suggesting this CD16low/−population might be immature neutrophils. Furthermore, the expression level of CD16 on neutrophils in patients with capecitabine treatment was positively correlated with the number of anti-tumor immune cell subsets, such as CD8+T cell, CD4+T cell, NK cell and monocyte.

Conclusions
Our findings indicated that CD16 expression on neutrophils in peripheral blood was a good prognostic marker for predicting efficacy of capecitabine in CRC patients.
Genome-wide sRNA and mRNA transcriptomic profiling insights into dynamic regulation of taproot thickening in radish (Raphanus sativus L.)
Authors: Xie Yang , Ying Jiali , Xu Liang , Wang Yan , Dong Junhui , Chen Yinglong , Tang Mingjia , Li Cui , M’mbone Muleke Everlyne , Liu Liwang 
Published: August 2020

Abstract
Background
Taproot is the main edible organ and ultimately determines radish yield and quality. However, the precise molecular mechanism underlying taproot thickening awaits further investigation in radish. Here, RNA-seq was performed to identify critical genes involved in radish taproot thickening from three advanced inbred lines with different root size.

Results
A total of 2606 differentially expressed genes (DEGs) were shared between ‘NAU-DY’ (large acicular) and ‘NAU-YB’ (medium obovate), which were significantly enriched in ‘phenylpropanoid biosynthesis’, ‘glucosinolate biosynthesis’, and ‘starch and sucrose metabolism’ pathway. Meanwhile, a total of 16 differentially expressed miRNAs (DEMs) were shared between ‘NAU-DY’ and ‘NAU-YH’ (small circular), whereas 12 miRNAs exhibited specific differential expression in ‘NAU-DY’. Association analysis indicated that miR393a-bHLH77, miR167c-ARF8, and miR5658-APL might be key factors to biological phenomenon of taproot type variation, and a putative regulatory model of taproot thickening and development was proposed. Furthermore, several critical genes including SUS1, EXPB3, and CDC5 were characterized and profiled by RT-qPCR analysis.

Conclusion
This integrated study on the transcriptional and post-transcriptional profiles could provide new insights into comprehensive understanding of the molecular regulatory mechanism underlying taproot thickening in root vegetable crops.
A risk predictor of restenosis after superficial femoral artery stent implantation: relevance of mean platelet volume
Authors: Yang Yao Bo , Shen Jing , Wang Sheng Hai , Song Jian Bo , Ge Fangfang , Xie Jia Pei , Qu Jiang Shuai , Mao Xin Zu , Kuang Zhao Cheng , Shang Nan , Wang Xiang , Wu Ye Jun , Yang Fan , Yuan Yue , Wang Hongxin , Sun Jun , Fang Jicheng , Xiao Liang 
Published: August 2020

Abstract
Background
To investigate the relationship between an increase in the pre- and post-operative mean platelet volume (MPV) and superficial femoral artery in-stent restenosis (ISR) rate.

Methods and results
We recruited patients that underwent superficial femoral artery stenting for lower extremity arteriosclerosis obliterans at our hospital from March 2015 to March 2018. All patients gave venous blood three days before and following implantation. Doppler ultrasound, computed tomography angiography or digital subtraction angiography were used for regular follow-up examination. Logistic regression was used to identify predictors of ISR after superficial femoral artery stenting. We enrolled 173 patients, of which 34 (19.6%) were determined as having ISR for a mean of 8.9 ± 2.7 months (3–12 months). Neutrophil count, neutrophil ratio, lymphocyte ratio and platelet count pre-implantation, and platelet count and MPV after stent implantation, and the pre- and post-operative mean platelet volume difference (MPVD) and mean platelet volume difference ratio (MPVDR) were all statistically different when comparing the ISR and non-restenosis groups (p < 0.05). A positive correlation was found for post-operative MPV and presence of ISR (r = 0.58; P < 0.001). A MPVD not less than 1.5 fL was associated with an odds ratio of 9.17 (95% CI [3.76 to 22.35]; P < 0.001) for presence of ISR. A MPVDR of not less than 17.9% was associated with an odds ratio of 7.68 (95% CI [3.19 to 18.49]; P < 0.001) for occurrence of ISR.

Conclusions
An increase in pre- and post-operative MPV was correlated with the occurrence of superficial femoral artery ISR.
Assessment of regional left ventricular myocardial strain in patients with left anterior descending coronary stenosis using computed tomography feature tracking
Authors: Han Xiaoyu , Cao Yukun , Ju Zhiguo , Liu Jia , Li Na , Li Yumin , Liu Tong , Shi Heshui , Gu Jin 
Published: August 2020

AbstractBackgroundComputed tomography feature tracking (CT-FT) has emerged as a valuable method for the assessment of cardiac function. However, no studies have investigated the usefulness of CT-derived assessments of left ventricular (LV) strain in coronary artery disease (CAD). Our aim was to evaluate regional LV systolic deformation in patients with left anterior descending coronary artery (LAD) stenosis using CT-FT.MethodsSeventy-six patients with LAD stenosis were enrolled. The patients were divided into four groups according to the percentage of LAD stenosis: ≤25% was defined as group I (24 patients), 26 to 49% as group II (17 patients), 50 to 74% as group III (21 patients), and ≥ 75% as group IV (14 patients). Thirty-two sex- and age-matched healthy subjects were included as controls.ResultsNo intergroup differences were found between groups I-IV and the controls in terms of the left ventricular ejection fraction, end-diastolic volume and end-systolic volume. However, the longitudinal strain (LS) of the LAD territory was significantly reduced in groups I-IV compared with the controls (− 20.8, − 18.6%, − 18.6%, and − 17.0% vs − 23.7%, respectively). The circumferential strain (CS) of the LAD territory was significantly reduced in groups III and IV compared with the controls and groups I and II (− 22.4% and − 22.1% vs − 25.4, − 24.1%, and − 25.3%, respectively). Compared with the non-LAD territory, the LAD territory in groups II-IV showed significantly increased LS (− 18.6% vs − 21.9%,p = 0.07; − 18.6% vs − 21.9%,p = 0.024; − 17.5% vs − 20%,p = 0.032, respectively). The severity of LAD stenosis was positively correlated with the LS of the LAD territory (r = 0.438,p = 0.002).ConclusionCT-FT can detect decreasing LV systolic function in patients with LAD stenosis. LV regional systolic deformation of the LAD territory was reduced with increasing LAD stenosis severity.
Changes in inflammatory cytokines, antioxidants and liver stiffness after chelation therapy in individuals with chronic lead poisoning
Authors: Teerasarntipan Tongluk , Chaiteerakij Roongruedee , Prueksapanich Piyapan , Werawatganon Duangporn 
Published: August 2020

Abstract
Background
Chronic exposure to lead causes lead to accumulate mainly in the liver. In vivo studies have shown that lead toxicity is related to alterations in the inflammatory response. We aimed to evaluate the association between lead poisoning and liver fibrosis as well as the change in the degree of liver fibrosis, levels of inflammatory mediators and glutathione (GSH) after chelation therapy.

Methods
Workers from a battery factory who were exposed to lead for > 12 months and had a blood lead level (BLL) > 70 μg/dL were enrolled (n = 86) in the study. Participants underwent chelation therapy with intravenous CaNa2EDTA for 2 days followed by treatment with oral D-penicillamine for 90 days. The primary outcome was the change in the degree of liver fibrosis, which was presented as liver stiffness (LS) measured by FibroScan®. Secondary outcomes were the changes in the levels of serum GSH and inflammatory mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) after chelation therapy.

Results
Among the 86 participants, there was a positive correlation between the duration of lead exposure and LS (r = 0.249, p = 0.021). To avoid the confounding effect of obesity-related steatosis, only 70 individuals who had controlled attenuation parameters < 296 dB/m, BMI < 25 kg/m2 and normal waist circumference were included in the interventional analysis. After chelation, the mean LS significantly decreased from 5.4 ± 0.9 to 4.8 ± 1.4 kPa (p = 0.001). Similarly, all of the inflammatory cytokines studied significantly decreased after chelation (p < 0.001); TNF-α decreased from 371.6 ± 211.3 to 215.8 ± 142.7; the levels of IL-1β decreased from 29.8 ± 1.7 to 25.9 ± 4.3; and the levels of IL-6 decreased from 46.8 ± 10.2 to 35.0 ± 11.9. On the other hand, the mean GSH level increased significantly from 3.3 ± 3.3 to 13.1 ± 3.7 (p < 0.001) after chelation therapy.

Conclusion
The duration of lead exposure was significantly correlated with the degree of liver fibrosis. Chelation treatment was associated with increased levels of GSH and decreased levels of proinflammatory cytokines and could potentially reduce the degree of LS.

Trial registration
This study was retrospectively registered and approved by the Thai Clinical Trial Registry (TCTR) on 2019-11-07. The TCTR identification number is TCTR20191108001.
Preoperative anthropomorphic and nutritious status and fistula risk score for predicting clinically relevant postoperative pancreatic fistula after pancreaticoduodenectomy
Authors: Abe Tomoyuki , Amano Hironobu , Kobayashi Tsuyoshi , Hanada Keiji , Hattori Minoru , Nakahara Masahiro , Ohdan Hideki , Noriyuki Toshio 
Published: August 2020

Abstract
Background
Postoperative pancreatic fistula (POPF) is a life-threatening postoperative complication. The aim of this study was to evaluate the efficacy of the fistula risk score (FRS) and preoperative body composition factors for predicting the occurrence of clinically relevant POPF (CR-POPF) after pancreaticoduodenectomy (PD).

Methods
In this study, 136 consecutive patients who underwent PD between 2006 and 2018 were enrolled. The risk factors of CR-POPF (grades B and C) were analyzed. Preoperative visceral adipose tissue area (VATA), skeletal mass index (SMI), and subcutaneous adipose tissue area (SATA) were calculated from computed tomography data.

Results
The overall 30-day mortality and morbidity rates were 0.7 and 38%, respectively. The incidence rates of grade B and C CR-POPF were 27 and 4%, respectively. A univariate analysis revealed that male sex, habitual smoking, prognostic nutritional index (PNI) < 45, VATA ≥90, VATA/SATA ≥0.9, VATA/SMI ≥ 1.4, and FRS > 4 were significantly associated with the incidence of CR-POPF. A multivariate analysis revealed that PNI < 45, VATA/SMI ≥ 1.4 and FRS > 4 were the independent risk factors of CR-POPF.

Conclusions
Preoperative anthropomorphic imbalance, PNI, and FRS were independent risk factors for CR-POPF. Patients with high-risk factors should be closely monitored during the postoperative period.
Prevalence of genital Chlamydia trachomatis infection in the general population: a meta-analysis
Authors: Huai Pengcheng , Li Furong , Chu Tongsheng , Liu Dianchang , Liu Jian , Zhang Furen 
Published: August 2020

Abstract
Background
Estimating prevalence of Chlamydia trachomatis (CT) worldwide is necessary in designing control programs and allocating health resources. We performed a meta-analysis to calculate the prevalence of CT in the general population.

Methods
The Pubmed and Embase databases were searched for eligible population-based studies from its inception through June 5, 2019. Q test and I2 statistic were used to calculate the heterogeneity between studies. Random effects models were used to pool the prevalence of CT. Meta regression was performed to explore the possible sources of heterogeneity. Publication bias was evaluated using a funnel plot and “trim and fill” method.

Results
Twenty nine studies that reported prevalence of CT infection from 24 countries were identified, including a total population of 89,886 persons. The pooled prevalence of CT among the general population was 2.9% (95% CI, 2.4–3.5%), and females had a higher CT prevalence (3.1, 95% CI, 2.5–3.8%) than males (2.6, 95% CI, 2.0–3.2%) (χ2 = 10.38, P <  0.01). Prevalence of CT was highest in region of America (4.5, 95% CI, 3.1–5.9%), especially in Latin America (6.7, 95% CI, 5.0–8.4%), followed by females in region of Africa (3.8, 95% CI, 0.7–6.9%), while South-East Asia had a lowest CT prevalence 0.8% (95% CI, 0.3–1.3%).

Conclusions
This study provided the updated prevalence of CT among general population worldwide. General population from Latin America, especially females, and women in Africa should be given priority by WHO when design and delivery CT control programs.
The genome-wide supported CACNA1C gene polymorphisms and the risk of schizophrenia: an updated meta-analysis
Authors: Liu Yong-ping , Wu Xue , Xia Xi , Yao Jun , Wang Bao-jie 
Published: August 2020

AbstractBackgroundTheCACNA1Cgene was defined as a risk gene for schizophrenia in a large genome-wide association study of European ancestry performed by the Psychiatric Genomics Consortium. Previous meta-analyses focused on the association between theCACNA1Cgene rs1006737 and schizophrenia. The present study focused on whether there was an ancestral difference in the effect of theCACNA1Cgene rs1006737 on schizophrenia. rs2007044 and rs4765905 were analyzed for their effect on the risk of schizophrenia.MethodsPooled, subgroup, sensitivity, and publication bias analysis were conducted.ResultsA total of 18 studies met the inclusion criteria, including fourteen rs1006737 studies (15,213 cases, 19,412 controls), three rs2007044 studies (6007 cases, 6518 controls), and two rs4765905 studies (2435 cases, 2639 controls). An allele model study also related rs2007044 and rs4765905 to schizophrenia. The overall meta-analysis for rs1006737, which included the allele contrast, dominant, recessive, codominance, and complete overdominance models, showed significant differences between rs1006737 and schizophrenia. However, the ancestral-based subgroup analysis for rs1006737 found that the genotypes GG and GG + GA were only protective factors for schizophrenia in Europeans. In contrast, the rs1006737 GA genotype only reduced the risk of schizophrenia in Asians.ConclusionsRs1006737, rs2007044, and rs4765905 of theCACNA1Cgene were associated with susceptibility to schizophrenia. However, the influence model for rs1006737 on schizophrenia in Asians and Europeans demonstrated both similarities and differences between the two ancestors.
The burden of hyperkalemia in Germany – a real world evidence study assessing the treatment and costs of hyperkalemia
Authors: Haas Jennifer Scarlet , Krinke Kim-Sarah , Maas Christopher , Hardt Thomas , Barck Isabella , Braun Sebastian 
Published: August 2020

Abstract
Background
Hyperkalemia (HK) can affect health outcomes and quality of life, as it is referred to as a potentially life-threatening condition caused by an increased serum potassium concentration in the blood. Patients suffering from heart failure or chronic kidney diseases are at a higher risk of HK, which can further be amplified by the treatment received. To date, data on HK prevalence is lacking for Germany and the aims of this study were to assess HK and compare health-relevant outcomes and healthcare costs between HK patients and non-HK patients.

Methods
The InGef research database containing healthcare claims of over 4 million individuals in Germany was utilized for this retrospective, matched cohort analysis. Patients with non-acute outpatient treated and a subgroup of patients with chronic HK, were identified in 2015 with an individual 1 year pre- and post-index period, taking the first observable HK diagnosis/treatment in 2015 into account as the index event. To identify non-acute outpatient treated HK patients, at least two ICD-10-GM diagnosis codes E87.5 “Hyperkalemia” and/or prescriptions of polystyrene sulfonate were required. Chronic HK patients had additional diagnoses and/or prescriptions in all quarters following the first observable HK diagnosis. Patients without HK were matched 1:1 to the respective HK cohorts.

Results
In the year 2015, 3333 patients with non-acute outpatient treated HK were identified of which 1693 were patients with chronic HK. After matching, 3191 and 1664 HK patients and controls were available for analysis. A significantly higher number of hospitalizations was observed for both HK cohorts in comparison to their matched controls. Dialysis initiation as well as the healthcare costs were higher for both HK cohorts when compared to their matched counterparts.

Conclusions
The disease burden was higher for patients with HK, based on a higher proportion of patients with dialysis initiation and higher healthcare costs.