bluuebunny/crossref_metadata_2025_split huggingface dataset:
Commensal Lactobacillus Suppress Colon Tumorigenesis and Progression by Modulation of Sphingosine 1-Phosphate Signaling in Mice
Authors: Xu Fuqiang , Li Qiaoqiao , Wang Shuyang , Dong Miaoyin , Xiao Guoqing , Bai Jin , Wang Junkai , Sun Xisi 
Published: February 2022

Abstract
Background: Gut microbiota and their secreted metabolites influence the initiation, progression, and treatment responsiveness of colon cancer. Microbiota-based therapy regulated by probiotics has been considered as an effective strategy for prevention and therapeutic of colon cancer, whereas the antitumor mechanisms influenced by microbiota and their metabolites with intervention of probiotic remain further investigated.Results: Here, we investigated the preventive and therapeutic efficiency of commensal Lactobacillus in subcutaneous tumor models, and the underlying antitumor mechanism through the alteration of gut microbiota and their metabolites regulated by commensal Lactobacillus. Interestingly, we found that tumor formation rate in subcutaneous tumor models reduced 86.21% and 82.76%, in comparison to tumor controls when administrated with living or inactivated Lactobacillus (JY300-8 and JMR-01) for 20 days in advance. Subsequently, continuously oral administration for living or inactivated commensal Lactobacillus suppressed significantly the growth of tumor, and the tumor volumes declined 65.2% and 61.18%, respectively. Furthermore, microbiome and metabolome analyses revealed that commensal Lactobacillus suppressed colon tumorigenesis and progression through the modulation of gut microbiota and metabolites which included the down-regulation of secondary bile acids, sphingosine 1-phosphate (S1P) signaling in cancer and pyrimidine metabolism, as well as the production of anticarcinogenic compounds in tumor-bearing mice. Particularly, limitation the effects of S1P signaling via the modulation of sphingosine expression using probiotics, exerted antitumor efficiency.Conclusions: The work indicated the feasibility of using an effectively safe strategy to prevent the occurrence of colon cancer, and provided a potential therapeutic target for new therapeutics strategy via altering S1P signaling in cancer.
Association between the ELAVL1 gene single nucleotide polymorphisms and the Genetic Susceptibility to cervical cancer by high resolution melting in a Tunisian population
Authors: Boudhiba Najet , Sfar Sana , Helaoui Ahlem , Hołysz Marcin , Iwańczyk-Skalska Ewa , Bouchahda Haifa , Jagodziński Paweł piotr , KENANI Abderraouf 
Published: February 2022

Abstract
Background: Human papillomavirus infection is the major cause of cervical cancer, but only few cases develop into cancer. Although, HuR (ELAVL1) gene has been implicated in the oncogenesis of certain cancers. However, the correlation between the ELAVL1 gene and the risk of cervical cancer in Tunisian women remains unclear. Therefore, this study investigated the effect of ELAVL1 gene polymorphisms (SNPs) in cervical cancer development.Method: ELAVL1 gene SNPs: ELAVL1 rs12983784 T>C, ELAVL1 rs14394 T>C, ELAVL1 rs74369359 G>T, ELAVL1 rs35986520 G>A, ELAVL1 rs10402477 C>T, ELAVL1 rs12985234 A>G, ELAVL1 rs2042920 T>G, were genotyped by High resolution melting (HRM). SHEsis online software was used to perform linkage disequilibrium (LD) and haplotype analyses. Results: Comparing the cervical cancer patients with healthy control participants, the TC genotype of rs12983784 SNP (P=0.017, OR = 2.78, 95% CI = 1.2~6.45), the GT genotype of the rs74369359 SNP (P=0.004, OR = 9.4, 95% CI = 1.73~16.96) and the CT genotype of the rs10402477 SNP (P=0.002, OR = 5.89, 95% CI = 1.89~18.36) were associated with increased cervical cancer risk. TT genotype of rs12983784 SNP (P=0.005), GG genotype of the rs74369359 SNP (P=0.000) and CC genotype of the rs10402477 SNP (P=0.000) were considered as protective factors against cervical cancer in the Tunisian population. The haplotype analysis of the 7 SNPs of ELAVL1 gene suggested that “C C G G C A G” (P=0.02), “T T G G T A T” (P=0.01) and “T T T G C A T” (P=0.002) were a significant risk factor for cervical cancer. However, “TCGACAT” (P=0.04) and “TTGGCAT” (P=0.04) participated in the decrease of cervical cancer disease.The frequency of ELAVL1 haplotype rs10402477-rs2042920 TT was significantly higher in the cases group than in the control group (P=0.0001).Thus, this genotype increases cervical cancer risk among Tunisian women. Conclusion: The results of our study indicated that genetic variants in the ELAVL1 gene might be associated with susceptibility to cervical cancer in the Tunisian population.
PCSK9 Promotes Endothelial Dysfunction in Sepsis via TLR4/MyD88/NF-κB and NLRP3 Pathways
Authors: Huang Longxiang , Li Yuanjing , Cheng Zhe , Lv Zi , Luo Suxin , Xia Yong 
Published: February 2022

Abstract
Endothelial dysfunction often accompanies sepsis. We aimed to explore the role of PCSK9 in septic endothelial dysfunction. Sepsis was induced by Lipopolysaccharide (LPS) treatment on human umbilical vein endothelial cells (HUVECs) in vitro and Cecal ligation and puncture (CLP) surgery mice in vivo. Evolocumab (EVC) and Pep 2-8, PCSK9 inhibitors, was subsequently used to determine the role of PCSK9 in septic endothelial dysfunction in vitro and in vivo, respectively. And TLR4 agonist, Kdo2-Lipid A ammonium (KLA), was used to determine the related mechanism. Expression of eNOS, VE-Cadherin, PCSK9, TLR4, MYD88, p-p65, p65, NLRP3, ASC and Caspase1 p20 in the aortas and HUVECs were measured by Western blot and mRNA expression of TNFα, IL-1 and IL-6 were determined by PCR. Nitric oxide (NO) content in the medium and cell viability were examined. Vasodilation function of the aorta was detected by vascular reactivity experiments. The 48-h survival rate after CLP was observed. The results demonstrated that the expression of eNOS and VE-Cadherin decreased and PCSK9 expression increased in septic HUVECs or mice. Nevertheless, inhibition of PCSK9 could improve the eNOS and VE-Cadherin expression. The activation of TLR4/MyD88/NF-κB and NLRP3 pathways should be responsible for the PCSK9-induced endothelial dysfunction in sepsis. Vascular reactivity test and survival study shows that inhibiting PCSK9 could prevent the decline of endothelium-dependent vasodilation function and improve the survival rates of septic mice. In summary, our results suggest that increased PCSK9 in sepsis activates the TLR4/MyD88/NF-κB and NLRP3 pathways to induce inflammation, which results in vascular endothelial dysfunction and decrease of survival rates. However, inhibition of PCSK9 could improve the vascular endothelial function in sepsis, which may be a potential way for clinical treatment.
Effect and Mechanism of LncRNA-PBC11 in Regulating EMT Progression of Prostate Cancer Cells
Authors: Cui Haoyu , Xie Xuefeng , Hou Chuansheng , Ma Qiang , Chen Zhuo 
Published: February 2022

Abstract
The invasion and metastasis of prostate cancer is the main reason for its poor prognosis. Up to now, ADT (androgen deprivation therapy, ADT), whether surgical or drug therapy, is the basic method for the treatment of prostate cancer. However, ADT therapy is generally not recommended for the clinical treatment of metastatic prostate cancer. EMT (epithelial-to-mesenchymal transition, EMT) of tumor cells is the internal driving factor of tumor invasion and metastasis. Therefore, in-depth study on the regulation mechanism of EMT in prostate cancer cells will help us develop the new prevention and treatment plan for prostate cancer. Here, we will demonstrate and elaborate an lncRNA-PBC11 closely related to EMT of prostate cancer cells. The research data show that the content of PBC11 in metastatic prostate tumors increases significantly compared to non-metastatic, and can competitively bind hsa-miR-137 with 3'UTR of Twist1 in the form of miRNA sponge, thereby weakening the antitumor activity of hsa-miR-137. Our functional experiments confirmed that PBC11 knockdown is an important means for the normal operation of EMT inhibitory pathway hsa-miR-137/Twist1 in prostate cancer cells, and PBC11 knockdown combined with hsa-miR-137 overexpression showed excellent resistance to EMT in prostate cancer cells induced by TGF-β1. In a word, our study shows that PBC11 up-regulates the expression of Twist1 protein by blocking hsa-miR-137/ Twist1 pathway and promotes the progress of EMT in prostate cancer cells, overexpression of PBC11 can effectively inhibit EMT in prostate cancer cells by restoring the negative regulation of Twist1 by hsa-miR-137.
Novel gene loci associated with susceptibility or cryptic quantitative resistance to Pyrenopeziza brassicae in Brassica napus
Authors: Fell Heather , Ali Ajisa Muthayil , Wells Rachel , Mitrousia Georgia K. , Woolfenden Hugh , Schoonbeek Henk-jan , Fitt Bruce D. L. , Ridout Christopher J. , Stotz Henrik 
Published: February 2022

Abstract
Quantitative disease resistance (QDR) can provide durable control of pathogens in crops in contrast to resistance (R) gene-mediated resistance which can break down due to pathogen evolution. QDR is therefore a desirable trait in crop improvement but little is known about the causative genes and so it is difficult to incorporate into breeding programmes. Light leaf spot, caused by Pyrenopeziza brassicae, is an important disease of oilseed rape (canola, Brassica napus). To identify new QDR gene loci, we used a high-throughput screening pathosystem with P. brassicae on 196 lines of B. napus combined with an association transcriptomics platform. We show that all resistance against P. brassicae was associated with QDR and not R gene-mediated. We used genome-wide association analysis with an improved B. napus population structure to reveal four gene loci significantly (P = 0.0001) associated with QDR in regions showing linkage disequilibrium. On chromosome A09, enhanced resistance was associated with heterozygosity for a cytochrome P450 gene co-localising with a previously-described locus for seed glucosinolate content. In addition, eight significant gene expression markers with a false discovery rate of 0.001 were associated with QDR against P. brassicae. For seven of these, expression was positively correlated with resistance whereas for one, a HXXXD-type acyl-transferase, negative correlation indicated a potential susceptibility gene. The study identifies novel QDR loci for susceptibility and resistance, including novel cryptic QDR genes associated with heterozygosity, that will inform future crop improvement.
Research advances in the diagnosis and treatment of Chiari malformations: a bibliometric analysis
Authors: Rangel India , Singh Rohin , McLelland Marissa D. , Dodd Armaan , Shlobin Nathan A. , Meyer Jenna H. , Hudson Miles , Gottfried Oren 
Published: February 2022

Abstract
Chiari malformation is a relatively rare condition involving herniation of the brain out of the skull and into the spinal canal. The purpose of this review was to identify top contributors to the world of Chiari research, as well as to highlight the publications which have shaped our perception of this condition.We performed a search of the Web of Science between the years 1900 and 2021 using the terms “Chiari I malformation”, “Arnold Chiari malformation”, “Chiari II malformation”, “Chiari malformation type 1”, and “Chiari malformation type 2”. After screening for duplicates and assessing for relevance using two independent reviewers, the top 100 most frequently cited articles were collected and sorted. These articles were published between the years 1938 and 2015 and were cited 145.7 times on average, ranging from 79 to 724 citations per article. Authored by Milhorat et al., the 1999 Neurosurgery article “Chiari I Malformation Redefined: Clinical and Radiographic Findings for 364 Symptomatic Patients” received most citations (724 citations). Journal of Neurosurgery contributed the most articles to the top-100 with 21 publications. The University of California system accounted for the most articles by institution (8 of 100) and the USA was the highest contributing country (62%). In this study, we identified and analyzed the most cited articles on Chiari malformations to gain a better understanding of the publications contributing our knowledge of this disorder. This analysis serves both as a way of gauging the current state of research and of recognizing gaps where further research is necessary.
Infective Endocarditis With Oral Bacteria: Association With Findings During Oral Infection Screening
Authors: Thoresen Therese , Jordal Stina , Lie Stein-Atle , Wünsche Friederike , Jacobsen Martha Rolland , Lund Bodil 
Published: February 2022

Abstract
Background: Oral streptococci represent the causing microorganism for infective endocarditis (IE) in many patients. The impact of oral infections is questioned, and it has been suggested that bacteraemia due to daily routines may play a bigger part in the aetiology of IE. The aim of this study was to examine the association between oral health and infective endocarditis caused by oral viridans streptococci. Methods: A retrospective study was conducted at Haukeland University Hospital (HUH) from 2006- 2015. All consecutive adult patients admitted to hospital for treatment of IE and subjected to an oral focus screening including orthopantomogram, were included. The clinical, radiological and laboratory characteristics of the patients, collected during oral infectious focus screening, were analysed. Patient survival was calculated using Kaplan-Meier and mortality rates were compared using Cox-regression. Results: A total of 208 patients were included, 77% (n=161) male patients and 23% (n=47) female, mean age was 58 years. A total of 67 (32%) had IE caused by viridans streptococci. No statistically significant correlation could be found between signs of oral infection and IE caused by viridans streptococci. The overall mortality at 30 days was 4.3 % (95% CI: 1.6-7.0). There was no statistical difference in mortality between IE caused by viridans streptococci or S. aureus (HRR=1.16, 95% CI: 0.57-2.37, p=0.680). Conclusion: The benefit of oral infection screening and elimination in patients admitted with IE seems uncertain. Based on this study it cannot be concluded that oral conditions and oral infection influence the overall mortality for patients with endocarditis.
LncRNA MIR181A2HG Negatively Regulates Human Keratinocytes Proliferation by Binding SRSF1
Authors: Fan Xiaomei , Yue Pengpeng , Li Mingzhao , Chen Fangru , Fang Jingxian , Deng Xueling , Liu Xiaoyu , Wei Zhida , Gan Shaoqin , Weng Chengke , Gao Jintao 
Published: February 2022

Abstract
Psoriasis is a common chronic inflammatory skin disease. Abnormal proliferation of keratinocytes plays an important role in the pathogenesis of psoriasis. Long non-coding RNAs (lncRNAs) are involved in the regulation of a variety of cell biological processes. The purpose of this study was to investigate the potential role of lncRNA MIR181A2HG in the proliferation of human keratinocytes. qRT-PCR was performed to measure the expression levels of MIR181A2HG, SRSF1, miR-181a, miR-181b, KRT6 and KRT6 in tissue specimens and cells. Cell Counting Kit-8 (CCK-8) was used to measure cell viability. RNA pulldown-mass spectrometry (MS) was applied to identify the proteins interacting with MIR181A2HG. RNA pulldown-Western blotting and RNA immunoprecipitation (RIP)-qRT-PCR were used to confirm the interaction between MIR181A2HG and SRSF1. In this study, we found MIR181A2HG was decreased in psoriatic lesions. Knockdown of MIR181A2HG promoted the proliferation of human keratinocytes, while overexpression of MIR181A2HG inhibited the proliferation of human keratinocytes. 356 proteins were identified to interact with MIR181A2HG potentially. SRSF1 was finally determined to interact with MIR181A2HG. In addition, silencing of SRSF1 inhibited keratinocytes proliferation, which could be reversed with knockdown of MIR181A2HG. In summary, MIR181A2HG negatively regulates keratinocytes proliferation by binding SRSF1, suggesting that MIR181A2HG and SRSF1 may serve as potential targets for the treatment of psoriasis.
Benefit of Adjuvant Radiotherapy for Gallbladder Cancer: A Comparability-Based Metaanalysis
Authors: Choi Seo Hee , RIM CHAI HONG , Shin In-Soo , Yoon Won Sup , Koom Woong Sub , Seong Jinsil 
Published: February 2022

Abstract
Background & purpose: The benefits of adjuvant radiotherapy (ART) in gallbladder cancer (GBC) treatment remain inconclusive owing to the rarity of GBC and lack of randomized studies.Methods: PubMed, Medline, Embase, and Cochrane Library were systematically searched until March 2021. The primary endpoint was overall survival (OS). Comparative clinical studies that reported survival outcomes in GBC patients treated with or without ART were included. The comparability of each study was assessed by considering all possible clinical indicators (group 2: ART arm with poor clinical profile; group 1: ART arm with statistically similar profile or no evidence of having inferior clinical factors compared to non-ART arm).Results: Twenty-one studies involving 6876 GBC patients were reviewed. In pooled analyses of OS, the odds ratio (OR) was 1.26 ( p =0.111). In subgroup analyses considering comparability, the OR significantly favored the ART arm (1.92, p =0.008) among comparability group 1 studies, whereas it was 1.03 ( p =0.865) in comparability group 2 studies. The pooled rate of 5-yr OS in the ART vs. non-ART arms was 44.9% vs. 20.9% in group 1 and 34.1% vs. 40.0% in group 2. With ART, significant reduction in locoregional recurrence (OR: 0.21, p =0.001) but not in distant metastasis (OR: 1.32, p =0.332) was noted.Conclusion: ART not only showed benefits in patients with a similar clinical profile to those treated without ART but also yielded comparable survival in patients with an inferior clinical profile. Our results strongly support the more active application of ART in GBC treatment.Protocol registration: This study is registered in PROSPERO (CRD4202124062, available at: https://www.crd.york.ac.uk/).
Post Treatment Mastalgia is a Common Complaint But Not an Indication of Recurrence
Authors: Komenaka Ian , Hsu Chiu-Hsieh , Ramos Gilbert , Nodora Jesse , Martinez Maria Elena 
Published: February 2022

Abstract
Purpose: Post-treatment mastalgia is a common complaint in up to 68% of patients after treatment. This symptom is worrisome to patients as many believe it is a sign of recurrence. The current study was performed to evaluate if post-treatment mastalgia is associated with breast cancer recurrence.Methods: Patients included were seen from January 1, 2000 to December 31, 2020. All patients who were treated for breast cancer and then presented with breast pain during follow up were considered to have post-treatment mastalgia. All patients who were diagnosed with a second breast cancer but did not experience post-treatment mastalagia were also evaluated.Results: 1799 patients had a mean age 52.9 years. 36% of patients experienced post-treatment mastalgia. Of patients who complained of post-treatment mastalgia, 19 were diagnosed with a chest wall recurrence (CW), ipsilateral breast tumor recurrence (IBTR), or contralateral breast cancer (CBC). 17 of the 19 patients had breast pain after the second diagnosis and treatment were completed. The average duration between their second diagnosis and initial complaint of breast pain was 6.2 years. The two patients who complained of breast pain prior to their second diagnosis did not have mastalgia at the time of their second diagnosis. Local recurrence or contralateral breast cancer were more common in patients without post treatment mastalgia (10.1% vs 0.3%, p < 0.0001) during follow up.Conclusions: Post treatment mastalgia is not associated with recurrence. Interval or repeat imaging does not appear necessary and instead patient education and reassurance are important in its management.
Circumscription and typification of sphagnicolous omphalinoid species of Arrhenia (Hygrophoraceae) in Newfoundland and Labrador: three obligate and one facultative species
Authors: Voitk Andrus , Saar Irja , Moncada Bibiana , Lickey Edgar B. 
Published: February 2022

Abstract
Molecular studies of sphagnicolous arrhenias in Newfoundland and Labrador created four clades in Arrhenia, three obligate sphagnophiles (two scaly-capped and one smooth-capped) and one facultative (smooth-capped). Nomenclatural review recovered 16 names applied to omphalinoid sphagnicolous taxa in the past. Critical review of these left five as suitable to this group. One scaly obligate sphagnophilic clade contained the type for Arr. gerardiana and the other the type for Clitocybe gerardiana var. fusca; the latter we introduce as the novel species Arr. bigelowii. It differed from the first by longer spores and a darkening reaction in 10% of collections. The smooth-capped third obligate sphagnophilic clade contained the types of Ag. telmatiaeus and Omphalina fusconigra; we recombined it as Arr. telmatiaea. This is the darkest species of the group, with a more northern distribution. The facultative sphagnophile was identified as Arr. philonotis, a lighter smooth-capped species also with a more northern distribution. In addition, we collected an unidentified smooth-capped facultatively sphagnophilic species of Omphalina of the O. pyxidata complex. All five species are distributed in both Europe and North America. We describe each species of Arrhenia with a sequenced type, providing new type material where needed, and add an informal description of the Omphalina. Overall, this study adds new sequences from 82 specimens of sphagnicolous arrhenias to the two existing in GenBank when we began, 11 new sequences of the unidentified species of Omphalina, and several other arrhenias.
Genetic Diversity and Relationships Among Nopalea sp. and Opuntia spp. Accessions Revealed by RAPD, ISSR and ITS Molecular Markers
Authors: Bezerra Janieire Dorlamis Cordeiro , de Andrade Alberício Pereira , Rêgo Mailson Monteiro do , Silva Divan Soares da , Júnior José Ribamar Silva do Nascimento , Araújo Fernando dos Santos , Valença Roberta de Lima , Rêgo Elizanilda Ramalho do , Pessoa Angela Maria dos Santos , Bruno Riselane de Lucena Alcântara , de Medeiros Ariosvaldo Nunes 
Published: February 2022

Abstract
Background
Dactylopius opuntiae (Cockerell) (carmine cochineal) is an insect pest highly noxious that has spread through cactus pear crops in the Brazilian semiarid region. Knowledge of diversity and genetic relationships of the cactus pear accessions is fundamental to create new varieties resistance to carmine cochineal. Therefore, this investigation was undertaken to assess the genetic diversity and genetic relationships that existed in between cactus pear (Nopalea sp. and Opuntia spp.) accessions with contrasting resistance to D. opuntiae.
Methods
We conducted a molecular analysis in seven cactus pear accessions from the “reference collection” of the Agronomic Institute of Pernambuco, Brazil using RAPD, ISSR and ITS molecular markers.
Results
A total of 242 bands were detected from 26 polymorphic primers. The high percentage of polymorphism by RAPD (89.8%), ISSR (81.2%) and ITS (75%) markers suggests that the cactus pear accessions have high genetic diversity. The combined analysis of markers enabled the accessions discrimination of about the genus and ploidy, but were incongruous in relation to resistance level to D. opuntiae.
Conclusions
The resistant accessions (IPA-200016, IPA-200149, IPA-100004, IPA-200205) are genetically divergent, therefore could be potentially incorporated into any further breeding programs directed to create new varieties of cactus pear resistant to D. opuntiae.