bluuebunny/crossref_metadata_2025_split huggingface dataset:
The impact of guidelines on sterility precautions during indwelling urethral catheterization at two acute-care hospitals in Sweden - a descriptive survey
Authors: Kulbay Aysel , Joelsson-Alm Eva , Tammelin Ann 
Published: June 2021

Abstract
Background
To support a uniform and evidence-based practice for indwelling urinary catheterization in adults The European association of Urology Nurses (EAUN) published guidelines for this procedure in 2012. The Swedish national guidelines are based on the sterility precautions advocated by EAUN. Some hospitals have local guidelines with other requirements concerning sterility and leave to staff to decide how to perform the catheterization. The aim of this descriptive survey was to investigate the nurses´ self-reported sterility precautions during indwelling urethral catheterization at two acute-care hospitals, where the local guidelines differ in their sterility requirements. The study also aimed to analyze factors affecting conformity with sterility precautions in the EAUN-guidelines.

Methods
A structured questionnaire with questions concerning the participant, working conditions and performance of indwelling urethral catheterization was left to 931 nurses in two acute care hospitals. Chi-square test, Fisher’s exact test and Mann-Whitney U-test were used for descriptive statistics. Logistic regression was used to analyze variables associated with practicing the sterility precautions in the EAUN-guidelines.

Results
Answers were obtained from 852 persons (91.5%). Most of the participants called their insertion technique “non-sterile”. Regardless of designation of the technique the participants said that the indwelling urinary catheter (IUC) should be kept sterile during procedure. Despite that not everyone used sterile equipment to maintain sterility of the catheter. The nurses´ conformity with all the sterility precautions in the EAUN-guidelines were associated with working at departments for surgery and cardiology (OR 2.35, 95% CI 1.69–3.27), use of sterile set for catheterization (OR 2.06, 95% CI 1.42–2.97), use of sterile drapes for dressing on insertion area (OR 1.91, 95% CI 1.24–2.96) and using the term “sterile technique” for indwelling urethral catheterization (OR 1.64, 95% CI 1.11–2.43).

Conclusions
Only 55–74% of the nurses practiced one or more precautions that secured sterility of the IUC thus demonstrating a gap between the EAUN-guidelines and the actual performance. Adherence to the guidelines was associated with factors that facilitated an aseptic performance such as using a sterile set and sterile drapes.
Healthcare-settings should ensure education and skill training including measures to ensure that the IUC is kept sterile during insertion.
Registered nurses’ role experiences of caring for older stroke patients: a qualitative study
Authors: Cheng Wei , Tu Jiong , Shen Xiaoyan 
Published: June 2021

Abstract
Background
With China’s population ageing rapidly, stroke is becoming one of the major public health problems. Nurses are indispensable for caring for older patients with acute and convalescent stroke, and their working experiences are directly linked to the quality of care provided. The study aims to investigate registered nurses’ experiences of caring for older stroke patients.

Methods
A qualitative descriptive design was adopted. Data were collected via semi-structured interviews with 26 registered nurses about their lived experiences of caring for older stroke patients. Thematic analysis was used to analyze the data.

Results
Two main themes were identified. First, the nurses identified an obvious gap between their ideal role in elderly care and their actual practice. The unsatisfactory reality was linked to the practical difficulties they encountered in their working environment. Second, the nurses expressed conflicting feelings about caring for older stroke patients, displaying a sense of accomplishment, indifference, annoyance, and sympathy. Caring for older stroke patients also affects nurses psychologically and physically. The nurses were clear about their own roles and tried their best to meet the elderly people’s needs, yet they lack time and knowledge about caring for older stroke patients. The factors influencing their working experiences extend beyond the personal domain and are linked to the wider working environment.

Conclusions
Sustaining the nursing workforce and improving their working experiences are essential to meet the care needs of older people. Understanding nurses’ lived working experiences is the first step. At the individual level, nurse mangers should promote empathy, relieve anxiety about aging, and improve the job satisfaction and morale of nurses. At the institutional level, policymakers should make efforts to improve the nursing clinical practice environment, increase the geriatric nursing education and training, achieve a proper skill mix of the health workforce, and overall attract, prepare and sustain nurses regarding caring for older people in a rapidly aging society.
Functional differentiation related to decomposing complex carbohydrates of intestinal microbes between two wild zokor species based on 16SrRNA sequences
Authors: Zou Yao , Liang Nannan , Zhang Xuxin , Han Chongxuan , Nan Xiaoning 
Published: June 2021

Abstract
Background
The intestinal microbes in mammals play a key role in host metabolism and adaptation. As a subterranean rodent, zokor digs tunnels for foraging and mating. These digging activities of zokors increase the energy expenditure relative to their aboveground counterparts. However, relatively little is known regarding intestinal microbes of zokor and how they make full use of limited food resources underground for high energy requirements.

Results
Eospalax cansus and Eospalax rothschildi had distinct intestinal microbes. Although the composition of intestinal microbes is similar in two species, the proportion of bacterium are distinctly different between them. At phylum level, 11 phyla were shared between two species. Firmicutes and Bacteroidota were two dominant microbes in both of two species, while Eospalax cansus have a significantly high proportion of Firmicutes/Bacteroidota than that of Eospalax rothschildi. At genus level, norank_f_Muribaculaceae were dominant microbes in both of two zokor species. The relative abundance of 12 genera were significantly different between two species. Some bacterium including unclassified_f__Lachnospiraceae, Lachnospiraceae_NK4A136_group, Ruminococcus and Eubacterium_siraeum_group associated with cellulose degradation were significantly enriched in Eospalax cansus. Although alpha diversity was with no significant differences between Eospalax cansus and Eospalax rothschildi, the intestinal microbes between them are significant distinct in PCoA analysis. We have found that trapping location affected the alpha diversity values, while sex and body measurements had no effect on alpha diversity values. PICRUSt metagenome predictions revealed significant enrichment of microbial genes involved in carbohydrate metabolism in Eospalax cansus rather than Eospalax rothschildi.

Conclusions
Our results demonstrate that Eospalax cansus harbor a stronger ability of fermentation for dietary plants than Eospalax rothschildi. The stronger ability of fermentation and degradation of cellulose of intestinal microbes of Eospalax cansus may be a long-time adaptation to limited food resources underground.
The emerging role of circular RNAs in common solid malignant tumors in children
Authors: Yu Jiabin , Yang Li , Lu Hongting 
Published: June 2021

AbstractMalignant tumors are one of the fatal diseases that threaten children’s physical and mental health and affect their development. Research has shown that the occurrence and development of malignant tumors are associated with the abnormal expression and regulation of genes. Circular RNAs (circRNAs) are noncoding RNAs that have a closed circular structure, with a relatively stable expression, and do not undergo exonuclease-mediated degradation readily. Recent studies have shown that circRNA plays an important role in the occurrence, metastasis, and invasion of solid malignant tumors (SMTs) in children. Thus, circRNA is being considered as a breakthrough in the treatment of SMTs in children. In this review, we describe the functions and mechanisms of circRNAs involved in SMTs in children oncogenesis, and summarize the roles of circRNAs in regulating cell proliferation, cell apoptotic death, the cell cycle, cell migrative and invasive ability, epithelial-mesenchymal transition (EMT), cancer stem cells and drug resistance in SMTs in children. In addition, we also discuss the role of circRNAs in the early diagnosis, pathological grading, targeted therapy, and prognosis evaluation of common SMTs in children. CircRNAs are likely to provide a novel direction in therapy in SMTs of children.
Type I IFN signaling limits hemorrhage-like disease after infection with Japanese encephalitis virus through modulating a prerequisite infection of CD11b+Ly-6C+ monocytes
Authors: Patil Ajit Mahadev , Choi Jin Young , Park Seong Ok , Uyangaa Erdenebelig , Kim Bumseok , Kim Koanhoi , Eo Seong Kug 
Published: June 2021

Abstract
Background
The crucial role of type I interferon (IFN-I, IFN-α/β) is well known to control central nervous system (CNS) neuroinflammation caused by neurotrophic flaviviruses such as Japanese encephalitis virus (JEV) and West Nile virus. However, an in-depth analysis of IFN-I signal-dependent cellular factors that govern CNS-restricted tropism in JEV infection in vivo remains to be elucidated.

Methods
Viral dissemination, tissue tropism, and cytokine production were examined in IFN-I signal-competent and -incompetent mice after JEV inoculation in tissues distal from the CNS such as the footpad. Bone marrow (BM) chimeric models were used for defining hematopoietic and tissue-resident cells in viral dissemination and tissue tropism.

Results
The paradoxical and interesting finding was that IFN-I signaling was essentially required for CNS neuroinflammation following JEV inoculation in distal footpad tissue. IFN-I signal-competent mice died after a prolonged neurological illness, but IFN-I signal-incompetent mice all succumbed without neurological signs. Rather, IFN-I signal-incompetent mice developed hemorrhage-like disease as evidenced by thrombocytopenia, functional injury of the liver and kidney, increased vascular leakage, and excessive cytokine production. This hemorrhage-like disease was closely associated with quick viral dissemination and impaired IFN-I innate responses before invasion of JEV into the CNS. Using bone marrow (BM) chimeric models, we found that intrinsic IFN-I signaling in tissue-resident cells in peripheral organs played a major role in inducing the hemorrhage-like disease because IFN-I signal-incompetent recipients of BM cells from IFN-I signal-competent mice showed enhanced viral dissemination, uncontrolled cytokine production, and increased vascular leakage. IFN-I signal-deficient hepatocytes and enterocytes were permissive to JEV replication with impaired induction of antiviral IFN-stimulated genes, and neuron cells derived from both IFN-I signal-competent and -incompetent mice were vulnerable to JEV replication. Finally, circulating CD11b+Ly-6C+ monocytes infiltrated into the distal tissues inoculated by JEV participated in quick viral dissemination to peripheral organs of IFN-I signal-incompetent mice at an early stage.

Conclusion
An IFN-I signal-dependent model is proposed to demonstrate how CD11b+Ly-6C+ monocytes are involved in restricting the tissue tropism of JEV to the CNS.
Cordycepin confers long-term neuroprotection via inhibiting neutrophil infiltration and neuroinflammation after traumatic brain injury
Authors: Wei Pengju , Wang Ke , Luo Chen , Huang Yichen , Misilimu Dilidaer , Wen Huimei , Jin Peng , Li Chuhua , Gong Ye , Gao Yanqin 
Published: June 2021

AbstractBackgroundThe secondary injury caused by traumatic brain injury (TBI), especially white matter injury (WMI), is highly sensitive to neuroinflammation, which further leads to unfavored long-term outcomes. Although the cross-talk between the three active events, immune cell infiltration, BBB breakdown, and proinflammatory microglial/macrophage polarization, plays a role in the vicious cycle, its mechanisms are not fully understood. It has been reported that cordycepin, an extract fromCordyceps militaris, can inhibit TBI-induced neuroinflammation although the long-term effects of cordycepin remain unknown. Here, we report our investigation of cordycepin’s long-term neuroprotective function and its underlying immunological mechanism.MethodsTBI mice model was established with a controlled cortical impact (CCI) method. Cordycepin was intraperitoneally administered twice daily for a week. Neurological outcomes were assessed by behavioral tests, including grid walking test, cylinder test, wire hang test, and rotarod test. Immunofluorescence staining, transmission electron microscopy, and electrophysiology recording were employed to assess histological and functional lesions. Quantitative-PCR and flow cytometry were used to detect neuroinflammation. The tracers of Sulfo-NHS-biotin and Evans blue were assessed for the blood-brain barrier (BBB) leakage. Western blot and gelatin zymography were used to analyze protein activity or expression. Neutrophil depletion in vivo was performed via using Ly6G antibody intraperitoneal injection.ResultsCordycepin administration ameliorated long-term neurological deficits and reduced neuronal tissue loss in TBI mice. Meanwhile, the long-term integrity of white matter was also preserved, which was revealed in multiple dimensions, such as morphology, histology, ultrastructure, and electrical conductivity. Cordycepin administration inhibited microglia/macrophage pro-inflammatory polarization and promoted anti-inflammatory polarization after TBI. BBB breach was attenuated by cordycepin administration at 3 days after TBI. Cordycepin suppressed the activities of MMP-2 and MMP-9 and the neutrophil infiltration at 3 days after TBI. Moreover, neutrophil depletion provided a cordycepin-like effect, and cordycepin administration united with neutrophil depletion did not show a benefit of superposition.ConclusionsThe long-term neuroprotective function of cordycepin via suppressing neutrophil infiltration after TBI, thereby preserving BBB integrity and changing microglia/macrophage polarization. These findings provide significant clinical potentials to improve the quality of life for TBI patients.
Anti-CD20 treatment effectively attenuates cortical pathology in a rat model of widespread cortical demyelination
Authors: Haindl Michaela T. , Üçal Muammer , Klaus Benjamin , Tögl Lennart , Dohrmann Jana , Adzemovic Milena Z. , Enzinger Christian , Hochmeister Sonja 
Published: June 2021

AbstractBackgroundCortical demyelination represents a prominent feature of the multiple sclerosis (MS) brain, especially in (late) progressive stages. We recently developed a new rat model that reassembles critical features of cortical pathology characteristic to progressive types of MS. In persons affected by MS, B-cell depleting anti-CD20 therapy proved successful in the relapsing remitting as well as the early progressive course of MS, with respect to reducing the relapse rate and number of newly formed lesions. However, if the development of cortical pathology can be prevented or at least slowed down is still not clear. The main goal of this study was thus to increase our understanding for the mode of action of B-cells and B-cell directed therapy on cortical lesions in our rat model.MethodsFor this purpose, we set up two separate experiments, with two different induction modes of B-cell depletion. Brain tissues were analyzed thoroughly using histology.ResultsWe observed a marked reduction of cortical demyelination, microglial activation, astrocytic reaction, and apoptotic cell loss in anti-CD20 antibody treated groups. At the same time, we noted increased neuronal preservation compared to control groups, indicating a favorable impact of anti-CD20 therapy.ConclusionThese findings might pave the way for further research on the mode of action of B-cells and therefore help to improve therapeutic options for progressive MS.
The LINC00922 aggravates ovarian cancer progression via sponging miR-361-3p
Authors: Wang Liping , Ren Chenchen , Xu Yajuan , Yang Li , Chen Yannan , Zhu Yuanhang 
Published: June 2021

Abstract
Background
Long noncoding RNA (lncRNA) LINC00922 has been reported to promote tumorigenesis of lung and breast cancer. However, the functions and mechanisms of LINC00922 in ovarian cancer (OC) remain unclarified. The current study aims to clarify the detailed functions and underlying mechanisms of LINC00922 in the progression of OC.

Methods
LINC00922 expression in OC tissues and cells was identified by a comprehensive strategy of data miming, computational biology and quantitative real-time polymerase chain reaction (RT-qPCR) experiment. In vitro CCK-8, wound healing, transwell invasion, western blotting and in vivo tumorigenesis assays LINC00922 were conducted to evaluate the functions of LINC00992. Subsequently, bioinformatics technology and dual luciferase reporter assay were performed to confirm the between miR-361-3p and LINC00922 or CLDN1. Finally, rescue experiments were performed to confirm whether LINC00922 effect functions of OC cells through regulation of miR-361-3p.

Results
LINC00922 was significantly upregulated in OC tissues and cell lines, which is significantly positively corelated with the poor prognosis of patients with OC. LINC00922 knockdown inhibited proliferation and tumorigenesis of OC cells in vitro and vivo. In addition, LINC00922 knockdown suppressed migration, invasion, and EMT of OC cells in vitro. Mechanically, LINC00922 could competitively bind with miR-361-3p to relieve the repressive effect of miR-361-3p on its target gene CLDN1 in OC cells. In addition, silencing miR-361-3p promoted OC cell proliferation, migration, invasion, EMT and Wnt/β-catenin signaling, while LINC00922 knockdown inhibited Wnt/β-catenin signaling by upregulating miR-361-3p. Rescue experiments revealed that LINC00922 knockdown inhibited OC cell proliferation, migration, invasion and EMT by regulating miR-361-3p.

Conclusion
This study suggested that LINC00922 could competitively bind with miR-361-3p to promote the CLDN1 expression and activate Wnt/β-catenin signaling in OC progression, which providing a promising therapeutically target for OC.
Photoactivation of TGFβ/SMAD signaling pathway ameliorates adult hippocampal neurogenesis in Alzheimer’s disease model
Authors: Wu Xiaolei , Shen Qi , Zhang Zhan , Zhang Di , Gu Ying , Xing Da 
Published: June 2021

AbstractBackgroundAdult hippocampal neurogenesis (AHN) is restricted under the pathological conditions of neurodegenerative diseases, especially in Alzheimer’s disease (AD). The drop of AHN reduces neural circuit plasticity, resulting in the decrease of the generation of newborn neurons in dentate gyrus (DG), which makes it difficult to recover from learning/memory dysfunction in AD, therefore, it is imperative to find a therapeutic strategy to promote neurogenesis and clarify its underlying mechanism involved.MethodsAmyloid precursor protein/presenilin 1 (APP/PS1) mice were treated with photobiomodulation therapy (PBMT) for 0.1 mW/mm2per day in the dark for 1 month (10 min for each day). The neural stem cells (NSCs) were isolated from hippocampus of APP/PS1 transgenic mice at E14, and the cells were treated with PBMT for 0.667 mW/mm2in the dark (5 min for each time).ResultsIn this study, photobiomodulation therapy (PBMT) is found to promote AHN in APP/PS1 mice. The latent transforming growth factor-β1 (LTGFβ1) was activated in vitro and in vivo during PBMT-induced AHN, which promoted the differentiation of hippocampal APP/PS1 NSCs into newborn neurons. In particular, behavioral experiments showed that PBMT enhanced the spatial learning/memory ability of APP/PS1 mice. Mechanistically, PBMT-stimulated reactive oxygen species (ROS) activates TGFβ/Smad signaling pathway to increase the interaction of the transcription factors Smad2/3 with Smad4 and competitively reduce the association of Smad1/5/9 with Smad4, thereby significantly upregulating the expression of doublecortin (Dcx)/neuronal class-III β-tubulin (Tuj1) and downregulating the expression of glial fibrillary acidic protein (GFAP). These in vitro effects were abrogated when eliminating ROS. Furthermore, specific inhibition of TGFβ receptor I (TGFβR I) attenuates the DNA-binding efficiency of Smad2/3 to the Dcx promotor triggered by PBMT.ConclusionOur study demonstrates that PBMT, as a viable therapeutic strategy, directs the adult hippocampal APP/PS1 NSCs differentiate towards neurons, which has great potential value for ameliorating the drop of AHN in Alzheimer’s disease mice.
Parkinson’s disease–associated VPS35 mutant reduces mitochondrial membrane potential and impairs PINK1/Parkin-mediated mitophagy
Authors: Ma Kai Yu , Fokkens Michiel R. , Reggiori Fulvio , Mari Muriel , Verbeek Dineke S. 
Published: June 2021

Abstract
Background
Mitochondrial dysfunction plays a prominent role in the pathogenesis of Parkinson’s disease (PD), and several genes linked to familial PD, including PINK1 (encoding PTEN-induced putative kinase 1 [PINK1]) and PARK2 (encoding the E3 ubiquitin ligase Parkin), are directly involved in processes such as mitophagy that maintain mitochondrial health. The dominant p.D620N variant of vacuolar protein sorting 35 ortholog (VPS35) gene is also associated with familial PD but has not been functionally connected to PINK1 and PARK2.

Methods
To better mimic and study the patient situation, we used CRISPR-Cas9 to generate heterozygous human SH-SY5Y cells carrying the PD-associated D620N variant of VPS35. These cells were treated with a protonophore carbonyl cyanide m-chlorophenylhydrazone (CCCP) to induce the PINK1/Parkin-mediated mitophagy, which was assessed using biochemical and microscopy approaches.

Results
Mitochondria in the VPS35-D620N cells exhibited reduced mitochondrial membrane potential and appeared to already be damaged at steady state. As a result, the mitochondria of these cells were desensitized to the CCCP-induced collapse in mitochondrial potential, as they displayed altered fragmentation and were unable to accumulate PINK1 at their surface upon this insult. Consequently, Parkin recruitment to the cell surface was inhibited and initiation of the PINK1/Parkin-dependent mitophagy was impaired.

Conclusion
Our findings extend the pool of evidence that the p.D620N mutation of VPS35 causes mitochondrial dysfunction and suggest a converging pathogenic mechanism among VPS35, PINK1 and Parkin in PD.