bluuebunny/crossref_metadata_2025_split huggingface dataset:
An exploration of South African university students’ experience with pre-exposure prophylaxis for HIV: A qualitative study
Authors: Haffejee Firoza , Chetty Lynette , Ghuman Shanaz 
Published: June 2022

Abstract
Background
South Africa is the epicentre of the HIV pandemic, with young women particularly at risk of infection. Pre-exposure prophylaxis (PrEP) is an anti-retroviral drug taken once daily to reduce the risk of HIV infection in HIV-negative people. Oral PrEP was offered in South Africa in 2015, as an additional prevention choice for persons at substantial risk of HIV infection. It was subsequently integrated into an existing HIV prevention programme at a university campus health clinic in 2019. Currently, the experiences of students on PrEP are unknown. This qualitative study investigated reasons for PrEP uptake, compliance, and student perceptions about taking the prophylaxis.
Methods
Students (n = 12), who had previously commenced PrEP, at a university in Kwa-Zulu Natal, South Africa were recruited using purposive sampling. A semi-structured interview guide was used to collect qualitative data. All interviews were audio-recorded, subsequently transcribed and thematically analysed using Tsech’s eight steps.
Results
All participants commenced PrEP in 2019. The following four themes emerged from the study: (1) Sexual risk behavior, (2) reasons for using PrEP, (3) PrEP compliance and (4) the effect of COVID-19 on PrEP use. Five participants indicated that they had multiple concurrent sexual partners whilst all 12 indicated that their partners most likely had sexual relationships with others. Condom use was not regular both before and after commencing PrEP. All the participants thus used PrEP to protect themselves from HIV infection as they realised that they were at a high risk of infection due to their sexual behaviour. In the first year of taking PrEP eight participants were compliant. Those that defaulted, missed the treatment intermittently, when travelling over weekends or rushing to university some mornings. All participants experienced challenges with PrEP compliance after the COVID-19 pandemic, which resulted in closure of the campus health clinic, and difficulties in obtaining the regimen from other clinics.
Conclusions
The high level of risk perception for HIV was a driving factor in commencing PrEP. Difficulties in adherence, particularly due to COVID-19 restrictions were evident.
Chemo- versus immuno-precipitation of G-quadruplex-DNA (G4DNA): a direct comparison of the efficiency of the antibody BG4 versus the small-molecule ligands TASQs for G4 affinity capture
Authors: Feng Yilong , Luo Zhenyu , Sperti Francesco Rota , Valverde Ibai E. , Zhang Wenli , Monchaud David 
Published: June 2022

Abstract
The search for genomic G-quadruplex (G4) motifs is motivated by their involvement in key cellular processes ( e.g ., transcription, replication) and corresponding dysregulations underlying genetic diseases. Sequencing-based methods have been developed to assess G4 DNA formation genome-wide, including G4-seq that detects G4s in purified DNA (so called in vitro ) from human lymphocytes using the G4 stabilizer PDS, and G4 ChIP-seq that detects G4s in the chromatin of human keratinocytes (so called in vivo ) using the G4-specific antibody BG4. We recently reported on the use of a small molecule, BioTASQ, as a proxy for BG4 for assessing the transcriptomic prevalence of G4-RNA in vivo using G4RP-seq. Here, we provide the first direct and unbiased comparison of the G4 capturing ability of small molecules BioTASQ and its new derivative BioCyTASQ versus the antibody BG4, developing G4DP-seq which makes the genome-wide detection of G4s in vitro and in vivo more straightforward, reproducible and reliable.
Autophagic plasmid expressing SIRT3 and SIRT4 to improve Alzheimer’s disease
Authors: Li Shiyu , Deng Jianshan , Mo Xuemei , Sun Hanxu , Wang Jiajia , Dai Zhenning , Chen Youyu , Zheng Weihan , Li Ziyue , Zhong Zhiying , Geng Chengxu , Jiang Zhenyou , Huang Wenhua , Sun Hanxiao 
Published: June 2022

Abstract
Background: Improving mitochondria dysfunction using gene therapy effectively treats Alzheimer’s disease (AD). Meanwhile, the molecular chaperone-mediated autophagy (CMA) mechanism in mammalian cells helps achieve effective and safe gene therapy. Methods: We introduced an internal ribosome entry site (IRES) into a plasmid vector co-expressing Sirtuin (SIRT)3 and SIRT4. This plasmid was then combined with a nucleic acid autophagic peptide (NAP) that activates and expresses CMA under the tetracycline-on (Tet-on) regulation system to construct a two-gene autophagic plasmid pSIRT3/4-NAP. The plasmid was then transfected into 293T cells, and its effect on autophagy mechanisms and dysfunctional mitochondria were assessed. Additionally, the plasmids were encapsulated into nanoparticles with transferrin-coupled cationic liposomes and injected into AD mouse models for behavioral tests and mitochondrial function detection in brain cells.Results: NAP expression is induced by doxycycline (DOX). Thereafter NAP activates the CMA mechanism to remove plasmid DNA in 293T cells. Meanwhile, SIRT3 and SIRT4 are simultaneously expressed in mitochondrial dysfunction cells induced by high glucose concentration, and significantly improve mitochondrial structure and function. Moreover, the liposome-plasmid effectively targets the brain tissue of AD mice, significantly improving mitochondrial dysfunction in the cerebral cortex and hippocampus, and restoring the learning and memory functions. Importantly, following induction by DOX, the intracellular autophagic pathway activates and clears the plasmid.Conclusions: The two-gene autophagic plasmid realizes safe and controllable expression of target genes by activating the intracellular CMA mechanism, thus, providing an effective strategy for controllable gene therapy in AD.
ADAR1p110 promotes Enterovirus D68 replication through its deaminase domain and inhibition of PKR pathway
Authors: Zhang Kehan , Wang Siyuan , Chen Tingting , Tu Zeng , Huang Xia , Fan Xinyue , Liu Jia , Tian Yunbo , Lu Nan , Zhang Guangyuan 
Published: June 2022

Abstract
Background
Severe respiratory and neurological diseases caused byEV-D68 pose a serious threat to public health, but there are currently no effective drugs and vaccines. ADAR1 has been reported to have diverse biological functions in various viral infections, but its role in EV-D68 infection remains undetermined.
Methods
RD cells, 293T cells and Hela cells were used to evaluate the expression level of ADAR1 upon EV-D68 (Ferm strain) and HPIV3 (NIH47885) infection, respectively. The knockdown through siRNA and overexpression of either ADAR1p110 or ADAR1p150 in cell lines above were utilized to determine the role of the two proteins after viral infection. ADAR1p110 dsRBDs deleted mutation was generated by seamless clone kit. The expression patterns of ADAR1, EV-D68 VP1 protein and HPIV3 HN protein were identified by western blotting. TCID50 was applied to detect viral titers. The transcription level of EV-D68 mRNA was analyzed by RT-qPCR and viral 5’UTR-mediated translation was analyzed by dual luciferase reporter gene.
Conclusion
Here, we found that the transcription and expression of ADAR1 was inhibited upon EV-D68 infection. RNA interference of endogenous ADAR1 decreased VP1 protein expression and viral titers, while overexpression of ADAR1p110 but not ADAR1p150 facilitated virus replication. Immunofluorescence assays showed that ADAR1p110 migrated from the nucleus to the cytoplasm after EV-D68 infection. Further, ADAR1p110 lost the pro-viral ability after mutating the key sites in the deaminase domain, and 5’-UTR sequencing of the viral genome revealed that ADAR1p110 probably plays a role in EV-D68 RNA editing. In addition, after knockdown of ADAR1, both p-PKR and p-eIF2α increased. Attenuated translation activity of viral genome 5’-UTR was also shown in dual-luciferase reporter gene assay. At last, deletion of ADAR1p110 dsRBDs increased PKR phosphorylation, which incurs a lower level of VP1 expression, indicating that the promotion of EV-D68 replication by ADAR1p110 is also related to the inhibition of PKR activation by its double stranded RNA binding domains (dsRBDs). Together, our work illustrates ADAR1p110 as a novel pro-viral factor of EV-D68 replication and provides a theoretical basis for EV-D68 antiviral research.
Validation of grip strength as a measure of frailty in rheumatoid arthritis
Authors: Sobue Yasumori , Suzuki Mochihito , Ohashi Yoshifumi , Koshima Hiroshi , Okui Nobuyuki , Funahashi Koji , Ishikawa Hisato , Inoue Hidenori , Kojima Masayo , Asai Shuji , Terabe Kenya , Kishimoto Kenji , Maeda Masataka , Kihira Daisuke , Imagama Shiro , Kojima Toshihisa 
Published: June 2022

Abstract
Rheumatoid arthritis (RA) patients often exhibit finger/wrist joint symptoms and reduced grip strength. This study aimed to validate grip strength as a measure of frailty in RA patients. Subjects were 424 female RA patients (mean age±standard deviation, 66.8±14.5 years). Frailty was defined as a score of ≥8 points on the Kihon Checklist (KCL). Finger/wrist joint symptoms were defined based on tender or swollen joints. Associations between frailty and grip strength were determined using receiver operating characteristic (ROC) curve analysis and multivariable logistic regression analysis. There were 179 subjects with frailty (42.2%). Multivariable logistic regression analysis revealed that frailty was significantly associated with grip strength independently of finger/wrist joint symptoms. In ROC curves, cut-off scores of grip strength for frailty in subjects without and with finger/wrist joint symptoms were 17 kg (sensitivity, 62.1%; specificity, 69.0%) and 14 kg (sensitivity, 63.2%; specificity, 73.0%), respectively. The results of the present study suggest that grip strength in female RA patients is associated with frailty, with a cut-off score of 17 kg (equivalent to Cardiovascular Health Study criteria, <18 kg) when RA patients have no finger/wrist joint symptoms. However, when RA patients have finger/wrist joint symptoms, measures other than grip strength such as lower limb function should be considered.
Backward propagating quantum repeater protocol with multiple quantum memories
Authors: Sekiguchi Yuhei , Okumura Satsuki , Kosaka Hideo 
Published: June 2022

Abstract
Quantum repeaters with multiple quantum memories provide high throughput, low latency, and high fidelity quantum state (qubit) transfer over long distances. However, conventional quantum repeater protocols require full connections among the multiple quantum memories in a repeater node, which is technically challenging. Here, we propose a quantum repeater protocol based on backward propagating photon emission and absorption, where the quantum memories are multiplexed in the time-domain to speed up a single transmission channel without requiring full connectivity, thereby drastically facilitating physical implementation. Although the protocol is described with nitrogen-vacancy (NV) centers in diamond, it is applicable to various physical systems and opens up the possibility of high-speed high-fidelity quantum networks for distributed quantum computation and the quantum Internet.
Short-term Effects of Solar Storms in Phytoplankton Photosynthesis
Authors: López-Águila Madeleine , Rodríguez-López Lien , Cardenas Rolando , González-Rodríguez Lisdelys 
Published: June 2022

Abstract
It is investigated the potential short-term influence of a solar storm on micro-algal photosynthesis. From the secondary cosmic rays at sea level we focus on muons, given their high penetrating power, and it is considered that a ‘’generic’’ solar storm would imply an increase of 10% in both muon fluxes and their average energy. It is then assumed an exponential decay of muon fluxes down the water column and a direct proportionality between their penetrating power and energy. This allows obtaining a function of ionizing radiation to be embedded in a physical-mathematical model for photosynthesis previously modified by some of us to include particulate ionizing radiation. It is finally shown that solar storms can cause a significant short-term depletion of photosynthesis in both ocean and coastal waters.
Evolution of p53 pathway-related genes provides insights into anticancer mechanisms of natural longevity in cetaceans
Authors: Liu Xing , Yu Zhenpeng , Yang Fei , Huang Xin , Sun Linxia , Ren Wenhua , Yang Guang , Xu Shixia 
Published: June 2022

Abstract
Background: Large, long-lived organisms typically have a higher risk of cancer, but cetaceans, which include the largest and longest-living mammals, may have evolved a mechanism to counter this. However, little is known about the genetic basis underlying this mechanism. Cetaceans, which include the largest and longest-lived mammals, may have evolved effective anticancer mechanisms in response to a high risk of cancer caused by massive somatic cell divisions.Results: The p53 pathway is ideal for studying the mechanisms behind cancer resistance, as nearly all types of cancer have evolved ways to evade this suppressive mechanism. Here, comparative genetic analyses of the 73 genes involved in the p53 pathway were examined in cetaceans to explore potential anticancer mechanisms behind natural longevity. We found that long-lived species have three positively selected genes (APAF1, CASP8, TP73) and three duplicated genes (IGFBP3, PERP, CASP3) involved in the regulation of apoptosis, suggesting that apoptosis regulation may be an important strategy for cancer resistance in these long-lived cetaceans. Inhibition of angiogenesis may be another strategy for protecting cetaceans from cancer because the evolutionary rates of three angiogenesis-regulated genes (SERPINE1, CD82 and TSC2) were significantly related to longevity traits (longevity quotient and maximum lifespan). Interestingly, some tumor suppressor genes were determined to be under positive selection (APAF1 and TP73), have high copy numbers (CASP3 and CCNG1), and be related to body size in the large-bodied and long-lived cetacean lineages. The above is all molecular evidence for Peto's paradox. Conclusions: Our study identified several candidate genes for the p53 pathway with different evolutionary paths in the large, long-lived cetaceans and suggested that tumor suppression in cetaceans might be mediated through multiple synergistic effects rather than a single pathway/target.
Ninja Omicron: BA.1 subvariant showing a BA.2-like pattern using a variant-specific PCR assay due to a single point mutation downstream the spike 69/70 deletion.
Authors: Daviña-Nuñez Carlos , Pérez-Castro Sonia , Martínez-Lamas Lucía , Cabrera-Alvargonzalez Jorge Julio , Rey-Cao Sonia , Carballo-Fernández Raquel , Godoy-Diz Montse , López-Bóveda Leticia , Campo-Pérez Víctor del , Suárez-Luque Silvia , Regueiro-García Benito 
Published: June 2022

Abstract
Background: SARS-CoV-2 variant tracking is key to the genomic surveillance of the pandemic. While next-generation sequencing (NGS) is commonly used for variant determination, it is expensive and time-consuming. Variant-specific PCR (vsPCR) is a faster, cheaper method that detects specific mutations that are considered variant-defining. These tests usually rely on specific amplification when a mutation is present or a specific melting temperature peak after amplification.Case presentation: A discrepant result between vsPCR and NGS was found in seventeen SARS-CoV-2 samples from Galicia, Spain. A cluster of BA.1 Omicron SARS-CoV-2 variant showed a BA.2-like melting temperature pattern due to a point mutation (C21772T) downstream the deletion of the spike aminoacids 69/70. As the 69/70 deletion is widely used for differentiation between BA.1 and BA.2 by vsPCR, C21772T can cause BA.1 samples to be misinterpreted as BA.2. Over a thousand BA.1 sequences in the EpiCoV database contain this mutation. Conclusions: To our knowledge, this is the first case of a point mutation causing a vsPCR algorithm to misclassify BA.1 samples as BA.2. This is an example of how mutations in the targets of vsPCR tests based on melting curve analysis can lead to variant misclassification. NGS confirmation of vsPCR results is relevant for the accuracy of the epidemiological surveillance. In order to overcome the possible impact of novel mutations, diagnostic tools must be constantly updated.
Resistin as a risk factor for mortality in the general population
Authors: Pérez María Cristo Rodríguez , González Delia Almeida , Rodríguez Itahisa Marcelino , Coello Santiago Domínguez , Fernández Francisco J Cuevas , Díaz Buenaventura Brito , de León Antonio Cabrera 
Published: June 2022

Abstract
Serum resistin has been described as a risk factor associated with mortality in several clinical sets including type 2 diabetes. Mortality studies in the general population are needed to find out the risk of death among those who have been exposed to high levels of this cytokine. In a follow-up study of a cohort of adult population (n=6636) in Spain over a period of fifteen years (447 events/102,255 person-years), serum resistin measurements and death records were obtained. The risks of total deaths, and deaths from cardiovascular and oncological diseases were estimated. Hazard ratios (HR) and its confidence intervals (CI) were calculated using multivariable Cox models, adjusting the effect of 11 traditional risk factors. The risk of total mortality among participants exposed to the highest quintile of resistin was always higher than among those in the lowest quintile (HR varied between 1.55 when smoking was the adjusted factor [95%CI=1.17-2.05], and 1.68 when the adjusted factor was physical activity [95%CI=1.27-2.21]). The maximally adjusted model, accounting for the effect of all traditional factors, corroborated this higher risk of total mortality among people in the highest resistin quintile (HR=1.52; 95%CI=1.13-2.05). The effect of resistin was even higher for cardiovascular deaths (HR=2.14; 95%CI=1.13-4.06), being exceeded only by suffering diabetes (HR=3.04; 95%CI=1.98-4.69) or previous acute coronary syndrome (HR=3.67; 95%CI=2.18-6.18). This findings corroborate the role of resistin as a risk factor for general and cardiovascular mortality in the general population.
Ambient air pollution and emergency department visits and hospitalisation for cardiac arrest: a population-based case-crossover study
Authors: Halldorsdottir Solveig , Finnbjornsdottir Ragnhildur Gudrun , Elvarsson Bjarki Thor , Gunnarsdottir Oddny Sigurborg , Gudmundsson Gunnar , Rafnsson Vilhjálmur 
Published: June 2022

Abstract
Background
The association between ambient air pollution and cardiac arrhythmia has been explored in numerous studies; however, the small subgroup of cardiac arrest has not been closely studied thus far. The aim of the present study was to assess the association between traffic-related ambient air pollution and emergency hospital visits for cardiac arrest.
Methods
A bidirectional time-stratified case-crossover design was used. The setting was the Reykjavik capital area and the study population were the inhabitants 18 years and older identified by zip codes. Cases were those who had made emergency visits to Landspitali University Hospital during the period 2006 to 2017 and who were given the primary discharge diagnosis of cardiac arrest according to The International Classification of Diseases 10th edition (ICD-10), code I46. The pollutants were NO2, PM10, PM2.5, and SO2 with adjustment for H2S, temperature and relative humidity.
Results
The 24-h mean NO2 was 20.7 µg/m3, mean PM10 was 20.5 µg/m3, mean PM2.5 was 12.5 µg/m3, and mean SO2 was 2.5 µg/m3. PM10 level was positively associated with the number of emergency hospital visits (n = 453) for cardiac arrest. Each 10 µg/m3 increase in PM10 was associated with increased risk of cardiac arrest (ICD-10: I46), odds ratio (OR) 1.093 (95%CI 1.033–1.162) on lag 2, and OR 1.118 (95%CI 1.031–1.212) on lag 0–2. Significant associations were shown between exposure to PM10 on lag 2 and on lag 0–2 and increased risk of cardiac arrest in the age, gender, and season strata. Females and those 71 years and older were at higher risk for cardiac arrest, OR 1.193 (95%CI 1.059–1.344), and OR 1.186 (95%CI 1.066–1.320) on lag 2, per 10 µg/m3 increase in PM10, respectively. Significant associations were sporadically found for NO2 and SO2 and emergency hospital visits for cardiac arrest, but these associations were weaker and did not show a discernable pattern.
Conclusions
A new endpoint was used for the first time in this study: cardiac arrest (ICD-10 code I46). Short-term increase in PM10 concentrations was associated with cardiac arrest. The effect seemed higher among the elderly and females. Future ecological studies of this type and their related discussions should perhaps concentrate more on precisely defined endpoints.
Floralozone plays a role in heart failure treatment by down-regulating Vascular Endothelial Growth Factor Receptor 1 Expression
Authors: Yin Ya-ling , Guo Ya-qi , Hou Hong-yan , Que Hua-dong , Li Zi-tian , Fu Yu-tian , Liu Wei-Zhen , Yue Rui-Zhu , Zhu Mo-li , Li peng 
Published: June 2022

Abstract
Background
Floralozone (FL) is medicine with the refreshing aroma of rabbit's ear grass, which can be used to prevent the progression of atherosclerosis and reduces endothelial dysfunction. Vascular endothelial growth factor receptor 1 (VEGFR1) is one of the receptors of vascular endothelial factor (VEGF), which mainly plays a negative role in cardiovascular system regulation mainly by acting as a decoy receptor in endothelial cells. Therefore, the purpose of this study is to evaluate whether FL can down-regulate VEGFR1 expression in treating diabetes-induced heart failure (HF).
Methods
We used high-sugar and high-fat diet and tail vein injection of streptozotocin (STZ) to establish the rat model of HF. After intragastric administration of FL, the left ventricular function, pathological changes, oxidative stress condition in HF rats were assessed by echocardiography, oxidative stress monitoring, hematoxylin-eosin histological staining, argyrophilic staining, Masson staining, lichen red staining. The expression of VEGFR1 in the myocardial tissue of HF rats was detected by immunohistochemistry, immunofluorescence, western blot and RT-PCR analysis
Results
The HF model was established successfully. Through intragastric administration of FL, it was observed the cardiac function of HF rats was significantly improved, ventricular remodeling level was reversed, and the ability of antioxidant stress was enhanced. These therapeutic effects were closely connected with the down-regulation of VEGFR1 expression. ZM306416 is an antagonist of VEGFR1, which can up-regulate VEGFR1 expression and inhibit the protective effect of FL in rats with HF.
Conclusions
These results suggest that FL can play a salutary role in HF rats by down-regulating VEGFR1 expression, inhibiting ventricular remodeling and reducing oxidative stress.