bluuebunny/crossref_metadata_2025_split huggingface dataset:
High capacity DNA data storage with variable-length Oligonucleotides using repeat accumulate code and hybrid mapping
Authors: Wang Yixin , Noor-A-Rahim Md , Zhang Jingyun , Gunawan Erry , Guan Yong Liang , Poh Chueh Loo 
Published: December 2019

Abstract
Background
With the inherent high density and durable preservation, DNA has been recently recognized as a distinguished medium to store enormous data over millennia. To overcome the limitations existing in a recently reported high-capacity DNA data storage while achieving a competitive information capacity, we are inspired to explore a new coding system that facilitates the practical implementation of DNA data storage with high capacity.

Result
In this work, we devised and implemented a DNA data storage scheme with variable-length oligonucleotides (oligos), where a hybrid DNA mapping scheme that converts digital data to DNA records is introduced. The encoded DNA oligos stores 1.98 bits per nucleotide (bits/nt) on average (approaching the upper bound of 2 bits/nt), while conforming to the biochemical constraints. Beyond that, an oligo-level repeat-accumulate coding scheme is employed for addressing data loss and corruption in the biochemical processes. With a wet-lab experiment, an error-free retrieval of 379.1 KB data with a minimum coverage of 10x is achieved, validating the error resilience of the proposed coding scheme. Along with that, the theoretical analysis shows that the proposed scheme exhibits a net information density (user bits per nucleotide) of 1.67 bits/nt while achieving 91% of the information capacity.

Conclusion
To advance towards practical implementations of DNA storage, we proposed and tested a DNA data storage system enabling high potential mapping (bits to nucleotide conversion) scheme and low redundancy but highly efficient error correction code design. The advancement reported would move us closer to achieving a practical high-capacity DNA data storage system.
RETRACTED ARTICLE: MicroRNA-338-3p suppresses ovarian cancer cells growth and metastasis: implication of Wnt/catenin beta and MEK/ERK signaling pathways
Authors: Zhang Ruitao , Shi Huirong , Ren Fang , Feng Wei , Cao Yuan , Li Gailing , Liu Zheying , Ji Pengcheng , Zhang Minghui 
Published: December 2019

Abstract
Background
Downregulation of microRNA-338-3p (miR-338-3p) was detected in many malignant tumors, which indicated miR-338-3p might serve as a role of antioncogene in those cancers. The present study aimed to explore the roles of miR-338-3p in the growth and metastasis of ovarian cancer cells and elaborate the underlying possible molecular mechanism.

Methods
Multiply biomedical databases query and KEGG pathway enrichment assay were used to infilter possible target genes and downstream pathways regulated by miR-338-3p. Overexpression miR-338-3p lentiviral vectors were transfected into ovarian cancer OVCAR-3 and OVCAR-8 cells, cell proliferation, migration and invasion were analyzed by MTT, colony formation, transwell, Matrigel assay and xenograft mouse model. One 3′-untranslated regions (UTRs) binding target gene of miR-338-3p, MACC1 (MET transcriptional regulator MACC1), and its regulated gene MET and downstream signaling pathway activities were examined by western blot.

Results
Biomedical databases query indicated that miR-338-3p could target MACC1 gene and regulate Met, downstream Wnt/Catenin beta and MEK/ERK pathways. Rescue of miR-338-3p could inhibit the proliferation, migration and invasion of ovarian cancer cells, and suppress the growth and metastasis of xenograft tumor. Restoration of miR-338-3p could attenuate MACC1 and Met overexpression induced growth, epithelial to mesenchymal transition (EMT) and activities of Wnt/Catenin beta and MEK/ERK signaling in vitro and in vivo.

Conclusions
The present data indicated that restoration of miR-338-3p could suppress the growth and metastasis of ovarian cancer cells, which might due to the inhibition of proliferation and EMT induced by MACC1, Met and its downstream Wnt/Catenin beta and MEK/ERK signaling pathways.
Responses of Methanosarcina barkeri to acetate stress
Authors: He Pinjing , Duan Haowen , Han Wenhao , Liu Yang , Shao Liming , Lü Fan 
Published: December 2019

Abstract
Background
Anaerobic digestion of easily degradable biowaste can lead to the accumulation of volatile fatty acids, which will cause environmental stress to the sensitive methanogens consequently. The metabolic characteristics of methanogens under acetate stress can affect the overall performance of mixed consortia. Nevertheless, there exist huge gaps in understanding the responses of the dominant methanogens to the stress, e.g., Methanosarcinaceae. Such methanogens are resistant to environmental deterioration and able to utilize multiple carbon sources. In this study, transcriptomic and proteomic analyses were conducted to explore the responses of Methanosarcina barkeri strain MS at different acetate concentrations of 10, 25, and 50 mM.

Results
The trend of OD600 and the regulation of the specific genes in 50 mM acetate, indicated that high concentration of acetate promoted the acclimation of M. barkeri to acetate stress. Acetate stress hindered the regulation of quorum sensing and thereby eliminated the advantages of cell aggregation, which was beneficial to resist stress. Under acetate stress, M. barkeri allocated more resources to enhance the uptake of iron to maintain the integrities of electron-transport chains and other essential biological processes. Comparing with the initial stages of different acetate concentrations, most of the genes participating in acetoclastic methanogenesis did not show significantly different expressions except hdrB1C1, an electron-bifurcating heterodisulfide reductase participating in energy conversion and improving thermodynamic efficiency. Meanwhile, vnfDGHK and nifDHK participating in nitrogen fixation pathway were upregulated.

Conclusion
In this work, transcriptomic and proteomic analyses are combined to reveal the responses of M. barkeri to acetate stress in terms of central metabolic pathways, which provides basic clues for exploring the responses of other specific methanogens under high organics load. Moreover, the results can also be used to gain insights into the complex interactions and geochemical cycles among natural or engineered populations. Furthermore, these findings also provide the potential for designing effective and robust anaerobic digesters with high organic loads.
A new methodology for sporogony research of avian haemoproteids in laboratory-reared Culicoides spp., with a description of the complete sporogonic development of Haemoproteus pastoris
Authors: Bukauskaitė Dovilė , Chagas Carolina Romeiro Fernandes , Bernotienė Rasa , Žiegytė Rita , Ilgūnas Mikas , Iezhova Tatjana , Valkiūnas Gediminas 
Published: December 2019

Abstract
Background
Haemosporidian parasites of the genus Haemoproteus (Haemoproteidae) are widespread and cause haemoproteosis in birds and therefore, their diversity, ecology and evolutionary biology have become subjects of intensive research. However, the vectors and transmission patterns of haemoproteids as well as the epidemiology of haemoproteosis remain insufficiently investigated. Several species of Culicoides (Ceratopogonidae) support complete sporogony of haemoproteids belonging to the subgenus Parahaemoproteus. However, experimental research with these fragile insects is difficult to design in the field, particularly because their abundance markedly depends on seasonality. This is an obstacle for continuous sampling of sufficient numbers of naturally infected or experimentally exposed midges from wildlife. We developed simple methodology for accessing sporogonic development of haemoproteids in laboratory-reared Culicoides nubeculosus. This study aimed to describe the mosaic of methods constituting this methodology, which was applied for investigation of the sporogonic development of Haemoproteus (Parahaemoproteus) pastoris, a widespread parasite of the common starling Sturnus vulgaris.

Methods
The methodology consists of the following main stages: (i) laboratory rearing of C. nubeculosus from the egg stage to adult insects; (ii) selection of naturally infected birds, the donors of mature gametocytes to expose biting midges; (iii) experimental exposure of insects and their laboratory maintenance; and (iv) dissection of exposed insects. Biting midges were exposed to H. pastoris (cytochrome b lineage hLAMPUR01) detected in one naturally infected common starling. Engorged insects were dissected at intervals in order to follow sporogony. Microscopic examination and PCR-based methods were used to identify the sporogonic stages and to confirm the presence of the parasite lineage in infected insects, respectively.

Results
Culicoides nubeculosus females were successfully reared and exposed to H. pastoris, which completed sporogonic development 7–9 days post-infection when sporozoites were observed in the salivary glands.

Conclusions
The new methodology is easy to use and non-harmful for birds, providing opportunities to access the sporogonic stages of Parahaemoproteus parasites, which might be used in a broad range of parasitology and genetic studies. Culicoides nubeculosus is an excellent experimental vector of subgenus Parahaemoproteus and is recommended for various experimental studies aiming investigation of sporogony of these pathogens.
Maintenance of active chromatin states by HMGN2 is required for stem cell identity in a pluripotent stem cell model
Authors: Garza-Manero Sylvia , Sindi Abdulmajeed Abdulghani A. , Mohan Gokula , Rehbini Ohoud , Jeantet Valentine H. M. , Bailo Mariarca , Latif Faeezah Abdul , West Maureen P. , Gurden Ross , Finlayson Lauren , Svambaryte Silvija , West Adam G. , West Katherine L. 
Published: December 2019

AbstractBackgroundMembers of the HMGN protein family modulate chromatin structure and influence epigenetic modifications. HMGN1 and HMGN2 are highly expressed during early development and in the neural stem/progenitor cells of the developing and adult brain. Here, we investigate whether HMGN proteins contribute to the chromatin plasticity and epigenetic regulation that is essential for maintaining pluripotency in stem cells.ResultsWe show that loss ofHmgn1orHmgn2in pluripotent embryonal carcinoma cells leads to increased levels of spontaneous neuronal differentiation. This is accompanied by the loss of pluripotency markersNanogandSsea1, and increased expression of the pro-neural transcription factorsNeurog1andAscl1. Neural stem cells derived from theseHmgn-knockout lines also show increased spontaneous neuronal differentiation andNeurog1expression. The loss of HMGN2 leads to a global reduction in H3K9 acetylation, and disrupts the profile of H3K4me3, H3K9ac, H3K27ac and H3K122ac at theNanogandOct4loci. At endodermal/mesodermal genes,Hmgn2-knockout cells show a switch from a bivalent to a repressive chromatin configuration. However, at neuronal lineage genes whose expression is increased, no epigenetic changes are observed and their bivalent states are retained following the loss of HMGN2.ConclusionsWe conclude that HMGN1 and HMGN2 maintain the identity of pluripotent embryonal carcinoma cells by optimising the pluripotency transcription factor network and protecting the cells from precocious differentiation. Our evidence suggests that HMGN2 regulates active and bivalent genes by promoting an epigenetic landscape of active histone modifications at promoters and enhancers.
Association of predicted 10 years cardiovascular mortality risk with duration of HIV infection and antiretroviral therapy among HIV-infected individuals in Durban, South Africa
Authors: Todowede Olamide O. , Sartorius Benn , Magula Nombulelo , Schutte Aletta E. 
Published: December 2019

AbstractBackgroundSouth Africa has the largest population of human immunodeficiency virus (HIV) infected patients on antiretroviral therapy (ART) realising the benefits of increased life expectancy. However, this population may be susceptible to cardiovascular disease (CVD) development, due to the chronic consequences of a lifestyle-related combination of risk factors, HIV infection and ART. We predicted a 10-year cardiovascular mortality risk in an HIV-infected population on long-term ART, based on their observed metabolic risk factor profile.MethodsWe extracted data from hospital medical charts for 384 randomly selected HIV-infected patients aged ≥ 30 years. We defined metabolic syndrome (MetS) subcomponents using the International Diabetes Federation definition. A validated non-laboratory-based model for predicting a 10-year CVD mortality risk was applied and categorised into five levels, with the thresholds ranging from very low-risk (< 5%) to very high-risk scores (> 30%).ResultsAmong the 384 patients, with a mean (± standard deviation) age of 42.90 ± 8.20 years, the proportion of patients that were overweight/obese was 53.3%, where 50.9% had low high-density lipoprotein (HDL) cholesterol and 21 (17.5%) had metabolic syndrome. A total of 144 patients with complete data allowed a definitive prediction of a 10-year CVD mortality risk. 52% (95% CI 44–60) of the patients were stratified to very low risk (< 5%) compared to 8% (95% CI 4–13) that were at a very high risk (> 30%) of 10-year CVD mortality. The CVD risk grows with increasing age (years), 57.82 ± 6.27 among very high risk and 37.52 ± 4.50; p < 0.001 in very low risk patients. Adjusting for age and analysing CVD risk mortality as a continuous risk score, increasing duration of HIV infection (p = 0.002) and ART (p = 0.007) were significantly associated with increased predicted 10 year CVD mortality risk. However, there was no association between these factors and categorised CVD mortality risk as per recommended scoring thresholds.ConclusionsApproximately 1 in 10 HIV-infected patients is at very high risk of predicted 10-year CVD mortality in our study population. Like uninfected individuals, our study found increased age as a major predictor of 10-year mortality risk and high prevalence of metabolic syndrome. Additional CVD mortality risk due to the duration of HIV infection and ART was seen in our population, further studies in larger and more representative study samples are encouraged. It recommends an urgent need for early planning, prevention and management of metabolic risk factors in HIV populations, at the point of ART initiation.
Effects of virtual reality-based cognitive training in older adults living without and with mild dementia: a pretest–posttest design pilot study
Authors: Zając-Lamparska Ludmiła , Wiłkość-Dębczyńska Monika , Wojciechowski Adam , Podhorecka Marta , Polak-Szabela Anna , Warchoł Łukasz , Kędziora-Kornatowska Kornelia , Araszkiewicz Aleksander , Izdebski Paweł 
Published: December 2019

Abstract
Objective
Modern technologies are increasingly used in the development of cognitive interventions for older adults. Research into possible applications of virtual reality in such interventions has begun only recently. The aim of present study was to evaluate the effects of 8 sessions of VR-based cognitive training using the GRADYS game in healthy older adults (n = 72; aged 60–88) and older adults living with mild dementia (n = 27; aged 60–89).

Results
Older adults with mild dementia demonstrated worse baseline cognitive performance than participants without dementia. Both groups showed progress in training, which was greater in healthy older adults. There were also significant differences in cognitive functioning before and after the training. However, positive changes were revealed almost exclusively in the group of older adults without dementia. Based on the findings, we can recommend the GRADYS game for cognitive enhancement and as a possible counter-measure for cognitive decline experienced in normal cognitive ageing. Our results provide also support for the usefulness of VR technology in cognitive interventions in older adults. The use of the GRADYS game in persons living with dementia, however, would require several of the hardware and software modifications.
Trial registration ISRCTN17613444, date of registration: 10.09.2019. Retrospectively registered
PAD-Beads enrichment enhances detection of PrPSc using real-time quaking-induced conversion
Authors: Hwang Soyoun , Dassanayake Rohana P. , Nicholson Eric M. 
Published: December 2019

Abstract
Objective
Scrapie is a transmissible spongiform encephalopathy (TSE) that naturally occurs in sheep and goats. This fatal neurodegenerative disease results from misfolding of the normal cellular prion protein (PrPC) to a pathogenic prion protein form (PrPSc). This pathogenic form, PrPSc, accumulates in the brain and lymphoid tissues. The presence of PrPSc can be detected by an in vitro conversion assay known as real-time quaking induced conversion (RT-QuIC). RT-QuIC has been used to detect PrPSc in a variety of biological tissues from brains to fluids. While this technique is both rapid and sensitive, enhancing the detection of prions would be valuable in the diagnostic laboratories.

Results
In this study, we assessed whether PrPSc detection sensitivity of RT-QuIC can be increased by enriching PrPSc in scrapie tissue homogenates using commercially available aggregated protein binding ligands coated magnetic beads (PAD-Beads). Coupling of RT-QuIC to PAD-Beads based cleanup allowed detection of PrPSc rapidly and without dilution of scrapie sheep brain homogenates prior to RT-QuIC. The PAD-Beads sample pretreatment step prior to RT-QuIC is a useful enhancement in the diagnosis of TSEs.
Human plasma dynamically quenches the fluorescein at the initial point of oxygen radical absorption capacity (ORAC) assay
Authors: Gunawardena Harshi , Silva Renuka , Ranasinghe Pathmasiri 
Published: December 2019

Abstract
Objective
Oxygen radical absorbance capacity (ORAC) assay measures the quenching of fluorescent probe by peroxyl radicals. Antioxidants present in biological systems block the quenching of fluorescence probe. We experienced the dynamic quenching of fluorescein, the fluorescence probe used in ORAC assay by the human plasma while plasma ORAC assay was optimized. Therefore, for the first time, we report the quenching of fluorescein by human plasma at the initial point of ORAC assay.

Results
Aqueous whole and non-protein fractions of plasma were used in the analysis. Since the both fractions showed a similar pattern of quenching at the initial stage, quenched percentage of fluorescein was calculated and added to each sample in subsequent analysis. Addition of extra 20% fluorescein allowed plasma samples to quench the required amount of fluorescein and follow the normal decay curves afterwards. Further, change of fluorescein quenching (ΔF/F0) disclosed a dose dependent linear relationship with plasma (R2 = 0.8). It can be speculated that dynamic quenching exhibited by human plasma biomolecule/s at the initial stage would be of non-protein aqueous phase molecule/s. We suggest initiating further studies to detect, identify and quantify the fluorescein quenching biomolecules present in human plasma for further improvements in plasma ORAC assay.
Methylomic profiling in trisomy 21 identifies cognition- and Alzheimer’s disease-related dysregulation
Authors: Haertle Larissa , Müller Tobias , Lardenoije Roy , Maierhofer Anna , Dittrich Marcus , Riemens Renzo J. M. , Stora Samantha , Roche Mathilde , Leber Markus , Riedel-Heller Steffi , Wagner Michael , Scherer Martin , Ravel Aimé , Mircher Clotilde , Cieuta-Walti Cecile , Durand Sophie , van de Hove Daniel L. A. , Hoffmann Per , Ramirez Alfredo , Haaf Thomas , El Hajj Nady , Mégarbané André 
Published: December 2019

Abstract

Background
Trisomy 21 (T21) is associated with intellectual disability that ranges from mild to profound with an average intellectual quotient of around 50. Furthermore, T21 patients have a high risk of developing Alzheimer’s disease (AD) early in life, characterized by the presence of senile plaques of amyloid protein and neurofibrillary tangles, leading to neuronal loss and cognitive decline. We postulate that epigenetic factors contribute to the observed variability in intellectual disability, as well as at the level of neurodegeneration seen in T21 individuals.

Materials and Methods
A genome-wide DNA methylation study was performed using Illumina Infinium® MethylationEPIC BeadChips on whole blood DNA of 3 male T21 patients with low IQ, 8 T21 patients with high IQ (4 males and 4 females), and 21 age- and sex-matched control samples (12 males and 9 females) in order to determine whether DNA methylation alterations could help explain variation in cognitive impairment between individuals with T21. In view of the increased risk of developing AD in T21 individuals, we additionally investigated the T21-associated sites in published blood DNA methylation data from the AgeCoDe cohort (German study on Ageing, Cognition, and Dementia). AgeCoDe represents a prospective longitudinal study including non-demented individuals at baseline of which a part develops AD dementia at follow-up.

Results
Two thousand seven hundred sixteen differentially methylated sites and regions discriminating T21 and healthy individuals were identified. In the T21 high and low IQ comparison, a single CpG located in the promoter of PELI1 was differentially methylated after multiple testing adjustment. For the same contrast, 69 differentially methylated regions were identified. Performing a targeted association analysis for the significant T21-associated CpG sites in the AgeCoDe cohort, we found that 9 showed significant methylation differences related to AD dementia, including one in the ADAM10 gene. This gene has previously been shown to play a role in the prevention of amyloid plaque formation in the brain.

Conclusion
The differentially methylated regions may help understand the interaction between methylation alterations and cognitive function. In addition, ADAM10 might be a valuable blood-based biomarker for at least the early detection of AD.
Human fetal skin-derived stem cell secretome enhances radiation-induced skin injury therapeutic effects by promoting angiogenesis
Authors: Rong Xiaoli , Li Jiannan , Yang Yanyan , Shi Liyan , Jiang Tiechao 
Published: December 2019

Abstract
Background
Radiation dermatitis is a refractory skin injury caused by radiotherapy. Human fetal skin-derived stem cell (hFSSC) is a preferable source for cell therapy and skin tissue regeneration. In the present study, we investigated the repair effect of using hFSSC secretome on a radiation skin injury model in rats.

Methods
We prepared the hFSSC secretome and studied its effects on the proliferation and tube formation of human umbilical vein endothelial cell (HUVEC) in vitro. Furthermore, we used a Sr-90 radiation-induced skin injury model of rats and evaluated the effects of hFSSC secretome on radiation skin injury in vivo.

Results
The results showed that hFSSC secretome significantly promoted the proliferation and tube formation of HUVEC in vitro; in addition, hFSSC secretome-treated rats exhibited higher healing quality and faster healing rate than the other two control groups; the expression level of collagen type III α 1 (Col3A1), transforming growth factor β3 (TGF-β3), angiotensin 1 (Ang-1), angiotensin 2 (Ang-2), vascular endothelial growth factor (VEGF), and placental growth factor (PLGF) was significantly increased, while collagen type I α 2 (Col1A2) and transforming growth factor β1 (TGF-β1) were decreased in hFSSC secretome group.

Conclusions
In conclusion, our results provided the first evidence on the effects of hFSSC secretome towards radiation-induced skin injury. We found that hFSSC secretome significantly enhanced radiation dermatitis angiogenesis, and the therapeutic effects could match with the characteristics of fetal skin. It may act as a kind of novel cell-free therapeutic approach for radiation-induced cutaneous wound healing.