cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.10278959
title: Questionnaire and Data of Neck Pain and Distance learning among university Students During COVID-19

description:  The shift to online learning during COVID-19 led to increased musculoskeletal discomforts and impacted students' quality of life. Neck pain, once a minor issue, has become more prevalent due to prolonged electronic device use in new learning methods. This study aims to measure the prevalence of neck pain among University of Sharjah (UOS) students during the COVID-19 online learning period and to investigate the factors that provoked it.
 This cross-sectional study used an online survey distributed to UOS students via social media from February 16 to March 12, 2021. Demographic data, Neck Disability Index (NDI) assessments, and pain management information were gathered and analyzed using SPSS 24 through univariate and bivariate methods.
The prevalence of neck pain during COVID-19, among 325 UOS students was found to be 62.7%, 64.41% of which had neck pain at the time of doing the survey. The mean NDI percentage point was 19.19%. The most common location of pain was the back of the neck 38.77%). Participants reported prolonged sitting (81.23%) while leaning forward as the most prevalent cause of their neck pain. Bivariate analysis showed that the most significant factors affecting the NDI were lifting, personal care, headaches, concentration, sleeping, recreational activities, reading, anxiousness, depression, and work. Moreover, subjects who did not seek medical attention treatment had significantly higher NDI scores as compared to those who did (83.89 vs 125.80, p=0.002).
By determining the prevalence of neck pain among UOS students, this research can attract attention to the importance of postural changes and time spent in e-learning on neck pain, and the gaps of previously published articles can be filled. Future studies about neck pain and additional preventative measures should be catalyzed in the UAE.
DOI: 10.17632/gtv8pw7frw.1
title: Bulgarian bonds

description: I study bond volatility and yields to examine its determinants.
DOI: 10.6084/m9.figshare.6275141
title: The clinical application of single-sperm-based SNP haplotyping for PGD of osteogenesis imperfecta

description: Osteogenesis imperfecta (OI) is a genetically heterogeneous disorder, presenting either autosomal dominant, autosomal recessive or X-linked inheritance patterns. The majority of OI cases are autosomal dominant and are caused by heterozygous mutations in either the <i>COL1A1</i> or <i>COL1A2</i> gene. In these dominant disorders, allele dropout (ADO) can lead to misdiagnosis in preimplantation genetic diagnosis (PGD). Polymorphic markers linked to the mutated genes have been used to establish haplotypes for identifying ADO and ensuring the accuracy of PGD. However, the haplotype of male patients cannot be determined without data from affected relatives. Here, we developed a method for single-sperm-based single-nucleotide polymorphism (SNP) haplotyping via next-generation sequencing (NGS) for the PGD of OI. After NGS, 10 informative polymorphic SNP markers located upstream and downstream of the <i>COL1A1</i> gene and its pathogenic mutation site were linked to individual alleles in a single sperm from an affected male. After haplotyping, a normal blastocyst was transferred to the uterus for a subsequent frozen embryo transfer cycle. The accuracy of PGD was confirmed by amniocentesis at 19 weeks of gestation. A healthy infant weighing 4,250 g was born via vaginal delivery at the 40th week of gestation. Single-sperm-based SNP haplotyping can be applied for PGD of any monogenic disorders or <i>de novo</i> mutations in males in whom the haplotype of paternal mutations cannot be determined due to a lack of affected relatives. <b>Abbreviations:</b> ADO: allele dropout; DI: dentinogenesis imperfect; ESHRE: European Society of Human Reproduction and Embryology; FET: frozen embryo transfer; gDNA: genomic DNA; ICSI: intracytoplasmic sperm injection; IVF: in vitro fertilization; MDA: multiple displacement amplification; NGS: next-generation sequencing; OI: osteogenesis imperfect; PBS: phosphate buffer saline; PCR: polymerase chain reaction; PGD: preimplantation genetic diagnosis; SNP: single-nucleotide polymorphism; STR: short tandem repeat; TE: trophectoderm; WGA: whole-genome amplification
DOI: 10.6084/m9.figshare.6275141.v1
title: The clinical application of single-sperm-based SNP haplotyping for PGD of osteogenesis imperfecta

description: Osteogenesis imperfecta (OI) is a genetically heterogeneous disorder, presenting either autosomal dominant, autosomal recessive or X-linked inheritance patterns. The majority of OI cases are autosomal dominant and are caused by heterozygous mutations in either the <i>COL1A1</i> or <i>COL1A2</i> gene. In these dominant disorders, allele dropout (ADO) can lead to misdiagnosis in preimplantation genetic diagnosis (PGD). Polymorphic markers linked to the mutated genes have been used to establish haplotypes for identifying ADO and ensuring the accuracy of PGD. However, the haplotype of male patients cannot be determined without data from affected relatives. Here, we developed a method for single-sperm-based single-nucleotide polymorphism (SNP) haplotyping via next-generation sequencing (NGS) for the PGD of OI. After NGS, 10 informative polymorphic SNP markers located upstream and downstream of the <i>COL1A1</i> gene and its pathogenic mutation site were linked to individual alleles in a single sperm from an affected male. After haplotyping, a normal blastocyst was transferred to the uterus for a subsequent frozen embryo transfer cycle. The accuracy of PGD was confirmed by amniocentesis at 19 weeks of gestation. A healthy infant weighing 4,250 g was born via vaginal delivery at the 40th week of gestation. Single-sperm-based SNP haplotyping can be applied for PGD of any monogenic disorders or <i>de novo</i> mutations in males in whom the haplotype of paternal mutations cannot be determined due to a lack of affected relatives. <b>Abbreviations:</b> ADO: allele dropout; DI: dentinogenesis imperfect; ESHRE: European Society of Human Reproduction and Embryology; FET: frozen embryo transfer; gDNA: genomic DNA; ICSI: intracytoplasmic sperm injection; IVF: in vitro fertilization; MDA: multiple displacement amplification; NGS: next-generation sequencing; OI: osteogenesis imperfect; PBS: phosphate buffer saline; PCR: polymerase chain reaction; PGD: preimplantation genetic diagnosis; SNP: single-nucleotide polymorphism; STR: short tandem repeat; TE: trophectoderm; WGA: whole-genome amplification
DOI: 10.6084/m9.figshare.7848026
title: Using high-resolution annotation of insect mitochondrial DNA to decipher tandem repeats in the control region

description: In this study, we used a small RNA sequencing (sRNA-seq) based method to annotate the mitochondrial genome of the insect <i>Erthesina fullo</i> Thunberg at 1 bp resolution. The high-resolution annotations cover both entire strands of the mitochondrial genome without any gaps or overlaps. Most of the new annotations were consistent with the previous annotations which had been obtained using PacBio full-length transcripts. Two important findings were that animals transcribe both entire strands of mitochondrial genomes and the tandem repeats in the control region of the <i>E. fullo</i> mitochondrial genome contains the repeated Transcription Initiation Sites (TISs) of the heavy strand. In addition, we found that the copy numbers of tandem repeats showed a great diversity within an individual, suggesting that mitochondrial DNA recombination occurs in an individual. In conclusion, the sRNA-seq based method uses 5′ and 3′ end small RNAs to annotate nuclear non-coding and mitochondrial genes at 1 bp resolution, and can be used to identify new steady RNAs, particularly long non-coding RNAs (lncRNAs). The high-resolution annotations of mitochondrial genomes can also be used to study the molecular phylogenetics and evolution of animals or to investigate mitochondrial gene transcription, RNA processing, RNA maturation and several other related topics. The complete mitochondrial genome sequence of <i>E. fullo</i> with the new annotations using the sRNA-seq based method is available at the NCBI GenBank database under the accession number MK374364. We publish our theories, methods, the high quality sRNA-seq and RNA-seq data (SRA: SRP174926) for extensive use.
DOI: 10.6084/m9.figshare.7848026.v1
title: Using high-resolution annotation of insect mitochondrial DNA to decipher tandem repeats in the control region

description: In this study, we used a small RNA sequencing (sRNA-seq) based method to annotate the mitochondrial genome of the insect <i>Erthesina fullo</i> Thunberg at 1 bp resolution. The high-resolution annotations cover both entire strands of the mitochondrial genome without any gaps or overlaps. Most of the new annotations were consistent with the previous annotations which had been obtained using PacBio full-length transcripts. Two important findings were that animals transcribe both entire strands of mitochondrial genomes and the tandem repeats in the control region of the <i>E. fullo</i> mitochondrial genome contains the repeated Transcription Initiation Sites (TISs) of the heavy strand. In addition, we found that the copy numbers of tandem repeats showed a great diversity within an individual, suggesting that mitochondrial DNA recombination occurs in an individual. In conclusion, the sRNA-seq based method uses 5′ and 3′ end small RNAs to annotate nuclear non-coding and mitochondrial genes at 1 bp resolution, and can be used to identify new steady RNAs, particularly long non-coding RNAs (lncRNAs). The high-resolution annotations of mitochondrial genomes can also be used to study the molecular phylogenetics and evolution of animals or to investigate mitochondrial gene transcription, RNA processing, RNA maturation and several other related topics. The complete mitochondrial genome sequence of <i>E. fullo</i> with the new annotations using the sRNA-seq based method is available at the NCBI GenBank database under the accession number MK374364. We publish our theories, methods, the high quality sRNA-seq and RNA-seq data (SRA: SRP174926) for extensive use.
DOI: 10.6084/m9.figshare.15188059
title: Short- and long-term follow-up outcomes of patients with Brucella endocarditis: a systematic review of 207 Brucella endocarditis Cases

description: <i>Brucella</i> endocarditis is a fatal complication and the most frequent cause of death for human brucellosis. This study aimed to systematically review the literature on the follow-up outcomes of <i>Brucella</i> endocarditis and analyze the determinants affecting the follow-up outcomes. The databases PubMed, Web of Science, Embase, and Cochrane were searched using keywords and suitable combinations. All studies reporting the follow-up outcomes of <i>Brucella</i> endocarditis were included. Finally, a total of 76 studies (207 patients), including cases or case series, were included. The event rate for patients who underwent short- and long-term follow-up was 12.0% (2 relapsed and 1 died) and 8.1% (6 relapsed and 8 died), respectively. The differences in outcomes between different age groups (18–39, 40–59, and ≥60) were significant (<i>P</i> &lt; 0.05, <i>P</i> = 0.035). The outcomes of the 18–39 age group were worse than those of the 40–59 age group (OR, 0.277; 95% CI, 0.103–0.748; <i>P</i> = 0.011). Accordingly, follow-up (both short- and long-term follow-up) is essential for <i>Brucella</i> endocarditis patients, especially for younger patients (18–39 years) in the first 6 months after treatment. The burden of <i>Brucella</i> endocarditis related complications were immense. Further studies are needed to explore age-based epidemiology of <i>Brucella</i> endocarditis and the exact influencing factors of the follow-up outcomes.
DOI: 10.6084/m9.figshare.7848014
title: METTL3 and ALKBH5 oppositely regulate m<sup>6</sup>A modification of <i>TFEB</i> mRNA, which dictates the fate of hypoxia/reoxygenation-treated cardiomyocytes

description: N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) mRNA modifications play critical roles in various biological processes. However, no study addresses the role of m<sup>6</sup>A in macroautophagy/autophagy. Here, we show that m<sup>6</sup>A modifications are increased in H/R-treated cardiomyocytes and ischemia/reperfusion (I/R)-treated mice heart. We found that METTL3 (methyltransferase like 3) is the primary factor involved in aberrant m<sup>6</sup>A modification. Silencing METTL3 enhances autophagic flux and inhibits apoptosis in H/R-treated cardiomyocytes. However, overexpression of METTL3 or inhibition of the RNA demethylase ALKBH5 has an opposite effect, suggesting that METTL3 is a negative regulator of autophagy. Mechanistically, METTL3 methylates <i>TFEB</i>, a master regulator of lysosomal biogenesis and autophagy genes, at two m<sup>6</sup>A residues in the 3ʹ-UTR, which promotes the association of the RNA-binding protein HNRNPD with <i>TFEB</i> pre-mRNA and subsequently decreases the expression levels of TFEB. Further experiments show that autophagic flux enhanced by METTL3 deficiency is TFEB dependent. In turn, TFEB regulates the expression levels of METTL3 and ALKBH5 in opposite directions: it induces ALKBH5 and inhibits METTL3. TFEB binds to the <i>ALKBH5</i> promoter and activates its transcription. In contrast, inhibition of METTL3 by TFEB does not involve transcriptional repression but rather downregulation of mRNA stability, thereby establishing a negative feedback loop. Together, our work uncovers a critical link between METTL3-ALKBH5 and autophagy, providing insight into the functional importance of the reversible mRNA m<sup>6</sup>A methylation and its modulators in ischemic heart disease. ACTB, actin beta; ALKBH5, alkB homolog 5, RNA demethylase; ANXA5, annexin A5; ATG, autophagy-related; BafA, bafilomycin A<sub>1</sub>; CASP3, caspase 3; ELAVL1, ELAV like RNA binding protein 1; FTO, FTO, alpha-ketoglutarate dependent dioxygenase; GFP, green fluorescent protein; GST, glutathione S-transferase; HNRNPD, heterogeneous nuclear ribonucleoprotein D; H/R, hypoxia/reoxygenation; I/R, ischemia/reperfusion; LAD, left anterior descending; m<sup>6</sup>A, N<sup>6</sup>-methyladenosine; MEFs, mouse embryo fibroblasts; Mer, mutated estrogen receptor domains; METTL3, methyltransferase like 3; METTL14, methyltransferase like 14; mRFP, monomeric red fluorescent protein; MTORC1, mechanistic target of rapamycin kinase complex 1; NMVCs, neonatal mouse ventricular cardiomyocytes; PCNA, proliferating cell nuclear antigen; PE, phosphatidylethanolamine; PI, propidium iodide; PTMs, post-translational modifications; PVDF, polyvinylidenedifluoride; RIP, RNA-immunoprecipitation; siRNA, small interfering RNA; SQSTM1, sequestosome 1; TFEB, transcription factor EB; TUBA: tublin alpha; WTAP, WT1 associated protein; YTHDF, YTH N6-methyladenosine RNA binding protein
DOI: 10.6084/m9.figshare.15188059.v1
title: Short- and long-term follow-up outcomes of patients with Brucella endocarditis: a systematic review of 207 Brucella endocarditis Cases

description: <i>Brucella</i> endocarditis is a fatal complication and the most frequent cause of death for human brucellosis. This study aimed to systematically review the literature on the follow-up outcomes of <i>Brucella</i> endocarditis and analyze the determinants affecting the follow-up outcomes. The databases PubMed, Web of Science, Embase, and Cochrane were searched using keywords and suitable combinations. All studies reporting the follow-up outcomes of <i>Brucella</i> endocarditis were included. Finally, a total of 76 studies (207 patients), including cases or case series, were included. The event rate for patients who underwent short- and long-term follow-up was 12.0% (2 relapsed and 1 died) and 8.1% (6 relapsed and 8 died), respectively. The differences in outcomes between different age groups (18–39, 40–59, and ≥60) were significant (<i>P</i> &lt; 0.05, <i>P</i> = 0.035). The outcomes of the 18–39 age group were worse than those of the 40–59 age group (OR, 0.277; 95% CI, 0.103–0.748; <i>P</i> = 0.011). Accordingly, follow-up (both short- and long-term follow-up) is essential for <i>Brucella</i> endocarditis patients, especially for younger patients (18–39 years) in the first 6 months after treatment. The burden of <i>Brucella</i> endocarditis related complications were immense. Further studies are needed to explore age-based epidemiology of <i>Brucella</i> endocarditis and the exact influencing factors of the follow-up outcomes.
DOI: 10.6084/m9.figshare.7848014.v1
title: METTL3 and ALKBH5 oppositely regulate m<sup>6</sup>A modification of <i>TFEB</i> mRNA, which dictates the fate of hypoxia/reoxygenation-treated cardiomyocytes

description: N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) mRNA modifications play critical roles in various biological processes. However, no study addresses the role of m<sup>6</sup>A in macroautophagy/autophagy. Here, we show that m<sup>6</sup>A modifications are increased in H/R-treated cardiomyocytes and ischemia/reperfusion (I/R)-treated mice heart. We found that METTL3 (methyltransferase like 3) is the primary factor involved in aberrant m<sup>6</sup>A modification. Silencing METTL3 enhances autophagic flux and inhibits apoptosis in H/R-treated cardiomyocytes. However, overexpression of METTL3 or inhibition of the RNA demethylase ALKBH5 has an opposite effect, suggesting that METTL3 is a negative regulator of autophagy. Mechanistically, METTL3 methylates <i>TFEB</i>, a master regulator of lysosomal biogenesis and autophagy genes, at two m<sup>6</sup>A residues in the 3ʹ-UTR, which promotes the association of the RNA-binding protein HNRNPD with <i>TFEB</i> pre-mRNA and subsequently decreases the expression levels of TFEB. Further experiments show that autophagic flux enhanced by METTL3 deficiency is TFEB dependent. In turn, TFEB regulates the expression levels of METTL3 and ALKBH5 in opposite directions: it induces ALKBH5 and inhibits METTL3. TFEB binds to the <i>ALKBH5</i> promoter and activates its transcription. In contrast, inhibition of METTL3 by TFEB does not involve transcriptional repression but rather downregulation of mRNA stability, thereby establishing a negative feedback loop. Together, our work uncovers a critical link between METTL3-ALKBH5 and autophagy, providing insight into the functional importance of the reversible mRNA m<sup>6</sup>A methylation and its modulators in ischemic heart disease. ACTB, actin beta; ALKBH5, alkB homolog 5, RNA demethylase; ANXA5, annexin A5; ATG, autophagy-related; BafA, bafilomycin A<sub>1</sub>; CASP3, caspase 3; ELAVL1, ELAV like RNA binding protein 1; FTO, FTO, alpha-ketoglutarate dependent dioxygenase; GFP, green fluorescent protein; GST, glutathione S-transferase; HNRNPD, heterogeneous nuclear ribonucleoprotein D; H/R, hypoxia/reoxygenation; I/R, ischemia/reperfusion; LAD, left anterior descending; m<sup>6</sup>A, N<sup>6</sup>-methyladenosine; MEFs, mouse embryo fibroblasts; Mer, mutated estrogen receptor domains; METTL3, methyltransferase like 3; METTL14, methyltransferase like 14; mRFP, monomeric red fluorescent protein; MTORC1, mechanistic target of rapamycin kinase complex 1; NMVCs, neonatal mouse ventricular cardiomyocytes; PCNA, proliferating cell nuclear antigen; PE, phosphatidylethanolamine; PI, propidium iodide; PTMs, post-translational modifications; PVDF, polyvinylidenedifluoride; RIP, RNA-immunoprecipitation; siRNA, small interfering RNA; SQSTM1, sequestosome 1; TFEB, transcription factor EB; TUBA: tublin alpha; WTAP, WT1 associated protein; YTHDF, YTH N6-methyladenosine RNA binding protein
DOI: 10.6084/m9.figshare.19382391
title: The effect and mechanism of miR-30e-5p targeting SNAI1 to regulate epithelial-mesenchymal transition on pancreatic cancer

description: Accumulating evidence indicates that abnormally expressed microRNAs (miRNAs, miRs) contribute to cancer progression. Nonetheless, the role of miR-30e-5p in pancreatic cancer (PCa) remains unclear. In this study, using quantitative real-time polymerase chain reaction analysis, we found that miR-30e-5p expression was downregulated in human PCa tissues compared with that in normal para-cancerous tissues. After transfecting with miR-30e-5p inhibitors, miR-30e-5p mimics, or empty vectors in the BxPC-3 and PANC-1 cells, respectively, the experiments revealed that the upregulation of miR-30e-5p expression inhibited cell growth, invasion, migration and epithelial-mesenchymal transition (EMT), and promoted apoptosis, while miR-30e-5p downregulation had the opposite effects. RNA sequencing of miR-30e-5p inhibitor-, miR-30e-5p mimic-, and the negative control (NC)-treated groups revealed that miR-30e-5p may affect epithelial cell differentiation, cell growth and death. Next, the snail family transcriptional repressor 1 (SNAI1) was predicted and verified as the target gene of miR-30e-5p using bioinformatics analysis and luciferase assays. SNAI1 expression levels were decreased in the PCa cells transfected with miR-30e-5p mimics, whereas the opposite was observed in the cells transfected with miR-30e-5p inhibitors. Subsequently, PCa cells were transfected with a vector overexpressing SNAI1 (OE-SNAI1) and miR-30e-5p mimics, miR-30e-5p inhibitors, or empty vectors. Compared with that in the OE-SNAI1 + miR-30e-5p NC group, transfection with OE-SNAI1 + miR-30e-5p mimics inhibited the PCa cell growth, migration, and increased apoptosis, whereas transfection with OE-SNAI1 + miR-30e-5p inhibitors had the opposite effects. In conclusion, miR-30e-5p potentially inhibits PCa cell proliferation, migration, and invasion via the SNAI1/EMT axis.
DOI: 10.5066/p135prta
title: Juvenile Salmonid Densities in Orwell Brook and Trout Brook, New York 2014-2023

description: Individual point estimates of stream density by juvenile salmonid species in two small tributaries to the Salmon River, Lake Ontario, New York were recorded. Enumeration of salmonid species was observed using a backpack electrofisher in order to identify fish species. Stream density estimates were calculated using stream width measurements taken at equally spaced transects. Comparisons of species densities between the two streams were analyzed to infer competition or segregation.