cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29967405.v1
title: Altered mitochondrial DNA methylation in blood in individuals with mild cognitive impairment

description: Previous studies reported that altered mitochondrial methylation in Alzheimer’s disease (AD), however, whether epigenetic modifications in mitochondrial genomes contribute to preclinical AD remains unclear. This study aimed to investigate mitochondrial methylation changes in individuals with cognitive decline. We examined whole mitochondrial genome methylation in 50 individuals with mild cognitive impairment (MCI) and 50 individuals without MCI, using bisulfite amplicon sequencing, assessing methylation at 366 Cytosine-guanine oligodeoxynucleotide (CpG) sites. We found the overall methylation level of mitochondrial DNA (mtDNA) in each subject was relatively low, ranging from 0% to 15%. Global methylation was significantly higher in individuals with cognitive decline compared to controls (3.86% vs. 3.46%, <i>p</i> = 0.037), with 34 differentially methylated CpG sites identified. Methylation differences (MD) between cognitive decline individuals and controls were 22.93 ± 5.60% at chrM6465 (Q = 0.013), 12.55 ± 3.02% at chrM9612 (Q = 0.013), 11.45 ± 3.88% at chrM11762 (Q = 0.159) and 11.03 ± 3.88% at chrM11766 (Q = 0.172), respectively, while the level of MD at chrM15812 was −13.11 ± 4.31% (Q = 0.159) after Benjamini-Hochberg FDR adjusted. Furthermore, Methylation at specific sites were significantly correlated with Mini-Mental State Examination scores, distinguishing individuals with cognitive decline from controls. Our study provides an mtDNA methylation map and suggests a role for these sites in preclinical AD pathogenesis. Alzheimer’s disease is a brain condition that causes memory loss and thinking problems. Before the disease becomes serious, people may show early signs like forgetting things or having trouble focusing. This stage is called “mild cognitive impairment” or MCI. Finding it early can help doctors provide better care. In this study, we looked at small chemical changes in cell parts called mitochondria. These changes, called DNA methylation, can affect how genes work. We took blood samples from 50 older adults with memory problems and compared them to 50 healthy people of the same age and gender. We used a special test to check over 300 spots in the mitochondrial DNA. We found that some of these spots were more changed in people with memory problems. These changes were linked to lower memory test scores and could help tell who has early memory decline. This research shows that changes in mitochondrial DNA might be early warning signs of Alzheimer’s disease. In the future, a simple blood test may help find the disease before it gets worse.
DOI: 10.6084/m9.figshare.13246940
title: Development of cancer prognostic signature based on pan-cancer proteomics

description: Utilizing genomic data to predict cancer prognosis was insufficient. Proteomics can improve our understanding of the etiology and progression of cancer and improve the assessment of cancer prognosis. And the Clinical Proteomic Tumor Analysis Consortium (CPTAC) has generated extensive proteomics data of the vast majority of tumors. Based on CPTAC, we can perform a proteomic pan-carcinoma analysis. We collected the proteomics data and clinical features of cancer patients from CPTAC. Then, we screened 69 differentially expressed proteins (DEPs) with R software in five cancers: hepatocellular carcinoma (HCC), children’s brain tumor tissue consortium (CBTTC), clear cell renal cell carcinoma (CCRC), lung adenocarcinoma (LUAD) and uterine corpus endometrial carcinoma (UCEC). GO and KEGG analysis were performed to clarify the function of these proteins. We also identified their interactions. The DEPs-based prognostic model for predicting over survival was identified by least absolute shrinkage and selection operator (LASSO)-Cox regression model in training cohort. Then, we used the time-dependent receiver operating characteristics analysis to evaluate the ability of the prognostic model to predict overall survival and validated it in validation cohort. The results showed that the DEPs-based prognostic model could accurately and effectively predict the survival rate of most cancers.
DOI: 10.6084/m9.figshare.13246940.v1
title: Development of cancer prognostic signature based on pan-cancer proteomics

description: Utilizing genomic data to predict cancer prognosis was insufficient. Proteomics can improve our understanding of the etiology and progression of cancer and improve the assessment of cancer prognosis. And the Clinical Proteomic Tumor Analysis Consortium (CPTAC) has generated extensive proteomics data of the vast majority of tumors. Based on CPTAC, we can perform a proteomic pan-carcinoma analysis. We collected the proteomics data and clinical features of cancer patients from CPTAC. Then, we screened 69 differentially expressed proteins (DEPs) with R software in five cancers: hepatocellular carcinoma (HCC), children’s brain tumor tissue consortium (CBTTC), clear cell renal cell carcinoma (CCRC), lung adenocarcinoma (LUAD) and uterine corpus endometrial carcinoma (UCEC). GO and KEGG analysis were performed to clarify the function of these proteins. We also identified their interactions. The DEPs-based prognostic model for predicting over survival was identified by least absolute shrinkage and selection operator (LASSO)-Cox regression model in training cohort. Then, we used the time-dependent receiver operating characteristics analysis to evaluate the ability of the prognostic model to predict overall survival and validated it in validation cohort. The results showed that the DEPs-based prognostic model could accurately and effectively predict the survival rate of most cancers.
DOI: 10.6084/m9.figshare.13207146
title: Bioinformatics analysis to screen key prognostic genes in the breast cancer tumor microenvironment

description: Increasing evidence has shown that the tumor microenvironment (TME) plays an important role in tumor occurrence and development and can also affect patient prognosis. In this study, we screened key prognostic genes in the breast cancer (BC) TME by analyzing the immune and stromal scores of tumor samples to detect differentially expressed genes (DEGs) and also constructed a TME-related prognostic model. First, we obtained mRNA-Seq and related clinical information for patients with BC from The Cancer Genome Atlas (TCGA) and calculated the stromal and immune scores of tumor tissues using the ESTIMATE algorithm. Next, we performed functional enrichment analysis and generated protein–protein interaction networks from the DEGs that were highly related to the TME. Finally, Cox proportional hazards regression analysis was performed on BC datasets from TCGA, and analyses were conducted on infiltrating immune cells and the human protein atlas. Together, these analyses indicated that the <i>KLRB1</i> and <i>SIT1</i> genes could be used as independent prognostic factors for BC, while risk score, age, and clinical stage could be used as prognostic factors. In summary, we found that the prognosis of BC is closely related to immune regulation in the TME.
DOI: 10.6084/m9.figshare.13207146.v1
title: Bioinformatics analysis to screen key prognostic genes in the breast cancer tumor microenvironment

description: Increasing evidence has shown that the tumor microenvironment (TME) plays an important role in tumor occurrence and development and can also affect patient prognosis. In this study, we screened key prognostic genes in the breast cancer (BC) TME by analyzing the immune and stromal scores of tumor samples to detect differentially expressed genes (DEGs) and also constructed a TME-related prognostic model. First, we obtained mRNA-Seq and related clinical information for patients with BC from The Cancer Genome Atlas (TCGA) and calculated the stromal and immune scores of tumor tissues using the ESTIMATE algorithm. Next, we performed functional enrichment analysis and generated protein–protein interaction networks from the DEGs that were highly related to the TME. Finally, Cox proportional hazards regression analysis was performed on BC datasets from TCGA, and analyses were conducted on infiltrating immune cells and the human protein atlas. Together, these analyses indicated that the <i>KLRB1</i> and <i>SIT1</i> genes could be used as independent prognostic factors for BC, while risk score, age, and clinical stage could be used as prognostic factors. In summary, we found that the prognosis of BC is closely related to immune regulation in the TME.
DOI: 10.6084/m9.figshare.13246932
title: Upregulation of the microRNA rno-miR-146b-5p may be involved in the development of intestinal injury through inhibition of Kruppel-like factor 4 in intestinal sepsis

description: Regulatory mechanisms of microRNAs (miRNAs) in the development of intestinal sepsis are unclear. This study investigated the role of rno-miR-146b-5p in sepsis-induced intestinal injury. A rat sepsis model was created using the cecal ligation and puncture method. The expression profiles of miRNA and mRNA in sepsis rats were examined using miRNA and mRNA sequencing; rno-miR-146b was selected for further investigation. The mimics and inhibitors of rno-miR-146b-5p were transfected into IEC-6 cells and then with or without lipopolysaccharide (LPS) treatment, and the expressions of Kruppel-like factor 4 (Klf4) and Cyclin D2 (Ccnd2) were assessed by quantitative real-time transcriptase-polymerase chain reaction (qRT-PCR) and western blotting. Next, cell counting kit-8 assay was used to detect cell viability, and scratch wound healing assay was used to assess cell migration. In sepsis rat model, crypt cell proliferation was inhibited and crypt cell apoptosis was increased. Compared with the sham control, results of miRNA and mRNA sequencing showed that there were 17 miRNAs and 1617 mRNAs that were upregulated and 123 miRNAs and 1917 mRNAs that were downregulated in the sepsis model group. The network diagrams and qRT-PCR validation indicated that rno-miR-146b-5p may inhibit the expression of Klf4. By adjusting the expression of rno-miR-146b-5p in IEC-6 cells with or without LPS treatment, we found that increased expression of rno-miR-146b-5p inhibited cell proliferation and migration and inhibited the expression of Ccnd2. rno-miR-146b-5p may play a vital role in the development of sepsis intestinal injury through targeting Klf4 expression and affecting promoter activity of Ccnd2.
DOI: 10.6084/m9.figshare.13246932.v1
title: Upregulation of the microRNA rno-miR-146b-5p may be involved in the development of intestinal injury through inhibition of Kruppel-like factor 4 in intestinal sepsis

description: Regulatory mechanisms of microRNAs (miRNAs) in the development of intestinal sepsis are unclear. This study investigated the role of rno-miR-146b-5p in sepsis-induced intestinal injury. A rat sepsis model was created using the cecal ligation and puncture method. The expression profiles of miRNA and mRNA in sepsis rats were examined using miRNA and mRNA sequencing; rno-miR-146b was selected for further investigation. The mimics and inhibitors of rno-miR-146b-5p were transfected into IEC-6 cells and then with or without lipopolysaccharide (LPS) treatment, and the expressions of Kruppel-like factor 4 (Klf4) and Cyclin D2 (Ccnd2) were assessed by quantitative real-time transcriptase-polymerase chain reaction (qRT-PCR) and western blotting. Next, cell counting kit-8 assay was used to detect cell viability, and scratch wound healing assay was used to assess cell migration. In sepsis rat model, crypt cell proliferation was inhibited and crypt cell apoptosis was increased. Compared with the sham control, results of miRNA and mRNA sequencing showed that there were 17 miRNAs and 1617 mRNAs that were upregulated and 123 miRNAs and 1917 mRNAs that were downregulated in the sepsis model group. The network diagrams and qRT-PCR validation indicated that rno-miR-146b-5p may inhibit the expression of Klf4. By adjusting the expression of rno-miR-146b-5p in IEC-6 cells with or without LPS treatment, we found that increased expression of rno-miR-146b-5p inhibited cell proliferation and migration and inhibited the expression of Ccnd2. rno-miR-146b-5p may play a vital role in the development of sepsis intestinal injury through targeting Klf4 expression and affecting promoter activity of Ccnd2.
DOI: 10.15468/dl.8wbdxz
title: Occurrence Download

description: A dataset containing 11573 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is one of (function (name, pos = -1, envir = as.environment(pos), all.names = FALSE, pattern, sorted = TRUE) \n{\n if (!missing(name)) {\n pos &lt;- tryCatch(name, error = function(e) e)\n if (inherits(pos, \"error\")) {\n name &lt;- substitute(name)\n if (!is.character(name)) \n name &lt;- deparse(name)\n warning(gettextf(\"%s converted to character string\", sQuote(name)), domain = NA)\n pos &lt;- name\n }\n }\n all.names &lt;- .Internal(ls(envir, all.names, sorted))\n if (!missing(pattern)) {\n if ((ll &lt;- length(grep(\"[\", pattern, fixed = TRUE))) && ll != length(grep(\"]\", pattern, fixed = TRUE))) {\n if (pattern == \"[\") {\n pattern &lt;- \"\\\\[\"\n warning(\"replaced regular expression pattern '[' by '\\\\\\\\['\")\n }\n else if (length(grep(\"[^\\\\\\\\]\\\\[&lt;-\", pattern))) {\n pattern &lt;- sub(\"\\\\[&lt;-\", \"\\\\\\\\\\\\[&lt;-\", pattern)\n warning(\"replaced '[&lt;-' by '\\\\\\\\[&lt;-' in regular expression pattern\")\n }\n }\n grep(pattern, all.names, value = TRUE)\n }\n else all.names\n}, Acanthoscelides macrophthalmus, Acanthoscelides obtectus, Anoplolepis gracilipes, Aulacaspis yasumatsui, Blattella germanica)",
 "BasisOfRecord is one of (Specimen, Human Observation, Observation, Living Specimen, Machine Observation, Literature Occurrence)",
 "HasCoordinate is true",
 "HasGeospatialIssue is false"
 ]
}

 The dataset includes 11573 records from 218 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0009083-260129131611470/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.f4x7tf
title: Occurrence Download

description: A dataset containing 2227 species occurrences available in GBIF matching the query:
{
 "and" : [
 "BasisOfRecord is one of (Human Observation, Machine Observation, Occurrence evidence)",
 "Country is Japan",
 "OccurrenceStatus is Present",
 "TaxonKey is Vulpes vulpes"
 ]
}

 The dataset includes 2227 records from 9 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0009084-260129131611470/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.11988903.v1
title: Improved production of recombinant <i>Rhizomucor miehei</i> lipase by coexpressing protein folding chaperones in <i>Pichia pastoris</i>, which triggered ER stress

description: <i>Rhizomucor miehei</i> lipase (RML) is a biocatalyst that widely used in laboratory and industrial. Previously, RML with a 70-amino acid propeptide (pRML) was cloned and expressed in <i>P. pastori</i><i>s</i>. Recombinant strains with (strain containing 4-copy <i>prml</i>) and without ER stress (strain containing 2-copy <i>prml</i>) were obtained. However, the effective expression of pRML in <i>P. pastoris</i> by coexpressing ER-related elements in pRML-produced strain with or without ER stress has not been reported to date. In this study, an efficient way to produce functional pRML was explored in <i>P. pastoris</i>. The coexpression of protein folding chaperones, including <i>PDI</i> and <i>ERO1</i>, in different strains with or without ER stress, was investigated. <i>PDI</i> overexpression only increased pRML production in 4-copy strain from 705 U/mL to 1430 U/mL because it alleviated the protein folded stress, increased the protein concentration from 0.56  mg/mL to 0.65 mg/mL, and improved enzyme-specific activity from 1238 U/mg to 2186 U/mg. However, <i>PDI</i> coexpression could not improve pRML production in the 2-copy strain because it increased protein folded stress, while <i>ERO1</i> coexpression in the two strains all had a negative effect on pRML expression. We also investigated the effect of the propeptide on the substrate specificity and the condition for pRML enzyme powder preparation. Results showed that the relative activity exceeded 80% when the substrates C8–C10 were detected at 35°C and pH 6, and C8–C12 at 45°C and pH 8. The optimal enzyme powder preparation pH was 7, and the maximum recovery rate for pRML was 73.19%.
DOI: 10.6084/m9.figshare.13122078
title: A new metabolic signature contributes to disease progression and predicts worse survival in melanoma

description: Metabolic reprogramming is a common hallmark of tumor cells and is a crucial mediator of resistance toward anticancer therapies. The pattern of a metabolism-related signature in melanoma remains unknown. Here, we explored the role of a multi-metabolism-related gene signature in melanoma.We used the training and validation sets to develop a multi-metabolism-related gene signature. Cox regression analysis and the least absolute shrinkage and selection operator (LASSO) method were used for constructing a model. The predictive role of the metabolic signature with clinicopathological features of melanoma was also analyzed. Functional analysis of this metabolic signature was also investigated.A ten metabolism-related gene signature was identified and can stratify melanoma into high- and low- risk groups. The signature was correlated with progressive T stage, Breslow thickness, Clark level, and worse survival (all <i>Ps</i>&lt; 0.01). This metabolic signature was shown as an independent prognostic factor and was also a predictive indicator for worse survival in various clinical and molecular features of melanoma. Furthermore, the metabolic signature was implicated in immune responses such as the regulation of T cell activation and cytokine activity. The metabolic signaturewas associated with the progression and worse survival of melanoma. Our study offered a valuable metabolism-targeted therapy approach for melanoma.
DOI: 10.6084/m9.figshare.13122078.v1
title: A new metabolic signature contributes to disease progression and predicts worse survival in melanoma

description: Metabolic reprogramming is a common hallmark of tumor cells and is a crucial mediator of resistance toward anticancer therapies. The pattern of a metabolism-related signature in melanoma remains unknown. Here, we explored the role of a multi-metabolism-related gene signature in melanoma.We used the training and validation sets to develop a multi-metabolism-related gene signature. Cox regression analysis and the least absolute shrinkage and selection operator (LASSO) method were used for constructing a model. The predictive role of the metabolic signature with clinicopathological features of melanoma was also analyzed. Functional analysis of this metabolic signature was also investigated.A ten metabolism-related gene signature was identified and can stratify melanoma into high- and low- risk groups. The signature was correlated with progressive T stage, Breslow thickness, Clark level, and worse survival (all <i>Ps</i>&lt; 0.01). This metabolic signature was shown as an independent prognostic factor and was also a predictive indicator for worse survival in various clinical and molecular features of melanoma. Furthermore, the metabolic signature was implicated in immune responses such as the regulation of T cell activation and cytokine activity. The metabolic signaturewas associated with the progression and worse survival of melanoma. Our study offered a valuable metabolism-targeted therapy approach for melanoma.
DOI: 10.6084/m9.figshare.13169436
title: Prognostic and clinical significance of long non-coding RNA SNHG12 expression in various cancers

description: Recently, increasing studies suggested that lncRNA SNHG12 was aberrantly expressed in kinds of cancers. However, definite prognostic value of SNHG12 remains unclear. We conducted this meta-analysis to evaluate the association between SNHG12 expression level and cancer prognosis. A literature retrieval was conducted by searching kinds of databases. The meta-analysis was performed by using Revman 5.2 and Stata 12.0 software. Besides, The Cancer Genome Atlas dataset was analyzed to validate the results in our meta-analysis via using Gene Expression Profiling Interactive Analysis. The pooled results showed that high SNHG12 expression significantly indicated worse overall survival and recurrence-free survival. Tumor type, sample size, survival analysis method, and cutoff value did not alter SNHG12 prognosis value according to stratified analysis results. Additionally, higher expression of SNHG12 suggested unfavorable clinicopathological outcomes including larger tumor size, lymph node metastasis, distant metastasis, and advanced clinical stage. Online cross-validation in TCGA dataset further indicated that cancer patients with upregulated SNHG12 expression had worse overall survival and disease-free survival. Therefore, elevated SNHG12 expression was associated with poor survival and unfavorable clinical outcomes in various cancers, and therefore might be a potential prognostic biomarker in human cancers. <b>Abbreviations</b> Akt: protein kinase B; CESC: cervical squamous cell carcinoma and endocervical adenocarcinoma; ceRNA: competitive endogenous RNA; CNKI: China National Knowledge Infrastructure; CI: confidence interval; CCNE1: cyclin E1; COAD: colon adenocarcinoma; DM: distant metastasis; DFS: disease-free survival; EMT: epithelial–mesenchymal transition; FISH: fluorescence in situ hybridization; FIGO: the International Federation of Gynecology and Obstetrics; GEPIA: Gene Expression Profiling Interactive Analysis; HR: hazard ratio; HIFα: hypoxia-inducible factor 1 α; KIRC: kidney renal clear cell carcinoma; KIRP: kidney renal papillary cell carcinoma; LIHC: hepatocellular carcinoma; LNM: lymph node metastasis; mTOR: mechanistic target of rapamycin kinase; MMP-9: matrix metalloproteinase 9; MCL1: myeloid cell leukemia 1; MLK3: mixed-lineage protein kinase 3; N/A: not available; NOS: Newcastle-Ottawa Scale; OR: odd ratio; OS: overall survival; PSA: prostate-specific antigen; PI3K: phosphoinositide 3-kinase; qRT-PCR: quantitative real-time polymerase chain reaction; READ: rectum adenocarcinoma; RFS: recurrence-free survival; SARC: sarcoma; SNHG12: small nucleolar RNA host gene 12; STAT3: signal transducer and activator of transcription 3; SOX4: SRY-box transcription factor 4; SOX5: SRY-box transcription factor 5; STAD: stomach adenocarcinoma; TCGA: The Cancer Genome Atlas; TNM: tumor node metastasis; WWP1: WW domain-containing E3 ubiquitin protein ligase 1; WHO grade: World Health Organization grade; ZEB2: zinc finger E-box-binding homeobox 2