cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.23119063
title: Additional file 1 of Effect of body mass index on clinical outcomes after robotic cardiac surgery: is there an obesity paradox?

description: Additional File: Clinically collected data
DOI: 10.25582/data.2022-10.2621116/2286303
title: Data for EMSL Project 51834 from October 2022
DOI: 10.25582/data.2021-09.2327528/2286304
title: Data for EMSL Project 51834 from September 2021
DOI: 10.25582/data.2022-04.2478901/2286305
title: Data for EMSL Project 51834 from April 2022
DOI: 10.6084/m9.figshare.23643302
title: The predictive value of noninvasive prenatal screening for copy number variations: a cohort study and a systematic meta-analysis

description: To assess the diagnostic accuracy of noninvasive prenatal screening (NIPS) in screening for copy number variations (CNVs). We conducted a systematic review and meta-analysis by combining our study results with those reported in other articles. We retrospectively collected the data of pregnant women with NIPS testing in the Hangzhou Women’s Hospital from December 2019 to February 2022. Simultaneously, a systematic search of PubMed, EMBASE, and Web of Science was carried out to identify all relevant peer-reviewed publications. Statistical analysis was performed based on the random-effects model to determine a pooled estimate of the positive predictive value (PPV). A total of 29 studies involving 2,667 women were included for analysis. The pooled PPV of NIPS in the detection of CNVs was 32.86% (95% confidence interval [24.61–41.64]). Statistical heterogeneity was high, while no significant publication bias was found in this meta-analysis. There were insufficient data to accurately determine sensitivity and specificity, as most studies only performed confirmatory tests on high-risk women. The PPV of NIPS in screening for CNVs was approximately 33%. Cautions should be kept in mind for the pretest guidance and subsequent after-test counseling when offering such genome-wide NIPS tests.
DOI: 10.25582/data.2021-09.2322508/2286306
title: Data for EMSL Project 51834 from September 2021
DOI: 10.25582/data.2022-09.2609822/2286307
title: Data for EMSL Project 51834 from September 2022
DOI: 10.25582/data.2021-11.2380754/2286308
title: Data for EMSL Project 51834 from November 2021
DOI: 10.6084/m9.figshare.23643302.v1
title: The predictive value of noninvasive prenatal screening for copy number variations: a cohort study and a systematic meta-analysis

description: To assess the diagnostic accuracy of noninvasive prenatal screening (NIPS) in screening for copy number variations (CNVs). We conducted a systematic review and meta-analysis by combining our study results with those reported in other articles. We retrospectively collected the data of pregnant women with NIPS testing in the Hangzhou Women’s Hospital from December 2019 to February 2022. Simultaneously, a systematic search of PubMed, EMBASE, and Web of Science was carried out to identify all relevant peer-reviewed publications. Statistical analysis was performed based on the random-effects model to determine a pooled estimate of the positive predictive value (PPV). A total of 29 studies involving 2,667 women were included for analysis. The pooled PPV of NIPS in the detection of CNVs was 32.86% (95% confidence interval [24.61–41.64]). Statistical heterogeneity was high, while no significant publication bias was found in this meta-analysis. There were insufficient data to accurately determine sensitivity and specificity, as most studies only performed confirmatory tests on high-risk women. The PPV of NIPS in screening for CNVs was approximately 33%. Cautions should be kept in mind for the pretest guidance and subsequent after-test counseling when offering such genome-wide NIPS tests.
DOI: 10.25582/data.2022-10.2618017/2286309
title: Data for EMSL Project 51834 from October 2022
DOI: 10.25582/data.2022-10.2622263/2286310
title: Data for EMSL Project 51834 from October 2022
DOI: 10.6084/m9.figshare.6866264.v1
title: Molecular dynamics investigations of structural and functional changes in Bcl-2 induced by the novel antagonist BDA-366

description: Apoptosis is a fundamental biological phenomenon, in which anti- or proapoptotic proteins of the Bcl-2 family regulate a committed step. Overexpression of Bcl-2, the prototypical antiapoptotic protein in this family, is associated with therapy resistance in various human cancers. Accordingly, Bcl-2 inhibitors intended for cancer therapy have been developed, typically against the BH3 domain. Recent experimental evidences have shown that the antiapoptotic function of Bcl-2 is not immutable, and that BDA-366, a novel antagonist of the BH4 domain, converts Bcl-2 from a survival molecule to an inducer of cell death. In this study, the underlying mechanisms of this functional conversion were investigated by accelerated molecular dynamics simulation. Results revealed that Pro127 and Trp30 in the BH4 domain rotate to stabilize BDA-366 via π-π interactions, and trigger a series of significant conformational changes of the α3 helix. This rearrangement blocks the hydrophobic binding site (HBS) in the BH3 domain and further prevents binding of BH3-only proteins, which consequently allows the BH3-only proteins to activate the proapoptotic proteins. Analysis of binding free energy confirmed that BDA-366 cross-inhibits BH3-only proteins, implying negative cooperative effects across separate binding sites. The newly identified blocked conformation of the HBS along with the open to closed transition pathway revealed by this study advances the understanding of the Bcl-2 transition from antiapoptotic to proapoptotic function, and yielded new structural insights for novel drug design against the BH4 domain. Communicated by Ramaswamy H. Sarma The ability of the small molecule BDA-366 to convert Bcl-2 from an antiapoptotic to a proapoptotic molecule was investigated by accelerated molecular dynamics simulation. Results show that BDA-366 blocks or reduces the affinity of Bcl-2 for BH3-only proteins like Bid via negative cooperative effects, thereby releasing such proteins and unleashing their proapoptotic effects.
DOI: 10.6084/m9.figshare.7390769
title: Protective effects of Polygonatum sibiricum polysaccharide on acute heart failure in rats

description: Abstract Purpose: To investigate the protective effects of Polygonatum sibiricum polysaccharide (PSP) on acute heart failure (AHF) in rats. Methods: Sixty rats were randomly divided into control, model, and low-, middle- and high-dose PSP groups, 12 rats in each group. The low-, medium- and high-dose PSP groups were intragastrically administrated with 100, 200 and 400 mg/kg PSP for 5 days, respectively. On the sixth day, the AHF model was established by intraperitoneal injection of adriamycin. After 24h, the cardiac function, serum biochemical indexes, myocardial ATPase and succinate dehydrogenase levels and apoptosis related protein expressions were determined. Results: Compared with model group, in high-dose PSP group the heart rate, left ventricular systolic pressure, ±dp/dtmax, serum superoxide dismutase level, myocardial Na+-K+-ATPase, Ca2+-Mg2+-ATPase and succinate dehydrogenase levels and myocardial Bcl-2 and Caspase-3 protein expression levels were significantly increased (P&lt;0.05), the left ventricular end diastolic pressure, serum cTnI, CK-MB, TNF-α, IL-6, malondialdehyde and nitric oxide levels and myocardial Bax and cleaved Caspase-3 protein expression levels were significantly decreased (P&lt;0.05). Conclusions: Polysaccharide can prevent the acute heart failure induced by adriamycin. The mechanism may be related to its anti-oxidative stress, anti-inflammation and inhibition of cardiac myocyte apoptosis.
DOI: 10.25582/data.2021-08.2305229/2286311
title: Data for EMSL Project 51834 from August 2021
DOI: 10.6084/m9.figshare.23119033
title: Additional file 2 of Empowering biologists to decode omics data: the Genekitr R package and web server

description: Additional file 2. 1) GO CC enrichment analysis result without simplification method. 2) GO CC enrichment analysis result after simplification.
DOI: 10.6084/m9.figshare.23119033.v1
title: Additional file 2 of Empowering biologists to decode omics data: the Genekitr R package and web server

description: Additional file 2. 1) GO CC enrichment analysis result without simplification method. 2) GO CC enrichment analysis result after simplification.
DOI: 10.25582/data.2022-09.2606839/2286312
title: Data for EMSL Project 51834 from September 2022
DOI: 10.25582/data.2021-08.2305323/2286313
title: Data for EMSL Project 51834 from August 2021
DOI: 10.25582/data.2021-12.2404931/2286314
title: Data for EMSL Project 51834 from December 2021
DOI: 10.6084/m9.figshare.7390784
title: HtrA1 suppresses the growth of pancreatic cancer cells by modulating Notch-1 expression

description: Pancreatic cancer is well known to be the most deadly malignancy with the worst survival rate of all cancers. High temperature requirement factor A1 (HtrA1) plays an important role in cancer cell proliferation, migration, apoptosis, and differentiation. This study aimed to explore the function of HtrA1 in pancreatic cancer cell growth and its underlying mechanism. We found that the expression of HtrA1 was lower in pancreatic cancer tissue compared to the adjacent normal tissue. Consistently, HtrA1 levels were also decreased in two human pancreatic cancer cell lines, PANC-1 and BXPC-3. Moreover, enforced expression of HtrA1 inhibited cell viability and colony formation of PANC-1 and BXPC-3 cells. Overexpression of HtrA1 promoted apoptosis and suppressed migratory ability of tumor cells. On the contrary, siRNA-mediated knockdown of HtrA1 promoted the growth potential of pancreatic cancer cells. In addition, we found that up-regulation of HtrA1 reduced the expression of Notch-1 in pancreatic cancer cells. On the contrary, knockdown of HtrA1 increased the expression levels of Notch-1. Furthermore, overexpression of Notch-1 abolished the anti-proliferative effect of HtrA1 on pancreatic cancer cells. Taken together, our findings demonstrated that HtrA1 could inhibit pancreatic cancer cell growth via regulating Notch-1 expression, which implied that HtrA1 might be developed as a novel molecular target for pancreatic cancer therapy.
DOI: 10.25582/data.2022-09.2608857/2286315
title: Data for EMSL Project 51834 from September 2022
DOI: 10.6084/m9.figshare.7390784.v1
title: HtrA1 suppresses the growth of pancreatic cancer cells by modulating Notch-1 expression

description: Pancreatic cancer is well known to be the most deadly malignancy with the worst survival rate of all cancers. High temperature requirement factor A1 (HtrA1) plays an important role in cancer cell proliferation, migration, apoptosis, and differentiation. This study aimed to explore the function of HtrA1 in pancreatic cancer cell growth and its underlying mechanism. We found that the expression of HtrA1 was lower in pancreatic cancer tissue compared to the adjacent normal tissue. Consistently, HtrA1 levels were also decreased in two human pancreatic cancer cell lines, PANC-1 and BXPC-3. Moreover, enforced expression of HtrA1 inhibited cell viability and colony formation of PANC-1 and BXPC-3 cells. Overexpression of HtrA1 promoted apoptosis and suppressed migratory ability of tumor cells. On the contrary, siRNA-mediated knockdown of HtrA1 promoted the growth potential of pancreatic cancer cells. In addition, we found that up-regulation of HtrA1 reduced the expression of Notch-1 in pancreatic cancer cells. On the contrary, knockdown of HtrA1 increased the expression levels of Notch-1. Furthermore, overexpression of Notch-1 abolished the anti-proliferative effect of HtrA1 on pancreatic cancer cells. Taken together, our findings demonstrated that HtrA1 could inhibit pancreatic cancer cell growth via regulating Notch-1 expression, which implied that HtrA1 might be developed as a novel molecular target for pancreatic cancer therapy.
DOI: 10.25582/data.2021-12.2404852/2286316
title: Data for EMSL Project 51834 from December 2021
DOI: 10.25582/data.2021-09.2318875/2286317
title: Data for EMSL Project 51834 from September 2021
DOI: 10.25582/data.2022-09.2611170/2286318
title: Data for EMSL Project 51834 from September 2022
DOI: 10.25582/data.2021-12.2399731/2286319
title: Data for EMSL Project 51834 from December 2021
DOI: 10.25582/data.2021-11.2387565/2286320
title: Data for EMSL Project 51834 from November 2021
DOI: 10.25582/data.2021-11.2388473/2286321
title: Data for EMSL Project 51834 from November 2021
DOI: 10.6084/m9.figshare.7915175.v1
title: Additional file 1: of RNA N6-methyladenosine demethylase FTO promotes breast tumor progression through inhibiting BNIP3

description: Table S1. Primer lists used in this study. (XLSX 10 kb)
DOI: 10.25582/data.2022-10.2616449/2286322
title: Data for EMSL Project 51834 from October 2022
DOI: 10.25582/data.2022-01.2417495/2286323
title: Data for EMSL Project 51834 from January 2022
DOI: 10.25582/data.2022-09.2609515/2286324
title: Data for EMSL Project 51834 from September 2022
DOI: 10.25582/data.2021-11.2387378/2286325
title: Data for EMSL Project 51834 from November 2021
DOI: 10.25582/data.2022-04.2479127/2286326
title: Data for EMSL Project 51834 from April 2022
DOI: 10.6084/m9.figshare.7915205
title: Additional file 5: of Reprogramming histone modification patterns to coordinate gene expression in early zebrafish embryos

description: Table S4. Enriched GO and INTERPRO domains for active gene group in zebrafish. (XLSX 15 kb)
DOI: 10.25582/data.2021-10.2361356/2286327
title: Data for EMSL Project 51834 from October 2021
DOI: 10.25582/data.2022-04.2479134/2286328
title: Data for EMSL Project 51834 from April 2022
DOI: 10.25582/data.2022-10.2623095/2286329
title: Data for EMSL Project 51834 from October 2022
DOI: 10.25582/data.2021-12.2411287/2286330
title: Data for EMSL Project 51834 from December 2021
DOI: 10.6084/m9.figshare.7915202.v1
title: Additional file 4: of RNA N6-methyladenosine demethylase FTO promotes breast tumor progression through inhibiting BNIP3

description: Table S2. Differentially expressed genes in FTO-knockdown MDA-MB-231 cells. (XLSX 764 kb)
DOI: 10.25582/data.2021-09.2315111/2286331
title: Data for EMSL Project 51834 from September 2021
DOI: 10.6084/m9.figshare.23119018
title: Additional file 3 of TMT proteomics analysis reveals the mechanism of bleomycin-induced pulmonary fibrosis and effects of Ginseng honeysuckle superfine powdered tea

description: Additional file 3. Pos-neg table.
DOI: 10.25582/data.2022-09.2608764/2286332
title: Data for EMSL Project 51834 from September 2022
DOI: 10.6084/m9.figshare.5818101
title: Data and Matlab package for Using imaging photoplethysmography for heart rate estimation in non-human primates

description: Raw data for imaging photoplethysmogram extraction collected in 10 recording sessions from four rhesus monkeys and Matlab scripts for their processing.<br>For details of the study please refer to [1].<br><br>INSTRUCTIONS:<br>1. Please download the zip-archive and unpack its contents. <br>2. Please launch the script dataset_analysis.m in MATLAB to reproduce the results described in [1]. For a detailed description of the code please see [2].Matlab scripts require Matlab Wavelet Toolbox.<br><br>DATA DESCRIPTION:<br>Data of session N is placed in a folder SessionN. <br>Data for sessions 1-8 consist of four files:<br>SessionN.bin - raw color signal data in binary file, in format r1 g1 b1 r2 g2 ....;<br>SessionN_ROIdata.txt - metadata of ROI used for data color signal computing;<br>SessionN_interframeDif.txt
 - interframe differences in the video, proxy for the amount of motion. 
Format: stream of double values with a new line symbol as delimiter, use <br>a = load('SessionN_interframeDif.txt', '-ascii') to load in Matlab;SessionN_REF.csv - average reference pulse rate values for time intervals of length reported in file summary.txt.<br><br>Data for session 1 additionally contain the following files:<br>Session1RegionN.bin - raw color signal data in binary file for Section 1 with ROI different from region 3; <br>Session1RegionN_ROIdata.txt
 - metadata of ROI used for data color signal computing for Section 1 
with ROI different from region 3;<br><br>Data for sessions 2IR, 9IR and 10IR consist of three files:<br>SessionN.bin - raw "color" (effectively - monochrome) signal data in binary file, in format i1 i1 i1 i2 i2 i2 ...;<br>SessionN_ROIdata.txt - metadata of ROI used for signal computing;<br>SessionN_REF.csv - average reference pulse rate values for time intervals of length reported in file summary.txt.<br><br>REFERENCES:<br>[1] Unakafov AM, Möller S, Kagan I, Gail A, Treue S, Wolf F (2018) Using imaging photoplethysmography for heart rate estimation in non-human primates. bioRxiv. doi:10.1101/252403<br>[2] Matlab package "Imaging photoplethysmogram extraction and pulse rate estimation". https://de.mathworks.com/matlabcentral/fileexchange/67527-matlab-package--imaging-photoplethysmogram-extraction-and-pulse-rate-estimation-<br><br><br>
DOI: 10.25582/data.2021-09.2322499/2286333
title: Data for EMSL Project 51834 from September 2021
DOI: 10.6084/m9.figshare.7915286.v1
title: Additional file 2: of Integrated analysis of lncRNA and mRNA repertoires in Marekâ s disease infected spleens identifies genes relevant to resistance

description: Genomic location and classification of 1315 putative lncRNAs. (XLSX 124 kb)
DOI: 10.25582/data.2021-11.2380638/2286334
title: Data for EMSL Project 51834 from November 2021
DOI: 10.25582/data.2022-10.2617052/2286335
title: Data for EMSL Project 51834 from October 2022
DOI: 10.6084/m9.figshare.7915271
title: Additional file 1: of Integrated analysis of lncRNA and mRNA repertoires in Marekâ s disease infected spleens identifies genes relevant to resistance

description: Genomic location of 1166 newly re-assembled known lncRNAs in ALDB and NONCODE. (XLSX 196 kb)
DOI: 10.6084/m9.figshare.7390787.v1
title: Necroptosis occurs in osteoblasts during tumor necrosis factor-α stimulation and caspase-8 inhibition

description: Necroptosis is a regulated cell death mechanism. However, it is unknown whether necroptosis is involved in the death of tumor necrosis factor-α (TNF-α)-treated osteoblasts. Therefore, we conducted the study with TNF-α, Nec-1 (a specific inhibitor of necroptosis), and Z-IETD-FMK (a specific inhibitor of apoptosis) to determine whether necroptosis plays a role in the death of TNF-α-treated osteoblast cell line MC3T3-E1. Cell viability, cell death, and lactate dehydrogenase (LDH) release were assayed to evaluate cytotoxicity. Specific marker proteins receptor interacting protein kinase (RIPK3) and phosphorylated mixed lineage kinase domain-like protein (p-MLKL) for necroptosis, and cleaved caspase 3 for apoptosis were detected by western blot, and mRNA was measured by quantitative real-time polymerase chain reaction (qRT-PCR). We found that TNF-α inhibited cell proliferation in a dose- and time-dependent manner. Nec-1 plus Z-IETD-FMK restored cell viability and significantly decreased LDH release. In addition, TNF-α alone increased the cell population of AV+PI−, while Z-IETD-FMK caused a shift in the cell population from AV+PI− to AV+PI+. Furthermore, TNF-α significantly increased protein cleaved caspase 3. TNF-α plus Z-IETD-FMK significantly increased the proteins RIPK3 and MLKL phosphorylation in MC3T3-E1 cells, while the changes in mRNA levels of RIPK3, MLKL, and caspase 3 were not consistent with the changes in the corresponding protein expression levels. In conclusion, TNF-α induced preferentially apoptosis in osteoblast cell line and necroptosis played a decisive role when TNF-α-induced death was inhibited by the inhibitor of apoptosis. Combined treatment with Nec-1 and Z-IETD-FMK protected mouse osteoblasts from death induced by TNF-α.
DOI: 10.6084/m9.figshare.7915313
title: Additional file 7: of Integrated analysis of lncRNA and mRNA repertoires in Marekâ s disease infected spleens identifies genes relevant to resistance

description: Gene Significance, Module Membership, and P-value of protein coding genes and lncRNAs in WGCNA co-expression network. MM1 (Module Membership between gene and cluster 1); P_MM1 (P-value of each MM1); GS (Gene Significance); PG (P-value of each Gene Significance). (XLSX 3957 kb)
DOI: 10.25582/data.2022-09.2610324/2286336
title: Data for EMSL Project 51834 from September 2022
DOI: 10.6084/m9.figshare.7390865.v1
title: Apoptotic mechanisms in rabbits with blast-induced acute lung injury

description: Abstract Purpose: To investigate the apoptotic mechanisms in rabbits with blast-induced acute lung injury (ALI). Methods: A total of 40 rabbits were randomly divided into a blank control group (A, n=10) and an experimental group (EXP, n=30). Explosion-induced chest-ALI models were prepared and sampled at different time points (4, 12, and 24h after modeling, T1-T3) to test the lung dry weight/wet weight ratio (W/D) and arterial oxygen pressure (PaO2), apoptosis of lung tissue by the TUNEL assay, and Caspase-3, Bax, and Bcl-2 levels by immunohistochemical analysis. Furthermore, lung tissue was sampled to observe pathological morphology by microscopy. Results: Under a light microscope, Group EXP exhibited obvious edema in the pulmonary interstitial substance and alveoli, a large number of red blood cells, inflammatory cells, and serous exudation in the alveolar cavity, as well as thickening of the pulmonary interstitial fluid. Compared to Group A, the W/D ratio was significantly increased in Group EXP (P&lt;0.01), while PaO2 was significantly reduced (P&lt;0.01). The apoptosis index was significantly increased (P&lt;0.01), and caspase-3 and Bax/Bcl-2 levels were increased (P&lt;0.01). Conclusion: Apoptosis plays an important role in the occurrence and development of acute lung injury in rabbits by participating in lung injury and promoting the progression of ALI.