cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.11313629
title: Effect of Artemisia apiacea Hance on growth performance, cecal opportunistic bacteria, and microbicidal peptides in rabbits

description: ABSTRACT This study aimed to investigate the effect of Artemisia apiacea Hance supplementation on growth performance, cecal opportunistic bacteria, and antimicrobial defense using 120 rabbits. There were four experimental diets containing a control and A. apiacea Hance added at doses of 25, 50, and 75 g kg−1 of feed. The trial lasted for 70 days. The results showed that diets supplemented with A. apiacea Hance improved feed intake, body weight gain, and feed efficiency. Linear and quadratic responses were found between feed intake and herbal meal doses. For cecal opportunistic pathogenic bacteria, compared with the control treatment, the herb decreased cecal C. perfringens, Gram-negative bacteria, and Salmonella spp. by 9.5 to 56.8%. Linear responses of herb doses were found on the four bacteria and a quadratic response on Salmonella spp. In addition, the herb increased the mRNA levels by 12.6 to 57.8% of cecal defensive peptides, including neutrophil peptide defensing-3a, regenerating family member-3 gamma defensin beta-1, and galectin-4. These genes linearly responded to the herb doses. The obtained data suggest that A. apiacea Hance is effective to improve animal growth by beneficially regulating gut opportunistic bacteria and microbicidal peptide activity.
DOI: 10.6084/m9.figshare.11313629.v1
title: Effect of Artemisia apiacea Hance on growth performance, cecal opportunistic bacteria, and microbicidal peptides in rabbits

description: ABSTRACT This study aimed to investigate the effect of Artemisia apiacea Hance supplementation on growth performance, cecal opportunistic bacteria, and antimicrobial defense using 120 rabbits. There were four experimental diets containing a control and A. apiacea Hance added at doses of 25, 50, and 75 g kg−1 of feed. The trial lasted for 70 days. The results showed that diets supplemented with A. apiacea Hance improved feed intake, body weight gain, and feed efficiency. Linear and quadratic responses were found between feed intake and herbal meal doses. For cecal opportunistic pathogenic bacteria, compared with the control treatment, the herb decreased cecal C. perfringens, Gram-negative bacteria, and Salmonella spp. by 9.5 to 56.8%. Linear responses of herb doses were found on the four bacteria and a quadratic response on Salmonella spp. In addition, the herb increased the mRNA levels by 12.6 to 57.8% of cecal defensive peptides, including neutrophil peptide defensing-3a, regenerating family member-3 gamma defensin beta-1, and galectin-4. These genes linearly responded to the herb doses. The obtained data suggest that A. apiacea Hance is effective to improve animal growth by beneficially regulating gut opportunistic bacteria and microbicidal peptide activity.
DOI: 10.6084/m9.figshare.22323739
title: Full-Stokes polarization multispectral images (FSPMI) dataset

description: The processed image data of all 67 objects is packaged into “FSPMI dataset.zip”. The image data for each object is stored separately in a file labeled as “Object_xx.mat”. For example, the file labeled as “Object_01.mat” stores image data for the first object. The data in each file includes a set of spectral bands, five sets of preprocessed images, four sets of Stokes images, two sets of polarization angle images and three sets of polarization degree images.
DOI: 10.6084/m9.figshare.10265120
title: Cerebrospinal fluid proteomics and biological heterogeneity in Alzheimer’s disease: A literature review

description: Alzheimer’s disease (AD) is the most common cause of dementia and is characterized by aggregation of amyloid and tau proteins in the brain. Results from genetic studies suggest that the pathophysiology underlying AD is complex, but studying this complexity in patients remains difficult. The cerebrospinal fluid (CSF) proteome contains a large number of proteins that can reflect ongoing biological processes. Proteomics techniques can be used to measure many proteins simultaneously in individual patients and may therefore provide an opportunity to study AD disease mechanisms. Here, we review the CSF proteomics literature to identify proteins consistently associated with AD, and perform pathway analyses on these proteins to study which biological processes may be involved in the disease. We performed a literature search of studies that investigated CSF proteomic alterations related to AD. We included original research articles when they measured at least 10 proteins in (antemortem) CSF in at least 10 individuals with AD, mild cognitive impairment (MCI) or controls. We examined if proteins were consistently related to AD, defined as consistent increase or decrease in AD vs. controls across studies. Next, we used the proteins identified as input to pathway analyses using Reactome to investigate which biological processes were enriched. In total, 29 studies were included that investigated AD-related changes to the CSF proteome, including a total of 1434 individuals with AD (of whom 47.1% had a CSF biomarker profile and 9.6% a postmortem examination consistent with AD) and 1380 controls. The studies reported 1 to 138 proteins associated with AD, of which 97 proteins were reported by two or more studies. Among proteins that were measured in more than one study, 27 (27.8%) showed consistent increases, 15 (15.5%) consistent decreases and 55 (56.7%) had contrasting results. Pathway analyses showed that AD-related proteins were enriched for hemostasis, lipoprotein and extracellular matrix pathways. These results indicate that proteomic alterations in CSF associated with AD reflect involvement of various biological pathways. The frequent occurrence of inconsistent protein level changes reported by different studies suggests that additional biological and/or (pre)analytical factors may influence the CSF proteome in AD, which should be further investigated in order to improve understanding of the biological complexity underlying AD.
DOI: 10.6084/m9.figshare.22323739.v1
title: Full-Stokes polarization multispectral images (FSPMI) dataset

description: The processed image data of all 67 objects is packaged into “FSPMI dataset.zip”. The image data for each object is stored separately in a file labeled as “Object_xx.mat”. For example, the file labeled as “Object_01.mat” stores image data for the first object. The data in each file includes a set of spectral bands, five sets of preprocessed images, four sets of Stokes images, two sets of polarization angle images and three sets of polarization degree images.
DOI: 10.6084/m9.figshare.10265156
title: STYK1 promotes autophagy through enhancing the assembly of autophagy-specific class III phosphatidylinositol 3-kinase complex I

description: Macroautophagy/autophagy plays key roles in development, oncogenesis, and cardiovascular and metabolic diseases. Autophagy-specific class III phosphatidylinositol 3-kinase complex I (PtdIns3K-C1) is essential for autophagosome formation. However, the regulation of this complex formation requires further investigation. Here, we discovered that STYK1 (serine/threonine/tyrosine kinase 1), a member of the receptor tyrosine kinases (RTKs) family, is a new upstream regulator of autophagy. We discovered that STYK1 facilitated autophagosome formation in human cells and zebrafish, which was characterized by elevated LC3-II and lowered SQSTM1/p62 levels and increased puncta formation by several marker proteins, such as ATG14, WIPI1, and ZFYVE1. Moreover, we observed that STYK1 directly binds to the PtdIns3K-C1 complex as a homodimer. The binding with this complex was promoted by Tyr191 phosphorylation, by means of which the kinase activity of STYK1 was elevated. We also demonstrated that STYK1 elevated the serine phosphorylation of BECN1, thereby decreasing the interaction between BECN1 and BCL2. Furthermore, we found that STYK1 preferentially facilitated the assembly of the PtdIns3K-C1 complex and was required for PtdIns3K-C1 complex kinase activity. Taken together, our findings provide new insights into autophagy induction and reveal evidence of novel crosstalk between the components of RTK signaling and autophagy. <b>Abbreviations</b>: AICAR: 5-aminoimidazole-4-carboxamide ribonucleotide; AMPK: adenosine 5‘-monophosphate (AMP)-activated protein kinase; ATG: autophagy related; ATP: adenosine triphosphate; BCL2: BCL2 apoptosis regulator; BECN1: beclin 1; Bre A: brefeldin A; Co-IP: co-immunoprecipitation; CRISPR: clustered regularly interspaced short palindromic repeats; DAPI: 4′,6-diamidino-2-phenylindole; EBSS: Earle’s balanced salt solution; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFP: green fluorescent protein; GSEA: gene set enrichment analysis; MAP1LC3/LC3, microtubule associated protein 1 light chain 3; MAPK8/JNK1: mitogen-activated protein kinase 8; mRFP: monomeric red fluorescent protein; MTOR: mechanistic target of rapamycin kinase; MTT: 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; PIK3R4: phosphoinositide-3-kinase regulatory subunit 4; qRT-PCR: quantitative reverse transcription PCR; RACK1: receptor for activated C kinase 1; RUBCN: rubicon autophagy regulator; siRNA: small interfering RNA; SQSTM1: sequestosome 1; STYK1/NOK: serine/threonine/tyrosine kinase 1; TCGA: The Cancer Genome Atlas; Ub: ubiquitin; ULK1: unc-51 like autophagy activating kinase 1; UVRAG: UV radiation resistance associated; WIPI1: WD repeat domain, phosphoinositide interacting 1; ZFYVE1: zinc finger FYVE-type containing 1
DOI: 10.6084/m9.figshare.10265156.v1
title: STYK1 promotes autophagy through enhancing the assembly of autophagy-specific class III phosphatidylinositol 3-kinase complex I

description: Macroautophagy/autophagy plays key roles in development, oncogenesis, and cardiovascular and metabolic diseases. Autophagy-specific class III phosphatidylinositol 3-kinase complex I (PtdIns3K-C1) is essential for autophagosome formation. However, the regulation of this complex formation requires further investigation. Here, we discovered that STYK1 (serine/threonine/tyrosine kinase 1), a member of the receptor tyrosine kinases (RTKs) family, is a new upstream regulator of autophagy. We discovered that STYK1 facilitated autophagosome formation in human cells and zebrafish, which was characterized by elevated LC3-II and lowered SQSTM1/p62 levels and increased puncta formation by several marker proteins, such as ATG14, WIPI1, and ZFYVE1. Moreover, we observed that STYK1 directly binds to the PtdIns3K-C1 complex as a homodimer. The binding with this complex was promoted by Tyr191 phosphorylation, by means of which the kinase activity of STYK1 was elevated. We also demonstrated that STYK1 elevated the serine phosphorylation of BECN1, thereby decreasing the interaction between BECN1 and BCL2. Furthermore, we found that STYK1 preferentially facilitated the assembly of the PtdIns3K-C1 complex and was required for PtdIns3K-C1 complex kinase activity. Taken together, our findings provide new insights into autophagy induction and reveal evidence of novel crosstalk between the components of RTK signaling and autophagy. <b>Abbreviations</b>: AICAR: 5-aminoimidazole-4-carboxamide ribonucleotide; AMPK: adenosine 5‘-monophosphate (AMP)-activated protein kinase; ATG: autophagy related; ATP: adenosine triphosphate; BCL2: BCL2 apoptosis regulator; BECN1: beclin 1; Bre A: brefeldin A; Co-IP: co-immunoprecipitation; CRISPR: clustered regularly interspaced short palindromic repeats; DAPI: 4′,6-diamidino-2-phenylindole; EBSS: Earle’s balanced salt solution; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFP: green fluorescent protein; GSEA: gene set enrichment analysis; MAP1LC3/LC3, microtubule associated protein 1 light chain 3; MAPK8/JNK1: mitogen-activated protein kinase 8; mRFP: monomeric red fluorescent protein; MTOR: mechanistic target of rapamycin kinase; MTT: 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; PIK3R4: phosphoinositide-3-kinase regulatory subunit 4; qRT-PCR: quantitative reverse transcription PCR; RACK1: receptor for activated C kinase 1; RUBCN: rubicon autophagy regulator; siRNA: small interfering RNA; SQSTM1: sequestosome 1; STYK1/NOK: serine/threonine/tyrosine kinase 1; TCGA: The Cancer Genome Atlas; Ub: ubiquitin; ULK1: unc-51 like autophagy activating kinase 1; UVRAG: UV radiation resistance associated; WIPI1: WD repeat domain, phosphoinositide interacting 1; ZFYVE1: zinc finger FYVE-type containing 1
DOI: 10.6084/m9.figshare.25231922
title: DevEval

description: A Code Generation Benchmark on Practical Software Projects
DOI: 10.6084/m9.figshare.11313926
title: Change in Functional Moderate Mitral Regurgitation after Aortic Valve Replacement

description: Abstract Objective: To evaluate the changes of the mitral valve geometrics and the degrees of moderate mitral regurgitation (MR) in patients undergoing aortic valve replacement (AVR) for aortic stenosis (AS). Methods: A retrospective analysis study of intraoperative transesophageal echocardiography (TEE) and postoperative transthoracic echocardiography (TTE) was performed in 49 patients diagnosed with pure AS combined with moderate MR, who underwent AVR from January 2013 to December 2017. TEE was used to evaluate the direct geometric changes of the mechanical effects on mitral annulus after AVR. TTE was used to evaluate the changes of MR after operation. All patients underwent TTE during the midterm follow-up. The mean follow-up time was 40.21 months. Results: All of the 49 patients had moderate MR. Anterolateral-posteromedial diameter, anterior-posterior diameter, and mitral annular area were significantly reduced after AVR, while no significant changes were found in the intraoperative left ventricular loading conditions before and after AVR. The degree of mitral valve regurgitation, left ventricular size, left atrial size, left ventricular end-diastolic volume, and left ventricular to aortic pressure gradient were significantly reduced before discharge, and midterm follow-up showed good results. Conclusion: This study supports the belief that aortic outflow tract obstruction and an actual mechanical compression of the anterior mitral annulus after AVR would cause reduction in MR. Ventricular remodeling would also cause reduction in MR with time going on. Patients with AS, especially young patients with moderate MR, were most likely to benefit from AVR in early time.
DOI: 10.6084/m9.figshare.11313926.v1
title: Change in Functional Moderate Mitral Regurgitation after Aortic Valve Replacement

description: Abstract Objective: To evaluate the changes of the mitral valve geometrics and the degrees of moderate mitral regurgitation (MR) in patients undergoing aortic valve replacement (AVR) for aortic stenosis (AS). Methods: A retrospective analysis study of intraoperative transesophageal echocardiography (TEE) and postoperative transthoracic echocardiography (TTE) was performed in 49 patients diagnosed with pure AS combined with moderate MR, who underwent AVR from January 2013 to December 2017. TEE was used to evaluate the direct geometric changes of the mechanical effects on mitral annulus after AVR. TTE was used to evaluate the changes of MR after operation. All patients underwent TTE during the midterm follow-up. The mean follow-up time was 40.21 months. Results: All of the 49 patients had moderate MR. Anterolateral-posteromedial diameter, anterior-posterior diameter, and mitral annular area were significantly reduced after AVR, while no significant changes were found in the intraoperative left ventricular loading conditions before and after AVR. The degree of mitral valve regurgitation, left ventricular size, left atrial size, left ventricular end-diastolic volume, and left ventricular to aortic pressure gradient were significantly reduced before discharge, and midterm follow-up showed good results. Conclusion: This study supports the belief that aortic outflow tract obstruction and an actual mechanical compression of the anterior mitral annulus after AVR would cause reduction in MR. Ventricular remodeling would also cause reduction in MR with time going on. Patients with AS, especially young patients with moderate MR, were most likely to benefit from AVR in early time.
DOI: 10.6084/m9.figshare.11313929
title: Effect of Simulated Geomagnetic Activity on Myocardial Ischemia/Reperfusion Injury in Rats

description: Abstract Objective: To study the response of myocardial ischemia/reperfusion injury (MI/RI) in rats to simulated geomagnetic activity. Methods: In a simulated strong geomagnetic outbreak, the MI/RI rat models were radiated, and their area of myocardial infarction, hemodynamic parameters, creatine kinase (CK), lactate dehydrogenase (LDH), melatonin, and troponin I values were measured after a 24-hour intervention. Results: Our analysis indicates that the concentrations of troponin I in the geomagnetic shielding+operation group were lower than in the radiation+operation group (P&lt;0.05), the concentrations of melatonin in the shielding+operation group and normal+operation group were higher than in the radiation + operation group (P&lt;0.01), and the concentrations of CK in the shielding + operation group were lower than in the radiation + operation group and normal + operation group (P&lt;0.05). Left ventricular developed pressure (LVDP) and ± dP/dtmax in the radiation+operation group were lower than in the shielding + operation group and normal+operation group (P&lt;0.01). Left ventricular end-diastolic pressure (LEVDP) in the shielding + operation group was higher than in the normal + operation group (P&lt;0.05). There was no significant difference in area of myocardial infarction and LDH between the shielding + operation group and the radiation + operation group. Conclusion: Our data suggest that geomagnetic activity is important in regulating myocardial reperfusion injury. The geomagnetic shielding has a protective effect on myocardial injury, and the geomagnetic radiation is a risk factor for aggravating the cardiovascular and cerebrovascular diseases.
DOI: 10.6084/m9.figshare.11313929.v1
title: Effect of Simulated Geomagnetic Activity on Myocardial Ischemia/Reperfusion Injury in Rats

description: Abstract Objective: To study the response of myocardial ischemia/reperfusion injury (MI/RI) in rats to simulated geomagnetic activity. Methods: In a simulated strong geomagnetic outbreak, the MI/RI rat models were radiated, and their area of myocardial infarction, hemodynamic parameters, creatine kinase (CK), lactate dehydrogenase (LDH), melatonin, and troponin I values were measured after a 24-hour intervention. Results: Our analysis indicates that the concentrations of troponin I in the geomagnetic shielding+operation group were lower than in the radiation+operation group (P&lt;0.05), the concentrations of melatonin in the shielding+operation group and normal+operation group were higher than in the radiation + operation group (P&lt;0.01), and the concentrations of CK in the shielding + operation group were lower than in the radiation + operation group and normal + operation group (P&lt;0.05). Left ventricular developed pressure (LVDP) and ± dP/dtmax in the radiation+operation group were lower than in the shielding + operation group and normal+operation group (P&lt;0.01). Left ventricular end-diastolic pressure (LEVDP) in the shielding + operation group was higher than in the normal + operation group (P&lt;0.05). There was no significant difference in area of myocardial infarction and LDH between the shielding + operation group and the radiation + operation group. Conclusion: Our data suggest that geomagnetic activity is important in regulating myocardial reperfusion injury. The geomagnetic shielding has a protective effect on myocardial injury, and the geomagnetic radiation is a risk factor for aggravating the cardiovascular and cerebrovascular diseases.
DOI: 10.6084/m9.figshare.17079491.v1
title: Additional file 1 of U2-VC: one-shot voice conversion using two-level nested U-structure

description: Additional file 1 Demo samples of the proposed approach. The conversion samples are available on the demo page: https://tjulfk.github.io/U2VC/ .
DOI: 10.6084/m9.figshare.23577069.v1
title: Source_data_for_non_volatile_polarization_switching

description: The data is used to support the conclusion in the manuscript
 entitled "Non-volatile electrical polarization switching via domain wall release in 3R-MoS2 bilayer"
DOI: 10.6084/m9.figshare.10265387
title: A Meta-Analysis of Cardiovascular Events Associated with Intravitreal Anti-VEGF Treatment in Patients with Retinal Vein Occlusion

description: <b>Purpose</b>: Retinal vein occlusion is associated with an increased risk of cardiovascular diseases. Anti-vascular endothelial growth factor has been widely used as a treatment option. However, the systemic safety of intravitreal anti-vascular endothelial growth factor for retinal vein occlusion patients is still unclear. <b>Materials and Methods</b>: A meta-analysis was conducted to investigate all randomized controlled trials published up to February 2019 of retinal vein occlusion patients who received intravitreal anti-vascular endothelial growth factor vs. control treatments. Fixed effect models were used and results were reported as odds ratios and 95% confidence intervals. <b>Results</b>: Eight trials that evaluated 2320 patients were retrieved. Anti-vascular endothelial growth factor did not significantly increase the risks of cardiovascular events (odds ratio,1.54; 95% confidence interval, 0.66–3.57), hypertension (odds ratio, 0.92; 95% confidence interval, 0.63–1.33), or heart rate disorders (odds ratio,1.53; 95% confidence interval, 0.37–6.28) when compared with control treatment. Subgroup analyses did not show a significant increase of cardiovascular events in aflibercept (odds ratio,1.96; 95% confidence interval, 0.44–8.81) vs. ranibizumab trials (odds ratio, 1.47; 95% confidence interval, 0.54–4.02); 0.5 mg ranibizumab trials (odds ratio, 1.73; 95% confidence interval, 0.61–4.96) vs. 0.3 mg ranibizumab trials (odds ratio, 0.70; 95% confidence interval, 0.14–3.59); nor branch retinal vein occlusion (odds ratio, 1.32; 95% confidence interval, 0.40–4.33) vs. central retinal vein occlusion trials (odds ratio, 1.93; 95% confidence interval, 0.59–6.29). <b>Conclusions</b>: Intravitreal administration of anti-vascular endothelial growth factor did not significantly increase the risks of cardiovascular events, hypertension or heart rate disorders in retinal vein occlusion patients.