cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1568367.v2
title: Late Palaeozoic <sup>40</sup>Ar/<sup>39</sup>Ar ages of the HP-LT metamorphic rocks from the Kekesu Valley, Chinese southwestern Tianshan: new constraints on exhumation tectonics

description: Although numerous ages have been obtained for the Chinese southwestern Tianshan high pressure/ultrahigh pressure-low temperature (HP/UHP-LT) metamorphic belt in the past two decades, its exhumation history is still controversial. The poor age constraint was related to the appealing low metamorphic temperatures and excess Ar commonly present under HP/UHP conditions. This study aims to provide new age constraints on the orogen’s exhumation by obtaining <sup>40</sup>Ar/<sup>39</sup>Ar mica ages using the conventional step-heating technique, with emphasis on the avoidance of excess Ar contamination. From a cross section along the Kekesu Valley, four samples, three from the HP-LT metamorphic belt (TK050, TK051, and TK081) and one from the southern margin of the low pressure metamorphic belt (TK097), were selected for <sup>40</sup>Ar/<sup>39</sup>Ar dating. Phengites from garnet glaucophane schist TK050 and the surrounding rock garnet phengite schist TK051 yield comparable plateau ages of 321.4 ± 1.6 and 318.6 ± 1.6 Ma, respectively, while epidote mica schist TK081 gives a younger plateau age of 293.3 ± 1.5 Ma. Considering the chemical compositions of phengites, mineral assemblages, and microstructures in the thin slices, we suppose that the former represents the time the HP rocks retrograded from the peak stage (eclogite facies) to the (epidote)-blueschist facies, whereas the latter reflects greenschist facies overprinting. Biotite and muscovite from two-mica quartzite TK097 give similar plateau ages of 253.0 ± 1.3 and 247.1 ± 1.2 Ma, interpreted to date movement on the post collisional transcrustal South Nalati ductile shear zone. By combining our new ages with published data, a two-stage exhumation model is suggested for the Chinese southwestern Tianshan HP/UHP-LT metamorphic belt: initial fast exhumation to a depth of about 30–35 km by ~320 Ma was followed by relatively slow (~1 mm year<sup>–1</sup>) uplift to ~10 km by ~293 Ma.
DOI: 10.6084/m9.figshare.1568367.v1
title: Late Palaeozoic <sup>40</sup>Ar/<sup>39</sup>Ar ages of the HP-LT metamorphic rocks from the Kekesu Valley, Chinese southwestern Tianshan: new constraints on exhumation tectonics

description: Although numerous ages have been obtained for the Chinese southwestern Tianshan high pressure/ultrahigh pressure-low temperature (HP/UHP-LT) metamorphic belt in the past two decades, its exhumation history is still controversial. The poor age constraint was related to the appealing low metamorphic temperatures and excess Ar commonly present under HP/UHP conditions. This study aims to provide new age constraints on the orogen’s exhumation by obtaining <sup>40</sup>Ar/<sup>39</sup>Ar mica ages using the conventional step-heating technique, with emphasis on the avoidance of excess Ar contamination. From a cross section along the Kekesu Valley, four samples, three from the HP-LT metamorphic belt (TK050, TK051, and TK081) and one from the southern margin of the low pressure metamorphic belt (TK097), were selected for <sup>40</sup>Ar/<sup>39</sup>Ar dating. Phengites from garnet glaucophane schist TK050 and the surrounding rock garnet phengite schist TK051 yield comparable plateau ages of 321.4 ± 1.6 and 318.6 ± 1.6 Ma, respectively, while epidote mica schist TK081 gives a younger plateau age of 293.3 ± 1.5 Ma. Considering the chemical compositions of phengites, mineral assemblages, and microstructures in the thin slices, we suppose that the former represents the time the HP rocks retrograded from the peak stage (eclogite facies) to the (epidote)-blueschist facies, whereas the latter reflects greenschist facies overprinting. Biotite and muscovite from two-mica quartzite TK097 give similar plateau ages of 253.0 ± 1.3 and 247.1 ± 1.2 Ma, interpreted to date movement on the post collisional transcrustal South Nalati ductile shear zone. By combining our new ages with published data, a two-stage exhumation model is suggested for the Chinese southwestern Tianshan HP/UHP-LT metamorphic belt: initial fast exhumation to a depth of about 30–35 km by ~320 Ma was followed by relatively slow (~1 mm year<sup>–1</sup>) uplift to ~10 km by ~293 Ma.
DOI: 10.6084/m9.figshare.1568410
title: Influence of the R823W mutation on the interaction of the ANKS6–ANKS3: insights from molecular dynamics simulation and free energy analysis

description: The sterile alpha motif (SAM) domain of the protein ANKS6, a protein–protein interaction domain, is responsible for autosomal dominant polycystic kidney disease. Although the disease is the result of the R823W point mutation in the SAM domain of the protein ANKS6, the molecular details are still unclear. We applied molecular dynamics simulations, the principal component analysis, and the molecular mechanics Poisson–Boltzmann surface area binding free energy calculation to explore the structural and dynamic effects of the R823W point mutation on the complex ANKS6–ANKS3 (PDB ID: 4NL9) in comparison to the wild proteins. The energetic analysis presents that the wild type has a more stable structure than the mutant. The R823W point mutation not only disrupts the structure of the ANKS6 SAM domain but also negatively affects the interaction of the ANKS6–ANKS3. These results further clarify the previous experiments to understand the ANKS6–ANKS3 interaction comprehensively. In summary, this study would provide useful suggestions to understand the interaction of these proteins and their fatal action on mediating kidney function.
DOI: 10.6084/m9.figshare.1568410.v2
title: Influence of the R823W mutation on the interaction of the ANKS6–ANKS3: insights from molecular dynamics simulation and free energy analysis

description: The sterile alpha motif (SAM) domain of the protein ANKS6, a protein–protein interaction domain, is responsible for autosomal dominant polycystic kidney disease. Although the disease is the result of the R823W point mutation in the SAM domain of the protein ANKS6, the molecular details are still unclear. We applied molecular dynamics simulations, the principal component analysis, and the molecular mechanics Poisson–Boltzmann surface area binding free energy calculation to explore the structural and dynamic effects of the R823W point mutation on the complex ANKS6–ANKS3 (PDB ID: 4NL9) in comparison to the wild proteins. The energetic analysis presents that the wild type has a more stable structure than the mutant. The R823W point mutation not only disrupts the structure of the ANKS6 SAM domain but also negatively affects the interaction of the ANKS6–ANKS3. These results further clarify the previous experiments to understand the ANKS6–ANKS3 interaction comprehensively. In summary, this study would provide useful suggestions to understand the interaction of these proteins and their fatal action on mediating kidney function.
DOI: 10.6084/m9.figshare.1568410.v1
title: Influence of the R823W mutation on the interaction of the ANKS6- ANKS3: Insights from molecular dynamics simulation and free energy analysis

description: The sterile alpha motif (SAM) domain of the protein ANKS6, a protein-protein interaction domain, is responsible for autosomal dominant polycystic kidney disease (ADPKD). Although the disease is the result of the R823W point mutation in the SAM domain of the protein ANKS6, the molecular details is still unclear. We applied molecular dynamics (MD) simulations, principal component analysis (PCA) and the molecular mechanics Poisson-Boltzmann surface area (MM-PBSA) binding free energy calculation to explore the structural and dynamic effects of the R823W point mutation on the complex ANKS6-ANKS3 (PDB ID: 4NL9) in comparison to the wild proteins. The energetic analysis presents that the wide type has a more stable structure than the mutant. The R823W point mutation not only disrupts the structure of the ANKS6 SAM domain but also negatively affects the interaction of the ANKS6-ANKS3. These results further clarify the previous experiments to understand the ANKS6-ANKS3 interaction comprehensively. In summary, this study would provide useful suggestions to understand the interaction of these proteins and their fatal action on mediating kidney function.
DOI: 10.6084/m9.figshare.1568415
title: Characterization of the platelet transcriptome by RNA sequencing in patients with acute myocardial infarction

description: Transcripts in platelets are largely produced in precursor megakaryocytes but remain physiologically active as platelets translate RNAs and regulate protein/RNA levels. Recent studies using transcriptome sequencing (RNA-seq) characterized the platelet transcriptome in limited number of non-diseased individuals. Here, we expand upon these RNA-seq studies by completing RNA-seq in platelets from 32 patients with acute myocardial infarction (MI). Our goals were to characterize the platelet transcriptome using a population of patients with acute MI and relate gene expression to platelet aggregation measures and ST-segment elevation MI (STEMI) (<i>n</i> = 16) vs. non-STEMI (NSTEMI) (<i>n</i> = 16) subtypes. Similar to other studies, we detected 9565 expressed transcripts, including several known platelet-enriched markers (e.g. <i>PPBP, OST4</i>). Our RNA-seq data strongly correlated with independently ascertained platelet expression data and showed enrichment for platelet-related pathways (e.g. wound response, hemostasis, and platelet activation), as well as actin-related and post-transcriptional processes. Several transcripts displayed suggestively higher (<i>FBXL4, ECHDC3, KCNE1, TAOK2, AURKB, ERG</i>, and <i>FKBP5</i>) and lower (<i>MIAT, PVRL3</i>, and <i>PZP</i>) expression in STEMI platelets compared to NSTEMI. We also identified transcripts correlated with platelet aggregation to TRAP (<i>ATP6V1G2, SLC2A3</i>), collagen (<i>CEACAM1, ITGA2</i>), and ADP (<i>PDGFB, PDGFC, ST3GAL6</i>). Our study adds to current platelet gene expression resources by providing transcriptome-wide analyses in platelets isolated from patients with acute MI. In concert with prior studies, we identify various genes for further study in regards to platelet function and acute MI. Future platelet RNA-seq studies examining more diverse sets of healthy and diseased samples will add to our understanding of platelet thrombotic and non-thrombotic functions.
DOI: 10.6084/m9.figshare.1568415.v4
title: Characterization of the platelet transcriptome by RNA sequencing in patients with acute myocardial infarction

description: Transcripts in platelets are largely produced in precursor megakaryocytes but remain physiologically active as platelets translate RNAs and regulate protein/RNA levels. Recent studies using transcriptome sequencing (RNA-seq) characterized the platelet transcriptome in limited number of non-diseased individuals. Here, we expand upon these RNA-seq studies by completing RNA-seq in platelets from 32 patients with acute myocardial infarction (MI). Our goals were to characterize the platelet transcriptome using a population of patients with acute MI and relate gene expression to platelet aggregation measures and ST-segment elevation MI (STEMI) (<i>n</i> = 16) vs. non-STEMI (NSTEMI) (<i>n</i> = 16) subtypes. Similar to other studies, we detected 9565 expressed transcripts, including several known platelet-enriched markers (e.g. <i>PPBP, OST4</i>). Our RNA-seq data strongly correlated with independently ascertained platelet expression data and showed enrichment for platelet-related pathways (e.g. wound response, hemostasis, and platelet activation), as well as actin-related and post-transcriptional processes. Several transcripts displayed suggestively higher (<i>FBXL4, ECHDC3, KCNE1, TAOK2, AURKB, ERG</i>, and <i>FKBP5</i>) and lower (<i>MIAT, PVRL3</i>, and <i>PZP</i>) expression in STEMI platelets compared to NSTEMI. We also identified transcripts correlated with platelet aggregation to TRAP (<i>ATP6V1G2, SLC2A3</i>), collagen (<i>CEACAM1, ITGA2</i>), and ADP (<i>PDGFB, PDGFC, ST3GAL6</i>). Our study adds to current platelet gene expression resources by providing transcriptome-wide analyses in platelets isolated from patients with acute MI. In concert with prior studies, we identify various genes for further study in regards to platelet function and acute MI. Future platelet RNA-seq studies examining more diverse sets of healthy and diseased samples will add to our understanding of platelet thrombotic and non-thrombotic functions.
DOI: 10.6084/m9.figshare.1568423
title: Chronic gastric electrical stimulation leads to weight loss via modulating multiple tissue neuropeptide Y, orexin, α-melanocyte-stimulating hormone and oxytocin in obese rats

description: <b><i>Objectives. </i></b>Gastric electrical stimulation (GES) has great potential for the treatment of obesity. We investigated the impact of chronic GES on the alteration of adipose tissue and the regulation of neuropeptide Y (NPY), orexin (OX), α-melanocyte-stimulating hormone (α-MSH) and oxytocin (OXT), and their receptors in several tissues. <b><i>Material and methods.</i></b> Most of the experiments included three groups of diet-induced obesity rats: (1) sham-GES (SGES); (2) GL-6mA (GES with 6 mA, 4 ms, 40 Hz, 2 s on, 3 s off at lesser curvature); and (3) SGES-PF (SGES rats receiving pair feeding to match the consumption of GL-6mA rats). Chronic GES was applied for 2 h every day for 4 weeks. During treatment with GES, food intake and body weight were monitored weekly. The alteration of epididymal fat weight, gastric emptying, and expression of peptides and their receptors in several tissues were determined. <b><i>Results.</i></b> GL-6mA was more potent than SGES-PF in decreasing body weight gain, epididymal fat tissue weight, adipocyte size and gastric emptying. Chronic GES significantly altered NPY, OX, α-MSH and OXT and their receptors in the hypothalamus, adipose tissue and stomach. <b><i>Conclusions. </i></b>Chronic GES effectively leads to weight loss by reducing food intake, fat tissue weight and gastric emptying. NPY, α-MSH, orexin and OXT, and their receptors in the hypothalamus, adipose tissue and stomach appear to be involved in the anti-obesity effects of chronic GES.
DOI: 10.6084/m9.figshare.1568423.v1
title: Chronic gastric electrical stimulation leads to weight loss via modulating multiple tissue neuropeptide Y, orexin, α-melanocyte-stimulating hormone and oxytocin in obese rats

description: <b><i>Objectives. </i></b>Gastric electrical stimulation (GES) has great potential for the treatment of obesity. We investigated the impact of chronic GES on the alteration of adipose tissue and the regulation of neuropeptide Y (NPY), orexin (OX), α-melanocyte-stimulating hormone (α-MSH) and oxytocin (OXT), and their receptors in several tissues. <b><i>Material and methods.</i></b> Most of the experiments included three groups of diet-induced obesity rats: (1) sham-GES (SGES); (2) GL-6mA (GES with 6 mA, 4 ms, 40 Hz, 2 s on, 3 s off at lesser curvature); and (3) SGES-PF (SGES rats receiving pair feeding to match the consumption of GL-6mA rats). Chronic GES was applied for 2 h every day for 4 weeks. During treatment with GES, food intake and body weight were monitored weekly. The alteration of epididymal fat weight, gastric emptying, and expression of peptides and their receptors in several tissues were determined. <b><i>Results.</i></b> GL-6mA was more potent than SGES-PF in decreasing body weight gain, epididymal fat tissue weight, adipocyte size and gastric emptying. Chronic GES significantly altered NPY, OX, α-MSH and OXT and their receptors in the hypothalamus, adipose tissue and stomach. <b><i>Conclusions. </i></b>Chronic GES effectively leads to weight loss by reducing food intake, fat tissue weight and gastric emptying. NPY, α-MSH, orexin and OXT, and their receptors in the hypothalamus, adipose tissue and stomach appear to be involved in the anti-obesity effects of chronic GES.
DOI: 10.6084/m9.figshare.1568423.v2
title: Chronic gastric electrical stimulation leads to weight loss via modulating multiple tissue neuropeptide Y, orexin, α-melanocyte-stimulating hormone and oxytocin in obese rats

description: <b><i>Objectives. </i></b>Gastric electrical stimulation (GES) has great potential for the treatment of obesity. We investigated the impact of chronic GES on the alteration of adipose tissue and the regulation of neuropeptide Y (NPY), orexin (OX), α-melanocyte-stimulating hormone (α-MSH) and oxytocin (OXT), and their receptors in several tissues. <b><i>Material and methods.</i></b> Most of the experiments included three groups of diet-induced obesity rats: (1) sham-GES (SGES); (2) GL-6mA (GES with 6 mA, 4 ms, 40 Hz, 2 s on, 3 s off at lesser curvature); and (3) SGES-PF (SGES rats receiving pair feeding to match the consumption of GL-6mA rats). Chronic GES was applied for 2 h every day for 4 weeks. During treatment with GES, food intake and body weight were monitored weekly. The alteration of epididymal fat weight, gastric emptying, and expression of peptides and their receptors in several tissues were determined. <b><i>Results.</i></b> GL-6mA was more potent than SGES-PF in decreasing body weight gain, epididymal fat tissue weight, adipocyte size and gastric emptying. Chronic GES significantly altered NPY, OX, α-MSH and OXT and their receptors in the hypothalamus, adipose tissue and stomach. <b><i>Conclusions. </i></b>Chronic GES effectively leads to weight loss by reducing food intake, fat tissue weight and gastric emptying. NPY, α-MSH, orexin and OXT, and their receptors in the hypothalamus, adipose tissue and stomach appear to be involved in the anti-obesity effects of chronic GES.
DOI: 10.6084/m9.figshare.1568423.v3
title: Chronic gastric electrical stimulation leads to weight loss via modulating multiple tissue neuropeptide Y, orexin, α-melanocyte-stimulating hormone and oxytocin in obese rats

description: <b><i>Objectives. </i></b>Gastric electrical stimulation (GES) has great potential for the treatment of obesity. We investigated the impact of chronic GES on the alteration of adipose tissue and the regulation of neuropeptide Y (NPY), orexin (OX), α-melanocyte-stimulating hormone (α-MSH) and oxytocin (OXT), and their receptors in several tissues. <b><i>Material and methods.</i></b> Most of the experiments included three groups of diet-induced obesity rats: (1) sham-GES (SGES); (2) GL-6mA (GES with 6 mA, 4 ms, 40 Hz, 2 s on, 3 s off at lesser curvature); and (3) SGES-PF (SGES rats receiving pair feeding to match the consumption of GL-6mA rats). Chronic GES was applied for 2 h every day for 4 weeks. During treatment with GES, food intake and body weight were monitored weekly. The alteration of epididymal fat weight, gastric emptying, and expression of peptides and their receptors in several tissues were determined. <b><i>Results.</i></b> GL-6mA was more potent than SGES-PF in decreasing body weight gain, epididymal fat tissue weight, adipocyte size and gastric emptying. Chronic GES significantly altered NPY, OX, α-MSH and OXT and their receptors in the hypothalamus, adipose tissue and stomach. <b><i>Conclusions. </i></b>Chronic GES effectively leads to weight loss by reducing food intake, fat tissue weight and gastric emptying. NPY, α-MSH, orexin and OXT, and their receptors in the hypothalamus, adipose tissue and stomach appear to be involved in the anti-obesity effects of chronic GES.
DOI: 10.6084/m9.figshare.1568423.v4
title: Chronic gastric electrical stimulation leads to weight loss via modulating multiple tissue neuropeptide Y, orexin, α-melanocyte-stimulating hormone and oxytocin in obese rats

description: <b><i>Objectives. </i></b>Gastric electrical stimulation (GES) has great potential for the treatment of obesity. We investigated the impact of chronic GES on the alteration of adipose tissue and the regulation of neuropeptide Y (NPY), orexin (OX), α-melanocyte-stimulating hormone (α-MSH) and oxytocin (OXT), and their receptors in several tissues. <b><i>Material and methods.</i></b> Most of the experiments included three groups of diet-induced obesity rats: (1) sham-GES (SGES); (2) GL-6mA (GES with 6 mA, 4 ms, 40 Hz, 2 s on, 3 s off at lesser curvature); and (3) SGES-PF (SGES rats receiving pair feeding to match the consumption of GL-6mA rats). Chronic GES was applied for 2 h every day for 4 weeks. During treatment with GES, food intake and body weight were monitored weekly. The alteration of epididymal fat weight, gastric emptying, and expression of peptides and their receptors in several tissues were determined. <b><i>Results.</i></b> GL-6mA was more potent than SGES-PF in decreasing body weight gain, epididymal fat tissue weight, adipocyte size and gastric emptying. Chronic GES significantly altered NPY, OX, α-MSH and OXT and their receptors in the hypothalamus, adipose tissue and stomach. <b><i>Conclusions. </i></b>Chronic GES effectively leads to weight loss by reducing food intake, fat tissue weight and gastric emptying. NPY, α-MSH, orexin and OXT, and their receptors in the hypothalamus, adipose tissue and stomach appear to be involved in the anti-obesity effects of chronic GES.
DOI: 10.6084/m9.figshare.1568423.v6
title: Chronic gastric electrical stimulation leads to weight loss via modulating multiple tissue neuropeptide Y, orexin, α-melanocyte-stimulating hormone and oxytocin in obese rats

description: <b><i>Objectives. </i></b>Gastric electrical stimulation (GES) has great potential for the treatment of obesity. We investigated the impact of chronic GES on the alteration of adipose tissue and the regulation of neuropeptide Y (NPY), orexin (OX), α-melanocyte-stimulating hormone (α-MSH) and oxytocin (OXT), and their receptors in several tissues. <b><i>Material and methods.</i></b> Most of the experiments included three groups of diet-induced obesity rats: (1) sham-GES (SGES); (2) GL-6mA (GES with 6 mA, 4 ms, 40 Hz, 2 s on, 3 s off at lesser curvature); and (3) SGES-PF (SGES rats receiving pair feeding to match the consumption of GL-6mA rats). Chronic GES was applied for 2 h every day for 4 weeks. During treatment with GES, food intake and body weight were monitored weekly. The alteration of epididymal fat weight, gastric emptying, and expression of peptides and their receptors in several tissues were determined. <b><i>Results.</i></b> GL-6mA was more potent than SGES-PF in decreasing body weight gain, epididymal fat tissue weight, adipocyte size and gastric emptying. Chronic GES significantly altered NPY, OX, α-MSH and OXT and their receptors in the hypothalamus, adipose tissue and stomach. <b><i>Conclusions. </i></b>Chronic GES effectively leads to weight loss by reducing food intake, fat tissue weight and gastric emptying. NPY, α-MSH, orexin and OXT, and their receptors in the hypothalamus, adipose tissue and stomach appear to be involved in the anti-obesity effects of chronic GES.