cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.3472460
title: Tunicamycin aggravates endoplasmic reticulum stress and airway inflammation via PERK-ATF4-CHOP signaling in a murine model of neutrophilic asthma

description: <i>Introduction</i>: Endoplasmic reticulum (ER) stress has been considered to be an important regulator of airway inflammation in the pathogenesis of bronchial asthma, but the mechanism of ER stress involved in neutrophilic asthma remain not fully understood. <i>Methods</i>: Tunicamycin is a mixture of homologous nucleoside antibiotics, which is used to induce ER stress. In the present study, Tunicamycin was administered to mouse bronchial epithelial cells and a neutrophilic asthma model (OVA<sub>LPS</sub>-OVA mice), and ER stress indicators and inflammatory cytokines were measured by Western blotting and Elisa. <i>Results</i>: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-α via PERK-ATF4-CHOP signaling. Additionally, the phosphorylation of PERK and the expression levels of ATF4 and CHOP proteins and inflammatory cytokines (IL-6, IL-8 and TNF-α) were elevated in the lung tissue of OVA<sub>LPS</sub>-OVA mice. Administering tunicamycin further increased protein expression levels of ER stress indicators and inflammatory cytokines, and resulted in more severe asthma phenotypes in OVA<sub>LPS</sub>-OVA mice, suggesting that PERK-ATF4-CHOP signaling is associated with airway inflammation in neutrophil-dominant asthma. <i>Conclusions</i>: These data support the emerging notion that regulation of ER stress could be strongly associated with the development of neutrophilic asthma.
DOI: 10.6084/m9.figshare.3472460.v2
title: Tunicamycin aggravates endoplasmic reticulum stress and airway inflammation via PERK-ATF4-CHOP signaling in a murine model of neutrophilic asthma

description: <i>Introduction</i>: Endoplasmic reticulum (ER) stress has been considered to be an important regulator of airway inflammation in the pathogenesis of bronchial asthma, but the mechanism of ER stress involved in neutrophilic asthma remain not fully understood. <i>Methods</i>: Tunicamycin is a mixture of homologous nucleoside antibiotics, which is used to induce ER stress. In the present study, Tunicamycin was administered to mouse bronchial epithelial cells and a neutrophilic asthma model (OVA<sub>LPS</sub>-OVA mice), and ER stress indicators and inflammatory cytokines were measured by Western blotting and Elisa. <i>Results</i>: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-α via PERK-ATF4-CHOP signaling. Additionally, the phosphorylation of PERK and the expression levels of ATF4 and CHOP proteins and inflammatory cytokines (IL-6, IL-8 and TNF-α) were elevated in the lung tissue of OVA<sub>LPS</sub>-OVA mice. Administering tunicamycin further increased protein expression levels of ER stress indicators and inflammatory cytokines, and resulted in more severe asthma phenotypes in OVA<sub>LPS</sub>-OVA mice, suggesting that PERK-ATF4-CHOP signaling is associated with airway inflammation in neutrophil-dominant asthma. <i>Conclusions</i>: These data support the emerging notion that regulation of ER stress could be strongly associated with the development of neutrophilic asthma.
DOI: 10.6084/m9.figshare.3472460.v1
title: Tunicamycin Aggravates Endoplasmic Reticulum Stress and Airway Inflammation via PERK-ATF4-CHOP Signaling in a Murine Model of Neutrophilic Asthma

description: <b>Introduction</b>: Endoplasmic reticulum (ER) stress has been considered to be an important regulator of airway inflammation in the pathogenesis of bronchial asthma, but the mechanism of ER stress involved in neutrophilic asthma remain not fully understood. <b>Methods</b>: Tunicamycin is a mixture of homologous nucleoside antibiotics, which is used to induce ER stress. In the present study, Tunicamycin was administered to mouse bronchial epithelial cells and a neutrophilic asthma model (OVA<sub>LPS</sub>-OVA mice), and ER stress indicators and inflammatory cytokines were measured by Western blotting and Elisa. <b>Results</b>: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-α via PERK-ATF4-CHOP signaling. Additionally, the phosphorylation of PERK and the expression levels of ATF4 and CHOP proteins and inflammatory cytokines (IL-6, IL-8 and TNF-α) were elevated in the lung tissue of OVA<sub>LPS</sub>-OVA mice. Administering tunicamycin further increased protein expression levels of ER stress indicators and inflammatory cytokines, and resulted in more severe asthma phenotypes in OVA<sub>LPS</sub>-OVA mice, suggesting that PERK-ATF4-CHOP signaling is associated with airway inflammation in neutrophil-dominant asthma. <b>Conclusions</b>: These data support the emerging notion that regulation of ER stress could be strongly associated with the development of neutrophilic asthma.
DOI: 10.6084/m9.figshare.3472349
title: CNT Raman for Mitocondrial Oxygen Consumption Data Set and Regression Models

description: nanotubes, QSAR, Regression Models, Raman spectra, Shannon entropies
DOI: 10.6084/m9.figshare.3472349.v1
title: CNT Raman for Mitocondrial Oxygen Consumption Data Set and Regression Models

description: nanotubes, QSAR, Regression Models, Raman spectra, Shannon entropies
DOI: 10.6084/m9.figshare.3472349.v3
title: CNT Raman for Mitocondrial Oxygen Consumption Data Set and Regression Models

description: nanotubes, QSAR, Regression Models, Raman spectra, Shannon entropies
DOI: 10.6084/m9.figshare.3472349.v2
title: CNT Raman for Mitocondrial Oxygen Consumption Data Set and Regression Models

description: nanotubes, QSAR, Regression Models, Raman spectra, Shannon entropies
DOI: 10.6084/m9.figshare.3472292
title: Computer-aided design of carbon nanotubes with the desired bioactivity and safety profiles

description: Growing experimental evidences suggest the existence of direct relationships between the surface chemistry of nanomaterials and their biological effects. Herein, we have employed computational approaches to design a set of biologically active carbon nanotubes (CNTs) with controlled protein binding and cytotoxicity. Quantitative structure–activity relationship (QSAR) models were built and validated using a dataset of 83 surface-modified CNTs. A subset of a combinatorial virtual library of 240 000 ligands potentially attachable to CNTs was selected to include molecules that were within the chemical similarity threshold with respect to the modeling set compounds. QSAR models were then employed to virtually screen this subset and prioritize CNTs for chemical synthesis and biological evaluation. Ten putatively active and 10 putatively inactive CNTs decorated with the ligands prioritized by virtual screening for either protein-binding or cytotoxicity assay were synthesized and tested. We found that all 10 putatively inactive and 7 of 10 putatively active CNTs were confirmed in the protein-binding assay, whereas all 10 putatively inactive and 6 of 10 putatively active CNTs were confirmed in the cytotoxicity assay. This proof-of-concept study shows that computational models can be employed to guide the design of surface-modified nanomaterials with the desired biological and safety profiles.
DOI: 10.6084/m9.figshare.3472283
title: Advances in oral delivery of anti-cancer prodrugs

description: <b>Introduction</b>: Most anticancer drugs have poor aqueous solubility and low permeability across the gastrointestinal tract. Furthermore, extensive efflux by P-glycoproteins (P-gp) in the small intestine also limits the efficient delivery of anticancer drugs via oral route. <b>Area covered</b>: This review explores the prodrug strategy for oral delivery of anticancer drugs. Different categories of oral anticancer prodrugs along with recent clinical studies have been comprehensively reviewed here. Furthermore, novel anticancer prodrugs such as polymer-prodrugs and lipid-prodrugs have been discussed in detail. Finally, various nanocarrier-based approaches employed for oral delivery of anticancer prodrugs have also been discussed. <b>Expert opinion</b>: Premature degradation of anticancer prodrugs in the gastrointestinal tract could lead to variable pharmacokinetics and undesired toxicity. Despite their increased aqueous solubility, the oral bioavailability of several anticancer prodrugs are limited by their poor permeability across the gastrointestinal tract. These limitations can be overcome by the use of functional excipients (polymers, lipids, amino acids/dipeptides), which are specifically absorbed via transporters and receptor-mediated endocytosis. Oral delivery of anticancer prodrugs using nanocarrier-based drug delivery system is a recent development; however it should be justified based on the comparative advantages of encapsulating prodrug in a nanocarrier versus the use of anticancer prodrug molecule itself.
DOI: 10.6084/m9.figshare.3472292.v1
title: Computer-aided design of carbon nanotubes with the desired bioactivity and safety profiles

description: Growing experimental evidences suggest the existence of direct relationships between the surface chemistry of nanomaterials and their biological effects. Herein, we have employed computational approaches to design a set of biologically active carbon nanotubes (CNTs) with controlled protein binding and cytotoxicity. Quantitative structure–activity relationship (QSAR) models were built and validated using a dataset of 83 surface-modified CNTs. A subset of a combinatorial virtual library of 240 000 ligands potentially attachable to CNTs was selected to include molecules that were within the chemical similarity threshold with respect to the modeling set compounds. QSAR models were then employed to virtually screen this subset and prioritize CNTs for chemical synthesis and biological evaluation. Ten putatively active and 10 putatively inactive CNTs decorated with the ligands prioritized by virtual screening for either protein-binding or cytotoxicity assay were synthesized and tested. We found that all 10 putatively inactive and 7 of 10 putatively active CNTs were confirmed in the protein-binding assay, whereas all 10 putatively inactive and 6 of 10 putatively active CNTs were confirmed in the cytotoxicity assay. This proof-of-concept study shows that computational models can be employed to guide the design of surface-modified nanomaterials with the desired biological and safety profiles.
DOI: 10.6084/m9.figshare.3472283.v1
title: Advances in oral delivery of anti-cancer prodrugs

description: <b>Introduction</b>: Most anticancer drugs have poor aqueous solubility and low permeability across the gastrointestinal tract. Furthermore, extensive efflux by P-glycoproteins (P-gp) in the small intestine also limits the efficient delivery of anticancer drugs via oral route. <b>Area covered</b>: This review explores the prodrug strategy for oral delivery of anticancer drugs. Different categories of oral anticancer prodrugs along with recent clinical studies have been comprehensively reviewed here. Furthermore, novel anticancer prodrugs such as polymer-prodrugs and lipid-prodrugs have been discussed in detail. Finally, various nanocarrier-based approaches employed for oral delivery of anticancer prodrugs have also been discussed. <b>Expert opinion</b>: Premature degradation of anticancer prodrugs in the gastrointestinal tract could lead to variable pharmacokinetics and undesired toxicity. Despite their increased aqueous solubility, the oral bioavailability of several anticancer prodrugs are limited by their poor permeability across the gastrointestinal tract. These limitations can be overcome by the use of functional excipients (polymers, lipids, amino acids/dipeptides), which are specifically absorbed via transporters and receptor-mediated endocytosis. Oral delivery of anticancer prodrugs using nanocarrier-based drug delivery system is a recent development; however it should be justified based on the comparative advantages of encapsulating prodrug in a nanocarrier versus the use of anticancer prodrug molecule itself.
DOI: 10.6084/m9.figshare.3472199
title: Export Excel fieldbook to csv-file

description: Screencast on how to export field observations with gps coordinates in Excel to a .csv file.<br>
DOI: 10.6084/m9.figshare.3472199.v1
title: Export Excel fieldbook to csv-file

description: Screencast on how to export field observations with gps coordinates in Excel to a .csv file.<br>
DOI: 10.6084/m9.figshare.3472193
title: Weight and prognosis for influenza A(H1N1)pdm09 infection during the pandemic period between 2009 and 2011: a systematic review of observational studies with meta-analysis

description: <b>Background:</b> In 2009, a novel influenza A(H1N1)pdm09 virus was detected and caused influenza pandemic. It is important to identify the risk factors for severe outcomes. However, inconsistent results regarding the effect of obesity were reported in previous studies. <b>Methods:</b> We conducted a systematic review to assess the association between obesity and poor prognosis for laboratory-confirmed A(H1N1)pdm09 influenza. We searched three English databases and three Chinese databases for relevant studies from April 2009 to October 2015: PubMed, the Cochrane library, Embase, CNKI, CBM, and Wanfang. Two investigators independently identified eligible articles, assessed quality using NOS, and extracted data. We performed meta-analyses and meta-regressions to estimate the association between weight and poor prognosis for influenza A(H1N1)pdm09 infection, when data were available. <b>Results:</b> We identified 22 articles enrolling 25,189 laboratory confirmed patients. The pooled estimates indicated obesity significantly increased the risk of fatal and critical complications of influenza A(H1N1)pdm09 infection (for fatal, <i>OR =</i> 1.81, 95% CI: 1.23−2.65; for critical complications, <i>OR =</i> 1.67, 95% CI: 1.13−2.47). However, we found significant interaction between early antiviral treatment and obesity (<i>β</i> = −0.28). After adjustment for early antiviral treatment, relationship between obesity and poor outcomes disappeared (<i>OR =</i> 1.14, 95% CI: 0.94−1.39). <b>Conclusions:</b> The results of the meta-analyses showed obesity significantly increased the risk of death, critical complications, and severe complications for influenza A(H1N1)pdm09 infection, especially among high-quality studies and in Asia region. Importantly, the result from our meta-regression indicated that the conclusion should be interpreted with caution, because early antiviral treatment might be a key confounding factor.
DOI: 10.6084/m9.figshare.3472193.v1
title: Weight and prognosis for influenza A(H1N1)pdm09 infection during the pandemic period between 2009 and 2011: a systematic review of observational studies with meta-analysis

description: <b>Background:</b> In 2009, a novel influenza A(H1N1)pdm09 virus was detected and caused influenza pandemic. It is important to identify the risk factors for severe outcomes. However, inconsistent results regarding the effect of obesity were reported in previous studies. <b>Methods:</b> We conducted a systematic review to assess the association between obesity and poor prognosis for laboratory-confirmed A(H1N1)pdm09 influenza. We searched three English databases and three Chinese databases for relevant studies from April 2009 to October 2015: PubMed, the Cochrane library, Embase, CNKI, CBM, and Wanfang. Two investigators independently identified eligible articles, assessed quality using NOS, and extracted data. We performed meta-analyses and meta-regressions to estimate the association between weight and poor prognosis for influenza A(H1N1)pdm09 infection, when data were available. <b>Results:</b> We identified 22 articles enrolling 25,189 laboratory confirmed patients. The pooled estimates indicated obesity significantly increased the risk of fatal and critical complications of influenza A(H1N1)pdm09 infection (for fatal, <i>OR =</i> 1.81, 95% CI: 1.23−2.65; for critical complications, <i>OR =</i> 1.67, 95% CI: 1.13−2.47). However, we found significant interaction between early antiviral treatment and obesity (<i>β</i> = −0.28). After adjustment for early antiviral treatment, relationship between obesity and poor outcomes disappeared (<i>OR =</i> 1.14, 95% CI: 0.94−1.39). <b>Conclusions:</b> The results of the meta-analyses showed obesity significantly increased the risk of death, critical complications, and severe complications for influenza A(H1N1)pdm09 infection, especially among high-quality studies and in Asia region. Importantly, the result from our meta-regression indicated that the conclusion should be interpreted with caution, because early antiviral treatment might be a key confounding factor.
DOI: 10.6084/m9.figshare.3472013
title: Resting high frequency heart rate variability selectively predicts cooperative behavior

description: Resting high frequency heart rate variability predicts cooperative behavior in a hawk-dove game when the hawk-hawk payoff is severe but not moderate.<br>
DOI: 10.6084/m9.figshare.3472013.v1
title: New draft item

description: Resting high frequency heart rate variability predicts cooperative behavior in a hawk-dove game when the hawk-hawk payoff is severe but not moderate.<br>
DOI: 10.6084/m9.figshare.3471983
title: Supplementary Material for: Natural Killer Cell Deficits Aggravate Allergic Rhinosinusitis in a Murine Model

description: <b><i>Objective:</i></b> Defective innate immune functions can contribute to chronic rhinosinusitis (RS). Recently, it has been reported that chronic RS patients show impaired function of natural killer (NK) cells. We investigated the role of NK cells in eosinophilic inflammation in an allergic RS mouse model. <b><i>Methods:</i></b> Mice sensitized to ovalbumin (OVA) by intraperitoneal injection received nasal challenges with OVA for 5 weeks. NK cell depletion was achieved by intraperitoneal injections of anti-asialo ganglio-N-tetraosylceramide (ASGM1) antibodies 10 days before OVA sensitization and every 5 days thereafter until sacrifice. Sinonasal complex samples were evaluated histologically, and IL-4, IL-5, IL-13, IFN-γ, MIP-2, and eotaxin levels were measured in the nasal lavage fluid. Differential white blood cell counts were also obtained. <b><i>Results:</i></b> Allergic RS mice showed significantly more eosinophilic inflammation in the sinonasal mucosa, elevated levels of IL-4, IL-5, IL-13, and eotaxin in the nasal lavage fluid, and peripheral blood eosinophilia compared to control mice. The depletion of NK cells by anti-ASGM1 treatment induced more prominent eosinophilic inflammation and increased secretion of IL-5 and peripheral blood eosinophilia in allergic RS mice. <b><i>Conclusion:</i></b> The depletion of NK cells aggravates allergen-induced sinonasal eosinophilic inflammation, suggesting that impaired NK cell activity may be an exacerbating factor in eosinophilic chronic RS.
DOI: 10.6084/m9.figshare.3471983.v1
title: Supplementary Material for: Natural Killer Cell Deficits Aggravate Allergic Rhinosinusitis in a Murine Model

description: <b><i>Objective:</i></b> Defective innate immune functions can contribute to chronic rhinosinusitis (RS). Recently, it has been reported that chronic RS patients show impaired function of natural killer (NK) cells. We investigated the role of NK cells in eosinophilic inflammation in an allergic RS mouse model. <b><i>Methods:</i></b> Mice sensitized to ovalbumin (OVA) by intraperitoneal injection received nasal challenges with OVA for 5 weeks. NK cell depletion was achieved by intraperitoneal injections of anti-asialo ganglio-N-tetraosylceramide (ASGM1) antibodies 10 days before OVA sensitization and every 5 days thereafter until sacrifice. Sinonasal complex samples were evaluated histologically, and IL-4, IL-5, IL-13, IFN-γ, MIP-2, and eotaxin levels were measured in the nasal lavage fluid. Differential white blood cell counts were also obtained. <b><i>Results:</i></b> Allergic RS mice showed significantly more eosinophilic inflammation in the sinonasal mucosa, elevated levels of IL-4, IL-5, IL-13, and eotaxin in the nasal lavage fluid, and peripheral blood eosinophilia compared to control mice. The depletion of NK cells by anti-ASGM1 treatment induced more prominent eosinophilic inflammation and increased secretion of IL-5 and peripheral blood eosinophilia in allergic RS mice. <b><i>Conclusion:</i></b> The depletion of NK cells aggravates allergen-induced sinonasal eosinophilic inflammation, suggesting that impaired NK cell activity may be an exacerbating factor in eosinophilic chronic RS.
DOI: 10.6084/m9.figshare.3471935
title: Supplementary Material for: Structured Exercise in Obese Diabetic Patients with Chronic Kidney Disease: A Randomized Controlled Trial

description: <b><i>Background:</i></b> Patients with type 2 diabetes mellitus (DM), obesity, and chronic kidney disease (CKD) are generally physically inactive and may benefit from exercise. Our objective was to determine the effects of structured exercise on physical fitness, kidney function, endothelial function, inflammation, and body composition in such patients. <b><i>Methods:</i></b> In this randomized, controlled trial, 36 male patients (age 49-81) were randomly assigned to exercise + diet management (n = 18) or diet alone (n = 18). Participants were eligible if they had type 2 DM, body mass index &gt;30 kg/m<sup>2</sup>, CKD stages 2-4, and persistent proteinuria (&gt;200 mg/g creatinine for &gt;3 months). The exercise intervention was a 12-week (3 days per week) program of aerobic and resistance training followed by 40 weeks of home exercise. The primary outcome measure was change from baseline in urine protein to creatinine ratio (UPCR) at 12 and 52 weeks. <b><i>Results:</i></b> Thirty-two participants completed the study (14 exercise + diet, 18 diet-alone group). The change from baseline in UPCR was slightly greater in the diet-alone group at 12 weeks but not at 52 weeks. Changes in both symptom-limited and constant-workrate treadmill times were significantly higher in the exercise + diet group at 12 weeks but not at 52 weeks. There were no significant differences in urine albumin to creatinine ratio, estimated glomerular filtration rate, endothelial function, inflammation, or body composition between the groups. <b><i>Conclusions:</i></b> In obese diabetic subjects with CKD, structured exercise improved exercise capacity but not body composition or renal function.