cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.10655349
title: Learning Locality-Sensitive Bucketing Functions

description: These are the trained models (i.e., (d1,d2)-locality-sensitive bucketing functions) from our manuscript titled "Learning Locality-Sensitive Bucketing Functions".
DOI: 10.25549/pmh-ouc1sto1646746
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646745
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646744
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646740
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646739
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646738
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646737
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646736
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646734
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646733
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646732
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646728
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646727
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646725
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646724
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646723
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646721
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646720
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646719
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646718
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646717
title: Pasadena Museum of History Collection
DOI: 10.6084/m9.figshare.13843853
title: Additional file 4 of Causal relationships between genetically determined metabolites and human intelligence: a Mendelian randomization study

description: Additional file 4: Table S1. Information of the instrumental variables used for Mendelian randomization estimates. Table S2. Unknown metabolites identified by the Mendelian randomization estimates. Table S3. Genetic predictors for dihomo-linoleate (20:2n6) and their association with Intelligence. Table S4. Genetic predictors for p-acetamidophenylglucuronide and their association with Intelligence.
DOI: 10.25549/pmh-ouc1sto1646716
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646715
title: Pasadena Museum of History Collection
DOI: 10.6084/m9.figshare.13843853.v1
title: Additional file 4 of Causal relationships between genetically determined metabolites and human intelligence: a Mendelian randomization study

description: Additional file 4: Table S1. Information of the instrumental variables used for Mendelian randomization estimates. Table S2. Unknown metabolites identified by the Mendelian randomization estimates. Table S3. Genetic predictors for dihomo-linoleate (20:2n6) and their association with Intelligence. Table S4. Genetic predictors for p-acetamidophenylglucuronide and their association with Intelligence.
DOI: 10.25549/pmh-ouc1sto1646714
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646713
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646712
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646711
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646710
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646709
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646708
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646707
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646706
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646705
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646701
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646700
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646699
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646698
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646697
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646696
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646695
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646694
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646693
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646692
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646691
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646690
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646689
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646688
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646687
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646686
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646685
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646684
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646683
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646682
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646681
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646680
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646679
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646678
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646677
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646676
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646675
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646674
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646673
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646672
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646671
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646670
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646669
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646668
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646667
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646666
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646665
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646664
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646663
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646662
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646661
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646660
title: Pasadena Museum of History Collection
DOI: 10.25549/pmh-ouc1sto1646659
title: Pasadena Museum of History Collection
DOI: 10.6084/m9.figshare.16989805.v1
title: Impact of mixed surfactant composition on emulsion stability in saline environment: anionic and nonionic surfactants

description: The influence of anionic and nonionic surfactant ratios on emulsion stability in saline environments was investigated in the context of bilge water. Sodium laureth sulfate (SLES) and Triton X-100 were selected as surfactants likely present in bilge water emulsions. Interfacial tension results revealed that with 0.42 M NaCl, SLES is a more surface-active surfactant with a smaller head group area than Triton X-100. Increasing the proportion of SLES resulted in a higher surface charge, thus creating a greater repulsive interaction energy barrier between oil droplets, preventing flocculation. Size distribution results showed emulsions with 500 ppm surfactants at different surfactant ratios had long-term (more than 20 days) stability against coalescence. However, SLES-rich emulsions had smaller oil droplets (&lt;8 μm) generated with the same energy input and were more stable against flocculation when compared to Triton X-100-rich emulsions. Visual observation showed more small oil droplets (&lt;10 μm) with a slow creaming rate in SLES-rich emulsions than in Triton X-100-rich emulsions. Turbidity measurements showed that SLES-rich emulsions had higher remnant oil content in the subnatant than Triton X-100-rich emulsions, which is undesirable for phase separation and bilge water treatment. This work provides experimental results on how anionic and nonionic surfactant ratio influences emulsion properties in saltwater environments, which is valuable in developing strategies to minimize and remove remnant oil in bilge water.
DOI: 10.6084/m9.figshare.6504053.v1
title: Interleukin-6 contributes to myocardial damage in pregnant rats with reduced uterine perfusion pressure

description: Preeclampsia is one of the most frequent and difficult illnesses in pregnancy, which jeopardizes both mother and fetus. There are several diagnostic criteria for preeclampsia. However, the preeclampsia-associated myocardial damage has not been described. In this study, we employed reduced uterine perfusion pressure (RUPP) to generate a rat model of preeclampsia for the evaluation of myocardial damage in late-gestation rats. The expressions of cardiac injury markers were analyzed by immunohistochemistry and ELISA. The arterial pressure and myocardial tissue velocities were also measured. The role of interleukin (IL)-6 in RUPP-associated myocardial damage was further explored. The results showed that RUPP rats had significant myocardial damage, as demonstrated by the high expressions of myoglobin, creatine kinase isoenzyme, cardiac troponin I, and brain natriuretic peptide. In addition, RUPP increased the mean arterial pressure and the early transmitral flow velocity to mitral annulus early diastolic velocity ratio (E/Ea). Furthermore, IL-6 deteriorated these abnormalities, whereas inhibition of IL-6 significantly relieved them. In conclusion, our study demonstrated that RUPP rats displayed myocardial damage in an IL-6-dependent manner.
DOI: 10.25549/pmh-ouc1sto1646658
title: Pasadena Museum of History Collection
DOI: 10.6084/m9.figshare.16989805
title: Impact of mixed surfactant composition on emulsion stability in saline environment: anionic and nonionic surfactants

description: The influence of anionic and nonionic surfactant ratios on emulsion stability in saline environments was investigated in the context of bilge water. Sodium laureth sulfate (SLES) and Triton X-100 were selected as surfactants likely present in bilge water emulsions. Interfacial tension results revealed that with 0.42 M NaCl, SLES is a more surface-active surfactant with a smaller head group area than Triton X-100. Increasing the proportion of SLES resulted in a higher surface charge, thus creating a greater repulsive interaction energy barrier between oil droplets, preventing flocculation. Size distribution results showed emulsions with 500 ppm surfactants at different surfactant ratios had long-term (more than 20 days) stability against coalescence. However, SLES-rich emulsions had smaller oil droplets (&lt;8 μm) generated with the same energy input and were more stable against flocculation when compared to Triton X-100-rich emulsions. Visual observation showed more small oil droplets (&lt;10 μm) with a slow creaming rate in SLES-rich emulsions than in Triton X-100-rich emulsions. Turbidity measurements showed that SLES-rich emulsions had higher remnant oil content in the subnatant than Triton X-100-rich emulsions, which is undesirable for phase separation and bilge water treatment. This work provides experimental results on how anionic and nonionic surfactant ratio influences emulsion properties in saltwater environments, which is valuable in developing strategies to minimize and remove remnant oil in bilge water.
DOI: 10.25549/pmh-ouc1sto1646657
title: Pasadena Museum of History Collection
DOI: 10.6084/m9.figshare.6504113.v1
title: Outcomes Following Coronary Artery Bypass Graft Surgery in Patients with Mild Preoperative Renal Insufficiency

description: Abstract Introduction: Preoperative renal insufficiency is an independent predictor of mortality after coronary artery bypass graft (CABG) surgery. However, there are few reports aimed to evaluate the impact of mild preoperative renal insufficiency on long-term follow-up outcomes after isolated CABG surgery. This study investigates the effect of mild preoperative renal insufficiency on long-term follow-up outcomes of patients after CABG. Methods: Five hundred eighty-four patients' data that underwent CABG between 1 January 2009 and 1 December 2016 were retrospectively analyzed. They were divided into two groups: normal group [Estimated glomerular filtration rate (eGFR) ≥ 90 ml/min/1.73 m2, n=304] and mild group (eGFR ranges from 60 to 89 ml/min/1.73 m2, n=280). Clinical material and long follow-up outcomes were compared inthe two groups. Results: Two groups had similar baseline and intraoperative data except eGFR. Six (0.01%) patients died in hospital, 15 in normal group and 28 in mild group during the long-term follow-up, which had statistical significance (P&lt;0.05). Univariate factor analysis displayed that the two groups had similar in-hospital outcomes. Kaplan-Meier curves showed a better long-term survival in patients with normal preoperative renal function compared to mild preoperative renal insufficiency (x 2=4.255, P=0.039). Cox proportional model presented the hazard ratio of long-term mortality in patients with mild preoperative renal insufficiency compared to normal preoperative renal function was 1.79 (95% CI 1.17-2.88, P=0.027). Conclusions: Patients with mild preoperative renal insufficiency had a higher mortality rate than normal patients in long-term survival, whereas no evidence of worse in-hospital mortality rate was found. Patients with mild preoperative renal insufficiency showed a higher mortality rate than other studies.
DOI: 10.6084/m9.figshare.6504146.v1
title: Long non-coding RNA HOTAIR promotes UVB-induced apoptosis and inflammatory injury by up-regulation of PKR in keratinocytes

description: Excessive exposure to ultraviolet (UV) rays can cause damage of the skin and may induce cancer, immunosuppression, photoaging, and inflammation. The long non-coding RNA (lncRNA) HOX antisense intergenic RNA (HOTAIR) is involved in multiple human biological processes. However, its role in UVB-induced keratinocyte injury is unclear. This study was performed to investigate the effects of HOTAIR in UVB-induced apoptosis and inflammatory injury in human keratinocytes (HaCaT cells). Quantitative real-time polymerase chain reaction was performed to analyze the expression levels of HOTAIR, PKR, TNF-α, and IL-6. Cell viability was measured using trypan blue exclusion method and cell apoptosis using flow cytometry and western blot. ELISA was used to measure the concentrations of TNF-α and IL-6. Western blot was used to measure the expression of PKR, apoptosis-related proteins, and PI3K/AKT and NF-κB pathway proteins. UVB induced HaCaT cell injury by inhibiting cell viability and promoting cell apoptosis and expressions of IL-6 and TNF-α. UVB also promoted the expression of HOTAIR. HOTAIR suppression increased cell viability and decreased apoptosis and expression of inflammatory factors in UVB-treated cells. HOTAIR also promoted the expression of PKR. Overexpression of HOTAIR decreased cell viability and increased cell apoptosis and expression of inflammatory factors in UVB-treated cells by upregulating PKR. Overexpression of PKR decreased cell viability and promoted cell apoptosis in UVB-treated cells. Overexpression of PKR activated PI3K/AKT and NF-κB pathways. Our findings identified an essential role of HOTAIR in promoting UVB-induced apoptosis and inflammatory injury by up-regulating PKR in keratinocytes.
DOI: 10.6084/m9.figshare.7028393
title: Maternal plasma-soluble ST2 concentrations are elevated prior to the development of early and late onset preeclampsia – a longitudinal study

description: <b>Objective:</b> The objectives of this study were to determine (1) the longitudinal profile of plasma soluble ST2 (sST2) concentrations in patients with preeclampsia and those with uncomplicated pregnancies; (2) whether the changes in sST2 occur prior to the diagnosis of preeclampsia; and (3) the longitudinal sST2 profile of women with early <i>or</i> late preeclampsia. <b>Materials and methods:</b> This longitudinal nested case–control study included singleton pregnancies in the following groups: (1) uncomplicated pregnancies (<i>n</i> = 160); and (2) those complicated by early (&lt;34 weeks, <i>n</i> = 9) and late (≥34 weeks, <i>n</i> = 31) preeclampsia. sST2 concentrations were determined by enzyme-linked immunosorbent assays. Mixed-effects models were used for the longitudinal analysis. <b>Results:</b> (1) Plasma sST2 concentration profiles across gestation differed significantly among cases and controls (<i>p</i> &lt; 0.0001); (2) women with early preeclampsia had higher mean sST2 concentrations than controls at &gt;22 weeks of gestation; cases with late preeclampsia had higher mean concentrations at &gt;33 weeks of gestation (both <i>p</i> &lt; 0.05); and (3) these changes started approximately 6 weeks prior to clinical diagnosis. <b>Conclusions:</b> Maternal plasma sST2 concentrations are elevated 6 weeks prior to the clinical diagnosis of preeclampsia. An increase in the maternal plasma concentration of sST2 may contribute to an exaggerated intravascular inflammatory response and/or the Th1/Th2 imbalance in some cases.
DOI: 10.25549/pmh-ouc1sto1646656
title: Pasadena Museum of History Collection
DOI: 10.6084/m9.figshare.6504113
title: Outcomes Following Coronary Artery Bypass Graft Surgery in Patients with Mild Preoperative Renal Insufficiency

description: Abstract Introduction: Preoperative renal insufficiency is an independent predictor of mortality after coronary artery bypass graft (CABG) surgery. However, there are few reports aimed to evaluate the impact of mild preoperative renal insufficiency on long-term follow-up outcomes after isolated CABG surgery. This study investigates the effect of mild preoperative renal insufficiency on long-term follow-up outcomes of patients after CABG. Methods: Five hundred eighty-four patients' data that underwent CABG between 1 January 2009 and 1 December 2016 were retrospectively analyzed. They were divided into two groups: normal group [Estimated glomerular filtration rate (eGFR) ≥ 90 ml/min/1.73 m2, n=304] and mild group (eGFR ranges from 60 to 89 ml/min/1.73 m2, n=280). Clinical material and long follow-up outcomes were compared inthe two groups. Results: Two groups had similar baseline and intraoperative data except eGFR. Six (0.01%) patients died in hospital, 15 in normal group and 28 in mild group during the long-term follow-up, which had statistical significance (P&lt;0.05). Univariate factor analysis displayed that the two groups had similar in-hospital outcomes. Kaplan-Meier curves showed a better long-term survival in patients with normal preoperative renal function compared to mild preoperative renal insufficiency (x 2=4.255, P=0.039). Cox proportional model presented the hazard ratio of long-term mortality in patients with mild preoperative renal insufficiency compared to normal preoperative renal function was 1.79 (95% CI 1.17-2.88, P=0.027). Conclusions: Patients with mild preoperative renal insufficiency had a higher mortality rate than normal patients in long-term survival, whereas no evidence of worse in-hospital mortality rate was found. Patients with mild preoperative renal insufficiency showed a higher mortality rate than other studies.
DOI: 10.25549/pmh-ouc1sto1646654
title: Pasadena Museum of History Collection
DOI: 10.6084/m9.figshare.14889385.v1
title: Additional file 4 of Molecular subtype identification and prognosis stratification by a metabolism-related gene expression signature in colorectal cancer

description: Additional file 4: Table S4. Twenty-eight immune cells and corresponding gene signatures.
DOI: 10.6084/m9.figshare.6504146
title: Long non-coding RNA HOTAIR promotes UVB-induced apoptosis and inflammatory injury by up-regulation of PKR in keratinocytes

description: Excessive exposure to ultraviolet (UV) rays can cause damage of the skin and may induce cancer, immunosuppression, photoaging, and inflammation. The long non-coding RNA (lncRNA) HOX antisense intergenic RNA (HOTAIR) is involved in multiple human biological processes. However, its role in UVB-induced keratinocyte injury is unclear. This study was performed to investigate the effects of HOTAIR in UVB-induced apoptosis and inflammatory injury in human keratinocytes (HaCaT cells). Quantitative real-time polymerase chain reaction was performed to analyze the expression levels of HOTAIR, PKR, TNF-α, and IL-6. Cell viability was measured using trypan blue exclusion method and cell apoptosis using flow cytometry and western blot. ELISA was used to measure the concentrations of TNF-α and IL-6. Western blot was used to measure the expression of PKR, apoptosis-related proteins, and PI3K/AKT and NF-κB pathway proteins. UVB induced HaCaT cell injury by inhibiting cell viability and promoting cell apoptosis and expressions of IL-6 and TNF-α. UVB also promoted the expression of HOTAIR. HOTAIR suppression increased cell viability and decreased apoptosis and expression of inflammatory factors in UVB-treated cells. HOTAIR also promoted the expression of PKR. Overexpression of HOTAIR decreased cell viability and increased cell apoptosis and expression of inflammatory factors in UVB-treated cells by upregulating PKR. Overexpression of PKR decreased cell viability and promoted cell apoptosis in UVB-treated cells. Overexpression of PKR activated PI3K/AKT and NF-κB pathways. Our findings identified an essential role of HOTAIR in promoting UVB-induced apoptosis and inflammatory injury by up-regulating PKR in keratinocytes.
DOI: 10.25549/pmh-ouc1sto1646653
title: Pasadena Museum of History Collection
DOI: 10.6084/m9.figshare.7028393.v1
title: Maternal plasma-soluble ST2 concentrations are elevated prior to the development of early and late onset preeclampsia – a longitudinal study

description: <b>Objective:</b> The objectives of this study were to determine (1) the longitudinal profile of plasma soluble ST2 (sST2) concentrations in patients with preeclampsia and those with uncomplicated pregnancies; (2) whether the changes in sST2 occur prior to the diagnosis of preeclampsia; and (3) the longitudinal sST2 profile of women with early <i>or</i> late preeclampsia. <b>Materials and methods:</b> This longitudinal nested case–control study included singleton pregnancies in the following groups: (1) uncomplicated pregnancies (<i>n</i> = 160); and (2) those complicated by early (&lt;34 weeks, <i>n</i> = 9) and late (≥34 weeks, <i>n</i> = 31) preeclampsia. sST2 concentrations were determined by enzyme-linked immunosorbent assays. Mixed-effects models were used for the longitudinal analysis. <b>Results:</b> (1) Plasma sST2 concentration profiles across gestation differed significantly among cases and controls (<i>p</i> &lt; 0.0001); (2) women with early preeclampsia had higher mean sST2 concentrations than controls at &gt;22 weeks of gestation; cases with late preeclampsia had higher mean concentrations at &gt;33 weeks of gestation (both <i>p</i> &lt; 0.05); and (3) these changes started approximately 6 weeks prior to clinical diagnosis. <b>Conclusions:</b> Maternal plasma sST2 concentrations are elevated 6 weeks prior to the clinical diagnosis of preeclampsia. An increase in the maternal plasma concentration of sST2 may contribute to an exaggerated intravascular inflammatory response and/or the Th1/Th2 imbalance in some cases.
DOI: 10.25549/pmh-ouc1sto1646652
title: Pasadena Museum of History Collection