Thermodynamic entropy as an indicator for urban sustainability?

As foci of economic activity, resource consumption, and the production of material waste and pollution, cities represent both a major hurdle and yet also a source of great potential for achieving the goal of sustainability. Motivated by the desire to better understand and measure sustainability in quantitative terms we explore the applicability of thermodynamic entropy to urban systems as a tool for evaluating sustainability. Having comprehensively reviewed the application of thermodynamic entropy to urban systems we argue that the role it can hope to play in characterising sustainability is limited. We show that thermodynamic entropy may be considered as a measure of energy efficiency, but must be complimented by other indices to form part of a broader measure of urban sustainability

Fusion or lack of fusion of embryonic palatal shelves.

<p>A: Fused embryonic palatal shelves. B: A failure to fuse embryonic palatal shelves. C: Fused embryonic palatal shelf in HE stain. D: A failure to fuse of embryonic palatal shelves in HE stain.</p

Comparison of the incidence of cleft palate in the embryos between four groups.

<p>Comparison of the incidence of cleft palate in the embryos between four groups.</p

The boxplot from ¹H-MRS of embryonic craniofacial tissues' metabolite concentrations.

<p>The boxplot from ¹H-MRS shows quantification of IMCL13, choline, taurine, IMCL21, EMCL23 concentrations in embryonic craniofacial tissues of pregnant mice. Values are mean ± standard deviation (SD). Metabolite concentrations were compared respectively. *Significant difference compared to control (P<0.05); △Significant difference compared to RA30 (P<0.05).</p

Metabolite concentrations determined by in vivo 1H-MR spectroscopy of embryonic craniofacial tissues.

<p>The concentration unit of metabolites is µmol per litre (umol/L).</p><p>Abbreviations: IMCL, intramyocellular lipids; EMCL, extramyocellular lipids.</p><p>All fetuses measured at E14.5, values are mean ± standard deviation (SD).</p><p>*Significant difference compared to control (P<0.05).</p>△<p>Significant difference compared to RA30 (P<0.05).</p

MRI and ¹H-MRS of mouse fetuses.

<p>A. Magnetic resonance imaging (MRI) of E14.5 mouse embryos at a dose of 70 mg/kg RA. Volumes of interest (VOI)  = 3.0×3.0×3.0 mm3. B. MRI of E14.5 mouse embryos at a dose of 100 mg/kg RA. Hyperintense regions were observed in the imaging. There were parts of or no embryos in the hyperintense regions. VOI  = 3.0×3.0×3.0 mm³. C. In vivo proton magnetic resonance spectroscopy (¹H-MRS) obtained from the control and three experimental groups after RA treatment. Resonances were readily identified by the LCModel software. 1. Taurine; 2. Choline; 3. Creatine; 4. Extramyocellular lipids (EMCL23); 5. Intramyocellular lipids (IMCL21); 6. IMCL13.</p

DataSheet_1_The integration of single-cell sequencing, TCGA, and GEO data analysis revealed that PRRT3-AS1 is a biomarker and therapeutic target of SKCM.zip

IntroductionSkin cutaneous melanoma (SKCM) is the world’s fourth deadliest cancer, and advanced SKCM leads to a poor prognosis. Novel biomarkers for SKCM diagnosis and prognosis are urgently needed. Long non-coding RNAs (lncRNAs) provide various biological functions and have been proved to play a significant role in tumor progression. Single-cell RNA sequencing (scRNA-seq) enables genome analysis at the single-cell level. This study explored prognostic lncRNAs in SKCM based on scRNA-seq and bulk RNA sequencing data.Materials and methodsThe TCGA cohort and melanoma samples in the GEO database (GSE72056, GSE19234, GSE15605, GSE7553, and GSE81383) were included in this study. Marker genes were filtered, and ensemble lncRNAs were annotated. The clinical significance of selected lncRNAs was verified through TCGA and GEO dataset analysis. SiRNA transfection, wound−healing and transwell assays were performed to evaluate the effect of PRRT3-AS1 on cellular function. Immune infiltration of the selected lncRNAs was also exhibited.ResultsA 5-marker-lncRNAs model of significant prognostic value was constructed based on GSE72056 and the TCGA cohort. PRRT3-AS1 combined with DANCR was then found to provide significant prognostic value in SKCM. PRRT3-AS1 was filtered for its higher expression in more advanced melanoma and significant prognosis value. Cellular function experiments in vitro revealed that PRRT3-AS1 may be required for cancer cell migration in SKCM. PRRT3-AS1 was found to be related to epithelial-mesenchymal transition (EMT) signaling pathways. DNA methylation of PRRT3-AS1 was negatively related to PRRT3-AS1 expression and showed significant prognosis value. In addition, PRRT3-AS1 may suppress immune infiltration and be involved in immunotherapy resistance.ConclusionPRRT3-AS1 may be a diagnostic and prognostic biomarker of SKCM.</p

The pooled OR from 15 studies including 1,247 samples form BCa patients and 405 from normal controls.

<p>OR: 5.81; 95%CI = 3.83–8.82, P<0.00001.</p

DAPK Promoter Methylation and Bladder Cancer Risk: A Systematic Review and Meta-Analysis

<div><p>Background</p><p>Methylation of tumor suppressor gene promoter leads to transcription inactivation and is involved in tumorigenesis. Several studies demonstrate a potential association between the Death-Associated Protein Kinase (DAPK) gene promoter methylation and bladder cancer risk, tumor stage and histological grade. Due to inconsistent results of these studies, we performed this meta-analysis to ascertain the association.</p><p>Methods</p><p>Studies were retrieved from the PubMed, Embase, Web of Science and the Cochrane Library databases. Study selection and data extraction were executed by two reviewers independently. Meta-analysis was performed using Stata 13.0 and Review Manager 5.3 software.</p><p>Results</p><p>A total of 21 articles involving 15 case control and 8 case series studies were included in this meta-analysis. DAPK promoter methylation was associated with bladder cancer risk (OR: 5.81; 95%CI = 3.83–8.82, P<0.00001). The frequency of DAPK promoter methylation was equal in bladder cancer tissue and paired adjacent normal tissue (OR: 0.87; 95%CI = 0.31–2.48, P = 0.794). Furthermore, DAPK promoter methylation was associated with higher histological grade (OR: 1.52; 95%CI = 1.10–2.09, P = 0.011) but not associated with tumor stage (OR: 1.12; 95%CI = 0.67–1.87, P = 0.668).</p><p>Conclusions</p><p>The result suggests that DAPK promoter methylation is significantly increased in bladder cancer patients compared to normal controls. DAPK promoter methylation could serve as a biomarker for bladder cancer detection and management.</p></div

Characteristics of the Included Studies

<p>Characteristics of the Included Studies</p