Experimental Study on the Influence of Ventilated Window on Indoor Air Quality and Energy Consumption

AbstractThe ventilated window has great potential on improving indoor air quality, but it may increase energy consumption. This paper studies the influence of different running modes of ventilated window on indoor PM2.5 and CO2 concentration and the overall energy consumption. When indoor PM2.5 concentration was more than 90ug/m3, and outdoor PM2.5 concentration was less than 300ug/m3 after ventilated window operating for an hour, indoor PM2.5 concentration decreased for 9-16%, it is appropriate to operating the ventilated window, but it was still 0.18-0.27 times more than the secondary standard. Operating the ventilated window for 55mins on mid-grade and high-grade respectively could reduce the increment of CO2 concentration for 3.31% and 22.19% than that without ventilated window operating. When the ventilated window operateing on low-grade, the increment of CO2 concentration was 11.34% larger than that without ventilated window operating. By increasing air volume and operating time of different modes, indoor air quality can be improved. Comparing with the condition with ventilated window off, the maximum energy consumption after ventilated window operating for 24hours on high-grade was 2.462 kW·h-1 (2.054 kW·h-1 for air conditioning consumption). Appropriate operating mode and running time can be chosen to reduce energy consumption effectively

Multiscale reconstruction of porous media based on multiple dictionaries learning

Digital modeling of the microstructure is important for studying the physical and transport properties of porous media. Multiscale modeling for porous media can accurately characterize macro-pores and micro-pores in a large-FoV (field of view) high-resolution three-dimensional pore structure model. This paper proposes a multiscale reconstruction algorithm based on multiple dictionaries learning, in which edge patterns and micro-pore patterns from homology high-resolution pore structure are introduced into low-resolution pore structure to build a fine multiscale pore structure model. The qualitative and quantitative comparisons of the experimental results show that the results of multiscale reconstruction are similar to the real high-resolution pore structure in terms of complex pore geometry and pore surface morphology. The geometric, topological and permeability properties of multiscale reconstruction results are almost identical to those of the real high-resolution pore structures. The experiments also demonstrate the proposal algorithm is capable of multiscale reconstruction without regard to the size of the input. This work provides an effective method for fine multiscale modeling of porous media

Impact of a staggered scaffold structure on the mechanical properties and cell response in bone tissue engineering

The primary goal of bone tissue engineering is to fabricate scaffolds that can provide a microenvironment similar to that of natural bone. Therefore, various scaffolds have been designed to replicate the bone structure. Although most tissues exhibit complicated structures, their basic structural unit includes stiff platelets arranged in a staggered micro-array. Therefore, many researchers have designed scaffolds with staggered patterns. However, relatively few studies have comprehensively analyzed this type of scaffold. In this review, we have analyzed scientific research pertaining to staggered scaffold designs and summarized their effects on the physical and biological properties of scaffolds. Compression tests or finite element analysis are typically used to evaluate the mechanical properties of scaffolds, and most studies have performed experiments in cell cultures. Staggered scaffolds improve mechanical strength and are beneficial for cell attachment, proliferation, and differentiation in comparison with conventional designs. However, very few have been studied in vivo experiments. Additionally, studies on the effect of staggered structures on angiogenesis or bone regeneration in vivo, particularly in large animals, are required. Currently, with the prevalence of artificial intelligence (AI)-based technologies, highly optimized models can be developed, resulting in better discoveries. In the future, AI can be used to deepen our understanding on the staggered structure, promoting its use in clinical applications.publishedVersio

Interactome mapping uncovers a general role for numb in protein kinase regulation

Cellular functions are frequently regulated by protein-protein interactions involving the binding of a modular domain in one protein to a specific peptide sequence in another. This mechanism may be explored to identify binding partners for proteins harboring a peptide-recognition domain. Here we report a proteomic strategy combining peptide and protein microarray screening with biochemical and cellular assays to identify modular domain- mediated protein-protein interactions in a systematic manner. We applied this strategy to Numb, a multifunctional protein containing a phosphotyrosine-binding (PTB) domain. Through the screening of a protein microarray, we identified \u3e100 protein kinases, including both Tyr and Ser/Thr kinases, that could potentially interact with the Numb PTB domain, suggesting a general role for Numb in regulating kinase function. The putative interactions between Numb and several tyrosine kinases were subsequently validated by GST pull-down and/or co-immunoprecipitation assays. Furthermore, using the Oriented Peptide Array Library approach, we defined the specificity of the Numb PTB domain which, in turn, allowed us to predict binding partners for Numb at the genome level. The combination of the protein microarray screening with computer-aided prediction produced the most expansive interactome for Numb to date, implicating Numb in regulating phosphorylation signaling through protein kinases and phosphatases. Not only does the data generated from this study provide an important resource for hypothesis-driven research to further define the function of Numb, the proteomic strategy described herein may be employed to uncover the interactome for other peptide-recognition domains whose consensus motifs are known or can be determined

IFN-γ regulates human dental pulp stem cells behavior via NF-κB and MAPK signaling

During caries, dental pulp expresses a range of pro-inflammatory cytokines in response to the infectious challenge. Interferon gamma (IFN-γ) is a dimerized soluble cytokine, which is critical for immune responses. Previous study has demonstrated that IFN-γ at relative high concentration (100 ng/mL) treatment improved the impaired dentinogenic and immunosuppressive regulatory functions of disease-derived dental pulp stem cells (DPSCs). However, little is known about the regulatory effects of IFN-γ at relative low concentration on healthy DPSC behavior (including proliferation, migration, and multiple-potential differentiation). Here we demonstrate that IFN-γ at relatively low concentrations (0.5 ng/mL) promoted the proliferation and migration of DPSCs, but abrogated odonto/osteogenic differentiation. Additionally, we identified that NF-κB and MAPK signaling pathways are both involved in the process of IFN-γ-regulated odonto/osteogenic differentiation of DPSCs. DPSCs treated with IFN-γ and supplemented with pyrrolidine dithiocarbamate (PDTC, an NF-κB inhibitor) or SB203580 (a MAPK inhibitor) showed significantly improved potential for odonto/osteogenic differentiation of DPSCs both in vivo and in vitro. These data provide important insight into the regulatory effects of IFN-γ on the biological behavior of DPSCs and indicate a promising therapeutic strategy for dentin/pulp tissue engineering in future endodontic treatment

Association of modifiable lifestyle with colorectal cancer incidence and mortality according to metabolic status: prospective cohort study

BackgroundMetabolic syndrome has been linked to an increased risk of colorectal cancer (CRC) incidence and mortality, but whether adopting a healthy lifestyle could attenuate the risk of CRC conferred by metabolic syndrome remains unclear. The aim of the study is to investigate the individual and joint effects of modifiable healthy lifestyle and metabolic health status on CRC incidence and mortality in the UK population.MethodsThis prospective study included 328,236 individuals from the UK Biobank. An overall metabolic health status was assessed at baseline and categorized based on the presence or absence of metabolic syndrome. We estimated the association of the healthy lifestyle score (derived from 4 modifiable behaviors: smoking, alcohol consumption, diet, physical activity and categorized into “favorable,” “intermediate”, and “unfavorable”) with CRC incidence and mortality, stratified by metabolic health status.ResultsDuring a median follow-up of 12.5 years, 3,852 CRC incidences and 1,076 deaths from CRC were newly identified. The risk of incident CRC and its mortality increased with the number of abnormal metabolic factors and decreased with healthy lifestyle score (P trend = 0.000). MetS was associated with greater CRC incidence (HR = 1.24, 95% CI: 1.16 – 1.33) and mortality (HR = 1.24, 95% CI: 1.08 – 1.41) when compared with those without MetS. An unfavorable lifestyle was associated with an increased risk (HR = 1.25, 95% CI: 1.15 – 1.36) and mortality (HR = 1.36, 95% CI: 1.16 – 1.59) of CRC across all metabolic health status. Participants adopting an unfavorable lifestyle with MetS had a higher risk (HR = 1.56, 95% CI: 1.38 – 1.76) and mortality (HR = 1.75, 95% CI: 1.40 – 2.20) than those adopting a favorable healthy lifestyle without MetS.ConclusionThis study indicated that adherence to a healthy lifestyle could substantially reduce the burden of CRC regardless of the metabolic status. Behavioral lifestyle changes should be encouraged for CRC prevention even in participants with MetS

MMS2plot: An R Package for Visualizing Multiple MS/MS Spectra for Groups of Modified and Non-Modified Peptides

A large number of post-translational modifications (PTMs) in proteins are buried in the unassigned mass spectrometric (MS) spectra in shot-gun proteomics datasets. Because the modified peptide fragments are low in abundance relative to the corresponding non-modified versions, it is critical to develop tools that allow facile evaluation of assignment of PTMs based on the MS/MS spectra. Such tools will preferably have the ability to allow comparison of fragment ion spectra and retention time between the modified and unmodified peptide pairs or group. Herein, MMS2plot, an R package for visualizing peptide-spectrum matches (PSMs) for multiple peptides, is described. MMS2plot features a batch mode and generates the output images in vector graphics file format that facilitate evaluation and publication of the PSM assignment. MMS2plot is expected to play an important role in PTM discovery from large-scale proteomics datasets generated by liquid chromatography-MS/MS. The MMS2plot package is freely available at https://github.com/lileir/MMS2plot under the GPL-3 license

PERK-Mediated Cholesterol Excretion from IDH Mutant Glioma Determines Anti-Tumoral Polarization of Microglia

Isocitrate dehydrogenase (IDH) mutation, a known pathologic classifier, initiates metabolic reprogramming in glioma cells and has been linked to the reaction status of glioma-associated microglia/macrophages (GAMs). However, it remains unclear how IDH genotypes contribute to GAM phenotypes. Here, it is demonstrated that gliomas expressing mutant IDH determine M1-like polarization of GAMs, while archetypal IDH induces M2-like polarization. Intriguingly, IDH-mutant gliomas secrete excess cholesterol, resulting in cholesterol-rich, pro-inflammatory GAMs without altering their cholesterol biosynthesis, and simultaneously exhibiting low levels of tumoral cholesterol due to expression remodeling of cholesterol transport molecules, particularly upregulation of ABCA1 and downregulation of LDLR. Mechanistically, a miR-19a/LDLR axis-mediated novel post-transcriptional regulation of cholesterol uptake is identified, modulated by IDH mutation, and influencing tumor cell proliferation and invasion. IDH mutation-induced PERK activation enhances cholesterol export from glioma cells via the miR-19a/LDLR axis and ABCA1/APOE upregulation. Further, a synthetic PERK activator, CCT020312 is introduced, which markedly stimulates cholesterol efflux from IDH wild-type glioma cells, induces M1-like polarization of GAMs, and consequently suppresses glioma cell invasion. The findings reveal an essential role of the PERK/miR-19a/LDLR signaling pathway in orchestrating gliomal cholesterol transport and the subsequent phenotypes of GAMs, thereby highlighting a novel potential target pathway for glioma therapy