A Review on the Impact of Outdoor Environment on Indoor Thermal Environment

Outdoor environment exchanges heat with indoor environment, enabling pollutants to infiltrate indoors, affecting buildings’ energy efficiency, comfort, and indoor air quality. Investigating the impact of the outdoor environment on the indoor thermal environment is crucial. Firstly, this paper reviews the coupling method to link the outdoor environment with the indoor environment. Secondly, it examines the impact of the outdoor physical environment, including neighboring buildings, greening, road surface, water body, and sky, on the indoor thermal environment. During the hottest summer, an increase of 17% in trees can reduce indoor temperature by 1.1 °C. Thirdly, the impact of weather conditions, including outdoor temperature, outdoor humidity, external wind, global warming, extreme weather conditions, and solar radiation, on the indoor thermal environment is studied. Due to global warming, cooling energy consumption and heating energy consumption in 2050 could increase by 223% to 1050%, and heating demand could decrease by 36% to 58%. Finally, the impact of outdoor air pollution on indoor environment and energy consumption is analyzed. For every 75 μg/m3 increase in PM2.5 concentration, average power consumption could increase by 11.2%. Recommendations for future research are provided. This study contributes to the understanding of the outdoor–indoor thermal relationship and offers insights into enhancing indoor thermal comfort and reducing building energy consumption.</p

Correction: The role of tumor-associated macrophages in tumor vascularization

This is a correction to a previously published article

The role of tumor-associated macrophages in tumor vascularization

Tumor vascularization is a highly complex process that involves the interaction between tumors and their surrounding stroma, as well as many distinct angiogenesis-regulating factors. Tumor associated macrophages (TAMs) represent one of the most abundant cell components in the tumor environment and key contributors to cancer-related inflammation. A large body of evidence supports the notion that TAMs play a critical role in promoting the formation of an abnormal tumor vascular network and subsequent tumor progression and invasion. Clinical and experimental evidence has shown that high levels of infiltrating TAMs are associated with poor patient prognosis and tumor resistance to therapies. In addition to stimulating angiogenesis during tumor growth, TAMs enhance tumor revascularization in response to cytotoxic therapy (e.g., radiotherapy), thereby causing cancer relapse. In this review, we highlight the emerging data related to the phenotype and polarization of TAMs in the tumor microenvironment, as well as the underlying mechanisms of macrophage function in the regulation of the angiogenic switch and tumor vascularization. Additionally, we discuss the potential of targeting pro-angiogenic TAMs, or reprograming TAMs toward a tumoricidal and angiostatic phenotype, to promote normalization of the tumor vasculature to enhance the outcome of cancer therapies

Hapln2 in neurological diseases and its potential as therapeutic target

Hyaluronan and proteoglycan link protein 2 (Hapln2) is important for the binding of chondroitin sulfate proteoglycans to hyaluronan. Hapln2 deficiency leads to the abnormal expression of extracellular matrix (ECM) proteins and dysfunctional neuronal conductivity, demonstrating the vital role of Hapln2 in these processes. Studies have revealed that Hapln2 promotes the aggregation of α-synuclein, thereby contributing to neurodegeneration in Parkinson’s disease (PD), and it was recently suggested to be in intracellular neurofibrillary tangles (NFTs). Additionally, the expression levels of Hapln2 showed lower in the anterior temporal lobes of individuals with schizophrenia than those of healthy subjects. Together, these studies implicate the involvement of Hapln2 in the pathological processes of neurological diseases. A better understanding of the function of Hapln2 in the central nervous system (CNS) will provide new insights into the molecular mechanisms of these diseases and help to establish promising therapeutic strategies. Herein, we review the recent progress in defining the role of Hapln2 in brain physiology and pathology

SRA Inhibition Improves Antitumor Potency of Antigen-Targeted Chaperone Vaccine

We Have Previously Demonstrated that Scavenger Receptor a (SRA) Acts as an Immunosuppressive Regulator of Dendritic Cell (DC) Function in Activating Antitumor T Cells. Here We Investigate the Potential of Inhibiting SRA Activity to Enhance DC-Targeted Chaperone Vaccines Including One that Was Recently Evaluated in Melanoma Patients. We Show that Short Hairpin RNA-Mediated SRA Silencing Significantly Enhances the Immunogenicity of DCs that Have Captured Chaperone Vaccines Designed to Target Melanoma (I.e., Hsp110-Gp100) and Breast Cancer (I.e., Hsp110-HER/Neu-ICD). SRA Downregulation Results in Heightened Activation of Antigen-Specific T Cells and Increased CD8+ T Cell-Dependent Tumor Inhibition. Additionally, Small Interfering RNA (SiRNA) Complexed with the Biodegradable, Biocompatible Chitosan as a Carrier Can Efficiently Reduce SRA Expression on CD11c+ DCs in Vitro and in Vivo. Our Proof-Of-Concept Study Shows that Direct Administration of the Chitosan-SiRNA Complex to Mice Promotes Chaperone Vaccine-Elicited Cytotoxic T Lymphocyte (CTL) Response, Culminating in Improved Eradication of Experimental Melanoma Metastases. Targeting SRA with This Chitosan-SiRNA Regimen Combined with the Chaperone Vaccine Also Leads to Reprogramming of the Tumor Environment, Indicated by Elevation of the Cytokine Genes (I.e., Ifng, Il12) Known to Skew Th1-Like Cellular Immunity and Increased Tumor Infiltration by IFN-Γ+CD8+ CTLs as Well as IL-12+CD11c+ DCs. Given the Promising Antitumor Activity and Safety Profile of Chaperone Vaccine in Cancer Patients, Further Optimization of the Chitosan-SiRNA Formulation to Potentially Broaden the Immunotherapeutic Benefits of Chaperone Vaccine is Warranted

A Hybrid Approach for Fault Diagnosis of Railway Rolling Bearings Using STWD-EMD-GA-LSSVM

Vibration signals resulting from railway rolling bearings are nonstationary by nature; this paper proposes a hybrid approach for the fault diagnosis of railway rolling bearings using segment threshold wavelet denoising (STWD), empirical mode decomposition (EMD), genetic algorithm (GA), and least squares support vector machine (LSSVM). The original signal is first denoised using STWD as a prefilter, which improves the subsequent decomposition into a number of intrinsic mode functions (IMFs) using EMD. Secondly, the IMF energy-torques are extracted as feature parameters. Concurrently, a GA is employed to optimize the LSSVM to improve the classification accuracy. Finally, the extracted features are used as inputs for classification by the GA-LSSVM. Actual railway rolling bearing vibration signals are used to experimentally verify the effectiveness of the proposed method. The results show that the novel method is effective and accurate for fault diagnosis of railway rolling bearings

Orexin-A protects against oxygen-glucose deprivation/reoxygenation-induced cell damage by inhibiting endoplasmic reticulum stress-mediated apoptosis via the Gi and PI3K signaling pathways

The neuropeptide orexin-A (OXA) has a neuroprotective effect, acting as an anti-apoptotic factor in response to multiple stimuli. Apoptosis induced by endoplasmic reticulum stress (ERS) underlies oxygen-glucose deprivation and reoxygenation (OGD/R)-induced cell damage, an in vitro model of ischemia/reperfusion injury. However, that OXA inhibits ERS-induced apoptosis in the OGD/R model has not been reported. In the present study, we investigated the neuroprotective effect of OXA (0.1 μM) on OGD/R-induced damage in the human neuroblastoma cell line SH-SY5Y. After OXA treatment following 4 h oxygen-glucose deprivation (OGD) and then 4 h reoxygenation (R), cell morphology, viability, and apoptosis were analyzed by histology, Cell Counting Kit-8 assay, and flow cytometry, respectively. Western blotting was used to measure expression levels of ERS- and apoptosis-related proteins. To determine signaling pathways involved in OXA-mediated neuroprotection, the Gi pathway inhibitor pertussis toxin (PTX; 100 ng/mL) and PI3K inhibitor LY294002 (LY; 10 μM) were added. In addition, in order to prove the specificity of these characteristics, the OXA antagonist Suvorexant (DORA; Ki of 0.55 nM and 0.35 nM for OX1R and OX2R) was used for intervention. Our results showed that OGD/R induced cell damage, manifested as morphological changes and a significant decrease in viability. Furthermore, Western blotting detected an increase in ERS-related proteins GRP78, p-IRE1α, p-JNK, and Cleaved caspase-12, as well as apoptosis-related proteins Cleaved caspase-3 and Bax, and a decrease in the anti-apoptosis factor Bcl-2. OXA intervention alleviated the degree of cellular damage, and protein expression was also reversed. In addition, the protective effect of OXA was reduced by adding PTX and LY. Meanwhile, after the use of DORA, changes in the expression of related proteins were detected, and it was found that the protective effect of OXA was weakened. Collectively, our results indicate that OXA has a neuroprotective effect on OGD/R-induced cell damage by inhibiting ERS-induced apoptosis through the combined action of Gi and PI3K signaling pathways. These findings help to clarify the mechanism underlying the neuroprotective action of OXA, which should aid the development of further candidate drugs, and provide a new therapeutic direction for the treatment of ischemic stroke

Cuproptosis-related genes signature and validation of differential expression and the potential targeting drugs in temporal lobe epilepsy

Introduction: Temporal lobe epilepsy (TLE) is the most common subtype of epilepsy in adults and is characterized by neuronal loss, gliosis, and sprouting mossy fibers in the hippocampus. But the mechanism underlying neuronal loss has not been fully elucidated. A new programmed cell death, cuproptosis, has recently been discovered; however, its role in TLE is not clear.Methods: We first investigated the copper ion concentration in the hippocampus tissue. Then, using the Sample dataset and E-MTAB-3123 dataset, we analyzed the features of 12 cuproptosis-related genes in TLEs and controls using the bioinformatics tools. Then, the expression of the key cuproptosis genes were confirmed using real-time PCR and immunohistochemical staining (IHC). Finally, the Enrichr database was used to screen the small molecules and drugs targeting key cuproptosis genes in TLE.Results: The Sample dataset displayed four differentially expressed cuproptosis-related genes (DECRGs; LIPT1, GLS, PDHA1, and CDKN2A) while the E-MTAB-3123 dataset revealed seven DECRGs (LIPT1, DLD, FDX1, GLS, PDHB, PDHA1, and DLAT). Remarkably, only LIPT1 was uniformly upregulated in both datasets. Additionally, these DECRGs are implicated in the TCA cycle and pyruvate metabolism—both crucial for cell cuproptosis—as well as various immune cell infiltrations, especially macrophages and T cells, in the TLE hippocampus. Interestingly, DECRGs were linked to most infiltrating immune cells during TLE’s acute phase, but this association considerably weakened in the latent phase. In the chronic phase, DECRGs were connected with several T-cell subclasses. Moreover, LIPT1, FDX1, DLD, and PDHB were related to TLE identification. PCR and IHC further confirmed LIPT1 and FDX1’s upregulation in TLE compared to controls. Finally, using the Enrichr database, we found that chlorzoxazone and piperlongumine inhibited cell cuproptosis by targeting LIPT1, FDX1, DLD, and PDHB.Conclusion: Our findings suggest that cuproptosis is directly related to TLE. The signature of cuproptosis-related genes presents new clues for exploring the roles of neuronal death in TLE. Furthermore, LIPT1 and FDX1 appear as potential targets of neuronal cuproptosis for controlling TLE’s seizures and progression

Characterization of a Novel, Cold-Adapted, and Thermostable Laccase-Like Enzyme With High Tolerance for Organic Solvents and Salt and Potent Dye Decolorization Ability, Derived From a Marine Metagenomic Library

Synthetic dyes are widely used in many industries, but they cause serious environmental problems due to their carcinogenic and mutagenic properties. In contrast to traditional physical and chemical treatments, biodegradation is generally considered an environmental-friendly, efficient, and inexpensive way to eliminate dye contaminants. Here, a novel laccase-like enzyme Lac1326 was cloned from a marine metagenomic library. It showed a maximum activity at 60°C, and it retained more than 40% of its maximal activity at 10°C and more than 50% at 20–70°C. Interestingly, the laccase behaved stably below 50°C, even in commonly used water-miscible organic solvents. The enzyme decolorized all tested dyes with high decolorization efficiency. This thermostable enzyme with high decolorization activity and excellent tolerance of organic solvents and salt has remarkable potential for bioremediation of dye wastewater. It is thus proposed as an industrial enzyme