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Identification for closed-loop two-dimensional (2-D) causal, recursive, and separable-in-denominator (CRSD) systems in the Roesser form is discussed in this study. For closed-loop 2-D CRSD systems, under feedback control condition, there exists some correlation between the unknown disturbances and future inputs which offers the fundamental limitation for utilizing standard open-loop 2-D CRSD systems subspace identification methods. In other words, the existing open-loop subspace approaches will result in biased estimates of plant parameters from closed-loop data. In this study, based on orthogonal projection and principal component analysis, novel 2-D CRSD subspace identification methods are developed, which are applicable to both open-loop and closed-loop data. Additionally, the whiteness external excitation case is discussed and subsequently modified instrument variables are adopted to improve the proposed subspace algorithm. An illustrative example of the injection molding process and several numerical examples are used to validate consistency and efficiency of the proposed subspace approaches for 2-D CRSD systems.

Self-trapped exciton (STE) emissions, featured by broad spectral band and minimal self-absorption, have garnered considerable attention for advanced lighting and imaging applications. However, developing strategies to facilitate multiple STE states, modulate the emission energy and extend the emission range remains a great challenge. Here, we introduce deviatoric stress to induce another intrinsic STE state (STE-2) and enable transitions between the intrinsic STE state (STE-1) and STE-2 in pyramidal ZnO nanocrystals. This approach results in a remarkable shift in emission energy, from yellow-green (2.34 eV) to deep-blue (2.88 eV). Combined in-situ stress monitoring and optical experiments show that the STE-2 state originates from a potential well generated by the deviatoric yield deformation of the pyramidal crystals under deviatoric stress. Spectroscopic and dynamical characterizations of the two STE emissions reveal a transition process in the carrier’s relaxation pathway from STE-2 to STE-1, and conversely at much higher pressures. These findings demonstrate that deviatoric stress serves as a robust tool for modulating STE emissions and provide new insights into the evolution of carrier dynamics of STE emissions. Deviatoric stress induces an intrinsic self-trapped exciton state (STE-2) and enables transitions between two intrinsic STE states in pyramidal ZnO nanocrystals. This approach results in a remarkable shift in emission energy, from 2.34 eV to 2.88 eV.

This paper provides an experimental investigation on the cracking process and residual mechanical properties of concrete after exposure to elevated temperatures. A total of 36 standard concrete prism specimens were tested after exposure to high temperatures of up to 600 °C. The failure modes, cracking process, residual mechanical properties, deformation characteristics and the strain distribution on the surface during the loading procedure were presented. The influences of exposure temperature and water–cement ratio (w/c) were interpreted. The digital image correlation (DIC) method was applied to quantitatively and visually characterize the development of cracking and relative displacement on the concrete surface. The findings suggest that the residual compressive strength and elastic modulus of the concrete decreases gradually with the increasing temperature, especially in the specimens with lower w/c ratio. The DIC technique provides an effective means to measure very precise and detailed information, including the crack opening and distribution of strain on the concrete surface.

This study aimed to estimate the attack rates, and identify the risk factors of COVID-19 infection. Based on a retrospective cohort study, we investigated 11,580 contacts of COVID-19 cases in Guangdong Province from 10 January to 15 March 2020. All contacts were tested by RT-PCR to detect their infection of SARS-COV-2. Attack rates by characteristics were calculated. Logistic regression was used to estimate the risk factors of infection for COVID-19. A total of 515 of 11,580 contacts were identified to be infected with SARS-COV-2. Compared to young adults aged 20-29 years, the infected risk was higher in children (RR: 2.59, 95%CI: 1.79-3.76), and old people aged 60-69 years (RR: 5.29, 95%CI: 3.76-7.46). Females also had higher infected risk (RR: 1.66, 95%CI: 1.39-2.00). People having close relationship with index cases encountered higher infected risk (RR for spouse: 20.68, 95%CI: 14.28-29.95; RR for non-spouse family members: 9.55, 95%CI: 6.73-13.55; RR for close relatives: 5.90, 95%CI: 4.06-8.59). Moreover, contacts exposed to index case in symptomatic period (RR: 2.15, 95%CI: 1.67-2.79), with critically severe symptoms (RR: 1.61, 95%CI: 1.00-2.57), with symptoms of dizzy (RR: 1.58, 95%CI: 1.08-2.30), myalgia (RR: 1.49, 95%CI: 1.15-1.94), and chill (RR: 1.42, 95%CI: 1.05-1.92) had higher infected risks. Children, old people, females, and family members are susceptible of COVID-19 infection, while index cases in the incubation period had lower contagiousness. Our findings will be helpful for developing targeted prevention and control strategies to combat the worldwide pandemic.

Sepsis-Associated Encephalopathy (SAE) is common in sepsis patients, with high mortality rates. It is believed that neuroinflammation is an important mechanism involved in SAE. High mobility group box 1 protein (HMGB1), as a late pro-inflammatory factor, is significantly increased during sepsis in different brain regions, including the hippocampus. HMGB1 causes neuroinflammation and cognitive impairment through direct binding to advanced glycation end products (RAGE) and Toll-like receptor 4 (TLR4). Electroacupuncture (EA) at Baihui (GV20) and Zusanli (ST36) is beneficial for neurological diseases and experimental sepsis. Our study used EA to treat SAE induced by lipopolysaccharide (LPS) in male Sprague–Dawley rats. The Y maze test was performed to assess working memory. Immunofluorescence (IF) and Western blotting (WB) were used to determine neuroinflammation and the HMGB1 signaling pathway. Results showed that EA could improve working memory impairment in rats with SAE. EA alleviated neuroinflammation by downregulating the hippocampus’s HMGB1/TLR4 and HMGB1/RAGE signaling, reducing the levels of pro-inflammatory factors, and relieving microglial and astrocyte activation. However, EA did not affect the tight junctions’ expression of the blood–brain barrier (BBB) in the hippocampus.

Taking the thermodynamic system of a 1000MW ultra-supercritical secondary reheating unit as the research object, the modeling energy consumption analysis was carried out, and the spatial distribution of energy consumption was determined, so as to provide a scientific basis for the operation optimization and energy-saving transformation of the unit. The analysis results show that: Boiler is one of the largest equipment factory irreversible loss, make up the loss by 85.1% of the total loss of the system, although the number of its external loss is not big but internal loss is very big, and the loss is high grade of energy, the number of the steam turbine cold source loss although large irreversible loss is not big but the grade is not high, its loss make up only 2.32% of the total loss system.

Background Aberrant RNA editing of adenosine-to-inosine (A-to-I) has been linked to multiple human cancers, but its role in intrahepatic cholangiocarcinoma (iCCA) remains unknown. We conducted an exome-wide investigation to search for dysregulated RNA editing that drive iCCA pathogenesis. Methods An integrative whole-exome and transcriptome sequencing analysis was performed to elucidate the RNA editing landscape in iCCAs. Putative RNA editing sites were validated by Sanger sequencing. In vitro and in vivo experiments were used to assess the effects of an exemplary target gene Kip1 ubiquitination-promoting complex 1 ( KPC1 ) and its editing on iCCA cells growth and metastasis. Crosstalk between KPC1 RNA editing and NF-κB signaling was analyzed by molecular methods. Results Through integrative omics analyses, we revealed an adenosine deaminases acting on RNA 1A (ADAR1)-mediated over-editing pattern in iCCAs. ADAR1 is frequently amplified and overexpressed in iCCAs and plays oncogenic roles. Notably, we identified a novel ADAR1-mediated A-to-I editing of KPC1 transcript, which results in substitution of methionine with valine at residue 8 (p.M8V). KPC1 p.M8V editing confers loss-of-function phenotypes through blunting the tumor-suppressive role of wild-type KPC1. Mechanistically, KPC1 p.M8V weakens the affinity of KPC1 to its substrate NF-κB1 p105, thereby reducing the ubiquitinating and proteasomal processing of p105 to p50, which in turn enhances the activity of oncogenic NF-κB signaling. Conclusions Our findings established that amplification-driven ADAR1 overexpression results in overediting of KPC1 p.M8V in iCCAs, leading to progression via activation of the NF-κB signaling pathway, and suggested ADAR1-KPC1-NF-κB axis as a potential therapeutic target for iCCA.

Glucocorticoid-induced osteonecrosis of the femoral head (ONFH) is a debilitating bone disorder characterized by impaired osteogenesis and apoptosis-driven bone collapse. This study identifies significantly reduced pentraxin 3 (PTX3) levels in patient samples and models. Recombinant PTX3 (rPTX3) alleviated dexamethasone-induced osteogenic suppression and apoptosis in vitro by activating TLR4/NF-κB pathway to downregulate fibroblast growth factor 21 (FGF21). In Ptx3 -knockout mice, glucocorticoid-induced bone deterioration was exacerbated, while PTX3 administration preserved bone architecture. Pharmacological blockade of TLR4/NF-κB signaling abolished PTX3’s protective effects. Notably, FGF21 suppression by activating transcription factor 3 (ATF3) retained bone-protective effects even in PTX3-deficient models, underscoring its role as a downstream effector. These findings establish the PTX3-TLR4/NF-κB-FGF21 axis as a key mechanism and suggest PTX3 supplementation as a potential therapeutic strategy against glucocorticoid-induced ONFH. PTX3 alleviates glucocorticoid-induced osteonecrosis by downregulating FGF21 via TLR4/NF-κB pathway, revealing a potential therapeutic strategy

BackgroundIdentification of futile recanalisation following endovascular therapy (EVT) in patients with acute ischaemic stroke is both crucial and challenging. Here, we present a novel risk stratification system based on hybrid machine learning method for predicting futile recanalisation.MethodsHybrid machine learning models were developed to address six clinical scenarios within the EVT and perioperative management workflow. These models were trained on a prospective database using hybrid feature selection technique to predict futile recanalisation following EVT. The optimal model was validated and compared with existing models and scoring systems in a multicentre prospective cohort to develop a hybrid machine learning-based risk stratification system for futile recanalisation prediction.ResultsUsing a hybrid feature selection approach, we trained and tested multiple classifiers on two independent patient cohorts (n=1122) to develop a hybrid machine learning-based prediction model. The model demonstrated superior discriminative ability compared with other models and scoring systems (area under the curve=0.80, 95% CI 0.73 to 0.87) and was transformed into a web application (RESCUE-FR Index) that provides a risk stratification system for individual prediction (accessible online at fr-index.biomind.cn/RESCUE-FR/).ConclusionsThe proposed hybrid machine learning approach could be used as an individualised risk prediction model to facilitate adherence to clinical practice guidelines and shared decision-making for optimal candidate selection and prognosis assessment in patients undergoing EVT.

Background Aberrant RNA editing of adenosine-to-inosine (A-to-I) has been linked to multiple human cancers, but its role in intrahepatic cholangiocarcinoma (iCCA) remains unknown. We conducted an exome-wide investigation to search for dysregulated RNA editing that drive iCCA pathogenesis. Methods An integrative whole-exome and transcriptome sequencing analysis was performed to elucidate the RNA editing landscape in iCCAs. Putative RNA editing sites were validated by Sanger sequencing. In vitro and in vivo experiments were used to assess the effects of an exemplary target gene Kip1 ubiquitination-promoting complex 1 (KPC1) and its editing on iCCA cells growth and metastasis. Crosstalk between KPC1 RNA editing and NF-κB signaling was analyzed by molecular methods. Results Through integrative omics analyses, we revealed an adenosine deaminases acting on RNA 1A (ADAR1)-mediated over-editing pattern in iCCAs. ADAR1 is frequently amplified and overexpressed in iCCAs and plays oncogenic roles. Notably, we identified a novel ADAR1-mediated A-to-I editing of KPC1 transcript, which results in substitution of methionine with valine at residue 8 (p.M8V). KPC1 p.M8V editing confers loss-of-function phenotypes through blunting the tumor-suppressive role of wild-type KPC1. Mechanistically, KPC1 p.M8V weakens the affinity of KPC1 to its substrate NF-κB1 p105, thereby reducing the ubiquitinating and proteasomal processing of p105 to p50, which in turn enhances the activity of oncogenic NF-κB signaling. Conclusions Our findings established that amplification-driven ADAR1 overexpression results in overediting of KPC1 p.M8V in iCCAs, leading to progression via activation of the NF-κB signaling pathway, and suggested ADAR1-KPC1-NF-κB axis as a potential therapeutic target for iCCA. Keywords: Intrahepatic cholangiocarcinoma, RNA editing, KPC1, p105, NF-κB pathway