Joint Association of Combined Healthy Lifestyle Factors and Hearing Loss with Cognitive Impairment in China.

BACKGROUND: Hearing loss and lifestyle factors have been associated with cognitive impairment. We aimed to explore the joint association of combined healthy lifestyle factors and hearing loss with cognitive impairment, which has been scarcely studied. METHODS: This baseline study used data from the CHOICE-Cohort study (Chinese Hearing Solution for Improvement of Cognition in Elders). Hearing loss was assessed by the better-ear pure-tone average (BPTA). A composite healthy lifestyle score was built based on never smoking, never drinking, regular physical activity, and balanced diet. Cognitive impairment was diagnosed by the Mini-Mental State Examination (MMSE) score of less than 24. RESULTS: We included 17057 participants aged 60 years or older in China (mean age 69.8 [SD 6.2] years, 55.7% female). Among the participants, 48.3% (n=8234) had mild hearing loss, and 25.8% (n=4395) had moderate or greater hearing loss. The proportion of participants with healthy lifestyle scores of 0-1, 2, 3, and 4 was 14.9% (n=2539), 29.3% (n=5000), 37.4% (n=6386), and 18.4% (n=3132), respectively. 29.6% (n=5057) participants had cognitive impairment. When compared to those with normal hearing and healthy lifestyle (scores of 3-4), participants with hearing loss plus unhealthy lifestyle (scores of 0-2) exhibited approximately twofold increased risk of cognitive impairment (OR=1.92, 95% CI 1.70-2.18). Conversely, the risk was greatly attenuated by adherence to healthy lifestyle in individuals with hearing loss (OR=1.57, 95% CI 1.40-1.76). CONCLUSIONS: Our findings demonstrated adherence to a broad range of healthy lifestyle factors was associated with a significantly lower risk of cognitive impairment among participants with hearing loss.

Classical swine fever virus inhibits serine metabolism-mediated antiviral immunity by deacetylating modified PHGDH.

Classical swine fever virus (CSFV), an obligate intracellular pathogen, hijacks cellular metabolism to evade immune surveillance and facilitate its replication. The precise mechanisms by which CSFV modulates immune metabolism remain largely unknown. Our study reveals that CSFV infection disrupts serine metabolism, which plays a crucial role in antiviral immunity. Notably, we discovered that CSFV infection leads to the deacetylation of PHGDH, a key enzyme in serine metabolism, resulting in autophagic degradation. This deacetylation impairs PHGDH's enzymatic activity, reduces serine biosynthesis, weakens innate immunity, and promotes viral proliferation. Molecularly, CSFV infection induces the association of HDAC3 with PHGDH, leading to deacetylation at the K364 site. This modification attracts the E3 ubiquitin ligase RNF125, which facilitates the addition of K63-linked ubiquitin chains to PHGDH-K364R. Subsequently, PHGDH is targeted for lysosomal degradation by p62 and NDP52. Furthermore, the deacetylation of PHGDH disrupts its interaction with the NAD+ substrate, destabilizing the PHGDH-NAD complex, impeding the active site, and thereby inhibiting de novo serine synthesis. Additionally, our research indicates that deacetylated PHGDH suppresses the mitochondria-MAVS-IRF3 pathway through its regulatory effect on serine metabolism, leading to decreased IFN-ß production and enhanced viral replication. Overall, our findings elucidate the complex interplay between CSFV and serine metabolism, revealing a novel aspect of viral immune evasion through the lens of immune metabolism. IMPORTANCE: Classical swine fever (CSF) seriously restricts the healthy development of China's aquaculture industry, and the unclear pathogenic mechanism and pathogenesis of classical swine fever virus (CSFV) are the main obstacle to CSF prevention, control, and purification. Therefore, it is of great significance to explore the molecular mechanism of CSFV and host interplay, to search for the key signaling pathways and target molecules in the host that regulate the replication of CSFV infection, and to elucidate the mechanism of action of host immune dysfunction and immune escape due to CSFV infection for the development of novel CSFV vaccines and drugs. This study reveals the mechanism of serine metabolizing enzyme post-translational modifications and antiviral signaling proteins in the replication of CSFV and enriches the knowledge of CSFV infection and immune metabolism.

Analysis of risk factors for weaning failure from mechanical ventilation in critically ill older patients with coronavirus disease 2019.

Objective: This study aimed to investigate the factors influencing weaning failure from invasive mechanical ventilation (IMV) in critically ill older patients with coronavirus disease 2019 (COVID-19). Methods: We enrolled critically ill older patients with COVID-19 who were admitted to the medical intensive care unit (ICU) and received IMV between December 2022 and June 2023. Results: We included 68 critically ill older patients with COVID-19 (52 male [76.5 %] and 16 female individuals [23.5 %]). The patients' median age (interquartile range) was 75.5 (70.3-82.8) years. The median length of ICU stay was 11.5 (7.0-17.8) days; 34 cases (50.0 %) were successfully weaned from IMV. The successfully weaned group had a higher proportion of underlying chronic obstructive pulmonary disease [6 (17.6 %) vs. 0, P = 0.033] and fewer cases of diabetes [7 (20.6 %) vs. 16 (47.1 %), P = 0.021] compared with the weaning failure group. Serum lactate levels [1.5 (1.2-2.3) vs. 2.6 (1.9-3.1) mmol/L, P < 0.001], blood urea nitrogen [8.2 (6.3-14.4) vs. 11.4 (8.0-21.3) mmol/L, P = 0.033], Acute Physiology and Chronic Health Evaluation (APACHE) II score [19.0 (12.0-23.3) vs. 22.5 (16.0-29.3), P = 0.014], and hospitalization days before endotracheal intubation [1.0 (0.0-5.0) vs. 3.0 (0.0-11.0), P = 0.023] were significantly decreased in the successfully weaned group, whereas PaO2/FiO2 [148.3 (94.6-200.3) vs. 101.1 (67.0-165.1), P = 0.038] and blood lymphocyte levels [0.6 (0.4-1.0) vs. 0.5 (0.2-0.6) 109/L, P = 0.048] were significantly increased, compared with the weaning failure group. Multivariate logistic regression analysis showed that diabetes (OR= 3.413, 95 %CI 1.029-11.326), P = 0.045), APACHE II Score (OR = 1.089, 95 % CI 1.008-1.175), P = 0.030), and hospitalization days before endotracheal intubation (OR = 1.137, 95 % CI 1.023-1.264), P = 0.017) were independent risk factors for weaning failure. Conclusion: In critically ill older patients with COVID-19 with diabetes, higher APACHE II Score, and longer hospitalization days before endotracheal intubation, weaning from IMV was more challenging. The study could help develop strategies for improving COVID-19 treatment.

A high-performance organic fluorescent probe with aggregation-induced emission properties for long-term tumor monitoring.

Near-infrared organic fluorescent probes have great need in biological sciences and medicine but most of them are still largely unable to meet demand. In this work, a delicate multipurpose organic fluorescent probe (DPPM-TPA) with aggregation-induced emission performances is designed and prepared by facile method to reflect fluorescence labeling, two-photon imaging, and long-term fluorescent tracking. Specifically, DPPM-TPA NPs was constructed from 4-(diphenylamino)phenylboronic acid and DPPM-Br by classical Suzuki coupling reaction and then coated with F127. Such nanoprobe possessed high stability in diverse medium under ambient temperatures, low cytotoxicity, and brilliant fluorescence performance. More importantly, DPPM-TPA NPs showed excellent two-photon imaging and extraordinary long-term fluorescence tracing capacity to malignant tumor, and it can last up to 9 days. These results indicated that DPPM-TPA NPs is expected to serve as a fluorescent probe for photodiagnostic and providing a new idea for the development of long-term fluorescent tracker.

IDO1 promotes CSFV replication by mediating tryptophan metabolism to inhibit NF-κB signaling.

Tryptophan metabolism plays a crucial role in facilitating various cellular processes essential for maintaining normal cellular function. Indoleamine 2,3-dioxygenase 1 (IDO1) catalyzes the conversion of tryptophan (Trp) into kynurenine (Kyn), thereby initiating the degradation of Trp. The resulting Kyn metabolites have been implicated in the modulation of immune responses. Currently, the role of IDO1-mediated tryptophan metabolism in the process of viral infection remains relatively unknown. In this study, we discovered that classical swine fever virus (CSFV) infection of PK-15 cells can induce the expression of IDO1, thereby promoting tryptophan metabolism. IDO1 can negatively regulate the NF-κB signaling by mediating tryptophan metabolism, thereby facilitating CSFV replication. We found that silencing the IDO1 gene enhances the expression of IFN-α, IFN-ß, and IL-6 by activating the NF-κB signaling pathway. Furthermore, our observations indicate that both silencing the IDO1 gene and administering exogenous tryptophan can inhibit CSFV replication by counteracting the cellular autophagy induced by Rapamycin. This study reveals a novel mechanism of IDO1-mediated tryptophan metabolism in CSFV infection, providing new insights and a theoretical basis for the treatment and control of CSFV.IMPORTANCEIt is well known that due to the widespread use of vaccines, the prevalence of classical swine fever (CSF) is shifting towards atypical and invisible infections. CSF can disrupt host metabolism, leading to persistent immune suppression in the host and causing significant harm when co-infected with other diseases. Changes in the host's metabolic profiles, such as increased catabolic metabolism of amino acids and the production of immunoregulatory metabolites and their derivatives, can also influence virus replication. Mammals utilize various pathways to modulate immune responses through amino acid utilization, including increased catabolic metabolism of amino acids and the production of immunoregulatory metabolites and their derivatives, thereby limiting viral replication. Therefore, this study proposes that targeting the modulation of tryptophan metabolism may represent an effective approach to control the progression of CSF.

PKM2 induces mitophagy through the AMPK-mTOR pathway promoting CSFV proliferation.

Viruses exploit the host cell's energy metabolism system to support their replication. Mitochondria, known as the powerhouse of the cell, play a critical role in regulating cell survival and virus replication. Our prior research indicated that the classical swine fever virus (CSFV) alters mitochondrial dynamics and triggers glycolytic metabolic reprogramming. However, the role and mechanism of PKM2, a key regulatory enzyme of glycolytic metabolism, in CSFV replication remain unclear. In this study, we discovered that CSFV enhances PKM2 expression and utilizes PKM2 to inhibit pyruvate production. Using an affinity purification coupled mass spectrometry system, we successfully identified PKM as a novel interaction partner of the CSFV non-structural protein NS4A. Furthermore, we validated the interaction between PKM2 and both CSFV NS4A and NS5A through co-immunoprecipitation and confocal analysis. PKM2 was found to promote the expression of both NS4A and NS5A. Moreover, we observed that PKM2 induces mitophagy by activating the AMPK-mTOR signaling pathway, thereby facilitating CSFV proliferation. In summary, our data reveal a novel mechanism whereby PKM2, a metabolic enzyme, promotes CSFV proliferation by inducing mitophagy. These findings offer a new avenue for developing antiviral strategies. IMPORTANCE: Viruses rely on the host cell's material-energy metabolic system for replication, inducing host metabolic disorders and subsequent immunosuppression-a major contributor to persistent viral infections. Classical swine fever virus (CSFV) is no exception. Classical swine fever is a severe acute infectious disease caused by CSFV, resulting in significant economic losses to the global pig industry. While the role of the metabolic enzyme PKM2 (pyruvate dehydrogenase) in the glycolytic pathway of tumor cells has been extensively studied, its involvement in viral infection remains relatively unknown. Our data unveil a new mechanism by which the metabolic enzyme PKM2 mediates CSFV infection, offering novel avenues for the development of antiviral strategies.

Triethanolamine-modified layered double oxide for efficient CO2 capture with low regeneration energy.

Various adsorbents for CO2 capture have been developed to mitigate the greenhouse effect. In this work, a novel CO2 adsorbent was fabricated by depositing triethanolamine (TEOA) onto the surface of nickel-cobalt-aluminum layered double oxide (NiCoAl-LDO) via the impregnation method. The CO2 capacity of the TEOA-LDO composite reached 1.27 mmol/g at 0 °C and 100 kPa, which was twice that of unmodified NiCoAl-LDO. In situ diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS) showed that the hydroxyl groups (-OH) on the surface of NiCoAl-LDO played a significant role in facilitating CO2 adsorption, similar to CO2 adsorption in the presence of H2O, where CO2 is not converted to carbamates but to bicarbonates through base-catalyzed hydration. This bicarbonate pathway doubles the theoretical amine efficiency, increases the CO2 capacity, and reduces the energy consumption during CO2 desorption. The work provides valuable insights into the development of CO2 adsorbents with high capacity, excellent cycling stability, and low regeneration energy.

CSFV restricts necroptosis to sustain infection by inducing autophagy/mitophagy-targeted degradation of RIPK3.

IMPORTANCE: CSFV infection in pigs causes persistent high fever, hemorrhagic necrotizing multi-organ inflammation, and high mortality, which seriously threatens the global swine industry. Cell death is an essential immune response of the host against pathogen invasion, and lymphopenia is the most typical clinical feature in the acute phase of CSFV infection, which affects the initial host antiviral immunity. As an "old" virus, CSFV has evolved mechanisms to evade host immune response after a long genetic evolution. Here, we show that necroptosis is a limiting host factor for CSFV infection and that CSFV-induced autophagy can subvert this host defense mechanism to promote its sustained replication. Our findings reveal a complex link between necroptosis and autophagy in the process of cell death, provide evidence supporting the important role for CSFV in counteracting host cell necrosis, and enrich our knowledge of pathogens that may subvert and evade this host defense.

Transcriptome Shock in Developing Embryos of a Brassica napus and Brassica rapa Hybrid.

Interspecific crosses that fuse the genomes of two different species may result in overall gene expression changes in the hybrid progeny, called 'transcriptome shock'. To better understand the expression pattern after genome merging during the early stages of allopolyploid formation, we performed RNA sequencing analysis on developing embryos of Brassica rapa, B. napus, and their synthesized allotriploid hybrids. Here, we show that the transcriptome shock occurs in the developing seeds of the hybrids. Of the homoeologous gene pairs, 17.1% exhibit expression bias, with an overall expression bias toward B. rapa. The expression level dominance also biases toward B. rapa, mainly induced by the expression change in homoeologous genes from B. napus. Functional enrichment analysis revealed significant differences in differentially expressed genes (DEGs) related to photosynthesis, hormone synthesis, and other pathways. Further study showed that significant changes in the expression levels of the key transcription factors (TFs) could regulate the overall interaction network in the developing embryo, which might be an essential cause of phenotype change. In conclusion, the present results have revealed the global changes in gene expression patterns in developing seeds of the hybrid between B. rapa and B. napus, and provided novel insights into the occurrence of transcriptome shock for harnessing heterosis.

A method for extracting tumor events from clinical CT examination reports.

Accurate and efficient extraction of key information related to diseases from medical examination reports, such as X-ray and ultrasound images, CT scans, and others, is crucial for accurate diagnosis and treatment. These reports provide a detailed record of a patient's health condition and are an important part of the clinical examination process. By organizing this information in a structured way, doctors can more easily review and analyze the data, leading to better patient care. In this paper, we introduce a new technique for extracting useful information from unstructured clinical text examination reports, which we refer to as a medical event extraction (EE) task. Our approach is based on Machine Reading Comprehension (MRC) and involves two sub-tasks: Question Answerability Judgment (QAJ) and Span Selection (SS). We use BERT to build a question answerability discriminator (Judger) that determines whether a reading comprehension question can be answered or not, thereby avoiding the extraction of arguments from unanswerable questions. The SS sub-task first obtains the encoding of each word in the medical text from the final layer of BERT's Transformer, then utilizes the attention mechanism to identify important information related to the answer from these word encodings. This information is then input into a bidirectional LSTM (BiLSTM) module to obtain a global representation of the text, which is used, along with the softmax function, to predict the span of the answer (i.e., the start and end positions of the answer in the text report). We use interpretable methods to calculate the Jensen-Shannon Divergence (JSD) score between various layers of the network and confirm that our model has strong word representation capabilities, enabling it to effectively extract contextual information from medical reports. Our experiments demonstrate that our method outperforms existing medical event extraction methods, achieving state-of-the-art results with a notable F1 score.

High-Flow Nasal Cannula versus Noninvasive Ventilation in AECOPD Patients with Respiratory Acidosis: A Retrospective Propensity Score-Matched Study.

Background: Limited data are available about the clinical outcomes of AECOPD patients with respiratory acidosis treated with HFNC versus NIV. Methods: We conducted a retrospective study to compare the efficacy of HFNC with NIV as initial ventilation support strategy in AECOPD patients with respiratory acidosis. Propensity score matching (PSM) was implemented to increase between-group comparability. Kaplan-Meier analysis was utilized to evaluate differences between the HFNC success, HFNC failure, and NIV groups. Univariate analysis was performed to identify the features that differed significantly between the HFNC success and HFNC failure groups. Results: After screening 2219 hospitalization records, 44 patients from the HFNC group and 44 from the NIV group were successfully matched after PSM. The 30-day mortality (4.5% versus 6.8%, p = 0.645) and 90-day mortality (4.5% versus 11.4%, p = 0.237) did not differ between the HFNC and NIV groups. Length of ICU stay (median: 11 versus 18 days, p = 0.001), length of hospital stay (median: 14 versus 20 days, p = 0.001), and hospital cost (median: 4392 versus 8403 $USD, p = 0.001) were significantly lower in the HFNC group compared with NIV group. The treatment failure rate was much higher in the HFNC group than in the NIV group (38.6% versus 11.4%, p = 0.003). However, patients who experienced HFNC failure and switched to NIV showed similar clinical outcomes to those who first received NIV. Univariate analysis showed that log NT-proBNP was an important factor for HFNC failure (p = 0.007). Conclusions: Compared with NIV, HFNC followed by NIV as rescue therapy may be a viable initial ventilation support strategy for AECOPD patients with respiratory acidosis. NT-proBNP may be an important factor for HFNC failure in these patients. Further well-designed randomized controlled trials are needed for more accurate and reliable results.

The regulation of cell homeostasis and antiviral innate immunity by autophagy during classical swine fever virus infection.

CSFV (classical swine fever virus) is currently endemic in developing countries in Asia and has recently re-emerged in Japan. Under the pressure of natural selection pressure, CSFV keeps evolving to maintain its ecological niche in nature. CSFV has evolved mechanisms that induce immune depression, but its pathogenic mechanism is still unclear. In this study, using transcriptomics and metabolomics methods, we found that CSFV infection alters innate host immunity by activating the interferon pathway, inhibiting host inflammation, apoptosis, and remodelling host metabolism in porcine alveolar macrophages. Moreover, we revealed that autophagy could alter innate immunity and metabolism induced by CSFV infection. Enhanced autophagy further inhibited CSFV-induced RIG-I-IRF3 signal transduction axis and JAK-STAT signalling pathway and blocked type I interferon production while reducing autophagy inhibition of the NF-κB signalling pathway and apoptosis in CSFV infection cells. Furthermore, the level of CSFV infection-induced glycolysis and the content of lactate and pyruvate, as well as 3-phosphoglyceraldehyde, a derivative of glycolysis converted to serine, was altered by autophagy. We also found that silencing HK2 (hexokinase 2), the rate-limiting enzyme of glycolytic metabolism, could induce autophagy but reduce the interferon signalling pathway, NF-κB signalling pathway, and inhibition of apoptosis induced by CSFV infection. In addition, inhibited cellular autophagy by silencing ATG5 or using 3-Methyladenine, could backfill the inhibitory effect of silencing HK2 on the cellular interferon signalling pathway, NF-κB signalling pathway, and apoptosis.

HSP90AA1 interacts with CSFV NS5A protein and regulates CSFV replication via the JAK/STAT and NF-κB signaling pathway.

Classical swine fever (CSF), caused by the classical swine fever virus (CSFV), is a highly contagious and fatal viral disease, posing a significant threat to the swine industry. Heat shock protein 90 kDa alpha class A member 1 (HSP90AA1) is a very conservative chaperone protein that plays an important role in signal transduction and viral proliferation. However, the role of HSP90AA1 in CSFV infection is unknown. In this study, we found that expression of HSP90AA1 could be promoted in PK-15 and 3D4/2 cells infected by CSFV. Over-expression of HSP90AA1 could inhibit CSFV replication and functional silencing of HSP90AA1 gene promotes CSFV replication. Further exploration revealed that HSP90AA1 interacted with CSFV NS5A protein and reduced the protein levels of NS5A. Since NS5A has an important role in CSFV replication and is closely related to type I IFN and NF-κB response, we further analyzed whether HSP90AA1 affects CSFV replication by regulating type I IFN and NF-κB pathway responses. Our research found HSP90AA1 positively regulated type I IFN response by promoting STAT1 phosphorylation and nuclear translocation processes and promoted the nuclear translocation processes of p-P65. However, CSFV infection antagonizes the activation of HSP90AA1 on JAK/STAT and NF-κB pathway. In conclusion, our study found that HSP90AA1 overexpression significantly inhibited CSFV replication and may inhibit CSFV replication by interacting with NS5A and activating JAK/STAT and NF-κB signaling pathways. These results provide new insights into the mechanism of action of HSP90AA1 in CSFV infection, which abundant the candidate library of anti-CSFV.

Genomic Characteristics and E Protein Bioinformatics Analysis of JEV Isolates from South China from 2011 to 2018.

Japanese encephalitis is a mosquito-borne zoonotic epidemic caused by the Japanese encephalitis virus (JEV). JEV is not only the leading cause of Asian viral encephalitis, but also one of the leading causes of viral encephalitis worldwide. To understand the genetic evolution and E protein characteristics of JEV, 263 suspected porcine JE samples collected from South China from 2011 to 2018 were inspected. It was found that 78 aborted porcine fetuses were JEV-nucleic-acid-positive, with a positive rate of 29.7%. Furthermore, four JEV variants were isolated from JEV-nucleic-acid-positive materials, namely, CH/GD2011/2011, CH/GD2014/2014, CH/GD2015/2015, and CH/GD2018/2018. The cell culture and virus titer determination of four JEV isolates showed that four JEV isolates could proliferate stably in Vero cells, and the virus titer was as high as 108.5 TCID 50/mL. The whole-genome sequences of four JEV isolates were sequenced. Based on the phylogenetic analysis of the JEV E gene and whole genome, it was found that CH/GD2011/2011 and CH/GD2015/2015 belonged to the GIII type, while CH/GD2014/2014 and CH/GD2018/2018 belonged to the GI type, which was significantly different from that of the JEV classical strain CH/BJ-1/1995. Bioinformatics tools were used to analyze the E protein phosphorylation site, glycosylation site, B cell antigen epitope, and modeled 3D structures of E protein in four JEV isolates. The analysis of the prevalence of JEV and the biological function of E protein can provide a theoretical basis for the prevention and control of JEV and the design of antiviral drugs.

Viruses Hijack ERAD to Regulate Their Replication and Propagation.

Endoplasmic reticulum-associated degradation (ERAD) is highly conserved in yeast. Recent studies have shown that ERAD is also ubiquitous and highly conserved in eukaryotic cells, where it plays an essential role in maintaining endoplasmic reticulum (ER) homeostasis. Misfolded or unfolded proteins undergo ERAD. They are recognized in the ER, retrotranslocated into the cytoplasm, and degraded by proteasomes after polyubiquitin. This may consist of several main steps: recognition of ERAD substrates, retrotranslocation, and proteasome degradation. Replication and transmission of the virus in the host is a process of a "game" with the host. It can be assumed that the virus has evolved various mechanisms to use the host's functions for its replication and transmission, including ERAD. However, until now, it is still unclear how the host uses ERAD to deal with virus infection and how the viruses hijack the function of ERAD to obtain a favorable niche or evade the immune clearance of the host. Recent studies have shown that viruses have also evolved mechanisms to use various processes of ERAD to promote their transmission. This review describes the occurrence of ERAD and how the viruses hijack the function of ERAD to spread by affecting the homeostasis and immune response of the host, and we will focus on the role of E3 ubiquitin ligase.

Harvesting the infrared part of solar light to promote charge transfer in Bi2S3/WO3 photoanode for enhanced photoelectrochemical water splitting.

Infrared light absorbed by semiconductors hardly contributes to the solar energy conversion due to its low photon energy. Herein, photothermal effect activated by infrared part of solar light is introduced to promote the photoelectrochemical (PEC) water splitting of photoanodes. Narrow band-gap semiconductor Bi2S3 is deposited on the surface of WO3 nanosheets, exhibiting a broad-spectral response. In addition to the enhanced density of photo-generated electrons, significant temperature elevation is observed for the Bi2S3/WO3 composite photoanode under the illumination of infrared part of solar light because of the photothermal conversion property of Bi2S3. The moderately enhanced temperature accelerates charge carrier migration and finally increases the efficiency of solar energy conversion. With the assistance of photothermal effect, a remarkable photocurrent density of 4.05 mA cm-2 at 1.23 V vs. reversible reference electrode (VRHE) is achieved by Bi2S3/WO3 composite photoanode, over 880% higher than that of the pristine WO3. The introduction of photothermal effect activated by infrared light provides general and robust strategy to promote the PEC performance of photoanodes.

Swine Enteric Coronavirus: Diverse Pathogen-Host Interactions.

Swine enteric coronavirus (SeCoV) causes acute gastroenteritis and high mortality in newborn piglets. Since the last century, porcine transmissible gastroenteritis virus (TGEV) and porcine epidemic diarrhea virus (PEDV) have swept farms all over the world and caused substantial economic losses. In recent years, porcine delta coronavirus (PDCoV) and swine acute diarrhea syndrome coronavirus (SADS-CoV) have been emerging SeCoVs. Some of them even spread across species, which made the epidemic situation of SeCoV more complex and changeable. Recent studies have begun to reveal the complex SeCoV-host interaction mechanism in detail. This review summarizes the current advances in autophagy, apoptosis, and innate immunity induced by SeCoV infection. These complex interactions may be directly involved in viral replication or the alteration of some signal pathways.

Spinel-Oxide-Integrated BiVO4 Photoanodes with Photothermal Effect for Efficient Solar Water Oxidation.

Spinel oxide materials have been widely used as oxygen evolution catalysts to enhance the photoelectrochemical (PEC) performance of photoelectrodes. Herein, we demonstrate that the water splitting efficiency of a photoanode can be further enhanced by introducing its photothermal effect. Under near-infrared radiation, the temperature of the NiCo2O4/BiVO4 photoanode increases moderately, leading to improved water oxidation kinetics and charge transport simultaneously. With the assistance of the photothermal effect, the obtained photoanode reaches a photocurrent density of 6.20 mA cm-2 at 1.23 V vs reversible hydrogen electrode. A series of spinel-type MCo2O4 oxides (M = Mn, Zn, Cu, and Fe) are deposited on the surface of the BiVO4 photoanode to show similar photothermally enhanced PEC performance. The research discovery provides a way for improving the catalytic activity of photoanode materials with a photothermal effect, which may be applied to various fields of energy conversion, including CO2 reduction, N2 fixation, and pollutant degradation.

Molecular Events Occurring in Lipophagy and Its Regulation in Flaviviridae Infection.

Diseases caused by Flaviviridae have a wide global and economic impact due to high morbidity and mortality. Flaviviridae infection usually leads to severe, acute or chronic diseases, such as liver injury and liver cancer resulting from hepatitis C virus (HCV) infection, dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS) caused by dengue virus (DENV). Given the highly complex pathogenesis of Flaviviridae infections, they are still not fully understood at present. Accumulating evidence suggests that host autophagy is disrupted to regulate the life cycle of Flaviviridae. Organelle-specific autophagy is able to selectively target different organelles for quality control, which is essential for regulating cellular homeostasis. As an important sub process of autophagy, lipophagy regulates lipid metabolism by targeting lipid droplets (LDs) and is also closely related to the infection of a variety of pathogenic microorganisms. In this review, we briefly understand the LDs interaction relationship with Flaviviridae infection, outline the molecular events of how lipophagy occurs and the related research progress on the regulatory mechanisms of lipophagy in Flaviviridae infection. Exploring the crosstalk between viral infection and lipophagy induced molecular events may provide new avenues for antiviral therapy.

Viral Infection Modulates Mitochondrial Function.

Mitochondria are important organelles involved in metabolism and programmed cell death in eukaryotic cells. In addition, mitochondria are also closely related to the innate immunity of host cells against viruses. The abnormality of mitochondrial morphology and function might lead to a variety of diseases. A large number of studies have found that a variety of viral infections could change mitochondrial dynamics, mediate mitochondria-induced cell death, and alter the mitochondrial metabolic status and cellular innate immune response to maintain intracellular survival. Meanwhile, mitochondria can also play an antiviral role during viral infection, thereby protecting the host. Therefore, mitochondria play an important role in the interaction between the host and the virus. Herein, we summarize how viral infections affect microbial pathogenesis by altering mitochondrial morphology and function and how viruses escape the host immune response.