Enhanced Electrical Conductivity of (001) Oriented Sr0.9La0.1TiO3 Microplatelets for Thermoelectric Applications.

Two-dimensional perovskite microplatelets have played an important role in various applications, especially acting as a template to guide grains' epitaxial growth in the preparation of textured ceramics. The (001) oriented Sr0.9La0.1TiO3 microplatelets with a high aspect ratio of ∼20 were synthesized and obtained from Aurivillius Bi4Ti3O12 precursors. To reveal the mechanism of topochemical microcrystal conversion of Bi4Ti3O12 to Sr0.9La0.1TiO3, the reaction interface, morphology development, and phase composition evolution of the (001) oriented Sr0.9La0.1TiO3 microplatelets were investigated. When the temperature of the molten salt is above 753 °C, multiple Sr0.9La0.1TiO3 topological nucleation events took place. At 950 °C, the polycrystalline aggregate of (001)-oriented Sr0.9La0.1TiO3 crystallites grew in place of the original single crystal Bi4Ti3O12 platelets. When the temperature reached 1150 °C, the Sr0.9La0.1TiO3 platelets preserved the shape of a high aspect ratio and exhibited not only enhanced electrical conductivity with a carrier concentration of 3.518 × 1020 cm-3 and carrier mobility of 8.460 cm2·V-1·s-1 but also significantly decreased thermal conductivity ranging from 5.65 W·m-1·K-1 at 300 K to 2.54 W·m-1·K-1 at 1073 K. It can be widely applied in the field of template grain growth methods for preparing textured thermoelectric ceramics to improve their thermoelectric properties.

Estradiol enhances T-type calcium channel activation in human myometrium telocytes.

Uterine peristalsis is essential for gamete transport and embryo implantation. It shares the characteristics of spontaneity, rhythmicity, and directivity with gastrointestinal peristalsis. Telocytes, the "interstitial Cajal-like cells" outside the digestive canal, are also located in the uterus and may act as pacemakers. To investigate the possible origin and regulatory mechanism of periodic uterine peristalsis in the human menstrual cycle, telocytes in the myometrium were studied to determine the effect of estradiol on T-type calcium channel regulation. In this study, biopsies of the human myometrium were obtained for cell culture, and double-labeling immunofluorescence screening was used to identify telocytes and T-type calcium channel expression. Intracellular calcium signal measurements and patch-clamp recordings were used to investigate the role of T-type calcium channels in regulating calcium currents with or without estradiol. Our study demonstrates that telocytes exist in the human uterus and express T-type calcium channels. The intracellular Ca2+ fluorescence intensity marked by Fluo-4AM was dramatically decreased by NNC 55-0396, a highly selective T-type calcium channel blocker, but enhanced by estradiol. T-type calcium current amplitude increased in telocytes incubated with estradiol in a dose-dependent manner compared to the control group. In conclusion, our study demonstrated that telocytes exist in the human myometrium, expressing T-type calcium channels and estradiol-enhanced T-type calcium currents, which may be a reasonable explanation for the origin of uterine peristalsis. The role of telocytes in the human uterus as pacemakers and message transfer stations in uterine peristalsis may be worth further investigation.

THOC1 deficiency leads to late-onset nonsyndromic hearing loss through p53-mediated hair cell apoptosis.

Apoptosis of cochlear hair cells is a key step towards age-related hearing loss. Although numerous genes have been implicated in the genetic causes of late-onset, progressive hearing loss, few show direct links to the proapoptotic process. By genome-wide linkage analysis and whole exome sequencing, we identified a heterozygous p.L183V variant in THOC1 as the probable cause of the late-onset, progressive, non-syndromic hearing loss in a large family with autosomal dominant inheritance. Thoc1, a member of the conserved multisubunit THO/TREX ribonucleoprotein complex, is highly expressed in mouse and zebrafish hair cells. The thoc1 knockout (thoc1 mutant) zebrafish generated by gRNA-Cas9 system lacks the C-startle response, indicative of the hearing dysfunction. Both Thoc1 mutant and knockdown zebrafish have greatly reduced hair cell numbers, while the latter can be rescued by embryonic microinjection of human wild-type THOC1 mRNA but to significantly lesser degree by the c.547C>G mutant mRNA. The Thoc1 deficiency resulted in marked apoptosis in zebrafish hair cells. Consistently, transcriptome sequencing of the mutants showed significantly increased gene expression in the p53-associated signaling pathway. Depletion of p53 or applying the p53 inhibitor Pifithrin-α significantly rescued the hair cell loss in the Thoc1 knockdown zebrafish. Our results suggested that THOC1 deficiency lead to late-onset, progressive hearing loss through p53-mediated hair cell apoptosis. This is to our knowledge the first human disease associated with THOC1 mutations and may shed light on the molecular mechanism underlying the age-related hearing loss.

A Novel Unsupervised Video Anomaly Detection Framework Based on Optical Flow Reconstruction and Erased Frame Prediction.

Reconstruction-based and prediction-based approaches are widely used for video anomaly detection (VAD) in smart city surveillance applications. However, neither of these approaches can effectively utilize the rich contextual information that exists in videos, which makes it difficult to accurately perceive anomalous activities. In this paper, we exploit the idea of a training model based on the "Cloze Test" strategy in natural language processing (NLP) and introduce a novel unsupervised learning framework to encode both motion and appearance information at an object level. Specifically, to store the normal modes of video activity reconstructions, we first design an optical stream memory network with skip connections. Secondly, we build a space-time cube (STC) for use as the basic processing unit of the model and erase a patch in the STC to form the frame to be reconstructed. This enables a so-called "incomplete event (IE)" to be completed. On this basis, a conditional autoencoder is utilized to capture the high correspondence between optical flow and STC. The model predicts erased patches in IEs based on the context of the front and back frames. Finally, we employ a generating adversarial network (GAN)-based training method to improve the performance of VAD. By distinguishing the predicted erased optical flow and erased video frame, the anomaly detection results are shown to be more reliable with our proposed method which can help reconstruct the original video in IE. Comparative experiments conducted on the benchmark UCSD Ped2, CUHK Avenue, and ShanghaiTech datasets demonstrate AUROC scores reaching 97.7%, 89.7%, and 75.8%, respectively.

Notch1 signaling modulates hypoxia-induced multidrug resistance in human laryngeal cancer cells.

BACKGROUND: Laryngeal carcinoma is one of the common malignant tumors of the head and neck. Multidrug resistance (MDR) remains a critical problem in the chemotherapy of patients with laryngeal cancer. This study aims to clarify the role and mechanisms of Notch1 signaling in MDR induced by hypoxia in laryngeal cancer cells. METHODS AND RESULTS: Laryngeal carcinoma cells were cultured under normoxia or hypoxia. Notch1 expression was inhibited by small interfering RNA (siRNA). The mRNA expression of Notch1, Hes1, Hey1, MDR1 and survivin was analyzed by real-time PCR. The protein expression of Notch1, the Notch1 intracellular domain (N1ICD), MDR1/P-gp and survivin was analyzed by Western blotting. Current research has shown that hypoxia can upregulate Notch1 expression and Notch1 signaling activity. Furthermore, suppression of Notch1 expression effectively downregulated Notch1 signaling activity and the expression of the MDR and survivin genes in laryngeal cancer cells under hypoxic conditions (P < 0.05). The Cell Counting Kit-8 (CCK-8) assay results confirmed that the sensitivity of hypoxic laryngeal cancer cells to a variety of drugs could be upregulated by suppressing Notch1 expression (P < 0.05). Additionally, flow cytometry (FCM) showed that suppression of Notch1 expression significantly increased drug-induced apoptosis and intracellular rhodamine 123 (Rh123) accumulation in hypoxic laryngeal carcinoma cells (P < 0.05). CONCLUSIONS: Notch1 signalling could be regarded as a pivotal regulator of hypoxia-induced MDR in laryngeal cancer cells through the regulation of survivin-mediated apoptosis resistance and MDR1/P-gp-mediated drug transport.

Effect of Notch1 signaling on cellular proliferation and apoptosis in human laryngeal carcinoma.

BACKGROUND: The occurrence and development of malignancies include excessive proliferation and apoptosis resistance in tumor cells. This study aimed to identify the effects of Notch1 signaling on proliferation and apoptosis of laryngeal cancer cells in a hypoxic microenvironment. METHODS: Notch1 and Ki-67 expression in laryngeal squamous cell carcinoma (LSCC) tissues was detected by immunohistochemistry. The apoptotic index (AI) of LSCC was evaluated by the TUNEL method. Small interfering RNA (siRNA) was used to inhibit Notch1 expression in laryngeal cancer cells. Real-time PCR was used to measure Notch1, Hes1, and Hey1 mRNA expression, and Western blotting was used to measure Notch1 and Notch1 intracellular domain (N1ICD) protein expression. Annexin V-FITC/propidium iodide staining and Cell Counting Kit-8 assays were used to measure cell apoptosis and proliferation, respectively. RESULTS: Notch1 expression was significantly related to the proliferation index (PI) and AI in LSCC tissues. Hypoxia could induce proliferation and inhibit apoptosis in cancer cells. Notch1 expression and Notch1 signaling activity could be upregulated by hypoxia. Suppressing Notch1 signaling activity in hypoxic cells could decrease proliferation and increase apoptosis. CONCLUSIONS: Our study has demonstrated that hypoxia may promote proliferation and inhibit apoptosis of laryngeal cancer cells. Notch1 signaling may play a pivotal role in regulating the proliferation and apoptosis resistance of laryngeal cancer cells under hypoxic conditions.

Regulation of the autophagy plays an important role in acute kidney injury induced acute lung injury.

AIM: This study aimed to investigate the regulatory role of autophagy in acute kidney injury (AKI) induced acute lung injury (ALI). METHODS: The male Sprague-Dawley rats were divided into four groups: normal saline-treated sham rats (sham group), normal saline-treated ischemia-reperfusion injury rats (IRI group), 3-methyladenine-treated IRI rats (3-MA group), and rapamycin-treated IRI rats (RA group). The rats in the IRI rat model received the nephrectomy of the right kidney and was subjected to 60 mins of left renal pedicle occlusion, followed by 12, 24, 48, and 72 h of reperfusion. The levels of Scr, BUN, wet-to-dry ratio of lung, inflammatory cytokines, and oxidative stress were determined. The damage to tissues was detected by histological examinations. The western blot and immunohistochemistry methods were conducted to determine the expression of indicated proteins. RESULTS: Renal IRI could induce the pulmonary injury after AKI, which caused significant increases in the function index of pulmonary and renal, the levels of inflammatory cytokines, and biomarkers of oxidative stress. In comparison to the IRI group, the RA group showed significantly decreased P62 and Caspase-3 expression and increased LC-II/LC3-I, Beclin-1, Bcl-2, and unc-51-like autophagy activating kinase 1 expression. Meanwhile, by suppressing the inflammation and oxidative stress, as well as inhibiting the pathological lesions in kidney and lung tissues, the autophagy could effectively ameliorate IRI-induced AKI and ALI. CONCLUSIONS: Autophagy plays an important role in AKI-induced ALI, which could be used as a new target for AKI therapy and reduce the mortality caused by the complication.

Joint Lossless Image Compression and Encryption Scheme Based on CALIC and Hyperchaotic System.

For efficiency and security of image transmission and storage, the joint image compression and encryption method that performs compression and encryption in a single step is a promising solution due to better security. Moreover, on some important occasions, it is necessary to save images in high quality by lossless compression. Thus, a joint lossless image compression and encryption scheme based on a context-based adaptive lossless image codec (CALIC) and hyperchaotic system is proposed to achieve lossless image encryption and compression simultaneously. Making use of the characteristics of CALIC, four encryption locations are designed to realize joint image compression and encryption: encryption for the predicted values of pixels based on gradient-adjusted prediction (GAP), encryption for the final prediction error, encryption for two lines of pixel values needed by prediction mode and encryption for the entropy coding file. Moreover, a new four-dimensional hyperchaotic system and plaintext-related encryption based on table lookup are all used to enhance the security. The security tests show information entropy, correlation and key sensitivity of the proposed methods reach 7.997, 0.01 and 0.4998, respectively. This indicates that the proposed methods have good security. Meanwhile, compared to original CALIC without security, the proposed methods increase the security and reduce the compression ratio by only 6.3%. The test results indicate that the proposed methods have high security and good lossless compression performance.

The projections from the anterior cingulate cortex to the nucleus accumbens and ventral tegmental area contribute to neuropathic pain-evoked aversion in rats.

Although the anterior cingulate cortex (ACC) plays a vital role in neuropathic pain-related aversion, the underlying mechanisms haven't been fully studied. The mesolimbic dopamine system encodes reward and aversion, and participates in the exacerbation of chronic pain. Therefore, we investigated whether the ACC modulates aversion to neuropathic pain via control of the mesolimbic dopamine system, in a rat model of chronic constriction injury (CCI) to the sciatic nerve. Using anterograde and retrograde tracings, we confirmed that a subgroup of ACC neurons projected to the nucleus accumbens (NAc) and ventral tegmental area (VTA), which are two crucial nodes of the mesolimbic dopamine system. Combining electrophysiology in juvenile rats 7 days post-CCI, we found that the NAc/VTA-projecting neurons were hyperexcitable after CCI. Chemogenetic inhibition of these projections induced conditioned place preference in young adult rats 10-14 days post-CCI, without modulating the evoked pain threshold, whereas activation of these projections in sham rats mimicked aversive behavior. Furthermore, the function of the ACC projections was probably mediated by NAc D2-type medium spiny neurons and VTA GABAergic neurons. Taken together, our findings suggest that projections from the ACC to the NAc and VTA mediate neuropathic pain-related aversive behavior.

Distinct Expression Patterns of Apoptosis and Autophagy-Associated Proteins and Genes during Postnatal Development of Spiral Ganglion Neurons in Rat.

Autophagy and apoptosis have a complex interplay in the early embryo development. The development of spiral ganglion neurons (SGNs) in addition to Corti's organ in the mammalian cochlea remains crucial in the first two-week postnatal period. To investigate the roles of apoptosis and autophagy in the development of SGNs, light microscopy was used to observe the morphological changes of SGNs. The number of SGNs was decreased from P1 to P7 and plateaued from P10 to P14. Immunohistochemistry results revealed positive expression of cleaved-caspase3, bcl-2, microtubule-associated protein light chain 3-II (LC3-II), Beclin1, and sequestosome 1 (SQSTM1/P62) in SGNs. The apoptotic bodies and autophagosomes and autolysosomes were also identified by transmission electron microscopy at P1 and P7. Real-time PCR and western blotting results revealed that the apoptotic activity peaked at P7 and the autophagy activity was gradually upregulated along with the development. Taken together, our results for the first time showed that autophagy and apoptosis in SGNs play distinct roles during specific developmental phases in a time-dependent manner.

The p.R206C Mutation in MYO7A Leads to Autosomal Dominant Nonsyndromic Hearing Loss.

BACKGROUND: Dominant mutations in MYO7A may lead to nonsyndromic deafness DFNA11. A p.R206C variant in MYO7A has previously been reported in a small deaf family from Taiwan but with ambiguous pathogenicity and inheritance pattern. AIMS/OBJECTIVES: Our study aims to clarify the pathogenicity of this variant by clinical characterization and genetic analysis of a separate autosomal dominant deaf family harboring this variant in mainland China. MATERIALS AND METHODS: Auditory features of hearing loss were characterized in representative affected family members. Mutation screening was performed by targeted next-generation sequencing of 138 known deafness genes in the proband. Candidate pathogenic mutations were confirmed by Sanger sequencing in family members and ethnically matched controls. RESULTS: Consistent with typical DFNA11 phenotype, the affected family members in this study showed delayed-onset, progressive hearing loss affecting mostly high frequencies. Targeted next-generation sequencing identified a p.R206C mutation in MYO7A as the only candidate pathogenic mutation cosegregating with the hearing phenotype. This mutation is not seen in 200 Chinese Han normal-hearing controls. CONCLUSIONS AND SIGNIFICANCE: The recurrent p.R206C variant in MYO7A is pathogenic and is likely in a mutation hot spot or due to a founder effect. Reports of such rare variants in multiple patients or families may facilitate exploitation of its pathogenicity.

Postnatal Development of Microglia-Like Cells in Mouse Cochlea.

Microglial cells are involved in surveillance and cleaning of the central nervous system. Recently, microglial-like cells (MLC) have been found in an adult cochlea and investigated for their role in cochlear inflammation. The presence and potential roles of MLCs during the development of the cochlea, however, remain unclear. In this study, immunostaining was performed using the MLC-specific marker IBA1 to characterize the presence, distribution, and morphology of MLCs in the developing cochlea. From P0 to P14, MLCs were present in a variety of cochlear regions including the modiolus, spiral lamina, spiral ganglion, spiral ligament, and the organ of Corti. Interestingly, the overall number of MLCs in a mouse cochlea steadily increased since P0, peaks at P5, then gradually decreased from P5 to P14. In the spiral ligament, the distribution of the MLCs trends to shift from the type I/II fibrocyte-rich regions to the type III/IV fibrocyte-rich regions during the course of cochlear development, accompanied by the morphological changes of MLCs from the amoeboid, activated form to the ramified, quiescent form. Our results suggested that MLCs experience drastic morphological and distributional changes during postnatal cochlear development, which may play a role in the maturing and remodeling of the cochlea.

Mutation in the Hair Cell Specific Gene POU4F3 Is a Common Cause for Autosomal Dominant Nonsyndromic Hearing Loss in Chinese Hans.

Autosomal dominant nonsyndromic hearing loss (ADNSHL) is extremely heterogeneous. So far the genetic etiological contribution of the gene POU4F3 associated with ADNSHL has been rarely reported. In our previous study, a c.603_604delGG mutation in the hair cell specific gene POU4F3 has been identified as the pathogenic cause in one of the seven Chinese Han ADNSHL families. In the present study, we performed targeted next-generation sequencing of 144 known deafness genes in another nine Chinese Han ADNSHL families and identified two more novel mutations in POU4F3, p.Leu311Pro and c.120+1G>C, as the pathogenic cause. Clinical characterization of the affected individuals in these three families showed that the three POU4F3 mutations may lead to progressive hearing loss with variable ages of onset and degrees of severity. Our results suggested that mutations in POU4F3 are a relatively common cause (3/16) for ADNSHL in Chinese Hans, which should be routinely screened in such cases during genetic testing.

NLRP3 Is Expressed in the Spiral Ganglion Neurons and Associated with Both Syndromic and Nonsyndromic Sensorineural Deafness.

Nonsyndromic deafness is genetically heterogeneous but phenotypically similar among many cases. Though a variety of targeted next-generation sequencing (NGS) panels has been recently developed to facilitate genetic screening of nonsyndromic deafness, some syndromic deafness genes outside the panels may lead to clinical phenotypes similar to nonsyndromic deafness. In this study, we performed comprehensive genetic screening in a dominant family in which the proband was initially diagnosed with nonsyndromic deafness. No pathogenic mutation was identified by targeted NGS in 72 nonsyndromic and another 72 syndromic deafness genes. Whole exome sequencing, however, identified a p.E313K mutation in NLRP3, a gene reported to cause syndromic deafness Muckle-Wells Syndrome (MWS) but not included in any targeted NGS panels for deafness in previous reports. Follow-up clinical evaluation revealed only minor inflammatory symptoms in addition to deafness in six of the nine affected members, while the rest, three affected members, including the proband had no obvious MWS-related inflammatory symptoms. Immunostaining of the mouse cochlea showed a strong expression of NLRP3 in the spiral ganglion neurons. Our results suggested that NLRP3 may have specific function in the spiral ganglion neurons and can be associated with both syndromic and nonsyndromic sensorineural deafness.

Alteration in rectification of potassium channels in perinatal hypoxia ischemia brain damage.

Oligodendrocyte progenitor cells (OPCs) are susceptible to perinatal hypoxia ischemia brain damage (HIBD), which results in infant cerebral palsy due to the effects on myelination. The origin of OPC vulnerability in HIBD, however, remains controversial. In this study, we defined the HIBD punctate lesions by MRI diffuse excessive high signal intensity (DEHSI) in postnatal 7-day-old rats. The electrophysiological functional properties of OPCs in HIBD were recorded by patch-clamp in acute cerebral cortex slices. The slices were intracellularly injected with Lucifer yellow and immunohistochemically labeled with NG2 antibody to identify local OPCs. Passive membrane properties and K(+) channel functions in OPCs were analyzed to estimate the onset of vulnerability in HIBD. The resting membrane potential, membrane resistance, and membrane capacitance of OPCs were increased in both the gray and white matter of the cerebral cortex. OPCs in both the gray and white matter exhibited voltage-dependent K(+) currents, which consisted of the initiated rectified potassium currents (IA) and the sustained rectified currents (IK). The significant alternation in membrane resistance was influenced by the diversity of potassium channel kinetics. These findings suggest that the rectification of IA and IK channels may play a significant role in OPC vulnerability in HIBD.

A Low Dose of Rapamycin Promotes Hair Cell Differentiation by Enriching SOX2+ Progenitors in the Neonatal Mouse Inner Ear Organoids.

PURPOSE: To investigate the impact of rapamycin on the differentiation of hair cells. METHODS: Murine cochlear organoids were derived from cochlear progenitor cells. Different concentrations of rapamycin were added into the culture medium at different proliferation and differentiation stages. RESULTS: Rapamycin exhibited a concentration-dependent reduction in the proliferation of these inner ear organoids. Nevertheless, organoids subjected to a 10-nM dose of rapamycin demonstrated a markedly increased proportion of hair cells. Furthermore, rapamycin significantly upregulated the expression of markers associated with both hair cells and supporting cells, including ATOH1, MYO7A, and SOX2. Mechanistic studies revealed that rapamycin preferentially suppressed cells without Sox2 expression during the initial proliferation stage, thereby augmenting and refining the population of SOX2+ progenitors. These enriched progenitors were predisposed to differentiate into hair cells during the later stages of organoid development. Conversely, the use of the mTOR activator MHY 1485 demonstrated opposing effects. CONCLUSION: Our findings underscore a practical strategy for enhancing the generation of inner ear organoids with a low dose of rapamycin, achieved by enriching SOX2+ progenitors in an in vitro setting.

Synergistic effect of hydrothermal sludge and food waste in the anaerobic co-digestion process: microbial shift and dewaterability.

While thermal hydrolysis technology is commonly employed for sewage sludge treatment in extensive wastewater treatment facilities, persistent challenges remain, including issues such as ammonia-induced digestive inhibition and reduced productivity stemming from nutrient deficiency within the hydrothermal sludge. In this study, the effects of hydrothermal sludge-to-food waste mixing ratios and fermentation temperatures on anaerobic co-digestion were systematically investigated through a semi-continuous experiment lasting approximately 100 days. The results indicated that anaerobic co-digestion of hydrothermal sludge and food waste proceeded synergistically at any mixing ratio, and the synergistic effect is mainly attributed to the improvement of carbohydrate removal and digestive system stability. However, thermophilic digestion did not improve the anaerobic performance and methane yield. On the contrary, mesophilic digestion performed better in terms of organic matter removal, especially in the utilization of soluble carbohydrates, soluble proteins, and VFAs. Microbial community analysis revealed that the transition from mesophilic to thermophilic anaerobic co-digestion prompts changes in the methane-producing pathways. Specifically, the transition entails a gradual shift from pathways involving acetoclastic and hydrogenotrophic methanogenesis to a singular hydrogenotrophic methanogenesis pathway. This shift is driven by thermodynamic tendencies, as reflected in Gibbs free energy, as well as environmental factors like ammonia nitrogen and volatile fatty acids. Lastly, it is worth noting that the introduction of food waste did lead to a reduction in cake solids following dewatering. Nevertheless, it was observed that thermophilic digestion had a positive impact on dewatering performance.

Effects of nanobubble water on digestate soaking hydrolysis of rice straw.

This study investigated the performance of combined nanobubble water (NW) and digestate in the soaking hydrolysis process. Two types of NW (CO2NW and O2NW) with digestate were used to soak rice straw for 1, 2, 3, 5, and 7 days. During soaking process, the volatile fatty acids (VFA) concentration in the treatment with O2NW and digestate for 3 days (O2NW-3 d) reached 7179.5 mg-HAc/L. Moreover, the highest specific methane yield (SMY) obtained in this treatment could reach 336.7 NmL/gVS. Although the addition of NW did not significantly increase SMY from digestate soaking, NW could accelerate the rate of methane production and reduce digestion time of T80. The enrichment of Enterobacter in the soaking process was observed when using CO2NW and O2NW as soaking solutions which played important roles in VFA production. This study provides a new insight into environment-friendly enhanced crop straw pretreatment, combining NW and digestate soaking hydrolysis.

Hepatitis B virus-mediated sodium influx contributes to hepatic inflammation via synergism with intrahepatic danger signals.

The NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome has been involved in the pathogenesis of various chronic liver diseases. However, its role in hepatitis B virus (HBV)-associated hepatitis remains unknown. Here we demonstrate the synergistic effect of HBV with potential intrahepatic danger signals on NLRP3 inflammasome activation. HBV exposure at the appropriate temporal points enhances potassium efflux-dependent NLRP3 inflammasome activation in macrophages and also increases NLRP3 inflammasome-mediated inflammation in HBV-transgenic mouse model. HBV-mediated synergism with intrahepatic signals represented by ATP molecules on NLRP3 activation was observed via relevance analysis, confocal microscopy, and co-immunoprecipitation, and its effector cytokines exhibit positive associations with hepatic inflammation in patients with severe hepatitis B. Furthermore, the synergism of HBV on NLRP3 inflammasome activation owes to increased sodium influx into macrophages. Our data demonstrate that HBV contributes to hepatic inflammation via sodium influx-dependent synergistic activation of NLRP3 inflammasome, which provides a deeper understanding of immune pathogenesis in HBV-associated hepatitis.

Two-step anaerobic digestion of rice straw with nanobubble water.

Lignocellulose usually requires pretreatment to improve biogas production. To enhance lignocellulose biodegradability and improve anaerobic digestion (AD) efficiency, different types (N2, CO2, and O2) of nanobubble water (NW) were applied in this study as soaking agent and AD accelerant to increase the biogas yield of rice straw. The results showed that the cumulative methane yields of treating with NW in two-step AD increased by 11.0%-21.4% compared with untreated straw. The maximum cumulative methane yield was 313.9±1.7 mL/gVS in straw treated with CO2-NW as soaking agent and AD accelerant (PCO2-MCO2). The application of CO2-NW and O2-NW as AD accelerants increased bacterial diversity and relative abundance of Methanosaeta. This study suggested that using NW could enhance soaking pretreatment and methane production of rice straw in two-step AD; however, combined treatment with inoculum and NW or microbubble water in the pretreatment needs to compare in future.