Room-temperature spin injection across a chiral perovskite/III-V interface.

Spin accumulation in semiconductor structures at room temperature and without magnetic fields is key to enable a broader range of optoelectronic functionality1. Current efforts are limited owing to inherent inefficiencies associated with spin injection across semiconductor interfaces2. Here we demonstrate spin injection across chiral halide perovskite/III-V interfaces achieving spin accumulation in a standard semiconductor III-V (AlxGa1-x)0.5In0.5P multiple quantum well light-emitting diode. The spin accumulation in the multiple quantum well is detected through emission of circularly polarized light with a degree of polarization of up to 15 ± 4%. The chiral perovskite/III-V interface was characterized with X-ray photoelectron spectroscopy, cross-sectional scanning Kelvin probe force microscopy and cross-sectional transmission electron microscopy imaging, showing a clean semiconductor/semiconductor interface at which the Fermi level can equilibrate. These findings demonstrate that chiral perovskite semiconductors can transform well-developed semiconductor platforms into ones that can also control spin.

NOX4-TIM23 interaction regulates NOX4 mitochondrial import and metabolic reprogramming.

Pulmonary fibrosis is a progressive lung disease characterized by macrophage activation. Asbestos-induced expression of nicotinamide adenine dinucleotide phosphate hydrogen oxidase 4 (NOX4) in lung macrophages mediates fibrotic progression by the generation of mitochondrial reactive oxygen species (ROS), modulating mitochondrial biogenesis, and promoting apoptosis resistance; however, the mechanism(s) by which NOX4 localizes to mitochondria during fibrosis is not known. Here, we show that NOX4 localized to the mitochondrial matrix following asbestos exposure in lung macrophages via direct interaction with TIM23. TIM23 and NOX4 interaction was found in lung macrophages from human subjects with asbestosis, while it was absent in mice harboring a conditional deletion of NOX4 in lung macrophages. This interaction was localized to the proximal transmembrane region of NOX4. Mechanistically, TIM23 augmented NOX4-induced mitochondrial ROS and metabolic reprogramming to oxidative phosphorylation. Silencing TIM23 decreased mitochondrial ROS and oxidative phosphorylation. These observations highlight the important role of the mitochondrial translocase TIM23 interaction with NOX4. Moreover, this interaction is required for mitochondrial redox signaling and metabolic reprogramming in lung macrophages.

Modulation of the emission spectrum of rare-earth ions using inverse-designed photonic crystals cavities.

Rare-earth elements play an indispensable role in the optical communication and laser industries, due to their superior luminescent properties. Nevertheless, the selective enhancement and suppression of different emission bands during energy level transitions for multi-band emitting rare-earth ions presents a significant research challenge, which we aim to address. This study explores the potential of leveraging an inverse-designed dual-cavity photonic crystals structure to manipulate the emission spectrum, thereby facilitating the augmentation or suppression of distinct emission bands. We utilized a convolutional neural network model to establish the relationship between geometric parameters and the local density of states, forecasting the optimal cavity geometry parameters for achieving the desired modulation outcomes. This paper delineates the neural network's generalization capabilities, along with the modulation efficacy of the dual-cavity configuration, both confirmed through numerical validation. Our findings highlight the modulatory capacity of Dy3+ ions, which exhibit three emission spectrum in the visible range, to achieve pure color light emission within the devised cavity structure. Notably, our approach yielded enhancements of up to 2.79-fold and 2.81-fold in pure yellow and red light emissions respectively, compared to free space emissions. The single-sided emission enhancement reaches 16.28-fold for yellow light and 30.79-fold for red light. This emphasizes the transformative potential of this methodology in crafting rare-earth-based luminescent materials with meticulously engineered emission attributes.

Acetyl-CoA synthetase 2 induces pyroptosis and inflammation of renal epithelial tubular cells in sepsis-induced acute kidney injury by upregulating the KLF5/NF-κB pathway.

BACKGROUND: Pyroptosis of the renal tubular epithelial cells (RTECs) and interstitial inflammation are central pathological characteristics of acute kidney injury (AKI). Pyroptosis acts as a pro-inflammatory form of programmed cell death and is mainly dependent on activation of the NLRP3 inflammasome. Previous studies revealed that acetyl-CoA synthetase 2 (ACSS2) promotes inflammation during metabolic stress suggesting that ACSS2 might regulate pyroptosis and inflammatory responses of RTECs in AKI. METHODS AND RESULTS: The expression of ACSS2 was found to be significantly increased in the renal epithelial cells of mice with lipopolysaccharide (LPS)-induced AKI. Pharmacological and genetic strategies demonstrated that ACSS2 regulated NLRP3-mediated caspase-1 activation and pyroptosis through the stimulation of the KLF5/NF-κB pathway in RTECs. The deletion of ACSS2 attenuated renal tubular pathological injury and inflammatory cell infiltration in an LPS-induced mouse model, and ACSS2-deficient mice displayed impaired NLRP3 activation-mediated pyroptosis and decreased IL-1ß production in response to the LPS challenge. In HK-2 cells, ACSS2 deficiency suppressed NLRP3-mediated caspase-1 activation and pyroptosis through the downregulation of the KLF5/NF-κB pathway. The KLF5 inhibitor ML264 suppressed NF-κB activity and NLRP3-mediated caspase-1 activation, thus protecting HK-2 cells from LPS-induced pyroptosis. CONCLUSION: Our results suggested that ACSS2 regulates activation of the NLRP3 inflammasome and pyroptosis by inducing the KLF5/NF-κB pathway in RTECs. These results identified ACSS2 as a potential therapeutic target in AKI.

Acetyl-CoA synthetase 2 promotes diabetic renal tubular injury in mice by rewiring fatty acid metabolism through SIRT1/ChREBP pathway.

Diabetic nephropathy (DN) is characterized by chronic low-grade renal inflammatory responses, which greatly contribute to disease progression. Abnormal glucose metabolism disrupts renal lipid metabolism, leading to lipid accumulation, nephrotoxicity, and subsequent aseptic renal interstitial inflammation. In this study, we investigated the mechanisms underlying the renal inflammation in diabetes, driven by glucose-lipid metabolic rearrangement with a focus on the role of acetyl-CoA synthetase 2 (ACSS2) in lipid accumulation and renal tubular injury. Diabetic models were established in mice by the injection of streptozotocin and in human renal tubular epithelial HK-2 cells cultured under a high glucose (HG, 30 mmol/L) condition. We showed that the expression levels of ACSS2 were significantly increased in renal tubular epithelial cells (RTECs) from the diabetic mice and human diabetic kidney biopsy samples, and ACSS2 was co-localized with the pro-inflammatory cytokine IL-1ß in RTECs. Diabetic ACSS2-deficient mice exhibited reduced renal tubular injury and inflammatory responses. Similarly, ACSS2 knockdown or inhibition of ACSS2 by ACSS2i (10 µmol/L) in HK-2 cells significantly ameliorated HG-induced inflammation, mitochondrial stress, and fatty acid synthesis. Molecular docking revealed that ACSS2 interacted with Sirtuin 1 (SIRT1). In HG-treated HK-2 cells, we demonstrated that ACSS2 suppressed SIRT1 expression and activated fatty acid synthesis by modulating SIRT1-carbohydrate responsive element binding protein (ChREBP) activity, leading to mitochondrial oxidative stress and inflammation. We conclude that ACSS2 promotes mitochondrial oxidative stress and renal tubular inflammation in DN by regulating the SIRT1-ChREBP pathway. This highlights the potential therapeutic value of pharmacological inhibition of ACSS2 for alleviating renal inflammation and dysregulation of fatty acid metabolic homeostasis in DN. Metabolic inflammation in the renal region, driven by lipid metabolism disorder, is a key factor in renal injury in diabetic nephropathy (DN). Acetyl-CoA synthetase 2 (ACSS2) is abundantly expressed in renal tubular epithelial cells (RTECs) and highly upregulated in diabetic kidneys. Deleting ACSS2 reduces renal fatty acid accumulation and markers of renal tubular injury in diabetic mice. We demonstrate that ACSS2 deletion inhibits ChREBP-mediated fatty acid lipogenesis, mitochondrial oxidative stress, and inflammatory response in RTECs, which play a major role in the progression of diabetic renal tubular injury in the kidney. These findings support the potential use of ACSS2 inhibitors in treating patients with DN.

Predicting the postoperative intraocular lens position based on IOL Master 700 biometry, compared with results from the anterior segment analysis system.

PURPOSE: Predict intraocular lens position after cataract surgery using the IOL Master 700 and explore the associated ocular parameters compared with the results obtained from the anterior segment analysis system (Sirius, CSO Inc, Florence, Italy). METHODS: A total of 98 patients (106 eyes) were included in the retrospective study. The postoperative intraocular lens position was obtained using the IOL Master 700 and measured using Adobe Illustrator software. Correlation analysis and linear regression analysis were applied to study the correlation between the actual position of the postoperative intraocular lens (ALP) and the ocular parameters. In addition, Bland-Altman consistency analysis was used to compare the consistency between any two among the predicted intraocular lens position (ALPi) obtained using IOL Master 700 biometry, the predicted artificial lens position (ALPs) calculated using the anterior segment analysis system, or the ALP. RESULTS: Ocular parameters, including preoperative anterior chamber depth, lens thickness, axial length, white-to-white, and postoperative refractive error were all correlated with ALP after cataract surgery (P < 0.05) using univariate analysis. However, in multivariate linear regression, only the first three variables were correlated with ALP. Compared with the equation obtained by the anterior segment analysis, the equation from IOL Master 700 biometry provided a better fit. The results of the consistency analysis showed that ALP, ALPi, and ALPs were in good agreement. CONCLUSION: IOL Master 700 biometry can help predict intraocular lens position after surgery, and its accuracy is better than that provided by the anterior segment analysis system.

Management of experimental trabeculectomy filtering blebs via crosslinking of the scleral flap inhibited vascularization.

PURPOSE: The aim of this study was to evaluate whether UVA-light-activated riboflavin-induced collagen crosslinking (UVA-CXL) can maintain the function of filtering blebs after trabeculectomy (TRAB) in rabbits. METHODS: Thirty-six healthy rabbits were randomized to one of the following groups with 12 rabbits in each group: Trabeculectomy group (TRAB group), trabeculectomy combined with CXL group (CXL group), and trabeculectomy combined with MMC group (MMC group). Six rabbits of each group were performed with intraocular pressure (IOP), optical coherence tomography (OCT), and OCT angiography (OCTA). Bleb structure was observed via hematoxylin & eosin (H&E) and Masson staining. Immunohistochemistry, proteomic study, western blot, and tensile test were performed between CXL group and the control. In vitro, cell viability was evaluated by CCK-8 and Calcein/PI staining. TRPV4 and VEGF-a expression levels were measured by Q-PCR. Ca2+ concentration was observed with Fluo-4 AM. RESULTS: The IOP and bleb median survival day were significantly modified in CXL (5.92 ± 0.32 mmHg and 15.5 days) than TRAB group (7.50 ± 0.43 mmHg and 9 days). The bleb area and height increased. CXL inhibited vascularization, and vascularization peaked at postoperative day (POD) 14 and then decreased gradually. In proteomic analyses, Z disc, actin filament binding, and sarcomere organization were significantly enriched. CXL inhibited scleral stress‒strain in tensile tests. Compared with TRAB group, TRPV4 expression was significantly increased, but VEGF-a and TGF-ß1 levels were reduced in the CXL group in western blot. Meanwhile, TRPV4 expression colocalized with CD31. In vitro, CXL inhibited HUVECs cell viability. After CXL, expression level of TRPV4 was increased and calcium influx was activated, but VEGF-a was decreased in HUVECs. CONCLUSIONS: This study demonstrates that intraoperative UV-RF CXL can significantly improve the success rate of TRAB via inhibiting filtering bleb vascularization. CXL increased sclera stiffness, in turn, induced TRPV4 activation, thus contributing to vascular endothelial cells suppression.

Long-Term Field Application of a Plant Growth-Promoting Rhizobacterial Consortium Suppressed Root-Knot Disease by Shaping the Rhizosphere Microbiota.

Root-knot nematodes (Meloidogyne spp.) are one of the most economically important plant parasitic nematodes, infecting almost all cultivated plants and resulting in severe yield losses every year. Plant growth-promoting rhizobacteria (PGPR) have been extensively used to prevent and control root-knot diseases and increase yield. In this study, the effect of a consortium of three PGPR strains (Bacillus cereus AR156, B. subtilis SM21, and Serratia sp. XY21; hereafter "BBS") on root-knot disease of cucumber was evaluated. The application of BBS significantly reduced the severity of root-knot disease by 56 to 72%, increased yield by 36 to 55%, and improved fruit quality by 14 to 90% and soil properties by 1 to 90% relative to the control in the cucumber fields of the Nanjing suburb, Jiangsu Province, from 2015 to 2018. BBS altered the rhizosphere bacterial community. Compared with the control group, it significantly (false discovery rate, P < 0.05) increased the abundance of 14 bacterial genera that were negatively correlated with disease severity. Additionally, the redundancy analysis suggested that BBS-treated rhizosphere soil samples were dominated by disease-suppressive bacteria, including the genera Iamia, Kutzneria, Salinibacterium, Mycobacterium, Kribbella, Pseudonocardia, Sporichthya, Sphaerisporangium, Actinomadura, Flavisolibacter, Phenylobacterium, Bosea, Hyphomicrobium, Agrobacterium, Sphingomonas, and Nannocystis, which were positively related to total organic carbon, total nitrogen, total organic matter, dissolved organic carbon, [Formula: see text]-N, and available phosphorus contents. This suggests that BBS suppresses root-knot nematodes and improves the soil chemical properties of cucumber by altering the rhizosphere microbial community.

Animal models of hepatitis E infection: Advances and challenges.

Hepatitis E virus (HEV) is one of the leading causes of acute viral hepatitis worldwide. Although most of HEV infections are asymptomatic, some patients will develop the symptoms, especially pregnant women, the elderly, and patients with preexisting liver diseases, who often experience anorexia, nausea, vomiting, malaise, abdominal pain, and jaundice. HEV infection may become chronic in immunosuppressed individuals. In addition, HEV infection can also cause several extrahepatic manifestations. HEV exists in a wide range of hosts in nature and can be transmitted across species. Hence, animals susceptible to HEV can be used as models. The establishment of animal models is of great significance for studying HEV transmission, clinical symptoms, extrahepatic manifestations, and therapeutic strategies, which will help us understand the pathogenesis, prevention, and treatment of hepatitis E. This review summarized the animal models of HEV, including pigs, monkeys, rabbits, mice, rats, and other animals. For each animal species, we provided a concise summary of the HEV genotypes that they can be infected with, the cross-species transmission pathways, as well as their role in studying extrahepatic manifestations, prevention, and treatment of HEV infection. The advantages and disadvantages of these animal models were also emphasized. This review offers new perspectives to enhance the current understanding of the research landscape surrounding HEV animal models.

Activation of aryl hydrocarbon receptor (AhR) alleviates depressive-like behaviors in LPS-induced mice.

The role of the aryl hydrocarbon receptor (AhR) in regulating oxidative stress and immune responses has been increasingly recognized. However, its involvement in depression and the underlying mechanisms remain poorly understood. This study aimed to investigate the effect of 6-formylindolo[3,2-b]carbazole (FICZ), an endogenous AhR ligand, on a lipopolysaccharide (LPS)-induced depression model and the underlying mechanism. After being treated with FICZ (50 mg/kg), male C57BL/6J mice received intraperitoneal injection of LPS and underwent behavioral tests 24 h later. The levels of inflammatory cytokines, including IL-1ß, IL-6, and TNF-α, were measured in the hippocampus and serum using enzyme-linked immunosorbent assay (ELISA). The expression levels of CYP1A1, AhR and NLRP3 were analyzed using qPCR and Western blot. The results showed that, compared with control group, LPS alone significantly down-regulated the expression levels of CYP1A1 mRNA and AhR protein in the hippocampus of mice, reduced glucose preference, prolonged immobility time in forced swimming test, increased IL-6 and IL-1ß levels in the hippocampus, increased serum IL-1ß level, and up-regulated NLRP3 mRNA and protein expression levels in mouse hippocampus, while FICZ significantly reversed the aforementioned effects of LPS. These findings suggest that AhR activation attenuates the inflammatory response associated with depression and modulates the expression of NLRP3. The present study provides novel insights into the role of AhR in the development of depression, and presents AhR as a potential therapeutic target for the treatment of depression.

Multifactorial analysis of willingness to undergo subcutaneous allergen immunotherapy in pediatric patients.

Objective: To explore factors influencing the acceptance of allergen immunotherapy (AIT) for the treatment of allergic respiratory diseases by pediatric patients and their families. Methods: A total of 406 children (210 males and 196 females) attending the pediatric outpatient clinics and wards of the Renji Hospital, Shanghai Jiao Tong University School of Medicine from June 2020 to April 2022. Those who met the criteria for the AIT treatment, were included in the survey. An online 20-item questionnaire was developed. Data on patient's general characteristics, allergic disease status, family history of allergies, general family information, parental knowledge of allergic diseases, and whether the AIT treatment was recommended by a physician, were collected. The patients were divided into two groups according to their willingness to receive AIT: a reluctant or neutral group (n = 182), and a willing group (n = 224). A univariate analysis of the willingness to undergo AIT was done to detect parameters that significantly differed between the groups, and the identified factors were used as independent variables in the multifactorial logistic regression analysis. Results: The severity of allergic disease, presence of drug allergy, occurrence of severe allergic reactions, mother's education, distance from home to the hospital, parental knowledge of allergic diseases, and whether the doctor recommended AIT were all statistically different between the groups (p < 0.05). Multifactorial logistic regression analysis showed that the degree of allergic rhinitis (AR), or asthma (AS), parental knowledge of allergic diseases, and doctor's recommendation of AIT were the factors that influenced the willingness of pediatric patients to receive AIT. Conclusions: The severity of AR and AS, parental knowledge of allergic diseases, and doctor's recommendation influenced the willingness of pediatric patients to receive AIT.

Binding FSI- to Construct a Self-Healing SEI Film for Li-Metal Batteries by In situ Crosslinking Vinyl Ionic Liquid.

The solid electrolyte interphase (SEI) membrane on the Li metal anode tends to breakdown and undergo reconstruction during operation, causing Li metal batteries to experience accelerated decay. Notably, an SEI membrane with self-healing characteristics can help considerably in stabilizing the Li-electrolyte interface; however, uniformly fixing the repairing agent onto the anode remains a challenging task. By leveraging the noteworthy film-forming attributes of bis(fluorosulfonyl)imide (FSI-) anions and the photopolymerization property of the vinyl group, the ionic liquid 1-vinyl-3-methylimidazolium bis(fluorosulfonyl)imide (VMI-FSI) was crosslinked with polyethylene oxide (PEO) in this study to form a self-healing film fixing FSI- groups as the repairing agent. When they encounter lithium metal, the FSI- groups are chemically decomposed into LiF & Li3N, which assist forming SEI membrane on lithium sheet and repairing SEI membrane in the cracks lacerated by lithium dendrite. Furthermore, the FSI- anions exchanged from film are electrochemically decomposed to generate inorganic salts to strengthen the SEI membrane. Benefiting from the self-healing behavior of the film, Li/LiCoO2 cells with the loading of 16.3 mg cm-2 exhibit the initial discharge capacities of 183.0 mAh ⋅ g-1 and are stably operated for 500 cycles with the retention rates of 81.4 % and the average coulombic efficiency of 99.97 %, operated between 3.0-4.5 V vs. Li+/Li. This study presents a new design approach for self-healing Li metal anodes and durable lithium metal battery.

The involvement of NLRP3 inflammasome in CUMS-induced AD-like pathological changes and related cognitive decline in mice.

BACKGROUND: Numerous studies have found that inhibiting the expression of NLRP3 inflammasome can significantly improve depressive-like behaviors in mice, but the research on its effect on cognitive decline in depression and its mechanism is still lacking. This study aimed to elucidate the role of NLRP3 inflammasome in cognitive decline in depression and explore the common neuro-immunological mechanisms of depression and Alzheimer's disease (AD). METHODS: Male C57BL/6 mice were subjected to chronic unpredictable mild stress (CUMS) for 5 weeks, treatment group was administered with the NLRP3 inhibitor MCC950 (10 mg/kg, i.p.), fluoxetine served as positive control. Then, the mice were assessed for cognitive behaviors and depression-like behaviors, and changes of microglia and neurons in hippocampus and levels of Aß metabolic pathway and tau protein were measured. To explore the mechanism of NLRP3 activation on neurons, we performed in vitro studies using BV2 microglia and mouse primary neurons. Furthermore, we focused on the role of NLRP3 inflammasome in the function of neurons and the expression of AD pathological indicators. RESULTS: CUMS induced depressive-like behaviors and cognitive decline in mice, which could be reversed by inhibiting NLRP3 inflammasome. MCC950, a specific NLRP3 inhibitor, alleviated CUMS-induced neuron injury and AD-like pathological changes, including the abnormal expression of Aß metabolic pathway and the hyper-phosphorylation of tau protein. LPS (1 µg/mL) + ATP (1 mM) treatment activated the expression of NLRP3 inflammasome and IL-1ß in vitro. In vitro experiment also proved that inhibiting the expression of NLRP3 inflammasome in microglia can restore the Aß metabolic pathway to normal, decrease neuronal tau protein phosphorylation and protect neurons. CONCLUSIONS: Inhibition of NLRP3 inflammasome effectively alleviated CUMS-induced depressive-like behaviors and cognitive decline in mice, and inhibited the activation of AD physiological indicators.

Serum extracellular vesicle-derived ASS1 is a promising predictor for the occurrence of HEV-ALF.

Development of biomarkers for predicting the occurrence of hepatitis E virus related-acute liver failure (HEV-ALF) is conducive to prevention and early intervention. Serum samples from 250 HEV-ALF patients, 250 patients with acute hepatitis E (AHE) and 250 health controls (HCs) were collected. We assessed the predictive ability of extracellular vesicle (EV)-derived argininosuccinate synthase 1 (ASS1) levels for HEV-ALF occurrence. Serum EVs were successfully isolated. EV-derived ASS1 levels in the HEV-ALF patients were significantly higher than those in the AHE patients and HCs. In HEV-ALF patients, EV-derived ASS1 levels were positively correlated with the number of failed organs and disease progression. The logistical regression showed that EV-derived ASS1 level is an independent risk factor for HEV-ALF, and orthogonal partial least squares discriminant analysis (OPLS-DA) also suggested that EV-derived ASS1 level has high predictive capability. Besides, the area under the curve (AUC) of EV-derived ASS1 level to predict HEV-ALF occurrence was 0.728 (0.684-0.772) with the sensitivity and specificity being 72.80% and 64.80%, which had a high decision-making ability. Furthermore, there existed no significant difference between the age ≥60 and age <60 groups in EV-derived ASS1 levels. Serum EV-derived ASS1 level is a promising predictor for the occurrence of HEV-ALF.

Narrow linewidth electro-optically tuned multi-channel interference widely tunable semiconductor laser.

A narrow linewidth electro-optically tuned multi-channel interference (MCI) widely tunable semiconductor laser based on carrier injection is demonstrated in this paper. The MCI laser with a common phase section and a semiconductor optical amplifier (SOA) is packaged into a 16-pin butterfly box. The laser is characterized by a strategy: shifting the longitudinal mode and then aligning the reflection peak, which obtains a quasi-continuous tuning range over 48 nm. The corresponding side mode suppression ratios (SMSRs) are higher than 40 dB and frequency deviations from ITU-grid are less than ± 1 GHz. Threshold currents are less than 28 mA. Fiber coupled output powers are higher than 20 mW and power variations with fixed gain and SOA currents are less than 0.8 dB over the whole tuning range. Lorentzian linewidths are less than 320 kHz over the entire tuning range, which is one of the lowest results for monolithic widely tunable semiconductor lasers tuned by carrier injection. These results demonstrate the potential prospects of the MCI laser with carrier injection in the field of optical sensing and optical communications.

Low-power consumption InP-based optical phase arrays with non-uniformly spaced output waveguides.

Optical Phase Arrays (OPAs) are expected to be an ideal solution to achieve beam shaping, laser radar (LIDAR), free-space optical communications, and spatially resolved optical sensors, etc. We demonstrated a low-power consumption 32-channel OPA with non-uniformly spaced waveguides based on InP substrate. The phase shifters are based on a p-i-n structure which are operated with reverse bias and have a low power consumption. Besides, in order to improve the performance especially to obtain larger steering angle and narrower beam divergence without increasing the number of channels, we have optimized the spacing between the output waveguides. The fabricated OPA achieved a steering angle of 35° with the side lobe suppression ratio more than 8.2 dB across the angle range from -20° to 20° in the far field, which is the largest phase tuning steering angle reported by InP-based OPAs as far as we know. The divergence angle is about 0.46° in the phase steering dimension and the power consumption of the OPA at each steering angle is lower than 7.5 mW.

Exosomes-mediated transfer of LINC00691 regulates the formation of CAFs and promotes the progression of gastric cancer.

OBJECTIVE: Gastric cancer (GC) is one of the malignant tumors with the highest mortality worldwide. Our previous studies have revealed that LINC00691 is up-regulated in serum of GC patients as a novel potential biomarker for GC diagnosis and prognosis. However, the roles of serum exosomal LINC00691 in GC has not been clarified. This study aimed to find the expression pattern of serum exosomal LINC00691 in GC patients and the correlation between the level of serum exosomal LINC00691 and the pathology of gastric cancer patients. METHODS: We collected the serum of 94 GC patients before surgery and extracted exosomes to detect the expression level of exosomal LINC00691, with 21 healthy volunteers and 17 patients with benign gastric diseases as controls. Surgical GC tissues and paired healthy tissues were collected to culture primary cancer-associated fibroblasts (CAFs) and normal fibroblasts (NFs). We then treated NFs with LINC00691-rich GC cell culture supernatant or exosomes and detected the activation markers and biological functions of the fibroblasts. RESULTS: The results of real-time qPCR indicated that the serum exosomal LINC00691 of GC patients was significantly higher than that of healthy subjects and patients with benign gastric diseases, and was associated with the clinicopathology of GC patients. More interestingly, when the NFs were treated with GC exosomes, the level of LINC00691 was significantly increased, the cell proliferation and migration were noticeably enhanced, and the ability to accelerate GC cell proliferation and invasion was promoted, which means that the induced fibroblasts gained the properties of CAFs. In addition, we found that knockdown of LINC00691 and the use of the JAK2/STAT3 signaling pathway inhibitor ruxolitinib effectively deprived exosome-containing GC cell supernatants of the effects on NFs. CONCLUSION: Our study suggested that exosomal LINC00691 promoted NFs to gained the properties of CAFs depending on JAK2/STAT3 signaling pathway as a potential diagnostic biomarker for GC.

Chronic ß-adrenergic stress contributes to cardiomyopathy in rodents with collagen-induced arthritis.

Patients with rheumatoid arthritis (RA) have a much higher incidence of cardiac dysfunction, which contributes to the high mortality rate of RA despite anti-arthritic drug therapy. In this study, we investigated dynamic changes in cardiac function in classic animal models of RA and examined the potential effectors of RA-induced heart failure (HF). Collagen-induced arthritis (CIA) models were established in rats and mice. The cardiac function of CIA animals was dynamically monitored using echocardiography and haemodynamics. We showed that cardiac diastolic and systolic dysfunction occurred in CIA animals and persisted after joint inflammation and that serum proinflammatory cytokine (IL-1ß, TNF-α) levels were decreased. We did not find evidence of atherosclerosis (AS) in arthritic animals even though cardiomyopathy was significant. We observed that an impaired cardiac ß1AR-excitation contraction coupling signal was accompanied by sustained increases in blood epinephrine levels in CIA rats. Furthermore, serum epinephrine concentrations were positively correlated with the heart failure biomarker NT-proBNP in RA patients (r2 = +0.53, P < 0.0001). In CIA mice, treatment with the nonselective ßAR blocker carvedilol (2.5 mg·kg-1·d-1, for 4 weeks) or the specific GRK2 inhibitor paroxetine (2.5 mg·kg-1·d-1, for 4 weeks) effectively rescued heart function. We conclude that chronic and persistent ß-adrenergic stress in CIA animals is a significant contributor to cardiomyopathy, which may be a potential target for protecting RA patients against HF.

Status quo of the public's knowledge of probiotics based on video-sharing platforms.

BACKGROUND: Probiotics have been deemed multipotent and unprecedentedly applied in the health field recently. However, there are challenges in promoting credible and reliable resources while avoiding misinformation regarding probiotics for the public. METHODS: This study analysed 400 eligible probiotic-related videos selected from YouTube, and the three most popular video-sharing platforms (Bilibili, Weibo and TikTok) in China. Video retrieval was performed on September 5th, 2022. GQS and tailored DISCERN tool assess each video's quality, usage, and reliability. A comparative analysis of videos from different sources was carried out. RESULTS: The identity distribution of probiotic video-producers was predominantly experts (n = 202, 50.50%), followed by amateurs (n = 161, 40.25%) and health-related institutions (n = 37, 9.25%). The videos' content category mainly discussed the function of probiotics (n = 120, 30%), the way to choose suitable products (n = 81, 20.25%), and the methods for taking probiotics (n = 71, 17.75%).The overall quality of videos was moderate (3/5 point) assessed by GQS, while the usage (1/6 point) and reliability (2/5 point) detailing probiotics assessed by tailored DISCERN tool were poor. The attitude of probiotic video-producers was primarily positive (n = 323, 80.75%), followed by neutral (n = 52, 13.00%) and negative (n = 25, 6.25%) (P < 0.001). CONCLUSIONS: The current study showed that videos on social media platforms publicise important information including the concepts, usage, and precautions of probiotics to the public. But the overall quality of uploaded videos about probiotics was unsatisfactory. More efforts are needed to improve the higher-quality content of probiotic-related online videos and better propagate probiotic knowledge to the public in the future.

Kurstakin Triggers Multicellular Behaviors in Bacillus cereus AR156 and Enhances Disease Control Efficacy Against Rice Sheath Blight.

Kurstakin is the latest discovered family of lipopeptides secreted by Bacillus spp. In this study, the effects of kurstakin on the direct antagonism, multicellularity, and disease control ability of Bacillus cereus AR156 were explored. An insertion mutation in the nonribosomal peptide synthase responsible for kurstakin synthesis led to a significant reduction of antagonistic ability of AR156 against the plant-pathogenic fungi Rhizoctonia solani, Ascochyta citrullina, Fusarium graminearum, and F. oxysporum f. sp. cubense. The loss of kurstakin synthesis ability significantly impaired the swarming motility of AR156 and reduced biofilm formation and amyloid protein accumulation. Although the loss of kurstakin synthesis ability did not reduce the competitiveness of AR156 under laboratory conditions, the colonization and environmental adaptability of the mutant was significantly weaker than that of wild-type AR156 on rice leaves. The cell surface of wild-type AR156 colonizing the leaf surface was covered by a thick biofilm matrix under a scanning electron microscope, but not the mutant. The colonization ability on rice roots and control efficacy against rice sheath blight disease of the mutant were also impaired. Thus, kurstakin participates in the control of plant diseases by B. cereus AR156 through directly inhibiting the growth of pathogenic fungi and improving long-term environmental adaptability and colonization of AR156 on the host surface by triggering multicellularity. This study explored the multiple functions of kurstakin in plant disease control by B. cereus.