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Abstract Background Follistatin-like protein 1 (FSTL1) has been identified as a secreted glycoprotein that plays an important role in obesity. However, its role in children with metabolic-associated fatty liver disease (MAFLD) has not been investigated. This study aimed at characterizing the relationship between serum FSTL1 concentration and MAFLD in children with obesity. Methods A total of 121 subjects were recruited from the Second Affiliated Hospital of Xi’an Jiaotong University, including 45 obese children with MAFLD, 31 obese children without MAFLD, and 45 healthy controls. Anthropometric parameters, biochemical data were measured and circulating FSTL1 levels were detected by ELISA. Results The levels of FSTL1 in obese children with MAFLD were higher than that in obese children without MAFLD: 1.31 (0.35–2.29) ng/mL vs. 0.55 (0.36–1.38) ng/mL. Correlation analysis illustrated that FSTL1 was associated with nonesterified free fatty acid and leptin (r = 0.278, P

BackgroundDespite emerging evidence linking alterations in gut microbiota to childhood obesity, the metabolic mechanisms linking gut microbiota to the lipid profile during childhood obesity and weight loss remain poorly understood.MethodologyIn this study, children with obesity were treated with lifestyle weight loss therapy. Metagenomics association studies and serum untargeted lipidomics analyses were performed in children with obesity and healthy controls before and after weight loss.Main findingsWe identified alterations in gut microbiota associated with childhood obesity, as well as variations in circulating metabolite concentrations. Children with obesity showed significant decreases in the levels of s-Rothia_kristinae and s-Enterobacter_roggenkampii, alongsige elevated levels of s-Clostridiales_bacterium_Marseille-P5551. Following weight loss, the levels of s-Streptococcus_infantarius and s-Leuconostoc_citreum increased by factors of 3.354 and 1.505, respectively, in comparison to their pre-weight loss levels. Correlation analyses indicated a significant positive relationship between ChE(2:0) levels and both with s-Lachnospiraceae_bacterium_TF09-5 and fasting glucose levels. CoQ8 levels were significantly negatively correlated with s-Rothia_kristinae and HOMA-IR.ConclusionWe linked altered gut microbiota and serum lipid levels in children with obesity to clinical indicators, indicating a potential impact on glucose metabolism via lipids. This study contributes to understanding the mechanistic relationship between altered gut microbiota and childhood obesity and weight loss, suggesting gut microbiome as a promising target for intervention.Clinical trial registrationhttps://www.chictr.org.cn/showproj.html?proj=178971, ChiCTR2300072179.

This study introduced an innovative pathway utilizing an algal anaerobic ammonium oxidation (ALGAMMOX) system to treat ammonium wastewater. Lake bottom sludge and anammox sludge were used to cultivate functional microorganisms and microalgae for nitrogen removal in an upflow reactor made of transparent materials. The results showed that the ALGAMMOX system achieved 87.40 % nitrogen removal when the influent NH4+-N concentration was 100 mg-N/L. Further analysis showed that anammox bacteria Candidatus Brocadia (8.87 %) and nitrosobacteria Nitrosomonas (3.74 %) were crucial contributors, playing essential roles in nitrogen removal. The 16S rRNA gene showed that the anammox bacteria in the sludge transitioned from Candidatus Kuenenia to Candidatus Brocadia. The 18S rRNA gene revealed that Chlamydomonas, Bacillariaceae and Pinnularia were the dominant microalgae in the system at a relative abundance of 7.99 %, 3.64 % and 3.14 %, respectively. This novel approach provides a theoretical foundation for ammonium wastewater treatment.

With the development of fifth-generation (5G) networks, the number of user equipments (UE) increases dramatically. However, the potential health risks from electromagnetic fields (EMF) tend to be a public concern. Generally, EMF exposure-related analysis mainly considers the passive exposure from base stations (BSs) and active exposure that results from the user’s personal devices while communicating. However, the passive radiation that is generated by nearby devices of other users is typically ignored. In fact, with the increase in the density of UE, their passive exposure to human bodies can no longer be ignored. In this work, we propose a stochastic geometry framework to analyze the EMF exposure from active and passive radiation sources. In particular, considering a typical user, we account for their exposure to EMF from BSs, their own UE, and other UE. We derive the distribution of the Exposure index (EI) and the coverage probability for two typical models for spatial distributions of UE, i.e., i) a Poisson point process (PPP); ii) a Matern cluster process. Also, we show the trade-off between the EMF exposure and the coverage probability. Our numerical results suggest that the passive exposure from other users is non-negligible compared to the exposure from BSs when user density is 102 times higher than BS density, and non-negligible compared to active exposure from the user’s own UE when user density is 105 times the BS density.

Recombinant human type II tumour necrosis factor receptor-antibody fusion protein (rh TNFR:Fc) is an immunosuppressant approved for treating rheumatoid arthritis (RA). This case report describes a case of hepatitis B reactivation in a patient with drug-induced acute-on-chronic liver failure. A 58-year-old woman with a history of RA was treated with rh TNFR:Fc; and then subsequently received 25 mg rh TNFR:Fc, twice a week, as maintenance therapy. No anti-hepatitis B virus (HBV) preventive treatment was administered. Six months later, she was hospitalized with acute jaundice. HBV reactivation was observed, leading to acute-on-chronic liver failure. After active treatment, the patient’s condition improved and she recovered well. Following careful diagnosis and treatment protocols are essential when treating RA with rh TNFR:Fc, especially in anti-hepatitis B core antigen antibody-positive patients, even when the HBV surface antigen and the HBV DNA are negative. In the case of HBV reactivation, liver function parameters, HBV surface antigen and HBV DNA should be closely monitored during treatment, and antiviral drugs should be used prophylactically when necessary, as fatal hepatitis B reactivation may occur in rare cases. A comprehensive evaluation and medication should be administered in a timely manner after evaluating the patient’s physical condition and closely monitoring the patient.

The safety of battery energy storage systems (BES) is of paramount importance for societal development and the wellbeing of the people. This is particularly true for retired batteries, as their performance degradation increases the likelihood of thermal runaway occurrences. Existing early warning methods for BES thermal runaway face two main challenges: mechanism-based research methods only consider a single operating state, making their application and promotion difficult; while data-driven methods based on supervised learning struggle with limited sample sizes. To address these issues, this paper proposes a data-driven early warning method for BES thermal runaway. The method utilizes unsupervised learning to create a framework that measures BES differences through reconstruction errors, enabling effective handling of limited samples. Additionally, ensemble learning is employed to enhance the method’s stability and quantify the probability of BES experiencing thermal runaway. To accurately capture the time-varying behaviors of BES, such as voltage, temperature, current, and state of charge (SOC), and detect performance differences in BES before and after thermal runaway, a bidirectional long short-term memory (Bi-LSTM) network with an attention mechanism is utilized. This approach effectively extracts features from training data. Subsequently, a Case study was conducted using the actual operation data of retired lithium batteries to verify the effectiveness of the proposed method.

A mouse model was used to investigate the role of the hyaluronidase, transmembrane protein 2 (TMEM2), on the progression of Graves' orbital (GO) disease. We established a GO mouse model through immunization with a plasmid expressing the thyroid stimulating hormone receptor. Orbital fibroblasts (OFs) were subsequently isolated from both GO and non-GO mice for comprehensive in vitro analyses. The expression of TMEM2 was assessed using qRT-PCR, Western blot and immunohistochemistry in vivo. Disease pathology was evaluated by H&E staining and Masson's trichrome staining in GO mouse tissues. Our investigation revealed a notable reduction in TMEM2 expression in GO mouse orbital tissues. Through overexpression and knockdown assays, we demonstrated that TMEM2 suppresses inflammatory cytokines and reactive oxygen species production. TMEM2 also inhibits the formation of lipid droplets in OFs and the expression of adipogenic factors. Further incorporating Gene Set Enrichment Analysis of relevant GEO datasets and subsequent in vitro cell experiments, robustly confirmed that TMEM2 overexpression was associated with a pronounced upregulation of the JAK/STAT signaling pathway. In vivo, TMEM2 overexpression reduced inflammatory cell infiltration, adipogenesis, and fibrosis in orbital tissues. These findings highlight the varied regulatory role of TMEM2 in GO pathogenesis. Our study reveals that TMEM2 plays a crucial role in mitigating inflammation, suppressing adipogenesis, and reducing fibrosis in GO. TMEM2 has potential as a therapeutic target and biomarker for treating or alleviating GO. These findings advance our understanding of GO pathophysiology and provide opportunities for targeted interventions to modulate TMEM2 for therapeutic purposes. [ABSTRACT FROM AUTHOR]