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Background and objective: Lung adenocarcinoma (LUAD), a subtype of non-small cell lung cancer (NSCLC), is associated with high incidence and mortality rates. Effective treatment options are limited due to the frequent development of multidrug resistance, making it crucial to identify new therapeutic targets and sensitizing agents. This study investigates the role of Lactate dehydrogenase A (LDHA) in enhancing the chemotherapy sensitivity of Lobaplatin (LBP) in LUAD. Methods: Bioinformatics analyses were performed using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) to assess LDHA expression in LUAD tissues. LUAD cell lines A549 and NCL-H1975 were treated with siRNA targeting LDHA and the small molecule inhibitor Oxamate. We measured changes in lactate production, ATP levels, NAD+ and pyruvate levels, and assessed cell viability. The chemotherapy sensitivity to Lobaplatin was evaluated, and key signaling pathways related to chemotherapy resistance were analyzed. Results: The inhibition of LDHA resulted in a significant reduction in lactate production and ATP levels, along with an increase in NAD+ and pyruvate levels. These metabolic alterations led to decreased cell viability and enhanced sensitivity to Lobaplatin. The study identified the PI3K/AKT signaling pathway as a critical mediator of this enhanced sensitivity, with reduced phosphorylation of AKT observed upon LDHA inhibition. Furthermore, the combination of LDHA inhibition and Lobaplatin treatment demonstrated a synergistic effect, significantly inhibiting tumor growth and highlighting the potential of LDHA as a therapeutic target to overcome drug resistance in LUAD. Conclusion: Targeting LDHA and disrupting lactate metabolism and its signaling pathways can effectively enhance the sensitivity of LUAD to Lobaplatin, providing a promising approach to overcoming multidrug resistance. These findings offer valuable insights into developing new treatment strategies for lung adenocarcinoma, emphasizing the role of metabolic pathways in cancer therapy. [ABSTRACT FROM AUTHOR]

Persistent transcription of HBV covalently closed circular DNA (cccDNA) is critical for chronic HBV infection. Silencing cccDNA transcription through epigenetic mechanisms offers an effective strategy to control HBV. Long non‐coding RNAs (lncRNAs), as important epigenetic regulators, have an unclear role in cccDNA transcription regulation. In this study, lncRNA sequencing (lncRNA seq) is conducted on five pairs of HBV‐positive and HBV‐negative liver tissue. Through analysis, HOXA‐AS2 (HOXA cluster antisense RNA 2) is identified as a significantly upregulated lncRNA in HBV‐infected livers. Further experiments demonstrate that HBV DNA polymerase (DNA pol) induces HOXA‐AS2 after establishing persistent high‐level HBV replication. Functional studies reveal that HOXA‐AS2 physically binds to cccDNA and significantly inhibits its transcription. Mechanistically, HOXA‐AS2 recruits the MTA1‐HDAC1/2 deacetylase complex to cccDNA minichromosome by physically interacting with metastasis associated 1 (MTA1) subunit, resulting in reduced acetylation of histone H3 at lysine 9 (H3K9ac) and lysine 27 (H3K27ac) associated with cccDNA and subsequently suppressing cccDNA transcription. Altogether, the study reveals a mechanism to self‐limit HBV replication, wherein the upregulation of lncRNA HOXA‐AS2, induced by HBV DNA pol, can epigenetically suppress cccDNA transcription. [ABSTRACT FROM AUTHOR]

Purpose: Precise lateralizing the epileptogenic zone in patients with drug-resistant mesial temporal lobe epilepsy (mTLE) remains challenging, particularly when routine MRI scans are inconclusive (MRI-negative). This study aimed to investigate the synergy of fast, high-resolution, whole-brain MRSI in conjunction with simultaneous [18F]FDG PET for the lateralization of mTLE. Methods: Forty-eight drug-resistant mTLE patients (M/F 31/17, age 12–58) underwent MRSI and [18F]FDG PET on a hybrid PET/MR scanner. Lateralization of mTLE was evaluated by visual inspection and statistical classifiers of metabolic mappings against routine MRI. Additionally, this study explored how disease status influences the associations between altered N-acetyl aspartate (NAA) and FDG uptake using hierarchical moderated multiple regression. Results: The high-resolution whole-brain MRSI data offers metabolite maps at comparable resolution to [18F]FDG PET. Visual examinations of combined MRSI and [18F]FDG PET showed an mTLE lateralization accuracy rate of 91.7% in a 48-patient cohort, surpassing routine MRI (52.1%). Notably, out of 23 MRI-negative mTLE, combined MRSI and [18F]FDG PET helped detect 19 cases. Logistical regression models combining hippocampal NAA level and FDG uptake improved lateralization performance (AUC=0.856), while further incorporating extrahippocampal regions such as amygdala, thalamus, and superior temporal gyrus increased the AUC to 0.939. Concurrent MRSI/PET revealed a moderating influence of disease duration and hippocampal atrophy on the association between hippocampal NAA and glucose uptake, providing significant new insights into the disease's trajectory. Conclusion: This paper reports the first metabolic imaging study using simultaneous high-resolution MRSI and [18F]FDG PET, which help visualize MRI-unidentifiable lesions and may thus advance diagnostic tools and management strategies for drug-resistant mTLE. [ABSTRACT FROM AUTHOR]

Introduction: A bilateral anterior capsulotomy effectively treats refractory obsessive-compulsive disorder (OCD). We investigated the geometry of lesions and disruption of white matter pathways within the anterior limb of the internal capsule (ALIC) in patients with different outcomes. Methods: In this retrospective study, we analyzed data from 18 patients with refractory OCD who underwent capsulotomies. Patients were grouped into "responders" and "nonresponders" based on the percentage of decrease in the Yale-Brown Obsessive-Compulsive Scale (YBOCS) after surgery. We investigated neurobehavioral adverse effects and analyzed the overlap between lesions and the ventromedial prefrontal (vmPFC) and dorsolateral prefrontal (dlPFC) pathways. Probabilistic maps were constructed to investigate the relationship between lesion location and clinical outcomes. Results: Of the 18 patients who underwent capsulotomies, 12 were responders (>35% improvement in YBOCS), and six were nonresponders. The vmPFC pathway was more involved than the dlPFC pathway in responders (p = 0.01), but no significant difference was observed in nonresponders (p = 0.10). The probabilistic voxel-wise efficacy map showed a relationship between ventral voxels within the ALIC with symptom improvement. Weight gains occurred in 11/18 (61%) patients and could be associated with medial voxels within the ALIC. Conclusion: The optimal outcome after capsulotomy in refractory OCD is linked to vmPFC disruption in the ALIC. Medial voxels within the ALIC could be associated with weight gains following capsulotomy. [ABSTRACT FROM AUTHOR]

Simple Summary: Fat-related traits, such as intramuscular fat content and fatty acid compositions, are important factors affecting meat quality. In this study, we aimed to identify candidate genes affecting fat-related traits in meat-type pigeons. Double-digest restriction-associated DNA sequencing was employed to screen genomic single nucleotide polymorphisms in two meat-type pigeon breeds (the Chinese indigenous Shiqi pigeon and the imported White King pigeon) which demonstrated significant differences in fat-related meat traits. Gene ontology enrichment analysis and pathway analysis were performed on genes harboring genetic variants, and with clear annotations. Nineteen functional genes involved in lipid metabolism were identified as candidate genes that may affect fat-related traits in squabs. A molecular docking analysis further revealed that three non-synonymous amino acid mutations, resulting from the polymorphic sites in three functional genes, could influence the binding properties between the enzymatic proteins and their substrates, which may subsequently alter the catalytic efficiency of enzymes. We suggested that these three genes (acetyl-CoA acyltransferase 1 and 2, acetyl-CoA carboxylase beta), which encode rate-limiting enzymes in fatty acid synthesis and degradation, were worthy of further investigation to explore their contributions to the discrepancies in fat-related traits in squabs. The Chinese indigenous Shiqi (SQ) pigeon and the imported White King (WK) pigeon are two meat-type pigeon breeds of economical and nutritional importance in China. They displayed significant differences in such meat quality traits as intramuscular fat (IMF) content and fatty acid (FA) compositions in the breast muscles. In this study, we aimed to screen candidate genes that could affect fat-related meat quality traits in meat-type pigeons. We investigated the polymorphic variations at the genomic level using double-digest restriction-associated DNA (ddRAD) sequencing in 12 squabs of SQ and WK pigeons that exhibited significant inter-breed differences in IMF content as well as FA and amino acid compositions in the breast muscles, and screened candidate genes influencing fat-related traits in squabs through gene ontology analysis and pathway analysis. By focusing on 6019 SNPs, which were located in genes with correct annotations and had the potential to induce changes in the encoded proteins, we identified 19 genes (ACAA1, ACAA2, ACACB, ACADS, ACAT1, ACOX3, ACSBG1, ACSBG2, ACSL1, ACSL4, ELOVL6, FADS1, FADS2, HACD4, HADH, HADHA, HADHB, MECR, OXSM) as candidate genes that could affect fat-related traits in squabs. They were significantly enriched in the pathways of FA metabolism, degradation, and biosynthesis (p < 0.05). Results from molecular docking analysis further revealed that three non-synonymous amino acid alterations, ACAA1(S357N), ACAA2(T234I), and ACACB(H1418N), could alter the non-bonding interactions between the enzymatic proteins and their substrates. Since ACAA1, ACAA2, and ACACB encode rate-limiting enzymes in FA synthesis and degradation, alterations in the enzyme–substrate binding affinity may subsequently affect the catalytic efficiency of enzymes. We suggested that SNPs in these three genes were worthy of further investigation into their roles in explaining the disparities in fat-related traits in squabs. [ABSTRACT FROM AUTHOR]

• PES1 is a BRCT-containing nucleolar protein. • PES1 plays an important role in embryonic development and ribosome biogenesis. • PES1 is associated with tumor progression and is a promising therapeutic target. • PES1 plays an important role in metabolic disorders by regulating lipid metabolism. Pescadillo ribosomal biogenesis factor 1 (PES1), a nucleolar protein initially identified in zebrafish, plays an important role in embryonic development and ribosomal biogenesis. Notably, PES1 has been found to be overexpressed in a number of cancer types, where it contributes to tumorigenesis and cancer progression by promoting cell proliferation, suppressing cellular senescence, modulating the tumor microenvironment (TME) and promoting drug resistance in cancer cells. Moreover, recent emerging evidence suggests that PES1 expression is significantly elevated in the livers of Type 2 diabetes mellitus (T2DM) and obese patients, indicating its involvement in the pathogenesis of metabolic diseases through lipid metabolism regulation. In this review, we present the structural characteristics and biological functions of PES1, as well as complexes in which PES1 participates. Furthermore, we comprehensively summarize the multifaceted role of PES1 in various diseases and the latest insights into its underlying molecular mechanisms. Finally, we discuss the potential clinical translational perspectives of targeting PES1, highlighting its promising as a therapeutic intervention and treatment target. [ABSTRACT FROM AUTHOR]

Nowadays, wireless communication system is facing the problems of spectrum resource shortage. Cognitive radio technology allows cognitive users to use the spectrums authorized to primary users to improve the spectrum utilization. In this paper, a cognitive network model based on hybrid overlay–underlay spectrum access mode is established. To solve the resource allocation problem, a multi‐agent resource allocation algorithm based on graph convolution reinforcement learning which combines deep Q network (DQN) and graph attention network is proposed. DQN is used for action selection and graph attention network is used to obtain the information about neighbours, so as to achieve local cooperation. The proposed algorithm can adaptively optimize cognitive network throughput, spectrum efficiency, or power efficiency by controlling the transmission power and channel selection of cognitive users. To improve the information interaction efficiency, the agent's states are divided into two categories, whether it needs to interact with neighbours or not, which shortens training time and improves convergence speed. Simulation results show that the proposed algorithm can effectively improve the power efficiency of cognitive networks. Compared with Q‐learning, DQN and exiting graph convolutional reinforcement learning algorithm, the proposed algorithm has faster convergence speed and higher stability, and obtains higher network power efficiency. [ABSTRACT FROM AUTHOR]

Purpose: Pharmacists are key members of the pain management interdisciplinary team in many developed countries. However, the implementation of clinical pharmacy services in pain management is impeded by the imbalance between the pain physicians and clinical pharmacists specializing in pain management in China. The purpose of this study was to elucidate the perceptions, expectations and current experience of Chinese pain physicians regarding clinical pharmacy services. Patients and Methods: An anonymous, self-administered questionnaire was designed according to previously published studies with minor modifications and distributed online to 1100 pain physicians selected randomly in hospitals across all 31 provinces of mainland China in 2021. Data were analyzed using descriptive and inferential statistics. Results: A total of 1071 valid questionnaires were included for analysis. The pain physicians were from all 31 provinces of mainland China and most of them were from tertiary hospitals holding an undergraduate degree. Among listed kinds of clinical pharmacy services, pain physicians were less comfortable with pharmacists treating minor illnesses (p < 0.001). Pain physicians' experiences with clinical pharmacy services were far less than their expectations (p < 0.001), which is in line with the results that most of pain physicians (65.9%) interacted with pharmacists at a frequency of less than once a week. Significant differences in the experiences were found among ages (p < 0.01) and among years of work experience (p < 0.05) of pain physicians. Pain physicians' expectations of pharmacists were positively correlated with their experiences with clinical pharmacy services (p < 0.001). Conclusion: Pain physicians in China had positive perceptions and high expectations, but relatively low experiences regarding clinical pharmacy services. Expanding clinical pharmacist pain management credentialing and increasing pain physicians' exposure to clinical pharmacy services are favourable to support the interdisciplinary collaboration in pain management in China. [ABSTRACT FROM AUTHOR]

Wogonoside (WG) is a flavonoid chemical component extracted from Scutellaria baicalensis, which exerts therapeutic effects on liver diseases. Ferroptosis, a novel form of programmed cell death, regulates diverse physiological/pathological processes. In this study, we attempted to investigate a novel mechanism by which WG mitigates liver fibrosis by inducing ferroptosis in hepatic stellate cells (HSCs). A CCl4 -induced mouse liver fibrosis model and a rat HSC line were employed for in vivo and in vitro experiments, both treated with WG. Firstly, the levels of the fibrotic markers α-smooth muscle actin (α-SMA) and α1(I)collagen (COL1α1) were effectively decreased by WG in CCl4 -induced mice and HSC-T6 cells. Additionally, mitochondrial condensation and mitochondrial ridge breakage were observed in WG-treated HSC-T6 cells. Furthermore, ferroptotic events including depletion of SLC7A11, GPX4 and GSH, and accumulation of iron, ROS and MDA were discovered in WG-treated HSC-T6 cells. Intriguingly, these ferroptotic events did not appear in hepatocytes or macrophages. WG-elicited HSC ferroptosis and ECM reduction were dramatically abrogated by ferrostatin-1 (Fer-1), a ferroptosis inhibitor. Importantly, our results confirm that SOCS1/P53/SLC7A11 is a signaling pathway which promotes WG attenuation of liver fibrosis. On the contrary, WG mitigated liver fibrosis and inducted HSC-T6 cell ferroptosis were hindered by SOCS1 siRNA and pifithrin-α (PFT-α). These findings demonstrate that SOCS1/P53/SLC7A11-mediated HSC ferroptosis is associated with WG alleviating liver fibrosis, which provides a new clue for the treatment of liver fibrosis. [ABSTRACT FROM AUTHOR]

Objectives: Ischemia–reperfusion injury (IRI) is a major cause of chronic renal fibrosis. Currently, numerous therapies have shown a minimal effect on the blockade of fibrosis progression. Here, the therapeutic potential of peptide‐based TGF‐β1 inhibitor P144 in IRI‐induced renal fibrosis and the underlying mechanism were analyzed. Materials and Methods: The unilateral ischemia–reperfusion injury with the contralateral nephrectomy model was established, and the P144 was administered intravenously 1d/14d after the onset of IRI. The histopathology and immunofluorescence staining were used to detect renal fibrosis and macrophage infiltration. The in vivo fluorescence imaging was used to measure the bio‐distribution of P144. The transwell assays were used to observe the migration of macrophages. RT‐qPCR and western blot were used to analyze TGF‐β1 signaling. Results: P144 ameliorated the accumulation of extracellular matrix in the kidney and improved the renal function in the unilateral ischemia–reperfusion injury plus contralateral nephrectomy model. Mechanistically, P144 downregulated the TGF‐β1‐Smad3 signaling at both the transcriptional and translational levels and further reduced the TGF‐β1‐dependent infiltration of macrophages to the injured kidney. Additionally, P144 blocked the polarization of macrophages to an M2‐like phenotype induced by TGF‐β1 in vitro, but showed no effect on their proliferation. Conclusions: Our study showed that the TGF‐β1 peptide‐based inhibitor P144 decreased renal fibrosis through the blockade of the TGF‐β1–Smad3 signaling pathway and the modulation of macrophage polarization, suggesting its potential therapeutic use in IRI‐induced renal fibrosis. [ABSTRACT FROM AUTHOR]

Objectives: Evidences demonstrate that sorafenib alleviates liver fibrosis via inhibiting HSC activation and ECM accumulation. The underlying mechanism remains unclear. Ferroptosis, a novel programmed cell death, regulates diverse physiological/pathological processes. In this study, we aim to investigate the functional role of HSC ferroptosis in the anti‐fibrotic effect of sorafenib. Materials and Methods: The effects of sorafenib on HSC ferroptosis and ECM expression were assessed in mouse model of liver fibrosis induced by CCl4. In vitro, Fer‐1 and DFO were used to block ferroptosis and then explored the anti‐fibrotic effect of sorafenib by detecting α‐SMA, COL1α1 and fibronectin proteins. Finally, HIF‐1α siRNA, plasmid and stabilizers were applied to assess related signalling pathway. Results: Sorafenib attenuated liver injury and ECM accumulation in CCl4‐induced fibrotic livers, accompanied by reduction of SLC7A11 and GPX4 proteins. In sorafenib‐treated HSC‐T6 cells, ferroptotic events (depletion of SLC7A11, GPX4 and GSH; accumulation iron, ROS and MDA) were discovered. Intriguingly, these ferroptotic events were not appeared in hepatocytes or macrophages. Sorafenib‐elicited HSC ferroptosis and ECM reduction were abrogated by Fer‐1 and DFO. Additionally, both HIF‐1α and SLC7A11 proteins were reduced in sorafenib‐treated HSC‐T6 cells. SLC7A11 was positively regulated by HIF‐1α, inactivation of HIF‐1α/SLC7A11 pathway was required for sorafenib‐induced HSC ferroptosis, and elevation of HIF‐1α could inhibit ferroptosis, ultimately limited the anti‐fibrotic effect. Conclusions: Sorafenib triggers HSC ferroptosis via HIF‐1α/SLC7A11 signalling, which in turn attenuates liver injury and fibrosis. [ABSTRACT FROM AUTHOR]

A new process has been developed for inclusion removal. This process involves the creation and dispersion of fine bubbles in molten steel by calcium carbonate powder injection through the nozzles of the up-snorkel in RH (Ruhstahl Hausen Process) degasser. The plant trials have been carried out in ANSTEEL and the ruling factors have been analysed. The results indicate that this novel technique is beneficial to separate the small non-metallic inclusion removal from the molten steel. Compared with the conventional inclusion removal technology, the number of the oxide inclusions can be decreased to a lower level and the inclusion becomes finer. Using this novel technology, the total oxygen in the as-cast slab can approach 6 ppm. [ABSTRACT FROM AUTHOR]

Liniparhomaloptera qiongzhongensis Zheng and Chen 1980 is distributed in Hainan Island, China. The complete mitogenome of the species was sequenced in this study. It had a circular molecule of 16,554 bp in length with a total of 56.5% A + T content, containing 13 protein-coding genes (PCGs), 22 tRNA genes, two rRNA genes, and one control region. Five overlapping regions and 14 intergenic sequences were observed with the length of 2–10 bp and 1–31 bp, respectively. The phylogenetic analysis based on 13 protein-coding genes revealed that L. qiongzhongensis had the closest relationship with L. disparis. This study would provide useful genetic information for future studies on taxonomy, phylogeny and evolution of Liniparhomaloptera species. [ABSTRACT FROM AUTHOR]

Background and Purpose: Epilepsy, a globally prevalent neurological disorder, necessitates precise identification of the epileptogenic zone (EZ) for effective surgical management. While the individual utilities of FDG PET and FMZ PET have been demonstrated, their combined efficacy in localizing the epileptogenic zone remains underexplored. We aim to improve the non-invasive prediction of epileptogenic zone (EZ) in temporal lobe epilepsy (TLE) by combining FDG PET and FMZ PET with statistical feature extraction and machine learning., Materials and Methods: This study included 20 drug-resistant unilateral TLE patients (14 mesial TLE, 6 lateral TLE), and two control groups (N=29 for FDG, N=20 for FMZ). EZ of each patient was confirmed by post-surgical pathology, and one-year follow-up, while propagation zone (PZ) and non-involved zone (NIZ) were derived from the epileptogenicity index based on presurgical stereo-encephalography (SEEG) monitoring. Whole brain PET scans were obtained with dual tracers [ 18 F]FDG and [ 18 F]FMZ on separate days, from which standard uptake value ratio (SUVR) was calculated by global mean scaling. Low-order statistical parameters of SUVRs and t-maps derived against control groups were extracted. Additionally, fused FDG and FMZ features were created using arithmetic operations. Spearman correlation was used to investigate the associations between FDG and FMZ, while multiple linear regression analysis was used to explore the interaction effects of imaging features in predicting epileptogenicity. Crafted imaging features were used to train logistic regression models to predict EZ, whose performance was evaluated using 10-fold cross-validation at ROI-level, and leave-one-patient-out cross-validation at patient-level., Results: FDG SUVR significantly decreased in EZ and PZ compared to NIZ, while FMZ SUVR in EZ significantly differed from PZ. Interaction effects were found between FDG and FMZ in their prediction of epileptogenicity. Fusion of FDG and FMZ provided the best prediction model with an area under the curve (AUC) of 0.86 [0.84-0.87] for EZ vs. NIZ and an AUC of 0.79 [0.77-0.81] for EZ vs. PZ, eliminating 100% false positives in 50% of patients, and ≥80% FPs in 90% patients at patient level., Conclusions: Combined FDG and FMZ offer a promising avenue for non-invasive localization of the epileptogenic zone in TLE, potentially refining surgical planning., Abbreviations: AUC = Area under the curve; EI = Epileptogenicity index; EZ = Epileptogenic zone; FMZ = Flumazenil; GABAA = Gammaaminobutyric acid type A; NIZ = Not-involved zone; PZ = Propagation zone; SEEG = Stereo-electroencephalography; SUVR = Standard uptake value ratio; TLE = Temporal lobe epilepsy., Competing Interests: The authors declare no conflicts of interest related to the content of this article., (© 2025 by American Journal of Neuroradiology.)

Background: Programmed cell death-ligand 1 (PD-L1) is overexpressed in tumor cells, which promotes tumor cell survival and cell proliferation and causes tumor cells to escape T-cell killing. Schisanhenol, a biphenyl cyclooctene lignin-like compound, was extracted and isolated from the plant named Schisandra rubriflora (Franch.)., Purpose: In this work, we studied the anticancer potential of schisanhenol and explored whether schisanhenol mediated its effect by inhibiting the expression of PD-L1 in vitro and in vivo., Materials and Methods: In vitro, we performed western blot, immunofluorescence, immunoprecipitation, and colony formation assays to study the proteins, genes, and pathways related to the anti-tumour activity of schisanhenol. In vivo, we explored the antitumor activity of schisanhenol through orthotopic liver transplantation and subcutaneous transplantation tumor models of hepatocellular carcinoma (HCC) cells., Results: We found that schisanhenol decreased the viability of HCC cells. It inhibited the expression of programmed cell death ligand-1 (PD-L1), which plays a pivotal role in tumorigenesis. Subsequently, schisanhenol suppressed the expression of PD-L1 by decreasing the activation of STAT3. Furthermore, we found that schisanhenol inhibited the activation of STAT3 via JAK/STAT3 (T705), Src/STAT3 (T705), and PI3K/AKT/mTOR/STAT3 (S727) pathways. Colony formation tests showed that schisanhenol suppressed cell proliferation by inhibiting PD-L1. Schisanhenol also enhanced cytotoxic T lymphocytes (CTL) activity and regained their ability to kill tumour cells in co-culture. Finally, in vivo observation confirmed the antitumor activity of schisanhenol., Conclusion: Schisanhenol inhibits the proliferation of HCC cells by targeting PD-L1 via the STAT3 pathways. These findings prove that schisanhenol is a valuable candidate for HCC therapeutics and reveal previously unknown characteristics of schisanhenol., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objective: (MSU) crystals usually in the kidney tubules especially collecting ducts in the medulla. Previous animal models have not fully reproduced the impact of MSU on kidneys under non-hyperuricemic conditions., Methods: In the group treated with MSU, the upper pole of the rat kidney was injected intrarenally with 50 mg/kg of MSU, while the lower pole was injected with an equivalent volume of PBS solution. The body weight and kidney mass of the rats were observed and counted. H&E staining was used to observe the pathological damage of the kidney and to count the number of inflammatory cells. Masoon staining was used to observe the interstitial fibrosis in the kidneys of the rat model. Flow cytometric analysis was used for counting inflammatory cells in rats. ElISA was used to measure the concentration of serum and urine uric acid, creatinine and urea nitrogen in rats., Results: At the MSU injection site, a significantly higher infiltration of inflammatory cells and a substantial increase in the area of interstitial fibrosis compared to the control group and the site of PBS injection were observed. The serum creatinine level was significantly increased in the MSU group. However, there were no significant differences in the rats' general conditions or blood inflammatory cell counts when compared to the control group., Conclusion: The injection of urate crystals into the kidney compromised renal function, caused local pathological damage, and increased inflammatory cell infiltration and interstitial fibrosis. Intrarenal injection of MSU crystals may result in urate nephropathy. The method of intrarenal injection did not induce surgical infection or systemic inflammatory response., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Li, Li, Chen, Ouyang, Lin, Wu, Fu, Quan, Wang, Wu, Yuan, Liu, Zhao, Liu, Zhu, Li and Mao.)

Changes in lifestyle induce an increase in patients with hyperuricemia (HUA), leading to gout, gouty arthritis, renal damage, and cardiovascular injury. There is a strong inflammatory response in the process of HUA, while dysregulation of immune cells, including monocytes, macrophages, and T cells, plays a crucial role in the inflammatory response. Recent studies have indicated that urate has a direct impact on immune cell populations, changes in cytokine expression, modifications in chemotaxis and differentiation, and the provocation of immune cells by intrinsic cells to cause the aforementioned conditions. Here we conducted a detailed review of the relationship among uric acid, immune response, and inflammatory status in hyperuricemia and its complications, providing new therapeutic targets and strategies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Li, Yuan, Deng, Wang, Wu, Chen, Li, Ouyang, Lin, Quan, Fu, Li and Mao.)

Objective: To investigate the relationship between glucose metabolism and functional activity in the epileptogenic network of patients with mesial temporal lobe epilepsy (MTLE) and to determine whether this relationship is associated with surgical outcomes., Methods: 18 F-FDG PET and resting-state functional MRI (rs-fMRI) scans were performed on a hybrid PET/MR scanner in 38 MTLE patients with hippocampal sclerosis (MR-HS), 35 MR-negative patients and 34 healthy controls (HC). Glucose metabolism was measured using 18 F-FDG PET standardized uptake value ratio (SUVR) relative to cerebellum; Functional activity was obtained by fractional amplitude of low-frequency fluctuation (fALFF). The betweenness centrality (BC) of metabolic covariance network and functional network were calculated using graph theoretical analysis. Differences in SUVR, fALFF, BC and the spatial voxel-wise SUVR-fALFF couplings of the epileptogenic network, consisting of default mode network (DMN) and thalamus, were evaluated by Mann-Whitney U test (using the false discovery rate [FDR] for multiple comparison correction). The top ten SUVR-fALFF couplings were selected by Fisher score to predict surgical outcomes using logistic regression model., Results: The results showed decreased SUVR-fALFF coupling in the bilateral middle frontal gyrus ( P FDR = 0.0230, P FDR = 0.0296) in MR-HS patients compared to healthy controls. Coupling in the ipsilateral hippocampus was marginally increased ( P FDR = 0.0802) in MR-HS patients along with decreased BC of metabolic covariance network and functional network ( P FDR = 0.0152; P FDR = 0.0429). With Fisher score ranking, the top ten SUVR-fALFF couplings in regions from DMN and thalamic subnuclei could predict surgical outcomes with the best performance being a combination of ten SUVR-fALFF couplings with an AUC of 0.914., Conclusion: These findings suggest that the altered neuroenergetic coupling in the epileptogenic network is associated with surgical outcomes of MTLE patients, which may provide insight into their pathogenesis and help with preoperative evaluation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Yuan, Huang, Cai, Li, Zhang and Luo.)

Since the COVID-19 epidemic, mathematical and simulation models have been extensively utilized to forecast the virus's progress. In order to more accurately describe the actual circumstance surrounding the asymptomatic transmission of COVID-19 in urban areas, this research proposes a model called Susceptible-Exposure-Infected-Asymptomatic-Recovered-Quarantine in a small-world network. In addition, we coupled the epidemic model with the Logistic growth model to simplify the process of setting model parameters. The model was assessed through experiments and comparisons. Simulation results were analyzed to explore the main factors affecting the spread of the epidemic, and statistical analysis that was applied to assess the model's accuracy. The results are consistent well with epidemic data from Shanghai, China in 2022. The model can not only replicate the real virus transmission data, but also anticipate the development trend of the epidemic based on available data, so that health policy-makers can better understand the spread of the epidemic.

Liniparhomaloptera qiongzhongensis Zheng and Chen 1980 is distributed in Hainan Island, China. The complete mitogenome of the species was sequenced in this study. It had a circular molecule of 16,554 bp in length with a total of 56.5% A + T content, containing 13 protein-coding genes (PCGs), 22 tRNA genes, two rRNA genes, and one control region. Five overlapping regions and 14 intergenic sequences were observed with the length of 2-10 bp and 1-31 bp, respectively. The phylogenetic analysis based on 13 protein-coding genes revealed that L. qiongzhongensis had the closest relationship with L. disparis . This study would provide useful genetic information for future studies on taxonomy, phylogeny and evolution of Liniparhomaloptera species., Competing Interests: No potential conflict of interest was reported by the author(s)., (© 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.)