Processing of fearful faces exhibits characteristics of subcortical functions.

A subcortical pathway is thought to have evolved to facilitate fear information transmission, but direct evidence for its existence in humans is lacking. In recent years, rapid, preattentive, and preconscious fear processing has been demonstrated, providing indirect support for the existence of the subcortical pathway by challenging the necessity of canonical cortical pathways in fear processing. However, direct support also requires evidence for the involvement of subcortical regions in fear processing. To address this issue, here we investigate whether fear processing reflects the characteristics of the subcortical structures in the hypothesized subcortical pathway. Using a monocular/dichoptic paradigm, Experiment 1 demonstrated a same-eye advantage for fearful but not neutral face processing, suggesting that fear processing relied on monocular neurons existing mainly in the subcortex. Experiments 2 and 3 further showed insensitivity to short-wavelength stimuli and a nasal-temporal hemifield asymmetry in fear processing, both of which were functional characteristics of the superior colliculus, a key hub of the subcortical pathway. Furthermore, all three experiments revealed a low spatial frequency selectivity of fear processing, consistent with magnocellular input via subcortical neurons. These results suggest a selective involvement of subcortical structures in fear processing, which, together with the indirect evidence for automatic fear processing, provides a more complete picture of the existence of a subcortical pathway for fear processing in humans. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Pancreatic ß-cell failure, clinical implications, and therapeutic strategies in type 2 diabetes.

ABSTRACT: Pancreatic ß-cell failure due to a reduction in function and mass has been defined as a primary contributor to the progression of type 2 diabetes (T2D). Reserving insulin-producing ß-cells and hence restoring insulin production are gaining attention in translational diabetes research, and ß-cell replenishment has been the main focus for diabetes treatment. Significant findings in ß-cell proliferation, transdifferentiation, pluripotent stem cell differentiation, and associated small molecules have served as promising strategies to regenerate ß-cells. In this review, we summarize current knowledge on the mechanisms implicated in ß-cell dynamic processes under physiological and diabetic conditions, in which genetic factors, age-related alterations, metabolic stresses, and compromised identity are critical factors contributing to ß-cell failure in T2D. The article also focuses on recent advances in therapeutic strategies for diabetes treatment by promoting ß-cell proliferation, inducing non-ß-cell transdifferentiation, and reprograming stem cell differentiation. Although a significant challenge remains for each of these strategies, the recognition of the mechanisms responsible for ß-cell development and mature endocrine cell plasticity and remarkable advances in the generation of exogenous ß-cells from stem cells and single-cell studies pave the way for developing potential approaches to cure diabetes.

Urinary protein and coagulation-fibrinolysis indicators in preeclampsia: Expression and significance.

This study investigates the expression and significance of urinary protein and coagulation-fibrinolysis indicators in preeclampsia, categorized into mild preeclampsia (109 cases) and severe preeclampsia (97 cases) based on disease severity. Additionally, 110 patients with gestational hypertension (gestational hypertension group) were included for comparative analysis. General information, laboratory indicators, urinary protein, and coagulation-fibrinolysis indicator levels were collected for each group. Significant differences were observed in blood pressure among groups (P < .05), while uric acid, serum creatinine, aspartate transaminase, alanine transaminase, and triglycerides showed no significant differences (P > .05). Total cholesterol, triglycerides, and low-density Lipoprotein levels in severe preeclampsia were higher than those in mild preeclampsia and gestational hypertension groups, whereas high-density lipoprotein, albumin, and platelet levels were lower in severe preeclampsia. No significant differences were observed in prothrombin time or D-dimer levels among groups (P > .05). Urinary protein, urinary protein quantification, activated partial thromboplastin time, thrombin time, and fibrinogen were identified as influencing factors for adverse maternal and infant outcomes in severe preeclampsia patients. The study concludes that urinary protein and coagulation-fibrinolysis indicators are elevated in preeclampsia, particularly in severe preeclampsia cases, suggesting their potential use as diagnostic influencing factors for severe preeclampsia.

PTI-ETI synergistic signal mechanisms in plant immunity.

Plants face a relentless onslaught from a diverse array of pathogens in their natural environment, to which they have evolved a myriad of strategies that unfold across various temporal scales. Cell surface pattern recognition receptors (PRRs) detect conserved elicitors from pathogens or endogenous molecules released during pathogen invasion, initiating the first line of defence in plants, known as pattern-triggered immunity (PTI), which imparts a baseline level of disease resistance. Inside host cells, pathogen effectors are sensed by the nucleotide-binding/leucine-rich repeat (NLR) receptors, which then activate the second line of defence: effector-triggered immunity (ETI), offering a more potent and enduring defence mechanism. Moreover, PTI and ETI collaborate synergistically to bolster disease resistance and collectively trigger a cascade of downstream defence responses. This article provides a comprehensive review of plant defence responses, offering an overview of the stepwise activation of plant immunity and the interactions between PTI-ETI synergistic signal transduction.

Exosomal non-coding RNAs in colorectal cancer metastasis.

Colorectal cancer (CRC) is a type of gastrointestinal cancer with high morbidity and mortality rates, and is often accompanied by distant metastases. Metastasis is a major cause of shortened survival time and poor treatment outcomes for patients with CRC. However, the molecular mechanisms underlying the metastasis of CRC remain unclear. Exosomes are a class of small extracellular vesicles that originate from almost all human cells and can transmit biological information (e.g., nucleic acids, lipids, proteins, and metabolites) from secretory cells to target recipient cells. Recent studies have revealed that non-coding RNAs (ncRNAs) can be released by exosomes into the tumour microenvironment or specific tissues, and play a pivotal role in tumorigenesis by regulating a series of key molecules or signalling pathways, particularly those involved in tumour metastasis. Exosomal ncRNAs have potential as novel therapeutic targets for CRC metastasis, and can also be used as liquid biopsy biomarkers because of their specificity and sensitivity. Therefore, further investigations into the biological function and clinical value of exosomal ncRNAs will be of great value for the prevention, early diagnosis, and treatment of CRC metastasis.

Prognostic value and therapeutic potential of IAP family in head and neck squamous cell carcinoma.

Head and neck squamous cell carcinoma (HNSCC) ranks as the eighth most prevalent malignancy globally and has the eighth greatest fatality rate when compared to all other forms of cancer. The inhibitor of apoptosis protein (IAP) family comprises a collection of apoptosis-negative modulators characterized by at least one single baculovirus IAP repeat (BIR) domain in its N-terminal region. While the involvement of the IAP family is associated with the initiation and progression of numerous tumours, its specific role in HNSCC remains poorly understood. Thus, this study aimed to comprehensively examine changes in gene expression, immunomodulatory effects, prognosis, and functional enrichment of HNSCC utilising bioinformatics analysis. Elevated levels of distinct IAP family members were observed to varying degrees in HNSCC, with high BIRC2 expression indicating a worse prognosis. Additionally, Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to probe the enrichment of gene expression and biological processes related to the IAP family in HNSCC. The infiltration levels of immune cells were shown to be strongly associated with the IAP gene expression, as determined by subsequent analysis. Hence, BIRC2 could be an effective immunotherapy target for HNSCC. Collectively, novel knowledge of the biological roles and prognostic implications of IAP family members in HNSCC is presented in this study.

Low-level resource partitioning supports coexistence among functionally redundant bacteria during successional dynamics.

Members of microbial communities can substantially overlap in substrate use. However, what enables functionally redundant microorganisms to coassemble or even stably coexist remains poorly understood. Here, we show that during unstable successional dynamics on complex, natural organic matter, functionally redundant bacteria can coexist by partitioning low-concentration substrates even though they compete for one simple, dominant substrate. We allowed ocean microbial communities to self-assemble on leachates of the brown seaweed Fucus vesiculosus and then analyzed the competition among 10 taxonomically diverse isolates representing two distinct stages of the succession. All, but two isolates, exhibited an average of 90% ± 6% pairwise overlap in resource use, and functional redundancy of isolates from the same assembly stage was higher than that from between assembly stages, leading us to construct a simpler four-isolate community with two isolates from each of the early and late stages. We found that, although the short-term dynamics of the four-isolate communities in F. vesiculosus leachate was dependent on initial isolate ratios, in the long term, the four isolates stably coexist in F. vesiculosus leachate, albeit with some strains at low abundance. We therefore explored the potential for nonredundant substrate use by genomic content analysis and RNA expression patterns. This analysis revealed that the four isolates mainly differed in peripheral metabolic pathways, such as the ability to degrade pyrimidine, leucine, and tyrosine, as well as aromatic substrates. These results highlight the importance of fine-scale differences in metabolic strategies for supporting the frequently observed coexistence of large numbers of rare organisms in natural microbiomes.

Epstein-Barr Virus Promotes Inflammatory Cytokine Production in Human Gingival Fibroblasts.

BACKGROUND: Periodontitis is one of the most common chronic oral inflammatory diseases. Over the past decade, herpes viruses, particularly Epstein-Barr virus (EBV), have been considered promising pathogenic candidates for periodontitis. However, the specific mechanism by which EBV contributes to the development of periodontitis is still unknown. This study aimed to explore the mechanism of EBV underlying the inflammatory response in human gingival fibroblasts (HGFs). MATERIALS AND METHODS: HGFs were stimulated with different concentrations of EBV (104, 105, 106, 107, and 108 DNA copies/mL) for 0, 8, 24, or 48 hours. The mRNA levels of interleukin (IL)-1ß, tumour necrosis factor-α (TNF-α), IL-8, monocyte chemoattractant protein-1 (MCP-1), and Toll-like receptor 9 (TLR9) were measured using quantitative real-time polymerase chain reaction (PCR). Enzyme-linked immunosorbent assays (ELISAs) were performed for determining the mRNA and protein levels of IL-1ß, TNF-α, IL-8, and MCP-1. Real-time PCR and ELISA were performed to determine the protein levels of IL-1ß, TNF-α, IL-8, and MCP-1. Activation of the TLR9/myeloid differentiation factor 88 (MyD88)/nuclear factor kappa B (NF-κB) pathway was evaluated using western blotting. RESULTS: The expressions of IL-1ß, TNF-α, IL-8, and MCP-1 were significantly upregulated in HGFs under EBV stimulation in a concentration- and time-dependent manner. EBV promoted TLR9 and MyD88 expression and induced NF-κB transcription. On the contrary, the upregulation of these factors and the activation of NF-κB pathway were drastically inhibited by TLR9 antagonists. CONCLUSIONS: Our findings demonstrate that EBV promotes the production of inflammatory cytokines IL-1ß and TNF-α and chemokines IL-8 and MCP-1 in HGFs through the TLR9/MyD88/NF-κB pathway.

Comprehensive analysis of prognostic value and immune infiltration of IAPs family in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a malignant tumor with high morbidity and mortality rates. The inhibitors of apoptosis (IAP) family act as oncogenes in various tumor types; however, their functions in HCC remain unclear. Here, we used integrated bioinformatics analysis and experimental verification to assess the expression and the prognostic and clinical value of the IAP family in HCC. Using the University of Alabama at Birmingham Cancer Data Analysis Portal (UALCAN) and the Tumor Immune Estimation Resource (TIMER), we analyzed the expression profiles of IAP family members in HCC tissue, normal tissues, and in patients with different stages and grades of HCC. We further verified the expression level of BIRC2 in 25 HCC samples and matched adjacent normal tissues using quantitative real-time PCR (qRT-PCR), and analyzed its correlation with the marker gene of T-helper type 1 cells (Th1)-STAT1. Meanwhile, the association between BIRC2 and the immunotherapeutic response or immunomodulators was confirmed using the Biomarker Exploration of Solid Tumors (BEST) database. The results showed that NAIP, BIRC2, BIRC3, XIAP, BIRC5, and BIRC6 mRNAs were overexpressed in HCC. The clinical stages, pathological grades, and other clinicopathological features of HCC were closely related to the expression levels of the IAP family members, especially the BIRC2 and BIRC5, which were found to be potential prognostic biomarkers for HCC. Expression of the IAPs was strongly associated with immune cell infiltration. Based on the infiltrative status of various immune cells, HCC patients with high BIRC2 and BIRC5 expression demonstrated poor overall survival (OS) rates. In patients with HCC, BIRC2 expression was noticeably elevated. Concurrently, the expression levels of BIRC2 and STAT1 showed a favorable correlation. BEST database analysis revealed that BIRC2 was a negative predictor of responsiveness to anti-programmed cell death ligand 1 (PD-L1)/cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) inhibitor treatment in HCC, and BIRC2 mRNA expression levels were positively correlated with the expression levels of the immune checkpoint genes programmed cell death protein 1 (PD-1), PD-L1, and CTLA-4 in HCC. Consequently, the IAP family may play a role in carcinogenesis and cancer-immune system interactions in HCC. Our results demonstrate that IAP family members may be viable predictive biomarkers and therapeutic targets for HCC.

Immunological role and prognostic value of somatostatin receptor family members in colon adenocarcinoma.

Colon adenocarcinoma (COAD) is among the most prevalent cancers worldwide, ranking as the third most prevalent malignancy in incidence and mortality. The somatostatin receptor (SSTR) family comprises G-protein-coupled receptors (GPCRs), which couple to inhibitory G proteins (Gi and Go) upon binding to somatostatin (SST) analogs. GPCRs are involved in hormone release, neurotransmission, cell growth inhibition, and cancer suppression. However, their roles in COAD remain unclear. This study used bioinformatics to investigate the expression, prognosis, gene alterations, functional enrichment, and immunoregulatory effects of the SSTR family members in COAD. SSTR1-4 are differentially downregulated in COAD, and low SSTR2 expression indicates poor survival. Biological processes and gene expression enrichment of the SSTR family in COAD were further analyzed using the Kyoto Encyclopedia of Genes and Genomes and Gene Ontology. A strong correlation was observed between SSTR expression and immune cell infiltration. We also quantified SSTR2 expression in 25 COAD samples and adjacent normal tissues using quantitative real-time polymerase chain reaction. We analyzed its correlation with the dendritic cell-integrin subunit alpha X marker gene. The biomarker exploration of the solid tumors portal was used to confirm the correlation between SSTR2 with immunomodulators and immunotherapy responses. Our results identify SSTR2 as a promising target for COAD immunotherapy. Our findings provide new insights into the biological functions of the SSTR family and their implications for the prognosis of COAD.

Evaluation of morphological, histological, and immune-related cellular changes in ligature-induced experimental periodontitis in mice.

Background/purpose: The ligature-induced periodontitis model is an effective approach to induce inflammation and bone loss similar to that of human periodontitis. Previous clinical and in vitro studies have shown the involvement of lymphocytes in periodontitis, while, the local and systemic profile of immune cells associated with periodontitis in the ligature-induced periodontitis model in mice remains unclear. Materials and methods: Experimental periodontitis was constructed in mice by ligating around the maxillary second molars for 14 and 28 days, respectively. Alveolar bone loss was assessed by micro-computed tomography (micro-CT). Hematoxylin and eosin (H&E) and tartrate-resistant acid phosphatase (TRAP) staining were used to evaluate the histological changes in the periodontal tissues. B and T cells in the cervical lymph nodes, spleen, and peripheral blood were analyzed by flow cytometry. Results: The 14-day ligation effectively induced significant periodontal inflammation and alveolar bone loss in C57BL/6J mice, which were progressive and maintained for a relatively long-term period until day 28. In addition, CD3+ T cells and CD19+ B cells were the dominant population in both health and disease, and the B cell population within the cervical lymph nodes (LN) increased significantly under periodontitis condition, while, no significant differences of the T and B cell population among the spleen and peripheral blood were observed. Conclusion: The ligature-induced periodontitis mice model was established to perform a longitudinal assessment of changes in periodontal tissues morphologically and histologically, meanwhile, explore the local and systemic changes of the predominant immune-associated cells.

Exploring and validating the prognostic value of pathomics signatures and genomics in patients with cutaneous melanoma based on bioinformatics and deep learning.

BACKGROUND: Cutaneous melanoma (CM) is the most common malignant tumor of the skin. Our study aimed to investigate the prognostic value of pathomics signatures for CM by combining pathomics and genomics. PURPOSE: The purpose of this study was to explore the potential application value of pathomics signatures. METHODS: Pathology full scans, clinical information, and genomics data for CM patients were downloaded from The Cancer Genome Atlas (TCGA) database. Exploratory data analysis (EDA) was used to visualize patient characteristics. Genes related to a poorer prognosis were screened through differential analysis. Survival analysis was performed to assess the prognostic value of gene and pathomics signatures. Artificial neural network (ANN) models predicted prognosis using signatures and genes. Correlation analysis was used to explore signature-gene links. RESULTS: The clinical traits for 468 CM samples and the genomic data and pathology images for 471 CM samples were obtained from the TCGA database. The EDA results combined with multiple machine learning (ML) models suggested that the top 5 clinical traits in terms of importance were age, biopsy site, T stage, N stage and overall disease stage, and the eight ML models had a precision lower than 0.56. A total of 60 differentially expressed genes were obtained by comparing sequencing data. A total of 413 available quantitative signatures of each pathomics image were obtained with CellProfile software. The precision of the binary classification model based on pathomics signatures was 0.99, with a loss value of 1.7119e-04. The precision of the binary classification model based on differentially expressed genes was 0.98, with a loss value of 0.1101. The precision of the binary classification model based on pathomics signatures and differentially expressed genes was 0.97, with a loss value of 0.2088. The survival analyses showed that the survival rate of the high-risk group based on gene expression and pathomics signatures was significantly lower than that of the low-risk group. A total of 222 pathomics signatures and 51 differentially expressed genes were analyzed for survival with p-values of less than 0.05. There was a certain correlation between some pathomics signatures and differential gene expression involving ANO2, LINC00158, NDNF, ADAMTS15, and ADGRB3, etc. CONCLUSION: This study evaluated the prognostic significance of pathomics signatures and differentially expressed genes in CM patients. Three ANN models were developed, and all achieved accuracy rates higher than 97%. Specifically, the pathomics signature-based ANN model maintained a remarkable accuracy of 99%. These findings highlight the CellProfile + ANN model as an excellent choice for prognostic prediction in CM patients. Furthermore, our correlation analysis experimentally demonstrated a preliminary link between disease quantification and qualitative changes. Among various features, including M stage and treatments received, special attention should be given to age, biopsy site, T stage, N stage, and overall disease stage in CM patients.

The NT5DC family: expression profile and prognostic value in pancreatic adenocarcinoma.

Pancreatic adenocarcinoma (PAAD) is a malignant tumor with high morbidity and mortality rates. The NT5DC family is an evolutionarily-conserved family of 5'-nucleosidases that catalyze the intracellular hydrolysis of nucleotides. Although the NT5DC family has been linked to the initiation and growth of several cancers, its function in PAAD remains unclear. A series of bioinformatic analyses was used to ascertain the expression, prognosis, gene changes, functional enrichment, and immune regulatory functions of the NT5DC family in PAAD. NT5C2 and NT5DC1/2 mRNA and protein levels are increased in PAAD. Furthermore, the high mRNA expressions of NT5C2, NT5DC2, and NT5DC4 indicate a poor prognosis in patients with PAAD. The enrichment of biological processes and gene expression in the NT5DC family in PAAD were investigated using Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analyses. Further investigations into immune infiltration revealed a close relationship between NT5DC gene expression and immune cell infiltration. These findings provide new insights into the biological function and prognostic value of the NT5DC gene family in PAAD.

Primary intra­abdominal desmoid fibromatosis associated with familial adenomatous polyposis: A case report.

Desmoid fibromatosis (DF) is a clonal proliferative disorder of myofibroblasts, which arises, with a low incidence, in soft tissue, including within the abdomen. The incidence of DF is associated with familial adenomatous polyposis (FAP), and is more common following FAP surgery. It is rare for a patient to make his/her first visit to hospital due to DF symptoms associated with FAP. In the present report, a case of mesenteric DF associated with FAP is described. This case also had incomplete intestinal obstruction due to DF. By summarizing previous studies examining DF and FAP treatment, combined with the disease characteristics of this patient, the clinical treatment strategy for DF associated with FAP was explored.

Liraglutide ameliorates hepatic steatosis via retinoic acid receptor-related orphan receptor α-mediated autophagy pathway.

Liraglutide, an analog of human glucagon-like peptide-1 (GLP-1), has been found to improve hepatic steatosis in clinical practice. However, the underlying mechanism remains to be fully defined. Increasing evidence suggests that retinoic acid receptor-related orphan receptor α (RORα) is involved in hepatic lipid accumulation. In the current study, we investigated whether the ameliorating impact of liraglutide on lipid-induced hepatic steatosis is dependent on RORα activity and examined the underlying mechanisms. Cre-loxP-mediated, liver-specific Rorα knockout (Rora LKO) mice, and littermate controls with a Roraloxp/loxp genotype were established. The effects of liraglutide on lipid accumulation were evaluated in mice challenged with a high-fat diet (HFD) for 12 weeks. Moreover, mouse AML12 hepatocytes expressing small interfering RNA (siRNA) of Rora were exposed to palmitic acid to explore the pharmacological mechanism of liraglutide. The results showed that liraglutide treatment significantly alleviated HFD-induced liver steatosis, marked by reduced liver weight and triglyceride accumulation, improved glucose tolerance and serum levels of lipid profiles and aminotransferase. Consistently, liraglutide also ameliorated lipid deposits in a steatotic hepatocyte model in vitro. In addition, liraglutide treatment reversed the HFD-induced downregulation of Rora expression and autophagic activity in mouse liver tissues. However, the beneficial effect of liraglutide on hepatic steatosis was not observed in Rora LKO mice. Mechanistically, the ablation of Rorα in hepatocytes diminished liraglutide-induced autophagosome formation and the fusion of autophagosomes and lysosomes, resulting in weakened autophagic flux activation. Thus, our findings suggest that RORα is essential for the beneficial impact of liraglutide on lipid deposition in hepatocytes and regulates autophagic activity in the underlying mechanism.

Dapagliflozin's effect on serum homocysteine in patients with hypertension complicated with insulin resistance.

Most patients with hypertension are complicated with insulin resistance (IR), which is one of the risk factors of hypertension and can increase the level of serum homocysteine (Hcy) by affecting Hcy's metabolic enzyme and insulin level. Investigations in recent years have shown that Hcy is an independent risk factor for cardiovascular diseases. At present, folic acid is the prominent medicine used to reduce Hcy, but its effection for Hcy has an obvious individual difference, which is closely related to individual genes. Moreover, folic acid is chiefly used in patients with Hcy ≥15 µmol/L, but Hcy ≥10 µmol/L has had an adverse effect on the cardiovascular system. Randomized clinical trials have shown that dapagliflozin can improve IR. Therefore, whether it can reduce Hcy has become a new direction. This study was a retrospective case-control study. Patients with high serum Hcy and hypertension complicated with IR were divided into two groups: the dapagliflozin group (n = 166) and the control group (n = 198). Before and after 12 weeks of treatment, the changes in serum Hcy and IR index were measured and compared. We found that dapagliflozin could reduce the serum Hcy level of patients with hypertension and IR to a certain extent. Dapagliflozin could be a viable option for hypertension complicated with IR and hyperhomocysteinemia. However, these findings need to be further confirmed in future randomized clinical trials with a large number of samples.

EZH2 serves as a promising therapeutic target for fibrosis.

Fibrosis affects the function of many organs and tissues, and its persistent development can lead to tissue sclerosis and cancer, even leading to death further. Recent studies suggested that enhancer of zeste homolog 2 (EZH2), a major regulator of epigenetic repression, played an important role in the occurrence and development of fibrosis through gene silencing or transcriptional activation. As the most studied and powerful pro-fibrotic cytokine closely related to EZH2, TGF-ß1 was primarily involved in the regulation of fibrosis along with the typical Smads and non-Smads signaling pathways. In addition, EZH2 inhibitors demonstrated inhibitory effects in several types of fibrosis. This review summarized the relationship underlying the action of EZH2, TGF-ß1/Smads, and TGF-ß1/non-Smads with fibrosis and described the research progress of EZH2 inhibitors in the treatment of fibrosis.

Improved Biomagnetic Signal-To-Noise Ratio and Source Localization Using Optically Pumped Magnetometers with Synthetic Gradiometers.

Optically pumped magnetometers (OPMs) can capture brain activity but are susceptible to magnetic noise. The objective of this study was to evaluate a novel methodology used to reduce magnetic noise in OPM measurements. A portable magnetoencephalography (MEG) prototype was developed with OPMs. The OPMs were divided into primary sensors and reference sensors. For each primary sensor, a synthetic gradiometer (SG) was constructed by computing a secondary sensor that simulated noise with signals from the reference sensors. MEG data from a phantom with known source signals and six human participants were used to assess the efficacy of the SGs. Magnetic noise in the OPM data appeared predominantly in a low frequency range (<4 Hz) and varied among OPMs. The SGs significantly reduced magnetic noise (p < 0.01), enhanced the signal-to-noise ratio (SNR) (p < 0.001) and improved the accuracy of source localization (p < 0.02). The SGs precisely revealed movement-evoked magnetic fields in MEG data recorded from human participants. SGs provided an effective method to enhance SNR and improve the accuracy of source localization by suppressing noise. Software-simulated SGs may provide new opportunities regarding the use of OPM measurements in various clinical and research applications, especially those in which movement is relevant.

Regulatory B cells induced by interleukin-35 inhibit inflammation and alveolar bone resorption in ligature-induced periodontitis.

BACKGROUND: Regulatory B cells (Bregs) have been reported to suppress immune responses and alveolar bone loss in murine periodontitis models. These cells could be induced by interleukin (IL)-35 which is increased upon periodontal inflammation. Thus, this study aimed to explore the role of Bregs induced by IL-35 in periodontitis. METHODS: Experimental periodontitis was induced in mice by ligature. Two weeks after ligation, the test group was systemically treated with IL-35 for 1 week. Four weeks after ligation, all mice were euthanized, and alveolar bone loss was evaluated by microcomputed tomography. Cytokines associated with periodontitis were analyzed using reverse transcription-quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. Bregs in spleens, cervical lymph nodes, and periodontal tissues were detected by flow cytometry and immunofluorescence staining. RESULTS: In the mouse model of periodontitis, IL-35 induced the expansion of CD1dhi CD5+ B10 cells with increased interleukin-10 (IL-10) and IL-35 production. IL-35 administration also attenuated alveolar bone loss and reduced the levels of proinflammatory cytokines in situ. CONCLUSIONS: Following ligature-induced periodontitis in mice, IL-35 inhibited periodontal inflammation and alveolar bone resorption at least partially through the induction of B10 cells and IL-35+ Bregs.

Uric acid/superoxide dismutase can predict progression of gestational hypertension to preeclampsia.

Introduction: Preeclampsia (PE), at early onset, is likely to be diagnosed as gestational hypertension (GH). Some cases of GH rapidly progress to PE within a short period of time, increasing the mortality rate of pregnant women and adverse events in neonates during the peripartum period. Oxidative stress participates in the occurrence and progression of PE. However, it is unknown whether the progression of GH to PE can be predicted. Methods: A total of 1548 patients diagnosed with PE (649 cases) or GH (899 cases) from January 2016 to June 2022 were selected as the study subjects. The 1548 patients were randomly divided into the training set (1083 cases) and the validation set (465 cases) in a 7:3 ratio. General and clinical data were collected to construct a risk factor prediction model for PE. Results: We found that (1) Systolic blood pressure (SBP), and uric acid (UA)/ superoxide dismutase (SOD) were the risk factors for the progression of GH to PE; (2) A nomogram was constructed from the prediction model, and the area under the curve (AUC) was 0.95, with a sensitivity of 87.4%, a specificity of 92.8%; (3) Build a model simplified scoring system. PE was most strongly predicted by UA/SOD (100 points), SBP (29 points), and serum potassium (19 points). The AUC was 0.92, with a sensitivity of 91.0%, a specificity of 81.7%. The clinical decision analysis curve shows that the model exhibits positive benefits when the threshold probability is at 0.01-0.91. Conclusion: These findings show that UA/SOD can predict progression of GH to PE.