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The intricate interplay between the human oral microbiome and systemic health is increasingly being recognized, particularly in the context of central nervous system pathologies such as glioblastoma. In this study, we aimed to elucidate gender-specific differences in the salivary microbiome of glioma patients by utilizing 16S rRNA sequencing data from publicly available salivary microbiome datasets. We conducted comprehensive bioinformatics analysis, encompassing quality control, noise reduction, species classification, and microbial community composition analysis at various taxonomic levels. Machine learning algorithms were employed to identify microbial signatures associated with glioma. When compared to healthy controls, our analysis revealed distinct differences in the salivary microbiota of glioma patients. Notably, the genera Leptotrichia and Atopobium exhibited significant variations in abundance between genders. Leptotrichia was prevalent in healthy females but exhibited a reduced abundance in female glioma patients. In contrast, Atopobium was more abundant in male glioma patients. These findings suggest that hormonal influences might play a role in shaping the salivary microbiome and its association with glioma. We utilized a combination of LASSO-logistic regression and random forest models for feature selection, and identified key microbial features that differentiated glioma patients from healthy controls. We developed a diagnostic model with high predictive accuracy and area under the curve and principal component analysis metrics confirmed its robustness. The analysis of microbial markers, including Atopobium and Leptotrichia, highlighted the potential of the salivary microbiota as a non-invasive biomarker for the diagnosis and prognosis of glioma. Our findings highlight significant gender-specific disparities in the salivary microbiome of patients with glioma, offering new insights into the pathogenesis of glioma and paving the way for innovative diagnostic and therapeutic strategies. The use of saliva as a diagnostic fluid, given its ease of collection and non-invasive nature, holds immense promise for monitoring systemic health and the trajectory of disease. Future research should focus on investigating the underlying mechanisms by which the salivary microbiome influences the development of glioma and identifying potential microbiome-targeted therapies to enhance the management of glioma.

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OBJECTIVE: Renal function and the skeleton are classic target organs in primary hyperparathyroidism (PHPT), affected by the chronic course of the disease. Most patients diagnosed today exhibit mild PHPT, characterized by slight hypercalcemia and no or unspecific symptoms. Concerns have been raised that PHPT could promote deteriorating kidney function and increase cardiovascular risk directly. To examine the effect of parathyroidectomy (PTX) on mild PHPT on renal function and markers for bone turnover, cardiovascular disease (CVD), and vascular inflammation. DESIGN: Prospective randomized controlled trial. ClinicalTrials.gov: NCT00522028. SETTING: Eight Scandinavian referral centers. PARTICIPANTS: From 1998 to 2005, 191 patients with mild PHPT were included in Sweden, Norway, and Denmark. Of these 150 were included in the present analyses. INTERVENTION: Seventy patients were randomized to PTX and 80 to observation without intervention (OBS). MEASURES: e-GFR was calculated based on creatinine and cystatin C. Markers of CVD and systemic inflammation: osteoprotegerin, vascular cell adhesion molecule 1, soluble CD40 ligand, interleukin-1 receptor antagonist, von Willebrand factor. Bone turnover markers: C-terminal telopeptide of type 1 collagen (CTX-1) and serum Procollagen type 1 N-terminal propeptide. RESULTS: No differences in the development of renal function or vascular and systemic inflammation were detected. CTX-1 was lower in PTX after 10 years. LIMITATIONS: Secondary analyses of a randomized controlled trial. CONCLUSION: PTX does not appear to affect renal function or markers of CVD and vascular inflammation in mild PHPT in a ten-year perspective.

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The incidence of esophageal cancer continues to increase worldwide. Current therapeutic approaches have limited efficacy, so in order to search for better markers of the disease, it is necessary to further elucidate its molecular pathogenesis. Regulation of gene expression by long non-coding Rnas plays a role in many diseases, however the role in esophageal cancer is unclear. The aim of this study was to elucidate the role and regulatory mechanism of long non-coding RNA NRSN2-AS1 in the progression of esophageal cancer. By real-time quantitative PCR, immunohistochemistry, RNA interference, western blotting, and double luciferase reporter gene analysis, we found that NRSN2-AS1 was up-regulated in esophageal cancer tissues and cell lines, and was closely related to disease stage and prognosis. Functional studies have shown that the silencing of NRSN2-AS1 inhibits the proliferation of esophageal cancer cells, induces apoptosis, and prevents cell migration and invasion. In mouse models, NRSN2-AS1 also promoted tumor growth. The transcription factor TCFL5 upregulates the transcription of NRSN2-AS1, which acts as a sponge for microRNA(miR)-874-5p, thereby upregulating the expression of the oncogene RELT. Activation of the NRSN2-AS1/miR-874-5p/RELT regulatory axis was validated in vivo.

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Sarcopenia, a geriatric syndrome characterized by progressive loss of muscle mass and strength, and osteoarthritis, a common degenerative joint disease, are both prevalent in elderly individuals. However, the relationship and molecular mechanisms underlying these two diseases have not been fully elucidated. In this study, we screened microarray data from the Gene Expression Omnibus to identify associations between sarcopenia and osteoarthritis. We employed multiple statistical methods and bioinformatics tools to analyze the shared DEGs (differentially expressed genes). Additionally, we identified 8 hub genes through functional enrichment analysis, protein-protein interaction analysis, transcription factor-gene interaction network analysis, and TF-miRNA coregulatory network analysis. We also discovered potential shared pathways between the two diseases, such as transcriptional misregulation in cancer, the FOXO signalling pathway, and endometrial cancer. Furthermore, based on common DEGs, we found that strophanthidin may be an optimal drug for treating sarcopenia and osteoarthritis, as indicated by the Drug Signatures database. Immune infiltration analysis was also performed on the sarcopenia and osteoarthritis datasets. Finally, receiver operating characteristic (ROC) curves were plotted to verify the reliability of our results. Our findings provide a theoretical foundation for future research on the potential common pathogenesis and molecular mechanisms of sarcopenia and osteoarthritis.

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The aim of this study is to investigate the impact of exercise on intermediate disease markers in populations with overweight and obesity, providing evidence-based recommendations for clinicians to utilize these markers in developing exercise prescriptions for this group. The study was conducted by retrieving data from PubMed, Embase, Cochrane Library, Web of Science, and CNKI and only including Randomized Controlled Trials (RCTs) to examine the effect of different exercise interventions on intermediate disease markers in overweight and obese people. The quality of the included studies was evaluated using the Cochrane Bias Risk Assessment tool and the data was analyzed using Stata 15.1 data analysis software. The RCTs were collected from January 2017 to March 2024. A total of 56 RCTs were included and the results of 10 outcomes were analyzed using random effects meta-analysis. The total sample size used in the study was 3193 The results showed that resistance training significantly reduced total cholesterol (SUCRA: 99.9%), triglycerides (SUCRA: 100.0%), low-density lipoprotein (SUCRA: 100.0%), systolic pressure (SUCRA: 92.5%), and increased high-density lipoprotein (SUCRA: 100.0%). Aerobic exercise significantly reduced insulin (SUCRA: 89.1%) and HbA1c (SUCRA: 95.3%). Concurrent training significantly reduced HOMA-IR (SUCRA: 93.8%), diastolic blood pressure (SUCRA: 71.2%) and Glucose (SUCRA: 87.6%). Exercise has a significant impact on intermediate disease markers in populations with overweight and obese. Compared with no exercise, exercise lowers total cholesterol, triglycerides, LDL, systolic blood pressure, diastolic blood pressure, HOMA-IR, insulin, and HbA1c, and increases HDL in people with overweight and obese. These findings provide evidence-based recommendations for exercise interventions aimed at weight reduction and the prevention of chronic diseases in individuals with overweight and obese.

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BACKGROUND: Fatigue is a major complaint in stroke survivors, but data focusing on intracerebral haemorrhage (ICH) survivors are scarce. In a cohort of spontaneous ICH survivors, we assessed the long-term prevalence of fatigue and its associated factors. METHODS: We included consecutive 1-year ICH survivors from the prospective, observational, single-centre Prognosis of Intracerebral Haemorrhage (PITCH) study. We evaluated fatigue (defined as a score ≥ 4 in Chalder Fatigue Scale); the severity of neurological, depressive, and anxiety symptoms; and functional disability 1, 3, and 6 years after ICH. We performed univariable and multivariable models to evaluate clinical factors and brain magnetic resonance imaging (MRI) small vessel disease (SVD) markers associated with fatigue. RESULTS: Of 255 1-year ICH survivors, 153 (60%) underwent fatigue screening and were included in this study. Seventy-eight patients (51%) reported fatigue at 1-year, 56/110 (51%) at 3-year, and 27/67 (40%) at 6-year follow-up. Patients with fatigue exhibited more severe concomitant depressive/anxiety symptoms, but the severity of depressive symptoms was the only clinical factor significantly associated with 1-year fatigue in multivariable analysis (adjusted odds ratio 1.4 for one-point increase; 95% confidence interval 1.2-1.6). Patients with severe cortical atrophy at baseline had increased risk of fatigue at 1-year follow-up compared to patients with mild/no cortical atrophy (adjusted odds ratio 2.5; 95% confidence interval 1.1-5.8). CONCLUSIONS: Fatigue after ICH is frequent and long-lasting, and it is associated with cortical atrophy (but not with other MRI markers of cerebral SVD). The link between fatigue and depressive symptoms may represent a potential therapeutic target.

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High hepcidin is linked to low-grade inflammation and lower iron levels. The consequences of testosterone replacement therapy (TRT) on inflammation and the risk of cardiovascular disease (CVD) are undetermined. We investigate the effect of TRT on the inflammatory cardiovascular risk markers hepcidin-iron, fibroblast growth factor 23 (FGF23)-phosphate-klotho, and calprotectin pathways. METHODS: A randomized, placebo-controlled, double-blinded study at an academic tertiary-care medical center. Interventions were testosterone gel (TRT, n = 20) or placebo gel (n = 19) for 24 weeks. We included 39 men (50-70 years) with type 2 diabetes (T2D) on metformin monotherapy with bioavailable testosterone levels <7.3 nmol/L. Body composition was assessed with DXA- and MRI-scans; the main study outcomes were serum hepcidin-iron, FGF23, phosphate, klotho, and calprotectin. RESULTS: Hepcidin levels decreased during TRT (ß = -9.5 ng/mL, p < 0.001), lean body mass (ß = 1.9 kg, p = 0.001) increased, and total fat mass (ß = -1.3 kg, p = 0.009) decreased compared to placebo. Delta hepcidin was not associated with changes in lean body mass or fat mass. Iron and the pathways of FGF23-phosphate-klotho and calprotectin were unchanged during TRT. CONCLUSIONS: During TRT, the reduction in hepcidin was not associated with circulating iron levels, lean body mass, or fat mass; these findings suggested a direct anti-inflammatory effect of TRT and no indirect effect mediated through these factors.

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Background: Diagnostic models based on gene signatures of nasopharyngeal carcinoma (NPC) were constructed by random forest (RF) and artificial neural network (ANN) algorithms. Least absolute shrinkage and selection operator (Lasso)-Cox regression was used to select and build prognostic models based on gene signatures. This study contributes to the early diagnosis and treatment, prognosis, and molecular mechanisms associated with NPC. Methods: Two gene expression datasets were downloaded from the Gene Expression Omnibus (GEO) database, and differentially expressed genes (DEGs) associated with NPC were identified by gene expression differential analysis. Subsequently, significant DEGs were identified by a RF algorithm. ANN were used to construct a diagnostic model for NPC. The performance of the diagnostic model was evaluated by area under the curve (AUC) values using a validation set. Lasso-Cox regression examined gene signatures associated with prognosis. Overall survival (OS) and disease-free survival (DFS) prediction models were constructed and validated from The Cancer Genome Atlas (TCGA) database and the International Cancer Genome Consortium (ICGC) database. Results: A total of 582 DEGs associated with NPC were identified, and 14 significant genes were identified by the RF algorithm. A diagnostic model for NPC was successfully constructed using ANN, and the validity of the model was confirmed on the training set AUC =0.947 [95% confidence interval (CI): 0.911-0.969] and the validation set AUC =0.864 (95% CI: 0.828-0.901). The 24-gene signatures associated with prognosis were identified by Lasso-Cox regression, and prediction models for OS and DFS of NPC were constructed on the training set. Finally, the ability of the model was validated on the validation set. Conclusions: Several potential gene signatures associated with NPC were identified, and a high-performance predictive model for early diagnosis of NPC and a prognostic prediction model with robust performance were successfully developed. The results of this study provide valuable references for early diagnosis, screening, treatment and molecular mechanism research of NPC in the future.

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BACKGROUND: Moderate-intensity intermittent exercise (MIIE) has been proposed as an effective method for preventing Alzheimer's dementia (AD). AIM: This study aimed to investigate the effects of MIIE on the spatial memory and protein level of AD markers in the hippocampus of trimethyltin (TMT)-induced rat model of hippocampal degeneration. METHODS: Male Sprague Dawley (SD) rats were randomly assigned into four groups: normal control (N), exercise control (E), TMT control (T), and exercise and TMT (ET). Rats of the exercise groups (E and ET) were forced to run on a treadmill for 30 min each day at maximum for 12 weeks. Intraperitoneal injection of 8 mg/kgBW TMT was administered as a single dose, 10 days before the last exercise treatment for the T and ET groups. The spatial memory of rats was examined using Morris water maze (MWM) test after the exercise period. After euthanasia, the hippocampal tissue was dissected out and the level of hippocampal presenilin-1 (PSEN-1) and phosphorylated tau (p-tau) protein were measured using ELISA. The total number of hippocampal pyramidal neurons was estimated using unbiased stereological analysis. Qualitative immunohistochemistry was performed to examine the expression of brain-derived neurotrophic factor (BDNF), tumor necrosis factor-alpha (TNF-α), and interleukin-10 (IL-10) in paraffin sections of the hippocampus. RESULTS: TMT exposure induced memory impairment indicated by the T group having the lowest percentage of time and percentage of path length in the target quadrant compared to other groups. MIIE prevented the memory impairment effect of TMT exposure indicated by the ET group having no significantly different MWM performance compared to the E and N groups. The ET group had significantly lower levels of hippocampal AD markers, p-tau and PSEN-1, as well as significantly higher estimated total number of pyramidal neurons of hippocampal CA1 and CA2-3 regions compared to the T group. Expressions of TNF-α was weak, while the expression of IL-10 was stronger in the ET group compared to the control group. The TMT-induced group exhibited stronger expression of BDNF. CONCLUSION: MIIE prevents neuronal loss and impaired spatial memory upon TMT exposure most probably via preventing elevated levels of hippocampal AD markers and neuroinflammation. WC:350.

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Timely and powerful diagnostic means can achieve better therapeutic effects, reduce disease torment, and improve survival rate. As a powerful non-invasive spectroscopy technology, surface-enhanced Raman scattering (SERS) have testified to be a great potential candidate for extensive early clinical disease diagnosis. In recent years, the introduction of SERS label, combined with other analysis modes or artificial intelligence, and the emergence of miniaturized devices have made SERS technology more advantageous in early diagnosis of diseases. This review focuses on the research progress of SERS dominated analytical strategies in the field of early disease diagnosis in the past five years. The main content includes the application of label-free SERS detection; the construction of label SERS methodologies for various disease markers; SERS dominated multimode early disease diagnosis strategies; integration of SERS and artificial intelligence; portable Raman equipment and SERS imaging; and opportunities and trends for SERS diagnostic technology in the future.

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Cardiovascular complications combined with COVID-19 (SARS-CoV-2) lead to a poor prognosis in patients. The common pathogenesis of ischemic cardiomyopathy (ICM) and COVID-19 is still unclear. Here, we explored potential molecular mechanisms and biomarkers for ICM and COVID-19. Common differentially expressed genes (DEGs) of ICM (GSE5406) and COVID-19 (GSE164805) were identified using GEO2R. We performed enrichment and protein-protein interaction analyses and screened key genes. To confirm the diagnostic performance for these hub genes, we used external datasets (GSE116250 and GSE211979) and plotted ROC curves. Transcription factor and microRNA regulatory networks were constructed for the validated hub genes. Finally, drug prediction and molecular docking validation were performed using cMAP. We identified 81 common DEGs, many of which were enriched in terms of their relation to angiogenesis. Three DEGs were identified as key hub genes (HSP90AA1, HSPA9, and SRSF1) in the protein-protein interaction analysis. These hub genes had high diagnostic performance in the four datasets (AUC > 0.7). Mir-16-5p and KLF9 transcription factor co-regulated these hub genes. The drugs vindesine and ON-01910 showed good binding performance to the hub genes. We identified HSP90AA1, HSPA9, and SRSF1 as markers for the co-pathogenesis of ICM and COVID-19, and showed that co-pathogenesis of ICM and COVID-19 may be related to angiogenesis. Vindesine and ON-01910 were predicted as potential therapeutic agents. Our findings will contribute to a deeper understanding of the comorbidity of ICM with COVID-19.

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OBJECTIVES: Cognitive and neuroimaging assessments are still the main clinical practice methods for screening and diagnosing vascular dementia (VaD) patients. This study aimed to establish the neuropsychological characteristics of mild-to-moderate subcortical ischaemic vascular dementia (SIVD) patients, find an optimal cognitive marker for differentiating them from Alzheimer's disease (AD) patients, and explore the correlation between cognitive function and total small vessel disease (SVD) burden. METHODS: SIVD (n = 60) and AD (n = 30) patients and cognitively unimpaired healthy controls (HCs; n = 30) were recruited from our longitudinal MRI AD and SIVD study (ChiCTR1900027943) and received a comprehensive neuropsychological assessment and a multimodal MRI scan. Cognitive performance and MRI SVD markers were compared between groups. Combined cognitive scores were established for differentiating between SIVD and AD patients. Correlations between cognitive function and total SVD scores were analysed in dementia patients. RESULTS: SIVD patients showed poorer performance in information processing speed and better performance in memory, language, and visuospatial function than AD patients, although all cognitive domains were impaired in both groups compared with HCs. Combined cognitive scores showed an area under the curve of 0.727 (95%CI 0.62-0.84, p < 0.001) for differentiating SIVD and AD patients. Auditory Verbal Learning Test recognition scores were negatively correlated with total SVD scores in SIVD patients. CONCLUSIONS: Our results suggested that neuropsychological assessments, specifically combined tests including episodic memory, information processing speed, language and visuospatial ability, are useful in the clinical differentiation between SIVD and AD patients. Moreover, cognitive dysfunction was partly correlated with MRI SVD burden in SIVD patients.

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In this research, we aimed to perform a comprehensive bioinformatic analysis of immune cell infiltration in osteoarthritic cartilage and synovium and identify potential risk genes. Datasets were downloaded from the Gene Expression Omnibus database. We integrated the datasets, removed the batch effects and analyzed immune cell infiltration along with differentially expressed genes (DEGs). Weighted gene co-expression network analysis (WGCNA) was used to identify the positively correlated gene modules. LASSO (least absolute shrinkage and selection operator)-cox regression analysis was performed to screen the characteristic genes. The intersection of the DEGs, characteristic genes and module genes was identified as the risk genes. The WGCNA analysis demonstrates that the blue module was highly correlated and statistically significant as well as enriched in immune-related signaling pathways and biological functions in the KEGG and GO enrichment. LASSO-cox regression analysis screened 11 characteristic genes from the hub genes of the blue module. After the DEG, characteristic gene and immune-related gene datasets were intersected, three genes, PTGS1, HLA-DMB and GPR137B, were identified as the risk genes in this research. In this research, we identified three risk genes related to the immune system in osteoarthritis and provide a feasible approach to drug development in the future.

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Sorghum requires fewer inputs for sustainable cultivation in harsh climates and has the potential to be utilized in modern food product innovations. Moreover, consumption of sorghum may elicit favorable health effects similar to other commonly consumed cereals, like wheat. Animal and human research exploring health effects of sorghum consumption indicates potential beneficial effects on blood glucose and lipid regulation, oxidative stress modulation, appetite regulation and weight management. However, a recent appraisal of the strength of evidence has not been conducted. Therefore, this study aims to evaluate the effects of sorghum consumption on metabolic indicators of chronic disease, including blood lipid and blood glucose levels, markers of oxidative stress, and factors associated with weight management. Using CINAHL, Cochrane Library, PubMed and MEDLINE databases, a systematic review of intervention studies published up to May 2020 was conducted and 16 interventional studies met the criteria for inclusion. Evidence for favorable effects of sorghum consumption on indicators of chronic disease, including blood glucose responses, markers of oxidative stress, satiety measures and weight management was demonstrated. Evidence from this systematic review may assist to promote sorghum's potential health benefits globally, including in food markets where it is underutilized, stimulating more sorghum-based food innovations in the future.

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The translation of extracellular signals to intracellular responses involves a number of signal transduction molecules. A major component of this signal transducing function is adenylyl cyclase, which produces the intracellular "second messenger," cyclic AMP. What was initially considered as a single enzyme for cyclic AMP generation is now known to be a family of nine membrane-bound enzymes, and one cytosolic enzyme. Each member of the adenylyl cyclase family is distinguished by factors that modulate its catalytic activity, by the cell, tissue, and organ distribution of the family members, and by the physiological/behavioral functions that are subserved by particular family members. This review focuses on the Type 7 adenylyl cyclase (AC7) in terms of its catalytic characteristics and its relationship to alcohol use disorder (AUD, alcoholism), and major depressive disorder (MDD). AC7 may be part of the inherited system predisposing an individual to AUD and/or MDD in a sex-specific manner, or this enzyme may change in its expression or activity in response to the progression of disease or in response to treatment. The areas of brain expressing AC7 are related to responses to stress and evidence is available that CRF1 receptors are coupled to AC7 in the amygdala and pituitary. Interestingly, AC7 is the major form of the cyclase contained in bone marrow-derived cells of the immune system and platelets, and in microglia. AC7 is thus, poised to play an integral role in both peripheral and brain immune function thought to be etiologically involved in both AUD and MDD. Both platelet and lymphocyte adenylyl cyclase activity have been proposed as markers for AUD and MDD, as well as prognostic markers of positive response to medication for MDD. We finish with consideration of paths to medication development that may selectively modulate AC7 activity as treatments for MDD and AUD.

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Toothache (TA) is a common and severe pain, but its effects on the brain are somewhat unclear. In this study, functional magnetic resonance imaging (fMRI) was used to compare regional homogeneity (ReHo) between TA patients and a normal control group and to explore the brain activity changes during TA, establishing the theoretical basis for the mechanism of neuropathic pain. In total, 20 TA patients and 20 healthy controls (HCs) were recruited and underwent assessment of pain, and then resting-state fMRI (rs-fMRI). The ReHo method was used to analyze the original whole-brain images. Pearson's correlation analysis was used to assess the relationship between mean ReHo values in each brain region and clinical symptoms, and the receiver operating characteristic (ROC) curve was used to conduct correlation analysis on the brain regions studied. The ReHo values of the right lingual gyrus (RLG), right superior occipital gyrus (RSOG), left middle occipital gyrus (LMOG) and right postcentral gyrus (RPG) in the TA group were significantly higher than in HCs. The mean ReHo values in the RLG were positively correlated with the anxiety score (AS) (r = 0.723, p < 0.001), depression score (DS) (r = 0.850, p < 0.001) and visual analogue score (VAS) (r = 0.837, p < 0.001). The mean ReHo values of RSOG were also positively correlated with AS (r = 0.687, p = 0.001), DS (r = 0.661, p = 0.002) and VAS (r = 0.712, p < 0.001). The areas under the ROC curve of specific brain area ReHo values were as follows: RLG, 0.975; RSOG, 0.959; LMOG, 0.975; RPG, 1.000. Various degrees of brain activity changes reflected by ReHo values in different areas of the brain indicate the impact of TA on brain function. These findings may reveal related neural mechanisms underlying TA.

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INTRODUCTION: There is a significant incidence of cats with renal disease (RD) and calcium oxalate (CaOx) kidney uroliths in domesticated cats. Foods which aid in the management of these diseases may be enhanced through understanding the underlying metabolomic changes. OBJECTIVE: Assess the metabolomic profile with a view to identifying metabolomic targets which could aid in the management of renal disease and CaOx uroliths. METHOD: This is a retrospective investigation of 42 cats: 19 healthy kidney controls, 11 with RD, and 12 that formed CaOx nephroliths. Cats were evaluated as adults (2 through 7 years) and at the end of life for plasma metabolomics, body composition, and markers of renal dysfunction. Kidney sections were assessed by Pizzolato stain at the end of life for detection of CaOx crystals. CaOx stone presence was also assessed by analysis of stones removed from the kidney at the end of life. RESULTS: There were 791 metabolites identified with 91 having significant (p < 0.05, q < 0.1) changes between groups. Many changes in metabolite concentrations could be explained by the loss of renal function being most acute in the cats with RD while the cats with CaOx stones were intermediate between control and RD (e.g., urea, creatinine, pseudouridine, dimethylarginines). However, the concentrations of some metabolites differentiated RD from CaOx stone forming cats. These were either increased in the RD cats (e.g., cystathionine, dodecanedioate, 3-(3-amino-3-carboxypropyl) uridine, 5-methyl-2'-deoxycytidine) or comparatively increased in the CaOx stone forming cats (phenylpyruvate, 4-hydroxyphenylpyruvate, alpha-ketobutyrate, retinal). CONCLUSIONS: The metabolomic changes show specific metabolites which respond generally to both renal diseases while the metabolomic profile still differentiates cats with RD and cats with CaOx uroliths.

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So far, intense pulsed light (IPL) has been widely used in the treatment of meibomian gland dysfunction (MGD), but there was still a lack of research on its specific mechanism. Determining whether there was a correlation between liposome changes and remission of clinical signs in patients with MGD treated with IPL was of great significance in the clinical evaluation of efficacy in patients with MGD. Our study enrolled the 10 healthy subjects and 26 adult patients, who were diagnosed with MGD and had not received any alternative treatments for at least 3 months. Each patient received a series of three treatments at 3-week intervals. The meibum was collected before the first treatment (T0) and the third treatment (T2). The significant changes in ocular surface parameters before and after IPL treatment were analyzed. The results showed that IPL significantly improved the symptoms of MGD, including ocular surface disease index (OSDI), tear breakup time (TBUT), redness of conjunctival (CR), corneal fluorescein staining (CF), the meibomian gland expressibility (MGE), and meibum quality (all p < 0.05). Lipidomics analysis of the meibum characterized the changes in lipid profiles induced by IPL. A total of 323 lipid species compounds were identified in the spectrum. A total of 41 lipid species were significantly different in patients with MGD (T0) vs. healthy controls. Following IPL treatment (T2), 24 lipid species were significantly different compared with T0: TG (10 lipid species), LPC (6 lipid species), OAHFA (4 lipid species), Cer (2 lipid species), SM (1 lipid species), and PE (1 lipid specie). Among these lipids, 4 of the lipids was a high correlation with TBUT, 5 was TH, 6 was CR, and 11 was meibum quality. In a ward, IPL treatment can achieve the therapeutic effect by changing the alternations of tear film lipids in patients with MGD. The changes in lipid expression profiles are potential indexes to evaluate the therapeutic effectiveness of IPL treatment or other treatments on MGD.

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Mycoprotein is a fungal-based ingredient rich in fibre and protein used in meat substitutes called Quorn. Fibre and protein positively regulate glycaemia, lipidaemia and energy intake which are non-communicable diseases' (NCD) markers. We performed a cross-sectional study to investigate the association of mycoprotein intake with diet quality, nutrient, energy intake and NCD risk within 5507 UK free-living adults from the National Diet and Nutrition Survey from years 2008/2009 to 2016/2017. Dietary approaches to stop hypertension (DASH) and healthy diet index (HDI) were calculated to estimate diet quality. Comparison between mycoprotein consumers (>1 % kcal) and non-consumers, and associations between consumers and nutrient intakes, NCD's risk markers and diet quality were investigated using a survey-adjusted general linear model adjusted for sex, age, BMI, ethnicity, socio-economic, smoking status, region of residency, total energy, energy density, HDI and non-mycoprotein fibre intake. Mycoprotein consumers (3·44 % of the cohort) had a higher intake of dietary fibre (+22·18 %, P < 0·001), DASH score (+23·33 %) and HDI (+8·89 %) (P < 0·001, both) and lower BMI (-4·77 %, P = 0·00) v. non-consumers. There was an association (P = 0·00) between mycoprotein consumers and diet quality scores (+0·19 and +0·26), high fibre (+3·17 g), total and food energy (+3·09 and +0·22 kcal), but low energy density intakes (-0·08 kcal/g, P = 0·04). Consumers were negatively associated with fasting blood glucose (-0·31 mmol/l, P = 0·00) and glycated HbA1c (-0·15 %, P = 0·01). In conclusion, mycoprotein intake is associated with lower glycaemic markers and energy density intake, and high fibre, energy intake and diet quality scores.

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Phospholipids (PL) are converted into lipid biomarkers by the action of phospholipases and reactive oxygen species (ROS), which are activated or released under certain physiological and pathophysiological conditions. Therefore, the in vivo concentration of such lipid biomarkers [e.g., lysophospholipids (LPLs)] is altered in humans and animals under different conditions such as inflammation, stress, medication, and nutrition. LPLs are particularly interesting because they are known to possess pro- and anti-inflammatory properties and may be generated by two different pathways: either by the influence of phospholipase A2 or by different reactive oxygen species that are generated in significant amounts under inflammatory conditions. Both lead to the cleavage of unsaturated acyl residues. This review provides a short summary of the mechanisms by which lipid biomarkers are generated under in vitro and in vivo conditions. The focus will be on lysophosphatidylcholine (LPC) because usually, this is the LPL species which occurs in the highest concentration and is, thus, easily detectable by chromatographic and spectroscopic methods. Finally, the effects of lipid biomarkers as signaling molecules and their roles in different human and animal pathologies such as infertility, cancer, atherosclerosis, and aging will be shortly discussed.