Correlations of gray matter volume with peripheral cytokines in Parkinson's disease.

INTRODUCTION: Peripheral cytokine levels may affect specific brain volumes. Few studies have examined this possible relationship. OBJECTIVE: In a case-control study, we used magnetic resonance imaging (MRI) voxel-based morphological analysis techniques to examine the relationship between gray matter volume changes and cognitive, motor and emotional dysfunction as well as between gray matter volume changes and peripheral blood cytokine levels. METHOD: A total of 134 subjects, comprising 66 PD patients and 68 healthy controls, were recruited. Peripheral venous blood was collected to measure the concentrations of 12 cytokines, including IL-1ß, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-17, IFN-α, IFN-γ, and TNF-α. All the subjects also underwent MRI, where 3D-T1-weighted MR images were used for the analysis. In addition, the Montreal Cognitive Assessment (MoCA), Mini-Mental Status Examination (MMSE), Unified Parkinson's disease Rating Scale (UPDRS), Hamilton Anxiety Scale (HAMA), and Hamilton Depression Scale (HAMD) scores were assessed in PD patients. Statistical parameter mapping 12 software was used for the statistical analysis of the images. RESULT: Compared with control patients, PD patients presented decreased gray matter volume (GMV) in the bilateral frontal lobe, temporal lobe, parietal lobe, occipital lobe, insula, and right cerebellar lobule VIII. Regional GMV in the temporal lobe, parietal lobe, and cerebellum was correlated with MoCA, MMSE, UPDRS, HAMA, and HAMD scores in PDs. In addition, the regional GMV in PDs was correlated with the concentrations of cytokines, including IL-4, IL-6, IFN-γ, and TNF-α. The IL-6 concentration was negatively correlated with the UPDRS-IV score. CONCLUSION: PD patients exhibit gray matter atrophy in a wide range of brain regions, which are symmetrically distributed and mainly concentrated in the frontal and temporal lobes, and these changes may be linked to motor disorders and neuropsychiatric manifestations. Cytokine concentrations in peripheral blood are correlated with regional gray matter volume in PDs, and the IL-6 level affects gray matter volume in the left precentral gyrus and the manifestation of motor complications.

Genome-wide mapping of quantitative trait loci conferring resistance to stripe rust in spring wheat line PI 660072.

KEY MESSAGE: Two major QTL for resistance to stripe rust were mapped on chromosome 2BL and 4BL in spring wheat PI 660072, and their KASP markers were developed. Stripe rust, caused by Puccinia striiformis f. sp. tritici (Pst), is one of the most devastating diseases of wheat worldwide. Identifying resistance genes is crucial for developing resistant cultivars to control the disease. Spring wheat PI 660072 (Triticum aestivum) has been identified to possess both adult-plant resistance (APR) and all-stage resistance (ASR) to stripe rust. To elucidate the genetic basis of the resistance in PI 660072, a mapping population consisting of 211 F5-F7 recombinant-inbred lines (RILs) was developed from a cross of PI 660072 with susceptible spring wheat Avocet S. The mapping population was phenotyped for stripe rust responses across five field environments from 2020 to 2022 and genotyped using the 15 K SNP (single nucleotide polymorphism) array to map stripe rust resistance loci. The mapping population was also tested at the seedling stage with predominant Chinese Pst races CYR31, CYR32, CYR34 and PST-YX1-3-1 in the greenhouse. Stripe rust resistance genes were identified using the quantitative trait locus (QTL) mapping approach. Two QTL were identified with QYrPI660072.swust-2BL mapped on the long arm of chromosome 2B for ASR and QYrPI660072.swust-4BL on the long arm of chromosome 4B for APR. To facilitate marker-assisted selection breeding, Kompetitive allele specific PCR (KASP) markers, KASP-1269 for QYrPI660072.swust-2BL and KASP-3209 for QYrPI660072.swust-4BL, were developed. These markers could be used to introgress the effective resistance QTL into new wheat cultivars.

Design and Implementation of an Ontology for Measurement Terminology in Digital Calibration Certificates.

Digital Calibration Certificates (DCCs) are a key focus in metrology digitalization, necessitating that they satisfy the criteria for machine readability and understandability. Current DCCs are machine-readable, but they are still missing the essential semantic information required for machine understandability. This shortfall is particularly notable in the lack of a dedicated semantic ontology for measurement terminologies. This paper proposes a domain ontology for measurement terminologies named the OMT (Ontology for Measurement Terminology), using a foundation of metrological terms from standards like the International Vocabulary of Metrology (VIM), the Guide to the Expression of Uncertainty in Measurement (GUM), and JJF1001. It also incorporates insights from models such as the SI Reference Point, the Simple Knowledge Organization System (SKOS), and the DCC Schema. The methodology was guided by Stanford's Seven-Step Method, ensuring a systematic development process tailored to the needs of metrological semantics. Through semantic expression capability verification and SPARQL query validations, the OMT has been confirmed to possess essential machine readability and understandability features. It has been successfully integrated into version 3.2.1 of DCCs across ten representative domains. This integration demonstrates an effective method for ensuring that DCCs are machine-readable and capable of interoperating within digital environments, thereby advancing the research in metrology digitization.

Causal effect of gut-microbiota-derived metabolite trimethylamine N-oxide on Parkinson's disease: A Mendelian randomization study.

BACKGROUND AND PURPOSE: It has been suggested that trimethylamine N-oxide (TMAO) is related to Parkinson's disease (PD) in observational studies. However, the direction of this association is inconsistent. An exploratory Mendelian randomization study was conducted to investigate whether TMAO and its precursors have a causal relationship with PD. METHODS: Summary statistics were obtained for single nucleotide polymorphisms related to circulating levels of TMAO, betaine, carnitine and choline, and the corresponding data for the risk, age at onset and progression of PD from genome-wide association studies. Inverse-variance weighting was used as the primary method for effect estimation. The false discovery rate was applied to the correction of multiple testing. A p value of association <0.05 but above the false discovery rate corrected threshold was deemed suggestive evidence of a possible association. A range of robust Mendelian randomization methods were used for sensitivity analysis. RESULTS: Suggestive evidence was observed of an inverse causal effect of TMAO on motor fluctuations (odds ratio [OR] 0.851, 95% confidence interval [CI] 0.731, 0.990, p = 0.037) and carnitine on insomnia (OR 0.817, 95% CI 0.700, 0.954, p = 0.010) and a positive causal effect of betaine on Hoehn-Yahr stage (OR 1.397, 95% CI 1.112, 1.756, p = 0.004), Unified Parkinson's Disease Rating Scale (UPDRS) III score (ß = 0.138, 95% CI 0.051, 0.225, p = 0.002), motor fluctuations (OR 1.236, 95% CI 1.011, 1.511, p = 0.039), and choline on UPDRS IV (ß = 0.106, 95% CI 0.026, 0.185, p = 0.009) and modified Schwab and England Activities of Daily Living Scale score (ß = 0.806, 95% CI 0.127, 1.484, p = 0.020). CONCLUSIONS: Our findings provide suggestive evidence that TMAO and its precursors have a causal effect on the progression of PD. Further investigation of the underlying mechanisms is required.

Machine learning models based on multi-parameter MRI radiomics for prediction of molecular glioblastoma: a new study based on the 2021 World Health Organization classification.

BACKGROUND: The 2021 World Health Organization (WHO) classification considers a histological low grade glioma with specific molecular characteristics as molecular glioblastoma (mGBM). Accurate identification of mGBM will aid in risk stratification of glioma patients. PURPOSE: To explore the value of machine learning models based on magnetic resonance imaging (MRI) radiomics features in predicting mGBM. MATERIAL AND METHODS: In total, 166 patients histologically diagnosed as low-grade diffuse glioma (WHO II and III) were included in the study. Fifty-three cases were reclassified as mGBM based on molecular status. Four dimensionality reduction methods including distance correlation (DC), gradient boosted decision tree (GBDT), least absolute shrinkage and selection operator (LASSO) and minimal redundancy maximal relevance (MRMR) were used to select the optimal signatures. Six machine learning algorithms including support vector machine (SVM), linear discriminant analysis (LDA), neural network (NN), logistic regression (LR), K-nearest neighbour (KNN) and decision tree (DT) were used to develop the classifiers. The relative SD was used to evaluate the stability of the models, and the area under the curve values in the independent test group were used to evaluate their performances. RESULTS: NN_DC was determined as the optimal classifier due to the highest area under the curve of 0.891 in the test group. The classification accuracy, sensitivity, specificity, positive predictive value and negative predictive value of NN_DC were 0.915, 0.842, 0.950, 0.889 and 0.927, respectively. CONCLUSION: Machine learning models can predict mGBM non-invasively, which may help to develop personalized treatment strategies for neurosurgeons and provide an effective tool for accurate stratification in clinical trials.

Increased expression of NOP14 is associated with improved prognosis due to immune regulation in colorectal cancer.

BACKGROUND: Colorectal cancer (CRC) is the third most common of cancer-related deaths. Nucleolar protein 14 (NOP14) is known to play different roles in diverse types of cancers. However, little is known about its roles in CRC. Here, we assessed the prognostic value and functions of NOP14 in CRC using the data from The Cancer Genome Atlas (TCGA) and validated them based on the data from Gene Expression Omnibus (GEO). METHODS: NOP14 mRNA and protein data in CRC was obtained from the TCGA, GEO, human protein atlas (HPA), and UALCAN databases. Survival and Cox regression analysis was performed to assess the prognostic value of NOP14 in CRC patients. Next, to evaluate the potential functions of NOP14, a protein-protein interaction (PPI) network was constructed and gene set enrichment analysis (GSEA) of differential expression genes (DEGs) associated with dysregulated NOP14 was performed. Finally, to investigate the immune response associated with NOP14 expression in CRC, we analyzed the correlations between immune cells infiltration and NOP14 expression level. Additionally, the correlations between immune molecule expression levels with NOP14 expression level were analyzed. RESULTS: High NOP14 mRNA expression was observed in CRC tissues based on the data from TCGA and GEO datasets. Similarly, high NOP14 protein levels were found in CRC tissues according to the immunohistochemical images from HPA. Interestingly, high NOP14 expression level was associated with an improved prognosis in CRC patients. Univariate and multivariate Cox regression analysis indicated that high NOP14 expression level was an independent protective factor for CRC patients. With the support of PPI network analysis, we found several risk genes interacted with NOP14. GSEA revealed that high NOP14 expression inhibited several signal pathways involved in tumor formation and development. Additionally, high NOP14 expression was positively associated with most kinds of immune cell infiltrations and the expression levels of some molecules related to immune activation. CONCLUSION: Altogether, these results indicated that high NOP14 expression leads to improved prognosis in CRC patients by inhibiting the signaling pathways involved in tumor growth and promoting the immune responses.

The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options.

Parkinson's disease is a common neurodegenerative disorder in which gastrointestinal symptoms may appear prior to motor symptoms. The gut microbiota of patients with Parkinson's disease shows unique changes, which may be used as early biomarkers of disease. Alterations in the gut microbiota composition may be related to the cause or effect of motor or non-motor symptoms, but the specific pathogenic mechanisms are unclear. The gut microbiota and its metabolites have been suggested to be involved in the pathogenesis of Parkinson's disease by regulating neuroinflammation, barrier function and neurotransmitter activity. There is bidirectional communication between the enteric nervous system and the CNS, and the microbiota-gut-brain axis may provide a pathway for the transmission of α-synuclein. We highlight recent discoveries about alterations to the gut microbiota in Parkinson's disease and focus on current mechanistic insights into the microbiota-gut-brain axis in disease pathophysiology. Moreover, we discuss the interactions between the production and transmission of α-synuclein and gut inflammation and neuroinflammation. In addition, we draw attention to diet modification, the use of probiotics and prebiotics and faecal microbiota transplantation as potential therapeutic approaches that may lead to a new treatment paradigm for Parkinson's disease.

Exosomal lncRNA SNHG10 derived from colorectal cancer cells suppresses natural killer cell cytotoxicity by upregulating INHBC.

BACKGROUND: Exosome-mediated crosstalk between cancer cells and immune cells contributes to tumor growth. In this study, we investigated the mechanism underlying the exosome-mediated immune escape of colorectal cancer (CRC) cells from natural killer (NK) cells via the transfer of long noncoding RNAs (lncRNAs). METHODS: An epithelial-mesenchymal transition (EMT) model of SW480 cells was established by transforming growth factor beta (TGF-ß), followed by the assessment of the effect of EMT-derived exosomes (EMT-exo) on the functions of NK cells. RNA sequencing was performed to identify exosomal lncRNAs and target genes. The function of exosomal lncRNAs in tumor growth was further verified in vivo. RESULTS: EMT-exo suppressed the proliferation, cytotoxicity, IFN-γ production, and perforin-1 and granzyme B secretion of NK cells. RNA sequencing revealed that SNHG10 expression was upregulated in EMT-exo compared with that in non-EMT-exo. Moreover, SNHG10 expression was upregulated in tumor tissues in CRC, which was associated with poor prognosis. Overexpression of SNHG10 in exosomes (oe-lnc-SNHG10 exo) significantly suppressed the viability and cytotoxicity of NK cells. Transcriptome sequencing of NK cells revealed that the expression levels of 114 genes were upregulated in the oe-lnc-SNHG10 exo group, including inhibin subunit beta C (INHBC), which was involved in the TGF-ß signaling pathway. Si-INHBC treatment abrogated the effect of oe-lnc-SNHG10 exo on NK cells. oe-lnc-SNHG10 exo induced tumor growth and upregulated INHBC expression in mice and downregulated the expression of perforin, granzyme B, and NK1.1 in tumor tissues. CONCLUSIONS: The CRC cell-derived exosomal lncRNA SNHG10 suppresses the function of NK cells by upregulating INHBC expression. This study provides evidence that exosomal lncRNAs contribute to immune escape by inducing NK cell inhibition and proposes a potential treatment strategy for CRC.

Effects of combat sports on functional network connectivity in adolescents.

PURPOSE: To explore the effects of combat sports on functional network connectivity (FNC) in healthy adolescents. METHODS: Resting-state fMRI data were acquired from the combat sports (CS) group (n = 32) and non-athlete healthy control (HC) group (n = 29). Resting-state networks (RSNs) were obtained based on independent component analysis (ICA), and FNC analysis was performed. Then, the intra-network and inter-network connections were compared between the two groups. RESULTS: Compared with the HC group, the CS group demonstrated increased intra-network FC within the sensorimotor network (SMN), visual network (VIN), and cerebellum network (P < 0.01, FDR correction). Besides, decreased inter-network FC was found in the SMN-VIN, SMN-auditory network, SMN-default mode network, attention network (AN)-VIN, and AN-executive control network connections (P < 0.01, FDR correction). CONCLUSION: This study showed a complex relationship between combat sports and FNC in adolescents. The observed FNC patterns in the CS group may reflect training-related brain network optimization, early signs of subclinical brain damage, or preexisting differences. The extensive effects of combat sports on FNC in adolescents could expand our understanding of neuromodulatory mechanisms.

Long Noncoding RNA GAPLINC Promotes Cells Migration and Invasion in Colorectal Cancer Cell by Regulating miR-34a/c-MET Signal Pathway.

BACKGROUND: Gastric adenocarcinoma predictive long intergenic noncoding RNA (GAPLINC) has been detected in colorectal cancer (CRC) cells and reportedly performs many functions related to tumor proliferation and metastasis. Aim The present study aimed to comprehensively explore the biological functions of GAPLINC and their underlying mechanism in CRC cell. METHODS: The human cancer LncRNA PCR array was used to detect the differentially expressed long noncoding RNAs in human CRC samples. Real-time PCR, dual-luciferase assay, RNA pull-down assay, Transwell assay, and western blot analysis were performed to explore the molecular mechanism underlying GAPLINC functions related to migration and invasion of a human CRC cell line (HCT116). RESULTS: Compared to the non-cancerous tissues, GAPLINC expression was obviously increased in CRC tissues. In HCT116, silencing of GAPLINC weakened cell migration and invasion, while overexpression of GAPLINC significantly promoted cell migration and invasion. Through dual-luciferase, RNA pull-down, and Transwell assays, we verified that miR-34a was the downstream molecule of GAPLINC and that miR-34a negatively regulated the migration and invasion of HCT116 cell. Furthermore, we found that GAPLINC positively regulated the miR-34a target gene c-MET in CRC tissues. CONCLUSIONS: Our findings revealed that GAPLINC was up-regulated in CRC tissues and was involved in the migration and invasion of CRC cells by regulating miR-34a/c-MET signaling pathway.

Association between serum osteocalcin level and visceral obesity in Chinese postmenopausal women.

BACKGROUND: A low serum osteocalcin level, visceral obesity and postmenopausal status are recognized risk factors for cardiovascular disease. OBJECTIVE: We investigated the relationship between the serum osteocalcin level and visceral fat content in a population of Chinese postmenopausal women. DESIGN AND PATIENTS: In total, 1481 postmenopausal women (mean age ± standard deviation, 57·1 ± 4·8 years) were selected from the Shanghai Obesity Study. MEASUREMENTS: Abdominal fat accumulation was quantified using magnetic resonance imaging. Subjects with a visceral fat area (VFA) of ≥80 cm(2) were classified as abdominally obese. The total serum osteocalcin level was measured by electrochemiluminescence immunoassay. RESULTS: The median serum osteocalcin level was 20·66 µg/l (interquartile range, 16·88-25·42 µg/l). The overall prevalence of abdominal obesity was 49·1% (n = 727). Abdominally obese subjects had lower serum osteocalcin levels than did nonabdominally obese subjects [19·14 (16·02-23·82) vs 21·97 (18·14-26·77) µg/l, respectively; P < 0·001]. Partial correlation analysis showed that the serum osteocalcin level was still negatively correlated with VFA after adjusting for age, years since menopause and body mass index (P < 0·01). Moreover, VFA was independently associated with the serum osteocalcin level after adjustment for confounding factors (P < 0·05). A low serum osteocalcin level was an independent risk factor for abdominal obesity (odds ratio, 0·972; 95% confidence interval, 0·953-0·991; P = 0·004). CONCLUSION: The serum osteocalcin level was inversely correlated with the visceral fat content in these Chinese postmenopausal women.

Relationship between serum osteocalcin level and carotid intima-media thickness in a metabolically healthy Chinese population.

BACKGROUND: The relationship between osteocalcin and atherosclerosis remains unclear. This might be due to different degrees of confounding from factors that are associated with serum osteocalcin level, such as metabolic-related variables. This study aimed to investigate the relationship between serum osteocalcin level and carotid intima-media thickness (C-IMT) in a metabolically healthy population. METHODS: A total of 476 subjects with normal values for weight, glucose tolerance, blood pressure, and lipids (age range, 20-75 years; 155 men, 201 premenopausal women, 120 postmenopausal women) from the Shanghai Obesity Study were recruited for this cross-sectional study. Subjects with a history of cardiovascular disease or carotid plaque were excluded. C-IMT was measured by ultrasonography. Serum osteocalcin level was assessed by an electrochemiluminescence immunoassay. RESULTS: Median C-IMT in the entire study population was 0.55 mm with an interquartile range of 0.50-0.60 mm. C-IMT in premenopausal women was significantly lower than that in men and postmenopausal women (all P < 0.001). The median (interquartile range) of serum osteocalcin level in the entire population was 17.02 (13.31-21.47) ng/mL. Serum osteocalcin level in postmenopausal women was significantly higher than that in men and premenopausal women (all P < 0.001), while the level of serum osteocalcin in men was also significantly higher than that in premenopausal women (P < 0.001). No significant correlation was found between C-IMT and serum osteocalcin level in either men or postmenopausal women. There was a significant, inverse correlations between C-IMT and serum osteocalcin level in premenopausal women after adjustment of age, but this association was eliminated after adjustment for other confounding factors. CONCLUSIONS: Serum osteocalcin level was not independently associated with C-IMT in a metabolically healthy Chinese population.

Glycated albumin is more closely correlated with coronary artery disease than 1,5-anhydroglucitol and glycated hemoglobin A1c.

BACKGROUND: The aim of this study was to investigate the associations of two nontraditional glycemic markers, glycated albumin (GA) and 1,5-anhydroglucitol (1,5-AG), as well as glycated hemoglobin A1c (HbA1c) with coronary artery disease (CAD). METHODS: In total, 272 subjects (178 men and 94 postmenopausal women) were enrolled in this study. All of them underwent coronary angiography which was used to diagnose CAD. The severity of coronary artery stenosis was assessed by the coronary stenosis index (CSI). GA and 1,5-AG were assayed using the enzymatic method, and HbA1c was detected by high-pressure liquid chromatography. RESULTS: The HbA1c and GA levels were significantly higher in CAD group than those in non-CAD group (both P < 0.01). While the 1,5-AG level was significantly lower in CAD group than that in non-CAD group (P < 0.05). After adjustment for traditional risk factors of CAD, HbA1c, 1,5-AG, and GA, multivariate logistic regression analysis showed that GA was an independent risk factor for CAD (odds ratio = 1.143, 95% confidence interval: 1.048-1.247, P = 0.002). With CSI as a dependent variable, multiple stepwise regression analysis demonstrated an independent positive correlation between GA and CSI (standardized ß = 0.184, P = 0.003), beyond gender, age, and lipid-lowering therapy, after adjustment for traditional risk factors of CAD, HbA1c, 1,5-AG, and GA. CONCLUSIONS: GA was more closely correlated with CAD than HbA1c and 1,5-AG in a Chinese population with high risk of CAD.

Inverse relationship between serum osteocalcin levels and nonalcoholic fatty liver disease in postmenopausal Chinese women with normal blood glucose levels.

AIM: Osteocalcin is involved in the progression of nonalcoholic fatty liver disease (NAFLD) in animal models and humans. In this study we investigated the relationship between serum osteocalcin levels and NAFLD in postmenopausal Chinese women. METHODS: A total of 733 postmenopausal women (age range: 41-78 years) with normal blood glucose levels were enrolled in this cross-sectional study. Women taking lipid-lowering or anti-hypertensive drugs were excluded. Serum osteocalcin levels were assessed using an electrochemiluminescence immunoassay. The degree of NAFLD progression for each subject was assessed through ultrasonography. The fatty liver index (FLI) of each subject was calculated to quantify the degree of liver steatosis. RESULTS: The median level of serum osteocalcin for all subjects enrolled was 21.99 ng/mL (interquartile range: 17.84-26.55 ng/mL). Subjects with NAFLD had significantly lower serum osteocalcin levels (18.39 ng/mL; range: 16.03-23.64 ng/mL) compared with those without NAFLD (22.31 ng/mL; range: 18.55-27.06 ng/mL; P<0.01). Serum osteocalcin levels decreased with incremental changes in the FLI value divided by the quartile (P-value for trend<0.01). The serum osteocalcin levels showed a negative correlation with the FLI values, even after adjusting for confounding factors (standardized ß=-0.124; P<0.01). Binary logistic regression analysis identified an individual's serum osteocalcin level as an independent risk factor for NAFLD (odds ratio: 0.951; 95% confidence interval: 0.911-0.992; P=0.02). CONCLUSION: Serum osteocalcin levels are inversely correlated with NAFLD in postmenopausal Chinese women with normal blood glucose levels.

Serum vitamin D levels are inversely related with non-alcoholic fatty liver disease independent of visceral obesity in Chinese postmenopausal women.

The aim of the present study was to investigate the association between serum vitamin D levels and both visceral adipose and with non-alcoholic fatty liver disease (NAFLD) in Chinese postmenopausal women. Four hundred and fifty-one postmenopausal women between 45 and 74 years of age (mean (± SD) age 57.3 ± 4.6 years) were enrolled in the study. All subjects participated in the Shanghai Obesity Study between June and August 2011 and underwent abdominal magnetic resonance imaging and an abdominal ultrasonography. Patients with a visceral fat area (VFA) ≥ 80 cm(2) were classified as abdominally obese. Serum 25-hydroxyvitamin D3 (25(OH)D3 ) levels were measured with an electrochemiluminescence immunoassay. The prevalence of NAFLD in the study population was 34.8% (n = 157). Women with abdominal obesity had significantly lower serum 25(OH)D3 levels than those without abdominal obesity (median (interquartile range) 11.23 (8.64-14.12) vs 12.56 (9.41-15.98) ng/mL, respectively; P < 0.01). Regardless of abdominal obesity status, serum 25(OH)D3 levels in patients with NAFLD were lower than those without non-NAFLD (11.14 (8.63-13.81) vs 12.92 (9.48-16.37) ng/mL (P < 0.05) for those without abdominal obesity; 10.86 (8.61-13.56) vs 11.55 (8.82-16.38) ng/mL (P < 0.05) for those with abdominal obesity). Partial correlation analyses demonstrated a negative correlation between serum 25(OH)D3 levels and VFA (P < 0.05). Logistic regression analysis revealed that high serum 25(OH)D3 levels were a protective factor against NAFLD after adjusting for risk factors such as VFA. In conclusion, independent of visceral obesity, vitamin D is inversely correlated with NAFLD in Chinese postmenopausal women.

Fibroblast growth factor 23 is associated with the presence of coronary artery disease and the number of stenotic vessels.

Fibroblast growth factor 23 (FGF23) has been reported to be involved in cardiovascular disease. The aim of this study was to investigate the association between FGF23 and the presence of coronary artery disease (CAD), as well as the number of stenotic vessels. A total of 254 eligible participants (167 men and 87 postmenopausal women) were enrolled in this study. Coronary angiography was used for diagnosis of CAD. Serum intact FGF23 levels were determined by a two-sided sandwich enzyme-linked immunosorbent assay. The median serum FGF23 levels of the entire study population were 39.9 (33.1-47.5) pg/mL. Serum FGF23 levels were higher in subjects with one-vessel disease than those without CAD (P < 0.05), which further increased significantly in the subjects with multi-vessel disease (P < 0.05). Serum FGF23 levels increased with cumulative number of stenotic vessels (P for trend < 0.001). Multiple stepwise regression analysis revealed estimated glomerular filtration rate (standardized ß = -0.298; P < 0.001) and body mass index (standardized ß = 0.132; P = 0.049) were independent factors correlated with FGF23. Multivariate logistic regression analysis showed that FGF23 was positively and independently associated with the presence of CAD (odds ratio = 1.058, 95% confidence interval = 1.025-1.092; P = 0.001). Additionally, FGF23 was also correlated with multi-vessel disease significantly (odds ratio = 1.034, 95% confidence interval = 1.007-1.062; P = 0.013). In conclusion, serum FGF23 levels exhibit positive and independent association with the presence of CAD and increase with the cumulative number of stenotic vessels.

Associations of glycated haemoglobin A1c and glycated albumin with subclinical atherosclerosis in middle-aged and elderly Chinese population with impaired glucose regulation.

The aim of this study was to investigate the correlations of glycated haemoglobin A1c (HbA1c) and glycated albumin (GA) with subclinical atherosclerosis in middle-aged and elderly Chinese populations with impaired glucose regulation (IGR). In total, 640 subjects with IGR and no history of cardiovascular disease or carotid artery plaque were recruited for this study (256 men, 384 women; age range, 40-70 years). The carotid intima-media thickness (C-IMT) measured by carotid ultrasonography was used as an indicator of subclinical atherosclerosis. Increased C-IMT was defined as ≥ 0.70 mm (upper quartile). HbA1c and GA were measured with high-performance liquid chromatography and enzymatic method, respectively. The average HbA1c and GA among all 640 subjects were 5.7 ± 0.3% and 14.0 ± 1.1%, respectively. HbA1c and GA were higher in subjects with increased C-IMT than in subjects with normal C-IMT (5.8 ± 0.3% vs 5.7 ± 0.3% and 14.2 ± 1.0% vs 13.9 ± 1.1%, respectively; both P < 0.01). Correlation analysis showed that both HbA1c and GA were positively correlated with C-IMT (r = 0.135 and 0.112, respectively; both P < 0.01). Logistic regression analysis revealed that both HbA1c (odds ratio (OR), 2.630; 95% confidence interval (95% CI), 1.401-4.935; P = 0.003) and GA OR, 1.215; 95% CI, 1.008-1.466; P = 0.041) were independent risk factors for increased C-IMT. Both HbA1c and GA reflect the risk of subclinical atherosclerosis in middle-aged and elderly Chinese populations with IGR.

Serum vitamin D is associated with non-alcoholic fatty liver disease in Chinese males with normal weight and liver enzymes.

AIM: Considering the characterization of vitamin D deficiency as a risk factor of ectopic fat deposition, the association of serum 25-hydroxy vitamin D3 [25(OH)D3] levels with non-alcoholic fatty liver disease (NAFLD) was evaluated in Chinese men with normal body mass index (BMI) and enzyme markers of liver function. METHODS: A total of 514 participants (22 to 79 years old) with normal BMI and liver enzymes were identified for analysis. Abdominal ultrasound was performed to diagnose NAFLD, and the fatty liver index (FLI) was calculated to quantify liver steatosis. Serum 25(OH)D3 levels were determined by an electrochemiluminescence immunoassay. RESULTS: Among the entire study population, the mean levels of serum 25(OH)D3 were 15.32±5.77 ng/mL. However, when serum 25(OH)D3 levels were compared between non-NAFLD subjects (n=438) and NAFLD subjects (n=76), the latter showed significantly lower levels (15.65±5.89 ng/mL vs 13.46±4.65 ng/mL, P=0.002). In addition, serum 25(OH)D3 levels were found to be significantly correlated with FLI after adjustment for age and BMI (r=-0.108, P=0.014). Logistic regression showed that serum 25(OH)D3 levels were independently correlated with NAFLD (OR: 0.937, 95% CI: 0.884-0.993, P=0.028). Furthermore, stepwise regression analysis revealed that serum 25(OH)D3 levels were inversely associated with FLI (ß=-0.055, P=0.040). CONCLUSION: The present study demonstrated that serum 25(OH)D3 levels were inversely associated with NAFLD, even in subjects with normal total body fat, suggesting a potential role of lower levels of vitamin D in the occurrence and development of NAFLD.

Additional role of serum 25-hydroxyvitamin D3 levels in atherosclerosis in Chinese middle-aged and elderly men.

1. Perturbed serum vitamin D levels have been shown to be associated with increased risk of cardiovascular disease. The aim of the present study was to investigate the association of serum 25-hydroxyvitamin D3 (25(OH)D3) levels and B ultrasonography-detected carotid plaque and carotid intima-media thickness (C-IMT) in Chinese middle-aged and elderly men. 2. In all, 1001 men, aged 45-78 years, were enrolled in the study. Increased C-IMT was defined as any C-IMT value in the highest quartile of the study subjects (≥ 0.75 mm). 3. The study population had a median serum 25(OH)D3 level of 14.51 ng/mL (interquartile range (IQR) 10.84-18.67 ng/mL). Subjects with carotid plaques had lower serum 25(OH)D3 levels than those without (13.80 (IQR 10.82-17.68) vs 14.74 (IQR 10.87-19.08) ng/mL, respectively; P = 0.029), and decreasing serum 25(OH)D3 levels were accompanied by increased C-IMT in both groups (13.24 (IQR 9.91-16.81) vs 14.45 (IQR 11.40-18.51) ng/mL, respectively (P < 0.05) in those with plaque; 13.80 (IQR 9.99-17.09) vs 14.99 (IQR 11.17-19.43) ng/mL, respectively (P < 0.01) in those without plaque). Multivariate logistic regression analysis showed that serum 25(OH)D3 levels were independently associated with carotid plaque (odds ratio (OR) 0.972; 95% confidence interval (CI) 0.946-0.998; P = 0.032). In addition, serum 25(OH)D3 levels were identified as an independent protective factor for increased C-IMT among subjects with plaque (OR 0.900; 95% CI 0.849-0.955; P = 0.001) and those without plaque (OR 0.944; 95% CI 0.908-0.981; P = 0.004). 4. Collectively, these findings suggest that serum 25(OH)D3 levels are inversely associated with atherosclerosis in Chinese middle-aged and elderly men.