Data_Sheet_1_Consistency between self-reported disease diagnosis and clinical assessment and under-reporting for chronic conditions: data from a community-based study in Xi’an, China.PDF

AimsThe current study aims to investigate the consistency between the surveyees’ self-reported disease diagnosis and clinical assessment of eight major chronic conditions using community-based survey data collected in Xi’an, China in 2017. With a focus on under-reporting patients, we aim to explore its magnitude and associated factors, to provide an important basis for disease surveillance, health assessment and resource allocation, and public health decision-making and services.MethodsQuestionnaires were administered to collect self-reported chronic condition prevalence among the study participants, while physical examinations and laboratory tests were conducted for clinical assessment. For each of the eight chronic conditions, the sensitivity, specificity, under-reporting, over-reporting, and agreement were calculated. Log-binomial regression analysis was employed to identify potential factors that may influence the consistency of chronic condition reporting.ResultsA total of 2,272 participants were included in the analysis. Four out of the eight chronic conditions displayed under-reporting exceeding 50%. The highest under-reporting was observed for goiter [85.93, 95% confidence interval (CI): 85.25–86.62%], hyperuricemia (83.94, 95% CI: 83.22–84.66%), and thyroid nodules (72.89, 95% CI: 72.02–73.76%). Log-binomial regression analysis indicated that senior age and high BMI were potential factors associated with the under-reporting of chronic condition status in the study population.ConclusionThe self-reported disease diagnosis by respondents and clinical assessment data exhibit significant inconsistency for all eight chronic conditions. Large proportions of patients with multiple chronic conditions were under-reported in Xi’an, China. Combining relevant potential factors, targeted health screenings for high-risk populations might be an effective method for identifying under-reporting patients.</p

Image_1_Total sugar intake is associated with higher prevalence of depressive symptoms in obese adults.TIF

BackgroundThe existing literature has repeatedly assessed the association between sugar-sweetened beverages and depressive symptoms, but studies of the association of total dietary sugar with depressive symptoms and of this association in obese adults are scarce. Thus, the purpose of this cross-sectional study was to assess the association between total sugar consumption and depressive symptoms in the study population and then in the population stratified by body mass index.MethodsThis study was conducted in a nationally representative sample of 16,009 adults from the 2011–2018 National Health and Nutrition Examination Survey in the US. Total sugar intake was assessed by 24 h dietary recalls, and depressive symptoms were assessed by the nine-item Patient Health Questionnaire. Logistic regression models were used to evaluate the association between total sugar consumption and depressive symptoms.ResultsTotal sugar intake was positively associated with higher prevalence of depressive symptoms, and the adjusted odds ratio (95% confidence interval) of depressive symptoms for the highest vs. lowest quintile of total sugar intake was 1.56 (1.18, 2.05). In stratified analysis, we found a positive association between total sugar intake and depressive symptoms in adults with body mass index ≥30 kg/m2 (P for trend = 0.013), whereas no association was found in normal weight or overweight adults.ConclusionsA higher intake of total sugar was associated with increased odds of clinically relevant depressive symptoms among obese adults. Further studies are necessary to confirm the role of total sugar in depressive symptoms among obese adults.</p

MOESM1 of MiR-30c/PGC-1β protects against diabetic cardiomyopathy via PPARα

Additional file 1: Figure S1. Different expression genes belonging to PPAR family between diabetic hearts and normal ones. Figure S2. High palmitate treatment impaired the insulin signal of NRCMs. Figure S3. The efficacy of siRNAs against PGC-1β. Figure S4. Identification of the primary neonatal rat cardiomyocytes. Figure S5. PGC-1β knockdown relieved high palmitate induced lipotoxicity in vitro. Figure S6. The effects of PGC-1β knockdown on mitochondrial biogenesis and membrane potentials. Figure S7. Overexpression of miR-30c alleviated high palmitate induced lipotoxicity in vitro. Figure S8. The effect of miR-30c on mitochondrial biogenesis and membrane potentials. Figure S9. The effects of rAAV9 mediated miR-30c/anti-miR-30c delivery on plasma lipid profile and blood glucose in vivo. Figure S10. The effects of rAAV9 mediated miR-30c/anti-miR-30c delivery on liver steatosis in vivo. Table S1. The wildtype sequence containing predicted miR-30c binding site of the human PGC-1β 3′ UTR and corresponding mutant sequence. Table S2. Sequences of miR-30c, anti-miR-30c, or miR-random inserted into rAAV expression plasmid. Table S3. Primers of CD36 and PDK4 promotors in ChIP-PCR. Table S4. Primers of rat 12S ribosomal DNA, COI and and 18S ribosomal DNA in real-time PCR. Table S5. Comparison of hemodynamic variables among mice with different treatments

MOESM3 of MiR-30c/PGC-1β protects against diabetic cardiomyopathy via PPARα

Additional file 3. Table S2. microRNA targeting PGC-1β predicted by TargetScan, PicTar and TarBase websites

MOESM2 of MiR-30c/PGC-1β protects against diabetic cardiomyopathy via PPARι

Additional file 2. Table S1. Differentially expressed genes in 3, 28 and 42 day after diabetes induction

Transcriptomic and Metabolic Analyses Provide New Insights into the Apple Fruit Quality Decline during Long-Term Cold Storage

Long-term low-temperature conditioning (LT-LTC) decreases apple fruit quality, but the underlying physiological and molecular basis is relatively uncharacterized. We identified 12 clusters of differentially expressed genes (DEGs) involved in multiple biological processes (i.e., sugar, malic acid, fatty acid, lipid, complex phytohormone, and stress-response pathways). The expression levels of genes in sugar pathways were correlated with decreasing starch levels during LT-LTC. Specifically, starch-synthesis-related genes (e.g., BE, SBE, and GBSS genes) exhibited downregulated expression, whereas sucrose-metabolism-related gene expression levels were up- or downregulated. The expression levels of genes in the malic acid pathway (ALMT9, AATP1, and AHA2) were upregulated, as well as the content of malic acid in apple fruit during LT-LTC. A total of 151 metabolites, mainly related to amino acids and their isoforms, amines, organic acids, fatty acids, sugars, and polyols, were identified during LT-LTC. Additionally, 35 organic-acid-related metabolites grouped into three clusters, I (3), II (22), and III (10), increased in abundance during LT-LTC. Multiple phytohormones regulated the apple fruit chilling injury response. The ethylene (ET) and abscisic acid (ABA) levels increased at CS2 and CS3, and jasmonate (JA) levels also increased during LT-LTC. Furthermore, the expression levels of genes involved in ET, ABA, and JA synthesis and response pathways were upregulated. Finally, some key transcription factor genes (MYB, bHLH, ERF, NAC, and bZIP genes) related to the apple fruit cold acclimation response were differentially expressed. Our results suggest that the multilayered mechanism underlying apple fruit deterioration during LT-LTC is a complex, transcriptionally regulated process involving cell structures, sugars, lipids, hormones, and transcription factors

Transcriptomic and Metabolic Analyses Provide New Insights into the Apple Fruit Quality Decline during Long-Term Cold Storage

Long-term low-temperature conditioning (LT-LTC) decreases apple fruit quality, but the underlying physiological and molecular basis is relatively uncharacterized. We identified 12 clusters of differentially expressed genes (DEGs) involved in multiple biological processes (i.e., sugar, malic acid, fatty acid, lipid, complex phytohormone, and stress-response pathways). The expression levels of genes in sugar pathways were correlated with decreasing starch levels during LT-LTC. Specifically, starch-synthesis-related genes (e.g., BE, SBE, and GBSS genes) exhibited downregulated expression, whereas sucrose-metabolism-related gene expression levels were up- or downregulated. The expression levels of genes in the malic acid pathway (ALMT9, AATP1, and AHA2) were upregulated, as well as the content of malic acid in apple fruit during LT-LTC. A total of 151 metabolites, mainly related to amino acids and their isoforms, amines, organic acids, fatty acids, sugars, and polyols, were identified during LT-LTC. Additionally, 35 organic-acid-related metabolites grouped into three clusters, I (3), II (22), and III (10), increased in abundance during LT-LTC. Multiple phytohormones regulated the apple fruit chilling injury response. The ethylene (ET) and abscisic acid (ABA) levels increased at CS2 and CS3, and jasmonate (JA) levels also increased during LT-LTC. Furthermore, the expression levels of genes involved in ET, ABA, and JA synthesis and response pathways were upregulated. Finally, some key transcription factor genes (MYB, bHLH, ERF, NAC, and bZIP genes) related to the apple fruit cold acclimation response were differentially expressed. Our results suggest that the multilayered mechanism underlying apple fruit deterioration during LT-LTC is a complex, transcriptionally regulated process involving cell structures, sugars, lipids, hormones, and transcription factors

Data_Sheet_1_Fully synthetic phosphorylated Tau181, Tau217, and Tau231 calibrators for Alzheimer’s disease diagnosis.docx

BackgroundThe calibrator in immunoassay plays an essential role in diagnosing Alzheimer’s disease (AD). Presently, the most well-studied biomarkers for AD diagnosis are three phosphorylated Tau (p-Tau): p-Tau231, p-Tau217, and p-Tau181. Glycogen synthase-3beta (GSK3β)-phosphorated Tau-441 is the most commonly used calibrator for p-Tau immunoassays. However, the batch-to-batch inconsistency issue of the commonly used GSK3β-phosphorylated Tau-441 limits its clinical application.MethodsWe have successfully generated and characterized 61 Tau monoclonal antibodies (mAbs) with distinct epitopes by using the hybridoma technique and employed them as capture or detection antibodies for p-Tau immunoassays. Through chemical synthesis, we synthesized calibrators, which are three peptides including capture and detection antibody epitopes, for application in immunoassays that detect p-Tau231, p-Tau217, and p-Tau181. The novel calibrators were applied to Enzyme-linked immunosorbent assay (ELISA) and Single-molecule array (Simoa) platforms to validate their applicability and establish a range of p-Tau immunoassays.ResultsBy employing the hybridoma technique, 49 mAbs recognizing Tau (1–22), nine mAbs targeting p-Tau231, one mAb targeting p-Tau217, and two mAbs targeting p-Tau181 were developed. Peptides, including recognition epitopes of capture and detection antibodies, were synthesized. These peptides were used as calibrators to develop 60 immunoassays on the ELISA platform, of which six highly sensitive immunoassays were selected and applied to the ultra-sensitive Simoa platform. Remarkably, the LODs were 2.5, 2.4, 31.1, 32.9, 46.9, and 52.1 pg/ml, respectively.ConclusionThree novel p-Tau calibrators were successfully generated and validated, which solved the batch-to-batch inconsistency issue of GSK3β-phosphorylated Tau-441. The novel calibrators exhibit the potential to promote the standardization of clinical AD diagnostic calibrators. Furthermore, we established a series of highly sensitive and specific immunoassays on the Simoa platform based on novel calibrators, which moved a steady step forward in p-Tau immunoassay application for AD diagnosis.</p