Association between the triglyceride glucose index and obstructive sleep apnea and its symptoms: results from the NHANES.

BACKGROUND: Certain studies have indicated a link between obstructive sleep apnea and insulin resistance in specific populations. To gain more clarity, extensive research involving a broad sample of the overall population is essential. The primary objective of this study was to investigate this correlation by utilizing data from the National Health and Nutrition Examination Survey database. METHODS: The analysis incorporated data from the National Health and Nutrition Examination Survey database spanning the time periods from 2005 to 2008 and from 2015 to 2018, with a focus on American adults aged 18 years and older after applying weight adjustments. Key variables such as obstructive sleep apnea, triglyceride glucose index, and various confounding factors were considered. A generalized linear logistic regression model was used to investigate the association between obstructive sleep apnea and the triglyceride glucose index, with additional exploration of the consistency of the results through hierarchical analysis and other techniques. RESULTS: The study included participants aged between 18 and 90 years, with an average age of 46.75 years. Among the total sample, 50.76% were male. The triglyceride glucose index demonstrated a diagnostic capability for obstructive sleep apnea, with an AUC of 0.701 (95% CI: 0.6619-0.688). According to the fully adjusted model, individuals in the fourth quartile of the triglyceride glucose index showed an increased likelihood of having obstructive sleep apnea compared to those in the first quartile (OR: 1.45; 95% CI: 1.02-2.06; P < 0.05). Subgroup analysis indicated that male sex (OR: 2.09; 95% CI: 1.76-2.45; P < 0.05), younger age (OR: 2.83; 95% CI: 2.02-3.96; P < 0.05), white ethnicity (OR: 2.29; 95% CI: 1.93-2.73; P < 0.05), and obesity (OR: 1.54; 95% CI: 1.28-1.85; P < 0.05) were correlated with an elevated risk of OSA. CONCLUSIONS: This study demonstrated a strong association between an elevated TG index and OSA. Additionally, the triglyceride glucose index could serve as an independent predictor of obstructive sleep apnea.

Detection, mechanisms, and therapeutic implications of oncometabolites.

Metabolic abnormalities are a hallmark of cancer cells and are essential to tumor progression. Oncometabolites have pleiotropic effects on cancer biology and affect a plethora of processes, from oncogenesis and metabolism to therapeutic resistance. Targeting oncometabolites, therefore, could offer promising therapeutic avenues against tumor growth and resistance to treatments. Recent advances in characterizing the metabolic profiles of cancer cells are shedding light on the underlying mechanisms and associated metabolic networks. This review summarizes the diverse detection methods, molecular mechanisms, and therapeutic targets of oncometabolites, which may lead to targeting oncometabolism for cancer therapy.

Small molecule metabolites: discovery of biomarkers and therapeutic targets.

Metabolic abnormalities lead to the dysfunction of metabolic pathways and metabolite accumulation or deficiency which is well-recognized hallmarks of diseases. Metabolite signatures that have close proximity to subject's phenotypic informative dimension, are useful for predicting diagnosis and prognosis of diseases as well as monitoring treatments. The lack of early biomarkers could lead to poor diagnosis and serious outcomes. Therefore, noninvasive diagnosis and monitoring methods with high specificity and selectivity are desperately needed. Small molecule metabolites-based metabolomics has become a specialized tool for metabolic biomarker and pathway analysis, for revealing possible mechanisms of human various diseases and deciphering therapeutic potentials. It could help identify functional biomarkers related to phenotypic variation and delineate biochemical pathways changes as early indicators of pathological dysfunction and damage prior to disease development. Recently, scientists have established a large number of metabolic profiles to reveal the underlying mechanisms and metabolic networks for therapeutic target exploration in biomedicine. This review summarized the metabolic analysis on the potential value of small-molecule candidate metabolites as biomarkers with clinical events, which may lead to better diagnosis, prognosis, drug screening and treatment. We also discuss challenges that need to be addressed to fuel the next wave of breakthroughs.

The Effects of Dipeptidyl Peptidase 4 Inhibitors on Renal Function in Patients with Type 2 Diabetes Mellitus.

Past studies have confirmed that glucagon-like peptide 1 (GLP-1) receptor agonists can improve renal outcomes in patients with type 2 diabetes mellitus (DM). This study aimed to evaluate whether dipeptidyl peptidase 4 (DPP-4) inhibitors, which elevate GLP-1 levels, also have similar effects on renal function. In this retrospective study, diabetic patients treated with anti-hyperglycemic agents between 2008 and 2011 were selected. We compared the time to first occurrence of estimated glomerular filtration rate (eGFR) decline ≥30% from the baseline between patients treated with DPP-4 inhibitors and those treated with other anti-hyperglycemic drugs. A total of 2202 patients were enrolled. The incidence of eGFR decline ≥30% from the baseline was 10.08% in the DPP-4 inhibitor group and 16.17% in the non-DPP-4 inhibitor group (p < 0.001). The mean time to event was significantly longer in patients receiving DPP-4 inhibitors (2.84 ± 1.60 vs. 1.96 ± 1.30 years, p < 0.001). Patients who were younger than 65 years old, had better baseline eGFR, did not have preexisting hyperlipidemia, or who were untreated with concomitant statin showed greater reductions in the risk of renal function decline (all p for interaction < 0.05). Conclusively, DPP-4 inhibitors used alone or in combination with other glucose-lowering agents were correlated with lower risks of eGFR decline in patients with type 2 DM.

Comprehensive analysis of natural polysaccharides from TCMs: a generic approach based on UPLC-MS/MS.

Here, we report a new application using liquid chromatography-electrospray mass spectrometry (UHPLC-ESI-MS) using aldononitrile acetate derivatives for simultaneous baseline separation and detection of eight neutral saccharides, two uronic acids, one ketose, and eight alditols within 14 min. The separation was performed on a Cortecs C18 column using acetonitrile (A) and water (B) as the mobile phase with gradient elution. The target components were detected in selected ion monitoring (SIM) mode by mass spectrometry with an electrospray ionization (ESI) source operating in positive ionization mode. A comparison with traditional methods was used to determine the validity of the results. The UHPLC-ESI-MS method was used for quantitative analysis of free carbohydrates in water extracts of Crataegus pinnatifida as well as determination of Polygonatum cyrtonema and Glossy ganoderma monosaccharides in polysaccharides. The results demonstrate that this protocol is a comprehensive and effective technique for qualitative and quantitative analysis of plant polysaccharides from TCMs.

Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFßR1 Axis.

BACKGROUND: Myocardial infarction (MI) was a severe cardiovascular disease resulted from acute, persistent hypoxia, or ischemia condition. Additionally, MI generally led to heart failure, even sudden death. A multitude of research studies proposed that long noncoding RNAs (lncRNAs) frequently participated in the regulation of heart diseases. The specific function and molecular mechanism of SOX2-OT in MI remained unclear. Aim of the Study. The current research was aimed to explore the role of SOX2-OT in MI. METHODS: Bioinformatics analysis (DIANA tools and Targetscan) and a wide range of experiments (CCK-8, flow cytometry, RT-qPCR, luciferase reporter, RIP, caspase-3 activity, trans-well, and western blot assays) were adopted to investigate the function and mechanism of SOX2-OT. RESULTS: We discovered that hypoxia treatment decreased cell viability but increased cell apoptosis. Besides, lncRNA SOX2-OT expression was upregulated in hypoxic HCMs. Hereafter, we confirmed that SOX2-OT could negatively regulate miR-27a-3p levels by directly binding with miR-27a-3p, and miR-27a-3p also could negatively regulate SOX2-OT levels. Furthermore, knockdown of SOX2-OT promoted cell proliferation, migration, and invasion, but limited cell apoptosis. However, these effects were reversed by anti-miR-27a-5p. Besides, we verified that miR-27a-3p binding with the 3'UTR of TGFBR1 and SOX2-OT regulated TGFßR1 level by collaborating with miR-27a-3p in HCMs. Eventually, rescue assays validated that the influence of SOX2-OT silence or miR-27a-3p overexpression on cellular processes in cardiomyocytes injury was counteracted by TGFBR1 overexpression. CONCLUSIONS: Long noncoding RNA SOX2-OT exacerbated hypoxia-induced cardiomyocytes injury by regulating miR-27a-3p/TGFßR1 axis, which may provide a novel insight for heart failure treatment.

INPP4B promotes colorectal cancer cell proliferation by activating mTORC1 signaling and cap-dependent translation.

BACKGROUND AND OBJECTIVE: Inositol polyphosphate 4-phosphatase type II (INPP4B) is over-expressed in CRC tissues, and emerges as an oncogene. However, the mechanism by which INPP4B regulates CRC cell proliferation remains largely unclear. In this study, we aimed to investigate the regulatory mechanisms of INPP4B in CRC. MATERIALS AND METHODS: The expression levels of mRNA were detected by qRT-PCR. The expression levels of protein were determined by Western blot. Cell Counting Kit-8 (CCK-8) assays and BrdU incorporation assays were performed to evaluate cell proliferation abilities. Bicistronic luciferase assays and the m7GTP pull down assay were performed to measure the cap-dependent translation in cells. RESULTS: INPP4B promotes CRC cell proliferation by increasing mTORC1 activity. Furthermore, it was shown that the activation of mTORC1 signaling by INPP4B led to increased cap-dependent translation, which is essential for INPP4B-mediated CRC cell proliferation. Finally, it was demonstrated that increased AKT and serum and glucocorticoid-inducible kinase 1 activity contributed to the activation of cap-dependent translation induced by INPP4B. CONCLUSION: Collectively, the present study reveals INPP4B promotes colorectal cancer cell proliferation by activating mTORC1 signaling and cap-dependent translation.

Identification and chronological analysis of genomic signatures in influenza A viruses.

An increase in the availability of data on the influenza A viruses (IAV) has enabled the identification of the potential determinants of IAV host specificity using computational approaches. In this study, we proposed an alternative approach, based on the adjusted Rand index (ARI), for the evaluation of genomic signatures of IAVs and their ability to distinguish hosts they infected. Our experiments showed that the host-specific signatures identified using the ARI were more characteristic of their hosts than those identified using previous measures. Our results provided updates on the host-specific genomic signatures in the internal proteins of the IAV based on the sequence data as of February 2013 in the National Center for Biotechnology Information (NCBI). Unlike other approaches for signature recognition, our approach considered not only the ability of signatures to distinguish hosts (according to the ARI), but also the chronological relationships among proteins. We identified novel signatures that could be mapped to known functional domains, and introduced a chronological analysis to investigate the changes in host-specific genomic signatures over time. Our chronological analytical approach provided results on the adaptive variability of signatures, which correlated with previous studies' findings, and indicated prospective adaptation trends that warrant further investigation.

Effects of functional electrical stimulation on peak torque and body composition in patients with incomplete spinal cord injury.

The aim of this study was to investigate the change in body composition, leg girths, and muscle strength of patients with incomplete spinal cord injury (SCI) after functional electrical stimulation cycling exercises (FESCE). Eighteen subjects with incomplete SCI were recruited. Each patient received FESCE three times per week for 8 weeks. Body composition, thigh and calf girths of bilateral legs, muscle strength of bilateral knee flexors and extensors were measured before and after 4 and 8 weeks of FESCE. A significant increase in bilateral thigh girth after 4 weeks of FESCE and significant increase in muscular peak torque of knee flexion and extension were found after 8 weeks of training. Besides, lean body mass increased significantly after complete treatment. FESCE can increase the thigh girth and muscular peak torque of patients with incomplete spinal cord injury.

Emergence of G9 serotype rotavirus as a major cause of infectious gastroenteritis in southern Taiwan.

Infectious gastroenteritis is a common illness in children. This study investigated the etiology and clinical manifestations of hospitalized children with symptoms of infectious gastroenteritis in southern Taiwan. We studied 467 consecutive patients with infectious gastroenteritis aged from 2 days to 10 years hospitalized from April 2001 to March 2002. Rotavirus was the most common etiology (57%) of infectious gastroenteritis in these patients. Bacterial infection was noted in 57 cases (12%). Rotavirus was found in 92% of nosocomial infectious gastroenteritis (p < or = 0.001). Bloody stool was a presentation of bacterial infection in 74% of cases and rotavirus gastroenteritis in 8% of cases (p < or = 0.001). The G serotype of rotavirus was identified in 87 patients. Serotype G1 was the most common (51%), followed by G9 (31%). The emergence of serotype G9 strains in rotavirus infection has not been previously reported from Taiwan. Incorporation of G9 rotavirus into vaccines should be considered.