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Objectives: Competent velopharyngeal (VP) function is the basis for normal speech. Understanding how VP structure influences the airflow during speech details is essential to the surgical improvement of pharyngoplasty. In this study, we aimed to illuminate the airflow features corresponding to various VP closure states using computed dynamic simulations. Methods: Three-dimensional models of the upper airways were established based on computed tomography of 8 volunteers. The velopharyngeal port was simulated by a cylinder. Computational fluid dynamics simulations were applied to illustrate the correlation between the VP port size and the airflow parameters, including the flow velocity, pressure in the velopharyngeal port, as well as the pressure in oral and nasal cavity. Results: The airflow dynamics at the velopharynx were maintained in the same velopharyngeal pattern as the area of the velopharyngeal port increased from 0 to 25 mm2. A total of 5 airflow patterns with distinct features were captured, corresponding to adequate closure, adequate/borderline closure (Class I and II), borderline/inadequate closure, and inadequate closure. The maximal orifice area that could be tolerated for adequate VP closure was determined to be 2.01 mm2. Conclusion: Different VP functions are of characteristic airflow dynamic features. Computational fluid dynamic simulation is of application potential in individualized VP surgery planning.

Cancer cells characterized by uncontrolled growth and proliferation require altered metabolic processes to maintain this characteristic. Metabolic reprogramming is a process mediated by various factors, including oncogenes, tumor suppressor genes, changes in growth factors, and tumor–host cell interactions, which help to meet the needs of cancer cell anabolism and promote tumor development. Metabolic reprogramming in tumor cells is dynamically variable, depending on the tumor type and microenvironment, and reprogramming involves multiple metabolic pathways. These metabolic pathways have complex mechanisms and involve the coordination of various signaling molecules, proteins, and enzymes, which increases the resistance of tumor cells to traditional antitumor therapies. With the development of cancer therapies, metabolic reprogramming has been recognized as a new therapeutic target for metabolic changes in tumor cells. Therefore, understanding how multiple metabolic pathways in cancer cells change can provide a reference for the development of new therapies for tumor treatment. Here, we systemically reviewed the metabolic changes and their alteration factors, together with the current tumor regulation treatments and other possible treatments that are still under investigation. Continuous efforts are needed to further explore the mechanism of cancer metabolism reprogramming and corresponding metabolic treatments.

BackgroundAccumulating evidence has indicated that persistent human cytomegalovirus (HCMV) infection is associated with several cardiovascular diseases including atherosclerosis and coronary artery disease. However, whether there is a causal association between the level of anti-HCMV immune response and the risk of cardiovascular diseases remains unknown.MethodsSingle-nucleotide polymorphisms associated with anti-cytomegalovirus immunoglobulin (Ig) G levels were used as instrumental variables to estimate the causal effect of anti-cytomegalovirus IgG levels on 9 cardiovascular diseases (including atrial fibrillation, coronary artery disease, hypertension, heart failure, peripheral artery disease, pulmonary embolism, deep vein thrombosis of the lower extremities, rheumatic valve diseases, and non-rheumatic valve diseases). For each cardiovascular disease, Mendelian randomization (MR) analyses were performed. Inverse variance-weighted meta-analysis (IVW) with a random-effects model was used as a principal analysis. In addition to this, the weighted median approach and MR-Egger method were used for further sensitivity analysis.ResultsIn the IVW analysis, genetically predicted anti-cytomegalovirus IgG levels were suggestively associated with coronary artery disease with an odds ratio (OR) of 1.076 [95% CI, 1.009–1.147; p = 0.025], peripheral artery disease (OR 1.709; 95% CI, 1.039–2.812; p = 0.035), and deep vein thrombosis (OR 1.002; 95% CI, 1.000–1.004; p = 0.025). In the further analysis, similar causal associations were obtained from weighted median analysis and MR-Egger analysis with lower precision. No notable heterogeneities and horizontal pleiotropies were observed (p > 0.05).Conclusions/InterpretationOur findings first provide direct evidence that genetic predisposition of anti-cytomegalovirus IgG levels increases the risk of coronary artery disease, peripheral artery disease, and deep vein thrombosis.

Vanadium is an important trace element in bone to involve in bone metabolism, bone formation, and bone growth, but roles of various vanadium ions, especially pentavalent vanadium, in bone tissue...