Search

ObjectivesThis Mendelian randomization (MR) study identified modifiable risk factors for isolated rapid eye movement sleep behavior disorder (iRBD).MethodsGenome-wide association study (GWAS) datasets for 29 modifiable risk factors for iRBD in discovery and replication stages were used. GWAS data for iRBD cases were obtained from the International RBD Study Group. The inverse variance weighted (IVW) method was primarily employed to explore causality, with supplementary analyses used to verify the robustness of IVW findings. Co-localization analysis further substantiated causal associations identified via MR. Genetic correlations between mental illness and iRBD were identified using trait covariance, linkage disequilibrium score regression, and co-localization analyses.ResultsOur study revealed causal associations between sun exposure-related factors and iRBD. Utilizing sun protection (odds ratio [OR] = 0.31 [0.14, 0.69], p = 0.004), ease of sunburn (OR = 0.70 [0.57, 0.87], p = 0.001), childhood sunburn occasions (OR = 0.58 [0.39, 0.87], p = 0.008), and phototoxic dermatitis (OR = 0.78 [0.66, 0.92], p = 0.003) decreased iRBD risk. Conversely, a deep skin color increased risk (OR = 1.42 [1.04, 1.93], p = 0.026). Smoking, alcohol consumption, low education levels, and mental illness were not risk factors for iRBD. Anxiety disorders and iRBD were genetically correlated.ConclusionOur study does not corroborate previous findings that identified smoking, alcohol use, low education, and mental illness as risk factors for iRBD. Moreover, we found that excessive sun exposure elevates iRBD risk. These findings offer new insights for screening high-risk populations and devising preventive measures.

Podoplanin (PDPN) is known to play a role in thrombosis, metastasis of tumor cells, the epithelial–mesenchymal transition (EMT), and immune response. The present study aim to evaluate the clinical significance of soluble PDPN (sPDPN) in hypercoagulability and cellular immune status in patients with non-small cell lung cancer (NSCLC). Enzyme-linked immunosorbent assay (ELISA) was used to determine plasma sPDPN levels, and T-lymphocyte distribution was determined using flow cytometry. The levels of sPDPN were markedly higher in the NSCLC group than control group, and sPDPN was higher in patients with advanced-stage and with distant metastases. The high-sPDPN group had lower absolute numbers of CD3+, CD4+, and CD4+/CD8+ ratio than low-sPDPN group. Correlation analysis indicated that sPDPN was positively linked to platelet (r = 0.50, P < .001), D-dimer (r = 0.52, P < .001), and fibrinogen (r = 0.37, P < .001); and inversely correlated with CD3+ (r = −0.37, P < .001), CD4+ (r = −0.44, P < .001), and CD4+/CD8+ (r = −0.37, P < .001). Multivariate logistic regression analysis indicated that sPDPN (odds ratio [OR] = 2.293; 95% CI, 1.559−3.373) and tumor stage (OR = 15.857; 95% CI, 1.484−169.401) were separate risk indicators for hypercoagulability. The receiver operating characteristic curves (ROC) indicated that sPDPN had high diagnostic values for hypercoagulability in NSCLC patients. In conclusion, plasma sPDPN was not only linked to hypercoagulability, but it may also be an indicator of the body's cellular immune status in NSCLC patients.

Angular ligands are a class of important linkers to design and construct new metal–organic frameworks (MOFs). Herein, solvothermal reaction of 4,4′-(4H-1,2,4-triazole-3,5-diyl)dibenzoic acid (TZDB), a triazole-inserted dicarboxylate, acetate, and Cu(NO3)2·3H2O afforded a copper(II)-organic framework of Cu-TZDB. Structural analysis shows that Cu-TZDB displays an unusual (4,6)-c topological network concomitant with the generation of metalloligand [Cu(TZDB)(H2O)2] in situ. Due to its bi-channel cavities replete with triazolate, coordinated water and methyl groups, Cu-TZDB exhibits CO2 selective adsorption over N2 and CH4, which was not only predicted by ideal adsorption solution theory (IAST), but also verified by dynamic column breakthrough tests. [ABSTRACT FROM AUTHOR]

Rationale: Tetrandrine, the Q‐marker in Stephaniae Tetrandrae Radix, was proven to present an obvious antitumor effect. Until now, the metabolism and antitumor mechanism of tetrandrine have not been fully elucidated. Methods: The metabolites of tetrandrine in rats were profiled using ultra‐high‐performance liquid chromatography coupled with time‐of‐flight mass spectrometry. The potential antitumor mechanism of tetrandrine in vivo was predicted using network pharmacology. Results: A total of 30 metabolites were characterized in rats after ingestion of tetrandrine (10 mg/kg), including 0 in plasma, 7 in urine, 11 in feces, 9 in liver, 8 in spleen, 4 in lung, 5 in kidney, 5 in heart, and 4 in brain. This study was the first to show the metabolic processes demethylation, hydroxylation, and carbonylation in tetrandrine. The pharmacology network results showed that tetrandrine and its metabolites could regulate AKT1, TNF, MMP9, MMP2, PAK1, and so on by involving in proteoglycan tumor pathway, PI3K‐Akt signaling pathway, tumor pathway, MAPK signaling pathway, and Rap1 signaling pathway. Conclusions: The metabolism features of tetrandrine and its potential antitumor mechanism were summarized, providing data for further pharmacological validation. [ABSTRACT FROM AUTHOR]

H nuclear magnetic resonance spectroscopic analysis showed that two types of water molecules, Al-bound and mobile molecules undergoing fact isotropic reorientation, were identified within VPI-5 and AlPO4-5 molecular sieves. Similarly, adsorbed ammonia molecules interspersed in VPI-5 existed either in free physisorbed state, Al-bound rotating about the N-Al axis or rigid Al-bound dynamic states. In addition, VPI-5 featured a higher degree of water order despite its larger channels as compared to AlPO4-5.