Efficient Photocatalytic degradation of direct blue 15 dye using samarium doped bismuth tungstate nanosheets: A sustainable approach towards wastewater treatment.

The rare earth metal, samarium (Sm3+) doped bismuth tungstate (Bi2WO6) nanoparticles were prepared by a one-pot hydrothermal method. The powder X-ray diffraction (XRD) analysis confirmed the formation of Bi2WO6 with an orthorhombic crystal structure. The crystallite size of Bi2WO6 decreased from 20.73 to 9.25 nm as the Sm substitution in the W lattice increased. The vibrational modes of W-O, Bi-O, and Sm-O were identified in the range of 500-900 cm-1. The optical bandgap of Sm3+ doped Bi2WO6 nanoparticles increased from 2.86 to 2.95 eV with higher Sm doping levels. The surface morphology revealed the formation of flower-like sheets in the Sm3+ doped bismuth tungstate. The energy dispersive X-ray (EDX) spectrum of Sm3+ doped Bi2WO6 nanoparticles confirmed the presence of Sm, Bi, W, and O without any other impurities. The small peak detected at 1082.14 eV in the survey scan of Sm3+ doped Bi2WO6 nanoparticles belonged to Sm3d. In the photocatalytic degradation of direct blue 15 (DB15) under visible light irradiation, the efficiency of the nanoparticles increased with higher Sm3+ concentration. The obtained results demonstrated that the Sm-Bi2WO6 nanosheets could provide an effective and sustainable solution for treating the wastewater containing direct blue 15 dye.

Lower self-report fatigue in multiple sclerosis is associated with localized white matter tract disruption between amygdala, temporal pole, insula, and other connected structures.

BACKGROUND: Fatigue, a frequent and disabling symptom for people with multiple sclerosis (PwMS), inconsistently correlates with white matter (WM) pathology. Network-based analysis, accounting for the manner in which lesions disrupt networks of structurally connected gray matter (GM) regions, may provide additional insight. OBJECTIVE: To identify patterns of WM tract disruption which explain self-reported fatigue severity in PwMS. METHODS: 137 PwMS and 50 age- and sex-matched healthy controls (HC) underwent fatigue assessment and brain MRI. Lesion maps were applied to determine the severity of WM tract disruption between pairs of GM regions. Then, the Network-Based-Statistics tool was applied to identify structural networks whose disruption explained fatigue severity. To determine whether these networks explain unique variance above conventional MRI measures and depression, regressions were applied controlling for age, sex, brain volume, T2-lesion volume, and depression. RESULTS: Patient-perceived fatigue in PwMS was positively associated with overall lesion burden (ß = 0.563, p-value < 0.001). In contrast, localized disruptions in WM tracts between regions including the amygdala, insula, hippocampus, putamen, temporal pole, caudal-middle-frontal gyrus, rostral-middle-frontal gyrus, inferior-parietal gyrus, and banks of the superior temporal sulcus were significantly negatively correlated with fatigue in PwMS (ß = -0.586, p-value < 0.001). Average disruption within this specific, localized network explained significant additional variance in fatigue above what was otherwise explained by depression and conventional MRI measures of neuropathology (ΔR2 = 0.078, p-value < 0.001). CONCLUSION: Although overall lesion burden correlates positively with fatigue in PwMS, localized WM damage between the amygdala, temporal pole, and other connected structures is associated with lower severity of patient-perceived fatigue.