Origins and Simulation of (002) Forbidden Reflections in Nanodiamonds: Implications for Sub‑4 nm Nanodiamond Synthesis and Characterization

So far, although the conception of the so-called “n-diamond” has been established for almost 30 years and widely cited as the critical evidence of Younger Dryas impact hypothesis, its crystallographic structure is still mysterious. Many speculations on the unexplained (002) forbidden reflections have been proposed. However, none of them has any convincible evidence or obeys the carbon orbital hybridization rules. According to the recent observation on sub-4 nm nanodiamond, we concluded that the “n-diamond” was not derived from the Fm3m crystallographic group. The unexplainable (002) forbidden reflection is caused by the spatial resolution limitation of HRTEM equipment and defocus on the target particles. According to the forbidden reflection rules, the defocus will lead to a topological obscure shadow in plane. Finally, experimental evidence of an individual sub-4 nm nanodiamond exhibits an observable transformation from cubic diamond to “n-diamond” with the appearance of (002) reflection, which proves our assumption. This work will contribute to the characterization technique for sub-4 nm nanodiamond synthesis

Gas-Phase Alcoholysis of Benzylic Halides in the Atmospheric Pressure Ionization Source

The present study investigates the gas-phase alcoholysis reaction of benzylic halides under atmospheric pressure chemical ionization (APCI) conditions. The APCI corona discharge is used to initiate the novel reaction, which is monitored by ion trap mass spectrometry (IT-MS). The model compound α,α,α-trifluorotoluene is applied to observe the cascade methoxylation reaction during the +APCI-MS analysis, resulting in the formation of [PhC­(OCH3)2]+. Based on the results of isotopic labeling and substrate expansion experiments, an addition–elimination mechanism is proposed: initially, the reaction was initiated by the dissociation of fluorine from PhCF3 under APCI condition, leading to the formation of [PhCF2]+; subsequently, two methanol molecules nucleophilicly attack [PhCF2]+ stepwisely, accompanied by the elimination of HF, yielding the product ion [PhC­(OCH3)2]+. The proposed mechanism was further corroborated by theoretical calculations. The results of substrate scope expansion experiments suggest that this in-source reaction has the potential to differentiate the positional isomers of alcohols and phenols

Template-Free Synthesis and Self-Assembly of CeO₂ Nanospheres Fabricated with Foursquare Nanoflakes

Large-scale CeO2 spherical architectures composed of numerous nanoflakes have been controllably prepared through a simple hydrothermal reaction without any template. The products were characterized with X-ray diffraction, nitrogen adsorption−desorption experiments, transmission electron microscopy (TEM), and high-resolution transmission electron microscopy (HRTEM). It was found that the CeO2 architecture ca. 100−230 nm in diameter was made up of many nanoflakes with a BET surface of 24 m2/g. The possible mechanism for the nanostructures formation was discussed. The catalytic performance of CeO2 nanospheres and the direct-depositing CeO2 nanoparticles in CO oxidation were also tested, and the catalytic results were compared and explained by analyzing the exposed planes of the two

Additional file 1 of Associations of poor sleep quality, chronic pain and depressive symptoms with frailty in older patients: is there a sex difference?

Additional file 1: Table S1. General characteristics between included patients and excluded patients

Additional file 1 of Application, knowledge and training needs regarding comprehensive geriatric assessment among geriatric practitioners in healthcare institutions: a cross-sectional study

Supplementary Material 1

Additional file 1: of A novel nonsense mutation in MYO15A is associated with non-syndromic hearing loss: a case report

Table S1. Summary of 127 hereditary deafness-related genes by target region capture sequencing. (DOCX 16 kb) (DOCX 15 kb

Additional file 2: of A novel nonsense mutation in MYO15A is associated with non-syndromic hearing loss: a case report

Table S2. Overview of target region capture sequencing results of the proband affected by ARNSHL. (DOCX 15 kb) (DOCX 14 kb

Sensomics-Assisted Characterization of Fungal-Flowery Aroma Components in Fermented Tea Using <i>Eurotium cristatum</i>

Fermented tea (FT) using a single Eurotium cristatum strain can produce a pleasant fungal-flowery aroma, which is similar to the composite aroma characteristic of minty, flowery, and woody aromas, but its molecular basis is not yet clear. In this study, solvent-assisted flavor evaporation and gas chromatography–mass spectrometry/olfactometry were applied to isolate and identify volatiles from the FT by E. cristatum. The application of an aroma extract dilution analysis screened out 43 aroma-active compounds. Quantification revealed that there were 11 odorants with high odor threshold concentrations. Recombination and omission tests revealed that nonanal, methyl salicylate, decanoic acid, 4-methoxybenzaldehyde, α-terpineol, phenylacetaldehyde, and coumarin were the major odorants in the FT. Addition tests further verified that methyl salicylate, 4-methoxybenzaldehyde, and coumarin were the key odorants for fungal-flowery aroma, each corresponding to minty, woody, and flowery aromas, respectively. 4-Methoxybenzaldehyde and coumarin were newly found odorants for fungal-flowery aroma in FT, and 4-methoxybenzaldehyde had not been reported as a tea volatile compound before. This finding may guide future industrial production optimization of FT with improved flavor

Image1_PPARγ/SOD2 Protects Against Mitochondrial ROS-Dependent Apoptosis via Inhibiting ATG4D-Mediated Mitophagy to Promote Pancreatic Cancer Proliferation.jpeg

Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive disease with poor prognosis. Our previous study found that peroxisome proliferator activated receptor gamma (PPARγ) was capable of enhancing glycolysis in PDAC cells. However, whether PPARγ could promote PDAC progression remains unclear. In our present study, PPARγ was positively associated with tumor size and poor prognosis in PDAC patients. Functional assays demonstrated that PPARγ could promote the proliferation of pancreatic cancer cells in vitro and in vivo. Additionally, flow cytometry results showed that PPARγ decreased mitochondrial reactive oxygen species (mitochondrial ROS) production, stabilized mitochondrial membrane potential (MMP) and inhibited cell apoptosis via up-regulating superoxide dismutase 2 (SOD2), followed by the inhibition of ATG4D-mediated mitophagy. Meanwhile, the activation of PPARγ might reduce pancreatic cancer cell stemness to improve PDAC chemosensitivity via down-regulating ATG4D. Thus, these results revealed that PPARγ/SOD2 might protect against mitochondrial ROS-dependent apoptosis via inhibiting ATG4D-mediated mitophagy to promote pancreatic cancer proliferation, further improving PDAC chemosensitivity.</p

Image4_PPARγ/SOD2 Protects Against Mitochondrial ROS-Dependent Apoptosis via Inhibiting ATG4D-Mediated Mitophagy to Promote Pancreatic Cancer Proliferation.jpeg

Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive disease with poor prognosis. Our previous study found that peroxisome proliferator activated receptor gamma (PPARγ) was capable of enhancing glycolysis in PDAC cells. However, whether PPARγ could promote PDAC progression remains unclear. In our present study, PPARγ was positively associated with tumor size and poor prognosis in PDAC patients. Functional assays demonstrated that PPARγ could promote the proliferation of pancreatic cancer cells in vitro and in vivo. Additionally, flow cytometry results showed that PPARγ decreased mitochondrial reactive oxygen species (mitochondrial ROS) production, stabilized mitochondrial membrane potential (MMP) and inhibited cell apoptosis via up-regulating superoxide dismutase 2 (SOD2), followed by the inhibition of ATG4D-mediated mitophagy. Meanwhile, the activation of PPARγ might reduce pancreatic cancer cell stemness to improve PDAC chemosensitivity via down-regulating ATG4D. Thus, these results revealed that PPARγ/SOD2 might protect against mitochondrial ROS-dependent apoptosis via inhibiting ATG4D-mediated mitophagy to promote pancreatic cancer proliferation, further improving PDAC chemosensitivity.</p