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The efficient construction of heterojunction photocatalysts has a crucial significance in achieving the decomposition of water for hydrogen generation. This work successfully prepared nitrogen-deficient g-C3N4(ND-g-C3N4) and combined it with dysprosium oxide (Dy2O3) through high-temperature calcination to create a type II heterojunction photocatalyst (Dy2O3/ND-g-C3N4). Notably, under visible light, the Dy2O3/ND-g-C3N4photocatalyst demonstrated impressive hydrogen production rates in both ethylene glycol and glucose solutions. Specifically, the photocatalyst achieved H2generation rates of 463.256 and 510.305 μmol⋅g−1⋅h−1in ethylene glycol and glucose solutions, respectively. And the quantum yield could be up to 21.76% and 23.96%, respectively. Furthermore, the photocatalytic reforming of glucose for H2production yielded valuable intermediate products. The f-shell layer in the Dy2O3had a significant function in enhancing photocatalytic hydrogen production efficiency. This improvement was attributed to the ability of the f-shell layer to capture excited electrons, thereby decreasing the rate of recombination of exciton pairs.

Bone marrow (BM) niche-derived signals are critical for facilitating engraftment after hematopoietic stem cell (HSC) transplantation (HSCT). HSCT is required for restoration of hematopoiesis in patients with inherited BM failure syndromes (iBMFSs). Shwachman-Diamond syndrome (SDS) is a rare iBMFS associated with mutations in SBDS. Previous studies have demonstrated that SBDS deficiency in osteolineage niche cells causes BM dysfunction that promotes leukemia development. However, it is unknown whether BM niche defects caused by SBDS deficiency also impair efficient engraftment of healthy donor HSC after HSCT, a hypothesis that could explain morbidity noted after clinical HSCT for patients with SDS. Here, we report a mouse model with inducible Sbds deletion in hematopoietic and osteolineage cells. Primary and secondary BM transplantation (BMT) studies demonstrated that SBDS deficiency within BM niches caused poor donor hematopoietic recovery and specifically poor HSC engraftment after myeloablative BMT. We have also identified multiple molecular and cellular defects within niche populations that are driven by SBDS deficiency and are accentuated by or develop specifically after myeloablative conditioning. These abnormalities include altered frequencies of multiple niche cell subsets, including mesenchymal lineage cells, macrophages, and endothelial cells; disruption of growth factor signaling, chemokine pathway activation, and adhesion molecule expression; and p53 pathway activation and signals involved in cell cycle arrest. Taken together, this study demonstrates that SBDS deficiency profoundly impacts recipient hematopoietic niche function in the setting of HSCT, suggesting that novel therapeutic strategies targeting host niches could improve clinical HSCT outcomes for patients with SDS.

Bone marrow (BM) niche-derived signals are critical for facilitating engraftment after hematopoietic stem cell (HSC) transplantation (HSCT). HSCT is required for restoration of hematopoiesis in patients with inherited BM failure syndromes (iBMFSs). Shwachman-Diamond syndrome (SDS) is a rare iBMFS associated with mutations in SBDS. Previous studies have demonstrated that SBDS deficiency in osteolineage niche cells causes BM dysfunction that promotes leukemia development. However, it is unknown whether BM niche defects caused by SBDS deficiency also impair efficient engraftment of healthy donor HSC after HSCT, a hypothesis that could explain morbidity noted after clinical HSCT for patients with SDS. Here, we report a mouse model with inducible Sbdsdeletion in hematopoietic and osteolineage cells. Primary and secondary BM transplantation (BMT) studies demonstrated that SBDS deficiency within BM niches caused poor donor hematopoietic recovery and specifically poor HSC engraftment after myeloablative BMT. We have also identified multiple molecular and cellular defects within niche populations that are driven by SBDS deficiency and are accentuated by or develop specifically after myeloablative conditioning. These abnormalities include altered frequencies of multiple niche cell subsets, including mesenchymal lineage cells, macrophages, and endothelial cells; disruption of growth factor signaling, chemokine pathway activation, and adhesion molecule expression; and p53 pathway activation and signals involved in cell cycle arrest. Taken together, this study demonstrates that SBDS deficiency profoundly impacts recipient hematopoietic niche function in the setting of HSCT, suggesting that novel therapeutic strategies targeting host niches could improve clinical HSCT outcomes for patients with SDS.

Advances in femtosecond laser-material interaction facilitate the extension of maskless optical processing to the high efficiency and deep-subwavelength scale. Here, a hybrid plasmon lithography technique has been demonstrated by irradiating near-infrared femtosecond laser pulses onto the Si material coated with thin Cr films in a vacuum chamber, and superior nanograting structures are found to deeply penetrate through the thin Cr film into the underlying Si substrate. In stark contrast to the common ripple structures formed on the Si surface, the Cr-layer mediated Si nanograting structures not only exhibit the spatially super-regular arrangements with a deep-subwavelength period of 355 nm but also present the nonsinusoidal sharp-edged groove geometry with a large depth-to-width aspect ratio of 2.1. Theoretical analyses and calculations reveal that the anomalous structure characterizations are physically ascribed to the excitation of dual-interface coupled plasmons in the thin metal layer, which possess the squeezed spatial wavelength and the periodic columnar intensity distributions. Moreover, the further deepening of periodic nanostructures into the Si substrate is also elucidated by the simulation of electric field enhancements at the bottom of shallow grooves under irradiation of subsequent laser pulses. In combination with a wet etching process, the Si nanograting structures can be modified into the smooth and narrow-mouthed V-profiles, whose optical measurements show a near omnidirectional antireflection especially in the visible range of 565–750 nm, which is expected for the design of advanced photonic devices.

The highly thermal stability precipitates strengthen creep resistance for alloys, which require precipitates to resist coarsen at elevated temperature. In the Mg-RE-Zn (Ag) series alloys, the key strengthening phase - γ" phase, remains its single-unit-cell height throughout aging process. The origin of such extremely thermal stability of γ" phase is still unclear. By using the first-principles calculations, it is found that the formation of γ" phase introduces compressive strain to its surrounding α -Mg lattice and simultaneously alter charge distribution of α -Mg lattice near the α -Mg/γ" hetero-interface. These two variations over α -Mg lattice lead to lower vacancy formation energies and migration energy barriers for solute atoms near the α -Mg/γ" hetero-interface in comparison with that of bulk condition. Consequently, the variations facilitate rapid diffusion of solute atoms near the γ" phase and promote nucleation rate of other γ" plates around it. On the basis of ledge-thickening model, the origin of nucleation/growth of γ" phase with single-unit-cell height was explained. Thermodynamically and kinetically, the solute atoms are not apt to migrate into the nearest basal plane adjacent to the γ" phase. Moreover, the lower aging temperature (∼200 °C) and almost completely coherent α -Mg/γ" hetero-interface lead to the ledges are extremely hard to nucleate on the hetero-interface. Therefore, γ" plates maintain single-unit-cell height throughout aging process. [ABSTRACT FROM AUTHOR]

Juvenile polyposis syndrome (JPS) is a childhood polyposis syndrome with up to a 50% lifetime risk of gastrointestinal cancer. Germline pathogenic variants in BMPR1Aand SMAD4are responsible for around 40% of cases of JPS, but for the majority of individuals, the underlying genetic cause is unknown. We identified a family for which polyposis spanned four generations, and the proband had a clinical diagnosis of JPS. Next-generation sequencing was conducted, followed by Sanger sequencing confirmation. We identified an internal deletion of the FOCADgene in all family members tested that altered the reading frame and is predicted to be pathogenic. We conclude that inactivation of the FOCADgene is likely to cause JPS in this family.