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In this work, we employed a two-step modification process to improve the properties of 2D bimetallic nanoplates M(OH)(OCH3) (M = Co, Ni), which were recently proven as a promising "nano-flame retardant". The nanoplates were in situ modified with metal-organic framework ZIF-67 first and then silanized with a coupling agent APTES. Epoxy resin (EP) nanocomposites were fabricated using the functionalized M(OH)(OCH3). We investigated the performance of the nanocomposites in flame retardance and thermal stability. The results showed that 3% of APTES@ZIF-67@M(OH)(OCH3) gave the EP nanocomposite the V-1 rating in UL-94 test and the highest limited oxygen index of 27.6%. Moreover, the pHRR value of EP/APTES@ZIF-67@M 3% was reduced by 20.0% and 9.6%, respectively, compared to neat EP and EP/ZIF-67@M 3%. Regarding the mechanical properties, the Tensile properties and energy storage modulus of EP nanocomposite were both improved with 3% of APTES@ZIF-67@M(OH)(OCH3). The GC-MS test results revealed that the functionalized M(OH)(OCH3) significantly increased the cross-linking propensity of the EP matrix upon combustion, leading to the formation of a dense char layer. This study demonstrates the great potential of M(OH)(OCH3) as a highly efficient "nano-flame retardant" with tunable functionality. [ABSTRACT FROM AUTHOR]

Parashorea chinensis, an endemic tree species in China's tropical rainforests, holds ecological and economic importance. Challenges like low resistance, poor quality, and low survival rates hinder its successful cultivation. This study explores the potential of autumn potassium fertilization on Parashorea seedlings from two provenances (Napo and Tianyang). The treatments included no fertilizer (CK-1), a single application of 160 mg K·plant−1 (CK-2), and various potassium levels K1, K2, K3, K4, K5, and K6 (corresponding to 0, 40, 80, 160, 320, and 640 mg·K·plant−1, respectively) combined with nitrogen (200 mg·plant−1) and phosphorus (80 mg·plant−1) fertilization. The findings indicate that autumn potassium application, in conjunction with nitrogen (N) and phosphorus (P) fertilization, significantly enhances seedling height and biomass in both provenances, resulting in an average increase of 101% and 89% under the K4 treatment compared to CK-1 and CK-2, comparatively. Both Napo and Tianyang provenances exhibited distinct responses in photosynthetic rate (2.70 μmol·m−2·s−1 and 1.97 μmol·m−2·s−1, respectively) and stomatal conductance (0.042 mol·m−2·s−1 and 0.029 mol·m−2·s−1, respectively) to the K4 treatment, which proved most effective. The chlorophyll content was significantly higher for Napo provenance with the K3 treatment (74.31%, 58.99%), while for Tianyang, it was higher with the K4 treatment (41.48%, 17.36%), compared to CK-1 and CK-2, respectively. Antioxidant enzymes activity, osmoregulatory capacity, and malondialdehyde content all exhibited variations with potassium application levels, with the K4 treatment offering significant benefits. In Napo provenance, lignin (199.82 mg·g−1) and cellulose (252.38 mg·g−1) peaked at K4, while Tianyang exhibited variation, higher lignin (184.25 mg·g−1) at K3, and cellulose (257.73 mg·g−1) at K4. Nutrient content analysis demonstrates that the K4 treatment enhances nutrient absorption and storage, increasing total N (21.56 mg·kg−1), P (4.69 mg·kg−1), and K (13.49 mg·kg−1) content. A comprehensive analysis reveals that the K4 treatment yields the highest quality scores (1.87, 1.85) and membership values (0.82, 0.68) for both Napo and Tianyang seedlings, with Napo seedlings outperforming their Tianyang provenance. Thus, treatment K4 underscores the effectiveness of autumn potassium applications for robust seedling cultivation and adaptation, offering valuable insights for sustainable cultivation practices. [ABSTRACT FROM AUTHOR]

GJB2 (encoding connexin26, Cx26) mutation is the most common genetic cause of hereditary deafness. Cochlear sensory hair cell (HC) death is the core pathologic phenomenon of GJB2‐related deafness. However, mechanism‐based therapy is still obscure. A targeted‐cell conditional Gjb2 knockout mouse model was established in which the Cx26 in Deiters cells and pillar cells were knocked out at birth. We explored the mechanism of HC death caused by deficiency of GJB2 in supporting cells (SCs), which exhibited moderate deafness, early HC death without SCs, and a decrease in distortion product otoacoustic emission. Here, a DNA damage response was observed in HCs during the onset of hearing loss. Apoptosis, necroptosis, and ferroptosis do not contribute to the death of HCs. We identified and demonstrated that parthanatos, a poly‐(ADP‐ribose) polymerase (PARP)‐dependent and caspase‐independent form of cell death, is a mechanism of HC degeneration. Furthermore, we observed that the use of PARP inhibitors effectively alleviated both deafness and HC loss. Our study reveals the specific mechanism of HC death caused by GJB2 deficiency. These findings demonstrate that targeting parthanatos is an HC protective strategy in the prevention of GJB2‐related hereditary deafness. [ABSTRACT FROM AUTHOR]

The GJB2 gene, encoding Connexin26 (Cx26), is one of the most common causes of inherited deafness. Clinically, mutations in GJB2 cause congenital deafness or late‐onset progressive hearing loss. Recently, it has been reported that Cx26 haploid deficiency accelerates the development of age‐related hearing loss (ARHL). However, the roles of cochlear Cx26 in the hearing function of aged animals remain unclear. In this study, we revealed that the Cx26 expression was significantly reduced in the cochleae of aged mice, and further explored the underlying molecular mechanism for Cx26 degradation. Immunofluorescence co‐localization results showed that Cx26 was internalized and degraded by lysosomes, which might be one of the important ways for Cx26 degradation in the cochlea of aged mice. Currently, whether the degradation of Cx26 in the cochlea leads directly to ARHL, as well as the mechanism of Cx26 degradation‐related hearing loss are still unclear. To address these questions, we generated mice with Cx26 knockout in the adult cochlea as a model for the natural degradation of Cx26. Auditory brainstem response (ABR) results showed that Cx26 knockout mice exhibited high‐frequency hearing loss, which gradually progressed over time. Pathological examination also revealed the degeneration of hair cells and spiral ganglions, which is similar to the phenotype of ARHL. In summary, our findings suggest that degradation of Cx26 in the cochlea accelerates the occurrence of ARHL, which may be a novel mechanism of ARHL. [ABSTRACT FROM AUTHOR]