Although organellar genomes (including chloroplast and mitochondrial genomes) are smaller than nuclear genomes in size and gene number, organellar genomes are very important for the investigation of plant evolution and molecular ecology mechanisms. Few studies have focused on the organellar genomes of horticultural plants. Approximately 1193 chloroplast genomes and 199 mitochondrial genomes of land plants are available in the National Center for Biotechnology Information (NCBI), of which only 39 are from horticultural plants. In this paper, we report an innovative and efficient method for high-quality horticultural organellar genome assembly from next-generation sequencing (NGS) data. Sequencing reads were first assembled by Newbler, Amos, and Minimus software with default parameters. The remaining gaps were then filled through BLASTN search and PCR. The complete DNA sequence was corrected based on Illumina sequencing data using BWA (Burrows–Wheeler Alignment tool) software. The advantage of this approach is that there is no need to isolate organellar DNA from total DNA during sample preparation. Using this procedure, the complete mitochondrial and chloroplast genomes of an ornamental plant, Salix suchowensis, and a fruit tree, Ziziphus jujuba, were identified. This study shows that horticultural plants have similar mitochondrial and chloroplast sequence organization to other seed plants. Most horticultural plants demonstrate a slight bias toward A+T rich features in the mitochondrial genome. In addition, a phylogenetic analysis of 39 horticultural plants based on 15 protein-coding genes showed that some mitochondrial genes are horizontally transferred from chloroplast DNA. Our study will provide an important reference for organellar genome assembly in other horticultural plants. Furthermore, phylogenetic analysis of the organellar genomes of horticultural plants could accurately clarify the unanticipated relationships among these plants.

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Age, severity of brain injury, neuroimaging results, treatment methods, and early-stage seizures are independent risk factors of PTE.

Rational design of high-performance stable metal–organic framework (MOF) membranes is challenging, especially for the sustainable treatment of hypersaline waters to address critical global environmental issues. Herein, a molecular-level intra-crystalline defect strategy combined with a selective layer thinning protocol is proposed to fabricate robust ultrathin missing-linker UiO-66 (ML-UiO-66) membrane to enable fast water permeation. Besides almost complete salt rejection, high and stable water flux is achieved even under long-term pervaporation operation in hash environments, which effectively addresses challenging stability issues. Then, detailed structural characterizations are employed to identify the type, chemical functionality, and density of intra-crystalline missing-linker defects. Moreover, molecular dynamics simulations shed light on the positive atomistic role of these defects, which are responsible for substantially enhancing structural hydrophilicity and enlarging pore window, consequently allowing ultra-fast water transport via a lower-energy-barrier pathway across three-dimensional sub-nanochannels during pervaporation. Unlike common unfavorable defect effects, the present positive intra-crystalline defect engineering concept at the molecular level is expected to pave a promising way toward not only rational design of next-generation MOF membranes with enhanced permeation performance, but additional water treatment applications.

Cisplatin is widely used for the treatment of a number of solid malignant tumors. However, ototoxicity induced by cisplatin is an obstacle to effective treatment of tumors. The basis for this toxicity has not been fully elucidated. It is generally accepted that hearing loss is due to excessive production of reactive oxygen species by cells of the cochlea. In addition, recent data suggest that inflammation may trigger inner ear cell death through endoplasmic reticulum stress, autophagy, and necroptosis, which induce apoptosis. Strategies have been extensively explored by which to prevent, alleviate, and treat cisplatin-induced ototoxicity, which minimize interference with antitumor activity. Of these strategies, none have been approved by the Federal Drug Administration, although several preclinical studies have been promising. This review highlights recent strategies that reduce cisplatin-induced ototoxicity. The focus of this review is to identify candidate agents as novel molecular targets, drug administration routes, delivery systems, and dosage schedules. Animal models of cisplatin ototoxicity are described that have been used to evaluate drug efficacy and side effect prevention. Finally, clinical reports of otoprotection in patients treated with cisplatin are highlighted. For the future, high-quality studies are required to provide reliable data regarding the safety and effectiveness of pharmacological interventions that reduce cisplatin-induced ototoxicity.