ABSTRACT
Eu3+ ,Dy3+ co-doped Sr2 LaZrO5.5 -based phosphors were prepared through a sol-gel method. Through characterization, it was found that the Sr2 LaZrO5.5 -based fluorescent powder co-doped with Eu3+ and Dy3+ had a cubic structure. At an excitation wavelength of 290 nm, the substrate Sr2 LaZrO5.5 exhibited strong blue emission at 468 nm, and the Sr2 LaZrO5.5 :18%Eu3+ phosphor exhibited a strong red emission peak at 612 nm. When the doping amount of Dy3+ was 5, 8, 12, 15, or 18%, the Sr2 LaZrO5.5 :18%Eu3+ phosphor changed from an orange-red light, to a warm white light, and to a cold white light. According to the emission spectra, the emission intensities of the substrates Sr2 LaZrO5.5 and Sr2 LaZrO5.5 :Eu3+ decreased with increasing Dy3+ concentration, confirming the energy transfer between the host Sr2 LaZrO5.5 -Eu3+ ,Dy3+ , and resulting in a lower CCT value, with significantly improved white light emission.
Subject(s)
Dysprosium , Luminescence , Dysprosium/chemistry , Light , Energy Transfer , Red LightABSTRACT
The cascade of Ir-catalyzed enantioselective allylic amination and Cu-catalyzed alkyne-azide cycloaddition was designed for the asymmetric synthesis of homoallylic amidines. The nucleophilic addition of an in situ-generated enantioenriched tertiary allylamine to a ketenimine intermediate triggers a rapid and stereospecific zwitterionic aza-Claisen rearrangement in a 1,3-chiral transfer manner. The approach allows modular access to enantioenriched α-chiral homoallylic amidines in high yields with a high level of enantiomeric purity.
Subject(s)
Allylamine , Amidines , Alkynes , Azides , Catalysis , Molecular StructureABSTRACT
IMPORTANCE: The increasing trend of delaying childbirth means that more women are being diagnosed with breast cancer before having given birth to their desired number of children. Although chemotherapy can significantly improve the prognosis of this population, it also causes ovarian damage, including premature ovarian insufficiency and infertility. Gonadotropin-releasing hormone agonists (GnRHa) have shown promising fertility protective activity in premenopausal women, but their clinical usage remains controversial. OBJECTIVE: Here, we conducted a meta-analysis to assess the efficacy of GnRHa when administered concurrently with chemotherapy that included cyclophosphamide in the prevention of chemotherapy-induced ovarian damage in premenopausal women. EVIDENCE REVIEW: An extensive literature search was performed using the PubMed, Embase, and Cochrane databases. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were determined. FINDINGS: Eleven randomized controlled trials with a total of 1,219 participants were included in the analyses. A significantly higher number of women treated with GnRHa experienced the resumption of ovarian function after chemotherapy than those who did not receive this treatment (OR, 3.04; 95% CI, 1.87-4.94; P < 0.001). Regarding spontaneous pregnancy, a statistically significant difference was observed only in hormone receptor-negative participants (OR, 2.06; 95% CI, 1.03-4.11; P = 0.04). CONCLUSIONS AND RELEVANCE: When treating premenopausal women with breast cancer, the administration of GnRHa concurrently with chemotherapy appeared to improve the resumption rate of ovarian function; however, the spontaneous pregnancy rate only improved in hormone receptor-negative patients. Thus, the use of GnRHa during chemotherapy may represent a feasible strategy for preserving ovarian function in women with breast cancer.
Subject(s)
Breast Neoplasms , Primary Ovarian Insufficiency , Breast Neoplasms/drug therapy , Child , Female , Gonadotropin-Releasing Hormone/adverse effects , Humans , Immunologic Factors , Pregnancy , Premenopause , Primary Ovarian Insufficiency/chemically induced , Primary Ovarian Insufficiency/drug therapy , Primary Ovarian Insufficiency/prevention & control , Randomized Controlled Trials as TopicABSTRACT
BACKGROUND: Triple-negative breast cancer (TNBC) is associated with higher aggressiveness and mortality than hormone-positive breast cancer because of the lack of approved therapeutic targets. Patients with TNBC who attain a pathological complete response (pCR) after neoadjuvant chemotherapy have improved survival. Platinum-based agents show promising activity in TNBC; however, their use remains controversial. We conducted a meta-analysis to assess the role of platinum-based agents in neoadjuvant chemotherapy in patients with TNBC. METHODS: We performed an extensive literature search of the Pubmed, Embase, and Cochrane databases. We calculated pooled odds ratios (OR) with 95% confidence intervals (CI) for the identified studies. RESULTS: Eight randomized controlled trials with 1345 patients were included in the analysis. The addition of platinum-based agents improved pCR compared with neoadjuvant therapy based on anthracyclines, cyclophosphamide, taxanes, and fluorouracil (49.1% vs. 35.9%; OR: 1.87, 95% CI: 1.23-2.86). Hematological adverse events were similar in both groups, except for more thrombocytopenia in the platinum-based group (OR: 7.96, 95% CI: 3.18-19.93). CONCLUSION: The addition of platinum-based agents to neoadjuvant chemotherapy improved pCR rates in patients with TNBC, with a slight increase in hematological toxicities. Platinum-based agents might thus be an accessible and economically viable option in patients with TNBC.
Subject(s)
Breast Neoplasms , Triple Negative Breast Neoplasms , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Breast Neoplasms/drug therapy , Humans , Neoadjuvant Therapy , Platinum/therapeutic use , Randomized Controlled Trials as Topic , Taxoids/therapeutic use , Treatment Outcome , Triple Negative Breast Neoplasms/drug therapyABSTRACT
Wood, which is mainly composed of lignified secondary cell wall, is the most abundant biomass in woody plants. Previous studies have revealed that R2R3-type MYB transcription factors are important regulators of the formation of the secondary cell wall in vascular plants. In this study, we isolated the R2R3-type MYB transcription factor gene PtoMYB055, which is mainly expressed in xylem and phloem tissue, from Populus tomentosa and demonstrate that PtoMYB055 is a key regulator of lignin biosynthesis. PtoMYB055 as a transcriptional activator is localized to the nucleus. Overexpression of PtoMYB055 upregulates expression of lignin biosynthetic genes in transgenic poplar plants, resulting in ectopic deposition of lignin in phloem tissue and an increase in thickness of the secondary cell wall. In sum, PtoMYB055 is a transcriptional activator that is involved in regulating lignin biosynthesis during the formation of the secondary cell wall in poplar.
Subject(s)
Biosynthetic Pathways/genetics , Lignin/biosynthesis , Lignin/genetics , Plant Proteins/biosynthesis , Plant Proteins/genetics , Populus/genetics , Cell Nucleus/genetics , Cell Wall/genetics , Gene Expression Profiling/methods , Gene Expression Regulation, Plant/genetics , Phloem/genetics , Plants, Genetically Modified/genetics , Transcription Factors/biosynthesis , Transcription Factors/genetics , Transcriptional Activation/genetics , Up-Regulation/genetics , Wood/genetics , Xylem/geneticsABSTRACT
Trichomes are specialized epidermal cells that contribute to plant resistance against herbivores. Their formation is controlled precisely by multiple genetic and environmental signals. Previous studies have shown that microRNA319 (miR319) and gibberellin (GA) signaling are involved in trichome development in Arabidopsis, but little is known about their interaction between these factors. Here we reported that the miR319a/TEOSINTE BRANCHED/CYCLOIDEA/PCF (TCP) module participates in trichome initiation synergistically with GA signaling in Populus tomentosa. We demonstrated that overexpression of miR319a decreased transcription levels of its targeted TCPs and significantly elevated leaf trichome density in transgenic poplar, resulting in decreasing insect herbivory. Conversely, repressing miR319a by short tandem target mimics (STTM) elevated TCP expression levels and decreased trichome density in transgenic plants. The trichome phenotype of 35S:miR319a plants could be abolished by introducing a miR319a-resistant form of TCP19. Furthermore, the miR319a-targeted TCP19 interacted directly with REPRESSOR OF ga1-3 (RGA), a downstream repressor of GA signaling. TCP19 and RGA synergistically inhibited the GLABROUS1 (GL1)-induced expression of trichome marker gene GLABRA2 (GL2), thereby repressing leaf trichome initiation. Our results provide an insight into the molecular mechanism by which miR319/TCP19 module and GA signaling coordinated regulating trichome initiation in P. tomentosa.
Subject(s)
Arabidopsis Proteins , Populus , Animals , Arabidopsis Proteins/genetics , Arabidopsis Proteins/metabolism , Gene Expression Regulation, Plant , Insecta/metabolism , Populus/genetics , Populus/metabolism , Trichomes/metabolism , Zea mays/metabolismABSTRACT
Anthocyanins are involved in several aspects of development and defence in poplar (Populus spp.). Although, over the past decades, significant progress has been made in uncovering these anthocyanin biosynthetic and regulatory mechanisms, the fundamental understanding of the epigenetic regulation in this pathway is still largely unclear. Here, we isolated a histone H3K9 demethylase gene JMJ25 from Populus and characterized its role in anthocyanin biosynthesis by genetic and biochemical approaches. JMJ25 was induced by continuous dark treatment. Overexpression of JMJ25 led to downregulated expression of anthocyanin biosynthetic genes in transgenic poplar, resulting in a significant reduction in anthocyanin content. ChIP-qPCR assays showed that JMJ25 could directly associate with MYB182 chromatin and dynamically demethylate at H3K9me2. Furthermore, JMJ25 also affected the DNA methylation levels of MYB182. By contrast, knockout of JMJ25 by CRISPR/Cas9 resulted in ectopic anthocyanin accumulation under dark condition and increased expression of anthocyanin biosynthetic genes. Our results support a model in which JMJ25 directly affects MYB182 expression by altering the histone methylation status of its chromatin and DNA methylation, resulting in repression of anthocyanin accumulation. This study uncovered an epigenetic mechanism that modulates anthocyanin biosynthesis in poplar.