Correction: Immobilized Ni on TMEDA@ßSiO2@αSiO2@Fe3O4: as a novel magnetic nanocatalyst for preparation of pyrido[2,3-d:6,5-d']dipyrimidines.

[This corrects the article DOI: 10.1039/D3RA01720F.].

Immobilized Ni on TMEDA@ßSiO2@αSiO2@Fe3O4: as a novel magnetic nanocatalyst for preparation of pyrido[2,3-d:6,5-d']dipyrimidines.

In the current body of research, a very quick and effectual procedure for the synthesis of pyrido[2,3-d:6,5-d']dipyrimidines has been developed. This method is accomplished through the one-pot multi-component reaction of 2-thiobarbituric acid, NH4OAc and aldehydes utilizing Ni-TMEDA@ßSiO2@αSiO2@Fe3O4 as a novel mesoporous nanomagnetic catalyst at room temperature. This protocol is one of the few reports of the preparation of these derivatives without the use of conventional heating as well as energies such as microwave and ultrasound radiation. The characterization of the prepared catalyst was well accomplished by different techniques such as FT-IR, ICP-OES, SEM, TEM, BET, XRD, VSM, TGA, EDX and Elemental mapping. This organometallic catalyst was reusable for seven times with negligible decrement in its catalytic performance. In addition, all of the products were produced with high TON and TOF values, which demonstrates that our catalyst has a very high level of activity in the preparation of pyrido[2,3-d:6,5-d']dipyrimidines.

Malignant function of nuclear factor-kappaB axis in prostate cancer: Molecular interactions and regulation by non-coding RNAs.

Prostate carcinoma is a malignant situation that arises from genomic alterations in the prostate, leading to changes in tumorigenesis. The NF-κB pathway modulates various biological mechanisms, including inflammation and immune responses. Dysregulation of NF-κB promotes carcinogenesis, including increased proliferation, invasion, and therapy resistance. As an incurable disease globally, prostate cancer is a significant health concern, and research into genetic mutations and NF-κB function has the efficacy to facilitate the introduction of novel therapies. NF-κB upregulation is observed during prostate cancer progression, resulting in increased cell cycle progression and proliferation rates. Additionally, NF-κB endorses resistance to cell death and enhances the capacity for metastasis, particularly bone metastasis. Overexpression of NF-κB triggers chemoresistance and radio-resistance, and inhibition of NF-κB by anti-tumor compounds can reduce cancer progression. Interestingly, non-coding RNA transcripts can regulate NF-κB level and its nuclear transfer, offering a potential avenue for modulating prostate cancer progression.