Current vehicles used to deliver antisense oligonucleotides (ASOs) cannot distinguish between bacterial and mammalian cells, greatly hindering the preclinical or clinical treatment of bacterial infections, especially those caused by antibiotic‐resistant bacteria. Herein, bacteria‐specific ATP‐binding cassette (ABC) sugar transporters are leveraged to selectively internalize ASOs by hitchhiking them on α (1–4)‐glucosidically linked glucose polymers. Compared with their cell‐penetrating peptide counterparts, which are non‐specifically engulfed by mammalian and bacterial cells, the presented therapeutics consisting of glucose polymer and antisense peptide nucleic‐acid‐modified nanoparticles are selectively internalized into the human‐derived multidrug‐resistant Escherichia coli and methicillin‐resistant Staphylococcus aureus, and they display a much higher uptake rate (i.e., 51.6%). The developed strategy allows specific and efficient killing of nearly 100% of the antibiotic‐resistant bacteria. Its significant curative efficacy against bacterial keratitis and endophthalmitis is also shown. This strategy will expand the focus of antisense technology to include bacterial cells other than mammalian cells.
Thioredoxin-interacting protein (TXNIP) was first isolated from Vitamin D3-exposed HL60 cells. TXNIP is the main redox-regulating factor in various organs and tissues. We begin with an overview of the TXNIP gene and protein information, followed by a summary of studies that have shown its expression in human kidneys. Then, we highlight our current understanding of the effect of TXNIP on diabetic kidney disease (DKD) to improve our understanding of the biological roles and signal transduction of TXNIP in DKD. Based on the recent review, the modulation of TXNIP may be considered as a new target in the management of DKD.
Introduction:PRKCG mutations have been implicated in the pathogenesis of spinocerebellar ataxia type 14 (SCA14), which is a rare autosomal dominant disease marked by cerebellar degeneration, dysarthria, and nystagmus. Until now, there has never been a report of patients with mutations of c.1232G>C worldwide.Case description: We report a case of a 30-year-old Chinese man with episodic dystaxia, speech disorder, and cognitive impairment; however, his father exclusively exhibited a speech disorder regardless of the same mutation. Whole-exome sequencing revealed a heterozygous c.1232G>C (p.G411A) variant of PRKCG.Conclusion: This case presents an extended genotype and phenotype of SCA14, and emphasizes the importance of gene sequencing in patients with spinocerebellar ataxia.
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