Chitosan is a positively charged natural polymer with several properties conducive to wound-healing applications, such as biodegradability, structural integrity, hydrophilicity, adhesiveness to tissue, and bacteriostatic potential. Along with other mechanical properties, some of the properties discussed in this review are antibacterial properties, mucoadhesive properties, biocompatibility, high fluid absorption capacity, and anti-inflammatory response. Chitosan forms stable complexes with oppositely charged polymers, arising from electrostatic interactions between (+) amino groups of chitosan and (-) groups of other polymers.
View Article and Find Full Text PDFTumor hypoxia drives metabolic shifts, cancer progression, and therapeutic resistance. Challenges in quantifying hypoxia have hindered the exploitation of this potential "Achilles' heel." While gene expression signatures have shown promise as surrogate measures of hypoxia, signature usage is heterogeneous and debated.
View Article and Find Full Text PDFMetalloenzymes are responsible for numerous physiological and pathological processes in living organisms; however, there are very few FDA-approved metalloenzyme-targeting therapeutics (only ~ 67 FDA-approved metalloenzyme inhibitors as of 2020, less than ~ 5 % of all FDA-approved therapeutics). Most metalloenzyme inhibitors have been developed to target the catalytic metal centers in metalloenzymes the incorporation of metal-binding groups. Light-controlled inhibition of metalloenzymes has been used as a means to specifically activate and inactivate inhibitor engagement at a desired location and time light irradiation, allowing for precise spatiotemporal control over metalloenzyme activity.
View Article and Find Full Text PDFRare monogenic disorders often exhibit significant phenotypic variability among individuals sharing identical genetic mutations. Bruck syndrome (BS), a prime example, is characterized by bone fragility and congenital contractures, although with a pronounced variability among family members. BS arises from recessive biallelic mutations in FKBP10 or PLOD2.
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