The importance of in vitro diagnostics (IVDs) has significantly increased, driving the demand for rapid and sensitive diagnostic platforms. Molecular probes play a pivotal role in improving the sensitivity and accuracy of IVDs because of their target-specific signal transduction capabilities. Antibodies, which are commonly used as detection probes, face several challenges, including limited stability, high production costs, and low signal output.
View Article and Find Full Text PDFBackground: This study investigates the effect of botulinum toxin A on lipid layer thickness (LLT) and blink dynamics in patients with benign essential blepharospasm (BEB) compared to dry eye disease (DED) patients.
Methods: We reviewed the medical records of patients with dry eye disease (DED) and BEB treated with botulinum toxin A (BoT A) injections. Data on demographics, lipid layer thickness (LLT), meiboscore, and blink dynamics measured using a LipiView II interferometer before and 2 months after BoT A were collected.
Background: Merkel cell carcinoma (MCC) is a rare, aggressive cutaneous malignancy with neuroendocrine differentiation. Several molecular pathways have been implicated in MCC development and multiple cell-of-origin candidates have been proposed, including neural crest cells, which express acetylcholine receptors (AChRs). The role of nicotinic acetylcholine receptors (nAChRs) in MCC has not been explored.
View Article and Find Full Text PDFBioinspired coatings that mimic the adhesive properties of mussels have received considerable attention for surface modification applications. While polydopamine chemistry has been widely used to develop functional coatings, 3,4-dihydroxyphenyl-l-alanine (l-DOPA), a key component of mussel adhesive proteins, has received less attention because, compared to dopamine, it is relatively difficult to form effective coatings on solid substrates in mildly alkaline solutions. Although several methods have been explored to improve the efficiency of l-DOPA coatings, there is still a need to expand the l-DOPA-based surface chemistry.
View Article and Find Full Text PDFMembers of the KMT2C/D-KDM6A complex are recurrently mutated in urothelial carcinoma and in histologically normal urothelium. Here, using genetically engineered mouse models, we demonstrate that Kmt2c/d knockout in the urothelium led to impaired differentiation, augmented responses to growth and inflammatory stimuli and sensitization to oncogenic transformation by carcinogen and oncogenes. Mechanistically, KMT2D localized to active enhancers and CpG-poor promoters that preferentially regulate the urothelial lineage program and Kmt2c/d knockout led to diminished H3K4me1, H3K27ac and nascent RNA transcription at these sites, which leads to impaired differentiation.
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