Purpose: To test the impact of professional management of soft contact lens wear on symptoms and ocular complications.
Methods: Subjective symptoms and ocular complications of soft CL users who did not seek professional follow-up care (self-managed, SM), were compared to users who were prescribed CLs and their care professionally managed in optometry practices (PM), and to a control group of non-CL wearers. Habitual visual acuity, subjective dry-eye symptoms, and corneal abnormalities were assessed in all participants.
Purpose: Large cell neuroendocrine carcinoma (LCNEC) is a high-grade neuroendocrine malignancy that, like small cell lung cancer (SCLC), is associated with the absence of druggable oncogenic drivers and dismal prognosis. In contrast to SCLC, however, there is little evidence to guide optimal treatment strategies, which are often adapted from SCLC and non-small cell lung cancer approaches.
Experimental Design: To better define the biology of LCNEC, we analyzed cell line and patient genomic data and performed IHC and single-cell RNA sequencing of core needle biopsies from patients with LCNEC and preclinical models.
Background/importance: Chronic pain affects many people globally, requiring alternative management strategies. Psilocybin is gaining attention for its potential in chronic pain management despite being classified as Schedule I.
Objective: This systematic review critically evaluates the evidence for psilocybin, a Schedule I substance, in the treatment of chronic pain.
Squamous cell carcinomas (SCCs), including lung, head & neck, bladder, and skin SCCs often display constitutive activation of the KEAP1-NRF2 pathway. Constitutive activation is achieved through multiple mechanisms, including activating mutations in NFE2L2 (NRF2). To determine the functional consequences of Nrf2 activation on skin SCC development, we assessed the effects of mutant Nrf2 expression, one of the most common activating mutations in human SCCs, on tumor promotion and progression in the mouse skin multistage carcinogenesis model using a DMBA-initiation/TPA-promotion protocol where the Hras A->T mutation (Q61L) is the canonical driver mutation.
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