Which lab tests are best when you suspect hypothyroidism?

Thyroid-stimulating hormone (TSH) level is the preferred test for initial evaluation of suspected primary hypothyroidism (strength of recommendation [SOR]: C, expert opinion). If TSH is abnormal, a free thyroxine (T4) level will further narrow the diagnosis. Obtain a triiodothyronine (T3) level if TSH is undetectable and free T4 is normal. When assessing the adequacy of replacement therapy in primary hypothyroidism, the TSH is the most important parameter to monitor (SOR: C, expert opinion). Because TSH levels can't be used to monitor central hypothyroidism, use free T4 and T3 concentrations (SOR: C, case series)

ACRL Framework for Impactful Scholarship and Metrics

The ACRL Impactful Scholarship and Metrics Task Force was formed primarily to create a framework for the measurement and evaluation of academic librarian scholarship. The framework is designed to address gaps between current scholarly evaluation practices and impactful scholarly activities within academic librarianship, including ways to measure and evaluate the impact of a wide range of research outputs

An insertion loss model for evaluating the performance of floating-slab track for underground railway tunnels

Azithromycin is a potent macrolide antibiotic with poorly understood antiinflammatory properties. Long-term use of azithromycin in patients with chronic inflammatory lung diseases, such as cystic fibrosis (CF), results in improved outcomes. Paradoxically, a recent study reported that azithromycin use in patients with CF is associated with increased infection with nontuberculous mycobacteria (NTM). Here, we confirm that long-term azithromycin use by adults with CF is associated with the development of infection with NTM, particularly the multi-drug-resistant species Mycobacterium abscessus, and identify an underlying mechanism. We found that in primary human macrophages, concentrations of azithromycin achieved during therapeutic dosing blocked autophagosome clearance by preventing lysosomal acidification, thereby impairing autophagic and phagosomal degradation. As a consequence, azithromycin treatment inhibited intracellular killing of mycobacteria within macrophages and resulted in chronic infection with NTM in mice. Our findings emphasize the essential role for autophagy in the host response to infection with NTM, reveal why chronic use of azithromycin may predispose to mycobacterial disease, and highlight the dangers of inadvertent pharmacological blockade of autophagy in patients at risk of infection with drug-resistant pathogens

Role of AP1 and Gadkin in the traffic of secretory endo-lysosomes

We report that exocytosis of secretory lysosomes in nonspecialized cells does not depend on the mechanisms of late endocytic membrane transport but on Rab27A-like, lysosome-related organelles in specialized cells. We also find that this unconventional secretory process depends on clathrin, the Adaptor Protein complex 1 (AP1) adaptor, and the AP1-binding partner Gadkin