Purpose Of The Review: Calcineurin inhibitors (CNIs) are central to immunosuppression in kidney transplantation (KT), improving short-term outcomes but falling short in enhancing long-term outcomes due to cardiovascular, metabolic, and renal complications. Belatacept, an FDA-approved costimulation blocker, offers a less toxic alternative to CNIs but is limited by its intravenous administration and reduced efficacy in high-immunological-risk patients.
Recent Findings: Emerging therapies target more specific pathways to improve efficacy and accessibility.
Introduction: Hypertrophic cardiomyopathy (HCM) is a common genetic heart disorder. It is characterized by left ventricular hypertrophy and impaired cardiac function, with forms categorized into obstructive (oHCM) and nonobstructive (nHCM). Traditional treatments address symptoms but not the underlying disease mechanism, highlighting the need for novel therapies.
View Article and Find Full Text PDFGlobal demand for food has driven expansion and intensification of livestock production, particularly in developing nations where antibiotic use is often routine. Waste from poultry production, including manure, is commonly utilized as fertilizers in agroecosystems, risking environmental contamination with potentially zoonotic bacteria and antimicrobial resistance genes (ARGs). Here, 33 bacterial isolates were recovered from broiler (n=17) and layer (n=16) chicken manure by aerobic culture using Luria Bertani agar.
View Article and Find Full Text PDFObjective/background: Comorbid insomnia with obstructive sleep apnea (COMISA) is associated with worse daytime function and more medical/psychiatric comorbidities vs either condition alone. COMISA may negatively impact sleep duration and reduce rapid eye movement (REM) sleep, thereby impairing cognition. These post-hoc analyses evaluated the effect of lemborexant (LEM), a dual-orexin-receptor antagonist approved for adults with insomnia, on sleep architecture in participants with COMISA.
View Article and Find Full Text PDFThe highly nuanced transition from an inflammatory process to tumorigenesis is of great scientific interest. While it is well known that environmental stimuli can cause inflammation, less is known about the oncogenic modifications that chronic inflammation in the tissue microenvironment can bring about, as well as how these modifications can set off pro-tumorigenic processes. It is clear that no matter where the environmental factors come from, maintaining an inflammatory microenvironment encourages carcinogenesis.
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