Dihydropyrimidine Dehydrogenase Deficiency (DPYD) Genotyping-Guided Fluoropyrimidine-Based Adjuvant Chemotherapy for Breast Cancer. A Cost-Effectiveness Analysis.

Background And Objective: While standard doses of adjuvant fluoropyrimidine-based chemotherapies are generally safe for most patients, the risk of severe adverse drug reactions (ADRs) is increased for those with dihydropyrimidine dehydrogenase deficiency (DPYD), a genetic variation that affects drug metabolism. The objective of this study was to examine the cost effectiveness of offering DPYD pharmacogenetic-guided care, where genetic testing informs personalized dosing versus the current standard of care (SoC), which involves administering fluoropyrimidine-based therapies without prior genetic screening, for local or metastatic breast cancer patients in Qatar.

Methods: We developed a two-stage decision analysis, with an analytic tree model over a 6-month period, followed by a life-table Markov model over a lifetime horizon.

Mechanisms in thyroid eye disease - the TSH receptor interacts directly with the IGF-1 receptor.

The pathogenesis of Thyroid Eye Disease (TED) has been suggested as due to signal enhancement in orbital fibroblasts as a result of autoantibody-induced, synergistic, interaction between the TSH receptor (TSHR) and the IGF-1 receptor (IGF-1R). This interaction has been explained by a "receptor cross talk", mediated via β-arrestin binding. Here, we have examined if this interaction can be mediated via direct receptor contact using modeling and experimental approaches.

Type of arrhythmias and the risk of sudden cardiac death in dialysis patients: a systematic review and meta-analysis.

Background: Patients on long-term dialysis for end-stage kidney disease have a high mortality rate, predominantly due to sudden cardiac death (SCD), which is associated with an increased risk of arrhythmias compared to the general population. Thus, the current systematic review and meta-analysis aimed to investigate the incidence of SCD among dialysis patients at risk of arrhythmia.

Methods: This systematic review and meta-analysis followed the PRISMA guidelines.

Calcitriol ameliorates cisplatin-induced hepatorenal toxicity via regulation of Nrf2-Mrp2/p38 MAPK signaling in mice.

Despite being one of the most frequently used chemotherapy agents, cisplatin exhibits substantial hepatorenal injury by triggering oxidative stress, inflammation, and apoptosis pathways. The current investigation studied the possible protective effects of calcitriol on cisplatin-induced hepatorenal toxicity. Mice were divided randomly as follows: control group, calcitriol group (received calcitriol 5 µg/kg, p.