Sentinel and networked symptoms in patients with breast cancer undergoing chemotherapy.

PURPOSE: It was designed to identify the symptom clusters and sentinel symptoms among patients with breast cancer receiving chemotherapy at the community level, and to explore core and bridge symptoms at the global level. METHODS: A cross-sectional survey was conducted using the MD Anderson Symptom Inventory. Patients with breast cancer receiving chemotherapy, recruited from the "Be Resilient to Breast Cancer" project between January 2023 and December 2023, were included in the study. Symptom clusters and their sentinel symptoms were identified using exploratory factor analysis and Apriori algorithm. Core and bridge symptoms were identified using network analysis. RESULTS: A total of 468 patients with breast cancer participated in the current study. At the community level, three symptom clusters and their corresponding sentinel symptoms were identified: a gastrointestinal symptom cluster (with nausea as the sentinel symptom), a psycho-sleep-related symptom cluster (with distress as the sentinel symptom), and a neurocognition symptom cluster (with dry mouth as the sentinel symptom). At the global level, fatigue emerged as the core symptom, while disturbed sleep and lack of appetite as bridge symptoms. CONCLUSION: Addressing nausea, distress, and dry mouth are imperative for alleviating specific symptom clusters at the community level. Furthermore, targeting fatigue, disturbed sleep, and lack of appetite are crucial to break the interactions among diverse symptoms at the global level.

Establishment of BV2 microglia polarization model and its effect on Toxoplasma gondii proliferation.

Toxoplasma gondii is an intracellular opportunistic, parasitic protozoan. Microglia have been classified into two main types: M1 (classically activated macrophages) and M2 (alternatively activated macrophages). BV2 cells were used in this study, together with lipopolysaccharide (LPS) and interferon (IFN)-γ or interleukin (IL)-4, which were used to induce resting microglia. Expression levels of M1/M2 markers were determined at both mRNA and protein levels, using PCR, western blot, and flow cytometry. Furthermore, cells were infected with T. gondii PLK strain, and the dynamic changes in M1/M2 marker expression levels were determined. An in vitro polarization model was successfully established. Expression of Nos2 and M1-associated markers was significantly upregulated at 12 h post-infection in BV2 cells. Further, the JAK/STAT1 and NF-κB signaling pathways were also activated following T. gondii infection. This demonstrated that T. gondii infection induces M1-type microglial polarization in vitro. The present study demonstrated that T. gondii infection affects microglial activation in vitro and elucidated the effects of activated microglia on T. gondii proliferation. This data may serve as a useful reference for more detailed elucidation of interactions between T. gondii and the innate immune system.