Prognostic Factors of Quantitative Lymphoscintigraphic Findings in Patients with Breast Cancer-Related Lymphedema.

Background: To evaluate the usefulness of quantitative findings of pretherapy lymphoscintigraphy in predicting the effects of complex decongestive therapy (CDT) in patients with upper extremity lymphedema after breast cancer treatment. Methods and Results: We retrospectively analyzed patients with unilateral breast cancer-related lymphedema (BCRL) who underwent pretherapy lymphoscintigraphy and completed 2 weeks of CDT. A total of 18 patients with unilateral BCRL clinical stage II underwent 30-minute sessions of CDT five times per week for 2 weeks. The quantitative asymmetry index (QAI) of the upper extremity, axillary lymph node (LN) uptake, and axillary plus supraclavicular LN uptake from lymphoscintigraphy were calculated. The volume of lymphedema was calculated by percentage excess volume (PEV) at initial and posttreatment. The CDT response was assessed using percentage reduction in excess volume (PREV). Correlation analyses were conducted using Kendall tau rank correlation. There was positive correlation between upper extremity QAI at 2 hours and initial PEV. Negative correlations were found between axillary LN QAI at 1, 2 hours, and initial PEV, and between axillary plus supraclavicular LN QAI at 1, 2 hours, and initial PEV. The PREV showed a positive correlation with axillary LN QAI at 2 hours after injection (tau-b = 0.354, p = 0.041). Conclusion: Quantitative findings of pretherapy lymphoscintigraphy have potential value for use in predicting the response to CDT in patients with upper extremity lymphedema after breast cancer treatment. Using QAIs from lymphoscintigraphy, we could estimate the excess volume of lymphedema.

Brain-derived neurotrophic factor mediates macrophage migration inhibitory factor to protect neurons against oxygen-glucose deprivation.

Macrophage migration inhibitory factor (MIF) is a chemokine that plays an essential role in immune system function. Previous studies suggested that MIF protects neurons in ischemic conditions. However, few studies are reported on the role of MIF in neurological recovery after ischemic stroke. The purpose of this study is to identify the molecular mechanism of neuroprotection mediated by MIF. Human neuroblastoma cells were incubated in Dulbecco's modified Eagle's medium under oxygen-glucose deprivation (OGD) for 4 hours and then returned to normal aerobic environment for reperfusion (OGD/R). 30 ng/mL MIF recombinant (30 ng/mL) or ISO-1 (MIF antagonist; 50 µM) was administered to human neuroblastoma cells. Then cell cultures were assigned to one of four groups: control, OGD/R, OGD/R with MIF, OGD/R with ISO-1. Cell viability was analyzed using WST-1 assay. Expression levels of brain-derived neurotrophic factor (BDNF), microtubule-associated protein 2 (MAP2), Caspase-3, Bcl2, and Bax were detected by western blot assay and immunocytochemistry in each group to measure apoptotic activity. WST-1 assay results revealed that compared to the OGD/R group, cell survival rate was significantly higher in the OGD/R with MIF group and lower in the OGD/R with ISO-1 group. Western blot assay and immunocytochemistry results revealed that expression levels of BDNF, Bcl2, and MAP2 were significantly higher, and expression levels of Caspase-3 and Bax were significantly lower in the MIF group than in the OGD/R group. Expression levels of BDNF, Bcl2, and MAP2 were significantly lower, and expression levels of Caspase-3 and Bax were significantly higher in the ISO-1 group than in the OGD/R group. MIF administration promoted neuronal cell survival and induced high expression levels of BDNF, MAP2, and Bcl2 (anti-apoptosis) and low expression levels of Caspase-3 and Bax (pro-apoptosis) in an OGD/R model. These results suggest that MIF administration is effective for inducing expression of BDNF and leads to neuroprotection of neuronal cells against hypoxic injury.