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Radiation therapy is a common treatment modality offered to patients with localized prostate cancer. It can be associated with early radiation-induced toxicities including dysuria, nocturia, frequency, urgency, spasm, and, rarely, hematuria. Early toxicities usually resolve once the treatment period has ended. Chronic toxicities are less common, and rarely, patients may experience radiation-induced hemorrhagic cystitis and hematuria months or years after radiation. We herein describe the case of a 65-year-old man with a past medical history of type-2 diabetes mellitus who experienced hemorrhagic cystitis for months following his radiation therapy. The patient was on sodium-glucose cotransporter-2 inhibitor therapy (empagliflozin), which we highlight as a potential risk factor for hemorrhagic cystitis. After cessation of Jardiance and initiation of semaglutide (GLP-1 agonist), his urinary symptoms significantly improved. To the best of our knowledge, this is the first such case reported., Competing Interests: Disclosures None., (Copyright © 2024 American Society for Radiation Oncology. Published by Elsevier Inc. All rights reserved.)

Whole red raspberry polyphenols (RRW), including ellagic acid, and their gut-derived metabolite, urolithin A (UroA), attenuate inflammation and confer health benefits. Although results from recent studies indicate that polyphenols and UroA also provide neuroprotective effects, these compounds differ in their bioavailability and may, therefore, have unique effects on limiting neuroinflammation. Accordingly, we aimed to compare the neuroprotective effects of RRW and UroA on BV-2 microglia under both 3 h and 12 and 24 h inflammatory conditions. In inflammation induced by lipopolysaccharide (LPS) and ATP stimulation after 3 h, RRW and UroA suppressed pro-inflammatory cytokine gene expression and regulated the JNK/c-Jun signaling pathway. UroA also reduced inducible nitric oxide synthase gene expression and promoted M2 microglial polarization. During inflammatory conditions induced by either 12 or 24 h stimulation with LPS, UroA-but not RRW-dampened pro-inflammatory cytokine gene expression and suppressed JNK/c-Jun signaling. Taken together, these results demonstrate that RRW and its gut-derived metabolite UroA differentially regulate neuroprotective responses in microglia during 3 h versus 12 and 24 h inflammatory conditions.

Objective: To investigate the value of peripheral blood for the prognosis of patients with bloodstream infection., Methods: A retrospective analysis of patients with bloodstream infection was conducted in the intensive care unit (ICU) of Mianyang Central Hospital of Sichuan from January 2012 to October 2016. According to the 28-day survival, the patients were divided into survival group and death group. The white blood cell (WBC), neutrophils count (NEU), lymphocyte count (LYM), neutrophil/lymphocyte ratio (NLR), monocyte count (MO), eosinophil count (EO), basophil count (BA), hemoglobin (Hb), platelet count (PLT) and procalcitonin (PCT) in peripheral blood were recorded when patients were diagnosed with blood infection. Receiver operating characteristic curve (ROC), Kaplan-Meier survival analysis and Cox regression were used to evaluate the value of these risk factors for predicting the outcome., Results: 305 patients were enrolled. 182 patients survived while 123 patients died during the 28-day period. (1) There was no significant difference in gender, age and comorbidities between the two groups. There was no significant difference in infection rate between the two groups except for fungal infection rate. The fungal infection rate in the death group was significantly higher than that in the survival group (9.8% vs. 3.3%, P = 0.019). (2) The LYM, MO, EO and PLT in the death group were significantly lower than those in the survival group [LYM (×10 9 /L): 0.58 (0.29, 0.93) vs. 0.76 (0.44, 1.23), MO (×10 9 /L): 0.47 (0.19, 0.80) vs. 0.58 (0.30, 0.94), EO (×10 9 /L): 0.00 (0.00, 0.01) vs. 0.03 (0.01, 0.09), PLT (×10 12 /L): 89 (47, 148) vs. 126 (82, 186), all P < 0.05]. The NLR in the death group was significantly higher than that in the survival group [17.09 (7.60, 33.51) vs. 12.86 (6.51, 24.85), P < 0.05]. There was no significant difference in the WBC, NEU, BA, Hb and PCT between the two groups. (3) It was shown by ROC curve analysis that the maximum area under the ROC curve (AUC) of EO was 0.755. When the best cut-off value was 0.015×10 9 /L as a predictor of death in 28 days, the sensitivity was 80.3%, and specificity was 64.7%. (4) It was shown by survival analysis that the 28-day survival rate in the patients with EO < 0.015×10 9 /L was significantly lower than that of patients with EO > 0.015×10 9 /L [38.3% (62/162) vs. 83.9% (120/143), χ 2 = 56.999, P = 0.000]. (5) It was shown by Cox regression that EO was the independent factor for 28-day survival (β = 1.466, χ 2 = 39.535, P = 0.000). Risk of death was 4.331 times greater in patients with EO < 0.015×10 9 /L than in those with EO > 0.015×10 9 /L [hazard ratio (HR) = 4.331, 95% confidence interval (95%CI) = 2.743-6.840]., Conclusions: Compared to other parameters in peripheral blood, EO has the best correlation with the prognosis of bloodstream infection. EO is the independent prognostic predictor for 28-day survival.