Exploring the Synergistic Mechanisms of Nanopulsed Plasma Bubbles and Photocatalysts for Trimethoprim Degradation and Mineralization in Water.

In this study, the synergetic action of nanopulsed plasma bubbles (PBs) and photocatalysts for the degradation/mineralization of trimethoprim (TMP) in water was investigated. The effects of ZnO or TiO2 loading, plasma gas, and initial TMP concentration were evaluated. The physicochemical characterization of plasma-treated water, the quantification of plasma species, and the use of appropriate plasma species scavengers shed light on the plasma-catalytic mechanism. ZnO proved to be a superior catalyst compared to TiO2 when combined with plasma bubbles, mainly due to the increased production of ⋅OH and oxygen species resulting from the decomposition of O3. The air-PBs + ZnO system resulted in higher TMP degradation (i.e., 95% after 5 min of treatment) compared to the air-PBs + TiO2 system (i.e., 87%) and the PBs-alone process (83%). The plasma gas strongly influenced the process, with O2 resulting in the best performance and Ar being insufficient to drive the process. The synergy between air-PBs and ZnO was more profound (SF = 1.7), while ZnO also promoted the already high O2-plasma bubbles' performance, resulting in a high TOC removal rate (i.e., 71%). The electrical energy per order in the PBs + ZnO system was very low, ranging from 0.23 to 0.46 kWh/m3, depending on the plasma gas and initial TMP concentration. The study provides valuable insights into the rapid and cost-effective degradation of emerging contaminants like TMP and the plasma-catalytic mechanism of antibiotics.

Estimated glomerular filtration rate independently predicts outcome of azacitidine therapy in higher-risk Myelodysplastic syndromes. Results from 536 patients of the Hellenic National Registry of Myelodysplastic and Hypoplastic syndromes.

Higher-risk Myelodysplastic syndromes (MDS) patients undergoing treatment with 5-azacytidine (AZA) are typically elderly with several comorbidities. However, the effect of comorbidities on the effectiveness and safety of AZA in real-world settings remains unclear. We analyzed data from 536 AZA-treated patients with higher-risk MDS, Myelodysplastic/Myeloproliferative neoplasms and low blast count Acute Myeloid Leukemia enrolled to the Hellenic National Registry of Myelodysplastic and Hypoplastic Syndromes. Multivariate analysis adjusted also for the International Prognostic Scoring System (IPSS), its revised version (IPSS-R) and the French Prognostic Scoring System (FPSS), demonstrated independent associations of overall and leukemia-free survival with estimated glomerular filtration rate (eGFR) <45 mL min-1 /1.73 m2 (P = .039, P = .023, respectively), ECOG performance status <2 (P = .015, P = .006), and presence of peripheral blood blasts (P = .008, P = .034), while secondary MDS also correlated with significantly shorter leukemia-free survival (P = .039). Addition of eGFR <45 mL min-1 /1.73 m2 , in IPSS-R and FPSS increased the predictive power of both models. Only FPSS ≤2 and eGFR <45 mL min-1 /1.73 m2 predicted worse response to AZA in multivariate analysis, whereas eGFR <45 mL min-1 /1.73 m2 correlated significantly with death from hemorrhage (P = .003) and cardiovascular complications (P = .006). In conclusion, in the second largest real-world series of AZA-treated MDS patients, we show that an eGFR <45 mL min-1 /1.73 m2 is an independent predictor of worse response and survival. This higher cut-off, instead of the commonly used serum creatinine >2 mg/dL, can be utilized as a more precise indicator of renal comorbidity during AZA therapy. Incorporation of eGFR in the prognostic assessment of AZA-treated MDS patients may prove useful not only in routine practice, but also for the appropriate patient stratification in clinical trials with AZA combinations.

Causes of double-negative T-cell lymphocytosis in children and adults.

AIMS: The causes and diagnosis of 'double-negative' (CD3+CD4-CD8-) T-cell lymphocytosis are not well studied. We aimed to define the causes of double-negative T-cell lymphocytosis in children and adults, and to identify simple clinical and laboratory features that would help to differentiate between the underlying conditions. METHODS: We collected clinical and laboratory data on 10 children and 30 adults with significantly increased peripheral-blood double-negative T-cells (>10% of total lymphocytes). We identified conditions associated with double-negative T-lymphocytosis with flow cytometry, peripheral-blood morphology and T-cell receptor-gene rearrangement studies. Patients were assigned to diagnostic categories on the basis of these test results. RESULTS AND CONCLUSIONS: The causes of double-negative T-cell lymphocytosis in children were autoimmune lymphoproliferative syndrome (ALPS) and reactive γ/δ Τ-lymphocytosis. T-cell large granular lymphocyte (T-LGL) leukaemia, reactive γ/δ T-lymphocytosis and hepatosplenic T-cell lymphoma (HSTL) were the the most common disorders underlying double-negative T-cell lymphocytosis in adults. Less common causes included hypereosinophilic syndrome, peripheral T-cell lymphoma, ALPS and monoclonal, double-negative T-lymphocytosis of uncertain significance. CD5/CD7/Vδ2 expression and absolute double-negative lymphocyte count (<1.8×109/L) were useful discriminators for distinguishing patients with reactive γ/δ T-lymphocytosis from those with γ/δ lymphoproliferative disorders. Differentiating between γ/δ T-LGL and HSTL can be difficult. Expression of CD57 and cellular morphology (pale cytoplasm with distinct granules) would support a diagnosis of γ/δ T-LGL.