38, 7.96 and 6.67, respectively, indicating outstanding adsorption capacity and selectivity of 4-VP/SMIP. The pseudo-second-order model and Langmuir‒Freundlich model fit better than other models for the adsorption of phenol. 4-VP/SMIP is promising for selective removal and enrichment recovery towards phenol in wastewater. Bombyx mori is an important economic insect. However, the environmental pollution caused by the widespread use of neonicotinoid insecticides has significantly affected the safe production of sericulture. In this paper, we determined the LC50 of acetamiprid, a kind of neonicotinoid insecticides, to 5th instar silkworm larvae, examined its residues in hemolymph and midgut of silkworm after continuous exposure to low-dose of acetamiprid, and investigated the transcription level of detoxifying-related genes and the activity of detoxifying enzymes. The results showed that acetamiprid was highly toxic (24-h LC50, 1.50 mg/L) to silkworm larvae. After continuous exposure to low-dose of acetamiprid (0.15 mg/L), the acetamiprid residue concentrations in hemolymph and midgut were 0.90 and 0.58 μg/mg, respectively, at 48 h, but all decreased at 96 h. At 24 h of acetamiprid exposure, the transcription levels of CYP4M5 and CYP6AB4 and the P450 enzyme activity were significantly enhanced. However, the transcription levels of CarE and CarE-11 and the activity of CarE enzymes were both inhibited by acetamiprid exposure. After 24 h-72 h of acetamiprid exposure, the transcription levels of GSTe3 and GSTd1 were significantly up-regulated, and the GST enzyme activity was also significantly elevated from 48 h to 96 h. Furthermore, the expression levels of FoxO, CncC and Keap1, the key upstream genes of detoxification enzymes, showed a similar trend as the GST genes. These results indicated that acetamiprid was reduced in midgut and the expression of GSTs was upregulated may via FoxO/CncC/Keap1 signaling pathway, which plays a key role in detoxification responses. Microplastics are very complex pollutants; they can be made of many polymer types and exist in various shapes and sizes. When they enter the environment they are affected by biotic and abiotic factors that cause their properties to change. In this context, the aim of our study was to evaluate the extent to which biofouling affects the properties and toxicity of microplastics. Cosmetic polyethylene microbeads were incubated in stream water for four weeks resulting in biofouling and aging. Subsequently, the changes in properties (sinking, particle size, adsorption, and leaching of model metal – silver) and the microplastics toxicity to daphnids Daphnia magna and duckweed Lemna minor were evaluated. Pristine microplastics did not affect daphnids but they significantly affected the root growth of duckweed. On the other hand, reference natural particles (beech sawdust) did not show any negative effects. We observed significant differences in the properties of aged versus pristine microplastics. When compared to pristine microplastics, aged microplastics adsorbed more silver and the subsequent leaching of silver was more intensive, especially in the medium with an acidic pH. Microplastics with adsorbed silver had a high ecotoxicological potential and at environmentally relevant concentrations affected both daphnids and duckweed. This study suggests that biofouling is an important parameter that affects microplastics properties, pollutant adsorption and release into the environment, and toxicity. Overall, there are significant alterations of the microplastics properties, behaviour, and fate in the environment. BACKGROUND The prognostic impact of residual vegetation (RV) after medical treatment for endocarditis remains unknown. METHODS 134 consecutive patients hospitalized for infective endocarditis, not surgically treated, with presence of vegetation at diagnosis, were included retrospectively. learn more The follow-up started at the end of antibiotic treatment, when healing was complete. Presence or absence of RV was assessed at this time. The primary endpoint was a composite of the occurrence of embolic events, recurrence of endocarditis, or death from any cause. RESULTS Eighty-five patients were men (63%), mean age was 69 +/- 15 years, and median follow-up was 16.3 (IQR 5 to 30) months. Sixty-six patients (49%) had RV, 15 (11%) had RV > 10 mm and 9 (7%) had RV with an increase in size relative to that of the diagnosis. The primary endpoint occurred in 23 patients (35%) in the group with RV and in 16 patients (24%) without, which was not statistically relevant (HR 1.70; 95% confidence interval (CI) 0.89-3.22; p = 0.10). Based on univariate Cox regression analysis, the occurrence of the primary endpoint was associated with RV that increased (HR 3.90 95%CI 1.61-9.43; p  10 mm remained significant in multivariate Cox regression HR3.29; 95%CI 1.20-8.96; p = 0.02. CONCLUSIONS RV is frequent but has no clear prognostic impact in itself, however, its size, particularly in comparison with the start-of-treatment data, merits particular attention as potentially associated with an over-risk. BACKGROUND Evidence regarding biomarkers for risk prediction in patients with infective endocarditis (IE) is limited. We aimed to investigate the value of a panel of biomarkers for the prediction of in-hospital mortality in patients with IE. METHODS Between 2016 and 2018, consecutive IE patients admitted to the emergency department were prospectively included. Blood concentrations of nine biomarkers were measured at admission (D0) and on the seventh day (D7) of antibiotic therapy C-reactive protein (CRP), sensitive troponin I (s-cTnI), procalcitonin, B-type natriuretic peptide (BNP), neutrophil gelatinase-associated lipocalin (NGAL), interleukin 6 (IL6), tumor necrosis fator α (TNF-α), proadrenomedullin, alpha-1-acid glycoprotein, and galectin 3. The primary endpoint was in-hospital mortality. RESULTS Among 97 patients, 56% underwent cardiac surgery, and in-hospital mortality was 27%. At admission, six biomarkers were independent predictors of in-hospital mortality s-cTnI (OR 3.4; 95%CI 1.8-6.4; P  less then  0.001), BNP (OR 2.7; 95%CI 1.4-5.1; P = 0.002), IL-6 (OR 2.06; 95%CI 1.3-3.7; P = 0.019), procalcitonin (OR 1.9; 95%CI 1.1-3.2; P = 0.018), TNF-α (OR 1.8; 95%CI 1.1-2.9; P = 0.019), and CRP (OR 1.8; 95%CI 1.0-3.3; P = 0.037). At admission, S-cTnI provided the highest accuracy for predicting mortality (area under the ROC curve s-cTnI 0.812, BNP 0.727, IL-6 0.734, procalcitonin 0.684, TNF-α 0.675, CRP 0.670). After 7 days of antibiotic therapy, BNP and inflammatory biomarkers improved their performance (s-cTnI 0.814, BNP 0.823, IL-6 0.695, procalcitonin 0.802, TNF-α 0.554, CRP 0.759). CONCLUSION S-cTnI concentration measured at admission had the highest accuracy for mortality prediction in patients with IE. Management of Major Depressive Disorder (MDD) might be improved by a biomarker to predict whether a selected medication is likely to lead to remission. We previously reported on a quantitative electroencephalogram-based biomarker, the Antidepressant Treatment Response (ATR) index, that integrated recordings at baseline and after one week of treatment. The present study prospectively tested whether treatment directed by the biomarker increased the likelihood of remission; we hypothesized that continued treatment with a drug predicted to lead to remission (i.e., high ATR values) would be associated with better outcomes than if the drug was predicted not to lead to remission (i.e., low ATR values). We enrolled 180 adult outpatients with unipolar MDD from the community. After one week of escitalopram treatment to determine the biomarker, stratified randomization (high vs. low ATR) was used to assign subjects to either continued escitalopram or a switch to bupropion as a blinded control condition, for seven additional weeks. For the 73 evaluable subjects assigned to continued escitalopram treatment, the remission rate was significantly higher for those in whom ATR had predicted remission versus non-remission (60.4% vs. 30.0%, respectively, p = 0.01). Accuracy was enhanced by combining 1-week depressive symptom change with ATR (68.6% vs 28.9%). This prospective validation study supports further development of the ATR biomarker, alone or together with early symptom change, to improve care by identifying individuals unlikely to remit with their current treatment, and support the decision to change treatment after one week rather than after failing a full, prolonged course of medication. Treatment-resistant schizophrenia may be related to structural brain alterations. However, the mechanisms underlying these changes remain unclear. The present study had two main aims (1) to explore differences in cortical thickness between patients with treatment-resistant schizophrenia non-responsive to clozapine (ultra-treatment-resistant schizophrenia, UTRS), patients with treatment-resistant schizophrenia responsive to clozapine (Cloz-Resp), patients responsive to first-line non-clozapine antipsychotics (FL-Resp), and healthy controls (HCs); and (2) to test our hypothesis of structural compromise as a manifestation of neurotoxic effects from elevated glutamate (Glu) (i.e. glutamate-mediated excitotoxicity) by examining the relationships between glutamatergic neurometabolite levels (Glu and glutamate + glutamine (Glx)) in the dorsal anterior cingulate cortex (dACC) and cortical thickness. T1-weighted images and 1H-MRS data were obtained from UTRS (n = 24), Cloz-Resp (n = 25), FL-Resp (n = 19), and HCs (n = 26). Vertex-wise analyses showed that patients with UTRS had widespread cortical thinning in the bilateral frontal, temporal, parietal, and occipital gyri compared to HCs and FL-Resp patients. In the patient group, negative associations were found between dACC Glx levels and cortical thickness in the right dorsolateral prefrontal cortex after correcting for multiple comparisons and controlling for age, sex, antipsychotic dose, and illness severity. In conclusion, glutamate-mediated excitotoxicity may be one of the mechanisms underlying structural compromise seen in treatment-resistant schizophrenia. Future studies should longitudinally examine the associations between glutamatergic neurometabolite levels and cortical thickness in the context of treatment and illness progression. PURPOSE To investigate the experiences of adults living with chronic myeloid leukaemia and treated with tyrosine kinase inhibitors, with particular reference to factors influencing adherence. METHODS A thematic synthesis of all published qualitative studies examining adults with chronic myeloid leukaemia, receiving tyrosine kinase inhibitors. Eligible publications were identified by searching five electronic databases using defined criteria. The synthesis involved complete coding of extracted data and inductive theme development. RESULTS Nine studies were included and three overarching themes defined. Overarching themes were 1) Disease impacts whole life; 2) Disease management strategies; and 3) Valued aspects of care. Side-effects often required physical and psychological adaptation. Patients developed individual decision-making processes to promote adherence and manage side effects. Unintentional non-adherence occurred due to forgetfulness and system failures. Intentional omission also occurred, which together with side effects, was unlikely to be reported to healthcare professionals (HCPs).