A Carbazole-based Fluorescent Turn-off Chemosensor for Iron (II/III) Detection in a Dimethyl Sulfoxide.

We designed a novel carbazole-based chemosensor from 2-(N-hexylcarbazol-3'-yl)-pyridine-5-carbaldehyde which was named probe 7b. The main purpose of this study is to investigate whether metal ions in liquid media can be detected with probe 7b. The details were presented in this paper. First, the molecular absorption and fluorescence properties of probe 7b were characterized by spectrophotometers. Then, several methods were applied to check its sensing properties. The results showed that probe 7b has a sense towards Fe3+ ion than other interfering metal ions. The selectivity and sensitivity of probe 7b towards Fe3+ were very satisfactory to use in applications. Also, it was observed that when aqueous Fe3+ ion solutions were added to probe 7b in dimethyl sulfoxide (DMSO), the fluorescence intensity of probe 7b decreased. This situation (turn-off of emission) is due to the paramagnetic effect between probe 7b and Fe3+ ions. The limit of detection (LOD) value was found as 1.38 nM for probe 7b. This value is very small to compete with its counterparts in the literature. A real sample experiment indicated that probe 7b can detect Fe3+ ions more than other ions in real media, too. As a result, it was deduced that probe 7b is a very strong candidate to use in sensor technology.

Automated Annotation of Epileptiform Burden and Its Association with Outcomes.

OBJECTIVE: This study was undertaken to determine the dose-response relation between epileptiform activity burden and outcomes in acutely ill patients. METHODS: A single center retrospective analysis was made of 1,967 neurologic, medical, and surgical patients who underwent >16 hours of continuous electroencephalography (EEG) between 2011 and 2017. We developed an artificial intelligence algorithm to annotate 11.02 terabytes of EEG and quantify epileptiform activity burden within 72 hours of recording. We evaluated burden (1) in the first 24 hours of recording, (2) in the 12-hours epoch with highest burden (peak burden), and (3) cumulatively through the first 72 hours of monitoring. Machine learning was applied to estimate the effect of epileptiform burden on outcome. Outcome measure was discharge modified Rankin Scale, dichotomized as good (0-4) versus poor (5-6). RESULTS: Peak epileptiform burden was independently associated with poor outcomes (p < 0.0001). Other independent associations included age, Acute Physiology and Chronic Health Evaluation II score, seizure on presentation, and diagnosis of hypoxic-ischemic encephalopathy. Model calibration error was calculated across 3 strata based on the time interval between last EEG measurement (up to 72 hours of monitoring) and discharge: (1) <5 days between last measurement and discharge, 0.0941 (95% confidence interval [CI] = 0.0706-0.1191); 5 to 10 days between last measurement and discharge, 0.0946 (95% CI = 0.0631-0.1290); >10 days between last measurement and discharge, 0.0998 (95% CI = 0.0698-0.1335). After adjusting for covariates, increase in peak epileptiform activity burden from 0 to 100% increased the probability of poor outcome by 35%. INTERPRETATION: Automated measurement of peak epileptiform activity burden affords a convenient, consistent, and quantifiable target for future multicenter randomized trials investigating whether suppressing epileptiform activity improves outcomes. ANN NEUROL 2021;90:300-311.

Burst Suppression: Causes and Effects on Mortality in Critical Illness.

BACKGROUND: Burst suppression in mechanically ventilated intensive care unit (ICU) patients is associated with increased mortality. However, the relative contributions of propofol use and critical illness itself to burst suppression; of burst suppression, propofol, and critical illness to mortality; and whether preventing burst suppression might reduce mortality, have not been quantified. METHODS: The dataset contains 471 adults from seven ICUs, after excluding anoxic encephalopathy due to cardiac arrest or intentional burst suppression for therapeutic reasons. We used multiple prediction and causal inference methods to estimate the effects connecting burst suppression, propofol, critical illness, and in-hospital mortality in an observational retrospective study. We also estimated the effects mediated by burst suppression. Sensitivity analysis was used to assess for unmeasured confounding. RESULTS: The expected outcomes in a "counterfactual" randomized controlled trial (cRCT) that assigned patients to mild versus severe illness are expected to show a difference in burst suppression burden of 39%, 95% CI [8-66]%, and in mortality of 35% [29-41]%. Assigning patients to maximal (100%) burst suppression burden is expected to increase mortality by 12% [7-17]% compared to 0% burden. Burst suppression mediates 10% [2-21]% of the effect of critical illness on mortality. A high cumulative propofol dose (1316 mg/kg) is expected to increase burst suppression burden by 6% [0.8-12]% compared to a low dose (284 mg/kg). Propofol exposure has no significant direct effect on mortality; its effect is entirely mediated through burst suppression. CONCLUSIONS: Our analysis clarifies how important factors contribute to mortality in ICU patients. Burst suppression appears to contribute to mortality but is primarily an effect of critical illness rather than iatrogenic use of propofol.

Burden of Epileptiform Activity Predicts Discharge Neurologic Outcomes in Severe Acute Ischemic Stroke.

BACKGROUND/OBJECTIVES: Clinical seizures following acute ischemic stroke (AIS) appear to contribute to worse neurologic outcomes. However, the effect of electrographic epileptiform abnormalities (EAs) more broadly is less clear. Here, we evaluate the impact of EAs, including electrographic seizures and periodic and rhythmic patterns, on outcomes in patients with AIS. METHODS: This is a retrospective study of all patients with AIS aged ≥ 18 years who underwent at least 18 h of continuous electroencephalogram (EEG) monitoring at a single center between 2012 and 2017. EAs were classified according to American Clinical Neurophysiology Society (ACNS) nomenclature and included seizures and periodic and rhythmic patterns. EA burden for each 24-h epoch was defined using the following cutoffs: EA presence, maximum daily burden < 10% versus > 10%, maximum daily burden < 50% versus > 50%, and maximum daily burden using categories from ACNS nomenclature ("rare" < 1%; "occasional" 1-9%; "frequent" 10-49%; "abundant" 50-89%; "continuous" > 90%). Maximum EA frequency for each epoch was dichotomized into ≥ 1.5 Hz versus < 1.5 Hz. Poor neurologic outcome was defined as a modified Rankin Scale score of 4-6 (vs. 0-3 as good outcome) at hospital discharge. RESULTS: One hundred and forty-three patients met study inclusion criteria. Sixty-seven patients (46.9%) had EAs. One hundred and twenty-four patients (86.7%) had poor outcome. On univariate analysis, the presence of EAs (OR 3.87 [1.27-11.71], p = 0.024) and maximum daily burden > 10% (OR 12.34 [2.34-210], p = 0.001) and > 50% (OR 8.26 [1.34-122], p = 0.035) were associated with worse outcomes. On multivariate analysis, after adjusting for clinical covariates (age, gender, NIHSS, APACHE II, stroke location, stroke treatment, hemorrhagic transformation, Charlson comorbidity index, history of epilepsy), EA presence (OR 5.78 [1.36-24.56], p = 0.017), maximum daily burden > 10% (OR 23.69 [2.43-230.7], p = 0.006), and maximum daily burden > 50% (OR 9.34 [1.01-86.72], p = 0.049) were associated with worse outcomes. After adjusting for covariates, we also found a dose-dependent association between increasing EA burden and increasing probability of poor outcomes (OR 1.89 [1.18-3.03] p = 0.009). We did not find an independent association between EA frequency and outcomes (OR: 4.43 [.98-20.03] p = 0.053). However, the combined effect of increasing EA burden and frequency ≥ 1.5 Hz (EA burden * frequency) was significantly associated with worse outcomes (OR 1.64 [1.03-2.63] p = 0.039). CONCLUSIONS: Electrographic seizures and periodic and rhythmic patterns in patients with AIS are associated with worse outcomes in a dose-dependent manner. Future studies are needed to assess whether treatment of this EEG activity can improve outcomes.

Fission-track data and U-Pb dating of granites from Cameron Highland, Peninsular Malaysia: Evidence to comprehend exhumation episodes.

Fission tracks are linear trails of intense radiation damage in the crystal structure of a mineral, produced by spontaneous fissioning of uranium-238 (238U) atoms. Detail information on the low-temperature thermal histories of rocks, below∼120 °C for tracks in apatite and below∼350 °C for zircon, can be provided by Fission-track (FT) analysis. The purpose of this article is to present apatite and zircon fission-track data, and U-Pb granite ages that provide information about the cooling histories of a rock which can be crucial in comprehending the exhumation episodes of the study area, in particular, and the region, in general. Granite samples were collected along the same vertical profile at different elevation, 178-944 m.a.s.l. These samples were used to determine Fission-Track and crystallization ages. HeFTy software was employed to interpret the cooling histories of the samples using forward and inverse models. The inverse model was an approach of reproducing the observed data, and it was carried out only for fission-track data from the apatite grains. And it was constructed after generating a number of forward models, where in each of these models the predicted apatite fission-track parameters were compared to the measured values. The apatite fission track (AFT) and zircon fission track (ZFT) data indicated expected age trends, i.e. the older ages at higher elevations and the younger ages at lower elevations. Similarly, the data shows that the apatite and zircon FT ages appear younger than the age of the rock crystallization. The U-Pb age in zircon consistently suggest the age of the granite is Late Triassic.